Other Names
20:0Acide icosanoïqueácido n-eicosanoicoArachic acidArachidateArachidinic acidArachinsaeureC20:0EicosanoateEicosanoic acidFA 20:0Icosanoic acidIcosansäuren-Eicosanoaten-Eicosanoic acidNSC 93983
Arachidic acid, also known as icosanoic acid, is a saturated fatty acid with a 20-carbon chain. It is classified as a very long-chain saturated fatty acid (VLCSFA). It belongs to the group of saturated fatty acids — it has no double bond, and its shorthand notation is 20:0 — and is also a member of the group called very long chain fatty acids (VLCFA), from 20 carbon atoms onwards.
Its synonyms include arachic acid, C20:0, n-eicosanoic acid, FA 20:0, icosanoic acid, and NSC 93983. Its CAS registry number is 506-30-9. Its molecular weight is 312.5304 g/mol, its molecular formula is C20H40O2, and its IUPAC name is icosanoic acid.
Its name derives from the Latin arachis — peanut. Arachidic acid was first discovered by Gössmann A. in 1854 in peanut oil; peanuts are the seed of Arachis hypogaea, from which its name derives.
In purified form it is a white crystalline solid practically insoluble in water, with a melting point at 75.5 °C (167.9 °F; 348.65 K) and a boiling point (with some decomposition) at 328 °C (622.4 °F; 601.15 K) at 760 mmHg. The salts and esters of arachidic acid are known as arachidates. It has the properties of fatty acids: it can react with NaHCO₃ to form salts and with alcohols to form esters.
It is important to distinguish arachidic acid (20:0, a saturated fatty acid) from the similarly named arachidonic acid (20:4, n-6), which is a polyunsaturated omega-6 fatty acid. Arachidonic acid was named after the similarly structured arachidic acid, a constituent of peanut oil. These two compounds are biochemically and physiologically distinct. Arachidic acid can be formed by the hydrogenation of arachidonic acid. Reduction of arachidic acid yields arachidyl alcohol.
Arachidic acid is a minor constituent of peanuts, macadamia nuts, cocoa butter, corn oil, canola oil, and peanut oil, with its name deriving from the Latin arachis, meaning peanut. It is a minor constituent of cupuaçu butter (7%), perilla oil (0–1%), peanut oil (1.1–1.7%), corn oil (3%), and cocoa butter (1%). It comprises 7.08% of the fats from the fruit of Durio graveolens (a durian species).
It is found in appreciable quantities only in some vegetable fats and oils, where it occurs as a glycerol ester. In peanut oil, additional fatty acids alongside oleic and linoleic acid include palmitic (16:0), stearic (18:0), arachidic (20:0), 11-eicosenoic (20:1), behenic (22:0), and lignoceric (24:0). In addition to the major fatty acids, oleic acid (C18:1) and linoleic acid (C18:2) accounting for about 80% of peanut oil, the six other fatty acids, including arachidic acid (C20:0), gadoleic acid (C20:1), behenic acid (C22:0), and lignoceric acid (C24:0), account for the remaining approximately 20%.
In terms of food content in the diet: it is found in small quantities in peanut butter, 0.72 g/100 g of edible portion. In fresh and dried oily fruits, it is present in small quantities, with a maximum value in dried coconut at 0.6 g/100 g of edible portion. It is absent in legumes, with the exception of soybean meal, where it is found in trace amounts at 0.07 g/100 g of edible portion. In cereals and derivatives, it is found in trace amounts, never higher than 0.1 g/100 g of edible portion.
Endogenously, circulating VLCSFAs are derived from limited foods in the diet, such as canola oil, peanuts, and macadamia nuts, and are synthesized endogenously from the elongation of stearic acid (18:0) catalyzed by substrate-specific FA elongases (ELOVL), such as ELOVL1 and ELOVL3. Arachidic acid is generally formed from hydrogenation of plasma arachidonic acid (AA) in the body.
Arachidic acid does not circulate as a commonly isolated dietary supplement in its pure form. It is consumed primarily as a minor component of the dietary oils and nuts in which it naturally occurs. It is found in appreciable quantities only in some vegetable fats and oils, where it occurs as glycerol ester.
