Research papers and popular science articles noting the ongoing decline in dementia risk have become a regular occurrence. Since dementia is driven in part by cardiovascular aging, it is tempting to suggest that this is a side-effect of the improvements in control over blood pressure and treatment of cardiovascular disease obtained in recent decades. From studies that have run the numbers, that incremental progress is as much due to reductions in smoking as it is to the deployment of successful medications such as statins. We do not yet live in an age in which medical technology has reliably outpaced lifestyle choice in the matter of aging and age-related disease. Interesting, those researchers who run the numbers on dementia suggest that improvements in cardiovascular health cannot explain all of the reduction in dementia risk.
Cardiovascular decline contributes to dementia in a number of ways. Firstly, capillary networks spread throughout tissues become less dense, and so less able to deliver sufficient nutrients and oxygen to cells. Declining fitness and heart failure achieve a similar outcome, in different ways. Blood vessels become less elastic with age, causing the increase in blood pressure known as hypertension. Blood vessel walls become compromised by the fatty plaques of atherosclerosis, initially seeded by an excessive inflammatory reaction to oxidized lipids in the bloodstream, but eventually growing to distort, narrow, and block blood vessels. The combination of increased blood pressure and weakened blood vessels is damaging to sensitive tissues, causing cell death and structural harm. In the brain, aging is accompanied by many tiny, silent strokes, each destroying a minuscule section of brain tissue - but it adds up over time.
Considering the damage done by the above processes, what might account for the missing benefits that do not arise from either slowing or compensating for cardiovascular degeneration in aging? Age-related dysfunction of the immune system might be a candidate. All neurodegenerative disease appears to have an inflammatory component, and the immune system of the central nervous system is arguably far more complex and far more involved in correct function of tissue than is the case elsewhere in the body. Further, better lifestyle choices and better control over infectious disease may well lead to, all other things being equal, a slower decline into immunosenescence. This is speculative thinking, however, and a thesis that would have to be proven from the data.
A recently released study indicates that dementia's impact might be compressing a bit. That is, people might be developing dementia later and living with it for a shorter period of time. In data from four different time periods over a period of 30 years, the mean age at dementia onset increased, while the length of time living with dementia decreased. Is it because prevention and care of stroke today is superior compared to decades ago? Stroke is a major risk factor for dementia.
"Prevention of stroke and reduced impact of stroke are great advances, but neither completely explains the trend we are seeing. We are looking at other causes, such as lower burden of multiple infections because of vaccination, and possibly lower levels of lead or other pollutants in the atmosphere. Early education and nutrition might also play a role. Stroke risk has decreased because of greater control of blood pressure. In the past, if you had a stroke you were at 90 percent greater risk to develop dementia. Today, you have a 40 percent greater risk."
A total of 5,205 participants from the Framingham Original and Offspring cohorts were studied. Four epochs were considered from 1977-1984 to 2004-2008. Gender and education adjusted 5-year mortality risks were estimated using delayed entry Cox models with the earliest epoch as reference category. Stratified analyses by sex, education, and age were undertaken. A nested case control study of 317 dementia cases and 317 controls matched on age, gender and epoch was initiated.
In the whole sample, 5-year mortality risk has decreased with time, it was 33% lower in the last epoch compared to the earliest. In the 317 persons who developed dementia, age at onset increased (1.5 years/epoch), and years alive with dementia decreased (1 year/epoch) over time. We observed however, a decreased adjusted relative mortality risk (by 18%) in persons with dementia in 1986-1991 compared to 1977-1983 and no significant change from then to the latest epoch. The nested case control study suggested in matched controls that 5-year mortality relative risk had increased by 60% in the last epoch compared to Epoch 1.
In conclusion, in the Framingham Heart Study population, in the last 30 years, disease duration in persons with dementia has decreased. However, age-adjusted mortality risk has slightly decreased after 1977-1983. Consequences of such trends on dementia prevalence should be investigated.