The healthcare company filled the booth with its products and set up a section for its over-the-counter continuous glucose monitor (CGM). Staff gave out little treats and packets of electrolyte powder.

I had just left their CES panel, “Tracking Your Body’s Signals for Better Health,” at the Venetian Expo. Tunde Oyeneyin talked about using glucose data for cardio and preparation. I know her from Peloton and like her as a personality. Alexis Ohanian, Reddit’s co-founder, brought in a tech and fatherhood perspective, which I find interesting. He also appeared in the product’s “Spike Sessions” campaign, which is worth mentioning when considering his role on the company’s stage [1][2].

After 3 years of doubt, I wondered whether I should try one and later speak from experience.

The booth was big. My estimate is six figures, probably more. I spoke with someone I remember as a brand manager or salesperson. They kept explaining how eating order affects glucose, and how levels rise after eating carbs. I kept asking what a healthy person should do after a normal increase.

I never got an answer I could use. I left with a few samples, but not a glucose monitor. I still haven’t tried one.

My doctor’s take begins with me

That’s a fair point. I’m judging a device I haven’t tried myself.

I’m a physician with medical and dental degrees, but I don’t specialize in endocrinology or diabetes. I look at health devices like any other treatment: identify the problem, decide what action to take based on the result, and see if that action improves health.

I use the same approach for myself. Twice a year, I check my fasting glucose and HbA1c, which shows long-term glucose levels. My results are 92 mg/dL (about 5.1 mmol/L) and 4.9%.

I also take valsartan with hydrochlorothiazide for high blood pressure, which is well controlled. I take my medication and check my blood pressure regularly because there’s a clear target, and lowering it reduces health risks.

Hydrochlorothiazide belongs to a family of blood-pressure drugs called thiazides. Across 95 randomized trials in which treatment was assigned by chance, these drugs raised fasting glucose by 3.6 mg/dL on average, or 2.7 mg/dL in trials lasting at least 6 months. The authors called the class effect too small to change care [3]. It cannot predict my result without the drug.

Blood-pressure treatment also counts as 1 of the 5 markers used to define metabolic syndrome, a cluster of linked health risks. The diagnosis requires 3 markers. My treated hypertension is a managed cardiovascular risk factor; by itself, it does not meet that definition [4].

Where the evidence holds

For the right patient with diabetes, continuous glucose monitoring earns its place.

A review published in JAMA Internal Medicine on 3 August 2026 summarized randomized evidence in type 2 diabetes. Average HbA1c fell by about 0.3 percentage points compared with finger-prick checks or usual care, and some patients gained more. Much of that evidence came from people taking insulin or other glucose-lowering drugs [5].

This was a narrative review, meaning the authors chose and explained existing research without the strict process of a systematic review. Published at the journal’s initiative, it found only limited and indirect support for CGM in people with type 2 diabetes not taking glucose-lowering treatment, or with prediabetes or obesity. No CGM-manufacturer conflict was disclosed.

Prediabetes is a different case, since the evidence is more promising there. Here, I’m focusing on healthy adults without symptoms.

Minna Johansson set the boundary in a university press statement: “This technology is tremendously valuable for certain groups of patients. But it is increasingly being used by groups where we simply do not know whether it provides any benefit at all—or if it could even be harmful” [6]. The review didn’t measure a harm rate. The authors suggested using CGM only when a specific patient problem gives the readings a purpose. This is not a clinical guideline.

The FDA cleared Lingo for over-the-counter sale to adults aged 18 or older who do not use insulin. This includes some people with diabetes. Its screen covers 55 to 200 mg/dL, and the agency says users should consult a qualified health professional before taking medical action based on the output [7].

Even precise numbers can be misleading

Hutchins and colleagues ran a randomized crossover study in 15 healthy adults. Each person completed the same set of meal tests, with the order chosen by chance, so the researchers could compare each person with themselves.

The continuous monitor read 0.9 mmol/L, about 16 mg/dL, higher than a finger-prick test both before and after meals. For one smoothie, the monitor gave a glycemic index of 69 and the finger-prick method gave 53. Glycemic index is a score for how strongly a food raises glucose [8].

Those estimates had wide confidence intervals. A confidence interval is the range that still fits the data. The monitor’s range was 48 to 99, while the finger-prick range was 40 to 69. These ranges overlap a lot.

The p-value was .05. A p-value asks how often a difference this big could happen by chance if both methods worked the same. Here, it was about 5 times in 100, which is the usual cutoff researchers use. This example comes from one smoothie and 15 people, not a general error rate.

After adjusting for each person’s starting point, the monitor still showed about twice as much time above 140 mg/dL compared to the finger-prick method. The p-value was below .01, meaning a gap this large would happen less than once in 100 times if there was no real difference. They measured time above 140, not the actual glucose concentration.

Innocent Drinks funded the study with an unrestricted grant and provided the test products. “Unrestricted” means the company didn’t control how the study was run. The authors also disclosed connections to ZOE, PepsiCo, and the European Fruit Juice Association.

Then 18 CGM experts looked at 20 reports from adults without diabetes and decided whether each person needed medical follow-up. The researchers had deliberately chosen difficult reports. Dexcom supplied discounted sensors, and several authors had ties to the manufacturer [9].

Fleiss kappa measures how much a group agrees beyond what chance alone would produce. A score of 0 means chance-level agreement; 1 means perfect agreement. These experts scored 0.36, which the authors called low. All 18 gave the same answer on only 3 of the 20 reports. They all wanted follow-up for 2 and all declined it for 1. This measured agreement in a small selected set. It did not test whether their decisions were medically correct.

One rough pattern appeared. When more than 2 out of every 100 readings were above 180 mg/dL, between 56% and 100% of the experts recommended follow-up, depending on the report. Simply put, the same cutoff convinced just over half of them in some cases and all of them in others. The study didn’t prove that 2% was the right alarm line. I think this number comes from diabetes care. The authors said there are no guidelines for interpreting these reports in people without diabetes. Diabetes care has its own guidelines.

My doctor’s take after the evidence

This fits into the Activate part of the Upward ARC, which focuses on food and movement. It also relates to Capacity, since our attention is limited. Every new number asks you to look, interpret, and decide what to do.

Before buying a monitor, a healthy person should think about what reading would make them change their behavior.

Try this today

• Write down the exact number that would make you change your actions. Add what you would do next and what result you expect. If you can’t fill the page, that tells you something.

• If you have diabetes, prediabetes, symptoms, pregnancy, medication concerns, or another metabolic risk, take the question to a clinician. This newsletter doesn’t cover you.

• Try the habit without tracking it on a graph. Eat protein before carbs if you like. Take a 10- or 20-minute walk after eating. See if you can keep it up.

• Consider what the experiment costs, both in money and attention. Lingo launched at $89 for two 14-day sensors in the US. On 21 August 2026, its US 4-week subscription showed an $89 standard price, and Boots in the UK listed two sensors for £118 [10][11]. Decide before you start when you’ll stop.

The unused patches

About a year ago, I noticed an opened FreeStyle Libre package next to a monitor at the office. A blister pack of patches was still sealed. Since the desks were shared, I didn’t know whose it was. Later that day, a colleague told me they saw an influencer wearing one and bought it with a discount code. They showed me the sensor on their arm.

They learned that eating protein before carbohydrates seemed to flatten the curve. A 10- or 20-minute walk after eating had a similar effect. Fruit or something sweet made glucose rise and then fall.

I could have told them all of that without a sensor.

A few weeks later, I asked if they were still using it. They had stopped. I inferred that it had been an expensive way to learn basic lessons. They never said why they quit.

Normal is broader than it seems

The Framingham study followed 560 normoglycemic adults. That simply means their standard blood tests placed them in the normal glucose range [12].

Even so, their readings sat between 140 and 180 for almost 3 hours a day, then above 180 for another 19 minutes. Total time above 140 averaged roughly 3.3 hours. This was a group average, so it doesn’t predict one person’s day. Participants averaged 58.8 years old and had an average body mass index of 26.5, which indicates overweight. The group was 93.2% non-Hispanic White, and Dexcom supplied discounted sensors.

A second study followed 153 healthy, non-obese people aged 7 to 80 [13]. The sample averaged 31 years old. Average glucose was 98 to 99 mg/dL below age 60 and 104 at 60 or older. The median person (the middle value after ranking) spent 96% of the day between 70 and 140. The interquartile range was 93% to 98%, meaning the middle half of participants fell between those values. The sample was 93% White, and an author disclosed ties to Dexcom and Sanofi.

I think the difference comes down to age and who was in each study. The younger group didn’t include people with obesity, while the Framingham study looked at an older community group. Neither paper tested this, so this is just my opinion. Both studies show that healthy glucose levels can vary. Seeing a colored line can make normal changes look like a problem.

Curiosity still needs a purpose

In PREDICT 1, 1,002 generally healthy UK adults ate identical standard meals. Their population coefficient of variation was 68% [14]. This compares the spread of responses with the average; 68% signals wide variation. It is neither the share of people who reacted differently nor a treatment effect. Several authors worked for or consulted with ZOE.

A 2026 systematic review used preset rules to find and assess 23 studies [15]. It found signs of benefit in prediabetes and no appreciable improvement in healthy groups. Only 5 studies could be combined numerically. Most randomized studies lasted 12 weeks or less and paired the sensor with education or coaching, leaving its separate effect unclear.

Another review covered 25 randomized behavior-change trials [16]. Only 3 involved people without diabetes, all with obesity, and every trial added other support. Eight supplied weight data. The combined result was 0.7 kg less, with P = .066. If the true effect were zero, a result this large could appear by chance about 6.6 times in 100. It missed the usual cutoff and was not statistically significant. The analysis could not reliably separate a small loss from random variation, though it didn’t prove zero effect. Eleven trials reported CGM-industry conflicts, which proves neither funding nor bias.

When I visited the booth, I was open to trying a CGM. But after talking with them, I kept coming back to the same question: what should you do after seeing a normal rise in glucose from eating a banana?

I still don’t have a good answer for healthy people without symptoms. My first thought remains: for this group, a CGM is mostly a waste of money.

A monitor might encourage you to take a walk, but it can also turn normal body changes into warnings that even experts can’t interpret. I already have enough information to decide when to take a walk.

I took the electrolyte powder and left the monitor behind.

If you’ve worn a CGM without a diagnosis, what decisions are you still making differently six months later? Reply and tell me exactly what’s changed. I want to know if I’m missing something in my conclusion.

Stay healthy.

Andre

PS: This argument is for healthy, asymptomatic adults. If you know someone who uses a CGM, please forward this to them. That’s how this newsletter grows, and it’s the only way I want it to.

PPS: If someone forwarded this to you, you can get Under Load, my Sunday edition, here:

https://www.andreheeg.com

References

[1] Consumer Technology Association. (2025, January 7). Tracking your body’s signals for better health, presented by Abbott [Conference session]. CES 2025. https://www.ces.tech/videos/tracking-your-body-s-signals-for-better-health-presented-by-abbott/

[2] RQ Agency. (n.d.). Lingo. https://rqagency.com/work/lingo

[3] Hall, J. J., Eurich, D. T., Nagy, D., Tjosvold, L., & Gamble, J.-M. (2020). Thiazide diuretic-induced change in fasting plasma glucose: A meta-analysis of randomized clinical trials. Journal of General Internal Medicine, 35(6), 1849-1860. https://doi.org/10.1007/s11606-020-05731-3

[4] Alberti, K. G. M. M., Eckel, R. H., Grundy, S. M., Zimmet, P. Z., Cleeman, J. I., Donato, K. A., Fruchart, J.-C., James, W. P. T., Loria, C. M., & Smith, S. C., Jr. (2009). Harmonizing the metabolic syndrome: A joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation, 120(16), 1640-1645. https://doi.org/10.1161/CIRCULATIONAHA.109.192644

[5] Dower, J. A., Johansson, M., Camp, A. W., Montori, V. M., & Lipska, K. J. (2026). Continuous glucose monitoring in type 2 diabetes and beyond: A review. JAMA Internal Medicine. Advance online publication. https://doi.org/10.1001/jamainternmed.2026.2772

[6] University of Gothenburg. (2026, August 3). No evidence that continuous glucose monitors improve health in people without diabetes [Press release]. https://www.gu.se/en/news/no-evidence-that-continuous-glucose-monitors-improve-health-in-people-without-diabetes

[7] U.S. Food and Drug Administration. (2024, May 29). 510(k) premarket notification K233655: Lingo Glucose System. https://www.accessdata.fda.gov/cdrh_docs/pdf23/K233655.pdf

[8] Hutchins, K., Betts, J., Thompson, D., Hengist, A., & Gonzalez, J. (2025). Continuous glucose monitor overestimates glycemia, with the magnitude of bias varying by postprandial test and individual: A randomized crossover trial. American Journal of Clinical Nutrition, 121(5), 1025-1034. https://doi.org/10.1016/j.ajcnut.2025.02.024

[9] Spartano, N. L., Prescott, B., Walker, M. E., et al. (2025). Expert clinical interpretation of continuous glucose monitor reports from individuals without diabetes. Journal of Diabetes Science and Technology, 20(3), 727-735. https://doi.org/10.1177/19322968251315171

[10] Abbott. (2024, September 5). Abbott’s Lingo continuous glucose monitor for health and wellness now available in the U.S. https://abbott.mediaroom.com/2024-09-05-Abbotts-Lingo-TM-Continuous-Glucose-Monitor-for-Health-and-Wellness-Now-Available-in-the-U-S

[11] Boots. (2026). Lingo continuous glucose monitor bundle. Retrieved August 21, 2026, from https://www.boots.com/lingo-continuous-glucose-monitor-bundle-10390678

[12] Spartano, N. L., Sultana, N., Lin, H., et al. (2025). Defining continuous glucose monitor time in range in a large, community-based cohort without diabetes. The Journal of Clinical Endocrinology & Metabolism, 110(4), 1128-1134. https://doi.org/10.1210/clinem/dgae626

[13] Shah, V. N., DuBose, S. N., Li, Z., et al. (2019). Continuous glucose monitoring profiles in healthy nondiabetic participants: A multicenter prospective study. The Journal of Clinical Endocrinology & Metabolism, 104(10), 4356-4364. https://doi.org/10.1210/jc.2018-02763

[14] Berry, S. E., et al. (2020). Human postprandial responses to food and potential for precision nutrition. Nature Medicine, 26, 964-973. https://doi.org/10.1038/s41591-020-0934-0

[15] Liao, X., Li, Y., Tang, S., Xiao, Y., Yu, X., Huang, R., & Zhong, T. (2026). Continuous glucose monitoring in non-diabetic populations: A systematic review of observational and interventional studies with meta-analysis. European Journal of Medical Research, 31, Article 397. https://doi.org/10.1186/s40001-026-03920-0

[16] Richardson, K. M., Jospe, M. R., Bohlen, L. C., et al. (2024). The efficacy of using continuous glucose monitoring as a behaviour change tool in populations with and without diabetes: A systematic review and meta-analysis of randomised controlled trials. International Journal of Behavioral Nutrition and Physical Activity, 21, Article 145. https://doi.org/10.1186/s12966-024-01692-6

What?

Let’s start with the most reliable method. A USC-led study published in npj Aging on July 20 tested the five most popular epigenetic clocks on 3,227 adults from the Health and Retirement Study. These clocks, Horvath, Hannum, PhenoAge, GrimAge, and DunedinPACE, did not share a single gene in common. The authors said there were “more unique than common biological processes.”

These clocks can also give inconsistent results. A 2022 study in Nature Aging found that technical noise alone could make six of these clocks show up to a nine-year difference when testing the same sample twice. Newer versions have reduced this gap to about 1.5 years, so there is a fix. Still, most reports don’t say which version was used for your result.

Consumer options are even less accurate. EGYM gym machines use four fitness tests: strength, cardio, metabolism, and flexibility. WHOOP figures out your age from months of sleep, training, and recovery data. Garmin mostly uses your VO2max. This means the same person could get three different ages from three devices.

So what?

None of these tools truly measure aging. They look at your fitness and habits, then turn those results into years, since that’s a number people understand.

I think that’s okay. If a simple number gets someone to go to the gym on a Tuesday, that’s more useful than a perfect measurement no one pays attention to. Treat it like a game. If your watch pushes you to work out a fourth time this week, it’s working.

The problem is when doctors present a vendor’s score as if it’s a real lab result. Then the suggestion becomes a claim. Most people can’t tell the difference. That’s why credentials matter, and using them to support an unproven number isn’t a good idea.

Now what?

• See your ‘age’ score as a tool to track your habits, not as something for your official health record.

• Focus on the numbers behind the score: your VO2max (in ml/kg/min), strength, waist size in centimeters, and blood pressure. Each of these can predict health outcomes by itself.

• Only compare your results to your own past results, using the same device and the same conditions. Numbers from different brands can’t be compared.

• If you get a score, ask your provider two questions: Has this score been tested against illness or death in people outside their database? And which version of the clock are they using?

• If a gym blood pressure cuff shows 140/90 or higher, check your blood pressure at home over several days. The 2024 European Society of Cardiology guidelines recommend out-of-office readings before making a diagnosis.

I made a similar point in July about the supplements in your cupboard. You can read more in The Doctor’s Edit on Your Longevity Drawer (https://www.andreheeg.com/archive/the-doctors-edit-on-your-longevity-drawer).

Let the number motivate you to go to the gym. That’s its only purpose.

Stay healthy.

Andre

The result was a pale brown drink with a foamy, shiny layer that caught the morning light. I drank it at the counter before anyone else woke up, and I felt great about it.

I have both a medical and a dental degree. Even so, I ended up drinking butter for breakfast after hearing someone on a podcast explain the science. It made sense to me at the time.

These things always seem to make sense at first. That’s the real problem.

My butter phase lasted about two years. Then I switched to MCT oil, which cost almost as much as the whiskey on the shelf. After that came coconut oil, then ghee, which I thought was an upgrade. Now I use olive oil. Each choice felt reasonable at the time.

Each phase had its own expert, a scientific reason, and a type of fat to avoid. The latest trend has the most talked-about villain so far.

Before all of this, there was a hallway. After three training sessions that day, we would sit on the floor outside our rooms, leaning against the wall. On the youth national team, we shared rooms in a long corridor lined with doors. You could recognize another wrestler from across the room without saying anything. It was the ears that gave us away.

In May, Robert Saleh, in his first year coaching the Tennessee Titans, told reporters that removing every seed oil from the facility had been one of the first changes he made, part of an overhaul of how the team eats [1]. Canola and soybean oil, out of an NFL building.

Recently, more executives have asked me about seed oils than ever before. So I read everything I could find on the topic, including both sides and even the arguments I expected to disagree with.

The biology he describes is real

Paul Saladino is one of the most-followed voices arguing that seed oils are doing serious damage. He’s a physician, and he writes this on his own site: “we STORE these polyunsaturated fats in our cell membranes and mitochondrial membranes” [2].

He’s right about that.

Linoleic acid, the main omega-6 fat in conventional sunflower, corn, soybean, and canola oils, gets built into cell membranes and body fat. A review of 37 studies found that its share of American adipose fatty acids rose from 9.1% in 1959 to 21.5% in 2008 [3]. The review estimated a half-life in fat tissue of about 680 days.

Polyunsaturated fats oxidize more readily than saturated fats. In a laboratory study, peroxidized linoleic acid damaged isolated DNA [4].

In the most recent American dietary survey, foods coded as fats supplied 8% to 13% of people’s linoleic acid. Grains supplied 22% to 35%, meat 15% to 25% [5]. Those are categories of reported food, so oil baked into bread still counts as grain. The survey can’t isolate what came from a bottle. The bottle is the visible part of exposure spread across many foods.

Each of my phases started with a solid scientific explanation. Medium-chain fats are processed differently. Clarified butter removes milk solids. Now, I always ask a practical question: has anyone actually measured what happens to people who eat this?

Someone decided to test it

Saladino’s sharpest claim is about DNA. His words, as written: excess linoleic acid makes fat cells release free fats, and “These free fats induce insulin resistance in the peripheral muscles, causing inflammation and DNA damage” [6].

In 2003, the same group went looking in people. Thirty volunteers across three arms for six weeks, one taking 15 grams of linoleic acid a day against a palmitic acid control, measuring oxidative DNA damage in white blood cells. In the linoleic acid arm, the damage rose 13% from where it started and finished 23% below the control group. Neither difference was statistically significant [7].

Each group had ten people, and the study lasted six weeks. They measured only one marker in white blood cells, not muscle as Saladino’s theory suggests. With those limits, the study found no evidence that extra linoleic acid increased oxidative DNA damage.

The population data point the same way. Among 85,425 UK Biobank adults followed for almost 13 years, the top fifth for plasma omega-6 as a share of total fatty acids had 23% lower all-cause mortality than the bottom fifth [8].

That study also challenged an argument I believed for a year. The group with the highest ratio had 26% higher mortality. Both omega-6 and omega-3 were linked to lower mortality, but the link was stronger for omega-3 [8]. The authors thought the ratio result was probably due to omega-3.

Randomized trials don’t show much. In 19 studies with 6,461 adults followed for one to eight years, increasing omega-6 made little or no difference to deaths or heart problems overall. It did lower total cholesterol and might have reduced heart attacks, but the evidence for that is weak [9].

My own ratio was 3.6, which experts say is good. But that number didn’t tell me if I was getting enough of either fatty acid. I realized I might have been taking the wrong part of my fish oil for ten years.

The two trials that should trouble me

Two randomized trials are central to the main arguments against seed oils. Anyone who thinks this debate is settled should take a close look at them.

The Minnesota Coronary Experiment randomized 9,423 people across six mental hospitals and a nursing home between 1968 and 1973. The intervention replaced saturated fat with corn oil. Cholesterol fell 13.8% among participants measured again after a year or more, with no mortality benefit [10]. People kept leaving the institutions, ending their follow-up. The diet also pushed linoleic acid to 13.2% of calories, well above typical US intake of 5.5% to 6% [5].

The Sydney Diet Heart Study is the harder one. It randomized 458 men, 221 to safflower oil and safflower margarine and 237 to continue their usual diet. 86% had had a heart attack, on average about 11 weeks earlier. More of the intervention group died: 17.6% against 11.8%, a hazard ratio of 1.62, with a confidence interval from 1.00 to 2.64 [11].

I wish I could say the margarine was the reason. Margarine back then contained trans fats, but the exact makeup of this one wasn’t measured. However, the study’s authors considered this and ruled it out: the intervention also removed the usual margarines and shortenings, which were the main sources of trans fats at the time. So, trans fat intake probably went down, not up, and they thought it was unlikely to explain the results [11].

The study had clear limits: it involved men who had recently had heart problems, linoleic acid made up about 15% of their energy, there were several dietary changes, and the original protocol couldn’t be recovered. It was just one trial, in men who were already sick, at much higher intakes than usual. Still, it matters.

Why the evidence disagrees

My training taught me to look at each study and think about what kinds of errors it might have.

Plasma fatty acids depend on diet and metabolism. The UK Biobank authors adjusted for many known differences between participants. They still could not rule out factors they had missed or measured poorly, and they sampled blood once, at the start [8].

Randomization addresses confounding. Cochrane rated most of the clinical-outcome evidence low or very low certainty because of bias and imprecision [9].

Looking at all the studies together, I see two main gaps. The UK Biobank can’t prove cause and effect, and the trials only give rough estimates for real-world outcomes. No one has run a large, long-term trial at typical modern intake levels yet.

What the ears were for

No one planned to talk that night. My roommate brought up weight cutting, and soon everyone joined in, sharing stories about injuries, long hours inside, and the smell that never leaves a gym bag. We said things to each other we’d never say to a coach.

Someone joked that our parents should be prosecuted for signing us up. We all laughed, and while we half-meant it, none of us would have quit.

That’s what the ears meant. When you saw another guy across the room, you knew he’d gone through the same things you had, and you didn’t have to say a word.

I stopped wrestling in my mid-twenties, after my shoulder gave out for the last time. There was no final match or big decision, just a scan and a surgeon giving me practical advice. The training hall kept going every night without me. No one was unkind. What I wasn’t prepared for was how something that had shaped my whole life could just end, with everyone else carrying on while I stood outside.

Then there was nothing.

Nutrition groups offer the same sense of belonging, but without the physical cost. A jar on the counter shows everyone which side you’re on, and no one needs to check your ears.

That’s why the debate never ends. Each position gives you a group identity along with a health rule, and it’s harder to let go of the identity than the rule. I’ve been through this five times myself.

I went through all five phases on my own. Standing at the kitchen counter before anyone else was awake, blending butter into my coffee, I felt like I was part of something.

What I keep in the kitchen

At a work dinner a few weeks ago, a man sitting two seats away put down his fork and turned to me. “Andre, what do you think this was cooked in? Should I worry if it’s seed oils?” He wanted to know if his dinner was safe, and he was asking the doctor at the table.

The practical answer is simpler than the debate makes it seem. In the largest relevant study I found, 221,054 American health professionals were followed for up to 33 years. Replacing 10 grams of butter a day with plant oil was linked to a 17% lower risk of death [12]. This was an observational study, and the swap was modeled, not actually done.

Two of my own phases don’t look so good. Coconut oil raises LDL cholesterol by about 10 mg/dL compared to other vegetable oils, and none of the studies measured heart attacks or deaths [13]. Turning butter into ghee removes water and milk solids, so gram for gram, ghee has more saturated fat. As a percentage of total fat, butter and ghee are only a few points apart [14]. I swapped one for a more concentrated version and thought I was making a smart choice.

Olive oil, which I use now, compares well to butter. In a study of 92,383 people, it didn’t show a significant advantage over other vegetable oils [15].

What I told him

No, don’t worry about it, and eat your dinner.

The longer answer is that the bottle is just a distraction, and the scientific explanation is what convinces you. I went through five versions of this over 15 years, and each one was biochemically accurate. This is the Activate part of the Upward ARC, which is about what you put into your body. It’s also where marketing is strongest and the incentives are hardest to spot.

In one study, twenty people in a metabolic ward ate 508 more calories a day on an ultra-processed diet than on an unprocessed one, gaining about a kilogram in two weeks [16]. The trial didn’t test seed oil or figure out which differences in the diets caused the result. It was the overall eating pattern that changed how much people ate.

So, to answer his specific question: at the amounts people usually eat, there’s no human evidence that seed oils are especially harmful. Replacing butter and other saturated fats with plant oils lowers cholesterol, and studies link that swap to living longer. Whether purposely adding more omega-6 changes lifespan is still an open question.

Try this today

Each phase I went through added another rule. This list is about letting go of some of them.

Don’t treat the ratio as a final answer. In the UK Biobank data, both omega-6 and omega-3 were linked to lower mortality, and the authors believed the ratio was mostly influenced by omega-3. If you don’t eat oily fish often, start there before getting another test.

Stop overthinking and just keep two bottles: extra virgin olive oil for everyday cooking and finishing, and refined canola or high-oleic oil for frying and roasting. The difference between these sensible choices is so small that worrying about it costs you more than picking the wrong one.

Use frying oil only once, throw it out after cooking, and keep the pan below the oil’s smoke point. I do this as a kitchen habit, not because of any proven health outcome.

Ask what would make someone change their mind. For me, it would be a well-designed, independently funded trial at the amounts people actually eat. If I ever call a food poison and can’t answer that question, just stop reading.

Maybe I was just lucky

Throughout all five phases, my blood tests stayed normal. Maybe the type of fat mattered less than I believed. Maybe I was just lucky. I still keep butter in the fridge and use it in normal amounts.

Five times, an expert with a clear explanation convinced me before I checked the evidence myself, and five times I changed my mind later. I don’t regret making those changes.

I still miss that hallway and my wrestling tribe.

Stay healthy.

Andre

PS: I’ve told you my five eras. What was yours? The one you’d rather not admit to. Reply and tell me; I read every message and never share them. And if you know someone with strong opinions about oil who has never read a study on it, send this along. That’s how this newsletter grows, and the only way I want it to.

PPS: If someone forwarded this to you, you can get Under Load, my Sunday edition, here:

https://www.andreheeg.com

.

References

[1] Titans’ Robert Saleh sparks nutritional value debate with seed oil ban for players, team-provided meals. (2026, May). Fox News. https://www.foxnews.com/sports/titans-robert-saleh-sparks-nutritional-value-debate-seed-oil-ban-players-team-provided-meals

[2] Saladino, P. (2025, November 10). Don’t read this if you love your bacon. paulsaladinomd.com. https://www.paulsaladinomd.com/psmd-newsletters/dont-read-this-if-you-love-your-bacon

[3] Guyenet, S. J., & Carlson, S. E. (2015). Increase in adipose tissue linoleic acid of US adults in the last half century. Advances in Nutrition, 6(6), 660-664. https://doi.org/10.3945/an.115.009944

[4] de Kok, T. M., ten Vaarwerk, F., Zwingman, I., van Maanen, J. M., & Kleinjans, J. C. (1994). Peroxidation of linoleic, arachidonic and oleic acid in relation to the induction of oxidative DNA damage and cytogenetic effects. Carcinogenesis, 15(7), 1399-1404. https://doi.org/10.1093/carcin/15.7.1399

[5] Momin, S. R., Senn, M. K., Manichaikul, A., Tintle, N. L., Herrington, D. M., Rich, S. S., Kabagambe, E. K., & Wood, A. C. (2023). Dietary sources of linoleic acid (LA) differ by race/ethnicity in adults participating in NHANES between 2017-2018. Nutrients, 15(12), 2779. https://doi.org/10.3390/nu15122779

[6] Saladino, P. (2024, July 28). Seed oils & processed foods: How they’re harming you. paulsaladinomd.com. https://www.paulsaladinomd.com/psmd-newsletters/seed-oils-processed-foods-how-theyre-harming-you

[7] de Kok, T. M. C. M., Zwingman, I., Moonen, E. J., Schilderman, P. A. E. L., Rhijnsburger, E., Haenen, G. R. M. M., & Kleinjans, J. C. S. (2003). Analysis of oxidative DNA damage after human dietary supplementation with linoleic acid. Food and Chemical Toxicology, 41(3), 351-358. https://doi.org/10.1016/S0278-6915(02)00237-5

[8] Zhang, Y., Sun, Y., Yu, Q., Song, S., Brenna, J. T., Shen, Y., & Ye, K. (2024). Higher ratio of plasma omega-6/omega-3 fatty acids is associated with greater risk of all-cause, cancer, and cardiovascular mortality: A population-based cohort study in UK Biobank. eLife, 12, RP90132. https://doi.org/10.7554/eLife.90132

[9] Hooper, L., Al-Khudairy, L., Abdelhamid, A. S., Rees, K., Brainard, J. S., Brown, T. J., Ajabnoor, S. M., O’Brien, A. T., Winstanley, L. E., Donaldson, D. H., Song, F., & Deane, K. H. O. (2018). Omega-6 fats for the primary and secondary prevention of cardiovascular disease. Cochrane Database of Systematic Reviews, 2018(11), CD011094. https://doi.org/10.1002/14651858.CD011094.pub4

[10] Ramsden, C. E., Zamora, D., Majchrzak-Hong, S., Faurot, K. R., Broste, S. K., Frantz, R. P., Davis, J. M., Ringel, A., Suchindran, C. M., & Hibbeln, J. R. (2016). Re-evaluation of the traditional diet-heart hypothesis: Analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ, 353, i1246. https://doi.org/10.1136/bmj.i1246

[11] Ramsden, C. E., Zamora, D., Leelarthaepin, B., Majchrzak-Hong, S. F., Faurot, K. R., Suchindran, C. M., Ringel, A., Davis, J. M., & Hibbeln, J. R. (2013). Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: Evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ, 346, e8707. https://doi.org/10.1136/bmj.e8707

[12] Zhang, Y., Chadaideh, K. S., Li, Y., Li, Y., Gu, X., Liu, Y., Guasch-Ferré, M., Rimm, E. B., Hu, F. B., Willett, W. C., Stampfer, M. J., & Wang, D. D. (2025). Butter and plant-based oils intake and mortality. JAMA Internal Medicine, 185(5), 549-560. https://doi.org/10.1001/jamainternmed.2025.0205

[13] Neelakantan, N., Seah, J. Y. H., & van Dam, R. M. (2020). The effect of coconut oil consumption on cardiovascular risk factors: A systematic review and meta-analysis of clinical trials. Circulation, 141(10), 803-814. https://doi.org/10.1161/CIRCULATIONAHA.119.043052

[14] U.S. Department of Agriculture, Agricultural Research Service. (2019). FoodData Central: Butter, salted (FDC 173410); Butter, clarified (ghee) (FDC 171314).

https://fdc.nal.usda.gov

[15] Guasch-Ferré, M., Li, Y., Willett, W. C., Sun, Q., Sampson, L., Salas-Salvadó, J., Martínez-González, M. A., Stampfer, M. J., & Hu, F. B. (2022). Consumption of olive oil and risk of total and cause-specific mortality among U.S. adults. Journal of the American College of Cardiology, 79(2), 101-112. https://doi.org/10.1016/j.jacc.2021.10.041

[16] Hall, K. D., Ayuketah, A., Brychta, R., Cai, H., Cassimatis, T., Chen, K. Y., Chung, S. T., Costa, E., Courville, A., Darcey, V., Fletcher, L. A., Forde, C. G., Gharib, A. M., Guo, J., Howard, R., Joseph, P. V., McGehee, S., Ouwerkerk, R., Raisinger, K., … Zhou, M. (2019). Ultra-processed diets cause excess calorie intake and weight gain: An inpatient randomized controlled trial of ad libitum food intake. Cell Metabolism, 30(1), 67-77.e3. https://doi.org/10.1016/j.cmet.2019.05.008

What?

Researchers led by Parco Siu in Hong Kong assigned 315 inactive adults with central obesity to 3 groups: one group performed one workout a week, another performed 3, and the third attended health education classes. After 16 weeks, the once-a-week group lost 0.8 kg of fat compared to the control, while the 3-times-a-week group lost 1.0 kg. The difference between the 2 exercise groups was too small to be significant. Both groups reduced their waist size by about 2 cm. The study was published in Nature Communications.

There are two important details that most reports missed. The exercise involved supervised treadmill sessions: 4 intervals of 4 minutes each at 85-95% of peak heart rate, with 3 minutes of easy walking between intervals. For the once-a-week group, the session meant doing 3 of these blocks in a row with rest breaks, making it almost 2 hours at the gym, not just a long walk.

So what?

The main difference between the groups was in fitness. The once-a-week group improved their VO2 peak by 1.5 ml/kg/min, while the 3-times-a-week group improved by 2.6. 16 weeks after the training ended, only the 3-times-a-week group still had better fitness than the control group. By then, the fat loss was gone, but both groups kept their smaller waists.

I’ve said before that VO2 max is the best measure of how long you’ll live and how well you’ll function. From that perspective, the headline is only partly true. The once-a-week plan matched the others for fat loss, but it didn’t keep up in fitness; fitness was the lasting benefit at week 32.

The other side is important too. For living longer, how you spread out your workouts might not matter much. A 2025 review of 21 studies found that people who exercise only on weekends and those who exercise more regularly both experienced similar reductions in death rates. If you can only fit in one session a week, it’s still worth doing.

The real difference came from working at 85-95% of your peak heart rate.

Now what?

• Try the workout as it was tested: start with 5 minutes of easy effort, then do 4 rounds of 4 minutes hard and 3 minutes easy, and finish with another 5 minutes of easy effort. The whole session takes about 35 minutes.

• ‘Hard’ means you shouldn’t be able to finish a sentence. If you can talk easily during the 4-minute intervals, you’re not pushing hard enough. You don’t need a heart rate monitor for this.

• Aim for 3 sessions a week if you can, since that group kept their fitness gains. The study didn’t test 2 sessions a week, so I can’t speak to that.

• If your week gets busy, still try to fit in at least one session. Even one workout was better than just attending the education class.

• Don’t let the scale be your only measure. Choose a set route or stairwell, time yourself today, and check your progress again in 8 weeks.

8 weeks from today is October 7. Mark your calendar for your retest.

Stay healthy.

Andre

The shop sold vials. The shipping terms said the contents were for lab research only and not for people. Sites include that so whatever happens next is your responsibility.

