Population aging increases the need for knowledge on positive aspects of aging, and contributions of older people to their own wellbeing and that of others. We defined active aging as an individual's striving for elements of wellbeing with activities as per their goals, abilities and opportunities. This study examines associations of health, health behaviors, health literacy and functional abilities, environmental and social support with active aging and wellbeing. We will develop and validate assessment methods for physical activity and physical resilience suitable for research on older people, and examine their associations with active aging and wellbeing. We will examine cohort effects on functional phenotypes underlying active aging and disability.
For this population-based study, we plan to recruit 1000 participants aged 75, 80 or 85 years living in central Finland, by drawing personal details from the population register. Participants are interviewed on active aging, wellbeing, disability, environmental and social support, mobility, health behavior and health literacy. Physical activity and heart rate are monitored for 7 days with wearable sensors. Functional tests include hearing, vision, muscle strength, reaction time, exercise tolerance, mobility, and cognitive performance. Clinical examination by a nurse and physician includes an electrocardiogram, tests of blood pressure, orthostatic regulation, arterial stiffness, and lung function, as well as a review of chronic and acute conditions and prescribed medications. C-reactive protein, small blood count, cholesterol and vitamin D are analyzed from blood samples. Associations of factors potentially underlying active aging and wellbeing will be studied using multivariate methods. Cohort effects will be studied by comparing test results of physical and cognitive functioning with results of a cohort examined in 1989-90.
The current study will renew research on positive gerontology through the novel approach to active aging and by suggesting new biomarkers of resilience and active aging. Therefore, high interdisciplinary impact is expected. This cross-sectional study will not provide knowledge on temporal order of events or causality, but an innovative cross-sectional dataset provides opportunities for emergence of novel creative hypotheses and theories.
OBJECTIVE: Exposure to environmental organochlorines has been examined as a potential risk factor for human breast cancer with mixed results. Our purpose was to examine associations between organochlorines and the development of breast cancer in a large prospective study using stored adipose tissue. METHODS: We conducted a nested case-control study of 409 postmenopausal women who developed breast cancer and 409 controls selected from the 29,875 women enrolled in the Danish Diet, Cancer, and Health cohort between 1993 and 1997. We measured concentrations of 14 pesticides and 18 polychlorinated biphenyls in adipose tissue, collected upon enrollment, and estimated relative risk (RR) of breast cancer using conditional logistic regression. RESULTS: The results showed no higher risk of breast cancer among women with higher levels of any pesticides or polychlorinated biphenyls; the RR associated with the upper quartile of 1,1-dichloro-2, 2-bis(p-chlorophenyl)ethylene concentration was 0.7 [95% confidence interval (95% CI), 0.5-1.2] contrasting the lower quartile, and for the sum of polychlorinated biphenyls the similar risk was 1.1 (95% CI, 0.7-1.7). We observed a pattern of substantially lower risk of estrogen receptor-negative breast cancer in association with higher levels of most of the pesticides and polychlorinated biphenyls; the RR for the higher quartile of 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene was 0.1 (95% CI, 0.0-0.5) and for the sum of polychlorinated biphenyls it was 0.3 (95% CI, 0.1-0.9). CONCLUSION: The results do not support that higher organochlorine body levels increase the risk of breast cancer in postmenopausal women. The interpretation of the inverse association for estrogen receptor-negative breast cancer is currently unclear.
Vehicle engine exhaust includes ultrafine particles with a large surface area and containing absorbed polycyclic aromatic hydrocarbons, transition metals and other substances. Ultrafine particles and soluble chemicals can be transported from the airways to other organs, such as the liver, kidneys, and brain. Our aim was to investigate whether air pollution from traffic is associated with risk for other cancers than lung cancer.
We followed up 54,304 participants in the Danish Diet Cancer and Health cohort for 20 selected cancers in the Danish Cancer Registry, from enrolment in 1993-1997 until 2006, and traced their residential addresses from 1971 onwards in the Central Population Registry. We used modeled concentration of nitrogen oxides (NO(x)) and amount of traffic at the residence as indicators of traffic-related air pollution and used Cox models to estimate incidence rate ratios (IRRs) after adjustment for potential confounders.
