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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
- Bouchard C. Genetics of obesity in humans: Current issues.
Ciba Foundation Symposium, 1996:108-17, 188-93.
- Perusse L, et al. The human obesity gene map: The 1998 update.
Obes Res, 1999; 7(1):111-29.
- Ryan D, et al. Conference report – Obesity: New Directions.
Obes Res, 1999; 7(3):303-8.
- Bouchard C. Obesity in adulthood – The importance of
childhood and parental obesity (editorial). New Engl J Med,
1997; 337(13):926-7.
- Whitaker R, et al. Predicting obesity in young adulthood from
childhood and parental obesity. New Engl J Med, 1997; 337(13):869-73.
- Prentice A, Jebb S. Obesity in Britain: Gluttony or sloth?
BMJ, 1995; 311(7002):437-9.
- Drewnowski A, Popkin BM. The nutrition transition: New trends
in the global diet. Nutr Rev, 1997; 55(2):31-43.
- 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.
- Sobal J, Stunkard AJ. Socioeconomic status and obesity: A
review of the literature. Psychology Bulletin, 1989; 105(2):260-75.
- 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.
- 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.
- 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.
- Hill JO, Peters JC. Environmental contributions to the obesity
epidemic. Science, 1998; 280:1371-4.
- WHO. Obesity: Preventing and managing the global epidemic.
1998. Geneva, Switzerland: World Health Organization.
- 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
- http://www.hc-sc.gc.ca/hppb/nutrition/ bmicalulatorapplet/index.html
- Reeder BA, Angel A, Ledoux M, et.al. Can Med Assoc J 1992;
146(11):2009-19.
- 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
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