C15:0 (Pentadecanoic Acid): The Newest Longevity Fatty Acid

Medically reviewed by Dr Zeeshan Afzal, MBBS — Welzo Medical Team. Last updated: July 2026. This article is for general information only and is not a substitute for personalised medical advice. Always speak to your GP or pharmacist before starting any new supplement, particularly if you take prescription medication or have an existing health condition.

C15:0 — pentadecanoic acid — has gone from an obscure dairy biomarker to one of the most talked-about longevity ingredients in the UK supplement aisle. Its supporters call it the first essential fatty acid discovered in more than 90 years. Its critics point out that the human trial evidence is thin, mostly small, and often funded by the company selling it.

If you are newer to this category, our pillar guide to longevity supplements is a useful starting point, and you can browse the full anti-ageing and longevity range. Our pillar article on NMN benefits, side effects and dosage covers the most established ingredient in the space, alongside the NMN supplements range.

Both of those things can be true at once. This guide walks through what C15:0 actually is, what the published research does and does not show, how much you already get from a normal British diet, and how to judge a C15:0 supplement in the UK if you decide it is worth a place in your routine.

Key takeaways

• C15:0 (pentadecanoic acid) is an odd-chain saturated fatty acid found mainly in full-fat dairy, ruminant meat and some fish.
• Higher blood levels of C15:0 are consistently associated with lower rates of type 2 diabetes, cardiovascular disease, fatty liver disease and all-cause mortality across large cohort studies.
• Association is not causation. A 2026 Mendelian randomisation analysis across two major US cohorts found no evidence that C15:0 causally lowers blood pressure or hypertension risk.
• Only two published randomised controlled trials have tested C15:0 supplementation in humans. Both were small, 12 weeks long, and produced modest, pathway-specific results rather than dramatic effects.
• Research doses sit at roughly 100–300 mg per day. Commercial capsules are typically 100 mg.
• A UK diet containing whole milk, butter and hard cheese can already supply 100–300 mg of C15:0 daily. Low-fat and plant-based diets supply very little.
• No significant adverse events were reported in the published trials, but long-term safety data in humans does not yet exist.

Table of contents

• What is C15:0 (pentadecanoic acid)?
• The dolphin discovery that started it all
• Is C15:0 genuinely an "essential" fatty acid?
• What C15:0 does inside the cell
• What the human evidence actually shows
• Food sources of C15:0 in a UK diet
• Buying a C15:0 supplement in the UK
• Dosage, timing and stacking
• Safety, side effects and who should avoid it
• C15:0 vs NMN, omega-3 and urolithin A
• The honest verdict
• Frequently asked questions
• References

What is C15:0 (pentadecanoic acid)?

Pentadecanoic acid is a saturated fatty acid with a 15-carbon backbone and no double bonds. Its molecular formula is C₁₅H₃₀O₂, and its shorthand name — C15:0 — simply reads as "fifteen carbons, zero double bonds".

That odd number matters more than it sounds. Almost every fatty acid in human biology has an even number of carbons — palmitic acid (C16:0), stearic acid (C18:0), oleic acid (C18:1). These are built two carbons at a time from acetyl-CoA. Odd-chain fatty acids like C15:0 and heptadecanoic acid (C17:0) require a different starting unit, propionyl-CoA, and humans produce them only in small quantities.

Odd-chain versus even-chain saturated fats

The distinction is not academic. Decades of nutritional epidemiology have linked high circulating even-chain saturated fatty acids — particularly palmitic acid — to insulin resistance, inflammation and cardiovascular risk. Odd-chain saturated fats behave differently in almost every dataset. Higher C15:0 and C17:0 levels track with better metabolic markers, not worse ones.

This is one of the more interesting wrinkles in modern nutrition science, and it is a large part of why C15:0 attracted attention in the first place. It sits inside the "saturated fat" category that UK dietary guidance advises limiting, yet it behaves nothing like the fats those guidelines were written about.

Why C15:0 is not another omega-3

C15:0 is frequently marketed alongside — or against — omega-3. They are chemically unrelated. Omega-3s (EPA, DHA, ALA) are long-chain polyunsaturated fatty acids with multiple double bonds, which makes them prone to oxidation. C15:0 is fully saturated, which makes it chemically stable, odourless and resistant to rancidity.

