Vitamin B5

Vitamin B5 (Pantothenic Acid): A Comprehensive Reference

1. Identity: Chemical Names, Natural Sources, and Common Forms

Chemical Identity

Pantothenic acid, also known as vitamin B5, is an essential nutrient that is naturally present in some foods, added to others, and available as a dietary supplement. Pantothenic acid is the combination of pantoic acid and β-alanine, and its name comes from the Greek pantothen, meaning "from everywhere," because pantothenic acid, at least in small amounts, is found in almost all foods. It is a water-soluble nutrient necessary for various metabolic functions within the body.

Unlike vitamin E or vitamin K, which occur in several chemically related forms known as vitamers, pantothenic acid is only one chemical compound. It is synthesized from the amino acid β-alanine and pantoic acid. Biologically active pantothenic acid exists only as the D-isomer; the L-form is biologically inactive.

Natural Food Sources

Pantothenic acid is found in almost all plant and animal foods to some degree, because the vitamin is found in all living cells. The best sources are beef, chicken, organ meats, fortified cereals, and some vegetables. Pantothenic acid is abundant in foods of both plant and animal origin. The most significant sources are animal organs such as liver and kidney, fish, shellfish, milk products, eggs, avocados, legumes, mushrooms, and sweet potatoes. Almost all plant- and animal-based foods contain pantothenic acid in varying amounts, though food processing can cause a significant loss.

Bacteria in the gut can also produce some pantothenic acid but not enough to meet dietary needs.

Common Forms and Preparations

In dietary supplements and animal feed, the form commonly used is calcium pantothenate, because chemically it is more stable, and hence makes for longer product shelf-life, than sodium pantothenate and free pantothenic acid. Dietary supplements of vitamin B5 are available as vitamin B5 exclusively or in combination with other vitamins in multivitamin/multimineral products.

Two derivative forms are prominent in commerce and clinical research. Pantethine is the stable disulfide form of pantetheine, an intermediate in the biosynthesis of CoA. Pantethine is the stable form of pantetheine, the active form of pantothenic acid, which is the fundamental component of coenzyme A (CoA). Dexpanthenol (also known as D-panthenol or pantothenyl alcohol) is the stable alcoholic analog of pantothenic acid used extensively in topical preparations. The topical use of dexpanthenol is based on good skin penetration and high local concentrations of dexpanthenol when administered in an adequate vehicle, such as water-in-oil emulsions.

2. Historical Discovery and Context

The essential nature of pantothenic acid was discovered by Roger J. Williams in 1933 by showing it was required for the growth of yeast. Three years later, Elvehjem and Jukes demonstrated that it was a growth and anti-dermatitis factor in chickens. Pantothenic acid was recognized as a vitamin for animals in 1939, when Jukes and Woolley independently reported that pantothenic acid isolated in pure form from liver by R.J. Williams was identical with a chick antidermatitis factor first described by Norris and Ringrose in 1930.

Pantothenic acid was isolated and extracted from liver by Williams and his colleagues in 1939, as an impure substance (about 40% pure). The initial isolation produced 3 g of pantothenic acid from 250 kg of sheep liver. The total synthesis of the structure was first achieved by the US Merck group in 1940. However, it drew significant scientific interest only after 1950, when F. Lipmann showed that pantothenic acid was part of coenzyme A, required for biological acetylation reactions.

Williams later won both the Mead Johnson Award from the American Institute of Nutrition and the Chandler Medal from Columbia University for this discovery.

Traditional and Historical Use

Because pantothenic acid was identified as a specific chemical entity only in the twentieth century, there is no documented history of its intentional isolation or supplementation in pre-modern traditional medicine systems. Its presence in virtually all foods means it has always been consumed as part of any diet, but no traditional culture identified it as a distinct medicinal substance. Historical importance is primarily scientific rather than ethnobotanical.

Historically, pantothenic acid was implicated in the "burning feet" syndrome that affected prisoners of war in Asia during World War II. This syndrome — characterized by sensory neuropathy in the extremities — was observed in malnourished prisoners and was subsequently attributed in part to pantothenic acid deficiency, though multiple nutrient deficiencies were typically present simultaneously.

