If elevated LDLc or dyslipidemia—which includes high levels of total cholesterol—is not treated promptly, it raises the risk of cardiovascular diseases (CVDs), including ischemic heart disease (IHD) and cardiometabolic disorders. Sometimes complicated dyslipidemia with a hereditary component necessitates pharmacological therapy. After this, monoclonal antibody (mAb) therapy-based pharmacological research produced a number of highly effective medications, some of which were even evaluated in this publication.
But, when the market for drugs based on novel pharmacological approaches grows, prices fall, and—most importantly—administering the drugs becomes as simple as popping a pill every day, these drugs would become more widely available.Statins and ezetimibe, two less expensive LDLc-lowering medications, are also accessible for clinical usage. Because they reduce LDLc by about 20%, they are a formidable rival to severe diets or an alternative. Proprotein convertase subtilisin kexin type 9 (PCSK9)-inhibiting mAbs are an additional therapy option. These mAbs have been demonstrated in clinical tests to lower LDLc by as much as 60%, which lowers cardiovascular risk in a dose-dependent way. Studies in biochemistry and genomics have demonstrated the importance of PCSK9 for LDL and lipid metabolism.
Possibly this is the reason why scientists are using small interfering RNA (siRNA) interference to inhibit PCSK9 in clinical trials. Sadly, despite their allure, these treatments are pricey and inappropriate for treating moderate hypercholesterolemia, which is typically brought on by poor dietary habits.In the 1950s and 1960s, Ancel Keys and Mark Hegsted calculated variations in total cholesterol levels as a result of dietary changes. Their calculations showed that saturated fats doubled total and LDLc whereas polyunsaturated fats decreased both. Also, they found that monounsaturated fatty acids (MUFA) have no to very little impact on human serum cholesterol.
It was reaffirmed by the Prospective Urban Rural Epidemiology (PURE) research almost seven years later that it is challenging to evaluate the impact of decreased saturated fat intake on mortality or CVD outcomes. This study also demonstrated that while MUFA and polyunsaturated fatty acids (PUFA) hardly elevated LDLc, a high-saturated fat diet increased it the most. Subsequent research revealed that diets high in MUFA or carbohydrates also decreased LDLc.
