What Depletes Vitamin B5? Risk Factors, Drugs and Food Processing

Table of Contents

1. The Short Answer: Who Is Really at Risk
2. The Evidence Ladder: Every Claim, Ranked
3. Milling, Canning and Cooking Losses
4. Refined and Ultra-Processed Diets
5. Alcohol and Alcohol-Use Disorder
6. Medicines and Stress: What the Data Show
7. PKAN: A Genetic Disease of the B5 Pathway
8. Kidney Dialysis and Other Medical Situations
9. How to Protect Your B5: Food and Kitchen Tips
10. Safety and When to Get Checked
11. Key Research Papers
12. Connections
13. Featured Videos

The Short Answer: Who Is Really at Risk

Pantothenic acid — vitamin B5 — takes its name from the Greek pantos, "everywhere," and the name is earned. Meat, eggs, mushrooms, avocado, whole grains, legumes, seeds and vegetables all carry some. The Adequate Intake for adults is about 5 mg a day (NIH Office of Dietary Supplements), and an ordinary mixed diet of real food usually reaches it without effort. The body then turns B5 into coenzyme A (CoA), the molecular "carrying handle" that moves fats, carbohydrates and proteins through energy production (see Coenzyme A Synthesis).

That is why isolated B5 deficiency is so hard to produce. In the classic human experiments of the 1950s, researchers had to feed volunteers a purified B5-free diet and give them a drug that blocks the vitamin (omega-methyl pantothenic acid) before clear deficiency appeared — the full story is on Human Deficiency Experiments. Diet alone, in a person eating real food, rarely gets there.

So who is genuinely at risk? In plain terms:

• Higher risk, documented in people: severe overall malnutrition (starvation, advanced eating disorders, serious malabsorption); long-term dialysis, which washes water-soluble vitamins out of the blood; and people whose diet is dominated by alcohol.
• A separate case: the rare inherited disease PKAN, which breaks the first step in turning B5 into CoA. It is not a dietary deficiency and is not fixed by eating or swallowing more B5.
• Lower risk, mostly theoretical: people on antibiotics, steroids or valproate, people under stress, and pill users. Here the evidence is mechanistic, animal-only, or (for the pill) tested in people and not supported.
• Very low risk: anyone eating a varied whole-food diet. Here B5 is simply not a weak link.

When someone does run low on B5, they are almost always low on several nutrients at once. That matters: the fix is better food overall, not a single pill aimed at a single vitamin.

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The Evidence Ladder: Every Claim, Ranked

Think of evidence as a ladder. The top rungs are studies in people that measured B5 status directly. The middle rungs are small or indirect human studies. The bottom rungs are reasoning from biochemistry, rat experiments, cell work or genome analysis — useful for generating ideas, but not proof that the same thing happens in you. Here is where each popular "depleter" sits.

Two things stand out. First, the claims that travel fastest online — "stress burns through your B5," "antibiotics wipe it out," "steroids drain it" — sit on the bottom rung. They are plausible ideas built on real biochemistry, but nobody has shown them causing B5 deficiency in people. Second, the one claim that was properly tested in people (the contraceptive pill) did not hold up once diet was controlled. The rest of this page walks through each rung in turn.

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Milling, Canning and Cooking Losses

Here a common claim is simply correct: processing removes B5 from food. In 1971 the researcher Henry Schroeder published a widely cited survey of the vitamins and trace minerals lost when foods are processed and preserved (Schroeder 1971). Rather than repeat figures from a paper whose full tables we could not re-check, the numbers below come straight from the U.S. Department of Agriculture's food-composition tables (SR Legacy, via FoodData Central), comparing the same food before and after processing. All values are milligrams of pantothenic acid per 100 g.

What the numbers show

• Wheat flour: whole-grain soft-wheat flour carries 1.01 mg per 100 g; white all-purpose flour carries 0.438 mg — under 0.5 mg, or about 57% lower. Much of the vitamin sits in the bran and germ that milling removes. "Enriched" white flour lists exactly the same 0.438 mg as unenriched flour, because U.S. enrichment restores thiamin, riboflavin, niacin, folic acid and iron — not B5.
• Sweet corn: raw yellow sweet corn has 0.717 mg; canned whole-kernel corn, drained, has 0.209 mg — about 71% lower. Part of that B5 is destroyed by heat and part has simply dissolved into the canning liquid you pour down the sink.
• White mushrooms: raw, 1.5 mg; canned and drained, 0.811 mg — about 46% lower.
• Rice: the honest surprise. In the same USDA tables, raw long-grain brown rice lists 1.06 mg and raw long-grain white rice 1.01 mg — both about 1.0 mg, only 5% apart. Brown rice is still the better grain for fibre, magnesium and other B vitamins (see Brown Rice), but B5 is not where it wins. (Cooked rice reads lower, around 0.38 mg per 100 g, mostly because cooked rice is two-thirds water — the same grain, diluted.)

