Recent evidence suggests that obesity is associated with low level chronic inflammation. This may deplete antioxidant defences through the generation of systemic oxidative stress, and result in the formation of diseases such as diabetes, cardiovascular disease and cancer. An inverse association between plasma vitamin C and body mass index has been reported in the literature, supporting the contention that systemic oxidation associated with obesity is able to deplete cellular antioxidant defences. The acceptance that a low level chronic inflammatory milieu could be the cause of disease has been slow to gain acceptance in the scientific community, possibly because of the difficulty in detecting the condition, something that has resulted in the condition being labelled ‘silent inflammation’. Classic inflammatory markers such as C-reactive protein (CRP) are often not helpful in this regard because they can be influenced by infection and their specificity has been questioned.
In this regard the nutritional literature has lead the way by suggesting that a more suitable method for quantification of systemic inflammation is the ratio of precursor essential fatty acids required to form cellular pro- and anti-inflammatory eicosanoids. A number of papers have reported on the ratio of omega 3 to omega 6 fatty acids in the diet and other research has measured the arachidonic acid (AA, C20:4 (n-6)) levels in plasma phospholipid membranes of various populations. Because AA leads to the formation of pro-inflammatory eicosanoids that can increase systemic inflammation, and omega 3 fatty acid such as eicosapentanoic acid (EPA, C20:5 (n-3)) can inhibit this metabolic pathway at the delta 5-desturase enzyme step as well as form the anti-inflammatory resolvins, the ratio of AA to EPA can be used as a marker of systemic inflammation and give some indication as the risk of developing serious disease.
The ratio of omega 6 to omega 3 fatty acids in the Western diet has been steadily increasing in recent decades due to high consumption of vegetable oils rich in linoleic acid (LA, C18:2 (n-6)). It is now considered by nutritionists that the omega 6 intake of most Western nations is too high and that at the same time the intake of omega 3 fatty acids is too low. This has contributed to an internal environment where systemic inflammation can dominate with the consequence that chronic Western style diseases have increased. In addition to these dietary changes, total carbohydrate intake has increased, particularly consumption of sugars and high glycaemic index refined carbohydrate foods which can raise insulin levels by increasing the glycaemic load an individual is subjected to. Insulin is able to activate both delta 5-desaturase and delta 6-desaturase, which increases the conversion of the essential fatty acid LA to AA.
The imbalance in the fatty acid ratio and the excess insulin levels is detrimental to fat cells because both of these factors can work together to influence metabolic disruption. Excess AA causes the fats cells response to insulin signalling to become abnormal, and this compromises the glucose flow into the cell with a subsequent deficiency of glycerol availability for fatty acid synthesis. At the same time high insulin levels inhibit lipoprotein lipase. As a result of this the fat cell is unable to correctly sequester fatty acids. The AA can build up in the cell and causes apoptosis, which attract macrophages, and causes the secretion of additional inflammatory mediators such as interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF-α). The inflammatory markers cause further insulin signal disruption and AA levels are further increased, eventually spilling into the circulation to produce insulin resistance in other tissues.
RdB