I have both a medical and dental degree, but I was still about to send money to strangers for something I planned to inject into myself.

By August 2024, my wife was putting my socks on for me. Underwear was even harder because you have to balance on one leg. I washed my face in stages. After 18 months of this, things only got worse. On work mornings with travel, I took the strongest painkiller I had.

I wore headphones most of the day. That August, while half-listening to a podcast, I heard Andrew Huberman tell Joe Rogan something about a compound called BPC-157:

“while only animal data, it’s very clear, you know, it has the propensity to encourage fibroblasts, which is cells that, you know, make up things like, you know, tendon and cartilage, et cetera, and can really repair tissues… I certainly have experienced it can help repair things.” [1]

I missed the warning. The words that stayed with me were tendon and cartilage.

I had heard about it before and ignored it. That afternoon, I ended up on a vendor’s website.

The vote that changed nothing

I first heard about BPC-157 in July 2021 from the same two men on the same show [2]. Three years later, I was at my lowest point when it came up again. Two years after that, on July 23, an FDA advisory panel voted 8 to 6 to recommend letting pharmacies compound it, even though the agency’s own reviewers disagreed. Eight panelists were recent appointees, and six of them ran clinics that sell peptides. One person voted yes but admitted the data was disappointingly incomplete [3].

But nothing changed after that. A panel can only recommend. The list of what pharmacies can legally make hasn’t changed since February 2019 [4], so no pharmacy in America can legally make BPC-157 today. The vote only changed what people expect might happen.

There was a vote, but still not a single randomized trial in humans. That’s why people keep asking me the same question: Are peptides safe?

No one can answer that, because the word itself doesn’t refer to a single thing.

The word is a size

Insulin is a peptide. It has 51 amino acids and is the reason a 14-year-old in Toronto, who weighed just 65 pounds when admitted, lived another 13 years [5]. Semaglutide (Ozempic/Wegovy) is also a peptide, and someone on your leadership team is probably using it quietly.

A peptide is simply a short chain of amino acids. That’s the definition. In the U.S., regulators set the cutoff at 40. Anything above that is considered a biologic, which is protected from copies for 12 years and can’t be made by compounding pharmacies. Regular drugs get 5 years [6][7]. Tirzepatide (Mounjaro/Zepbound) is just under the limit, at 39 [8].

That number only affects the paperwork and nothing else.

Abud Bakri is an internist who has used these compounds himself and says so, sits on the medical commission of Enhanced, which sells peptides, and has consulted for a group planning a BPC-157 trial. On Huberman’s show in June:

“everyone online talks about peptides are good or peptides are bad. There’s no actual scientific category of peptides that gives you a functional definition that’s discussable between two people. Because what do you mean by peptide? Do you mean carnosine or do you mean [retatrutide]?” [9]

What I ask myself before taking anything

Three questions, in order.

Has this ever been given to humans in a study I can read? Who funded that study, and do they also sell the compound? And does the result actually matter in real life, or is it just a number in my blood that’s never been shown to make a difference?

Most so-called longevity peptides don’t even pass the first question.

One lab in Zagreb

In the early 1980s, a group in Croatia went looking for whatever keeps the stomach from digesting itself. By 1989 they said they had it: a fragment of a larger protein, 15 amino acids long [10][11].

The full sequence of that larger protein has never been published. When a reporter asked why, Predrag Sikirić said that if you have your own child, you want it to be yours forever. Anna Mapp, a chemist at Michigan and president of the American Peptide Society, told the same reporter that without the full sequence, it’s impossible to reproduce the original work [11].

Then came the animal studies: rats with severed tendons, cut ligaments, burns, and crushed muscles healed faster, again and again, mostly in studies by the same group. About four out of five BPC-157 papers on PubMed list Sikirić or his Zagreb colleague as an author, a number his critics published last year, and he disputed in the same journal [12].

There are no randomized controlled trials in humans. A systematic review last year looked at 544 papers and included 36; 35 were animal studies [13]. The only human study was a survey: 12 patients who had already received knee injections were asked how they felt afterward; 7 said they felt better, but there was no placebo and no blinding [14]. The rest are a small intravenous pilot in two people [15] and a couple of Croatian trials from the early 2000s where the compound was given as an enema and never fully published.

Bakri says that when researchers checked those patients’ blood afterward, they couldn’t find the compound [9]. Maybe it stayed local, broke down too quickly to measure, or was never absorbed. No one outside that group can verify it.

And almost no one takes it the way those trials did.

What I won’t write down

I should be clear that I’m not a purist. I’m curious and have tried plenty of things on myself that aren’t standard medicine. I’ve written before about experimenting with psychedelics. I know my own body, and I understand physiology and pharmacology well enough to take a calculated risk. I’m comfortable being the one who finds out.

What I get from that is a study with one participant, me, unblinded, and run by someone who wanted it to work. That’s a long way from real advice. I wouldn’t give it to my own family.

People still ask me for prescriptions. Metformin, because they read about its link to longevity. Stimulants. Testosterone. And lately, peptides.

Some of these would be easy to prescribe, and the risk would be small. I could write the prescription in 20 seconds and say what everyone says: this is off-label, I’ve explained it to you, you’re doing it at your own risk, I take no responsibility. All of that is true, but it still makes me the one who signed.

Most of my surgical years went on cancers of the mouth: the lip, the tongue, the floor of the mouth, the lining of the cheek. Surgery is the backbone; radiation comes after it, sometimes with chemotherapy alongside. Surgery means cutting in three dimensions with a margin of a centimeter around the tumor. Take something the size of a walnut out of the tongue, and you have changed how that person speaks for the rest of their life, how they move food around their mouth, whether they can swallow at all.

Most were men in their sixties, smokers, with a lesion on the side of the tongue they’d called a mouth ulcer for months. I would sit down and explain the situation. The consequences would be permanent, and they’d be reminded every time they spoke. It was their best chance, but no one could promise it wouldn’t return.

They said yes, almost all of them.

I would see them months later, eating, talking, holding a cup of coffee.

I’ve already been the person who said yes and then watched someone go home and live with the outcome. That’s why I won’t do it casually for something untested, just because someone wants it.

The argument back is always the same. If you don’t, someone else will.

Fine. Then someone else can take responsibility for that.

The correction that didn’t travel

In July 2021, Huberman told Rogan that things like it “definitely do accelerate the healing of an injury and there’s no question about that.” Rogan, same conversation: “I’ve used it myself, and I had a tendonitis in my elbow that I just could not fix. I started using [BPC-157]. It was gone in two weeks” [2].

By August 2024, Huberman had moved. The sentence now started with “while only animal data” [1]. And 5 months before that, on his own show, he had gone further still: BPC-157 may raise tumor growth risk through the same blood-vessel mechanism that makes it interesting, and he does not suggest anyone buy black-market peptides [16]. He has since said he took it himself, on a prescription, and no longer does [9].

He was more cautious than people think, and he became even more careful as time went on.

Still, I found myself on a vendor’s website.

The warning and the claim both leave the podcast studio, but only the claim spreads.

The evidence trail is contaminated too

Say you do the responsible thing and check. The American trials registry is where a careful person looks, and as of August 4 it returns Phase 2 studies for BPC-157 and TB-500, marked recruiting.

Three of the records in that cluster say inside their own text that they are fictional or mock entries [17].

They seem like practice submissions that accidentally got out of a test system. I have no proof anyone meant to mislead. But the effect is the same. You search for evidence and find something that looks real, from a sponsor with a real name, marked as enrolling patients. The BPC-157 record doesn’t have any disclaimer.

The Wolverine stack

Few people take BPC-157 alone, and the bundles have names.

BPC-157 with TB-500 is sold as the Wolverine stack. Add copper peptide, and it becomes the glow stack. Someone picked those names. An adult decided that a man injecting two untested compounds into his shoulder should picture himself as a comic book hero with claws. It works, because people buy it. I used the male pronouns on purpose.

Bakri described what he calls the Trinity stack: a GLP-1, a growth hormone drug, a hormone layer on top. “A lot of these transformations you see in CEOs and celebrities and stuff is using a combination of those three things,” he said. On whether it’s healthy: “We’ll find out” [9].

We’ll find out. By watching what happens to people like you.

He also explained how people get there: buy one, see a result, add three more, and “the average sale value goes up from these research sites” [9]. I couldn’t find any study on what these combinations do together.

The GLP-1s are the exception, and the reason everyone else is comfortable holding a syringe. Semaglutide and tirzepatide went through the full process, and they are the best evidence in this field.

I couldn’t find any published analysis of what’s actually in gray-market BPC-157. Researchers bought semaglutide from online sellers. The vials were overfilled with material that was only 7.7% to 14.4% semaglutide, against a label claiming 99%, which still left the dose 28% to 39% above what the label promised. Every sample carried bacterial endotoxin. Mostly unknown material, and more drug than you think [18].

Bakri told a story about a man who ordered a weight loss compound and saw his skin darken, only to realize he was injecting a tanning peptide [9]. That’s the kind of mistake you can see in the mirror. The others, you can’t.

Insulin and the GLP-1s are medicine, with the trials to prove it. BPC-157 is unfinished. TB-500 is a 7-amino-acid piece of a bigger molecule whose own trial record is mixed, and the fragment inherits none of it [19]. Melanotan II, the tanning one, has published case reports of muscle breakdown, kidney infarction, priapism, and new atypical moles [20][21][22][23]. KPV, dihexa, PEG-MGF, and epitalon have no registered Western human trial, which didn’t stop the July panel recommending KPV alongside BPC-157 [3].

Where I’m on thin ice

I can’t say BPC-157 doesn’t work. The animal data is better than I expected after a week of research, and there’s no published series of humans harmed by it either because no one has done the study that would answer that question.

And by my own three questions, my own back wouldn’t count as evidence. One participant, no blinding, no comparison group, and a condition that sometimes gets better on its own. I know that. I’d still begin with what I did before. If physiotherapy fails, you’ve lost 12 weeks. If a vial fails, you can’t take back whatever it already did.

This is the Activate pillar of the Upward ARC, the part about what you put into your body, and it’s where that risk hits hardest.

Try this today

Some of you are already taking something. Some of you are just thinking about it. This is for both groups.

If you have any history of cancer, or anything undiagnosed, this is where I stop being neutral. BPC-157 appears to work partly by growing blood vessels. Tumors need blood vessels. Nobody has run the study that would tell us whether that matters in a person, and I wouldn’t volunteer to find out. Huberman said the same on his own show, and almost nobody quotes that one [16]. If you compete under anti-doping rules, all three of these are prohibited at all times on the WADA list: BPC-157 as a non-approved substance, TB-500 as a thymosin derivative, MOTS-c as a metabolic modulator. A prescription is no defense [24].

Ask yourself those three questions before trying any compound. Most options will drop off the list.

Find out what’s actually in the vial, and ask about the markup. Who made it, which lab tested it, and is that lab independent from the seller? Then ask your clinician what the pharmacy charges them and what they charge you. That price gap is legal in many places and goes into someone’s pocket. Treat the seller’s certificate as marketing: in one analysis, two custom-made peptides were found to be 20% and 43% undeclared mannitol by weight, which standard purity tests wouldn’t catch [25].

Decide what failure looks like before you start. What will you measure, by when, and what result will make you stop? Write it down. Without this, every intervention seems to work forever.

Two years of boring

Looking at that transfer form, I realized what I had become: a man in an alley, buying something from a stranger and just hoping.

I had become someone willing to put an unknown substance into my body just because I couldn’t put on a sock. No vial could fix what that said about me.

So I chose the other path. I sought guidance from physiotherapists, back pain specialists, nutritionists, and others. I rebuilt my training routine twice, changed my diet, lost weight, and kept habits I still follow, like a walk before my first call and a proper shutdown routine after 10pm. It took months, but it worked. I haven’t needed a painkiller in almost two years.

At some point, my wife stopped needing to help me with my socks. I can’t say which morning it was, and that’s how I know it was the slow, steady approach that worked.

I’d listened to every podcast. The only thing I never did was take action on a random Tuesday, in a life that doesn’t stop for experiments.

I was lucky because of where I lived. The compound was hard to get in Germany, and that delay gave the rational part of me time to catch up with the desperate part. If I’d been somewhere with next-day delivery that August, things might have turned out differently.

Stay healthy.

Andre

PS: I’m not judging anyone, because I was one click away from doing the same thing. Have you ever come close? It doesn’t have to be peptides, just anything you considered when pain or exhaustion dragged on too long. Reply and tell me about it. I read every message, and I never share them. If you know someone who needs this, forward this edition to them. This is how this newsletter grows, and it’s the only way I want it to.

PPS: If a friend forwarded this to you, you can get Under Load, my Sunday edition, here:

https://www.andreheeg.com

.

References

[1] Rogan, J. (Host). (2024, August 27). #2195 – Andrew Huberman [Audio podcast episode]. In The Joe Rogan Experience. Speaker-labeled transcript, approximately 3:02:52.

[2] Rogan, J. (Host). (2021, July 14). #1683 – Andrew Huberman [Audio podcast episode]. In The Joe Rogan Experience. Approximately 2:39:14-2:40:37. Automated transcript; both speakers render the compound inconsistently, and bracketed corrections are marked.

[3] Lovelace, B., Jr., & Miller, S. G. (2026, July 23). FDA panel recommends easing some peptide restrictions despite disapproval from scientists. NBC News. https://www.nbcnews.com/health/health-news/peptides-restrictions-ease-fda-panel-recommend-bpc-157-scientists-rcna588879

[4] List of bulk drug substances that can be used to compound drug products in accordance with section 503A of the Federal Food, Drug, and Cosmetic Act, 84 Fed. Reg. 4696 (February 19, 2019), codified at 21 C.F.R. § 216.23. No subsequent amendment as of August 2026.

[5] Rogol, A. D., Laffel, L. M., Bode, B., & Sperling, M. A. (2023). Celebration of a century of insulin therapy in children with type 1 diabetes. Archives of Disease in Childhood, 108(1), 3-10. https://doi.org/10.1136/archdischild-2022-323975

[6] Definitions, 21 C.F.R. § 600.3(h)(6).

[7] Biologics Price Competition and Innovation Act of 2009, 42 U.S.C. § 262(k)(7); Drug Price Competition and Patent Term Restoration Act of 1984, 21 U.S.C. § 355(j)(5)(F)(ii); Federal Food, Drug, and Cosmetic Act § 503A, 21 U.S.C. § 353a.

[8] Coskun, T., Sloop, K. W., Loghin, C., Alsina-Fernandez, J., Urva, S., Bokvist, K. B., Cui, X., Briere, D. A., Cabrera, O., Roell, W. C., Kuchibhotla, U., Moyers, J. S., Benson, C. T., Gimeno, R. E., D’Alessio, D. A., & Haupt, A. (2018). LY3298176, a novel dual GIP and GLP-1 receptor agonist for the treatment of type 2 diabetes mellitus: From discovery to clinical proof of concept. Molecular Metabolism, 18, 3-14. https://doi.org/10.1016/j.molmet.2018.09.009

[9] Huberman, A. D. (Host). (2026, June 1). Peptides: The science, uses & safety | Dr. Abud Bakri [Audio podcast episode]. In Huberman Lab. Quotations at approximately 0:00:29, 0:21:12, 0:34:15, 2:30:20 and 2:37:50.

[10] Józwiak, M., Bauer, M., Kamysz, W., & Kleczkowska, P. (2025). Multifunctionality and possible medical application of the BPC 157 peptide: Literature and patent review. Pharmaceuticals, 18(2), 185. https://doi.org/10.3390/ph18020185

[11] Talpos, S. (2026, May 29). A peptide, a secretive scientist, and a debate over evidence. Undark Magazine. https://undark.org/2026/05/29/stress-test-bpc-157-history/ (Co-published by STAT News, June 1, 2026.)

[12] Józwiak, M., Bauer, M., Kamysz, W., & Kleczkowska, P. (2025). Reply to Sikiric et al. Comment on “Józwiak et al. Multifunctionality and possible medical application of the BPC 157 peptide: Literature and patent review.” Pharmaceuticals, 18(10), 1451. https://doi.org/10.3390/ph18101451

[13] Vasireddi, N., Hahamyan, H., Salata, M. J., Karns, M., Calcei, J. G., Voos, J. E., & Apostolakos, J. M. (2025). Emerging use of BPC-157 in orthopaedic sports medicine: A systematic review. HSS Journal, 21(4), 485-495. https://doi.org/10.1177/15563316251355551

[14] Lee, E., & Padgett, B. (2021). Intra-articular injection of BPC 157 for multiple types of knee pain. Alternative Therapies in Health and Medicine, 27(4), 8-13.

[15] Lee, E., & Burgess, K. (2025). Safety of intravenous infusion of BPC157 in humans: A pilot study. Alternative Therapies in Health and Medicine, 31(5), 20-24.

[16] Huberman, A. D. (Host). (2024, April 1). Benefits & risks of peptide therapeutics for physical & mental health [Audio podcast episode]. In Huberman Lab. https://www.hubermanlab.com/episode/benefits-risks-of-peptide-therapeutics-for-physical-mental-health

[17] U.S. National Library of Medicine. (2026). ClinicalTrials.gov records NCT07437547, NCT07487363, NCT07481734 and NCT07437560, first posted February-March 2026. Retrieved August 4, 2026.

[18] Ashraf, A. R., Mackey, T. K., Vida, R. G., Kulcsár, G., Schmidt, J., Balázs, O., Domián, B. M., Li, J., Csákó, I., & Fittler, A. (2024). Multifactor quality and safety analysis of semaglutide products sold by online sellers without a prescription: Market surveillance, content analysis, and product purchase evaluation study. Journal of Medical Internet Research, 26, e65440. https://doi.org/10.2196/65440

[19] Sosne, G., Kleinman, H. K., Springs, C., Gross, R. H., Sung, J., & Kang, S. (2023). 0.1% RGN-259 (thymosin β4) ophthalmic solution promotes healing and improves comfort in neurotrophic keratopathy patients in a randomized, placebo-controlled, double-masked Phase III clinical trial. International Journal of Molecular Sciences, 24(1), 554. https://doi.org/10.3390/ijms24010554 (Primary endpoint not met, p=0.0656; funded by ReGenTree, with authors employed by the sponsor or its parent.)

[20] Nelson, M. E., Bryant, S. M., & Aks, S. E. (2012). Melanotan II injection resulting in systemic toxicity and rhabdomyolysis. Clinical Toxicology, 50(10), 1169-1173. https://doi.org/10.3109/15563650.2012.740637

[21] Peters, B., Hadimeri, H., Wahlberg, R., & Afghahi, H. (2020). Melanotan II: A possible cause of renal infarction. CEN Case Reports, 9(2), 159-161. https://doi.org/10.1007/s13730-020-00446-0

[22] Dreyer, B. A., Amer, T., & Fraser, M. (2019). Melanotan-induced priapism: A hard-earned tan. BMJ Case Reports, 12(2), e227644. https://doi.org/10.1136/bcr-2018-227644

[23] Reid, C., Fitzgerald, T., Fabre, A., & Kirby, B. (2013). Atypical melanocytic naevi following melanotan injection. Irish Medical Journal, 106(5), 148-149.

[24] World Anti-Doping Agency. (2026). The 2026 prohibited list. BPC-157 under S0 (non-approved substances); thymosin beta-4 and its derivatives, including TB-500, under S2.3 (growth factors); MOTS-c under S4.4 (AMPK activators, metabolic modulators). All prohibited at all times.

[25] Choules, M. P., Bisson, J., Simmler, C., McAlpine, J. B., Giancaspro, G., Bzhelyansky, A., Niemitz, M., & Pauli, G. F. (2020). NMR reveals an undeclared constituent in custom synthetic peptides. Journal of Pharmaceutical and Biomedical Analysis, 178, 112915. https://doi.org/10.1016/j.jpba.2019.112915

What?

On July 31, Bailey Knopf and Dudley Lamming published a paper called “The hallmarks of protein and amino acid restriction in aging and longevity” in Cell Press Blue. They say that eating less protein can improve metabolic health and, in some species, might even help them live longer.

If you look closer, the paper gets specific fast. It’s a narrative review, so it sums up existing studies instead of combining their data. Most of the strong evidence comes from research on flies, worms, mice, and rats. The best human data is from Lamming’s own 43-day trial, where people on a low-protein diet lost weight and fat, and had lower fasting glucose, even though they ate more calories. That is a real result, but the study only lasted six weeks and only measured blood sugar and body fat. No one tracked how long anyone lived.

Paul Greenhaff, a professor of muscle metabolism at Nottingham, summed it up that same day. The main question “has not been addressed in humans.”

So what?

The paper doesn’t actually tell you to eat less protein. Instead, it says your protein needs depend on how active you are. Lamming himself said, “It’s absolutely crystal clear that there are benefits of protein to muscle growth and exercise response of active individuals.” But here’s what the headlines missed: most people aren’t very active, yet many eat as if they train much more than they really do.

I’ve made this point before. Last February, I said most people need 1.6 to 2.2 grams of protein per kilogram, then quickly added, “less if you’re sedentary,” and moved on. Those four words were actually the most important.

Think of protein as your body’s repair budget. You use it for the work your body actually does. If you train, eating at the higher end of the range makes sense. If you don’t train, you’re paying the metabolic cost for muscle you never built.

There’s something else you should know, though it doesn’t make the science wrong. Lamming is on the scientific advisory board of a company working on mTOR inhibitors, and mTOR is central to his paper. He disclosed this, but I think it’s important for you to know.

The other side of the story is strong too. In the Nurses’ Health Study, nearly 49,000 women were tracked from 1984 to 2016. More protein in midlife, especially from plants, was linked to better odds of aging well. This result is about chronic disease, not muscle, and it only shows an association. For muscle, animal protein still has more leucine and a more complete amino acid profile. That difference matters most if you’re not eating enough protein to start with. Once you get enough, studies stop finding a difference in strength or lean mass.

Now what?

• Count the lifting sessions you actually did last week, not the ones you planned. If you did two or more, stick with 1.6 grams per kilogram or more. If you did zero or one, drop to about 1.2.

• Are you over 65 or already losing strength? Ignore the headline. This review agrees with the usual advice. Your minimum is 1.0 to 1.2 grams per kilogram.

• Keep your protein intake steady throughout the week instead of loading up only on gym days. Your muscles stay sensitive to protein for 24 to 48 hours after you lift, so Sunday’s chicken still helps pay for Saturday’s workout.

• Compare what you eat on a typical day to your target number. If you go over it during a week when you didn’t train, cutting out fortified snacks is the easiest way to adjust.

Stay healthy.

Andre

At the border, they took my passport, phone, and laptop. Someone asked about my job, and I wasn’t sure if ‘consultant’ would make sense or cause trouble, so I said I was a doctor. The next morning, they brought us to a hospital, where I met the head physician. He asked how I’d treat a patient with shortness of breath, then chest pain, then a stubborn headache. The questions were simple enough for me to answer. I passed. It actually felt a bit more stressful than my final exams, but we did get to see a North Korean hospital from the inside.

We spent two weeks there with a driver and two guides, following a route we didn’t pick, in a place with almost no phone signal anyway. For the first few days, I kept reaching for my pocket, only to find it empty. By the third day, I stopped, and my mind finally quieted in a way it hadn’t for years.

That sense of calm happened within a tightly controlled system. We followed a set itinerary, always with our guides and driver, and paid to be part of a state-run tourism program. I don’t want to make the regime sound better than it was (it’s bad, and we saw enough to judge even on a tightly controlled trip), but the quiet is what stayed in my memory.

Fourteen years later, no holiday I’ve picked has given me that same distance from work.

How would you even know

That bothers me more than it probably should, because I honestly can’t say if any holiday since then has really worked. I usually come home saying I feel better, even after a week where I checked email twice a day and spent six out of seven days thinking about a budget decision.

Feeling rested is a terrible measure. It depends on things like the last morning, the weather, or a good breakfast, and it often just tells you what you want to hear. So I started looking for something else.

The password test

On a family holiday, in a place with no reception or somewhere so new I’d stopped checking, I opened my laptop for something and couldn’t remember my password. The whole thing just vanished. I typed something, got it wrong, and stared at the screen. I’ve entered that password loads of times, usually without even thinking about it.

My company made us change our passwords every few months, so it never really became automatic. Do you know that little shock, and then a feeling almost like satisfaction when this happens? The part of me that remembered those characters had finally let go.

Researchers have a name for the state I had stumbled into. Sonnentag and Fritz call it psychological detachment, one of four parts of recovery alongside relaxation, mastery, and control [1]. Your head leaves the job, which turns out to be a completely separate event from your body leaving the office. They measure it by asking people whether they have stopped thinking about work, and I should be straight with you: nobody has validated password recall as a measure of anything. People forget passwords for dull reasons.

I took that blank screen as a personal sign that I’d finally let go of a work habit, and I’ve used it ever since. I’ve also stopped trying to plan the perfect destination. Grant’s meta-analysis couldn’t say if location matters, and it did find that trip length makes a difference, but didn’t say how much or in which direction [2]. So I’m going beyond the evidence when I say I don’t worry about either anymore. In 20 years, I haven’t seen an executive come back changed just because they stayed in a nicer hotel. Now, I just pay attention to whether my mind let go of work at all.

Nobody is going to reward you for this

Eva Buechel and Elisa Solinas did 16 studies on how detachment is seen at work, and their findings surprised me [3]. Managers say detachment is good for their teams when asked directly. But when they see an employee actually switch off, they rate that person as less promotable. This was true for out-of-office replies, vacation requests, and even when the reason for disconnecting was valid. Managers seem to see detachment as a sign of low commitment.

There’s another surprising result. In a meta-analysis of 89 samples with 39,085 employees, the six studies that measured work performance found that people who worked during their off-hours actually scored higher [4]. But these studies were mostly self-reported and cross-sectional, so no one was independently assessed. We can’t say if the extra work really caused better performance.

If you find it hard to switch off, it’s probably because of the incentives at work, not a flaw in your character. The tricky part is that if you’re in a senior role, you help set those incentives. Your out-of-office message is a policy statement. The email you send at 11pm from an airport is, too. Your team pays more attention to that than to any wellbeing presentation.

Somebody in this house is still working

I’ve never asked my wife if she’s ever forgotten her password on holiday. I think I already know the answer.

Musick, Meier and Flood analyzed 12,163 people across 36,036 activities, asking how they had felt during three randomly selected activities from the previous day [5]. Parents reported more positive affect in time with their children than in time without. Mothers reported less happiness, more stress, and more fatigue in that same time than fathers did.

Some of the difference had to do with context. Mothers spent twice as much time on basic care as on play, while fathers split those activities evenly. A partner was present for 31% of mothers’ time with their kids, compared to 61% for fathers. But even after accounting for activity type, solo parenting, sleep, and leisure, mothers were still more tired. That’s the part I keep thinking about, because avoiding fatigue is the whole point of a holiday.

Holiday-specific research is thin and mostly qualitative, though it exists. A study of self-catering trips found that mothers’ domestic roles largely persisted through the holiday [6]. A more recent interview study found women, and mothers especially, still did more of the housework in home-like accommodation, while hotels shifted couples toward a more equal split, because somebody else does the cooking and the cleaning [7].

Thinking about our own holiday trips, not just the data. A family holiday takes away the school run, the office, and the usual bedtime routine. But it also removes the structure that decides who does what, so the usual patterns take over. Someone still has to find the pharmacy, pack the bags, remember what each child ate, and handle bedtime in a room without blackout curtains. That person is running a household in an unfamiliar kitchen with worse tools and no schedule to lean on. It feels more like a business trip than a real break.

This is part of the Recover part of my Upward ARC framework, and a holiday is usually the biggest chunk of recovery time you get all year. Many executives spend it feeling refreshed, while someone else in the house is running an under-resourced operation in a place where they can’t even find the scissors.

What the trip does to you

The good news is that holidays do work, and they work better than I once thought. Ty Ferguson’s team tracked movement using Fitbits on 308 Australian parents of primary school kids, over 13 months and 9,778 holiday days across 806 trips [8]. The average age was 40, and most had two or three kids at home.

During holidays, they slept about 21 minutes more each night, did about 5 more minutes of moderate-to-vigorous activity, and sat about half an hour less each day. The extra sleep lasted even after the trip, staying 8 minutes above normal in the first week back and 7 minutes in the second.

Their light activity dropped, though. All the small movements that fill a normal day went down by about 10 minutes a day in the first week back and stayed about 10 minutes below normal even four weeks later. So they came home sleeping a bit more, but moving less, and that lasted a month.

Where this gets shaky

In an earlier edition, I said a holiday doesn’t fix burnout, and last summer I called that idea complete “bullshit.” I still don’t think two weeks in Greece will cure a burnt-out executive. But I underestimated the effect. The evidence I used came from seven studies [9]. A much bigger analysis last year looked at 32 studies and found a larger benefit that fades more slowly [2]. Another analysis, which reworks the original data instead of testing it independently, still finds the benefit gone within a week [10].

There is more uncertain ground. Detachment is the best sign researchers have that you’ve left work behind, but calling it the main driver of recovery is a stretch. In one Dutch study of 54 people, detachment didn’t link to health or wellbeing during or after the holiday [11]. The biggest review found it lowers exhaustion, but doesn’t clearly boost engagement or performance; relaxation and mastery do that instead [12]. Most of this research is based on self-reported questionnaires, and the holiday-specific studies on households are just a few interviews.

Try this today

Divide up the responsibilities before you leave, and write them down. Give each parent two hours completely off and unreachable by anyone under 140cm, then switch. If you just play it by ear, the usual patterns take over, just like in Musick’s study [5]. No one has tested this, so it’s my practical suggestion, not a proven method. Have this talk at home on a Tuesday when you’re both calm.

Consider choosing a hotel instead of a rental. This is the most useful thing I learned while writing this. In the interview study mentioned earlier, staying in a home-like place kept the usual domestic roles going, while hotels led to a more equal split, mainly because someone else does the cooking and cleaning [7]. It’s a small study with just ten couples and wasn’t meant to test your family, but it’s still worth considering.

Take care of the month after you get back. Schedule some movement before you leave. Ferguson’s study found people were still about 10 minutes a day below their usual light activity four weeks after returning [8], and most don’t notice. As a doctor, I recommend adjusting your wake-up time gradually over the first few mornings and keeping your caffeine intake close to your usual amount and timing until you’ve settled in. That’s standard circadian hygiene, and it’s what I do myself.

Deal with the mental loop in your head. Airplane mode is the simple fix. What really predicts a rough return is negative work reflection. That’s the technical term for lying by the pool and thinking about everything wrong with your job. In a study of 221 employees, those who did this came back with more health complaints and more exhaustion, even two weeks later [13]. If you catch yourself going over a decision, write down the one action you’ll take when you’re back, put it somewhere you’ll see it, and then let it go.

Pay attention to your first login when you get home. If your password doesn’t come to you right away, take it as a personal sign that you really let go of a work habit. It won’t tell you if the holiday worked, but it’s an easy thing to notice.

If you are in a senior role, say it out loud. Tell people you will be unreachable, then be unreachable. Buechel and Solinas found that a formal no-weekend-email policy may reduce the promotion penalty [3], and detachment turns out to be learnable, with the biggest gains in older people and those who began with health or recovery-related issues [14].

The price of the quiet

It took eleven days without work on my mind, a surrendered passport, a driver, two guides, and a skills test from a stranger in a Pyongyang hospital to get that kind of mental break. That’s a ridiculous amount of effort for something we’re supposed to manage on a regular holiday.

The “wild places to visit before kids” list is in a drawer now. We have three children, the holidays are louder and shorter and considerably more negotiated, and I have stopped expecting any of them to feel like North Korea.

What I want to know is whether at some point my hands forget the password, and whether my wife’s do, too.

One question, and I read every reply. What is the one thing your head refuses to put down when you are away? Name it in a sentence.

Stay healthy.

Andre

PS: If you are the one in your house who books the pharmacy run and knows which child ate what, this edition was written with you in mind. Send it to the person you are on holiday with. That’s the way this newsletter grows, and it’s the only way I want it to.

PPS: If a friend forwarded this to you, you can get Under Load, my Sunday edition, here:

https://www.andreheeg.com

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References

[1] Sonnentag, S., & Fritz, C. (2007). The Recovery Experience Questionnaire: Development and validation of a measure for assessing recuperation and unwinding from work. Journal of Occupational Health Psychology, 12(3), 204-221. https://doi.org/10.1037/1076-8998.12.3.204

[2] Grant, R. S., Buchanan, B. E., & Shockley, K. M. (2025). I need a vacation: A meta-analysis of vacation and employee well-being. Journal of Applied Psychology, 110(7), 887-905. https://doi.org/10.1037/apl0001262

[3] Buechel, E. C., & Solinas, E. (2025). The detachment paradox: Employers recognize the benefits of detachment for employee well-being and performance, yet penalize it in employee evaluations. Organizational Behavior and Human Decision Processes, 188, 104403. https://doi.org/10.1016/j.obhdp.2025.104403

[4] Kühner, C., Rudolph, C. W., Derks, D., Posch, M., & Zacher, H. (2023). Technology-assisted supplemental work: A meta-analysis. Journal of Vocational Behavior, 142, 103861. https://doi.org/10.1016/j.jvb.2023.103861

[5] Musick, K., Meier, A., & Flood, S. (2016). How parents fare: Mothers’ and fathers’ subjective well-being in time with children. American Sociological Review, 81(5), 1069-1095. https://doi.org/10.1177/0003122416663917

[6] Mottiar, Z., & Quinn, D. (2012). Is a self-catering holiday with the family really a holiday for mothers? Examining the balance of household responsibilities while on holiday from a female perspective. Hospitality & Society, 2(2), 197-214. https://doi.org/10.1386/hosp.2.2.197_1

[7] Yao, X., Hua, C., & Jordan, E. J. (2025). Housework stress in home and travel living spaces: A gender space and housework industrialization perspective. Annals of Tourism Research, 112, 103937. https://doi.org/10.1016/j.annals.2025.103937

[8] Ferguson, T., Curtis, R., Fraysse, F., Olds, T., Dumuid, D., Brown, W., Esterman, A., & Maher, C. (2023). How do 24-h movement behaviours change during and after vacation? A cohort study. International Journal of Behavioral Nutrition and Physical Activity, 20(1), 24. https://doi.org/10.1186/s12966-023-01416-2

[9] de Bloom, J., Kompier, M., Geurts, S., de Weerth, C., Taris, T., & Sonnentag, S. (2009). Do we recover from vacation? Meta-analysis of vacation effects on health and well-being. Journal of Occupational Health, 51(1), 13-25. https://doi.org/10.1539/joh.K8004

[10] Speth, F., Wendsche, J., & Wegge, J. (2023). We continue to recover through vacation!: Meta-analysis of vacation effects on well-being and its fade-out. European Psychologist, 28(4), 274-287. https://doi.org/10.1027/1016-9040/a000518

[11] de Bloom, J., Geurts, S. A. E., & Kompier, M. A. J. (2013). Vacation (after-)effects on employee health and well-being, and the role of vacation activities, experiences and sleep. Journal of Happiness Studies, 14(2), 613-633. https://doi.org/10.1007/s10902-012-9345-3

[12] Headrick, L., Newman, D. A., Park, Y. A., & Liang, Y. (2023). Recovery experiences for work and health outcomes: A meta-analysis and recovery-engagement-exhaustion model. Journal of Business and Psychology, 38(4), 821-864. https://doi.org/10.1007/s10869-022-09821-3

[13] Fritz, C., & Sonnentag, S. (2006). Recovery, well-being, and performance-related outcomes: The role of workload and vacation experiences. Journal of Applied Psychology, 91(4), 936-945. https://doi.org/10.1037/0021-9010.91.4.936

[14] Karabinski, T., Haun, V. C., Nübold, A., Wendsche, J., & Wegge, J. (2021). Interventions for improving psychological detachment from work: A meta-analysis. Journal of Occupational Health Psychology, 26(3), 224-242. https://doi.org/10.1037/ocp0000280

What?

