The headline finding is stark. Using QRISK3, a widely used algorithm that estimates a person’s likelihood of suffering a heart attack or stroke over the next decade, the researchers calculated that participants with severe mental illness carried roughly 1.9 times the cardiovascular risk of matched people in the reference population. Even more striking, about 26 percent of the 86 participants met the criteria for initiating active primary prevention treatment — meaning their risk was high enough that clinical guidelines would recommend drug therapy such as statins to prevent a first cardiovascular event. Yet very few of them were actually receiving lipid-lowering therapy.

That gap between identified risk and delivered care sits at the heart of the study’s message. Cardiovascular risk factors and preventive treatment, the authors note, remain insufficiently addressed in psychiatric care. A person being treated intensively for psychosis or manic episodes may never have their cholesterol measured, their blood pressure tracked over time, or their overall risk formally scored. The result is a preventable burden of disease that accumulates silently while clinical attention remains fixed on psychiatric symptoms.

What makes the new findings particularly provocative is what the study ruled out. A common assumption is that the excess cardiovascular mortality in severe mental illness is driven mainly by lifestyle — poor diet, smoking, sedentary behaviour — compounded by the metabolic side effects of antipsychotic medication. This study complicates that narrative. When researchers compared participants’ dietary habits against Norwegian population-based reference data, adherence to dietary recommendations was broadly comparable to that of the general population. Prevalence of hypertension and type 2 diabetes mellitus likewise did not differ significantly from the general population.

Smoking, by contrast, did contribute measurably to the elevated risk estimates, as expected given the high smoking prevalence among people with severe mental illness. But here is the crucial detail: even when the researchers excluded smoking from the QRISK3 calculation, the relative risk remained elevated compared with the reference population. Something beyond diet and tobacco is pushing cardiovascular risk upward in this group — a residual excess that the authors attribute to the complex interplay of factors in severe mental illness, and one that current clinical practice is failing to intercept.

The study’s dietary assessment deserves attention for its rigour. Rather than relying on crude questionnaires, the researchers performed a comprehensive dietary evaluation using a digital food frequency questionnaire, allowing them to score adherence against the Norwegian Food-Based Dietary Guidelines. This level of detail is rare in psychiatric populations, where nutritional data are often limited. It allowed the team to test, rather than assume, whether poor eating habits explain the cardiovascular gap — and to probe how diet interacts with specific psychiatric treatments.

That interaction proved revealing. Participants treated with antipsychotics classified as having high metabolic liability — agents known from previous literature to promote weight gain, dyslipidaemia and insulin resistance — had poorer dietary habits than those receiving low-risk agents. The direction of this association is not fully resolved: patients on high-liability drugs may experience appetite changes and cravings that degrade their diets, or clinicians may already avoid high-liability agents in patients with worse baseline metabolic profiles. Dietary adherence did not differ across treatment settings, however, meaning the pattern held whether patients were treated as inpatients or in community-based outpatient services.

In exploratory regression analyses, dietary quality was nonetheless associated with estimated cardiovascular risk, suggesting that nutrition still matters even if it is not the dominant driver. The authors are careful with their interpretation. This was a cross-sectional study of 86 participants, so it cannot establish causation, and the associations explored are explicitly described as exploratory. Yet the convergence of findings — near-normal dietary adherence alongside nearly doubled risk, elevated risk persisting after smoking is removed, and low uptake of preventive medication — paints a consistent picture of a patient group whose cardiovascular danger is real, multifactorial and under-treated.

The clinical implications are difficult to ignore. The researchers argue that their findings support systematic cardiovascular risk assessment and preventive interventions embedded within psychiatric care itself, rather than left to overburdened primary care systems that patients with severe mental illness may engage with irregularly. Concretely, that could mean routine QRISK3-style scoring at psychiatric intake and follow-up, active management of dyslipidaemia, smoking cessation support integrated into mental health services, and attention to dietary counselling particularly for patients prescribed high metabolic liability antipsychotics. The finding that 26 percent of participants qualified for primary preventive treatment while few received lipid-lowering therapy is the clearest possible indicator of an unmet need.

The study also carries a broader scientific message. For decades, excess cardiovascular mortality in severe mental illness has been attributed, at least partly, to simple explanations — patients eat badly, smoke heavily, and take drugs that make them gain weight. Those factors are real and this study does not minimise them; diet quality was linked to risk, and smoking contributed substantially. But the persistence of elevated relative risk after accounting for smoking, alongside dietary habits comparable to the general population, indicates that severe mental illness itself — through mechanisms that may include biological stress pathways, the effects of illness on physiology, health-system barriers, and the metabolic consequences of medication that go beyond what diet can offset — imposes cardiovascular vulnerability that demands direct clinical attention. Closing that gap, the authors suggest, will require psychiatric services to treat cardiovascular prevention not as someone else’s job, but as an integral part of caring for the whole patient.

Subject of Research: Cardiovascular risk, dietary habits and antipsychotic metabolic liability in severe mental illness

Article Title: Cardiovascular risk beyond dietary adherence and antipsychotic metabolic liability in severe mental illness

Article References: Angelsen, M. E., Joaquim, S. C. S., Johannessen, E. N., Myrdal, C. N., Ringen, P. A., Peleikis, D. E., & Retterstøl, K. (2026). Cardiovascular risk beyond dietary adherence and antipsychotic metabolic liability in severe mental illness. BMC Psychiatry. https://doi.org/10.1186/s12888-026-08663-0

Image Credits: AI Generated

DOI: 10.1186/s12888-026-08663-0

Keywords: severe mental illness, cardiovascular disease, metabolic syndrome, antipsychotic medication, dietary habits, smoking, cardiometabolic risk, QRISK3, schizophrenia, bipolar disorder, preventive treatment, psychiatry