Arachidic acid is used in the manufacture of pharmaceuticals, soaps, cosmetics, and food packaging because of its surfactant-like properties. Arachidic acid is also used for the production of detergents, photographic materials, and lubricants. In research settings, purified arachidic acid with a purity of ≥98% is available for laboratory study.
While its direct historical use in medicinal remedies is less documented compared to other fatty acids, arachidic acid has played a significant role as a natural component of traditional plant-based oils that have been used for centuries in folk medicine.
Peanut oil, derived from the seeds of the Arachis hypogaea plant, has a history of use, particularly in traditional and folk remedies across Asia, Africa, and the Americas. Ancient cultures recognized its emollient and nourishing qualities, often applying it topically for soothing dry skin, minor burns, and joint stiffness. In Indian Ayurvedic medicine, peanut oil has been utilized as a massage oil to alleviate muscular aches and improve circulation, thanks to its warming properties and high content of beneficial fatty acids. Historically, peanut oil was also consumed to support overall vitality.
In some traditional medicine systems, particularly in certain regions of Asia and Africa, peanut oil has been used for various purposes. However, it must be emphasized that the traditional uses documented for peanut oil as a whole cannot be attributed specifically to arachidic acid, which is a minor fatty acid constituent. Arachidic acid is not classified as an essential fatty acid itself, but its consistent presence in commonly consumed oils has established its role as a regular component of the human diet for generations.
Arachidic acid is a very long-chain saturated fatty acid (VLCSFA). VLCSFAs, such as arachidic acid, behenic acid, and lignoceric acid, contain aliphatic, long fatty acid chains (the aliphatic tail) of 20, 22, and 24 carbon atoms, respectively. This classification is important because, as research has demonstrated, individual saturated fatty acids tend to have different biological functions. The VLCSFA class is distinct from shorter-chain saturated fatty acids (e.g., palmitic acid, 16:0; stearic acid, 18:0) in terms of metabolic behavior and observed associations with cardiometabolic outcomes.
As an important constituent of sphingolipids, such as ceramides and sphingomyelins, the circulating proportions of VLCSFAs are also influenced by genetic factors related to sphingolipid synthesis. Conventional C20 ceramide contains the saturated fatty acid arachidic acid. This places arachidic acid at the intersection of the sphingolipid synthesis pathway, in which very-long-chain ceramides have been studied for their roles in membrane biophysics and cellular signaling. Long-chain ceramides (C16:0, C18:0, C20:0) are consistently associated with myocardial infarction, heart failure, and cardiovascular mortality, whereas very-long-chain ceramides (C22:0, C24:0) exhibit neutral or potentially protective associations.
Recent studies have shown that arachidic acid is a fatty acid component of phosphatidylglucoside (PtdGlc). This phospholipid is found in the plasma membrane of neutrophils and is an enriched lipid in the brain. It is thought to be involved in cell-cell interactions, central nervous system signaling, and brain development. Research in animal models has suggested that PtdGlc, a novel glucosylated lipid enriched in the brain, may protect against beta-amyloid and tau pathology, cognitive deficits, and neuroinflammation, potentially through activation of PPARγ and restoration of neurotrophin signaling.
In vitro assays demonstrate that arachidic acid demonstrates the capability to displace ligands from PPAR subtypes — PPARδ, PPARγ, and PPARα — with an IC₅₀ value of 30,000.0 nM for each receptor, indicating potential modulation of metabolic, inflammatory, and cell differentiation processes. PPARs (peroxisome proliferator-activated receptors) are nuclear receptors and transcription factors that regulate cell differentiation, proliferation, and development and significantly modulate glucose, lipid metabolism, mitochondrial function, and biogenesis. The measured IC₅₀ value suggests only weak binding affinity, however, and these data are from in vitro studies only.
