Vitamin B6 (pyridoxine) toxicity has been reported at dosages above 300 mg per day for extended periods. However, the biologically active form of vitamin B6,
pyridoxal‐5‐phosphate (P5P), has no reported toxicity. Therefore, P5P is the preferred form of vitamin B6 for higher utilization.
While Vitamin B1 is widely distributed in the food chain, highly refined foods are virtually absent in thiamin, thus a diet high in these foods will ultimately be low in thiamin. Functionally, thiamin is a part of the coenzyme thiamin pyrophosphate (TPP), also known as cocarboxyase, and is a required component in the metabolism of carbohydrates as a part of the coenzyme thiamine cocarboxylase. Specifically, TPP “is required for the oxidative decarboxylation of pyruvate to form acetyl‐coenzyme A, providing entry of oxidizable substrate(s) into the Krebs cycle for the generation of energy. Additionally, it is also a coenzyme for transketolase, which functions in the pentose phosphate pathway, an alternate pathway for glucose oxidation.”
Thiamine is most strongly linked with carbohydrate metabolism, but TPP is also required for the oxidative decarboxylation of other alpha‐keto acids such as alpha‐ketoglutarate and branched‐chain alpha‐keto acids (i.e., 2‐ketocarboxylates) derived from certain amino acids (e.g., valine, isoleucine, leucine). The pyrophosphate ester of thiamine, thiamine diphosphate is a cofactor for enzymatic reactions that cleave alpha‐keto acids. TPP activates the decarboxylation of pyruvate in the pyruvate dehydrogenase complex.
Vitamin B1 (thiamin) is also noted for its benefits for inflammation of the nerves (neuritis), and deficiency is associated with “high calorie malnutrition.” Deficiency may be established by determination of the erythrocyte (red blood cell) transketolase activity.
Zinc serves as an essential cofactor for greater than seventy (70) enzymes, and participates in binding DNA as a component of the zinc binding proteins (zinc fingers), which consists of a combination of the protein and zinc. Zinc also functions in many other roles in the body, including participation in the role of insulin release.
Zinc functions in membrane stabilization, and is part of the bone mineral apatite. Zinc has also been demonstrated to “increase osteogenic effect” via
multiple mechanisms, including via cellular proliferation stimulation, increased alkaline phosphatase (ALP) activity, increased synthesis of collagen in osteoblastic cells, and via a concentration increase of cellular collagen.
A deficiency in zinc results in a decrease in bone weight, delays growth in bone metabolism, and retards bone growth, development and maintenance. Both in vivo and in vitro studies have also demonstrated that zinc possess stimulatory effects on bone formation and mineralization.