Medline References:
1.Animal and human studies suggest that vitamin B6 deficiency affects both humoral and cell-mediated immune responses. Lymphocyte differentiation and maturation are altered by deficiency, delayed-type hypersensitivity responses are reduced, and antibody production may be indirectly impaired. Additional human studies indicate that vitamin B6 status may influence tumor growth and disease processes. Deficiency of the vitamin has been associated with immunological changes observed in the elderly, persons infected with human immunodeficiency virus (HIV), and those with uremia or rheumatoid arthritis.
2.Vit B6 deficiency impairs interleukin-2 production and lymphocyte proliferation.
3. It is suggested that damaged arterial smooth muscle cells (SMC) and altered structural proteins are interpreted as foreign and degraded by the complement system and by macrophages. The long-lived proteins in the ground substance are glucosylated by Amadori reactions leading to virtually stable compounds and to polymerization. This process is enhanced by high blood sugar and possibly by vitamin B6 deficiency.
4.The principal metabolic function of vitamin B6 is in amino acid metabolism, although the greater part of the body's vitamin B6 is in muscle, associated with glycogen phosphorylase, and the vitamin also has an important role in the actions of steroid hormones.Current RDAs range between 1.5 and 2.2 mg/d.
5.Pyridoxine significantly reduced total plasma lipid and cholesterol levels, whereas it enhanced HDL-cholesterol level. Serum zinc level was also significantly increased by pyridoxine (p 0.001). These findings suggest that oral vitamin B6 inhibits platelet aggregation in normal subjects.
6.... the critical role of vitamin B6 in both neurogenesis and neuron longevity in neocortex. Postnatal cellular events in the neocortex, that is, neuron differentiation and synaptogenesis, were also altered by vitamin B6 deficits; higher order dendrites were reduced on stellate neurons in Layer II and on pyramidal neurons in Layer V.
"...In general, T cell-dependent, cell-mediated responses decline
with age. The elderly are at great risk for low consumption of proteins
and of several micronutrients, such as zinc or vitamins C, E and B6 which
play a critical role in the maintenance of normal immune function. As a
consequence, the incidence of inflammatory and infectious disease,
auto-immune disorders, cutaneous pathological changes, and skin cancers
increases. Morbidity and mortality rates due to tetanus, pulmonary
infections and influenza remain high in elderly populations. Depressing
the rate of immunosenescence and restoring a normal immunocompetence in
the elderly may involve improved nutrition through proteins,
micronutrients and vitamins, and should deal with the economic and
psychosocial problems of the elderly."
(
Ann Pharm Fr 1992;50(1):13-24:
Fattal-German M
[Immunocompetence in the elderly].)
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