NO(x) at the residence was significantly associated with risks for cervical cancer (IRR, 2.45; 95% confidence interval [CI], 1.01;5.93, per 100 µg/m(3) NO(x)) and brain cancer (IRR, 2.28; 95% CI, 1.25;4.19, per 100 µg/m(3) NO(x)).
This hypothesis-generating study indicates that traffic-related air pollution might increase the risks for cervical and brain cancer, which should be tested in future studies.
Cites: JAMA. 2002 Mar 6;287(9):1132-4111879110
Cites: Environ Health Perspect. 2011 Jun;119(6):860-521227886
Cites: Cancer Causes Control. 2003 Dec;14(10):907-1414750529
Cites: Int J Cancer. 2004 May 20;110(1):3-1415054863
Cites: Cancer Causes Control. 2004 May;15(4):331-915141134
Cites: Int J Cancer. 2004 Aug 20;111(2):286-9215197784
Oxidative damage to guanine (8-oxoGua) is one of the most abundant lesions induced by oxidative stress and documented mutagenic. 8-Oxoguanine DNA glycosylase 1 (OGG1) removes 8-oxoGua from DNA by excision. The urinary excretion of 8-oxoGua is a biomarker of exposure, reflecting the rate of damage in the steady state. The aim of this study was to investigate urinary 8-oxoGua as a risk factor for lung cancer. In a nested case-cohort design we examined associations between urinary excretion of 8-oxoGua and risk of lung cancer as well as potential interaction with the OGG1 Ser326Cys polymorphism in a population-based cohort of 25,717 men and 27,972 women aged 50-64 years with 3-7 years follow-up. We included 260 cases with lung cancer and a subcohort of 263 individuals matched on sex, age, and smoking duration for comparison. Urine collected at entry was analysed for 8-oxoGua by HPLC with electrochemical detection. There was no significant effect of smoking or OGG1 genotype on the excretion of 8-oxoGua. Overall the incidence rate ratio (IRR) (95% confidence interval) of lung cancer was 1.06 (0.97-1.15) per doubling of 8-oxoGua excretion. The association between lung cancer risk and 8-oxoGua excretion was significant among men [IRR: 1.17 (1.03-1.31)], never-smokers [IRR: 9.94 (1.04-94.7)], and former smokers [IRR: 1.19 (1.07-1.33)]. There was no significant interaction with the OGG1 genotype, although the IRR was 1.14 (0.98-1.34) among subjects homozygous for Cys326. The association between urinary 8-oxoGua excretion and lung cancer risk among former and never-smokers suggests that oxidative stress with damage to DNA is important in this group.
Perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) are used in a variety of consumer products and have been detected worldwide in human blood. Recent studies mainly of highly exposed populations have indicated that PFOA and PFOS may affect serum cholesterol levels, but the magnitude of the effect may be inconsistent across exposure levels. The aim of the present cross-sectional study was to investigate the association between plasma PFOA and PFOS and total cholesterol in a general, middle-aged Danish population. The study population comprised 753 individuals (663 men and 90 women), 50-65 years of age, nested within a Danish cohort of 57,053 participants. Blood samples were taken from all cohort members at enrolment (1993-1997) and stored in a biobank at -150°C. Plasma levels of PFOA and PFOS and serum levels of total cholesterol were measured. The associations between plasma PFOA and PFOS levels and total cholesterol levels were analysed by generalized linear models, both crude and adjusted for potential confounders. We observed statistically significant positive associations between both perfluorinated compounds and total cholesterol, e.g. a 4.4 [95% CI ?=? 1.1-7.8] higher concentration of total cholesterol (mg/dL) per interquartile range of PFOA plasma level. Sex and prevalent diabetes appeared to modify the association between PFOA and PFOS, respectively, and cholesterol. In conclusion, this study indicated positive associations between plasma PFOA and PFOS levels and total cholesterol in a middle-aged Danish population, although whether the observed pattern of results reflects a causal association is unclear.
Cites: Drug Chem Toxicol. 2000 Nov;23(4):603-2011071397
Cites: Environ Sci Technol. 2011 Oct 1;45(19):8137-4320939531
To profile participants based on reported outdoor physical activity barriers using a data-driven approach, describe the profiles and study their association with unmet physical activity need.
