Since Dr. Fogh-Andersen's legendary 1942 thesis, the Danish facial cleft population has been one of the most extensively studied in terms of epidemiology and genetic-epidemiology. The etiology of cleft lip and/or palate (CLP) is still largely an enigma, and different results concerning environmental and genetic risk factors are obtained in different countries and regions. This may be due to etiological heterogeneity between settings. Therefore, an in-depth studied area with an ethnically homogeneous population, such as Denmark, has provided one of the best opportunities for progress in CLP etiological research. The present review summarizes epidemiological and genetic-epidemiological studies conducted in the 20th century Danish facial cleft population. Furthermore, analyses of sex differences, time trends and seasonality for more than 7000 CLP cases born in Denmark in the period 1936 to 1987 are presented. The review also points toward the excellent opportunities for continued etiological CLP research in Denmark in the 21st century using already established resources and an on-going prospective cohort study of 100,000 pregnant women.
OBJECTIVE. Body image and perceived attractiveness were examined, and the impact of age, gender, and body mass index (BMI) was analyzed and discussed from an evolutionary and a sociocultural perspective. METHOD. The population-based sample consisted of 11,468 Finnish men and women aged 18 to 49 years. RESULTS. Both age-related decrease and increase in body satisfaction was detected as well as interactions between age and gender. Some effects were nonlinear. Women were generally less satisfied with their bodies than men. BMI had a stronger influence on women's body image than men's. DISCUSSION. It was proposed that it is insufficient to merely study how age affects general body image because adults might become more satisfied with some aspects of their bodies as a function of age and less satisfied with other aspects. Body satisfaction might also fluctuate during different phases of the adult life, and the patterns possibly differ between men and women.
BACKGROUND AND PURPOSE: Since stroke is a principal cause of death in elderly people, we analyzed the association between alcohol and stroke mortality in a cohort of 15,077 middle-aged and older men and women. METHODS: Data on alcohol habits were obtained from a questionnaire in 1967. The subsequent 20 years yielded 769 deaths from stroke, of which 574 were ischemic. Relative mortality risks (RR) were estimated from logistic regression analyses with lifelong alcohol abstainers as a reference group. Adjustments were made for age and smoking. RESULTS: No association was found between alcohol intake and hemorrhagic stroke. An elevated risk of ischemic stroke was found for men who drank infrequently, that is, a few times a year or less often (RR, 2.0; 95% confidence interval [CI], 1.3 to 3.2), for those who were intoxicated now and then (RR, 1.8; 95% CI, 1.1 to 2.8), and for those who reported "binge" drinking a few times in the year or less often (RR, 1.6; 95% CI, 1.1 to 2.5). Among women only ex-drinkers had an elevated risk of dying of ischemic stroke (RR, 3.3; 95% CI, 1.5 to 7.2). The risk was reduced for women who had an estimated average consumption of 0 to 5 g pure alcohol per day (RR, 0.6; 95% CI, 0.5 to 0.8); for those who did not drink every day (RR, 0.7; 95% CI, 0.5 to 0.9); and for those who never "went on a binge" (RR, 0.6; 95% CI, 0.5 to 0.8) or became intoxicated (RR, 0.7; 95% CI, 0.5 to 0.9). CONCLUSIONS: Drinking habits were associated only with deaths from ischemic stroke, and the risk patterns were different for men and women. In analyses, ex-drinkers should not be included with lifelong abstainers, since the former tend to run high health risk.
A frailty model for multivariate correlated life times is considered. The model both extends, in a rather straight-forward way, ordinary survival analysis with its emphasis on hazard modeling and incorporates well-known variance components models to account for the dependence between events of related individuals. Different approaches to estimation and inference are considered. An example from an ongoing study of genetic and environmental influences on premature death in adults serves to motivate and illustrate the model. Multivariate frailty models offer a conceptually simple and promising framework for analysis of correlated event times data, even if current knowledge is too sparse for such models to be tested critically.
