Arachidonic Acid (Omega-6)

If omega-6 fatty acids have an inflammatory reputation, arachidonic acid is the reason why. AA is the omega-6 that actually produces the pro-inflammatory eicosanoids — the prostaglandins, leukotrienes, and thromboxanes that drive inflammation, pain, fever, and blood clotting. When you take aspirin or ibuprofen, you’re blocking the enzymes that convert AA into these inflammatory mediators. AA is that central to the inflammatory process.

But labeling AA simply as “bad” misses important nuance. AA is a normal and necessary component of cell membranes, particularly abundant in the brain, muscles, and immune cells. You need AA for proper immune function — the inflammatory response it generates is essential for fighting infections and healing wounds. Infants require AA for brain development; it’s added to infant formulas alongside DHA for this reason.

The problem isn’t AA’s existence but its excess relative to competing omega-3 fatty acids, particularly EPA. AA and EPA compete for the same enzymes (cyclooxygenase, lipoxygenase) that convert them into signaling molecules. When AA predominates, pro-inflammatory mediators dominate. When EPA is abundant, it “crowds out” AA and shifts the balance toward less inflammatory or actively pro-resolving products.

Testing arachidonic acid reveals where you stand in this competition. Combined with EPA measurement as the AA/EPA ratio, it provides the most specific assessment of your cellular inflammatory potential.

Order Your Arachidonic Acid Test

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Key Benefits of Testing

Arachidonic acid testing measures the specific omega-6 responsible for inflammatory eicosanoid production. While total omega-6 or linoleic acid provide broader context, AA directly predicts inflammatory mediator availability. This specificity makes AA the most clinically relevant omega-6 for assessing inflammatory potential.

For understanding inflammation at the cellular level, AA testing reveals whether your cell membranes are loaded with pro-inflammatory substrate. High AA means inflammatory mediators are just one enzymatic step away whenever cells are activated. Low AA (relative to EPA) means this inflammatory potential is tempered.

For cardiovascular risk assessment, the AA/EPA ratio provides information beyond traditional markers. Japanese research has extensively documented that lower AA/EPA ratios predict better cardiovascular outcomes, including fewer events after coronary stenting and more stable arterial plaques.

For those managing inflammatory conditions — rheumatoid arthritis, inflammatory bowel disease, psoriasis, asthma — knowing your AA status helps assess whether fatty acid imbalance is contributing to disease activity. Optimizing the AA/EPA balance may be part of comprehensive management.

For athletes and those interested in muscle recovery, AA has a complex role. It’s necessary for the inflammatory response that triggers muscle adaptation, but excessive AA may prolong inflammation and impair recovery. Testing helps find the balance.

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What Does Arachidonic Acid Testing Measure?

Arachidonic acid testing measures the concentration or percentage of this specific 20-carbon omega-6 fatty acid (20:4n-6) in blood samples.

Biochemical Identity

Arachidonic acid is a 20-carbon polyunsaturated fatty acid with four double bonds (20:4). The “n-6” designation indicates omega-6 family membership. AA’s 20-carbon length makes it the direct substrate for eicosanoid production — the term “eicosanoid” comes from the Greek word for twenty.

AA’s four double bonds make it highly flexible and important for membrane fluidity, but also susceptible to oxidation and enzymatic modification.

Sources of Body AA

Your body’s arachidonic acid comes from two sources:

Direct dietary intake: AA is found preformed in animal foods — meat (especially organ meats), poultry, eggs, and fish. A typical Western diet provides 100-300 mg of AA daily from these sources.

Conversion from linoleic acid: Your body converts linoleic acid (LA, the dominant dietary omega-6) to AA through a series of enzymatic steps: LA → GLA → DGLA → AA. This pathway provides additional AA beyond dietary intake.

The relative contribution of each pathway varies. Some individuals are efficient “converters” (genetic variants in FADS1/FADS2), producing substantial AA from dietary LA. Others are less efficient converters and depend more on preformed dietary AA.

Sample Types

Red blood cell (RBC) membranes: Reflects longer-term AA status (2-3 months). AA incorporates into RBC membranes during cell formation. Most relevant for assessing chronic inflammatory potential.

Plasma/serum: More variable, reflecting recent intake. Includes AA in phospholipids, cholesterol esters, and triglycerides.

Plasma phospholipids: Some labs specifically measure phospholipid-bound AA, which may better reflect tissue membrane AA.

Related Metrics

AA/EPA Ratio: Divides AA by EPA to show the balance between pro-inflammatory (AA) and anti-inflammatory (EPA) 20-carbon fatty acids. This ratio is often more clinically meaningful than AA alone.

AA as percentage of total fatty acids: Shows AA relative to all fatty acids measured.

AA/DHA ratio: Occasionally used, comparing AA to the other major marine omega-3.

