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Exclusive Online Expanded Version—The Essential in Fats: A Global Perspective for Healthy Skin Cells

By: Alexandra J. Zani
Posted: March 5, 2014, from the March 2014 issue of Skin Inc. magazine.

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Diet and lifestyle influence numerous inflammatory responses within the body, including increased C-reactive proteins (CRP). In particular, risk factors for inflammation that include metabolic syndrome escalate with lifestyle factors, especially during weight gain that intensifies the amount of adipocytes in the body. CRPs are biomarkers of amplified inflammation and appear to increase with the presence of these risk factors.7

EFAs play a dynamic regulatory role during inflammatory and wound-healing responses. N-3 eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are precursors to inflammation-regulating messenger chemicals called eicosanoids (prostaglandins) derived from a collection of elongated essential fatty acids.5 Moreover, the body’s immune system can actually manufacture inflammation-reducing compounds called resolvins from the n-3 EPA and DHA, and NPD1—a neuroprotectin—from DHA.8, 9 Exciting research continues to investigate the roles of resolvin in managing inflammation and pain in diseases such as arthritis.

The dermis provides physical and nutritional support to the epidermis. Moreover, EFAs in the dermis mediate the reduction and production of cytokine messenger chemicals that cause excessive inflammation (an immune response) and inhibit the activation of white blood cells. n-3 also protects dermal collagen from becoming damaged from UV-induced photoaging. For example, n-3 helps diminish photoaging through a process known as signal transduction cascades—cell-to-cell communication—that mitigates damage to collagen. Notably, excessive sunlight interferes with and destroys the enzymatic mechanisms that convert long-chain highly unsaturated n-3 and n-6 into their metabolites that present structural and protective resources for the skin. The signs of oxidative stress appear as sunspots, skin anomalies and skin cancer.10

Unraveling EFAs

The years of 1929–30 proved to be exciting times with the discovery of essential fatty acids. It was during a time when the role of fats was looked upon as a calorie source interchangeable with carbohydrates without the realization that they play an innate role throughout the entire body. Compelling studies performed by George and Mildred Burr determined that specific nutrients they named EFAs were compulsory dietary components fundamental for balanced reproduction, growth and healthy skin function. Furthermore, their research confirmed that the absence of dietary unsaturated fatty acids created a deficiency syndrome leading to death. Moreover, the Burrs’ identification of linoleic acid as an essential fatty acid showed that it played a significant role and function within all cell membranes. Their research became a catalyst for many other scientists and nutritionists both in Europe and North America to explore the attributes and health benefits of these distinctive fatty acid molecules. As the years passed into the 1990s and into the 21st century, more precise instrumentation allowed researchers to realize the importance of the interrelationship between both n-3 and n-6 families of EFAs, especially with relevance to the architecture of the skin barrier.

EFA deficiency

Ralph T. Holman, PhD (1917—2012), a graduate student and later research associate of George and Mildred Burr, who discovered that fatty acids were critical to health, at the University of Minnesota, devoted his career researching the molecular structures of essential fatty acids. Furthermore, he established the terminology for EFAs and their metabolites. Holman’s life’s work embraced the behavior of EFAs and the significance of the conversion process for each omega family into their metabolites. He continued to prove that there were serious physiological and biochemical consequences when unsaturated fatty acids were withheld from the diet. Moreover, the importance of the competition between n-3s and n-6s for the same desaturation enzymes became the incentive for realizing that any defects lead to marked skin abnormalities, such as atopic dermatitis, and dry and inflamed skin.11