By the time we reach age 50, doctors recommend we start taking statins to keep our cholesterol levels in check. But research is discovering that high fats are a common factor in centenarians, reports nutritionist and master herbalist Donnie Yance
As we enter our fifth decade of life, we’re urged to take a statin to lower our levels of cholesterol, the fat that drives the heart disease epidemic, at least according to medical convention. That, combined with a low-fat diet, should dramatically reduce our risk of CVD (cardiovascular disease), they say, and help us live a long and relatively healthy life.
Living to 100 is now within the grasp of a growing number of us—one in 5,000 reach their century. But there’s something about centenarians that contradicts the cholesterol theory: They all have high levels of the fats in their blood.
This isn’t a statistical anomaly. Studies from around the world all show the same pattern. The oldest old, those who’ve actually achieved extreme longevity, have cholesterol levels that current US and UK guidelines would classify as “borderline high” or “high.” Many would be prescribed statins.
This paradox raises an uncomfortable question that challenges five decades of medical dogma: Are our cholesterol guidelines preventing deaths or causing harm?
What makes centenarians remarkable isn’t just their age. It’s that they’ve managed to escape or significantly delay the diseases that normally cause mortality: CVD, stroke, cancer, diabetes and dementia.
Despite their advanced age, centenarians show remarkable heterogeneity in health status. Some remain physically robust and cognitively sharp well into their 100s. Others experience significant frailty, requiring assistance with daily activities. Yet even the frail have demonstrated an ability to survive conditions that would be fatal in younger populations.
Research has identified several characteristics of centenarians across different populations and cultures:
These lifestyle factors matter enormously. But here’s what makes the cholesterol paradox so striking: Despite doing many things “right” for cardiovascular health, centenarians consistently have higher cholesterol levels than younger people.
A 2025 study of 168 nonagenarians and centenarians from central Sardinia—a recognized Blue Zone where exceptional longevity clusters—found median total cholesterol levels of 199.5 mg/dL in men and 202.5 mg/dL in women. These are levels that would prompt most American physicians to recommend lifestyle changes or prescribe statins. More remarkably, those with LDL cholesterol above 130 mg/dL survived longer than those with lower levels: 3.82 years versus 2.79 years.1
A 2009 study of 302 Japanese centenarians found that those in better physical and cognitive condition had high blood pressure and high total cholesterol—what researchers called “the centenarian paradox.”2 The very markers we’ve been taught predict early death were associated with better health in the oldest old.
This isn’t what the cholesterol hypothesis predicts. If high cholesterol causes atherosclerosis and CVD, centenarians should have low cholesterol.
But they don’t. And this observation—replicated across multiple populations and continents—suggests we may have fundamentally misunderstood the relationship between cholesterol and longevity.
For decades, LDL (low-density lipoprotein) cholesterol has been labeled “bad cholesterol.” This oversimplification has shaped medical practice, dietary guidelines and pharmaceutical development.
But LDL cholesterol isn’t inherently bad. It plays physiological roles that are critical to health and survival.
LDL is the primary carrier of cholesterol to peripheral tissues. Every cell in your body needs cholesterol to maintain membrane integrity, produce hormones (including sex hormones and cortisol), make vitamin D and create bile acids to digest fat. When tissues are damaged—from injury, infection or inflammation—LDL delivers cholesterol for repair and regeneration.
It also plays a crucial role in immune function. It binds and neutralizes bacterial toxins and viruses, preventing them from causing systemic infection.3
People with very low LDL levels have higher rates of serious infections and sepsis.4 During the Covid-19 pandemic, several studies found that patients with very low cholesterol had worse outcomes and higher mortality.5
The problem isn’t LDL cholesterol itself—it’s oxidation. When LDL particles are exposed to free radicals and oxidative stress, they undergo chemical modification.
These oxidized particles trigger inflammatory responses in arterial walls. Immune cells called macrophages engulf oxidized LDL and become foam cells that contribute to plaque formation. This is the beginning of atherosclerosis.
But here’s the critical point: LDL becomes problematic only when it’s oxidized and when the arterial wall is already inflamed and permeable. Native, unoxidized LDL doesn’t cause atherosclerosis. This explains why some people with high cholesterol never develop heart disease, while others with normal or low cholesterol do.
The evidence supporting this more nuanced view is substantial. A comprehensive 2020 systematic review examined 19 cohort studies involving more than 6 million patients aged 60 and older. The conclusion was stark: “High LDL-C is not associated with reduced lifespan.” In eight of the cohorts, people with the highest LDL lived as long as those with normal LDL. In nine cohorts, they lived longer.6
The Framingham Heart Study—often cited as proof that cholesterol causes heart disease—actually reveals something more complex. When William Castelli, the study’s longtime director, analyzed the data, he found that cholesterol levels of people who developed coronary heart disease (CHD) overlapped substantially with those of people who didn’t.
