BMJ 2004;329:736-739 (25 September), doi:10.1136/bmj.329.7468.736
Education and debate
The runaway weight gain train: too many accelerators, not enough brakes
Boyd Swinburn, professor of population health1,
Garry Egger, adjunct professor2
1 School of Exercise and Nutrition Sciences, Deakin University, 221 Burwood Highway, Melbourne, Victoria 3125, Australia,
2 Southern Cross University, Military Road, East Lismore, New South Wales 2480, Australia
Correspondence to: B Swinburn swinburn{at}deakin.edu.au
Obesity seems to be perpetuated by a series of vicious cycles, which, in combination with increasingly obesogenic environments, accelerate weight gain and represent a major challenge for weight management
Introduction
The chronic positive energy balance that leads to obesity is
apparently relatively small.
1 It is therefore paradoxical that
obesity is so persistent and difficult to treat, because, in
Western countries at least, the basic causes of obesity are
readily apparent to everyone (eating too much and exercising
too little). Obesity is associated with a substantial loss of
quality of life and with social stigmatisation; awareness of
the health consequences of obesity has never been greater. Even
the body's physiological systems try to prevent weight gain
by minimising the impact of energy imbalance on weight change.
2
To help explain this apparent paradox, we propose that numerous vicious cycles are acting as "accelerators" that maintain and even increase overweight. We liken the situation to a "runaway weight gain train" (figure), which already has high momentum from the downhill slope of obesogenic (obesity promoting) environments but is getting faster as the vicious cycles start acting as accelerators. The brakes, which, on the face of it, should be strong enough to slow down the train, turn out to be weak by comparison.
The downhill slope of obesogenic environments
The obesogenic environments of the modern world have been well
described.
3
4 They make the unhealthy choices the easy, default
choices, resulting in a high intake of energy dense foods and
beverages and in reduced physical activity. Examples include
the heavy promotion of fast food outlets, energy dense snacks,
and high sugar drinks to children; the low cost and large serving
sizes of such foods; and the transport systems and urban design
that inhibit active transport and active recreation.
In our runaway train model (figure), the twin tracks of "energy in" and "energy out" are on the downhill slope of the obesogenic environments, indicating that the default direction is downhill towards positive energy balance. Levelling out the obesogenic slope is fundamental to slowing down the momentum of the obesity epidemic. However, in some areas, such as "retro fitting" walking, cycling and public transport into a car oriented built environment, this will require a massive engineering effort and is likely to take a very long time.5
Ineffective brakes
Several "brakes" are acting against increasing weight gain.
Possibly the strongest in Western societies is the social discrimination
of being overweight or obese.
6 Unlike other conditions related
to a combination of inappropriate diet, lack of exercise, and
genetic backgroundfor example, hypertension and dyslipidaemiaobesity
is visible to others and carries the social stigmata of sloth
and gluttony. Interestingly, the rise of support groups for
big people, the sanctions against discrimination on the basis
of size, and the rise of the average body size into the overweight
range may reduce the pressure on this brake.
A further brake is the personal physical discomfort associated with obesity, which reduces quality of life substantially.7 Knowledge about the fundamental causes of weight gain (eating too much and exercising too little) is common, but this cognitive brake is often ineffectual. Some authors argue for a greater application of cognitive efforts to control weight gain,5 but knowledge alone seems to be a weak predictor of human behaviour, and educational strategies, at least at the population level, seem to have little effect on preventing weight gain.8
Even physiology attempts to slow weight gain. The metabolic profile of an obese person is one of physiological brakes being fully applied to prevent further weight gain. These include reductions in appetite, increased fat oxidation, increased energy expenditure, insulin resistance, increased activity of the sympathetic nervous system, increased leptin concentrations, and so on.2
9
10 In response to weight loss, these physiological mechanisms are reversed (and more vigorousfor obvious survival reasons),9
10 so their role seems to be to dampen the impact of energy imbalances on subsequent weight change.
While all these brakes seem to be substantive, they are clearly not strong enough to halt the increasing momentum of the weight gain train. This argues for the existence of a powerful set of accelerating forces in addition to the downhill obesogenic slope.
Vicious cycles as accelerators
A vicious cycle is a positive feedback loop in which the problem
(in this case, weight gain) becomes self perpetuating. In almost
all physiological systems, cycles are based on negative feedback
relations, so the interaction of multiple systems ensures a
dynamic stability. Positive feedback cycles, on the other hand,
are destabilising and potentially accelerating, because an initial
increase in one factor leads to changes in the system that feed
back and further exaggerate the initial increase. Several vicious
cycles, outlined in the
table and explained below, seem to be
operating in obesity, creating a potent driving force for perpetuation
and even acceleration.
Movement inertia cycle
A heavy body weight is a disincentive for movement and physical
activity, creating "movement inertia." Although obese people
expend more energy in performing a given level of physical activity
than lighter people, they tend to do fewer of those energy demanding
activities.
