Analyze Etiologies of Anorexia Nervosa

1. Analyze Etiologies of Anorexia Nervosa Abnormal Psychology

2. Introduction • It is unlikely that one factor is enough to explain anorexia nervosa (AN) • Biology, cognition and culture all contribute to the etiology AN • All three levels of analysis influence this abnormal behavior in a bidirectional way • The Walker-Tessner model and the diathesis-stress model both help explain AN through a bidirectional approach and thus avoid reductionism

3. Walker-Tessner Model • Walker-Tessner model demonstrates the contributions of each level of analysis in acquiring AN • Prenatal + Postnatal affect an individual’s Acquired Biological Factors (imbalances in hypothalamus, which controls weight and regulation and appetite) • Prenatal Factors = mother engaging in alcoholism, drug abuse, unhealthy dieting • Postnatal Factors = birthing complications, the child’s diet, parental neglect/abuse

4. Walker-Tessner Model • Inherited factors (genes) = 5HTT receptor genes, estrogen receptor genes and 2 dopamine receptor genes have been identified as possible risk genes • Constitutional Vulnerability = personality traits (OCD-like personality), overestimation of body size, negative thinking patterns

5. Walker-Tessner Model • Stress = exposure to media, diet/complaints of mother of girls with AN • Neuromaturational factors = decreased leptin (protein) is the neuropeptide (similar to neurotransmitters) most associated with AN; serotonin, norepinephrine, dopamine

6. Risk Factors of AN The same risk factor approach should be used to analyze the etiologies of AN.

7. A list of factors that increase one’s risk of AN • Biological LOA: • Genes • The hypothalamus: Appetite and weight regulation imbalance • Neurotransmitters: Serotonin, norepinephrine, dopamine.

8. A list of factors that increase one’s risk of AN • Cognitive LOA: • Cognitive factors: Attentional biases toward food and body-related cues • Cognitive distortions: Dichotomous thinking • Perfectionism • Reward sensitivity: Those with AN report higher reward dependence. • This means that they have a higher need for reward and praise than those without AN.

9. A list of factors that increase one’s risk of AN • Sociocultural LOA: • Media portrayal of cultural attitudes towards thinness. • Family interaction • Social learning, including modeling from parents and self efficacy.

10. A list of factors that increase one’s risk of AN • All three LOA (genes, cognitive style, and the role of the media) work together. • Walker-Tessner model shows this relationship.

11. Anorexia – Biological Perspective • Levels of serotonin (regulates mood and appetite) • Increased levels – reduces appetitie • Starvation – lowers serotonin levels which also reduces anxiety • Brain adapts – adds more receptor cites for serotonin • Now starvation increases to keep the levels low • Visious cycle

12. Genetic Risk Factors: Biological LOA • Family-based association studies and twin studies suggest an importance in genetic contributions to eating disorders. • Despite this, molecular genetic studies have been inconsistent in identifying specific risk alleles (gene variations). • Therefore, it remains unclear as to which specific gene poses the greatest risk. • .

13. Genetic Risk Factors: Biological LOA • Several genes have been identified as risk factors in molecular genetic studies. • These include: 5 HTT (serotonin transporter gene), several 5 HTT receptor genes, estrogen receptor genes, and two dopamine receptor genes. • None have demonstrated sufficient evidence to be clear candidates

14. Genetic Risk Factors: Biological LOA • Is molecular genetic research moving towards reductionist thinking? • No. Molecular genetic research aims to move towards complex models where identified risk alleles interact with other genes and environmental factors.

15. Gene-Environment (GXE) Correlations • Mazzeo and Bulik: clarify which environmental risk factors are most likely to interact with genetic vulnerabilities. • Passive, evocative, and active GXE correlations probaby work for eating disorders. • Advances in genetic research methodology will aid future researchers in identifying specific alleles that make certain people more reactive to environmental factors.

16. Passive GXE Correlations • Possible passive GXE Correlation: Parental models and child disordered eating behavior. • Unfair to say that parents are a direct cause of offsprings’ eating disorder. • Studies have demonstrated that a mother’s comments and complaints about her own body image correlate with the esteem levels of their children, especially with daughters’ concern about their own weight. • This is a passive correlation because the parents transfer the risky genes to their children as well as providing the environment. • Mazzeo and Bulik call this a “double dose” of risk factors for the children without them even doing anything.

17. Passive GXE Correlations • Examples of Passive GXE correlations: • A mother’s own problematic feeding behavior, such as restricting, may lead to their five-year-old offspring also showing restricting eating behaviors. • Parental overemphasis on weight is present when a mother’s satisfaction level with their child’s body size is negatively correlated with the severity level of their own eating disorder.

18. Evocative GXE Correlations • In Evocative GXE Correlations, a person with a specific genetic make up evokes, or brings about, specific types of responses from the environment. • Example: Perfectionism. • While temperament is influenced by genetic factors, a person’s temperament also influences how a person interacts with the environment. • People with perfectionist temperaments seek out demanding environments and hold themselves to very high standards. This temperament is influenced by feedback from others.

19. Evocative GXE Correlations • Monozygotic (identical) twin research on AN and BN reveals that one twin is often more strongly criticized that the other. • Both twins carry the predisposition, but only one expresses it, which may result in the behavior that attracts parental attention

20. Active GXE Correlation • Media is believed to be a large part of active GXE correlations to eating disorders. • Why do most girls not develop eating disorders despite being constantly exposed to media that idolizes thinness? • Girls with a genetic predisposition to eating disorders might seek out media that highlights thinness in order to reinforce their own negative views about their body shape.

21. Active GXE Correlation • Longitudinal Studies support the media hypothesis. • Girls whose eating disorder symptoms increased over a 16-month period were reportedly reading more fashion magazines during that time. • Girls with genetic predispositions to eating disorders actively select peer groups with the same ideals. • European-American (Wetern) girls who are members of sororities reportedly develop more eating disorders that those not in sororities.

22. Information Processing Biases: Cognitive LOA • Two types of cognitive factors that increase the risk of eating disorders are attentional biasestoward food and body and cognitive styles that distort reality. • Research on cognition is valuable for understanding the symptoms and personality traits of people with eating disorders, making predictions about the severity of an individual’s disorder, and designing treatment plans.

23. Analyze Etiologies of Anorexia Nervosa • Laura Southgate and Colleagues (2008)

24. Television Exposure: Sociocultural LOA • Becker and Colleagues (2002) documented large changes in attitude towards body image and risky eating behaviors after the introduction of television to the island of Fiji. • Previously, television exposure was very limited on the island. Fijian tradition valued robust figures and hearty appetites.