IngredientsCapric acid, also known as decanoic acid or decylic acid, is a saturated fatty acid, medium-chain fatty acid (MCFA), and carboxylic acid. The term "capric acid" is derived from the Latin caper/capra (goat) because the sweaty, unpleasant smell of the compound is reminiscent of goats. Salts and esters of decanoic acid are called caprates or decanoates.
Its key identifying data are: molecular weight 172.2646 g/mol; molecular formula C₁₀H₂₀O₂; IUPAC name decanoic acid; CAS registry number 334-48-5; PubChem CID 2969. Its structural formula is CH₃(CH₂)₈COOH.
Capric acid is a carboxylic acid with a 10-carbon chain that belongs to the group of saturated fatty acids, with no double bonds in the aliphatic chain (shorthand notation 10:0), and is a member of the group called medium-chain fatty acids (MCFA), namely fatty acids containing from 6 to 12 carbon atoms. In purified form it is a crystalline solid insoluble in water, with a melting point of 31.4 °C (88.52 °F; 304.55 K) and a boiling point of 270 °C (518 °F; 543.15 K) at 760 mmHg.
Two other fatty acids are named after goats: caproic acid (a C6:0 fatty acid) and caprylic acid (a C8:0 fatty acid). Along with capric acid, these total 15% in goat milk fat.
Capric acid occurs naturally in coconut oil (about 10%) and palm kernel oil (about 4%); otherwise it is uncommon in typical seed oils. It is found in the milk of various mammals and to a lesser extent in other animal fats. It occurs notably in goat milk, accounting for about 15% of the fatty acids, and is also present in human breast milk.
Coconut oil and palm kernel oil are also characterized by high amounts of capric acid (5–10% and 3–5% of fatty acids, respectively) alongside lauric acid. The compound has also been identified in small quantities in cow's milk and butter.
Medium-chain triglycerides (MCTs) are comprised primarily of the MCFAs caprylic (C8; 50–80%) and capric (C10; 20–50%) fatty acids, along with a very small amount (2–4%) of caproic (C6) and lauric (C12) fatty acids.
Capric acid is commercially encountered in several distinct forms:
While capric acid has been present in the human diet for centuries, its targeted use as a supplement is relatively new. Capric acid as a distinct chemical entity was not isolated or named by traditional healing systems; rather, its historical exposure occurred via dietary consumption of foods intrinsically rich in the compound.
Goat milk, which contains a notable proportion of capric acid among its fatty acids, has long been valued across the Mediterranean, the Middle East, and parts of Asia and Africa for its perceived digestibility and therapeutic properties. In many traditional systems, goat milk and its derived products — cheese and fermented preparations — were preferred for infants, the elderly, and the convalescent, partly because of the belief that such dairy was more easily tolerated than cow's milk. The characteristic aroma of goat-milk products arises in part from capric acid itself.
Coconut oil, the richest concentrated plant source of capric acid, has been used in the Ayurvedic medical tradition of the Indian subcontinent for thousands of years. In this tradition, coconut oil was employed both as food and as a topical preparation for skin and hair, as well as in oil-pulling (oral hygiene). Pacific Islander cultures, particularly in Polynesia and Melanesia, have used coconut oil as a primary dietary fat and as a topical agent for wound healing, skin conditions, and protection against heat and sun — uses that have since been investigated in part through the lens of the antimicrobial properties attributable to its medium-chain fatty acid constituents, including capric acid.
Epilepsy treatment using the ketogenic diet was originally developed in the 1920s, and its modified version using medium-chain triglycerides was developed in the 1970s (Huttenlocher et al., 1971). The formal identification of capric acid as a bioactive component within MCT-based dietary therapy thus belongs to the mid-to-late twentieth century scientific tradition rather than any ancient system of medicine.
Capric acid is itself the primary active constituent of interest. Its biological effects arise from several distinct, partially overlapping mechanisms:
Unlike long-chain fatty acids, capric acid is absorbed directly into the portal vein and rapidly transported to the liver, where it is used for energy production. Orally ingested medium-chain fatty acids would be very rapidly degraded by first-pass metabolism by being taken up in the liver via the portal vein, and are quickly metabolized via coenzyme A intermediates through β-oxidation and the citric acid cycle to produce carbon dioxide, acetate, and ketone bodies. Unlike long-chain fats, MCFAs do not require bile salts for micelle formation or carnitine shuttles to enter mitochondria.
