scholarly journals Methods to Address Self-Selection and Reverse Causation in Studies of Neighborhood Environments and Brain Health

Author(s):  
Lilah M. Besser ◽  
Willa D. Brenowitz ◽  
Oanh L. Meyer ◽  
Serena Hoermann ◽  
John Renne

Preliminary evidence suggests that neighborhood environments, such as socioeconomic disadvantage, pedestrian and physical activity infrastructure, and availability of neighborhood destinations (e.g., parks), may be associated with late-life cognitive functioning and risk of Alzheimer’s disease and related disorders (ADRD). The supposition is that these neighborhood characteristics are associated with factors such as mental health, environmental exposures, health behaviors, and social determinants of health that in turn promote or diminish cognitive reserve and resilience in later life. However, observed associations may be biased by self-selection or reverse causation, such as when individuals with better cognition move to denser neighborhoods because they prefer many destinations within walking distance of home, or when individuals with deteriorating health choose residences offering health services in neighborhoods in rural or suburban areas (e.g., assisted living). Research on neighborhood environments and ADRD has typically focused on late-life brain health outcomes, which makes it difficult to disentangle true associations from associations that result from reverse causality. In this paper, we review study designs and methods to help reduce bias due to reverse causality and self-selection, while drawing attention to the unique aspects of these approaches when conducting research on neighborhoods and brain aging.

2020 ◽  
Vol 2 (1) ◽  
pp. 585-614
Author(s):  
Caleb E. Finch ◽  
Todd E. Morgan

Brain development is impaired by maternal exposure to airborne toxins from ambient air pollution, cigarette smoke, and lead. Shared postnatal consequences include gray matter deficits and abnormal behaviors as well as elevated blood pressure. These unexpectedly broad convergences have implications for later life brain health because these same airborne toxins accelerate brain aging. Gene-environment interactions are shown for ApoE alleles that influence the risk of Alzheimer disease. The multigenerational trace of these toxins extends before fertilization because egg cells are formed in the grandmaternal uterus. The lineage and sex-specific effects of grandmaternal exposure to lead and cigarettes indicate epigenetic processes of relevance to future generations from our current and recent exposure to airborne toxins.


2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 164-164
Author(s):  
Sarah Tom ◽  
Amol Mehta ◽  
Stepanie Izard ◽  
Paul Crane ◽  
David Bennett ◽  
...  

Abstract While higher life course socioeconomic status (SES) is associated with lower Alzheimer’s Disease (AD) risk, relationships with AD-related neuropathological lesions are unclear. We hypothesize that high SES in early, mid and late life will be associated with lower frequency of AD-related pathological lesions. The Rush Memory and Aging Project is a cohort of 2025 people age ≥ 65 years from Northeastern Illinois recruited 1997 – 2018; 972 participants died. We created binary variables for Braak stage (0-II versus III-VI), NIA-Reagan score (low likelihood/no AD pathology versus high/intermediate likelihood), presence of microinfarcts and, separately, macroinfarcts, and life course SES based on median for late life (baseline income), midlife (income at age 40 years), and early life (composite of parental education and number of siblings). Logistic regression models adjusted for ages at baseline and death, sex, presence of APOE-Ɛ4 alleles, and separately, vascular factors and education. Of 761 participants with relevant data, 69% were women, and mean ages at baseline and death were 83 + 6 years and 90 + 6 years, respectively. High early life SES was related to lower frequency of AD pathology (OR= 0.69, 95% CI 0.50, 0.96) and macroinfarcts (OR= 0.69, 95% CI 0.51, 0.94). Results were similar when adjusting for vascular factors; adjustment for education modestly attenuated these associations. Mid-life and late life SES were not associated with AD-related neuropathological lesions. High early life SES was related to lower frequency of AD pathology and macroinfarct presence. Environment during early development may influence later life brain aging.


BMC Urology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Saira Khan ◽  
K. Y. Wolin ◽  
R. Pakpahan ◽  
R. L. Grubb ◽  
G. A. Colditz ◽  
...  

