Atherosclerosis and the various complications associated with this disease, especially towards its final stages, may causes disability and death within Western societies. Although advancement of atherosclerosis is a slow process, beginning in childhood, remaining asymptomatic for several decades, complication like myocardial infarction, peripheral ischemia, or stroke happening later on in life. Some recognized risk factors towards the development of the illness include diabetes, hypertension, obesity, dyslipidaemia, smoking, sedentary lifestyle, and ageing. Several studies suggest heritability of coronary atherosclerosis, established through fatal cardiac episodes between 38 and 57%.
Furthermore, epidemiology studies also correlate a positive family history is independently related with the occurrence of cardiovascular events. Such occurrences derived from genetics include lipid profile as well as genes related to obesity. Development of these molecular biology methods promotes effective identification of these “candidate genes” through use of high-throughput technologies like genome-wide scans. An article explains the connection between the illness and heredity.
A family history of atherosclerosis is independently associated with an increased incidence of cardiovascular events. The genetic factors underlying the importance of inheritance in atherosclerosis are starting to be understood. Genetic variation, such as mutations or common polymorphisms has been shown to be involved in modulation of a range of risk factors, such as plasma lipoprotein levels, inflammation and vascular calcification (Biros, Karan & Golledge, 2008, p. 29).
Some links such as APOE (gene), which is a main protein of the lipid-transportation system, regulates serum cholesterol as well as participating in development of high-density lipoprotein or HDL particles. Furthermore, hepatic parenchymal cells facilitate construction of all outlying APOE. The body rapidly removes APOE-containing particles from circulation through binding to LDLR or LDLR-like protein receptor mediating endocytosis within the liver. The body maps APOE to chromosome 19 at 19q13.2. From there it is linked to apolipoprotein C1 and C2.
APOE is a clear link between the disease and genes. One can produce within the body, the conditions to promote or accelerate this kind of disease. Sure environmental conditions outside the body like poor eating habits and a sedentary lifestyle will contribute; however, genetic predisposition plays a part. When the body cannot remove excess cholesterol as efficiently as someone who does not possess the defective genes to produce such a result, a person with these genes will experience higher levels of blood cholesterol. Even if a person eats healthy and maintains a proper weight, the excess cholesterol may lead or add to the increased risk of developing atherosclerosis.
There are several disease linked to faulty genes. Some are clearly indicated by the gene expression within a person’s body. Therefore nothing a person does could relieve such problems and some of these diseases even lead to death. Naturally, faulty mechanisms within the body cannot be alleviated through diet and exercise alone. Some may never be alleviated.
If someone has a predisposition to store more cholesterol, there is something wrong in their body’s internal mechanisms. Some people see others eating junk food all the time and they are not at risk for heart disease. Some experience heart disease even if they adopt a vegan diet, free of cholesterol. This is simply how some people’s body’s work. They work like this due to the genes they inherited from their parents.
Genes play an important role in a person health. They can enable a long life in a person. They can also enable higher risk for cancers and heart disease. It truly is the kind of problem that cannot be treated simply through diet and exercise.
Biros, E., Karan, M., & Golledge, J. (2008). Genetic Variation and Atherosclerosis. CG, 9(1), 29-42. doi:10.2174/138920208783884856
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