The statin question worth asking at your next appointment
When your doctor tells you a statin will halve your risk of a heart attack, half sounds like a lot, and depending on where you’re starting from it can be. It can also come to almost nothing, because that one phrase, cutting your risk in half, describes both a genuinely large benefit and a barely measurable one without ever telling you which you’re being offered. Working out the difference is the most useful thing you can do before you fill the prescription or decide it isn’t for you.
The gap lives inside the arithmetic. Imagine a hundred people at moderate risk who take a statin every day for five years, and suppose that without the drug two of them would have a heart attack in that time while with it only one does. That’s the 50 percent reduction you were told about, since one is half of two. Looked at the other way, the same result means the drug made no difference at all to 99 of those 100 people, who were either never going to have a heart attack or went on to have one anyway. It changed the story for a single person out of the hundred, which in absolute terms is a fall of one percentage point.
Both numbers honestly describe the same trial. The 50 percent is the relative risk reduction, and it gets quoted because it’s the larger and more persuasive of the two. The one-in-a-hundred is the absolute risk reduction, and it’s the one that tells you what to expect, because you’re deciding as one person rather than as a population.
The number that answers the question you’re really asking
There’s a plainer way to put the question, and doctors have a term for it. The number needed to treat asks how many people like you have to take a drug, and for how long, before one of you avoids the thing you’re trying to prevent. For statins given to people who haven’t yet had a heart attack or stroke, which is most people weighing up whether to start, the answer is sobering. Reviewing the primary-prevention trials, David Diamond and Uffe Ravnskov put it at roughly 100 people treated for five years to prevent a single cardiovascular event, with the absolute benefit over that time coming in under one percent. When the outcome measured is death from any cause, some analyses land closer to 167 people treated for four years to prevent one death.
That doesn’t make statins a con, and it isn’t an argument against taking one. It turns the size of the benefit into a real question with a real answer, and that answer is yours to ask for. The next time a risk reduction gets quoted at you, two follow-ups tell you most of what you need to know: is that a relative figure or an absolute one, and what’s my number needed to treat over five years?
Current Australian practice is already built around the absolute version, which helps. The 2023 Australian guideline for assessing and managing cardiovascular disease risk, and the Aus CVD Risk calculator behind it at cvdcheck.org.au, report your risk as a five-year percentage and sort it into low (under 5 percent), intermediate (5 to just under 10 percent), or high (10 percent and above). Ask your GP to run it and walk you through the number, because every decision that follows, statin or otherwise, hangs off where you sit on that scale.
Why “normal” cholesterol can be cold comfort
If your standard panel came back clean and you still have the nagging sense that something isn’t right, one finding is worth sitting with. When researchers examined 136,905 hospital admissions for coronary artery disease in the American Get With The Guidelines registry in 2009, the average LDL cholesterol on admission was about 105 mg/dL, close to three-quarters of those patients came in under 130, and almost half were under 100. These were people already in hospital with heart disease, and by the numbers most of us are taught to watch, their cholesterol looked fine.
That reading cuts both ways, so it’s worth being careful with it. It doesn’t say LDL cholesterol is meaningless, because it isn’t. It says LDL on its own is a coarse measure, and a reassuring figure on a routine panel isn’t the all-clear it feels like.
The main questions a standard panel can’t answer for you
If the standard panel only tells part of the story, the next question is what fills in the rest. What follows isn’t a shopping list to demand or a set of results to read alone; these are the markers worth raising with your GP or a cardiologist so the two of you can decide whether your situation calls for them.
ApoB is probably the most useful of them. Rather than estimating the cholesterol carried inside your particles, it counts the particles themselves, and Allan Sniderman’s work, supported by a long run of studies since, shows that when your particle count and your LDL number disagree, it’s the particle count that tracks your risk more faithfully. A standard panel weighs the cargo, while ApoB counts the trucks on the road.
Lp(a) is a different kind of test, largely set by your genes, left off routine panels, and ordered on its own. Because it barely shifts over a lifetime, a single measurement can tell you whether you’re carrying an inherited risk your cholesterol number will never reveal, which matters most if heart disease runs in your family.
