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.
To study which individual characteristics and environmental factors correlate with fear of moving outdoors and whether fear of moving outdoors predicts development of mobility limitation.
Observational prospective cohort study and cross-sectional analyses.
Community and research center.
Seven hundred twenty-seven community-living people aged 75 to 81 were interviewed at baseline, of whom 314 took part in a 3.5-year follow-up.
Fear of moving outdoors and its potential individual and environmental correlates were assessed at baseline. Perceived difficulties in walking 0.5 km and 2 km were assessed twice a year over a 3.5-year period.
At baseline, 65% of the women and 29% of the men reported fear of moving outdoors. Poor socioeconomic status; musculoskeletal diseases; slow walking speed; and the presence of poor street conditions, hills in the nearby environment, and noisy traffic correlated with fear of moving outdoors. At the first 6-month follow-up, participants with fear of moving outdoors had more than four times the adjusted risk (odds ratio (OR)=4.6, 95% confidence interval (CI)=1.92-11.00) of developing difficulties in walking 0.5 km and a three times greater adjusted risk (OR=3.10, 95% CI=1.49-6.46) for developing difficulty in walking 2 km compared with those without fear. The difference in the prevalence of walking difficulties remained statistically significant over the 3.5-year follow-up (P=.02 and P=.009, respectively).
Fear of moving outdoors is common in older adults and increases the risk of developing self-reported difficulties in walking 0.5 km and 2 km. Knowledge about individual and environmental factors underlying fear of moving outdoors and finding ways to alleviate fear of moving outdoors are important for community planning and prevention of disability.
The aim of the present study was to examine the contribution of genetic and environmental factors to depressive symptoms among older women. The participants were 102 monozygotic and 115 dizygotic female twin pairs aged 64 to 76 years. Depressive symptoms were assessed by the Center for the Epidemiologic Studies Depression Scale. The contribution of genetic and environmental effects was estimated for the constructed depressiveness factor and for the subscales which were depressed mood, psychomotor retardation, lack of wellbeing and interpersonal difficulties. Of the variance in depressiveness, shared environmental influences accounted for 39% and nonshared environmental influences 61%. For the subscales, 24% to 62% of the variance was explained by individual, and 13% to 23% by shared, environmental factors. Lack of wellbeing had its own moderate additive genetic effect explaining 30% of the variance. This study showed that in older women predominantly environmental factors underlay individual differences in depressiveness; however, the factors varied to some extent between dimensions measured by the subscales.
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.
Cites: Am J Otolaryngol. 1999 Nov-Dec;20(6):371-810609481
Cites: J Gerontol A Biol Sci Med Sci. 2008 Feb;63(2):171-818314453
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.