🩺 Fat, Carbs, and Heart Disease: Why Everything You’ve Been Told About Nutrition Is WRONG
🩺 Fat, Carbs, and Heart Disease: Why Everything You’ve Been Told About Nutrition Is WRONG
For decades, Americans have been told that fat—especially saturated fat—is the enemy. Doctors, dietitians, and public health officials warned us to avoid butter, eggs, and red meat, insisting these foods would clog our arteries. Instead, we were urged to embrace “heart-healthy” vegetable oils, margarine, and low-fat processed foods.
Yet despite following this advice, heart disease remains the #1 killer worldwide, while obesity, type 2 diabetes, dementia, and fatty liver disease continue to climb at alarming rates. If avoiding saturated fat was the solution, why are we sicker than ever?
The truth is, the fat in your arteries does not come directly from the fat you eat. Instead, it comes from a toxic combination of refined carbohydrates, chronically elevated insulin, and industrial seed oils that have quietly taken over the American diet.
Recent scientific & medical research—including a landmark study in eClinicalMedicine (part of The Lancet)—has confirmed this reality: diets high in fat, including saturated fat, are protective for the brain and blood vessels, while diets high in refined carbs are damaging [1].
It is time to face the facts: what we’ve been told about fat, cholesterol, and heart disease has been WRONG all along.
Cholesterol: Essential for Life, Not the Villain
Cholesterol has been demonized for decades, but it is one of the most vital molecules in the human body. Cholesterol is the building block for:
Hormones (estrogen, testosterone, cortisol)
Vitamin D (critical for immune health and metabolism)
Bile acids (necessary to digest and absorb dietary fat)
Cell membranes (giving structure and communication ability to cells)
Coenzyme Q10 (ubiquinone), which powers the mitochondria to generate ATP—the energy currency of life [2].
Without cholesterol, your cells cannot function, your hormones cannot be made, and your heart and muscles cannot generate energy.
So when does cholesterol become harmful? Not in its natural state. In fact, native cholesterol is stable, non-inflammatory, and may even be protective.
The danger comes when cholesterol becomes oxidized. This occurs under conditions of oxidative stress, excess free radicals, and the pro-inflammatory state of insulin resistance. Once oxidized, cholesterol becomes unstable and is engulfed by macrophages—scavenger cells of the immune system—forming “foam cells,” the very first step in atherosclerosis [5].
Unoxidized cholesterol does not trigger this process. In fact, in its pure form, cholesterol may actually be anti-inflammatory.
Cholesterol and Longevity
Far from being a “killer molecule,” cholesterol in its natural, unoxidized state is often linked to better health and longer life.
Large population studies have shown:
In elderly populations, higher total cholesterol is associated with lower all-cause mortality [3].
A systematic review of 19 studies involving over 68,000 older adults found that low LDL was not associated with longer life—if anything, the opposite was true [4].
This suggests that cholesterol, in its pure form, may actually be protective, perhaps because of its role in hormone synthesis, immune function, and antioxidant activity. What kills is not cholesterol itself, but when it becomes oxidized in the pro-inflammatory state of insulin resistance.
Statins: Benefits, Risks, and What They Really Do
Statins, the most prescribed drugs in the world, lower cholesterol by blocking its production in the liver. Large trials show statins can reduce cardiovascular events, but their benefits are not simply from lowering cholesterol.
Statin benefit often correlates with dose and degree of inflammation reduction—not the final LDL number achieved [6].
The JUPITER trial proved this point: patients with normal LDL but high CRP (a marker of inflammation) had nearly a 50% reduction in heart attacks and strokes when given rosuvastatin [7].
This means the real power of statins comes from reducing inflammation and plaque instability, not simply lowering LDL cholesterol.
Yet statins are not without side effects. They slightly increase the risk of type 2 diabetes [8]. They also reduce Coenzyme Q10, impairing mitochondrial energy production and leading to fatigue, muscle pain, and even cognitive decline in some patients [9].
Despite these limitations, statins are prescribed on a massive scale, often for primary prevention, driven by a “pill for an ill” philosophy pushed by pharmaceutical marketing. Instead of addressing root causes like diet, insulin resistance, and inflammation, we treat numbers on a lab sheet.
And here’s the shocking truth: 70% of patients who arrive in the emergency room with a heart attack have cholesterol levels that are considered “normal” [10,11]. This one fact proves cholesterol is not the driver. Instead, the danger lies in oxidized LDL, insulin resistance, and chronic inflammation.
Fat Was Never the Problem. Carbs and Seed Oils Were.
One of the biggest myths in nutrition is that we started eating “too much saturated fat,” and that’s why heart disease exploded.
The reality? Per capita, Americans eat about the same amount of saturated fat today as we did 100–150 years ago [12].
So what changed? A 10,000–50,000-fold increase in omega-6 seed oils—mainly soybean, corn, and canola oil [13]. Today, soybean oil alone accounts for more than 50% of all dietary fat consumed in the U.S. [14].
Why did this happen? Seed oils are cheap, extend shelf life, and make processed foods stable in warehouses and on store shelves. But what makes them stable in processed food makes them unstable in the human body.
Here’s why:
Native cholesterol is stable.
But when exposed to oxidative stress and linoleic acid from seed oils, cholesterol becomes oxidized and inflammatory [5,15].
Oxidized LDL contains toxic compounds like 9-HODE and 13-HODE, both derived from linoleic acid, which accelerate plaque formation [16].