Decanoic acid functions as a direct anticonvulsant by attenuating excitatory postsynaptic currents, inhibiting AMPA receptor activity, and promoting GABA synthesis in astrocytes. Based on the observation of a blood rise of ketone bodies as well as two fatty acids (decanoic acid and octanoic acid) in patients under MCT ketogenic diet therapy, these compounds have been explored for their anticonvulsant properties, revealing that decanoic acid, but not the ketones β-hydroxybutyrate or acetone, has antiseizure activity. Decanoic acid acts on the glutamatergic pathway through a non-competitive antagonism of the AMPA receptors.
This direct inhibition of excitatory neurotransmission by capric acid in the brain contributes to the anticonvulsant effect of the MCT ketogenic diet. Decanoic acid and the AMPA receptor antagonist drug perampanel act at separate sites on the AMPA receptor, and so it is possible that they have a cooperative effect at the AMPA receptor, suggesting that perampanel and the ketogenic diet could be synergistic.
Capric acid readily crosses the blood-brain barrier, probably by a combination of diffusion and saturable carrier-mediated transport via a medium-chain fatty acid transporter.
Capric acid may be responsible for the mitochondrial proliferation associated with the ketogenic diet, and this may occur via PPARγ receptor agonism and its target genes involved in mitochondrial biogenesis. Complex I activity of the electron transport chain is substantially elevated by decanoic acid treatment.
Decanoic acid (C10) is recognized for its capacity to optimize mitochondrial functionality, modulate astrocyte activity, increase neuronal GABA production through augmented glutamine supply, and inhibit mTORC1 activity, contributing to improved neurological function.
Capric and caprylic acids inhibit processes involved in Candida albicans virulence like morphogenesis, adhesion, and biofilm formation. However, their primary mode of antifungal action is through membrane perturbations in the target organism. Capric acid decreases fluidity while increasing the potential of the plasma membrane.
P. acnes-induced mRNA levels and secretion of IL-8 and TNF-α in THP-1 cells were suppressed by capric acid, which inhibited NF-κB activation and the phosphorylation of MAP kinases.
Unlike long-chain fats, MCFAs do not require bile salts for micelle formation or carnitine shuttles to enter mitochondria. This "shortcut" explains why MCT oils — blends rich in C8 (caprylic) and C10 — can be rapidly converted into cellular energy and ketone bodies (beta-hydroxybutyrate and acetoacetate).
This is the most extensively studied and clinically significant area of capric acid research. The MCT ketogenic diet, in which capric acid represents a major component, has been formally evaluated in randomized controlled trials.
The first randomized trial on classical and medium-chain triglyceride (MCT) versions of the ketogenic diet examined efficacy and tolerability after 3, 6, and 12 months. One hundred forty-five children with intractable epilepsy were randomized to receive a classical or an MCT diet. This study showed classical and MCT ketogenic diet protocols to be comparable in efficacy and tolerability; both ways of implementing the diet have their place in the treatment of childhood epilepsy.
Capric acid is a major constituent of the MCT ketogenic diet, providing about 40% of the medium-chain fat within the diet. Neal and colleagues conducted the first randomized study comparing efficacy of the classical ketogenic diet (CKD) with that of the MCT ketogenic diet (MCTKD), in which MCTs provided 40–50% of energy.
Two recent meta-analyses of many clinical prospective studies reported approximately 50–65% efficacy of versions of the original and modified ketogenic diets in the treatment of various adult and childhood epilepsies. In children with certain types of epilepsy, the MCT ketogenic diet seems to be similarly effective as the classical ketogenic diet in regard to seizure control.
A prospective open-label feasibility study in drug-resistant epilepsy patients investigated the safety of a medical food blend containing a unique ratio of decanoic acid and octanoic acid. This is the first clinical use of decanoic acid as an antiseizure medication. The feasibility study found that two-thirds of children and adults involved in this clinical trial completed the study. Gastrointestinal side effects were the main cause of discontinuation.