11 These reductions in levels of physical activity
are most apparent in people who are substantially overweight.
12 Reducing levels of physical activity obviously then promotes
further weight gain. The potential "cycle breakers" (analogous
to a clutch in the train model) could be the use of motivational
techniques, weight supportive exercise (such as pool based activities),
and focusing on reducing energy intake in the first instance.
Mechanical dysfunction cycle
A related vicious cycle is one due to the mechanical problems
associated with increased body weight. These include arthritis,
arthralgia, low back pain, chest wall and diaphragm restriction,
incontinence, obstructive sleep apnoea, oedema, and cellulitis.
13-15 These may result in pain and difficulty walking and moving,
shortness of breath (often diagnosed as asthma), exercise and
stress incontinence, daytime somnolence, fatigue, and so on,
which further limit physical activity and increase weight gain.
Some specific treatments for the mechanical dysfunction itself
to break the cycle may be available, such as continuous positive
airways pressure for obstructive sleep apnoea and anti-inflammatory
drugs and surgery for orthopaedic problems.
Psychological dysfunction cycle
For some obese individuals, body dissatisfaction, the physical
discomfort of obesity, and social stigmatisation may trigger
or exacerbate depression, anxiety, and feelings of low self
esteem and guilt. Some of the consequences of these psychological
problems may increase energy intake (such as binge or comfort
eating, excess alcohol intake) or reduce physical activity (such
as lethargy and lack of motivation).
16 In addition, some medications
that might be used to manage the psychological condition may
promote weight gain (for example, psychotropic drugs). Appropriate
management of the psychological condition and the medication
may be needed to help break the effects of this vicious cycle.
Dieting cycle
New diets (and recycled old diets) are constantly coming in
and going out of fashion. They often have specific "magic" weight
loss ingredients or a set of restrictive rules with "free" and
"forbidden'" foods. Some of the diets are very hypocaloric and
result in marked weight loss, and most are unsustainable. The
metabolic response to a large weight loss is vigorous, and the
subsequent weight that is regained is disproportionately higher
in fat.
17 In addition, the sense of failure (personal failure
and "diet" failure) may contribute to the depression and psychological
problems described in the previous cycle. For some people with
so called food cravings or addictions, self deprivation of particular
favourite foods, such as chocolate, may lead to a heightened
desire for those foods
18 and contribute to the failure of the
diet.
Low socioeconomic status cycle
In developed countries, socioeconomic status is strongly associated
with obesity, especially among women, with a higher prevalence
of obesity in groups with a lower socioeconomic status.
3 This
relation seems to be bidirectional. Obesity leads to reduced
opportunities for jobs, education, marriage, and social inclusion,
19 and these may be more potent in women than in men. A lower income
reduces the range of healthy choices, such as fresh fruit and
vegetables, and expensive active recreational pursuits. Neighbourhoods
with a low socioeconomic status are usually more obesogenic
than neighbourhoods with a high status.
20 A low income is also
associated with higher levels of chronic stress, which may lead
to comfort eating, excessive consumption of alcohol, and even
the chronic activation of the hypothalamic-pituitary-adrenal
axis,
21 resulting ultimately in increased obesity and hence
perpetuating the cycle. Improving equity of access to healthy
choices and reducing the obesogenicity of poor neighbourhoods
are important strategies to break this cycle.
Conclusion
The combination of the described vicious cycles acting as accelerator
wheels, a set of ineffective brakes, and increasingly obesogenic
environments represents a major challenge for weight management.
We have identified several vicious cycles that may be operating
in obesity and acknowledge that there may even be more. Defining
these potential vicious cycles is vital for several reasons.
Firstly, they help explain the apparent paradox of continuing
(and often increasing) obesity in the face of brakes such as
strong social stigmatisation and knowledge of causes and solutions.
Secondly, they may contribute to the increasing right skewness
of the frequency distribution of body mass index as the population
gains weight over time. In other words, the lean people gain
a little weight but the already overweight and obese gain a
lot of weight, creating an exaggerated interaction between individual
and environment. Thirdly, they underline the variety and strength
of the factors that people with established obesity have to
struggle against in their attempts to lose weight. Fourthly,
they point to opportunities for specific measures that can be
taken at an individual or societal level that might help to
diminish the driving forces that are promoting weight gain.
Fifthly, they point to the need for more research into the nature
of these vicious cycles and the effectiveness of strategies
to break them. Lastly, all this makes it imperative to focus
on prevention, especially in children. This is one train ride
they won't want to take.
| Summary points
Obesity seems to be perpetuated by a series of vicious cycles
Obesity may result in movement inertia, mechanical dysfunction, psychological dysfunction, cyclical dieting, and socioeconomic disadvantage, all of which may promote further weight gain
The "obesogenic" environment is also driving the obesity epidemic, whereas the "brakes" against weight gain (social, personal, cognitive, physiological) are weak by comparison
Management of obesity should include the identification of active vicious cycles and implementation of strategies to break the cycle
| |
The authors each have more than 15 years' experience in research
and action on obesity at metabolic, clinical, and population
levels. BS's obesity research includes metabolic studies at
the National Institutes of Health, Phoenix, Arizona; clinical
and public health interventions at the University of Auckland;
and whole of community obesity prevention at Deakin University.
