In older adults, mobility limitations often coexist with overweight or obesity, suggesting that similar factors may underlie both traits. This study examined the extent to which genetic and environmental influences explain the association between adiposity and mobility in older women. Body fat percentage (bioimpedance test), walking speed over 10 m, and distance walked in a 6-min test were evaluated in 92 monozygotic (MZ) and 104 dizygotic (DZ) pairs of twin sisters reared together, aged 63-76 years. Genetic and environmental influences on each trait were estimated using age-adjusted multivariate genetic modeling. The analyses showed that the means (and s.d.) for body fat percentage, walking speed, and walking endurance were 33.2+/-7.3%, 1.7+/-0.3 m/s and 529.7+/-75.4 m, respectively. The phenotypic correlation between adiposity and walking speed was -0.32 and between adiposity and endurance it was -0.33. Genetic influences explained 80% of the association between adiposity and speed, and 65% of adiposity and walking endurance. Cross-trait genetic influences accounted for 12% of the variability in adiposity, 56% in walking speed, and 34% in endurance. Trait-specific genetic influences were also detected for adiposity (54%) and walking endurance (13%), but not speed. In conclusion, among community-living older women, an inverse association was found between adiposity and mobility that was mostly due to the effect of shared genes. This result suggests that the identification of genetic variants for body fat metabolism may also provide understanding of the development of mobility limitations in older women.
The purpose of the present study was to examine the relative contribution of genetic and environmental effects on the air-conducted hearing threshold levels at low (0.125-0.5 kHz), mid (1-2 kHz), and high (4-8 kHz) frequencies separately for the better and worse hearing ear in older women. We also examined the distribution of audiogram configurations. Data was analysed using quantitative genetic modelling. As part of the Finnish twin study on aging (FITSA), hearing was measured in 103 monozygotic and 114 dizygotic female twin pairs aged 63-76 years. Approximately every third subject had a flat type, and two-thirds a descending type of audiogram configuration. No significant difference was observed in the distribution of audiogram configurations between zygosity groups. In the better ear, additive genetic effects accounted for 64%-74% of the total variance at different frequencies. For the worse ear, environmental effects were larger. Although overall heritability is rather constant across the frequency spectrum, it is noteworthy that at low and high frequencies frequency-specific genetic and environmental effects together accounted for the majority of the total variance.
Previous studies in young and middle-aged men and women have shown that resting electrocardiographic (ECG) variables are influenced by genetic factors. However, the extent to which resting ECG variables are influenced by genetic factors in older women is unknown. Thus, the aim of this study was to estimate the relative contribution of genetic and environmental influences to individual differences in resting ECG variables among older female twins without overt cardiac diseases.
Resting ECG recordings were obtained from 186 monozygotic and 203 dizygotic twin individuals, aged 63-76 years. Quantitative genetic modeling was used to decompose the phenotypic variance in each resting ECG variable into additive genetic, dominance genetic, shared environmental, and unique environmental influences.
The results showed that individual differences in the majority of the resting ECG variables were moderately to highly explained by additive genetic influences, ranging from 32% for T axis to 72% for TV(5). The results also suggested dominance genetic influences on QRS duration, TV(1), and Sokolow-Lyon voltage (36%, 53%, and 57%, respectively). Unique environmental influences were important for each resting ECG variable, whereas shared environmental influences were detected only for QT interval and QTc.
In older women without overt cardiac diseases, genetic influences explain a moderate to high proportion of individual differences in the majority of the resting ECG variables. Genetic influences are especially strong for T-wave amplitudes, left ventricular mass, and hypertrophy indices, whereas other variables, including heart rate, intervals, and axes, are more affected by environmental influences.
To examine the genetic and environmental sources of variation in self-rated health (SRH) in older female twins and to explore the roles of morbidity, functional limitation, and psychological well-being as mediators of genetic and environmental effects on SRH.
Cross-sectional analysis of twin data.
One hundred two monozygotic and 115 dizygotic female twin pairs aged 63 to 76.
