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At least 847 records · Page 47Linked to original sources
PubMed1999

Toward a new definition of essential nutrients: is it now time for a third 'vitamin' paradigm?

The concepts of vitamin 'deficiency' diseases and the recommended dietary allowances (RDAs) have not kept pace with the growing understanding of the cellular and molecular functions of vitamins and other micronutrients. As a consequence, many researchers and clinicians rely on outdated signs and symptoms in assessing nutritional deficiencies. A new paradigm, presented here, proposes that: (1) deficiencies can be identified on biochemical and molecular levels long before they become clinically visible; (2) the definition of essential micronutrients be broadened to include some carotenoids and flavonoids, as well as various human metabolites, such as coenzyme Q10, carnitine, and alpha-lipoic acid, which are also dietary constituents; (4) individual nutritional requirements are partly fixed by genetics but also dynamically influenced by variations in the body's biochemical milieu and external stresses; and (5) the distinction between nutritional and pharmacological doses of vitamins is meaningless, since high doses of micronutrients may be required to achieve normal metabolic processes in some people.

Animals↗
PubMed1969

[Burning feet].

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Avitaminosis↗
PubMed1980

[On the etiology of syndromes of dementia (author's transl)].

Some new aspects of dementia are discussed. It is emphasized that the idea of dementia as a primary entity is obsolete. The following classification is proposed: dementia as a sign of a (still) unknown illness; dementia is a sign of a known, but not yet treatable illness and dementia as a sign of a known and also treatable illness. The differential diagnosis of the last group is described. Finally, some tests are proposed for the examination of demented patients to diagnose early treatable illnesses.

Alcoholism↗
PubMed1955

Oral medicine.

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Avitaminosis↗
PubMed2000

Pyridoxal phosphate de-activation by pyrroline-5-carboxylic acid. Increased risk of vitamin B6 deficiency and seizures in hyperprolinemia type II.

We previously identified vitamin B6 deficiency in a child presenting with seizures whose primary diagnosis was the inherited disorder hyperprolinemia type II. This is an unrecognized association, which was not explained by diet or medication. We hypothesized that pyridoxal phosphate (vitamin B6 coenzyme) was de-activated by L-Delta(1)-pyrroline-5-carboxylic acid, the major intermediate that accumulates endogenously in hyperprolinemia type II. The proposed interaction has now been investigated in vitro with high resolution 1H nuclear magnetic resonance spectroscopy and mass spectrometry at a pH of 7.4 and temperature of 310 K. Three novel adducts were identified. These were the result of a Claisen condensation (or Knoevenagel type of reaction) of the activated C-4 carbon of the pyrroline ring with the aldehyde carbon of pyridoxal phosphate. The structures of the adducts were confirmed by a combination of high performance liquid chromatography, nuclear magnetic resonance, and mass spectrometry. This interaction has not been reported before. From preliminary observations, pyrroline-5-carboxylic acid also condenses with other aromatic and aliphatic aldehydes and ketones, and this may be a previously unsuspected generic addition reaction. Pyrroline-5-carboxylic acid is thus found to be a unique endogenous vitamin antagonist. Vitamin B6 de-activation may contribute to seizures in hyperprolinemia type II, which are so far unexplained, but they may be preventable with long term vitamin B6 supplementation.

Aldehydes↗
PubMed1981

Vitamin and mineral nutrition in chronic alcoholics including patients with Korsakoff's psychosis.

1. A group of 129 patients with chronic alcoholism were assessed for their nutritional status with respect to certain minerals and vitamins, and compared with control subjects. 2. In all subjects the plasma values were normal for calcium, magnesium and zinc. 3. As in other studies a seasonal variation was found in the plasma levels of 25-hydroxyvitamin D in the control subjects and the alcoholic subjects; in all seasons lower levels were found in the alcoholics than in the controls, but none of the alcoholic patients had results in the range found in osteomalacia. 4. The alcoholic subjects had low levels of ascorbic acid both in the plasma and in the leucocytes. 5. Although vitamin A and beta-carotene levels were within the reference range, the results in alcoholics were found to be lower than in the control subjects. 6. We suggest that subclinical vitamin deficiencies other than thiamine deficiency contribute to the cerebral impairment frequently found in alcoholism.

25-Hydroxyvitamin D 2↗