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Why Arachidonic Acid Matters

The Eicosanoid Factory

Arachidonic acid is the primary substrate for eicosanoid production. When cells are activated by injury, infection, or other stimuli, phospholipase enzymes release AA from membrane phospholipids. Free AA is then converted by:

Cyclooxygenase (COX) enzymes → Prostaglandins and Thromboxanes:

• Prostaglandin E2 (PGE2): Promotes inflammation, pain, fever
• Prostaglandin I2 (PGI2, prostacyclin): Vasodilation, inhibits platelet aggregation
• Thromboxane A2 (TXA2): Vasoconstriction, promotes platelet aggregation

Lipoxygenase (LOX) enzymes → Leukotrienes:

• Leukotriene B4 (LTB4): Powerful chemoattractant for immune cells
• Leukotrienes C4, D4, E4: Bronchoconstriction (relevant to asthma)

These AA-derived mediators are powerful and necessary for normal physiology — they fight infection, stop bleeding, and initiate tissue repair. Problems arise when they’re chronically elevated without adequate resolution.

The Competition with EPA

EPA (eicosapentaenoic acid, 20:5n-3) is also a 20-carbon fatty acid and uses the same COX and LOX enzymes as AA. When both are present, they compete for enzyme access:

EPA-derived eicosanoids are less inflammatory:

• Prostaglandin E3 (PGE3): Much less inflammatory than PGE2
• Thromboxane A3 (TXA3): Much less platelet aggregation than TXA2
• Leukotriene B5 (LTB5): Much weaker chemoattractant than LTB4

EPA also produces specialized pro-resolving mediators:

• E-series resolvins: Actively resolve inflammation and promote healing

The AA/EPA ratio in cell membranes directly determines which set of mediators predominates when cells are activated. High AA/low EPA = pro-inflammatory dominance. Balanced AA/EPA = tempered inflammation with resolution capacity.

Essential Roles of AA

Despite its inflammatory potential, AA has essential functions:

Brain development and function: AA is highly concentrated in the brain, second only to DHA among polyunsaturated fatty acids. It’s essential for neuronal membrane structure, signaling, and neurotransmitter release. Infant formulas contain AA for this reason.

Immune function: The inflammatory response AA enables is necessary for fighting infections. Severely depleted AA could impair immune defenses.

Muscle adaptation: The inflammatory response to exercise involves AA-derived mediators and appears necessary for muscle adaptation and growth. Some athletes deliberately consume AA supplements for this reason (though evidence is mixed).

Cell membrane structure: AA contributes to membrane fluidity and receptor function throughout the body.

The Problem: Excess Without Balance

The concern isn’t AA’s existence but its predominance over competing omega-3s. When the AA/EPA ratio is 15:1 or 20:1 (typical Western levels) rather than 1:1 to 3:1 (typical of high-fish-consuming populations), the inflammatory response is amplified and resolution is impaired.

This chronic pro-inflammatory state — sometimes called “silent inflammation” — doesn’t cause obvious symptoms but accelerates atherosclerosis, worsens autoimmune conditions, and may contribute to numerous chronic diseases.

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What Can Affect Arachidonic Acid Levels?

Factors That Increase AA

Direct dietary AA intake:

• Red meat, especially organ meats (liver is very high)
• Poultry, especially dark meat
• Eggs (primarily in yolk)
• Some fish (though they also provide EPA/DHA)

High linoleic acid intake: LA from vegetable oils converts to AA. High LA consumption provides more substrate for AA synthesis.

Genetic efficient conversion: FADS1/FADS2 variants that increase desaturase activity produce more AA from dietary LA.

Insulin and carbohydrate: Insulin activates delta-5 desaturase, the final enzyme in AA synthesis. High-carbohydrate diets that elevate insulin may increase LA→AA conversion.

Factors That Decrease AA or Its Effects

Omega-3 intake (EPA and DHA): Competes with AA for membrane incorporation and enzyme access. The most effective strategy for improving the AA/EPA ratio.

Reducing vegetable oil consumption: Less LA means less substrate for AA production.

Reducing animal food AA sources: Eating less meat, poultry, and eggs reduces direct AA intake. (Note: this also reduces other nutrients, so balance is needed.)

GLA supplementation: Paradoxically, the omega-6 GLA (from evening primrose oil, borage oil) competes with AA for enzyme access and may reduce AA-derived inflammatory mediators in some contexts.

ALA intake: The omega-3 ALA competes with LA for conversion enzymes, potentially reducing LA→AA conversion (though this effect is modest).

