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Blog Archive

Wednesday, September 24, 2008

Some may be genetically in need of more choline than normal

Re: A paper written by experts at the University of North Carolina, Chapel Hill, NC
Common genetic polymorphisms affect the human requirement for the nutrient choline

Since low-choline is so important to the presently advised 'TMAU diet', this paper is of interest for 2 reasons: Partly because it goes into detail of what choline is needed for, and also it raises awareness that some people may need more choline than the RDA because of a weakness in an enzyme that deals with choline metabolism.

While crippling mutant genes are (supposedly) in the minority (supposed to be around 10% of genetic weaknesses), single nucleotide polymorphisms (SNP) are very common. Generally they are what make us different. In the case of cell enzymes, they are what make some people have enzyme weaknesses. Rather than having a crippling 'null-allele' type chromosome pairing that hardly functions (say down in the 0-30% range), SNPs make it more of a % game depending on the chromosome combination. Usually only a minor weakness, depending on the 2 chromosomes. For instance a null-allele chromosome coupled with a normal chromosome is likely to make things awkward. Coupled with a known SNP weakness, it may be the most common type of bad formation. Or 2 known 'weak' SNP pairings. This may explain why the TMAU testers seem to have gone from a 50% hurdle originally, to around 85%-90% now (depending on the tester. In the UK they even diagnose 'secondary tmau' where the enzyme output was regarded normal but too much tma was in the urine)

This intro was written so as to give the paper some context. The intro should not be regarded as being wholly accurate.

Humans eating diets deficient in the essential nutrient choline can develop organ dysfunction...

CHOLINE IS AN essential nutrient needed for structural integrity and signaling functions of cell membranes, methyl group metabolism, and neurotransmitter synthesis. Humans eating diets deficient in choline develop fatty liver, liver damage, and muscle damage. These effects occur, in part, because a specific lack of phosphatidylcholine limits the export of excess triglyceride from liver and induces apoptosis and subsequent leakage of enzymes (e.g., AST, ALT, and CPK) from tissues of liver and muscle. Women’s dietary requirements for choline are of special interest because deficient maternal dietary intake of choline during pregnancy in humans was associated with a 4-fold increased risk of having a baby with a neural tube defect...

Of the 57 participants, 68% developed organ dysfunction when fed the low choline diet and this resolved when choline was added back to their diets...

Common genetic polymorphisms have been reported to influence human requirements for nutrients. For example, a common SNP in the methyltetrahydrofolate reductase gene increases dietary requirements for the vitamin folic acid...

Common genetic polymorphisms affect the human requirement for the nutrient choline


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