Over time, eight chemically distinct, water-soluble B vitamins were isolated and numbered, with pantothenic acid designated as vitamin B5. The essential nature of pantothenic acid was discovered by Roger J. Williams in 1933 by showing it was required for the growth of yeast. Three years later, Elvehjem and Jukes demonstrated that it was a growth and anti-dermatitis factor in chickens. Williams dubbed the compound "pantothenic acid," deriving the name from the Greek word pantothen, which translates as "from everywhere."

3. Key Constituents, Active Compounds, and Mechanisms of Action

Pantothenic Acid as a CoA Precursor

Pantothenate is vitamin B5 and is the key precursor for the biosynthesis of coenzyme A (CoA) and carrier proteins that have a phosphopantetheine prosthetic group. Pantothenic acid is a precursor to CoA via a five-step process. The biosynthesis requires pantothenic acid, cysteine, and four equivalents of ATP. Pantothenic acid is phosphorylated to 4′-phosphopantothenate by the enzyme pantothenate kinase. This is the committed step in CoA biosynthesis and requires ATP.

The synthesis of CoA from pantothenate is regulated primarily by pantothenate kinase, an enzyme inhibited by the pathway end products CoA and acyl-CoA.

Coenzyme A: The Central Active Form

Pantothenic acid is used to make coenzyme A, a chemical compound that helps enzymes to build and break down fatty acids as well as perform other metabolic functions, and acyl carrier protein, which is also involved in building fats. Coenzyme A, the physiologically active form of pantothenic acid, serves as a cofactor for a variety of enzyme-catalyzed reactions involving transfer of acetyl (two-carbon) groups; the precursor fragments of various lengths are bound to the sulfhydryl group of coenzyme A.

Metabolic Roles of CoA

CoA forms part of oxidative decarboxylation systems of α-ketoacids (pyruvate, α-ketoglutarate, and branched-chain α-ketoacid dehydrogenases). In lipid metabolism, CoA is involved in fatty acid β-oxidation and in fatty acid, cholesterol, and ketone synthesis. Acetyl-CoA is required for acetylation reactions. The transfer of long-chain acyls from CoA to carnitine is the mechanism by which fatty acids enter into mitochondria to be β-oxidized.

Pantothenic acid is a metabolically active component of coenzyme A (CoA) essential for the metabolism of carbohydrates, fats, and proteins and for acyl carrier protein (ACP), a component of fatty acid synthesis. All tissues are capable of synthesizing CoA from pantothenic acid, which binds with various carboxylic acids, the most important of which is acetic acid. As acetyl-CoA, it enters the TCA cycle to produce energy or can be used to synthesize fatty acids, cholesterol, alcohols, amines, and amino acids.

Coenzyme A is also involved in the synthesis of lipids, cholesterol, and acetylcholine (a neurotransmitter).

Acyl Carrier Protein (ACP)

In all cells, pantothenic acid is converted to 4′-phosphopantetheine. Coenzyme A synthase catalyzes a series of reactions that lead to the synthesis of CoA. 4′-Phosphopantetheine binds to a polypeptide of approximately 8,600 Da to form the acyl carrier protein (ACP). ACP is a direct participant in fatty acid synthesis, carrying the growing acyl chain through each elongation cycle.

Protein Modification

Bound forms of pantothenic acid, such as coenzyme A and 4′-phosphopantetheine, play important roles in various metabolic processes, especially in fatty acid synthesis and degradation. CoA also participates in post-translational protein modifications, including acetylation of histones — reactions relevant to gene expression regulation.

Adrenal and Steroidogenic Functions

Pantothenic acid will affect both the structure and the function of the adrenal cortex. Changes in adrenocortical function are suggested by the decrease in adrenal cholesterol concentration in pantothenate deficiency. Additional evidence of impaired adrenocortical function in pantothenate deficiency is provided by the abnormal response of animals to various types of stress stimuli. The effects of pantothenate deficiency on the metabolism of tissues other than the adrenal cortex may also contribute to the abnormal responses elicited by stress. These observations come principally from animal studies; direct evidence from controlled human clinical trials on adrenal function is limited.

