Title: Skin Disorders and Essential Fatty Acids

Key words: Cell membranes, prostaglandins, inflammatory mediators, PUFAs, linolenic acid, linoleic acid, psoriasis, fish oils, atopic eczema

Date: Dec 1999

Category: 13. Specific conditions

Type: Article

Author: Dr van Rhijn


Skin Disorders and Essential Fatty Acids



Essential polyunsaturated fatty acids (PUFA’s) are important in maintaining cell membrane fluidity and are precursors for eicosanoids, such as prostaglandins (PG), thromboxanes (TX), leucotrienes (LT) and hydroxyeicosatetraaenoic acid (HETE). Their role in skin disorders is based on modulation of these inflammatory mediators1 and will be discussed.

Rational for PUFA’s

Dietary n-3 essential fatty acids (EFA’s), especially eicosapentaenoic acid (EPA, C20:5 w -3), competitively inhibit oxygenation of n-6 EFA arachidonic acid (AA, C20:4 w -6) and act as a substrate for cyclo-oxygenase (CO) and lipoxygenase (LO) pathways at the expense of n-6 EFA’s incorporation in epidermal cells and neutrophils2. The amount and type of eicosanoids synthesized are determined by the availability of arachidonic acid (AA). This results in the production of less biologically active eicosanoids3, such as the 5-series LT, the 3-series TX & PG4 and interleukin1 (T-cell activator), hence reducing the inflammatory (chemotactic & aggragation)5 components of atopic lesions 6.

Atopic Eczema (Dermatitis)

Studies confirmed reduced plasma levels of gamma-linolenic acid (GLA, C18:3 w -6), dihomogammalinolenic acid (DGLA, C20:3 w -6) and arachidonic acid (AA, C20:4 w -6) the metabolites of linoleic acid (LA, C18:2 w -6)7 in patients with atopic dermatitis. This suggests reduced8 conversion of LA, via the enzyme delta-6-desaturase (absent in the skin), to GLA, resulting in a local biochemical deficit and dependence on the liver9 for AA supply. GLA supplementation (bypass enzyme block) with evening primrose oil, has been shown to be significantly effective (all clinical parameters) in treating patients with moderate atopic dermatitis10, 11, 12. Improvement was associated with a plasma rise, particularly in AA, DGLA, and its metabolite PGE1, suggesting an anti-eczema, anti-inflammatory action. Supplementation studies with n-3 EFA’s, showed beneficial effects13, but not better than placebo (corn oil)14, though baseline serum phospholipids (w -3 & w -6) were significantly lower in atopic dermatitis compared to psoriasis. Clinical improvement was significantly correlated with an increase in serum docosahexaenoic acid (DHA, 22:6 w -3), resulting in inhibition of T-cell proliferation.


Psoriasic skin contains increased amounts of free AA, preferentially converted to 5-lipoxygenase products, resulting in high levels of pro-inflammatory chemotaxin LTB4 15, 16, but it is unclear whether this is due to the characteristic lesional polymorphonuclear leukocytes (PMNL) infiltrates17. Eskimos are virtually free from psoriasis, probably due to a diet rich in EPA or the inability to make AA (potentially inflammatory metabolites – LTB4) via 5-desaturase18.


EPA is known to suppress LTB4 through active inhibition of synthesis and promoting synthesis of the weaker LTB519, but has no effect on the vasodilatory LTC420. Supplementation with fish oils (EPA), even intravenously21, has shown a significant clinical improvement in plaque psoriasis21, 22 but not with lower doses, for a brief period against active23 olive oil as control24.


In contrast to trials, achieving sustained increased plasma EPA/AA ratios in ordinary life requires ongoing daily supplementation with lower doses (GLA 200 mg & EPA 1.5 g) to avoid any risk of immunosuppression.


Dietary supplementation with EFA’s might well suppress inflammation and could be an effective addition to the therapeutic avenues already used in the management of atopic eczema and psoriasis.


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