Abstract
Objective: To synthesize current evidence on how hormones regulate lipid metabolism, examine the bidirectional relationship between endocrine disorders and atherogenic dyslipidemia, and evaluate cardiovascular outcomes of emerging therapies that target hormone-lipid pathways.
Methodology: A narrative review of PubMed, Scopus, and Web of Science was conducted for English-language articles published from January 2000 to March 2025, using search terms including lipid metabolism, dyslipidemia, cardiovascular disease, hormones, insulin resistance, thyroid hormone, glucocorticoids, growth hormone, sex hormones, and adipokines. Two authors independently screened titles and abstracts; 542 full-text articles were reviewed, and 312 studies relevant to endocrine function, lipid metabolism, and cardiovascular outcomes were included and synthesized narratively.
Results: Insulin resistance drives the atherogenic lipid triad of hypertriglyceridemia, low HDL-C, and small dense LDL. Hypothyroidism elevates LDL-C by thirty to fifty percent through reduced LDL receptor expression. Glucocorticoid excess promotes hepatic VLDL overproduction and visceral adiposity. Growth hormone deficiency increases LDL-C and lipoprotein(a). Sex hormone imbalances produce characteristic dyslipidemias, and oxidized LDL and ceramides act as bioactive signaling molecules that promote inflammation and endothelial dysfunction. GLP-1 receptor agonists, SGLT2 inhibitors, icosapent ethyl, and PCSK9 inhibitors reduce cardiovascular events through mechanisms that extend beyond LDL-C lowering.
Conclusion: Cardiovascular disease requires an integrated perspective that accounts for the hormonal regulation of lipid metabolism. Clinicians should evaluate endocrine function in patients with treatment-resistant dyslipidemia or premature cardiovascular disease.