Glutathione Facts

Lipids in Inflammation

Inflammation is a broad term describing the body's reaction to injury. Is a necessary process that allows defense against toxins and pathogens, protection against further damage and tissue repair. However, if the inflammatory process over product beyond what is necessary to heal, can become a disease in itself. Runaway inflammation underlying allergic reactions and other self-destructive diseases, such as arthritis, atherogenesis cycle, and some skin disorders.

The use of essential fatty acids in the diet has long been known to exert a beneficial effect on healthy skin and hair. inflammatory skin diseases has been shown to respond to essential fatty acids fed by mouth and even apply topically.1-3 Children suffering from atopic eczema has been shown to have low blood levels of essential fatty acid metabolites. With the use of acids essential fatty acids raise blood levels and skin problems decrease.4 Eskimos eat the traditional high-fat fish oil diet has very little psoriasis. But when they take Western diet, the incidence of this disease largely increases.5 acne vulgaris has also been shown to respond to the administration of fatty acids essential. In some cases, even where there was resistance to treatment with antibiotics, 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 transition zone between active living cells in the skin and outer epidermal layers that eventually separate (exfoliate) and are lost as part of normal growth skin, is a water barrier. This lipid layer (stratum lucidum) is among the granule cells (stratum granulosum) and the horny cells (stratum corneum) of the skin. If this layer of lipids is not well formed, the skin undergoes a change in the transdermal permeability. Water is lost resulting in dry, peeling skin, moisturizer, and a mat of hair, and increased water intake, although the volume of urine is not increased proportionately. This lipid layer is formed from a class of compounds called sphingolipids including acylglucosylceramides containing linolenic acid, a vital component. If linoleic acid is deficient in diet, lipid granule produced by the granule cells (Odland bodies) has replaced other fatty acids such as oleate. This results in a configuration different stereochemistry resulting in leakage of excess water from the skin.7-9 (Fig. 17)

Eicosanoids METABOLISM
Within the skin, arachidonic acid can be a part of the phospholipids that make up the membranes of tissue (especially the meat in the diet high). Arachidonic acid is released from phospholipids by ester phospholipase enzymes break and C, is initiated by various stimuli such as collagen, thrombin, bradykinin, serotonin and adrenaline. Once released acid arachidonic breaks down (falls) in the various eicosa-noids. These autocoids peroxide are powerful inflammatory agents on the skin. They can cause dilation of blood vessels, release chemotactic factors, lead to extravasation of white blood cells and skin cause itching, redness, enlargement and hyperkeratosis of sebaceous follicles.10-11

Excess dietary omega 6 fatty acids (especially arachidonic acid) the two positions saturated fatty acids glycerol in membrane phospholipids and may result in excessive production of proinflammatory eicosanoids. Omega 3 fatty acids may compete for the enzyme systems the same necessary for arachidonic acid to convert the pro-inflammatory eicosanoids due to the similarity of carbon omega-6 fatty acids 20 to 20 carbon omega 3 fatty acids. Therefore, if the diet enriched membrane phospholipids with omega-3 fatty acids, a larger fraction of the group of enzymes are used to omega-3 fatty acids produce anti-inflammatory eicosanoids.12 (Fig. 16)

[The water of the skin barrier image]
http://www.wysong.net/articles/lipid/figures/figure17.jpg

In particular, if the cyclooxygenase and lipoxygenase enzymes are used to form the prostaglandin 2 series, the laugh leukot-4 series, lipoxins and hydroxy reactive as 5-HETE (hydroxyeicosatetranoids) and 12-HETE, which are the normal offspring of arachidonic acid cascade, rather than the 3 series prostaglandins and leukotrienes are 5 series normal progeny of omega 3 fatty acid cascade, inflammatory disease can result. (Fig. 18)

Image Enyeme Competition
http://www.wysong.net/articles/lipid/figures/figure18.jpg

In addition, dihomogammalinolenic acid consumed directly or derived in vivo from linoleic acid has the ability to form a series of prostaglandins, that are inflammatory, thorium and 15-hydroxy DHGLA that has the ability to inhibit the production of inflammatory lipoxygenase eicosanoids.13

Various drugs antiinflammatoiy can exert effects through its action on these pathways. For example, cor-steroids can inhibit the release of fatty acids phospholipids through the action of lipocortins that interferes with phospholipase. So if arachidonic acid is not released from the membrane lipids, not have the opportunity to cascade into inflammatory eicosanoids. Indomethacin and aspirin have the potential to interfere with the action of cyclooxygenase COX-and this then can inhibit the production of inflammatory prostanoids two series. Benoxaprofen (zinc and nutrients) have the ability to inhibit the action of lipoxygenase to produce leukotrienes.14 inflammatory Series 4 (Fig. 19)

An interesting interaction of nutrients is the ability of Glutathione Antioxidant system to convert fatty eicosatetra hydroperoxy-the less inflammatory NOIC eicosatetranoic hydroxy acids. There are certain amino acids associated with glutathione, namely, glycine, glutamic acid and cysteine, and the trace mineral selenium, and so deficiencies in these elements could result in a condition.15 proinfiammatory

CELL SIGNALS
It is postulated that dietary fats can affect the signals that cause cells to perform particular functions such as division or secretion. These signals, in addition, possibly due to turnover of phospholipids, can also result from mediators such as acetylcholine, adrenaline, histamine, dopomine serotonin.

It is believed that when cells receive signals from the release of phospholipid components which in turn affect ki-nases, calmodulin, (Which affects calcium levels) and cyclic nucleotide such as AMP and GMP.16

This is a very complex subject, even in the most rudimentary level of understanding now exists. The end result, however, is that the increase of arachidonic acid or excess of omega 6 arachidonic acid precursors in the diet to create phospholipids that send signals to promote tissue inflammatory response.

It is unlikely that any of the above explanations is the only answer to how inflammation in the skin or other tissue product. Elements of several mechanisms likely contribute. But it is very interesting and important therapeutically in each case diet modification provides a rational basis for altering the inflammatory response.

It is thus possible by converting the diet to its most natural, whole, raw or (as a second option), specifically supplementing it unchanged, stabilized omega 3, omega 9 and omega 6 fatty acids certain that the inflammatory response may be modified. The effects of this have been tested clinically and provide an exciting alternative to the use of pharmacological agents that do not treat the underlying problem and carry with them the possible toxic effects.

References available in textbooks, click the link below to view this article in 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.

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