That stability is genuinely useful in a supplement context: no fishy burps, no oxidation concerns, no refrigeration. Whether it delivers comparable health benefits is a separate question, and one the evidence has not yet answered.

The dolphin discovery that started it all

The C15:0 story begins with the US Navy Marine Mammal Program in San Diego. Veterinary epidemiologist Dr Stephanie Venn-Watson was studying a population of bottlenose dolphins under Navy care that routinely lived into their 40s and 50s — far longer than wild dolphins typically do.

Longer life brought human-like age-related disease: elevated cholesterol, insulin resistance, fatty liver and even Alzheimer's-type brain changes. When the team applied metabolomics to decades of archived dolphin serum, C15:0 emerged as one of the strongest molecular predictors separating the healthiest ageing animals from the rest, as documented by Tufts Cummings School of Veterinary Medicine.

Feeding dolphins a fish diet higher in C15:0 improved their metabolic and red blood cell markers. That observation was published in Scientific Reports in 2020 and became the foundation of the entire C15:0 supplement category. It is a genuinely elegant piece of comparative medicine — and it is also, importantly, where the strongest causal evidence currently ends.

Is C15:0 genuinely an "essential" fatty acid?

This is the single most contested claim in the category, so it deserves proper treatment rather than a slogan.

What "essential" actually means

In nutrition science, a nutrient earns the label "essential" when it meets two criteria: the body cannot synthesise enough of it, and its absence from the diet produces a specific, reproducible deficiency syndrome that is corrected when the nutrient is restored. Linoleic acid (omega-6) and alpha-linolenic acid (omega-3) were established this way in 1929 and 1930 respectively. Nothing has been added to the list since.

The case for essentiality

• Limited endogenous synthesis. Humans produce only small amounts of C15:0, primarily from gut bacterial propionate. Circulating levels largely reflect dietary intake.
• Deficiency-pattern epidemiology. Low circulating C15:0 is repeatedly associated with higher risk of type 2 diabetes, cardiovascular disease and metabolic dysfunction-associated fatty liver disease.
• Animal deficiency models. Work published in the Journal of Nutritional Biochemistry reported that rodents fed C15:0-deficient diets through pregnancy produced pups with impaired growth, and that C15:0 supplementation restored normal growth. This mirrors the classic experimental design used to establish the original essential fatty acids.
• Downstream metabolites. C15:0 can be elongated and desaturated into previously undescribed odd-chain polyunsaturated fatty acids, suggesting it sits at the head of its own metabolic family rather than being a metabolic dead end.

The case against

• No demonstrated human deficiency syndrome. No recognised clinical condition in humans has been shown to result from low C15:0 intake and to resolve on repletion. "Cellular Fragility Syndrome" is a term coined by the company commercialising C15:0; it does not appear in ICD-11, NICE guidance or mainstream clinical nutrition texts.
• No authority has adopted the classification. Neither EFSA, the UK Scientific Advisory Committee on Nutrition, the Institute of Medicine nor the WHO currently recognises C15:0 as an essential nutrient or has set an intake reference value.
• Publication concentration. A substantial share of the mechanistic and clinical C15:0 literature originates from researchers with commercial interests in the ingredient. That does not make the findings wrong, but it does mean independent replication carries extra weight.
• Formal review remains cautious. A 2024 mini-review in Biochimie by Ciesielski and colleagues at INRAE/Institut Agro Rennes examined the evidence specifically and framed essentiality as unresolved — the paper's own title describes it as "controversial".

Where the science actually stands

The fairest summary available today: C15:0 is a biologically active dietary fatty acid with a plausible mechanistic profile and a consistent, favourable epidemiological signal. It is a legitimate candidate essential fatty acid. It has not yet met the evidential bar that omega-3 and omega-6 cleared, and treating the "first essential fatty acid in 90 years" line as settled science overstates the current position.

This pattern — promising mechanism, encouraging observational data, thin randomised evidence — is extremely common across the longevity category. We cover how to think about it in longevity supplements that don't work and is NMN a scam?.

