On the unlikelihood of the single nutrient deficiency

I have given many reasons why this widely held myth is false. Here is another:

one nutrient deficiency inevitably leads to other deficiencies as the body tries to cope.

Consider a deficiency in niacin due to either dietary insufficiency or an absorption problem (with either any of various NAD+ precursors or specifically to NAD+ precursor tryptophan) or a metabolic problem or an excretion problem. In the case of excretion: if the intestines absorb tryptophan poorly, for example, in Hartnup disease, the kidneys tend to reabsorb tryptophan poorly.

This niacin deficiency leads directly to a measurable deficiency in tryptophan, as tryptophan must be diverted to make NAD+. This leads to a major deficiency in tryptophan if dietary tryptophan is limiting or if tryptophan absorption is also compromised. Tryptophan is only about 1% of all protein; so in a sense it is seriously limited except in what I would call high protein diets: more than 100 grams of protein per day. 1 gram of tryptophan in 100 grams of protein is only enough to make 16 mg of niacin – a little more than 1xRDA – if that is all that tryptophan had to supply. Not even close – the demands on tryptophan are stringent.

Tryptophan deficiency leads to serotonin and melatonin deficiencies for the same reason.

[I need to look into the possibility of inchoate protein deficiencies; seems unlikely, generally the most important use for every amino acid found in proteins is for protein synthesis.]

Tryptophan deficiency leads to measurable zinc deficiency because less picolinic acid is made because more of the tryptophan has to be diverted to making NAD+.

[Also needs investigation: There may also be a local B6 deficiency in the circulatory system, as more B6 is diverted to making NAD+ – of the 140+ reactions requiring vitamin B6, I doubt there is one more important than the manufacture of NAD+ when niacin is deficient in the diet or is insufficiently absorbed.]


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