Cross-sectional analyses of 848 community-dwelling men and women aged 75-90 living in Central Finland in 2012. Barriers to outdoor physical activity and unmet physical activity need were enquired with a questionnaire. The latent profiles were identified by profiling participants into latent groups using a mixture modeling technique on the multivariate set of indicators of outdoor physical activity barriers. A path model was used to study the associations of the profiles with unmet physical activity need.
Five barrier profiles were identified. Profile A was characterized with minor barriers, profile B with weather barriers, profile C with health and weather barriers, profile D with barriers concerning insecurity, health and weather; and profile E with mobility and health barriers. The participants in the profiles differed in the proportion of individual and environmental barriers. The risk for unmet physical activity need was highest among people whose severe mobility difficulties restricted their outdoor physical activity.
Outdoor physical activity barriers reflect the imbalance in person-environment fit among older people, manifested as unmet physical activity need.
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.
Short-term exposure to air pollution has been associated with exacerbation of chronic obstructive pulmonary disease (COPD), whereas the role of long-term exposures on the development of COPD is not yet fully understood.
We assessed the effect of exposure to traffic-related air pollution over 35 years on the incidence of COPD in a prospective cohort study.
We followed 57,053 participants in the Danish Diet, Cancer, and Health cohort in the Hospital Discharge Register for their first hospital admission for COPD between 1993 and 2006. We estimated the annual mean levels of nitrogen dioxide (NO2) and nitrogen oxides (NO(x)) at all residential addresses of the cohort participants since 1971 to an event or 2006 and used indicators of traffic near the residential address at recruitment. We assessed the association between exposure to air pollution and COPD incidence by Cox regression analyses for the full cohort, and for participants with and without comorbid conditions, including asthma, diabetes, or cardiovascular disease.
A first hospital admission for COPD was recorded for 1,786 (3.4%) of 52,799 eligible subjects between recruitment (1993-1997) and 2006. COPD incidence was associated with the 35-year mean NO2 level (hazard ratio, 1.08; 95% confidence interval, 1.02-1.14, per interquartile range of 5.8 µg/m³), with stronger associations in subjects with diabetes (1.29; 1.05-1.50) and asthma (1.19; 1.03-1.38).
Long-term exposure to traffic-related air pollution may contribute to the development of COPD with possibly enhanced susceptibility in people with diabetes and asthma.
Perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) are used in a variety of industrial and consumer products and have been detected worldwide in human blood. The sources for human exposure are not well described, but dietary intake is suggested as an important source. In this study of 652 Danish men from the Diet, Cancer and Health cohort, we examined intake of 10 major dietary groups, tap water drinks, alcohol consumption, cooking method, geographical area, age, smoking status, and BMI as potential determinants of PFOA and PFOS plasma levels. Living in the Aarhus area was associated with higher PFOA and PFOS plasma levels compared with living in the Copenhagen area, and never smokers had higher levels than current smokers. Frying as compared with other cooking methods was a determinant of PFOA and PFOS levels. BMI and alcohol consumption were inversely associated with both compounds. Among the dietary groups, only intake of eggs was significantly positively associated with PFOS plasma levels. In future studies, PFOA and PFOS levels in air, dust and water samples should be measured to elucidate further the sources of exposure; exposure through diet needs to be studied in greater detail. Our finding of a higher body burden of PFOA and PFOS among never smokers also warrants further evaluation.
Cadmium is a known carcinogen that can disrupt endocrine signalling. Cigarette smoking and food are the most common routes of non-occupational exposure to cadmium. Cadmium accumulates in the kidney and can be measured in urine, making urine cadmium (U-Cd) a biomarker of long-term exposure. However dietary-cadmium (D-Cd) intake estimates are often used as surrogate indicator of cadmium exposure in non-smoking subjects. It is therefore important to investigate the concordance between D-Cd estimates obtained with Food Frequency Questionnaires and U-Cd.
U-Cd levels were compared with estimated dietary-cadmium (D-Cd) intake in 1764 post-menopausal women from the Danish Diet, Cancer and Health cohort. For each participant, a food frequency questionnaire, and measures of cadmium content in standard recipes were used to judge the daily intake of cadmium, normalized by daily caloric intake. Cadmium was measured by ICP-MS in spot urine sampled at baseline and normalized by urinary creatinine. Information on diet, socio-demographics and smoking were self-reported at baseline.