Arachidic acid has exhibited antioxidant activity as assessed by formazan formation-induced absorbance changes at 25 ppm at 570 nm at 37°C for 6 hours using the MTT assay. Arachidic acid acts as an antagonist at recombinant rat TRPV2 expressed in HEK293 cells, inhibiting LPC-induced and CBD-induced Ca²⁺ levels with IC₅₀ values greater than 10,000.0 nM, suggesting moderate to low potency. It shows significant inhibitory activity against electric eel Acetylcholinesterase (AChE) with an inhibition of 33.93% and an IC₅₀ value of 12,800.0 nM, and exhibits moderate inhibitory activity against equine serum Butyrylcholinesterase (BuChE) with 4.67% inhibition. All of these findings are from in vitro experiments and their relevance to human physiology at typical dietary exposures remains unestablished.
Circulating VLCSFAs are synthesized endogenously from the elongation of stearic acid (18:0) catalyzed by substrate-specific fatty acid elongases (ELOVL), such as ELOVL1 and ELOVL3. This means that arachidic acid levels in blood reflect both dietary intake and endogenous metabolic activity, making circulating concentrations a complex metabolic biomarker rather than a simple reflection of dietary consumption.
Observational and prospective cohort data (human):
Increased levels of circulating VLCSFAs have been found associated with lower risks of incident heart failure, atrial fibrillation, coronary heart disease, mortality, sudden cardiac arrest, type 2 diabetes, and with better aging.
A key nested case-control study within the Nurses' Health Study (NHS) and Health Professionals Follow-Up Study (HPFS): researchers measured three VLCSFAs (C20:0, C22:0, and C24:0) in plasma and erythrocytes using gas-liquid chromatography among 794 incident coronary heart disease (CHD) cases who were prospectively identified and confirmed among women in NHS (1990–2006) and among men in HPFS (1994–2008). A total of 1,233 CHD-free controls were randomly selected and matched to cases. Conditional logistic regression was used to estimate hazard ratios and 95% confidence intervals. Plasma VLCSFAs were correlated with favorable profiles of blood lipids, C-reactive protein, and adiponectin in the NHS and HPFS, as well as with fasting insulin and C-peptide levels in a nationally representative U.S. comparison population.
A community-based cohort study and meta-analysis: this study included 2,198 adults without carotid artery plaques (CAPs) at baseline. The percentage of baseline erythrocyte VLCSFA (arachidic acid (C20:0), behenic acid (C22:0), and lignoceric acid (C24:0)) was measured by gas chromatography. The presence of CAPs was determined at baseline and every 3 years thereafter by ultrasound examination. During a median of 7.2 years of follow-up, 573 women (35.1%) and 281 men (49.6%) were identified as CAP incident cases. VLCSFAs were inversely related with CAP risk in women (all p-trend < 0.05) but not in men.
Beneficial associations of circulating proportions of VLCSFAs, including arachidic acid (C20:0), behenic acid (C22:0), and tetracosanoic acid (C24:0), with the risks of coronary heart disease (CHD), heart failure, atrial fibrillation, sudden cardiac arrest, and/or CVD mortality were observed in the Cardiovascular Health Study, the Prevención con Dieta Mediterránea trial, the Nurses' Health Study, and the Health Professionals Follow-Up Study. However, no associations were observed in cohort studies from the Ludwigshafen Risk and Cardiovascular Health study and the Physicians' Health Study. Since the numbers of published studies and participants involved were limited for the association between the proportion of each individual VLCSFA and each CVD endpoint, these associations remained speculative.
A prospective study specifically examining erythrocyte VLCSFA and coronary artery disease: this 10-year prospective study included 2,383 participants without CHD at baseline. Erythrocyte VLCSFAs (arachidic acid (C20:0), behenic acid (C22:0), and lignoceric acid (C24:0)) were measured using gas chromatography at baseline, and 274 CHD incidents were documented in triennial follow-ups. Previous studies suggested that VLCSFAs might contribute to plasmalogen biosynthesis and reduce endogenous ceramide concentrations containing shorter-chain SFAs (<20 carbons), which may enhance cardiometabolic health.
