For more than three decades, statins have been widely prescribed under the assumption that lowering cholesterol — specifically low-density lipoprotein (LDL) — protects against cardiovascular disease. Over time, this assumption has calcified into medical dogma, reinforced by clinical guidelines, pharmaceutical marketing, and statistical framings that favor surrogate markers over biological reality. Yet a growing body of biomedical evidence points to a far more uncomfortable conclusion. This pattern of well-intended but scientifically oversold interventions is not unique to statins. It also appears in other areas of cardiovascular care, including common supplements — such as calcium — where presumed benefits have masked unanticipated harms. According to research indexed in PubMed and the National Library of Medicine, statin drugs are now associated with more than 350 adverse health effects, impacting nearly every major physiological system. These findings are not anecdotal or fringe. They are cumulative, reproducible, and increasingly difficult to reconcile with the claim that statins are biologically benign--let alone intrinsically cardioprotective. The deeper issue is not merely the number of adverse effects, but their nature. A drug that damages muscle tissue, impairs mitochondrial energy production, disrupts metabolic signaling, and injures peripheral nerves cannot logically be assumed to protect the most energy-demanding, nerve-dense muscle in the human body: the heart. Since 2006, I have been issuing public alerts about these overlooked risks. I began systematically documenting and indexing the peer-reviewed literature linking statins to muscle injury, mitochondrial dysfunction, metabolic disruption, neurological harm, and paradoxical cardiovascular impairment. Today, 1000s of published sutides substansitae these concerns, forming an evidentiary record that remains largely absent from mainstream patient risk-benefit discussions despite its clear clinical relevance.