Statins and Heart Disease: What Patients Should Know About Cholesterol, Risks, and Benefits

TL;DR

Cholesterol is not a significant risk factor for developing heart disease. Cholesterol is a necessary steroid for cell membrane structure, hormone production, bile acid production, brain function, nerve health, and immune function.

Statins are only proven to be effective at reducing the risk of developing heart disease in those who have already have cardiovascular disease (a prior heart attack, stroke, or documented coronary artery disease).

As a preventative measure for those without a history of heart disease, statins only prevent less than one percent of nonfatal cardiovascular disease events and have no significant reduction in overall mortality.

What Cholesterol Actually Is and Why Your Body Makes It on Purpose

Before we talk about statins, risk, and guidelines, we need to correct a foundational misunderstanding:

Cholesterol is not a toxin. It is not metabolic waste. It is not something your body accidentally accumulates.

Cholesterol is a structural molecule that your body manufactures intentionally and continuously because life depends on it.

Your Liver Makes Most of Your Cholesterol

The average adult liver synthesizes approximately 1,500–2,000 mg of cholesterol per day – far more than most people consume in their diet. In fact, that is roughly ten times the cholesterol in a large egg.

If you eat less cholesterol, your liver makes more. If you eat more, your liver makes less. This tight internal regulation is one reason dietary cholesterol has only a modest effect on blood cholesterol levels in most individuals.

The Roles of Cholesterol

Cholesterol is required for:

• Cell membrane structure – Every cell in your body depends on cholesterol for structural stability and flexibility.

• Hormone production – Cholesterol is the precursor to testosterone, estrogen, progesterone, cortisol, and vitamin D.

• Bile acid production – Necessary for digestion and absorption of fats and fat-soluble vitamins.

• Brain function – Approximately 25% of the body’s cholesterol is found in the brain and nervous system.

• Myelin sheath formation – The protective coating around nerves is cholesterol-rich.

• Immune defense – LDL particles can bind and neutralize certain bacterial toxins

Cholesterol is foundational for human health. Without it, life is not possible.

Cholesterol vs HDL vs LDL vs Triglycerides: What’s the Difference?

These are the most common markers on a lipid panel blood test. Here is what each of them are.

Cholesterol

Cholesterol is a steroid, a molecule that promotes growth and the synthesis of other compounds. Because cholesterol is a fat-soluble molecule, it cannot travel freely in the bloodstream (which is water-based). Therefore, your body packages cholesterol into lipoproteins so that it can be transported throughout the body.

LDL (Low-Density Lipoprotein)

LDL is a transport particle that carries cholesterol from the liver to tissues that need it for repair, hormone production, or membrane maintenance.

HDL (High-Density Lipoprotein)

HDL functions primarily opposite of LDL by helping move cholesterol from peripheral tissues back to the liver.

Triglycerides

Triglycerides are not cholesterol at all. They are a form of stored energy. When you consume carbohydrates, particularly excess sugar and fructose, your liver converts surplus energy into triglycerides for storage.

The Cholesterol Story Most People Are Told

Most patients hear a simple narrative:

• HDL is “good.”

• LDL is “bad.”

• High cholesterol causes heart disease.

• Lowering LDL with a statin prevents heart attacks.

However, nothing about human health is this simple, and this over simplistic approach is harming you.

The Cholesterol Story You Haven't Been Told

Cholesterol

Cholesterol is touted as the thing that clogs your arteries. But how is it that the human body can make something so beneficial yet be so consequential? As stated above, not only is cholesterol an incredibly important steroid necessary for life, it is not an important risk factor of heart disease. Yes, you read that correctly. This is what the research shows:

• ALLHAT Study: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial found that despite cholesterol being lowered in 28% of study participants, not a single life was saved from statin therapy. Statin therapy neither reduces all cause mortality or fatal or nonfatal coronary heart disease.

• ASCOT-LLA: The Anglo-Scandinavian Cardiac Outcomes Trial–Lipid Lowering Arm spent $100 million to study the prevention of coronary and stroke events with Lipitor. Not a single life was saved from the drug. 

• The Heart Protection Study: The long term use of statins only improves 5 year survival rate by 1.7%. However, careful analysis of this study showed that survival rates were independent of lowering cholesterol.