Causative gene mutations have been identified in about 2% of those with amyotrophic lateral sclerosis (ALS), often, but not always, when there is a strong family history. There is an assumption that there is a genetic component to all ALS, but genome-wide association studies have yet to produce a robustly replicated result. A definitive estimate of ALS heritability is therefore required to determine whether ongoing efforts to find susceptibility genes are worth while.
The authors performed two twin studies, one population- and one clinic-based. The authors used structural equation modelling to perform a meta-analysis of data from these studies and an existing twin study to estimate ALS heritability, and identified 171 twin pairs in which at least one twin had ALS.
Five monozygotic twin pairs were concordant-affected, and 44 discordant-affected. No dizygotic twin pairs were concordant-affected, and 122 discordant-affected. The heritability of sporadic ALS was estimated as 0.61 (0.38 to 0.78) with the unshared environmental component 0.39 (0.22 to 0.62). ALS has a high heritability, and efforts to find causative genes should continue.
Clinically significant anxiety symptoms are prevalent among the elderly, yet knowledge about the longitudinal course of anxiety symptoms in later life remains scarce. The goals of this study were to (a) characterize age trajectories of state anxiety symptoms in the second half of life, and (b) estimate genetic and environmental contributions to individual differences in the age trajectory of state anxiety. This study was based on data from 1,482 participants in the Swedish Adoption/Twin Study of Aging who were aged 50 and older at their first occasion (512 complete twin pairs, 458 singletons) and had up to 6 measurement occasions spanning 11 years. Consistent with life span developmental theories of age-related emotional change, anxiety symptom levels declined during the transition from midlife to the mid-60s, followed by a mild increase that gradually plateaued in the 80s. There were substantial individual differences in the age trajectory of anxiety. After accounting for effects of sex, cohort, mode of testing, and proximity to death, this longitudinal variation was partitioned into biometric sources. Nonshared environmental variance was highest in the late 60s and declined thereafter, whereas genetic variance increased at an accelerated pace from approximately age 60 onward. There was no evidence for effects of rearing or other shared environment on anxiety symptoms in later life. These findings highlight how the etiology of anxiety symptoms changes from midlife to old age.
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Although the ApoE gene has been intensively studied in aging research, most of the studies conducted so far have been based on the traditional case-control design with subjects consisting of young controls and long-lived cases. The genotype frequency pattern in and between the two age-groups has been rarely investigated due to limitations in either research design or data analytical method. In this study, we genotyped 748 individuals (including both twin pairs and unrelated individuals) aged from 73 to 95 with aim at examining the genotype frequency trajectory of ApoE gene at high ages. Binomial and multinomial logistic regression models have been applied to model the gene frequency as a function of age and to investigate the modes of gene function (dominant, recessive, additive). The generalized estimation equations (GEEs) are introduced to account for the intra-pair genotype correlation in the twin pairs included in the data. Both the observed and the fitted frequencies show a constantly declining pattern of ApoE epsilon4 allele as age advances indicating a significant and steadily deleterious effect of the dominant allele that increases the hazard of death at high ages.
We studied the association of adolescent smoking with overweight and abdominal obesity in adulthood.
We used the FinnTwin16, a prospective, population-based questionnaire study of 5 consecutive and complete birth cohorts of Finnish twins born between 1975 and 1979 (N = 4296) and studied at four points between the ages of 16 and 27 years to analyze the effect of adolescent smoking on abdominal obesity and overweight in early adulthood.
Smoking at least 10 cigarettes daily when aged 16 to 18 years increased the risk of adult abdominal obesity (odds ratio [OR]=1.77; 95% confidence interval [CI] = 1.39, 2.26). After we adjusted for confounders, the OR was 1.44 (95% CI = 1.11, 1.88), and after further adjustment for current body mass index (BMI), the OR was 1.34 (95% CI = 0.95, 1.88). Adolescent smoking significantly increased the risk of becoming overweight among women even after adjustment for possible confounders, including baseline BMI (OR = 1.74; 95% CI = 1.06, 2.88).
Smoking is a risk factor for abdominal obesity among both genders and for overweight in women. The prevention of smoking during adolescence may play an important role in promoting healthy weight and in decreasing the morbidity related to abdominal obesity.
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