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School of Medicine
High Blood Pressure In Midlife May Spur Cognitive Decline Later - 08/05/2014
High Blood Pressure In Midlife May Spur Cognitive Decline Later
Findings suggest anti-hypertensive drugs could help preserve cognitive function
Release Date: August 5, 2014
A review of data from a long-term study of thousands of Americans suggests that a history of high blood pressure in midlife increases the risk of cognitive decline in old age, according to a report on the study led by Johns Hopkins researchers. The findings, the scientists say, indicate a treatable cause — hypertension — for at least some pervasive forms of cognitive deficit.
Alzheimer’s disease and other forms of dementia affect more than 35 million people around the globe, according to the World Health Organization. Despite the persistent nature of this problem, says study leader Rebecca F. Gottesman, M.D., Ph.D., an associate professor of neurology and epidemiology at the Johns Hopkins University School of Medicine, no truly effective treatment exists. Research suggests that vascular disease, already known to cause heart attacks and strokes, also contributes to dementia’s pathology. However, she says, researchers are still unclear about the details of this association and whether treatments that target high blood pressure, also known as hypertension, might also prevent dementia.
To investigate, Gottesman and her colleagues used data from the Atherosclerosis Risk in Communities Study (ARIC), a long-term study started in the late 1980s that’s followed more than 15,000 adults over 25 years. ARIC, originally designed to track how risk factors for atherosclerosis might lead to later cardiovascular disease, has also included assessments of the volunteers’ cognitive skills over the years, a window into cognitive change.
With these data, the researchers investigated how blood pressure measurements taken five times over the course of ARIC — the first taken when subjects were between 48 and 67 years old — correlated with the results of three cognitive tests participants took several times over the course of the study period.
Their findings, published in the Aug. 4 issue of JAMA Neurology, showed that even though all the participants had some cognitive decline over time — an inevitable part of old age — those who had hypertension in those first blood pressure readings during midlife had a 6.25 percent steeper decline than those whose blood pressure readings were normal.
“It may not seem like a huge effect, but that’s just the average amount of cognitive decline,” Gottesman explains. “Some people probably have a significantly larger amount of decline. Since the number of people with hypertension is huge on a population scale, that leads to a lot of people with hypertension-related dementia.”
Having hypertension only during the most recent blood pressure readings, when subjects were in their 70s to 90s, didn’t affect the rate of cognitive decline. When the researchers used statistical methods to account for study participants who dropped out or died over time, it strengthened these results, emphasizing the importance of midlife blood pressure on cognitive decline risk.
The good news, Gottesman says, is that at least some of the decline may be preventable by controlling blood pressure early. The team’s results also showed that ARIC participants who took blood pressure-lowering drugs had less cognitive decline than those whose high blood pressure was uncontrolled — another reason to aggressively treat hypertension, particularly in middle age.
“The take-home message is that we need to pay attention to hypertension at a relatively young age, long before the health problems of old age set in,” Gottesman says. “People should really know what their blood pressure is and what their doctor plans to do if it’s elevated.”
Other Johns Hopkins researchers who participated in this study include Andrea L. C. Schneider, Marilyn Albert, Karen Bandeen-Roche, Josef Coresh, Melinda C. Power, Andreea Rawlings and A. Richey Sharrett.
The ARIC Study is part of a collaborative study supported by contracts HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C from the National Heart, Lung and Blood Institute (NHLBI). Neurocognitive data collection was supposed by contracts U01 HL096812, HL096814, HL096899, HL096917 from the NHLBO and the National Institute of Neurological Disorders and Stroke and previous magnetic resonance imaging examinations of the brain were supported by contract R01-HL70825 from the NHLBI. This study was also supported by contract T32HL007024 from the NHLBI, NIH (Dr. Schneider and Ms. Rawlings) and by contract T32AG027668 from the National Institute on Aging, NIH. (Dr. Power.)