Obesity and high blood pressure may directly cause dementia, not just raise the risk, according to a large genetic study published Wednesday that points to weight and hypertension control as key prevention targets. Obesity Causes Dementia.
People living with obesity and high blood pressure face a higher likelihood of developing dementia, researchers reported in The Journal of Clinical Endocrinology & Metabolism. The findings suggest these conditions play a causal role in brain decline, challenging the long-held view that they are merely associated risk factors.
Dementia is a growing global health concern with no cure. The condition causes progressive loss of memory, reasoning, and thinking skills that can interfere with daily life and independence. As populations age, identifying preventable causes has become a public health priority.
Study Links BMI, Blood Pressure to Dementia
Researchers analyzed health and genetic data from large population groups in Copenhagen and the United Kingdom. They focused on body mass index, a common measure of body fat based on height and weight, and its relationship to dementia outcomes.
“In this study, we found high body mass index and high blood pressure are direct causes of dementia,” said Ruth Frikke-Schmidt, a professor and chief physician at Copenhagen University Hospital–Rigshospitalet and the University of Copenhagen. “The treatment and prevention of elevated BMI and high blood pressure represent an unexploited opportunity for dementia prevention.”
The analysis showed that higher body weight directly increases the likelihood of developing dementia. Much of that effect appeared to operate through elevated blood pressure, which is known to damage blood vessels in the brain over time.
Dementia is not a single disease but a group of conditions caused by progressive brain cell damage. The most common forms include Alzheimer’s disease, vascular dementia, and mixed dementia, which combines features of both.
Genetic Method Strengthens Cause-and-Effect Claim
To establish causation, the research team used a method called Mendelian randomization. The approach uses naturally occurring genetic differences that influence traits such as BMI to mimic the design of a randomized clinical trial.
In this case, genetic variants that predispose people to higher BMI served as stand-ins for lifelong exposure to higher body weight. Because these variants are randomly inherited at birth, they are not influenced by lifestyle, socioeconomic status, or other environmental factors that can distort observational studies.
“That random assignment allows us to see the effect of higher BMI on dementia without the usual confounding influences,” Frikke-Schmidt said. The method enabled researchers to draw stronger conclusions about cause and effect than traditional population studies.
The findings indicate that excess weight itself contributes to dementia risk and that controlling blood pressure may significantly reduce that risk, particularly for vascular-related forms of the disease.
Implications for Early Prevention obesity causes dementiaStrategies
The results raise new questions about when interventions should begin. Previous trials of weight-loss medications in people with early Alzheimer’s disease have not slowed cognitive decline once symptoms were present.
“An open question that remains is whether weight-loss medication initiated before the appearance of cognitive symptoms may be protective against dementia,” Frikke-Schmidt said. “Our present data would suggest that early weight-loss interventions would prevent dementia, and especially vascular-related dementia.”
The study underscores the potential impact of preventing Obesity Causes Dementia. hypertension earlier in life, long before cognitive symptoms emerge. Researchers emphasized that lifestyle changes and medical treatment targeting weight and blood pressure could have benefits that extend beyond heart health.
The Independent Research Fund Denmark, the Capital Region of Denmark, the Lundbeck Foundation, and several other Danish health organizations funded the research. Additional authors were affiliated with institutions in Denmark and the United Kingdom.
