Arachidonic Acid
Compiled from published pharmacological and botanical literature. Not independently verified by Herbuno. Spotted an error or have a correction? Flag it below →
| CAS Number | 506-32-1 (verified against PubChem CID 444899) |
| Molecular Formula / MW | C20H32O2 / 304.47 g/mol |
| Chemical Class | Omega-6 polyunsaturated fatty acid, 20:4(ω-6) — four cis double bonds at positions 5, 8, 11, 14 |
| Sources | Endogenous (from linoleic acid); dietary in animal products; commercial material from fungal fermentation (Mortierella alpina) |
| Physiological Role | Precursor of prostaglandins, thromboxanes, and leukotrienes; major structural component of cell-membrane phospholipids |
| Typical Standardisation | ARA by GC; microencapsulated powder formats for stability |
| Claim Strength (Overview) | High for physiological essentiality and infant-formula use; Emerging and contested for supplementation in adults |
| Buy from Herbuno |
Arachidonic Acid Powder → Omega 6 Fatty Acid Powder → |
Name origin: Arachidonic acid was named after arachidic acid, a saturated C20 fatty acid first characterised in peanut oil — and that name derives from Arachis, the peanut genus, from the Greek for a leguminous plant. The etymology is therefore slightly misleading: arachidonic acid is not a peanut compound, it simply shares a twenty-carbon backbone with one. It is 20:4(ω-6), bearing four cis double bonds. Traditional use: None. Arachidonic acid is an endogenous metabolite and a structural constituent of every cell membrane you possess, characterised by 20th-century lipid biochemistry. Its dietary presence is in animal products — meat, eggs, dairy — and its commercial production is by fungal fermentation, typically Mortierella alpina. Research trajectory: Arachidonic acid occupies an unusual and slightly awkward commercial position, and this page will be direct about it. It is simultaneously (a) a physiologically essential membrane constituent added to infant formula worldwide alongside DHA, and (b) the substrate from which the pro-inflammatory 2-series prostaglandins, thromboxanes, and 4-series leukotrienes are made — the very pathway that aspirin, NSAIDs, and leukotriene antagonists exist to block. Selling it as a supplement therefore requires unusual candour. Commercial source: Microencapsulated ARA powder from fungal fermentation.
Evidence for Arachidonic Acid Applications
The physiological facts are not contested and are worth stating precisely. Arachidonic acid is a polyunsaturated omega-6 fatty acid, 20:4(ω-6), which serves as a precursor in the formation of leukotrienes, prostaglandins, and thromboxanes, contributes to cell-membrane structure, and participates in the synthesis of eicosanoids that act as signalling molecules across numerous physiological roles (PubChem CID 444899). Virtually all cellular arachidonic acid is esterified in membrane phospholipids, where its presence is tightly regulated through multiple interconnected pathways, with free arachidonic acid being a transient but critical substrate for eicosanoid biosynthesis. That tight regulation is itself a clue about supplementation. Claim strength: High.
The metabolic context is the omega-6 pathway documented in this index. Linoleic acid is desaturated to gamma-linolenic acid, elongated to dihomo-γ-linolenic acid, and then converted by delta-5-desaturase to arachidonic acid — the precursor of the pro-inflammatory 2-series prostaglandins and 4-series leukotrienes. The whole rationale for GLA and evening primrose oil supplementation was to divert flux away from this endpoint, a hypothesis whose clinical failure is documented on the Omega-6 Fatty Acids page in this index (Bamford 2013 Cochrane). There is an obvious tension in a market that sells GLA to reduce arachidonic acid and arachidonic acid to raise it, and formulators should notice it. Claim strength: Moderate.
The most defensible commercial application by a wide margin is infant nutrition. Arachidonic acid is added to infant formula worldwide, typically alongside DHA, because both are present in human breast milk and are required for normal neural and retinal development, and because infant capacity to synthesise them from precursors is limited. This is a regulated, evidence-supported, and internationally standard use, and it is a genuinely different proposition from adult supplementation. Formulators working in infant nutrition are on solid ground; those extrapolating from it to adult products are not. Claim strength: High (infant nutrition).
Adult supplementation is a much weaker proposition and the evidence is thin. A small sports-nutrition literature has explored ARA supplementation for muscle hypertrophy on the reasoning that exercise-induced eicosanoid signalling contributes to the anabolic response and that raising substrate availability might amplify it. The results have been modest and inconsistent, the trials small, and the mechanistic argument — that deliberately increasing inflammatory-eicosanoid substrate is desirable — sits uneasily with essentially every other piece of nutritional advice on the market. This page will not dress that up. Claim strength: Emerging.
