Both obesity and exercise behavior are influenced by genetic and environmental factors. However, whether obesity and physical inactivity share the same genetic vs environmental etiology has rarely been studied. We therefore analyzed these complex relationships, and also examined whether physical activity modifies the degree of genetic influence on body mass index (BMI) and waist circumference (WC).
The FinnTwin16 Study is a population-based, longitudinal study of five consecutive birth cohorts (1975–1979) of Finnish twins. Data on height, weight, WC and physical activity of 4343 subjects at the average age of 25 (range, 22–27 years) years were obtained by a questionnaire and self-measurement of WC. Quantitative genetic analyses based on linear structural equations were carried out by the Mx statistical package. The modifying effect of physical activity on genetic and environmental influences was analyzed using gene-environment interaction models.
The overall heritability estimates were 79% in males and 78% in females for BMI, 56 and 71% for WC and 55 and 54% for physical activity, respectively. There was an inverse relationship between physical activity and WC in males (r=−0.12) and females (r=−0.18), and between physical activity and BMI in females (r=−0.12). Physical activity significantly modified the heritability of BMI and WC, with a high level of physical activity decreasing the additive genetic component in BMI and WC.
Physically active subjects were leaner than sedentary ones, and physical activity reduced the influence of genetic factors to develop high BMI and WC. This suggests that the individuals at greatest genetic risk for obesity would benefit the most from physical activity.
Excessive energy intake and physical inactivity are believed to be the main factors behind the current obesity epidemic.1, 2 Earlier studies have documented an association between sedentary behavior and obesity,3 as well as an inverse relationship between habitual physical activity and obesity.4, 5 Sedentary lifestyle is a strong predictor of obesity,6 and physical activity is considered important in the prevention of weight gain.7, 8, 9 Further, we have recently shown that persistent physical activity is associated with decreased rate of weight gain and a smaller waist circumference (WC) during a follow-up period of 30 years,10 even after controlling for genetic background and shared environmental factors.
Population-based twin studies have shown that body mass index (BMI), WC and exercise behavior are influenced by genetic factors. The heritability of BMI ranged from 45 to 85% in a comparative study of twin cohorts in eight countries,11 and heritability estimates for WC have varied between 45 and 77% in previous twin studies.12, 13, 14, 15 Genetic effects have also been demonstrated for weight gain.16, 17 The heritability of exercise participation ranged from 27 to 70% in a large pooled twin sample from seven countries.18
Given the high heritabilities of BMI, WC and physical activity, it is likely that these interrelated traits share some of the underlying genetic factors. However, it is difficult to disentangle these effects and this question has therefore rarely been studied. Heitmann et al.19 demonstrated that although both genetic factors and physical activity played an independent role in weight changes, physical activity level modified the genetic effects on weight change in male twins. The researchers hypothesized that genes suppressing weight gain may be expressed only at high physical activity levels. Karnehed et al.20 used a model based on the co-twins' obesity status as an indicator of genetic risk to analyze gene-environment interaction. Among twins with genetic susceptibility to obesity, WC and weight gain were modified by physical activity level. These studies have not, however, been able to quantify the effect of physical activity on the relative contribution of genetic and environmental effects on obesity.
In this study, we assessed the genetic and environmental components in the relationship between obesity, as indexed by BMI and WC, and physical activity in young adulthood in Finnish twins. We also examined whether physical activity modifies the genetic influences on BMI and WC. By using modern methods of quantitative genetics, we were able to analyze how much physical activity affects genetic and environmental variation in these measures of obesity.