Researchers at Cedars-Sinai followed 354,957 adults in the UK Biobank for a median of 13 years, published July 1 in Clinical Gastroenterology and Hepatology. Against people who drank none, those drinking 5 or more cups a day had 32% less cirrhosis, 47% less liver cancer and 42% fewer liver-related deaths. They backed it with MRI scans on 28,961 of them: less liver fat, less iron, less scarring. Caffeinated and decaf tracked the same. The study is observational, and its authors said they would not tell anyone to start drinking coffee for their liver.

So what?

Hold that headline loosely, and I’ll go first. In January I wrote a full coffee playbook and told you liver risk drops 40 to 50 percent in habitual drinkers. That came from a real umbrella review. I’d write it with more caution now, because of a paper I missed: in 2024, a reanalysis in the journal Nutrients ran 455,870 people from the same biobank with tighter statistical control, and the liver-mortality benefit vanished. The authors concluded that earlier studies might have overestimated coffee’s effect on the liver.

So the direction is probably real, and the scans make it more believable than the usual coffee headline. The size is probably flattered. People who drink 5 cups a day and volunteer for a biobank are not average people.

Two things in the new paper do hold up, and both are usable today. Decaf carried the same signal, so moving your afternoon cup to decaf costs you nothing on the liver side. And people who sweetened their coffee kept the risk reductions but had 1.36 times the odds of a raised scan marker for liver inflammation and scarring. One marker, one cohort, not proof. It’s also the only coffee variable in the study that moved the wrong way, and the only one you can change before lunch.

Now what?

• Hold your count. If you drink 2 to 4 cups, stay there. The study authors don’t recommend climbing to 5.

• Take it black. If you sweeten, take it out of the first cup this week and the rest next week.

• Push the afternoon cup to decaf. Count back 9 to 10 hours from your bedtime for the caffeine cutoff. Bed at 11pm means last call at 1 or 2pm.

• Keep the paper filter. Drip and pour-over strip out the oils that raise LDL cholesterol. French press, moka pot and espresso leave them in.

Science moves. Correcting a line in public beats defending it. Take the sugar out of the cup.

Stay healthy.

Andre

After your run, while you’re still catching your breath, you could step through a glass door and be in a chair with an IV in your arm before your heart rate even drops. On one side, people put in the slow, steady effort that really keeps you healthy. On the other, someone built a business on the idea that you could skip all that. Just a bag of vitamins, forty minutes, and you leave feeling younger.

I stood in the hallway between the two doors longer than I planned. There was no doctor’s name on the glass and no hours listed. Just a logo and a price list. I was traveling for work and felt tired, and I remember thinking how odd it was that this was now a hotel amenity, somewhere between the sauna and the minibar.

Some time ago, I wrote about similar clinics opening in Berlin and thought the whole trend was just another fad that would fade away. The IV bars, the rapamycin talk at dinner, the NAD+ everyone mentioned. I thought the craze had ended.

But last Sunday, a 27-year-old woman went into a clinic in the Bronx for an NAD+ infusion. She never walked out.

She lost consciousness just minutes after the IV began and was pronounced dead later that afternoon [1]. As I write this, no one knows exactly what caused her death. It could have been the molecule, the dose, the method, or something else entirely. The person who gave her the IV told police he wasn’t licensed to practice medicine in New York.

I read the news on my phone and thought about it for a while. It wasn’t the science that surprised me, but I had let myself believe we were past this. We’re not.

There’s a simple reason these things are so popular. We want something that promises big results, feels certain, comes quickly, and doesn’t take much effort. A drip offers all of that at once. Be younger today, without the training, the sleep, or the years of work. Real health doesn’t offer shortcuts, because what really works is slow, takes effort, and rarely feels certain.

The drip sounds great when someone is selling it. But the problems show up in real studies. So I spent the last week looking at actual human research on these molecules. The results are tough to read.

The test that keeps saying no

Let’s start with the drug that has the best story: rapamycin. In mice, it works. When given to genetically varied mice, it makes them live longer. This is one of the most repeated results in the field [2]. That part is real.

But when it comes to people, the story changes. The biggest and longest trial of low-dose rapamycin in healthy adults, called PEARL, lasted 48 weeks. It was mostly a safety study, and for safety it looked fine. But for what people actually want, it came up empty: the visceral fat it was supposed to reduce didn’t change, and the epigenetic aging clock didn’t move [3]. There were a couple of small positive signs in a subgroup of women, on lean mass and pain. None of this tells you if rapamycin helps people live longer. No human trial has ever been set up to answer that, because you can’t just run a 40-year study. That answer is still far away. Right now, people are treating a guess as if it’s proof.

This is the pattern for almost everything in the drawer. Most of these are mouse studies. There’s a strict, independent check they have to pass: the Interventions Testing Program. It’s a government-run test that tries the same compound in genetically diverse mice across three labs at once, so one lucky lab can’t fake a win.

A lot of promising results don’t survive this test. Acarbose, a diabetes drug, extends life in that test, but mostly in males (22% longer median life in males, 5% in females) [4]. In the one large human trial that mattered, with 6,522 people who had heart disease and prediabetes, it did nothing for cardiac events [5]. Fisetin, the supplement sold to clear your “zombie cells,” did not extend lifespan in the mouse test, and in a completed knee-arthritis trial it did no better than placebo on pain, function, or cartilage [6][7]. Alpha-ketoglutarate, the main ingredient in the supplement Rejuvant, failed the same mouse test in 2026 [8].

Taurine is the clearest example. In 2023, a paper in Science said taurine drops as we age and that giving more to mice made them live about 10% longer. The internet ran with it [9]. Two years later, a bigger study followed people and animals over time and found taurine doesn’t consistently fall with age. The main claim, that taurine drops with age, didn’t hold up [10]. That’s how science works. The problem starts when someone sells the first result before the second even comes out.

Chasing a number

Supplements play a subtler game. They change a number in your blood and make you think that number means you’re healthier.

NAD+ is the main attraction. NMN and nicotinamide riboside, the two top sellers, really do raise NAD+ in your blood. For nicotinamide riboside, one careful study measured a jump of 40 to 60% [11]. That’s true, and that’s where the marketing ends. When researchers checked if anything you actually care about improved, the answer was still no. The one positive NMN trial looked at 25 prediabetic women. It improved insulin sensitivity in muscle and a few related signaling measures, but nothing you would notice in your life, and it started with the two groups unevenly matched [12]. When eight NMN trials were combined, about 342 people, there was no benefit to blood sugar, insulin, HbA1c, or cholesterol [13]. The best nicotinamide riboside trials found the same flat results on the things that matter [14]. You’re paying to raise a number that no human trial has linked to a longer or better life.

Resveratrol, the old red-wine molecule, is even worse. The whole idea was that it switches on a longevity enzyme called SIRT1. The famous result came from a test that was set up in a way that produced misleading activation. Later work found resveratrol can nudge SIRT1 only for certain substrates, far more narrowly than the original story claimed [15]. When researchers followed older adults for years, those with more resveratrol in their bodies were no less likely to die or get heart disease or cancer [16].

Then there’s alpha-ketoglutarate, sold with the boldest claim of all: “8 years younger.” That number comes from a single report on 42 people who had already bought the product, with no comparison group, measured on a special aging clock from a lab connected to the company [17]. Even the authors say a real trial is needed. It’s basically a testimonial with a p-value.

Who paid for the study

Once you start reading these papers, you notice the same names keep showing up in two places: in the study, and at the company selling the product the study is about.

The PEARL rapamycin trial was run by staff from a telehealth company that prescribes rapamycin. All seven authors were employees and shareholders, though to be fair, most of the funding came from crowdfunding [3]. The two main trials behind Urolithin A, sold as Mitopure, were funded by the company selling it, and both missed their main muscle targets. The strength number on the label came from a secondary result the trial wasn’t mainly designed to prove [18]. The best trial of spermidine, a full year in older adults with memory complaints, found nothing [19].

Even the rules can’t keep up. In 2022, the FDA ruled that NMN could not be sold as a supplement, because it had first been studied as a drug. In 2025 it reversed course and made it legal again [20]. The bottle in your cabinet comes from a regulator that changed its position inside three years.

At the far, unregulated end of all this is a clinic on a top floor, or on a Bronx side street, with a bag on a pole and no one qualified to use it. Most of the time, the gap between the science and the sales pitch is just about money. Once in a while, like in the Bronx last week, it ends with someone dead and no one able to say why.

The one you can keep

I didn’t write all this to say everything is fake. One thing in the drawer actually belongs there. Creatine, the cheap powder from the gym, has real evidence in people.

When combined with lifting, in people over 50, creatine adds a small amount of muscle and a bit of strength [21]. It may also help the aging brain: across trials, it gives a modest boost to memory, small on average and drawn mostly from a couple of small studies in older adults, with almost nothing in the young [22]. If someone takes a big single dose after a sleepless night, it measurably protects their thinking for a few hours [23].

The brain effect mostly shows up when you’re already low, older, or sleep-deprived, and usually at doses much higher than the 3 to 5 grams people actually take. When a creatine company asked European regulators if they could claim the powder sharpens thinking, the regulators looked at all the evidence and said no [24]. The newer headlines about “creatine helps you live longer” are based on surveys of what people eat, not real trials. The study’s author has a commercial tie to creatine, an advisory-board seat, and related patents, and the effect almost disappears when you account for the obvious [25]. So use creatine to help your training, and if you’re older, maybe your memory. But not to add years.

Look at where creatine’s benefits come from. The muscle gain only happens if you lift. The brain benefit mostly shows up when you’re older or short on sleep. Both point back to the same basics: sleep and training.

The clearest sign that this whole category has it backward is metformin. It’s a good, affordable diabetes drug and a popular choice for longevity. But two separate randomized trials found that in older adults, metformin reduces the muscle you gain from resistance training [26] and lessens the improvement in insulin sensitivity that exercise usually brings [27]. The so-called longevity pill actually interferes with exercise, one of the few things that genuinely extends healthy life. For a healthy person without diabetes, it works against the very thing that keeps you alive longer.

A fair question is that most of these are cheap and safe, so why not hedge your bets? I think a pill you believe in quietly tells you that you’ve taken care of your longevity, and that belief can keep a busy person out of the gym. And the hedge isn’t always free. You just saw what metformin does to the training that actually works.

This is the Capacity pillar of the Upward ARC, the framework I write about here. It’s about the limit on what your body and mind can still do in 20 years. You can’t buy a higher limit while sitting in a chair. You raise it slowly, with habits that build up over time, and most of them are free.

Try this today

Before you take any supplement, ask yourself three questions. Is there a human trial, not just a mouse study? Who paid for that trial? And is the result just a marker, or a real outcome on something that actually matters, like living longer or getting sick less? Most of the options in the drawer fail the first question.

Put your money and effort where the evidence is strongest: into your muscles. A study of 147,374 adults followed for up to 30 years found that 90 to 120 minutes a week of strength training was linked to about a 13% lower chance of dying, with no extra benefit above two hours, and bigger drops in death from heart and neurological disease [28]. That’s an association, not a trial. It’s the same kind of evidence I’ve questioned throughout this piece. But here, every layer agrees: the mechanism, the trials on strength and function, and the population data all point the same way. With the supplements, each layer comes back empty or biased. Exercise is the real medicine. It costs nothing and comes with the side effect of a body that works.

If you want one supplement that’s earned its place, take creatine, 3 to 5 grams a day, alongside your training, not instead of it. That’s the honest way to use it.

And if a number on your body is really worrying you, talk to a doctor who has nothing to sell you, not a clinic that profits from saying yes.

The two doors

Those two doors are still there, ten steps apart on that hotel floor. The gym and the drip clinic.

Everything on the drip side is designed to fit the sales formula: fast, certain, easy, and dressed up as science. Almost none of it holds up when you look at the actual studies. Everything on the gym side doesn’t fit that formula because it’s slow, hard, and quiet. But it’s the only side with real evidence behind it.

A woman is dead, and no one can yet say why. What fills these clinics isn’t a strange or foolish wish. It’s the same one we all have: wanting the good outcome without the long, boring cost. The real work, if you know how or have someone to help, is to notice when a promise sounds too perfect and ask who’s selling it.

One honest question before you go: What’s the one thing in your own longevity drawer that you’ve never actually checked the evidence on? Reply and tell me. I read every message.

I still walk into hotel gyms. I’ve never once walked into the clinic next door.

Stay healthy.

Andre

PS: If you know a friend about to spend real money on a drip or a shelf of these bottles, send this to them first. Be kind about it. That’s how this newsletter grows, and it’s the only way I want it to.

PPS: Wednesdays are now a thing too. The Next Move is a two-minute mid-week short I started this month: one finding, what it means for you, and one action. It runs alongside these Sunday pieces, not instead of them.

PPPS: If a friend sent you this, you can get The Upward ARC here: https://www.andreheeg.com

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References

[1] Kriegstein, B. (2026, July 21). NYPD says unlicensed Bronx doc admitted “I made a very big mistake” after woman died. Gothamist. https://gothamist.com/news/nypd-says-unlicensed-bronx-doc-admitted-i-made-a-very-big-mistake-after-woman-died

[2] Harrison, D. E., Strong, R., Sharp, Z. D., Nelson, J. F., Astle, C. M., Flurkey, K., Nadon, N. L., Wilkinson, J. E., Frenkel, K., Carter, C. S., Pahor, M., Javors, M. A., Fernandez, E., & Miller, R. A. (2009). Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature, 460(7253), 392-395. https://doi.org/10.1038/nature08221

[3] Moel, M., Harinath, G., Lee, V., Nyquist, A., Morgan, S. L., Isman, A., & Zalzala, S. (2025). Influence of rapamycin on safety and healthspan metrics after one year: PEARL trial results. Aging, 17(4). https://doi.org/10.18632/aging.206235

[4] Harrison, D. E., Strong, R., Allison, D. B., Ames, B. N., Astle, C. M., Atamna, H., Fernandez, E., Flurkey, K., Javors, M. A., Nadon, N. L., Nelson, J. F., Pletcher, S., Simpkins, J. W., Smith, D., Wilkinson, J. E., & Miller, R. A. (2014). Acarbose, 17-α-estradiol, and nordihydroguaiaretic acid extend mouse lifespan preferentially in males. Aging Cell, 13(2), 273-282. https://doi.org/10.1111/acel.12170

[5] Holman, R. R., Coleman, R. L., Chan, J. C. N., Chiasson, J.-L., Feng, H., Ge, J., Gerstein, H. C., Gray, R., Huo, Y., Lang, Z., McMurray, J. J., Rydén, L., Schröder, S., Sun, Y., Theodorakis, M. J., Tendera, M., Tucker, L., Tuomilehto, J., Wei, Y., … Hu, D. (2017). Effects of acarbose on cardiovascular and diabetes outcomes in patients with coronary heart disease and impaired glucose tolerance (ACE): A randomised, double-blind, placebo-controlled trial. The Lancet Diabetes & Endocrinology, 5(11), 877-886. https://doi.org/10.1016/S2213-8587(17)30309-1 (Note: trial funded by Bayer, the drug’s maker; acarbose reduced new-onset diabetes by ~18% but had no effect on the cardiovascular primary endpoint.)

[6] Harrison, D. E., Strong, R., Reifsnyder, P., Rosenthal, N., Korstanje, R., Fernandez, E., Flurkey, K., Ginsburg, B. C., Murrell, M. D., Javors, M. A., Lopez-Cruzan, M., Nelson, J. F., Willcox, B. J., Allsopp, R., Watumull, D. M., Watumull, D. G., Cortopassi, G., Kirkland, J. L., Tchkonia, T., … Miller, R. A. (2024). Astaxanthin and meclizine extend lifespan in UM-HET3 male mice; fisetin, SG1002 (hydrogen sulfide donor), dimethyl fumarate, mycophenolic acid, and 4-phenylbutyrate do not significantly affect lifespan in either sex at the doses and schedules used. GeroScience, 46(1), 795-816. https://doi.org/10.1007/s11357-023-01011-0

[7] Tashman, et al. (2025). Results from a randomized clinical trial evaluating the senolytic fisetin for treating knee osteoarthritis [Conference abstract]. Osteoarthritis and Cartilage, 33(Suppl.). https://doi.org/10.1016/j.joca.2025.02.667 [PIN: conference abstract, not a full article; primarily a safety trial with efficacy as a secondary outcome; confirm full author list]

[8] Korstanje, R., Strong, R., Salmon, A. B., Bogue, M. A., Curran, S. P., Diaz, V., Fernandez, E., Ginsburg, B., Han, M., Harrison, D. E., Kaczorowski, C., Kaeberlein, M., Kennedy, B. K., Kumar, N., LaCroix-Fralish, M., Leiser, S. F., Nelson, J. F., Polymenis, M., Reifsnyder, P. C., … Miller, R. A. (2026). Astaxanthin, meclizine, mitoglitazone, pioglitazone, alpha-ketoglutarate, mifepristone, methotrexate, and atorvastatin-telmisartan do not increase lifespan in UM-HET3 mice. GeroScience, 48(3), 3821-3830. https://doi.org/10.1007/s11357-026-02201-2 (The ITP tested alpha-ketoglutarate; the AKG in the supplement Rejuvant is the calcium salt. The salt form of the tested compound was not verified from the accessible abstract.)

[9] Singh, P., Gollapalli, K., Mangiola, S., Schranner, D., Yusuf, M. A., Chamoli, M., … Yadav, V. K. (2023). Taurine deficiency as a driver of aging. Science, 380(6649), eabn9257. https://doi.org/10.1126/science.abn9257

[10] Fernandez, M. E., Bernier, M., Price, N. L., Camandola, S., Aon, M. A., Vaughan, K., Mattison, J. A., Preston, J. D., Jones, D. P., Tanaka, T., Tian, Q., González-Freire, M., Ferrucci, L., & de Cabo, R. (2025). Is taurine an aging biomarker? Science, 388(6751), eadl2116. https://doi.org/10.1126/science.adl2116

[11] Martens, C. R., Denman, B. A., Mazzo, M. R., Armstrong, M. L., Reisdorph, N., McQueen, M. B., Chonchol, M., & Seals, D. R. (2018). Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nature Communications, 9, 1286. https://doi.org/10.1038/s41467-018-03421-7 (Tests nicotinamide riboside, not NMN; the ~40-60% NAD+ rise in the text is scoped to NR accordingly.)

[12] Yoshino, M., Yoshino, J., Kayser, B. D., Patti, G. J., Franczyk, M. P., Mills, K. F., Sindelar, M., Pietka, T., Patterson, B. W., Imai, S., & Klein, S. (2021). Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science, 372(6547), 1224-1229. https://doi.org/10.1126/science.abe9985

[13] Chen, F., Zhou, D., Kong, A. P.-S., Yim, N. T., Dai, S., Chen, Y. N., & Hui, L. L. (2024). Effects of nicotinamide mononucleotide on glucose and lipid metabolism in adults: A systematic review and meta-analysis of randomised controlled trials. Current Diabetes Reports, 25(1), Article 4. https://doi.org/10.1007/s11892-024-01557-z

[14] Dollerup, O. L., Christensen, B., Svart, M., Schmidt, M. S., Sulek, K., Ringgaard, S., Stødkilde-Jørgensen, H., Møller, N., Brenner, C., Treebak, J. T., & Jessen, N. (2018). A randomized placebo-controlled clinical trial of nicotinamide riboside in obese men: Safety, insulin-sensitivity, and lipid-mobilizing effects. The American Journal of Clinical Nutrition, 108(2), 343-353. https://doi.org/10.1093/ajcn/nqy132

[15] Pacholec, M., Bleasdale, J. E., Chrunyk, B., Cunningham, D., Flynn, D., Garofalo, R. S., Griffith, D., Griffor, M., Loulakis, P., Pabst, B., Qiu, X., Stockman, B., Thanabal, V., Varghese, A., Ward, J., Withka, J., & Ahn, K. (2010). SRT1720, SRT2183, SRT1460, and resveratrol are not direct activators of SIRT1. Journal of Biological Chemistry, 285(11), 8340-8351. https://doi.org/10.1074/jbc.M109.088682 (Later work, e.g. Hubbard et al., 2013, Science, found substrate-dependent direct activation; the text is worded to reflect that the broad-activation story was overstated, not that no activation occurs.)

[16] Semba, R. D., Ferrucci, L., Bartali, B., Urpí-Sardà, M., Zamora-Ros, R., Sun, K., Cherubini, A., Bandinelli, S., & Andres-Lacueva, C. (2014). Resveratrol levels and all-cause mortality in older community-dwelling adults. JAMA Internal Medicine, 174(7), 1077-1084. https://doi.org/10.1001/jamainternmed.2014.1582

[17] Demidenko, O., Barardo, D., Budovskii, V., Finnemore, R., Palmer, F. R., III, Kennedy, B. K., & Budovskaya, Y. V. (2021). Rejuvant, a potential life-extending compound formulation with alpha-ketoglutarate and vitamins, conferred an average 8 year reduction in biological aging, after an average of 7 months of use, in the TruAge DNA methylation test. Aging, 13(24), 24485-24499. https://doi.org/10.18632/aging.203736 (Biological age read on the TruMe/TruAge methylation clock, from a lab with a service agreement to the product company.)

[18] Liu, S., D’Amico, D., Shankland, E., Bhayana, S., Garcia, J. M., Aebischer, P., Rinsch, C., Singh, A., & Marcinek, D. J. (2022). Effect of urolithin A supplementation on muscle endurance and mitochondrial health in older adults: A randomized clinical trial. JAMA Network Open, 5(1), e2144279. https://doi.org/10.1001/jamanetworkopen.2021.44279 (with Singh, A., et al. (2022), ATLAS trial, Cell Reports Medicine — peak-power primary endpoint not met; positive strength/endurance results were prespecified secondary endpoints; funded by Amazentis, with author employees/shareholders/patent holders.)

[19] Schwarz, C., Benson, G. S., Antonenko, D., Horn, N., Köbe, T., Klimecki, O., Sommer, W., Wirth, M., & Flöel, A. (2022). Effects of spermidine supplementation on cognition and biomarkers in older adults with subjective cognitive decline (SmartAge): A randomized clinical trial. JAMA Network Open, 5(5), e2213875. https://doi.org/10.1001/jamanetworkopen.2022.13875

[20] U.S. Food and Drug Administration. (2022, November). Responses to new dietary ingredient notifications for β-nicotinamide mononucleotide (NDIN 1247, SyncoZymes; NDIN 1259, Inner Mongolia Kingdomway): NMN excluded from the dietary-supplement definition under FD&C Act § 201(ff)(3)(B), the drug-preclusion provision. Regulations.gov docket FDA-2022-S-0023. https://www.regulations.gov/docket/FDA-2022-S-0023. Reversed by FDA determination letters dated September 29, 2025 (D. Prater), concluding NMN is not excluded; reported in Daniells, S. (2025, September 30), FDA declares NMN lawful in dietary supplements, NutraIngredients-USA, https://www.nutraingredients.com/Article/2025/09/30/fda-declares-nmn-lawful-in-dietary-supplements/. A legal-classification decision, not a ruling on safety or effectiveness.

[21] Liu, S., Huang, N., Wu, W., OuYang, X., Luo, Y., Zhong, Y., Wang, M., & Xiao, L. (2025). The impact of creatine supplementation associated with resistance training on muscular strength and lean tissue mass in the aged: A systematic review and meta-analysis. European Review of Aging and Physical Activity, 22, Article 26. https://doi.org/10.1186/s11556-025-00392-9

[22] Prokopidis, K., Giannos, P., Triantafyllidis, K. K., Kechagias, K. S., Forbes, S. C., & Candow, D. G. (2023). Effects of creatine supplementation on memory in healthy individuals: A systematic review and meta-analysis of randomized controlled trials. Nutrition Reviews, 81(4), 416-427. https://doi.org/10.1093/nutrit/nuac064 (Older-adult memory benefit rests on a small subgroup, ~57 participants across 2 studies, with high heterogeneity.)

[23] Gordji-Nejad, A., Matusch, A., Kleedörfer, S., Jayeshkumar Patel, H., Drzezga, A., Elmenhorst, D., Binkofski, F., & Bauer, A. (2024). Single dose creatine improves cognitive performance and induces changes in cerebral high energy phosphates during sleep deprivation. Scientific Reports, 14, 4937. https://doi.org/10.1038/s41598-024-54249-9 (Single 0.35 g/kg dose, roughly 25-35 g, well above the usual 3-5 g maintenance dose.)

[24] EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA); Turck, D., Bohn, T., et al. (2024). Creatine and improvement in cognitive function: Evaluation of a health claim pursuant to Article 13(5) of Regulation (EC) No 1924/2006. EFSA Journal, 22(12), e9100. https://doi.org/10.2903/j.efsa.2024.9100 (EU Commission refusal, 2026)

[25] Ostojic, S. M. (2025). Dietary creatine intake and all-cause mortality among U.S. adults: A linked mortality analysis from the NHANES study. Applied Physiology, Nutrition, and Metabolism, 50, 1-6. https://doi.org/10.1139/apnm-2025-0001 (Single-author paper. Observational dietary-intake association, not a supplementation trial; author disclosed an AlzChem creatine advisory-board seat and creatine-related patents; no study sponsor/funder reported.)

[26] Walton, R. G., Dungan, C. M., Long, D. E., Tuggle, S. C., Kosmac, K., Peck, B. D., Bush, H. M., Villasante Tezanos, A. G., McGwin, G., Windham, S. T., Ovalle, F., Bamman, M. M., Kern, P. A., & Peterson, C. A. (2019). Metformin blunts muscle hypertrophy in response to progressive resistance exercise training in older adults: The MASTERS trial. Aging Cell, 18(6), e13039. https://doi.org/10.1111/acel.13039 (NIH-funded.)

[27] Konopka, A. R., Laurin, J. L., Schoenberg, H. M., Reid, J. J., Castor, W. M., Wolff, C. A., Musci, R. V., Safairad, O. D., Linden, M. A., Biela, L. M., Bailey, S. M., Hamilton, K. L., & Miller, B. F. (2019). Metformin inhibits mitochondrial adaptations to aerobic exercise training in older adults. Aging Cell, 18(1), e12880. https://doi.org/10.1111/acel.12880 (Cited for the significant blunting of exercise-induced insulin sensitivity, p=0.02; the VO2max reduction in the same trial was a non-significant trend, p=0.08, and is not claimed in the text. Supported in part by Dairy Management, Inc. and Dexcom, Inc., not government funding.)

[28] Zhang, Y., Lee, D. H., Rezende, L. F. M., Ma, Y., & Giovannucci, E. (2026). Long-term resistance training with all-cause and cause-specific mortality: Assessing dose-response and joint associations with aerobic physical activity. British Journal of Sports Medicine, 60(12), 874-883. https://doi.org/10.1136/bjsports-2025-110503 (Harvard T.H. Chan cohort, 147,374 adults, up to 30 years; 90-119 min/week resistance training associated with ~13% lower all-cause mortality, HR ~0.87, plateau ~120 min, with larger reductions in cardiovascular and neurological mortality. Observational association.)

Sometimes I’d get half an hour of sleep, maybe a few hours if the night was quiet. Then the pager would go off, and I’d rush down the corridor into the bright trauma bay, where someone needed their face rebuilt. As a young reconstructive surgeon, I worked 24- and 36-hour weekend shifts. You learn two rules quickly, and they’re really the same: eat when there’s food, not just when you’re hungry, and sleep when there’s time, not just when you’re tired. You never know when the next call will come. So you lie down, fall asleep in minutes, and get rest whenever you can.

Maybe I was lucky, or maybe I learned it under pressure. Either way, I could fall asleep on a hard bed in a noisy hospital with a pager on my chest, and then do it again a few hours later. I still sleep that way. After reading a page or two of a book, I’m out. You could move me to another room and I wouldn’t wake up.

On paper, that probably makes me the wrong person to write about sleep problems.

Sleep is the topic you ask me about most. Whenever someone new joins this newsletter, I ask what they’re looking for, and the answer I hear most often is sleep. Not how to make it perfect, but how to get any at all. How to fall asleep when your body is tired but your mind won’t stop. How to get back to sleep after waking at 3am with your thoughts racing, when it feels like the night is over even though there are still hours left.

That’s not my struggle, so I did the next best thing. I read what sleep experts say, looked through the research, and listened to dozens of your replies. Most sleep problems come down to one main issue with a real name, and the real solutions are rarely things you can buy.

The Night Shift

While you sleep, your body takes care of things it can’t do when you’re awake.

You might have heard that sleep clears the brain of the plaque linked to Alzheimer’s. It’s a good story, but it’s often overstated. The idea comes from a 2013 mouse study showing that sleeping brains cleared waste faster, including amyloid-beta [1]. But a 2024 mouse study found the opposite. The debate continues in animal studies.

The evidence in humans is less dramatic. If a healthy adult stays awake for one night, amyloid levels rise about 5% by morning [2]. Sleep brings those levels back down. Over many years, though, the risk adds up. One study followed nearly 8,000 adults for 25 years and found that those who slept six hours or less in midlife had about a 30% higher rate of dementia [3]. This is a link, not proof, since early disease can shorten sleep before symptoms appear. Still, a 30% increase over 25 years is hard to ignore.

The effects you feel the next day show up quickly. After just one night without sleep, your amygdala (the brain’s threat detector) becomes about 60% more active, while the part that keeps it in check gets quieter [4]. That’s why you might have a short fuse or make a decision at 4pm you wouldn’t make if you were rested. Your judgment slips before you even realize it.

The Hangover You Didn’t Drink For

If you lose sleep, your hormones start to show it within just a few days.

When healthy young men sleep only four hours a night for six nights, their blood sugar control becomes as poor as someone decades older and at risk for diabetes, all in less than a week [5]. A week of five-hour nights lowers their daytime testosterone by 10 to 15%, which is about what aging does over 10 to 15 years [6]. These are small studies in young men, so take the numbers with caution. Still, the trend is clear, and it explains why you might feel foggy on a Tuesday.

You also can’t make up for lost sleep on the weekend. When researchers had people sleep short nights and then let them sleep in, the extra rest didn’t fix the damage. Their blood sugar levels remained poor, and some even worsened because they ate more and shifted their sleep schedules later [7]. Sleeping in on Saturday doesn’t undo a week of short nights.

Your immune system notices too. In one study, healthy adults tracked their sleep for a week, then were exposed to a cold virus. Those who slept less than six hours were about four times more likely to get sick than those who got seven or more [8]. Same exposure, but a different defense.

The Basics, Fast

You already know the basics: get seven to eight hours, keep your room cool and dark, and avoid screens before bed. All of that is true, but it’s not the reason you’re lying awake. There are two less obvious things worth mentioning.

Consistency might matter more than total sleep time. In a study of 60,000 adults wearing wrist monitors, regular sleep patterns predicted longer life better than total hours slept [9]. Going to bed and waking up at the same time every day is better than sleeping in on Sunday to make up for lost sleep during the week. Your body runs on a clock, and it doesn’t like when that clock keeps changing.

And remember, you’re not the same as your neighbor. I’ve always woken up at first light. As a kid, I’d be up at seven while my cousin would sleep until someone dragged him out at eleven. Sleep is personal, even though most advice makes it seem like it isn’t.

Even careful people can get tripped up by two basics. Caffeine stays in your body for five to six hours, so a coffee at 4pm still has a quarter of its effect at 10pm. In one study, 400mg of caffeine six hours before bed cut sleep by more than an hour [10]. Alcohol can also backfire. It might help you fall asleep faster, but it breaks up the second half of the night and reduces your REM sleep. That’s why two glasses of wine can leave you wide awake at 4am, feeling like you never slept [11].

Why You Can’t Switch Off

For most high performers, the problem isn’t sleep itself. It’s the 90 minutes before bed, and a nervous system that stays active even after you lie down. Insomnia in someone who’s trying hard is really about being too alert. The body is too tense to relax, and trying to force sleep only makes it worse.

That’s why using a sleep tracker can sometimes make things worse. There’s even a name for it now: orthosomnia. Sleep doctors use this term for people who worry so much about getting a perfect sleep score that it actually ruins their sleep [12]. And those scores aren’t even that reliable. When researchers compared seven trackers to a sleep lab, the devices could tell sleep from waking, but missed 30 to 50% of deep and REM sleep [13]. People end up worrying about a deep-sleep number that the device is only guessing at.

Trying to sleep is often what keeps you awake. Clinicians call this sleep effort. The harder you try to fall asleep, the more you activate the alert, goal-focused part of your brain, which is exactly what sleep doesn’t need [14]. You can’t force yourself to sleep. The best you can do is stop getting in your own way.

This is the Recover part of my Upward ARC framework, which is about helping your nervous system return to calm between stresses. Sleep is also an input, so it connects to Activate as well. But the reason you’re awake is usually in Recover, and you can’t reset by trying harder. The reset happens when you slow down and stop pushing.

The Theory That Didn’t Survive

My wife is away tonight. She travels a few times a year, never far, and tonight she’s a few hours from here, still in Germany. The kids are asleep down the hall, and I’m the only adult in the house.

And here I am, lying in the dark with my eyes open.

This never happens to me. But tonight, I’m very aware of how deeply I usually sleep. If Karla calls out at 3am, the part of me that normally sleeps through anything won’t hear her. So I keep myself just below waking, listening, not willing to fall all the way asleep. For once, I can’t let go.

As I lay there, I thought I understood something. Maybe this is why so many women sleep more lightly than men. They keep an ear out for the kids, just like I was doing tonight, always a little alert. It seemed obvious, even a bit profound, at 1am. So I did what I always do now. I checked the data. And it humbled me.

Women do carry the heavier load. Insomnia is about 1.4 times more common in women than in men across more than a million people [15]. If you’re a woman reading this at 3am, that struggle is real, and I won’t wave it away with a lab result.

But when sleep is measured with electrodes rather than surveys, healthy women actually get more deep sleep than men of the same age, fall asleep faster, and spend more time asleep [16]. The hard nights are real, but so is the deeper sleep. The difference between the two is the real story.

My caretaker theory didn’t hold up. When researchers tested it directly, women woke up a little faster, but only to the faintest sounds, and just as quickly to a beeping alarm as to a baby’s cry [17]. That’s just a small difference in hearing. It’s not the mother’s radar I imagined. Who gets up at night depends on who’s on duty, and that’s shaped by life, not biology.

Two things explain the gap, and both are stronger than my late-night theory. On average, women go to bed with a more alert, worried mind, which breaks up sleep [18]. And women deal with hormonal changes, I never will. Throughout the monthly cycle, during pregnancy, and especially during menopause, sleep can really suffer. 40 to 60% of women say their sleep falls apart during menopause, mostly because they wake up during the night [19]. If that’s you, know this: you’re not failing at sleep, and you’re not imagining it. Your biology changed, and that deserves a real conversation with a doctor, not just a shrug or a supplement.

Try This Today

None of these are supplements or gadgets. These are the tools sleep clinicians actually use, organized by the kind of sleep problem you have.

If you can’t fall asleep, stop trying so hard. The effort itself is the problem, so take the pressure off. First, get tomorrow’s worries out of your head and onto paper. In one study, people who spent five minutes writing a to-do list for the next day fell asleep about nine minutes faster than those who wrote about their day [20]. The more specific your list, the better, because it helps your brain stop running through tasks. Next, slow your body down with your breath. Five minutes of cyclic sighing, a double breath in through the nose, and a long, slow breath out through the mouth calmed people better than meditation in a controlled trial [21]. The goal is to slow down, so sleep can come naturally.

If you wake up at 3am and can’t get back to sleep, get out of bed. It might feel wrong, but it works. If you’ve been awake for more than about 15 or 20 minutes (just by feel, not by watching the clock), get up. Leave the bedroom, sit somewhere dim, do something boring, and only go back to bed when you feel sleepy. This is called stimulus control, and it’s one of the best-proven tools [22]. Lying in bed, frustrated, teaches your brain that bed is a place to be awake and anxious, so you’re breaking that link. Also, remember that waking up in the night isn’t the emergency it feels like. For most of history, people slept in two shifts, with an hour of quiet awake time in between, and didn’t think anything of it [23]. Waking up is normal. It’s the panic that turns a 20-minute gap into a lost night.

