The major change in the United States and European diets associated with the increased rates of obesity was an increased consumption of refined carbohydrates. A feature of refined carbohydrates is their predisposition to cause increased fluctuations in plasma insulin and glucose levels and postprandial reactive hypoglycaemia. As the central nervous system is dependent on a stable supply of glucose this threatens the central nervous system functioning and these fluctuations also have a negative impact on the cardiovascular system. Phenotypic plasticity enables organisms to use adaptive phenotypes already in existence such as the increased insulin resistance and increased adiposity associated with pregnancy or the insulin resistance associated with infection, trauma and burns or to evolve new phenotypes to adapt to variations in the environment. This paper explores the evidence that increased insulin resistance that is commonly associated with increased adiposity possibly because of shared locations on the genome is a phenotypic plastic adaptation to the increased consumption of refined carbohydrates and their predisposition to cause increased fluctuations in plasma insulin and plasma glucose and post-prandial reactive hypoglycaemia both of which have negative impacts on the metabolism. Obesity, that is a relatively stable state of increased adiposity and insulin resistance has adaptive and defensive features to these fluctuations in plasma insulin and glucose in that metabolic disorders associated with refined carbohydrate consumption are often mitigated and modified as exemplified by the obesity paradox.
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