T Brosche and D Platt. Effect of borage oil consumption on fatty acid metabolism, transepidermal water loss and skin parameters in elderly people. Arch Gerontol Geriatr, 2000; 30(2): 139-150.

Human skin is not able to biosynthesize gamma-linolenic acid (GLA, 18:3omega 6) from the precursor linoleic acid (LA), or arachidonic acid (AA) from dihomo-gamma-linolenic acid (DHGLA).
Dietary supplementation with GLA-rich seed oil of borage skips the step of hepatic 6-desaturation of fatty acids (FA) and, therefore, compensates the lack of these essential FA in conditions with impaired activity of delta 6-desaturase.

Twenty-nine healthy elderly people (mean age 68.6 years), received a daily dose of 360 or 720 mg GLA for 2 months, using Borage oil in gelatine capsules (Quintesal 180, manufacturer Galderma Laboratorium GmbH, Freiburg, Germany).
The effects of fatty acids derived from ingested borage oil capsules on skin barrier function were assessed by measurement of transepidermal water loss (TEWL).
The consumption of borage oil induced a statistically significant improvement of cutaneous barrier function in the elderly people, as reflected in a mean decrease of 10.8% in the transepidermal water loss.

Thirty-four percent of the people noted itch before borage oil consumption and 0% afterwards. Dry skin was claimed to be reduced from 42 to 14%, but no significant alteration of skin hydration was measured.
The FA-composition of erythrocyte membrane phospholipids demonstrated an increase of GLA (+70%) and DHGLA (+18%) and a reduction of saturated and monounsaturated FA. There was no significant alteration in nervonic acid or in AA content, but an increase in the DHGLA/AA ratio (+23%).

Thus, the consumption of borage oil by elderly people lead to alteration of FA metabolism and improved skin function.

David F Horrobin. Essential fatty acid metabolism and its modification in atopic eczema. Am J of Clinical Nutrition, 2000;71(1): 367S-372S

Research from the 1930s to the 1950s established that a deficit of n-6 essential fatty acids (EFAs) leads to an inflammatory skin condition in both animals and humans.

In a common inherited skin condition, atopic dermatitis (eczema) , there was evidence of low blood EFA concentrations and of a therapeutic response to exceptionally high doses of linoleic acid.

More recently, it has been established that there is no deficit of linoleic acid in atopic eczema.

Concentrations of linoleic acid instead tend to be elevated in blood, milk, and adipose tissue of patients with atopic eczema, whereas concentrations of linoleic acid metabolites are substantially reduced.

This suggests reduced conversion of linoleic acid to gamma-linolenic acid (GLA). In most but not all studies, administration of GLA has been found to improve the clinically assessed skin condition, the objectively assessed skin roughness, and the elevated blood catecholamine concentrations of patients with atopic eczema.

Atopic eczema may be a minor inherited abnormality of EFA metabolism.

Boelsma E, Hendriks HFJ, and Roza L. Nutritional skin care: health effects of micronutrients and fatty acids. Am J Clin Nut, 2001;73(5):853-864.

Human skin is continously exposed to internal and external influences that may alter its conditon and functioning. As a consequence, the skin may undergo alterations leading to photoaging, inflammation, immune dysfuntion, imbalanced epidermal homeostasis, or other skin disorders.

Modern nutritional science is developing new insights into the relation between food intake and health, and effects of food ingredients may prove to be biologically relevant for optimal skin condition.

The objective of this review was to evaluate the present knowledge about the interrelation of nutrients and skin, particularly the photoprotective effoects of nutrients, the influences of nutrients on cutaneous immune responses, and therapeutic actions of nutrients in skin disorders.

The nutrients of focus were vitamins, carotenoids, and polyunsaturated fatty acids. Supplmentation with these nutrients was shown to provide protection against ultraviolet light, although the sun-protection factor was relatively small compared with that of topical sunscreens.

An increase in delayed-type hypersensitivity skin responses after supplementation with nutrients has proven beneficial, especialy in elderly people, and may boost cell-mediated immunity.

Dietary consumption of certain plants or fish oil is known to modulate the balance of lipid inflammatory mediators and, therefore, is valuable in the treatment of inflammatory skin disorders.

It was concluded that nutritional factors exert promising actions on the skin, but information on the effects of low-to-moderate doses of nutrients consumed long term by healthy individuals is obviously lacking, as are data on direct effects on basal skin properties, including hydration, sebum production, and elasticity.