Evidence strength: The cardiovascular evidence for circulating arachidic acid (20:0) is primarily observational (prospective cohort studies and meta-analyses). These studies consistently show inverse associations between circulating VLCSFAs and adverse cardiovascular outcomes. However, these findings are limited by confounding, by the fact that arachidic acid is one of three co-measured VLCSFAs (making isolating the specific effect of 20:0 difficult), and by the absence of randomized controlled trials specifically targeting arachidic acid. The evidence is hypothesis-generating but not causal.
Observational and prospective cohort data (human):
A pooled analysis from the Nurses' Health Study (NHS) and Health Professionals Follow-Up Study (HPFS): researchers used existing measurements of fatty acid concentrations in plasma and erythrocytes among 2,854 and 2,831 participants in the NHS and HPFS, respectively. During 39,941 person-years of follow-up, 243 cases of type 2 diabetes were documented. Comparing the highest with the lowest quartiles of plasma concentrations, pooled hazard ratios (95% CIs) were 0.51 (0.35, 0.75) for arachidic acid, 0.43 (0.28, 0.64) for behenic acid, 0.40 (0.27, 0.61) for lignoceric acid, and 0.41 (0.27, 0.61) for the sum of VLCSFAs, after multivariate adjustments for demographic, lifestyle, and dietary factors. This represents a statistically significant approximately 49% lower risk of type 2 diabetes in those with the highest versus lowest plasma arachidic acid concentrations, after adjustment.
Results from a pooled analysis indicate that higher concentrations of circulating VLSFAs 20:0, 22:0, and 24:0 are each associated with a lower risk of diabetes.
However, the findings across studies are not entirely consistent. Results of studies investigating the associations between VLCSFAs and incident type 2 diabetes were inconsistent. For example, two prospective studies reported that plasma phospholipid arachidic acid (20:0), behenic acid (22:0), and lignoceric acid (24:0) were inversely associated with incident T2D, while another study reported a null association of erythrocyte 20:0, 22:0, and 24:0 with incident T2D. One prospective cohort study in Chinese adults found that erythrocyte arachidic acid was positively associated with type 2 diabetes risk (multivariable-adjusted HR of the fourth quartile vs. first quartile: 1.46 [1.00–2.12]; p = 0.035). That study's findings indicate that individual erythrocyte SFAs are associated with T2D in different directions, with 18:0 and 20:0 SFAs positively associated with the risk in that population.
Evidence strength: Moderate-level observational evidence from large prospective cohorts in Western populations (predominantly) suggests an inverse association between circulating arachidic acid and type 2 diabetes incidence. However, conflicting findings from non-Western populations and methodological differences (plasma phospholipid vs. erythrocyte measurement, population demographics) mean the totality of evidence is mixed. No randomized controlled trials have examined arachidic acid specifically for diabetes risk reduction.
Recent studies have shown that arachidic acid is a fatty acid component of phosphatidylglucoside (PtdGlc). This phospholipid is found in the plasma membrane of neutrophils and is an enriched lipid in the brain. It is thought to be involved in cell-cell interactions, central nervous system signaling, and brain development.
Dietary intake of the lipid PtdGlc has been associated with decreased cognitive deficits and hippocampal neuroinflammation, and more research is being done to further elucidate the relationship between this compound and human health and disease. Animal model research specifically showed that treatment with phosphatidylglucoside (PtdGlc) may protect against amyloid-beta and tau pathology, cognitive deficits in APP/PS1 mice, and alleviate neuroinflammation through activation of PPARγ and restoration of neurotrophin signaling.
Separately, a clinical study analyzed the neuroprotective role of arachidic acid in autism spectrum disorder (ASD). The study found that an increased plasma ratio of omega-3/omega-6 PUFAs (i.e., DHA/arachidonic acid and EPA/arachidonic acid) led to decreased ceruloplasmin, transferrin, and superoxide dismutase levels, which have neuroprotective properties.
Evidence strength: The neurological evidence for arachidic acid specifically is highly preliminary. The PtdGlc findings are primarily from animal models and cell culture studies. No adequately powered human clinical trials have examined arachidic acid's effects on cognitive function, neurodegeneration, or neuroinflammation as a primary endpoint.
