HEALTH PROFESSIONALS

Obesity: Genetics or Environment?

Contributed by Dr. Harvey Anderson, Ph.D., University of Toronto

What roles do genetics and environment play as determinants of obesity? Obesity is a multifactorial disease. It results primarily from a lifestyle that promotes greater energy input than output, and manifests itself more readily in individuals who have inherited susceptibility to the disease, suggesting a strong role for genetics as a determinant. However, interpreting the strength of genetics is complicated by the fact that families share lifestyle, environmental and cultural factors (1). Also, changes in the gene pool do not account for the rapid worldwide increase in obesity, suggesting that environment is the major factor.

Role of Genetics

Some researchers have estimated that genetics accounts for 25-40% of the variation in body mass index (BMI) (2). However, no one gene has been consistently associated with BMI when studies of likely genes are evaluated in popu-lation studies (2). The number of genes and other markers that have been linked with the human obesity phenotype is now approaching 200. Thus, there appears to be a great deal of diversity in the types of genetic abnormalities that produce obesity. In a recent report of an obesity conference held in 1998, the authors state that “even when the entire genome is sequenced and we have all of the individual units of heredity in hand, the problem of predicting which combinations will produce obesity on which background will still be difficult, if not impossible” (3).

The fact that obesity runs in families cannot be fully accounted for by environmental conditions and it appears that affected relatives share specific genetic characteristics (4). This has been shown in studies of fraternal and identical twins reared together, and identical twins reared apart, adoptees and their biologic and adoptive parents, large cohorts of nuclear families, as well as in intervention studies with identical twins (4).

Both childhood and parental obesity predict obesity in adulthood (5). Parental obesity probably influences the risk of obesity because of both shared genes and environmental factors within families. Parental obesity more than doubles the risk of adult obesity among both obese and non-obese children under 10 years of age. Among older children, obesity is an important predictor of adult obesity, regardless of parents’ weight, suggesting strong environmental and behavioural components. However, overweight children under 3 years of age whose parents are not obese, are at low risk for obesity.

Recent epidemiological trends suggest that the primary causes of obesity must be environmental and behavioural changes affecting large sections of the population.

Biological factors which influence an individual’s susceptibility to obesity include: gender, ethnicity and vulnerable periods of life. Higher body fat in females is assumed to have the purpose of ensuring reproductive functions. Development of obesity in certain ethnic groups may be due to a genetic predisposition for obesity, which only becomes apparent with an affluent lifestyle. Examples include: Australian Aborigines and South Asians who move to industrialized countries. Both have a predisposition for central adiposity. The physiological determinants of this fat distribu-tion are unknown, but are believed to involve insulin. Vulnerable periods when there is a predisposition to gain weight because of altered physiology and metabolism include: prenatal life, adolescence, pregnancy, and menopause. A decrease in activity is a major contributor for some of these periods.

An increase in obesity rates has occurred in a relatively constant gene pool. For example, from 1980-1991, the prevalence of clinical obesity doubled in England (5), yet similar large changes in the gene pool could not have occurred in only 11 years.

Recent epidemiological trends suggest that the primary causes of obesity must be environmental and behavioural changes, affecting large sections of the population.

Environmental Factors

The two environmental factors affecting body weight and energy balance are food supply and activity. Low energy expenditure appears to be the key determinant of the current obesity epidemic. Economic and technological advances have caused a significant reduction in activity levels (6). Daily energy expenditure continues to decrease and is associated with affluence. Both work and leisure time are often spent physically inactive as mechanization replaces intensely physical tasks and computers, television and video are choice leisure pursuits (6). The relationship between obesity and inactivity is much closer than between obesity and diet (6).

While activity is key, food supply is also an important environmental factor in obesity. Aspects of food that affect intake include: taste, texture, smell, sight and compositional factors like fat, protein, carbohydrate and fibre. Added sugars and dietary fat have received intense examination as possible causes of obesity, yet there is no direct evidence that any one dietary factor is responsible for the development of obesity.

The incidence of obesity increases in an environment where food is plentiful, safe, palatable and energy-rich (i.e. high energy-density and high fat) (7). Substantial experimental evidence shows that high-fat diets tend to increase body fat in humans. Human meal feeding studies show fat suppresses food intake the least, suggesting that it has a lesser effect, than either carbohydrate or protein, on food intake regulatory centres in the short term. Fat is the most efficient of the macronutrients in expanding fat stores. The estimated cost of storing fat is 3% of energy ingested, whereas storing carbohydrate as body fat requires 23% of its energy content (8).

Diet and energy expenditure are key determinants of body weight which operate within an environment encompassing a wide range of socio-economic status (SES) and behavioural factors including income, education and occupation. Income is the SES factor most responsible for changes in dietary intake and body weight.

