Eating Disorders:

the Cause and

Effect of
Medicalization
18 March 2015

By Jenica Woolley
 Introduction

Eating disorders (ED) kill more people than any other mental illness1. Although
research validates genetic contributions to this neurological disease, anorexia
nervosa (AN) and bulimia nervosa (BN) are seen as
consequences of poor decisions. Medicalization of ED ED eating disorder
could revolutionize its diagnoses and treatment. This AN anorexia nervosa
review describes single gene polymorphisms,
BN bulimia nervosa
epigenetic polymorphisms, sex-specific aspects, and
obesitys impact on the medicalization of EDs.

Single Gene Polymorphism

Because of gene alterations, inability to produce adequate amounts of protein

could contribute to ED symptoms. Current research targets neurochemistry
receptor genes as potential causes. For instance, of the three -1438 G/A
polymorphisms belonging to the 5-HT2A serotonin receptor gene, AN patients
are more likely to have the AA variant1 (see Figure 1). In total, 46.7% of AN
patients and 43.6% of controls have the -1438 G/A polymorphism of 5-HT2A
serotonin gene2. This statistical significance suggests that
G x E genetic and inadequate serotonin regulation can cause EDs. This makes
environmental sense because serotonin regulates mood, appetite, and
interaction weight.
Additionally, patients with the short allele 5-HTTLPR
serotonin transporter variant
Allele Frequency in ED Patients and Control
are four times more likely to
switch from AN to BN over 0.7
time . Genetic and
2

environmental (G x E) 60.8%
0.525
interaction found between BN ED
50.6%
patients with short 5-HTTLPR Control
polymorphism and child abuse 0.35 39.3%
result in sensation seeking,
insecure attachment, and
dissocial behavior. G x E with 0.175 21.6%
17.6%
the Taq1A allele combined with
10.1%
childhood sexual abuse caused
0
higher sensation seeking in ED AA GA GG

2 Figure 1.
patients. This indicates that child abuse triggers inadequate serotonin transport.
ED behaviors such as restricting food and over-exercising satisfies the genetic-
driven impulse of sensation seeking.
BN patients have higher frequency of G/A single-nucleotide
polymorphisms (SNP) in the endocannabinoid CNR1 receptor gene and C/A SNP
in the fatty acid amide hydrolase (FAAH) gene1. The
endocannabinoid system affects appetite, pain, and mood.
single
The CNR1 and FAAH SNPs cause dysregulation of the insular SNP nucleotide
cortex in BN patients. Disrupting one's appetite and mood polymorphism
regulation would explain the binging and purging aspect of
BN. Identifying these genes in patients could improve ED
diagnosis efficiency.

Sex-specific

Initially, researchers hypothesized that because 90% ED patients are female and
onset is around puberty, AN and BN are caused by hormone gene variants.
Despite continuous experimentation, no link between sex and genetic
predisposition to EDs has been found1. These results do not completely rule out
a link between ED and hormone variants, but presently there is no supporting
evidence. However, a genome-wide study conducted on twins in the UK showed
high percentage of a SNP variant within a neurological coding region that causes
female-specific major depressive disorder3. Further research needs to be
conducted.
Women have more environmental pressures surrounding body weight
which contribute to neurological stress and potential epigenetic consequences.
Medicalization of EDs would create more research opportunities to understand
why ED patients are predominantly female.

Epigenetics

Researchers are currently trying to identify ED epigenetic candidate genes.

Three possible methylation processes found at higher rate in ED patients
include:
1. Altering genes that make leptin receptors which affect the brain food-
regulation circuitry.
2. Methylation of the adrenal hormone POMC gene promoter region that
causes weight-loss.

3
 3. Changing the BDNF gene that regulates neuronal histone deacetylase2.
It is unknown whether ED behaviors cause the epigenetic alterations and if
these processes can be reversed3.
Stress is a key component of epigenetics. For example, children of women
who were pregnant after intense Quebec ice storms in 1998 have increased risk
of BN5. This indicates that gestational stress can lead to an ED later in life.
Adolescents with controlling parents are more likely to develop EDs. AN and BN
rates are high in sports that rely heavily on personal performance. People with
perfectionistic tendencies may be drawn to gymnastics, ballet, figure skating, or
wrestling where weight-loss is encouraged6. Unremitting stress can facilitate
epigenetic polymorphism that activates ED genes. Understanding the interaction
between epigenetics and external stress can improve ED prevention.

Obesity

Obese individuals are five times more likely to have BN (see Figure 2). People
have higher risk for BN if they have obese parents or were obese as a child (see
Figure 3)7. The melanocorin-4 receptor gene (MC4R) that causes obesity is also
found at higher rates in BN patients8. However, MC4R regulates the metabolic
system, yet BN is a neurological disease. Uncontrollable weight-gain can cause
intense body image concerns that trigger binging and purging behavior.

Obese vs. Control

Percent of People
with BN
Obese vs. Healthy Percent CO and PO
0.4
0.02 40%
2%
Obese
Control 0.3
34%
0.015 Obese
Healthy
Control

0.01 0.2
20%
15%
0.005 0.1
11% 11%
0.4%
0 0
Bulimia nervosa Childhood Obesity Parental Obesity

Figure 2. Figure 3.

4
 Medicalization

One opinion is that regardless of evidence, suggesting that EDs are genetically
caused removes patient responsibility9. They claim it will make patients feel out
of control and rely on excuses. Medicalization would not hold external forces
such as media representation, diet advertising, and weight-related teasing
accountable for disordered eating10.
Others believe that attributing ED to genetics would cement its status as
a legitimate medical condition. ED would be treated seriously instead of the lazy
way to lose weight11.
Because 90% of ED patients are women, AN and BN are typically seen as
girly and shallow. Gender stereotypes stigmatize women with EDs by presenting
them as vain and trivial. Despite the high mortality rate and DSM-V
canonization, EDs dont produce the same empathetic
DSM V Diagnostic
response as schizophrenia or autism. People frequently
and Statistical say things like "men don't like when girls are too skinny"
Manual of Mental without considering that a woman is starving herself and
Disorders interaction overexercising because of a biological mental illnessnot
to please men. People believe EDs are just poor behavior
choices that can be cured with willpower. This is a
method of muting womens voices. Emphasizing EDs genetic genesis advocates
for the elimination of bullying women with AN and BN.

Discussion

I believe that more research about the genetic contributors of ED will encourage
change. If ED were medicalized, society could reach a point where I had
anorexia as a teenager is said as lightly as I had pneumonia as a teenager.
Bulimia can evolve from something someone does to something someone has.
Understanding the molecular process of ED can help doctors treat patients
more effectively. When a patient understands that their mental illness is a
disease and not a flaw of willpower, they are more motivated to recover.

5
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