A large number of studies have shown that obesity is both under genetic control and influenced by several environmental factors, including energy expenditure and intake. Several studies in animals and humans have furthermore suggested that certain environmental factors, such as a high fat intake, may modify the expression of the genes responsible for weight gain. The present study examined whether physical activity, measured at the baseline examination in 1975, was likely to play a differential role in subsequent weight changes in the following 6 y in 1571 monozygotic and 3029 dizygotic, same-sex twin pairs from the Finnish Twin Cohort Study. A hierarchical multiple-regression analysis was used to test for gene-environment interactions by identifying significant three-way interactions between genetic factors, physical activity, and weight change. The results showed that associations between weight change in twin A and twin B were significantly stronger for monozygotic than for same-sex dizygotic twins at all levels of physical activity. Additionally, in the monozygotic men the strength of the association varied with physical activity level, and the association between the change in body mass index between the twin pairs with the highest physical activity level was about three times stronger (beta = 0.40) than the association in twin pairs with the lowest physical activity level (beta = 0.15, P for trend = 0.002). In pairs of dizygotic men, and in both monozygotic and dizygotic women, similarity in body mass index change was independent of physical activity level (all P > 0.14). The present study showed that genetic factors may modify the effects of physical activity on weight change, and suggests that a sedentary lifestyle may have an obesity-promoting effect in men with a genetic predisposition.
To study twin resemblance for weight change (delta wt) and to assess the consistency of body mass index (BMI) over 6 years.
6 year follow-up based on identical mailed questionnaires in 1975 (baseline) and in 1981 (follow-up).
5967 same-sexed non-pregnant Finnish twin pairs aged 18-54 in 1975 (1106 male and 862 female monozygotic (MZ) and 2430 male and 1569 female dizygotic (DZ) pairs).
Intra-pair correlations of delta wt and BMI, estimates of genetic and environmental components of variance of delta wt and BMI.
Unadjusted mean delta wt was +2.0 (s.d. = 4.6) kg among MZ and 2.1 (4.9) kg among DZ male individuals. Corresponding values among MZ and DZ female individuals were +1.5 (4.4) kg and +1.7 (4.4) kg, respectively. Age and initial BMI together explained 8.0% of the male and 2.3% of the female phenotypic variance of delta wt. The intraclass correlations for delta wt (adjusted for age and initial BMI) for all pairs were 0.29 and 0.07 for MZ and DZ men and 0.25 and 0.05 for MZ and DZ women, respectively. The BMI of the twins increased slightly during the follow-up compared to the baseline values (23.9 (2.7) for MZ and 24.1 for DZ men and 23.0 (3.3) for MZ and 23.2 (3.42) for DZ women). The intra-class correlations for BMI at baseline (0.69 for MZ and 0.34 for DZ men and 0.67 for MZ and 0.29 for DZ women) were almost identical with the correlations at follow-up (0.67 for MZ and 0.32 for DZ men and 0.69 for MZ and 0.29 for DZ women). The intra-class correlations for both BMI and delta wt were consistently higher among pairs living together than among pairs living apart at baseline and at follow-up in both zygosity groups (MZ and DZ). Among pairs living apart at baseline, the longitudinal model for BMI showed that the correlation between genetic effects at baseline and at follow-up was very high (> 0.9 in all age groups among both genders). The correlations for environmental effects ranged from 0.50 to 0.67 during the follow-up period.
Weight changes in adults over a 6-year period appear to be determined by environmental effects rather than genetic factors. However, the genetic component in BMI is considerable and stable over time. Shared environment is likely to contribute to the resemblance of both delta wt and BMI among adult twin pairs, especially among MZ pairs.
BACKGROUND: Published heritability estimates (h2) for body mass index (BMI) range from as low as 0.05 to as high as 0.90. The purpose of this paper is to introduce new data to help narrow the range of plausible estimates. SUBJECTS: Subjects were 53 pairs (23 M; 30 F) of monozygotic twins reared apart (MZAs), whose mean BMI was 24.2 (SD = 4.7). BMI's were transformed to approximate normality via the Box-Cox transformation. Twin paris came from the Finnish Twin Cohort (17 pairs), a data base of Japanese twins (10 pairs) and published case histories of primarily American twins (26 pairs). RESULTS: The h2 for MZAs is given by the correlation among the twin pairs. For the transformed data, the zero-order correlation of twins' BMIs was 0.79 for all twins, 0.63 for the Finnish twins, 0.73 for the Japanese twins and 0.85 for the 'archival' twins. When modeled with regression to control for relevant covariates, the estimate of h2 is either 0.50 or 0.70, depending on one's definition. The semipartial r was 0.50, suggesting that 50% of the total variance in BMI appears to the genetic in origin after controlling the covariates. The partial r was 0.70, suggesting that 70% of the variance in BMI that is not accounted for by the covariates can be attributed to genetic variation. Separation age had a small positive correlation with absolute intra-pair difference in BMI, suggesting that these estimates of h2 are not biased upwards due to early shared environment. CONCLUSIONS: Findings are consistent with past studies of MZAs and suggest that h2 estimates between 0.50 and 0.70 are reasonable. Implications of this finding are discussed.
To study how stress, life satisfaction and personality related factors, are related to long-term major weight gain.
Prospective cohort study, with follow-up by questionnaire at 6 y and 15 y with a within-study replication.
5867 twin pairs aged 18-54 y at baseline, considered as two sets of unrelated individuals in analyses.
Adjusted odds ratios (OR) for 10 kg weight gain over 6 y and 15 y.
A high level of stress at baseline, was a predictor for major weight gain over 6 y, and this effect was consistent in some groups even over 15 y. Low levels of life satisfaction and high scores for neuroticism, were predictors for weight gain in older women. These effects were consistent, even after adjustments for confounding variables (education, dieting, smoking, alcohol consumption and pregnancy in women). High levels of extroversion showed a trend towards lesser weight gain in younger men.
Psychological traits did not affect the risk of major long-term weight gain in a uniform fashion. The observed effects of the factors related to psychological health were modest and consistent, but varied by age and gender. Thus, there may be trait-specific effects in selected subgroups of the population that should be further investigated.
The effects of weight-loss attempts on long-term weight gain remain unclear.
The objective was to study prospectively how attempts to lose weight relate to future risk of major weight gain (>10 kg) and whether familial factors affect this relation.
Participants in the Finnish Twin Cohort (3536 men and 4193 women aged 18-54 y at baseline) were followed up for 6-15 y. The role of familial factors was studied in 1705 twin pairs in this cohort who were discordant for weight-loss attempts at baseline. Baseline (1975) and follow-up (1981 and 1990) data-including weight, weight-loss attempts (dieting), and selected confounders-were obtained via mailed questionnaires.
Average weight gain was at most weakly associated with weight-loss attempts. The risk of major weight gain for subjects attempting to lose weight at baseline was greatest among initially young (18-29 y) men (over 6 and 15 y, respectively-odds ratios: 2.01 and 1.74; 95% CI: 1.13, 3.57 and 1.11, 2.75) and middle-aged (30-54 y) women (over 6 and 15 y, respectively-2.43 and 1.52; 1.33, 4.42 and 1.06, 2.22) and persisted after potential confounders were controlled for. These risks decreased and became nonsignificant in the pairwise twin analysis, suggesting that the relation between dieting and subsequent major weight gain may also have a familial component.
Weight-loss attempts may be associated with subsequent major weight gain, even when several potential confounders are controlled for. Genetic and familial factors may contribute to this association.