Associations between self-reported sleep characteristics and incident mild cognitive impairment: The Heinz Nixdorf Recall Cohort Study.
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ABSTRACT:
SUBMITTER: Brachem C
PROVIDER: S-EPMC7162850 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background/objectivesSleep duration influences weight change in children and young adults, but there is less evidence in middle-aged, and, in particular, older adults. We assessed associations between sleep duration, daytime napping and sleep disturbances, respectively, with change of weight and waist circumference in older subjects. Contrary to previous studies, we also used two points in time to assess sleep characteristics.MethodsWe used data from the population-based Heinz Nixdorf Recall study, a cohort study in Germany with a baseline and two follow-up visits (age 45-74 years, median follow-up 5.1 years for first, 5.2 years for second follow-up visit). In adjusted linear regression models (N=3751), we estimated weight change between baseline and first follow-up visit in relation to various self-reported sleep characteristics measured at baseline. Furthermore, we estimated change of weight and waist circumference, respectively, between first and second follow-up visit in relation to patterns of sleep characteristics measured at baseline and at the first follow-up visit (N=2837).ResultsIn all analyses, short and long sleep duration, sleep disturbances, and regular daytime napping were associated with <1 kg of weight gain and <1 cm of gain in waist circumference over 5 years compared with the respective reference categories. For example, compared with 7-<8 h night sleep, short night sleep (⩽5 h at baseline) was associated with 0.5 kg of weight gain (95% confidence interval: -0.1; 1.1 kg).ConclusionsOur study gave no evidence that sleep characteristics were associated with clinically relevant weight gain in the older population.
| S-EPMC5022146 | biostudies-literature
Project description:IntroductionPoor sleep is a risk factor for adverse health events. For health prevention, it may be helpful to know whether poor sleep or sleep disorders in individuals are associated with sleep problems in their partners or children.MethodsIn the MultiGeneration Study (MGS, conducted from 2013 to 2016), 1237 partners (aged 27 to 90 years) and 1660 adult children (aged 18 to 66 years) of index persons were recruited. Index persons are participants of the Heinz Nixdorf Recall Study, a population-based cohort study in the Ruhr area (study start 1999-2001, 4841 participants aged 45-75 years). We used two analysis populations: one with 1181 index persons whose partners were in MGS, and one with 1083 index persons with at least one adult child in MGS. Sleep characteristics were assessed using questionnaires (including the Pittsburgh Sleep Quality Index). The exposure was the presence of a sleep characteristic of the index subject.ResultsChildren showed the investigated sleep characteristics more often if these were also present in their parent (e.g., RR (relative risk) = 1.28 (95% CI: 1.06-1.55) for poor sleep quality). In partners, strong associations were observed for rising times and napping, but only weak associations for snoring, poor sleep quality and sleep disorders. Snoring of the bed partner is a risk factor for poor sleep (e.g., RR = 1.67 (0.91-3.07) for difficulties falling asleep).ConclusionAggregation is observed for many sleep characteristics in people living in partnerships as well as in parents and their adult children.
| S-EPMC8177478 | biostudies-literature
Project description:BackgroundKallikrein-8 (KLK8) might be an early blood-biomarker of Alzheimer's disease (AD). We examined whether blood KLK8 is elevated in persons with amnestic mild cognitive impairment (aMCI) which is a precursor of AD, compared to cognitively unimpaired (CU) controls.MethodsForty cases and 80 controls, matched by sex and age (± 3years), were participants of the longitudinal population-based Heinz Nixdorf Recall study (baseline: 2000-2003). Standardized cognitive performance was assessed 5 (T1) and 10 years after baseline (T2). Cases were CU at T1 and had incidental aMCI at T2. Controls were CU at T1 and T2. Blood KLK8 was measured at T2. Using multiple logistic regression the association between KLK8 in cases vs. controls was investigated by estimating odds ratios (OR) and 95% confidence intervals (95%CI), adjusted for inter-assay variability and freezing duration. Using receiver operating characteristic (ROC) analysis, the diagnostic accuracy of KLK8 was determined by estimating the area under the curve (AUC) and 95%CI (adjusted for inter-assay variability, freezing duration, age, sex).ResultsThirty-seven participants with aMCI vs. 72 CU (36.7%women, 71.0±8.0 (mean±SD) years) had valid KLK8 measurements. Mean KLK8 was higher in cases than in controls (911.6±619.8 pg/ml vs.783.1±633.0 pg/ml). Fully adjusted, a KLK8 increase of 500pg/ml was associated with a 2.68 (1.05-6.84) higher chance of having aMCI compared to being CU. With an AUC of 0.92 (0.86-0.97), blood KLK8 was a strong discriminator for aMCI and CU.ConclusionThis is the first population-based study to demonstrate the potential clinical utility of blood KLK8 as a biomarker for incipient AD.
