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Dr. Sanjaya Kumar Shrestha, <\/em><\/strong><\/span> Heart attacks and strokes remain the leading cause of death worldwide. For decades, cholesterol has been blamed as the primary culprit \u2014 but is that really the case? As a cardiologist who has spent years studying cardiovascular disease, I believe it\u2019s time to challenge one of the biggest misconceptions in modern medicine: that cholesterol is the enemy.<\/p>\n Rethinking Cholesterol: The Misunderstood Molecule What Really Causes Heart Attacks and Strokes?<\/strong> But what causes the initial damage to the inner lining of arteries?<\/strong> The Role of Cholesterol in Arterial Health<\/strong> The Real Story Behind High Cholesterol<\/strong> Familial Hypercholesterolemia: A Special Case<\/strong> So, Should You Fear Cholesterol?<\/strong> Practical Advice: How to Keep Your Arteries Healthy<\/strong> Final Thoughts<\/strong> Dr. Sanjaya Kumar Shrestha, Professor of Cardiology, Kathmandu Medical College Heart attacks and strokes remain the leading cause of death worldwide. For decades, cholesterol has been blamed as the primary culprit \u2014 but is that really the case? As a cardiologist who has spent years studying cardiovascular disease, I believe it\u2019s time to challenge …<\/p>\n","protected":false},"author":110,"featured_media":8068,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"advanced_seo_description":"","jetpack_seo_html_title":"","jetpack_seo_noindex":false,"_jetpack_memberships_contains_paid_content":false,"footnotes":"","jetpack_publicize_message":"","jetpack_publicize_feature_enabled":true,"jetpack_social_post_already_shared":true,"jetpack_social_options":{"image_generator_settings":{"template":"highway","default_image_id":0,"font":"","enabled":false},"version":2}},"categories":[39],"tags":[],"class_list":["post-8066","post","type-post","status-publish","format-standard","has-post-thumbnail","","category-feature"],"jetpack_publicize_connections":[],"jetpack_featured_media_url":"https:\/\/i0.wp.com\/medicosnext.com\/wp-content\/uploads\/2025\/06\/MedicosNext-High-Quality-Images-1.jpg?fit=900%2C600&ssl=1","jetpack_likes_enabled":true,"jetpack_sharing_enabled":true,"_links":{"self":[{"href":"https:\/\/medicosnext.com\/index.php?rest_route=\/wp\/v2\/posts\/8066","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/medicosnext.com\/index.php?rest_route=\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/medicosnext.com\/index.php?rest_route=\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/medicosnext.com\/index.php?rest_route=\/wp\/v2\/users\/110"}],"replies":[{"embeddable":true,"href":"https:\/\/medicosnext.com\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=8066"}],"version-history":[{"count":1,"href":"https:\/\/medicosnext.com\/index.php?rest_route=\/wp\/v2\/posts\/8066\/revisions"}],"predecessor-version":[{"id":8069,"href":"https:\/\/medicosnext.com\/index.php?rest_route=\/wp\/v2\/posts\/8066\/revisions\/8069"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/medicosnext.com\/index.php?rest_route=\/wp\/v2\/media\/8068"}],"wp:attachment":[{"href":"https:\/\/medicosnext.com\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=8066"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/medicosnext.com\/index.php?rest_route=%2Fwp%2Fv2%2Fcategories&post=8066"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/medicosnext.com\/index.php?rest_route=%2Fwp%2Fv2%2Ftags&post=8066"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}
\nProfessor of Cardiology, <\/em><\/strong><\/span>
\nKathmandu Medical College<\/em><\/strong><\/span><\/p>\n
\nWe\u2019ve been conditioned to fear high cholesterol. Medical guidelines define “normal” ranges, and any deviation above those levels is met with alarm. But cholesterol is not inherently harmful. In fact, it plays a vital role in our health. It is crucial for hormone production, vitamin D synthesis, and\u2014most importantly\u2014for maintaining the structural integrity of cell membranes, especially those lining our arteries.
