Synopsis

Source of validity: Scientific
Rating (out of 5): 3

Vitamin B5, also known as pantothenic acid, plays a well-established role in cellular energy metabolism, particularly within the mitochondria. It is an essential precursor for the synthesis of coenzyme A (CoA), a molecule critical for the Krebs (citric acid) cycle, which is the central mechanism by which mitochondria generate ATP from carbohydrates, fats, and proteins. Without adequate pantothenic acid, CoA synthesis is impaired, leading to reduced mitochondrial function and energy production.

Several biochemical and animal studies have demonstrated that B5 deficiency leads to diminished CoA levels and compromised mitochondrial metabolism. Human deficiency is rare but can cause symptoms such as fatigue, irritability, and metabolic disturbances, all of which are linked to impaired energy metabolism at the cellular level. Supplementation with vitamin B5 reverses these symptoms in deficient individuals.

However, direct clinical evidence in healthy individuals showing that B5 supplementation enhances mitochondrial function or energy production beyond correcting deficiency is lacking. Most evidence supporting its mitochondrial role is based on its indispensable biochemical function and studies in deficiency states. There are no robust clinical trials demonstrating benefits of supplementation in non-deficient individuals for enhancing mitochondrial function.

In summary, the scientific basis for vitamin B5’s role in supporting the mitochondrial “body system” is strong in the context of deficiency, but evidence for benefit in the general population is limited, thus warranting a moderate evidence rating.

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