If you wake up at every little sound, focus on fixing your room before trying to fix yourself. Make it cool, dark, and as quiet as possible. Earplugs or steady background noise can help cover sudden sounds that wake you up. One honest note: the machines that promise deeper sleep are overhyped. Steady sound can help mask a barking dog or a snoring partner, which is useful, but it doesn’t actually make your sleep deeper like the ads claim.

If you wake up every couple of hours, try spending less time in bed, not more. It might sound backward, but if you lie in bed for nine hours to get six hours of broken sleep, you’re actually training your body for broken sleep. Instead, shorten your time in bed to match the sleep you actually get, with a minimum of about five hours. Keep a fixed wake time, and let your sleep pressure build until your nights become more solid. Then, you can gradually increase your time in bed again. Even a nurse-led version of this approach worked better than standard advice in a large 2023 trial [24]. Also, rule out one thing: if you wake up tired no matter how long you sleep, and you snore, get checked for sleep apnea. Nearly a billion adults have it, most without knowing, and it’s common in middle-aged or heavier people [25]. No breathing trick can fix a blocked airway.

Most importantly, anchor your wake time. Get up at the same time every day. This is the strongest signal you can send your body clock [9], and it’s more effective than any bedtime rule, because morning light and a steady start set the tone for the rest of the day.

If you’ve been struggling for months, seek real treatment. Insomnia that happens three nights a week for three months or more is a diagnosable condition, and the best first treatment is cognitive behavioral therapy for insomnia (CBT-I), which major medical organizations recommend over sleeping pills [26]. It works. In studies, people fall asleep about 19 minutes faster and spend much less time awake at night, and the benefits last even after stopping [27]. Talk to your doctor, or try a reputable CBT-I app.

What the Pager Taught Me

I still fall asleep in an instant, and now I understand why. Those years in the trauma unit taught me, without me realizing it, how to lower my alertness on command. I could go from fully awake to asleep fast, because the next emergency could happen at any moment, and I had to get rest when I could. The pager trained my nervous system to let go quickly.

That’s the real secret, and it’s what most people are missing—the ability to turn down the volume and stop fighting. I learned it the hard way, under bright lights with a pager on my chest. You can build this skill on purpose, using the tools above, and skip the trauma unit. And if it’s not just your nights but your whole week that’s wearing you down, check out my earlier piece on choosing the few habits that last when everything else is falling apart: Three Bikes, Four Habits.

Readers who tell me sleep is what they want most are really asking for one thing: permission. Permission to stop trying so hard and just let sleep happen. So here it is. You don’t have to earn your sleep tonight. Let it happen.

One question, since I read every reply and it shapes what I write next: When you wake up at 3am, is it because of a specific worry, or are you just awake for no clear reason? Reply with the one that fits you. The solution is different for each, and I’ll write a future piece based on what most of you say.

Stay healthy.

Andre

PS: I wrote this because so many of you replied to my welcome email with one word: sleep. Thank you for being honest about what keeps you up. If you know someone who lies awake at 3am and quietly blames themselves, please forward this to them tonight. That’s how this newsletter grows, and it’s the main way I want it to.

PPS: If a friend sent you this, you can get the Sunday editions here: https://www.andreheeg.com

References

[1] Xie, L., Kang, H., Xu, Q., Chen, M. J., Liao, Y., Thiyagarajan, M., O’Donnell, J., Christensen, D. J., Nicholson, C., Iliff, J. J., Takano, T., Deane, R., & Nedergaard, M. (2013). Sleep drives metabolite clearance from the adult brain. Science, 342(6156), 373-377. https://doi.org/10.1126/science.1241224

[2] Shokri-Kojori, E., Wang, G.-J., Wiers, C. E., Demiral, S. B., Guo, M., Kim, S. W., Lindgren, E., Ramirez, V., Zehra, A., Freeman, C., Miller, G., Manza, P., Srivastava, T., De Santi, S., Tomasi, D., Benveniste, H., & Volkow, N. D. (2018). β-Amyloid accumulation in the human brain after one night of sleep deprivation. Proceedings of the National Academy of Sciences, 115(17), 4483-4488. https://doi.org/10.1073/pnas.1721694115

[3] Sabia, S., Fayosse, A., Dumurgier, J., van Hees, V. T., Paquet, C., Sommerlad, A., Kivimäki, M., Dugravot, A., & Singh-Manoux, A. (2021). Association of sleep duration in middle and old age with incidence of dementia. Nature Communications, 12, 2289. https://doi.org/10.1038/s41467-021-22354-2

[4] Yoo, S.-S., Gujar, N., Hu, P., Jolesz, F. A., & Walker, M. P. (2007). The human emotional brain without sleep: A prefrontal amygdala disconnect. Current Biology, 17(20), R877-R878. https://doi.org/10.1016/j.cub.2007.08.007

[5] Spiegel, K., Leproult, R., & Van Cauter, E. (1999). Impact of sleep debt on metabolic and endocrine function. The Lancet, 354(9188), 1435-1439. https://doi.org/10.1016/S0140-6736(99)01376-8

[6] Leproult, R., & Van Cauter, E. (2011). Effect of 1 week of sleep restriction on testosterone levels in young healthy men. JAMA, 305(21), 2173-2174. https://doi.org/10.1001/jama.2011.710

[7] Depner, C. M., Melanson, E. L., Eckel, R. H., Snell-Bergeon, J. K., Perreault, L., Bergman, B. C., Higgins, J. A., Guerin, M. K., Stothard, E. R., Morton, S. J., & Wright, K. P. (2019). Ad libitum weekend recovery sleep fails to prevent metabolic dysregulation during a repeating pattern of insufficient sleep and weekend recovery sleep. Current Biology, 29(6), 957-967.e4. https://doi.org/10.1016/j.cub.2019.01.069

[8] Prather, A. A., Janicki-Deverts, D., Hall, M. H., & Cohen, S. (2015). Behaviorally assessed sleep and susceptibility to the common cold. Sleep, 38(9), 1353-1359. https://doi.org/10.5665/sleep.4968

[9] Windred, D. P., Burns, A. C., Lane, J. M., Saxena, R., Rutter, M. K., Cain, S. W., & Phillips, A. J. K. (2024). Sleep regularity is a stronger predictor of mortality risk than sleep duration: A prospective cohort study. Sleep, 47(1), zsad253. https://doi.org/10.1093/sleep/zsad253

[10] Drake, C., Roehrs, T., Shambroom, J., & Roth, T. (2013). Caffeine effects on sleep taken 0, 3, or 6 hours before going to bed. Journal of Clinical Sleep Medicine, 9(11), 1195-1200. https://doi.org/10.5664/jcsm.3170

[11] Ebrahim, I. O., Shapiro, C. M., Williams, A. J., & Fenwick, P. B. (2013). Alcohol and sleep I: Effects on normal sleep. Alcoholism: Clinical and Experimental Research, 37(4), 539-549. https://doi.org/10.1111/acer.12006

[12] Baron, K. G., Abbott, S., Jao, N., Manalo, N., & Mullen, R. (2017). Orthosomnia: Are some patients taking the quantified self too far? Journal of Clinical Sleep Medicine, 13(2), 351-354. https://doi.org/10.5664/jcsm.6472

[13] Chinoy, E. D., Cuellar, J. A., Huwa, K. E., Jameson, J. T., Watson, C. H., Bessman, S. C., Hirsch, D. A., Cooper, A. D., Drummond, S. P. A., & Markwald, R. R. (2021). Performance of seven consumer sleep-tracking devices compared with polysomnography. Sleep, 44(5), zsaa291. https://doi.org/10.1093/sleep/zsaa291

[14] Broomfield, N. M., & Espie, C. A. (2003). Initial insomnia and paradoxical intention: An experimental investigation of putative mechanisms using subjective and actigraphic measurement of sleep. Behavioural and Cognitive Psychotherapy, 31(3), 313-324. https://doi.org/10.1017/S1352465803003060

[15] Zhang, B., & Wing, Y.-K. (2006). Sex differences in insomnia: A meta-analysis. Sleep, 29(1), 85-93. https://doi.org/10.1093/sleep/29.1.85

[16] Mong, J. A., & Cusmano, D. M. (2016). Sex differences in sleep: Impact of biological sex and sex steroids. Philosophical Transactions of the Royal Society B, 371(1688), 20150110. https://doi.org/10.1098/rstb.2015.0110

[17] Vermillet, A.-Q., Skewes, J. C., & Parsons, C. E. (2025). Men and women’s waking patterns to infant crying: Preparenthood differences are insufficient to explain uneven sharing of nighttime care. Emotion, 25(5), 1108-1121. https://doi.org/10.1037/emo0001478

[18] Hantsoo, L., Khou, C. S., White, C. N., & Ong, J. C. (2013). Gender and cognitive-emotional factors as predictors of pre-sleep arousal and trait hyperarousal in insomnia. Journal of Psychosomatic Research, 74(4), 283-289. https://doi.org/10.1016/j.jpsychores.2013.01.014

[19] Baker, F. C., Lampio, L., Saaresranta, T., & Polo-Kantola, P. (2018). Sleep and sleep disorders in the menopausal transition. Sleep Medicine Clinics, 13(3), 443-456. https://doi.org/10.1016/j.jsmc.2018.04.011

[20] Scullin, M. K., Krueger, M. L., Ballard, H. K., Pruett, N., & Bliwise, D. L. (2018). The effects of bedtime writing on difficulty falling asleep: A polysomnographic study comparing to-do lists and completed activity lists. Journal of Experimental Psychology: General, 147(1), 139-146. https://doi.org/10.1037/xge0000374

[21] Balban, M. Y., Neri, E., Kogon, M. M., Weed, L., Nouriani, B., Jo, B., Holl, G., Zeitzer, J. M., Spiegel, D., & Huberman, A. D. (2023). Brief structured respiration practices enhance mood and reduce physiological arousal. Cell Reports Medicine, 4(1), 100895. https://doi.org/10.1016/j.xcrm.2022.100895

[22] Bootzin, R. R. (1972). Stimulus control treatment for insomnia. Proceedings of the 80th Annual Convention of the American Psychological Association, 7, 395-396.

[23] Ekirch, A. R. (2001). Sleep we have lost: Pre-industrial slumber in the British Isles. The American Historical Review, 106(2), 343-386. https://doi.org/10.1086/ahr/106.2.343

[24] Kyle, S. D., Siriwardena, A. N., Espie, C. A., Yang, Y., Petrou, S., Ogburn, E., Begum, N., Maurer, L. F., Robinson, B., Gardner, C., Lee, V., Armstrong, S., Pattinson, J., Mort, S., Temple, E., Harris, V., Yu, L.-M., Bower, P., & Aveyard, P. (2023). Clinical and cost-effectiveness of nurse-delivered sleep restriction therapy for insomnia in primary care (HABIT): A pragmatic, superiority, open-label, randomised controlled trial. The Lancet, 402(10406), 975-987. https://doi.org/10.1016/S0140-6736(23)00683-9

[25] Benjafield, A. V., Ayas, N. T., Eastwood, P. R., Heinzer, R., Ip, M. S. M., Morrell, M. J., Nunez, C. M., Patel, S. R., Penzel, T., Pépin, J. L., Peppard, P. E., Sinha, S., Tufik, S., Valentine, K., & Malhotra, A. (2019). Estimation of the global prevalence and burden of obstructive sleep apnoea: A literature-based analysis. The Lancet Respiratory Medicine, 7(8), 687-698. https://doi.org/10.1016/S2213-2600(19)30198-5

[26] Qaseem, A., Kansagara, D., Forciea, M. A., Cooke, M., & Denberg, T. D. (2016). Management of chronic insomnia disorder in adults: A clinical practice guideline from the American College of Physicians. Annals of Internal Medicine, 165(2), 125-133. https://doi.org/10.7326/M15-2175

[27] Trauer, J. M., Qian, M. Y., Doyle, J. S., Rajaratnam, S. M. W., & Cunnington, D. (2015). Cognitive behavioral therapy for chronic insomnia: A systematic review and meta-analysis. Annals of Internal Medicine, 163(3), 191-204. https://doi.org/10.7326/M14-2841

After only two minutes, he asks for water. Then he needs to use the bathroom. He checks the clock. Soon his nose is running, but the tissues are in another room. It takes us thirty minutes to finish half the worksheet. He really wants to do well. He asks if he is getting the answers right, and he means it. But his body just will not let him stay still.

I know exactly what I am watching. I was him.

I grew up in the Bavarian countryside in the 1980s. I was the lively one, the class clown, the boy who read everything but never finished, and I could never follow a lesson to the end. Where I lived, no one used the word ADHD. You were just called spirited. If you remembered things easily, like I did, you still passed your exams, and no one looked any further.

Nobody looked any closer. For forty years.

Now I sit across the kitchen table from my son and see the same patterns in a smaller body. This time, it has a name.

At home, we have another name for it, one that came before the diagnosis: the monkey. It is the part in his head that jumps from thought to thought and never sits still. When I ask Magnus if the monkey is loud today, he knows exactly what I mean. Most days, it is.

Now I see this from three sides. I have it myself. I am raising a boy who has it. And for years, I have worked with people who have it, even if they did not know it.

So here is my view as a doctor on ADHD: what it really is when you take away the panic and the hype, how to spot it, what truly helps, what is just for show, and the one thing that decides if this trait helps or hurts you. This advice is the same whether the person in the chair is your child, your coworker, or yourself.

It Is Real, and It Runs in Families

Let’s start with what answers the blame question. If your child has ADHD, it is not because of anything you did as a parent. ADHD is one of the most inherited conditions in medicine: across 37 twin studies, the average heritability is 74% [1]. That is closer to height than to anything you can control as a parent. You probably passed it down, which is a strange kind of comfort.

The brain develops more slowly in ADHD. If you track brain growth in hundreds of children, those with ADHD follow the same pattern as others, just later. Peak thickness comes about three years later overall, and about five years later in the prefrontal cortex, which controls planning and self-control [2].

ADHD is common, and it does not stop at age eighteen. In the United States, 11.4% of children have been diagnosed, and nearly 78% of them also have another condition, usually anxiety or a learning difficulty [3]. It continues into adulthood. About 2.6% of adults have the full diagnosis [4], and by age 25, only about 15% still meet the strict criteria, while around 65% still have some impairment [5]. Most people do not outgrow it. They either learn to work around it, or they do not.

How to Spot It, in a Child and in Yourself

Having lots of energy is not enough for a diagnosis. The clinical standard is stricter. Symptoms must appear in more than one setting, cause real problems, and start before age twelve [6]. They need to show up at home and at school, not just at home.

The diagnosis can be wrong in both directions. Sometimes, it is given out too easily. The youngest child in a class gets diagnosed much more often than the oldest, just for being a few months less mature. Across nearly a million children, the youngest boys were 30% more likely to be diagnosed than the oldest, and the youngest girls 70% more [7]. Some of what we call ADHD is just being five in a room made for six-year-olds.

In the other direction, real cases get missed. In childhood, the diagnosis is about three boys for every girl. By adulthood, it is nearly even, because the quiet, inattentive girl who does not disrupt anyone gets overlooked and is treated for anxiety first [8]. The clever get missed most of all. In adults who had never been medicated, a high IQ hid the problem so well they failed only one test, while others failed many [9]. That was me. I remembered enough to pass, so no one looked, and no one saw the cost underneath: the meetings I sat through without catching a word, the restlessness that never showed on my face.

One sign the checklist leaves out is emotion. Trouble managing feelings is one of the biggest causes of impairment, and this is true even after you consider every other diagnosis [10]. Having a short fuse is part of the condition itself.

Superpower or Limitation

Here, I disagree with most of what you may have read online. The internet often says ADHD is a superpower. But the evidence does not support that.

The costs come first, and they are serious. A Danish study of 1.9 million people found those with ADHD died at about twice the rate of everyone else, mostly from accidents [11]. A 2025 UK analysis estimated that diagnosed adults lose about 7 years of life expectancy if they are men, and 9 years if they are women [12]. Both numbers need caution: the mortality figure is relative, not a high absolute risk, and the life-expectancy estimate is for diagnosed adults, who tend to be more severe cases. But the direction is clear. Untreated, this shortens lives.

Now for the superpower side, judged by the same standard. The link to entrepreneurship is real but limited: the sensation-seeking part of ADHD draws people to start things, while the inattentive part makes it hard to finish them [13]. Studies that highlight strengths often recruit people who have already succeeded. The most-cited study interviewed six successful men and asked what was good about having ADHD [14]. A 2026 review of 125 studies found that 70% looked for strengths on purpose, and concluded the benefits show up “in contexts where they are most likely to flourish” [15]. The loudest source fails completely: of the 100 most-viewed ADHD videos on TikTok, 52% were misleading, and most were posted by people with no medical training [16].

The honest answer is less exciting than the headlines. ADHD is a real impairment, and whether it helps or hurts depends almost entirely on where you direct it. Here is what the superpower posts leave out, both from my own experience and from watching my son: this is a lot of work. It is hard for the person who has it and hard for the parent raising them, and it shows you your own limits. It is not fun, and it is not something I would wish on my son or anyone else.

What Decides It Is the Environment

If the trait is fixed but the outcome is not, something in between makes the difference. That something is the environment you put the wiring into.

Consider one strange study. A dopamine-receptor variant tied to ADHD was carried by men in two branches of the same Kenyan people, one still nomadic, one recently settled into farming. Among the nomads, carriers were better nourished than non-carriers. Among the settled, the same variant left them worse off [17]. Same gene. Opposite lives. The environment cast the deciding vote.

I know that difference from my own life. For more than five years, early in my medical career, I worked in a hospital emergency and trauma room, where the ambulance doors would swing open and you never knew if it was a sprained wrist or a major accident. Chaos was normal, and I was always the calmest person in the room. The worse things got, the more settled I became. For years I thought that was discipline. It was not. It was a brain built for emergencies finally given a job that was all emergencies.

The opposite is also true. The worst four months of my career were during a corporate reorganization: the same org chart on the same slide, the same boxes moved in the same order, week after week, with nothing ever really decided. The brain that thrived in the trauma room could not handle that setting. It is not built for it. It shows up in smaller ways too. Over the years I have ignored a steady stream of invoices, traffic fines, and forms, and my brain declared victory every time. The fines disagreed.

Most of the time, the environment does not organize itself, so I do it. My phone has no notifications. None, from anything. Every screen I own has a plain black background, because a photo of my kids would distract me. When I need to get something done, I use a Time Timer, a clock for children that shows the minutes disappearing, because otherwise thirty minutes and four hours feel the same to me until the deadline hits. And when a subject grabs me, the systems do not matter: I disappear into it for hours, unreachable, as my wife can easily confirm.

You could call it a treatment plan, the way I manage myself: remove distractions, make time visible, and focus attention on work the brain can actually handle.

That is what a parent has to do, too, even though it goes against every instinct. The instinct is to push harder: correct, repeat, sit the child down, and demand focus. But pushing harder backfires. Children whose parents stayed very critical over the years were more likely to stay stuck in the severe form [18]. Cause goes both ways, and none of it is about blame. But the practical answer is clear: you cannot argue a child out of this, and shame only makes it worse. What helps is quieter and less satisfying. Fewer open tabs on his desk. A timer he can see. A task that matches his attention span. A parent who has stopped keeping score.

This is part of the Capacity pillar in my Upward ARC framework, which is about raising the ceiling on what a person can handle over a lifetime. For ADHD, you raise that ceiling by fitting the environment to the person, and this is true from all three perspectives. For me, it means a working life full of variety and deadlines. For Magnus, it means a childhood built around how he actually learns. And on a team, the colleague who cannot stand paperwork is often the one you want beside you when the ambulance doors swing open.

Try This Today

Get assessed, and do not stop at therapy alone. Get a real evaluation, not just an online checklist. The diagnosis usually comes from a psychologist or psychiatrist. Once medication is considered, that part is a psychiatrist’s or physician’s job. We spent more than two years on occupational therapy with Magnus because it seemed like a gentler start. It helped a little, but it was not enough. For young children, the guidelines rightly put behavioral parent training first [6], but do not let “we tried therapy” be the reason you wait for years.

See medication as the most effective tool, and do not be afraid of it. Stimulants are among the most effective treatments in psychiatry, with strong effects on symptoms in both children and adults [19]. And it is not just about grades: across 2.3 million patients, the months people took their medication saw 38% fewer car crashes for men and 42% fewer for women [20]. At the right dose, this is a safety measure.

Fix sleep at the same time. ADHD and poor sleep make each other worse. In a trial of children with both, a short behavioral sleep program clearly lowered their ADHD symptoms months later [21]. Protect the wind-down, keep a steady bedtime, and treat sleep as part of the treatment.

Shape the environment, and skip the showy solutions. Build the day around the way the brain works: single-task blocks, outside deadlines, and let someone or something else handle the boring follow-through. Skip the brain-training apps that claim to fix attention. In blinded tests, their benefit for real-world symptoms is limited at best [22].

If you lead someone like this, focus on the fit. When they keep struggling, it is usually the wiring, not a lack of effort. Give them work that sparks their brain: novelty, variety, or the crisis no one else wants. Take the ongoing admin tasks off their plate, or pair them with someone who can handle it. Provide structure from outside, and never use shame as a tool. You get their best work the same way a parent does: by shaping the environment.

The Chair He Can Stay In

For the first time in my life, I sat at the same desk, working on the same task, for two hours last week. I did not get up. I did not reach for my phone. I did not get distracted by something I never meant to open.

I am forty-seven, a few weeks into treatment, and the quiet in my head is so unfamiliar it is almost loud.

I did not do this for myself. I did it because of a nine-year-old who cannot sit through eight math problems, and whom I recognized right away, because he is me. We got his diagnosis. Then, in solidarity, I got mine. The psychologist said it was about as clear a case as she had seen.

Two months ago, we added medication to the years of therapy. One evening, a few weeks later, Magnus looked up from his worksheet and said, “The monkey in my head isn’t jumping around all the time anymore. I can focus now.” He was nine years old, and he found the words before I ever did.

The worksheet still takes time. He still gets up. But now he finishes it, and he knows why he is in the chair.

That is why naming it early matters. Not to label a child, but to give him what I spent forty years without: a chair he can stay in when it matters, and the choice of when to leave it.

We are doing this together. That was never the plan, but it turned out to be the point.

Stay healthy.

Andre

PS: If you read this and thought of someone, your child, your colleague, or the version of yourself who could never sit still, please forward it to them. Not everyone gets to find the name for this at nine. Those who find it at forty-seven still feel lucky. That is how this newsletter grows, and it is the only way I want it to.

References

[1] Faraone, S. V., & Larsson, H. (2019). Genetics of attention deficit hyperactivity disorder. Molecular Psychiatry, 24(4), 562-575. https://doi.org/10.1038/s41380-018-0070-0

[2] Shaw, P., Eckstrand, K., Sharp, W., Blumenthal, J., Lerch, J. P., Greenstein, D., Clasen, L., Evans, A., Giedd, J., & Rapoport, J. L. (2007). Attention-deficit/hyperactivity disorder is characterized by a delay in cortical maturation. Proceedings of the National Academy of Sciences, 104(49), 19649-19654. https://doi.org/10.1073/pnas.0707741104

[3] Danielson, M. L., Claussen, A. H., Bitsko, R. H., Katz, S. M., Newsome, K., Blumberg, S. J., Kogan, M. D., & Ghandour, R. (2024). ADHD prevalence among U.S. children and adolescents in 2022: Diagnosis, severity, co-occurring disorders, and treatment. Journal of Clinical Child & Adolescent Psychology, 53(3), 343-360. https://doi.org/10.1080/15374416.2024.2335625

[4] Song, P., Zha, M., Yang, Q., Zhang, Y., Li, X., & Rudan, I. (2021). The prevalence of adult attention-deficit hyperactivity disorder: A global systematic review and meta-analysis. Journal of Global Health, 11, 04009. https://doi.org/10.7189/jogh.11.04009

[5] Faraone, S. V., Biederman, J., & Mick, E. (2006). The age-dependent decline of attention-deficit hyperactivity disorder: A meta-analysis of follow-up studies. Psychological Medicine, 36(2), 159-165. https://doi.org/10.1017/S003329170500471X

[6] Wolraich, M. L., Hagan, J. F., Allan, C., Chan, E., Davison, D., Earls, M., Evans, S. W., Flinn, S. K., Froehlich, T., Frost, J., Holbrook, J. R., Lehmann, C. U., Lessin, H. R., Okechukwu, K., Pierce, K. L., Winner, J. D., & Zurhellen, W. (2019). Clinical practice guideline for the diagnosis, evaluation, and treatment of attention-deficit/hyperactivity disorder in children and adolescents. Pediatrics, 144(4), e20192528. https://doi.org/10.1542/peds.2019-2528

[7] Morrow, R. L., Garland, E. J., Wright, J. M., Maclure, M., Taylor, S., & Dormuth, C. R. (2012). Influence of relative age on diagnosis and treatment of attention-deficit/hyperactivity disorder in children. CMAJ, 184(7), 755-762. https://doi.org/10.1503/cmaj.111619

[8] Attoe, D. E., & Climie, E. A. (2023). Miss. Diagnosis: A systematic review of ADHD in adult women. Journal of Attention Disorders, 27(7), 645-657. https://doi.org/10.1177/10870547231161533

[9] Milioni, A. L. V., Chaim, T. M., Cavallet, M., de Oliveira, N. M., Annes, M., dos Santos, B., Louzã, M., da Silva, M. A., Miguel, C. S., Serpa, M. H., Zanetti, M. V., Busatto, G., & Cunha, P. J. (2017). High IQ may “mask” the diagnosis of ADHD by compensating for deficits in executive functions in treatment-naïve adults with ADHD. Journal of Attention Disorders, 21(6), 455-464. https://doi.org/10.1177/1087054714554933

[10] Shaw, P., Stringaris, A., Nigg, J., & Leibenluft, E. (2014). Emotion dysregulation in attention deficit hyperactivity disorder. American Journal of Psychiatry, 171(3), 276-293. https://doi.org/10.1176/appi.ajp.2013.13070966

[11] Dalsgaard, S., Østergaard, S. D., Leckman, J. F., Mortensen, P. B., & Pedersen, M. G. (2015). Mortality in children, adolescents, and adults with attention deficit hyperactivity disorder: A nationwide cohort study. The Lancet, 385(9983), 2190-2196. https://doi.org/10.1016/S0140-6736(14)61684-6

[12] O’Nions, E., El Baou, C., John, A., Lewer, D., Mandy, W., McKechnie, D. G. J., Petersen, I., & Stott, J. (2025). Life expectancy and years of life lost for adults with diagnosed ADHD in the UK: Matched cohort study. The British Journal of Psychiatry, 226(5), 261-268. https://doi.org/10.1192/bjp.2024.199

[13] Wiklund, J., Yu, W., Tucker, R., & Marino, L. D. (2017). ADHD, impulsivity and entrepreneurship. Journal of Business Venturing, 32(6), 627-656. https://doi.org/10.1016/j.jbusvent.2017.07.002

[14] Sedgwick, J. A., Merwood, A., & Asherson, P. (2019). The positive aspects of attention deficit hyperactivity disorder: A qualitative investigation of successful adults with ADHD. ADHD Attention Deficit and Hyperactivity Disorders, 11(3), 241-253. https://doi.org/10.1007/s12402-018-0277-6

[15] Rafael, R. B., Jia, H., Rouel, M., Wootton, B. M., & Mitchison, D. (2026). Attention deficit/hyperactivity disorder (ADHD)-related strengths in adults: A scoping review. Journal of Attention Disorders. Advance online publication. https://doi.org/10.1177/10870547261425737

[16] Yeung, A., Ng, E., & Abi-Jaoude, E. (2022). TikTok and attention-deficit/hyperactivity disorder: A cross-sectional study of social media content quality. The Canadian Journal of Psychiatry, 67(12), 899-906. https://doi.org/10.1177/07067437221082854

[17] Eisenberg, D. T. A., Campbell, B., Gray, P. B., & Sorenson, M. D. (2008). Dopamine receptor genetic polymorphisms and body composition in undernourished pastoralists: An exploration of nutrition indices among nomadic and recently settled Ariaal men of northern Kenya. BMC Evolutionary Biology, 8, 173. https://doi.org/10.1186/1471-2148-8-173

[18] Musser, E. D., Karalunas, S. L., Dieckmann, N., Peris, T. S., & Nigg, J. T. (2016). Attention-deficit/hyperactivity disorder developmental trajectories related to parental expressed emotion. Journal of Abnormal Psychology, 125(2), 182-195. https://doi.org/10.1037/abn0000097

[19] Cortese, S., Adamo, N., Del Giovane, C., Mohr-Jensen, C., Hayes, A. J., Carucci, S., Atkinson, L. Z., Tessari, L., Banaschewski, T., Coghill, D., Hollis, C., Simonoff, E., Zuddas, A., Barbui, C., Purgato, M., Steinhausen, H.-C., Shokraneh, F., Xia, J., & Cipriani, A. (2018). Comparative efficacy and tolerability of medications for attention-deficit hyperactivity disorder in children, adolescents, and adults: A systematic review and network meta-analysis. The Lancet Psychiatry, 5(9), 727-738. https://doi.org/10.1016/S2215-0366(18)30269-4

[20] Chang, Z., Quinn, P. D., Hur, K., Gibbons, R. D., Sjölander, A., Larsson, H., & D’Onofrio, B. M. (2017). Association between medication use for attention-deficit/hyperactivity disorder and risk of motor vehicle crashes. JAMA Psychiatry, 74(6), 597-603. https://doi.org/10.1001/jamapsychiatry.2017.0659

[21] Hiscock, H., Sciberras, E., Mensah, F., Gerner, B., Efron, D., Khano, S., & Oberklaid, F. (2015). Impact of a behavioural sleep intervention on symptoms and sleep in children with attention deficit hyperactivity disorder, and parental mental health: Randomised controlled trial. BMJ, 350, h68. https://doi.org/10.1136/bmj.h68

[22] Cortese, S., Ferrin, M., Brandeis, D., Buitelaar, J., Daley, D., Dittmann, R. W., Holtmann, M., Santosh, P., Stevenson, J., Stringaris, A., Zuddas, A., & Sonuga-Barke, E. J. S. (2015). Cognitive training for attention-deficit/hyperactivity disorder: Meta-analysis of clinical and neuropsychological outcomes from randomized controlled trials. Journal of the American Academy of Child & Adolescent Psychiatry, 54(3), 164-174. https://doi.org/10.1016/j.jaac.2014.12.010

In my twenties, I wrestled competitively and weighed every meal. The sauerkraut had to be raw and unpasteurized. I just knew, without needing proof, that the live cultures mattered most. Heat destroyed them. The canned, shelf-stable kind seemed inferior. So most days, I ate it cold and sour, alongside the raw meat.

I never questioned any of it, not during my wrestling years, not in medical school, and not in the twenty years since. Fermented food was good for me. My doctor said so, my social feed said so, and my mother said so. It was one of the few health beliefs I never examined, because it seemed too old and obvious to be wrong.

Last month, I did what I usually do for everything else, but rarely for beliefs I enjoy: I looked for proof. I read every human trial I could find on the four fermented foods people call medicine: sauerkraut, kimchi, kefir, and kombucha.

What I found was not the reason I ate all that raw cabbage.

The gap between what we believe about these foods and what research has actually shown is wide, wider than I expected. Fermented food is fine to eat, but its reputation got ahead of the evidence, and no one updated the story.

The Yogurt That Won a Nobel Prize

This story begins with a Nobel laureate and a mistake.

In 1907, Élie Metchnikoff, one of the founders of immunology, published a book called The Prolongation of Life [1]. In it, he argued that Bulgarian peasants lived unusually long because they drank soured milk full of lactic acid bacteria, and that these bacteria fought the rot in the gut, which he believed caused aging. He won the Nobel Prize the next year (specifically for his discovery of phagocytosis, the process by which certain cells engulf and destroy foreign bodies and bacteria). The idea that fermented dairy means a long life is his.

There was one problem. It was wrong. By the early 1920s, work at Yale by the bacteriologist Leo Rettger had shown that the bacteria in Bulgarian yogurt do not survive the human gut, let alone settle there [2]. Metchnikoff’s specific claim was dead within about 15 years of the book. His reputation and the reputation of the foods were not. The belief outlived its own disproof by a century.

That pattern runs through this entire field. You do not have to take my word for how weak the evidence is. Listen to the people who most want it to be strong.

In 2021, the International Scientific Association for Probiotics and Prebiotics, the field’s own leading scientific association, published a consensus statement [3]. Inside the careful language is a sentence that should stop anyone selling you a bottle: “with the exception of yoghurt and other cultured dairy products, few well-designed, randomized controlled trials on the health benefits of the array of fermented foods have been published.” For foods like kombucha, they wrote, the evidence “is mostly limited to chemical analyses and animal and cell culture models.” Cells in a dish. Mice. Not people.

So how did such a weak belief become so widespread?

Part of the reason is that lab results are often mistaken for proof. The science is real and interesting: fermented foods have live bacteria, and those bacteria make compounds that calm inflammation in test tubes. But what works in a dish or in a mouse quietly turns into ‘good for you’ by the time it becomes a headline.

Then there are population studies, which cannot separate cause from coincidence. People who eat a lot of kimchi or sauerkraut also tend to eat more vegetables, avoid junk food, exercise more, and smoke less. Their better health is often credited to the fermented foods. Even the researchers behind these studies say clearly that this kind of evidence “does not establish causation” [4].

Money also plays a role. Many of the existing trials are funded by the companies that sell these foods. In one well-studied example, reviews of artificially sweetened drinks written by authors with industry ties were much more likely to be positive than those without [5]. There is a big business in promoting kombucha, and little incentive to prove that cabbage does nothing.

The Part That Holds Up

So keep eating fermented food. I do most weeks. Just judge it by the same standard as anything else you eat, and the claims become more modest and honest.

I still train hard for a man in his forties, and what I am actually trying to hold down is the low, constant background inflammation that rises with age. Researchers call it inflammaging, and it is one of the shared roots of heart disease, dementia, and metabolic decline [6]. It is not abstract. In adults over 80, high levels of two inflammatory markers, IL-6 and CRP, roughly doubled the risk of dying over the following years [7]. And your gut sits at the center of this, because it holds as much as 70% of your immune system [8]. Anything that genuinely lowers that inflammatory load has my attention.

There is one good study suggesting fermented food does exactly that. In 2021, a Stanford team put 36 healthy adults on one of two diets for ten weeks. One group worked up to six servings of fermented foods per day. The other added fiber. The fermented group’s gut diversity rose, and 19 inflammatory proteins in their blood fell. The fiber group did not move [9]. A genuinely striking result.

To be honest, because you deserve it, that study only included 36 people. When another team ran a larger trial in 2025 with 147 participants, the fermented-food group did not show the same broad drop in inflammatory proteins. In fact, some markers of immune-cell activation even increased [10]. When researchers combined 26 controlled trials involving 1,461 participants, they found a real drop in the marker TNF-alpha, but no significant change in CRP or IL-6 [11]. The effect is real, but it is small. I will not pretend it is more than that.

There is one finding I trust most, and it is not the loudest. A study of over 9,000 people found that a healthy gut becomes more unique as you age, and this pattern predicts who lives into their late eighties [12]. Diversity, the thing fermented foods seem to support, goes hand in hand with healthy aging. That is the real reason to eat these foods. The label still promises more than the science shows.

Best to Worst

So which of the four is worth including? I read the human trials on each, and they are not all equal.

Kefir (unsweetened) has the strongest case. I make a point of buying it when I see it in the supermarket or think of it. It is closest to yogurt, the only fermented food with solid evidence. Pooled trials show kefir lowers fasting insulin fairly consistently [13]. Blood sugar drops by about 10 mg/dL in one analysis, but only across six small trials with wide error margins [13]. Beyond that, the numbers are quiet: long-term blood sugar and blood pressure stay about the same [13][14]. There are only six to eight small trials, none large. Still, kefir is the lowest in salt of the four and easy to add to a normal day, so it is the one I choose on purpose.