Approximately 25 percent of people who developed CHD had total cholesterol below 200 mg/dL—the level we’re told is “desirable.” Meanwhile, many people with cholesterol above 240 mg/dL never developed heart disease at all.7
This overlap is critical because it exposes a fundamental flaw in how we interpret cholesterol data. Association does not equal causation.
Yes, some studies show that people with higher cholesterol have slightly higher rates of cardiovascular events. But this doesn’t prove that cholesterol causes those events or that lowering cholesterol will prevent them.
The centenarian paradox isn’t limited to small populations in Blue Zones. Massive prospective cohort studies consistently show that higher cholesterol—particularly in older adults—is associated with lower mortality, not higher.
South Korea. One of the most compelling studies comes from South Korea, where researchers followed 347,971 adults for an average of 5.6 years. They divided participants into five groups based on LDL cholesterol levels and tracked all-cause mortality.
The results contradicted the cholesterol hypothesis completely. The group with the lowest LDL cholesterol of 70 mg/dL, compared to the reference group with 100–129 mg/dL, had a hazard ratio of 1.95—meaning they were 95 percent more likely to die during the follow-up period.
This increased risk persisted even after adjusting for age, sex, smoking, diabetes and other confounding factors. The pattern held across all age groups and both sexes. In every subgroup analysis, the group with the lowest cholesterol had the worst survival rate. 8
Perhaps the most powerful evidence comes from a study in which South Korean researchers analyzed data from 12.8 million adults in the National Health Insurance Service database. This massive cohort followed adults of all ages and both sexes for cardiovascular events and mortality.
The results showed U-shaped associations between total cholesterol and all-cause mortality across all groups. The optimal total cholesterol level for lowest mortality was 210–249 mg/dL—a range that current US and UK guidelines classify as “borderline high” and that often triggers statin prescriptions.
Mortality risk increased both below and above this optimal range. People with total cholesterol below 160 mg/dL had significantly higher death rates than those in the 210–249 mg/dL range.9
Denmark. A Danish study of 108,243 individuals followed for a median of nine years found a clear U-shaped association between LDL cholesterol and all-cause mortality. Both very low and very high LDL levels increased death risk, but the optimal level for lowest mortality was 140 mg/dL.
This U-shaped curve appeared consistently across age groups, though it was most pronounced in people under age 65. 10
Sardinia. The Sardinian centenarian study brings the paradox into sharp focus because it examines the people who’ve actually achieved extreme longevity. These 168 nonagenarians and centenarians from central Sardinia were followed from 2018 to 2024.
Their median total cholesterol was 199.5 mg/dL in males and 202.5 mg/dL in females—levels that would prompt statin recommendations under current guidelines. But when researchers divided the group by cholesterol levels, they found that those with mild hypercholesterolemia (LDL >130 mg/dL) survived longer than those with lower cholesterol.
Cox regression analysis showed that mild hypercholesterolemia was associated with reduced mortality risk even after adjusting for age, sex, frailty and other health conditions. The researchers concluded that their findings “challenge the common belief that longevity requires low cholesterol levels.”1
The Netherlands. In the Netherlands, elderly residents of Leiden with average cholesterol of 252 mg/dL had lower mortality than those with lower cholesterol.11
Italy. In Italy, a study of 4,500 older people found those with higher total cholesterol were less likely to die than those with the lowest levels.12
The pattern is remarkably consistent: Higher cholesterol in older adults is associated with longer life, not shorter, and only at much higher levels does it have a negative impact on longevity. The optimal levels for lowest mortality—140 mg/dL for LDL, 210–249 mg/dL for total cholesterol—are far above current guideline targets.
Current US guidelines recommend total cholesterol below 200 mg/dL and LDL below 100 mg/dL for most people, with even lower targets. In the UK, the recommendations are total cholesterol below 193 mg/dL and LDL below 116 mg/dL.
Beyond the centenarian paradox, there’s an abundance of evidence that low cholesterol is harmful (see below). If, as conventional medicine tells us, high cholesterol is so dangerous and lowering it is so beneficial, we should see clear mortality benefits in randomized controlled trials of statins. But that’s not what the data show.
