Alpha Lipoic Acid 100 mg, Beta Carotene 5.17 mcg, Calcium Pantothenate 5 mg, Chromium Picolinate 2.5 mg, Copper Sulphate 15 mg, Folic Acid 50 mg, Lutein 1 mg, Manganese Sulphate 60 mcg, Methylcobalamin 500 mcg, Niacinamide 25 mg, Selenium Dioxide 1.4 mg, Vitamin B1 2 mg, Vitamin B2 2 mg, Vitamin B6 1.5 mg, Vitamin C 50 mg, Vitamin D3 200 IU, Vitamin E 10 IU, Zinc Oxide 65 mcg Tablets

Folic acid acts on megaloblastic bone marrow to produce a normoblastic marrow.

In man, an exogenous source of folate is required for nucleoprotein synthesis and the maintenance of normal erythropoiesis. Folic acid is the precursor of tetrahydrofolic acid, which is involved as a cofactor for transformylation reactions in the biosynthesis of purines and thymidylates of nucleic acids. Impairment of thymidylate synthesis in patients with folic acid deficiency is thought to account for the defective deoxyribonucleic acid (DNA) synthesis that leads to megaloblast formation and megaloblastic and macrocytic anemias.

Absorption — Folic acid is absorbed from the small intestine, primarily from the proximal portion. Folic acid appears in the plasma approximately 15 to 30 minutes after an oral dose; peak levels are generally reached within 1 hour.

Distribution — Folic acid as well as its physiologically active metabolite, L-5-methyl tetrahydro folate (L-5-MTHF), can be bound to plasma proteins when entering the systemic circulation. The fraction of folic acid bound to plasma proteins, particularly albumin, ranges between ~50% to 64%. The volume of distribution of L-5-MTHF is estimated to be 32.0 L. Tetrahydrofolic acid derivatives are distributed to all body tissues but are stored primarily in the liver. Cerebrospinal fluid levels of folic acid are several times greater than serum levels of the drug.

Metabolism — The first step in the metabolism of folic acid is its reduction to dihydrofolate via dihydrofolate reductase. Subsequently, dihydrofolate is further reduced to tetrahydrofolate (THF). THF is further converted to methylene-THF by serine-hydroxymethyltransferase and reduced to physiologically active L-5-MTHF via methylenetetrahydrofolate reductase (MTHFR).

Elimination — After intravenous administration, folic acid is rapidly cleared from the plasma. Following oral administration, majority of the dose was recovered in the urine. A majority of the metabolic products appeared in the urine after 6 hours; excretion was generally complete within 24 hours. Small amounts of orally administered folic acid have also been recovered in the feces.

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.

Riboflavin forms the coenzymes FMN and FAD, which participate in energy production and the metabolism of fats, drugs and steroids. These cofactors also contribute to the metabolic activation or conversion of other B vitamins.

Most riboflavin is absorbed in the proximal small intestine. The NIH fact sheet describes limited additional absorption from a single dose above approximately 27 mg and only small stores in liver, heart and kidneys. This is a nutrient-level absorption description, not a formulation-specific plasma concentration study.

Thiamine diphosphate is the principal active coenzyme form. It serves as a cofactor for enzymes in carbohydrate, amino-acid and lipid metabolism, supporting cellular energy metabolism.

Thiamine is absorbed in the small intestine by active transport at nutritional doses and passive diffusion at pharmacological doses. Dietary phosphorylated forms are hydrolyzed before absorption. Body stores, mainly in the liver, are small and turnover is rapid. These data concern thiamine and must not be substituted for the kinetics of benfotiamine.

Pantothenic acid is used to form coenzyme A and acyl carrier protein. These compounds support fatty-acid synthesis and breakdown and the transfer of acetyl and acyl groups in metabolism.

Digestive enzymes convert dietary coenzyme forms to pantothenic acid. Intestinal absorption uses active transport, with possible passive diffusion at higher doses. Red cells carry the nutrient, and most tissue pantothenate is present as coenzyme A. Urinary excretion is related to intake. This does not establish the kinetics of panthenol or pantethine.

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.

Ascorbic acid supports collagen, carnitine and neurotransmitter biosynthesis and acts as a physiological antioxidant. It also improves absorption of nonheme iron. These biological functions do not establish a disease-treatment benefit for an individual formulation.

Oral absorption is dose-dependent: the NIH review reports about 70–90% at intakes of 30–180 mg/day and less than 50% above 1 g/day. Plasma and tissue concentrations are tightly regulated, and absorbed unmetabolized ascorbic acid is eliminated in urine. Oral data cannot be used as intravenous vitamin C pharmacokinetics.

Vitamin E encompasses fat-soluble compounds with antioxidant activity. Alpha-tocopherol is the form recognized as meeting human requirements; biological activity differs among tocopherols and tocotrienols.

Vitamin E forms are absorbed in the small intestine and taken up by the liver. Hepatic alpha-tocopherol transfer protein preferentially returns alpha-tocopherol to the circulation, while the liver metabolizes and excretes other forms. This selective handling means different vitamin E forms should not be assigned identical pharmacokinetic values.

Vitamin A supports cell differentiation and normal epithelial tissues and is required for visual signaling through rhodopsin. Preformed retinoids and provitamin A carotenoids are different nutritional sources of vitamin A activity.

Vitamin A forms enter intestinal micelles and are absorbed by duodenal cells. Retinyl esters and provitamin A carotenoids undergo conversion to retinol at different stages of uptake. The NIH review reports variable absorption across forms; these nutrient findings should not be treated as equivalent bioavailability for retinol, beta-carotene and retinoid medicines.

Copper is a cofactor in enzymes involved in energy production, iron metabolism, connective-tissue synthesis and neurotransmitter processing. Copper-containing superoxide dismutases participate in defense against oxidative damage.

Dietary copper is absorbed primarily in the upper small intestine. Ceruloplasmin carries most plasma copper. Intestinal uptake and liver secretion into bile regulate copper balance; bile is the major elimination route and urinary loss is smaller. This general nutrient disposition does not establish salt-specific bioavailability.

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.

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.

Alpha-lipoic acid is a coenzyme in mitochondrial multienzyme complexes. The reference also describes antioxidant biochemical effects and experimental findings in diabetic nerve models; these do not establish that every supplement or combination produces the same clinical benefit.

After a 600 mg oral tablet, the reference reports rapid absorption, a peak at approximately 0.3–0.5 hours and a plasma half-life of 20–30 minutes. Metabolism includes oxidative chain shortening and sulfur methylation. Only small quantities of unchanged substance appear in human urine. The high urinary recovery percentages reported in animal experiments are not presented here as human elimination data.