A more recent study (2025) found that a C10-enriched ketogenic diet demonstrated comparable efficacy and tolerability to the classic KD, offering a promising option for patients with refractory epilepsy who do not respond adequately to the classic KD alone. This study, described as the first to directly compare a C10-enriched KD with a classic KD, highlights the potential synergistic effects of decanoic acid.
The preclinical mechanistic evidence is robust: animal and in vitro studies have consistently demonstrated anticonvulsant activity attributable specifically to decanoic acid, with a defined receptor-level mechanism (AMPA antagonism) that is distinct from ketosis. Studies in animal models have shown that decanoic acid inhibits epileptiform activity. The overall clinical evidence is moderately strong for the MCT ketogenic diet as a class, with the specific contribution of capric acid within that diet supported by both mechanistic and early clinical data.
Both capric acid (decanoic acid, C10:0) and lauric acid (dodecanoic acid, C12:0) have been shown to be powerful bactericidal agents in vitro. Capric acid exhibits antibacterial activity against several Gram-positive and Gram-negative bacteria, as well as antifungal and antiviral activity.
A study published in the Journal of Dermatological Science examined capric acid against Propionibacterium acnes (now Cutibacterium acnes), an organism implicated in acne vulgaris: among the fatty acids tested, capric acid exhibited the most potent antibacterial activity. The data demonstrated that both capric acid and lauric acid exert bactericidal and anti-inflammatory activities against P. acnes. The anti-inflammatory effect may partially occur through the inhibition of NF-κB activation. Lauric acid had stronger antimicrobial activity against P. acnes than capric acid in vitro and in vivo. However, both fatty acids attenuated P. acnes-induced ear swelling in mice along with microabscess and significantly reduced interleukin (IL)-6 and CXCL8 production in P. acnes-stimulated SZ95 sebocytes. This work was conducted in animal and cell models; direct human clinical trials of capric acid for acne are lacking.
Regarding antifungal activity, Saccharomyces boulardii secretes capric acid (C10:0), which is most effective in inhibiting essential virulence factors of C. albicans, especially morphological transition, partial adhesion, and biofilm formation. The minimum inhibitory concentrations (MICs) of five medium-chain saturated fatty acids (7:0, 8:0, 9:0, 10:0, and 11:0) against Candida albicans ranged from 100 to 200 µg/mL.
Importantly, the antagonism between capric acid and amphotericin B is a strong indication for physicians not to use both compounds simultaneously in the treatment of candidiasis. All currently published antimicrobial evidence is preclinical (in vitro or animal); there are no registered human clinical trials demonstrating therapeutic efficacy of capric acid alone against systemic or invasive fungal infections.
Most studies on MCT oil supplementation reported that MCT oil did not improve exercise performance and had no effect on respiratory exchange ratio, glucose concentration, fat and carbohydrate oxidation, and lactate concentration. MCT oil showed very little to no ergogenic effects on exercise performance and substrate utilization in healthy populations. This 2022 systematic review covered studies in which capric acid (as part of MCT oil) was a key variable.
Capric acid-rich structured lipids regulate metabolic imbalances associated with obesity by attenuation of hepatic steatosis, as investigated in a study of male C57BL/6J mice subjected to a high-fat diet. Incorporation of capric acid into structured lipids resulted in lower leptin levels compared to control, and a protective effect against hepatocellular micro-vesicular steatosis and macro-vesicular steatosis was observed in mice fed these structured lipids. This evidence is entirely preclinical (murine model) and cannot yet be extrapolated to clinical recommendations.
Epidemiological studies have associated higher dietary decanoic acid intake with reduced risk of type 2 diabetes, and preclinical research indicates protective effects against obesity through gut microbiota modulation and anti-inflammatory actions. Much of this evidence stems from studies through 2020; further clinical trials are needed to validate these effects and elucidate long-term mechanisms.
The clinical evidence supporting ketogenic diet use includes management of adult epilepsy, malignant glioma, Alzheimer's disease, migraine headache, motor neuron disease, and other neurologic disorders. However, evidence specifically attributable to capric acid rather than the broader ketogenic/MCT diet is limited in this context. The use of ketogenic diets and MCTs is expanding to other neurological disorders, including Alzheimer's disease, Parkinson's disease, and mild cognitive impairments. Clinical trials specifically isolating capric acid's contribution in these areas remain preliminary or exploratory.
