Should You Start a Statin After 70? What the STAREE Trial Found

September 20, 2026

The question arrives in my office most weeks, usually from someone in their late seventies who feels fine. They have never had a heart attack. Their cholesterol is a little high. Somebody has suggested a statin, or they have been on one for years and want to know whether they still need it. And the question underneath the question is always the same one. At my age, is this pill actually buying me anything?

For twenty years I have had to answer that from indirect evidence. Large statin prevention trials either excluded people over 70 or enrolled so few of them that any conclusion about that group was borrowed rather than measured. In the pooled analysis of 28 statin trials, only 8 percent of participants were 75 or older, and within that sliver the drugs cut major vascular events about 13 percent for every 39-point drop in LDL, with nothing to show on overall survival. Two trials that did enroll older adults, JUPITER and HOPE-3, pooled their participants over 70 and found a 26 percent reduction in heart attack, stroke, and cardiovascular death, in groups selected for elevated risk. PROSPER, average age 75, cut coronary events and moved nothing else. I could tell a 78-year-old what statins did for 58-year-olds and explain why the biology should carry over. I could not point to a trial built for people her age.

That changed last month. At the European Society of Cardiology meeting in Munich on August 29, investigators presented STAREE, and the New England Journal of Medicine published it the same day. It is the first large randomized trial of statins for prevention built around people over 70. It produced two headline numbers that point in opposite directions, which is why you may have seen it reported as proof that statins work in older adults and, in a different outlet, as proof that they do not.

Both numbers are real. Neither one is the whole answer. What follows is my read on what the trial measured, what it did not, and how I am using it with the people who sit across from me in Encinitas.

What the trial did

STAREE enrolled 9,971 adults aged 70 and older through 1,583 general practices across Australia. Their average age was 74.7 years, about 40 percent were 75 or older, and 52 percent were women. To get in, you had to be living independently in the community with no history of cardiovascular disease, no diabetes, and no dementia. That last set of exclusions shapes everything about how the results apply, and I will come back to it.

Half received atorvastatin, half received a matching placebo, and neither the participants nor their doctors knew which. Dosing started at 20 milligrams and moved up to 40 after a month for anyone tolerating it. Follow-up ran a median of 5.9 years, which is long for a prevention trial and long enough for the endpoints to accumulate.

This trial carried two co-primary endpoints, and that design choice is the reason it produced a split verdict. One was a composite of cardiovascular death, nonfatal heart attack, stroke, and coronary revascularization, which means a stent or bypass. The second was disability-free survival, counted as living without dying from any cause, without developing dementia, and without becoming persistently physically disabled.

Two endpoints, two different questions. Does the drug prevent cardiovascular events? And does the drug extend the number of years you live as yourself, independent and thinking clearly?

The first answer was yes

Major cardiovascular events occurred in 6.0 percent of the atorvastatin group and 8.3 percent of the placebo group. That is 297 events against 412, a hazard ratio of 0.70 with a confidence interval of 0.61 to 0.82 and a p value below 0.001. A 30 percent relative reduction, and the confidence interval is tight enough that the finding is not going to be argued away. That part is settled.

Translate the relative number into the one that describes a person. Events ran at 10.9 per 1,000 patient-years on atorvastatin against 15.5 on placebo, and the trialists put the number needed to treat at 37 across the 5.9 years. Treat 37 people like these for six years and one of them avoids a heart attack, a stroke, a stent, or a cardiovascular death who otherwise would have had one. The other 36 take a pill every night and get nothing measurable from it, though none of them can know in advance which group they are in.

I consider 37 a respectable number for a cheap generic drug with a five-decade safety record. It sits in the same range as a good deal of what we do in preventive cardiology. For comparison, the site’s piece on aspirin for primary prevention walks through a drug that failed to clear that bar in this same age group, which I will return to shortly.

Two details sharpen the result. The first is what the composite was made of. Across both groups there were 709 first events, and they broke down into 247 strokes, 208 heart attacks, 171 revascularizations, and 83 cardiovascular deaths. Benefit came mostly from the nonfatal events, heart attacks and procedures to open arteries above all. Cardiovascular death did not move, and neither did death from any cause. Nothing in the design was built to move them, and in a country with subsidized access to modern cardiac care few of these events were fatal in the first place.

Second, the cholesterol arithmetic is less clean than the headline suggests. Both groups started with an average LDL of 127 mg/dL. On atorvastatin the average fell about 48 points, roughly 38 percent. In the placebo group it drifted down about 16 points, and the investigators put that down mostly to placebo-group participants picking up a statin from their own doctor. The net difference actually tested was 31 points, not 48. That cuts in the drug’s favor, since a trial whose comparison group quietly gets some of the treatment understates the true effect, and the authors say as much when they call the observed benefit conservative. A 30 percent event reduction off a 31-point LDL difference tracks with the exposure relationship described in what LDL does to long-term survival.