A useful analogy: B5 behaves like sugar in tea. It dissolves readily in water, so anything that soaks food in water and then throws the water away — canning brine, long boiling, blanching before freezing — carries some of the vitamin off with it. Freezing itself is generally gentler than canning, but we did not find a modern measured figure for B5 that we could verify, so we give none.

How much does this matter for a person? A 1981 study measured B5 in 75 ready-to-eat processed and cooked foods. Meats, potatoes, oat cereals, tomato products and whole grains came out as good sources, supplying about 2 to 9 mg per 1,000 calories, while fruit products and corn-based and presweetened cereals were among the poorest (Walsh 1981). The authors' conclusion was measured: people eating very few calories need to choose foods with care. For everyone else, processing trims the margin rather than causing deficiency. Evidence tier: food-composition analysis — strong for the food, indirect for the person.

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Refined and Ultra-Processed Diets

A popular claim is that a high-sugar, packaged-food diet "depletes" B5. The more precise word is dilutes. There is no good human evidence that sugar actively destroys B5 already in your body. What happens is arithmetic: table sugar contains 0 mg of B5 per 100 g, and refined cooking oils such as olive oil also list 0 mg in the USDA tables. Every calorie from them is a calorie that brought no B5 along. Swap a bowl of oats or a plate of eggs and mushrooms for sweetened cereal, white bread and soda, and the B5 per calorie drops sharply — just as that 1981 food analysis found (Walsh 1981).

Think of your daily calories as seats on a bus. Whole foods fill each seat with a passenger carrying a little B5. Sugar, white flour and refined oils fill seats with passengers carrying nothing. The bus still arrives full, but with less B5 on board.

Evidence tier: food-composition reasoning, solid as arithmetic. What we did not find is a study showing that people on ultra-processed diets develop clinical B5 deficiency — in practice, such diets usually still supply some B5 from the meat, dairy and potatoes they contain. The real concern is that the same eating pattern is short on many nutrients at once, which is reason enough to change it.

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Alcohol and Alcohol-Use Disorder

Heavy drinking is linked to low status of nearly all B vitamins, and B5 is no exception, though it has been studied far less than thiamine (Vitamin B1). Alcohol supplies calories with no vitamins, people drinking heavily often eat poorly, and alcohol damages the gut and liver where vitamins are absorbed and stored.

The most direct human data are modest. A 1976 study measured urinary B5 in patients with alcohol-use disorder during a 10-week rehabilitation programme. In the acute phase, excretion averaged 2.7 mg a day, lower than the 3.9 mg a day previously reported for healthy people. In a chronic-drinking group, excretion began near intake (6.6 mg a day) and fell to less than half that by the end of rehabilitation — which the authors interpreted, cautiously, as the body holding on to more B5 as recovery progressed (Tao and Fox 1976). Evidence tier: small human observational study, without a matched control group in the same study.

The practical message is not "take B5 if you drink." It is that alcohol-use disorder is one of the few everyday settings where multiple B-vitamin shortfalls are expected, and treatment usually includes a full B-complex and proper meals. See Alcohol-Use Disorder and Alcohol.

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Medicines and Stress: What the Data Show

Antibiotics

The claim: antibiotics kill the gut bacteria that make B5, so courses of antibiotics deplete it. The kernel of truth: many gut bacteria can make B vitamins. A 2015 analysis of the genomes of 256 common human gut bacteria predicted that each of eight B vitamins, pantothenate included, can be made by roughly 40–65% of them, and that the bacteria trade vitamins among themselves (Magnúsdóttir 2015). The authors proposed that shifts in the microbiome could change our dietary needs.

What is missing is the human step. That study counted genes; it did not measure how much bacterial B5 the colon absorbs, or whether antibiotics change anyone's B5 status. We found no human study showing that antibiotic courses cause B5 deficiency. Evidence tier: genome analysis / mechanism only. Eating plenty of fibre-rich whole food helps the microbiome recover after antibiotics anyway.