What C15:0 does inside the cell

Membrane stability and lipid peroxidation

Cell membranes are built from a lipid bilayer. The ratio of saturated to polyunsaturated fatty acids in that bilayer determines how rigid or fluid it is, and how vulnerable it is to oxidative damage. Polyunsaturated fatty acids have double bonds that are chemically easy to attack; saturated fatty acids do not.

The proposed role of C15:0 is to sit within the membrane and increase its resistance to lipid peroxidation — the chain reaction of oxidative damage that, when severe, triggers ferroptosis, an iron-dependent form of cell death. This is a coherent biophysical argument. It is currently supported by cell and animal work rather than by human outcome trials.

AMPK activation and mTOR inhibition

This is where C15:0 intersects with mainstream longevity biology. Venn-Watson and Schork reported in Nutrients (2023) that C15:0 activates AMP-activated protein kinase (AMPK) and inhibits mTOR — the same two nodes targeted by metformin and rapamycin, the two most-studied pharmacological longevity candidates.

AMPK is the cell's low-energy sensor: activating it promotes fat oxidation, mitochondrial biogenesis and autophagy. mTOR is the growth sensor: inhibiting it shifts cells from building toward repair and recycling. If you want the underlying biology in plain English, see autophagy explained and the hallmarks of ageing.

Two caveats worth holding on to. First, these were in vitro assays across human cell systems, not human physiology. Second, "shares activities with rapamycin in a cell assay" is a very long way from "produces rapamycin-like effects in a person". For context on those comparator compounds, see rapamycin for longevity in the UK and metformin and longevity.

Mitochondrial function and PPAR signalling

The 2020 Scientific Reports paper reported that C15:0 reduced mitochondrial reactive oxygen species in a dose-dependent fashion at concentrations in the 10–50 µM range, and acts as a partial dual agonist at PPAR-α and PPAR-δ — nuclear receptors that regulate fatty acid oxidation, lipid handling and inflammatory tone. In rodent models, this translated to reduced markers of inflammation, improved lipid profiles and reduced liver fibrosis.

If mitochondrial support specifically is your goal, it is worth comparing the evidence base here against better-established options — see urolithin A in the UK, CoQ10 vs ubiquinol and PQQ vs CoQ10.

What the human evidence actually shows

This section matters more than any mechanism. Here is every meaningful strand of human data, presented without editing out the inconvenient parts.

Large observational cohorts: consistently favourable

The causality problem

The 2026 CARDIA/ARIC paper did something the earlier studies did not: it ran two-sample Mendelian randomisation, using genetic variants as a natural experiment to test whether C15:0 causes the outcomes it is associated with. The result was clear — no evidence of a causal effect on systolic or diastolic blood pressure, resting heart rate or hypertension. The authors concluded that the collective evidence is not consistent with a causal cardiovascular benefit.

There is a well-known confounding explanation for the whole observational literature. C15:0 is used across nutritional epidemiology as a biomarker of dairy fat intake. People with high blood C15:0 are, by definition, people who eat more full-fat dairy — and dairy eaters differ from non-dairy eaters in calcium, protein, fermented food intake, vitamin K2, socioeconomic status and dozens of other variables. C15:0 may be measuring a dietary pattern rather than doing the work itself.

Randomised controlled trials: small, short and mixed

Read those honestly and a consistent picture emerges. C15:0 supplementation reliably raises blood C15:0. In people who reach adequate levels, liver enzyme markers appear to improve. It does not produce weight loss, blood pressure reduction or cholesterol improvement. And in a head-to-head against dietary change, dietary change did the heavy lifting.

An earlier registered trial, NCT04947176, established the pilot framework for this work. Larger and longer trials are what the field now needs.

Absorption and dose–response

Pharmacokinetic data reported by the manufacturer indicates that roughly every 100 mg of supplemental C15:0 raises circulating levels by around 1 µg/mL, and the 2024 RCT's observation that 200 mg daily for 12 weeks raised levels by an average of 1.88 µg/mL is broadly consistent with that. Individual response varies considerably — which is why half the treatment group in that trial did not reach the 5 µg/mL threshold associated with the liver enzyme improvements.

Food sources of C15:0 in a UK diet

C15:0 makes up roughly 1–1.5% of the fatty acids in cow's dairy fat. That percentage lets you estimate intake from any dairy food if you know its fat content. The figures below are approximations based on that ratio and will vary with breed, feed and season — grass-fed and pasture-grazed animals produce noticeably more C15:0 than grain-fed ones.

