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OBJECTIVE: To examine the bi-directional associations of a weight loss intervention with quality of life and mental health in obese older adults with functional limitations. DESIGN: Combined-group analyses of secondary variables from the MEASUR-UP randomized controlled trial. SETTING: Academic medical center. PARTICIPANTS: Obese community-dwelling men and women (N = 67; age ≥60; BMI ≥30) with functional limitations (Short Physical Performance Battery [SPPB] score of 4–10 out of 12). INTERVENTION: Six-month reduced calorie diet at two protein levels MEASUREMENTS: Weight, height, body composition, physical function, medical history, and mental health and quality of life assessments (Center for Epidemiologic Studies Depression Scale [CES-D]; Profile of Mood States [POMS], Pittsburgh Sleep Quality Index [PSQI]; Perceived Stress Scale [PSS]; Satisfaction with Life Scale [SWLS]; and Short Form Health Survey [SF-36]) were acquired at 0, 3 and 6 months RESULTS: Physical composite quality of life (SF-36) improved significantly at 3 months (β = 6.29, t2,48 = 2.60, p = 0.012) and 6 months (β = 10.03, t2,48 = 4.83, p < 0.001), as did several domains of physical quality of life. Baseline depression symptoms (CES-D and POMS) were found to predict lower amounts of weight loss; higher baseline sleep latency (PSQI) and anger (POMS) predicted less improvement in physical function (SPPB). CONCLUSION: The significant bi-directional associations found between a weight loss intervention and mental health/quality of life, including substantial improvements in physical quality of life with obesity treatment, indicate the importance of considering mental health and quality of life as part of any weight loss intervention for older adults.

Data in humans and nonhuman primates have suggested a possible synergistic effect of vitamin D and calcium (CaD) and estrogen on the cardiovascular disease (CVD) risk factors. Using randomized trial data we explored whether the effect of menopausal hormone therapy (HT) on CVD events is modified by CaD supplementation.A prospective, randomized, double-blind, placebo-controlled trial was implemented among postmenopausal women in the Women's Health Initiative. A total of 27,347 women were randomized to the HT trials (0.625 mg/d of conjugated equine estrogens [CEE] alone for women without a uterus vs placebo; or 0.625 mg of CEE in addition to 2.5 mg of medroxyprogesterone acetate daily [CEE + MPA] for women with a uterus vs placebo). After 1 year, 16,089 women in the HT trial were randomized to the CaD trial and received either 1,000 mg of elemental calcium carbonate and 400 IU of vitamin D3 daily or placebo. The mean (SD) duration of follow-up after CaD randomization was 6.2 (1.3) years for the CEE trial and 4.6 (1.1) years for the CEE + MPA trial. CVD and venous thromboembolism events evaluated in this subgroup analysis included coronary heart disease, stroke, pulmonary embolism, all-cause mortality, plus select secondary endpoints (total myocardial infarction, coronary revascularization, deep venous thrombosis, cardiovascular death, and all CVD events). Time-to-event methods were used and models were fit with a Cox proportional hazards regression model.In the CEE trial, CaD significantly modified the effect of CEE on stroke (P interaction = 0.04). In the CaD-placebo group, CEE's effect on stroke was harmful (hazard ratio [95% confidence interval] = 2.19[1.34-3.58]); however, it was neutral in the CaD-supplement group (hazard ratio [95% confidence interval] = 1.07[0.66-1.73]). We did not observe significant CEE-CaD interactions for coronary heart disease, total CVD events, or any of the remaining endpoints. In the CEE + MPA trial, there was no evidence that the effect of CEE + MPA on any of CVD endpoints was modified by CaD supplementation.CaD did not consistently modify the effect of CEE therapy or CEE + MPA therapy on CVD events. However, the increased risk of stroke due to CEE therapy appears to be mitigated by CaD supplementation. In contrast, CaD supplementation did not influence the risk of stroke due to CEE + MPA.

