New research led by the University of California (UC) Davis found accelerated brain aging among young middle-aged people with high blood pressure, and even among those whose blood pressure would not be considered high enough to warrant clinical intervention. The researchers say their findings emphasize the need for “early and optimum control of blood pressure”.
Reporting in The Lancet‘s 2 November online issue, senior author Charles DeCarli, professor of neurology and director of the Alzheimer’s Disease Center at UC Davis, and colleagues, describe how they found evidence of structural damage in white matter and volume of gray matter in the brains of hypertensive and prehypertensive people in their 30s and 40s that suggests vascular brain injury “develops insidiously over the lifetime with discernible effects”.
The study is thought to be the first to show structural damage to the brains of people in young middle age as a result of high blood pressure. Such damage has been linked with cognitive decline in older people.
DeCarli says in a statement:
“The message here is really clear: people can influence their late-life brain health by knowing and treating their blood pressure at a young age, when you wouldn’t necessarily be thinking about it.”
“The people in our study were cognitively normal, so a lack of symptoms doesn’t mean anything.”
High Blood Pressure and Cognitive Decline
Normal blood pressure is up to 120/80 (“one twenty over eighty”: the first number being the systolic pressure, when the heart is contracting, and the second being the diastolic pressure, when the heart is resting). Prehypertension lies in the range 120-139/80-89, while blood pressures above 140/90 are classed as high (hypertension).
High blood pressure is linked to a 62% higher risk of cerebrovascular disease such as ischemic stroke, and a 49% higher risk of cardiovascular disease. It is the single greatest risk factor for premature death in the US, where it affects some 50 million people.
Previous studies have shown links between high blood pressure and a raised chance of brain injury and wasting away (atrophy), which in turn leads to reduced ability in thinking and memory, and a greater risk of developing dementia. High blood pressure is therefore indirectly an important risk factor for cognitive decline later in life, but it is a modifiable one because it can be treated.
The researchers say there is evidence that treating high blood pressure in middle age can prevent cognitive decline and dementia later.
For their study, DeCarli and colleagues analyzed data on 579 people taking part in the Framingham Heart Study, a longitudinal investigation that started following the cardiovascular health of people living in Framingham, Massachusetss, over 60 years ago. The study is now in its third generation of participants.
The participants were mostly in their late 30s when they were joined this part of the study, in 2009.
They had their blood pressure taken on entry, and were at that time assigned to one of three groups: normal blood pressure, prehypertensive, or high blood pressure. The researchers also noted their smoking status and if they were taking any medication for blood pressure.
After that, the participants underwent magnetic resonance imaging (MRI) brain scans that took extensive measurements of any white matter injury and gray matter.
Detailed Scans of White Matter
Some of the MRI scans were of a type known as “diffusion tensor imaging” that examines in microscopic detail the architecture of the brain’s white matter.
The white matter of the brain comprises the axons, the long filaments that carry electrical signals from one area of the brain to another. Diffusion tensor imaging yields a measure known as “fractional anisotropy”, which can sense whether axons are damaged or intact. It can be regarded as a measure of connectivity in the brain.
There is also another type of MRI scan that shows damaged white matter as areas of intense whiteness, or “white-matter hyperintensities”.
When combined, the various imaging studies of white and gray matter produced a global measure that allowed comparison of of brain health among the different blood pressure groups.
When they analyzed the results, the researchers found that the brains of the people in the high blood pressure were significantly less healthy than those of the normal blood pressure group: in fact they looked like they had aged more.
For example, the brain of a typical 33-year-old member of the high blood pressure group, looked similar on the scans to the brain of a typical 40-year-old in the normal blood pressure group.
The more detailed measures showed that the brains of the people in the high blood pressure group had an average 6.5% reduction of fractional anisotropy in the frontal lobes. They also, on average, had 9% less gray matter, in the frontal and temporal lobes, compared to the normal blood pressure group.
The researchers did not propose a mechanism for how high blood pressure might cause the brain to age more quickly. But they did mention that high blood pressure leads to stiffer arteries, which in turn impedes blood flow, so the axons receive less oxygen and essential nutrients.
Lead author Pauline Maillard, a postdoctoral fellow in the UC Davis Department of Neurology, says the findings suggest the microscopic white matter damage that has been linked to high blood pressure in the elderly in other studies may be detectable earlier in life.
This supports the idea that “vascular brain injury may develop insidiously over several decades”, says Maillard, and that there is a need for “early and optimum control of blood pressure, which is neither routinely achieved nor subject to testing in randomized controlled clinical trials”.
Written by Catharine Paddock PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today
“Effects of systolic blood pressure on white-matter integrity in young adults in the Framingham Heart Study: a cross-sectional study”; Pauline Maillard, Sudha Seshadri, Alexa Beiser, Jayandra J Himali, Rhoda Au, Evan Fletcher, Owen Carmichael, Philip A Wolf, Charles DeCarli; The Lancet Neurology, 2 November 2012; DOI: 10.1016/S1474-4422(12)70241-7; Link to Abstract
Additional source: University of California – Davis Health System.
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