Pharmacokinetics

The absorption of free pantothenic acid occurs within intestinal cells through a saturable, sodium-dependent active transport system. When pantothenic acid intake is high and the transport system reaches its maximum capacity, a portion may also be absorbed through passive diffusion. Consequently, when the intake of pantothenic acid increases by a factor of 10, the rate of absorption decreases to 10%. Pantothenic acid is excreted intact in urine, and the amount excreted varies proportionally with dietary intake. In the body, the largest pools of pantothenic acid are in the form of CoA in mitochondria.

4. Scientific Evidence by Area of Use

4.1 Lipid Metabolism and Cardiovascular Risk (Pantethine)

The most clinically researched application for a pantothenic acid derivative involves pantethine, not pantothenic acid itself, and its effects on serum lipid levels. Several clinical trials have shown that the form of pantothenic acid known as pantethine reduces lipid levels when taken in large amounts, but pantothenic acid itself does not appear to have the same effects.

A 2005 review included 28 small clinical trials (average sample size of 22 participants) that examined the effect of pantethine supplements (median daily dose of 900 mg for an average of 12.7 weeks) on serum lipid levels in a total of 646 adults with hyperlipidemia. On average, the supplements were associated with triglyceride declines of 14.2% at 1 month and 32.9% at 4 months. The corresponding declines in total cholesterol were 8.7% and 15.1%, and for low-density lipoprotein (LDL) cholesterol were 10.4% and 20.1%. The corresponding increases in high-density lipoprotein (HDL) cholesterol were 6.1% and 8.4%.

A subsequent triple-blinded, placebo- and diet-controlled investigation examined pantethine in low- to moderate-cardiovascular risk North American subjects eligible for statin therapy. Participants receiving pantethine had a 6% decrease in total cholesterol and 8% decrease in non-HDL-C, which was significantly different from participants on placebo who only had 2% and 1% decreases, respectively. Although the absolute magnitude of these effects was small in these low- to moderate-risk North Americans (4–6 mg/dL), the results are noteworthy as prior studies have shown that, for each 1 mg/dL reduction in LDL-C, there is a concomitant 1% reduction in overall future CVD risk.

An earlier double-blind protocol in 29 patients with hyperlipoproteinemia (11 with type IIB, 15 with type IV) used pantethine at 300 mg three times daily for 8 weeks. In type IIB patients, this produced a highly significant lowering of plasma total and LDL-associated cholesterol (−13.5% for both parameters). In the same patients, HDL-C levels increased about 10% at the end of treatment. Switching from pantethine to placebo was associated with a rapid return to baseline cholesterolemia. In both type IIB and type IV patients, plasma triglyceride levels were reduced around 30% when pantethine was given as the first treatment.

The synthetic pathway from pantethine to CoA is much shorter than that of pantothenic acid, making pantethine the preferred therapeutic substance. Pantethine has significant lipid-lowering activity, whereas pantothenic acid has very little if any effect in lowering cholesterol and triglyceride levels. The proposed mechanism is inhibition of cholesterol synthesis and acceleration of fatty acid breakdown in the mitochondria.

Evidence strength: Moderate. The 2005 meta-analysis was limited by the small sample sizes of its component trials. The length of the 2014 trial was a shortcoming of the study, as after 16 weeks of pantethine administration the measured parameters had not plateaued, making prediction of the long-term outcome difficult. Future clinical trials investigating long-term administration may demonstrate a more robust decline. A small sample size and absence of sex stratification were also limitations of this study design. Additional larger, longer-duration trials are warranted before firm conclusions can be drawn.

4.2 Skin Health, Wound Healing, and Dermatology (Dexpanthenol)

Topical dexpanthenol (pantothenyl alcohol) has a substantial and relatively well-studied evidence base for dermatological applications. The topical use of dexpanthenol is based on good skin penetration and high local concentrations when administered in an adequate vehicle, such as water-in-oil emulsions. Topical dexpanthenol acts like a moisturizer, improving stratum corneum hydration, reducing transepidermal water loss, and maintaining skin softness and elasticity.

Activation of fibroblast proliferation, which is of relevance in wound healing, has been observed both in vitro and in vivo with dexpanthenol. Accelerated re-epithelialization in wound healing, monitored by means of the transepidermal water loss as an indicator of the intact epidermal barrier function, has also been demonstrated.