To analyze the treatment effect of calcium+vitamin D supplementation, hormone therapy, both, and neither on cardiovascular disease risk factors.We conducted a prospective, randomized, double-blind, placebo-controlled trial among Women's Health Initiative (WHI) participants. The predefined primary outcome was low-density lipoprotein cholesterol (LDL-C).Between September 1993 and October 1998, a total of 68,132 women aged 50-79 years were recruited and randomized to the WHI-Dietary Modification (n=48,835) and WHI-Hormone Therapy trials (n=27,347). Subsequently, 36,282 women from WHI-Hormone Therapy (16,089) and WHI-Dietary Modification (n=25,210) trials were randomized in the WHI-Calcium+Vitamin D trial to 1,000 mg elemental calcium carbonate plus 400 international units vitamin D3 daily or placebo. Our study group included 1,521 women who participated in both the hormone therapy and calcium+vitamin D trials and were in the 6% subsample of trial participants with blood sample collections at baseline and years 1, 3, and 6. The average treatment effect with 95% confidence interval, for LDL-C, compared with placebo, was -1.6, (95% confidence interval [CI] -5.5 to 2.2) mg/dL for calcium+vitamin D alone, -9.0 (95% CI -13.0 to -5.1) mg/dL for hormone therapy alone, and -13.8 (95% CI -17.8 to -9.8) mg/dL for the combination. There was no evidence of a synergistic effect of calcium+vitamin D+hormone therapy on LDL-C (P value for interaction=.26) except in those with low total intakes of vitamin D, for whom there was a significant synergistic effect on LDL (P value for interaction=.03).Reductions in LDL-C were greater among women randomized to both calcium+vitamin D and hormone therapy than for those randomized to either intervention alone or to placebo. The treatment effect observed in the calcium+vitamin D+hormone therapy combination group may be additive rather than synergistic. For clinicians and patients deciding to begin calcium+vitamin D supplementation, current use of hormone therapy should not influence that decision.ClinicalTrials.gov, https://clinicaltrials.gov, NCT00000611.

Objective Exposure to stressful events is associated with both occurrence of depression and also vascular disease. The objective of this study was to determine whether higher levels of stress exposure was related to measures of pathological brain aging, specifically white matter hyperintensity volumes, in older adults with and without depression. Methods The sample included 130 depressed and 110 never-depressed older adults aged 60 years or older enrolled in a longitudinal study at an academic medical center. Participants completed clinical assessments, assessment of stressful event exposure and perceived stress, and magnetic resonance imaging at baseline and after 2 years. Analyses examined both cross-sectional and longitudinal relationships between stress measures and white matter hyperintensity volumes. Results There were no statistically significant relationships observed between cross-sectional baseline stress measures and either baseline hyperintensity volume or 2-year change in hyperintensity volume. However, after controlling for demographic variables and baseline measures, change in stressor exposure was associated with change in hyperintensity volumes. In this analysis, increased stressor exposure was associated with greater increases in white matter hyperintensity volume, while reductions in stressor exposure were associated with less increase in hyperintensity volume. This relationship did not significantly differ based on the presence of either depression or medical comorbidities. Conclusions This work adds to a growing literature associating exposure to stressful events in later life with more rapid pathological brain aging. Work is needed to understand the physiological mechanisms by which stress exposure has this effect and examine whether stress reduction techniques may modify these observed outcomes. Copyright © 2016 John Wiley & Sons, Ltd.

Objective To estimate trajectories of body mass index (BMI) and determine their association with incident frailty in later life. Methods Data come from the 2004 to 2012 waves of the Health and Retirement Study, a longitudinal survey of older adults. Analysis was restricted to respondents who were not frail at baseline (n = 10,827). BMI (kg/m2) was calculated from self-reported weight and height. Incident frailty was assessed using the Frailty Index. Longitudinal growth mixture modeling was used to estimate the relationship between BMI trajectories and incident frailty over a 10-year period. Results Four trajectory classes were identified: weight gain (n = 162 [1.4%], mean final BMI = 42 kg/m2), weight loss (n = 171 [1.7%], mean final BMI = 25.0 kg/m2), consistent obesity (n = 640 [6.8%], mean final BMI = 34.7 kg/m2), and consistent overweight (n = 9,864 [90.1%] mean final BMI = 26.0 kg/m2). Cumulative incidence of frailty was 19.9%. Relative to the consistent overweight class, the weight gain class had the highest likelihood of incident frailty (odds ratio, OR: 3.61, 95% confidence interval, CI: 2.39–5.46). The consistent obesity (OR: 2.72, 95% CI: 2.06–3.58) and weight loss (OR: 2.81, 95% CI: 1.84–4.30) classes had similarly elevated risk of frailty. Conclusions Weight change and obesity are associated with risk of frailty.

