Behavioural theories

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people of similar height. To explain these apparently contradictory findings it has been
suggested that obese people may have lower metabolic rates to start with, which results
in weight gain and this weight gain itself results in an increase in metabolic rate
(Ravussin and Bogardus 1989).
Fat cell theory
A genetic tendency to be obese may also express itself in terms of the number of fat cells.
People of average weight usually have about 25–35 billion fat cells, which are designed
for the storage of fat in periods of energy surplus and the mobilization of fat in periods of
energy deficit. Mildly obese individuals usually have the same number of fat cells but
they are enlarged in size and weight. Severely obese individuals, however, have more fat
cells – up to 100–125 billion (Sjostrom 1980). Cell number is mainly determined by
genetics; however, when the existing number of cells have been used up, new fat cells are
formed from pre-existing preadipocytes. Most of this growth in the number of cells
occurs during gestation and early childhood and remains stable once adulthood has been
reached. Although the results from studies in this area are unclear, it would seem that if
an individual is born with more fat cells then there are more cells immediately available
to fill up. In addition, research suggests that once fat cells have been made they can never
be lost (Sjostrom 1980). An obese person with a large number of fat cells, may be able to
empty these cells but will never be able to get rid of them.
Appetite regulation
A genetic predisposition may also be related to appetite control. Over recent years
researchers have attempted to identify the gene, or collection of genes, responsible for
obesity. Although some work using small animals has identified a single gene that is
associated with profound obesity, for humans the work is still unclear. Two children have,
however, been identified with a defect in the ‘ob gene’, which produces leptin which is
responsible for telling the brain to stop eating (Montague et al. 1997). It has been argued
that the obese may not produce leptin and therefore overeat. To support this, researchers
have given these two children daily injections of leptin, which has resulted in a decrease
in food intake and weight loss at a rate of 1–2 kg per month (Farooqi et al. 1999). Despite
this, the research exploring the role of genetics on appetite control is still in the very early
stages.
Behavioural theories
Behavioural theories of obesity have examined both physical activity and eating
behaviour.
Physical activity
Increases in the prevalence of obesity coincide with decreases in daily energy expenditure due to improvements in transport systems, and a shift from an agricultural society
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to an industrial and increasingly information-based society. As a simple example, a telephone company in the USA has suggested that in the course of one year an extension
phone saves an individual approximately one mile of walking, which could be the equivalent of 2–3 lb of fat or up to 10,500 kcals (Stern 1984). Further, at present only 20 per
cent of men and 10 per cent of women are employed in active occupations (Allied
Dunbar National Fitness Survey 1992) and for many people leisure times are dominated
by inactivity (Central Statistical Office 1994). Although data on changes in activity levels
are problematic, there exists a useful database on television viewing which shows that
whereas the average viewer in the 1960s watched 13 hours of television per week, in
England this has now doubled to 26 hours per week (General Household Survey 1994).
This is further exacerbated by the increased use of videos and computer games by both
children and adults. It has therefore been suggested that obesity may be caused by
inactivity. In a survey of adolescent boys in Glasgow in 1964 and 1971, whereas daily
food diaries indicated a decrease in daily energy intake from 2795 kcals to 2610 kcals,
the boys in 1971 showed an increase in body fat from 16.3 per cent to 18.4 per cent.
This suggests that decreased physical activity was related to increased body fat (Durnin et
al. 1974). To examine the role of physical activity in obesity, research has asked ‘Are
changes in obesity related to changes in activity?’, ‘Do the obese exercise less?’, ‘What
effect does exercise have on food intake?’ and ‘What effect does exercise have on energy
expenditure?’ These questions will now be examined.
Are changes in obesity related to changes in activity? This question can be
answered in two ways: first using epidemiological data on a population and second using
prospective data on individuals.
In 1995, Prentice and Jebb presented epidemiological data on changes in physical
activity from 1950 to 1990, as measured by car ownership and television viewing, and
compared these with changes in the prevalence of obesity. The results from this study
suggested a strong association between an increase in both car ownership and television viewing and an increase in obesity (see Figure 15.4). They commented that ‘it
seems reasonable to conclude that the low levels of physical inactivity now prevalent in
Britain must play an important, perhaps dominant role in the development of obesity
by greatly reducing energy needs’ (Prentice and Jebb 1995). However, their data was
only correlational. Therefore, it remains unclear whether obesity and physical activity
are related (the third factor problem – some other variable may be determining both
obesity and activity) and whether decreases in activity cause increases in obesity or
whether, in fact, increases in obesity actually cause decreases in activity. In addition,
the data is at the population level and therefore could miss important individual differences (i.e. some people who become obese could be active and those who are thin could
be inactive).
