In response to a recent poll, this topic was chosen, “Statins and CoQ10: Who really needs them?” In order to do the topic justice, I’ve split them into two articles. My take on the CoQ question will arrive next tuesday.
At a Glance
A statin decision should not be based on one LDL cholesterol number alone.
The central question is your overall cardiovascular risk: not only your risk over the next 10 years, but your likely exposure to atherosclerosis over decades.
Blood pressure, smoking, diabetes, kidney function, family history, pregnancy-related risk factors, metabolic health, and lifestyle all help shape that risk.
ApoB can add useful information when LDL cholesterol and metabolic health do not tell the same story.
A coronary artery calcium score can sometimes clarify an uncertain decision, but it is not a universal test and a score of zero does not mean zero risk.
Lifestyle measures are foundational. They can substantially lower risk, but they do not always replace medication when risk is high or plaque is already present.
Readers chose this topic in a recent poll, and I understand why. A statin prescription can feel strangely impersonal: a lab result appears, a number is flagged, and suddenly you are being asked to take a daily medication for a disease you may not feel.
The question I hear is rarely, “Can a statin lower LDL cholesterol?” Most people already know that it can.
The real question is: Do I, personally, need one?
That is the right question. A statin is not a vitamin. It is not automatically appropriate because an LDL cholesterol number crosses a line on a laboratory report. But it is also not a medication to dismiss simply because you feel well, exercise, eat thoughtfully, or would prefer to avoid prescriptions.
The decision should start with the likelihood that atherosclerosis—the gradual buildup of plaque in arteries—will cause harm over time, and with how much a treatment is likely to reduce that risk for you.
The number that matters is not just LDL
LDL cholesterol matters. LDL-containing particles can enter the artery wall, contribute to plaque formation, and raise the risk of atherosclerotic cardiovascular disease over time. The evidence supporting that relationship comes from genetics, epidemiology, imaging, and randomized treatment trials.¹
But an LDL value is still only one piece of a larger clinical picture.
Two people can have the same LDL cholesterol and very different levels of cardiovascular risk.
A 42-year-old nonsmoker with normal blood pressure, no diabetes, no plaque, and no strong family history is not in the same situation as a 62-year-old with hypertension, insulin resistance, elevated triglycerides, a parent who had a heart attack at 52, and a calcium score showing coronary plaque—even if their LDL values are identical.
That distinction is why prevention has moved away from asking only, “What is your cholesterol?” and toward asking, “What is your overall risk?”
Risk estimates are imperfect.²,³ They are not crystal balls, and they are not instructions to treat yourself. They are structured ways to begin a better conversation.
They incorporate familiar factors such as age, blood pressure, cholesterol values, smoking, diabetes, and kidney function. Newer approaches may also consider metabolic health, long-term risk, and social conditions that affect cardiovascular health.⁴,⁵ The useful point is not the name of any particular calculator. It is that good prevention is individualized.
A calculated score should start a shared decision, not end one.
Why age can hide long-term risk
One limitation of short-term risk calculators is that age carries so much weight.
A younger person can have a reassuring 10-year estimated risk while still having meaningful lifetime exposure to high LDL cholesterol, high blood pressure, smoking, insulin resistance, or diabetes. Plaque does not usually develop because of one bad month or one isolated blood test. It develops through cumulative exposure over years and decades.¹,⁵
That does not mean every young person with an elevated LDL needs medication immediately. It does mean that “my 10-year risk is low” should not automatically become “there is nothing to address.”
The question becomes: What direction is this person heading?
For some people, the answer is to improve diet quality, activity, sleep, weight, blood pressure, alcohol use, and metabolic health; then repeat testing after a meaningful period of change. For others, the presence of markedly elevated LDL cholesterol, diabetes, familial hypercholesterolemia, kidney disease, established plaque, or a strong family history makes earlier medication more reasonable.
The goal is not to medicate everyone early. It is to avoid waiting until the first event reveals that the risk was real.
A brief history of risk
The idea that heart disease could be predicted was revolutionary when the Framingham Heart Study began following residents of Framingham, Massachusetts, in 1948. Investigators identified characteristics—high blood pressure, smoking, diabetes, and elevated cholesterol—that made future coronary disease more likely.⁶
That work gave medicine the language of “risk factors.”⁶
Over time, clinicians learned that risk factors should not be considered one at a time. Their effects overlap and compound. A person with modest abnormalities in several areas may face more risk than someone with a single striking laboratory value.
Risk equations evolved in response. They expanded beyond heart attack alone to include stroke and other cardiovascular outcomes, and newer models aim to account more fully for kidney function, metabolic factors, and longer time horizons.⁴,⁷
Still, no calculator sees everything.
It may not adequately capture a powerful family history, elevated lipoprotein(a), chronic inflammatory disease, prior pregnancy complications, metabolic dysfunction, or a person’s actual plaque burden. That is where clinical judgment—and sometimes additional testing—matters.