The second answer was no

Death from any cause, dementia, or lasting physical disability reached 12.8 percent of the atorvastatin group and 13.6 percent of the placebo group. That is 637 people against 676, a hazard ratio of 0.94 with a confidence interval of 0.84 to 1.05 and a p value of 0.25. The numbers are too close to call. A statin did not add years of independent, cognitively intact life.

Read quickly, that looks like it cancels the first result. It does not, and understanding why is the most useful thing this trial has to teach.

Investigators offered the explanation, and the arithmetic backs it. Look at what filled that composite. Of the 1,313 people who reached one of the three marks, 650 died, 548 developed dementia, and only 115 became persistently disabled. Roughly 80 percent of all the deaths in the trial came from causes with nothing to do with the heart. So the endpoint was carried almost entirely by non-cardiovascular death and by dementia. A drug that lowers LDL cholesterol has no purchase on either one. Asking a statin to move that composite is asking it to do something it was never built to do. Statins do carry effects beyond cholesterol lowering, and STAREE is a fair test of whether those add up to more independent years late in life. They did not.

Worth knowing how the trial defined its terms, since the words are looser in ordinary use. Dementia was formally adjudicated against diagnostic criteria once a cognitive screening test flagged a decline. Persistent physical disability meant losing the ability to do at least one of six basic daily tasks, walking, bathing, dressing, getting in and out of a chair, using the toilet, or feeding yourself, for six months or longer. That is a high bar, and it is part of why the disability component stayed so small.

So the two results are not in conflict. The trial found that a statin prevents the specific kind of event a statin is supposed to prevent, and that preventing those events was not frequent enough to shift a much broader measure of how long people stayed well. A nonfatal heart attack avoided is worth avoiding. It is also not the same thing as a year of independence gained, and STAREE is the trial that finally lets us say both of those things with numbers attached.

Aspirin got the same test and failed it

This is the part of STAREE that reaches past a single trial result. That disability-free survival endpoint, the composite of death, dementia, and persistent physical disability, is not a new invention. It is the exact primary endpoint used by ASPREE, the trial that tested low-dose aspirin in healthy people over 70 and reported in 2018. Same yardstick, same kind of patient, same broad question about whether a daily preventive pill buys good years. That was deliberate. Monash University led both trials, seven investigators appear on both, and John McNeil, ASPREE’s lead author, is a co-investigator on STAREE. The statin trial was designed as the companion to the aspirin one.

ASPREE enrolled 19,114 adults, gave them 100 milligrams of aspirin or placebo, and followed them a median of 4.7 years. Disability-free survival came out flat at a hazard ratio of 1.01. Cardiovascular events were not reduced either, 0.95 with a confidence interval running from 0.83 to 1.08. Major bleeding rose 38 percent. Deaths ran somewhat higher in the aspirin arm at 1.14, partly from cancer, a finding that stopped holding up once the statisticians corrected for the number of comparisons made and that nobody has fully explained. Extended follow-up published in 2025 found the same picture years later, no cardiovascular benefit and a bleeding excess that persisted.

Put the two side by side and the picture is instructive. Two preventive pills, tested against the same standard in the same population by overlapping investigators. Aspirin failed on both counts, reduced nothing and caused bleeding. The statin failed the same broad endpoint and passed the narrower one convincingly, with no serious-harm signal. Aspirin lost, the statin split.

That is the reason I have spent the last several years talking most of my healthy older patients off daily aspirin while keeping them on their statin. STAREE did not change that position. It supplied the evidence I had been missing for the second half of it.

The side-effect ledger

A trial that shows benefit owes you its harms. STAREE reported them, and I want to put them next to the benefit where you can weigh both.

Musculoskeletal adverse events, meaning muscle aches and related complaints, occurred in 32.0 percent of the atorvastatin group and 29.4 percent of the placebo group. Take a second look at those numbers. Nearly three in ten people taking a placebo reported muscle complaints. Atorvastatin added 2.6 percentage points on top of a very high background rate, which is the clearest illustration I have seen of the point made in the statin muscle pain myth. Most muscle aches in people taking statins are not caused by the statin. Some are, and those people deserve to be believed and worked up rather than dismissed, which is what the piece on what to do when you cannot tolerate a statin is for.

