Higher phosphatidylcholine protects against dementia

[giftsplash]

dentification of dietary phosphatidylcholine metabolites as markers for increased CVD risk

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3086762/

[Jafa]

Thankyou for the studylink Giftsplash. Sobering for those of us supplementing lecithin/Bettaine as well as upping egg consumption. Reassessment is probably in order.

[Julie G]

I'd be hesitant to use a 2011 mouse study to guide choline intake. See a brand new paper below that suggests benefit for our genotype:

Components of the Choline Oxidation Pathway Modify the Association Between the Apolipoprotein ε4 Gene Variant and Cognitive Decline in Patients with Dementia
https://www.sciencedirect.com/science/a ... ihub#f0020

Highlights
•One-carbon metabolism and the APOEε4 allele variant could interact in dementia.
•This potential interaction has not been addressed in prognostic dementia studies.
•We measured metabolites in sera in a longitudinal study on cognition in dementia.
•Choline oxidation metabolites seem to improve cognitive prognosis in APOEε4 carriers.
•In comparison, they may be detrimental to cognitive prognosis in non-carriers.

The take-away for me:

Interestingly however, our data suggests that higher concentrations of components of the choline oxidation pathway may be of benefit to patients with APOEε4, but potentially detrimental to patients without this allele.

[Jafa]

Thanks Julie. I missed the date on the mouse study, and now that you’ve pointed that out I recall Chris Masterjohn during one of his recent podcasts questioning the validity of the outcomes from an older mouse TMAO/choline study.

The extracts (I have yet to find a workaround for the paywall) you have kindly posted from the recent dementia study which suggests that there might be different outcomes in respect to the manipulation of the choline metabolism pathway for ApoE4 vs non-ApoE4 genotypes poses an interesting question for me. Up until now I have not sought to have my genotype and SNPs tested. I have assumed I am ApoE4 as I have a strong maternal family history of dementia and heart disease. Following the ApoE4 way and Bredesen’s ReCode protocol as much as is practicable, has been sensible and I would not change this either way if I was genotype aware. However, now there is a fork in the road, with the risk of a poor outcome if I am not E4 and continue to supplement with phosphatidylcholine. Testing might now change my practice, so will have to ponder exploring my DNA.

[circular]

I have assumed I am ApoE4 as I have a strong maternal family history of dementia...

Ah but assumptions can throw a spanner in the works. My maternal side has the AD but my mother, who also had it, was 3/3. I wish I could find out what those before her had in their genetics. I'm saving all the stamps I can in case DNA on them can ever be extracted or inferred at an affordable cost. It would be interesting if they were all 3/3, since it could suggest some other strong risk genetics at play with a mechanism worth elucidating.

[Jafa]

Thanks circ, and I hear what you say. By sheer weight of numbers there are more 3/3 AD sufferers than any other genotype, but I would have happily barked up the wrong (E4) tree as only good could have come from it. Now, it seems with respect to phosphatidylcholine metabolism that may not be true. If there are additional interventions which may be beneficial for E4, but deleterious for E3 then that might push me towards opening Pandora’s box.