SRH was categorized as good, average, or poor. Morbidity was described using a physician-assessed disease-severity scale together with information about the presence of diabetes mellitus and cancer. Maximal walking speed measured over 10 m was used to assess physical functional limitation; the Mini-Mental State Examination and the Center for Epidemiologic Studies Depression Scale were used to characterize psychological well-being. The contributions of genetic and environmental (defined as familial (shared by siblings) or nonshared (unique to each sibling)) effects were assessed using univariate and multivariate structural equation modeling of twin data.
SRH did not have its own specific genetic effect but shared a genetic component in common with the genetic components underlying liability to disease severity, maximal walking speed, and depressive symptoms. It accounted for 64% of the variation in SRH, with environmental effects accounting for the remaining variation.
The current results suggest that there are no specific genetic effects on SRH but rather that genetic influences on SRH are mediated through genetic influences affecting chronic diseases, functional limitation, and mood.
The purpose of the present study was to examine, first, whether hearing acuity predicts falls and whether the potential association is explained by postural balance and, second, to examine whether shared genetic or environmental effects underlie these associations.
Hearing was measured using a clinical audiometer as a part of the Finnish Twin Study on Aging in 103 monozygotic and 114 dizygotic female twin pairs aged 63-76 years. Postural balance was indicated as a center of pressure (COP) movement in semi-tandem stance, and participants filled in a fall-calendar daily for an average of 345 days after the baseline.
Mean hearing acuity (better ear hearing threshold level at 0.5-4 kHz) was 21 dB (standard deviation [SD] 12). Means of the COP velocity moment for the best to the poorest hearing quartiles increased linearly from 40.7 mm(2)/s (SD 24.4) to 52.8 mm(2)/s (SD 32.0) (p value for the trend = .003). Altogether 199 participants reported 437 falls. Age-adjusted incidence rate ratios (IRRs) for falls, with the best hearing quartile as a reference, were 1.2 (95% confidence interval [CI] = 0.4-3.8) in the second, 4.1 (95% CI = 1.1-15.6) in the third, and 3.4 (95% CI = 1.0-11.4) in the poorest hearing quartiles. Adjustment for COP velocity moment decreased IRRs markedly. Twin analyses showed that the association between hearing acuity and postural balance was not explained by genetic factors in common for these traits.
People with poor hearing acuity have a higher risk for falls, which is partially explained by their poorer postural control. Auditory information about environment may be important for safe mobility.
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The aim of this study was to investigate the association of noise sensitivity with self-reported hearing disability and hearing levels, with consideration of the role of self-reported history of noise exposure and use of hearing protectors. The study is based on the Finnish Twin Cohort. In 1988, a noise questionnaire was sent to 1005 twin pairs, 1495 individuals (688 men, 807 women) replied. The age range was 31-88 years. Information on some potential confounders was obtained from the questionnaire in 1981 for the same individuals. A subsample of thirty-eight elderly women with noise sensitivity response from 1988 had audiometry data from 2000 to 2001. Noise sensitivity was associated with self-reported hearing disability among all subjects [odds ratio (OR) 1.55, 95% confidence interval (CI) 1.14-2.12] and among women (OR 1.90, 95% CI 1.19-3.04), but no-more significantly among men (OR 1.31, 95% CI 0.86-1.98). The association was primarily seen among younger subjects (50 years or less). The difference between noise sensitive and non-noise sensitive elderly women in the average of thresholds at frequencies of 0.5-4 kHz in the better ear was not significant (Pr = 0.18). Noise sensitivity did not modify the association of hearing disability with the self-reported history of occupational noise exposure. Noise sensitivity was associated with the use of hearing protectors at work. The study shows the importance of recognizing the noise sensitive in noise effect studies, since sensitivity in annoyance has implications in most of the effect categories.
Stress has damaging effects on individual's health. However, information about the long-term consequences of mental stress is scarce.
