Metabolic syndrome

Several lines of evidence indicate lifestyle-induced hyperinsulinemia and reduced insulin function (i.e. insulin resistance) as a decisive factor in many disease states. For example, hyperinsulinemia and insulin resistance are strongly linked to chronic inflammation, which in turn is strongly linked to a variety of adverse developments such as arterial microinjuries and clot formation (i.e. heart disease) and exaggerated cell division (i.e. cancer). Hyperinsulinemia and insulin resistance (the so-called metabolic syndrome) are characterized by a combination of abdominal obesity, elevated blood sugar, elevated blood pressure, elevated blood triglycerides, and reduced HDL cholesterol. The negative impact of hyperinsulinemia on prostaglandin PGE1/PGE2 balance may be significant.
The state of obesity clearly contributes to insulin resistance, which in turn can cause type 2 diabetes. Virtually all obese and most type 2 diabetic individuals have marked insulin resistance. Although the association between overweight and insulin resistance is clear, the exact (likely multifarious) causes of insulin resistance remain less clear. Importantly, it has been demonstrated that appropriate exercise, more regular food intake and reducing glycemic load (see below) all can reverse insulin resistance in overweight individuals (and thereby lower blood sugar levels in those who have type 2 diabetes).
Obesity can unfavourably alter hormonal and metabolic status via resistance to the hormone leptin, and a vicious cycle may occur in which insulin/leptin resistance and obesity aggravate one another. The vicious cycle is putatively fuelled by continuously high insulin/leptin stimulation and fat storage, as a result of high intake of strongly insulin/leptin stimulating foods and energy. Both insulin and leptin normally function as satiety signals to the hypothalamus in the brain; however, insulin/leptin resistance may reduce this signal and therefore allow continued overfeeding despite large body fat stores. In addition, reduced leptin signalling to the brain may reduce leptin's normal effect to maintain an appropriately high metabolic rate.
There is a debate about how and to what extent different dietary factors— such as intake of processed carbohydrates, total protein, fat, and carbohydrate intake, intake of saturated and trans fatty acids, and low intake of vitamins/minerals—contribute to the development of insulin and leptin resistance. In any case, analogous to the way modern man-made pollution may potentially overwhelm the environment's ability to maintain homeostasis, the recent explosive introduction of high glycemic index and processed foods into the human diet may potentially overwhelm the body's ability to maintain homeostasis and health (as evidenced by the metabolic syndrome epidem