In an alternative approach to assessing the relationship between activity and obesity
a large Finnish study of 12,000 adults examined the association between levels of
physical activity and excess weight gain over a five-year follow-up period (Rissanen et al.
1991). The results showed that lower levels of activity were a greater risk factor for
weight gain than any other baseline measures. However, although this data was prospective it is still possible that a third factor may explain the relationship (i.e. those with
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Fig. 15-4 Changes in physical activity and obesity
lower levels of activity at baseline were women, the women had children and therefore
put on more weight). Unless experimental data is collected, conclusions about causality
remain problematic.
Do the obese exercise less?
Research has also examined the relationship between
activity and obesity using a cross-sectional design to examine differences between the
obese and non-obese. In particular, several studies in the 1960s and 1970s examined
whether the obese exercised less than the non-obese. Using time-lapse photography,
Bullen et al. (1964) observed girls considered obese and those of normal weight on a
summer camp. They reported that during swimming the obese girls spent less time
swimming and more time floating, and while playing tennis the obese girls were
inactive for 77 per cent of the time compared with the girls of normal weight, who
were inactive for only 56 per cent of the time. In addition, research indicates that the
obese walk less on a daily basis than the non-obese and are less likely to use stairs or
walk up escalators. However, whether reduced exercise is a cause or a consequence of
obesity is unclear. It is possible that the obese take less exercise due to factors such as
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embarrassment and stigma and that exercise plays a part in the maintenance of obesity
but not in its cause.
What effect does exercise have on food intake?
The relationship between
exercise and food intake is complex, with research suggesting that exercise may increase,
decrease or have no effect on eating behaviour. For example, a study of middle-aged male
joggers who ran approximately 65km per week, suggested that increased calorie intake
was related to increased exercise with the joggers eating more than the sedentary control
group (Blair et al. 1981). However, another study of military cadets reported that
decreased food intake was related to increased exercise (Edholm et al. 1955). Much
research has also been carried out on rats, which shows a more consistent relationship
between increased exercise and decreased food intake. However, the extent to which such
results can be generalized to humans is questionable.
What effect does exercise have on energy expenditure? Exercise burns up
calories. For example, 10 minutes of sleeping uses up to 16 kcals, standing uses 19 kcals,
running uses 142 kcals, walking downstairs uses 88 kcals and walking upstairs uses
229 kcals (Brownell 1989). In addition, the amount of calories used increases with the
individual’s body weight. Therefore, exercise has long been recommended as a weight
loss method. However, the number of calories exercise burns up is relatively few compared with those in an average meal. In addition, exercise is recommended as a means
to increase metabolic rate. However, only intense and prolonged exercise appears to have
an effect on metabolic rate.
Therefore, the role of exercise in obesity is still unclear. There appears to be an
association between population decreases in activity and increases in obesity. In addition,
prospective data support this association and highlight lower levels of activity as an
important risk factor. Further, cross-sectional data indicate that the obese appear to
exercise less than the non-obese. However, whether inactivity is a cause or consequence
of obesity is questionable. It is possible that an unidentified third factor may be creating
this association, and it is also debatable whether exercise has a role in reducing food
intake and promoting energy expenditure. However, exercise may have psychological
effects, which could benefit the obese either in terms of promoting weight loss or simply
by making them feel better about themselves (see Chapter 7 for the effects of exercise
on mood).
Eating behaviour
In an alternative approach to understanding the causes of obesity, research has examined eating behaviour. Research has asked ‘Are changes in food intake associated with
changes in obesity?’, ‘Do the obese eat for different reasons than the non-obese?’ and ‘Do
the obese eat more than the non-obese?’ These questions will now be examined.
Are changes in food intake associated with changes in obesity? The UK
National Food Survey collects data on food intake in the home, which can be analysed
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to assess changes in food intake over the past 50 years. The results from this database illustrate that, although overall calorie consumption increased between 1950
and 1970, since 1970 there has been a distinct decrease in the amount we eat (see
Figure 15.5).
Prentice and Jebb (1995) examined the association between changes in food intake in
terms of energy intake and fat intake and changes in obesity. Their results indicated no
obvious association between the increase in obesity and the changes in food intake (see
Figure 15.6).
Therefore, using population data there appears to be no relationship between
changes in food intake and changes in obesity.
Do the obese eat for different reasons than the non-obese? Throughout the
1960s and 1970s theories of eating behaviour emphasized the role of food intake in
predicting weight. Original studies of obesity were based on the assumption that the
obese ate for different reasons than people of normal weight (Ferster et al. 1962).