• JUPITER Trial: The absolute risk reduction of developing a heart attack is 0.9% if you take a statin.

• Cholesterol only makes up 3% of arterial plaque while calcium makes up 50%

Taken together, these data force a different conclusion than the one most people have been taught. Lowering cholesterol does not reliably translate into saving lives, preventing heart attacks, or meaningfully reducing long-term mortality in the general population. The absolute risk reductions are small, survival benefits are marginal, and in some trials outcomes were independent of how much cholesterol was lowered. If cholesterol were the primary driver of heart disease, aggressively reducing it should consistently and dramatically change outcomes. It does not.

HDL

HDL is touted as the "good cholesterol" because it removes cholesterol from tissues like your heart and arteries. However, the cells in all of these tissues make their own cholesterol because they need it. The role of HDL is to shuttle the excess cholesterol to other tissues in need and to your liver to make bile. This process is inherently a good thing but HDL is not all good.

In 2011, the NIH funded study AIM-HIGH found raising HDL did nothing to protect against heart attacks, strokes, or deaths. This is because, once again, HDL, like all other cholesterol markers, is not cut and dry. You have two different types of HDL

• HDL-2 is anti-inflammatory, anti-atherogenic (preventing atherosclerosis), and protective.

• HDL-3 is small, dense, and inflammatory.

  
  

Raising total HDL raises both types of HDL.

LDL

Hopefully you see a trend occurring. LDL cholesterol, demonized for causing atherosclerosis and heart disease, is a beneficial fat based protein (lipoprotein) that your body makes on its own. The human body does not waste its time or energy making something that would cause it harm. Honestly, the argument could stop here, but I will keep going.

LDL, on its own, is never a problem. It is only when LDL becomes oxidized that it becomes dangerous. Oxidation is the process by which a molecule looses a hydrogen atom. This seems harmless, but now that molecule is unstable. It bounces around your body looking for another hydrogen atom for stability. When it cannot find a free one, it steals one from a health tissue, which damages that tissue. If you have heard of free radicals before, I just described why they are a bad thing. Oxidized LDL cholesterol is a bad thing. It is a free radical that specifically damages your blood vessels which can lead to heart disease if left unchecked.

Trying to remove LDL without addressing oxidation is a medical oversight.

Cigarette smoke, heavy metals, environmental toxins, and omega-6 fatty acids oxidize LDL the most. So smokers with normal LDL actually have a higher risk of heart disease than non smokers with high LDL.

Like HDL, there are two types of LDL:

• LDL-A is buoyant, fluffy, does no harm, and is not damaged by oxidation.

• LDL-B is small, hard, dense, and promotes atherosclerosis through oxidation.

Japanese Lipid Intervention Trial found no correlation between LDL levels and death. This is because when you lower LDL you lower both types. In fact, the Isehara Study demonstrated that overall mortality was highest in the group with the lowest LDL (<80 mg/dL). Additionally, low LDL levels are associated with an increased risk of cancer and infections.

Instead of looking at LDL, you can use your triglycerides:HDL ratio which is a better predictor of heart disease than cholesterol. A 3:1 or greater ratio is a reliable predictor of insulin resistance and can also indicate you have more LDL-B than LDL-A.

Insulin Resistance

The conversation about health always seems to stop short of the things that matter most. We love to blame things like cholesterol, or salt, for causing heart disease, when in reality, sugar and insulin resistance is culprit.

When you consume carbohydrates and sugar, your body converts them to glucose to be used for rapidly available energy. If you do not rapidly use glucose it gets absorbed into your muscles, for storage, with the help of insulin. If you continuously consume more sugar and carbohydrates than you are using, your storage centers get full. With the help of more insulin you can pack a little more glucose into your muscles but there is a limit to it. When this limit is reached excess glucose is stored in adipose tissue (fat cells) because it is dangerous for glucose to be freely floating around your blood stream.

When storage space becomes available in your muscles again glucose may have a hard time getting in. That is because your muscles have become accustom to large amounts of insulin. Sometimes more than your pancreas can consume. Insulin resistance is the process by which your muscles, and other cells, stop taking up excess glucose, even if they are capable, because they now require more insulin than you can provide.