Abstract Background Existing evidence suggests that there is an association between body size and prevalent Benign Prostatic Hyperplasia (BPH)-related outcomes and nocturia. However, there is limited evidence on the association between body size throughout the life-course and incident BPH-related outcomes. Methods Our study population consisted of men without histories of prostate cancer, BPH-related outcomes, or nocturia in the intervention arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) (n = 4710). Associations for body size in early- (age 20), mid- (age 50) and late-life (age ≥ 55, mean age 60.7 years) and weight change with incident BPH-related outcomes (including self-reported nocturia and physician diagnosis of BPH, digital rectal examination-estimated prostate volume ≥ 30 cc, and prostate-specific antigen [PSA] concentration > 1.4 ng/mL) were examined using Poisson regression with robust variance estimation. Results Men who were obese in late-life were 25% more likely to report nocturia (Relative Risk (RR): 1.25, 95% Confidence Interval (CI): 1.11–1.40; p-trendfor continuous BMI < 0.0001) and men who were either overweight or obese in late-life were more likely to report a prostate volume ≥ 30 cc (RRoverweight: 1.13, 95% CI 1.07–1.21; RRobese: 1.10, 95% CI 1.02–1.19; p-trendfor continuous BMI = 0.017) as compared to normal weight men. Obesity at ages 20 and 50 was similarly associated with both nocturia and prostate volume ≥ 30 cc. Considering trajectories of body size, men who were normal weight at age 20 and became overweight or obese by later-life had increased risks of nocturia (RRnormal to overweight: 1.09, 95% CI 0.98–1.22; RRnormal to obese: 1.28, 95% CI 1.10–1.47) and a prostate volume ≥ 30 cc (RRnormal to overweight: 1.12, 95% CI 1.05–1.20). Too few men were obese early in life to examine the independent effect of early-life body size. Later-life body size modified the association between physical activity and nocturia. Conclusions We found that later-life body size, independent of early-life body size, was associated with adverse BPH outcomes, suggesting that interventions to reduce body size even late in life can potentially reduce the burden of BPH-related outcomes and nocturia.


2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Aliabbas Zia ◽  
Ali Mohammad Pourbagher-Shahri ◽  
Tahereh Farkhondeh ◽  
Saeed Samarghandian

AbstractAging is the leading risk factor for several age-associated diseases such as neurodegenerative diseases. Understanding the biology of aging mechanisms is essential to the pursuit of brain health. In this regard, brain aging is defined by a gradual decrease in neurophysiological functions, impaired adaptive neuroplasticity, dysregulation of neuronal Ca2+ homeostasis, neuroinflammation, and oxidatively modified molecules and organelles. Numerous pathways lead to brain aging, including increased oxidative stress, inflammation, disturbances in energy metabolism such as deregulated autophagy, mitochondrial dysfunction, and IGF-1, mTOR, ROS, AMPK, SIRTs, and p53 as central modulators of the metabolic control, connecting aging to the pathways, which lead to neurodegenerative disorders. Also, calorie restriction (CR), physical exercise, and mental activities can extend lifespan and increase nervous system resistance to age-associated neurodegenerative diseases. The neuroprotective effect of CR involves increased protection against ROS generation, maintenance of cellular Ca2+ homeostasis, and inhibition of apoptosis. The recent evidence about the modem molecular and cellular methods in neurobiology to brain aging is exhibiting a significant potential in brain cells for adaptation to aging and resistance to neurodegenerative disorders.


2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 439-439
Author(s):  
Changmin Peng ◽  
Sae Hwang Han ◽  
Jeffrey Burr

Abstract Neighborhood environments shape the availability of resources for social engagement and social interaction, which are associated with better health outcomes. However, these contextual factors are also considered sources of potential social distress and tension, increasing the risk of subsequent health deficits, including cognitive decline. Our understanding of the linkage between childhood neighborhood environments and cognitive functioning in later life is limited. This study employed three waves of nationally representative data from the China Health and Retirement Longitudinal Study (2011-2015; N = 11,105) to investigate the relationship between self-reported neighborhood social cohesion during childhood (i.e., neighborhood safety, neighbors willing to help, and close-knit neighborhood) and cognitive functioning (Chinese version of TICS). We employed latent growth curve modeling to test hypotheses relating to life course models of childhood conditions and later life cognitive functioning (the long arm of childhood). The results showed that perceptions regarding the willingness of neighbors to help and close-knit neighborhood characteristics during childhood were positively associated with levels of later life cognitive function. Further, growing up in a neighborhood characterized by the willingness of neighbors to help others was negatively associated with the rate of cognitive decline, net of childhood and adulthood covariates. Self-report of neighborhood safety during childhood was unrelated to cognitive function (level and change). These findings underscored the long-term ramifications of childhood conditions as potential risk factors for later-life cognitive health. Social cohesion at the neighborhood level as experienced during childhood may be a protective factor for healthy cognitive aging among older Chinese adults.