Ziboh VA, Miller CC, and Cho Y. Metabolism of polyunsaturated fatty acids by skin epidermal enzymes: generation of antiinflammatory and antiproliferative metabolites. Am J Clin Nut, 2000; 71(1):361S-366S.

In the skin epidermis, the metabolism of polyunsaturated fatty acids (PUFAs) is highly active.

Dietary deficiency of linoleic acid (LA), the major 18-carbon n-6 PUFA in normal epidermis, results in a characteristic scaly skin disorder and excessive epidermal water loss.

Because of the inability of normal skin epidermis to desaturate LA to gamma-linolenic acid, it is transformed by epidermal 15-lipoxygenase to mainly 13-hydroxyoctadecadienoic acid, which functionally exerts antiproliferative properties in the tissue.

In contrast, compared with LA, arachidonic acid (AA) is a relatively minor 20-carbon n-6 PUFA in the skin and is metabolized via the cyclooxygenase pathway, predominantly to the prostaglandins E2, F2 , and D2. AA is also metabolized via the 15-lipoxygenase pathway, predominantly to 15-hydroxyeicosatetraenoic acid.

At low concentrations, the prostaglandins function to modulate normal skin physiologic processes, whereas at high concentrations they induce inflammatory processes.

PUFAs derived from other dietary oils are also transformed mainly into monohydroxy fatty acids. For instance, epidermal 15-lipoxygenase transforms dihomo-gamma-linolenic acid (20:3n-6) to 15- hydroxyeicosatrienoic acid, eicosapentaenoic acid (20:5n-3) to 15-hydroxyeicosapentaenoic acid, and docosahexaenoic acid (22:6n-3) to 17-hydroxydocosahexaenoic acid, respectively. These monohydroxy acids exhibit antiinflammatory properties in vitro.

Thus, supplementation of diets with appropriate purified vegetable oils, fish oil, or both may generate local cutaneous antiinflammatory and antiproliferative metabolites which could serve as less toxic in vivo monotherapies or as adjuncts to standard therapeutic regimens for the management of inflammatory skin disorders.

Wolters M. Diet and psoriasis: experimental data and clinical evidence. British Journal of Dermatology, 2005.

Psoriasis is considered as a T-cell-mediated inflammatory skin disease which is characterized by hyperproliferation and poor differentiation of epidermal keratinocytes.

While susceptibility to psoriasis is inherited, the disease is influenced by environmental factors such as infections and stress.

Diet has been suggested to play a role in the aetiology and pathogenesis of psoriasis. Fasting periods, low-energy diets and vegetarian diets improved psoriasis symptoms in some studies, and diets rich in n-3 polyunsaturated fatty acids from fish oil also showed beneficial effects.

All these diets modify the polyunsaturated fatty acid metabolism and influence the eicosanoid profile, so that inflammatory processes are suppressed.

Some patients with psoriasis show an elevated sensitivity to gluten. In patients with IgA and/or IgG antigliadin antibodies the symptoms have been shown to improve on a gluten-free diet.

The active form of vitamin D, 1,25-dihydroxyvitamin D3, exhibits antiproliferative and immunoregulatory effects via the vitamin D receptor, and thus is successfully used in the topical treatment of psoriasis.

In this review, dietary factors which play a role in psoriasis are assessed and their potential benefit is evaluated. Furthermore, the risk of drug-nutrient interactions in psoriasis therapy is discussed.

Rhodes LE, Durham BH, et al. Dietary fish oil reduces basal and ultraviolet B-generated PGE2 levels in skin and increases the threshold to provocation of polymorphic light eruption. J Invest Dermatol, 1995; 105(4): 532-535

The sunburn response is markedly reduced by dietary fish oil rich in omega-3 polyunsaturated fatty acids.

Because prostaglandins mediate the vasodilatation, we examined the effect of fish oil on ultraviolet (UV) B-induced prostaglandin metabolism. In addition we assessed the potential photoprotective effect of fish oil in light-sensitive patients.

Thirteen patients with polymorphic light eruption received dietary supplements of fish oil rich in omega-3 polyunsaturated fatty acids for 3 months.

At baseline and 3 months, the minimal erythema dose of UVB irradiation was determined, and a graded UVA challenge given to a forearm to assess the threshold dose for papule provocation. Suction blisters were raised on the other forearm, on control skin, and on skin irradiated with four times the minimal erythema dose of UVB 24 h previously, and blister fluid prostaglandin E2 was measured by radioimmunoassay.