This 28-year prospective cohort study examined on the associations between midlife stress and old age disability among 2,994 Finnish municipal professionals aged 44-58 years at baseline. Self-reported stress symptoms were assessed at baseline in 1981 and 4 years later in 1985 and perceived disability in 2009. For the baseline data, principal component analysis was used for differentiation into stress symptom profiles. The regression coefficient estimates for self-care disability (activities of daily living) and instrumental activities of daily living disability were estimated using left-censored regression. The odds ratios for mobility limitation were estimated using logistic regression.
Four midlife stress profiles were identified: negative reactions to work and depressiveness, perceived decrease in cognition, sleep disturbances, and somatic symptoms. We saw a clear gradient of increasing disability severity in old age for increasing intensity of midlife stress symptoms. In comparison with the participants with no stress symptoms, the extensively adjusted left-censored and logistic regression models showed that in old age, disability scores were almost 2-4 units higher and risk for mobility limitation was 2-3 times higher for those with constant stress symptoms in midlife.
Among occupationally active 44- to 58-year-old men and women, perceived stress symptoms in midlife correlated with disability 28 years later. Stress symptoms may be the first signs of decompensation of individual functioning relative to environmental demands, which may later manifest in disabilities.
To cope at their homes, community-dwelling older people surviving a hip fracture need a sufficient amount of functional ability and mobility. There is a lack of evidence on the best practices supporting recovery after hip fracture. The purpose of this article is to describe the design, intervention and demographic baseline results of a study investigating the effects of a rehabilitation program aiming to restore mobility and functional capacity among community-dwelling participants after hip fracture.
Population-based sample of over 60-year-old community-dwelling men and women operated for hip fracture (n = 81, mean age 79 years, 78% were women) participated in this study and were randomly allocated into control (Standard Care) and ProMo intervention groups on average 10 weeks post fracture and 6 weeks after discharged to home. Standard Care included written home exercise program with 5-7 exercises for lower limbs. Of all participants, 12 got a referral to physiotherapy. After discharged to home, only 50% adhered to Standard Care. None of the participants were followed-up for Standard Care or mobility recovery. ProMo-intervention included Standard Care and a year-long program including evaluation/modification of environmental hazards, guidance for safe walking, pain management, progressive home exercise program and physical activity counseling. Measurements included a comprehensive battery of laboratory tests and self-report on mobility limitation, disability, physical functional capacity and health as well as assessments for the key prerequisites for mobility, disability and functional capacity. All assessments were performed blinded at the research laboratory. No significant differences were observed between intervention and control groups in any of the demographic variables.
Ten weeks post hip fracture only half of the participants were compliant to Standard Care. No follow-up for Standard Care or mobility recovery occurred. There is a need for rehabilitation and follow-up for mobility recovery after hip fracture. However, the effectiveness of the ProMo program can only be assessed at the end of the study.
Current Controlled Trials ISRCTN53680197.
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This study examined the relative contribution of genetic and environmental effects on maximal leg extensor power and also investigated whether leg extensor power and maximum voluntary isometric knee extensor strength share a genetic component.
Muscle functions were measured as part of the Finnish Twin Study on Aging in 101 monozygotic (MZ) and 116 dizygotic (DZ) female twin pairs aged 63-76 yr. Leg extensor power was measured using the Nottingham Leg Extensor Power Rig and maximum voluntary isometric knee extensor strength using an adjustable dynamometer chair. The analyses were carried out using the maximum likelihood method in Mx-program on the raw data set.
A bivariate Cholesky decomposition model showed that leg extensor power and isometric knee extensor strength shared a genetic component in common, which accounted for 32% of the total variance in leg extensor power and 48% in isometric knee extensor strength. In addition, power and strength had a nonshared environmental effect in common accounting for four percent of the variance in power and 52% in strength. Remaining variance for leg extensor power was due to trait-specific shared and nonshared environmental effects.
Observed genetic effect in common for leg extensor power and maximum voluntary isometric knee extensor strength indicated that these two traits are regulated by the same genes. However, also environmental effects have a significant role in explaining the variability in power and strength.