Genetic Factors

FADS1/FADS2 polymorphisms: These genes encode the desaturase enzymes that convert LA to AA (and ALA to EPA/DHA). Variants significantly affect conversion efficiency:

• “High converter” genotypes produce more AA from dietary LA
• “Low converter” genotypes produce less AA and depend more on preformed dietary AA
• These variants are distributed differently across populations, affecting population-level fatty acid profiles

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Understanding Your Results

Interpreting Arachidonic Acid Levels

AA interpretation is most meaningful in context, particularly relative to EPA:

High AA with low EPA: High inflammatory potential. The AA/EPA ratio will be elevated. Increasing omega-3 intake (fish, fish oil) is indicated to restore balance.

High AA with adequate EPA: AA is elevated but balanced by EPA competition. The ratio may be acceptable. Monitor and maintain omega-3 intake.

Moderate AA with low EPA: AA itself isn’t extreme, but the ratio is still unfavorable due to low EPA. Adding omega-3 will improve the ratio.

Moderate AA with good EPA: Favorable balance. The ratio should be good. Maintaining current dietary pattern is appropriate.

Low AA: Unusual in Western diets. Could reflect very low animal food intake (vegan diet), genetic low-converter status, or fat malabsorption. Some AA is necessary — very low levels warrant evaluation if unexpected or symptomatic.

The AA/EPA Ratio

The AA/EPA ratio is often more clinically useful than AA alone:

• Ratio >15: Strongly pro-inflammatory, typical of Western diets with minimal fish
• Ratio 5-15: Elevated, room for improvement
• Ratio 2-5: Reasonable balance
• Ratio 1-2: Excellent, typical of high-fish consumers
• Ratio <1: Very high EPA relative to AA, seen with aggressive supplementation

Using Results

Establish baseline: Know your starting point.

Guide intervention: If AA is high and EPA is low, priority is increasing omega-3. If AA is very high from dietary sources, reducing meat and egg consumption may also help.

Retest after changes: Allow 3-4 months for RBC fatty acids to reflect dietary modifications. Confirm intervention achieved desired improvement.

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Health Connections

Cardiovascular Disease

Atherosclerosis and plaque stability: AA-derived eicosanoids promote inflammation within arterial plaques. Higher AA/EPA ratios are associated with more unstable plaques prone to rupture. Japanese research shows lower ratios predict better outcomes after cardiac interventions.

Thrombosis: TXA2 (from AA) promotes platelet aggregation and clot formation. EPA-derived TXA3 is far less potent. The AA/EPA balance affects clotting tendency.

Inflammatory Conditions

Rheumatoid arthritis: Joint inflammation involves AA-derived prostaglandins and leukotrienes. Increasing omega-3 relative to AA has documented benefits for RA.

Asthma: Leukotrienes from AA cause bronchoconstriction. Leukotriene receptor antagonists (montelukast) are asthma medications. The AA/EPA balance affects leukotriene production.

Inflammatory bowel disease: Intestinal inflammation involves AA-derived mediators. Omega-3 supplementation shows some benefit in IBD.

Brain and Mental Health

Brain structure: AA is abundant in brain membranes alongside DHA. Both are important for brain function, though DHA receives more attention.

Depression: Elevated AA and inflammatory markers are associated with depression. The AA/EPA ratio may be relevant to mood disorders.

Muscle and Exercise

Muscle adaptation: The inflammatory response to exercise (involving AA-derived mediators) appears necessary for muscle adaptation. Some athletes supplement AA, though evidence for performance benefit is limited.

Recovery: Excessive inflammation may impair recovery. Balance with omega-3 may optimize the adaptation/recovery trade-off.

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Why Regular Testing Matters

Baseline testing reveals your AA status and, combined with EPA testing, your inflammatory potential at the cellular level. This provides actionable information for dietary optimization.

Follow-up testing after dietary changes confirms whether modifications achieved the desired effect. Did increasing fish intake actually shift your AA/EPA ratio? Testing shows the biological reality.

Periodic testing may be valuable for:

Cardiovascular risk optimization: The AA/EPA ratio adds inflammatory risk information beyond traditional lipid markers.

Managing inflammatory conditions: Confirming that dietary intervention is maintaining optimal fatty acid balance.

Athletes optimizing recovery: Finding the balance between sufficient AA for adaptation and adequate EPA for recovery.

Those on omega-3 supplementation: Confirming supplements are achieving the desired ratio change.

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Related Biomarkers Often Tested Together

AA/EPA Ratio — The most clinically relevant metric, showing the balance between AA and its anti-inflammatory competitor EPA.

Omega-3 Index — EPA + DHA as percentage of RBC fatty acids. Shows absolute omega-3 status alongside the AA relationship.

Linoleic Acid — The parent omega-6 that converts to AA. Shows whether high LA is contributing to AA levels.

Omega-6/Omega-3 Ratio — Broader ratio including all fatty acids in both families.

hs-CRP — Direct measure of inflammation. Complements AA/EPA ratio’s assessment of inflammatory potential.

Note: Information provided in this article is for educational purposes and doesn’t replace personalized medical advice.