There are two essential fatty acids in human nutrition and both are polyunsaturated fats formed in plants. Alpha linolenic (ALA, C18:3 (n-3)) is fatty acid belonging to the omega 3 family of fatty acid and linoleic acid (LA, C18:2 (n-6)) is a fatty acid belonging to the omega 6 family of fatty acids. The essential fatty acids are essential because they cannot be synthesised in the body, but are required for health in human nutrition. When ingested, ALA, and LA are absorbed and metabolised to a number of longer chain and more unsaturated fatty acids. Three of these fatty acids are then converted to a group of short-lived hormone-like chemicals called eicosanoids. Alpha linolenic acid is converted to eicosapentaenoic acid (EPA, C20:5 (n-3)), and this forms the series 3 eicosanoids and series 5 leukotrienes. Linoleic acid is converted firstly to gamma linolenic acid (GLA, C18:3 (n-6)) and thus to the series 1 eicosanoids, and also further to arachidonic acid (AA, C20:4 (n-6)) and thus to the series 2 eicosanoids and series 4 leukotrienes.
The series 1 eicosanoids derived from GLA are highly anti-inflammatory and they are responsible for moderating down the inflammatory response in cells. In contrast, the series 2 eicosanoids and series 4 leukotrienes derived from AA are highly pro-inflammatory. The series 3 eicosanoids derived from ALA are mildly anti-inflammatory. The balance between the dietary levels of these fatty acids can therefore determine the degree of cellular inflammation experienced by an individual. When the intake between the omega 6 and omega 3 fatty acids are in the correct ratio, synthesis of pro- and anti-inflammatory eicosanoids and leukotrienes are balanced such that inflammation is modulated correctly. However, too many omega 6 fatty acids and too few omega 3 fatty acids and, or vice versa, and the balance of eicosanoid production becomes disturbed and this leads to the formation of too many pro-inflammatory series 2 eicosanoids and series 4 leukotrienes, which leads to systemic inflammation and disease.
Arachidonic acid can be ingested directly from most foods of animal origin. Dietary AA accumulates in the membranes of cells and increases the production of the pro-inflammatory series 2 eicosanoids and series 4 leukotrienes. An imbalance of LA to ALA in combination with a high animal fat diet can therefore significantly increases inflammation. An essential fatty acid imbalance or too much AA is detrimental to insulin resistance because inflammation is a cause of oxidative stress. Oxidative stress in turn has been shown to detrimentally affect the function of the insulin receptor, although the exact mechanisms is not fully understood. Ironically high insulin levels caused by insulin resistance also interfere with the metabolism of essential fatty acids, contributing to inflammation and worsening the already dysfunctional insulin system. Ensuring the correct balance of essential fats, moderating animal food intakes and keeping insulin under control are therefore pivotal to maintaining insulin sensitivity.
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