Inflammation is a broad term describing the body's reaction to injury. It is a necessary process enabling defense against toxins and pathogens, protection against further damage, and repair of tissue. However, if the inflammatory process proceeds beyond that which is necessary to heal, it can become a disease in itself. Runaway inflammation underlies allergic reactions and certain other self-destructive diseases such as arthritis, the cycle of atherogenesis, and some dermatologic disorders.

The use of essential fatty acids in the diet has long been known to exert a beneficial effect on the health of skin and hair. Inflammatory skin disease has been shown to respond to essential fatty acids fed orally and even applied topically.^1-3 Children who suffer from atopic eczema have been shown to have low blood levels of essential fatty acid metabolites. With the use of essential fatty acids blood levels rise and the skin problems decrease.⁴ Eskimos eating the traditional fishy high fat and oil diet have very little psoriasis. But when they adopt the Western diet, the incidence of this condition greatly increases.⁵ Acne vulgaris has also been shown to respond to administration of essential fatty acids. In some cases, where there was even resistance to antibiotic treatments, the administration of linoleic acid resulted in a favorable outcome.⁶

There are several proposed mechanisms by which essential fatty acids can affect inflammatory skin diseases.

SKIN BARRIER FUNCTION
In the transitional area between live active cells in the skin and the outer epidermal layers that eventually detach (desquamate) and are lost as a part of normal skin growth, there is a water barrier. This lipid layer, (stratum lucidum) lies between the granular cells (stratum granulosum) and the horny cells (stratum corneum) of the skin. If this lipid layer is not properly formed, the skin experiences a change in transdermal permeability. Water is thus lost resulting in dry, scaling skin, a moistening and matting of hair, and increased water intake even though urine volume is not proportionally increased. This lipid layer is formed from a class of compounds called sphingolipids including acylglucosylceramides which contain linoleic acid as a vital constituent. If linoleic acid is deficient in the diet, the lipid granule produced by the granular cells (Odland bodies) has other fatty acids substituted such as oleate. This results in a different stereochemical configuration resulting in excess water leakage from the skin.^7-9 (Fig. 17)

EICOSANOID METABOLISM
Within the skin, arachidonic acid can be a part of the phospholipids which make up tissue membranes (especially in high meat diets). Arachidonic acid is released from phospholipids by the ester breaking enzymes phospholipase \ and C. This is initiated by various stimuli such as collagen, thrombin, bradykinin, serotonin, and adrenalin. Once released the arachidonic acid breaks down (cascades) into the various eicosa-noids. These oxygenated autocoids are powerful inflammatory agents within the skin. They can cause vessel dilation, release chemotactic factors, result in extravasation of white blood cells, and dermatologically produce pruritis, erythema, scaling and hyperkeratosis of sebaceous follicles.^10-11

An excess of dietary omega 6 fatty acids (particularly arachidonic acid) saturates the two glycerol fatty acid positions on membrane phospholipids and may result in excess production of pro-inflammatory eicosanoids. Omega 3 fatty acids can compete for the same enzyme systems necessary for arachidonic acid to convert to pro-inflammatory eicosanoids because of the similarity of 20 carbon omega 6 fatty acids to 20 carbon omega 3 fatty acids. Therefore, if the diet enriches membrane phospholipids with omega 3 fatty acids, a larger fraction of the pool of enzymes will be used to produce antiinflammatory omega 3 eicosanoids.¹² (Fig. 16)

Specifically, if the cyclooxygenase and lipoxygenase enzymes are used to form the prostaglandin 2 series, the leukot-riene 4 series, lipoxins and other reactive hydroxyacids such as 5-HETE (hydroxyeicosatetranoids) and 12-HETE that are the normal progeny of the arachidonic acid cascade, instead of the prostaglandin 3 series and leukotriene 5 series which are the normal progeny of the omega 3 fatty acid cascade, inflammatory disease can result. (Fig. 18)

Additionally, dihomogammalinolenic acid consumed directly or derived in vivo from linoleic acid has the capability of forming prostaglandin 1 series, which are antiinflamma-tory, as well as 15-hydroxy DHGLA which has the ability to inhibit lipoxygenase production of inflammatory eicosanoids.¹³

Various drugs can exert antiinflammatoiy effects through their action on these metabolic pathways. For example, cor-ticosteroids can inhibit the release of fatty acids from phospholipids through the action of lipocortin which interferes with the phospholipases. Thus if arachidonic acid is not released from lipid membranes, it does not have the opportunity to cascade into the inflammatory eicosanoids. Indomethacin and aspirin have the ability to interfere with the action of cyclooxy-genase and this then can inhibit the production of the inflammatory 2 series prostanoids. Benoxaprofen (and the nutrient zinc) have the ability to inhibit the action of lipoxygenase which produces the 4 series inflammatory leukotrienes.¹⁴ (Fig. 19)

An interesting nutrient interaction is the ability of the anti-oxidant glutathione system to convert hydroperoxy eicosatetra-noic acids to the less inflammatory hydroxy eicosatetranoic acids. There are certain amino acids associated with glutathione, namely glycine, cysteine and glutamic acid, as well as the trace mineral selenium, and thus deficiencies in these elements could conceivably result in a proinfiammatory condition.¹⁵

CELL SIGNALS
It is postulated that dietary fats may effect signals which cause cells to perform particular functions such as division or secretion. These signals, aside from possibly resulting from phospholipid turnover, can also result from mediators such as acetylcholine, adrenalin, histamine, dopomine and serotonin.

It is believed that when cells receive signals they release components of their phospholipids which in turn affect ki-nases, calmodulin, (which affects calcium levels) and cyclic nucleotides such as AMP and GMP.¹⁶

This is an incredibly complex subject even at the rather rudimentary level of understanding that exists now. The end result, however, is that increased arachidonic acid or excess omega 6 arachidonate precursors in the diet create phospholipids which send signals to tissue encouraging inflammatory response.

It is unlikely that any one of the above explanations is the sole answer to how inflammation in the skin or other tissues proceeds. Elements from several mechanisms likely contribute. But it is highly interesting and therapeutically important that in each case dietary modification provides a rational basis for altering the inflammatory response.

It is thus possible through converting the diet to its more natural, whole, raw form, or (as a second choice) by supplementing specifically with unaltered, stabilized omega 3, omega 9, and certain omega 6 fatty acids, that the inflammatory response can be modified. The effects of so doing have been proven clinically and provide an exciting alternative to the use of pharmacologic agents which do not address the underlying problem and carry with them potential toxic effects.

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