Common Heart Disease Myths That May Be Shaping Your Care

Cardiovascular disease remains one of the leading causes of death in many countries, yet some of the advice most commonly offered to prevent it has been questioned by researchers and clinicians for decades. A handful of persistent myths, about dietary fat, cholesterol, aspirin, triglycerides, and the adequacy of standard testing, continue to shape clinical conversations and public behavior in ways that may not always serve patients well. Examining each of these misconceptions carefully, with attention to what the evidence actually shows, is a useful starting point for anyone trying to make sense of their cardiovascular health.

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The advice to avoid saturated fat has been a cornerstone of dietary guidance for roughly half a century, but according to Dr. Sten Ekberg, the foundational research behind it was deeply flawed. The recommendation traces back to the Seven Countries Study, which, as Ekberg describes it, drew on data from only 7 of the 22 countries originally examined, selecting those that supported a predetermined conclusion linking saturated fat to heart disease. The broader dataset, he argues, did not show the same pattern.

What followed from that recommendation, according to Ekberg, may have made things worse rather than better. Replacing saturated fat with vegetable oils substantially increased the consumption of omega-6 fatty acids, which he identifies as a driver of systemic inflammation, itself a primary mechanism in the development of arterial plaque. Saturated fat, Ekberg notes, does raise LDL cholesterol, but primarily the large, buoyant form that is not considered atherogenic. It also raises HDL cholesterol, which typically improves the total cholesterol to HDL ratio, a more informative marker than LDL alone. When people reduce saturated fat, they tend to replace those calories with carbohydrates, which Ekberg argues increases insulin resistance and further elevates inflammation.

This does not mean all fats are equivalent. Ekberg suggests that a combination of monounsaturated fats, such as those in olive oil, alongside saturated fats from whole food sources like meat, butter, and eggs, represents a more defensible dietary pattern than one built around refined vegetable oils. Individual responses to dietary fat vary, and food quality, processing methods, and overall dietary context all matter considerably.

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Total LDL cholesterol has long been treated as the primary cardiovascular risk marker, but Ekberg argues this framing misses the mechanism by which LDL actually contributes to plaque formation. LDL, in his view, does not become harmful in its native state. It becomes problematic when it is oxidized or glycated, processes driven by insulin resistance, excess omega-6 fatty acids, high sugar intake, and smoking. The result is small, dense, damaged LDL particles that are far more likely to penetrate the arterial wall and initiate plaque than large, intact LDL particles.

This distinction has practical implications. A person with a high total LDL but predominantly large particles, good insulin sensitivity, and low inflammation may carry less actual cardiovascular risk than someone with a lower total LDL composed mostly of small, dense particles in the context of insulin resistance and elevated inflammatory markers. Ekberg points to a range of markers that he considers more informative than total LDL: LDL particle size and count, the small LDL percentage, fasting insulin, hemoglobin A1c, high-sensitivity C-reactive protein, homocysteine, and lipoprotein(a). Standard panels, he notes, often miss all of these.

According to Ekberg, a person could present with a total cholesterol under 200 and an LDL under 130, numbers that would typically be considered acceptable, while simultaneously having an HDL of 35 (below the range associated with protection), a triglyceride-to-HDL ratio of 5 (where a ratio around 1 is considered favorable), and a fasting insulin of 14 (where values between 2 and 5 are considered more optimal). None of these warning signs would be caught by a standard lipid panel.

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A common mental model of heart attacks involves arteries that gradually narrow until blood flow is cut off entirely, like a pipe slowly clogging. This picture is largely inaccurate. According to Ben Azadi, studies going back decades show that roughly 70% of heart attacks occur in arteries that were less than 50% blocked at the time of the event. The actual mechanism is plaque rupture: soft, inflamed plaque within the arterial wall destabilizes and ruptures, the body responds by forming a clot at the injury site, and that clot, not the plaque itself, is what obstructs blood flow.

This distinction matters for how we think about prevention. Interventions that stabilize or reduce inflamed plaque address the actual mechanism. Interventions that focus only on the degree of arterial narrowing may miss the most dangerous lesions entirely, because a soft, vulnerable plaque in a relatively open artery is more likely to rupture than a calcified, stable plaque in a more narrowed one. Coronary artery calcium scoring, which measures calcified plaque burden, provides one window into this risk, though it captures calcified rather than soft plaque.

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For many years, daily low-dose aspirin was widely recommended as a general cardiovascular preventive measure. That guidance has shifted. According to Azadi, the 2022 US Preventive Services Task Force update clarified that for adults 60 and older who have never had a heart attack or stroke, initiating daily aspirin for primary prevention is not recommended. For adults in their 40s and 50s with elevated cardiovascular risk, it remains an individual clinical decision. The guidance for secondary prevention, meaning people who have already experienced a cardiac event or have documented plaque, did not change; in that population, aspirin reduces the risk of a second event by approximately 19 to 20% based on pooled trial data.

