Asian Journal of Research in Biochemistry

Background: Cholesterol supports membrane organisation, myelin formation and the synthesis of steroid hormones and bile acids. Its biological necessity has sometimes been used to question the cardiovascular consequences of elevated circulating cholesterol. This interpretation overlooks differences between cellular cholesterol requirements and exposure to cholesterol carried by atherogenic lipoproteins.

Objective: To critically examine cholesterol homeostasis, the evidence connecting lipoproteins to atherosclerosis, and the nutritional and therapeutic implications of this distinction.

Method: A focused narrative synthesis of selected mechanistic studies, genetic evidence, clinical trials, meta-analyses and professional guidance was undertaken using publicly accessible scholarly records and guideline sources.

Result: Cholesterol function depends on its location and regulation. Retention of apolipoprotein B-containing particles within the arterial wall promotes lipid accumulation and inflammatory plaque development. Concordant genetic and intervention evidence establishes low-density lipoprotein as a causal contributor to atherosclerotic cardiovascular disease. High density lipoprotein cholesterol concentration is an incomplete measure of particle function and raising it does not reliably improve cardiovascular outcomes. Dietary recommendations should consider the overall food pattern, while pharmacological decisions should prioritise absolute cardiovascular risk and interventions with demonstrated clinical benefit.

Conclusion: Cholesterol is physiologically indispensable, but this does not justify elevated atherogenic lipoprotein exposure. Effective prevention combines nutritional quality, appropriate risk assessment and sustained reduction of the circulating particles that drive atherosclerosis.