Dexpanthenol has been shown to have an anti-inflammatory effect on experimental ultraviolet-induced erythema. Beneficial effects have been observed in patients who have undergone skin transplantation or scar treatment, or therapy for burn injuries and different dermatoses. The stimulation of epithelialization, granulation, and mitigation of itching were the most prominent effects. In double-blind placebo-controlled clinical trials, dexpanthenol was evaluated for its efficacy in improving wound healing. Epidermal wounds treated with dexpanthenol emulsion showed a reduction in erythema and more elastic and solid tissue regeneration.

A 2020 systematic review of clinical and in vitro data concluded that in vitro and clinical studies provided evidence that topically applied dexpanthenol promotes superficial and postprocedure wound healing. The latest findings confirmed that dexpanthenol upregulates genes that are critical for the healing process. The gene expression data are of clinical relevance as evidenced by prospective clinical studies indicating that topical dexpanthenol accelerates wound healing with rapid re-epithelialization and restoration of skin barrier function following skin injury. It can therefore be inferred that topical dexpanthenol represents an appropriate and state-of-the-art treatment option for superficial postprocedure wounds.

For atopic dermatitis, dexpanthenol improves skin barrier function, reduces acute and frequent flares, has a significant topical corticosteroid (TCS) sparing effect, and enhances wound healing for skin lesions. As an active ingredient in ointments or emollients, it is suitable for the treatment and maintenance of atopic dermatitis. Evidence supports considering dexpanthenol as a treatment option for mild to moderate atopic dermatitis.

Research has found that dexpanthenol can potentially treat mild to moderate childhood atopic dermatitis. Other research suggests that dexpanthenol cream can help manage mucocutaneous side effects during isotretinoin therapy. Isotretinoin therapy is used for acne treatment, and its mucocutaneous side effects include dry mucous membranes, cheilitis, and xerosis.

Clinical studies have been conducted on dexpanthenol in wound healing applications. These small clinical trials used the drug as a pastille or spray to heal wounds in postoperative endotracheal intubation, endoscopic sinus surgery, and tonsillectomy.

Evidence strength: Moderate to good for topical dexpanthenol in wound healing and skin barrier support, supported by multiple clinical trials and mechanistic studies. Evidence for oral pantothenic acid in acne or general skin health is preliminary and insufficiently powered. There is no good scientific evidence that oral pantothenic acid improves human skin or hair.

4.3 Adrenal Function and Stress Response

Pantothenic acid has long been connected to adrenal cortex function due to the high concentration of the vitamin in adrenal tissue and the CoA dependence of steroid hormone synthesis. For steroid biosynthesis, vitamin B5 (pantothenic acid) plays an important role in maintaining steroid secretion from the adrenal cortex. Effects of pantothenic acid deficiency are specifically related to decreased adrenal function both in humans and animals.

An animal study examining pantothenic acid supplementation (0.03% in drinking water) in female rats found that ACTH-stimulated release of corticosterone and progesterone was greater for supplemented animals than controls, suggesting a supportive role for pantothenic acid in adrenal steroidogenesis. The effect of pantothenic acid supplementation on adrenal secretion of corticosterone and progesterone in female rats was investigated using an in-vitro primary adrenal cell culture system. Pregnant rats were given 0.03% pantothenic acid in their drinking water throughout pregnancy and lactation. The effect of ACTH at low doses on corticosterone and progesterone release was greater for pantothenic acid-treated cyclic rats than for control cyclic rats.

Evidence strength: Primarily animal/preclinical. No adequately powered, controlled human clinical trials have demonstrated that supplemental pantothenic acid improves adrenal function or stress resilience in humans with normal pantothenic acid status.

4.4 Neurological Disease: Pantothenate Kinase-Associated Neurodegeneration (PKAN)

The clearest pathological connection between pantothenic acid metabolism and human disease is PKAN. Pantothenate kinase-associated neurodegeneration (PKAN), an inborn error of coenzyme A (CoA) metabolism, represents the most common form of neurodegeneration with brain iron accumulation (NBIA). This rare neurodegenerative disorder involves progressive extrapyramidal dysfunction (e.g., dystonia, rigidity, choreoathetosis), iron accumulation in the basal ganglia, and axonal spheroids within the central nervous system.

