Why staying lean is not a matter of ethics Joseph Proietto
MJA 1999; 171: 611-613 Introduction -
What is obesity? -
Is obesity a risk to health? -
Are obese people entirely responsible for their excess weight? -
Are the obese abused in our society? -
What should be the consequences of our new knowledge of the aetiology of obesity? -
Acknowledgement -
References -
Authors' details
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| Introduction | It has been argued that indulging in behaviour that is detrimental to health is, according to Aristotle's Nicomachean Ethics, unethical: because obesity causes many health problems, and because it is the result of the individual's own actions, the obese must therefore be indulging in unethical behaviour.1 We can all have some sympathy with the view that everyone should take personal responsibility for their health. However, in this article, I hope to show that obesity is the result of genetic mutations that alter appetite and that it is unreasonable to expect individuals with such mutations to exercise their free will to sustain hunger indefinitely in the presence of an abundance of food. | ||
What is obesity? | |||
| "Overweight" and "obese" indicate different degrees of severity of excess fat accumulation. Body mass index (BMI) is commonly used to relate weight to height. Although not a perfect measure of adiposity, the BMI has been widely used in many epidemiological studies. A BMI of 20-25 kg/m2 is considered healthy, 25-30 kg/m2 is considered overweight, and >30 kg/m2 is obese. Both genes and environment contribute to excess weight gain. Figure 1 shows one possible way in which this relationship may be viewed. At modest increases in BMI (eg, 25-30), environment plays the dominant role, with genetic predisposition contributing only a little. At the other extreme, in morbidly obese individuals, the disorder is largely due to a genetic defect, with environment playing a permissive role.2-4 | |||
Is obesity a risk to health? | |||
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There is no doubt that obesity is harmful to health. It is associated
with increased mortality, type 2 diabetes, dyslipidaemia,
hypertension, arthritis, and some cancers.5,6 These abnormalities are
serious and often chronic and place a financial burden on society. In
Australia, obesity costs the community $840 million annually, 63% of
which are direct costs to the healthcare system. A further $500
million a year is spent on weight control programs.7 However, the
relationship of obesity to ill-health is not simple and needs further
clarification.
Central obesity is more harmful than hip/thigh fat.8,9 A woman with a BMI of 32 and a gynoid shape has a lower risk of cardiovascular disease than a man with a BMI of 27 who has an android shape. Abdominal fat is metabolically more active and, by releasing more fatty acids, causes the metabolic defects that increase the risk of death from cardiovascular causes.10 So, we can exclude those fortunate women who put on weight around their hips from being bound by Burry's proposed ethical rule that we should maintain a BMI of 22-25.1 Thus excluded will be about 80% of women with a BMI between 25-30. Women with a BMI >30 tend to have excess fat all over the body and hence they may be at increased risk of ill-health. | |||
Are obese people entirely responsible for their excess weight? | |||
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It has been argued that "control of weight, no matter that some have a
genetically determined potential to acquire and retain more weight
in comparison to others, remains a matter of self control and
personal responsibility".1
This view may apply to mildly overweight individuals (BMI 25-30 kg/m2) but it does not apply to the truly obese (BMI >30). Body weight regulation is highly complex and tightly controlled. From our first beginnings, our single-celled ancestors spent most of the day swimming in the primordial slime in a quest for nutrients. The search for food and water is so important that multiple overlapping mechanisms control and integrate this behaviour. The key role for regulation is given to the hypothalamus.11,12 Recent work has identified many neurotransmitters involved in the regulation of weight, which are gradually being placed into an ordered hierarchy as shown in Figure 2. The arcuate nucleus expresses neuropeptide Y (NPY) and agouti-related peptide (AGRP), which powerfully stimulate food intake, and pro-opiomelanocortin (POMC), whose product, α-melanocyte-stimulating hormone (αMSH) and cocaine-and- amphetamine-regulated transcript (CART), inhibit food intake. In turn, the paraventricular nucleus produces the peptides oxytocin and corticotropin-releasing hormone (CRH), which inhibit food intake, and orexin and melanocyte-concentrating hormone (MCH), which stimulate it.13 These act on the brainstem, the output of which controls feeding behaviour and energy expenditure (Figure 2). Gut hormones such as cholecystokinin (CCK), which respond to the physical presence of food in the gut, modulate food intake at the brainstem level but are unable to control body weight.14 There is evidence that body weight is defended. Two recent studies illustrate the point. In the first, lean and obese subjects losing or gaining 10%-20% of their body weight by food restriction or overeating had compensatory changes in energy expenditure that opposed the change in body weight.15 The compensation was not via changes in resting energy expenditure,15 but by changes in non-exercise activity thermogenesis (NEAT) that is associated with fidgeting, maintenance of posture and other physical activities of daily life.16 The central integrating unit in the brain can only function properly if it is aware of the size of the nutrient stores, so there must be signals from the fat stores to the hypothalamus. One such important signal is the hormone leptin, discovered in 1994.17 This hormone is synthesised in adipocytes in proportion to the amount of stored fat. It is transported into the brain, where it powerfully inhibits NPY and AGRP and stimulates CART and MSH production (Figure 2), leading to reduction in food intake and an increase in energy expenditure.18 Absence of leptin leads to severe obesity. Recently, two children were found with leptin deficiency.2 It is instructive to review the behaviour of one of these children before and after leptin treatment. Before treatment she was always hungry, demanded food constantly, and was disruptive if food was denied her.19 This behaviour was drastically reduced after leptin treatment.