He is a member of the Prevention Group of the International
Obesity TaskForce. GE was the founder of GutBusters, a waist
loss programme for men which treated thousands of overweight
Australian men between 1991 and 2002. He was the lead author
of the Australian Physical Activity Guidelines and the National
Health and Medical Council's National Clinical Guidelines for
Weight Control and Obesity Management.
Contributors: Both authors contributed to defining the concepts included in the paper and both were involved in writing and editing. BS is guarantor.
Competing interests: None declared.
References
- Hill JO, Wyatt HR, Reed GW, Peters JC. Obesity and the environment: where do we go from here? Science
2003;299: 853-5.[Abstract/Free Full Text]
- Ravussin E, Swinburn BA. Metabolic predictors of obesity: cross-sectional versus longitudinal data. Int J Obes Relat Metab Disord
1993;17(suppl 3): S28-31; discussion S41-2.
- Swinburn B, Egger G. Preventive strategies against weight gain and obesity. Obes Rev
2002;3: 289-301.[CrossRef][Medline]
- French SA, Story M, Jeffery RW. Environmental influences on eating and physical activity. Annu Rev Public Health
2001;22: 309-35.[CrossRef][Web of Science][Medline]
- Peters JC, Wyatt HR, Donahoo WT, Hill JO. From instinct to intellect: the challenge of maintaining healthy weight in the modern world. Obes Rev
2002;3: 69-74.[CrossRef][Medline]
- Puhl R, Brownell KD. Bias, Discrimination, and obesity. Obes Res
2001;9: 788-805.[Web of Science][Medline]
- Han TS, Tijhuis MA, Lean ME, Seidell JC. Quality of life in relation to overweight and body fat distribution. Am J Public Health
1998;88: 1814-20.[Abstract/Free Full Text]
- Jeffery RW, French SA. Preventing weight gain in adults: the pound of prevention study. Am J Public Health
1999;89: 747-51.[Abstract/Free Full Text]
- Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med
1995;332: 621-8.[Abstract/Free Full Text]
- Blundell JE, Gillett A. Control of food intake in the obese. Obes Res
2001;9(suppl 4): 263S-270S.
- Ferraro R, Boyce VL, Swinburn B, De Gregorio M, Ravussin E. Energy cost of physical activity on a metabolic ward in relationship to obesity. Am J Clin Nutr
1991;53: 1368-71.[Abstract/Free Full Text]
- Prentice AM, Black AE, Coward WA, Cole TJ. Energy expenditure in overweight and obese adults in affluent societies: an analysis of 319 doubly-labelled water measurements. Eur J Clin Nutr
1996;50: 93-7.[Web of Science][Medline]
- World Health Organization. Obesity: preventing and managing the global epidemic. Report of a WHO consultation. Geneva: World Health Organization, 2000. (WHO Technical Report Series 894.)
- Visscher TL, Seidell JC. The public health impact of obesity. Annu Rev Public Health
2001;22: 355-75.[CrossRef][Web of Science][Medline]
- Mommsen S, Foldspang A. Body mass index and adult female urinary incontinence. World J Urol
1994;12: 319-22.[Web of Science][Medline]
- Wardle J. Aetiology of obesity VII: psychological factors. In: Force BNFT, ed. Obesity. Oxford: Blackwell Science, 1999: 83-91.
- Dulloo AG, Jacquet J, Girardier L. Poststarvation hyperphagia and body fat overshooting in humans: a role for feedback signals from lean and fat tissues. Am J Clin Nutr
1997;65: 717-23.[Abstract/Free Full Text]
- Rogers P, Smit H. Food craving and food `addiction': A critical review of the evidence from a biopsychosocial perspective. Pharmacol Biochem Behav
2000;66(1): 3-14.[CrossRef][Web of Science][Medline]
- Stunkard AJ. Socioeconomic status and obesity. In: Cadwick DJ, Cardew G, eds. The origins and consequences of obesity. Chichester: Wiley, 1996: 174-93.
- Reidpath D, Burns C, Garrard J, Mahoney M, Townsend M. An ecological study of the relationship between social and environmental determinants of obesity. Health Place
2002;8: 141-5.[CrossRef][Web of Science][Medline]
- Bjorntorp P, Rosmond R. Neuroendocrine abnormalities in visceral obesity. Int J Obes Relat Metab Disord
2000;24(suppl 2): S80-5.

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