In developed societies a strong inverse relationship between obesity and SES exists among women, meaning that rich women tend to be thin and poor women, obese. The relationship is inconsistent for men and children (9). In contrast, in developing societies, the SES/obesity relationship is strong, as SES increases so does the incidence of obesity, with both men and women affected. A population-wide shift occurs as socio-economic conditions improve, with overweight replacing thinness (10). Obesity in high SES groups in developing countries appears to be due to more adequate food supplies and also perhaps to cultural values favouring fat body shapes (9). Thinness in lower SES groups may be due to insufficient food, high levels of energy expenditure or both. Obesity may be a sign of health and wealth in developing countries and the reverse in developed countries.

Education level tends to be inversely associated with body weight in industrialized countries (11). Little is known about the role of occupation, although in industrialized countries manual workers are heavier, smoke more and consume more food high in fat than non-manual workers(12).

Prevention Strategies

Prevention of obesity must be based on an understanding of genetics and environment. A fundamental premise must be that obesity arises from low energy expenditure and abundant food supply (13). A recent WHO report concludes that obesity is “a disease that is largely preventable through change in lifestyles” and that obesity prevention is the responsibility of communities, governments, media and the food industry (14). All of these sectors must collaborate to make the environ-ment less conducive to weight gain. Dietary guidance should be informed by public health issues, social, economic, agricultural and environmental factors affecting food availability, eating and food patterns.

As with food-based dietary guidance (15), strategies to reduce the prevalence of obesity, must be relevant in the socio-cultural context. Each country should develop a process for examining the prevalence and determinants of obesity and strategies for its prevention. It should be recognized that planning a public health strategy that focuses on a single factor is a reductionist approach that has failed.

Summary

Determinants of obesity are complex. Genetics account for approximately 25-40%. However, there is no reason to believe that identification of the multitude of genes that in some way modulate responses to the environment will provide a solution. Environmental factors that increase the susceptibility to obesity of the individual are many and include activity, socio-economic status and food supply. One factor alone cannot account for obesity in all individuals. Prevention and control of obesity will depend on understanding and managing the environmental factors operating within a country and a culture.

References

  1. Bouchard C. Genetics of obesity in humans: Current issues. Ciba Foundation Symposium, 1996:108-17, 188-93.
  2. Perusse L, et al. The human obesity gene map: The 1998 update. Obes Res, 1999; 7(1):111-29.
  3. Ryan D, et al. Conference report – Obesity: New Directions. Obes Res, 1999; 7(3):303-8.
  4. Bouchard C. Obesity in adulthood – The importance of childhood and parental obesity (editorial). New Engl J Med, 1997; 337(13):926-7.
  5. Whitaker R, et al. Predicting obesity in young adulthood from childhood and parental obesity. New Engl J Med, 1997; 337(13):869-73.
  6. Prentice A, Jebb S. Obesity in Britain: Gluttony or sloth? BMJ, 1995; 311(7002):437-9.
  7. Drewnowski A, Popkin BM. The nutrition transition: New trends in the global diet. Nutr Rev, 1997; 55(2):31-43.
  8. Flatt J. The biochemistry of energy expenditure. In: Bray G, ed. Recent advances in obesity research II. Proceedings of the 2nd international congress on obesity. London: Newman, 1978.
  9. Sobal J, Stunkard AJ. Socioeconomic status and obesity: A review of the literature. Psychology Bulletin, 1989; 105(2):260-75.
  10. De Onis M, Habicht JP. Anthropometric reference data for international use: Recommendations from a World Health Organization expert committee. Am J Clin Nutr, 1996; 64:650-8.
  11. Popkin B, et al. A review of dietary and environmental correlates of obesity with emphasis on developing countries. Obes Res, 1995; 2(suppl 2):145s-53s.
  12. Hulshof K, et al. Diet and other lifestyle factors in high and low socio-economic groups (Dutch Nutrition Surveillance System). Eur J Clin Nutr, 1995; 45:441-50.
  13. Hill JO, Peters JC. Environmental contributions to the obesity epidemic. Science, 1998; 280:1371-4.
  14. WHO. Obesity: Preventing and managing the global epidemic. 1998. Geneva, Switzerland: World Health Organization.
  15. Anderson GH. Developing and implementing science-based dietary guidelines: An opportunity for facilitating and forging partnerships. In: Florentino RF, ed. Dietary guidelines in Asian countries: Towards a food-based approach. Singapore: ILSI Press/ILSI Southeast Asia, 1997:77-85.

Definitions

Obesity - The definition of obesity is based on the body mass index (BMI), a simple index of weight to height that provides the best measure of body fat. BMI has become a world-wide standard, adopted by the World Health Organization (WHO) and Health Canada, and is defined as weight in kilograms divided by height in metres squared (1).

BMI = weight (kg)
        height 2 (m 2 )

Using this scale, BMI cut-off points have been established by the WHO:

under 20 = underweight
20 to 25 = normal
25 to 30 = overweight
greater than 30 = obese.

In the early 1990s, using these WHO definitions, it was reported that 47% of Canadians were over-weight and 15% were obese. Men were more likely to be overweight than women, but a greater proportion of women were taking steps to lose weight (2).

