Concerning Omega-3 Brain Study

In 2024, I made a video called Your Brain on Omega-3. I said omega-3 plus B-vitamins was one of the most defensible things you could take for your brain. Last week, a study landed that found the opposite [1]. Older adults who took omega-3 declined faster — on every cognitive test the researchers measured [1].

The authors' proposed mechanism wasn't subtle. They argued the omega-3 in commercial fish oil is going rancid — and damaging the brain's mitochondria. So I went back. I re-read my own video script from 2024. I re-read every paper I'd cited. I read this new study from start to finish.

And here's where I actually landed. The signal is real. But the study didn't measure the two things that decide whether omega-3 helps you or hurts you. And once you put those two things back into the picture, the answer changes.

Table of Contents

• The Study Landed
• What The Study Didn't Measure — The Bottle
• What The Study Didn't Measure — The Co-Factor
• What I'm Actually Doing
• References

The Study Landed

The paper is from Liao and colleagues, published in The Journal of Prevention of Alzheimer's Disease in 2026 [1]. They used the ADNI database — the Alzheimer's Disease Neuroimaging Initiative — which is one of the best longitudinal cognitive datasets in the world.

They took 273 people in the database who said they were taking omega-3, and paired each of them with two similar non-users — matched for age, sex, baseline memory status, and even genetic Alzheimer's risk. They then followed both groups for a median of five years. And on every cognitive test they ran, the omega-3 group declined faster [1].

Before going any further, I want to address the objection that will already be ringing in your mind. Reverse causality. People often start a supplement because they've noticed something is wrong. Maybe their memory has slipped. Maybe their partner has noticed. They start taking omega-3, but the decline that was already underway continues, and the supplement gets blamed.

The authors did try to address this. They went back and looked at the omega-3 users before they ever started taking the supplement — and compared their memory test scores and their brain scans to the people who never used it. The two groups were tracking the same way. No difference before the supplement entered the picture [1].

That's a real check, and they deserve credit for running it. But here's the limitation they themselves concede — they can't pick up the subtle trajectories that prompt someone to walk into a pharmacy in the first place. These ADNI participants typically enter the study because they're already worried about their memory. So the reverse causality concern is still there [1].

Now look at what the imaging actually shows — because this is where the study gets really interesting. The authors looked at four imaging biomarkers — amyloid, tau, gray matter atrophy, and FDG-PET, which measures brain glucose metabolism. Three of the four were completely flat. There was no association between omega-3 supplementation and amyloid. No association with tau. No association with gray matter volume [1].

Just one biomarker, connected to glucose, moved. The brain runs on glucose — that's its fuel. PET scans showed the omega-3 group's brains were burning less of it over time, a pattern linked to cognitive decline [1]. But why would the brains of people who use omega-3 supplements burn less glucose?

What The Study Didn't Measure — The Bottle

Start with the molecule itself.

DHA — the omega-3 fatty acid your brain enriches the most — is the most chemically vulnerable fat in common dietary use. In plain terms, it has weak spots where oxygen attacks. In direct lab measurements, DHA oxidizes around five times faster than linoleic acid — which is the main fat in seed oils — and far faster than monounsaturated fats in olive oil [2].

And gray matter — the part of the brain that does most of the cognitive heavy lifting — is around 14% DHA by weight. So the brain's favourite fat is also its most chemically vulnerable [3].

This is the mechanism the authors of the new study explicitly propose. They argue that if the DHA fats are going rancid inside the brain, this could degrade mitochondrial function, which would show up as exactly the kind of drop in brain energy use they observed [1].

That's a biologically coherent story. But there's a giant assumption sitting underneath it. The mechanism requires that the omega-3 supplements were already oxidised when they went into the body, or that the body wasn't handling them well, or both.

Which brings us to a paper that this ADNI study actually cites — and which I think is the most important paper in this whole conversation. It's from Ben Albert at the University of Auckland, where I graduated in 2015.

It is, frankly, a damning paper. They went into a New Zealand pharmacy, pulled 32 fish oil supplements off the shelf, and tested them. Three had what the label said. Eighty-three percent were over the oxidized limit. Half were over the total oxidation limit [4].

Now, to be fair, the industry pushed back on Albert's methodology, and a follow-up study found fewer oxidised products. So "all fish oil is rancid" is an overclaim. But ConsumerLab, which independently tests supplements, consistently flags fish oil as the single most quality-variable category they test.

The point is, it's possible that rancid omega-3 supplements may play a role in the results seen from this new ADNI study. It would be great to analyze, but unfortunately, the ADNI study didn't measure oxidation. It didn't ask which brand. It didn't ask whether the supplement was an ethyl ester or a triglyceride. It didn't ask whether the bottle had been sitting in someone's kitchen drawer at 22 degrees for 18 months. The exposure is just "self-reported omega-3 user, yes or no" [1].

What that means in practice: the bottle matters. Ideally, third-party tested omega-3 supplements. Algal-derived omega-3 is, in theory, less prone to oxidation because of how it's processed — although no head-to-head cognitive trial has tested this.

But the bottle is only half the story.

What The Study Didn't Measure — The Co-Factor

The other half goes back to a body of work I covered in detail in the 2024 video. It's from the VITACOG trial.

Here's the setup. VITACOG was a randomized controlled trial in older adults with mild cognitive impairment. They were given high-dose B-vitamins — folic acid, B6, and B12 — or placebo, for two years. The primary outcome was brain shrinkage on MRI. And what the team found, in a series of follow-up papers, was that whether the B-vitamins worked or didn't depended on something specific. It depended on omega-3 [5].

If omega-3 levels in the blood were low, the B vitamins didn't have an effect on brain health. But if omega-3 levels were in a healthy range, then the B vitamins had an impact on the brain MRI scan results. This result was replicated a year later [6].

So put the VITACOG story together. Omega-3 and B-vitamins are not independent. They work as a pair. B-vitamins protect the brain — but only if you have adequate omega-3. Omega-3 helps the brain — but only if you have adequate B-vitamins to keep homocysteine in range.

Now go back to the new ADNI paper. They didn't measure homocysteine. They didn't measure B-vitamin levels.

Which means it's entirely possible — and I'd argue it's likely for at least a fraction of the cohort — that the people taking omega-3 in this study were B-deficient. Their homocysteine was elevated. And by the VITACOG framework, that is exactly the wrong combination. Omega-3 in a B-deficient person looks very different from omega-3 in a person with adequate levels of B vitamins.

The new study tested omega-3 as if it were a standalone variable. The VITACOG work says it isn't.

What I'm Actually Doing

So here's where I've actually landed. Nothing for me has changed.

I still take omega-3 at around 1 gram for its potential cognitive effects, as well as its impact on heart health as demonstrated in the VITAL trial [7] and a Mayo Clinic meta-analysis [8].

I take a brand that's third-party tested by Labdoor.com.

I eat a good diet, and also take MicroVitamin, which has a methylated B-vitamin complex and TMG to lower homocysteine levels.

Just because I take a supplement though, doesn't mean that you should. Make sure to discuss with your doctor.

References

1. https://doi.org/10.1016/j.tjpad.2026.100569

2. https://pmc.ncbi.nlm.nih.gov/articles/PMC3656724/

3. https://www.mdpi.com/2072-6643/3/5/529

4. https://www.nature.com/articles/srep07928

5. https://pubmed.ncbi.nlm.nih.gov/25877495/

6. https://pubmed.ncbi.nlm.nih.gov/26757190/

7. https://www.nejm.org/doi/full/10.1056/NEJMoa1811403

8. https://www.mayoclinicproceedings.org/article/S0025-6196%2820%2930985-X/fulltext