Exposure to a diet containing high fat foods constitutes a risk factor for body weight gain but this relationship does not constitute a 'biological inevitability'. How does this relationship manifest itself in children?
First, evidence suggests the existence of a relationship between parental obesity and obesity in the offspring (28). In a retrospective cohort study of 854 subjects born between 1965 and 1971, obesity (defined as a BMI of 27.8 for men and 27.3 for women) in later adulthood was compared with the medical records of the parents. Among those who were obese during childhood, the chance of obesity in adulthood ranged from 8% (for 1- to 2-year-olds without obese parents) to 79% (for 10- to 14-year-olds with at least one obese parent). Therefore obese children under 3 years of age without obese parents are at low risk for obesity in adulthood, but among older children, obesity is an increasingly important predictor of adult obesity. In this study, parental obesity more than doubled the risk of adult obesity among children under 10 years of age.
One mediating factor (and possibly a mechanism) in the development of adult obesity from childhood involves the so-called 'adiposity rebound' (AR). This is the name given to the second augmentation of BMI after birth, and there is an inverse relationship between adult BMI and the age of AR. In a longitudinal study of Czech children, followed from 1 month of age to adulthood, the heaviest adults had an AR around 5 years and the leanest at 7.6
A number of studies have also examined the dietary fat intake of children and both the diet composition and adiposity of the parents. In one study, a high-risk group of children (one or two overweight parents) was compared with a low-risk group (no parent overweight) at 4.5 years of age. The high-risk group was consuming a higher percentage of fat in their diet and a smaller percentage of carbohydrate
(30). In an unselected sample of 4- to 7-year-old children (35 girls, 36 boys) there was an influence of maternal adiposity on dietary fat intake in the children, and, for the boys a correlation between their own fat mass and fat intake (31). These data suggest that mothers may contribute more strongly than fathers to the development of obesity in children by influencing their dietary fat intake. Moreover, it is known that young children's preferences for particular foods are powerful predictors of consumption when self-selection is permitted (32). Interestingly, it has been demonstrated that the fat preferences (and fat consumption) of 3- to 5-year-old children are related to parental adiposity (33). The fat intake from 18 children was obtained from 30 h weighed food intake records and compared with the body composition measures of children and parents. Children's fat intakes were correlated with preferences for high fat foods and to their triceps skinfold measurements. In addition, there were strong correlations between the children's fat preferences and fat intakes and the BMIs of the parents. Children of heavier parents had stronger preferences for (and higher consumption of) fatty foods. In a further study of 9- to 10-year-old children, the fattest children consumed significantly more energy from fat than the lean children (34).
These findings strongly support an environmental impact of the habitual diet upon the development ofweight gain and obesity. However, the data could also suggest a biological influence over the preferences for those high fat foods which form part of the habitual diet. This scenario, which focuses attention on the energy intake side of the energy balance equation, should not obscure the role of physical activity and energy expenditure. One major factor in the ever-increasing frequency of sedentary behaviours is television viewing. In a representative cohort of 746 youths aged 10-15 years there was a strong dose-response relationship between the prevalence of overweight and the hours of television viewed (35). The incidence of obesity was 8.3 times greater in those youths watching more than 5 hours of television per day compared with those watching 0 to 2 hours. As is the case with adults (36), overweight in children appears to be strongly influenced by the environmental factors of low physical activity (high frequency of sedentary activities) and exposure to a high energy-dense (high fat) diet. However, we should be wary of assuming that the effect of TV watching is necessarily due to sedentarism since viewing also provides an opportunity for further eating. Consequently, in children appetite control can play a significant role in weight gain and obes ity. It is very obvious in cases of major gene mutations (leptin and MC4 receptor) that these forms of childhood obesity are driven exclusively by loss of restraint over appetite.
THE OBESITY EPIDEMIC: WHAT CAN WE LEARN FROM APPETITE CONTROL?
In simple terms it can be said that the increased prevalence of worldwide obesity arises largely from the excess of energy intake over energy expenditure. This can be driven to happen, or allowed to happen, through the defects in single major genes or by multiple genes with lower effects acting together. It can also arise because of the 'obesigenic' nature of the environment (37); and it can also occur through the mediation of some intrinsic modulation of the excitatory or inhibitory processes involved in appetite control (described earlier). There exists a simple formula indicating that the amount of excess energy intake (above expenditure), required for weight gain over years, is very small—perhaps between 20 and 40 kilocalories. However, the simplicity of this equation, and the apparent ease with which it seems possible for an individual to make the necessary correction to achieve weight stability, is illusory. This is because the expression of appetite displays a high degree of individual variability, and because the processes are complex. Therefore the volitional control over appetite required to make minimal savings in energy on a daily basis is, in practice, extremely difficult. A small deliberate adjustment can be swamped by uncontrollably large swings in day-to-day or intra-day consumption (particularly of dietary fat). In part, this explains why appetite control is difficult to maintain in the long term.
However, the control of appetite is clearly central to the containment of obesity and certain factors arise from an analysis of the field. These factors can be considered as principles to guide our understanding of appetite in relation to obesity.
• Emerging relationships between the nutritional environment and biological vulnerability (metabolic and behavioural risk factors) form the basis for a modern psychobiological approach to appetite control.
• Understanding the processes which permit over-consumption leading to a positive energy balance can inform a public health approach to prevent the further escalation of the obesity epidemic.
• The actions of specific nutrients on processes of preference and satiety can form the basis of a science of functional foods for appetite control.
• A pharmacological approach to obesity treatment can be formulated on drugs directed to specific molecules which influence drive and food seeking, food preferences and rewards, satiety signals and lipostatic hunger mechanisms.
In these ways, an understanding of appetite control can help to combat the epidemic of obesity.
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