Corticosteroids (prednisone and similar)

The claim: long-term steroid medicines drain B5 because the adrenal glands use CoA to make hormones. The adrenal link is real biochemistry — CoA is needed to build steroid hormones — and rat studies show that B5-deficient animals have reduced adrenal cortex function, which a dose of pantothenate partly restored (Tarasov 1985). But that is a deficiency causing an adrenal problem in rats, not a steroid drug causing a deficiency in people. We found no human study measuring B5 status in people on long-term prednisone. Evidence tier: animal and mechanistic only. People on long-term steroids have many genuine nutritional concerns (bone, blood sugar, muscle); B5 is not an established one.

The contraceptive pill

This is the one popular claim that was put to a proper test. In a 12-day study, 13 young women (9 taking oral contraceptives, 4 not) lived in a metabolic unit on an identical formula diet supplying 10 mg of B5 a day. At the start, blood and urine B5 were lower in the pill users — but after 12 days on the same diet, the difference had disappeared. The authors concluded that when diet and timing are controlled, oral contraceptives do not significantly change B5 status (Lewis and King 1980). The earlier gap most likely reflected what the women had been eating. Evidence tier: small controlled human study — claim not supported.

Valproate (an anti-seizure and mood medicine)

Valproate is the most interesting case biochemically. In the liver, valproate and some of its breakdown products get attached to CoA, forming compounds the body clears slowly. That "traps" free CoA, the way a parking garage fills up with cars that never leave. In rat liver mitochondria, valproate and three of its metabolites measurably sequestered CoA, though trapping did not explain all of the drug's effects (Ponchaut 1992). In young mice, giving pantothenate and carnitine alongside valproate kept liver CoA and ketone production from falling as low (Thurston and Hauhart 1992).

This is a story about CoA being tied up, not about B5 running out of the diet, and it comes from rat and mouse studies. It has not been shown that people on valproate need B5 supplements, and no one should add supplements to an anti-seizure regimen on their own. Evidence tier: animal and test-tube. If you take valproate, liver monitoring is already part of standard care; raise any questions with the prescriber. See Epilepsy and Carnitine.

Stress and the "adrenal fatigue" claim

A common claim, repeated in a widely viewed clinician Q&A, is that stress "burns through" B5 because stress is energy-expensive and needs lots of CoA, and that running low leads to being "stress maladapted" or to "adrenal fatigue." Part of this is fair: B5 really is the raw material for CoA, and CoA really is central to energy production and steroid hormone synthesis. B5 has even been nicknamed the "anti-stress vitamin," largely because of those rat adrenal studies.

The rest goes further than the evidence. We found no human study showing that psychological stress lowers B5 status, and "adrenal fatigue" is not a recognised medical diagnosis — endocrinologists use the term adrenal insufficiency for genuine adrenal failure, which is a serious, testable condition with different causes. Fatigue is real and worth investigating, but it has dozens of explanations (thyroid, iron, sleep, depression, other nutrient gaps). Evidence tier: animal and mechanistic. More on this on Adrenal Support and Stress.

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PKAN: A Genetic Disease of the B5 Pathway

Pantothenate kinase-associated neurodegeneration (PKAN), once called Hallervorden-Spatz syndrome, is a rare inherited brain disease. In 2001, researchers showed that it is caused by faults in a gene called PANK2, which makes pantothenate kinase — the enzyme that performs the very first step in turning B5 into CoA (Zhou 2001). The disease usually begins in childhood, causes progressive movement problems such as dystonia, and leaves iron deposits in part of the brain called the basal ganglia.

It is important to be clear what PKAN is not. It is not a dietary deficiency. People with PKAN can have perfectly normal B5 intake; the problem is a broken machine, not a shortage of raw material. Picture a factory whose loading dock is jammed: delivering more trucks of B5 does not get the cargo inside.

That logic is why researchers tried to bypass the broken step. Fosmetpantotenate was designed to deliver phosphopantothenate — the product the faulty enzyme fails to make — directly. In a randomised, double-blind, placebo-controlled trial, 84 patients aged 6 to 65 took fosmetpantotenate 300 mg three times a day or placebo for 24 weeks. The drug was safe, but it did not improve daily functioning: the difference from placebo was −0.09 points on the PKAN activities-of-daily-living scale, with a P value of 0.91 (Klopstock 2021). That is an honest, disappointing result, and it reinforces the bigger point: ordinary B5 supplements are not an established treatment for PKAN. Care is led by movement-disorder and genetics specialists.