The MRFIT disaster. The Multiple Risk Factor Intervention Trial (MRFIT), conducted in the US in the 1970s, was one of the most ambitious cholesterol-lowering studies ever attempted. Researchers identified 362,000 men and selected 12,000 with cholesterol levels above 290 mg/dL for intensive intervention: a low-fat, low-cholesterol diet and aggressive risk factor management.
The results, published in the Wall Street Journal in 1982, were shocking. The intervention group had more deaths than the control group. This included higher rates of lung cancer and other non-CVD deaths.13 The study was such a failure that it couldn’t be replicated—by the time researchers wanted to try again, statins had become so widely prescribed that finding an untreated control group was impossible.
MRFIT should have been a wake-up call that the cholesterol hypothesis was too simplistic. Instead, it was largely forgotten as the pharmaceutical industry ramped up statin development and marketing.
If statins save lives, the benefit should be most apparent in high-risk populations: elderly patients, those with heart failure and those with kidney disease. Yet trial after trial in these populations, including the following studies, has shown no reduction in all-cause mortality:
These weren’t small studies. Combined, these trials enrolled more than 30,000 high-risk patients—and found no mortality benefit from statins.
The Cholesterol Treatment Trialists’ (CTT) Collaboration conducted a meta-analysis of 26 randomized trials involving 169,138 participants. While the analysis showed that statins reduce cardiovascular events, it found no significant benefit for all-cause mortality in people without existing CVD.20
A Cochrane review of 18 trials in patients with peripheral arterial disease found that statins reduced cardiovascular events but showed no mortality benefit.21 A meta-analysis of 11 primary prevention trials similarly found no all-cause mortality benefit.22
The pattern is consistent: Statins reduce cardiovascular events but don’t extend life in most populations. This suggests that statins may prevent some heart attacks and strokes, but they may also cause other problems that offset any survival benefit. Several mechanisms may explain why statins fail in this way.
Increased diabetes risk. Statins increase diabetes risk by 9–12 percent.23 In mouse studies, they appear to disrupt the gut microbiome, which reduces the body’s production of GLP-1 (glucagon-like peptide-1), a hormone that regulates blood sugar and insulin secretion.24 Since diabetes itself increases mortality risk, this side effect may offset cardiovascular benefits.
Muscle damage and fall risk. Statin-associated muscle symptoms (SAMS) are one of the most common and clinically significant side effects of statin therapy. SAMS occur in up to 30 percent of patients, ranging from asymptomatic elevations in creatine kinase (a marker of muscle disease) to symptomatic muscle disorders with pain and weakness, and in severe cases, life-threatening rhabdomyolysis (when muscle tissue breaks down and muscle fibers are released into the bloodstream).
The spectrum of muscle injury is broad: Some patients experience mild discomfort, while others develop severe muscle inflammation or rhabdomyolysis that can lead to acute kidney injury and death. 25 Notably, severe cases can develop rapidly—within a week of starting therapy or even after a single dose in susceptible individuals.
SAMS is one of the most common reasons patients discontinue statin treatment, and many choose to stop therapy despite CVD risk reduction because the muscle symptoms significantly impair quality of life. In elderly patients, even moderate muscle weakness increases fall risk and fractures, which can be life-threatening and lead to loss of independence, hospitalization and mortality. The risk of SAMS increases substantially with high-intensity statins, particularly when they’re combined with other medications that inhibit statin metabolism.
Accelerated vascular calcification. Paradoxically, high-dose, long-term statin therapy accelerates coronary artery calcification. A 2015 study found that patients on intensive statin therapy had greater progression of coronary calcium scores than those on moderate-intensity therapy.26 Vascular calcification is linked to increased CVD risk and mortality.
Statins can increase calcification by depleting proteins, such as matrix Gla protein (MGP), that stop calcium from being deposited in arterial walls.27 Vitamin K2 activates MGP, allowing it to shuttle calcium away from blood vessels and maintain vascular elasticity. Without adequate vitamin K2 availability, MGP loses its ability to prevent calcification, leading to progressive arterial stiffening and increased CVD risk.28
Statins inhibit the production of vitamin K2 by blocking an important metabolic pathway, the same mechanism through which they lower cholesterol.29 This creates a dual problem: Not only does aggressive cholesterol lowering increase hemorrhagic stroke risk by making vessel walls more fragile, but it depletes vitamin K2-dependent proteins that protect against arterial calcification.
Notably, a clinical study of 134 statin-intolerant patients showed that normalizing their levels of vitamin D—which works with vitamin K2 to activate MGP—allowed 88–95 percent of previously statin-intolerant patients to tolerate statin therapy.30 This finding suggests that addressing micronutrient deficiencies may be more appropriate and effective than simply increasing statin doses. It also highlights how statins’ disruption of fat-soluble vitamin metabolism contributes to their adverse effects.