Kimchi has one strong modern trial, but there is an important detail. In a 2024 randomized, double-blind study, 55 overweight adults took kimchi for twelve weeks. The kimchi group lost body fat, while the placebo group gained it [15]. That is a real result. However, the kimchi was freeze-dried and put into capsules, with one version made low in sodium, and the World Institute of Kimchi ran the study (I swear this is real). A capsule of dried kimchi is not the same as a bowl of the real thing. And real kimchi is very high in salt. The same Korean data that show benefits also link heavy kimchi intake to a higher risk of stomach cancer, likely due to the salt and N-nitroso compounds formed during fermentation [16]. Enjoy kimchi, but do not treat it as a supplement or eat it in huge amounts.

Sauerkraut, which I have eaten my whole life, has the weakest evidence. I found only two small controlled human studies that used sauerkraut alone, with about 120 people in total, and not one well-powered trial on a major outcome [17][18]. Its reputation is based on tradition and theory, not on strong human results. I still eat it, but I no longer call it medicine.

Kombucha has the weakest case and the most hype. I found about eight human trials, with mixed effects on blood sugar and one promising result in just twelve people [19][20]. A 16-ounce bottle has about 12 to 19 grams of carbohydrates, most of it leftover sugar [21]. I do not drink much kombucha, and reading the studies did not change my mind. For the most part, it is a fermented soft drink with a health image. If you like the taste, choose the low-sugar version and do not count it as a health habit.

The Jar in My Fridge

Right now, there is a jar of sauerkraut in my Berlin fridge that I paid too much for because the label promised raw, unpasteurized, live cultures.

The reason for that purchase makes sense. Most fermented foods in stores are pasteurized to last longer, but the heat kills the bacteria you want. A shelf-stable can is mostly dead food [22]. If you want live cultures, choose the refrigerated jar labeled raw or unpasteurized, and eat it cold.

Here is what the label does not say: when researchers compared raw, living sauerkraut to pasteurized, dead sauerkraut in people, the raw version did not come out ahead. In one trial, the pasteurized one did more [18]. The label promises more than the science supports. Still, buy the raw jar if you want more live bacteria and less sugar than the pasteurized kind. Just know the word on the front is not the main reason.

In my Upward ARC framework, fermented food belongs in Activate, the part about what you put into your body. Also, it touches on Recover, which is about calming your system back to normal, since lowering inflammation helps you reset. That is the right place for it: a cheap, low-risk, enjoyable food with potential benefits. It is not a miracle, but it is not worthless either.

Try This Today

Try making your own sauerkraut. Here is how we do it at home: use a scale and a big glass jar, and get one of the kids to help stomp the cabbage. It is almost impossible to mess up, and homemade sauerkraut is better than anything you can buy. Shred the cabbage, weigh it, add 2% of its weight in salt, and pack it into a jar until the brine covers it. Keep it under the liquid and away from air. Let it sit at room temperature, ideally around 20 degrees Celsius, for one to four weeks [23]. For safety, Fred Breidt, a USDA microbiologist, says there has never been a recorded case of food poisoning from properly fermented vegetables, because the acid produced by the bacteria lowers the pH below what pathogens can handle [24]. Botulism is a risk with sealed, low-acid canning, not with salted open ferments, where the acidity keeps the bacteria from growing. A fresh homemade jar can have hundreds of millions of live bacteria per gram, especially in the first three months [25]. All you need is cabbage, salt, a jar, and time.

Make kefir your daily choice. Of the four, it has the most evidence from human studies and the least salt. Buy it plain and unsweetened, or make it at home with grains, and use it as you would use yogurt.

Read labels carefully, like a clinician would. For any fermented food, look for raw, unpasteurized, refrigerated, live cultures, and skip shelf-stable versions if you want live bacteria. For kombucha, ignore the health claims on the front and check the carbohydrate content on the back. Twelve grams of sugar in a health drink is still twelve grams of sugar.

Know who needs to be careful. Fermented vegetables are high in salt and biogenic amines such as histamine and tyramine. If you have high blood pressure, histamine intolerance, or take an older antidepressant called an MAO inhibitor, which can make tyramine dangerous, these foods can be a real problem instead of a health food [26]. For everyone else, a serving or two a day is enough; you do not need a whole jar.

My Mother’s Kitchen

I still eat sauerkraut most weeks without thinking about it, just as I have since I was a boy. That has not changed, and it will not.

Every time I visit my parents, I ask for the same dish: my mother’s sauerkraut, cooked slowly from her mother’s recipe, from the Bavarian farm where the cabbage fermented in a stone crock in the cellar. She always expects it and starts making it before I even ask.

For decades, I ate these foods as medicine, convinced of a benefit I never actually checked. When I finally did, my certainty did not last, but the food did.

Eat these foods because they are real, you enjoy them, and they might offer a small benefit. That has always been reason enough.

The rest was just a story I told myself, even though I am supposed to be someone who tests his stories. I let this one go unchecked for decades, in the very field where checking is my job. We all have a few beliefs like that. The real work is figuring out which ones they are.

Stay healthy.

Andre

PS: If you know someone certain their kombucha is doing something, forward this to them. Be kind about it. That is how this newsletter grows, and it is the only way I want it to.

References

[1] Metchnikoff, É. (1908). The prolongation of life: Optimistic studies (P. C. Mitchell, Ed. & Trans.). G. P. Putnam’s Sons. (Original work published 1907)

[2] Rettger, L. F., & Cheplin, H. A. (1921). A treatise on the transformation of the intestinal flora, with special reference to the implantation of Bacillus acidophilus. Yale University Press.

[3] Marco, M. L., Sanders, M. E., Gänzle, M., Arrieta, M. C., Cotter, P. D., De Vuyst, L., Hill, C., Holzapfel, W., Lebeer, S., Merenstein, D., Reid, G., Wolfe, B. E., & Hutkins, R. (2021). The International Scientific Association for Probiotics and Prebiotics (ISAPP) consensus statement on fermented foods. Nature Reviews Gastroenterology & Hepatology, 18(3), 196-208. https://doi.org/10.1038/s41575-020-00390-5

[4] Paveljšek, D., Pertziger, E., Fardet, A., et al. (2025). A systematic review of prospective evidence linking non-alcoholic fermented food consumption with lower mortality risk. Frontiers in Nutrition, 12, 1657100. https://doi.org/10.3389/fnut.2025.1657100

[5] Mandrioli, D., Kearns, C. E., & Bero, L. A. (2016). Relationship between research outcomes and risk of bias, study sponsorship, and author financial conflicts of interest in reviews of the effects of artificially sweetened beverages on weight outcomes: A systematic review of reviews. PLoS ONE, 11(9), e0162198. https://doi.org/10.1371/journal.pone.0162198

[6] Franceschi, C., & Campisi, J. (2014). Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases. The Journals of Gerontology: Series A, 69(Suppl 1), S4-S9. https://doi.org/10.1093/gerona/glu057

[7] Giovannini, S., Onder, G., Liperoti, R., Russo, A., Carter, C., Capoluongo, E., Pahor, M., Bernabei, R., & Landi, F. (2011). Interleukin-6, C-reactive protein, and tumor necrosis factor-alpha as predictors of mortality in frail, community-living elderly individuals. Journal of the American Geriatrics Society, 59(9), 1679-1685. https://doi.org/10.1111/j.1532-5415.2011.03570.x

[8] Vighi, G., Marcucci, F., Sensi, L., Di Cara, G., & Frati, F. (2008). Allergy and the gastrointestinal system. Clinical & Experimental Immunology, 153(Suppl 1), 3-6. https://doi.org/10.1111/j.1365-2249.2008.03713.x

[9] Wastyk, H. C., Fragiadakis, G. K., Perelman, D., Dahan, D., Merrill, B. D., Yu, F. B., Topf, M., Gonzalez, C. G., Van Treuren, W., Han, S., Robinson, J. L., Elias, J. E., Sonnenburg, E. D., Gardner, C. D., & Sonnenburg, J. L. (2021). Gut-microbiota-targeted diets modulate human immune status. Cell, 184(16), 4137-4153.e14. https://doi.org/10.1016/j.cell.2021.06.019

[10] van den Belt, M., et al. (2025). Distinct modulatory effects of high-fiber and fermented-food diets on gut microbiota, immune function, transit time, and sleep quality in a citizen science randomized controlled trial [Preprint]. medRxiv. https://doi.org/10.1101/2025.08.05.25332853

[11] SaeidiFard, N., Djafarian, K., & Shab-Bidar, S. (2020). Fermented foods and inflammation: A systematic review and meta-analysis of randomized controlled trials. Clinical Nutrition ESPEN, 35, 30-39. https://doi.org/10.1016/j.clnesp.2019.10.010

[12] Wilmanski, T., Diener, C., Rappaport, N., Patwardhan, S., Wiedrick, J., Lapidus, J., Earls, J. C., Zimmer, A., Glusman, G., Robinson, M., Yurkovich, J. T., Kado, D. M., Cauley, J. A., Zmuda, J., Lane, N. E., Magis, A. T., Lovejoy, J. C., Hood, L., Gibbons, S. M., … Price, N. D. (2021). Gut microbiome pattern reflects healthy ageing and predicts survival in humans. Nature Metabolism, 3(2), 274-286. https://doi.org/10.1038/s42255-021-00348-0

[13] Salari, A., Ghodrat, S., Gheflati, A., Jarahi, L., Hashemi, M., & Afshari, A. (2021). Effect of kefir beverage consumption on glycemic control: A systematic review and meta-analysis of randomized controlled clinical trials. Complementary Therapies in Clinical Practice, 44, 101443. https://doi.org/10.1016/j.ctcp.2021.101443

[14] Rashidbeygi, E., Mehrzad Samarin, M., Sheikhhossein, F., et al. (2025). The effect of kefir consumption on blood pressure and C-reactive protein: A systematic review and meta-analysis of randomised controlled trials. Endocrinology, Diabetes & Metabolism, 8(6), e70124. https://doi.org/10.1002/edm2.70124

[15] Lee, W., Kwon, M.-S., Yun, Y.-R., Choi, H., Jung, M.-J., Hwang, H., et al. (2024). Effects of kimchi consumption on body fat and intestinal microbiota in overweight participants: A randomized, double-blind, placebo-controlled, single-center clinical trial. Journal of Functional Foods, 122, 106401. https://doi.org/10.1016/j.jff.2024.106401

[16] Nan, H. M., Park, J. W., Song, Y. J., Yun, H. Y., Park, J. S., Hyun, T., Youn, S. J., Kim, Y. D., Kang, J. W., & Kim, H. (2005). Kimchi and soybean pastes are risk factors of gastric cancer. World Journal of Gastroenterology, 11(21), 3175-3181. https://doi.org/10.3748/wjg.v11.i21.3175

[17] Nielsen, E. S., Garnås, E., Jensen, K. J., Hansen, L. H., Olsen, P. S., Ritz, C., Krych, L., & Nielsen, D. S. (2018). Lacto-fermented sauerkraut improves symptoms in IBS patients independent of product pasteurisation: A pilot study. Food & Function, 9(10), 5323-5335. https://doi.org/10.1039/c8fo00968f

[18] Schropp, N., Bauer, A., Stanislas, V., Huang, K. D., Lesker, T. R., Bielecka, A. A., Strowig, T., & Michels, K. B. (2025). The impact of regular sauerkraut consumption on the human gut microbiota: A crossover intervention trial. Microbiome, 13, 52. https://doi.org/10.1186/s40168-024-02016-3

[19] Costa, M. A. C., et al. (2025). Benefits of kombucha consumption: A systematic review of clinical trials focused on microbiota and metabolic health. Fermentation, 11(6), 353. https://doi.org/10.3390/fermentation11060353

[20] Mendelson, C., Sparkes, S., Merenstein, D. J., Christensen, C., Sharma, V., Desale, S., Auchtung, J. M., Kok, C. R., Hallen-Adams, H. E., & Hutkins, R. (2023). Kombucha tea as an anti-hyperglycemic agent in humans with diabetes: A randomized controlled pilot investigation. Frontiers in Nutrition, 10, 1190248. https://doi.org/10.3389/fnut.2023.1190248

[21] Yang, J., Lagishetty, V., Kurnia, P., Henning, S. M., Ahdoot, A. I., & Jacobs, J. P. (2022). Microbial and chemical profiles of commercial kombucha products. Nutrients, 14(3), 670. https://doi.org/10.3390/nu14030670

[22] Rezac, S., Kok, C. R., Heermann, M., & Hutkins, R. (2018). Fermented foods as a dietary source of live organisms. Frontiers in Microbiology, 9, 1785. https://doi.org/10.3389/fmicb.2018.01785

[23] NC State Extension. (2023). Lactic acid fermentation. NC State Extension Publications. https://content.ces.ncsu.edu/lactic-acid-fermentation

[24] Beecher, C. (2014, March 11). Fermenting veggies at home: Follow food safety ABCs [quoting F. Breidt, USDA ARS]. Food Safety News. https://www.foodsafetynews.com/2014/03/fermenting-veggies-at-home-follow-food-safety-abcs/

[25] Thierry, A., Madec, M.-N., Chuat, V., Bage, A.-S., Picard, O., Grondin, C., Rué, O., Mariadassou, M., Marché, L., & Valence, F. (2023). Microbial communities of a variety of 75 homemade fermented vegetables. Frontiers in Microbiology, 14, 1323424. https://doi.org/10.3389/fmicb.2023.1323424

[26] Turna, N. S., Chung, R., & McIntyre, L. (2024). A review of biogenic amines in fermented foods: Occurrence and health effects. Heliyon, 10(2), e24501. https://doi.org/10.1016/j.heliyon.2024.e24501

Karla is six. She can’t eat fish.

Two kids, two lists, one kitchen. Dinner here is a problem to solve before it is a meal. We start with protein. Which one, how to cook it, what to put with it. Then we check the basics. Are they getting enough to grow, the vitamins, the nutrients they would get if they could eat everything. Milk is a huge challenge here.

For years, we’ve just done this. It’s normal now.

Last week, we ran into a new problem. Omega-3. The best source is oily fish, and the child who needs it most cannot have it. How do you supplement it for a six-year-old? Flaxseed or a capsule? Which one, what dose?

I did not have a clear answer. Thinking about it reminded me of something in my inbox.

A few weeks earlier, I was in San Francisco and signed up for Function Health to test the service and see what it was like. They check more than a hundred biomarkers. I skimmed the cholesterol and hormone numbers, the ones I know well. I had never opened the omega panel.

I’m a doctor. I write about this every Sunday. For ten years, my omega-3 plan was simple: buy the best-rated bottle online, take two or three a day, and move on.

That night I opened the panel.

What I found surprised me.

My total omega-3 was 9.2%. Most labs call anything above 8 good. I had cleared it without effort. I felt confident.

Then I read the breakdown. My DHA was high, at 5.6%. My EPA was lower, 1.9. The two omega-3s I had taken as one for years were not equal, and the one that does most of the anti-inflammatory work was the one I had the least of.

I had been taking fish oil. I did not realize I was taking mostly the wrong part.

Here’s what I learned in the rabbit hole that followed.

The Two Halves of Fish Oil

Start here, because almost every mistake comes from missing it.

“Omega-3” on a label usually means two different fatty acids doing two different jobs. EPA and DHA. They share a family name and not much else.

DHA is structural. It’s the omega-3 your brain is mostly built from. Brain tissue contains 250-300 times more DHA than EPA [1]. It sits in the membranes of your neurons and your retina.

EPA is the worker. Your body uses it to make the signaling molecules that calm inflammation, the resolvins and protectins, and often milder versions of the inflammatory compounds that arachidonic acid produces [1][2]. EPA is the one with cardiovascular and mood data to back it up. DHA builds the structure. EPA runs the maintenance.

A standard capsule treats them as the same. Your blood does not. My results were uneven, just as I had been dosing for years.

The 8% Test

Most people taking omega-3 supplements have never measured their levels. I was one of them. We take it on faith and a five-star rating.

There is a real test. The Omega-3 Index measures EPA plus DHA in your red blood cell membranes, as a percentage. Bill Harris and Clemens von Schacky proposed it in 2004 as a graded risk marker for dying of heart disease. 8% or higher was the protected end; 4% or lower was the exposed end [3].

It holds up. In the Framingham Heart Study, people in the top fifth of the Omega-3 Index had a 34% lower risk of dying from any cause and a 39% lower risk of a new cardiovascular event than those in the bottom fifth [4].

Raise your number. There is a second number people often focus on, but it is less solid than it seems.

It’s the AA/EPA ratio. Arachidonic acid against EPA. The two compete for the same enzymes, so the balance between them determines how much inflammatory versus calming signaling your cells produce [5]. A higher ratio means more inflammatory raw material relative to EPA. Mine came back at 6.1. On the functional-medicine chart that reads as high: the target, they’ll tell you, sits between 1.5 and 3, so 6.1 looks like I’m running hot.

So I looked for the trial behind it. There isn’t one. The 1.5-to-3 target comes from clinical reference ranges, not randomized data, and the literature treats the ratio as a continuous signal: lower values tend to be better, with no proven cutoff. So my 6.1 isn’t an alarm. It mostly tells me what the EPA number already did, that my EPA is low.

And even that effect has conditions. In the Hisayama study, a large Japanese cohort, each drop in the EPA-to-AA ratio was associated with about 1.5 times the cardiovascular risk, but mostly in people whose inflammation was already elevated on a CRP test [6].

I had cleared the validated number and was being told to chase one that is not. That should make you pause.

Three Things, One Bottle

So I went looking for the right product, this time for Karla.

Three things had to be true at once. A disclosed split of DHA and EPA, so I knew what was in the capsule. The triglyceride form, the one that absorbs (more on this later). And no fish, because she can’t have it.

That overlap is small. I gave the problem to an AI to sort the market, as I do now. Even then, few products met all three. We found one.

The harder part is earlier. Most people never learn these are the three questions to ask.

Does Any of It Even Work?

This is where marketing and evidence separate.

The best case comes from one trial. REDUCE-IT, 2019. 8,000 high-risk patients on statins, given 4 grams a day of pure EPA, a high-dose prescription ethyl ester. Their rate of major cardiac events dropped by 25% compared with placebo [7]. A real, large, hard-outcome win.

Then the results changed. A similar trial, STRENGTH, used the same 4 grams per day, but with a mix of EPA and DHA rather than EPA alone. It found no benefit and stopped early for futility [8]. Same dose, same patients, opposite result. Two of the largest fish oil trials do not agree. Pure high-dose EPA may work, the mixed product may not, and the answer is not settled.

Looking at more data, the effect is smaller. A Cochrane review of 86 trials and 162,796 people found that omega-3 supplements have little or no effect on overall mortality [9]. They lower triglycerides by about 15%. There is a real effect on one blood marker, but nothing clear on lifespan.

The brain data is similar. In one Framingham analysis, people with the highest red-cell DHA had about half the Alzheimer’s rate, a 49% lower risk [10]. But in a large trial, giving 1 g/day to older adults with adequate levels did not slow cognitive decline compared with placebo [11].

The pattern is consistent. Omega-3 matters most when you are low. Adding more to someone who already has enough does little.

The Seed Oil Panic Is Mostly Wrong

A quick note, since people ask. Many worry about omega-6, seed oils, and a high omega-6-to-omega-3 ratio [12]. My ratio was 3.6, and it does not matter much. Higher linoleic acid, the main seed-oil fat, is associated with about a 22% lower risk of cardiovascular death across 30 cohorts [13]. It does not raise inflammatory markers [14], and the American Heart Association advises against focusing on the ratio [15]. The key is raising omega-3. I will cover this in detail another time.

The Brain You’ll Need at 70

In my Upward ARC framework, this is mostly Activate, the pillar about what you put into the system. Food first, then the few supplements that earn their place. Omega-3 earns its place, in the right form and dose, checked against your Omega-3 Index.

It also affects Capacity, the long-term view. DHA is part of the brain you will need at 70. You are not supplementing for now. You are building the hardware for later life.

Try This Today

Measure before you medicate. Order an Omega-3 Index test. It’s the same red-cell measure used in the research, and the only way to know if your routine is doing anything. Aim for 8% or higher. Below 4 is the danger zone [3]. Retest three to four months after any change. One number ends years of guessing.

Read the label like a clinician. Four checks. One, form. You want “triglyceride” or “rTG,” the shape omega-3 takes in the fish itself, rebuilt after concentration. Avoid “ethyl ester,” the cheaper version where the fatty acid is attached to an alcohol to pack it more tightly. The triglyceride form absorbs at 124% of natural fish oil; the ethyl ester sits at 73 [16][17]. (The one big trial that worked, REDUCE-IT, used a high-dose prescription ethyl ester. At that dose, the form barely matters. For the modest dose in your daily capsule, it decides how much you actually absorb.) Two, a third-party seal: IFOS five-star, USP, or a printed oxidation number. In one test of 32 fish oils, half were oxidized beyond the accepted limit, and 69% contained less omega-3 than the label promised [18]. Three, read the actual EPA and DHA milligrams, not the “1,000 mg fish oil” on the front. The targets are set for the two combined: 250 to 500 mg per day for general health, and 2 to 4 grams per day for a specific job, like lowering triglycerides, under medical supervision. Same number for men and women, and no special older-adult dose, whatever the marketing says. Pregnancy is the one exception, adding about 200 mg of DHA. Four, smell it. Crack a capsule; rancid means oxidized, so trash it. Then keep the bottle somewhere cool and dark. Light and heat accelerate oxidation.

Match the molecule to the goal. If your aim is brain and baseline, balanced or DHA-leaning is fine. If your aim is inflammation, triglycerides, or mood, you want an EPA-dominant supplement. The antidepressant signal in the trials only shows up above 60% EPA [19], and the one cardiovascular win used pure EPA [7]. Swap to the right one rather than stacking a second bottle on the first. I’m moving to an EPA-heavy form and will retest in autumn.

Take it with a fatty meal, and not just any fat. Co-ingest your omega-3 with 10 to 15 grams of long-chain fat: olive oil, avocado, eggs, oily fish. With a high-fat meal, EPA absorption from fish oil climbs to about 90% [20]. Don’t take it with MCT or coconut oil. Those are medium-chain fats; they bypass the route your long-chain omega-3 needs, so part of the dose is wasted. A capsule on an empty stomach is the worst version.

Eat the fish. Or, if you can’t, the algae. Two to three servings a week of salmon, sardines, or mackerel will move your index better than any stack. And for the people who can’t eat fish, my six-year-old included, algal oil works just as well. In a head-to-head trial, omega-3 from microalgae was absorbed as well as fish oil, around 111% [21].

The Patient I’d Have Corrected

Dinner tonight is the same engineering problem it always is. Magnus’s list, Karla’s list, the protein, the sides, the macros. None of that changes.

The change is small and specific. I read a panel I had ignored for ten years and found fish oil was two molecules I had taken out of balance. I am changing one bottle, not adding more. I booked the retest.

I spent a decade as the patient I would have corrected. The fix was a single blood test and the willingness to look at it.

The question that started this now has an answer. Karla cannot eat fish, and she has never minded. She’ll get her omega-3 from where the fish get theirs, the algae. She will grow up with what I never thought to measure in myself.

Stay healthy.

Andre

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PS: If you take fish oil every morning and have never measured whether it works, you are where I was. Forward this to someone who would say their routine is fine. That is how this newsletter grows, and it is the only way I want it to.

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References

[1] Dyall, S. C. (2015). Long-chain omega-3 fatty acids and the brain: A review of the independent and shared effects of EPA, DPA and DHA. Frontiers in Aging Neuroscience, 7, 52. https://doi.org/10.3389/fnagi.2015.00052​

[2] Calder, P. C. (2013). Omega-3 polyunsaturated fatty acids and inflammatory processes: Nutrition or pharmacology? British Journal of Clinical Pharmacology, 75(3), 645-662. https://doi.org/10.1111/j.1365-2125.2012.04374.x​

[3] Harris, W. S., & von Schacky, C. (2004). The Omega-3 Index: A new risk factor for death from coronary heart disease? Preventive Medicine, 39(1), 212-220. https://doi.org/10.1016/j.ypmed.2004.02.030​

[4] Harris, W. S., Tintle, N. L., Etherton, M. R., & Vasan, R. S. (2018). Erythrocyte long-chain omega-3 fatty acid levels are inversely associated with mortality and with incident cardiovascular disease: The Framingham Heart Study. Journal of Clinical Lipidology, 12(3), 718-727.e6. https://doi.org/10.1016/j.jacl.2018.02.010​

[5] Nelson, J. R., & Raskin, S. (2019). The eicosapentaenoic acid:arachidonic acid ratio and its clinical utility in cardiovascular disease. Postgraduate Medicine, 131(4), 268-277. https://doi.org/10.1080/00325481.2019.1607414​

[6] Ninomiya, T., Nagata, M., Hata, J., Hirakawa, Y., Ozawa, M., Yoshida, D., Ohara, T., Kishimoto, H., Mukai, N., Fukuhara, M., Kitazono, T., & Kiyohara, Y. (2013). Association between ratio of serum eicosapentaenoic acid to arachidonic acid and risk of cardiovascular disease: The Hisayama Study. Atherosclerosis, 231(2), 261-267. https://doi.org/10.1016/j.atherosclerosis.2013.09.023​

[7] Bhatt, D. L., Steg, P. G., Miller, M., Brinton, E. A., Jacobson, T. A., Ketchum, S. B., Doyle, R. T., Juliano, R. A., Jiao, L., Granowitz, C., Tardif, J.-C., & Ballantyne, C. M. (2019). Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. New England Journal of Medicine, 380(1), 11-22. https://doi.org/10.1056/NEJMoa1812792​

[8] Nicholls, S. J., Lincoff, A. M., Garcia, M., Bash, D., Ballantyne, C. M., Barter, P. J., Davidson, M. H., Kastelein, J. J. P., Koenig, W., McGuire, D. K., Mozaffarian, D., Ridker, P. M., Ray, K. K., Katona, B. G., Himmelmann, A., Loss, L. E., Rensfeldt, M., Lundström, T., & Nissen, S. E. (2020). Effect of high-dose omega-3 fatty acids vs corn oil on major adverse cardiovascular events in patients at high cardiovascular risk: The STRENGTH randomized clinical trial. JAMA, 324(22), 2268-2280. https://doi.org/10.1001/jama.2020.22258​

[9] Abdelhamid, A. S., Brown, T. J., Brainard, J. S., Biswas, P., Thorpe, G. C., Moore, H. J., Deane, K. H. O., Summerbell, C. D., Worthington, H. V., Song, F., & Hooper, L. (2020). Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease. Cochrane Database of Systematic Reviews, 2020(3), Article CD003177. https://doi.org/10.1002/14651858.CD003177.pub5​

[10] Sala-Vila, A., Satizabal, C. L., Tintle, N., Melo van Lent, D., Vasan, R. S., Beiser, A. S., Seshadri, S., & Harris, W. S. (2022). Red blood cell DHA is inversely associated with risk of incident Alzheimer’s disease and all-cause dementia: Framingham Offspring Study. Nutrients, 14(12), 2408. https://doi.org/10.3390/nu14122408​

[11] Kang, J. H., Kim, E., Cook, N. R., & Manson, J. E. (2022). Marine n-3 fatty acids and cognitive change among older adults in the VITAL randomized trial. Alzheimer’s & Dementia: Translational Research & Clinical Interventions, 8(1), e12288. https://doi.org/10.1002/trc2.12288​

[12] Simopoulos, A. P. (2008). The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases. Experimental Biology and Medicine, 233(6), 674-688. https://doi.org/10.3181/0711-MR-311​

[13] Marklund, M., Wu, J. H. Y., Imamura, F., Del Gobbo, L. C., Fretts, A., de Goede, J., Shi, P., Tintle, N., Wennberg, M., Aslibekyan, S., Chen, T.-A., de Oliveira Otto, M. C., Hirakawa, Y., Qureshi, W., Guan, W., Bork, C. S., … Mozaffarian, D. (2019). Biomarkers of dietary omega-6 fatty acids and incident cardiovascular disease and mortality: An individual-level pooled analysis of 30 cohort studies. Circulation, 139(21), 2422-2436. https://doi.org/10.1161/CIRCULATIONAHA.118.038908​

[14] Johnson, G. H., & Fritsche, K. (2012). Effect of dietary linoleic acid on markers of inflammation in healthy persons: A systematic review of randomized controlled trials. Journal of the Academy of Nutrition and Dietetics, 112(7), 1029-1041. https://doi.org/10.1016/j.jand.2012.03.029​

[15] Harris, W. S., Mozaffarian, D., Rimm, E., Kris-Etherton, P., Rudel, L. L., Appel, L. J., Engler, M. M., Engler, M. B., & Sacks, F. (2009). Omega-6 fatty acids and risk for cardiovascular disease: A science advisory from the American Heart Association Nutrition Subcommittee. Circulation, 119(6), 902-907. https://doi.org/10.1161/CIRCULATIONAHA.108.191627​

[16] Dyerberg, J., Madsen, P., Møller, J. M., Aardestrup, I., & Schmidt, E. B. (2010). Bioavailability of marine n-3 fatty acid formulations. Prostaglandins, Leukotrienes and Essential Fatty Acids, 83(3), 137-141. https://doi.org/10.1016/j.plefa.2010.06.007​

[17] Schuchardt, J. P., & Hahn, A. (2013). Bioavailability of long-chain omega-3 fatty acids. Prostaglandins, Leukotrienes and Essential Fatty Acids, 89(1), 1-8. https://doi.org/10.1016/j.plefa.2013.03.010​

[18] Albert, B. B., Derraik, J. G. B., Cameron-Smith, D., Hofman, P. L., Tumanov, S., Villas-Boas, S. G., Garg, M. L., & Cutfield, W. S. (2015). Fish oil supplements in New Zealand are highly oxidised and do not meet label content of n-3 PUFA. Scientific Reports, 5, 7928. https://doi.org/10.1038/srep07928​

[19] Sublette, M. E., Ellis, S. P., Geant, A. L., & Mann, J. J. (2011). Meta-analysis of the effects of eicosapentaenoic acid (EPA) in clinical trials in depression. The Journal of Clinical Psychiatry, 72(12), 1577-1584. https://doi.org/10.4088/JCP.10m06634​

[20] Lawson, L. D., & Hughes, B. G. (1988). Absorption of eicosapentaenoic acid and docosahexaenoic acid from fish oil triacylglycerols or fish oil ethyl esters co-ingested with a high-fat meal. Biochemical and Biophysical Research Communications, 156(2), 960-963. https://doi.org/10.1016/s0006-291x(88)80937-9​

[21] Bailey, E., Wojcik, J., Rahn, M., Roos, F., Spooren, A., & Koshibu, K. (2025). Comparative bioavailability of DHA and EPA from microalgal and fish oil in adults. International Journal of Molecular Sciences, 26(19), 9343. https://doi.org/10.3390/ijms26199343​

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A note for new readers:

I’m a trained reconstructive facial surgeon, medical doctor, and dentist. Before launching this newsletter, I had a varied career: competitive freestyle wrestler, management consultant (McKinsey), entrepreneur (Zocdoc, Thermondo, and docdre ventures), and corporate executive (Sandoz). Today, I’m a Managing Director and Partner at BCG.

Husband of one. Father of three. Split between Berlin’s urban pulse and our Baltic Sea retreat. I’d rather be moving than sitting. Not just hobbies. Research. My body is my primary laboratory; I’ve been conducting experiments for decades.

If this is your first time here, welcome. I’m excited to share what I’ve learned and will continue to learn with you.

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DISCLAIMER:

Let’s get one thing straight: None of this, whether text, graphics, images, or anything else, is medical or health advice. This newsletter is here to inform, educate, and (hopefully) entertain you, not to diagnose or treat you.

Yes, I’m a trained medical doctor and dentist. No, I’m not your doctor. The content here isn’t a replacement for professional medical advice, diagnosis, or treatment.

If you have questions about your health, talk to your physician or a qualified health professional. Don’t ignore their advice or delay getting care because of something you read in The Upward ARC. Be smart. Do your research. And, as always, take care of yourself.

There were three preschool classes, about 50-60 kids, all around six years old, plus teachers and support staff. They were supposed to be back by three. For a week, the parent WhatsApp group had been arguing about the school’s updates. There weren’t enough updates, or they were the wrong kind, or they arrived too late. It was the usual drama, and I can’t stand the usual drama.

At three o’clock, the bus still wasn’t back. By 3:10, the chat had gone from worried to full-on crisis mode. “Are they back?” “Does anyone have eyes on them?” “We were told three.” There was supposed to be a buffer, and everyone knew about it, but it didn’t help.

So I did what I always do. I typed, “My daughter is missing. I’m calling the police.” Then I put my phone down, feeling pretty pleased with myself.

I was acting. I played the over-the-top, panicked parent for a group of parents who had been working themselves up all week. Anyone who knows me would have seen right through it.

But a preschool WhatsApp group isn’t full of people who know you.

The panic came right back. “Oh my god.” “What happened??” “How can we help?” I gave in immediately. “Sorry, everyone, that was a joke.”

That’s when one of them called me sick.

Karla, who’s six, was on the bus. The bus was just twelve minutes late.

I wish I could say this was out of character, but it wasn’t. My family would laugh if I tried. My brain is often about half a step ahead of my judgment, which is just how ADHD works for me. Most days, that half-step is where my best ideas come from. Other days, it’s where I end up posting a joke about a missing child to 40 strangers.

I’m usually the last person to realize when a joke has flopped. That afternoon, I managed to do it live, in writing, in front of everyone. I deleted the message within a minute, apologized, still got called sick, and then decided to do something more useful than argue. I started looking into whether laughter is actually good for you, physically, like all those posters claim.

We’ve all heard that claim without ever really checking it. Laughter is the best medicine. It’s been on mugs and hospital walls for decades. I wanted to see if there’s any real evidence behind it, or if the parent chat just punished me for using bad folk medicine.

What the Mug Gets Wrong

Let’s start with the slogan, because it’s mostly not true.

“Laughter is the best medicine” traces to Norman Cousins, a magazine editor who in 1976 wrote in the New England Journal of Medicine that he had recovered from a painful spinal condition on a regimen of Marx Brothers films and vitamin C [1]. A lovely story. Also, one uncontrolled case. Self-reported. A condition that can clear up on its own, while he was also taking high doses of vitamin C, which means the films get no clean credit either way. One patient. No control group. 50 years of a medical myth.

The claims grew from there. You have read that laughter boosts your immune system, lifts your natural killer cells, and helps fight cancer. Those headlines come from a few tiny studies, 10-30 people, that measured a small blip in a blood marker for an hour or two [2]. None followed a patient to a real outcome. Laughter yoga, the organized-circle kind, has been properly reviewed: weak evidence, small, biased trials, and no clear edge over any other group activity [3].

The most honest voice is the field’s own. Rod Martin, who built the standard tool for measuring humor, reviewed the entire literature and found the immune effects inconsistent, the physical health benefits thin, and no good evidence that funnier people live longer [4]. The leading man in the field looked at the folklore and said, in effect: Slow down.

I could have stopped there, punished by a parent chat for a remedy that doesn’t even work. But the evidence doesn’t end there.

What a Laugh Actually Does

Beneath the slogans, there’s what laughter actually does to your body right after you laugh. Here, the evidence is solid because it’s measurable.

Laughter and stress move the cardiovascular system in opposite directions. In a randomized, controlled experiment, arterial stiffness fell after people laughed and rose after a stressful task. The same laughter lowered cortisol too [5]. Real, and gone within a day.

Cortisol shows your stress load. A 2023 meta-analysis pooled trials that had participants sit in front of something funny and measured the hormone before and after. Laughter cut it by roughly a third, most of that in a single session [6]. The authors are careful, and so am I. The studies are small, and none can be blinded, because there is no placebo joke. The effect is real, and the evidence is thin. Both are true.

The sturdiest finding is, in evolutionary terms, the oldest. Robin Dunbar at Oxford ran six experiments showing that genuine laughter, the helpless kind, raised people’s pain threshold, most likely by releasing endorphins [7]. Feeling good on its own did not do it. The laughing did. The effect was strongest when people laughed together, and Dunbar thinks the physical act of real laughter is what matters. He argues it evolved to do the job grooming does for other primates: hold the group together. It is, first, how humans bond.