Linear regressions between U-Cd and D-Cd alone revealed minimal but significant positive correlation in never smokers (R2 = 0.0076, ß = 1.5% increase per 1 ng Cd kcal(-1), p = 0.0085, n = 782), and negative correlation in current smokers (R2 = 0.0184, ß = 7.1% decrease per 1 ng Cd kcal(-1) change, p = 0.0006, n = 584). In the full study population, most of the variability in U-Cd was explained by smoking status (R2 = 0.2450, n = 1764). A forward selection model revealed that the strongest predictors of U-Cd were age in never smokers (? R2 = 0.04), smoking duration in former smokers (? R2 = 0.06) and pack-years in current smokers (? R2 = 0.07). Food items that contributed to U-Cd were leafy vegetables and soy-based products, but explained very little of the variance in U-Cd.
Dietary-Cd intake estimated from food frequency questionnaires correlates only minimally with U-Cd biomarker, and its use as a Cd exposure indicator may be of limited utility in epidemiologic studies.
Cites: Environ Health Perspect. 2014 Apr;122(4):363-7024531129
Cites: Environ Health Perspect. 2009 Aug;117(8):1293-30119672411
Cites: PLoS One. 2014;9(6):e10081524963789
Cites: Int J Hyg Environ Health. 2014 Sep;217(7):720-524690412
We investigated whether there is an interaction between distance from residence at birth to nearest power line and domestic radon and traffic-related air pollution, respectively, in relation to childhood leukemia risk. Further, we investigated whether adjusting for potential confounders alters the association between distance to nearest power line and childhood leukemia. We included 1024 cases aged
The aim of this study was to analyze whether the associations between perceived environmental and individual characteristics and perceived walking limitations in older people differ between those with intact and those with poorer lower extremity performance.
Persons aged 75 to 90 ( N = 834) participated in interviews and performance tests in their homes. Standard questionnaires were used to obtain walking difficulties; environmental barriers to and, facilitators of, mobility; and perceived individual hindrances to outdoor mobility. Lower extremity performance was tested using Short Physical Performance Battery (SPPB).
Among those with poorer lower extremity performance, the likelihood for advanced walking limitations was, in particular, related to perceived poor safety in the environment, and among those with intact performance to perceived social issues, such as lack of company, as well as to long distances.
The environmental correlates of walking limitations seem to depend on the level of lower extremity performance.
INTRODUCTION: Ambient air pollution is a risk factor for mortality and morbidity. The aim of this study was to quantify the health effects related to particulate matter (PM10) in Denmark. MATERIALS AND METHODS: We used relative risk estimates in relation to PM10 based on the epidemiological literature. Population exposure to PM10 was calculated. Cases attributable to PM10 were estimated for mortality, cardiovascular and respiratory hospital admissions, chronic bronchitis, acute bronchitis, restricted activity days, and asthma attacks. Moreover, we attempted to estimate health-related gains from equipping all heavy-duty vehicles in Denmark with particle filters. RESULTS: We estimated the average population PM10 exposure to be about 22 micrograms/m3, about one third of which can be attributed to natural (not man-made) PM10. The number of cases per year attributable to the estimated exposure included about 5,000 deaths, about 5,000 hospital admissions, about 5,000 cases of chronic bronchitis, about 17,000 cases of acute bronchitis, about 200,000 asthma attacks, and about three million restricted activity days. The health-related gains from installing particle filters on all heavy-duty vehicles in Denmark are uncertain; the estimates for mortality ranged from 22 to 1,250, depending on the assumptions. DISCUSSION: Although air pollution constitutes only a minor risk factor on the individual level, it seems to be a major public health problem. The particle characteristics responsible for the estimated health effects are not well understood. The ultrafine particle fraction may cause a much greater impact on health than indicated by the mass.
Comment In: Ugeskr Laeger. 2002 Aug 19;164(34):393512212471
Environmental barriers are associated with disability-related outcomes in older people but little is known of the effect of environmental barriers on mortality. The aim of this study was to examine whether objectively measured barriers in the outdoor, entrance and indoor environments are associated with mortality among community-dwelling 80- to 89-year-old single-living people.