Gerontology ◽  
2018 ◽  
Vol 64 (6) ◽  
pp. 576-588
Author(s):  
Deirdre A. Robertson ◽  
David Weiss

Background: Social status is the standing of a person or group in the social hierarchy, and is perceived to change across the life span from low social status in early life, to peak in midlife, and to a decline thereafter. As threats to subjective social status are known to be detrimental to individuals’ health, it is important to better understand how older adults perceive themselves and others in terms of age-related social status. Objective: We examined status ambivalence – the potential discrepancy between how older adults’ perceive social status for themselves compared to older adults in general. Method: Study 1 used qualitative data from 37 semi-structured interviews with older adults to assess perceptions of social status. Study 2 used quantitative survey data from 114 older adults who completed explicit and implicit measures of social status. Results: Study 1 (n = 37, meanage = 71.72, SDage = 5.69; 81.1% women) provided preliminary evidence for status ambivalence such that older adults reported unequivocal low social status for other older adults but a more ambivalent perception of their own social status. Study 2 (n = 114, meanage = 64.32, SDage = 8.98, 57.9% women) compared implicit and explicit measures of social status revealing that older adults consistently perceive older adults to have low social status but again show a more ambivalent perception of their own social status. Conclusion: We discuss status ambivalence as a potential protective mechanism in the context of negative societal perceptions of age-related social status that may be important for well-being in later life.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Oluwaseun E Fashanu ◽  
Di Zhao ◽  
Andrea L Schneider ◽  
Andreea M Rawlings ◽  
Richey A Sharrett ◽  
...  

Background: Prior cross-sectional studies among older adults have found associations between low vitamin D (vitD) levels and reduced cognitive performance but were unable to distinguish the temporal order between vitD and the onset of dementia. We examined the association between mid-life vitD levels, assessed by serum 25-hydroxyvitD, with later life performance on neuropsychological testing. Methods: We conducted a non-concurrent cross-sectional analysis of 5,887 white and black participants enrolled in the ARIC Neurocognitive Study. We included participants who had serum vitD concentrations measured at visit 2 (1990-1992; age range 47-69 years) and who had neuropsychological and functional testing at visit 5 (2011-2013; age range 67-91 years). Neuropsychological tests were grouped into memory, language, and executive function domains and were standardized. We categorized vitD using clinical cut points as deficient (<20 ng/mL), intermediate (20-<30 ng/mL), or sufficient (≥ 30 ng/mL). We used Poisson and linear regression models adjusted for demographic and socioeconomic factors to examine the associations between vitD with prevalent dementia and performance on neuropsychological testing. Results: In mid-life, the mean (SD) age of participants was 56 (5) years, 60% were female, and 22% black. Mean (SD) vitD was 24.6 (8.4) ng/mL; 30% had deficient, 46% intermediate, and 24% sufficient vitD levels. Compared to participants with sufficient vitD levels, the prevalence ratios (95% CI) of late-life dementia were 1.35 (0.99, 1.84) and 1.27 (0.90, 1.80) for participants with intermediate and deficient vitD levels, respectively. We found no significant association between mid-life vitD and late-life performance on neuropsychological testing ( Table ). Further adjustments for cardiovascular, genetic, and metabolic factors yielded similar results. Conclusion: In this cohort, mid-life serum vitD levels were not associated with prevalent dementia or with performance on neuropsychological testing 20 years later.


2021 ◽  
Vol 50 (Supplement_2) ◽  
pp. ii5-ii7
Author(s):  
Q Dercon ◽  
J Nicholas ◽  
S-N James ◽  
J Schott ◽  
M Richards

Abstract Introduction Grip strength is an objective measure of physical function with potential predictive value for health in ageing populations. We aimed to assess whether levels and changes in grip strength from midlife predicted later-life brain health and cognition. Methods 446 participants in an ongoing British birth cohort study, the MRC National Survey of Health and Development (NSHD), had their maximum grip strength measured at ages 53, 60–64, and 69, and underwent neuroimaging as part of its neuroscience sub-study, Insight 46, at 69–71. A group-based trajectory model identified latent groups of individuals in the whole NSHD cohort with below- and above-average grip strength over time, plus a reference group. Trajectory group membership, plus standardised grip strength levels and change from age 53, were each related to MRI-derived measures of whole-brain volume (WBV) and white-matter hyperintensity volume (WMHV), plus several cognitive tests. Models were adjusted for sex, body size, head size (where appropriate), sociodemographics, and behavioural and vascular risk factors. Results Consistently below-average grip strength from midlife was associated with lower WBV and non-verbal reasoning ability at age 69–71 (e.g. low group WBV vs. reference group β = −13.38 cm^3; 95% CI = (−24.12 cm^3, −2.64 cm^3); p = 0.015). There was some accompanying evidence that above-average maximum grip strength showed a positive association with WBV, which was more pronounced in female participants (high group female WBV vs. reference group β = 18.30 cm^3; 95% CI = (1.34 cm^3, 35.29 cm^3); p = 0.034). Steeper than average declines in grip strength between 53 and 69 were additionally weakly associated with an estimated 10% higher WMHV at age 69–71 (β = 1.10, 95% CI = (1.00, 1.22); p = 0.053). Conclusion This study provides preliminary evidence that tests of maximum grip strength may have value in predicting brain health. Future work should assess how these observed differences relate to later-life negative health outcomes, and whether changes in grip strength reflect concurrent changes in brain structure and connectivity.


Sign in / Sign up

Export Citation Format

Share Document