The obvious implication

A British breakfast of buttered toast and a glass of whole milk, plus 30 g of cheddar at lunch, already delivers 300 mg or more of C15:0 — at or above the entire proposed daily target, and above the dose used in the published RCT. Anyone eating a conventional full-fat dairy diet is very unlikely to be deficient.

Conversely, someone following a low-fat, dairy-free or fully plant-based diet may be getting close to zero. That is the population where supplementation has the clearest theoretical rationale — and it overlaps substantially with the readers of our vegan longevity supplements guide.

The saturated fat tension

There is an unavoidable trade-off in getting C15:0 from food. Dairy fat is only about 1% C15:0; the other 99% is largely even-chain saturated fat, and UK guidance from the NHS advises men to consume no more than 30 g and women no more than 20 g of saturated fat per day. The SACN review of saturated fats and health reaffirmed that saturated fat should not exceed around 10% of food energy.

Eating 300 g of butter to hit a C15:0 target would be self-defeating. This is the legitimate argument for an isolated supplement: it delivers the odd-chain fatty acid without the even-chain saturated fat and calories that accompany it in food. It is a real point, and probably the strongest practical case the category has.

Why UK dietary C15:0 may be falling

• Long-running public health advice to switch to low-fat and skimmed dairy.
• Rapid growth in plant-based milk consumption, which contains no C15:0 at all.
• Shifts in agricultural practice from pasture grazing toward grain-based feeding, which lowers C15:0 in milk fat.

Populations with famously high dairy-fat intake from grazing animals — Sardinia among them — show notably higher circulating C15:0, which is one thread in the wider Blue Zones longevity discussion.

Buying a C15:0 supplement in the UK

Availability and regulatory status

C15:0 is present in ordinary foods, so purified pentadecanoic acid is generally sold in the UK as a food supplement rather than requiring separate novel food authorisation. In the United States the ingredient holds GRAS (Generally Recognised As Safe) status. UK availability is currently dominated by imported branded products and a small number of specialist retailers.

UK-sold supplements must comply with food supplement labelling rules and may not carry unauthorised health claims. If a product page tells you it treats, prevents or cures a disease, that is a compliance failure and a reason for scepticism, not confidence.

What to look for on the label

• Dose per capsule. Most products supply 100 mg of pentadecanoic acid per capsule. Trial doses were 200 mg daily, so check whether the labelled serving is one capsule or two.
• Free fatty acid form. The material used in human trials was purified free pentadecanoic acid, not a triglyceride-bound or esterified derivative.
• Purity stated as a percentage. Look for a specified purity figure rather than a vague "pure C15:0" claim.
• Third-party testing. Independent verification of identity, potency and contaminants matters more here than in most categories because the raw material supply chain is young. See third-party tested supplements.
• A batch-specific Certificate of Analysis. A generic PDF is not the same thing. Our guide to reading a supplement certificate of analysis explains what to check.
• A short excipient list. Vegetable cellulose capsule and the active ingredient is all that is required. See supplement fillers explained.

Cost in context

C15:0 is one of the more expensive ingredients per day in the longevity category. UK retail pricing for branded products has typically worked out at roughly £1.00–£1.50 per day, depending on subscription and pack size — considerably more than a daily NMN, creatine or omega-3 dose. Prices change frequently, so check current listings rather than relying on this range.

Whether that is defensible depends entirely on how you weigh the evidence. If you are budgeting a whole regimen, our breakdowns of longevity stack costs in the UK, building a cheap longevity stack and why supplements are so expensive are worth reading before you commit.

Dosage, timing and stacking

How much per day

Published human trials used 200 mg daily for 12 weeks. Mechanistic and epidemiological work suggests an intake of roughly 100–300 mg per day is needed to achieve and maintain circulating concentrations in the 10–30 µM range associated with the biological activity described above.

There is no established RDA, no upper limit set by any authority, and no evidence that exceeding 300 mg per day confers additional benefit. Higher is not better here.

