13.4.1 Biological Explanations for Obesity

• Obesity is defined as a Body-mass index (BMI) score of 30 kg/m²
• Research seems to suggest an inherited genetic basis for obesity as some individuals appear more genetically predisposed to become obese than others
• Genetic explanations suggest multiple genes are responsible, rather than one single gene, for making an individual more vulnerable to becoming obese, although studies on mice have identified the Obese (ob) gene which affects mouse appetite and weight (Loos and Yeo, 2022)
• Genetic explanations are generally tested by looking at the incidence of obesity among related individuals, using twin and family studies, as well as gene-profiling studies that search for common genes among obese people
• One genetic variation that has been directly linked to obesity is found in Bardet-Biedl syndrome, a rare genetic condition that is caused by mutations of genes that have a role in cell development (Siopa et al, 2002)
• Bardet-Biedl syndrome causes abnormal weight gain (as well as many other bodily complications) that typically begins in early childhood and continues to be a problem throughout life
• Obesity has also been blamed on the inherited genes from human ancestors that predispose individuals to favour fatty, sweet and salty foods, all of which are now cheap and easily accessible through fast food outlets
• Evolution causes bodies to behave as if they were still living in their ancestral past and because the human gene pool has not substantially altered, genes that once favoured survival now favour obesity
• This Thrifty gene model explains how humans’ inherited genes are not useful adaptations with regards to eating and obesity

Estimated global prevalence and numbers of adults living with obesity in 2010–2030 

• The hypothalamus is the brain structure identified as playing a central role in the regulation of eating
• Therefore neural explanations focus on the idea that a malfunction within the hypothalamus is associated with the development of obesity
• The lateral hypothalamus (LH) is the ‘hunger centre’ that initiates eating behaviour, and the ventromedial hypothalamus (VMH), is the ‘satiety centre’
• Neural explanations for obesity go back to the ob gene (above), which codes for leptin arguing that obese individuals lack the hormone leptin, because of a mutation in the ob gene, and therefore do not receive the message in the VMH to stop eating when full
• The neurotransmitters serotonin and dopamine are also related to obesity, with low levels of both associated with increased appetite
• Serotonin normally  signals to the VMH that a person has eaten to satiety
• Dysfunctions of the serotonin system may be genetically inherited, due to stress or other disorders such as depression (Booij, 2015) 
• When levels of serotonin are abnormally low this creates inaccurate satiety signals to the hypothalamus, disinhibiting eating behaviour
• Low levels of serotonin have also been linked with cravings for energy-rich foods, such as cake and chocolate that are high in fats and sugars, that cause weight gain through consuming too many calories (Wurtman, 1995)
• Dopamine stimulates the hypothalamus, hippocampus and amygdala, providing rewarding feelings of well-being associated with the pleasure we derive from eating and cues associated with eating, such as the smell of food
• Low levels of dopamine reduce pleasure in eating, and overeating is an attempt to activate reward centres in the brain by increasing dopamine levels
• The explanation that focuses on low levels of dopamine proposes that obesity is caused by food addiction that operates neurochemically in the same ways as other addictions

Low levels of both serotonin and dopamine can lead to cravings for carbohydrates.

Research which investigates biological explanations for obesity

• Stice et al (2008) found obese people had a poorly functioning dorsal striatum, leading to lower dopamine signalling in the brain, causing them to overeat, supporting the neural explanation for obesity 
• Elks et al (2011) found that the heritability of obesity was highest during childhood and then decreased in adulthood due to greater Gene expression in childhood and a greater emphasis on dietary and exercise habits in adulthood, suggesting limited usefulness of the genetic explanation for obesity

Evaluation of biological explanations for obesity

Strengths

• The discovery of genes related to obesity has practical application, as it has led to the search for effective gene therapies for the treatment of the condition
• There is research support for the role of leptin in regulating appetite and its deficiency as a risk factor for obesity (Gibson et al, 2007)

Weaknesses

• Neural explanations for obesity that examine serotonin and dopamine levels are correlational and so it is not clear whether low neurotransmitter levels are a cause or an effect of being obese
• Many of the research findings from biological investigations into obesity have been based on studies using genetically modified mice, and so they  cannot be generalised to humans

Link to Issues & Debates: 

The genetic and neural explanations for obesity are on the nature side of the nature-nurture debate.  However, genes alone cannot explain the increase in obesity as the genotype of humans has not changed, but environmental factors like the availability of food have, suggesting the environment plays a key contributory role. 

The biological explanations are also reductionist, ignoring psychological and environmental factors and an argument that explains obesity as an interaction between nature and nurture would be a more holistic and less reductionist approach.

Link to Approaches: 

The role of genes and neural mechanisms in obesity  is a biological approach to behaviour, explaining appetite and overeating through the resulting low levels of the hormone leptin and the neurotransmitters serotonin and dopamine.