Relationships Between Sedentary Behavior, Physical Activity, and White Matter Hyperintensities in the Brain
A broad array of epidemiological evidence indicates that greater time spent being sedentary and inactive harms long-term health and increases mortality risk. Equally, a similar body of evidence indicates that greater physical activity has the opposite effect, at least up to a point that is far above the level of activity that most people undertake in their day to day lives. When looking at any specific aspect of age-related disease and functional decline, one might expect to find the same patterns, and indeed there are any number of studies in which this is the case.
Today's open access paper considers sedentary behavior and physical activity in the context of white matter hyperintensities, areas of damage in the brain produced by rupture of capillaries and related vascular issues. People accumulate these lesions as they age, each one unnoticed when it happens, but this damage accumulates to harm the function of the brain. As one might expect, more activity correlates with less of this damage to the brain, and the researchers speculate on the usual suspects when it comes to underlying mechanisms.
White matter hyperintensity (WMH) volume measured with magnetic resonance imaging (MRI) serves as a significant indicator of the extent of cerebral white matter lesions, typically associated with ischemia due to small vessel disease. WMHs are frequently found in older cognitively unimpaired individuals, are linked with worse cognitive performance, particularly executive functions and processing speed, are associated with genetic risk of neurodegenerative disease, and can potentially impact both the onset and advancement of dementia related to both Alzheimer's disease (AD) and cerebrovascular disease (CVD). Here, we examine the potential associations of physical activity (PA) and sedentary behaviors (SBs), two modifiable lifestyle factors, with WMH volumes in middle-aged to older adults. In the UK Biobank, we found associations of both moderate-to-vigorous physical activity (MVPA) and SB with WMH volume, and the associations are not fully independent of each other.
A large number of studies have shown that engaging in greater amounts of MVPA is associated with improved vascular health and that SB is associated with vascular pathology and chronic disease. One potential vascular mechanism that could underlie these results is that MVPA may increase cerebral blood flow, which in turn may help prevent the development of high WMH loads. SB, on the other hand, has been linked with reduced cerebral blood flow which may lead to increased lesion load, though this finding has not been consistently replicated.
Our results also align with the growing body of literature emphasizing the synergistic effects of higher PA and reduced SB on various health outcomes. While previous studies have independently linked excessive SB and lack of MVPA with adverse brain health, our study demonstrates how these behaviors interact in their associations with WMH volumes. It is possible that the mechanisms linking PA and SB with WMH volumes may only partially overlap. For example, while both SB and MVPA have been linked with cerebral blood flow and vascular health in previous work, MVPA is also associated with the upregulation of neurotrophic factors (eg, Brain Derived Neurotrophic Factor or BDNF) that may provide additional compensatory protection against the impact of increased WMH volumes.
While our study was not designed to determine whether mechanistic pathways are fully or partially independent, the interactions found here suggest more work is needed to better understand how these two lifestyle behaviors may differentially impact brain lesion loads that may, in turn, influence the risk for cognitive decline and dementia related to both AD and CVD. Overall, our results highlight the importance of considering interactions between these key modifiable behaviors when examining their associations with brain health outcomes.
I suppose that I am skeptical of the idea that the same behaviours and mechanisms that make unhealthy people (early or later stages of some pathologies, obvious statistical low-performance health data, etc.,) into healthy people (full physical and mental functionality, obvious evidence of robust internal repair mechanisms ongoing) through lifestyle changes can be automatically extrapolated to those individuals experiencing top 10% functionality up to and including living to top 10% life span (> 95 yrs). The behaviours may show obvious correlations, but I am unconvinced that advanced aging is 'exclusively' the same as top 1% health 'going in' to advanced age. Healthy people may statistically be more likely to get to 100+ but the number of comparable top healthy people who should live over 100 appears to be less predictable (interesting to see how people who are in the top 1% healthy from 30 onwards are able to live into the top <1% of life expectanices - probably a weak correlation).