Association between Blood Lead and Walking Speed in the National Health and Nutrition Examination Survey (NHANES 1999–2002)

Background: Walking speed is a simple and reliable measure of motor function that is negatively associated with adverse health events in older people, including falls, disability, hospital admissions, and mortality. Lead has adverse affects on human health, particularly on the vascular and neurological systems. Objective: We explored the hypothesis that lead is associated with slower walking speed. Methods: We used U.S. National Health and Nutrition Examination Survey (NHANES) cross-sectional data from 1999–2002. The time to walk 20 ft (walking speed) was measured among 1,795 men and 1,798 women ≥ 50 years of age. The association between walking speed and quintiles of blood lead concentration was estimated separately in men and women using linear regression models adjusted for age, education, ethnicity, alcohol use, smoking status, height, and waist circumference. Results: Mean blood lead concentrations and walking speeds were 2.17 μg/dL and 3.31 ft/sec in women, and 3.18 μg/dL and 3.47 ft/sec in men, respectively. Among women, walking speed decreased with increasing quintiles of blood lead, resulting in an estimated mean value that was 0.11 ft/sec slower (95% CI: –0.19, –0.04; p-trend = 0.005) for women with blood lead concentrations in the highest versus lowest quintile. In contrast, lead was not associated with walking speed in men. Conclusion: Blood lead concentration was associated with decreased walking speed in women, but not in men. Our results contribute to the growing evidence that lead exposure, even at low levels, is detrimental to public health

Slow walking speed and cardiovascular death in well functioning older adults: prospective cohort study

Objective To study the relation between low walking speed and the risk of death in older people, both overall and with regard to the main causes of death

No evidence of a longitudinal association between diurnal cortisol patterns and cognition

We examined the effect of salivary cortisol on cognitive performance and decline in 3229 adults (79% men), mean age 61years. Six saliva samples over the day along with a cognition test battery were administered twice in 5years. In fully-adjusted cross-sectional analyses from 2002 to 2004, higher waking cortisol was associated with higher reasoning score (β= 0.08, 95% confidence interval: 0.01, 0.15) but this finding was not replicated using data from 2007 to 2009. Over the mean 5years follow-up there was decline in all cognitive tests but this decline did not vary as a function of cortisol levels; the exception was among APOE e4 carriers where a flatter diurnal slope and higher bedtime cortisol were associated with faster decline in verbal fluency. Changes in cortisol measures between 2002/2004 and 2007/2009 or chronically elevated levels were not associated with cognitive performance in 2007/2009. These results, based on a large sample of community-dwelling adults suggest that variability in hypothalamic-pituitary-adrenal function is not a strong contributor to cognitive aging. © 2014 The Authors

Structural brain lesions and restless legs syndrome: a cross-sectional population-based study

Objective: To evaluate the association between white matter lesion (WML) volume, silent infarcts and restless legs syndrome (RLS) in a population-based study of elderly individuals. Design: Cross-sectional study. Setting: Population-based Three-City study. Participants: 1035 individuals from the Dijon, France, centre of the Three-City study who had available information on volume of WMLs from MRIs and who answered questions about the prevalence of RLS. Primary outcome measure Prevalence of RLS. Results: WML volume was measured using an automated tissue segmentation method. Logistic regression was used to evaluate adjusted associations between tertiles of WML volume and RLS and between silent infarcts and RLS. 218 individuals (21.1%) were determined to have RLS. Compared with those in the first tertile of WML volume, individuals in the second tertile (OR=1.09; 95% CI 0.75 to 1.60) or third tertile (OR=1.17; 95% CI 0.79 to 1.74) did not have an increased prevalence of RLS. We also did not observe associations between the volume of deep or periventricular WML and RLS; nor did we observe an association between silent brain infarcts and RLS (OR=0.74; 95% CI 0.40 to 1.39). These findings were not modified by age or gender. Conclusions: Higher volume of WML and the presence of silent infarcts were not associated with an increased prevalence of RLS in this population-based cohort of elderly individuals

Association of body mass index and waist circumference with successful ageing: 16 year follow-up of the Whitehall II study

Objective: We examined whether midlife body mass index (BMI) and waist circumference (WC) predict successful ageing. Design and Methods BMI/WC were assessed in 4869 persons (mean age 51.2, range 42–63 in 1991/93) and survival and successful ageing (alive, no chronic disease at age >60 years, not in the worst age- and sex-standardized quintile of cognitive, physical, respiratory, and cardiovascular, and mental health) ascertained over a 16-year follow-up, analysed using logistic regression adjusted for socio-demographic factors and health behaviours. Results: 507 participants died, 1008 met the criteria for successful ageing. Those with BMI≥30 kg/m2 had lower odds of successful ageing (Odds Ratio (OR)=0.37; 95% Confidence Interval (CI): 0.27, 0.50) and survival (OR=0.55; 95% CI: 0.41, 0.74) compared to BMI between 18.5–25 kg/m2. Those with a large waist circumference (≥102/88 cm in men/women) had lower odds of successful ageing (OR=0.41; 95% CI: 0.31, 0.54) and survival (OR=0.57; 95% CI: 0.44, 0.73) compared to those with a small waist (<94/80 cm in men/women). Analysis with finer categories showed lower odds of successful ageing starting at BMI ≥23.5 kg/m2 and waist circumference 82/68 cm in men/women. Conclusions: Optimal midlife BMI and waist circumference for successful ageing might be substantially below the current thresholds used to define obesity

Motor function in the elderly: evidence for the reserve hypothesis.