So how does this tie into heart disease? Insulin is anti-inflammatory in people with normal insulin sensitivity, but inflammatory otherwise. Insulin resistance:

• Increases blood pressure (narrowing blood vessels)

• Increases the production of cholesterol

• Promotes inflammation

• Increases triglycerides

• Oxidizes LDL

• Lowers HDL

• Leads to the formation of advanced glycation end products (AGEs)

If you have excess glucose floating around your body it begins to bind to proteins through a process called glycation. Glycation makes proteins sticky, which makes otherwise small and smooth proteins too big and sticky to get through smaller arteries, such as in the hands, feet, eyes, and kidneys (the places where diabetics have the most issues).

When you step back and look at the full picture, cholesterol begins to look less like the villain and more like a bystander in a metabolically chaotic environment. However, this is not the story you are told.

Saturated Fat

The most evil of them all, am I right? Wrong again. Just like everything else we have discussed, the argument of saturated fats is over simplistic and heavily confounded.

Saturated fats are very stable. However, they are largely found in vegetable oil which is not resistant to damage from heat. When exposed to heat, vegetable oils are susceptible to oxidation and cause the formation of noxious compounds including carcinogens. This is one basis for the conclusion that all saturated fat is bad. When in reality, saturated fats are only harmful in the presence of carbs and sugar.

Eating a high carb diet causes your body to hold onto saturated fats instead of burning them for fuel.  Excess carbs get converted to saturated fatty acids. All this lessens the anti-inflammatory effects of HDL. Otherwise, even though saturated fat raises total cholesterol, it also raises HDL and changes the pattern of LDL-B to LDL-A (shifting the distribution).

Saturated fat is not associated with a greater risk of heart disease, and is associated with less progression of coronary atherosclerosis (carbohydrate intake associated with greater progression). For those still worried about their risk of developing heart disease, your omega-3:omega-6 ratio is far more important than saturated fat intake.

Trans Fat

Trans fats certainly do not get talked about enough. For a long time they were not required information on nutrition labels. Luckily, adding trans fats to foods is illegal in the U.S. but they still do occur naturally. Unfortunately, despite being banned, manufacturers can claim no trans fat as long as there is less than 0.5g per serving.  Manufacturers, therefore, make serving sizes smaller to accommodate

Each 2% increase in trans fat consumption doubles the risk off coronary heart disease.

LP(a)

Lipoprotein(a) is the most important cholesterol particle, but like HDL and LDL, is still not cholesterol.  It is very small, highly inflammatory, and thrombogenic (creating blood clots).  In a healthy body it circulates and carries out repair to arteries.  In too high concentrations it binds with amino acids, promotes oxidation, increases blood clot and plaque formation.

LP(a) is not a part of a standard lipid panel which is why it is almost never discussed in medicine. However, it can be easily added by your cholesterol literate doctor if asked for.

How Cholesterol Guidelines Have Changed

Over the last two decades, cholesterol guidelines have evolved to encourage the use of statins (cholesterol lowering medications) for more and more people.

• 1990s – Early Adult Treatment Panel (ATP) Era

  • Focused on LDL “targets” and treating clearly high-risk patients

  • Drug therapy primarily for those with established heart disease or very high LDL

  • Lifestyle first, medication second

• 2001 – ATP III

  • Expanded risk categories

  • Lowered LDL thresholds for treatment in moderate-risk groups

  • Introduced more aggressive LDL goals

  • More people became candidates for statins

• 2004 – ATP III Update

  • Lowered LDL targets further for high and very high-risk patients

  • Encouraged earlier and more aggressive statin use

  • Increased statin intensity recommendations

• 2013 – American College of Cardiology (ACC) / American Heart Association (AHA) Major Shift

  • Abandoned LDL “treat-to-target” approach

  • Introduced 4 “statin benefit groups”

  • Recommended statins based on 10-year ASCVD risk ≥ 7.5%

  • Many people qualified even with normal LDL levels

• 2018–2019 – ACC/AHA Updates

  • Added “borderline” and “intermediate” risk categories

  • Introduced “risk-enhancing factors” (family history, metabolic syndrome, inflammation, etc.)

