Many individuals with high levels of blood sugar go on to develop high levels of blood cholesterol. In particular, levels of the very low density lipoprotein (VLDL) and low density lipoprotein (LDL) becomes elevated in the blood. While LDL is referred to colloquially as ‘bad’ cholesterol, VLDL is synonymous with fasting triglycerides. The standard treatment for high cholesterol by mainstream medicine is a cholesterol lowering statin drug, which effectively blocks the synthesis of cholesterol in the liver. However, it is often not understood that high cholesterol levels are often secondary to high blood glucose levels. This link originates from the fact that both conditions are characteristic of the metabolic syndrome, and both are caused by insulin resistance in the individual. Treating high cholesterol is not effective at improving the quality of life or the survival of the patient in isolation because the underlying metabolic deterioration that caused the high cholesterol levels is still present.
Dietary fructose is the common factor that can be linked to both high blood sugar and high cholesterol levels. Fructose, in its refined and crystalline state is absorbed from the gut and transported in the blood to the liver where it is processed to either glycogen or fatty acids. As the quantity of fructose in the diet increases, the flux down the de novo lipogenesis pathway also increases, thus increasing the production of fatty acids. These fatty acids are exported to tissues where they accumulate and then may interfere with the insulin signal cascade. This desensitises the cell to insulin and this raises blood glucose levels by preventing the uptake of glucose from the blood to the tissues. Therefore one of the metabolic problems associated with consuming fructose is insulin resistance and elevated levels of blood glucose. When insulin resistance first develops such individuals are described as being glucose intolerant, but as the disorder progresses, insulin resistance can ultimately lead to the development of type 2 diabetes.
The fatty acids produced in the liver may also accumulate in the liver, and this leads to deterioration of the normal metabolic regulation, In particular glucose, fatty acid and amino acid metabolism may be affected. Fatty acid accumulation in the liver creates a condition called non-alcoholic fatty liver disease (NAFLD). As the fat accumulation worsens, NAFLD develops into steatohepatitis and can worsen further to hepatitis. The efflux of the VLDL particles increases their number in the plasma, and the triglycerides they carry are transferred to tissues. As this process proceeds the density of the particle increases and it becomes a LDL particle (a LDL particle is a remnant of a VLDL particle that has had its triglyceride content lowered). Therefore the LDL levels of the blood rise with the increase in plasma triglycerides. Therefore while lowering the LDL number through inhibition of cholesterol synthesis may be effective, it does nothing to treat the underlying metabolic dysfunction and disease state.
Eat Well, Stay Healthy, Protect Yourself