Metabolic syndrome is the name given to a group of metabolic disorders that can severely affect the cardiovascular system through excessive production of free radicals generated via systemic inflammation. Abdominal fat accumulates in metabolic syndrome because of nutrient overload within the liver. This increases rates of de novo lipogenesis and ultimately results in lipid deposits in the liver and surrounding viscera that cause the development of insulin resistance. It is the accumulation of abdominal fat stores that causes the generation of free radical damage to tissues, including those in the cardiovascular system. In contrast, subcutaneous fat does not increase the risk of cardiovascular disease, because subcutaneous fat does not cause systemic inflammation or generate of free radical damage. Because subcutaneous and abdominal fat stores are formed through different mechanisms and have different functions, patterns of fat loss can differ.
Measuring the patterns of fat loss in obese individuals undergoing forced calorie restriction shows that an energy deficit causes abdominal fat stores to be used as an energy source, while subcutaneous fat stores are relatively unaffected. For example, one study published in the American Journal of Clinical Nutrition1 assessed the upper and lower fat loss from 68 obese women who lost an average of 12.3 kg from a starting weight of 103.6 kg. That weight loss was accompanied by a reduction in abdominal obesity was demonstrated by a significant reduction in the waist to hip ratio of the subjects. Those with the greatest abdominal obesity had the greatest reduction in the waist to hip ratio, supporting the view that abdominal fat is a labile store of fat that is readily depleted if calorie intake is significantly diminished, accounting for early weight loss on a forced calorie restricted diet.
However, once the abdominal energy reserves are depleted, further fat loss is not evident because subcutaneous stores are not so labile. In fact, subcutaneous fat is highly stubborn in its desire to be mobilised for energy, and as a result resting metabolic rate and energy expenditure fall once abdominal stores are depleted, and appetite increases to replenish lost energy. This accounts for the high failure rate of forced calorie restrictive diets. The whole premise of forced calorie restriction being a successful solution to obesity rests on the assumption that the individual is in control of energy intake and expenditure. However, this is not the case because it is the hypothalamus that dictates the resting metabolic rate (RMR), the thermic effect of food (TEF), the amount of energy available for physical activity and the appetite level of the individual. As soon as energy intake falls, the hypothalamus compensates with behavioural changes.
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