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Background: Uterine leiomyomata, or fibroids, are hormone-dependent neoplasms of the myometrium that can cause severe gynecologic morbidity. In previous studies, incidence of these lesions has been positively associated with exposure to polychlorinated biphenyls (PCBs), a class of persistent endocrine-disrupting chemicals. However, previous studies have been retrospective in design and none has used ultrasound to reduce disease misclassification., Methods: The Study of Environment, Lifestyle, and Fibroids is a prospective cohort of 1,693 reproductive-aged Black women residing in Detroit, Michigan (enrolled during 2010-2012). At baseline and every 20 months for 5 years, women completed questionnaires, provided blood samples, and underwent transvaginal ultrasound to detect incident fibroids. We analyzed 754 baseline plasma samples for concentrations of 24 PCB congeners using a case-cohort study design. We used multivariable Cox proportional hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals for the association between plasma PCB concentrations and ultrasound-detected fibroid incidence over a 5-year period., Results: We observed little association between PCB congener concentrations and fibroid incidence. The HR for a one-standard deviation increase in log-transformed total PCBs was 0.94 (95% CI = 0.78, 1.1). The PCB congener with the largest effect estimate was PCB 187 (HR for a one-standard deviation increase in log-transformed exposure = 0.88, 95% CI = 0.73, 1.1). Associations did not seem to vary strongly across PCB groupings based on hormonal activity., Conclusions: In this cohort of reproductive-aged Black women, plasma PCB concentrations typical of the contemporary general population were not appreciably associated with higher risk of fibroids., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

Background: The extent to which couples change their behaviors with increasing pregnancy attempt time is not well documented., Methods: We examined change in selected behaviors over pregnancy attempt time in a North American preconception cohort study. Eligible females were ages 21-45 years and not using fertility treatment. Participants completed baseline and bimonthly follow-up questionnaires for up to 12 months or until pregnancy., Results: Among 3,339 females attempting pregnancy for 0-1 cycles at enrollment, 250 contributed 12 months of follow-up without conceiving. Comparing behaviors at 12 months versus baseline, weighted for loss-to-follow-up, we observed small-to-moderate reductions in mean caffeine intake (-19.5 mg/day, CI = -32.7, -6.37), alcohol intake (-0.85 drinks/week, CI = -1.28, -0.43), marijuana use (-3.89 percentage points, CI = -7.33, 0.46), and vigorous exercise (-0.68 hours/week, CI = -1.05, -0.31), and a large increase in activities to improve conception chances (e.g., ovulation testing) (21.7 percentage points, CI = 14.8, 28.6). There was little change in mean cigarette smoking (-0.27 percentage points, CI = -1.58, 1.04), perceived stress scale score (-0.04 units, CI = -0.77, 0.69), or other factors (e.g., sugar-sweetened soda intake, moderate exercise, intercourse frequency, and multivitamin use), but some heterogeneity within subgroups (e.g., 31% increased and 32% decreased their perceived stress scores by ≥2 units; 14% reduced their smoking but none increased their smoking by ≥5 cigarettes/day)., Conclusions: Although many behaviors changed with increasing pregnancy attempt time, mean changes tended to be modest for most variables. The largest differences were observed for the use of caffeine, alcohol, and marijuana, and methods to improve conception chances.

Background: US-based studies have reported that older blacks perform worse than older whites on cognitive tests and have higher risk of Alzheimer disease dementia (AD). It is unclear whether these findings reflect differences in cognitive decline., Methods: The Chicago Health and Aging Project followed individuals, 65+ years old (64% black, 36% white), for up to 18 years. Participants underwent triennial cognitive assessments; stratified randomized samples underwent assessments for AD. We compared black and white participants' cognitive performance, cognitive decline rate (N = 7,735), and AD incidence (N = 2,144), adjusting for age and sex., Results: Black participants performed worse than white participants on the cognitive tests; 441 participants developed AD. Black participants' incident AD risk was twice that of whites (RR = 1.9; 95% CI, 1.4, 2.7), with 58 excess cases/1,000 occurring among blacks (95% CI, 28, 88). Among noncarriers of APOE ε4, blacks had 2.3 times the AD risk (95% CI, 1.5, 3.6), but among carriers, race was not associated with risk (RR = 1.1; 95% CI, 0.6, 2.0; Pinteraction = 0.05). However, cognitive decline was not faster among blacks: the black-white difference in 5-year change in global cognitive score was 0.007 standard unit (95% CI, -0.034, 0.047). Years of education accounted for a sizable portion of racial disparities in cognitive level and AD risk, in analyses using a counterfactual approach., Conclusions: The higher risk of AD among blacks may stem from lower level of cognitive test performance persisting throughout the observation period rather than faster rate of late-life cognitive decline. Disparities in educational attainment may contribute to these performance disparities. See video abstract at, http://links.lww.com/EDE/B299.