\nIronically, it\u2019s not an excess of cholesterol that causes heart disease \u2014 but rather, a deficiency of cholesterol in the cell membranes of blood vessel linings that may trigger the process of atherosclerosis.<\/p>\n
\nTo understand this, imagine your arteries as pipes carrying blood to vital organs. Just like water pipes, these arteries can be damaged over time. When the inner lining (endothelium) of arteries is injured, plaque can build up in the damaged areas \u2014 a process known as atherosclerosis. These plaques can narrow arteries, causing chest pain during physical exertion. If a plaque ruptures or erodes, it can trigger a blood clot that completely blocks the artery. This sudden blockage is what causes a heart attack or stroke.<\/p>\n
\nThe answer lies in mechanical and biochemical stress. The endothelium, especially the arterial endothelium, endures constant pressure of flowing blood and exposure to harmful compounds, especially advanced glycation end-products (AGEs) formed by excess sugar in the bloodstream. These stresses damage the endothelial cells, which are then repaired by the body\u2019s natural healing process, the inflammatory reaction \u2014 similar to how a cut on the skin heals with a scar. In the arteries, however, this “scar” is known as a plaque.<\/p>\n
\nOur body contains around 30 trillion cells, all with delicate membranes composed of double layers of phospholipids regularly interspersed with cholesterol molecules. While phospholipids are fragile and temperature-sensitive, cholesterol provides stability and strength to these membranes.
\nThe endothelium, constantly under attack of mechanical and biochemical stresses, needs a steady supply of cholesterol and phospholipids to repair itself and maintain its function. While most cells produce their own cholesterol and phospholipid, endothelial cells require additional cholesterol and phospholipid from the bloodstream, carried by lipoproteins like LDL (low-density lipoprotein) and HDL (high-density lipoprotein).
\nContrary to popular belief, LDL is not inherently harmful. It is simply a transport vehicle, delivering cholesterol to cells that need it. Demonizing LDL has distracted us from the real problem: when cells cannot absorb enough cholesterol, they become vulnerable to damage.<\/p>\n
\nThe notion that high cholesterol causes heart disease can be traced back to mid-19th-century research by German scientist Rudolf Virchow, who observed cholesterol in arterial plaques. But his observations did not prove causation \u2014 just correlation.
\nThis misunderstanding was amplified by the Framingham Heart Study in the late 1940s, which showed that high cholesterol levels were associated with increased risk of ischemic heart disease. However, when the data were closely examined, they revealed two overlapping bell curves: many people with \u201chigh\u201d cholesterol never had heart attacks, while many with \u201cnormal\u201d cholesterol did. The real risk became significant only when cholesterol levels exceeded 300 mg\/dL, a level usually seen in a genetic condition called Familial Hypercholesterolemia (FH).<\/p>\n
\nPeople with FH lack enough LDL receptors on their cells. These receptors allow cholesterol to enter cells for membrane repair and maintenance. Without them, cholesterol builds up in the blood but not in the cells \u2014 especially in the endothelial cells that need it most.
\nThe result? High blood cholesterol and cholesterol-starved arteries, which are more prone to damage, inflammation, and plaque formation. FH affects roughly 1 in 200 to 1 in 300 people, but is more common in certain populations, such as French Canadians, where it may affect 1 in 80.
\nIt is possible that the Framingham Heart Study may have unintentionally combined data from people with FH and those without \u2014 leading to a misleading conclusion about the dangers of cholesterol.<\/p>\n
\nOnly if your cholesterol level is extremely high (around 300 mg\/dL) \u2014 a range suggestive of familial hypercholesterolemia. For the vast majority of people, moderately elevated cholesterol is not a direct threat.
\nInstead, we should focus on protecting the endothelium \u2014 the true frontline in the fight against heart disease.<\/p>\n
\nThe key to preventing heart attacks and strokes is minimizing the stress on your arterial walls. Here\u2019s how:
\n– Lower your blood pressure: Keep salt intake low from an early age.
\n– Control blood sugar: Avoid sugary foods and processed carbohydrates that increase harmful AGEs.
\n– Stay physically active: Regular movement helps maintain healthy blood vessels.
\n– Avoid smoking: Smoking directly damages the endothelium.
