The mechanisms through which genes influence body weight are not well understood, but appetite has been implicated as one mediating pathway. Here we use data from two independent population-based Finnish cohorts (4632 adults aged 25-74 years from the DILGOM study and 1231 twin individuals aged 21-26 years from the FinnTwin12 study) to investigate whether two appetitive traits mediate the associations between known obesity-related genetic variants and adiposity. The results from structural equation modelling indicate that the effects of a polygenic risk score (90 obesity-related loci) on measured body mass index and waist circumference are partly mediated through higher levels of uncontrolled eating (ßindirect = 0.030-0.032, P
Cites: Am J Clin Nutr. 2009 Dec;90(6):1483-819828706
Cites: J Nutr. 2010 Apr;140(4):831-420181787
Cites: Int J Epidemiol. 2010 Apr;39(2):504-1819959603
The aim of the study was to compare the appropriateness of different obesity indicators in the assessment of coronary heart disease (CHD) risk.
The study cohort included 11,510 Finnish men and women aged 25 to 64 year at baseline who participated in a cardiovascular disease risk factor survey in 1987 or 1992. At baseline, data on smoking and diabetes were recorded, blood pressure. body mass index (BMI), waist circumference (WC), and waist to hip ratio (WHR) were measured, and serum total and high-density lipoprotein (HDL) cholesterol were determined. A follow-up was done to the end of 1997. Death or diagnosed event from CHD was used as an outcome variable.
At baseline, BMI was the best explaining variable for systolic and diastolic blood pressure (DBP) and for total cholesterol, whereas WC was the best explaining variable for HDL cholesterol, among both men and women. During the follow-up, WHR was the best predictor of CHD incidence. However, after the adjustment for other CHD risk factors none of the obesity indicators remained statistically significant. In both sexes, BMI was a statistically significant predictor of CHD incidence among subjects with DBP lower than the mean. Among men, a similar interaction was seen between DBP and WC.
WHR was the best predictor of CHD incidence in our data. Abdominal obesity has an effect on CHD incidence independently of general obesity.
An inverse association between body height and the incidence of coronary heart disease (CHD) has been observed. However, the mechanisms behind this association are still largely unknown. We will examine the role of genetic and familial factors behind the association in a large twin data set.
The data were derived from the Finnish Twin cohort including 2438 singletons, 4073 monozygotic (MZ) twins, and 9202 dizygotic (DZ) twins aged 25-69 years at baseline in 1976. Incident CHD cases were derived from hospital discharge data and cause of death data between 1977 and 1995. Cox regression analysis and conditional logistic regression analysis were used.
In population-level analyses no differences in the general risk of CHD between zygosity groups were found. The association between body height and CHD was similar between sexes and zygosity groups. When men and women in all zygosity groups were studied together an increased risk of CHD was found only among the shortest quartile (hazard ratio [HR] = 1.34, 95% CI: 1.14-1.57). Among the twin pairs discordant for CHD a suggestive increased risk for the shorter twin was seen among DZ twins (odds ratio [OR] = 1.19, 95% CI: 0.95-1.48) when men and women were studied together.
An inverse association between body height and CHD was broadly similar between sexes and twin zygosity groups and was associated with short stature. Among discordant twin pairs we found a weak association among DZ twins but not MZ twins. This may suggest the role of genetic liability behind the association between body height and CHD.
Education is associated with health related lifestyle choices including leisure-time physical inactivity. However, the longitudinal associations between education and inactivity merit further studies. We investigated the association between education and leisure-time physical inactivity over a 35-year follow-up with four time points controlling for multiple covariates including familial confounding.