PKAN is caused by mutations in PANK2, encoding the mitochondrial pantothenate kinase 2, which is the first enzyme of the biosynthesis of Coenzyme A. Classic PKAN emerges in children, typically with age of onset ≤10 years, followed by rapid progression and early disability or death. Atypical PKAN emerges in adolescence or early adulthood, followed by slower progression, milder symptomatology, and more diverse symptom manifestations.

Studies have revealed that the presence of low but considerable PANK2 expression, which can be increased in certain mutations, provides necessary information that justifies the use of a high dose of pantothenate as a treatment. Furthermore, recent studies on treatment of mutant cell cultures using various supplements, including pantothenate, pantethine, vitamin E, omega-3 fatty acids, α-lipoic acid, L-carnitine, or thiamine, have improved pathophysiological alterations in PKAN fibroblasts.

Evidence strength: PKAN is genetically confirmed and its connection to pantothenic acid metabolism is mechanistically well-established. Therapeutic trials of pantothenate supplementation in PKAN patients are limited; most evidence is from cell culture and animal models, or early-phase clinical development of pantothenate prodrugs.

4.5 Energy Metabolism and Exercise Performance

Pantothenic acid participates in energy generation, synthesizing hormones, and maintaining optimal conditions for skin, hair, and nails. The essential role of CoA in the TCA cycle underpins the theoretical basis for a role in exercise performance; however, direct human clinical evidence is weak. Acute supplementation with pantothenic acid and cysteine in healthy humans has not been shown to affect muscle CoA content, fuel selection, or exercise performance, as documented in at least one published study in the field.

Evidence strength: Insufficient. No high-quality human clinical trials have demonstrated that pantothenic acid supplementation enhances athletic or exercise performance in individuals who are not pantothenic acid deficient.

4.6 Inflammation and C-Reactive Protein

Low-grade inflammation, represented by minor C-reactive protein (CRP) elevation, has a critical role in the early stages of atherosclerosis, and pantothenic acid may have an antioxidant effect in the inflammatory process. However, the long-term relationship between pantothenic acid intake and CRP had not yet been studied. A subsequent epidemiological study by Jung et al. (2017) examined this relationship in Korean adults aged 40 years and older, finding a long-term association between dietary pantothenic acid intake and CRP concentration. This study was observational, precluding causal inference.

Evidence strength: Preliminary. Limited to observational data; no randomized controlled trials have examined pantothenic acid's effects on inflammatory markers in humans.

5. Body Systems and Health Areas of Association

• Energy metabolism: Via acetyl-CoA's central role in glycolysis product entry into the TCA cycle, fatty acid β-oxidation, and amino acid catabolism.
• Lipid metabolism: CoA is involved in fatty acid β-oxidation and in fatty acid, cholesterol, and ketone synthesis.
• Nervous system: Coenzyme A is also involved in the synthesis of lipids, cholesterol, and acetylcholine (a neurotransmitter).
• Endocrine/adrenal system: Pantothenic acid will affect both the structure and the function of the adrenal cortex.
• Skin and integument: Topical dexpanthenol acts like a moisturizer, improving stratum corneum hydration, reducing transepidermal water loss, and maintaining skin softness and elasticity.
• Cardiovascular system (pantethine): Pantethine has been shown in clinical trials to significantly reduce serum triglyceride and cholesterol levels and to increase high-density-lipoprotein cholesterol levels.
• Neurodegeneration: Mutations in the pantothenic acid metabolic pathway (PKAN) lead to iron accumulation in the basal ganglia and progressive movement disorders.
• Protein acetylation and gene regulation: Acetyl-CoA is required for acetylation reactions, which includes histone acetylation relevant to epigenetic gene regulation.

6. Deficiency

Pantothenic acid deficiency has only been observed in individuals who were fed diets virtually devoid of pantothenic acid or who were given a pantothenic acid metabolic antagonist, ω-methyl pantothenic acid. The subjects exhibited various degrees of signs and symptoms, including irritability and restlessness; fatigue; apathy; malaise; sleep disturbances; gastrointestinal complaints such as nausea, vomiting, and abdominal cramps; neurobiological symptoms such as numbness, paresthesias, muscle cramps, and staggering gait; and hypoglycemia and an increased sensitivity to insulin.