Obesity affects a large proportion of older adults, contributing to poor physical and mental health outcomes. Yet, weight loss (WL) interventions have been under-studied in this population due to concerns about exacerbating age-related reductions in muscle mass, bone density, and physical function. Thus, the potential influence of WL interventions on mental health and quality of life is mostly unknown. We assessed these attributes in a group of community-dwelling, obese (BMI ≥30 kg/m2) older adults (≥60 yr; n = 67) with mild to moderate physical impairment (SPPB score 4–10 out of 12) who were participating in a 6-month WL intervention (-500 kcal/day deficit; 2 diet groups [0.8 g versus 1.2 protein/kg body wt/day]). Significant weight loss and improved SPPB scores (ps < 0.05) were achieved by both groups. Mixed model analysis of the combined groups revealed short-term improvements in mental composite quality of life (SF-36), positive affect (CES-D), and total mood disturbance (POMS) at 3 months and sustained improvement of physical composite quality of life and its subdomains at both 3 and 6 months (ps < 0.05). Conversely, higher baseline depression (CES-D and POMS) and anger (POMS) and longer sleep latency (PSQI) were associated with less successful WL and blunted functional benefit. These findings demonstrate the potential benefits to mental health and quality of life of intentional WL in obese older adults and underscores the need for evaluation of mental health when considering a WL intervention for obese older adults.

Background: Obesity is a significant cause of functional limitations in older adults; yet, concerns that weight reduction could diminish muscle along with fat mass have impeded progress toward an intervention. Meal-based enhancement of protein intake could protect function and/or lean mass but has not been studied during geriatric obesity reduction. Methods: In this 6-month randomized controlled trial, 67 obese (body mass index ≥30 kg/m 2 ) older (≥60 years) adults with a Short Physical Performance Battery score of 4–10 were randomly assigned to a traditional (Control) weight loss regimen or one with higher protein intake (>30 g) at each meal (Protein). All participants were prescribed a hypo-caloric diet, and weighed and provided dietary guidance weekly. Physical function (Short Physical Performance Battery) and lean mass (BOD POD), along with secondary measures, were assessed at 0, 3, and 6 months. Results: At the 6-month endpoint, there was significant (p < .001) weight loss in both the Control (−7.5 ± 6.2 kg) and Protein (−8.7 ± 7.4 kg) groups. Both groups also improved function but the increase in the Protein (+2.4 ± 1.7 units; p < .001) was greater than in the Control (+0.9 ± 1.7 units; p < .01) group (p = .02). Conclusion: Obese, functionally limited older adults undergoing a 6-month weight loss intervention with a meal-based enhancement of protein quantity and quality lost similar amounts of weight but had greater functional improvements relative to the Control group. If confirmed, this dietary approach could have important implications for improving the functional status of this vulnerable population (ClinicalTrials.gov identifier: NCT01715753).

Objective Vascular lesions seen through brain imaging as hyperintensities are associated with both depression and functional impairment in older adults. Our objective was to determine if the relationship between the volume of cerebral white matter hyperintensities (WMHs) and functional decline differed in the presence of late life depression. Design Secondary analysis of data collected through the Neurocognitive Outcomes of Depression Study. Analysis techniques included general linear mixed models examining trajectories of functional change predicted by lesion volume at baseline. Participants 381 participants (244 patients diagnosed with major depression and 137 never depressed comparison participants) ages 60 years and older followed for up to 16 years. Measurements WMH volume was measured through analysis of brain magnetic resonance imaging data. Functional limitations included difficulties with basic activities of daily living tasks, instrumental activities of daily living tasks, and mobility. Results Those participants who were both depressed and had a higher volume of WMHs at baseline were most at risk for functional decline across all measures of function. Among the never depressed, those with a higher WMH volume at baseline had a more accelerated rate of functional decline than those with lower WMH volume, and those who were depressed with lower volume of WMH started with more limitations than the never depressed but appeared to progress at a rate similar to those who were never depressed with lower WMH. Conclusion Older patients with both cerebrovascular risk factors and depression are at an increased risk for functional decline, and may benefit from the treatment of both conditions.