| S-EPMC8690879 | biostudies-literature
Project description:BackgroundThe apolipoprotein E (APOE) ɛ4 allele is reported to be a strong genetic risk factor for mild cognitive impairment (MCI) and Alzheimer's disease (AD). Additional genetic loci have been detected that influence the risk for late-onset AD. As socioeconomic position (SEP) is also strongly related to cognitive decline, SEP has been suggested to be a possible modifier of the genetic effect on MCI.ObjectiveTo investigate whether APOEɛ4 and a genetic sum score of AD-associated risk alleles (GRSAD) interact with SEP indicators to affect MCI in a population-based cohort.MethodsUsing data of 3,834 participants of the Heinz Nixdorf Recall Study, APOEɛ4 and GRSAD by SEP interactions were assessed using logistic regression models, as well as SEP-stratified genetic association analysis. Interaction on additive scale was calculated using the relative excess risk due to interaction (RERI). All analysis were additionally stratified by sex.ResultsIndication for interaction on the additive scale was found between APOEɛ4 and low education on MCI (RERI: 0.52 [95% confidence interval (CI): 0.01; 1.03]). The strongest genetic effects of the APOEɛ4 genotype on MCI were observed in groups of low education (Odds ratio (OR): 1.46 [95% CI: 0.79; 2.63] for≤10 years of education versus OR: 1.00 [95% CI: 0.43; 2.14] for≥18 years of education). Sex stratified results showed stronger effects in women. No indication for interaction between the GRSAD and SEP indicators on MCI was observed.ConclusionResults indicate that low education may have an impact on APOEɛ4 expression on MCI, especially among women.
| S-EPMC8461721 | biostudies-literature
Project description:Male-pattern baldness (MPB) is characterized by a progressive hair loss from the frontal and vertex scalp that affects about 80% of men at the age of 80 years. Epidemiological studies show positive associations between MPB and coronary heart disease (CHD) and CHD related risk factors such as blood pressure (BP), diabetes mellitus (DM) or elevated blood lipid levels. The results however vary with regard to the pattern of hair loss (i.e. moderate, severe, frontal or vertex). Further, no study has investigated for a shared genetic determinant between MPB and CHD as well as CHD related risk factors. Using the longitudinal data from the population-based Heinz Nixdorf Recall study we aimed to systematically investigate the association between MPB and incident CHD and CHD risk factors on (i) an epidemiological (N = 1,673 males) and (ii) a genetic (N = 1,357 males) level. The prevalence of any baldness in our study population was 88% (mean age ± SD: 64±7.5 years). Compared to men with 'no baldness', in men with any kind of baldness a slightly increased risk for CHD (Hazard ratio [95% confidence interval (95%CI)] = 1.2 [0.8; 1.9]), a slightly higher extend of coronary artery calcification (CAC) (Beta [95%CI] = 0.2 [-0.1; 0.6]), a moderately increased risk for DM (prevalence ratio [95%CI] = 1.4 [0.9; 2.0]) and higher body mass index (BMI) (Beta [95%CI] = 0.6 [0.00003; 1.2]) seem to be indicated in the adjusted model. In contrast, the MPB genetic risk score did not show any association with CHD or CHD risk factors. Taken together, the results of our study suggest a weak association between MPB and a few CHD risk factors (CAC, DM and BMI) but do not point to MPB as a strong surrogate measure for CHD and CHD risk factors in general.