Liver and gallbladder related adverse events ran 3.3 percent against 0.9 percent, which looks alarming until you see that the serious ones numbered nine against four. Nearly all of that category was an abnormal liver blood test, the expected and reversible finding, not liver disease. New diabetes appeared in 4.0 percent against 2.7 percent, about one extra case for every 77 people treated over six years, which lines up with the size of the effect described in do statins cause diabetes. Serious adverse events came out identical in both arms at 2.7 percent. A middle tier of events the investigators tracked separately ran 8.8 percent against 6.7 percent, and 7.2 percent of the atorvastatin group stopped the drug over a side effect against 6.1 percent on placebo. So the drug’s real cost is roughly one extra person in a hundred who quits because it bothers them, plus the diabetes signal. Both columns belong on the ledger.

Worth remembering that everybody in this trial had no diabetes at entry, by design. The new-diabetes signal turned up in a population selected to be free of it.

How I actually use this in clinic

A trial gives you an average. Nobody in the chair is an average, so the number has to be turned into a conversation. Three questions do most of that work for me.

The first is how long this person is likely to live. A statin prevented one event per 37 people over six years in STAREE, which means a person needs to be around long enough to collect. The best estimate of how long a statin takes to pay off in prevention is about two and a half years, so that is the horizon I am really asking about. A vigorous 76-year-old with good kidneys and a full calendar will be. Someone the same age with advanced heart failure, metastatic cancer, or a dementia already taking hold most likely will not, and prevention of a heart attack in 2032 is not what that person needs from me. François Mach put the principle well at the session in Munich when he said age should no longer be a reason to withhold a statin and that the decision still has to account for life expectancy, competing risk, and treatment burden. Age is a poor proxy for any of the three.

The second is what the arteries look like. STAREE randomized people by age and risk factors, which is how trials have to work. In clinic I can do better, because a calcium score tells me whether this particular person has plaque. A 74-year-old with a calcium score in the hundreds is a different proposition from a 74-year-old with a score of zero, and the coronary calcium score is the single most useful tiebreaker I have for the patient who cannot decide. The 2026 cholesterol guideline goes further here than I do. It suggests a score of zero in an older adult means treatment is unlikely to be worth the trouble, and it floats a threshold of 10 as a reasonable place to draw the line, while conceding that no one has tested that strategy prospectively. I am more cautious, for the reasons in why a zero score does not erase a high LDL. A zero score lowers the odds without emptying them.

The third is how this person feels about taking a pill. Some people want every available point of risk reduction and would be annoyed with me for not offering it. Others are on nine medications, hate all of them, and would trade a small statistical gain for one fewer bottle. Both positions are reasonable. My job is to make sure the number they are trading against is the right number, which is roughly one event prevented per 37 people over six years, and not the vaguer impression that a statin either adds years to your life or does nothing at all.

Who this trial does not answer for

STAREE excluded anyone with existing cardiovascular disease, diabetes, or dementia. Three groups, three different conclusions.

If you have already had a heart attack, a stroke, or a stent, this trial says nothing about you, and nothing here is a reason to reconsider your statin. Evidence for statins after an event is much stronger than the evidence in this trial, it has been settled for decades, and it holds at every age studied. The same goes for diabetes, which carries enough cardiovascular risk on its own that the calculation is different from the start.

If you have dementia, or are far enough along a path toward it that six more years of independence is not a realistic target, a statin has little left to offer, and the deprescribing conversation I described in do you still need that beta-blocker applies here too.

I want to be careful about how far that goes, because the evidence on stopping statins does not say what people assume it says. The one randomized trial enrolled patients with a life expectancy under a year, and stopping there improved quality of life without shortening survival in any way the trial could detect. Outside that setting the picture reverses. Pooled data on more than a million and a half patients found higher death rates and more cardiovascular events among people who stopped, and a deprescribing guideline published this year lands on continuing the statin in older adults who are not near the end of life. Stopping is a decision for a narrow situation. It is not a policy for turning 80.

Two more limits belong on the list. Everyone in the trial was an Australian recruited through general practice, a population that skews healthier and better cared for than the American average. And atorvastatin at 40 milligrams is a moderate-to-high intensity dose. Nothing in the trial tells us whether 10 milligrams of a weaker statin would have done the same job, and nobody has run that comparison in this age group. What the wider evidence suggests is that the benefit tracks how far the LDL comes down rather than which pill brought it there, and that pairing a moderate dose with ezetimibe matches a high dose with fewer people quitting. That is what I reach for in an older patient who cannot take a full dose.

What I would tell you

If you are over 70, healthy, living your life, and wondering whether the statin is worth it, STAREE gives you a defensible yes and an accurate sense of scale. Atorvastatin cuts your odds of a heart attack, a stroke, or a stent by about a third. It will probably not add years to the part of your life you care most about, which is the years spent independent and sharp. Those two sentences are both true and they are not in tension.