Study subjects were Finnish twins participating in the FinnTwin16 study, a nationwide longitudinal cohort study of health behaviors in twins and their families that identified virtually all twin births from 1975 to 1979 from the Central Population Registry of Finland.21 A questionnaire was mailed semi-annually between autumn 2000 and autumn 2002 to each of the five birth cohorts of twin pairs as well as twins born in the last 3 months of 1974 (who acted as a pilot sample).22 The respondents were 22.8- to 27.2-years-old at the time of response. The response rate was 84.5% with 5236 subjects returning questionnaires out of 6196 mailed.23 Zygosity was defined using questions on physical similarity and confusion by strangers at school age. This method has shown high reliability in Finnish twin data.24 We excluded participants with known illnesses (diabetes mellitus, systemic lupus erythematosus, inflammatory bowel disease, celiac disease, hyper- or hypothyroidism, malignancies and mobility disorders) or with medication affecting weight (for example, insulin, thyroxin and antipsychotic medication) from the analyses (n=237). We also excluded subjects with missing data on zygosity (n=253). Our final data included 2188 male and 2610 female twin individuals, 696 monozygotic (MZ) and 1396 dizygotic (DZ) pairs. Data collection and analysis were approved by the ethics committee of the Department of Public Health of the University of Helsinki, and the IRB of Indiana University.
Body Mass Index (kg/m2) was calculated from self-reported height and weight. For assessment of WC, subjects were sent a tape measure. They were asked to measure their WC in the standing position according to an instruction clarified by a picture indicating that WC was to be measured midway between the lowest rib and iliac spine. We assessed the validity of the self-reported BMI and WC in a subsample of 566 twins. They participated in another study on the consequences of adolescent alcohol use with a median of 650 days after the self-report. Height was measured without shoes on a stadiometer and weight in light clothes on a calibrated beam balance. WC was measured standing, half way between the iliac crest and the lowest rib, at the end of light expiration. The agreement between the measured and reported values was good. The intra-class correlation for BMI was 0.89, mean difference 0.93 (95% CI 0.79–1.07) kg/m2, for height 0.99 and 0.24 (0.14–0.35) cm and for waist 0.75 and 2.48 (0.96–3.00) cm, respectively.
Physical activity index was calculated from the product of self-reported exercise intensity, duration (hours) and yearly frequency (days). Intensity was expressed as estimated metabolic equivalent (MET) values (work metabolic rate divided by resting metabolic rate).25 Adequate validity of these measures was found with respect to interviews and fitness assessments of VO2max among these twins in adolescence.26 A cardiorespiratory exercise test was performed in 48 MZ twin individuals from the FinnTwin16 cohort, as described earlier,27 and we found a strong correlation (r=0.53) between VO2max and the physical activity index.
The data were analyzed using quantitative genetic modeling of twin and family data.28 Whereas MZ twins are genetically identical, DZ twins and full-sibs have, on average, 50% of their segregating genes identical-by-descent. In addition to additive genetic variation, which is the sum of the effects of all alleles affecting the phenotype, part of the genetic variation may be due to interaction between alleles in the same locus (dominance). Additive and dominance genetic effects are fully correlated within MZ pairs and have expected correlations of 0.5 and 0.25 within DZ pairs, respectively. Epistatic effects, that is, interaction effects between alleles in different loci, are assumed to be absent. MZ and DZ pairs are assumed to share the same amount of environmental variation, which is partly shared by a twin pair (common environment) and partly unique to each twin individual (unique environment) including any random measurement error. On the basis of the above assumptions, four sources of variation interpreted as latent and standardized variance components in the structural equation model can be identified: additive genetic (A), genetic dominance (D), common environment (C) and unique environment (E). Our data include only twins reared together and do therefore not allow modeling of genetic dominance and common environmental effects simultaneously. The genetic models were carried out using the Mx statistical package.29
We started the genetic modeling by carrying out univariate models for BMI, WC and physical activity to estimate genetic and environmental influences and find the best model for each trait used in further modeling. The fit of models was tested comparing χ2-goodness-of-fit statistics and degrees of freedom (d.f.) between nested models; large change in the χ2-values compared with the change in d.f. (Δχd.f.2) between two nested models indicates that the simpler model does not describe the data as adequately as the more complex model and the eliminated parameters are thus important in the model. The assumptions of twin modeling, that is, equal means and variances for MZ and DZ twins as well as for both co-twins, were tested by comparing twin models to saturated models, which do not make these assumptions.
