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Socio-Cultural and Behavioral Genetic Perspectives on Eating ...

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Socio-Cultural and Behavioral Genetic Perspectives on Eating ...

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    1. Socio-Cultural and Behavioral Genetic Perspectives on Eating Disorders: Implications for Theory, Treatment, and Recovery Michael P. Levine, Ph.D., FAED – Kenyon College Keynote Panel with Drs. Kelly Klump and Anne Becker Renfrew Conference, Philadelphia, November 10, 2007 Levine Acknowledges the Considerable Support of Linda Smolak, Ph.D., & Sarah Murnen, Ph.D., Kenyon College and Carolyn Costin, M.A., M.Ed. – Monte Nido, Malibu, CA, & Margo Maine, Ph.D, FAED, Maine & Weinstein Associates, W. Hartford

    3. Establishing a Causal Risk Factor: Logical, Admissable, & Cogent “Scientific Evidence” (after J. S. Mill, H. Kraemer, and others) Inductive Sensibility = makes logical, coherent sense, based on observations and reasoning Covariation 1 = co-relationship = correlation Temporal precedence = longitudinal verification Covariation 2 = modifiability Replicability = “robustness” This is loosely based on the Kraemer et al definition of risk factors though they don’t include meta-analyses. The correlates/case study is just to identify potential causes. There is a substantial amount of correlational/case study data indicating sociocultural variables are related to every aspect of the eating disorders continuum. We cannot/will not review all of that here. Experimental data can potentially identify causal data; prospective, longitudinal data can identify variable risk factors. Meta-analysis can tell us (a) effect size across studies; and (b) consistency of findings. Of course, they are bound by the extant data.This is loosely based on the Kraemer et al definition of risk factors though they don’t include meta-analyses. The correlates/case study is just to identify potential causes. There is a substantial amount of correlational/case study data indicating sociocultural variables are related to every aspect of the eating disorders continuum. We cannot/will not review all of that here. Experimental data can potentially identify causal data; prospective, longitudinal data can identify variable risk factors. Meta-analysis can tell us (a) effect size across studies; and (b) consistency of findings. Of course, they are bound by the extant data.

    4. Establishing a Causal Risk Factor: Logical, Admissable, & Cogent “Scientific Evidence” (after J. S. Mill, H. Kraemer, and others) Biographies, clinical case histories, and clinical observations/experiences Cross-sectional – current and retrospective – based on the use of bi-variate or multi-variate correlations Prospective, longitudinal data - based on use of bi-variate or multi-variate correlations Experimental data --- laboratory, treatment-oriented, prevention-oriented Meta-analyses Other statistical summaries and analyses This is loosely based on the Kraemer et al definition of risk factors though they don’t include meta-analyses. The correlates/case study is just to identify potential causes. There is a substantial amount of correlational/case study data indicating sociocultural variables are related to every aspect of the eating disorders continuum. We cannot/will not review all of that here. Experimental data can potentially identify causal data; prospective, longitudinal data can identify variable risk factors. Meta-analysis can tell us (a) effect size across studies; and (b) consistency of findings. Of course, they are bound by the extant data.This is loosely based on the Kraemer et al definition of risk factors though they don’t include meta-analyses. The correlates/case study is just to identify potential causes. There is a substantial amount of correlational/case study data indicating sociocultural variables are related to every aspect of the eating disorders continuum. We cannot/will not review all of that here. Experimental data can potentially identify causal data; prospective, longitudinal data can identify variable risk factors. Meta-analysis can tell us (a) effect size across studies; and (b) consistency of findings. Of course, they are bound by the extant data.

    5. This is a definition from a well-known sociocultural researcher/theorist from an often cited paper (his risk factor meta-analysis). Note the references to (a) social pressure; (b) thin ideal; (c ) continuum This is a definition from a well-known sociocultural researcher/theorist from an often cited paper (his risk factor meta-analysis). Note the references to (a) social pressure; (b) thin ideal; (c ) continuum

    6. What A Sociocultural Perspective Is Focuses on socially constructed or culturally endorsed variables Involves socialization but may also involve active construction or use of schema – cognitive social learning, reciprocal determinism, and a transactional approach Culture will determine what is ideal for whom and how to attain it Culture will determine what is normative (even if unhealthy) and pathological There will be within- and across-group differences based on exposure to various sociocultural factors

    7. A Sociocultural Perspective Does Not Does not deny any role for genetics or neurobiology as important – but not the only important – sources of individual differences in vulnerability Does not minimize the seriousness of full-blown eating disorders, nor fail to make any distinctions between different types or levels of disordered eating Does not expect that one model will fit all cultures or both genders or all ages Admittedly, Stice’s definition actually does not give any role to neurobiology or genetics. Similarly, most sociocultural models (e.g., Objectification Theory; Thompson et al.’ s Tripartite Theory; Stice’s Dual Process Theory; a Feminist-Ecological Theory). But they do not actively deny the possibility. We will have to develop the specific roles of each component, however, later in the workshop.Admittedly, Stice’s definition actually does not give any role to neurobiology or genetics. Similarly, most sociocultural models (e.g., Objectification Theory; Thompson et al.’ s Tripartite Theory; Stice’s Dual Process Theory; a Feminist-Ecological Theory). But they do not actively deny the possibility. We will have to develop the specific roles of each component, however, later in the workshop.

