scholarly journals Nine-Year Ethanol Intake Trajectories and Their Association With 15-Year Cognitive Decline Among Black and White Adults

2020 ◽  
Vol 189 (8) ◽  
pp. 788-800
Author(s):  
Shelly-Ann M Love ◽  
Kari E North ◽  
Donglin Zeng ◽  
Natalia Petruski-Ivleva ◽  
Anna Kucharska-Newton ◽  
...  

Abstract Faster rates of age-related cognitive decline might result in early onset of cognitive impairment and dementia. The relationship between ethanol intake and cognitive decline, although studied extensively, remains poorly understood. Previous studies used single measurements of ethanol, and few were conducted in diverse populations. We assessed the association of 9-year trajectories of ethanol intake (1987–1998) with 15-year rate of decline in cognitive performance from mid- to late life (1996–2013) among 2,169 Black and 8,707 White participants of the US Atherosclerosis Risk in Communities study using multivariable linear regression models. We hypothesized that stable, low to moderate drinking would be associated with lesser 15-year cognitive decline, and stable, heavy drinking with greater 15-year cognitive decline. Stable, low to moderate drinking (for Blacks, adjusted mean difference (MD) = 0.03 (95% confidence interval (CI): −0.13, 0.19); for Whites, adjusted MD = 0.02 (95% CI: −0.05, 0.08)) and stable, heavy drinking (for Blacks, adjusted MD = 0.08 (95% CI: −0.34, 0.50); for Whites, adjusted MD = −0.03 (95% CI: −0.18, 0.11)) in midlife compared with stable never-drinking were not associated with 15-year decline in general cognitive function from mid- to late life. No association was observed for the stable former and “mostly” drinking trajectories with 15-year cognitive decline. Stable low, low to moderate, and stable heavy drinking in midlife are not associated with lesser and greater cognitive decline, respectively, from mid- to late life among Black and White adults.

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 296-296
Author(s):  
Caroline Hartnett

Abstract Cognitive decline common in the U.S. and greatly impacts quality of life, both for those who experience it and for those who care for them. Black Americans experience higher burdens of cognitive decline but the mechanisms underlying this disparity have not been fully elucidated. Stress experienced in early life is a promising explanatory factor, since stress and cognition are linked, childhood stressors been shown to have a range of negative implications later in life, and Black children experience more childhood stressors than White children, on average. In this paper, we use data from the Behavioral Risk Factor Surveillance System (BRFSS) to examine whether stressful experiences in childhood help explain Black-White disparities in memory loss. These data were available for 5 state-years between 2011 and 2017 (n=11,708). Preliminary results indicate that, while stressful childhood experiences are strongly associated with memory loss, stressful experiences do not mediate the association between race and memory loss. However, race does appear to moderate the association between stressful childhood experiences and memory loss. Specifically, stressful experiences are associated with a higher likelihood of memory loss for Black adults compared to White adults.In addition, there seem to be some noteworthy patterns across different types of experiences (i.e. parental drinking may predict later memory loss more strongly for Black adults than White adults, but parental hitting may predict memory loss more strongly for White adults than Black adults).


2021 ◽  
Author(s):  
Raihaan Patel ◽  
Clare E. Mackay ◽  
Michelle G. Jansen ◽  
Gabriel A. Devenyi ◽  
M. Clare O’Donoghue ◽  
...  

AbstractWhile all individuals are susceptible to age-related cognitive decline, significant inter- and intra-individual variability exists. However, the sources of this variation remain poorly understood. Here, we examined the association between 30-year trajectories of cognitive decline and multimodal indices of brain microstructure and morphology in older age. We used the Whitehall II Study, an extensively characterised cohort using 3T brain magnetic resonance images acquired at older age (mean age = 69.52 ± 4.9) and 5 repeated cognitive performance assessments between mid-life (mean age = 53.2 ± 4.9 years) and late-life (mean age = 67.7 ± 4.9). Using non-negative matrix factorization, we identified 10 brain microstructural components that integrate measures of cortical thickness, surface area, fractional anisotropy, and mean and radial diffusivities. We observed two modes of variance that describe the association between cognition and brain microstructure. The first describes variations in 5 microstructural components associated with low mid-life performance across multiple cognitive domains, decline in reasoning abilities, but a relative maintenance of lexical and semantic fluency from mid-to-late life. The second describes variations in 5 microstructural components that are associated with low mid-life performance in lexical fluency, semantic fluency and short-term memory performance, but a retention of abilities in multiple domains from mid-to-late life. The extent to which a subject loads onto a latent variables predicts their future cognitive performance 3.2 years later (mean age = 70.87 ± 4.9). This data-driven approach highlights a complex pattern of brain-behavior relationships, wherein the same individuals express both decline and maintenance in function across cognitive domains and in brain structural features.Significance StatementAlthough declines in cognitive performance are an established aspect of aging, inter- and intra-individual variation exists. Nevertheless, the sources of this variation remain unclear. We analyse a unique sample to examine associations between 30-year trajectories of cognitive decline and multimodal indices of brain anatomy in older age. Using data-driven techniques, we find that age-related cognitive decline is not uniform. Instead, each individual expresses a mixture of maintenance and decline across cognitive domains, that are associated with a mixture of preservation and degeneration of brain structure. Further, we find the primary determinants of late-life cognitive performance are mid-life performance and higher brain surface area. These results suggest that early and mid-life preventative measures may be needed to reduce age-related cognitive decline.


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.


2012 ◽  
Vol 8 (4S_Part_4) ◽  
pp. P147-P147
Author(s):  
Mathew Summers ◽  
Michael Valenzuela ◽  
Jeffery Summers ◽  
Karen Ritchie ◽  
Tracey Dickson ◽  
...  

Diabetes Care ◽  
2017 ◽  
Vol 40 (12) ◽  
pp. 1661-1667 ◽  
Author(s):  
Alexandra K. Lee ◽  
Clare J. Lee ◽  
Elbert S. Huang ◽  
A. Richey Sharrett ◽  
Josef Coresh ◽  
...  

2013 ◽  
Vol 9 ◽  
pp. P699-P700
Author(s):  
Patricia Boyle ◽  
Robert Wilson ◽  
Lei Yu ◽  
Julie Schneider ◽  
David Bennett

2017 ◽  
Vol 30 (7) ◽  
pp. 981-990 ◽  
Author(s):  
Marcus Praetorius Björk ◽  
Boo Johansson

ABSTRACTBackground:A recently published study suggests that Gamma-Glutamyltransferase (GGT) in midlife is related to an increased risk of dementia. In the present longitudinal study, we explore the effects of serum GGT on cognitive decline and dementia also in more advanced ages.Methods:We analyzed GGT in a sample of 452 individuals, aged 80 years and older at baseline, with the purpose to explore subsequent effects on cognitive performance. We specifically modeled GGT to cognitive change, time to death, and dementia.Results:Our main finding is that a higher level of GGT is associated with cognitive decline prior to death and vascular dementia in late life. These findings were evident across cognitive domains.Conclusions:This is the first longitudinal study to report on significant associations in late life between GGT, cognitive performance and dementia. Further research is needed to examine the underlying mechanisms of GGT as a marker of age-related cognitive decline.


1999 ◽  
Vol 28 (3) ◽  
pp. 304-312 ◽  
Author(s):  
Mark A. Pereira ◽  
Aaron R. Folsom ◽  
Paul G. McGovern ◽  
Myra Carpenter ◽  
Donna K. Arnett ◽  
...  

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