Evidence tier: genetics and a randomised controlled trial — the strongest rung on this page, but about a disease of the B5 pathway rather than about diet.

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Kidney Dialysis and Other Medical Situations

Dialysis filters small, water-soluble molecules out of the blood — that is its job — and it cannot tell waste from water-soluble vitamins. A 1985 review of vitamin levels in chronic kidney failure noted that deficiencies of water-soluble vitamins can arise from restricted diets and from losses during both haemodialysis and peritoneal dialysis, and recommended a multivitamin including pantothenic acid after each dialysis session (Stein 1985). A 2023 systematic review of water-soluble vitamins in chronic kidney disease likewise describes rising needs and losses as the disease progresses and with dialysis, with no intervention needed in the early stages (Kędzierska-Kapuza 2023). Evidence tier: human clinical reviews; B5 itself has been measured less often than folate, B12 or vitamin C in these patients.

Renal vitamin products are formulated for this, and kidney teams prescribe them. People on dialysis should not add over-the-counter supplements without their team, because some vitamins and minerals accumulate dangerously when the kidneys fail. See Dialysis and Transplant.

Other situations worth knowing

• Severe malnutrition and eating disorders: B5 falls with every other nutrient. The famous "burning feet" reports came from prisoners of war on starvation rations (see Burning Feet and Neuropathy).
• Serious malabsorption: conditions that damage the small intestine reduce absorption of many vitamins together.
• Very low-calorie diets: the 1981 food study specifically flagged people eating little as needing careful food choice (Walsh 1981).

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How to Protect Your B5: Food and Kitchen Tips

The best protection is boring and effective: eat a variety of whole foods and lose as little of their B5 in the kitchen as possible. Values below are USDA figures per 100 g, raw unless noted (more on B5 Sources).

Foods that carry the most

• Liver: beef liver about 7.17 mg, chicken liver about 6.23 mg — the richest everyday source by far (Beef Liver). A small portion once a week covers a lot of ground; liver is also very high in vitamin A, so more is not better.
• Whole eggs: about 1.53 mg. Most of it is in the yolk — egg white alone has about 0.19 mg — so eat the whole egg (Eggs).
• White mushrooms: about 1.5 mg raw (White Button Mushroom).
• Avocado: about 1.39 mg (Avocado).
• Sunflower seeds: about 1.13 mg for dried kernels (Sunflower Seeds).
• Whole grains: whole-grain wheat flour 1.01 mg versus 0.438 mg for white; brown rice about 1.06 mg raw. Choose oats, brown rice and whole-wheat breads.
• Also good: meat, poultry, fish, whole milk and yoghurt, potatoes, lentils and other legumes, broccoli and tomatoes.

Kitchen habits that keep it

• Use the cooking liquid. B5 dissolves into water. Simmer vegetables in soups and stews, cook brown rice by absorption so it takes up all its water, and turn meat juices into gravy rather than pouring them off.
• Steam, roast or sauté rather than boil hard. Less water and shorter cooking mean less leaching.
• Prefer fresh or frozen over canned. If you do use canned vegetables, the liquid holds some of the vitamin; using it in a soup recovers part of what the can took.
• Choose the whole grain. The bran and germ are where much of the wheat's B5 lives, and enrichment does not put it back.
• Do not reheat leftovers repeatedly. Each round of heat adds a little more loss.

Do these things and most people will clear the 5 mg Adequate Intake comfortably — two eggs, a handful of mushrooms and half an avocado together supply well over half of it.

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Safety and When to Get Checked

B5 from food carries no known risk of excess. Supplements are also among the gentlest of vitamins; no tolerable upper intake level has been set because harmful effects have not been established, and the side effect most often reported at very high doses (grams a day) is diarrhoea and stomach upset. That said, "low risk" is not "useful": if you are not deficient, extra B5 has no proven benefit for energy, stress or fat loss. Details are on B5 Toxicity and Dosing and Supplement Forms.

Points worth acting on:

• Burning feet or tingling deserves a real medical work-up. Burning feet can come from B5 shortfall, but far more often from diabetes, alcohol, thyroid disease, B12 or B1 deficiency, kidney disease or certain medicines. It is not specific to B5.
• On dialysis, valproate or long-term steroids: keep vitamin questions with the team managing those treatments rather than self-supplementing.
• Testing: urinary pantothenate excretion is the standard research marker of B5 status, with blood levels as a secondary measure; both reflect recent intake. Commercial "intracellular" or "functional" micronutrient panels exist, but their validation for B5 is limited. See Testing for B5.
• Movement problems in a child or young adult — stiffness, twisting postures, worsening walking — need a neurologist. PKAN and related conditions are diagnosed with brain MRI and genetic testing, not with vitamin levels.