However, only a few individuals have been described with leptin
deficiency. In most obese people, leptin levels are high and
proportional to the level of fat accumulation.20 The problem
appears to be leptin insensitivity. Mutations in the leptin receptor
have rarely been found,21 but, as there are several
steps downstream of leptin (Figure 2),
there are many other possible mechanisms. For example, families have
now been described with mutations in the melanocortin-4 receptor
(MCR-4), the receptor through which
Animal studies suggest that severe obesity can only occur if there is a
defect in the central regulating mechanism. So far, all single-gene
mutations causing gross obesity in rodents have been in genes
involved in hypothalamic weight regulation.13 This is likely to be true in
humans also. Milder forms of overweight may be caused by changes in
peripheral regulatory mechanisms that reduce energy expenditure,
such as mutations in the Some of these abnormalities do not make leptin completely inactive but rather produce insensitivity. Thus, most obese individuals eventually limit their weight gain as the increasing leptin levels produced by the enlarging fat stores finally reduce hunger. Soon after starting caloric restriction there is a marked fall in the level of circulating leptin, resulting in relative leptin deficiency.23 The dieting individual now experiences the effects of leptin deficiency (which, as we saw from the child with a mutation in the leptin gene, include severe hunger). Different individuals can sustain hunger while being surrounded by food for different lengths of time, determined largely by inherited personality traits, but eventually the majority succumb. This is clearly demonstrated by the inevitable weight regain that occurs following most forms of therapy.24 | |||
Are the obese abused in our society? | |||
| Much has been written about the current fashion to be thin. There is a considerable problem with underweight girls. Many obese individuals share the desire to be lean because leanness is considered more attractive in our society (this is not true of all cultures). There is no doubt that obesity causes much anguish, especially in women. On top of this cosmetic issue, the obese need to cope with the ill-health that the condition causes. Ignorance continues to prevail, despite our recent insights into the physiological regulation of body weight. Many believe that the solution to obesity is simply a matter of controlling what on the surface appear to be entirely voluntary actions: the decision to eat or not to eat and the decision to move or not move. This often means that thin individuals have little sympathy for the obese. Sadly, despite their own irresistible feelings of hunger, the obese often blame themselves for their failure to achieve thinness, and guilt is added to an already long list of torments. To this can be added discrimination by society. It has been shown that the obese are often poorer, have less education, earn less, and are less likely to marry.25 | |||
What should be the consequences of our new knowledge of the aetiology of obesity? | |||
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The scientific evidence points to a genetic cause of obesity
interfering with the normal central regulation of body weight.
Several consequences should flow from this knowledge: the obese
should not blame themselves for their excess weight; they should not
pay money for weight loss therapies that are short term; society and
the medical profession should view obesity as a chronic medical
disorder; and we should accept the need for chronic drug therapy
provided it is safe.
Are the obese behaving unethically? Given the power of our most basic instinct, is it reasonable to expect individuals to remain chronically hungry while there is food all around? This is the crux of the ethical argument. How free is free will? There is no doubt that the higher cortical centres can override the hypothalamus and stop an individual from eating. We know that some political activists have starved themselves to death. So can an adult control his or her food intake by an act of will? How easy is it to push a car? The answer clearly depends on the slope of the land. My view is that hunger is a very steep hill and that few individuals are strong enough to sustain chronic hunger while food is freely available. It is grossly unfair to punish the obese for not having the strength to fight hunger. | |||
Acknowledgement | |||
| I wish to thank Dr Anne Thorburn, of the University of Melbourne Department of Medicine, Royal Melbourne Hospital, for proof reading the manuscript and for drawing Figure 2. | |||
| References | |||
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| Authors' details |
University of Melbourne Department of Medicine, Royal Melbourne
Hospital, Parkville, VIC.
Joseph Proietto, MB BS, FRACP, PhD, Associate Professor.
Reprints: Associate Professor J Proietto, Department of Medicine,
Royal Melbourne Hospital, Parkville, VIC 3050.
©MJA 1999
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