If you are on a statin and tolerating it, stay on it. Anyone reading headlines that say the trial showed statins do not help older people is seeing the second endpoint with the first one left out.

If you are trying to decide whether to start one, the conversation worth having is not about your age. It is about your arteries, your other conditions, how long you expect to be around, and how you feel about pills. Bring your LDL number, ask whether a calcium score would settle anything, and ask your cardiologist to put the benefit in absolute terms rather than percentages. Anybody can do that arithmetic for you in thirty seconds, and the number is a good deal more informative than a 30 percent headline.

And if you are still taking a daily aspirin alongside it because someone recommended it in 2009, that is the item on your list I would want to talk about first.

Frequently Asked Questions

Does STAREE mean everyone over 70 should be on a statin?

No. It means age by itself is no longer a reason to say no. The trial showed a real reduction in heart attacks, strokes, and stents in healthy people over 70, at a rate of one event prevented for every 37 people treated for six years. Whether you are one of the people who should take it depends on your cholesterol, whether imaging shows plaque in your arteries, what else you are being treated for, and how long you are likely to be around to collect the benefit.

If it did not help people live longer or better, what is the point?

It prevented heart attacks, strokes, and procedures, and those events carry real cost in pain, hospital time, and function. That broader endpoint counted death from any cause, dementia, and physical disability together. Of the 1,313 people who reached one of those marks, 650 died, 548 developed dementia, and 115 became disabled, and about 80 percent of the deaths came from causes unrelated to the heart. A cholesterol drug cannot touch any of that. Preventing a nonfatal heart attack is worth something. It is a smaller thing than adding a year of independent life, and the trial is clear about which one it delivered.

I am 80 and take eight other medications. Should I stop my statin?

Do not stop it on your own, and take the question to your doctor rather than deciding from a headline. The case for continuing is strongest if you have already had a heart attack or a stent, since STAREE did not study that group and the evidence there is far stronger. The case for stopping gets more reasonable if you have no history of cardiovascular disease and a life expectancy short enough that a drug taking two and a half years to pay off will not pay off. Short of that, the evidence leans toward staying on it. Pooled data on more than a million and a half patients found more deaths and more cardiovascular events among people who stopped, and a deprescribing guideline published this year recommends continuing in older adults who are not near the end of life. That is a conversation, not a rule.

Did the statin cause side effects in the trial?

Muscle complaints occurred in 32.0 percent on atorvastatin and 29.4 percent on placebo, so the drug added about 2.6 percentage points to a background rate that was already high. Liver and gallbladder related events ran 3.3 percent against 0.9 percent, though the serious ones numbered only nine against four, so almost all of that was an abnormal liver blood test rather than liver disease. New diabetes ran 4.0 percent against 2.7 percent. Serious adverse events were the same in both groups at 2.7 percent, and 7.2 percent stopped the drug over a side effect against 6.1 percent on placebo.

How does this compare with taking a daily aspirin?

The comparison is close to direct. ASPREE tested aspirin in nearly 19,000 healthy adults over 70 against the identical primary endpoint, run by overlapping investigators at the same university. Aspirin did not extend disability-free survival, did not reduce cardiovascular events, and raised major bleeding by 38 percent, a pattern that held up in extended follow-up published in 2025. Atorvastatin missed the same broad endpoint and clearly reduced cardiovascular events with no serious-harm signal. For a healthy older adult, that is a reason to look hard at the aspirin and a reason to keep the statin.

What dose did the trial use, and does the dose matter?

Atorvastatin started at 20 milligrams and increased to 40 milligrams after a month in anyone tolerating it. That is a moderate-to-high intensity dose and it lowered LDL by about 48 points from an average starting value of 127 mg/dL, though the placebo group’s own cholesterol drifted down too, so the net difference tested was 31 points. Whether a lower dose or a weaker statin would work as well is something this trial cannot answer. The wider evidence points to the size of the LDL drop as the thing that counts, not which pill delivers it, and that a moderate dose paired with ezetimibe can match a high dose with fewer people quitting.

Would a calcium score help me decide?

Often, yes. A calcium score shows whether plaque is present in your own arteries rather than estimating your risk from your age and lab values, and for someone truly on the fence it is the most useful test I have. Find a high score and the case for treatment gets much stronger. A zero score lowers your odds without erasing them. The 2026 cholesterol guideline treats a zero score in an older adult as a reason to hold off, and I am more cautious than that, since a very high LDL still deserves treatment in my hands regardless of the score.

