There is a good deal of evidence to show that lifestyle choices such as lack of exercise and putting on excess weight accelerate the decline of the brain. Lack of exercise means a more rapid deterioration in blood vessel integrity, and that in turn causes a growing number of tiny lesions in the brain, damage that adds up year by year until the cognitive effects become noticeable. Excess visceral fat tissue does the same thing via other mechanisms, spurring chronic inflammation that corrodes blood vessel structure. It does a lot more besides - most age-related conditions are accelerated by greater levels of inflammation, and that is handily provided by a fat and sedentary life.
Better lifestyle choices can add years of health and life expectancy per the consensus epidemiological data. You can't exercise your way to reliably living to age 90 or 100, however, and you're still going to be severely impacted by degenerative aging when you get there. So why bother? Well, for one, because you'll likely undergo much less pain, suffering, and frailty along the way. Perhaps more importantly, however, this is an age of very rapid, accelerating progress in medical biotechnology. A few years counts when that is how long it takes to develop a prototype therapy, or for a well-supported set of clinical trials to run to completion, or for a medical business to start up and put its products into the global supply chain. A few years means the difference between today's technology and the next version. As we move into an era in which researchers are now trying to treat the causes of aging with increasing vigor, it becomes an ever better idea to improve your own personal odds of living to see the results.
People with poor physical fitness in their 40s may have lower brain volumes by the time they hit 60, an indicator of accelerated brain aging. "Many people don't start worrying about their brain health until later in life, but this study provides more evidence that certain behaviors and risk factors in midlife may have consequences for brain aging later on." A subset of 1,271 participants from the Framingham Offspring Study participated in exercise treadmill testing in the 1970s, when their average age was 41. Starting in 1999, when their average age was 60, they underwent magnetic resonance imaging (MRI) of their brains as well as cognitive tests. The participants did not have heart disease or cognitive problems at the beginning of the study, and none were taking medication that alters heart rate.
In individuals with low fitness levels, the blood pressure and heart rate responses to low levels of exercise are often much higher than in individuals with better fitness. The researchers found that people who had a lower fitness level or greater increase in diastolic blood pressure (bottom number) or heart rate a few minutes into the low-intensity treadmill test (2.5 miles an hour) had smaller brain tissue volume later in life. People who had a larger increase in diastolic blood pressure during low-intensity exercise also performed more poorly on a cognitive test for decision-making function later in life.
The study associates heart function with the development of dementia and Alzheimer's disease. Participants with decreased heart function, measured by cardiac index, were two to three times more likely to develop significant memory loss over the follow-up period. "Cardiac index is a measure of heart health. It reflects cardiac output or the amount of blood that leaves the heart and is pumped through the body taking into consideration a person's body size. A low cardiac index value means there is less blood leaving the heart."
"We thought heart disease might be driving the increased risk of dementia and Alzheimer's disease. When we excluded participants with heart disease and other heart conditions, we were surprised that the risk of dementia and Alzheimer's disease got even worse. The risk we found between lower cardiac index and the development of dementia may reflect a subtle but protracted process that occurs over decades - essentially a lifetime burden of subtle reductions in oxygen and nutrient delivery to the brain."
Despite a wealth of research into why caloric restriction extends life, we are still rather far from pinpointing the mechanism behind the longevity effect of this dietary intervention. Of significant interest is how diets may affect aging in the brain, which is particularly sensitive to alterations in energy availability. Caloric restriction attenuates the progression of Alzheimer's disease in mouse models, for example, while diet-induced obesity exacerbates symptoms. By studying the influence of diet on aging in the brain, researchers have discovered a number of bioenergetic molecules and druggable targets that may serve as candidates for interventions to delay the onset of neurodegenerative disorders.
Calorie-restricted animals are smaller than their well-fed counterparts, perhaps corresponding to decreased cell proliferation, a phenomenon that occurs in response to energy deficits in both normal and cancer cells. Decreased cell proliferation may be important, as it also leads to slower division of stem cells, allowing these progenitor cell populations to supply the various cell types of the body for longer periods of time. This sparing of stem-cell pools could explain why dietary restriction is particularly effective in maintaining tissue homeostasis in rapidly proliferating tissues such as skin, hair, and bone marrow. Neural tissues, such as the brain and spinal cord, have a limited capacity to rejuvenate themselves through stem-cell renewal, however, perhaps explaining why dietary restriction may not impact these areas of the body as much as others.