This study of the population-based Finnish Twin Cohort consisted of 5254 twin individuals born in 1945-1957 (59 % women), of which 1604 were complete same-sexed twin pairs. Data on leisure-time physical activity and multiple covariates was available from four surveys conducted in 1975, 1981, 1990 and 2011 (response rates 72 to 89 %). The association between years of education and leisure-time physical inactivity (
Cites: Twin Res. 2002 Oct;5(5):358-6512537859
Cites: Twin Res Hum Genet. 2013 Feb;16(1):157-6223298696
Cites: Am J Epidemiol. 2002 Dec 1;156(11):985-9312446254
Cites: J Health Econ. 2010 Jan;29(1):1-2819963292
Cites: Int J Epidemiol. 2009 Oct;38(5):1310-2219528192
Cites: Scand J Public Health. 2014 Nov;42(7):611-2025201896
To investigate the predictive value of hand grip/body weight ratio and hand grip strength in early adulthood for obtaining a disability pension (DP) due to musculoskeletal disorders in later life.
A nationwide population-based sample of men born 1951-76 (n=1,387,166) in Sweden and anthropometric and strength indicators from their conscription examination. Register data on the date and diagnoses of granted DP between the years 1971-2006. Cox proportional hazards regression was used to estimate hazard ratios (HR) with 95% confidence intervals (95% CI).
The lowest quintile of hand grip/body weight ratio predicted a greatly increased risk (HR 2.51, 95% CI 2.40-2.63) for DP due to musculoskeletal disorders compared to the mid-quintile. The highest quintile of hand grip/body weight ratio predicted a decreased risk (HR 0.80, 95% CI 0.75-0.84). Stratification of the hand grip/body weight ratio with body mass index confirmed the results. However, the highest quintiles of hand grip strength adjusted for height and weight predicted a somewhat increased risk for DP due to musculoskeletal disorders (HR 1.25, 95% CI 1.18-1.32).
This study indicates that the hand grip/body weight ratio in young adulthood is strongly and inversely associated with men's risk of obtaining a disability pension due to musculoskeletal disorders in later life. However, the risk seems to be mediated through the body weight. The properties of hand grip/body weight ratio should be further evaluated before it can be recommended for use in clinical and epidemiological studies.
Birth order is associated with outcomes such as birth weight and adult socioeconomic position (SEP), but little is known about the association with adult height. This potential birth order-height association is important because height predicts health, and because the association may help explain population-level height trends. We studied the birth order-height association and whether it varies by family characteristics or birth cohort.
We used the Swedish Military Conscription Register to analyse adult height among 652,518 men born in 1951-1983 using fixed effects regression models that compare brothers and account for genetic and social factors shared by brothers. We stratified the analysis by family size, parental SEP and birth cohort. We compared models with and without birth weight and birth length controls.
Unadjusted analyses showed no differences between the first two birth orders but in the fixed effects regression, birth orders 2, 3 and 4 were associated with 0.4, 0.7 and 0.8 cm (p
An inverse association between height and risk of coronary heart disease (CHD) is well demonstrated, but it is not known whether this association is because of genetic factors, socioeconomic background, or other environmental factors. Four population-based twin cohorts with register-based follow-up data on CHD mortality from Denmark (1966-1996), Finland (1975-2001), and Sweden (1963-2001 and 1972-2001) were used to investigate this question; response rates varied between 65% and 86%. Together, the cohorts included 74,704 twin individuals (35,042 complete twin pairs) with 5,943 CHD deaths during 1.99 million person-years of follow-up. Cox and conditional logistic regression models were used. Per 1-standard deviation decrease in height, height was inversely associated with CHD mortality in men (hazard ratio = 1.08, 95% confidence interval (CI): 1.04, 1.12) and in women (hazard ratio = 1.06, 95% CI: 1.01, 1.10). A twin who had died from CHD was on average shorter than the co-twin within monozygotic pairs (odds ratio = 1.27, 95% CI: 1.12, 1.44, with no sex difference), whereas a weaker association was found within dizygotic pairs in men (odds ratio = 1.01, 95% CI: 0.91, 1.13) and in women (odds ratio = 1.14, 95% CI: 1.01, 1.28). The inverse association between height and CHD mortality found within monozygotic discordant twin pairs suggests that this association is because of environmental factors that directly affect height and CHD risk.
To investigate longitudinal associations of smoking and a change in smoking status with leisure-time physical inactivity. In addition, to control whether familial confounding (genetics and shared environment) influences the associations.
