According to the WHO (2010), childhood obesity is one of the most serious public health challenges of the 21st century. Globally, in 2010 the number of overweight children under the age of 5 is estimated to be over 42 million (WHO, 2010). Obesity can be defined in a number of ways, e.g. by population means, BMI and waist circumference (Odgen, 2012). And according to Kleiser et al (2009), obesity may have several short-term consequences (e.g. social discrimination, lower quality of life, increased cardiovascular risk factors, diseases like asthma) and long-term consequences were obesity is likely to persist into adulthood, were individuals are more likely to develop noncommunicable diseases e.
g. diabetes and cardiovascular disease at a much younger age. It is due to this that a great body of research within health psychology has focused on not only the consequences of obesity but also understanding the causes of obesity, both genetic and environmental – this is what this essay will explore…. Genetics
There have been several theories put forward by research to best explain the causes obesity and one major potential causes is genetics.
Maffeis et al (1998) found that obesity in parents was the strongest predictor of childhood obesity, regardless of diet or level of activity. Furthermore recent research has found support for this claim. Moreover, Wardle et al., (2001, 2006) reported that, controlling for other environmental factors, children with obese parents preferred fatty foods, had less liking for vegetables, were more likely to overeat had a higher preference for sedentary activities than did children of normal weight parents.
This is further strengthened by more recent research by Kleiser et al (2009) who found that the strongest determinant of obesity was obesity in parents.
Despite the evidence for this relationship, Odgen (2012) states that parents and children not only share genetic constitution but also share very similar environments, therefore this relationship between child and parental obesity could be contributed to either factor. However, according to Barlow (2013) twin studies have also have clearly demonstrated a genetic influence on body weight, therefore strengthening the argument for the role of genetics in obesity. For instance studies have found 25 – 40 % of BMI is heritable and identical twins raised apart have been found to have a correlation of .7, only slightly lower than that of twins raised together (Stunkard et al, 1990). Moreover adoption studies have also provided evidence for a genetic component in obesity, Skunkard (1986) found a strong relationship between the weight class of the adoptee and their biological parents and interestingly found no relationship with their adoptee parents’ weight class.
Research has also stated that factors such as metabolic rate (Bouchard, 1990) and appetite regulation may also have a role to play in causing obesity. Research in terms of metabolic rate has suggested a low resting metabolic rate is a risk factor for weight gain (Tataranni, 2003), but in fact there is little research to support this. In particular there is no evidence to suggest that overweight people tend to have slightly higher metabolic rates than thin people of a similar height (Garrow, 1987; Odgen, 2012). A genetic predisposition may also be related to appetite control. For instance, the discovery of leptin, ghrelin, adiponectin, and other hormones that inﬂuence appetite, satiety, and fat distribution provides insight into metabolic mechanisms for physiological risk of obesity (Maes et al, 1997; Gale et al, 2004).
Research, although seen to be in its infancy has yielded support, e.g. Farooqi et al (1999) injected 2 participants daily with leptin, which resulted in decreased food uptake and weight loss at a rate of 1-2kg per month. According to Odgen (2012) there is strong evidence for a genetic basis to obesity, but it is how this genetic bias expresses itself that remains unclear, due to the fact research on lowered metabolic rate has been widely refuted and the genetics of appetite control remain in its infancy. Furthermore, genetic studies are not without their criticisms. For instance small sample size, zygosity needs to be confirmed and again the role of environmental factors cannot be ignored.
Behaviour & Environmental factors
Therefore in light of the above criticisms research has begun to more fully examine the extent to which an individual’s behaviour and/or environment can influence the development of obesity. As Barlow (2013) states that at a population level, the increase in prevalence is too rapid to be explained by a genetic shift; rather, it must result from changes in eating and physical activity behaviours that have shifted. A recent study by Kileser (2009) found independently of other factors, a positive association was observed
between obesity and low SES, migration background (up to age 13), parental overweight, high weight gain during pregnancy (when the mother is of normal weight), maternal smoking during pregnancy, high birth weight, and high media consumption, as well as a negative association with sleep duration for 3- to 10-year olds.