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In this month’s selection of content from GPnotebook, I look at whether age alone should make us reluctant to use statins for primary prevention, and I point to a practical refresher on gallstone disease.

These short discussions are intended as starting points rather than comprehensive reviews. Follow the link at the end of each discussion to explore the evidence and its implications for clinical practice in more detail.

Are we too reluctant to start statins in older people?

Few areas of cardiovascular prevention generate as much uncertainty as whether to start or continue a statin in an otherwise well person in their late 70s or 80s.

The uncertainty is understandable. Statins clearly reduce cardiovascular events in younger people at increased risk, but older adults have historically been under-represented in primary prevention trials. As age increases, competing risks, polypharmacy, frailty and life expectancy also become increasingly important. Yet there is a paradox: older people have the highest absolute cardiovascular risk and therefore potentially the most to gain from an effective preventive treatment.

Previous studies have generally supported statin treatment into the 70s. Observational data have suggested benefit even beyond 75, while the Copenhagen General Population Study demonstrated how dramatically absolute cardiovascular risk rises with age. Its modelling suggested that the number needed to treat to prevent one cardiovascular event may actually become substantially lower in older people.

Two important studies published in 2026, and explored on GPnotebook here, now add to this debate. First, the SAGA/SITE trial approached the question from the perspective of deprescribing. Among adults aged 75 years or older already receiving statins for primary prevention, discontinuing treatment was non-inferior to continuing it for all-cause mortality over 3 years, without major differences in cardiovascular events or quality of life.

The STAREE trial, however, asked a different question. In community-dwelling older adults without established cardiovascular disease, atorvastatin reduced major cardiovascular events over a median of 5.9 years, although it did not prolong disability-free survival.

These findings are not necessarily contradictory. They highlight how the question changes as patients age. Should our objective be preventing cardiovascular events, extending survival, maintaining disability-free life or minimising medication burden? And should starting a statin in a healthy 75-year-old be viewed differently from continuing one in a frail 85-year-old?

This is where absolute risk becomes particularly important. Older adults often have a high baseline cardiovascular risk simply because of age, so a similar relative reduction in risk can translate into a greater absolute benefit than it would in a younger low-risk person. The key question may therefore be shifting from “Is this patient’s cardiovascular risk high enough to justify a statin?” to “Is this patient’s overall health and life expectancy sufficient for them to realise the benefit?”

For a healthy, independent older person with a reasonable life expectancy, preventing myocardial infarction or stroke over the next 5–10 years may be very worthwhile. In a frail person with substantial multimorbidity and limited life expectancy, the same calculated cardiovascular risk may not make initiation of long-term preventive therapy equally compelling.

The accumulating evidence makes the old assumption that primary prevention statins simply become ineffective after an arbitrary age increasingly difficult to sustain. But it also makes individualising the decision in very old patients more important, not less. The updated discussion on GPnotebook of age and primary prevention is worth reading, particularly in light of the new SAGA/SITE and STAREE findings.

Gallstones – from incidental finding to medical emergency

Gallstones are common, particularly with increasing age, but their clinical significance ranges from an incidental finding requiring no treatment to a cause of pancreatitis, sepsis and emergency biliary intervention.

A recently posted podcast on GPnotebook provides a useful refresher on this spectrum, beginning with why gallstones form and following their progression through biliary colic, acute cholecystitis, choledocholithiasis, ascending cholangitis and gallstone pancreatitis.

Most gallstones remain asymptomatic and generally require no treatment. Once symptoms develop, however, recognising where the patient sits along this clinical spectrum becomes important. The podcast revisits the characteristic presentation of biliary colic and how persistent cystic duct obstruction changes the picture to acute cholecystitis. It also considers the consequences of stones migrating into the common bile duct, including obstructive jaundice, cholangitis and pancreatitis.

There are some particularly useful practical reminders. Ultrasound remains the preferred initial investigation for suspected gallstone disease, while MRCP and ERCP have more specific roles when common bile duct stones are suspected. Ascending cholangitis remains an important medical emergency, particularly when biliary obstruction is accompanied by systemic illness.

The discussion also touches on changing patterns of risk. Obesity, insulin resistance and diabetes predispose to cholesterol gallstones, but rapid weight loss can also increase risk. This has led to renewed interest in gallbladder disease as the use of glucagon-like peptide-1 receptor agonists for diabetes and obesity has expanded.

For anyone wanting a concise update on gallstone disease – from pathophysiology and diagnosis through to when cholecystectomy, ERCP or urgent biliary decompression is required – the full podcast provides a useful clinical refresher.