| S-EPMC6863534 | biostudies-literature
Project description:BackgroundMild cognitive impairment (MCI) describes the intermediate state between normal cognitive aging and dementia. Adverse effects of air pollution (AP) on cognitive functions have been proposed, but investigations of simultaneous exposure to noise are scarce.ObjectivesWe analyzed the cross-sectional associations of long-term exposure to AP and traffic noise with overall MCI and amnestic (aMCI) and nonamnestic (naMCI) MCI.MethodsAt the second examination of the population-based Heinz Nixdorf Recall study, cognitive assessment was completed in 4,086 participants who were 50-80 years old. Of these, 592 participants were diagnosed as having MCI (aMCI, n = 309; naMCI, n = 283) according to previously published criteria using five neuropsychological subtests. We assessed long-term residential concentrations for size-fractioned particulate matter (PM) and nitrogen oxides with land use regression, and for traffic noise [weighted 24-hr (LDEN) and night-time (LNIGHT) means]. Logistic regression models adjusted for individual risk factors were calculated to estimate the association of environmental exposures with MCI in single- and two-exposure models.ResultsMost air pollutants and traffic noise were associated with overall MCI and aMCI. For example, an interquartile range increase in PM2.5 and a 10 A-weighted decibel [dB(A)] increase in LDEN were associated with overall MCI as follows [odds ratio (95% confidence interval)]: 1.16 (1.05, 1.27) and 1.40 (1.03, 1.91), respectively, and with aMCI as follows: 1.22 (1.08, 1.38) and 1.53 (1.05, 2.24), respectively. In two-exposure models, AP and noise associations were attenuated [e.g., for aMCI, PM2.5 1.13 (0.98, 1.30) and LDEN 1.46 (1.11, 1.92)].ConclusionsLong-term exposures to air pollution and traffic noise were positively associated with MCI, mainly with the amnestic subtype.CitationTzivian L, Dlugaj M, Winkler A, Weinmayr G, Hennig F, Fuks KB, Vossoughi M, Schikowski T, Weimar C, Erbel R, Jöckel KH, Moebus S, Hoffmann B, on behalf of the Heinz Nixdorf Recall study Investigative Group. 2016. Long-term air pollution and traffic noise exposures and mild cognitive impairment in older adults: a cross-sectional analysis of the Heinz Nixdorf Recall Study. Environ Health Perspect 124:1361-1368;?http://dx.doi.org/10.1289/ehp.1509824.
| S-EPMC5010410 | biostudies-literature
Project description:BackgroundDepression might be an independent risk factor for cognitive decline, a prodromal dementia symptom or a reaction to cognitive/functional impairment.ObjectiveTo investigate the association between (1) depressive symptoms and (2) depressive symptom patterns over 13 years with incident mild cognitive impairment (MCI) 5 years later.Materials and methodsWe included 724/823 cognitively unimpaired men/women who participated in the population-based Heinz Nixdorf Recall study (t1: 2005-2008, ø62.9 years; t2: 2010-2015, ø68.1 years). Depressive symptoms were assessed in the study center and during six postal follow-ups using the short form of the Center for Epidemiologic Studies Depression Scale (CES-D). Relative risks (RR; 95% confidence intervals) for MCI at t2 (men/women: 71/76) were estimated for CES-D at t1 (linear and dichotomized at ≥17, cut-off for clinically relevant depressive symptoms) and CES-D fluctuations over 13 years (stable low, large fluctuations, stable high/stable around cut-off) using log-linear regression models with Poisson working likelihood adjusted for age, sex, education, diabetes mellitus, coronary heart disease, and stroke.ResultsFully adjusted risk for MCI at t2 (per CES-D point increase at t1) was elevated for the total cohort (1.053, 1.031-1.076), men (1.046, 1.012-1.081), and women (1.059, 1.029-1.090). Applying the dichotomized CES-D, risk for MCI was substantially increased for the total cohort [2.22 (1.38-3.58)] and in women [2.59 (1.46-4.58)]. Large CES-D fluctuations and stable high/stable around cut-off were associated with increased RR for MCI in the total cohort and in women compared to stable low symptoms.ConclusionDepressive symptoms predicted MCI in cognitively unimpaired participants of our population-based study. Adequate treatment of depression may therefore contribute to the maintenance of normal cognition and delay dementia onset.