A genuine complication that undercuts simplistic framing in both directions: the eicosanoid picture is not a straightforward "arachidonic acid = inflammation" story. Arachidonic acid is also the precursor of the lipoxins, which are actively pro-resolving mediators that terminate inflammation, and its metabolites include prostacyclin, a vasodilator and platelet-aggregation inhibitor. Meanwhile, intervention data linking increased dietary linoleic acid to raised tissue arachidonic acid is weaker than commonly assumed, because the delta-5-desaturase step is tightly regulated. The honest formulator position is that this pathway is more nuanced than either the "inflammatory omega-6" or the "essential building block" marketing narrative allows. Claim strength: Moderate (contested).
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Dosage & Formulator Specification
Herbuno carries Arachidonic Acid powder and Omega 6 Fatty Acid powder. The general Omega-6 Fatty Acids page in this index documents the class-level context, including the null Cochrane finding for evening primrose oil in eczema and the contested omega-6-to-omega-3 ratio debate, and buyers are directed to it before building a claim around this ingredient.
Dosing depends entirely on application, and the two principal applications are not remotely comparable. In infant formula, ARA is included at levels benchmarked to human breast-milk composition, typically in a defined ratio to DHA, and these levels are set by regulation and international standards rather than by the formulator — this is the well-founded use. In adult supplementation, the small sports-nutrition literature has used gram-scale daily doses, but the evidence is thin and inconsistent, and no dose can honestly be presented as clinically validated for muscle or performance endpoints. Formulators should be explicit about which application they are in.
Analytical verification should specify the full fatty acid profile by gas chromatography with ARA quantified specifically, not merely a total omega-6 figure. As a highly unsaturated fatty acid with four double bonds, ARA is exceptionally oxidation-prone — more so than the omega-6 fatty acids with fewer double bonds — so peroxide value and anisidine value are essential rather than optional, and oxidised lipid is not a benign impurity. Fungal fermentation origin (typically Mortierella alpina) should be documented, along with residual solvent and mycotoxin testing. For microencapsulated powder formats, the carrier system, oil load, and oxidative stability across the intended shelf life should be specified.
Arachidonic acid is an endogenous metabolite and is present in ordinary animal-source foods, so it is not intrinsically toxic; infant-formula use at breast-milk-equivalent levels has an extensive safety record. The cautions for adult supplementation are mechanistic rather than toxicological and are worth stating clearly. Because arachidonic acid is the substrate for thromboxane A₂ — a potent platelet aggregator — caution is reasonable for individuals on anticoagulant or antiplatelet therapy, and by the same logic for anyone with cardiovascular risk. Because it is the substrate for the 2-series prostaglandins and 4-series leukotrienes, caution is reasonable in inflammatory conditions including asthma, where leukotriene signalling is centrally implicated. A supplier should be candid that these are not remote theoretical concerns but the direct pharmacological consequence of what the molecule does.
Frequently Asked Questions — Arachidonic Acid
Why would anyone supplement arachidonic acid if it is pro-inflammatory?
That is the right question, and it deserves candour. The main defensible use is infant formula, where ARA is added worldwide alongside DHA because both are in breast milk and required for neural and retinal development. Adult supplementation rests on a thin, inconsistent sports-nutrition literature. There is an obvious tension in a market that sells GLA to reduce arachidonic acid and ARA to raise it.
Is arachidonic acid simply "the inflammatory one"?
That framing is too simple in both directions. ARA is also the precursor of the lipoxins, which are actively pro-resolving mediators that terminate inflammation, and of prostacyclin, a vasodilator and platelet-aggregation inhibitor. Meanwhile the delta-5-desaturase step is tightly regulated, so dietary linoleic acid raises tissue ARA less than commonly assumed.
What are the safety cautions for adult ARA supplementation?
They are mechanistic rather than toxicological. ARA is the substrate for thromboxane A2, a potent platelet aggregator — so caution is reasonable alongside anticoagulant or antiplatelet therapy and with cardiovascular risk. It is also substrate for the 4-series leukotrienes, warranting caution in asthma, where leukotriene signalling is centrally implicated.
Where does commercial arachidonic acid come from?
Fungal fermentation, typically Mortierella alpina, rather than any plant or animal source. As a fatty acid with four double bonds it is exceptionally oxidation-prone, so peroxide and anisidine values are essential rather than optional analytical requirements — oxidised lipid is not a benign impurity.
Related compounds: Omega-6 Fatty Acids, Linoleic Acid, EPA/DHA Omega-3, Alpha-Linolenic Acid
Claim-strength scale – High = multiple human RCTs; Moderate = limited trials or strong preclinical convergence; Emerging = early-stage lab or animal data.
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