ietary cholesterol is believed by a great many people to cause cardiovascular disease. This is a belief is based on faith, rather like one might believe in the tooth fairy or flying spaghetti monster. Although such people like to think their views are rational and based on observation, there is little scientific evidence to support their fantasy. For example, no study has convincingly demonstrated that feeding cholesterol to humans raises plasma cholesterol levels. In addition, although there is an association between plasma levels of low density lipoprotein (LDL) and the risk of cardiovascular disease, the elevated levels of LDL are not the cause of the disease. Instead, the elevated LDL is caused by another factor, that is also the cause of cardiovascular disease. This other factor is likely the metabolic changes associated with insulin resistance, one symptom of which is the accumulation of abdominal body fat.
To demonstrate this, researchers1 have investigated the association between lipoprotein abnormalities and fat distribution in 361 children and adolescent subjects. The fat distribution of the subjects was measured and the lipoprotein levels determined following a blood test. Fat distribution included assessments of the waist circumference with subscapular, subcostal and suprailiac skin fold thicknesses (truncal measurements) and femoral, tricep, calf and bicep skin folds measurements (peripheral measurements). When the authors analysed the data they fond that subjects with more truncal fat but less peripheral fat had higher concentrations of both LDL and very low density lipoprotein (VLDL), when compared to those subjects with more peripheral fat and less truncal fat. High levels of truncal fat were also associated with decreased concentrations of high density lipoprotein (HDL) and apolipoprotein A-1. These results therefore suggest that accumulation of truncal fat is associated with a detrimental lipoprotein profile.
Recent evidence suggests that such detrimental lipoprotein changes are caused by insulin resistance. Insulin resistance diverts energy from oxidation in skeletal muscle to storage in visceral adipose tissue through interference with the leptin system. Development of insulin resistance therefore leads to the accumulation of truncal fat and eventually abdominal obesity. The lipoprotein changes associated with cardiovascular disease likely result from the metabolic dysfunction associated with these changes, a condition that has been termed the metabolic syndrome. The understanding of this biochemistry has moved on considerably since the cholesterol theory of cardiovascular disease was conceptualised in the 1950’s. In reality, the cholesterol theory of cardiovascular disease is based on pseudoscience and was never any better than a fairy tale. That people still believe in the magic cholesterol fairy are testament to the power of the cholesterol lobby and its paid agents that have infiltrated the health services to peddle their propaganda.
RdB