International audienceThe reserve hypothesis accounts for the lack of direct relationship between brain pathology and its clinical manifestations. Research has mostly focused on cognition; our objective is to examine whether the reserve hypothesis applies to motor function. We investigated whether education, a marker of reserve, modifies the association between white matter lesions (WMLs), a marker of vascular brain damage, and maximum walking speed (WS), an objective measure of motor function. We also examined the cross-sectional and longitudinal association between education and WS. Data are from 4,010 participants aged 65-85 years in the longitudinal Three-City-Dijon Study with up to 4 WS measures over 10 years. We examined the interaction between education and WMLs for baseline WS. We studied the association between education and repeated WS measures using linear mixed models, and the role of covariates in explaining the education-WS association. Education was strongly associated with baseline WS; the difference in mean WS between the high and low education groups (0.145 m/s, 95% confidence interval = 0.125-0.165) was equivalent to 7.4 years of age. WMLs were associated with slow WS only in the low education group (p interaction = 0.026). WS declined significantly over time (-0.194 m/s/10 years, 95% confidence interval = -0.206, -0.182), but education did not influence rate of decline. Anthropometric characteristics, parental education, general health, and cognition had the strongest role in explaining the baseline education-WS association. Participants with more education were less susceptible to WMLs' effect on motor function. Higher education was associated with better motor performances but not with motor decline. These results are consistent with the passive reserve hypothesis

Alcohol consumption and cognitive decline in early old age.

OBJECTIVE: To examine the association between alcohol consumption in midlife and subsequent cognitive decline. METHODS: Data are from 5,054 men and 2,099 women from the Whitehall II cohort study with a mean age of 56 years (range 44-69 years) at first cognitive assessment. Alcohol consumption was assessed 3 times in the 10 years preceding the first cognitive assessment (1997-1999). Cognitive tests were repeated in 2002-2004 and 2007-2009. The cognitive test battery included 4 tests assessing memory and executive function; a global cognitive score summarized performances across these tests. Linear mixed models were used to assess the association between alcohol consumption and cognitive decline, expressed as z scores (mean = 0, SD = 1). RESULTS: In men, there were no differences in cognitive decline among alcohol abstainers, quitters, and light or moderate alcohol drinkers (<20 g/d). However, alcohol consumption ≥36 g/d was associated with faster decline in all cognitive domains compared with consumption between 0.1 and 19.9 g/d: mean difference (95% confidence interval) in 10-year decline in the global cognitive score = -0.10 (-0.16, -0.04), executive function = -0.06 (-0.12, 0.00), and memory = -0.16 (-0.26, -0.05). In women, compared with those drinking 0.1 to 9.9 g/d of alcohol, 10-year abstainers showed faster decline in the global cognitive score (-0.21 [-0.37, -0.04]) and executive function (-0.17 [-0.32, -0.01]). CONCLUSIONS: Excessive alcohol consumption in men (≥36 g/d) was associated with faster cognitive decline compared with light to moderate alcohol consumption.The Whitehall II study is supported by the British Medical Research Council (K013351), British Heart Foundation; National Heart, Lung, and Blood Institute (R01HL036310); and US NIH National Institute on Aging (R01AG013196; R01AG034454)

Midlife type 2 diabetes and poor glycaemic control as risk factors for cognitive decline in early old age: a post-hoc analysis of the Whitehall II cohort study

Background: Type 2 diabetes increases the risk for dementia, but whether it affects cognition before old age is unclear. We investigated whether duration of diabetes in late midlife and poor glycaemic control were associated with accelerated cognitive decline. Methods: 5653 participants from the Whitehall II cohort study (median age 54·4 years [IQR 50·3-60·3] at first cognitive assessment), were classified into four groups: normoglycaemia, prediabetes, newly diagnosed diabetes, and known diabetes. Tests of memory, reasoning, phonemic and semantic fluency, and a global score that combined all cognitive tests, were assessed three times over 10 years (1997-99, 2002-04, and 2007-09). Mean HbA1c was used to assess glycaemic control during follow-up. Analyses were adjusted for sociodemographic characteristics, health-related behaviours, and chronic diseases. Findings: Compared with normoglycaemic participants, those with known diabetes had a 45% faster decline in memory (10 year difference in decline -0·13 SD, 95% CI -0·26 to -0·00; p=0·046), a 29% faster decline in reasoning (-0·10 SD, -0·19 to -0·01; p=0·026), and a 24% faster decline in the global cognitive score (-0·11 SD, -0·21 to -0·02; p=0·014). Participants with prediabetes or newly diagnosed diabetes had similar rates of decline to those with normoglycaemia. Poorer glycaemic control in participants with known diabetes was associated with a significantly faster decline in memory (-0·12 [-0·22 to -0·01]; p=0·034) and a decline in reasoning that approached significance (-0·07 [-0·15 to 0·00]; p=0·052). Interpretation: The risk of accelerated cognitive decline in middle-aged patients with type 2 diabetes is dependent on both disease duration and glycaemic control. Funding: US National Institutes of Health, UK Medical Research Council. © 2013 Elsevier Ltd. All rights reserved

Timing of onset of cognitive decline: results from Whitehall II prospective cohort study

Objectives To estimate 10 year decline in cognitive function from longitudinal data in a middle aged cohort and to examine whether age cohorts can be compared with cross sectional data to infer the effect of age on cognitive decline