(8) Biological Explanations for Obesity

Twin studies: Average heritability in obesity studies - 40%-75%. Meta-analysis of studies involving 75,000 people. Results: BMI heretability rate of 74% in MZ twins and 32% in DZ twins. Even then MZ are raised apart they have more similar BMI than DZ twins raised together. 

Adoption studies: Allow a look into the influence of biological parents (genetics) and adpotive parents (environment). Danish study - 540 adult adoptees, their adoptive parents and their biological parents. Results: Strong relationship between weight catergory of adoptees and their biological parents weight catergory - no significant relationship with adoptive parents catergory.

Hypothalamus: Arcuate nucleus a collection of neurons that monitors circulating sugar levels in the blood + acts when energy levels are low. When activated sends messages to parts of the body, producing the need to eat. Plays a key role in appetite and maintaining body weight, thus resulting in obesity if it malfunctions.

Leptin: Signal of stored bodily energy and acts to decrease feeding behaviour and promote energy expenditure through neural and endocrime mechanisms. Inhibits food intake by acting on leptin receptors in appetite control centers of the brain. Researchers showed that the disruption of leptin signalling in the hypothalamus results in obesity - proves leptins role is feeding regulation.

James Neel - 'thrifty gene hypothesis' - the history of humans was often 'food or famine' - those who gorged when food was abundant, reserved body fat for when food was scarce = more likley to survive. Suggested these genes were well selected for the feast-famine environment. This would make people with these genes fat to provide enough energy to survive during famines as they already relied on large amounts of stored energy. These genes are now disadvantages because they promote fat deposition to prepare for a famine that isn't likely to occur - leads to obesity and diabetes.

The expression of genetic influences varies with age: Research suggests the genetic contribution to BMI isn't stable across a persons life. Meta-analysis of 88 studies found that heritability estimates varied according to the age group. Found that heritability figure was highest during childhood and decreased in adulthood - likely due to the greater gene expression during childhood - in adults adopt their own dietry and exercise habits - decreasing the genetic contribution to their BMI and increasing the environmental contribution.

The problem of time an geography: 2015 government report showed increase in obesity in the UK over 20yrs. However, the nature of the gene pool has remained the same - means an explanation based only on genetics can't explain it - levels of obesity also vary within cultures - suggests differences are likely to be because of psychological factors.

Research support for the leptin-obesity relationship: Researcher reported on 2 obese cousins of Pakistani origin but living in the UK - both had low leptin levels despite having elevated fat levels. Gibson et al reported on a child from the same region who was also obese - 4yrs of leptin injections had beneficial effects on appetite, metabolism and weight. 

Advantages of biological explanations: Offer explanations that suggest being obese is out of the persons control - less stimatising. Psychological explanations suggests personal failure from overeating/lack of exercise. More simplistic - scientific nature means remedies such as leptin injections used to help people with their disorder.

Problems with the thrifty gene hypothesis: Speakman argues if the thrifty gene explanation is right, the majority of humans should have inherited them = majority of people should be obese. Study found that more than half the worlds obese people live in 10 countries - suggests that it can be explained by cultural factors rather than evolved adaptations.