What bothered me that evening wasn’t being called sick. I’ve been called worse by people whose opinions actually matter to me. What really bothered me was simpler: I thought the joke was good, but I was wrong about the only thing that mattered. Who was reading it.

The same eight words, if I sent them to my wife or to the two friends who always reply with something even darker, would be a good joke. Sending it to 40 strangers stressed about pickup made me look like someone who doesn’t take a missing child seriously.

Same words, completely different meaning. The difference was the audience, and I got it wrong.

Four Kinds of Funny

Psychology has spent 20 years measuring the exact thing I got wrong. It starts, again, with Rod Martin, who in 2003 showed that humor comes in four distinct styles [8]. Two tend to help you. Two tend to cost you.

The two that help: affiliative humor, which brings people together, and self-enhancing humor, which you use on yourself to keep a bad day in proportion. The two that cost: aggressive humor, at someone else’s expense, and self-defeating humor, putting yourself down to buy a laugh.

The style matters more than the amount. A meta-analysis of 37 studies and nearly 13,000 people found that the two adaptive styles show lower depression and higher self-esteem. At the same time, self-defeating humor is the only one that reliably tracks worse mental health [9]. A second, 85 studies and over 27,000 people, put numbers on it: adaptive and maladaptive humor move well-being in opposite directions, the signs cleanly reversed [10]. The effects are modest in magnitude, and they recur across studies. In this kind of research, consistency counts for more than a big number that fails to replicate.

There is a mechanism behind this. In one experiment, people looked at upsetting images and found a kind, funny way to see them. Their bad feeling dropped. A cruel joke did not work nearly as well [11]. Humor is one way the mind decides how big a threat really is, and the kind you reach for changes the answer. Under real stress, the helpful styles soften the blow, and the self-defeating ones deepen it [12].

None of this research told me my joke was wrong. I figured that out on my own, sitting on the sofa that evening. The research just explained why.

Whose Joke Is It

Now, let’s move from a parent chat to something more familiar for most of you, a team you’re responsible for. The same rules apply, but the stakes are higher.

A meta-analysis of 49 studies found that positive humor at work is associated with higher performance, more trust, better teamwork, and lower burnout. The link was about 0.36, which is strong for this kind of research [13]. Leaders who use warm humor well get more from their people. That much holds up.

The catch is that it depends on you. A review of leadership studies found that humor helps when the leader is already trusted and seen as competent, but it backfires if they’re not [14]. Another study followed the same leaders for six weeks and found that affiliative humor improved their standing within the team, whereas aggressive humor worsened it [15].

And dark humor, the kind I reached for, is not the clean tool people assume it is. Among more than 500 investigators who work on the worst cases imaginable, lighthearted humor was associated with lower traumatic stress, whereas gallows humor was associated with higher traumatic stress [16]. Joking about horror did not protect these people. The darkest humor went with the most stress, not the least.

Which brings us back to the late bus and my bad joke. What really matters is your standing and where you’re coming from: whether you’re laughing with the people who are dealing with the problem, or at them from the outside. That afternoon, I was on the outside, even though I thought I was in.

In my Upward ARC framework, this falls under Recover, the work of bringing your nervous system back to normal between stressful moments. A real laugh does that quickly: it lowers cortisol, relaxes your arteries, gives you a boost of endorphins, and usually happens with someone else. It also affects Capacity. The kind of humor you use under pressure either builds your resilience over time or slowly wears it down. You reset every day, and your style adds up.

Does It Buy You Years

The last promise on the mug is the biggest. Does humor make you live longer?

The honest answer is a quiet maybe, and it gets weaker the more you look into it. One study of over 66,000 Norwegians found that people with a stronger sense of humor were less likely to die over 7 years [17]. But when the same group was followed for 15 years, the effect persisted among women but largely disappeared among men [18]. A Japanese study of 17,000 adults found that people who rarely laughed had nearly double the death rate of frequent laughers, even after adjusting for obvious risk factors [19]. It’s interesting, but far from settled, and could just mean that sick and lonely people laugh less.

The stronger evidence is actually for optimism. A meta-analysis of nearly 230,000 people found that optimism is linked to lower rates of heart disease and early death [20]. But that’s about optimism as a personality trait, and optimism isn’t the same as humor.

So I won’t tell you that humor adds years to your life. The evidence just isn’t strong enough. What humor really changes is how today feels, how your team works, and how you handle tough moments.

Try This Today

The Hard Laugh. Not just a smile. A real, full laugh. Find what really cracks you up, whether it’s a comedian, a video, or a friend who does the voice, and give yourself ten minutes of it when your day gets heavy. The studies that showed a drop in cortisol did it just like this: healthy adults, something funny, nothing else [6]. The key is that it has to be genuine. In the study, the effect only stemmed from real, uncontrollable laughter, not just from feeling amused [7]. Think of it as a dose. Use it when you need it, not just once in a while.

The Style Audit. For a week, pay attention to which of the four types of humor you use. Affiliative brings people together. Self-enhancing helps you keep your own bad day in perspective. Aggressive is at someone else’s expense. Self-defeating is at your own. The first two are worth keeping. If you often use the fourth, making fun of yourself for a laugh, that’s the one most clearly linked to feeling worse [9][10]. Try to cut those.

The Standing Check. Before you make a joke that might go too far, ask yourself quietly: am I laughing with the person who’s dealing with this, or at them from the outside? If you’re sharing the burden, almost anything goes. If you’re not, almost nothing does. I didn’t ask myself that question at three o’clock that afternoon. I’ve asked it many times since.

The Room Rule. If you’re a leader, your humor isn’t just yours. Warm humor from a trusted leader brings the team together, but the same joke from someone who isn’t trusted yet, or aimed at someone with less power, does the opposite [14][15]. Earn trust first. Then you’ll get the laughs.

The Morning After

The next morning, I thought about writing a proper apology to the group. A calm one, after a night’s sleep. But I didn’t.

I had already apologized right away, as soon as I saw the joke land badly. That was real, and it was enough. A second apology wouldn’t have been for them. It would have been for me, just to feel better. The two who called me sick weren’t waiting for me to change. They just wanted me to grovel. I don’t grovel to a group chat.

So I let it go. I admit I messed up. They’re right that it landed badly. I still stand by why I made the joke, but I won’t defend how I sent it.

Karla doesn’t know that any of this happened. She came back twelve minutes late, after seeing elephants and monkeys and eating ice cream, three scoops, according to her, and she was as happy as one can be. The crisis that took over the chat that afternoon turned out to be the best day of the month for the only person it was really about.

I’ll keep making jokes. I wouldn’t be any use to my kids, or to you, if I tried to make myself smaller and safer just to please strangers. But I will choose my audience more carefully. The best laughs I’ve ever had come from a few people who know me well enough to joke right back. They’re what really matters.

Stay healthy.

Andre

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PS: If you have a friend who would have answered my text with something far worse and made you laugh harder for it, send them this. That’s how this newsletter grows, and it’s the only way I want it to.

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References

[1] Cousins, N. (1976). Anatomy of an illness (as perceived by the patient). New England Journal of Medicine, 295(26), 1458-1463.

[2] Bennett, M. P., Zeller, J. M., Rosenberg, L., & McCann, J. (2003). The effect of mirthful laughter on stress and natural killer cell activity. Alternative Therapies in Health and Medicine, 9(2), 38-45.

[3] Bressington, D., Mui, J., Yu, C., Leung, S. F., Cheung, K., Wu, C. S. T., Bollard, M., & Chien, W. T. (2018). The effects of group-based laughter yoga interventions on mental health in adults: A systematic review. Journal of Psychiatric and Mental Health Nursing, 25(8), 517-527.

[4] Martin, R. A. (2001). Humor, laughter, and physical health: Methodological issues and research findings. Psychological Bulletin, 127(4), 504-519.

[5] Vlachopoulos, C., Xaplanteris, P., Alexopoulos, N., Aznaouridis, K., Vasiliadou, C., Baou, K., Stefanadi, E., & Stefanadis, C. (2009). Divergent effects of laughter and mental stress on arterial stiffness and central hemodynamics. Psychosomatic Medicine, 71(4), 446-453.

[6] Kramer, C. K., & Leitao, C. B. (2023). Laughter as medicine: A systematic review and meta-analysis of interventional studies evaluating the impact of spontaneous laughter on cortisol levels. PLOS ONE, 18(5), e0286260.

[7] Dunbar, R. I. M., Baron, R., Frangou, A., Pearce, E., van Leeuwen, E. J. C., Stow, J., Partridge, G., MacDonald, I., Barra, V., & van Vugt, M. (2012). Social laughter is correlated with an elevated pain threshold. Proceedings of the Royal Society B: Biological Sciences, 279(1731), 1161-1167.

[8] Martin, R. A., Puhlik-Doris, P., Larsen, G., Gray, J., & Weir, K. (2003). Individual differences in uses of humor and their relation to psychological well-being: Development of the Humor Styles Questionnaire. Journal of Research in Personality, 37(1), 48-75.

[9] Schneider, M., Voracek, M., & Tran, U. S. (2018). “A joke a day keeps the doctor away?” Meta-analytical evidence of differential associations of habitual humor styles with mental health. Scandinavian Journal of Psychology, 59(3), 289-300.

[10] Jiang, F., Lu, S., Jiang, T., & Jia, H. (2020). Does the relation between humor styles and subjective well-being vary across culture and age? A meta-analysis. Frontiers in Psychology, 11, 2213.

[11] Samson, A. C., & Gross, J. J. (2012). Humour as emotion regulation: The differential consequences of negative versus positive humour. Cognition & Emotion, 26(2), 375-384.

[12] Fritz, H. L., Russek, L. N., & Dillon, M. M. (2017). Humor use moderates the relation of stressful life events with psychological distress. Personality and Social Psychology Bulletin, 43(6), 845-859.

[13] Mesmer-Magnus, J., Glew, D. J., & Viswesvaran, C. (2012). A meta-analysis of positive humor in the workplace. Journal of Managerial Psychology, 27(2), 155-190.

[14] Rosenberg, C., Walker, A., Leiter, M., & Graffam, J. (2021). Humor in workplace leadership: A systematic search scoping review. Frontiers in Psychology, 12, 610795.

[15] Pundt, A., & Herrmann, F. (2015). Affiliative and aggressive humour in leadership and their relationship to leader-member exchange. Journal of Occupational and Organizational Psychology, 88(1), 108-125.

[16] Craun, S. W., & Bourke, M. L. (2014). The use of humor to cope with secondary traumatic stress. Journal of Child Sexual Abuse, 23(7), 840-852.

[17] Svebak, S., Romundstad, S., & Holmen, J. (2010). A 7-year prospective study of sense of humor and mortality in an adult county population: The HUNT-2 study. International Journal of Psychiatry in Medicine, 40(2), 125-146.

[18] Romundstad, S., Svebak, S., Holen, A., & Holmen, J. (2016). A 15-year follow-up study of sense of humor and causes of mortality: The Nord-Trondelag Health Study. Psychosomatic Medicine, 78(3), 345-353.

[19] Sakurada, K., Konta, T., Watanabe, M., Ishizawa, K., Ueno, Y., Yamashita, H., & Kayama, T. (2020). Associations of frequency of laughter with risk of all-cause mortality and cardiovascular disease incidence in a general population: Findings from the Yamagata Study. Journal of Epidemiology, 30(4), 188-193.

[20] Rozanski, A., Bavishi, C., Kubzansky, L. D., & Cohen, R. (2019). Association of optimism with cardiovascular events and all-cause mortality: A systematic review and meta-analysis. JAMA Network Open, 2(9), e1912200.

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A note for new readers:

I’m a trained reconstructive facial surgeon, medical doctor, and dentist. Before launching this newsletter, I had a varied career: competitive freestyle wrestler, management consultant (McKinsey), entrepreneur (Zocdoc, Thermondo, and docdre ventures), and corporate executive (Sandoz). Today, I’m a Managing Director and Partner at BCG.

Husband of one. Father of three. Split between Berlin’s urban pulse and our Baltic Sea retreat. I’d rather be moving than sitting. Not just hobbies. Research. My body is my primary laboratory; I’ve been conducting experiments for decades.

If this is your first time here, welcome. I’m excited to share what I’ve learned and will continue to learn with you.

​

DISCLAIMER:

Let’s get one thing straight: None of this, whether text, graphics, images, or anything else, is medical or health advice. This newsletter is here to inform, educate, and (hopefully) entertain you, not to diagnose or treat you.

Yes, I’m a trained medical doctor and dentist. No, I’m not your doctor. The content here isn’t a replacement for professional medical advice, diagnosis, or treatment.

If you have questions about your health, talk to your physician or a qualified health professional. Don’t ignore their advice or delay getting care because of something you read in The Upward ARC. Be smart. Do your research. And, as always, take care of yourself.

He stacks chairs at the far end of the room, moving slowly, as if he no longer cares. The candle on our table is gone. We’re the last two in the restaurant, taking our time.

An old friend, one of my closest. We started the night with a Negroni each, just like we used to. Then we shared a bottle of red that was better than it needed to be. The steaks are gone. The table is covered in empty glasses and bread.

We talked about his relationship. We talked about my kids. We talked about work, especially the parts we never share online. We talked about the future, our plans, and ideas that aren’t fully formed. We even talked about our fears, the kind of conversation you only have this late, with this friend, after a bottle of wine.

I’m a doctor. I know what those drinks will do to me over the next two days. I sleep better now than I used to. I stopped wearing my Oura ring a year ago. I feel the trade-off as it happens, and I choose it on purpose.

I wouldn’t trade this night for a perfect recovery score. Not even for ten perfect scores.

There’s an honesty at this table you don’t find in a quiet office with a professional. Two old friends, past midnight, telling each other the truth about their lives.

It’s one of the best things I’ll do for my health all month. No wearable device would ever count it as a success.

A Few Days Later

I saw a man say that a night like this has ruined three days of his life.

He was speaking into a podcast microphone. He hadn’t been drunk. Just a couple of glasses of wine at dinner, he said, and it affected him for three days. He slept worse, ate worse the next day, and skipped the gym. Then he said the line that went viral: “I podcasted worse.”

Oh boy. That escalated fast.

The man was Steven Bartlett, host of Diary of a CEO, one of the world’s biggest podcasts. Within two days, he became a symbol of something many people were tired of. A BBC Radio 1 host even called for an anti-optimization movement. A man with a fitness tracker had called a normal evening with wine a three-day disaster, and people online had had enough.

I watched with mixed feelings. The physical effects he described are real. I’ve written about them before. But I see things differently.

He blamed the wine. But the wine wasn’t the real problem. What really cost him three days was the tracker on his wrist and the story it told him about a normal night.

The Part Where I Agree With Him

Let me be clear about the science. This is where I stand, and I won’t change it just to make a point.

Alcohol isn’t good for you. The largest analysis we have, covering 195 countries, found that the amount of drinking that does the least harm to your health is zero [1]. Not one glass. Zero. Even light drinking raises the risk of several cancers. For women, every 10 grams of alcohol a day, about one small glass of wine, raises breast cancer risk by roughly 10 percent. Wine is no exception [2].

And it does disturb your sleep. Alcohol helps you fall asleep faster at any dose, but then it breaks up the second half of the night. At moderate and higher doses, it also reduces your REM sleep [3]. So when Bartlett says the wine cost him a bad night and a worse next day, he’s right. I’ve felt it. You’ve felt it.

That’s why I made alcohol the exception, not the rule. I don’t have a glass most nights. I save it for special occasions, like the dinner I described. I knew the cost ahead of time, and I’m fine with it.

So if the evidence is on his side, what did he get so wrong?

The Cost of Keeping Score

Here’s where the optimized life goes wrong. The harm from an occasional glass of wine is small and lasts a day or two. But treating your body like a business report does much more harm and lasts for years.

Start with the tracker. Sleep researchers have a name for this: orthosomnia. In several cases, patients became so focused on perfecting their sleep scores that the obsession made their insomnia worse [4]. The device meant to help them ended up causing trouble.

Then there’s stress. A study of nearly 29,000 adults found something I think about often. People under high stress had a 43% higher risk of dying early, but only if they believed stress was harming them. Those under the same high stress who didn’t see it as a threat had no higher risk [5]. The belief did as much damage as the stress.

The way you think about a bad recovery score might hurt you more than what caused it in the first place.

And we’re getting worse at this. The pressure to meet other people’s standards, what researchers call socially prescribed perfectionism, keeps rising. By 2017, two-thirds of young adults scored above the 1989 average [6]. We’re making ourselves anxious by trying to be perfect. That slow, steady stress has a name too: allostatic load, the biological cost your body pays after years of stress. Over time, it wears down your heart, metabolism, and brain [7].

One more honest note, because it cuts both ways. The old idea that moderate drinking helps you live longer was mostly a statistical artifact. Once you stop counting the “non-drinkers” who are really sick people who quit, the apparent benefit mostly disappears [8]. The largest recent review, almost five million people, found no real protection at low levels [9]. So don’t drink for your health. And don’t punish yourself over the glass you had with a friend. Both follow from the same evidence.

What the Trackers Miss

If the small things are just for show, what really matters? The things that affect how long you live are usually simple, and most can’t be tracked by any device.

Connection is near the top. A review of 148 studies involving more than 300,000 people found that those with strong social relationships had a 50% higher chance of surviving the follow-up period. The authors put it on par with quitting smoking, ahead of obesity and inactivity [10]. The reverse holds. Isolation, loneliness, and living alone each raise the risk of early death by around 30%, on the scale of obesity itself [11].

It runs deeper than a headcount. Adults over 50 with the weakest sense of purpose had nearly two and a half times the risk of dying compared to those with the strongest [12]. Even meaning shows up in the mortality tables.

Think back to that restaurant table. Two old friends, talking honestly late into the night. There’s real science behind this. The same endorphins released when we laugh or sing also appear when we share a drink. This chemistry brings people closer, and those who keep up these social habits have bigger support networks and more trust in their communities [13]. The dinner was the real medicine that night. The wine was just there.

Do the Basics, Then Stop

There’s one more thing, and it’s what lets you relax.

The basics work, and then doing more doesn’t help. A pooled study of 661,000 adults found that the risk of early death dropped quickly as people went from doing nothing to meeting the basic activity guidelines, then kept improving up to three to five times that level, and then leveled off. Doing ten times the minimum added nothing [14]. Almost all the benefits come from the first ordinary dose.

That’s how most things in health work. Sleep seven to eight hours. Move and lift something heavy a few times a week. Eat mostly real food. Stay close to people you care about. Do work that matters to you. If you get these right, you’ve covered most of what matters.

It’s fun to try new things, like the cold plunge, the latest breathing app, or the supplement of the month. I do it too. But the basics give you almost all the benefits. The new stuff is just the last one percent, and you only get there after you’ve handled the basic 99%.

A landmark study followed five simple habits: never smoking, keeping a healthy weight, regular movement, a decent diet, and, believe it or not, moderate drinking. Those five added 12-14 years to life expectancy [15]. You could argue, as the alcohol researchers earlier would, whether that last one truly belongs. But notice the pattern. The gold standard for a long, healthy life includes a glass of wine. It was never about living like a monk.

We’re Coming Back to Our Senses

I think we’re at a turning point, and the way people reacted to that clip shows it clearly.

For years, the culture pushed us in one direction: more tracking, more routines, more new health trends. Some of it helped. But things kept escalating until someone could say a glass of wine ruined three days, and a million people finally said enough.

That reaction wasn’t really about him. It was a sign. People are starting to remember that connection, a few good habits, and some moderation have always been the answer. Common sense is coming back.

This doesn’t mean you should ignore the science. Your tracker can teach you something real. Wear it for a month, see how alcohol and late nights affect your numbers, and then trust what you’ve learned. The readiness score is just information. It’s not a judgment on your day, and it’s not worth chasing for its own sake.

In my Upward ARC framework, this idea fits into two pillars. Recover, because connection and a calm mind help you reset, while constant self-scoring keeps you stressed. And Capacity, because moderation, the discipline to do the basics and then stop, is what helps you keep going for years instead of burning out over a number.

Try This Today

The Occasion Rule: The goal isn’t zero. It’s to stop pouring a glass out of habit on a random Tuesday and save it for nights that matter. A dinner with an old friend is worth it. A glass alone in front of your laptop isn’t. Make your choice on purpose.

The Sunday Check: If you use a tracker, stop worrying about single mornings. One bad number means almost nothing. Check your numbers once a week, maybe every Sunday, compare this week to last, and see if you missed one of your basics. Then adjust. Checking every day mostly just adds stress.

The Standing Table: Schedule one relaxed evening with people you care about, and protect it as you would a board meeting. Keep your phone in your pocket. Don’t leave early for an alarm. Don’t feel guilty the next day. That evening is part of your health. Treat it that way.

The Subtraction Audit: List everything you do for your health right now. Then cut the one with the weakest evidence and the most effort. Maybe it’s the cold plunge you hate, the eleventh supplement, or the routine you follow just because. Cutting back often helps more than adding something new.

Last Call

It’s almost one in the morning. My friend and I finally get up, because the staff deserves to go home and we’ve said what we needed to say. I’ll sleep worse tonight. I knew that when I ordered the second bottle. Tomorrow I’ll move a little slower, drink some water, and get back to the basics I always stick to.

It will have been worth every minute.

Somewhere else, someone with a perfect recovery score is going to bed on time, proud of his podcast and tracking every detail of his evening. I don’t envy him. I think he’s missing the point.

A glass of wine might cost you a day. But obsessing over the numbers can cost you the dinner, the friend, and the honest talk at midnight. Those are the real reasons any of this matters.

Do the basics as if your life depends on them, because it does. Then put the tracker away, pour a drink for someone you care about, and stay at the table.

Moderation is the harder skill. It means knowing the science well and still choosing to enjoy the night.

Stay healthy.

Andre

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PS: If this message came at the right time for you, send it to the friend you’d want to sit with at midnight. Tell them dinner’s on you. That’s how this newsletter grows, and it’s the only way I want it to.

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References

[1] GBD 2016 Alcohol Collaborators. (2018). Alcohol use and burden for 195 countries and territories, 1990-2016: A systematic analysis for the Global Burden of Disease Study 2016. The Lancet, 392(10152), 1015-1035.

[2] Sun, Q., Xie, W., Wang, Y., Chong, F., Song, M., Li, T., Yang, Y., & Tang, H. (2020). Alcohol consumption by beverage type and risk of breast cancer: A dose-response meta-analysis of prospective cohort studies. Alcohol and Alcoholism, 55(3), 246-253.

[3] Ebrahim, I. O., Shapiro, C. M., Williams, A. J., & Fenwick, P. B. (2013). Alcohol and sleep I: Effects on normal sleep. Alcoholism: Clinical and Experimental Research, 37(4), 539-549.

[4] Baron, K. G., Abbott, S., Jao, N., Manalo, N., & Mullen, R. (2017). Orthosomnia: Are some patients taking the quantified self too far? Journal of Clinical Sleep Medicine, 13(2), 351-354.

[5] Keller, A., Litzelman, K., Wisk, L. E., Maddox, T., Cheng, E. R., Creswell, P. D., & Witt, W. P. (2012). Does the perception that stress affects health matter? The association with health and mortality. Health Psychology, 31(5), 677-684.

[6] Curran, T., & Hill, A. P. (2019). Perfectionism is increasing over time: A meta-analysis of birth cohort differences from 1989 to 2016. Psychological Bulletin, 145(4), 410-429.

[7] Guidi, J., Lucente, M., Sonino, N., & Fava, G. A. (2021). Allostatic load and its impact on health: A systematic review. Psychotherapy and Psychosomatics, 90(1), 11-27.

[8] Stockwell, T., Zhao, J., Panwar, S., Roemer, A., Naimi, T., & Chikritzhs, T. (2016). Do “moderate” drinkers have reduced mortality risk? A systematic review and meta-analysis of alcohol consumption and all-cause mortality. Journal of Studies on Alcohol and Drugs, 77(2), 185-198.

[9] Zhao, J., Stockwell, T., Naimi, T., Churchill, S., Clay, J., & Sherk, A. (2023). Association between daily alcohol intake and risk of all-cause mortality: A systematic review and meta-analyses. JAMA Network Open, 6(3), e236185.

[10] Holt-Lunstad, J., Smith, T. B., & Layton, J. B. (2010). Social relationships and mortality risk: A meta-analytic review. PLoS Medicine, 7(7), e1000316.

[11] Holt-Lunstad, J., Smith, T. B., Baker, M., Harris, T., & Stephenson, D. (2015). Loneliness and social isolation as risk factors for mortality: A meta-analytic review. Perspectives on Psychological Science, 10(2), 227-237.

[12] Alimujiang, A., Wiensch, A., Boss, J., Fleischer, N. L., Mondul, A. M., McLean, K., Mukherjee, B., & Pearce, C. L. (2019). Association between life purpose and mortality among US adults older than 50 years. JAMA Network Open, 2(5), e194270.

[13] Dunbar, R. I. M., Launay, J., Wlodarski, R., Robertson, C., Pearce, E., Carney, J., & MacCarron, P. (2017). Functional benefits of (modest) alcohol consumption. Adaptive Human Behavior and Physiology, 3(2), 118-133.

[14] Arem, H., Moore, S. C., Patel, A., Hartge, P., Berrington de Gonzalez, A., Visvanathan, K., Campbell, P. T., Freedman, M., Weiderpass, E., Adami, H. O., Linet, M. S., Lee, I. M., & Matthews, C. E. (2015). Leisure time physical activity and mortality: A detailed pooled analysis of the dose-response relationship. JAMA Internal Medicine, 175(6), 959-967.

[15] Li, Y., Pan, A., Wang, D. D., Liu, X., Dhana, K., Franco, O. H., Kaptoge, S., Di Angelantonio, E., Stampfer, M., Willett, W. C., & Hu, F. B. (2018). Impact of healthy lifestyle factors on life expectancies in the US population. Circulation, 138(4), 345-355.

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A note for new readers:

I’m a trained reconstructive facial surgeon, medical doctor, and dentist. Before launching this newsletter, I had a varied career: competitive freestyle wrestler, management consultant (McKinsey), entrepreneur (Zocdoc, Thermondo, and docdre ventures), and corporate executive (Sandoz). Today, I’m a Managing Director and Partner at BCG.

Husband of one. Father of three. Split between Berlin’s urban pulse and our Baltic Sea retreat. I’d rather be moving than sitting. Not just hobbies. Research. My body is my primary laboratory; I’ve been conducting experiments for decades.

If this is your first time here, welcome. I’m excited to share what I’ve learned and will continue to learn with you.

​

DISCLAIMER:

Let’s get one thing straight: None of this, whether text, graphics, images, or anything else, is medical or health advice. This newsletter is here to inform, educate, and (hopefully) entertain you, not to diagnose or treat you.

Yes, I’m a trained medical doctor and dentist. No, I’m not your doctor. The content here isn’t a replacement for professional medical advice, diagnosis, or treatment.

If you have questions about your health, talk to your physician or a qualified health professional. Don’t ignore their advice or delay getting care because of something you read in The Upward ARC. Be smart. Do your research. And, as always, take care of yourself.

Inside are eight packages of dried herbs, some tree bark shavings, and scorpions. Dried scorpions. I promise, this is real.

I brought it back from Beijing about eight years ago. A traditional Chinese medicine doctor gave me the prescription during a free afternoon on a work trip. I was supposed to boil everything into a broth and drink it. When my wife saw it, she took a careful sniff and decided that if I ever made it, I’d have to do it outside, in the garden, far from the kitchen.

I still haven’t done it. The bag is still there.

I went for one reason: curiosity. I often try things on myself before I can explain why. That afternoon, I got a tongue exam, a pulse reading on both wrists, a diagnosis that mentioned a shoulder surgery the doctor couldn’t have known about, two hours lying on a bench with needles, and a bag of scorpions I’ll probably never use.

Somewhere in that strange afternoon, a real question stuck with me. I finally spent a weekend digging into the research to find an answer.

The question is simple to ask but tough to answer. Is traditional Chinese medicine 5,000 years of wisdom that modern medicine ignores? Or is it just elaborate theater with ancient branding?

The truth is, it’s both, mixed together so closely that most people never separate them. Supporters focus on the successes and ignore the rest. Critics focus on the nonsense and ignore the successes. Neither approach really helps.

So I did what I always do when unsure about a treatment. I looked at the evidence rather than the reputation, kept what held up to a doctor’s review, and set aside what didn’t. You could call it the doctor’s edit.

Surprisingly, quite a bit holds up. But some of it can also land you in a cancer ward. It’s important to know the difference.

The 5,000-Year Story

Every brochure claims traditional Chinese medicine is 5,000 years old, but that number is mostly marketing. The oldest main text, the Huangdi Neijing or Yellow Emperor’s Inner Classic, was put together between 400 BCE and 260 CE [1]. So the written tradition is about 2,000 years old. Still old, just not 5,000.

What’s even more surprising is how recent the unified system is. The version of TCM we know today was mostly put together in the 1950s and early 1960s in communist China, under Mao [2]. There weren’t enough Western-trained doctors, so the government combined different classical and folk practices, settled the disagreements, and created a single curriculum. The tidy, “ancient” system sold to wellness tourists is mostly a product of mid-20th-century health policy.

But that hasn’t slowed its growth. Today, 170 World Health Organization member countries officially recognize that their people use traditional or complementary medicine [3]. In 2019, the WHO even added 150 traditional-medicine disorder categories, based on classical Chinese medicine, to the ICD-11, the global disease classification manual [4].

TCM is built on a few main ideas: qi, a vital energy said to flow through the body; yin and yang; the five phases; and a network of meridians, or channels for qi [5]. These ideas lead to the practices most people know: acupuncture, herbal formulas, cupping, tui na massage, tai chi, and qigong.

What Survives the Audit

Let’s start with the best thing TCM has given us, which is also one of the most important drugs of the last century.

In the 1960s, a Chinese chemist named Tu Youyou was asked to find a malaria treatment. She worked through hundreds of old texts and kept returning to one line from Ge Hong, written around 340 CE, which described soaking sweet wormwood in cold water and drinking the juice for fevers [6]. Every extraction she had tried with heat had failed. That detail, cold water, told her heat was destroying the active compound. She switched to a low-temperature extraction in 1971, and it worked [6]. The active molecule, isolated soon after, was artemisinin.

Today, it reduces malaria deaths by over 20% overall and more than 30% in children, saving more than 100,000 lives a year in Africa alone [7]. Tu Youyou won the Nobel Prize in 2015 [7]. The old text gave her the clue, and modern chemistry did the rest. That’s the best way to look at TCM: a huge, ancient list of ideas, most untested, with a few real gems.

Acupuncture is a trickier case. The biggest analysis combined 39 trials and 20,827 patients with chronic pain [8]. Acupuncture worked much better than doing nothing, and a little better than fake “sham” acupuncture [8]. The researchers, who supported the practice, said the effect is real but can’t be explained by needling alone [8]. It works, to some extent, but not for all the reasons its theory suggests. We’ll return to this later.

Then there’s tai chi, which I’ve come to respect most. A New England Journal of Medicine trial found it worked better than wellness education and stretching for fibromyalgia, a tough pain condition [9]. A bigger BMJ study showed tai chi was as effective as aerobic exercise [10]. A Cochrane review, our strictest evidence, found tai chi reduced falls in older adults by 19% [11]. For an aging executive or parent, fewer falls can mean the difference between staying independent and a hip fracture.

What Fails the Audit

After 2,000 years of searching, no one has ever found a meridian. Anatomists have looked for the channels where qi is supposed to flow and found nothing. Even acupuncture researchers agree there’s no physical structure matching the meridian map [12]. The lines on the chart aren’t in the body.

The data on needling tells a similar story. In a large German trial, 1,162 patients with chronic back pain got either real acupuncture or fake acupuncture, with needles placed randomly and shallowly [13]. Both groups improved, and both did better than standard drugs and physiotherapy. The difference between real and fake was just 3.4%, which wasn’t statistically significant [13]. If the “wrong” points work as well as the “right” ones, meridian theory isn’t the reason. Something else is at play.

There’s another issue for anyone who relies on Chinese research. A review of controlled trials found that 99% of studies published in China said the treatment worked [14]. Not just most.. almost all. When almost nothing ever fails, the research stops showing whether treatments actually work.

What Can Hurt You

The risks are real, and this is where the appeal of tradition has to end.

Some Chinese herbs contain aristolochic acid, a potent carcinogen so distinctive it leaves its own signature mutation in your DNA. In Taiwan, where these herbs were widely prescribed, researchers studying patients with upper urinary tract cancer found that 60% carried the chemical’s fingerprint in their DNA and 31% carried its signature mutation [15]. Taiwan has the world’s highest rate of that cancer [15]. These herbs cause cancer, traceably, at the level of the gene.

Contamination is common. In one review, a Taiwan survey found that 24% of Chinese herbal products contained undeclared pharmaceutical drugs, like corticosteroids, anti-inflammatories, and sedatives [16]. You might think you’re taking a gentle plant remedy, but you could be getting an unregulated dose of something else.

Some herbs are simply dangerous on their own. Ma huang, or ephedra, caused strokes, seizures, and heart problems so severe that the FDA banned it from supplements in 2004 [17].

The harm goes beyond the clinic. Demand for traditional remedies has pushed animals like the pangolin, rhino, and tiger toward extinction for their scales, horns, and bones. China banned the medicinal trade in tiger bone and rhino horn in 1993, but the pressure continues. The pangolin is now the most trafficked mammal in the world.

Where Our Own Medicine Runs Out

So why does any of this last? Why did a fairly skeptical doctor bring home a bag of scorpions and a story he still tells?

Part of the answer is uncomfortable, because it’s really about us.

When I was in that Beijing clinic, the doctor spent almost an hour with me before prescribing anything. He checked my tongue, held both wrists, and asked about my work, sleep, and previous illnesses. Compare that to today’s reality: in 67 countries, doctors in 18 of them, covering about half the world’s population, spend five minutes or less with each patient [18]. Even in well-funded places, an American study found doctors spend only 27% of their day with patients, and 49% on paperwork and screens [19].

Then there was my shoulder. He guessed a surgery he couldn’t have seen, and for years, I thought of it as a small miracle. But the more likely explanation is more interesting. He was a skilled observer who had examined thousands of bodies, looking at someone my age and build, with the signs of old contact sports and a guarded injury. He made some confident guesses; the ones that hit stand out, and the misses are forgotten. And he spent more time looking at me, calmly, than any doctor had in years. When you give someone that much attention, you notice things too.

Here’s something modern medicine is only now admitting: the attention itself is a treatment. In a Harvard trial, patients with irritable bowel syndrome were split into three groups: a waiting list, fake acupuncture alone, and fake acupuncture given by a warm, attentive practitioner [20]. Relief rates went from 28% on the waiting list, to 44% with the ritual, to 62% when a caring person delivered it [20]. The needles were fake in both groups, but the relationship made the difference.

The benefit came from simple things: time, ritual, and a caring person. Our five-minute, screen-focused system has quietly stopped offering all three. Now, Western medicine is trying to bring them back with new names like systems medicine, whole-person care, and the P4 model of prevention over rescue [21]. We’re reinventing the bedside manner we once cut to save time.

This belongs in the Recover pillar of my Upward ARC framework, and it matters more than most high performers admit. Recover means bringing the nervous system back to baseline: giving unhurried attention, resetting stress, and treating stress as a real factor, not just a personality trait. Movement, like tai chi, fits in Activate, alongside the one proven molecule from the tradition. The metaphysics doesn’t fit anywhere. That’s my edit.

Try This Today

The Enforced Stillness. The most helpful thing in that clinic was being forced to stay still for two hours. Most high performers never plan rest, so set up something that makes you rest. Try one 90-minute block a week with no screen, no phone, and no agenda. A long walk without headphones counts. Lying on the floor counts. The key is to have a break from input.

The Tai Chi Floor. Of all the traditional practices, tai chi has real studies behind it: it helps with pain, balance, fewer falls, and lower stress [9][10][11]. The studies used it twice a week. It’s gentle enough for anyone from 50 to 80, and it trains both balance and a calm nervous system. Try a class or a video, and give it eight weeks before deciding if it works for you.