Beneficial physiological effects of dietary medium-chain fatty acids have been studied for a long time, and MCT oil has been used as a special energy source for patients suffering from pancreatic insufficiency, impaired lymphatic chylomicron transport, and fat malabsorption. In this setting, capric acid-containing MCT formulas are a standard component of clinical nutritional support with a long record of use; however, most of this literature treats MCT as a class rather than capric acid specifically.
In clinical studies of the MCT ketogenic diet in children, subjects received diets in which MCTs provided 40–55%, 60%, or >60% of total energy. Results suggested that 21% of children were seizure free, 19% had a >90% seizure reduction, and another 42% had a 50–90% seizure reduction.
Neal and colleagues' randomized controlled trial used a diet in which MCTs provided 40–50% of energy.
Capric acid is a major constituent of the MCT ketogenic diet, providing about 40% of the medium-chain fat within the diet.
In in vitro antimicrobial research, minimum inhibitory concentrations of capric acid (10:0) against Candida albicans ranged from 100 to 200 µg/mL. Capric acid at a concentration of 100 µM significantly reduced IL-8 release by P. acnes-stimulated THP-1 cells.
In a seizure model, rat cortex-hippocampus slices were incubated with 100 µM and 1 mM of capric acid.
The safety of human dietary consumption of MCT, up to levels of 1 g/kg, has been confirmed in clinical trials.
In a 90-day sub-chronic oral toxicity study of a capric acid-rich oil in Sprague–Dawley rats, the no-observed-adverse-effect level (NOAEL) was determined to be more than 4 mL/kg body weight.
According to part 172 of the Code of Federal Regulations (CFR), free fatty acids (including capric and caprylic acid) and their metallic salts are recognized as safe additives for use in food by the U.S. Food and Drug Administration. Glyceryl Tridecanoate (GT) — the triglyceride form of decanoic acid — belongs to the class of MCTs, which has been accepted as a Generally Recognized As Safe (GRAS) food product by the FDA.
The MCT ketogenic diet has adverse gastrointestinal-related side effects, such as diarrhoea, vomiting, bloating, and cramps. There is also a high attrition rate for the diet, due to many patients finding it difficult to tolerate. Higher intakes often cause gastrointestinal upset (bloating, cramping, diarrhea); gradual increases in intake are advised.
The reported toxicity data for capric acid indicate an oral LD₅₀ of 3,730 mg/kg in rats and a dermal LD₅₀ of 1,770 mg/kg in rabbits, based on MSDS sources.
In MCAD deficiency (MCADD — medium-chain acyl-CoA dehydrogenase deficiency), octanoic acid and decanoic acid accumulate as primary metabolites, along with their glycine and L-carnitine derivatives. This inherited disorder of fatty acid oxidation typically presents in early childhood, though adult-onset can occur. Key symptoms include hypoglycemia, vomiting, lethargy, and encephalopathy, especially following fasting, infection, or other metabolic stressors.
Rare absolute contraindications to ketogenic and MCT-based diets include selected inborn errors of metabolism affecting pyruvate carboxylase activity, carnitine transport or utilization, fatty acid oxidation pathways, as well as porphyria. Relative contraindications encompass acute pancreatitis, advanced hepatic or renal disease, familial hypercholesterolaemia, and other conditions that may be aggravated by MCT-induced metabolic changes, including concomitant use of propofol.
Decanoic acid and the AMPA receptor antagonist drug perampanel act at separate sites on the AMPA receptor, and it is possible that they have a cooperative effect at the AMPA receptor, suggesting that perampanel and the ketogenic diet could be synergistic. While this pharmacodynamic interaction may be clinically useful in epilepsy, it requires monitoring.
The antagonism between capric acid and amphotericin B — a widely used antifungal — is a strong pharmacological signal for physicians not to use both compounds simultaneously in the treatment of candidiasis.
Long-term MCT administration requires monitoring for growth retardation, gastrointestinal intolerance, and lipid abnormalities. Periodic assessments of BMI, liver function, and developmental milestones are advised in children on MCT-enriched regimens.
People with significant liver disease, known fatty-acid oxidation disorders, or on strict therapeutic ketogenic diets should only use capric acid-containing preparations under clinical guidance.
Health conditions that Capric acid may help support.
Body systems that Capric acid may help support.
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