You can also supplement with small amounts of citicoline. Eggs are like any other food. You might already be getting some nutrients from other sources - vit. B12, vit. D, vit. B2, vit. A, choline, lutein, and so on. It also has protein… with a lot of methionine. In some diets eggs will be a big plus, in other diets less so. Is there something unique in eggs that you need even at the cost of the amino-acid profile? Then go ahead. If you don’t consume much protein from other sources, eggs are a good source. Again, there are no magical superfoods, you have to see everything in the context of the whole diet.
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Avoid air pollution…
Source research:
Long-term air pollution exposure and incident dementia: a systematic review and meta-analysis
Findings
The search generated 15 619 records, of which 51 studies met the inclusion criteria for data extraction. After excluding studies due to population overlap and missing continuous effect estimates, 32 studies reported on exposure–outcome pairs that met the threshold of three or more studies, and were included in meta-analyses of adjusted effect estimates for incident dementia and/or in subgroup analyses of dementia subtypes. In meta-analyses of incident dementia, we identified a dementia diagnosis to be significantly associated with long-term exposure to PM2·5 (21 studies, n=24 030 527, pooled adjusted hazard ratio (HR) per 5 μg/m3 increase in exposure, 1·08 [95% CI 1·02–1·14]; I 2=95%), nitrogen dioxide (16 studies, n=17 228 429, pooled adjusted HR per 10 μg/m3 increase, 1·03 [1·01–1·05]; I 2=84%), and black carbon/PM2·5 absorbance (six studies, n=19 421 865, pooled adjusted HR per 1 μg/m3 increase, 1·13 [1·01–1·27]; I 2=97%). We found no significant association for exposure to nitrogen oxides (five studies, n=241 409, pooled adjusted HR per 10 μg/m3 increase, 1·05 [0·97–1·13]; I 2=44%), PM10 (four studies, n=246 440, pooled adjusted HR per 15 μg/m3 increase, 1·52 [0·80–2·87]; I 2=82%), or annual ozone (four studies, n=419 972, pooled adjusted HR per 45 μg/m3 increase, 0·82 [0·35–1·92]; I 2=69%), with moderate to considerable heterogeneity between studies in these pooled analyses. Of the 32 studies overall, three (9%) had a probably high risk of bias in one of seven domains; all other studies had ratings of probably to definitely low risk of bias. The overall certainty of evidence of studies in the systematic review was moderate.
https://www.thelancet.com/journals/lanplh/article/PIIS2542-5196(25)00118-4/fulltext
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"Initially developed as a way to help the immune system better recognize and attack tumors, ONC-841 has also shown promise in addressing the mechanisms underlying Alzheimer’s disease in preclinical models. OncoC4 is presenting research presented at AAIC, which it says demonstrates that inhibiting SIGLEC 10 activity in the brain could restore microglia, the brain’s resident immune cells, to a more functional state. These cells play a critical role in clearing protein aggregates such as amyloid plaques and tau tangles – known hallmarks of Alzheimer’s disease.
In two mouse models of Alzheimer’s disease, ONC-841 treatment improved microglial migration and ability to clear amyloid plaques, reduced levels of phosphorylated tau in plasma and alleviated structural and functional abnormalities linked to disease progression. According to OncoC4, the treated mice also exhibited measurable improvements in memory and learning, suggesting that immune modulation targeting SIGLEC 10 could influence both pathological and cognitive outcomes."
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I had a look at the Stanford study and am interested in your further thoughts because I had i slightly different interpretation.
Admittedly this is a cohort study only (so confounders…) but highest quartile for EPA had a big impact on All Cause Mortality regardless of DHA. 0.48 Hazard Ratio even with high DHA!
I appreciate that the study shows that we can do even better (0.36 HR if EPA high and DHA low) but I’m thinking that the overwhelming message is to increase your EPA intake. Not avoid DHA at all costs ( because there wasnt a clear signal when looking at DHA alone: “However, after the adjustment for baseline differences, the risk of MACE was not significant for DHA”)
My reading is that there was a statistical signal when looking at DHAs impact in potentially modifying EPAs benefit. But not really
strong enough to find significance from DHA levels alone.
Given the limitations of the study (use of quartiles in this study, and the relatively small cohort size) this Isn’t completely surprising. But I think if someone offered me a ‘balanced’ omega 3 tablet, and i only had this study to go on - I’d take it.
“While the unadjusted hazard ratio (HR) of MACE for the highest (fourth) quartile of EPA was 0.48 (95% CI: 0.35, 0.67) compared to the lowest quartile, the adjustment for DHA improved the HR to 0.36 (95% CI: 0.22, 0.58), suggesting an adverse effect modification by DHA”
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I agree with that and the way I sum it up is: “Supplement with EPA but don’t cut on fish intake”.
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