Timing and food

C15:0 is a fatty acid, so absorption should logically improve when taken with a meal containing some fat — though the manufacturer states it can be taken with or without food. Since there is no compelling reason to take it fasted, taking it with your largest meal is the sensible default. Our broader guidance on taking supplements on an empty stomach and our supplement timing chart cover the general principles.

How long before you would know

Blood levels shift within weeks, but the 2024 RCT measured biochemical outcomes at 12 weeks. If you are trialling C15:0, give it at least three months and, ideally, book blood work before and after — liver enzymes (ALT, AST, GGT) are the markers that actually moved in the trial data. Realistic expectations are covered in how long supplements take to work.

Stacking

C15:0 has no known interactions with common longevity ingredients and, being a stable saturated fat, is unlikely to interfere with absorption of anything else. It targets membrane integrity and AMPK/mTOR signalling, which is mechanistically distinct from NAD⁺ precursors like NMN, so the two are not redundant.

That said, adding a relatively expensive and relatively unproven ingredient to an already crowded regimen is rarely the highest-value move. If you are starting out, our minimal supplement stack and how to start longevity supplements guides argue for establishing the fundamentals first. See also can you take supplements together? and our full longevity stack framework.

Safety, side effects and who should avoid it

What the trials reported

In the 2024 Journal of Nutrition RCT, no significant adverse events occurred, and reported side effects — headaches, rashes, stomach upset — did not differ between the active and placebo groups. The TANGO trial similarly reported a drop-out rate below 5% with no safety signal attributed to supplementation.

This is reassuring at 12 weeks in small populations. It is not the same as established long-term safety, and nobody should present it as such. There are currently no human trials of C15:0 supplementation running beyond three months.

Sensible cautions

• Existing liver disease. The most consistent signal in the trial data is a change in liver enzymes. If you have diagnosed liver disease, this is a conversation to have with your hepatologist or GP, not a decision to make from a product page.
• Diabetes medication. C15:0 activates AMPK, the same pathway metformin acts on. There is no documented interaction, but if you take glucose-lowering medication it is worth flagging to your prescriber and monitoring readings.
• Pregnancy and breastfeeding. Despite marketing claims about safety in pregnancy, there are no randomised human trials in pregnant or breastfeeding women. UK practice is to avoid non-essential supplements in pregnancy unless advised otherwise; follow NHS guidance on supplements in pregnancy and speak to your midwife.
• Children. No paediatric efficacy trials exist. Children eating normal full-fat dairy are among the least likely groups to have low intake.
• Anyone on prescription medication. Check with a pharmacist. This is standard practice for any new supplement.

C15:0 vs NMN, omega-3 and urolithin A

The honest positioning: if you are choosing one thing, omega-3 has vastly more human outcome data and costs a fraction as much. If you want NAD⁺ support, our NMN pillar guide, the Welzo NMN range and NMN Pro 1000 are the practical route. C15:0 is a reasonable addition for people who have already covered the fundamentals, eat little or no dairy, and are comfortable funding an ingredient whose evidence base is still forming.

For direct comparisons elsewhere in the category, see urolithin A vs NMN, NMN vs creatine, spermidine vs NMN and taurine for longevity.

The honest verdict on C15:0 supplements

C15:0 is genuinely interesting science that is being marketed well ahead of its evidence.

What holds up: it is a real, biologically active fatty acid; the epidemiology is consistent and comes from good cohorts; the mechanistic work is coherent; supplementation reliably raises blood levels; the short-term safety profile looks clean; and there is a defensible liver-enzyme signal in the one dedicated RCT.

What does not hold up: the claim that essentiality is settled; the framing of "Cellular Fragility Syndrome" as a recognised clinical diagnosis; the implication that a supplement can replicate the effects of rapamycin or metformin on the basis of cell assays; and any suggestion that the observational cardiovascular data represents proven causal benefit, which the 2026 Mendelian randomisation analysis directly contradicts.

A pragmatic position:

• If you eat full-fat dairy regularly, you are almost certainly already consuming trial-level doses. Supplementing is difficult to justify.
• If you are dairy-free, vegan or on a strict low-fat diet, your dietary C15:0 is likely near zero, and the theoretical case for supplementing is at its strongest.
• If you have elevated liver enzymes, this is the one area with direct randomised human evidence — but it belongs in a conversation with your GP alongside the interventions that produce far larger effects, chiefly weight loss and dietary change, as the TANGO trial demonstrated.
• If your budget is finite, spending £1.50 a day on C15:0 before you have addressed sleep, resistance training, zone 2 cardiovascular work and basic nutrition is the wrong order of operations.