Schachter’s externality theory suggested that, although all people were responsive to
environmental stimuli such as the sight, taste and smell of food, and that such stimuli
might cause overeating, the obese were highly and sometimes uncontrollably responsive
to external cues. It was argued that normal weight individuals mainly ate as a response
to internal cues (e.g. hunger, satiety) and obese individuals tended to be underresponsive to their internal cues and over-responsive to external cues. Within this perspective, research examined the eating behaviour and eating style of the obese and nonobese in response to external cues such as the time of day, the sight of food, the taste of
food and the number and salience of food cues (e.g. Schachter 1968; Schachter and
Gross 1968; Schachter and Rodin 1974). The results from these studies produced fairly
inconsistent results. Therefore, research also examined whether the obese ate more than
the non-obese.
Do the obese eat more than the non-obese?
Research exploring the amount
eaten by the obese has either focused on the amount consumed per se or on the type of
food consumed.
Because it was believed that the obese ate for different reasons than the non-obese it
was also believed that they ate more. Research therefore explored the food intake of the
obese in restaurants and at home, and examined what food they bought. For example,
Coates et al. (1978) suggested that perhaps the obese were overeating at home and went
into the homes of 60 middle-class families to examine what was stored in their
cupboards. They weighed all members of the families and found no relationship between
body size and the mass and type of food they consumed at home. In an attempt to clarify
the problem of whether the obese eat more than the non-obese, Spitzer and Rodin (1981)
examined the research into eating behaviour and suggested that ‘of twenty nine studies
examining the effects of body weight on amount eaten in laboratory studies . . . only nine
reported that overweight subjects ate significantly more than their lean counterparts’.
Therefore, the answer to the question ‘do the obese eat more/differently to the nonobese?’ appears to be ‘no’; the obese do not necessarily overeat (compared with others). If
overeating is defined as ‘compared with what the body needs’, it could be argued that the
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Fig. 15-5 Changes in food intake from the 1950s to the 1990s
Fig. 15-6 Changes in calorie consumption and obesity
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obese overeat because they have excess body fat. Over recent years, research has focused
on the eating behaviour of the obese not in terms of calories consumed, or in terms of
amount eaten, but more specifically in terms of the type of food eaten.
Population data indicates that calorie consumption has decreased since the 1970s
and that this decrease is unrelated to the increase in obesity (see Figures 15.5 and
15.6). However, this data also shows that the ratio between carbohydrate consumption
and fat consumption has changed; whereas we now eat less carbohydrate, we eat
proportionally more fat (Prentice and Jebb 1995). One theory that has been developed
is that, although the obese may not eat more than the non-obese overall, they may eat
proportionally more fat. Further, it has been argued that not all calories are equal
(Prentice 1995) and that calories from fat may lead to greater weight gain than
calories from carbohydrates. To support this theory, one study of 11,500 people in
Scotland showed that men consuming the lowest proportion of carbohydrate in their
diets were four times more likely to be obese than those consuming the highest proportion of carbohydrate. A similar relationship was also found for women, although
the difference was only two- to three-fold. Therefore, it was concluded that relatively
lower carbohydrate consumption is related to lower levels of obesity (Bolton-Smith and
Woodward 1994). A similar study in Leeds also provided support for the fat proportion
theory of obesity (Blundell and Macdiarmid 1997). This study reported that high fat
eaters who derived more than 45 per cent of their energy from fat were 19 times more
likely to be obese than those who derived less than 35 per cent of their energy from
fat. Therefore, these studies suggest that the obese do not eat more overall than the
non-obese, nor do they eat more calories, carbohydrate or fat per se than the nonobese. But they do eat more fat compared with the amount of carbohydrate; the
proportion of fat in their diet is higher. So how might a relative increase in fat
consumption relate to obesity?
As a possible explanation of these results, research has examined the role of fat and
carbohydrates in appetite regulation. Three possible mechanisms have been proposed
(Blundell et al. 1996; Blundell and Macdiarmid 1997):
1 The benefits of complex carbohydrates to energy use. First, it has been suggested
that it takes more energy to burn carbohydrates than fat. Further, as the body
prefers to burn carbohydrates than fat, carbohydrate intake is accompanied by an
increase of carbohydrate oxidation. In contrast, increased fat intake is not accompanied by an increase in fat oxidation. Therefore, carbohydrates are burned, fat is
stored.
2 The benefits of complex carbohydrates to hunger. Second, it has been suggested
that complex carbohydrates (such as bread, potatoes, pasta, rice) reduce hunger and
cause reduced food intake due to their bulk and the amount of fibre they contain. In
addition, they switch off the desire to eat. Therefore, carbohydrates make you feel
fuller faster.
3 The costs of fat to hunger. Third, it has been suggested that fat does not switch off
the desire to eat, making it easier to eat more and more fat without feeling full.
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