Introduction

Genetic factors influence several features of obesity - e.g. insulin resistance, central abdominal adiposity - in postmenopausal women. However, the increased prevalence of overweight and obesity cannot be entirely attributed to changes in the genetics of the population. This does not prevent many obese persons blaming their condition on their genes, claiming that diet and exercise cannot help them. A recent study in twins shows that this is not quite the case; it explores the potential interaction between genetic susceptibility to obesity and levels of physical activity. Because monozygotic twins share 100% of their genes, any differences in body fat within a pair must result from environmental differences.

Method

A database in the United Kingdom containing information on unselected twins yielded 970 white female twin subjects; these included 241 monozygotic twin pairs. The following assessments were made: body weight, height, and body composition, using dual-energy x-ray absorptiometry, of total-body fat (mass and percentage body weight), and central abdominal fat (expressed as mass of fat tissue in a defined region). Physical activity was gauged using two questionnaires, one concerned with general activity at home or work, in sport and in walking, and the other with leisure activity in detail. Quadriceps muscle strength was measured mechanically. Dietary intake was assessed in roughly half the participants using a food-frequency questionnaire, and demographic information (smoking habits, socioeconomic class, etc) was obtained.

Cross-sectional analysis of body fat and physical activity in the whole collective was done using simple regression analysis. Multiple regression models that considered smoking, hormone replacement therapy, dietary carbohydrate intake, and socioeconomic status were next done. Then 156 monozygotic twin pairs that were concordant for hormone use and smoking status were entered in a co-twin case-control analysis of physical activity. Finally, analysis was done to determine if participants genetically predisposed to obesity had a differential effect of physical activity on fat mass; the genetic risk was derived from tertiles of body fat, resulting in 67 twins with a low genetic risk and 69 with a high genetic risk.

Results

The mean age of the 970 female twins was 55.5 years, and the mean body mass index (BMI) was 24.4 kg/m2. Fifty-six percent were normal weight, 30% overweight (BMI >25 - 29.9 kg/m2), 7% obese (BMI >30 kg/m2), and 7% underweight (BMI <19.9 kg/m2).

The cross-sectional analysis showed an inverse relationship between physical activity and total-body and central abdominal fat. The lowest fat values were found in those twins who were active at home or work, or who did 2 hours of sport, walked 10 miles, or undertook sweat-inducing activities each week. Weight-bearing exercise was particularly effective - mean total-body and central abdominal fat mass were 5.6 kg and 0.43 kg less, respectively, in those performing vigorous resistance programs.

In the regression models, physical activity was the strongest independent predictor of total-body and central abdominal fat. In the monozygotic twins who were concordant for smoking and hormone use, 1 and 2 hours of moderate-intensity exercise were associated with lesser amounts of 1.0 kg and 1.4 kg of total-body fat, respectively.

Analyses did not support an interaction between genetic risk and physical activity - thus twins in the higher tertile of total-body fat (i.e. those allocated a greater genetic risk) had a mean decrease of 3.96 kg with physical activity, compared with a decrease of 2.05 kg in the lower risk tertile group.

Comment

The monozygotic twin-pair model is recognized as a powerful tool for specifically exploring the relationship between two variables. In this study, the role of one environmental factor against obesity, physical activity, was examined in depth, while controlling for smoking and hormone replacement therapy. A similar study by the same investigators found no relationship between carbohydrate and fat intake and total-body or central abdominal fat mass.¹ It seems clear, therefore, that physical activity is the strongest environmental influence on total-body fat mass in healthy middle-aged women. The findings also suggest that persons with a strong family history of obesity may not be disadvantaged in their response to exercise, despite strong genetic factors regulating fat mass. In other words, obese people cannot blame it all on their genes; they should be given every encouragement to participate in a well-designed exercise program.

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