Both genetic and environmental factors are involved in the etiology of obesity and the associated lipid disturbances. We determined whether acquired obesity is associated with changes in global serum lipid profiles independent of genetic factors in young adult monozygotic (MZ) twins. 14 healthy MZ pairs discordant for obesity (10 to 25 kg weight difference) and ten weight concordant control pairs aged 24-27 years were identified from a large population-based study. Insulin sensitivity was assessed by the euglycemic clamp technique, and body composition by DEXA (% body fat) and by MRI (subcutaneous and intra-abdominal fat). Global characterization of lipid molecular species in serum was performed by a lipidomics strategy using liquid chromatography coupled to mass spectrometry. Obesity, independent of genetic influences, was primarily related to increases in lysophosphatidylcholines, lipids found in proinflammatory and proatherogenic conditions and to decreases in ether phospholipids, which are known to have antioxidant properties. These lipid changes were associated with insulin resistance, a pathogonomic characteristic of acquired obesity in these young adult twins. Our results show that obesity, already in its early stages and independent of genetic influences, is associated with deleterious alterations in the lipid metabolism known to facilitate atherogenesis, inflammation and insulin resistance.
Cites: Cell. 1992 Mar 6;68(5):879-871312391
Cites: J Immunol. 2005 Mar 1;174(5):2981-915728511
Cites: Biochem J. 1992 Oct 1;287 ( Pt 1):237-401417777
The aim of this study was to examine the effects of genetic and environment influences and sex on injury involvement using two sets of Finnish twin data. The younger participants were 955 twins born between 1983 and 1987, aged 20 to 24 years. The older participants were 12,428 twins born between 1930 and 1957, aged 33 to 60 years. Within-twin correlations in monozygotic and dizygotic twins suggested that genetic effects play no role in injury involvement among young twins, but do have some effect at older ages. The results indicated that environmental factors have greater importance in injury involvement than genetic factors in the younger twin data set (FT12), whereas in a middle-aged (33-60 years) twin data set, genetic effects explained about quarter of the variance in injury involvement. Sex was a strong contributing factor, with males being generally more prone to injuries than females.
To investigate life expectancy and mortality among former elite athletes and controls.
HR analysis of cause-specific deaths sourced from the national death registry for former Finnish male endurance, team and power sports athletes (N=2363) and controls (N=1657). The median follow-up time was 50 years.
Median life expectancy was higher in the endurance (79.1 years, 95% CI 76.6 to 80.6) and team (78.8, 78.1 to 79.8) sports athletes than in controls (72.9, 71.8 to 74.3). Compared to controls, risk for total mortality adjusted for socioeconomic status and birth cohort was lower in the endurance ((HR 0.70, 95% CI 0.61 to 0.79)) and team (0.80, 0.72 to 0.89) sports athletes, and slightly lower in the power sports athletes (0.93, 0.85 to 1.03). HR for ischaemic heart disease mortality was lower in the endurance (0.68, 0.54 to 0.86) and team sports (0.73, 0.60 to 0.89) athletes. HR for stroke mortality was 0.52 (0.33 to 0.83) in the endurance and 0.59 (0.40 to 0.88) in the team sports athletes. Compared to controls, the risk for smoking-related cancer mortality was lower in the endurance (HR 0.20, 0.08 to 0.47) and power sports (0.40, 0.25 to 0.66) athletes. For dementia mortality, the power sports athletes, particularly boxers, had increased risk (HR 4.20, 2.30 to 7.81).
Elite athletes have 5-6 years additional life expectancy when compared to men who were healthy as young adults. Lower mortality for cardiovascular disease was in part due to lower rates of smoking, as tobacco-related cancer mortality was especially low.
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
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 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.
The genetic component of alcohol use disorder is substantial, but monozygotic twin discordance indicates a role for nonheritable differences that could be mediated by epigenetics. Despite growing evidence associating epigenetics and psychiatric disorders, it is unclear how epigenetics, particularly DNA methylation, relate to brain function and behavior, including drinking behavior.
The authors carried out a genome-wide analysis of DNA methylation of 18 monozygotic twin pairs discordant for alcohol use disorder and validated differentially methylated regions. After validation, the authors characterized these differentially methylated regions using personality trait assessment and functional MRI in a sample of 499 adolescents.
Hypermethylation in the 3'-protein-phosphatase-1G (PPM1G) gene locus was associated with alcohol use disorder. The authors found association of PPM1G hypermethylation with early escalation of alcohol use and increased impulsiveness. They also observed association of PPM1G hypermethylation with increased blood-oxygen-level-dependent response in the right subthalamic nucleus during an impulsiveness task.
Overall, the authors provide first evidence for an epigenetic marker associated with alcohol consumption and its underlying neurobehavioral phenotype.
Comment In: Am J Psychiatry. 2015 Jun;172(6):499-50125982661
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.
Cites: Am J Public Health. 1989 Feb;79(2):152-72913832
Cites: Am J Epidemiol. 1982 Nov;116(5):765-757148802
Cites: Ann Intern Med. 1989 Nov 15;111(10):783-72817625
Cites: JAMA. 1993 Mar 17;269(11):1391-58441214
Cites: BMJ. 1995 Nov 25;311(7017):1401-58520275
Cites: Int J Obes Relat Metab Disord. 1997 Mar;21(3):189-969080257
Cites: J Epidemiol Community Health. 1997 Jun;51(3):252-609229053
Cites: Am J Clin Nutr. 1998 May;67(5):846-529583840
Cites: Int J Obes Relat Metab Disord. 1998 Sep;22(9):915-229756252
Cites: Health Psychol. 1998 Sep;17(5):454-89776004
It has been suggested that certain health behaviours, such as smoking, may operate as mediators of the well-established inverse association between IQ and mortality risk. Previous research may be afflicted by unadjusted confounding by socioeconomic or psychosocial factors. Twin designs offer a unique possibility to take genetic and shared environmental factors into account. The aim of the present national twin study was to determine the interrelations between IQ at age 18, childhood and attained social factors and smoking status in young adulthood and mid-life. We studied the association between IQ at age 18 and smoking in later life in a population of 11 589 male Swedish twins. IQ was measured at military conscription, and data on smoking and zygosity was obtained from the Swedish Twin Register. Information on social factors was extracted from censuses. Data on smoking was self-reported by the twins at the age of 22-47 years. Logistic regression models estimated with generalised estimating equations were used to explore possible associations between IQ and smoking among the twins as individuals as well as between-and within twin-pairs. A strong inverse association between IQ and smoking status emerged in unmatched analyses over the entire range of IQ distribution. In within-pair and between-pair analyses it transpired that shared environmental factors explained most of the inverse IQ-smoking relationship. In addition, these analyses indicated that non-shared and genetic factors contributed only slightly (and non-significantly) to the IQ-smoking association. Analysis of twin pairs discordant for IQ and smoking status displayed no evidence that non-shared factors contribute substantially to the association. The question of which shared environmental factors might explain the IQ-smoking association is an intriguing one for future research.