There is impaired energy production, due to low CoA levels, which could cause symptoms of irritability, fatigue, and apathy. Acetylcholine synthesis is also impaired; therefore, neurological symptoms can also appear in deficiency, including sensations of numbness or burning in hands and feet, paresthesia, and muscle cramps.

Pantothenic acid is widely distributed in foods; deficiency has been reported only as a result of feeding semisynthetic diets or an antagonist to the vitamin. People with a rare inherited disorder called pantothenate kinase-associated neurodegeneration cannot use pantothenic acid properly. This disorder can lead to symptoms of pantothenic acid deficiency.

In rodents, there can be loss of hair color, which led to marketing of pantothenic acid as a dietary supplement which could prevent or treat graying of hair in humans, despite the lack of any human trial evidence.

7. Dietary Reference Intakes and Dosages Reported in Studies

The primary criterion used to estimate the Adequate Intake (AI) for pantothenic acid is intake adequate to replace urinary excretion. The AI for adults is 5 mg/day. The Recommended Dietary Allowance (RDA) designation has not been established; rather, the Adequate Intake (AI) for vitamin B5 for men and women ages 19+ years is 5 mg daily. For pregnancy and lactation, the amount increases to 6 mg and 7 mg daily, respectively.

For infants up to 12 months, the AI is 1.8 mg/day. For children ages 1–13 years, the AI increases with age from 2 to 4 mg/day.

There is not sufficient scientific evidence on which to base a Tolerable Upper Intake Level (UL) for pantothenic acid.

Dosages used in key clinical studies:

• Pantethine for hyperlipidemia: The 2005 meta-analysis reviewed trials using a median daily dose of 900 mg of pantethine for an average of 12.7 weeks.
• Pantethine for hyperlipidemia (double-blind trial): 300 mg three times daily (900 mg/day) for 8 weeks.
• Pantethine in perimenopausal women: 24 hypercholesterolemic women were treated with 900 mg/day of pantethine for 16 weeks.
• Pantethine for cardiovascular risk markers: The standard dose used for pantethine in this application is 900 mg per day.

8. Safety Considerations and Known Interactions

General Safety Profile

Nutritional deficiency of pantothenic acid is rare and toxicity negligible. A toxic level of pantothenic acid has not been observed from food sources. With very large daily doses of 10 grams a day, stomach upset or mild diarrhea has been reported. Very high doses of pantothenic acid supplements (such as 10,000 mg per day) can cause an upset stomach and diarrhea.

A 2023 Nordic Nutrition Recommendations scoping review identified no health concerns related to pantothenic acid.

Tolerable Upper Intake Level

There is not sufficient scientific evidence on which to base a Tolerable Upper Intake Level (UL) for pantothenic acid. Because no UL has been established by the Institute of Medicine, this reflects the overall low toxicity potential rather than a lack of study.

Interaction with Biotin and Shared Transporters

Large doses of pantothenic acid may compete with biotin for uptake by the human sodium-dependent transporter. This transporter — the sodium-dependent multivitamin transporter (SMVT) — is responsible for intestinal absorption of both pantothenic acid and biotin. High supplemental doses of either nutrient could theoretically reduce absorption of the other, although the clinical significance of this interaction at commonly supplemented doses has not been rigorously quantified in humans.

Regulatory Status

Vitamin B5 (pantothenic acid) supplements are not subject to initial review by the U.S. Food and Drug Administration (FDA). The agency does not have the authority to examine dietary supplement products for safety and effectiveness before they are marketed.

Claims Not Supported by Evidence

Pantothenic acid is sold as a supplement purported to help dozens of conditions, from allergies and dandruff to leg cramps and arthritis. Unfortunately, there is little evidence to support these claims.

References

• NIH Office of Dietary Supplements – Pantothenic Acid: Health Professional Fact Sheet
• NIH Office of Dietary Supplements – Pantothenic Acid: Consumer Fact Sheet
• Institute of Medicine – Dietary Reference Intakes: Pantothenic Acid (NCBI Bookshelf)
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