Following 3 months of fish oil, the mean minimal erythema dose of UVB irradiation increased from 19.8 +/- 2.6 to 33.8 +/- 3.7 mJ/cm2 (mean +/- SEM), p < 0.01. The UVA provocation test was positive in 10 patients at baseline, and after 3 months nine of these showed reduced sensitivity to papule provocation, p < 0.001.

Before fish oil, PGE2 increased from 8.6 (SEM 2.1) ng/ml in control skin to 27.2 (11) ng/ml after UVB, p < 0.01. Following 3 months of fish oil, PGE2 decreased to 4.1 (1) and 9.6 (2.4) ng/ml in control and irradiated skin, respectively, p < 0.05. Reduction of UV-induced inflammation by fish oil may be due, at least partially, to lowered prostaglandin E2 levels.

The photoprotection against UVA-provocation of a papular response suggests a clinical application for fish oil in polymorphic light eruption.

Kim HH, Shin CM, Park CH, et al. Eicosapentaenoic acid (EPA) inhibits UV-induced MMP-1 expression in human dermal fibroblasts. J Lipid Research, 2005; 46:1712-1720.

Ultraviolet (UV) irradiation regulates UV-responsive genes, including matrix metalloproteinases (MMPs). Moreover, UV-induced MMPs cause connective tissue damage and the skin to become wrinkled and aged.

Here, we investigated the effect of eicosapentaenoic acid (EPA), a dietary omega-3 fatty acid, on UV-induced MMP-1 expression in human dermal fibroblasts (HDFs).

We found that UV radiation increases MMP-1 expression and that this is mediated by p44 and p42 MAP kinase (ERK) and Jun-N-terminal kinase (JNK) activation but not by p38 activation.
Pretreatment of HDFs with EPA inhibited UV-induced MMP-1 expression in a dose-dependent manner and also inhibited the UV-induced activation of ERK and JNK by inhibiting ERK kinase (MEK1) and SAPK/ERK kinase 1 (SEK1) activation, respectively.
Moreover, inhibition of ERK and JNK by EPA resulted in the decrease of c-Fos expression and c-Jun phosphorylation/expression induced by UV, respectively, which led to the inhibition of UV-induced activator protein-1 DNA binding activity.

This inhibitory effect of EPA on MMP-1 was not mediated by an antioxidant effect. We also found that EPA inhibited 12-O- tetradecanoylphorbol-13-acetate- or tumor necrosis factor-alpha -induced MMP-1 expression in HDFs and UV-induced MMP-1 expression in HaCaT cells.

In conclusion, our results demonstrate that EPA can inhibit UV-induced MMP-1 expression by inhibiting the MEK1/ERK/c-Fos and SEK1/JNK/c-Jun pathways.

Therefore, EPA is a potential agent for the prevention and treatment of skin aging.

Chung S, Kong S, et al. Gamma-Linolenic Acid in Borage Oil Reverses Epidermal Hyperproliferation in Guinea Pigs. J. Nutr, 2002;132:3090-3097

As dietary sources of gamma-linolenic acid [GLA; 18:3(n-6)], borage oil (BO; 24?25 g/100 g GLA) and evening primrose oil (PO; 810 g/100 g GLA) are efficacious in treating skin disorders.

The triglycerol stereospecificity of these oils is distinct, with GLA being concentrated in the sn-2 position of BO and in the sn-3 position of PO.

To determine whether the absolute level and/or the triglycerol stereospecificity of GLA in oils affect biological efficacy, epidermal hyperproliferation was induced in guinea pigs by a hydrogenated coconut oil (HCO) diet for 8 wk.
Subsequently, guinea pigs were fed diets of PO, BO or a mixture of BO and safflower oil (SO) for 2 wk. The mixture of BO and SO (BS) diet had a similar level of GLA as PO but with sn-2 stereospecificity.
As controls, two groups were fed SO and HCO for 10 wk.

Epidermal hyperproliferation was reversed by all three oils in the order of BO > BS > PO. However, proliferation scores of group PO were higher than of the normal control group, SO. The accumulations of dihomo-gamma-linolenic acid [DGLA; 20:3(n-6)], an elongase product of GLA, into phospholipids and ceramides, of 15-hydroxyeicosatrienoic acid (15-HETrE), the potent antiproliferative metabolite of DGLA, and of ceramides, the major lipid maintaining epidermal barrier, in the epidermis of group BO were greater than of groups BS and PO. Group BS had higher levels of DGLA, 15-HETrE and ceramides than group PO.

With primary dependence on absolute levels, our data demonstrate that the antiproliferative efficacy of GLA in the epidermis is preferably exerted from sn-2 stereospecificity of GLA in BO.