I Took Fish Oil for 10 Years. I Was Taking the Wrong Half.

Magnus is nine. He can’t eat dairy, eggs, most nuts, or sesame.

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.