This longitudinal study is based on a sample of 397 people who were single-living in ordinary housing in Sweden. Participants were interviewed during 2002-2003, and 393 were followed up for mortality until May 15, 2012.Environmental barriers and functional limitations were assessed with the Housing Enabler instrument, which is intended for objective assessments of Person-Environment (P-E) fit problems in housing and the immediate outdoor environment. Mortality data were gathered from the public national register. Cox regression models were used for the analyses.
A total of 264 (67%) participants died during follow-up. Functional limitations increased mortality risk. Among the specific environmental barriers that generate the most P-E fit problems, lack of handrails in stairs at entrances was associated with the highest mortality risk (adjusted RR 1.55, 95% CI 1.14-2.10), whereas the total number of environmental barriers at entrances and outdoors was not associated with mortality. A higher number of environmental barriers indoors showed a slight protective effect against mortality even after adjustment for functional limitations (RR 0.98, 95% CI 0.96-1.00).
Specific environmental problems may increase mortality risk among very-old single-living people. However, the association may be confounded by individuals' health status which is difficult to fully control for. Further studies are called for.
Epidemiological studies suggest that long-term exposure to transport noise increases the risk for cardiovascular disorders. The effect of transport noise on blood pressure and hypertension is uncertain.
In 1993-1997, 57,053 participants aged 50-64 year were enrolled in a population-based cohort study. At enrollment, systolic and diastolic blood pressure was measured. Incident hypertension during a mean follow-up of 5.3 years was assessed by questionnaire. Residential long-term road traffic noise (Lden) was estimated for 1- and 5-year periods preceding enrollment and preceding diagnosis of hypertension. Residential exposure to railway noise was estimated at enrollment. We conducted a cross-sectional analysis of associations between road traffic and railway noise and blood pressure at enrollment with linear regression, adjusting for long-term air pollution, meteorology and potential lifestyle confounders (N = 44,083). Incident self-reported hypertension was analyzed with Cox regression, adjusting for long-term air pollution and potential lifestyle confounders.
We found a 0.26 mm Hg higher systolic blood pressure (95% confidence intervals (CI): -0.11; 0.63) per 10 dB(A) increase in 1-year mean road traffic noise levels, with stronger associations in men (0.59 mm Hg (CI: 0.13; 1.05) per 10 dB(A)) and older participants (0.65 mm Hg (0.08; 1.22) per 10 dB(A)). Road traffic noise was not associated with diastolic blood pressure or hypertension. Exposure to railway noise above 60 dB was associated with 8% higher risk for hypertension (95% CI: -2%; 19%, P = 0.11).
While exposure to road traffic noise was associated with systolic blood pressure in subgroups, we were not able to identify associations with hypertension.
Cites: Behav Sleep Med. 2007;5(1):1-2017313321
Cites: Occup Environ Med. 2007 Feb;64(2):122-617053022
Exposure to traffic noise has been associated with adverse effects on neuropsychological outcomes in children, but findings with regard to behavioral problems are inconsistent.
We investigated whether residential road traffic noise exposure is associated with behavioral problems in 7-year-old children.
We identified 46,940 children from the Danish National Birth Cohort with complete information on behavioral problems at 7 years of age and complete address history from conception to 7 years of age. Road traffic noise (Lden) was modeled at all present and historical addresses. Behavioral problems were assessed by the parent-reported Strengths and Difficulties Questionnaire (SDQ). Associations between pregnancy and childhood exposure to noise and behavioral problems were analyzed by multinomial or logistic regression and adjusted for potential confounders.
A 10-dB increase in average time-weighted road traffic noise exposure from birth to 7 years of age was associated with a 7% increase (95% CI: 1.00, 1.14) in abnormal versus normal total difficulties scores; 5% (95% CI: 1.00, 1.10) and 9% (95% CI: 1.03, 1.18) increases in borderline and abnormal hyperactivity/inattention subscale scores, respectively; and 5% (95% CI: 0.98, 1.14) and 6% (95% CI: 0.99, 1.12) increases in abnormal conduct problem and peer relationship problem subscale scores, respectively. Exposure to road traffic noise during pregnancy was not associated with child behavioral problems at 7 years of age.
Residential road traffic noise in early childhood may be associated with behavioral problems, particularly hyperactivity/inattention symptoms.
Cites: Lancet. 2005 Jun 4-10;365(9475):1942-915936421
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.