The metabolic syndrome is a cluster of metabolic disorders characterised by insulin resistance. It is becoming increasingly evident that the Western diet is the cause of metabolic syndrome, and this results largely from the poor quality food that it contains. The Western diet is problematic from a health perspective because it is devoid of meaningful levels of micronutrients, essential fatty acids, fibre and phytochemicals, all of which are required by humans for correct metabolic function. In addition, the Western diet contains a number of metabolic poisons including trans fats, oxidised fats and fructose, all of which can detrimentally interfere with normal metabolic regulation. The lack of fibre and high quality protein in the Western diet is thought to lead to rapid increases in the absorption rates of the energy within the food. This rapid influx of energy overloads the liver with nutrients, and this increases flux through the de novo lipogenesis pathway, creating large quantities of endogenously synthesised fatty acids.
The de novo lipogenesis pathway is interesting because it is a mechanisms by which the carbohydrate in the diet can be converted without limit to fatty acids (literally: new lipid synthesis). Under normal dietary conditions, a person eating high quality foods would experience only relatively small flux through the de novo lipogenesis pathway postprandially. This is because the less energy dense foods associated with high quality diets, often with a high water and fibre content, would only be absorbed slowly from the gut, thus presenting the liver with suitable time to process and metabolise the lower energy content through alternative routes such as glycogen resynthesis and respiration. However, the rampant synthesis of new fats through the de novo lipogenesis pathway seen postprandially with the Western diet is far more problematic because such fats can accumulate in tissues where they may interfere with the insulin signal cascade, leading to the formation of insulin resistance.
Another problem with the Western diet is that it lacks a balanced ratio of essential fatty acids. The essential fatty acids alpha linolenic acid (ALA, C18:3 (n-3)) and linoleic acid (C18:2 (n-6)), are converted through a series of elongation and desaturation reactions to form a number of short live eicosanoid hormones that regulate cell function. Correct eicosanoid formation occurs only with a balanced ratio of ALA to LA in the diet, and in this regard the ratio should around 1 to 3 (ALA to LA). The Western diet generally contains far too much LA far too little ALA, and as a result the actual ratio present in the diet may be as low as 1 to 10 or 1 to 20. The imbalance to the dietary intake of essential fatty acids is now thought to lead to a transition to a proinflammatory state, and an induction of systemic oxidative stress associated with this inflammation. Another major metabolic effect of an imbalance to the essential fat intake associated with the Western diet is a desensitising of the insulin receptor and a slow decline to insulin resistance.
The Western diet therefore can cause insulin resistance because it induces the de novo lipogenesis pathway and because it is devoid of the correct ratio of essential fatty acids. Individuals at an increased risk of insulin resistance and its associated deterioration of glycaemic control would therefore be expected to have fatty acid compositions in their cell membranes that reflected their dietary faux pas. In particular, flux through the de novo lipogenesis pathway increases production of the fatty acid palmitoleic acid (C16:1 (n-7)) and this can then accumulate in cells membranes. In addition, the essential fatty acids LA can accumulate in cell membranes and high intakes are reflected in high concentrations of the parent compound, but low concentrations of its metabolites, production of the latter being inhibited by decreased activity of the relevant delta-6 desaturase enzyme under conditions of essential fatty acid imbalance. The ratio of LA to its metabolites in cell membranes can therefore reflect dietary intake.
As erythrocyte cell membranes lack the ability to undergo de novo lipogenesis or the delta-6 desaturase enzyme for LA metabolism, they can be used to assess the long-term dietary intakes of essential fats and the flux through the de novo lipogenesis pathways. Because such dietary factors might be associated with long-term glycaemic control, researchers have used the fatty acid composition of erythrocytes to assess the relationship. For example, in one study1 researchers investigated if they could use the fatty acid profiles of healthy men to predict the level of glycaemic control over time. Subjects had the fatty acid composition of their erythrocyte cell membranes assessed and were then subjected to a series of oral glucose tolerance tests to assess their glycaemic control over 5 years. The results of the study showed that the ration of LA to its metabolite dihomo-gamma linolenic acid (DGLA, C20:3 (n-6)) and the total concentration of palmitoleic acid were able to predict the worsening of glycaemic control in the men.
Dr Robert Barrington’s Nutritional Recommendation: The risk of developing of insulin resistance is greatly increased if a Western diet is consumed. In turn insulin resistance is a driver of central adiposity and weight gain. Markers of endogenous fat production and essential fatty acid imbalance to the diet show a good correlation with worsening glycaemic control, suggesting that both mechanisms are heavily implicated in the development of insulin resistance. Insulin resistance is easily reversed by following traditional eating practices, which means consuming high quality foods while avoiding those foods associated with Western living.
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