  • Encouraged coronary artery calcium (CAC) scoring to guide decisions

  • Further expanded the pool of eligible patients

• 2016 / 2022 – United States Preventive Services Task Force

  • Recommended statins for adults 40–75 with risk factors and elevated 10-year risk

  • Suggested selective use even in moderate-risk patients

  • Continued risk-based expansion rather than disease-based prescribing

Overall Trend (TL;DR)

There has been a significant shift from treating known risk factors for cardiovascular disease to treating lab numbers with statin medications. Over time the threshold of each of these markers has been lowered to include more and more people. Which would be a great thing, trying to prevent heart disease, except we are treating lab tests that are not risk factors of cardiovascular disease. Additionally, we are trying to prevent the risk of developing cardiovascular disease with medications that do not prevent cardiovascular disease to any significant degree.

To understand that, we have to examine the math.

Relative Risk vs Absolute Risk – The Math That Changes Everything

Secondary Prevention: Clear Benefit

For people who already have cardiovascular disease (a prior heart attack, stroke, or documented coronary artery disease), statins reduce relative risk of major cardiovascular events by about 20% over five years.

That sounds substantial.

But relative risk reduction is not the same as absolute risk reduction.

Relative risk reduction describes the percentage decrease in risk compared to a control group, while absolute risk reduction describes the actual difference in event rates between groups. For example, reducing heart attack risk from 2% to 1% is a 50% relative risk reduction, but only a 1% absolute risk reduction. Studies often highlight relative risk because it produces larger, more impressive-looking numbers, even when the actual difference in real-world outcomes is small.

The absolute risk reduction in the secondary prevention group is 3.3% over five years (from 17.6% to 14.3%). That means:

• Number Needed to Treat (NNT) = 30: Thirty people must take a statin for five years to prevent one heart attack or stroke.

• For mortality:

  • Absolute risk reduction = 1.25% over five years

  • NNT = 80 to prevent one death.

Most clinicians, and I agree, consider those numbers meaningful in secondary prevention. But they should be communicated clearly.

Primary Prevention: Much Smaller Benefit

In lower-risk individuals without prior cardiovascular disease, the numbers change dramatically.

Re-analysis of controlled clinical trial data showed:

• No significant reduction in overall mortality in low-risk populations

• Approximately 100–140 people must be treated for five years to prevent one nonfatal event.

That means 99% of low-risk individuals taking statins for five years derive no measurable cardiovascular benefit but are subject to adverse effects.

I'm not suggesting that we shouldn't do everything we can to help that one person, but putting everyone on a lifelong statin to help that one is asinine when nutritional and lifestyle modifications are safer and more effective.

Why Statins Can Matter in Chronic Pain Physiology

Statins inhibit the synthesis of cholesterol in your body by inhibiting an enzyme high up in the cholesterol pathway called HMG-CoA reductase. The problem with blocking the pathway here is that HMG-CoA reductase also makes a very important nutrient called Coenzyme Q10 (CoQ10).

CoQ10 is critical for mitochondrial ATP (cellular energy) production and functions as an antioxidant protecting cell membranes, nerves, DNA, and proteins.

Your cells need energy to do their job and to heal damaged tissues. Mitochondrial dysfunction, statin induced or not, is already a hallmark of all chronic pain conditions.

Additionally, serotonin receptors can be rendered dysfunctional by statins, which is of significance since serotonin deficiency is involved in central sensitization. Statins also increase the risk of type 2 diabetes, a disease of insulin resistance.

Shared Decision-Making: How to Think About Statins

Here is the rational framework:

1. Are you in secondary prevention?

If you already have cardiovascular disease (a prior heart attack, stroke, or documented coronary artery disease) then you should consider statin therapy in combination with nutritional and lifestyle improvements for maximum benefit.

2. Are you in primary prevention?

Understand that the absolute risk reduction of developing cardiovascular disease is less than 1% over five years with adverse effects and mitochondrial dysfunction common.

3. What is your metabolic context?

If you are truly worried about your risk of developing cardiovascular disease there are much better tests than a standard lipid panel at identifying your risk. Ask your cholesterol literate doctor for:

• Cholesterol particle size tests

  • NMR test

  • Lipoprotein particle profile test (LLP)

  • Berkeley cholesterol test from Berkeley Heartlab

  • Vertical auto profile (VAP)

• Lp(a)

• Fasting insulin

• Triglyceride:HDL ratio

  
  

4. Are you addressing insulin resistance?

Nutritional and lifestyle interventions prevent the majority of cardiovascular disease.