Increased bleeding risk. Very low LDL levels increase hemorrhagic stroke risk. High-intensity statins in stroke patients have been associated with increased intracranial hemorrhage.31 This is particularly concerning in elderly patients who may already be on anti-blood-clotting medications.
COPD progression. Statins have been associated with worsening chronic obstructive pulmonary disease (COPD), likely through mechanisms related to lowering LDL cholesterol.32 This is another example of how aggressive cholesterol-lowering may cause unintended harm.
It’s astonishing to consider that medicine has gotten it so wrong for the past 40 years about cholesterol and the role of statins. As we get older, we need fats—as any centenarian might tell you.
While we’ve been focused on the dangers of high cholesterol, we’ve largely ignored the very real dangers of cholesterol that’s too low. The evidence of harm from aggressive cholesterol lowering is substantial and growing.
Hemorrhagic stroke risk. The Women’s Health Study followed 27,937 women over age 45 for an average of 19 years, tracking cholesterol levels and stroke outcomes. The findings were alarming: Women with LDL cholesterol below 70 mg/dL were 2.2 times more likely to experience hemorrhagic stroke than those with LDL of 100–130 mg/dL.
The risk increased dramatically at even lower levels. Women with LDL below 50 mg/dL had a 169 percent increased risk of bleeding stroke.1 This makes biological sense: Cholesterol is essential for maintaining the structural integrity of blood vessel walls. When cholesterol drops too low, vessels become more fragile and prone to rupture.
Cancer. Multiple studies have linked low cholesterol to increased cancer mortality. While some researchers initially dismissed this as “reverse causation”—arguing that cancer causes low cholesterol rather than the reverse—long-term follow-up studies have shown that the association persists even when cancer diagnoses in the first several years are excluded.2
Infection. Low cholesterol also impairs immune function. LDL cholesterol plays a crucial role in binding and neutralizing bacterial toxins and viruses. People with very low LDL have higher rates of serious infections and sepsis.3 This immune impairment may explain why some studies have found increased mortality from infectious diseases in people with very low cholesterol.
All-cause mortality. Perhaps most importantly, very low cholesterol is consistently associated with increased all-cause mortality. A Chinese study of 935 people aged 80 and older found that mortality risk decreased 19 percent for every 1 mmol/L (38.7 mg/dL) increase in total cholesterol.4
A Korean study found that people with LDL below 70 mg/dL had 95 percent higher all-cause mortality than those with LDL of 100–129 mg/dL. This increased risk wasn’t driven by CVD deaths—it was driven by deaths from cancer, infection and other non-cardiovascular causes.5
The message is clear: Cholesterol can be too low. The U-shaped curves seen in multiple large studies tell us that there’s an optimal range and that both very high and very low levels increase mortality risk. Current guidelines focus exclusively on the high end while ignoring the dangers at the low end.
In addition to ignoring their dangers, conventional medicine often overstates the benefits of statins by using statistical sleight of hand. These are some ways to help your body normalize cholesterol levels and support cardiovascular health and longevity without resorting to pharmaceuticals and suffering their side effects.
Focus on inflammation, not cholesterol
There’s substantial evidence that cholesterol levels are not the cause of CVD and that inflammation is the real culprit.1 These are some practical ways to lower inflammation:
Correct nutrient deficiencies
Two examples of key nutrients for cardiovascular health are vitamin D and vitamin K2 (see “Accelerated vascular calcification,” above).
Try supplements
Red yeast rice (Monascus purpureus) was shown to lower cardiovascular events and all-cause mortality by about a third in at least two Chinese studies of people who had suffered a previous heart attack. It lowered the risk of stroke by 44 percent.3
Guggul (Commiphora mukul) is an Ayurvedic botanical used for centuries that enhances cholesterol processing in the liver. Clinical studies show it helps prevent LDL oxidation and is as effective as lipid-lowering drugs when combined with a diet including more fruits and vegetables.4
Artichoke leaf contains bioactive compounds that inhibit LDL oxidation—addressing the root mechanism of atherosclerosis rather than simply lowering cholesterol concentration.5 This mechanism is fundamentally different from statin action and complements anti-inflammatory dietary approaches.
Tocotrienols are a form of vitamin E. Those sourced from annatto have been found to lower cholesterol levels and downregulate inflammatory markers linked to CVD.6
When using supplements, follow the label instructions. Ideally, consult your practitioner before using them, as some can interact with medications.
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