In 1957, the first results of the Framingham Heart Study were published [1]. It was (or I should say, is, as it’s still ongoing) an epidemiological study that sought to find out risk factors for cardiovascular disease. The study is named after the city of Framingham, Massachusetts, in the United States. A total of 5,209 residents of the city between the age of 30 and 62 were recruited. Various data of this group of people (cohort) was gathered over time to discover these risk factors. In their milestone publication, they identified three risk factors for cardiovascular disease: hypertension, obesity, and hypercholesterolemia (high cholesterol levels).
For the purpose of this article, we’ll focus on cholesterol. Before I get to the effect anabolic steroids have on HDL cholesterol, I’ll first provide some more background.
After these initial findings of the Framingham Heart Study, the role cholesterol plays in the development of cardiovascular disease risk has been further refined. An early step forward in this area of research was the division of cholesterol into low-density lipoprotein (LDL) cholesterol and high-density lipoprotein (HDL) cholesterol and their respective contributions to cardiovascular disease risk. These two cholesterol fractions are also known to the lay public as “bad” and “good” cholesterol, respectively.
High LDL cholesterol was found to be associated with an increased risk of cardiovascular disease. After decades of research, a plethora of evidence has firmly established this association to be causal [2]. Indeed, LDL-lowering therapy, for example by the use of statins, is a cornerstone of dyslipidemia treatment. The association between HDL cholesterol and cardiovascular disease risk is opposite that of LDL cholesterol: high HDL cholesterol has been found to be associated with a decreased risk of cardiovascular disease. Epidemiologic studies find a decreased cardiovascular risk of approximately 2–3 % for every 1 mg/dL increase in HDL cholesterol [3].
Contrary to LDL cholesterol, however, there doesn’t appear to be a direct causal link between HDL cholesterol levels and cardiovascular disease risk [4]. Human genetic studies, in which certain gene mutations which lead to higher or lower HDL cholesterol levels, didn’t clearly demonstrate an association with cardiovascular disease risk. This would’ve been expected if there was a direct causal link. The disconnect between HDL cholesterol levels and cardiovascular disease risk perhaps became most painfully evident in clinical drug trials. A handful of drugs have been developed (or already existed) that raise HDL cholesterol levels quite significantly, but fail to reduce mortality or the incidence of cardiovascular events, such as stroke or myocardial infarction [5]. This also includes the use of over the counter supplements, such as niacin [5, 6].