5. Are side effects impacting quality of life?

• Muscle Pain and Weakness

• Digestive Problems: Nausea, constipation, diarrhea, and stomach cramps.

• Increased Blood Sugar/Diabetes

• Neurological/Cognitive Effects

• Other Side Effects: Headache, rash, fatigue, and, in some cases, sexual dysfunction

Putting It All Together

Statins help most when risk is already high. Lifestyle and metabolic context dominate primary prevention.

The goal is not the lowest cholesterol number. The goal is the lowest risk of heart disease and stroke – with the greatest preservation of energy, muscle function, and overall health.

When patients understand absolute risk, cholesterol biology, metabolic drivers, and mitochondrial physiology, they can engage in informed conversations with their clinicians.

And that, not blind adherence to simplified cholesterol narratives and treatment guidelines, is how better cardiovascular decisions are made.

Written By:

Dr. Jason Winkelmann

Naturopathic doctor, Chiropractor, Chronic Pain Specialist, and Educator

Frequently Asked Questions

Is high cholesterol actually the main cause of heart disease?

Not exactly. Elevated LDL cholesterol is associated with cardiovascular risk, but it is not the sole—or even primary—driver in many cases. Atherosclerosis is fundamentally an inflammatory and metabolic process involving endothelial injury, immune activation, oxidative stress, insulin resistance, and vascular dysfunction. Cholesterol becomes problematic when it is oxidized and retained within an inflamed arterial wall.

Many patients with “normal” cholesterol levels still develop heart disease, while others with elevated cholesterol do not. This is because cardiovascular risk is influenced by multiple systems: metabolic health, blood sugar regulation, autonomic tone, mitochondrial function, chronic inflammation, sleep quality, and stress physiology. Cholesterol is one variable inside a much larger physiologic picture.

Do statins reduce heart risk for everyone?

Statins reduce cardiovascular risk most clearly in individuals who already have established cardiovascular disease (secondary prevention). In those patients, the absolute risk reduction can be meaningful. In primary prevention—people without prior heart attack or stroke—the benefit is statistically present but often modest in absolute terms.

Statins lower LDL cholesterol and also reduce inflammatory signaling (such as C-reactive protein), which may partly explain their benefit. However, they do not correct underlying drivers such as insulin resistance, visceral adiposity, autonomic imbalance, sleep apnea, or chronic systemic inflammation. For some patients, especially those with low overall risk, the magnitude of benefit may be smaller than they were led to believe.

Understanding whether a medication meaningfully reduces your personal risk requires looking beyond total cholesterol and considering overall cardiometabolic context.

What are the potential downsides of statins?

Most patients tolerate statins reasonably well, but side effects are real and physiologically explainable.

Statins inhibit HMG-CoA reductase in the liver to reduce cholesterol synthesis. That same biochemical pathway also produces coenzyme Q10 (CoQ10), a critical molecule for mitochondrial energy production. Reduced CoQ10 levels may contribute to muscle pain, fatigue, and reduced exercise tolerance in susceptible individuals.

Other reported effects include increased blood sugar in some patients, mild liver enzyme elevations, and rarely more significant muscle injury. For individuals already living with chronic pain, fatigue, or mitochondrial stress, these effects can feel amplified.

This does not mean statins are “bad” medications. It means that risk–benefit decisions should account for whole-body physiology rather than focusing on one laboratory number.

If cholesterol isn’t the whole story, what actually drives heart risk?

Cardiovascular disease is a systems-level condition. Key drivers include:

• Chronic low-grade inflammation

• Insulin resistance and metabolic dysfunction

• Oxidative stress

• Endothelial dysfunction

• Autonomic nervous system imbalance

• Visceral adiposity

• Sleep disturbance

• Chronic stress signaling (cortisol, sympathetic dominance)

From a physiologic perspective, heart disease often reflects decades of metabolic and inflammatory strain. The arterial wall becomes dysfunctional long before a cholesterol number crosses a threshold.

For many patients—especially high-performing professionals who are under chronic stress, sleeping poorly, and managing high cognitive loads—the autonomic and metabolic contributors may be more relevant than a mildly elevated LDL level.

Cholesterol matters. But it matters within context.

Non hyperlinked statistics

Abramson, J. (2022). Sickening: How big pharma broke American health care and how we can repair it. Mariner Books.