Magnetic resonance imaging studies of maltreated children with posttraumatic stress disorder (PTSD) suggest that maltreatment-related PTSD is associated with adverse brain development. Maltreated youth resilient to chronic PTSD were not previously investigated and may elucidate neuromechanisms of the stress diathesis that leads to resilience to chronic PTSD. In this cross-sectional study, anatomical volumetric and corpus callosum diffusion tensor imaging measures were examined using magnetic resonance imaging in maltreated youth with chronic PTSD (N = 38), without PTSD (N = 35), and nonmaltreated participants (n = 59). Groups were sociodemographically similar. Participants underwent assessments for strict inclusion/exclusion criteria and psychopathology. Maltreated youth with PTSD were psychobiologically different from maltreated youth without PTSD and nonmaltreated controls. Maltreated youth with PTSD had smaller posterior cerebral and cerebellar gray matter volumes than did maltreated youth without PTSD and nonmaltreated participants. Cerebral and cerebellar gray matter volumes inversely correlated with PTSD symptoms. Posterior corpus callosum microstructure in pediatric maltreatment-related PTSD differed compared to maltreated youth without PTSD and controls. The group differences remained significant when controlling for psychopathology, numbers of Axis I disorders, and trauma load. Alterations of these posterior brain structures may result from a shared trauma-related mechanism or an inherent vulnerability that mediates the pathway from chronic PTSD to comorbidity.

Racial/ethnic differences in obesity prevalence and in responses to weight-loss treatment between Black and White women are well documented. Whether these differences influence responses to weight-loss treatment among older women is unknown. Therefore, we evaluated racial/ethnic differences among participants in a 6-month weight-loss study with traditional versus higher protein intake. Participants were obese (BMI ≥ 30 kg/m2) community-dwelling women, age 45 years or older, who self-identified as either Black or White. Change in body-weight, 6 minute walk test (6MWT), general health (SF-36), and satisfaction with life (SWL) were evaluated at 0, 4 and 6 months. Both racial groups reduced (ps < 0.01) body weight at 4 and 6 months, with a trend toward more weight loss among White women (p = 0.07), relative to Black women. Other racial/ethnic differences included greater improvements in general health (p = 0.05) and 6MWT (p < 0.05) for White versus Black women at 6 months; these differences persisted after adjusting for treatment group, age/education, and comorbidity. Although racial/ethnic differences in SWL were not observed, significant improvement was observed only among White women (p < 0.01). Interestingly, weight loss was associated with improved 6MWT only among Black women (r = -0.66, p < 0.05) and with general health only among White women (r = -0.44, p < 0.05). Overall, White women experienced greater improvements in health and physical function as a result of weight-loss than did Black women. Further research is needed to identify equitable intervention strategies for the treatment of sarcopenic obesity.

Background Anemia is associated with poorer sleep in children, and clinically, anemia is linked to insomnia. However, the association between anemia and insomnia in older adults is understudied. Methods We examined the cross-sectional association between anemia and insomnia in 1,053 adults (71.4 ± 10.6 years) in the Baltimore Longitudinal Study of Aging. Participants were classified as nonanemic, non-iron-deficient anemic, or iron-deficient anemic based on hemoglobin, ferritin, transferrin saturation, and mean cell volume. Insomnia symptoms were evaluated by the Women's Health Initiative Insomnia Rating Scale (WHIIRS). A total score (range 0-20) was generated, and participants were also classified as having 0, 1, or 2+ symptoms. Results Overall, 10.5% of participants had non-iron-deficient anemia, 0.9% had iron-deficient anemia, and 88.5% had no anemia. Due to its low prevalence, the iron-deficient anemic group was dropped from analyses. In models adjusted for demographics, number of medical conditions, and Center for Epidemiologic Studies Depression Scale score, non-iron-deficient anemic individuals had significantly higher WHIIRS total scores, indicating greater insomnia severity, compared to those without anemia (predicted adjusted mean WHIIRS of 7.24 [95% confidence interval (CI): 6.40-8.08] vs 5.92 [95% CI: 5.65-6.19]). They also had twice the risk of reporting ≥2 insomnia symptoms (vs 0 symptoms; relative risk ratio = 2.20, 95% CI: 1.25-3.89). Conclusions Results suggest that individuals with non-iron-deficient anemia are more likely to experience insomnia symptoms than those who are nonanemic. These results may have implications for insomnia treatment or the identification of underlying frailty in individuals with sleep problems.