The Long Consult Rule. What worked in Beijing was unhurried attention, and you can get that at home if you ask. When something matters, book the longest appointment you can, write down your three main questions ahead of time, and don’t let the visit end with the doctor typing. If your system only gives you 7 minutes, find a way to get at least 45 once a year.

The Natural-Label Audit. If you use herbal or traditional supplements, remember that “natural” is just a marketing term, not a safety guarantee. A quarter of these products contain undeclared pharmaceutical drugs [16], and some have a known carcinogen [15]. Only buy from suppliers who share third-party testing for contaminants. If a product can’t tell you exactly what’s in it, don’t take it.

The Bag in the Garden

The bag of scorpions is still in my house. Every so often, I move it, think about making the broth, imagine my wife’s reaction, and put it back.

I think about that afternoon more than I expected. The needles were probably just theater. The meridians weren’t real. The diagnosis was a skilled man making good guesses about a tired executive. But he did something no doctor had done for me in years: he made me lie still, doing nothing, for two hours. He saw a stressed, overworked man with a bad back and prescribed the one thing I’d never give myself.

That’s the part worth keeping: the stillness, the attention, the unhurried hour. The scorpions and the qi can be left behind.

Here’s my doctor’s edit on 5,000 years: keep the one proven molecule, keep the movement that’s backed by studies, and keep the unhurried hour that modern medicine lost. The rest can go out in the garden, where it belongs.

Stay healthy.

Andre

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​

PS: I still try things on myself that I can’t fully explain, and I keep that bag as a reminder. If you know someone who swears by all of this, or someone who dismisses it, share this with them. Both are half right, and that’s what makes it interesting.

​

​

References

[1] Unschuld, P. U. (2003). Huang Di nei jing su wen: Nature, knowledge, imagery in an ancient Chinese medical text. University of California Press.

[2] Taylor, K. (2005). Chinese medicine in early communist China, 1945-1963: A medicine of revolution. RoutledgeCurzon.

[3] World Health Organization. (2019). WHO global report on traditional and complementary medicine 2019. World Health Organization.

[4] World Health Organization. (2019). International statistical classification of diseases and related health problems (11th ed.), Chapter 26: Supplementary chapter traditional medicine conditions, Module I. World Health Organization.

[5] Zhang, Q., et al. (2021). An introduction to traditional Chinese medicine, including acupuncture. The Anatomical Record, 304(11), 2675-2682.

[6] Su, X.-Z., & Miller, L. H. (2015). The discovery of artemisinin and the Nobel Prize in Physiology or Medicine. Science China Life Sciences, 58(11), 1175-1179.

[7] The Nobel Assembly at Karolinska Institutet. (2015). The Nobel Prize in Physiology or Medicine 2015 [Press release]. NobelPrize.org.

[8] Vickers, A. J., Vertosick, E. A., Lewith, G., MacPherson, H., Foster, N. E., Sherman, K. J., Irnich, D., Witt, C. M., Linde, K., & Acupuncture Trialists’ Collaboration. (2018). Acupuncture for chronic pain: Update of an individual patient data meta-analysis. The Journal of Pain, 19(5), 455-474.

[9] Wang, C., Schmid, C. H., Rones, R., Kalish, R., Yinh, J., Goldenberg, D. L., Lee, Y., & McAlindon, T. (2010). A randomized trial of tai chi for fibromyalgia. New England Journal of Medicine, 363(8), 743-754.

[10] Wang, C., Schmid, C. H., Fielding, R. A., Harvey, W. F., Reid, K. F., Price, L. L., Driban, J. B., Kalish, R., Rones, R., & McAlindon, T. (2018). Effect of tai chi versus aerobic exercise for fibromyalgia: Comparative effectiveness randomized controlled trial. BMJ, 360, k851.

[11] Sherrington, C., Fairhall, N. J., Wallbank, G. K., Tiedemann, A., Michaleff, Z. A., Howard, K., Clemson, L., Hopewell, S., & Lamb, S. E. (2019). Exercise for preventing falls in older people living in the community. Cochrane Database of Systematic Reviews, (1), CD012424.

[12] Longhurst, J. C. (2010). Defining meridians: A modern basis of understanding. Journal of Acupuncture and Meridian Studies, 3(2), 67-74.

[13] Haake, M., Müller, H.-H., Schade-Brittinger, C., Basler, H. D., Schäfer, H., Maier, C., Endres, H. G., Trampisch, H. J., & Molsberger, A. (2007). German Acupuncture Trials (GERAC) for chronic low back pain. Archives of Internal Medicine, 167(17), 1892-1898.

[14] Vickers, A., Goyal, N., Harland, R., & Rees, R. (1998). Do certain countries produce only positive results? A systematic review of controlled trials. Controlled Clinical Trials, 19(2), 159-166.

[15] Chen, C.-H., Dickman, K. G., Moriya, M., Zavadil, J., Sidorenko, V. S., Edwards, K. L., Gnatenko, D. V., Wu, L., Turesky, R. J., Wu, X.-R., Pu, Y.-S., & Grollman, A. P. (2012). Aristolochic acid-associated urothelial cancer in Taiwan. Proceedings of the National Academy of Sciences, 109(21), 8241-8246.

[16] Ernst, E. (2002). Adulteration of Chinese herbal medicines with synthetic drugs: A systematic review. Journal of Internal Medicine, 252(2), 107-113.

[17] Haller, C. A., & Benowitz, N. L. (2000). Adverse cardiovascular and central nervous system events associated with dietary supplements containing ephedra alkaloids. New England Journal of Medicine, 343(25), 1833-1838.

[18] Irving, G., Neves, A. L., Dambha-Miller, H., Oishi, A., Tagashira, H., Verho, A., & Holden, J. (2017). International variations in primary care physician consultation time: A systematic review of 67 countries. BMJ Open, 7(10), e017902.

[19] Sinsky, C., Colligan, L., Li, L., Prgomet, M., Reynolds, S., Goeders, L., Westbrook, J., Tutty, M., & Blike, G. (2016). Allocation of physician time in ambulatory practice: A time and motion study in 4 specialties. Annals of Internal Medicine, 165(11), 753-760.

[20] Kaptchuk, T. J., Kelley, J. M., Conboy, L. A., Davis, R. B., Kerr, C. E., Jacobson, E. E., Kirsch, I., Schyner, R. N., Nam, B. H., Nguyen, L. T., Park, M., Rivers, A. L., McManus, C., Kokkotou, E., Drossman, D. A., Goldman, P., & Lembo, A. J. (2008). Components of placebo effect: Randomised controlled trial in patients with irritable bowel syndrome. BMJ, 336(7651), 999-1003.

[21] Hood, L., & Flores, M. (2012). A personal view on systems medicine and the emergence of proactive P4 medicine: Predictive, preventive, personalized and participatory. New Biotechnology, 29(6), 613-624.

​

A note for new readers:

I’m a trained reconstructive facial surgeon, medical doctor, and dentist. Before launching this newsletter, I had a varied career: competitive freestyle wrestler, management consultant (McKinsey), entrepreneur (Zocdoc, Thermondo, and docdre ventures), and corporate executive (Sandoz). Today, I’m a Managing Director and Partner at BCG.

Husband of one. Father of three. Split between Berlin’s urban pulse and our Baltic Sea retreat. I’d rather be moving than sitting. Not just hobbies. Research. My body is my primary laboratory; I’ve been conducting experiments for decades.

If this is your first time here, welcome. I’m excited to share what I’ve learned and will continue to learn with you.

​

DISCLAIMER:

Let’s get one thing straight: None of this, whether text, graphics, images, or anything else, is medical or health advice. This newsletter is here to inform, educate, and (hopefully) entertain you, not to diagnose or treat you.

Yes, I’m a trained medical doctor and dentist. No, I’m not your doctor. The content here isn’t a replacement for professional medical advice, diagnosis, or treatment.

If you have questions about your health, talk to your physician or a qualified health professional. Don’t ignore their advice or delay getting care because of something you read in The Upward ARC. Be smart. Do your research. And, as always, take care of yourself.

“You break him, or he breaks you. There is no third option.”

I heard some version of that line four times a week starting at age twelve. By the time I stopped competing at twenty-five, it was second nature. Read the room. Find the leverage. Finish the point. Everything became a point: school, exams, even client meetings in my thirties.

Thirty years later, I’m sitting on a terrace in Malta with eight other men. Six are surgeons, and three run hospital departments. Each of us learned some version of what my coach taught me. In different places, we were all trained to find leverage and finish the point.

It’s Friday night. One of the men at the end of the table has a brain tumor that has come back. This trip is on his list. The surgeon with the longest CV refills his glass before his own.

There’s no leverage here. No point to finish. None of our training prepared us for tonight, and this is the only thing that matters.

The Experiment on the Terrace

For two days, I’ve watched nine versions of the same experiment.

Each of us was picked for the same trait, in our own way. You don’t run a department, build a practice, make partner, or close a Series B without it. Psychiatrist Paul Conti describes three drives that compete in every adult: Generative, the urge to create, contribute, and build something lasting; Aggressive, the energy to compete, control, assert, and accumulate; and Pleasure, the pull toward satisfaction and enjoyment [1].

In a healthy system, Generative is in charge. Aggressive and Pleasure are still there, but they support the one in the chair.

The corner office, senior partner role, chief surgeon position, and founder seat are all twenty-year filters for the opposite setup. They select for Aggressive being in charge. By forty-seven, your inner system has run this way for so long you don’t notice it. You think it’s just who you are.

That’s the experiment I’m watching this weekend: nine men trained in Aggressive, but none of them using it.

The Three Drives

Every adult has all three drives running at all times. The real question is which one is in charge.

The Generative drive builds, teaches, creates, and contributes. It writes the chapter that took three years to learn. It operates on the patient who can’t pay the full fee because the case is interesting and the family is scared. It stays the extra hour with the junior who’s going to leave the firm anyway. It grows with age because it doesn’t depend on winning.

The Aggressive drive engages with the world; not violence, but the urge to compete, control, defend, and take ground. Healthy people use it as a tool. It builds practices, closes deals, and runs operating rooms under pressure. When it’s in charge, every flat surface looks like a hill.

The Pleasure drive pulls us toward sensation, satisfaction, and enjoyment. The wine, the holiday, the meal, the achievement as a trophy. It’s useful when it serves the others, but when it’s in charge, it ends up consuming what it was supposed to enjoy.

Conti’s model is hierarchical. For mental health, Generative should be in charge, Aggressive provides the drive, and Pleasure adds flavor. The order matters [1].

Why Aggressive Wins by Forty-Five

Two forces come together to put Aggressive in charge by midlife. The first is selection.

The path to seniority in any high-stakes field is a twenty-year competition: medical school, residency, fellowship, attending, division chief; associate, manager, principal, partner; analyst, founder, exit, next company. At each stage, those with the most Aggressive drive move forward. Usually not the most generative or curious, but the most willing to compete, defend ground, and take the next hill.

The second force is neurobiological. Robert Sapolsky spent decades with a baboon troop in Kenya’s Masai Mara. In stable hierarchies, dominant animals carry the lowest cortisol and the lowest atherosclerosis incidence. The system rewards the position. In unstable hierarchies, where the dominants must constantly defend their standing, the pathology load inverts. The dominants now carry the most severe cardiovascular, immunological, and adrenocortical damage in the troop [2]. They keep the rank. The body pays for it.

Modern corporate, surgical, and professional hierarchies are always unstable. Markets shift. Boards reorganize. Partners get pushed out at fifty-five. Hospital departments change with every new chief executive.

Erik Erikson named the developmental cost seventy-five years ago. He called it stagnation. The forty-seven-year-old who has won every external game and stopped generating internally is in Erikson’s clinical category, not a metaphor [3]. The Aggressive-dominant operator wins the climb and stalls when he gets there.

The Hollow Win

The cost builds up quietly over decades. The data has names.

Steptoe, Deaton, and Stone looked at Gallup data from 160 countries and found a U-shaped curve for well-being. The lowest point is ages 45 to 54 in high-income English-speaking countries [4]. The time of peak organizational seniority matches the lowest point of personal experience.

Hedonic adaptation adds to this. In the classic 1978 study by Brickman, Coates, and Janoff-Bulman, both recent lottery winners and recent accident-paralysis victims returned toward baseline well-being within months [5]. The next title doesn’t really change things.

For me, the 1996 Kasser and Ryan paper stands out most. Adults who put extrinsic goals (financial success, image, social recognition) above intrinsic ones (self-acceptance, affiliation, community feeling) reported lower energy and more physical symptoms [6]. You can win the game and still lose your health, your relationships, and your sense of self the next morning.

Envy keeps coming up. Richard Smith and Sung Hee Kim defined it as feeling inferior, hostile, and resentful when someone else has something you want. Environments where people compare status (like partner tracks, boardrooms, or surgical conferences) make it worse [7]. The people you envy show you where you’re still keeping score.

Nora Volkow’s PET scans showed that repeated dopamine hits lower D2 receptors, and the reduction lasts for months [8]. Anna Lembke at Stanford described the pleasure-pain seesaw in her 2021 book: the more pleasure you get, the more pain you borrow from the future [9]. Wins bring less pleasure as time goes on. This holds for the drink, the deal, and the screen.

What Generative Drive Produces

The Harvard Grant Study started in 1938 with 268 sophomore men and ran for over seventy years. George Vaillant, who led the study from 1972 to 2004, reported in 2012 that the warmth of relationships at age 47 was a stronger predictor of flourishing later in life than income, social class, or IQ [10]. The usual Aggressive drive scorecards (salary, rank, cognitive ability) were measured and found less important.

Robert Waldinger, who leads the study now, has made this point many times: the quality of relationships at age 50 predicts physical health at age 80 better than cholesterol levels do [11]. Investments in the Generative drive add up over time. Aggressive drive scorecards don’t.

This idea has been measured directly. Dan McAdams’ Loyola Generativity Scale, validated for over thirty years, links generativity scores to life satisfaction, coherence, and meaning [12]. Generativity is an outcome, not just a value.

A 2016 meta-analysis of 10 studies and 136,265 people found that having a higher sense of purpose in life was associated with a 17% lower risk of death from any cause (RR 0.83, 95% CI 0.75-0.91) [13]. A 2019 JAMA Network Open study of 6,985 adults over 50 found that those with the lowest sense of purpose had more than twice the four-year mortality risk compared to those with the highest (HR 2.43, 95% CI 1.57-3.75) [14]. The Generative drive helps you live longer.

These ideas aren’t new. Deci and Ryan’s Self-Determination Theory lists autonomy, competence, and relatedness as the three basic psychological needs that predict well-being across cultures [15]. Csikszentmihalyi described flow as the state where skill meets challenge, creating lasting satisfaction unlike passive pleasure [16]. Frankl’s clinical observation from the camps, that the main human motivation is the will to meaning, underlies all of this [17].

This structure is older than any of us reading this.

The Upward ARC

This belongs in the Capacity pillar of my Upward ARC framework, the long arc of what you can know, decide, and become over thirty years. The second part is Recover. An Aggressive-dominant system runs on constant stress, and no amount of vacation, retreat, or executive coaching can fix that after the fact. The real decision about your system comes before any other change you try to make.

Try This Today

Five protocols. They cost time, not money. You don’t need a coach or therapist for any of them.

The Three-Drive Inventory. Sit down with a notepad and look back at the last ninety days. Make three columns: Generative, Aggressive, Pleasure. Where did your hours, attention, and energy actually go? Be specific. Not just “leadership work,” but “the board prep that was really about not losing the chair.” Not just “client time,” but “the call I took on the holiday because I couldn’t stand the idea of someone else handling it.” The unbalanced output is your audit. Most senior leaders find the Generative column is only ten to twenty percent of the page.

The Morning-After Test. Pick your three biggest wins from the past year. Without overthinking, write down how each one actually felt the next morning. If it felt flat, joyless, or like “what’s next,” that’s the Aggressive drive at work. Generative wins are remembered with warmth, not just relief. The pattern across your three wins is your audit.

The Generative Slot. Set aside a recurring ninety-minute slot each week for something that’s only about contributing or creating. Teach a mentee who can’t promote you, write something, or build something for someone who won’t return the favor. This slot is sacred and doesn’t move for your calendar. After eight weeks, run the Morning-After Test on this slot and compare it to your Aggressive-drive wins.

The Envy Audit. List the five most recent times you felt envy. Name the person, what they had, and what you felt. Conti says envy is the Aggressive drive without a chance to win. Your list shows where you’re still keeping score and which Generative slot might be missing from your week.

The Two Cupboards. Take twenty minutes with just paper, no devices. Write down five things you’d still want to do if no one ever knew. Then list five things you spend a lot of time on that you’d stop tomorrow if no one ever saw. The gap between these lists shows who’s really running your life.

Back to the Terrace

There were nine men at the table on the terrace: the chiefs of surgery, the partners, and the man with the brain tumor. None of them got there without the trait my coach drilled into me back in 1996. But none of them were using it tonight.

In a healthy system, the Generative drive comes before the Aggressive drive. The Aggressive drive doesn’t disappear, but the order just changes. The surgeon who refilled the wine glass before his own is the same one who runs his department by Monday morning. The ability to take the hill is still there. It just isn’t in charge on a Friday night in Malta.

The leaders who age well, exit well, and enjoy what they built are the ones who do this audit at forty-seven, not sixty-seven. The Aggressive drive won’t give up control on its own. You have to move it.

For most of us, the climb picked for this trait so thoroughly that we mistake it for our character. That mistake matters. The Aggressive drive is just one of three, and it shouldn’t be in charge of any of us.

The friend at the end of the table laughs at something. The surgeon next to him passes him a piece of bread. The protocols above are a deliberate way back to what these nine men already had on Friday night.

Stay healthy.

Andre

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PS: If you read this and thought of a peer who has everything but feels nothing, please forward it to them. That’s how this newsletter grows, and it’s the only way I want it to.

References

[1] Conti, P. (Guest), & Huberman, A. (Host). (2023, September). Guest series: Dr. Paul Conti on mental health [Four-part audio podcast series]. Huberman Lab. https://www.hubermanlab.com/episode/guest-series-dr-paul-conti-how-to-understand-and-assess-your-mental-health

[2] Sapolsky, R. M. (2005). The influence of social hierarchy on primate health. Science, 308(5722), 648-652. https://doi.org/10.1126/science.1106477

[3] Erikson, E. H. (1950). Childhood and society. W. W. Norton.

[4] Steptoe, A., Deaton, A., & Stone, A. A. (2015). Subjective wellbeing, health, and ageing. The Lancet, 385(9968), 640-648. https://doi.org/10.1016/S0140-6736(13)61489-0

[5] Brickman, P., Coates, D., & Janoff-Bulman, R. (1978). Lottery winners and accident victims: Is happiness relative? Journal of Personality and Social Psychology, 36(8), 917-927. https://doi.org/10.1037/0022-3514.36.8.917

[6] Kasser, T., & Ryan, R. M. (1996). Further examining the American dream: Differential correlates of intrinsic and extrinsic goals. Personality and Social Psychology Bulletin, 22(3), 280-287. https://doi.org/10.1177/0146167296223006

[7] Smith, R. H., & Kim, S. H. (2007). Comprehending envy. Psychological Bulletin, 133(1), 46-64. https://doi.org/10.1037/0033-2909.133.1.46

[8] Volkow, N. D., Fowler, J. S., Wang, G. J., & Swanson, J. M. (2004). Dopamine in drug abuse and addiction: Results from imaging studies and treatment implications. Molecular Psychiatry, 9(6), 557-569. https://doi.org/10.1038/sj.mp.4001507

[9] Lembke, A. (2021). Dopamine nation: Finding balance in the age of indulgence. Dutton.

[10] Vaillant, G. E. (2012). Triumphs of experience: The men of the Harvard Grant Study. Belknap Press of Harvard University Press.

[11] Waldinger, R. J., & Schulz, M. S. (2023). The good life: Lessons from the world’s longest scientific study of happiness. Simon & Schuster.

[12] McAdams, D. P., & de St. Aubin, E. (1992). A theory of generativity and its assessment through self-report, behavioral acts, and narrative themes in autobiography. Journal of Personality and Social Psychology, 62(6), 1003-1015. https://doi.org/10.1037/0022-3514.62.6.1003

[13] Cohen, R., Bavishi, C., & Rozanski, A. (2016). Purpose in life and its relationship to all-cause mortality and cardiovascular events: A meta-analysis. Psychosomatic Medicine, 78(2), 122-133. https://doi.org/10.1097/PSY.0000000000000274

[14] Alimujiang, A., Wiensch, A., Boss, J., Fleischer, N. L., Mondul, A. M., McLean, K., Mukherjee, B., & Pearce, C. L. (2019). Association between life purpose and mortality among US adults older than 50 years. JAMA Network Open, 2(5), e194270. https://doi.org/10.1001/jamanetworkopen.2019.4270

[15] Deci, E. L., & Ryan, R. M. (2000). The “what” and “why” of goal pursuits: Human needs and the self-determination of behavior. Psychological Inquiry, 11(4), 227-268. https://doi.org/10.1207/S15327965PLI1104_01

[16] Csikszentmihalyi, M. (1990). Flow: The psychology of optimal experience. Harper & Row.

[17] Frankl, V. E. (2006). Man’s search for meaning (I. Lasch, Trans.). Beacon Press. (Original work published 1946)

A note for new readers:

I’m a trained reconstructive facial surgeon, medical doctor, and dentist. Before launching this newsletter, I had a varied career: competitive freestyle wrestler, management consultant (McKinsey), entrepreneur (Zocdoc, Thermondo, and docdre ventures), and corporate executive (Sandoz). Today, I’m a Managing Director and Partner at BCG.

Husband of one. Father of three. Split between Berlin’s urban pulse and our Baltic Sea retreat. I’d rather be moving than sitting. Not just hobbies. Research. My body is my primary laboratory; I’ve been conducting experiments for decades.

If this is your first time here, welcome. I’m excited to share what I’ve learned and will continue to learn with you.

​

DISCLAIMER:

Let’s get one thing straight: None of this, whether text, graphics, images, or anything else, is medical or health advice. This newsletter is here to inform, educate, and (hopefully) entertain you, not to diagnose or treat you.

Yes, I’m a trained medical doctor and dentist. No, I’m not your doctor. The content here isn’t a replacement for professional medical advice, diagnosis, or treatment.

If you have questions about your health, talk to your physician or a qualified health professional. Don’t ignore their advice or delay getting care because of something you read in The Upward ARC. Be smart. Do your research. And, as always, take care of yourself.

Jane (not her real name) is in her class. They sit together at lunch.

“Jane is out of school,” Tilda says. “She isn’t coming back this year.”

I ask what happened.

“She’s going into therapy.”

I put my fork down. Tilda leans back, balancing her chair on two legs. Her mother has reminded her not to do that so many times. I did not think I would hear that word from my 12-year-old, slipped so casually into a story about her friend.

“What do you mean, therapy?”

“She has a lot of dark thoughts. She’s depressed. She’ll be in a clinic.”

She says it like she’s telling me a friend has a dentist appointment. The words just sit there. Dark thoughts. Depressed. Clinic. When I was twelve, I didn’t have words like that for a friend.

I ask another question. She answers. We keep eating. Both the 12-year-old at our table and the one in the clinic know words I never did at their age.

After the kids go to bed, my wife and I stay at the table. It’s all we talk about.

Two Curves

I am 47. Every paper I read in residency said this would be the lowest year of my life.

The U-curve of life satisfaction is one of the most replicated findings in modern social science. Plot self-reported well-being across the human lifespan, and you get a U. High in your 20s, low in your late 40s, high again in your 70s. The shape is the headline.

Tilda is 12. Every recent paper says this is the edge of her own cliff.

There’s a turning point between us at this table. The low point I was told to expect at her age is where I am now. The low point she faces is right here, as she eats risotto and names a friend who is being treated for depression.

Both stories matter. Most of what I learned about midlife came from the curve I was taught. What I see now, in friends raising teens, is shaped by a curve no textbook has described yet.

This piece is about both.

The Floor I Was Taught

The U-curve found its modern shape in the work of David Blanchflower at Dartmouth. His 2021 paper in the Journal of Population Economics pooled data from 145 countries and 14 survey series and found the average minimum at age 46.7 in advanced economies and 49.9 in developing ones [1]. Whatever sample, whatever instrument, whatever decade, the U showed up again and again.

The pattern persisted after controlling for income, marriage, employment, and health. A separate 2010 PNAS paper from Stone, Schwartz, Broderick, and Deaton tracked psychological well-being across 340,847 US adults: daily stress peaked in the 20s and declined with age, but worry peaked around age 50 [2]. The 47-year-old reads as the most worried adult in the room because she is.

Why 47, specifically? The drivers stack in the same year. Children are still dependent, parents are starting to decline, both at once. Career complexity peaks: senior responsibility, the narrowing pyramid, the colleagues who were not going to make partner now know. Hedonic adaptation is maxed out. The aspiration-reality gap has nowhere left to hide. The first funerals shift from grandparents to peers. The hours do not lengthen. The demands do.

The most striking confirmation came from chimpanzees. In 2012, Weiss, King, and colleagues published a PNAS paper on 508 great apes [3]. Caretakers rated each animal’s well-being. The chimps and orangutans showed the same U-shape, with a low point at their species-equivalent midlife. The apes had no mortgage and no career. The U was older than either.

Not everyone bought it. Frijters and Beatton (2012) showed the U flattened in within-person data [4]. Cheng, Powdthavee, and Oswald (2017) reported four longitudinal panels and a within-person nadir at ages 40 to 42 [5]. The U held.

For my generation of doctors, the U-curve was a comfort. If you hit the floor, you knew there was a way back up.

The Floor That Moved

In August 2025, Blanchflower himself published the obituary of his own curve.

The paper, published in PLOS One, was titled “The declining mental health of the young and the global disappearance of the unhappiness hump shape in age” [6]. Across the BRFSS (US, 1993 to 2024), UKHLS (UK, 2009 to 2022), and the Global Minds Project (44 countries, 1.7 million observations), the hump shape was gone. Ill-being now decreases monotonically with age. The youngest people are the unhappiest. The 47-year-olds are no longer at the bottom because the bottom moved.

These are the numbers to remember.

Despair among US women under 25 rose from 5.6% in 2009 to 9.3% in 2023/24. Among UK women under 25, the same measure went from 4.4% to 12.7%. Across the 44-country Global Minds dataset, 48% of under-25s are now clinically at-risk, 13.4% classified as distressed.

A companion working paper by Twenge and Blanchflower (2025) examined six English-speaking countries (US, UK, Canada, Australia, Ireland, and New Zealand) and found the U-shape had gone in all six [7]. Young adults’ life satisfaction has fallen sharply across all six since around 2014. The Anglo-Nordic axis is where the floor moved first. The global generalization rests on thinner evidence than the US/UK claim, but the direction is consistent.

The person who shaped the U-curve is now the one closing the chapter.

Where the Descent Begins

The empirical bottom of the new curve lies in the 18-24 band. The descent begins earlier.

The CDC’s 2023 Youth Risk Behavior Survey reported that 52.6% of US female high school students experienced persistent sadness or hopelessness in the past year. 27.1% seriously considered suicide. 12.6% attempted [8]. Half the girls are feeling it. A quarter considering it. One in eight is trying.

The US Surgeon General’s 2023 advisory documented the exposure: 95% of US teens 13 to 17 use social media, a third “almost constantly,” and more than three hours a day doubles the risk of depression and anxiety symptoms [9]. Pew Research, surveying US teens in 2024 (published April 2025), found 48% of them now say social media has a “mostly negative” effect on others their age, up from 32% in 2022 [10]. The kids themselves are naming it.

The Lancet Psychiatry Commission on Youth Mental Health (McGorry et al., 2024) synthesized the international evidence across more than 20 countries and called the deterioration an early warning signal accelerating across two decades, predating COVID but worsened by it [11].

Jane is what the data describes. Tilda stands at the edge.

What Is Driving It

The trend is real. The mechanism is contested.

The strongest peer-reviewed causal evidence is Braghieri, Levy, and Makarin (2022) in the American Economic Review [12]. They used the staggered rollout of Facebook across 775 US colleges between 2004 and 2006 as a natural experiment. When Facebook arrived on a campus, the share of students with severe depression rose by about 7%. Generalized anxiety disorder rose by about 20%. A natural experiment with random timing of treatment is as close to a causal claim as a social scientist gets.

The synthesizing hypothesis lives in Jonathan Haidt’s 2024 book The Anxious Generation [13]. The argument is that phone-based childhood replaced play-based childhood, with early adolescence as the most vulnerable window. Girls take the worst of the social-comparison and body-dysmorphia load. Boys retreat into gaming and pornography. The losses are different. The neural substrate is the same.

One layer specific to this audience: Suniya Luthar’s work on affluent-youth distress (Luthar & Latendresse, 2005) [14]. Children of high-achieving parents show elevated rates of anxiety, depression, and substance use compared to peers. The drivers Luthar identified (achievement pressure and parental isolation) predate the smartphone era. They compound the load.

The counter-position is in Nature. Candice Odgers (2024) argued that most empirical evidence shows small or null effects, that the smartphone-causation thesis outruns its data, and that structural causes (post-2008 precarity, climate anxiety, declining civic infrastructure) may be undercounted [15]. Orben and Przybylski (2019) in Nature Human Behaviour found that digital technology use explains roughly 0.4% of variance in adolescent well-being [16]. The mechanism is contested even when the trend is not.

If your child is at this table, all three pressures are here at once.

The Upward ARC

This sits in the Capacity pillar of my Upward ARC framework. The long arc of what you can know, decide, and become over thirty years. Recover is the second pillar. The infrastructure that lets the climb back happen at all.

Lachman, Teshale, and Agrigoroaei (2015) identified the protective factors that predict midlife recovery: sense of control, physical activity, and social engagement [17]. My generation needs them for the climb back. She has to build the foundation for the first time. The protocols below are split for that reason.

Try This Today

The Floor Acknowledgment. Say where you are. The floor is a real dip with a known shape and a real way back up. Calling it a crisis leads to the wrong choices: the convertible, the affair, the boat. Calling it a floor leads to the right ones: the protective factors, the relationships you still have, the work that still matters. Different posture, different next step.

The Protective Three. Lachman’s factors, weekly cadence. Sense of control: one immovable 90-minute block this week that is yours. Physical activity: 150 minutes of moderate-intensity work across the week, the WHO floor. Social engagement: one in-person conversation with someone outside your work circle, this week.

The Aspiration-Reality Audit. One scheduled hour, no device, paper, and pen. Two columns. What you thought at 30, you would have by now. What you actually have. The gap is the source of the dip. Engage it honestly. The 47-year-olds who climb back are the ones who do this audit on purpose.

The Phone-Free Bedroom (for the parent). The charger lives in the kitchen. The phone is not in the child’s bedroom overnight. The Surgeon General advisory is explicit on this one because the sleep displacement effect is among the cleanest mechanisms we have. The conversation with your 12-year-old is not optional. The “her phone, her choice” position is what the data calls a mistake.

The In-Person Calendar (for the parent). Restore the lost hours deliberately. One sleepover, one in-person hang, one unmediated weekend afternoon per week. Calendar them. The protective effect of in-person socialization runs throughout the literature. “She will find her friends online” is the default that is hurting her.

Back to the Table

The conversation ends. Tilda is in bed. Her chair is back on all four legs. The dishwasher hums in the background.

My wife and I stay at the table. We talk about a 12-year-old we love who now uses the words of a 25-year-old in therapy, and about her friend who already has the diagnosis. The curve I expected at her age was still 35 years away. The curve she faces was never in any chart I saw in residency.

The work is bigger than this dinner table. It is also just as small as this dinner table.

For the 47-year-olds: the floor is real, the climb back is proven, the steps are simple, and the work is the work. For parents of 12-year-olds: the protective factors are the same, but you have to build the foundation, and the window is now.

Both happen at the same table.

Stay healthy.

Andre

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PS: If you read this and you are either standing at the empirical floor of the old curve or raising a kid at the cliff edge of the new one, forward it to one parent of a teenager you trust. The conversation my wife and I had at that table after the kids were in bed is the one they may not have had yet.

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References

[1] Blanchflower, D. G. (2021). Is happiness U-shaped everywhere? Age and subjective well-being in 145 countries. Journal of Population Economics, 34(2), 575-624. https://doi.org/10.1007/s00148-020-00797-z​

[2] Stone, A. A., Schwartz, J. E., Broderick, J. E., & Deaton, A. (2010). A snapshot of the age distribution of psychological well-being in the United States. Proceedings of the National Academy of Sciences, 107(22), 9985-9990. https://doi.org/10.1073/pnas.1003744107​

[3] Weiss, A., King, J. E., Inoue-Murayama, M., Matsuzawa, T., & Oswald, A. J. (2012). Evidence for a midlife crisis in great apes consistent with the U-shape in human well-being. Proceedings of the National Academy of Sciences, 109(49), 19949-19952. https://doi.org/10.1073/pnas.1212592109​

[4] Frijters, P., & Beatton, T. (2012). The mystery of the U-shaped relationship between happiness and age. Journal of Economic Behavior & Organization, 82(2-3), 525-542. https://doi.org/10.1016/j.jebo.2012.03.008​

[5] Cheng, T. C., Powdthavee, N., & Oswald, A. J. (2017). Longitudinal evidence for a midlife nadir in human well-being: Results from four data sets. The Economic Journal, 127(599), 126-142. https://doi.org/10.1111/ecoj.12256​

[6] Blanchflower, D. G., Bryson, A., & Xu, X. (2025). The declining mental health of the young and the global disappearance of the unhappiness hump shape in age. PLOS One, 20(8), e0327858. https://doi.org/10.1371/journal.pone.0327858​

[7] Twenge, J. M., & Blanchflower, D. G. (2025). Declining life satisfaction and happiness among young adults in six English-speaking countries (NBER Working Paper No. 33490). National Bureau of Economic Research. https://doi.org/10.3386/w33490​

[8] Centers for Disease Control and Prevention. (2024). Mental health and suicide risk among high school students and protective factors: Youth Risk Behavior Survey, United States, 2023. MMWR Supplements, 73(4), 79-86.

[9] Office of the U.S. Surgeon General. (2023). Social media and youth mental health: The U.S. Surgeon General’s advisory. U.S. Department of Health and Human Services.

[10] Faverio, M., & Sidoti, O. (2025, April 22). Teens, social media and mental health. Pew Research Center.

[11] McGorry, P. D., Mei, C., Dalal, N., Alvarez-Jimenez, M., Blakemore, S.-J., Browne, V., Dooley, B., Hickie, I. B., Jones, P. B., McDaid, D., Mihalopoulos, C., Wood, S. J., … Killackey, E. (2024). The Lancet Psychiatry Commission on youth mental health. The Lancet Psychiatry, 11(9), 731-774. https://doi.org/10.1016/S2215-0366(24)00163-9​

[12] Braghieri, L., Levy, R., & Makarin, A. (2022). Social media and mental health. American Economic Review, 112(11), 3660-3693. https://doi.org/10.1257/aer.20211218​

[13] Haidt, J. (2024). The anxious generation: How the great rewiring of childhood is causing an epidemic of mental illness. Penguin Press.

[14] Luthar, S. S., & Latendresse, S. J. (2005). Children of the affluent: Challenges to well-being. Current Directions in Psychological Science, 14(1), 49-53. https://doi.org/10.1111/j.0963-7214.2005.00333.x​

[15] Odgers, C. L. (2024). The great rewiring: Is social media really behind an epidemic of teenage mental illness? Nature, 628(8006), 29-30. https://doi.org/10.1038/d41586-024-00902-2​

[16] Orben, A., & Przybylski, A. K. (2019). The association between adolescent well-being and digital technology use. Nature Human Behaviour, 3(2), 173-182. https://doi.org/10.1038/s41562-018-0506-1​

[17] Lachman, M. E., Teshale, S., & Agrigoroaei, S. (2015). Midlife as a pivotal period in the life course: Balancing growth and decline at the crossroads of youth and old age. International Journal of Behavioral Development, 39(1), 20-31. https://doi.org/10.1177/0165025414533223​

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A note for new readers:

I’m a trained reconstructive facial surgeon, medical doctor, and dentist. Before launching this newsletter, I had a varied career: competitive freestyle wrestler, management consultant (McKinsey), entrepreneur (Zocdoc, Thermondo, and docdre ventures), and corporate executive (Sandoz). Today, I’m a Managing Director and Partner at BCG.