The reasoning behind this shift centers on the mechanism described above. Aspirin reduces platelet stickiness, blunting the first step of clot formation. For someone with unstable plaque, this is a meaningful intervention. For someone with no plaque at all, the bleeding risk, primarily gastrointestinal and, more rarely, intracranial, may outweigh any benefit. Azadi cites data from the MESA study making this concrete: people with a coronary calcium score of 100 or higher were estimated to be two to four times more likely to prevent a heart attack than to suffer a major bleed from aspirin, while people with a calcium score of zero were two to four times more likely to bleed than to benefit. Coronary calcium scoring, in this framing, becomes a practical tool for determining whether aspirin belongs in an individual's cardiovascular plan at all.

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High triglycerides are often assumed to result from eating too much fat, a logical-sounding inference that Ekberg argues gets the biology backwards. Triglycerides are produced in the liver primarily from carbohydrates, sugar, and alcohol, particularly in the presence of elevated insulin. When cells are overfed and insulin-resistant, they resist taking up additional fat, leaving triglycerides circulating in the bloodstream at elevated levels. Dietary fat, by contrast, does not drive this process in the same way.

The practical consequence of this misunderstanding, according to Ekberg, is that reducing dietary fat while increasing carbohydrate intake, which is what many standard dietary recommendations effectively produce, tends to raise triglycerides rather than lower them. Conversely, increasing dietary fat while reducing carbohydrates tends to drop triglycerides relatively quickly. Elevated triglycerides, in this view, are primarily a signal of insulin resistance, and addressing that underlying metabolic state is more directly relevant than restricting dietary fat.

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Statins are among the most prescribed medications in the world, and for people who have already had a heart attack or who carry significant genetic risk factors, the evidence for their benefit is reasonably well established. The picture for primary prevention is more complicated. According to Ekberg, in primary prevention populations, roughly 100 people must take a statin for five years for one person to avoid a heart attack during that period. The remaining 99 receive no measurable benefit from the intervention in terms of that outcome.

Ekberg also raises concerns about a mechanism that is not always discussed with patients. Statins inhibit an enzyme called HMG-CoA reductase, which is involved not only in cholesterol synthesis but also in the production of coenzyme Q10 (CoQ10), a compound essential for mitochondrial energy production. Reducing CoQ10 availability may impair energy production in the heart, brain, liver, kidneys, and muscles. Muscle pain and weakness are recognized side effects of statins, but Ekberg notes that internal organs lack the pain receptors that would signal similar dysfunction. Additionally, he cites evidence that statins increase the risk of developing type 2 diabetes by roughly 10 to 25%, a tradeoff that is not always foregrounded in clinical conversations.

For people who do take statins, Ekberg notes that some clinicians suggest CoQ10 supplementation alongside them. He describes a range of around 200 to 600 mg daily taken with fatty meals as one approach that has been discussed in the literature, and notes that co-prescribing CoQ10 with statins is standard practice in several countries, though not in the United States. This is presented as the view of clinicians in this space, not as a universal recommendation; anyone considering supplementation should discuss it with their own healthcare provider.

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• According to Dr. Sten Ekberg, the foundational research linking saturated fat to heart disease relied on selectively chosen data, and replacing saturated fat with vegetable oils may have increased omega-6-driven inflammation rather than reducing cardiovascular risk.
• Studies cited by Ben Azadi suggest roughly 70% of heart attacks occur in arteries that were less than 50% blocked; the actual event is plaque rupture and clot formation, not gradual occlusion.
• The 2022 US Preventive Services Task Force update, as described by Azadi, advises against initiating daily aspirin for primary prevention in adults 60 and older; coronary calcium scoring may help identify who is more likely to benefit than to be harmed.
• Ekberg argues that elevated triglycerides reflect carbohydrate and sugar intake combined with insulin resistance, not excess dietary fat, and that reducing carbohydrates tends to lower them more effectively than reducing fat.
• Standard lipid panels may miss important risk markers including LDL particle size and count, fasting insulin, high-sensitivity C-reactive protein, homocysteine, and lipoprotein(a), all of which Ekberg identifies as more informative for cardiovascular risk assessment.
• For primary prevention, Ekberg notes that approximately 100 people must take a statin for five years for one person to avoid a heart attack, and that statins carry potential risks including CoQ10 depletion and increased type 2 diabetes incidence that warrant careful individual discussion with a clinician.