Risk enhancers that change the conversation
A “risk enhancer” is not a diagnosis by itself. It is information that can make a seemingly modest estimated risk more concerning, or make a discussion about treatment more urgent.⁵
Important examples include:
A parent or sibling with premature coronary disease or stroke
Persistently elevated LDL cholesterol, particularly when it is markedly high
Diabetes, prediabetes, insulin resistance, or elevated triglycerides
Chronic kidney disease
Cigarette smoking or ongoing nicotine exposure
Elevated lipoprotein(a), often written as Lp(a)
Chronic inflammatory diseases such as rheumatoid arthritis, psoriasis, or lupus
A history of preeclampsia, gestational diabetes, premature menopause, or other pregnancy-related cardiovascular risk factors
Known plaque in the coronary arteries, carotid arteries, aorta, or peripheral arteries
Elevated high-sensitivity C-reactive protein in an appropriate clinical context
These factors do not mean a person has failed at prevention. They reflect biology, inherited risk, medical history, and the realities of a person’s environment and life circumstances.
They also explain why a good prevention visit should never be reduced to a five-minute discussion of total cholesterol.
ApoB: a useful measure when the story is unclear
LDL cholesterol tells us how much cholesterol is carried inside LDL particles. ApoB estimates the number of cholesterol-carrying particles that are capable of entering the artery wall.
Each atherogenic particle—LDL, very-low-density lipoprotein remnants, and lipoprotein(a)—carries one ApoB protein. Measuring ApoB therefore gives an estimate of the number of particles with the potential to contribute to plaque formation.⁸
For many people, LDL cholesterol and ApoB move together. If LDL is high, ApoB is usually high too. In those cases, ApoB may not change the plan very much.
But the two measurements can become discordant.
This is especially common in people with elevated triglycerides, insulin resistance, type 2 diabetes, obesity, metabolic syndrome, or fatty liver disease. A person may have an LDL cholesterol level that appears only mildly elevated while still carrying a larger number of smaller, cholesterol-poor atherogenic particles.⁸,⁹
In that setting, ApoB can refine the risk discussion.
It is not a replacement for LDL cholesterol. It is not automatically “better” for every person. And it is not a stand-alone reason to begin or intensify medication without considering the full clinical picture.
But when the usual lipid panel and the metabolic story do not match, ApoB can be a particularly useful additional piece of information.⁵,⁹
What a calcium score can—and cannot—tell you
A coronary artery calcium, or CAC, score uses a low-radiation CT scan to identify calcified plaque in the coronary arteries.¹⁰
For some people, it is one of the most helpful tests in preventive cardiology because it answers a different question from a blood test. Rather than estimating risk from risk factors alone, it looks for evidence that coronary plaque has already developed.
That can be clarifying when a statin decision remains uncertain after reviewing the usual clinical information.⁵
A calcium score may be most useful when:
You are in an intermediate or uncertain risk range
You and your clinician are genuinely undecided about starting a statin
You want more personalized information before committing to long-term medication
You have risk factors or a family history that make a simple calculator feel incomplete
You would be more likely to take a recommended treatment if there were objective evidence of plaque
But it is not a test that every person needs.
It is generally less useful when treatment is already clearly indicated—for example, after a heart attack or stroke, in established peripheral artery disease, with very high LDL cholesterol, or in certain high-risk diabetes or familial hypercholesterolemia situations. In those settings, delaying proven therapy to obtain another test often adds little.⁵
It also has limitations.
A calcium score detects calcified plaque. It does not see all plaque, particularly some earlier noncalcified plaque. A score of zero is reassuring in many contexts, but it does not mean a person has no cardiovascular risk.¹¹ It does not erase the importance of smoking, diabetes, markedly elevated LDL cholesterol, a strong family history, symptoms that need evaluation, or other high-risk conditions.
Think of it as a decision-refining tool—not as a cardiovascular report card, and not as a substitute for a clinical evaluation.
Why baseline risk changes the value of a statin
Statins lower LDL cholesterol and ApoB-containing particles. In appropriately selected people, they reduce heart attack, stroke, and other cardiovascular events.¹²
But the benefit is not the same for everyone.
A useful way to understand this is to separate relative benefit from absolute benefit.
If a treatment lowers cardiovascular events by a similar relative percentage across many groups, a person who begins at higher risk has more events available to prevent. That means the absolute benefit is larger.¹²
Here is an illustration, not a prediction for any one person:
If 100 people each have a 20% chance of a cardiovascular event over a given period, about 20 events might occur without treatment. A 20% relative reduction would prevent about 4 of those events.
If 100 people each have a 3% chance of an event, about 3 events might occur without treatment. The same relative reduction would prevent fewer than 1 event.
The medication may have a similar biologic effect in both groups. The practical value differs because the starting risk differs.
That is why statin decisions should feel more urgent in people with established atherosclerotic disease, clearly visible plaque, diabetes with high risk, markedly elevated LDL cholesterol, or a high overall estimated risk. And it is why the decision can be more preference-sensitive when short-term risk is low and the expected absolute benefit is smaller.