Husband of one. Father of three. Split between Berlin’s urban pulse and our Baltic Sea retreat. I’d rather be moving than sitting. Not just hobbies. Research. My body is my primary laboratory; I’ve been conducting experiments for decades.

If this is your first time here, welcome. I’m excited to share what I’ve learned and will continue to learn with you.

​

DISCLAIMER:

Let’s get one thing straight: None of this, whether text, graphics, images, or anything else, is medical or health advice. This newsletter is here to inform, educate, and (hopefully) entertain you, not to diagnose or treat you.

Yes, I’m a trained medical doctor and dentist. No, I’m not your doctor. The content here isn’t a replacement for professional medical advice, diagnosis, or treatment.

If you have questions about your health, talk to your physician or a qualified health professional. Don’t ignore their advice or delay getting care because of something you read in The Upward ARC. Be smart. Do your research. And, as always, take care of yourself.

The senior partner across from me, maybe mid-fifties, picks up his phone, checks the screen, and places it on the napkin in front of me. His latest annual physical is open in ChatGPT, the AI’s answer in blue under the labs. He says, Tell me what I’m missing.

I read through it. The numbers are his. The interpretation is solid. The recommendations aren’t quite what I’d give.

I look up. He’s watching my face, like clients do when the slides go silent. Three things are obvious. He’s got the right instinct. He’s reading his own body the way he reads a P&L. The tool covers about 80% of what a good doctor would do for him, without needing to fly anywhere. The missing 20% is what can cost you years, a decade from now, if nobody calls it out.

“What’s it not catching?” he says. The bacon is getting cold.

The Week That Made the Question

This is the conversation of the week. Two thousand partners in San Francisco for our annual offsite. AI is the topic in every panel, every hallway, every drink. The questions keep landing with me.

I’ve been on both sides of this all week. Bloodwork drawn. DEXA scan two blocks away. In my hotel room at 10:47 pm, lab dashboard open, Claude on my MacBook, checking where my markers line up beyond just a normal range. The results came back. Ten years ago, this would have meant a long trip to the doctor and a substantial bill.

Two truths from this week. The access upgrade is the biggest expansion of clinical reasoning for patients in 50 years. The new cognitive tax is real. The layer AI changes is narrower than the conference rooms make it sound.

Where the Model Wins

Start with imaging and the trace. This is where the evidence is clearest.

A 2017 Nature paper trained a convolutional network on 129,450 images and matched 21 board-certified dermatologists in diagnosing biopsy-proven melanoma [1]. A 2019 Nature Medicine deep neural network beat the average cardiologist on 12 rhythm classes across 91,232 single-lead ECGs, achieving F1 0.837 vs 0.780 [2]. A Mayo AI-ECG screen for asymptomatic left-ventricular dysfunction achieved an AUC of 0.93, a better screening test than mammography (0.85) or cervical cytology (0.70) [3]. A Google Health mammography system reduced false positives by 5.7% and false negatives by 9.4% versus US radiologists [4]; Nature published a reproducibility challenge the same year, so cite the headline with the caveat.

That’s the specialist layer. The harder part is that the model now matches primary care on the conversational side.

A 2020 dermatology system achieved top-1 accuracy of 0.66, compared with 0.44 for primary care physicians, across conditions accounting for 80% of primary-care visits [5]. Med-PaLM 2 hit 86.5% on USMLE-style questions; physicians preferred its consumer-question answers to physician-written ones on eight of nine clinical-utility axes [6]. GPT-4 achieved 57% accuracy in diagnosing NEJM clinicopathologic cases, outperforming 99.98% of simulated human readers [7]. Google’s AMIE, in a double-blind OSCE with 159 cases, beat 20 primary care physicians on 30 of 32 specialist-rated axes [8]. A 2025 NEJM AI RCT of an AI therapy chatbot reported a 51% reduction in depression symptoms over 4 weeks; therapeutic alliance comparable to that of human clinicians [9].

This is what the phone in the senior partner’s hand does. He uploads his ECG strip, maybe from his Apple Watch. It’s real. The model works.

The Twenty Percent

The opener made a promise. Here’s what it is.

The de-prescribing layer. I’ve reviewed a senior executive’s medication list and asked the basic questions. The statin started in 2014, twelve years after the event. Is anyone planning to revisit? The PPI for reflux that cleared up in 2019. Still needed? The beta-blocker for situational anxiety from 2017. Has anyone looked at it this decade? AI adds to the list. The clinician who knows your story edits it down.

The hands-on layer. Roughly 1 in 20 adult men has a thyroid nodule that you can feel that’s never been imaged. A hand exam detects tendon xanthomas, a sign of inherited dyslipidemia, before the lipid panel results come back. The difference between standing and sitting blood pressure is a frailty marker you won’t see on the panel. None of this is in the PDF you uploaded.

The non-quantifiable signal. The patient who pauses when you ask about alcohol. The wife who insisted on the appointment. Fingers tapping on the chair. The way he says the kids are fine three times. AI gets data. The clinician gets the person.

Realistic behavior change. A good doctor knows this person, with this calendar, this travel, this marriage, won’t do 14 things. They’ll do one. The doctor picks which lever to move.

From my week: My DEXA shows total body fat at the 6th percentile for men forty-five to forty-nine (13.1%). Visceral fat at the 39th (VAT mass 0.6kg or 639cm³). The model finds the mismatch. I’m carrying more visceral fat than you’d expect for how lean I am (leaner than 94% of men my age). Probably genetic; central adiposity runs in my family. The doctor knows what to do: a specific cardio plan, watch ApoB and insulin trends, and factor in family history on Lp(a) no matter the number. AI spots the pattern. The clinician knows what it means for me.

A coda on what the model gets wrong. All four major LLMs returned race-based medicine errors on clinical questions [10]. Medical hallucination benchmarks find models confidently endorsing wrong multiple-choice answers even with “none of the above” available [11]. USMLE-style benchmarks miss the clinical dialogue and longitudinal reasoning that real care requires [12]. And the human-in-the-loop is poorly trained: in a 2024 JAMA Network Open trial, physicians plus GPT-4 scored 76% on diagnostic reasoning; GPT-4 alone scored 92% [13]. The model has the capability that the clinician has not yet extracted.

The Cognitive Tax

A breakfast later, a different partner. He looks gray. That’s what happens when you sleep five hours for six nights. He admits he’s been asking Claude one more thing every night until 1 am this week. Eight specific things. None moved.

The cost. Attention residue is the measurable performance drag when you switch from an unfinished Task A to a new Task B; the cleaner the close-out of A, the less the drag [14]. Cognitive offloading is the broader pattern: when future access is expected, recall of the information drops, and recall of where to find it rises [15], driven by metacognitive misjudgment in which we offload even when internal cognition would be more accurate [16]. Interrupted work finishes faster at the same quality level, but at higher stress and frustration [17].

Then sleep. Four hours of evening iPad reading in a 2015 PNAS study suppressed melatonin by 55% and delayed circadian phase by over ninety minutes compared to print [18]. Late-night work-related smartphone use among mid- and high-level managers reduced sleep and increased next-morning depletion, more than for TV, laptop, or tablet use [19]. The evidence is smartphone-specific. The mechanism is the same.

The Fourteen Vials

Three days before the breakfast, at a Quest Diagnostics lab, the phlebotomist labeled the last of 14 vials and pointed me to the bathroom. The blood draw took two minutes. The urine cup would take 90 seconds.

I came out of the bathroom, and she was on the phone.

I didn’t need to hear the words. Her shoulders told me. She was on the phone with her supervisor. Behind her, the 14 vials of my blood were still lined up on the counter like a teaching demo. The reagent for one of the assays was missing from the kit. The panel couldn’t be run. They apologized. Could I come back tomorrow.

I came back the next day. The other arm. Two more minutes. Another bathroom trip. This time, the reagent was there. Somewhere in a centrifuge, my 100+ biomarkers became data.

This is the part the AI conversation in San Francisco kept missing. At least in health.

The model on my phone reads 100 biomarkers for $20 a month. Function Health, through Quest, runs the panel for a dollar a day. The interpretation and the test are now cheap. What isn’t cheap or automated is the person who puts the needle in your arm. The phlebotomist who finds your vein on the first try while you look away. Who tells you to keep breathing while she’s doing her thing. Who knows which vial will get agitated and which won’t. Who calls her supervisor when the reagent is missing. Nobody has built an AI for the inside of your elbow (yet).

The bottleneck didn’t disappear. It moved.

This sits in the Capacity pillar of my Upward ARC framework, the long arc of what you can know, decide, and do for yourself over thirty years. The second tether is Recover. Expanded medical reasoning is useless if running it every night costs you the sleep and parasympathetic foundation on which everything else depends. Both halves are the same edit. Be deliberate about what you let into your head, and when you let it out.

Try This Today

Build the Baseline First. Before you paste a lab into the model, build your context doc. AI without context defaults to population norms, which is the worst answer for a senior executive. Write three sections and save them. Family history: cause and age of death for grandparents and parents, first-degree relatives’ chronic conditions, and any cardiovascular event under sixty. Current meds and supplements: every pill, every dose, since when, why. Lifestyle context: work schedule including travel, sleep timing, training routine, alcohol honestly, diet, and mental state. Past data points go here too: prior bloodwork, BP, and weight trends, imaging. Save it as your patient context prompt. Add the question that matters for the next ten years: what biomarkers should I track in future readings so the next interpretation has trajectory, not just snapshots? Everything else depends on it.

The Six-Question Prompt. With the baseline set, when new labs or imaging come in, ask these: Trajectory, not snapshot. Family history is weighted on the markers near the top of the panel. What tests are missing that I should request. Cross-correlations between markers, the syndrome that a single marker might miss. De-prescribing review. The one or two changes that would move the most. The model does useful work on questions one to four and decent work on five and six. The doctor’s edit on five and six is in your physical exam. Bring both.

The Physical-First Rule. AI doesn’t replace the annual physical with a doctor who puts hands on you. The orthostatic blood pressure, the thyroid check, the hand exam, the conversation where you finally say what you haven’t told a GP in 15 years. Do both. AI interprets what the physical produces. The 20% is in the room.

The AI Curfew. No LLM after 9 pm on a workday. I spend six to eight hours a day in Claude Code right now. The capabilities are addictive. I learn, I experiment, I build. It’s a tool. Without boundaries, it turns into a video game. The same discipline that keeps your twelve-year-old off Fortnite at 9 pm applies to you and the model. It’ll be there at 7 am, with a clearer head, not at the cost of your sleep.

The Deliberate-Tool Rule. Don’t use five AI tools at once. Pick one or two and go deep. Learn their prompt patterns, their failure modes, your workflow. The knowledge transfers to other tools later. Depth beats breadth.

Back to the Breakfast Room

The senior partner is still waiting. I put my coffee down. Ask it three things it did not ask you, I tell him. Family history weighting on the markers near the top of the panel. What it would take off your medication list, not just add to it. What test it would order if it were sitting across from you. He pulls up ChatGPT and starts typing. The bacon is cold now.

This is the wave for the corner office’s relationship with its own body. Done well, it’s the biggest gift of clinical reasoning to the senior executive in 50 years. The second opinion you waited 6 weeks for is now available at 7 am, between a board call and a flight. Done badly, it’s a new cortisol drip with no off switch.

The senior executives who win this decade will be the ones who use it well and know when to turn it off. That’s one skill, not two.

Stay healthy.

Andre

PS: If you read this and you’re either anything like the partner who got 80% from ChatGPT or the partner asking Claude at 1 in the morning, forward it to one peer on the other side of that line. That’s how this newsletter grows, and it’s the only way I want it to.

References

[1] Esteva, A., Kuprel, B., Novoa, R. A., Ko, J., Swetter, S. M., Blau, H. M., & Thrun, S. (2017). Dermatologist-level classification of skin cancer with deep neural networks. Nature, 542(7639), 115-118.

[2] Hannun, A. Y., Rajpurkar, P., Haghpanahi, M., Tison, G. H., Bourn, C., Turakhia, M. P., & Ng, A. Y. (2019). Cardiologist-level arrhythmia detection and classification in ambulatory electrocardiograms using a deep neural network. Nature Medicine, 25(1), 65-69.

[3] Attia, Z. I., Kapa, S., Lopez-Jimenez, F., McKie, P. M., Ladewig, D. J., Satam, G., Pellikka, P. A., Enriquez-Sarano, M., Noseworthy, P. A., Munger, T. M., Asirvatham, S. J., Scott, C. G., Carter, R. E., & Friedman, P. A. (2019). Screening for cardiac contractile dysfunction using an artificial intelligence-enabled electrocardiogram. Nature Medicine, 25(1), 70-74.

[4] McKinney, S. M., Sieniek, M., Godbole, V., Godwin, J., Antropova, N., Ashrafian, H., Back, T., Chesus, M., Corrado, G. S., Darzi, A., Etemadi, M., Garcia-Vicente, F., Gilbert, F. J., Halling-Brown, M., Hassabis, D., Jansen, S., Karthikesalingam, A., Kelly, C. J., King, D., … Shetty, S. (2020). International evaluation of an AI system for breast cancer screening. Nature, 577(7788), 89-94.

[5] Liu, Y., Jain, A., Eng, C., Way, D. H., Lee, K., Bui, P., Kanada, K., de Oliveira Marinho, G., Gallegos, J., Gabriele, S., Gupta, V., Singh, N., Natarajan, V., Hofmann-Wellenhof, R., Corrado, G. S., Peng, L. H., Webster, D. R., Ai, D., Huang, S. J., … Coz, D. (2020). A deep learning system for differential diagnosis of skin diseases. Nature Medicine, 26(6), 900-908.

[6] Singhal, K., Azizi, S., Tu, T., Mahdavi, S. S., Wei, J., Chung, H. W., Scales, N., Tanwani, A., Cole-Lewis, H., Pfohl, S., Payne, P., Seneviratne, M., Gamble, P., Kelly, C., Babiker, A., Schärli, N., Chowdhery, A., Mansfield, P., Demner-Fushman, D., … Natarajan, V. (2023). Large language models encode clinical knowledge. Nature, 620(7972), 172-180.

[7] Eriksen, A. V., Möller, S., & Ryg, J. (2024). Use of GPT-4 to diagnose complex clinical cases. NEJM AI, 1(1), AIp2300031.

[8] Tu, T., Palepu, A., Schaekermann, M., Saab, K., Freyberg, J., Tanno, R., Wang, A., Li, B., Amin, M., Cheng, Y., Vedadi, E., Tomasev, N., Azizi, S., Singhal, K., Hou, L., Webson, A., Kulkarni, K., Mahdavi, S. S., Semturs, C., … Natarajan, V. (2025). Towards conversational diagnostic artificial intelligence. Nature, 642(8068), 442-450.

[9] Heinz, M. V., Mackin, D. M., Trudeau, B. M., Bhattacharya, S., Wang, Y., Banta, H. A., Jewett, A. D., Salzhauer, A. J., Griffin, T. Z., & Jacobson, N. C. (2025). Randomized trial of a generative AI chatbot for mental health treatment. NEJM AI, 2(4), AIoa2400802.

[10] Omiye, J. A., Lester, J. C., Spichak, S., Rotemberg, V., & Daneshjou, R. (2023). Large language models propagate race-based medicine. npj Digital Medicine, 6(1), 195.

[11] Pal, A., Umapathi, L. K., & Sankarasubbu, M. (2023). Med-HALT: Medical domain hallucination test for large language models. In Proceedings of the 27th Conference on Computational Natural Language Learning (CoNLL) (pp. 314-334). Association for Computational Linguistics.

[12] Mehandru, N., Miao, B. Y., Almaraz, E. R., Sushil, M., Butte, A. J., & Alaa, A. (2024). Evaluating large language models as agents in the clinic. npj Digital Medicine, 7(1), 84.

[13] Goh, E., Gallo, R., Hom, J., Strong, E., Weng, Y., Kerman, H., Cool, J. A., Kanjee, Z., Parsons, A. S., Ahuja, N., Horvitz, E., Yang, D., Milstein, A., Olson, A. P. J., Rodman, A., & Chen, J. H. (2024). Large language model influence on diagnostic reasoning: A randomized clinical trial. JAMA Network Open, 7(10), e2440969.

[14] Leroy, S. (2009). Why is it so hard to do my work? The challenge of attention residue when switching between work tasks. Organizational Behavior and Human Decision Processes, 109(2), 168-181.

[15] Sparrow, B., Liu, J., & Wegner, D. M. (2011). Google effects on memory: Cognitive consequences of having information at our fingertips. Science, 333(6043), 776-778.

[16] Risko, E. F., & Gilbert, S. J. (2016). Cognitive offloading. Trends in Cognitive Sciences, 20(9), 676-688.

[17] Mark, G., Gudith, D., & Klocke, U. (2008). The cost of interrupted work: More speed and stress. In Proceedings of the SIGCHI Conference on Human Factors in Computing Systems (CHI ‘08) (pp. 107-110). Association for Computing Machinery.

[18] Chang, A.-M., Aeschbach, D., Duffy, J. F., & Czeisler, C. A. (2015). Evening use of light-emitting eReaders negatively affects sleep, circadian timing, and next-morning alertness. Proceedings of the National Academy of Sciences, 112(4), 1232-1237.

[19] Lanaj, K., Johnson, R. E., & Barnes, C. M. (2014). Beginning the workday yet already depleted? Consequences of late-night smartphone use and sleep. Organizational Behavior and Human Decision Processes, 124(1), 11-23.

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A note for new readers:

I’m a trained reconstructive facial surgeon, medical doctor, and dentist. Before launching this newsletter, I had a varied career: competitive freestyle wrestler, management consultant (McKinsey), entrepreneur (Zocdoc, Thermondo, and docdre ventures), and corporate executive (Sandoz). Today, I’m a Managing Director and Partner at BCG.

Husband of one. Father of three. Split between Berlin’s urban pulse and our Baltic Sea retreat. I’d rather be moving than sitting. Not just hobbies. Research. My body is my primary laboratory; I’ve been conducting experiments for decades.

If this is your first time here, welcome. I’m excited to share what I’ve learned and will continue to learn with you.

​

DISCLAIMER:

Let’s get one thing straight: None of this, whether text, graphics, images, or anything else, is medical or health advice. This newsletter is here to inform, educate, and (hopefully) entertain you, not to diagnose or treat you.

Yes, I’m a trained medical doctor and dentist. No, I’m not your doctor. The content here isn’t a replacement for professional medical advice, diagnosis, or treatment.

If you have questions about your health, talk to your physician or a qualified health professional. Don’t ignore their advice or delay getting care because of something you read in The Upward ARC. Be smart. Do your research. And, as always, take care of yourself.

It’s the third time today she’s found a spot I didn’t know was there.

Earlier, she put her full weight on my quads, working deep into the muscle. Then she rolled my arm aside and pressed into the space between my shoulder and neck. I had to count my breaths to stay present.

This is the best massage I’ve had in years. Maybe even one of the top three ever.

It’s also a kind of audit.

You think you know how your body is doing because you train, sleep, and walk your twelve thousand steps. But when someone skilled puts an elbow into your scapula, you realize your soft tissue has been keeping score for years.

I walked out and, for the first time in twenty years, decided to make this a regular part of my life again.

Twenty Years Ago, This Was Tuesday

When I was wrestling competitively, the massage bench was the slot at the end of every full training day. You finished the session. You got worked on. You ate. You slept. You came back. Nobody called it recovery. Nobody talked about parasympathetic activation or fascial glide. The science was not the point. The bench was the point.

Five days a week, every week. The months blurred together until I stopped noticing.

When I stopped competing in my mid-twenties, the bench disappeared. Massage became a spa treat, something for holidays. Your partner might call it self-care, but to me, it just looked like another expense.

The wellness industry rushed in to fill the gap with the wrong things: wearables, supplements, a ring that tells you on Tuesday if you’re allowed to feel rested. None of it actually reaches your fascia.

Most of the executives I work with have the same missing piece. They went from college teams or serious sports to desk jobs, and somewhere along the way, their recovery routines vanished with the locker room. Now it’s just calendar invites. The cost builds up, even if your bloodwork looks fine.

If you sit for ten hours a day, bodywork isn’t a luxury. It’s the recovery system for tissue that’s lost its other means of recovery. The science supports this, though not always in the way the wellness industry says. Sometimes it even points the other way. Let’s look at three layers: muscle, fascia, and the nervous system.

Eleven Men and a Quadriceps

In 2012, a team at McMaster gave eleven young men a single bout of intense leg exercise. Then they massaged one quadriceps for ten minutes and left the other alone. They biopsied the muscle on both legs at three time points: baseline, immediately after, and two and a half hours later [1].

The massaged muscle showed three things the rested muscle did not. Inflammatory signaling was reduced. Tumor necrosis factor and interleukin-6 production dropped. The transcription factor that switches on mitochondrial biogenesis, called PGC-1 alpha, moved into the cell nucleus and was activated.

That is the canonical paper for what massage does to muscle at the cellular level. There are also eleven people. Single lab. Unreplicated in fourteen years. The mechanism story everyone repeats with confidence has not actually been re-run. Hold it as the best candidate we have, not as bedrock.

What survives at higher rigor is the clinical effect. A 2018 systematic review pooled ninety-nine controlled trials of post-exercise recovery techniques. Massage produced the largest pooled effect on delayed-onset muscle soreness among the tested modalities, outranking cryotherapy, contrast water, and compression garments [2]. A separate meta-analysis of twenty-two trials found the dose-response is specific: short sessions of five to twelve minutes outperformed longer ones, and the benefit was largest within the first ten minutes after intensity-loaded work [3].

What gets repeated in gym lore is that massage flushes lactic acid out of your muscles. It does not. A direct-measurement study showed that massage actually impeded local blood flow during application and reduced lactate clearance compared to passive rest [4]. The folk theory is wrong. If your therapist tells you they are flushing your lactic acid, you have a therapist who does not read.

Fascia Is Not a Wrapper

The Fascia Research Society defines the fascial system as a body-wide three-dimensional continuum of soft connective tissues that interpenetrates and surrounds organs, muscles, bones, nerves, and vessels [5]. Not a wrapper. An organ system.

It is contractile. Fascia contains myofibroblasts capable of smooth-muscle-like contraction [6]. It is also densely innervated with mechanoreceptors. Ruffini endings, Pacinian corpuscles, free interstitial nerve fibers [7]. Translation: the connective tissue around your muscles is alive, twitchy, and wired straight to your brainstem. When the therapist’s elbow goes in, your nervous system is the first to know.

Now imagine what happens to that tissue when you sit for ten hours a day, every day, for twenty years.

The leading mechanistic hypothesis involves hyaluronan. Hyaluronan sits between fascial layers and acts as the gliding lubricant. Under sustained pressure, immobility, and shifts in temperature or pH, hyaluronan polymerizes, and the gliding layer turns sticky. The clinical term is densification, and it is mechanistically distinct from fibrosis. Reversible, in theory, through heat and mechanical shear [8]. Strong cell-biology support, limited human in vivo verification. The honest summary: this is the leading mechanism, not the proven mechanism.

The imaging evidence is real but in flux. A 2011 ultrasound elasticity study of 121 subjects found that patients with chronic low back pain showed approximately 20% less shear strain in the thoracolumbar fascia than pain-free controls [9]. A 2025 replication of 64 subjects using different region-of-interest methods found the opposite direction [10]. The signal that the fascia is mechanically altered in chronic pain holds. Whether the altered tissue is stiffer or more compliant depends on which paper you read. Both are in good journals. Both are real findings. The field has not yet agreed.

The Cortisol Story Is Mostly Wrong

The third layer is the autonomic nervous system, and this is where the case for executives becomes specific.

A 2020 randomized controlled trial in Scientific Reports compared two massage protocols with rest in 60 healthy women. Both massage arms produced significantly higher high-frequency heart rate variability than the rest control [11]. High-frequency HRV is the vagally mediated parasympathetic component, the marker of how well your nervous system can shift out of threat mode. Ten minutes of structured touch was enough to move it. A 2024 meta-analysis of post-exercise recovery techniques confirmed the effect at the pooled level [12].

So far, so good. Now here’s where the wellness industry has been getting it wrong for fifteen years.

The dominant claim about massage and stress is that it lowers cortisol. The number changes depending on which article you read. The claim does not withstand scrutiny. The best independent meta-analysis of 19 studies and 704 adults found that massage’s effect on cortisol is “very small, in most cases not statistically distinguishable from zero” [13]. A 2024 meta-analysis of 137 touch-intervention studies, totaling almost 13,000 participants, found that cortisol effects are concentrated in newborns and are very modest in adults [14].

If you’ve read that massage lowers your cortisol, you’ve read someone quoting studies they didn’t actually check. What’s really happening is parasympathetic activation through the vagus nerve, not HPA-axis suppression. That difference matters. A massage will calm your nervous system, but it won’t change your cortisol numbers. Those are two separate things.

The mechanotransduction signal goes deeper. Mechanical loading of connective tissue in animal models activates pro-resolving lipid mediators that help clear inflammation [15]. The same substrate that responds to manual therapy responds to stretching. The body has a built-in resolution pathway that requires mechanical input to fire.

Then there is the lymphatic system. Most adults could not draw it in a diagram, and most do not know that it has no central pump. Lower-extremity lymph transport is roughly two-thirds intrinsic, from autonomous lymphatic muscle, and one-third extrinsic, from skeletal muscle compression and respiratory pressure [16]. Sit for ten hours, and the extrinsic share collapses. Manual lymphatic drainage in clinical lymphedema populations adds modest additional volume reduction beyond compression alone [17]. Bounded, real, not “detox.”

Now layer in who you are. A 2017 cohort study of nearly 8,000 adults found that the highest sedentary quartile had a hazard ratio of 2.63 for all-cause mortality [18]. That is who is reading this. The complication: a 2012 PNAS study found that senior leaders had lower cortisol levels than non-leaders matched on demographics, a finding that was mediated by a sense of control [19]. The corner office is not, on paper, harder on your HPA axis. The accumulated load lands somewhere else. In the soft tissue. In the autonomic system. In the lymphatic plumbing your body had forgotten. McEwen’s allostatic load framework explains the rest. Chronic stress remodels the hippocampus, the amygdala, and the prefrontal cortex [20]. Downregulating sympathetic drive is neuroanatomy, not soft.

This is the Recover pillar in my Upward ARC framework. Most people hear ‘recovery’ and think of sleep or rest days. That’s part of it. But your body also needs skilled hands on tissue that movement can’t reach. Activate (sleep, training, nutrition), and Capacity (fitness, skills, cognitive reserve) both depend on a soft-tissue and nervous-system base that can actually reset. Without that, you’re just building up debt.

Try This Today

The Skilled Hands Slot: Book a recurring sixty-minute session with a therapist who can actually find your trouble spots. Once a month is the minimum. Every two weeks is better. Skip the hotel spa. Look for words like ‘myofascial,’ ‘deep tissue,’ or ‘sports massage,’ and a therapist who asks where it hurts before starting. If you hear whale music or get asked if you just want to relax, you’re in the wrong place. The data is clear [3]: longer sessions for built-up tension, shorter ones after workouts. Block this time on your calendar like a board meeting. Most people skip it because it doesn’t feel like work, so it’s the first thing to go when the week gets busy. Don’t let it.

The Self-Audit: Spend ten minutes with a foam roller three nights a week before bed: quads, glutes, lats, upper back. Even if you’re not an expert, the pressure sends a real signal to your tissue [15], and your fascia responds to steady load over time [8]. This isn’t a replacement for skilled hands, just maintenance between sessions. If you can’t feel where you’re stuck, that’s your answer: spend more time there.

The Lymphatic Walk: Take a twenty-minute walk after lunch, or do five minutes of calf raises every ninety minutes at your desk. Your lymphatic pump only works when you move [16], and sitting all day shuts it down. Calf raises are the simplest fix. No gear, no scheduling, no need to shower. They work because of anatomy, not magic. Your soleus muscle is a pump for your veins and lymph, and it only turns on when you move.

Back to the Table

The therapist’s elbow on my scapula. The audit. Walking home after, my body felt different.

Back when I wrestled, the bench was just part of the routine. I never realized it was infrastructure. Twenty years of treating it as a luxury caught up to me in one hour with a skilled therapist on a Friday. The cost was clear the moment someone knew where to press.

Most of you are on the same path. Maybe you played college rugby. Maybe you swam in your twenties. Maybe you used to take care of your body, and now your calendar fills the space your body used to have. The bench disappeared, and nobody told you what you lost.

This is what you left behind.

The protocols above aren’t heroic. They’re just the slot at the end of the day. You do them because tissue under chronic load needs a reset, and your body has no backup pump.

Put the bench back. It’s not exciting. Neither is brushing your teeth.

Stay healthy.

Andre

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PS: If you read this and thought of someone who has not put the bench back yet, forward it to them. That is how this newsletter grows, and it is the only way I want it to. Past editions live in the archive: https://andreheeg.kit.com/profile.

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References

[1] Crane, J. D., Ogborn, D. I., Cupido, C., Melov, S., Hubbard, A., Bourgeois, J. M., & Tarnopolsky, M. A. (2012). Massage therapy attenuates inflammatory signaling after exercise-induced muscle damage. Science Translational Medicine, 4(119), 119ra13.

[2] Dupuy, O., Douzi, W., Theurot, D., Bosquet, L., & Dugué, B. (2018). An evidence-based approach for choosing post-exercise recovery techniques to reduce markers of muscle damage, soreness, fatigue, and inflammation: A systematic review with meta-analysis. Frontiers in Physiology, 9, 403.

[3] Poppendieck, W., Wegmann, M., Ferrauti, A., Kellmann, M., Pfeiffer, M., & Meyer, T. (2016). Massage and performance recovery: A meta-analytical review. Sports Medicine, 46(2), 183-204.

[4] Wiltshire, E. V., Poitras, V., Pak, M., Hong, T., Rayner, J., & Tschakovsky, M. E. (2010). Massage impairs postexercise muscle blood flow and “lactic acid” removal. Medicine & Science in Sports & Exercise, 42(6), 1062-1071.

[5] Adstrum, S., Hedley, G., Schleip, R., Stecco, C., & Yucesoy, C. A. (2017). Defining the fascial system. Journal of Bodywork and Movement Therapies, 21(1), 173-177.

[6] Schleip, R., Gabbiani, G., Wilke, J., Naylor, I., Hinz, B., Zorn, A., Jäger, H., Breul, R., Schreiner, S., & Klingler, W. (2019). Fascia is able to actively contract and may thereby influence musculoskeletal dynamics: A histochemical and mechanographic investigation. Frontiers in Physiology, 10, 336.

[7] Tesarz, J., Hoheisel, U., Wiedenhöfer, B., & Mense, S. (2011). Sensory innervation of the thoracolumbar fascia in rats and humans. Neuroscience, 194, 302-308.

[8] Pratt, R. L. (2021). Hyaluronan and the fascial frontier. International Journal of Molecular Sciences, 22(13), 6845.

[9] Langevin, H. M., Fox, J. R., Koptiuch, C., Badger, G. J., Greenan-Naumann, A. C., Bouffard, N. A., Konofagou, E. E., Lee, W.-N., Triano, J. J., & Henry, S. M. (2011). Reduced thoracolumbar fascia shear strain in human chronic low back pain. BMC Musculoskeletal Disorders, 12, 203.

[10] Tomita, N., Roy-Cardinal, M. H., Chayer, B., Daher, S., Attiya, A., Boulanger, A., Gaudreault, N., Cloutier, G., & Bureau, N. J. (2025). Thoracolumbar fascia ultrasound shear strain differs between low back pain and asymptomatic individuals: Expanding the evidence. Insights into Imaging, 16, 18.

[11] Meier, M., Unternaehrer, E., Dimitroff, S. J., Benz, A. B. E., Bentele, U. U., Schorpp, S. M., Wenzel, M., & Pruessner, J. C. (2020). Standardized massage interventions as protocols for the induction of psychophysiological relaxation in the laboratory: A block randomized, controlled trial. Scientific Reports, 10, 14774.

[12] Laborde, S., Allen, M. S., Borges, U., Dosseville, F., Hosang, T. J., Iskra, M., Mosley, E., Salvotti, C., Spolverato, L., Zammit, N., & Javelle, F. (2024). Influence of physical post-exercise recovery techniques on vagally-mediated heart rate variability: A systematic review and meta-analysis. Clinical Physiology and Functional Imaging.

[13] Moyer, C. A., Seefeldt, L., Mann, E. S., & Jackley, L. M. (2011). Does massage therapy reduce cortisol? A comprehensive quantitative review. Journal of Bodywork and Movement Therapies, 15(1), 3-14.

[14] Packheiser, J., Hartmann, H., Fredriksen, K., Gazzola, V., Keysers, C., & Michon, F. (2024). A systematic review and multivariate meta-analysis of the physical and mental health benefits of touch interventions. Nature Human Behaviour, 8, 1088-1107.

[15] Berrueta, L., Muskaj, I., Olenich, S., Butler, T., Badger, G. J., Colas, R. A., Spite, M., Serhan, C. N., & Langevin, H. M. (2016). Stretching impacts inflammation resolution in connective tissue. Journal of Cellular Physiology, 231(7), 1621-1627.

[16] Scallan, J. P., Zawieja, S. D., Castorena-Gonzalez, J. A., & Davis, M. J. (2016). Lymphatic pumping: Mechanics, mechanisms and malfunction. The Journal of Physiology, 594(20), 5749-5768.

[17] Ezzo, J., Manheimer, E., McNeely, M. L., Howell, D. M., Weiss, R., Johansson, K. I., Bao, T., Bily, L., Tuppo, C. M., Williams, A. F., & Karadibak, D. (2015). Manual lymphatic drainage for lymphedema following breast cancer treatment. Cochrane Database of Systematic Reviews, 2015(5), CD003475.

[18] Diaz, K. M., Howard, V. J., Hutto, B., Colabianchi, N., Vena, J. E., Safford, M. M., Blair, S. N., & Hooker, S. P. (2017). Patterns of sedentary behavior and mortality in U.S. middle-aged and older adults: A national cohort study. Annals of Internal Medicine, 167(7), 465-475.

[19] Sherman, G. D., Lee, J. J., Cuddy, A. J. C., Renshon, J., Oveis, C., Gross, J. J., & Lerner, J. S. (2012). Leadership is associated with lower levels of stress. Proceedings of the National Academy of Sciences, 109(44), 17903-17907.

[20] McEwen, B. S. (2007). Physiology and neurobiology of stress and adaptation: Central role of the brain. Physiological Reviews, 87(3), 873-904.

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A note for new readers:

I’m a trained reconstructive facial surgeon, medical doctor, and dentist. Before launching this newsletter, I had a varied career: competitive freestyle wrestler, management consultant (McKinsey), entrepreneur (Zocdoc, Thermondo, and docdre ventures), and corporate executive (Sandoz). Today, I’m a Managing Director and Partner at BCG.

Husband of one. Father of three. Split between Berlin’s urban pulse and our Baltic Sea retreat. I’d rather be moving than sitting. Not just hobbies. Research. My body is my primary laboratory; I’ve been conducting experiments for decades.

If this is your first time here, welcome. I’m excited to share what I’ve learned and will continue to learn with you.

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DISCLAIMER:

Let’s get one thing straight: None of this, whether text, graphics, images, or anything else, is medical or health advice. This newsletter is here to inform, educate, and (hopefully) entertain you, not to diagnose or treat you.

Yes, I’m a trained medical doctor and dentist. No, I’m not your doctor. The content here isn’t a replacement for professional medical advice, diagnosis, or treatment.

If you have questions about your health, talk to your physician or a qualified health professional. Don’t ignore their advice or delay getting care because of something you read in The Upward ARC. Be smart. Do your research. And, as always, take care of yourself.