↵The biological approach has two key arguments for the origins of anorexia nervosa.  First, there is the genetic argument that argues that the disorder is inherited and runs in families. The second argument is that there are neurochemical reasons for anorexia - specifically, levels of serotonin and dopamine.

Before reading the research on genetic and neurochemical explanations of anorexia, watch the video below with Laura Hill explaining why it is important to understand that anorexia may not be simply a "social disorder", but is actually based on biological dysfunction.

 Teacher only box

This question obviously has no correct answer. Students should be able to talk about why they agree or disagree with Dr. Hill. 

As for the second question, this gets students to think about the nature of biological vs social arguments. Many people prefer biological arguments because it explains that what is wrong with them is not their choice.  There is a more deterministic approach to explaining disorders. However, students often mistakenly think that sociocultural arguments have total choice.  But this is also not true. People do not choose abuse, poverty, or other social risk factors for mental illness.  Some argue that this is also a form of social determinism - which potentially has more wiggle room than biological determinism, but still may be beyond an individual's control.

Many people are happy to simply have an explanation of their condition, regardless of whether it is biological, cognitive, or sociocultural in nature.  Some, however, mistakenly believe that if it is biological,t hen it can be easily treated by drugs. Although this may be true in some cases, there are no easy treatments for complex mental disorders.

Genetic explanations of Anorexia

Both anorexia and bulimia run in families. First-degree relatives of young women with anorexia are over 10 times more likely than average to develop the disorder (Strober et al, 2000).

One of the earlier studies of the genetics of anorexia was carried out by Holland et al (1988). The research team studied 45 pairs of female twins. At least one had to have anorexia. There were 25 Monozygotic (MZ) and 20 dizygotic pairs of twins. The twins were interviewed and took surveys with regard to their diagnosis as well as eating habits. The researchers found a 56% concordance rate for the MZ (identical) twins and only 5% for the DZ (fraternal) twins. This is a significant difference; the researchers argued that up to 80% of cases of anorexia may be due to genetics. However, there are two significant limitations of the study. First, the diagnoses and eating habits were self-reported. This makes any diagnosis unreliable - and there may not be a clear differentiation between anorexia and bulimia. In addition, the sample size is small and may not be representative.

One of the key questions is: How do genes lead to a complex dysfunctional behaviour like anorexia? The answer is - we don't know. There are several potential biological factors that may lead to anorexia - such as lower levels of serotonin - and these could have a genetic basis. More importantly, researchers have taken a closer look at genetic variability in anorexics and found some trends, but cannot explain how these trends may lead to anorexia. So, whether it's twin studies or genetic mapping, the results are only correlational and cannot determine a cause and effect relationship. Most likely researchers will never find a single gene that "causes" anorexia nervosa, but rather a number of genes that make someone vulnerable to it. These genes may include ones for personality variables such as OCD or perfectionism, or for hormonal, metabolic and appetite factors.

It is important to note that twin studies of eating disorders have been conducted in primarily European populations. Little is known about the heritability of these disorders and traits in other cultures.

Much of the research today is done using Genome-wide association studies. These studies compare the DNA of two groups of participants: people with the disease and similar people without (controls). Each person gives a sample of DNA, from which genetic variants are read. If one type of the variant is more frequent in people with the disease, it is said to be "associated" with the disorder. GWAS Association studies have focused on the genes specifically relating to the neurochemistry of eating behaviour. Devlin et al (2002) have found one such allele is the serotonin receptor 5-HT_2A gene HTR2A. So far, however, many GWAS studies have not been replicated.

The largest GWAS study of anorexia nervosa has linked the eating disorder to variants in a gene coding for an enzyme that regulates cholesterol metabolism (Scott-Van Zeeland et al, 2014). The finding suggests that anorexia could be caused by a disruption in the normal processing of cholesterol, which may disrupt mood and eating behaviour. For this study genetic information was gathered from more than 1,200 anorexia patients and nearly 2,000 non-anorexic control subjects. One of the most significant findings was a difference in the gene EPHX2, which codes for an enzyme known to regulate cholesterol metabolism. The scientists have found that variants of EPHX2 occur more frequently in people with anorexia.

People with anorexia often have remarkably high cholesterol levels in their blood, despite being severely malnourished. There have been other studies that suggest that weight loss can lead to increases in cholesterol levels. At the same time, there is evidence that cholesterol, a basic building block of cells, particularly in the brain, has a positive association with mood. Conceivably, some anorexics for genetic reasons may feel an improved mood, via higher cholesterol, by not eating. However, as this is relatively new research, it will need to be investigated further.

Biochemical explanations of Anorexia

Bailer & Kaye (2011) found evidence from imaging studies that have linked anorexia to high levels of serotonin. High levels of serotonin suppress appetite and increase anxiety and obsessive behaviour, which are characteristics of anorexia. Restricting food may be a form of “self-help” because serotonin levels will drop as a result of less food.

Their research also suggests that women who develop anorexia nervosa may have altered levels of dopamine in their brains. Dopamine disturbances can cause hyperactivity, repetition of behaviour (such as food restriction), and a decreased sense of pleasure. This neurotransmitter also affects reward-motivated behaviour. Using PET scanning, they found that subjects who had recovered from Anorexia nervosa had increased dopamine receptor sites in the reward centres of the brain, compared to patients currently suffering from Anorexia. Improper levels of dopamine may explain why anorexics feel intensely driven to lose weight yet feel little satisfaction in actually losing it.