Background: Engaging in late-life cognitive activity is often proposed as a strategy to delay or prevent Alzheimer's disease (AD) and other dementias. However, it is unclear to what extent the available evidence supports a causal effect of cognitive activity in dementia prevention., Methods: We systematically searched PubMed and EMBASE through June 2014 to identify peer-reviewed epidemiologic studies of cognitive activity and incidence of AD or all-cause dementia. Eligible articles analyzed data from cohort or nested case-control studies, explicitly defined cognitive activity, evaluated participants for AD or all-cause dementia using clearly defined criteria, and provided effect estimates adjusted for at least age and sex. We describe methodologic issues and biases relevant to interpretation of these studies, and quantify the degree of bias due to confounding and reverse causation required to nullify typically observed associations., Results: We reviewed 12 studies involving 13,939 participants and 1,663 dementia cases, of which 565 were specifically evaluated as AD. Most studies found associations between late-life cognitive activity and lower AD and/or all-cause dementia incidence. Differences in cognitive activity operationalization across studies precluded meta-analysis of effect estimates. Our bias analysis indicated that the observed inverse associations are probably robust to unmeasured confounding, and likely only partially explained by reverse causation., Conclusion: Our systematic review and bias analyses provide support for the hypothesis that late-life cognitive activity offers some reduction in AD and all-cause dementia risk. However, more data are needed to confirm this relationship and on the optimal type, duration, intensity, and timing of that activity.

Background: Selective attrition may introduce bias into analyses of the determinants of cognitive decline. This is a concern especially for risk factors, such as smoking, that strongly influence mortality and dropout. Using inverse-probability-of-attrition weights, we examined the influence of selective attrition on the estimated association of current smoking (vs. never smoking) with cognitive decline., Methods: Chicago Health and Aging Project participants (n = 3713), aged 65-109 years, who were current smokers or never- smokers, underwent cognitive assessments up to 5 times at 3-year interval. We used pooled logistic regression to fit predictive models of attrition due to death or study dropout across the follow-up waves. With these models, we computed inverse-probability-of-attrition weights for each observation. We fit unweighted and weighted, multivariable-adjusted generalized-estimating-equation models, contrasting rates of change in cognitive scores in current versus never-smokers. Estimates are expressed as rates of change in z score per decade., Results: During the 12 years of follow-up, smokers had higher mortality than never-smokers (hazard ratio = 1.93 [95% confidence interval = 1.67 to 2.23]). Higher previous cognitive score was associated with increased likelihood of survival and continued participation. In unweighted analyses, current smokers' cognitive scores declined 0.11 standard units per decade more rapidly than never-smokers' (95% CI = -0.20 to -0.02). Weighting to account for attrition yielded estimates that were 56% to 86% larger, with smokers' estimated 10-year rate of decline up to 0.20 units faster than never-smokers' (95% CI = -0.36 to -0.04)., Conclusions: Estimates of smoking's effects on cognitive decline may be underestimated due to differential attrition. Analyses that weight for the inverse probability of attrition help compensate for this attrition.

Background: Many epidemiologic studies have considered the association between blood pressure (BP) and Alzheimer disease, yet the relationship remains poorly understood., Methods: In parallel with work on the AlzRisk online database (www.alzrisk.org), we conducted a systematic review to identify all epidemiologic studies meeting prespecified criteria reporting on the association between hypertension, systolic BP, or diastolic BP and incident Alzheimer disease. When possible, we computed summary measures using random-effects models and explored potential heterogeneity related to age at BP assessment., Results: Eighteen studies reporting on 19 populations met the eligibility criteria. We computed summary relative risks (RR(Σ)) for 3 measures of BP: hypertension (RR(Σ) = 0.97 [95% confidence interval = 0.80-1.16]); a 10-mm Hg increase in systolic BP (RR(Σ) = 0.95 [0.91-1.00]); and a 10-mm Hg increase in diastolic BP (RR(Σ) = 0.94 [0.85-1.04]). We were unable to compute summary estimates for the association between categories of systolic or diastolic BP and Alzheimer disease; however, there did not appear to be a consistent pattern across studies. After stratifying on age at BP assessment, we found a suggestion of an inverse association between late-life hypertension and Alzheimer disease and a suggestion of an adverse association between midlife diastolic hypertension and Alzheimer disease., Conclusions: Based on existing epidemiologic research, we cannot determine whether there is a causal association between BP and Alzheimer disease. Selection bias and reverse causation may account for the suggested inverse association between late-life hypertension on Alzheimer disease, but, given the expected direction of these biases, they are less likely to account for the suggestion that midlife hypertension increases risk. We advocate continuing systematic review; the AlzRisk database entry on this topic (www.alzrisk.org), which was completed in parallel with this work, will be updated as new studies are published.

Background: Inflammatory processes may be involved in the development of dementia, although findings from epidemiologic studies directly examining inflammatory markers and dementia or its precursor, impaired cognitive function, are inconsistent., Methods: We measured plasma levels of the inflammatory marker, C-reactive protein, using a high-sensitivity assay (hs-CRP) in 4,231 older participants of the Women's Health Study, who provided blood samples between 1992 and 1996 when they were age 60 to 90 years. From 1998 to 2000, we administered a battery of 5 cognitive tests measuring general cognition, verbal memory, and category fluency. Using multiple linear regression, we compared mean cognitive test scores across quintiles of hs-CRP, adjusting for potential confounding factors., Results: There was a wide distribution of hs-CRP levels among these women, and a large proportion had levels considered to reflect a high risk of cardiovascular disease. We observed no suggestion, however, that higher hs-CRP levels were associated with poorer cognitive performance. For example, on a global score combining results of all the cognitive tests, mean scores among women in the highest quintile of hs-CRP did not differ from those in the lowest quintile (multivariable-adjusted mean difference = 0.04; 95% confidence interval [CI]: -0.02 to 0.11, P for trend across quintiles = 0.38)., Conclusion: Overall, in these women, we found no evidence of a link between hs-CRP, a marker of inflammation, and decrements in cognitive function.