B-complex supplement products are popular commodities, often marketed for “stress” or “energy.” Is there scientific justification for these claims? Why should anyone choose a B-complex supplement as opposed to either broader multivitamin-mineral supplements or narrower single B-vitamin supplements?
You might remember in the early ‘90s when a neuropathy epidemic broke out in Cuba among unsuspecting tobacco growers. They complained of burning sensations in their feet, pain in their arms and legs, frequent urination, blurred vision, weight loss, sensitivity to sunlight, and, well, lots of stress and fatigue (1). After assessing their diets it was discovered they were deficient in B complex vitamins and the amount of alcohol they drank daily contributed to loss of the little Bs they had (1).
The tobacco growers may have not known that B vitamins play essential roles in the health of their bodies relating to energy metabolism and stress, but let’s be sure we do.
For generating ATP energy in the body, B vitamins act mainly in synergy. Specifically, the vitamins thiamin, riboflavin, niacin and pantothenic acid are all needed to act as co enzymes in the formation of a multi-enzyme complex known as pyruvate dehydrogenase complex (2). Pyruvate dehydrogenase complex is essential for the oxidative decarboxylation of pyruvate to form acetyl CoA, which feeds into the citric acid cycle (2). Take any of the B vitamins away and cellular respiration is no more.
Further, niacin either as nicotinic acid and nicotinamide is necessary for use in the forms of NAD, nicotinamide adenine dinucleotide, and, with a phosphate at the end, NADP. NAD and NADP act as coenzymes for about 200 enzymes (oxidation-reduction reactions). But a major role of NAD in its reduced form as NADH is to shuttle electrons through the electron transport chain creating ATP energy (2). Apart from joining the other Bs in oxidative decarboxylation of pyruvate, NAD and NADH also act as coenzymes in glycolysis, oxidation of acetyl CoA, beta-oxidation of fatty acids and oxidation of ethanol for energy (2).
Riboflavin is needed for its coenzyme derivatives flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD). Like NAD and NADP, FMN and FAD act as coenzymes in oxidative-reduciton reactions for many reactions (2). Apart from use in pyruvate dehydrogenase complex in which FAD acts as an electron carrier, FAD also is needed for the flavoprotein succinate dehydrogenase to remove electrons from succinate to form fumarate (2). Then electrons are passed into electron transport chain by coenzyme Q (2).
Biotin’s role in energy has to do with its coenzyme role in enzymes. Two regulatory enzymes are dependent on biotin: pyruvate carboxylase, regulator of carboxylation of pyruvate, acetyl CoA carboxylase, regulator of fatty acid synthesis (2). Two enzymes need biotin for catabolism of amino acids need biotin, propionyl CoA carboxylase and beta-methylcrotnonyl CoA carboxylase (2). Lack of biotin will produce lethargy, depression, hallucinations and muscle pain (2).
Cobalamin once converted to adenosylcobalamin can act along with biotin in a energy metabolism in which it acts to help convert methylmalonyl CoA mutase convert L-methylmalonyl CoA to succinyl CoA (2). L-methylmalonyl CoA is produced from D-methylmalonyl CoA, which was produced from propionyl CoA that arose from from oxidation of amino acids and odd-chain fatty acids from the biotin-dependent reaction (2).
Pantothenic acid, aside its role in pyruvate dehydrogenase complex as a component of CoA, also acts as a component of CoA in lipid metabolism such as synthesis of ketone bodies and fatty acids (2). Although deficiency is unlikely—it’s ubiquitous in food—among the symptoms would be fatigue and weakness (2). Its deficiency is characterized by numbness in the toes called “burning feet syndrome” of which was no doubt suffered by the Cuban tobacco farmers who lacked it (1;2).
Some examples of stress were given above, but stress help from B vitamins is largely the work of thiamin. Thiamin, in this case not as a coenzyme, may activate ion transport in nerve membranes as well as regulating sodium channels and acetylcholine receptors in nerve impulse transmissions (2). A thiamin deficiency produces beriberi (beri meaning “weakness”) and one of its first signs is anorexia and weight loss, then neurological symptoms of confusion and apathy in what can only end up as irritability (2).
Riboflavin has its role in stress too—and I’m using the word “stress” as a very wide-reaching general term. FAD-dependent monomaine oxidase is required by neurotransmitters such as dopamine (2). Regeneration of the antioxidant glutathione—which supports against oxidative stress—is dependent also on FAD-dependent glutathione reductase (2).
Without niacin life could be especially stressful due to pellagra, which comes with its four Ds: dermatitis, dementia, diarrhea and death (2). But the B vitamin’s more direct role is in reducing oxidative stress via regeneration of glutathione, vitamin C and thioredoxin (2).
Finally, the pernicious anemia from a deficiency or poor absorption of cobalamin would lead to neuropathy of which is characterized by demyelination of the nerves—painfully stressful indeed (2).
OK, so we know the roles of B vitamins as related to energy and stress. We definitely need them. The question remains, however, whether or not a normally healthy person should supplement? Plus, will taking more of B-complex act as an ergogenic aid such as for athletes?
The studies aren’t showing much promise. There is indication that exercise causes greater need for B-complex supplements (5). Athletes should continue to take them. But, despite widespread use of B-complex supplements among athletes even in massive doses, they should not be expected to increase actual performance unless a deficiency was in existence beforehand (3;4).
Those of us who aren’t athletes would benefit from B-complex vitamins simply to help us avoid deficiency and because of their lack of toxicity. But don’t expect huge increases in “energy” or reductions of “stress” unless you are deficient. Deficiency can happen if you’re malnourished, abuse alcohol, are a strict vegetarian (B12 or riboflavin) or if you have a disorder such as pernicious anemia (B12 deficiency) (2).
1. Arnaud J, Fleites-Mestre P, Chassagne M et al. Vitamin B intake and status in healthy Havanan men, 2 years after the Cuban neuropathy epidemic. Br J Nutr 2001;85:741-8.
2. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
3. Williams MH. Vitamin supplementation and athletic performance. Int J Vitam Nutr Res Suppl 1989;30:163-91.
4. Williams MH. Vitamin and mineral supplements to athletes: do they help? Clin Sports Med 1984;3:623-37.
5. Woolf K, Manore MM. B-vitamins and exercise: does exercise alter requirements? Int J Sport Nutr Exerc Metab 2006;16:453-84.