Inflammation is a broad termdescribing the body's reaction to injury. It is a necessary process enablingdefense against toxins and pathogens, protection against further damage, andrepair of tissue. However, if the inflammatory process proceeds beyond thatwhich is necessary to heal, it can become a disease in itself. Runawayinflammation underlies allergic reactions and certain other self-destructivediseases such as arthritis, the cycle of atherogenesis, and some dermatologicdisorders.

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

There are several proposedmechanisms by which essential fatty acids can affect inflammatory skindiseases.

SKIN BARRIER FUNCTION

In the transitional area betweenlive active cells in the skin and the outer epidermal layers that eventuallydetach (desquamate) and are lost as a part of normal skin growth, there is awater barrier. This lipid layer, (stratum lucidum) lies between the granularcells (stratum granulosum) and the horny cells (stratum corneum) of the skin.If this lipid layer is not properly formed, the skin experiences a change intransdermal permeability. Water is thus lost resulting in dry, scaling skin, amoistening and matting of hair, and increased water intake even though urinevolume is not proportionally increased. This lipid layer is formed from a classof compounds called sphingolipids including acylglucosylceramides which containlinoleic acid as a vital constituent. If linoleic acid is deficient in thediet, the lipid granule produced by the granular cells (Odland bodies) hasother fatty acids substituted such as oleate. This results in a differentstereochemical configuration resulting in excess water leakage from theskin.7-9 (Fig. 17)

EICOSANOID METABOLISM

Within the skin, arachidonic acidcan be a part of the phospholipids which make up tissue membranes (especiallyin high meat diets). Arachidonic acid is released from phospholipids by theester breaking enzymes phospholipase \ and C. This is initiated by variousstimuli such as collagen, thrombin, bradykinin, serotonin, and adrenalin. Oncereleased the arachidonic acid breaks down (cascades) into the variouseicosa-noids. These oxygenated autocoids are powerful inflammatory agentswithin the skin. They can cause vessel dilation, release chemotactic factors,result in extravasation of white blood cells, and dermatologically producepruritis, erythema, scaling and hyperkeratosis of sebaceous follicles.10-11

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

[ The Skin Water Barrier Image ]

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

Enyeme Competition Image

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Additionally, dihomogammalinolenicacid consumed directly or derived in vivo from linoleic acid has the capabilityof forming prostaglandin 1 series, which are antiinflamma-tory, as well as15-hydroxy DHGLA which has the ability to inhibit lipoxygenase production ofinflammatory eicosanoids.13

Various drugs can exertantiinflammatoiy effects through their action on these metabolic pathways. Forexample, cor-ticosteroids can inhibit the release of fatty acids fromphospholipids through the action of lipocortin which interferes with thephospholipases. 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 ofcyclooxy-genase and this then can inhibit the production of the inflammatory 2series prostanoids. Benoxaprofen (and the nutrient zinc) have the ability toinhibit the action of lipoxygenase which produces the 4 series inflammatoryleukotrienes.14 (Fig. 19)

An interesting nutrientinteraction is the ability of the anti-oxidant glutathione system to converthydroperoxy eicosatetra-noic acids to the less inflammatory hydroxyeicosatetranoic acids. There are certain amino acids associated withglutathione, namely glycine, cysteine and glutamic acid, as well as the tracemineral selenium, and thus deficiencies in these elements could conceivablyresult in a proinfiammatory condition.15

CELL SIGNALS

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

It is believed that when cellsreceive signals they release components of their phospholipids which in turnaffect ki-nases, calmodulin, (which affects calcium levels) and cyclicnucleotides such as AMP and GMP.16

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

It is unlikely that any one of theabove explanations is the sole answer to how inflammation in the skin or othertissues proceeds. Elements from several mechanisms likely contribute. But It Ishighly interesting and therapeutically Important that in each case dietarymodification provides a rational basis for altering the inflammatory response.

It is thus possible throughconverting the diet to its more natural, whole, raw form, or (as a secondchoice) by supplementing specifically with unaltered, stabilized omega 3, omega9, and certain omega 6 fatty acids, that the inflammatory response can bemodified. The effects of so doing have been proven clinically and provide anexciting alternative to the use of pharmacologic agents which do not addressthe underlying problem and carry with them potential toxic effects.

References available within booktext, click the following link to view this article on wysong.net:

http://www.wysong.net/articles/lipid/06_article_lipid_chapter_six_nflammation.shtml

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About the Author Dr. Wysong: A former veterinary clinician and surgeon, college instructor in human anatomy, physiology and the origin of life, inventor of numerous medical, surgical, nutritional, athletic and fitness products and devices, research director for the present company by his name and founder of the philanthropic Wysong Institute. http://www.wysong.net. Also check out http://www.cerealwysong.com.