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Key Research Papers

1. Schroeder HA (1971). Losses of vitamins and trace minerals resulting from processing and preservation of foods. Am J Clin Nutr. 24(5):562–73. — PubMed PMID: 5578515
2. Walsh JH, Wyse BW, Hansen RG (1981). Pantothenic acid content of 75 processed and cooked foods. J Am Diet Assoc. 78(2):140–4. — PubMed PMID: 7217568
3. Tao HG, Fox HM (1976). Measurements of urinary pantothenic acid excretions of alcoholic patients. J Nutr Sci Vitaminol (Tokyo). 22(4):333–7. — PubMed PMID: 1011046
4. Magnúsdóttir S, Ravcheev D, de Crécy-Lagard V, Thiele I (2015). Systematic genome assessment of B-vitamin biosynthesis suggests co-operation among gut microbes. Front Genet. 6:148. — PubMed PMID: 25941533
5. Tarasov IuA, Sheĭbak VM, Moĭseenok AG (1985). Adrenal cortex functional activity in pantothenate deficiency and the administration of the vitamin or its derivatives [in Russian]. Vopr Pitan. (4):51–4. — PubMed PMID: 4060684
6. Lewis CM, King JC (1980). Effect of oral contraceptive agents on thiamin, riboflavin, and pantothenic acid status in young women. Am J Clin Nutr. 33(4):832–8. — PubMed PMID: 7361702
7. Ponchaut S, van Hoof F, Veitch K (1992). In vitro effects of valproate and valproate metabolites on mitochondrial oxidations. Relevance of CoA sequestration to the observed inhibitions. Biochem Pharmacol. 43(11):2435–42. — PubMed PMID: 1610408
8. Thurston JH, Hauhart RE (1992). Amelioration of adverse effects of valproic acid on ketogenesis and liver coenzyme A metabolism by cotreatment with pantothenate and carnitine in developing mice: possible clinical significance. Pediatr Res. 31(4 Pt 1):419–23. — PubMed PMID: 1570210
9. Zhou B, Westaway SK, Levinson B, Johnson MA, Gitschier J, Hayflick SJ (2001). A novel pantothenate kinase gene (PANK2) is defective in Hallervorden-Spatz syndrome. Nat Genet. 28(4):345–9. — PubMed PMID: 11479594
10. Klopstock T, Videnovic A, Bischoff AT, Bonnet C, et al. (2021). Fosmetpantotenate randomized controlled trial in pantothenate kinase-associated neurodegeneration. Mov Disord. 36(6):1342–1352. — PubMed PMID: 33200489
11. Stein G, Sperschneider H, Koppe S (1985). Vitamin levels in chronic renal failure and need for supplementation. Blood Purif. 3(1–3):52–62. — PubMed PMID: 4096835
12. Kędzierska-Kapuza K, Szczuko U, Stolińska H, Bakaloudi DR, Wierzba W, Szczuko M (2023). Demand for water-soluble vitamins in a group of patients with CKD versus interventions and supplementation — a systematic review. Nutrients. 15(4):860. — PubMed PMID: 36839219
13. Hodges RE, Bean WB, Ohlson MA, Bleiler R (1959). Human pantothenic acid deficiency produced by omega-methyl pantothenic acid. J Clin Invest. 38(8):1421–5. — PubMed PMID: 13673099

PubMed Topic Searches

1. PubMed: Pantothenic acid and food processing losses
2. PubMed: Valproate and coenzyme A sequestration
3. PubMed: PKAN treatment

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Connections

• All Vitamins
• Vitamin B5 (Pantothenic Acid)
• B5 Deficiency
• Human Deficiency Experiments
• Burning Feet and Neuropathy
• Testing for B5
• Dosing and Supplement Forms
• B5 Sources
• B5 Toxicity
• Coenzyme A Synthesis
• Adrenal Support and Stress
• Vitamin B1 (Thiamine)
• Vitamin B6
• Alcohol-Use Disorder
• Dialysis and Transplant
• Carnitine
• Whole Grain vs Refined Wheat
• Brown Rice

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