We then analyzed pair-wise genetic and environmental correlations between these indicators using full trivariate Cholesky decomposition (Figure 1a). According to this method, the trait correlation between BMI and physical activity is because of additive genetic correlation (rA) indicating the same or closely linked genes and unique environmental correlation (rE) indicating same or correlated environmental factors. Finally we conducted a gene-environment interaction model (Figure 1b). The moderator factor, that is, physical activity in this study, is denoted as M. This factor can affect the mean trait value (βM) but also modify the effects of genetic (βX) and environmental factors (βY and βZ) on the trait. The model implies that physical activity can affect both the mean BMI (active persons are leaner than sedentary persons) and variances (active persons may have less genetic or environmental variance than sedentary persons).
All applicable institutional and governmental regulations concerning the ethical use of human volunteers were followed during this research. The study was approved by the Ethics Committees of the Helsinki University Department of Public Health and of the Helsinki and Uusimaa Hospital District.
There were no systematic differences in means and variances of BMI, WC and physical activity between the MZ and DZ twins (Table 1). In the pooled data of MZ and DZ twins, males had higher BMI (23.9±3.1 vs 22.2±3.5 kg/m2, for male vs female, P<0.001), WC (85±9 vs 75±10 cm, P<0.001) and physical activity (5.1±5.6 vs 4.3±4.7 MET h/d, respectively, P<0.001) than females.
The within-pair intra-class correlations (Table 2) for all traits were higher for MZ twins than DZ twins, indicating the probable effect of genetic factors on BMI, WC and physical activity. The DZ correlations for BMI and WC were less than half of the corresponding MZ correlations, suggesting presence of dominance (D) effects. For physical activity, the same-sex DZ correlations were virtually exactly half of the MZ correlations suggesting lack of both dominance genetic and common environmental effects. Correlations within opposite-sex pairs were systematically lower than within same-sex DZ pairs suggesting the possible presence of sex-specific genetic effects.
We started genetic modeling by estimating the best model for BMI, WC and physical activity (model fit statistics available from the authors). The additive genetic/specific environment (AE) model offered the best fit for all traits: dropping dominance genetic (D) effect from the model did not decrease the fit statistically significantly. For physical activity we also tested for the presence of a common environmental effect, but dropping this effect had virtually no effect on model fit either (Δχ22=0.01, P=0.95). When compared to the saturated model, the fit of the AE model was good for all traits. Sex-specific genetic effect was statistically significant for BMI, WC and physical activity and also the absolute size of the variance components differed for BMI and WC whereas no difference was seen in physical activity. Thus in the subsequent modeling, we decided to use the AE model with sex-specific genetic effect and own variance component estimates for men and women for all traits.
Table 3 summarizes the proportions of the phenotypic variance of BMI, WC and physical activity explained by additive genetic and unique environmental factors in the best fitting AE model. The heritability estimates were higher for BMI and WC than for physical activity, with no difference between sexes except for WC for which the heritability was higher for women. When we decomposed the additive genetic effects to the proportions common to men and women and unique to one sex only, we found that a major part of the A effect for each trait consisted of sex-specific factors (51% for BMI, 49% for WC and 46% for physical activity).
Phenotypic correlations of WC, BMI and physical activity in twin individuals were calculated. In Table 4 we additionally show the model-based genetic and environmental correlations between these traits, which were estimated from trivariate Cholesky models. BMI and WC were strongly correlated in both males (r=0.79, 95% CI 0.77–0.81) and females (r=0.81, 95% CI 0.80–0.82), with a strong genetic correlation (adjusted for physical activity) between the two in both sexes. The environmental correlation (also adjusted for physical activity) was somewhat weaker but still highly significant. Physical activity was negatively and more weakly associated with BMI in females (r=−0.11, 95% CI −0.15 to −0.07) but not in males(r=0.04, 95% CI −0.002 to –0.08), although it was negatively correlated with WC in both sexes (r=−0.11 (95% CI −0.15 to −0.07) for men, r=−0.15 (95% CI −0.19 to −0.11) for women). The genetic and environmental correlations between physical activity and each of the anthropometric measures, adjusted for each other, were relatively weak and of approximately the same magnitude.
