Cholesterol is an important and necessary molecule made from lipids and used as a structural component of cell membranes and in the manufacture of certain hormones, fat-soluble vitamins, and bile acids, according to Medline Plus. Its reputation as a cause of cardiovascular disease is derived from a combination of genetic and lifestyle factors that lead to imbalances in metabolism with resultant hazardous plaques and blockages. Understanding how low-density lipoprotein, or LDL, levels become too high and how that affects the body can encourage the right steps toward reversing elevated levels and preventing cardiovascular disease.
Effects on Cells
High levels of circulating LDL causes cells to stop producing their own LDL by shutting off an enzyme involved in cholesterol production, according to the website, ExRx. Three important things happen as a result. The cell responds to excess circulating LDL by storing more cholesterol and by taking down its LDL receptors from the cell membrane, thereby absorbing even less and leaving more in circulation. Once the cells reach their LDL limit, they stop clearing LDL out of the blood and still higher levels of circulating LDL results.
Effects on Circulating LDL
LDL that is left in circulation is susceptible to oxidation, a process that breaks down old molecules but produces dangerous compounds in the intermediate stages. Oxidized LDL molecules are highly reactive with surrounding tissue. When they interact with cells lining the walls of arteries, these cells become damaged and inflammation ensues as part of the repair process.
As the repair continues, white blood cells, more cholesterol and other substances, such as calcium, accumulate. White blood cells that migrate into the area of the arterial wall to assist with the repair transform into a type of cell called a foam cell, according to a March 2001 report in Fronteirs in Bioscience. In some cases, such as chronically elevated cholesterol and arterial inflammation, foam cells may not function efficiently to remove cholesterol; instead, they die, initiating buildup of plaques, occlusions, and their end products--heart attacks and stroke.
Familial Hypercholesterolemia
In some individuals, this process is made more pronounced by an inherited mutation in the gene that codes for the production of LDL receptors, leaving the cells with no ability to recognize or absorb LDL. Known as familial hypercholesterolemia, this condition leads to very high levels of circulating LDL.
The gene that codes for familial hypercholesterolemia is dominant, which means that if one parent passes it to a child, it will be expressed. When both parents pass on the gene, the condition is even more pronounced, with cholesterol levels reaching 600 or more, thus increasing the likelihood of early occurrence of heart attacks and stroke, according to Medline Plus.