\n– Don\u2019t fear cholesterol \u2014 understand it: It\u2019s not the enemy. It\u2019s a vital part of your body\u2019s repair system.<\/p>\n
\nCholesterol has been wrongly accused for far too long. It\u2019s time we updated our understanding of its role in heart disease. Instead of focusing on lowering cholesterol at all costs, we should prioritize supporting arterial health and addressing the real risk factors \u2014 high blood pressure, high blood sugar, and inflammation. And remember: healthy arteries, not low cholesterol, are your best defense against heart disease.
\nIf you\u2019re concerned about your cholesterol levels and for related questions or more information, feel free to reach out to me at sanjayakumar70@gmail.com.<\/p>\nReferences: \r\n1. Historical and Epidemiological Studies\r\n- Kannel WB, Castelli WP, Gordon T.\r\nCholesterol in the prediction of atherosclerotic disease: new perspectives based on the Framingham Study.\r\nAnn Intern Med. 1979;90(1):85\u201391.\r\n[PMID: 758428]\r\n- A foundational publication from the Framingham Heart Study showing correlations between cholesterol and cardiovascular disease.\r\n- Anitschkow N, Chalatow S.\r\nOn experimental cholesterin steatosis and its significance in the origin of some pathological processes.\r\n(1913) Centralbl Allg Pathol Pathol Anat\r\n- The original experimental work that linked dietary cholesterol to arterial changes in rabbits.\r\n2. Cholesterol Physiology and Cellular Role\r\n- Yeagle PL.\r\nCholesterol and the cell membrane.\r\nBiochim Biophys Acta. 1985;822(3-4):267\u201387.\r\n[DOI: 10.1016\/0304-4157(85)90011-5]\r\n- Discusses cholesterol\u2019s essential structural role in maintaining membrane fluidity and integrity.\r\n- Maxfield FR, Tabas I.\r\nRole of cholesterol and lipid organization in disease.\r\nNature. 2005;438(7068):612\u201321.\r\n[DOI: 10.1038\/nature04399]\r\n- Explores the importance of cholesterol in cell membranes and its dysfunction in disease.\r\n3. Endothelial Dysfunction and Atherosclerosis\r\n- Libby P, Ridker PM, Hansson GK.\r\nInflammation in atherosclerosis: from pathophysiology to practice.\r\nJ Am Coll Cardiol. 2009;54(23):2129\u201338.\r\n[DOI: 10.1016\/j.jacc.2009.09.009]\r\n- Seminal review explaining that atherosclerosis is fundamentally an inflammatory process following endothelial injury.\r\n- Brownlee M.\r\nThe pathobiology of diabetic complications: a unifying mechanism.\r\nDiabetes. 2005;54(6):1615\u201325.\r\n[DOI: 10.2337\/diabetes.54.6.1615]\r\n- Describes how advanced glycation end products (AGEs) from high blood sugar damage endothelial cells.\r\n4. Familial Hypercholesterolemia (FH)\r\n- Nordestgaard BG, Chapman MJ, Humphries SE, et al.\r\nFamilial hypercholesterolaemia is underdiagnosed and undertreated in the general population: guidance for clinicians to prevent coronary heart disease.\r\nEur Heart J. 2013;34(45):3478\u201390.\r\n[DOI: 10.1093\/eurheartj\/eht273]\r\n- Guidelines highlighting the prevalence, pathophysiology, and cardiovascular risks of FH.\r\n- Goldstein JL, Brown MS.\r\nA century of cholesterol and coronaries: from plaques to genes to statins.\r\nCell. 2015;161(1):161\u201372.\r\n[DOI: 10.1016\/j.cell.2015.01.036]\r\n- Historical perspective on cholesterol metabolism and the LDL receptor hypothesis in FH.\r\n5. Critique of the Cholesterol Hypothesis\r\n- Ravnskov U.\r\nThe questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease.\r\nJ Clin Epidemiol. 1998;51(6):443\u201360.\r\n[DOI: 10.1016\/s0895-4356(97)00327-2]\r\n- Challenges the lipid hypothesis and explores alternative explanations for cardiovascular disease.\r\n- Ravnskov U, et al.\r\nLack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review.\r\nBMJ Open. 2016;6(6):e010401.\r\n[DOI: 10.1136\/bmjopen-2015-010401]\r\n- Systematic review showing that high LDL cholesterol is not consistently associated with increased mortality in older adults.<\/pre>\n","protected":false},"excerpt":{"rendered":"