| S-EPMC9640513 | biostudies-literature
Project description:Social inequalities in health and disease are well studied. Less information is available on inequalities in biomarker levels indicating subclinical stages of disease such as cystatin C, an early diagnostic marker of renal dysfunction and predictor for cardiovascular disease. We evaluated the relationship between cystatin C, socioeconomic position (SEP) and established cardiovascular risk factors in a population-based study. In 4475 men and women aged 45-75 years participating in the baseline examination of the Heinz Nixdorf Recall Study cystatin C was measured from serum samples with a nephelometric assay. SEP was assessed by education and household income. Linear regression models were used to analyse the association between SEP and cystatin C as well as the impact of cardiovascular risk factors (i.e., body mass index, blood pressure, blood glucose, diabetes mellitus, blood lipids, C-reactive protein, smoking) on this association. After adjustment for age and sex cystatin C decreased by 0.019 mg/l (95% confidence interval (CI) - 0.030 to - 0.008) per five years of education. While using a categorical education variable cystatin C presented 0.039 mg/l (95% CI 0.017-0.061) higher in men and women in the lowest educational category (≤ 10 years of education) compared to the highest category (≥ 18 years). Concerning income, cystatin C decreased by 0.014 mg/l (95% CI - 0.021 to - 0.006) per 1000 € after adjustment for age and sex. For men and women in the lowest income quartile cystatin C was 0.024 mg/l (95% CI 0.009-0.038) higher compared to the highest income quartile. After adjusting for established cardiovascular risk factors the observed associations were substantially diminished. Social inequalities seem to play a role in subclinical stages of renal dysfunction, which are also related to development of cardiovascular disease. Adjustment for traditional cardiovascular risk factors showed that these risk factors largely explain the association between SEP and cystatin C.
| S-EPMC8481271 | biostudies-literature
Project description:AimThe sleep disturbing effect of many drugs is derived from clinical trials with highly selected patient collectives. However, the generalizability of such findings to the general population is questionable. Our aim was to assess the association between intake of drugs labelled as sleep disturbing and self-reported nocturnal sleep disturbances in a population-based study.MethodsWe used data of 4221 participants (50.0% male) aged 45 to 75 years from the baseline examination of the Heinz Nixdorf Recall Study in Germany. The interview provided information on difficulties falling asleep, difficulties maintaining sleep and early morning arousal. We used the summary of product characteristics (SPC) for each drug taken and assigned the probability of sleep disturbances. Thereafter, we calculated cumulative probabilities of sleep disturbances per subject to account for polypharmacy. We estimated prevalence ratios (PR) using log Poisson regression models with robust variance.ResultsThe adjusted PRs of any regular nocturnal sleep disorder per additional sleep disturbing drug were 1.01 (95% confidence interval (CI) 0.97, 1.06) and 1.03 (95% CI 1.00, 1.07) for men and women, respectively. Estimates for each regular nocturnal sleep disturbance were similarly close to 1. PRs for regular nocturnal sleep disturbances did not increase with rising cumulative probability for drug-related sleep disturbances.ConclusionsSPC-based probabilities of drug-related sleep disturbances showed barely any association with self-reported regular nocturnal sleep disturbances. We conclude that SPC-based probability information may lack generalizability to the general population or may be of limited data quality.
| S-EPMC5338107 | biostudies-literature
Project description:Study objectivesSeveral studies have assessed the association between midday nap and cardiovascular outcomes and reported heterogenous results. Concern exists that confounding might have distorted these results and contributed to discrepancies among them. This study prospectively examines the association between midday nap habits and the occurrence of coronary artery disease in a non-Mediterranean population.ParticipantsThe baseline examination of 4,123 participants aged 45-75 years.MeasurementsMeasurements included interviews, physical examinations, laboratory tests, and electron beam computed tomography. We studied the influence of midday nap habits on risk of coronary artery disease. We adjusted for several potential confounders including measures of subclinical atherosclerosis-such as coronary calcium score and ankle brachial index-at baseline. Cardiac events during a median follow-up of 8.1 years were defined as nonfatal myocardial infarction and sudden cardiac death.ResultsOverall, 135 of 4,123 subjects (3.3%) either suffered from acute myocardial infarction (81 subjects) or died due to a sudden cardiac death (54 subjects) during follow-up. After adjustment for several confounders including measures of subclinical atherosclerosis, regular long (> 60 min) midday nap was associated with an increased hazard ratio of cardiac events (hazard ratio 2.12, 95% confidence interval 1.11-4.05).ConclusionsAs our detailed confounder analyses showed, confounding is not the sole explanation for this finding. Future research on midday naps should focus on biological mechanisms that may be responsible for increasing the risk of coronary artery disease among subjects taking regular long midday naps.
| S-EPMC3490363 | biostudies-literature