A cross-sectional association between depression and serum low-density lipoprotein cholesterol (LDL-c) has been noted in psychiatric literature, raising the question of temporality: does low LDL-c predict depression, does depression lead to changes in LDL-c levels, or is this relationship bidirectional? In a previous longitudinal analysis of postmenopausal women ages 50–79 who participated in the Women’s Health Initiative (WHI), we detected an association between low LDL-c and the subsequent onset of depressive symptoms (HR=1.25, 95% CI 1.05–1.49, p=0.01). This current study uses the WHI cohort to explore the question of temporality in the opposite direction, examining the influence of depressive symptoms on subsequent changes in LDL-c levels. This study provides no evidence to suggest an association between depression and subsequent changes in LDL-c level (−2.78 mg/dL, 95% CI=−7.49 to 1.92, p=0.25), nor was any association detected for total cholesterol, HDL, or triglyceride changes over time. Further, this study demonstrates that the relationship between depression and serum LDL changes is not mediated by changes in weight, exercise, or energy intake.

Exposure to stressful events is associated with both occurrence of depression and also vascular disease. The objective of this study was to determine whether higher levels of stress exposure was related to measures of pathological brain aging, specifically white matter hyperintensity volumes, in older adults with and without depression.The sample included 130 depressed and 110 never-depressed older adults aged 60 years or older enrolled in a longitudinal study at an academic medical center. Participants completed clinical assessments, assessment of stressful event exposure and perceived stress, and magnetic resonance imaging at baseline and after 2 years. Analyses examined both cross-sectional and longitudinal relationships between stress measures and white matter hyperintensity volumes.There were no statistically significant relationships observed between cross-sectional baseline stress measures and either baseline hyperintensity volume or 2-year change in hyperintensity volume. However, after controlling for demographic variables and baseline measures, change in stressor exposure was associated with change in hyperintensity volumes. In this analysis, increased stressor exposure was associated with greater increases in white matter hyperintensity volume, while reductions in stressor exposure were associated with less increase in hyperintensity volume. This relationship did not significantly differ based on the presence of either depression or medical comorbidities.This work adds to a growing literature associating exposure to stressful events in later life with more rapid pathological brain aging. Work is needed to understand the physiological mechanisms by which stress exposure has this effect and examine whether stress reduction techniques may modify these observed outcomes. Copyright © 2016 John WileySons, Ltd.

To estimate trajectories of body mass index (BMI) and determine their association with incident frailty in later life.Data come from the 2004 to 2012 waves of the Health and Retirement Study, a longitudinal survey of older adults. Analysis was restricted to respondents who were not frail at baseline (n = 10,827). BMI (kg/m(2) ) was calculated from self-reported weight and height. Incident frailty was assessed using the Frailty Index. Longitudinal growth mixture modeling was used to estimate the relationship between BMI trajectories and incident frailty over a 10-year period.Four trajectory classes were identified: weight gain (n = 162 [1.4%], mean final BMI = 42 kg/m(2) ), weight loss (n = 171 [1.7%], mean final BMI = 25.0 kg/m(2) ), consistent obesity (n = 640 [6.8%], mean final BMI = 34.7 kg/m(2) ), and consistent overweight (n = 9,864 [90.1%] mean final BMI = 26.0 kg/m(2) ). Cumulative incidence of frailty was 19.9%. Relative to the consistent overweight class, the weight gain class had the highest likelihood of incident frailty (odds ratio, OR: 3.61, 95% confidence interval, CI: 2.39-5.46). The consistent obesity (OR: 2.72, 95% CI: 2.06-3.58) and weight loss (OR: 2.81, 95% CI: 1.84-4.30) classes had similarly elevated risk of frailty.Weight change and obesity are associated with risk of frailty.

Insomnia and anemia can lead to poor health. We determined the cross-sectional association between anemia and insomnia symptoms in 1,066 adults (71.6±10.7 yr) from the Baltimore Longitudinal Study ...