If you want to track whether any of it is working, biological age testing and our guide to lowering your biological age cover the measurement side.

Frequently asked questions about C15:0 supplements

What is the best C15:0 supplement in the UK?

There is no single best product, and no independent UK head-to-head testing exists. Judge products on four criteria: a stated dose of pentadecanoic acid in free fatty acid form (typically 100 mg per capsule), a specified purity percentage, batch-specific third-party testing with an accessible certificate of analysis, and a minimal excipient list. Price per 100 mg is the fairest way to compare across brands, since capsule counts and serving sizes differ.

How much C15:0 should I take per day?

Published human trials used 200 mg daily. Mechanistic and epidemiological work suggests 100–300 mg per day is the range needed to reach and maintain circulating concentrations of 10–30 µM. No authority has set a recommended intake or an upper limit, and there is no evidence that going above 300 mg daily adds benefit.

Is C15:0 the same as fatty15?

Not exactly. C15:0 is the fatty acid itself — pentadecanoic acid. Fatty15 is a branded supplement whose sole active ingredient is a patented, vegan-friendly form of pure C15:0 marketed as FA15. Other manufacturers now supply purified pentadecanoic acid under their own labels. The molecule is the same; the branding, purity specification and price differ.

Does C15:0 actually work?

Partially, and modestly. It reliably raises blood C15:0 levels. In the one dedicated randomised trial, participants who reached adequate levels showed meaningful improvements in liver enzymes and haemoglobin. It did not produce weight loss, blood pressure reduction or cholesterol improvement. Claims of broad anti-ageing effects in humans are not currently supported by randomised evidence.

Can I get enough C15:0 from food instead of a supplement?

Yes, if you eat full-fat dairy. A tablespoon of butter, a 250 ml glass of whole milk and 30 g of cheddar together supply roughly 300 mg — at or above the proposed daily target. The trade-off is that dairy fat is only around 1% C15:0, so hitting the target through food also means a substantial intake of even-chain saturated fat and calories.

What are the side effects of C15:0 supplements?

In the published 12-week randomised trials, no significant adverse events were reported and side effect rates did not differ from placebo. Mild digestive upset is possible with any oral fatty acid supplement. Long-term human safety data beyond three months does not exist, so absence of reported harm is not the same as demonstrated long-term safety.

Is C15:0 better than omega-3?

They are not interchangeable and the question is somewhat misframed. Omega-3 has a far larger and more mature human evidence base, including large cardiovascular outcome trials, and costs a fraction as much per day. C15:0 has a plausible mechanism and a much smaller evidence base. Cell-based comparisons showing broader activity for C15:0 than omega-3 do not translate directly to clinical superiority in people.

Is C15:0 vegan?

The fatty acid occurs naturally in dairy and ruminant fat, but the pentadecanoic acid used in supplements is synthesised rather than extracted from animals, and leading products are vegan-friendly with vegetable cellulose capsules. Vegans and people avoiding dairy are, in principle, the group with the lowest dietary intake and therefore the clearest rationale for supplementing.

Is "Cellular Fragility Syndrome" a real medical condition?

It is a term coined by the researchers and company commercialising C15:0 to describe a proposed state of low C15:0 causing fragile, peroxidation-prone cell membranes. It is not a recognised diagnosis in ICD-11, NICE guidance or standard clinical nutrition references, and no diagnostic criteria have been adopted by any professional body. Treat it as a research hypothesis rather than a diagnosis.

How long does C15:0 take to work?

Blood levels rise within weeks of consistent daily use, with roughly 1 µg/mL of increase per 100 mg taken daily. The biochemical changes reported in trials were measured at 12 weeks. If you are trialling it, give it a full three months and use before-and-after blood work — liver enzymes are the markers with the most direct supporting evidence.