Other markers speak to something a lipid panel was never designed to catch, which is how your metabolism is treating your arteries. Your triglyceride-to-HDL ratio, already on the panel you have, gives a rough read on insulin resistance, and fasting insulin, glucose and HbA1c fill that picture in. It’s not an abstract concern, because persistently high insulin and blood sugar wear down the glycocalyx, the thin protective lining of your blood vessels, well before anything shows up as a diagnosis. hsCRP and homocysteine point at the inflammation doing its quieter work alongside the cholesterol.
And if you want to know whether there’s disease in your arteries now, rather than a statistical estimate of how likely it is, imaging can look directly. A coronary artery calcium score picks up the hardened, older plaque, while a CT coronary angiogram goes further and shows the softer, newer plaque a calcium score can miss. Whether either is right for you is a real conversation to have with your doctor, weighing your risk against the radiation and the cost, not a box you tick because you read about it.
The part that’s genuinely in your hands
For all the attention that goes to what a tablet does to your body, one of the strongest predictors of how long you’ll live is something you largely control, and it barely comes up in a cholesterol conversation. Cardiorespiratory fitness, your body’s capacity to take in and use oxygen, is that predictor, and its scale is easy to underrate. When the Cleveland Clinic followed 122,007 people who had completed a treadmill test, the least fit among them carried a risk of dying that was comparable to, and in the very lowest group greater than, established hazards like coronary artery disease, diabetes and smoking. There was no point at which more fitness stopped helping; the fitter people were, the longer they tended to live, right to the top of the range. As a rough rule of thumb, each meaningful step up in aerobic capacity is associated with something in the order of a 13 percent lower risk of death.
None of that calls for anything exotic. It’s built on the least fashionable training there is: zone 2 cardio, the steady conversational pace you could hold for 45 minutes, on most days of the week; resistance training a couple of times a week to defend the muscle you otherwise shed with age; and the diet changes that quietly bring insulin and triglycerides down. It’s slow and unglamorous, and it’s entirely yours, none of it needing a prescription.
The side effects you should know
A fair account owes you the other side of the ledger, so here it is without the gloss. Muscle aches are the complaint people raise most often, and observational studies report them in something like 10 to 20 percent of people taking statins. The wrinkle is that blinded trials, where neither patient nor doctor knows who’s actually on the drug, suggest a large share of those aches aren’t caused by the statin at all but by the expectation of them, the nocebo effect. The soreness is real either way, and how often the drug is genuinely to blame is contested enough that it’s worth investigating with your doctor rather than assuming.
There’s also a modest effect on blood sugar. A 2010 meta-analysis in The Lancet led by Naveed Sattar pooled 13 trials and found that statins raised the risk of developing type 2 diabetes by about 9 percent, which worked out to one extra case for every 255 people treated over four years. Small, but real, and it belongs on the scale alongside the benefit. Statins also appear to lower CoQ10, a compound your muscles and heart rely on for energy, though by how much and to what effect the evidence doesn’t settle, which is reason enough to distrust anyone who quotes you a precise figure.
When the answer is clearly yes
For a large group of people none of this is really the argument, and it’s worth saying so plainly, so the caution above isn’t mistaken for a blanket case against the drug. If you’ve already had a heart attack or a stroke, if you’ve been diagnosed with coronary artery disease, if you carry familial hypercholesterolaemia, or if you have a high Lp(a) together with a family history, the absolute benefit of a statin is far larger than the primary-prevention figures at the top of this piece, and your number needed to treat falls sharply. For you the useful question isn’t whether to take it but how to take it well, managing any side effects and keeping the rest of your risk in view. That’s a different conversation from the one a low-risk 45-year-old should be having, and the two were never meant to run off the same script.
Where we fit
None of this is an argument for or against any medication, and it isn’t meant to settle your decision for you. Its whole purpose is to raise the quality of the conversation you have when it counts, in the room with the doctor who knows your history. Go in asking for your absolute risk as well as the relative headline, ask what your number needed to treat actually is, ask whether ApoB, Lp(a) or imaging would show you something your standard panel can’t, and then ask what you can move on your own, because a surprising amount of it turns out to be within reach.
Those decisions sit with you and the doctor who prescribes for you, where they belong.
What we do at Supercell Health is work alongside that relationship, helping you make sense of your own numbers, sharpen the questions worth asking, and get to work on the parts of your health that were yours to shape all along.
Bring us the questions, and we’ll help you ask them better.