Recent observational studies have documented inverse associations of circulating very long-chain saturated fatty acids (VLCSFAs), namely arachidic acid (20:0), behenic acid (22:0), and lignoceric acid (24:0), with cardiometabolic outcomes.
A 2023 systematic review registered on PROSPERO (CRD42021233550): a systematic search of observational studies was conducted in MEDLINE, EMBASE, and The Cochrane databases up to February 2022. A total of 12 studies, consisting mostly of cross-sectional analyses, were included in this review. The majority of the studies documented the associations of dietary intake with total plasma or red blood cell VLCSFAs, in which a range of macronutrients and food groups were examined. Two cross-sectional analyses showed a consistent positive association between total fat and peanut intake with 22:0 and 24:0, and an inverse association between alcohol intake and 20:0 and 22:0. Furthermore, a moderate positive association between physical activity and 22:0 and 24:0 was observed. Lastly, there were conflicting results on the effects of smoking on VLCSFA.
Overall, there is currently no mechanistic link between overall healthier lifestyle habits such as increased physical activity and lower alcohol consumption with circulating VLCSFAs; however, recent reviews suggest that higher VLCSFAs may be a biomarker of lower de novo lipogenesis and/or overall health status. Therefore, the positive association between healthier lifestyle habits and VLCSFAs might reflect the overall benefits of a healthy lifestyle and improved cardiometabolic health.
On the other hand, results from animal model and cell culture studies have led to the hypothesis that the unique biochemical characteristics of VLCSFAs may influence cell membrane integrity and insulin signaling, thereby playing a significant role in cardiometabolic health; nonetheless, the mechanisms underlying the association between VLCSFAs and cardiometabolic disease are not well understood.
The relationship between arachidic acid and LDL cholesterol is complex and context-dependent. Diets rich in saturated fatty acids, such as arachidic acid, are known to increase serum low-density lipoproteins, resulting in high blood cholesterol levels. This is the classical perspective applied broadly to saturated fats.
However, circulating VLCSFA data suggest a different picture: plasma VLCSFAs were correlated with favorable profiles of blood lipids, C-reactive protein, and adiponectin. The distinction here is between the classical dietary SFA-raising-LDL paradigm (which applies to shorter-chain SFAs like palmitic acid more robustly) and the observational finding that circulating VLCSFAs — reflecting both diet and endogenous metabolism — correlate with favorable metabolic markers.
A meta-analysis of prospective studies: a total of 49 prospective studies reported in 45 articles were included. Higher concentration of circulating total SFAs was associated with an increasing risk of cardiometabolic diseases; the risk increased significantly by 50% for CVD (95% CI: 1.31–1.71), 63% for CHD (95% CI: 1.38–1.94), 38% for stroke (95% CI: 1.05–1.82). However, this refers to total circulating saturated fatty acids, not VLCSFAs specifically, and the evidence for the very-long-chain class diverges from shorter-chain SFAs.
Emerging research has suggested an indirect pathway by which VLCSFA-rich foods may affect health via gut microbiota. A randomized crossover trial highlighted an increased abundance of Roseburia and Ruminococcaceae following dietary interventions with peanuts compared to baseline measurements. Both Roseburia and Ruminococcaceae are recognized as major butyrate-producing bacteria genera, suggesting that dietary intake of VLCSFA-rich foods like peanuts and macadamia nuts may alter the gut microbial composition. Whether arachidic acid specifically (rather than other bioactive components of peanuts) drives this effect has not been established.
Arachidic acid is not typically formulated or administered as a standalone dietary supplement. The scientific literature on VLCSFAs has primarily used circulating biomarker concentrations (in plasma and erythrocytes as a percentage of total fatty acids) rather than measuring or prescribing discrete dietary doses. No clinical trials have administered isolated arachidic acid to human participants at a defined dose and measured health outcomes.
Peanuts, macadamia nuts, and canola oil are primary dietary sources of VLCSFA. Intervention studies have demonstrated that the consumption of peanuts and macadamia nuts can increase circulating concentrations of VLCSFAs, but specific arachidic acid doses used in those interventions are not reported separately from total food servings in the available literature.
