Creative Touch Permanent Makeup and Aesthetics

Arachidonic acid (AA) is a 20-carbon omega-6 polyunsaturated fatty acid (PUFA) with four double bonds; distinct from arachidic acid, a saturated 20-carbon fat with a similar name but no inflammatory role. AA is produced primarily in the liver and immune cells from dihomo-gamma-linolenic acid (DGLA) via delta-5 desaturase, and is found preformed in animal-source foods including meat, eggs, and dairy. Rather than circulating freely, AA is stored esterified within cell membrane phospholipids, where it remains metabolically inert until inflammatory signals trigger its release. It is at this release and conversion stage that AA’s biological significance becomes relevant to skin. ^[1]

The Eicosanoid Cascade

When inflammatory signals activate phospholipase A2, AA is cleaved from membrane phospholipids and becomes available to two enzyme systems. Cyclooxygenase (COX) converts AA to prostaglandin E2 (PGE2), which drives vasodilation, oedema, and pain sensitisation. Lipoxygenase (LOX) converts AA to leukotriene B4 (LTB4), a potent chemotactic signal that recruits neutrophils and mast cells to the site of inflammation. Both PGE2 and LTB4 are primary mediators in inflammatory skin conditions including atopic dermatitis, psoriasis, and rosacea. This is the pathway EPA competes with directly, by displacing AA from membrane phospholipids, EPA reduces the substrate available to both COX and LOX, moderating the inflammatory response at source. ^[1]

Dietary Context

AA’s inflammatory activity is real and clinically significant, but the dietary framing matters. Whole food sources of AA – meat, eggs, dairy – deliver it in quantities that a normal mixed diet does not elevate to problematic membrane concentrations in healthy individuals. The dietary pattern that meaningfully expands the AA pool is high consumption of refined seed oils – sunflower, safflower, corn, soybean – used in bulk in ultra-processed foods and commercial cooking. These deliver linoleic acid at a scale where even low systemic conversion rates to AA accumulate over time into a measurably expanded phospholipid AA fraction. The omega-6 inflammatory concern is therefore most accurately a processed food concern, not a whole food fat concern. ^[1]

It is also worth noting that the epidermis largely lacks the delta-6 and delta-5 desaturase enzymes required for LA-to-AA conversion, meaning AA in skin keratinocytes is primarily sourced systemically rather than synthesised locally. The inflammatory cascade operates predominantly through immune cells rather than through the keratinocytes themselves.