Finally, we tested physical activity as a moderator of genetic and/or environmental effects on BMI and WC. We conducted this model only for same-sex twins, because the model could not be identified in the presence of sex-specific genetic effects. Physical activity significantly modified additive genetic (A) effects on BMI and WC in both sexes, so that additive genetic variances decreased with increasing physical activity (Table 5, Figure 2). This indicates that genetic factors play a less important role in determining the BMI and WC of physically active subjects as compared with sedentary ones. In addition, parallel modification of the E effect by physical activity was seen for WC in females (Table 5, Figure 2).
This study on a large cohort of young adult twins shows a strong cross-sectional association between physical activity and WC, and a somewhat weaker association with BMI. Although, heritable factors play an important role behind the variation of BMI, WC and physical activity, the anthropometric measures were only modestly related genetically to physical activity. The strong relationship between BMI and WC was due to both genetic and environmental correlations. Further, we found that physical activity significantly modifies the effect of genetic factors on the variation of WC and BMI. The influence of genetic factors on the variation of BMI and WC was less important in physically active subjects, suggesting that high physical activity would be particularly beneficial in those genetically predisposed to obesity. However, prospective cohort studies and interventions are needed to confirm the direction of effect and causality.
A major finding in our study was that among healthy young adults the inverse relationship between physical activity and WC (adjusted for BMI) was more significant than that of physical activity and BMI (adjusted for WC), and seen in both males and females, whereas physical activity was negatively associated with BMI in females only. The close relationship between WC and physical activity suggests that WC is a more adequate measure of obesity than BMI, especially in young men. Physically active young males may have a large muscle mass, which affects BMI more than WC. Physical activity may also reduce body fat, preferentially from the abdominal area. For example, in a small but intensive study where energy balance was held constant, exercise reduced abdominal fat despite unchanged body weight.30
In keeping with earlier twin studies, the overall heritability estimates for physical activity in our study were 79 and 78% (males and females) for BMI, 56 and 71% for WC and 55 and 54% for physical activity. The heritability estimates for BMI have ranged from 45–85% in earlier twin studies.11, 31 In a study of 325 female and 299 male Danish twin pairs, heritability of WC was 61% for men and 48% for women.15 The heritability of exercise participation ranged from 27 to 70% in a large pooled twin sample from seven countries.18
Because genetic factors account for such a large proportion of the population variance in weight and physical activity, it is possible that genetic factors explain associations between physical inactivity and obesity. Many studies have shown that lean subjects are physically more active than obese ones4, 5, 32 and that physically active subjects gain less weight than sedentary subjects.33 These findings may partly be explained by a genetic selection bias: individuals who have a favorable genetic profile to engage in physical activity are more likely to do so and also more likely to stay lean. There are very few studies, which take into account this kind of complex genetic confounding. However, a recent Finnish twin study with a 30-year follow-up of twin pairs discordant for physical activity showed that the sedentary twin gained 5.4 kg more weight and had 8.4 cm larger WC compared with their more active co-twin10 indicating that independent of familial background, physical activity protects from weight gain, especially of that in the abdominal region. In this study, both genetic and environmental factors explained the cross-sectional associations between physical activity and WC as well as physical activity and BMI in females, among which additive genetic correlations were slightly stronger than specific environmental correlations. In males, the corresponding associations were weaker and we could not distinguish which had stronger impact, genes or environment.
