The increased blood pressure of hypertension is very damaging. So much so that blunt therapies that override regulatory systems controlling blood pressure, reducing blood pressure without in any way addressing the underlying causes of hypertension, can reduce mortality and incidence of age-related disease. Hypertension is a downstream consequence of forms of age-related cell and tissue damage that also cause many other forms of dysfunction. But a sizable fraction of their contribution to degenerative aging is mediated by increased blood pressure.
Hypertension turns biochemical issues in aging into physical trauma to tissues. It causes pressure damage such as rupture of capillaries to delicate structures necessary to tissue function in the kidney, brain, and elsewhere. It accelerates the progression of atherosclerosis, in which fatty lesions form in blood vessel walls. It contributes to destructive remodeling of heart muscle. Further, hypertension speeds the progression of neurodegenerative conditions leading to dementia, the subject of today's open access meta-analysis. The data demonstrates the point made above, that controlling hypertension makes a sizable difference to the risk of suffering dementia, a measure of just how much damage raised blood pressure does to the brain when sustained over time.
The utility of antihypertensives and ideal blood pressure (BP) for dementia prevention in late life remains unclear and highly contested. This study assessed the associations of hypertension history, antihypertensive use, and baseline measured BP in late life (older than 60 years) with dementia. Longitudinal, population-based studies of aging participating in the Cohort Studies of Memory in an International Consortium (COSMIC) group were included. Participants were individuals without dementia at baseline aged 60 to 110 years and were based in 15 different countries. Participants were grouped in 3 categories based on previous diagnosis of hypertension and baseline antihypertensive use: healthy controls, treated hypertension, and untreated hypertension. Baseline systolic BP (SBP) and diastolic BP (DBP) were treated as continuous variables.
The key outcome was all-cause dementia. Mixed-effects Cox proportional hazards models were used to assess the associations between the exposures and the key outcome variable. The association between dementia and baseline BP was modeled using nonlinear natural splines. The main analysis was a partially adjusted Cox proportional hazards model controlling for age, age squared, sex, education, racial group, and a random effect for study. Sensitivity analyses included a fully adjusted analysis, a restricted analysis of those individuals with more than 5 years of follow-up data, and models examining the moderating factors of age, sex, and racial group.
The analysis included 17 studies with 34,519 community dwelling older adults (58.4% female) with a mean age of 72.5 ± 7.5 years and a mean follow-up of 4.3 ± 4.3 years. In the main, partially adjusted analysis including 14 studies, individuals with untreated hypertension had a 42% increased risk of dementia compared with healthy controls (hazard ratio 1.42) and 26% increased risk compared with individuals with treated hypertension (hazard ratio 1.26). Individuals with treated hypertension had no significant increased dementia risk compared with healthy controls. The association of antihypertensive use or hypertension status with dementia did not vary with baseline BP. There was no significant association of baseline SBP or DBP with dementia risk in any of the analyses. There were no significant interactions with age, sex, or racial group for any of the analyses.
In conclusion, this individual patient data meta-analysis of longitudinal cohort studies found that antihypertensive use was associated with decreased dementia risk compared with individuals with untreated hypertension through all ages in late life. Individuals with treated hypertension had no increased risk of dementia compared with healthy controls.