The biopsychosocial model of health and wellness was developed by George Engel in response to the “medical model” which was dominating health psychology.  His argument was that the medical was too reductionist, focusing only on the physiological causes of health behaviour and seeing poor health outcomes as “disorders.”  The BPS model looks at health issues more holistically and argues that no one factor alone is enough to lead to good or bad health.  It is the interrelation of all three components that is important.  We can see this in the study of obesity.

The medical model argues that obesity has physiological causes – including genetics, the hormone leptin and potential damage to the hypothalamus. For example, Sorensen carried out a study of adopted Danish children. The study was a longitudinal, prospective study to see if there was a correlation between the weight of the adult children of the birth mother or the adoptive parents. The researchers found a strong correlation between obesity in the birth mother and the children than with adoptive parents. The study does not, however, identify any specific genes which may be the reason for this.  Later research has found polymorphisms linked to obesity – but these polymorphisms are in only a small part of the population.  This leads us to doubt that genetics explains the increased rate of obesity.

The genetics argument is a reductionist argument that does not account for the high rise in obesity that we are seeing today.  The research does not support that there is a common genetic variation that leads to obesity, so other factors must be involved.  The BPS model looks at both the cognitive and social factors as well.

Wansick argues that cognitive factors play a role in eating behaviour.  He looked at the different schemas used by two cultures – Americans in French – in knowing when they were “done eating.” The study carried out interviews with 150 Parisians and Chicagoans and asked them how they knew they were done eating dinner.  The French most often referred to bodily cues – such as no longer being hungry or the food is no longer interesting. The Americans said “when the plate is empty” or “when everyone else is done.” These social norms and perceptions of when to stop eating may play a key role in overeating.

Psychologists are also very interested in how a change in society may be changing our eating behaviour.  Prentice and Jebb found a positive correlation between an increase in obesity in the UK, and car ownership and television viewing.

None of these three factors – genetics, perceptions about food and eating, and sedentary lifestyle – can on its own explain the obesity epidemic.  Psychologists also discuss the increased level of processed sugar in our diets and the availability of fast food.  The BPS model sees that each of these factors may play an important role in the development of a health issue.  However, there are strengths and limitations of the medical model and the BPS model.

If the medical model could be supported, it could provide a relatively easy solution to what appears to be a complex problem.  However, the genetic research so far does not support that the obesity epidemic is due to genetic factors.  Research on the physiological roots of obesity, for example, the role of the hormone leptin, are well supported in animal models like the OB rat, but the findings in these animal models have not been consistently replicated in human research.  The BPS has the advantage that the majority of its research is conducted on humans, but because of this, it is very difficult to carry out research with high internal validity which could establish cause and effect relationships.

As we can see from the research above, the problem with the study by Wansick is that although it is an interesting theory of poor eating habits, it does not explain why this leads to obesity.  The research describes the habits of these two cultures, but it does not give a clear explanation for how this leads to obesity.  If this is a pervasive schema for eating in the respective cultures, why are not all people obese in one culture and not in the other?  Clearly, other factors are involved. It appears that the more risk factors that an individual has with regard to eating behaviour, the more likely obesity is the result.

The idea that a sedentary lifestyle is key to the obesity epidemic has been pretty well accepted.  Several studies have shown a correlation between the level of BMI and a sedentary lifestyle.  However, correlations suffer from bidirectional ambiguity – so it is difficult to know if the BMI is the result or the cause of the sedentary lifestyle.  Mortensen carried out a prospective study and found that a higher BMI led to a more sedentary lifestyle over a period of  ten years in people 40 and over.

The difficulty with the BPS model is that it is difficult to isolate the different factors and determine which may play the most significant role in obesity for most people.  In addition, it is difficult to see how these factors interact.  We know from studies such as the Dutch Hunger Winter study that stress can result in changes to the epigenome that lead to the retention of fat.  This interaction is well documented – but again, not all infants from this historic natural experiment are obese. So, there must be other factors involved.

The BPS approach to obesity has led to a large number of theories that are tested to see how they play a role in the current obesity epidemic.  Engel’s model predated the understandings of epigenetics that we have today. By better understanding the complexity of the holistic picture of the obesity epidemic, we also acknowledge that any solution to this problem will also have to be complex.