References

1. Venn-Watson S, Lumpkin R, Dennis EA. Efficacy of dietary odd-chain saturated fatty acid pentadecanoic acid parallels broad associated health benefits in humans: could it be essential? Scientific Reports. 2020;10:8161. https://www.nature.com/articles/s41598-020-64960-y
2. Venn-Watson S, Schork NJ. Pentadecanoic acid (C15:0), an essential fatty acid, shares clinically relevant cell-based activities with leading longevity-enhancing compounds. Nutrients. 2023;15(21):4607. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10649853/
3. Venn-Watson SK, Butterworth CN. Broader and safer clinically-relevant activities of pentadecanoic acid compared to omega-3: evaluation of an emerging essential fatty acid across twelve primary human cell-based disease systems. PLOS ONE. 2022;17(5):e0268778. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0268778
4. Robinson MK, Lee E, Ugalde-Nicalo PA, et al. Pentadecanoic acid supplementation in young adults with overweight and obesity: a randomized controlled trial. Journal of Nutrition. 2024. https://jn.nutrition.org/article/S0022-3166(24)00411-5/fulltext
5. Chooi YC, Zhang QA, Magkos F, et al. Effect of an Asian-adapted Mediterranean diet and pentadecanoic acid on fatty liver disease: the TANGO randomized controlled trial. American Journal of Clinical Nutrition. 2024;119(3):788–799. https://pubmed.ncbi.nlm.nih.gov/38035997/
6. Steffen BT, Jacobs DR, Li A, et al. Plasma pentadecanoic acid is modestly related to cardiovascular health in CARDIA and ARIC cohorts: observational associations without evidence of causality. Frontiers in Nutrition. 2026. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931280/
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8. Ciesielski V, Legrand P, Blat S, Rioux V. New insights on pentadecanoic acid with special focus on its controversial essentiality: a mini-review. Biochimie. 2024;227(Pt B):123–129. https://www.sciencedirect.com/science/article/pii/S0300908424002347
9. Forouhi NG, Koulman A, Sharp SJ, et al. Differences in the prospective association between individual plasma phospholipid saturated fatty acids and incident type 2 diabetes: the EPIC-InterAct case-cohort study. Lancet Diabetes & Endocrinology. 2014;2(10):810–818. https://pubmed.ncbi.nlm.nih.gov/25107467/
10. Schwimmer JB. A double blind, randomized, single center, controlled, two arm trial of dietary C15:0 supplementation in young adults at risk for metabolic syndrome. ClinicalTrials.gov identifier NCT04947176. https://clinicaltrials.gov/study/NCT04947176
11. National Center for Biotechnology Information. PubChem compound summary for CID 13849, pentadecanoic acid. https://pubchem.ncbi.nlm.nih.gov/compound/Pentadecanoic-Acid
12. NHS. Fat: the facts — different fats and nutrition. https://www.nhs.uk/live-well/eat-well/food-types/different-fats-nutrition/
13. Scientific Advisory Committee on Nutrition. Saturated fats and health: SACN report. UK Government. https://www.gov.uk/government/publications/saturated-fats-and-health-sacn-report
14. Cummings School of Veterinary Medicine at Tufts University. Research helping naval dolphins uncovers a new essential fatty acid. https://vet.tufts.edu/news-events/news/research-helping-naval-dolphins-led-dr-stephanie-venn-watson-v99-uncovers-new-essential-fatty-acid
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16. NHS. Vitamins, supplements and nutrition in pregnancy. https://www.nhs.uk/pregnancy/keeping-well/vitamins-supplements-and-nutrition/

Image credits

All images sourced from Wikimedia Commons under public domain or Creative Commons licences: pentadecanoic acid skeletal structure; pentadecanoic acid 3D ball-and-stick model; pentadecanoic acid powder; bottlenose dolphin (Tursiops truncatus, US federal government work); animal mitochondrion diagram; assorted cheeses.

Medical disclaimer

This article is intended for general information and does not constitute medical advice, diagnosis or treatment. Food supplements are not a substitute for a varied and balanced diet or a healthy lifestyle, and should not be used to treat or prevent disease. Do not exceed the stated dose. If you are pregnant, breastfeeding, taking prescription medication or have an existing medical condition, consult your GP or pharmacist before starting any supplement. If you experience concerning symptoms, contact your GP or NHS 111.