B-Carotene 38 mg, Biotin 10 mcg, Cholecalciferol 200 IU, Chromium 10 mcg, Cyanocobalamin 1 mcg, Inositol 10 mg, Iodine 50 mcg, Lysine Hcl 30 mg, Manganese 0.8 mg, Molybdenum 8 mcg, Niacinamide 15 mg, Pyridoxine 1 mg, Selenium 10 mcg, Zinc 3 mg Tablets

Vitamin B12 supplies cofactors for methionine synthase and methylmalonyl-CoA mutase. These reactions support methionine formation and conversion of methylmalonyl-CoA to succinyl-CoA. B12 is involved in DNA synthesis, red-cell formation and nervous-system function.

Free B12 combines with intrinsic factor and is taken up in the distal ileum. Absorption becomes less efficient as the dose exceeds intrinsic-factor capacity; the NIH review reports about 2% absorption at 500 micrograms and 1.3% at 1,000 micrograms. Cyanocobalamin and hydroxocobalamin are converted into active cobalamin forms. These are oral nutrient data, not injectable-product pharmacokinetics.

Pyridoxal phosphate and pyridoxamine phosphate are active vitamin B6 coenzymes involved in amino-acid metabolism. B6 also contributes to neurotransmitter synthesis, glycogen metabolism and hemoglobin formation.

Vitamin B6 is absorbed in the jejunum. Phosphorylated forms are dephosphorylated before free B6 enters by passive diffusion. The NIH review describes similar absorption from foods and supplements; much of a large pharmacological dose is rapidly eliminated in urine. This physiology does not supply a measured half-life for this formulation.

Vitamin D is converted to active metabolites that support calcium absorption and mineral homeostasis. The physiological role described by NIH includes maintaining bone mineralization; nutrient physiology alone does not establish a treatment claim for a particular supplement.

Vitamin D2 and D3 are absorbed in the small intestine by passive and carrier-mediated processes. Dietary fat enhances absorption, although absorption also occurs without fat. Liver hydroxylation produces 25-hydroxyvitamin D, followed primarily in the kidney by conversion to calcitriol. These steps describe the precursors, not the pharmacokinetics of administered calcitriol.

Zinc participates in the catalytic activity of numerous enzymes and contributes to protein and DNA synthesis, cell signaling, cell division and normal immune function.

Zinc balance depends on intestinal absorption, secretion into the gastrointestinal tract and reabsorption. Fractional absorption falls as intake rises. Much of the body zinc pool is in muscle and bone. This nutrient-level reference does not establish the absorption rate or bioavailability of a particular zinc salt or combination.

Niacin supplies precursors for NAD and NADP. These coenzymes participate in cellular oxidation-reduction reactions, energy metabolism and biosynthetic processes. This nutrient role should not be confused with evidence for a lipid-lowering effect of every niacin form.

Ingested niacin is absorbed mainly in the small intestine, with some stomach absorption. Tissues convert physiological amounts to NAD. Excess is metabolized in the liver to methylated and oxidized products that are eliminated in urine; very high intake can also produce urinary excretion of unchanged nicotinic acid or nicotinamide.

Biotin is a cofactor for five carboxylases involved in fatty-acid, glucose and amino-acid metabolism. It also participates in gene regulation and cell signaling; this biochemical role does not itself prove cosmetic benefits from supplementation.

Digestive enzymes release biotin from food proteins, with biotinidase producing free biotin for absorption in the small intestine. Most stored biotin is in the liver. The NIH review reports high absorption of free oral biotin; it does not establish measured pharmacokinetics for this finished combination.

Selenium is incorporated into selenoproteins including glutathione peroxidases and thioredoxin reductases. These proteins contribute to thyroid-hormone metabolism and protection against oxidative damage.

Absorbed organic and inorganic selenium is metabolized toward an intermediate used to synthesize selenocysteine. A substantial body pool is in skeletal muscle. Urinary excretion is the main mechanism maintaining balance; excretion through feces and lungs also increases at high intake. This general physiology does not establish equal bioavailability among selenium compounds.

Manganese is a cofactor for enzymes including manganese superoxide dismutase, arginase and pyruvate carboxylase. These functions connect manganese to nutrient metabolism, antioxidant defense and bone formation.

Manganese is absorbed in the small intestine by active transport, with possible diffusion at high intakes. After absorption, most circulating manganese binds to transferrin, albumin or alpha-2-macroglobulin. The cited nutrient review does not establish a plasma half-life or bioavailability for this finished product.

Iodine is a constituent of the thyroid hormones T4 and T3. These hormones regulate metabolic activity and are important for normal skeletal and nervous-system development.

Iodide is rapidly and almost completely absorbed from the stomach and duodenum. Ingested iodate is reduced to iodide before absorption. The thyroid concentrates circulating iodide for hormone synthesis, and most of the remainder is eliminated in urine. This oral nutrient reference does not characterize topical povidone-iodine or radiopharmaceuticals.

Chromium has been investigated for possible effects on insulin action and glucose metabolism. The NIH review describes inconsistent clinical findings, so a definite glucose-lowering mechanism or benefit should not be assumed for a chromium supplement.

Absorption of dietary chromium is low, estimated at approximately 0.4–2.5%. The NIH review gives illustrative absorption estimates of about 1.2% for chromium picolinate and 0.4% for chromium chloride, with dietary factors affecting uptake. These reference estimates do not establish bioavailability of this finished product.