Data were based on the population-based Finnish Adult Twin Cohort of 5254 twin individuals born in 1945-1957 (41% men) and who participated in all four surveys over a 35-year follow-up (1975-2011). Logistic and conditional logistic regression models with multiple covariates were used for analyses.
Compared to never-smokers, long-term daily smokers (1975-1990) had the highest likelihood for both long-term inactivity and to change into inactive by 2011. Recurrent smoking was associated with long-term inactivity. Instead, in comparison to persistent daily smokers, quitting smoking decreased the likelihood of becoming physically inactive at leisure time. The associations remained in the analyses which accounted for multiple covariates and/or familial confounding.
Daily smoking increases the likelihood of remaining or becoming physically inactive over the decades. Our results emphasize not only the importance of preventing smoking initiation, but also to support early smoking cessation in promotion of lifelong physical activity.
Little is known about the associations of serum fatty acids with lipoprotein profile and the underlying genetic and environmental etiology of these relationships. We aimed to analyze the phenotypic association of serum n-6 and n-3 polyunsaturated (PUFAs), monounsaturated (MUFAs) and saturated (SFAs) fatty acids (relative proportion to total fatty acids) with lipids and lipoproteins, and to quantify common genetic and environmental factors determining their covariation.
Two cohorts of healthy Finnish twins were assessed in young adulthood. Data were available for 1269 individual twins including 561 complete pairs. Serum metabolites were measured by nuclear magnetic resonance spectroscopy. Bivariate quantitative genetic models were used to decompose the phenotypic covariance between the pairs of traits into genetic and environmental components.
Among the strongest correlations observed, serum total n-6 PUFAs and linoleic acid were inversely (max. r=-0.65) and MUFAs positively (max. r=0.63) correlated with triglycerides and very low-density lipoprotein (VLDL) particle concentration, particularly with large VLDL (for n-6 PUFAs) and medium VLDL (for MUFAs). Genetic factors significantly contributed to their covariance with bivariate heritability estimates ranging from 44% to 56% for n-6 PUFAs and 58% to 66% for MUFAs. Genetic correlations with lipid traits were moderate to high (max. rA=-0.59 and 0.70 for n-6 PUFAs and MUFAs, respectively). Statistically significant, but substantially weaker phenotypic correlations of total n-3 PUFAs, docosahexaenoic acid (DHA) and SFAs with lipoprotein profile were not decomposed into their genetic and environmental components.
Shared genetic factors are important in explaining why higher concentrations of serum n-6 PUFAs and lower concentrations of serum MUFAs strongly associate with lower triglyceride and VLDL particle concentrations.
Little is known about the relationship between growth and lipoprotein profile. We aimed to analyze common genetic and environmental factors in the association of height from late childhood to adulthood and pubertal timing with serum lipid and lipoprotein subclass profile.
A longitudinal cohort of Finnish twin pairs (FinnTwin12) was analyzed using self-reported height at 11-12, 14, 17 years and measured stature at adult age (21-24 years). Data were available for 719 individual twins including 298 complete pairs. Serum lipids and lipoprotein subclasses were measured by proton nuclear magnetic resonance spectroscopy. Multivariate variance component models for twin data were fitted. Cholesky decomposition was used to partition the phenotypic covariation among traits into additive genetic and unique environmental correlations.
In men, the strongest associations for both adult height and puberty were observed with total cholesterol, low-density lipoprotein cholesterol, intermediate-density lipoprotein cholesterol, and low-density lipoprotein particle subclasses (max. r = -0.19). In women, the magnitude of the correlations was weaker (max. r = -0.13). Few associations were detected between height during adolescence and adult lipid profile. Early onset of puberty was related to an adverse lipid profile, but delayed pubertal development in girls was associated with an unfavorable profile, as well. All associations were mediated mainly by additive genetic factors, but unique environmental effects cannot be disregarded.
Early puberty and shorter adult height relate to higher concentrations of atherogenic lipids and lipoprotein particles in early adulthood. Common genetic effects behind these phenotypes substantially contribute to the observed associations.