Niacin, also called nicotinic
acid, functions in the body as coenzymes in the form of nicotinamide
adenine dinucleotide (NAD) and nicotinamide adenine dinu-cleotide phosphate
(NADP). These coenzymes are hydrogen acceptors; they combine with hydrogen
atoms as they are removed from food substrates by many types of dehydrogenases.
When a defi-ciency of niacin exists, the normal rate of dehydrogena-tion cannot
be maintained; therefore, oxidative delivery of energy from the foodstuffs to
the functioning ele-ments of all cells cannot occur at normal rates.
In the early stages of niacin deficiency, simple phys-iologic
changes such as muscle weakness and poor glan-dular secretion may occur, but in
severe niacin deficiency, actual tissue death ensues. Pathological lesions
appear in many parts of the central nervous system, and permanent dementia or
many types of psy-choses may result. Also, the skin develops a cracked,
pigmented scaliness in areas that are exposed to mechanical irritation or sun
irradiation; thus, it appears that in persons with niacin deficiency, the skin
is unable to repair irritative damage.
Niacin deficiency causes intense irritation and inflammation of the
mucous membranes of the mouth and other portions of the gastrointestinal tract,
result-ing in many digestive abnormalities that can lead to widespread
gastrointestinal hemorrhage in severe cases. It is possible that this results
from generalized depres-sion of metabolism in the gastrointestinal epithelium
and failure of appropriate epithelial repair.
The clinical entity called pellagra
and the canine disease called black
tongue are caused mainly by niacin deficiency. Pellagra is greatly
exacerbated in people on a corn diet, because corn is deficient in the amino
acid tryptophan, which can be converted in limited quanti-ties to niacin in the