References

1. Zoungas, Sophia, Rory Wolfe, Chris Moran, et al. “Atorvastatin, Cardiovascular Events, and Disability-free Survival in Older Adults.” New England Journal of Medicine (2026). doi:10.1056/NEJMoa2607314.

2. Zoungas, Sophia, Andrea Curtis, Simone Spark, Rory Wolfe, John J. McNeil, Lawrence Beilin, Trevor T. J. Chong, et al. “Statins for Extension of Disability-Free Survival and Primary Prevention of Cardiovascular Events Among Older People: Protocol for a Randomised Controlled Trial in Primary Care (STAREE Trial).” BMJ Open 13, no. 4 (2023): e069915. doi:10.1136/bmjopen-2022-069915.

3. Zoungas, Sophia, Chris Moran, Andrea J. Curtis, et al. “Baseline Characteristics of Participants in STAREE: A Randomized Trial for Primary Prevention of Cardiovascular Disease Events and Prolongation of Disability-Free Survival in Older People.” Journal of the American Heart Association (2024). doi:10.1161/JAHA.124.036357.

4. European Society of Cardiology. “Cholesterol-Lowering Medication Reduces Major Cardiovascular Events by 30 Per Cent in Older People Without Known Cardiovascular Disease.” Press release, ESC Congress 2026, Munich, August 29, 2026.

5. McNeil, John J., Robyn L. Woods, Mark R. Nelson, Christopher M. Reid, Brenda R. Kirpach, Rory Wolfe, Elsdon Storey, et al. “Effect of Aspirin on Disability-Free Survival in the Healthy Elderly.” New England Journal of Medicine 379, no. 16 (2018): 1499-1508.

6. McNeil, John J., Rory Wolfe, Robyn L. Woods, Andrew M. Tonkin, Geoffrey A. Donnan, Mark R. Nelson, Christopher M. Reid, et al. “Effect of Aspirin on Cardiovascular Events and Bleeding in the Healthy Elderly.” New England Journal of Medicine 379, no. 16 (2018). doi:10.1056/NEJMoa1805819.

7. Wolfe, Rory, Jonathan C. Broder, Zhen Zhou, et al. “Aspirin, Cardiovascular Events, and Major Bleeding in Older Adults: Extended Follow-Up of the ASPREE Trial.” European Heart Journal (2025).

8. Blumenthal, Roger S., Pamela B. Morris, Mario Gaudino, et al. “2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.” Journal of the American College of Cardiology (2026).

9. Bao, A., and Dean G. Karalis. “Statin Therapy for Primary and Secondary Prevention in Older Adults.” Current Atherosclerosis Reports (2024).

10. Mortensen, Martin Bodtker, and Erling Falk. “Primary Prevention With Statins in the Elderly.” Journal of the American College of Cardiology (2018).

11. Lee, S. H., Y. J. Lee, J. H. Heo, et al. “Combination Moderate-Intensity Statin and Ezetimibe Therapy for Elderly Patients With Atherosclerosis.” Journal of the American College of Cardiology (2023).

12. Kutner, Jean S., Patrick J. Blatchford, Donald H. Taylor, et al. “Safety and Benefit of Discontinuing Statin Therapy in the Setting of Advanced, Life-Limiting Illness: A Randomized Clinical Trial.” JAMA Internal Medicine (2015).

13. Peixoto, C., Y. Choudhri, S. Francoeur, et al. “Discontinuation Versus Continuation of Statins: A Systematic Review.” Journal of the American Geriatrics Society (2024).

14. Thompson, Wade, Arden R. Barry, Lisa M. McCarthy, et al. “Deprescribing Statins for Adults 65 Years of Age and Older: Evidence-Based Clinical Practice Guideline.” Canadian Family Physician (2026).

15. Bittner, Vera, Sunny A. Linnebur, Dave L. Dixon, et al. “Managing Hypercholesterolemia in Adults Older Than 75 Years Without a History of Atherosclerotic Cardiovascular Disease: An Expert Clinical Consensus From the National Lipid Association and the American Geriatrics Society.” Journal of the American Geriatrics Society (2025).

16. American College of Cardiology. “STAREE: Can Statin Therapy Help Prevent CV Events in Healthy, Community-Dwelling, Older Adults?” Trial summary, ESC Congress 2026, August 2026.

17. “STAREE: Statins Cut MACE Risk by 30% in Older Adults With No CVD History.” TCTMD, August 2026.

Published on damianrasch.com. The above information was composed by Dr. Damian Rasch, drawing on individual insight and bolstered by digital research and writing assistance. The information is for educational purposes only and does not constitute medical advice.