Lifestyle is treatment, not a consolation prize
There is a false choice that shows up constantly in prevention conversations:
Either I do lifestyle, or I take medication.
In reality, the most effective plan is often both.
Lifestyle is not something clinicians recommend because they have nothing else to offer. It affects blood pressure, insulin sensitivity, triglycerides, body composition, inflammation, sleep, mood, fitness, and vascular function. It can meaningfully improve cardiovascular risk, whether or not medication is eventually part of the plan.
The basics are familiar because they work:¹³
Do not smoke, and seek structured help if quitting has been difficult.
Build regular aerobic activity and resistance training around your actual health, mobility, and schedule.
Favor a Mediterranean-style or otherwise cardioprotective eating pattern centered on vegetables, fruit, legumes, nuts, seeds, high-fiber foods, unsaturated fats, and minimally processed protein sources.¹⁴
Treat high blood pressure thoughtfully and consistently.
Address diabetes, insulin resistance, and elevated triglycerides.
Prioritize sleep, including evaluation for sleep apnea when symptoms or risk factors point in that direction.
Reduce prolonged sedentary time.
Attend to depression, anxiety, loneliness, chronic stress, and the practical barriers that make healthy routines hard to sustain.
Stress is not a personal failure, and no one should be blamed for living in a body shaped by caregiving, financial strain, trauma, shift work, illness, or social isolation. The evidence for smoking cessation, blood-pressure treatment, and lipid lowering is more direct than the evidence for any single stress-reduction practice preventing heart attacks. Still, psychological health, social connection, sleep, and sustainable routines are part of real cardiovascular care—not decorative add-ons.¹⁵
Lifestyle can sometimes reduce or postpone the need for medication. It does not reliably remove the need for medication in every person with established plaque, familial hypercholesterolemia, markedly elevated LDL cholesterol, diabetes with high risk, or a high calculated risk.
So, who is likely to benefit from a statin?
A statin is most clearly supported when a person already has atherosclerotic cardiovascular disease: prior heart attack, coronary stent or bypass surgery, ischemic stroke or TIA caused by atherosclerosis, peripheral artery disease, or clearly documented plaque in an appropriate clinical context.⁵,¹²
It is also often appropriate in people without a prior event who have substantially elevated baseline risk because of factors such as:
Markedly elevated LDL cholesterol
Diabetes with additional risk factors or high overall risk
A high estimated cardiovascular risk
A strong family history together with unfavorable lipid or metabolic findings
A clearly elevated ApoB in a context where particle burden is likely underestimated by LDL cholesterol alone
Coronary artery calcium or other imaging evidence of plaque when the decision was previously uncertain
For a person at lower short-term risk, with modest LDL elevation, no plaque, and no major risk enhancers, a reasonable plan may be more lifestyle-focused with follow-up testing and a discussion of longer-term risk.
There is no virtue in taking a medication you do not need. There is also no prize for declining one that could meaningfully lower your chance of a heart attack or stroke.
The right answer is personal, evidence-based, and revisited over time.
Questions worth bringing to your visit
If you are unsure about a statin recommendation, these questions can make the conversation more useful:
What is my estimated short-term and longer-term cardiovascular risk?
What factors are driving that estimate?
Do I have risk enhancers that a calculator may not fully capture?
Would ApoB or Lp(a) change the way we understand my risk?
Is a calcium score likely to clarify a genuinely uncertain decision in my case?
What absolute benefit might I expect from a statin?
What lifestyle changes are most likely to help my risk profile?
If I develop side effects, what is the plan before we conclude that I cannot take any statin?
That last question matters. In the next article, I will address the second part of the poll question: what muscle symptoms on statins really mean, how they should be evaluated, and whether CoQ10 has a meaningful role.
Because the most integrative answer is not “take a statin” or “take CoQ10.”
It is to understand your actual cardiovascular risk, address the factors you can change, use medication when its likely benefit is meaningful, and remain appropriately skeptical about any supplement that promises to make a difficult decision simple.
Coming next
Statins, Muscle Pain, and CoQ10: What the Evidence Actually Says
We will cover:
Why statins can cause muscle symptoms in a minority of people
Why many symptoms occurring on statins are not pharmacologically caused by them
How to recognize red flags that need urgent evaluation
Medication interactions and common alternative explanations
Different statin strategies and non-statin options
What CoQ10 does, what the trials show, and when a supervised trial may be reasonable
This post is for general educational purposes only. It is not medical advice, is not a substitute for care from your own physician, and does not create a physician-patient relationship. Do not start, stop, or change any treatment based on what you read here. If you think you may have a medical emergency, call 911 or go to the nearest emergency department. Full disclaimer at drazhak.com/medical-disclaimer.
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Lloyd-Jones DM, Allen NB, Anderson CAM, et al. Life’s Essential 8: updating and enhancing the American Heart Association’s construct of cardiovascular health. Circulation. 2022;146:e18–e43. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001078
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So helpful!