#1

Very interesting video that shows you need to take B vitamins in order to get the benefits of Omega-3.

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#2

Not super convincing, as I said there:

Also, one paper he cites refers to amyloid plaques, is it relevant? See: mTOR activation and AD - #6 by adssx

And most papers he mentions are 10 to 15 years old, no? Don’t we have anything more recent?

(I’m not a big fan of him selling his supplement at the end but everyone has to make money somehow…)

Here’s what the 2024 report of the Lancet Commission on dementia prevention says on supplementation:

A French study (n=1279; mean age at baseline of 74·3 years [SD 4·9]; follow-up of 17 years) reported that increased concentrations of omega-3 index in plasma were associated with a decreased risk of dementia (HR 0·87 [95% CI 0·76–0·98] for 1 SD) and less decline in medial temporal lobe volume.
The Commission previously identified convincing evidence that vitamins did not prevent cognitive deterioration in the general population, as did WHO. Since then, further studies have not produced convincing benefit.

Alzheimer’s disease risk reduction in clinical practice: a priority in the emerging field of preventive neurology 2024 says:

Although randomized controlled trials assessing the benefit of ω-3 PUFA supplementation on AD risk have found variable results, this may be due to differences in cumulative doses, trial duration, and the stage and rate of cognitive decline. On average, studies that have shown minimal benefit from supplementation used lower cumulative doses (<1,500 mg DHA and/or <400 mg eicosapentaenoic acid (EPA)), had relatively shorter study lengths (from 12 to 26 weeks) and followed older individuals (>65 years) and/or participants with more advanced stage disease. Furthermore, baseline factors may also explain the variety of findings in the role ω-3 PUFA. For example, the OmegAD study found that ω-3 PUFA supplementation did not slow cognitive decline in patients with AD, but a follow-up post hoc analysis found that ω-3 PUFA supplementation improved cognition in patients with lower baseline levels of homocysteine, which is a marker for vitamin B status and itself is associated with an increased risk for AD. Another study found that high-dose ω-3 PUFA supplementation (1,500 mg DHA and 1,800 mg EPA) led to significant improvements in cognition, and delayed cognitive aging by 2.5 years in patients with statin-controlled coronary artery disease. This suggests that consideration of ω-3 PUFA supplementation should rely on the patient’s baseline presentation, including genetic factors.
Although they may not directly influence AD risk, the presence of other genetic polymorphisms can impact recommendations for risk reduction. For example, supplementation with vitamin B12, which can slow brain atrophy in MCI via downregulation of homocysteine, may require a differential route of administration based on the presence of C667T and A1298C polymorphisms of the MTHFR gene (which encodes methylene tetrahydrofolate reductase.

High-dose omega 3 supplementation is also associated with an increased risk of atrial fibrillation (itself associated with an increased risk of dementia): Diet and risk of atrial fibrillation: a systematic review 2024

So: important to measure B6, B9, B12, and omega 3 and to supplement (or not) accordingly with the “correct” supplement (form, dose, quality).

I ordered my Omega 3 Index ( Shop Our Products | OmegaQuant ), recommended by @DrFraser and I’ll see…

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#3

I think there is an argument that all vitamins are essential there is merely a question as to what the optimal dose is and how much you get from diet.

Vitamins are organic molecules (or a set of closely related molecules called vitamers) that are essential to an organism in small quantities for proper metabolic function.

There is an interesting question as to whether if you increase your input of one metabolite you also increase the ideal threshold of another. It is an area which needs some detailed study.

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#4

If true, this would suggest not taking large doses of anything and not taking anything without a deficiency. That seems like sensible advice anyway.

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#5

The problem is that there are a lot of deficiencies and surpluses (LDL, glucose, etc…) that we need to deal with.

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#6

As you keep adding things, the equation becomes more complex to solve. Start by removing. Stop the thing that is causing high blood sugar (for example, soda), rather than taking something to offset high blood sugar.

This might not work for everything but it’s a better path when it works. This is my way of thinking FWIW.

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#7

I do think measuring is best, but it is not that easy to get all the needed measurements.

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#8

@John_Hemming I do admire your efforts to measure and adjust. The data is limited as you say….test availability, knowledge of biology (to know what to test or how to interpret), testing error, biological variation due to the many variables in play, etc. I try to keep a high level perspective to avoid being overly distracted by looking where the light is good. I also try to learn from people like you and @ConquerAging who are admirably diligent in measuring and assessing impact. And mostly I try to avoid feeling optimistic about positive results from marketing campaigns and scientific studies on short lived creatures.