Linoleic acid is also converted into arachidonic acid, the precursor to inflammatory cytokines that fuel heart disease, arthritis, and other chronic illnesses [17].
In other words: the heart-damaging fats aren’t butter or steak—they’re the industrial seed oils hiding in salad dressings, chips, crackers, fried foods, and margarine.
The Lancet’s Evidence
The Lancet eClinicalMedicine study examined nearly 10,000 middle-aged adults from Canada, Poland, India, and China. Results were striking:
High carbohydrate intake increased silent brain infarcts and white matter damage by 40–50%.
High fat intake—including saturated fat—was associated with fewer brain lesions and better cognition.
Monounsaturated fats (olive oil, avocado) and polyunsaturated fats (fish) further improved brain performance, but saturated fats specifically reduced vascular brain injury [1].
This research dismantles the decades-old myth that “low fat equals heart healthy.” It shows that the real dietary culprits are refined carbs and unstable seed oils, not natural fats.
So why isn’t this truth more widely publicized? The reasons are complex. Some of it may be political correctness in nutrition policy, where admitting decades of guidelines were WRONG would undermine public trust. Some of it is market-driven: processed foods and seed oils are cheap, shelf-stable, and enormously profitable. Some of it is pharma-driven, because a “pill for every ill” creates far more revenue than prevention through lifestyle. And some of it reflects the inertia of traditional medicine, which reacts to disease after it strikes rather than proactively preventing it.
The Rise of Cardiometabolic Disease
This toxic combination of processed carbs and seed oils has fueled the modern epidemic of cardiometabolic disease, which includes:
Cardiovascular disease: heart attacks, strokes, and atherosclerosis
Type 2 diabetes: driven by chronic insulin resistance
Nonalcoholic fatty liver disease (NAFLD): now more common than alcoholic liver disease
Metabolic syndrome: a cluster of abdominal obesity, high triglycerides, low HDL, hypertension, and insulin resistance
Dementia & Alzheimer’s: now called “type 3 diabetes” for its metabolic roots
Each of these chronic illnesses shares the same foundation: oxidative stress, inflammation, and disrupted metabolism caused by poor diet.
Conclusion & Call to Action
The evidence is overwhelming: the war on fat was WRONG.
Saturated fat was never the enemy. The real villains are refined carbs, insulin resistance, and inflammatory seed oils that destabilize cholesterol and inflame the body. Statins reduce risk not by lowering LDL, but by calming inflammation. Yet even then, 70% of heart attack patients have “normal” cholesterol, proving we’ve been looking in the wrong place all along.
Meanwhile, industrial seed oils—once marketed as “heart healthy”—have quietly become the most consumed fat in America, fueling oxidative stress and chronic disease.
It’s time to stop chasing sparks and start putting out the fire.
At CardioCore Metabolic Wellness, we go beyond the band-aid of treating lab numbers. We uncover the root causes—insulin resistance, inflammation, and early plaque formation—long before disaster strikes.
Your health is not an accident. It is the result of choices, environment, and proactive care.
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References
Miller V et al. Association of dietary macronutrients with MRI-detected vascular brain injury and cognition. eClinicalMedicine (Lancet). 2025.
Littarru GP, Tiano L. Bioenergetic and antioxidant properties of coenzyme Q10. Mol Biotechnol. 2007;37(1):31–37.
Weverling-Rijnsburger A et al. Total cholesterol and risk of mortality in the elderly. Lancet. 1997;350:1119–1123.
Ravnskov U et al. Lack of an association or an inverse association between LDL cholesterol and mortality in the elderly: a systematic review. BMJ Open. 2016;6:e010401.
Steinberg D. The LDL modification hypothesis of atherogenesis: an update. J Lipid Res. 2009;50(Suppl):S376–S381.
Silverman MG et al. Association between lowering LDL-C and cardiovascular risk reduction across statins. JAMA. 2016;316(12):1289–1297.
Ridker PM et al. Rosuvastatin in prevention of vascular events among men and women with elevated CRP. N Engl J Med. 2008;359:2195–2207.
Carter AA et al. Risk of diabetes with statins: population study. BMJ. 2013;346:f2610.
Banach M et al. Statins, muscle disease, and mitochondria. Curr Opin Lipidol. 2015;26(3):221–227.
Sachdeva A et al. Lipid levels in patients hospitalized with coronary artery disease: analysis of 136,905 hospitalizations. Am Heart J. 2009;157(1):111–117.
Yusuf S et al. Effect of modifiable risk factors associated with myocardial infarction in 52 countries (INTERHEART study). Lancet. 2004;364(9438):937–952.
Mozaffarian D. Dietary fat: from vilification to vindication. JAMA. 2018;319(3):246–247.
Blasbalg TL et al. Changes in omega-3 and omega-6 fatty acid intake in the U.S. during the 20th century. Am J Clin Nutr. 2011;93(5):950–962.
Keenan AH, Davis CR. The dominance of soybean oil in the U.S. diet. Nutrients. 2021;13(9):3085.
Innes JK, Calder PC. Omega-6 fatty acids and inflammation. Prostaglandins Leukot Essent Fatty Acids. 2018;132:41–48.
Staprans I et al. Oxidized cholesterol in LDL accelerates atherosclerosis. Arterioscler Thromb Vasc Biol. 2000;20:708–714.
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