Bulimia Nervosa (bio - abnormal)

bulimia nervosa

an eating disorder usually characterized by a cycle of binge eating followed by compensatory behaviors to prevent weight gain

bulimia nervosa

characteristics

• Binge Eating – Eating excessive amounts of food within a short time, often feeling a loss of control.

• Compensatory Behaviors – Engaging in purging (vomiting, laxatives) or non-purging (excessive exercise, fasting) to counteract binge eating.

• Preoccupation with Body Weight & Shape – Strong fear of weight gain and distorted body image.

• Secrecy & Shame – Binges often occur in private, leading to feelings of guilt and self-loathing.

• Health Risks – Electrolyte imbalances, dehydration, gastrointestinal issues, and damage to the esophagus and teeth from vomiting.

Possible causes

• Psychological factors (low self-esteem, anxiety, depression)

• Societal pressure for thinness

• Genetics and family history

• History of dieting or restrictive eating

possible treatments

• Psychotherapy (Cognitive-Behavioral Therapy, Dialectical Behavior Therapy)

• Nutritional counseling

• Medication (e.g., antidepressants)

• Support groups & professional monitoring

3 studies on genetics and bulimia

• Twin Study:

  • Kendler et al. (1991)

    • Investigating the risk factors and genetic inheritance in bulimia nervosa

• Kinship Study:

  • Strober et al. (2000)

    • Found first-degree relatives of individuals with bulimia were significantly more likely to develop the disorder, supporting familial influence.

• Specific Gene Study:

  • Ribases et. al (2004)

    • To investigate the association between the BDNF gene and eating disorders

Strober et. al (2000)

AMRCE

• Investigate whether BN runs in families by studying the prevalence of BN in first-degree relatives of individuals with BN.

Strober et. al (2000)

AMRCE

• Participants:

  • Individuals diagnosed with BN (probands).

  • First-degree relatives of BN probands (parents, siblings).

  • Control group: Never-ill individuals and their relatives.

• Procedure:

  • Structured clinical interviews and family history assessments conducted.

  • Diagnoses made by clinicians blinded to the proband’s status to reduce bias.

Strober et. al (2000)

AMRCE

• Familial Risk for BN:

  • Female first-degree relatives of BN probands were 4.4 times more likely to have BN compared to relatives of control participants.

• Partial BN Symptoms Also Ran in Families:

  • Some relatives did not meet full BN criteria but exhibited binge eating and compensatory behaviors.

Strober et. al (2000)

AMRCE

• BN has a strong familial component, suggesting a genetic and environmental basis.

• Higher rates of BN among relatives support the idea that BN runs in families.

Strober et. al (2000)

AMRCE

✅ Strengths:

• Strong evidence for genetic influence on BN due to higher concordance among first-degree relatives.

• Blinded assessment reduced bias in diagnosing BN among relatives.

❌ Limitations:

• Focus on female relatives (less data on BN risk in males).

• Does not account for environmental triggers (e.g., family dynamics, media influence).

• Partial syndrome diagnoses may be subjective, affecting accuracy.

The Equal Environment Assumption (EEA) i

he assumption that monozygotic (MZ) twins (who share 100% of their genes) and dizygotic (DZ) twins (who share approximately 50% of their genes) are exposed to the same environmental factors to a similar degree.

Kendler et al. (1991)

AMRCE

• To investigate risk factors and genetic inheritance in bulimia nervosa.

Kendler et al. (1991)

AMRCE

• A sample of  2,163 female twins participated in the study.

  • One of the twins in each pair had developed bulimia.

• longitudinal

• researchers conducted interviews with the twins to see if the other twin would develop bulimia

  • + if concordance rates were higher in monozygotic twins (MZ) than in dizygotic twins (DZ).

Kendler et al. (1991)

AMRCE

• Overall the concordance rate or bulimia was 23% in MZ twins compared to 9% in DZ twins.

Kendler et al. (1991)

AMRCE

• The results indicate a heritability of 55%, but this leaves 45% for other factors.

• Genetic vulnerability may predispose an individual but other factors trigger the disorder and it is important to investigate environmental factors that might interact with the genetic predisposition.

Kendler et al. (1991)

AMRCE

• The study was a natural experiment so the researchers did not manipulate variables and there was no control, so it is not possible to establish a cause-effect relationship.

• The participants were all women so the findings cannot be generalized to men. It is also questionable whether twins are representative of the population.

• The study does not take environmental factors into account. It could be that twins grow up in the same dysfunctional environment.

• It is very difficult to find out the relative importance of genetic inheritance and environmental factors.

Ribases et. al (2004)

AMRCE

To investigate the association between the BDNF gene (Val66Met polymorphism) and eating disorders, including bulimia nervosa and anorexia nervosa, across six European populations.

Ribases et. al (2004)

AMRCE

• A quasi-experiment

  • IV: diagnosis of bulimia nervosa

    • Condition 1: bulimia diagnosed

    • Condition 2: Control

  • DV: Val66Met polymorphism in BDNF gene

• The study analyzed genetic samples from individuals diagnosed with bulimia nervosa and anorexia nervosa.

  • through collected saliva or blood samples

• The researchers compared the presence of the Val66Met polymorphism in individuals with eating disorders versus a control group without eating disorders.

Ribases et. al (2004)

AMRCE

• A significant association was found between the BDNF Val66Met polymorphism and eating disorders, including bulimia nervosa.

• Individuals with certain variations of this gene were more likely to develop bulimia.

Ribases et. al (2004)

AMRCE

• The study suggests that the BDNF gene plays a genetic role in the development of bulimia nervosa and anorexia nervosa.

• This highlights BDNF’s involvement in appetite regulation and eating behaviors.

Ribases et. al (2004)

AMRCE

✅ Strengths:

• Large sample size from six European populations, increasing generalizability.

• Genetic approach provides biological insight into eating disorders.

❌ Limitations:

• Correlation, not causation – the study only shows an association between BDNF and bulimia, not a direct cause.

• The study does not account for environmental factors like stress, social pressure, or family influences, which also contribute to bulimia.

BDNF gene

Brain-Derived Neurotrophic Factor (BDNF) gene

• found on chromosome 11

function:

• Encodes BDNF, a neurotrophic protein essential for the growth, survival, and maintenance of neurons.

• Plays a key role in synaptic plasticity, learning, memory, and mood regulation.

• Involved in the regulation of appetite and eating behaviors via pathways in the hypothalamus.

Val66Met Polymorphism (rs6265 SNP)

• A single nucleotide polymorphism (SNP) in the BDNF gene where guanine (G) is replaced by adenine (A) at a specific position.

• Leads to an amino acid change from Valine (Val) to Methionine (Met) at position 66 in the BDNF protein.

• Affects the secretion and activity of BDNF, influencing brain function.