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Diabetes and chronic dry skin, unfortunately, seem to go hand-in-hand. In fact, it is estimated that 83% of all diabetics suffer from dry skin, particularly in the lower extremities. Why is this?

According to well-documented clinical research, diabetics may suffer from an impaired ability to manufacture gamma-linolenic acid (GLA), an OMEGA-6 fatty acid crucial in the development of healthy skin cells.1 Used for a number of key functions throughout the body, GLA is a building block in the formation of cell membranes. Without it, skin cell membranes are unable to retain adequate moisture levels, resulting in dry skin. Hence, the link between diabetics (many of whom suffer from GLA deficiency) and dry skin.

Gamma-linolenic acid is a "good" OMEGA-6 fat that the human body is fully capable of producing for itself, under normal circumstances. The creation of GLA within the body begins with linoleic acid (LA), an essential fatty acid that we ingest in our daily diets. Generally, the body has a plentiful supply of linoleic acid since it is commonly found in almost all edible vegetable oils. Once inside the body, linoleic acid is acted upon by a key enzyme called delta-6-desaturase (D6D), which biochemically converts LA into GLA.

Without D6D, the body would not be able to manufacture GLA, regardless of how much linoleic acid was present. From that point, GLA is further converted, via a sequence of biochemical steps, into an extremely important compound called prostaglandin E1 (PGE1). This molecule acts as a potent anti-inflammatory on the skin, is key in regulating water loss, and protects skin cells from injury and damage.2

The D6D enzyme, which catalyzes the conversion of LA into GLA, is often referred to as a "lazy" enzyme. That is to say, it can be slow in doing its job, and under some conditions may actually be impaired. According to research, individuals with type 1 and 2 diabetes show increased levels of linoleic acid with simultaneous decreased levels of gamma-linolenic acid.3 The evidence also strongly suggests a reduction in the activity of the D6D enzyme, without which the chain reaction of GLA and PGE1 manufacture is impossible. The resulting decrease in the synthesis of PGE1 may be responsible for the characteristic dry skin and transepidermal water loss which is routinely observed.
 

This diagram illustrates the biochemical pathway undertaken by GLA

Click on the image to enlarge the diagram


Although the body is unable to manufacture GLA without D6D, there are other ways of providing the body with the steady supply of GLA that it needs - oral supplements and topical application being the two main ones. Studies have shown that topically applied GLA has a positive impact on chronic dry skin and other skin conditions. Topical application of GLA circumvents the issue of impaired, or altogether absent D6D levels, by introducing the OMEGA-6 fatty acid directly into the body, where it undergoes its normal conversion into PGE1. From that point forward, PGE1 assumes its role in anti-inflammatory and water-retention functions

Borage oil is the richest known source of GLA (24%). This oil is extracted from the seeds of the borage plant (borago officanalis), a wildflower commonly known as the blue starflower and used for thousands of years for its medicinal qualities. Because of its exceptional concentration of GLA, borage oil is used as the fundamental ingredient in all DiabetiCare™ formulations.

References
1Horrobin, DF. 1997. "Essential Fatty Acids in the Management of Impaired Nerve Function in Diabetes". . Diabetes. 46(2S):S90.
2Ziboh, V and Miller, C. 1990. "Essential fatty acids and polyunsaturated fatty acids: Significance in . Cutaneous Biology". Annu. Rev. Nutr. 10:433.
3Horrobin, DF, 2001. "Gamma-linolenic acid in Diabetics". Gamma-linolenic Acid - Recent Advances in Biotechnology and Clinical Applications.
 

 

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