Proponents of the cholesterol theory of cardiovascular disease believe that dietary cholesterol is the cause of atherosclerosis. Despite a large volume of evidence that contradicts this theory it is still popular amongst mainstream medicine. The most recent research in the nutritional science suggests that chronic inflammation as a result of excessive lipid accumulation in white adipocytes may be the real cause of cardiovascular disease. Adipocytes are metabolically active and when fully mature can act as endocrine tissue, secreting a number of different cytokines called adipocytokines. The main adipocytokines include leptin and adiponectin, which act as feedback regulation on the size of adipose tissue, and in fat and glucose metabolism, respectively. However, adipocytes that become infiltrated by macrophages can secrete a number of other adipocytokines including tumour necrosis factor alpha (TNF-α) and interleukin 6 (IL-6), which are thought to be a contributory cause of the inflammation that is now associated with cardiovascular disease.
A number of studies have reported on the high concentrations of inflammatory cytokines found in patients with cardiovascular disease. For example, one group of researchers1 investigated the tissue levels of various cytokines in 46 patient who had undergone coronary bypass surgery and 12 healthy control subjects. The results showed that the patients with cardiovascular disease had higher abdominal and epicardial adipose tissue levels of TNF-α and IL-6 when compared to the control subjects, suggesting a pro-inflammatory environment. In addition, levels of leptin and visfatin were also higher in the subjects with cardiovascular disease. The exact role of visfatin is not fully understood, but leptin can become elevated in those with metabolic syndrome. This is due to leptin resistance in the hypothalamus. In addition, the control subjects had significantly higher tissue levels of adiponectin when compared to subjects with cardiovascular disease. Adiponectin is inversely associated with metabolic syndrome,
These results support other studies in showing that inflammation is associated with cardiovascular disease. The current paradigm suggests that development of insulin resistance occurs due to poor dietary choices, and this causes the development of a metabolic dysfunction termed the metabolic syndrome. Such dysfunction includes the accumulation of lipids in abdominal adipocytes, particularly around the liver. Influx of macrophages are then thought to stimulate the release of cytokines from adipocytes, and at the same time release of adiponectin is inhibited. Increase in the adipocyte tissue volume causes increased leptin release but the hypothalamus becomes resistant to the signal, which would normally cause an increase in resting metabolic rate, decreased food intake and increase in exercise, in order to reduces adipocyte volume. Interference in the leptin signal is thought to be caused by high insulin levels, a result of the insulin resistance associated with metabolic syndrome.
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