A novel finding was that physical activity modified the heritability of BMI and WC, with a high level of physical activity decreasing the additive genetic component in BMI and WC. This suggests that inherited factors significantly influence body weight and adiposity in sedentary subjects, although in physically active individuals the effect of genes is diminished. It can thus be expected that physical activity could be especially advantageous in the prevention of weight gain for individuals genetically susceptible to obesity.
Few studies have assessed the modifying effect of physical activity on the genetic influences on obesity. Heitmann et al.19 studied BMI change in relation to past physical activity and found that the genetic influence on BMI change in men was detected at medium and high physical activity levels only. However, genetic influences on weight change appear to be rather distinct from those on BMI.34 Thus, although physical activity may lessen the effects of genes on body size, the future trajectory of weight change may be more affected by genes than environment in physically very active subjects. The interaction of genes and physical activity may also evolve as subjects age, young men and women in their mid 20s probably being much more active than in their later years. Karnehed et al.20 found that twins genetically susceptible to obesity were more prone to large WC if they were sedentary than twins without such susceptibility—a result in line with our findings. It was, however, unclear whether the high and low genetic risk groups differed in baseline BMI, WC and physical activity.
A possible mechanism for how physical activity reduces the genetic effects on obesity is that it changes the expression patterns of genes regulating weight and adiposity. Andreasen et al.35 recently demonstrated that the impact of the FTO rs9939609 genotype was influenced by the habitual level of physical activity. Physical inactivity was associated with a BMI increase of 1.95±0.33 kg/m2 in homozygous FTO rs9939609 A-allele carriers, whereas no major effect of sedentary lifestyle was found comparing non-carriers and those heterozygous for the FTO rs9939609 A-allele. A similar mechanism was detected in a recent study by Kilpeläinen et al.36 where physical activity was shown to modify the risk of developing type 2 diabetes associated with genes regulating insulin secretion, although Rankinen et al.37 found that the effect of a hypertension-associated genotype on blood pressure is dependent on physical activity levels.
This study has several strengths. It is based on a large and representative (response rate 88%) population based on a twin cohort of young and healthy adults with small differences in age. Studying MZ and DZ twins makes it possible to examine both genetic and environmental influences on certain traits as well as their interactions. The study also has limitations. The data on BMI, WC and physical activity are based on self-reports, likely to lead to under-reporting of body weight and over-reporting of height and thus underestimation of BMI.38 In this study, however, the correlation between self-reported and measured BMI was very high. The self-reporting of WC, however, appears to be subject to more error than reporting of BMI, though it should be noted that there was some time difference between self-measurement and later clinical measurement. In this analysis, we examined the relationship between physical activity, genes and obesity. It is possible that other factors modify or account for these relationships by both affecting the ability to be physically active and promoting the development of obesity. We have excluded overt disease as such a cause, and subclinical disease is not likely to account for our findings in a sample of young healthy adults. However, other environmental factors, known or unknown, such as viral or other infections may be of relevance in this complex interplay.
Our study is in keeping with previous data suggesting that physical activity is beneficial in preventing obesity, in particular abdominal obesity. Most importantly, this study demonstrates that a physically active lifestyle is able to counteract genetic predisposition to obesity.
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This study was funded by the Academy of Finland Center of Excellence in Complex Disease Genetics, Academy of Finland (Grants no. 44069, 100499, 118555 and 108297) and DIOGENES (‘Diet, Obesity and Genes’) project supported by the European Union (Contract no. FP6-513946) and Helsinki University Central Hospital Grants. L Mustelin and KH. Pietiläinen were supported by the Juho Vainio Foundation and KH. Pietiläinen by Yrjö Jahnsson Foundation and by Jalmari and Rauha Ahokas Foundation.
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Mustelin, L., Silventoinen, K., Pietiläinen, K. et al. Physical activity reduces the influence of genetic effects on BMI and waist circumference: a study in young adult twins. Int J Obes 33, 29–36 (2009). https://doi.org/10.1038/ijo.2008.258
- gene-environment interaction
- physical activity
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