#21

I don’t use DHA. I’ll change my mind when good data in favor of it appears (RCT, MR, or longitudinal study adjusted for supplementation, fish consumption, exercise and income).

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#22

For clarity, I’m in no way saying she is correct, but I’m simply sharing what just arrived in my inbox from gethealthspan.com

I think you’ve mentioned her before, so this is probably not new to you

Also @CronosTempi

#23

The link you shared says “EMAIL_CAMPAIGN_2023_08_10_04_00” so it seems to be an old campaign. We’ve already discussed this article. Rhonda Patrick is a bullshiter and what she says is wrong, neither lysophosphatidylcholine-bound omega-3 fatty acids nor krill oil increase brain DHA in APOE4 mice (and she never answered my emails and tweets about these papers): Predicting Alzheimers & Dementia (and minimizing risk) - #554 by adssx

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#24

Also in supplements the DHA can oxidise faster potentially compared to EPA in regular ethyl ester form. The EPA only versions are too expensive for most to run long term at a good enough dose. Though it doesnt seem that the EPA+DHA combinations (as long as EPA>DHA in them) will have as negative effect as DHA only

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#25

I wouldn’t take RP’s advice for a variety of reasons. That said, I have a slightly different view than Antoine. The fact is, we don’t have data on supplementing a modest amount of DHA in a pulsatile way, like once a week (similar to fish eating). After all, it’s the dose that makes the poison, and hormesis is a perfect example. What if the same is true for DHA? Now, I never supplemented with DHA. But if I were an ApoE4 with family history, I would supplement with EPA and I would take a once weekly small additional DHA dose. This would be based on risk/reward odds distribution of possible harm vs covering options. It’s insurance against being wrong, essentially game theory, built in fault tolerance.

EDIT: I have glanced over that RP text, but there’s a lot of nuance to discuss, and I can’t do it right now. However, there are several assumptions built in I disagree with.

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#26

463. EFFECTS OF 24-MONTH SUPPLEMENTATION OF EPA AND DHA ON HIPPOCAMPAL SPONTANEOUS NEUROACTIVITY IN MILD COGNITIVE IMPAIRMENT AND DEMENTIA: A RESTING-STATE FMRI STUDY 2025

Emerging evidence suggests that omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), may provide neuroprotective benefits in individuals with cognitive impairment and dementia. These fatty acids are hypothesized to influence brain function through anti-inflammatory, antioxidative, and membrane-stabilizing effects. Resting-state functional MRI (rs-fMRI) offers a non-invasive approach to investigate spontaneous brain activity, and the amplitude of low-frequency fluctuations (ALFF) has been validated as a robust metric for assessing neural activity.
This study investigates whether a 24-month intervention with EPA, DHA, or their combination can modulate hippocampal ALFF in individuals with mild cognitive impairment (MCI) or dementia.
Participants (n=59) were randomized into four groups: (1) EPA 0.8 g/day + DHA 0.35 g/day (n=13), (2) EPA 0.8 g/day (n=15), (3) DHA 0.35 g/day (n=17), and (4) placebo (n=14).
These findings suggest that 24-month supplementation with EPA, DHA, or their combination does not significantly influence hippocampal ALFF in individuals with MCI or dementia. This absence of modulation implies that the neuroprotective effects of omega-3 fatty acids may not operate through alterations in spontaneous neuroactivity of the hippocampus, as measured by ALFF. Interestingly, the observed positive correlations between increasing ALFF and higher ADAS-cog scores, which indicate more profound cognitive impairment, highlight a potential compensatory mechanism, where heightened spontaneous neuroactivity in the hippocampus may reflect the brain’s attempt to counteract cognitive decline. This compensatory process aligns with prior studies suggesting that increased neural activity in the hippocampus may be a response to pathological stress, such as beta-amyloid accumulation or synaptic dysfunction. Despite these intriguing correlations, the lack of significant group effects underscores the need for further research to explore other neural mechanisms by which omega-3 fatty acids may exert neuroprotective effects. Future studies should also investigate whether specific subpopulations or alternative biomarkers may demonstrate differential responses to omega-3 supplementation.

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