In addition to BMI, distribution of body fat is an important predictor of health problems associated with obesity. Fat in the central abdominal area has been shown to increase risks for diabetes, dyslipi-demia, hypertension and heart disease. A waist circumference greater than 40 inches (102 cm) in men, and greater than 35 inches (88 cm) in women is considered high risk (3). So, a person could have a “normal” BMI, but be at higher risk for chronic diseases if fat is selectively located in the abdominal area.

References

  1. http://www.hc-sc.gc.ca/hppb/nutrition/ bmicalulatorapplet/index.html
  2. Reeder BA, Angel A, Ledoux M, et.al. Can Med Assoc J 1992; 146(11):2009-19.
  3. Lau DCW. Can Med Assoc J 1999; 160(4):503-6.

Obesity Canada

In 1999, a new organization with a focus on obesity was formed: Obesity Canada. Obesity Canada is committed to improving the health of Canadians by decreasing the occurrence of obesity and its consequences. Obesity Canada’s mandate covers education, research and promotion.

Goals include:

  • development of partnerships
  • actions to prevent obesity
  • advocacy and advice
  • promotion of research
  • translation of research findings into health policy and practice
  • promotion of optimal practice in prevention and management among health professionals
  • discussion and dissemination of new knowledge
  • being a source of factual information for the public and media on issues and services.

To join Obesity Canada, you must be a registered health professional or student. The Board of Directors has representation from across Canada and reflects a broad membership including, epidemiology, medicine, dietetics, research, and nursing. Membership is $50 a year.

Apply to: Obesity Canada Secretariat, Dept. of Community Health and Epidemiology, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK S7N 5E5.

Carbohydrate Lit Scan

Cox DN, Perry L, Moore PB, Vallies L, Mela DJ. Sensory and hedonic associations with macronutrients and energy intakes of lean and obese consumers. Int J Obes, 1999;23:403-10.

The research objective was to establish differences between lean and obese subjects using subjective measures of sensory and hedonic attributes of food, food intake and composition. Results suggest both obese and lean subjects do not self-select diets with markedly different perceived attributes. Obese subjects appear to consume a diet higher in energy density, associated with intakes of salty/savoury food items.

Popkin BM, Doak CM. The obesity epidemic is a worldwide phenomenon. Nutr Rev, 1998;56(4):106-14.

Review of national surveys conducted around the world to develop a better understanding of the factors contributing to obesity. It is concluded that diet and physical activity are the major determinants of obesity, across all populations. The authors recommend that policy makers give high priority and direct more resources to preventive efforts.

Rippe J, Crossley S, Ringer R. Obesity as a chronic disease: Modern medical and lifestyle management. J Am Diet Assoc, 1998; 98(suppl 2):S9-S15.

Examination of the modern epidemic of obesity and its association with type-2 diabetes, coronary heart disease, dyslipidemia and hypertension. Authors recommend lifestyle interventions and, when required, medical treatment by an interdisciplinary team of physicians, dietitians, exercise specialists, and behaviour therapists.

Jebb SA. Obesity: From molecules to man. Proc Nutr Soc, 1999;58:1-14.

Review of causes of obesity, including genetic, metabolic, behavioural and environmental factors, based on research done at MRC Dunn Nutrition Centre at Cambridge, U.K. Extensive research has not shown that genetic or metabolic defects are responsible for most obesity. Causes of obesity lie in the integration of energy intake with energy expenditure. Lifestyle changes – diet and physical activity – are encouraged for the prevention and treatment of obesity.

Carbohydrate News

Carbohydrate News is an annual publication of the Canadian Sugar Institute (CSI). CSI maintains a scientific library and comprehensive computer database of current literature pertaining to carbohydrate, sugar and health.

CSI also publishes resource material for health professionals, educators and the public. CSI gratefully acknowledges the contributions made by the Editorial Board; Gérald Fortier, for his French adaptation; and Nathalie Jobin, dt.p., M.Sc., for her additional review of the French adaptation of Carbohydrate News.

EDITORIAL BOARD

Harvey Anderson, Ph.D.
Professor, Department of Nutritional Sciences
Faculty of Medicine
University of Toronto

N. Theresa Glanville, Ph.D., P. Dt.
Associate Professor and Chair
Department of Applied Human Nutrition
Mount St. Vincent University

David D. Kitts, Ph.D.
Associate Professor,
Department of Food Science
Faculty of Agriculture
University of British Columbia

Rena Mendelson, D.Sc., RD
Associate Vice President,
Academic School of Nutrition
Ryerson Polytechnic University

Alison M. Stephen, Ph.D.
Professor, Division of Nutrition and Dietetics
College of Pharmacy and Nutrition
University of Saskatchewan

Huguette Turgeon O’Brien, Ph.D., Dt.P.
Professor, Department of Food Sciences and Nutrition
Faculty of Agriculture and Food Science
Laval University

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