Intakes of peanuts, peanut butter, vegetable fat, dairy fat, and palmitic/stearic (16:0–18:0) fatty acids were significantly, albeit weakly, correlated with plasma and erythrocyte VLCSFA concentrations (|rs| ≤ 0.19). This weak correlation underscores that circulating arachidic acid is substantially determined by endogenous biosynthesis rather than dietary intake alone.
In industrial and research settings, purified arachidic acid of ≥98% purity is produced for laboratory use. In vitro studies have examined effects at concentrations such as 25 ppm in antioxidant assays and at IC₅₀ values of 30,000 nM for PPAR receptor displacement. These are experimental values only and do not correspond to physiologically achievable dietary concentrations in humans.
Research on arachidic acid specifically remains limited compared to other fatty acids such as omega-3 or omega-6 polyunsaturated fats. Current studies suggest that arachidic acid is efficiently metabolized in the human body and does not present adverse health effects when consumed as part of a balanced diet.
Diets rich in saturated fats like arachidic acid are associated with increased levels of serum low-density lipoproteins. This is the classical concern about saturated fatty acid intake broadly. However, as noted throughout this article, the chain-length specificity of saturated fatty acids is increasingly recognized, and very long-chain saturated fatty acids (VLCSFAs) have received limited attention compared to other saturated fatty acids in terms of specific clinical guidance. The evidence that circulating VLCSFAs associate with favorable lipid profiles does not automatically mean that isolated arachidic acid supplementation would be beneficial or safe.
A distinction must be drawn between free circulating arachidic acid and arachidic acid incorporated into ceramides. Long-chain ceramides (C16:0, C18:0, C20:0 Cer) are consistently associated with myocardial infarction, heart failure, and cardiovascular mortality, whereas the free VLCSFA form appears to correlate inversely with cardiovascular risk in epidemiological studies. This divergence highlights that the biological context in which arachidic acid exists (free fatty acid vs. ceramide-bound) matters considerably for its associated health outcomes and warrants attention in interpreting the literature.
Since peanut oil and peanut products are primary dietary sources of arachidic acid, individuals with peanut allergies should be aware that consuming foods high in arachidic acid may involve exposure to peanut-derived products. Peanut, a high-oil crop with about 50% oil content, is either crushed for oil or used as edible products. Highly refined peanut oil typically has allergen proteins removed, but cold-pressed and unrefined preparations may retain allergenic proteins.
No specific toxicity data, pharmacokinetic studies, drug interaction studies, or upper intake levels for isolated arachidic acid in humans were identified in the peer-reviewed literature searched for this article. Research on arachidic acid specifically remains limited compared to other fatty acids. No regulatory body — including the NIH Office of Dietary Supplements, EFSA, or European Medicines Agency — has issued a specific monograph or upper tolerable intake level for arachidic acid as a standalone supplement.
Arachidic acid occupies a distinctive position in nutritional biochemistry. Unlike most saturated fatty acids, which have been studied extensively in the context of cardiovascular harm, arachidic acid (20:0) as a circulating VLCSFA has been inversely associated in multiple large prospective cohort studies with coronary heart disease, heart failure, atrial fibrillation, sudden cardiac arrest, and type 2 diabetes. These associations are real but not yet causal — no randomized controlled trial has tested isolated arachidic acid supplementation in humans for any clinical outcome.
Its roles in sphingolipid metabolism, as a component of ceramide C20:0 and of phosphatidylglucoside (PtdGlc), link it to cell membrane integrity, neurological signaling, and immune cell function. In vitro evidence suggests weak interactions with PPAR nuclear receptors and cholinesterase inhibition, but these findings have no confirmed clinical relevance at dietary exposure levels.
The strongest evidence available — from prospective cohort studies and meta-analyses published in peer-reviewed journals — supports the use of circulating arachidic acid as a potential cardiometabolic biomarker rather than supporting supplementation with isolated arachidic acid for any specific health purpose.
Health conditions that Arachidic acid may help support.
Body systems that Arachidic acid may help support.