    9. MOREOVER: A Sociocultural Model Can Account for The 7 Gordon-Devereaux (2000) phenomena The Massive Gender Difference (at least 8:1) The Secular Trends – we can’t ignore population-based increases in antisocial behavior, drug use/abuse, depression, eating disorders, and obesity Cross-Cultural Differences in Prevalence, Incidence, and Expressions Migration Data Cumulative Effects at Developmental Transitions

    10. Characteristics of Ethnic Disorder (G. Devereux; from Gordon , 2000) Substantial prevalence in culture or in particular demographic groups. Continuum of severity; borderline forms. Core conflicts reflect cultural tensions. Diverse forms of underlying psychopathology.

    11. Characteristics of Ethnic Disorder (G. Devereux; from Gordon , 2000) Valued behaviors in culture utilized as defenses. Widely imitated template of deviance: Don’t go crazy but if you must do it this way.” Disorder evokes ambivalent response, admiration and derision, becomes “politicized.”

    12. A Sociocultural Model Can Also Account for the The Rarity of ED’s? A Look at Risk Factors & Probability (Hanson, 2004) If there were 4 (relatively) independent risk factors for bulimia nervosa, then to achieve a population frequency of .02 (the point prevalence), each would have to occur at a frequency of .375 in the population, because .375 to the 4th power (.3754) = .198 = ~.02. “The factors that lead to schizophrenia, as Dr. Gottesman taught us, are multiple. These factors must be quite common in the population and thus are not necessarily abnormal. [We need to] get out of our mindset of searching for abnormal schizophrenia genes and broaden our view to look at normal individual genetic variation in conjunction with exposure to common environmental agents” (p. 214)

    13. What Should Be Considered “Scientific Evidence”? Key Methodological & Theoretical/Empirical Issues: Criterion measures: Cases, symptoms, or precursors? Reliability and validity in risk factors and outcomes Ecological validity Sexual abuse, sexual harassment, rape, trauma Specificity, at least to a degree Continuum of eating problems Part of the question here is going to be whether the experimental method---the “gold standard” of empiricism—has any value in clinical case research (i.e., where actual cases of AN or BN) are involved. Further, it has little ecological validity---the dieting literature (Stice’s “naturalistic” vs. “experimental” dieting work) is probably a good example. And cannot be used to investigate sexual abuse, sexual harassment, and rape---important variables in understanding the gender differences in body image and eating pathology. We also fact the challenge of whether a risk or causal factor is exclusive or specific to eating problems/disorders (vs. affective, anxiety, or personality disorders)----though one is left wondering whether this issue is always raised fairly (e.g., CSA). On the other hand, work involving actual cases of AN or BN (and our title does say eating disorders, I think) rarely looks at sociocultural variables per se (looking instead at body image, wt concerns, etc as predictors). Part of the question here is going to be whether the experimental method---the “gold standard” of empiricism—has any value in clinical case research (i.e., where actual cases of AN or BN) are involved. Further, it has little ecological validity---the dieting literature (Stice’s “naturalistic” vs. “experimental” dieting work) is probably a good example. And cannot be used to investigate sexual abuse, sexual harassment, and rape---important variables in understanding the gender differences in body image and eating pathology. We also fact the challenge of whether a risk or causal factor is exclusive or specific to eating problems/disorders (vs. affective, anxiety, or personality disorders)----though one is left wondering whether this issue is always raised fairly (e.g., CSA). On the other hand, work involving actual cases of AN or BN (and our title does say eating disorders, I think) rarely looks at sociocultural variables per se (looking instead at body image, wt concerns, etc as predictors).

    14. Evidentiary Bases for a Sociocultural Perspective: Some Relevant Variables? Gender: The socially constructed and lived experience of being female or male, e.g., objectification for females Media: Exposure, social comparison, internalization, and media literacy Peers: Teasing, comments, investment in ideal and its attainment, social comparison Parents: Teasing, comments, investment in ideal and its attainment for self and child Trauma: Sexual and physical assault; traumatic loss (e.g., suicide of a parent, or seeing one parent murder another)

    15. Evidentiary Bases for a Sociocultural Perspective: Mass Media Content and Utilization Analyses (Levine & Harrison, 2004, in press) Meta-analyses Internalization of media ideal, perceived pressures from media and other sources (Cafri et al., 2005) Experimental manipulations of cultural ideal (Groesz, & Levine, & Murnen, 2002) Extent of exposure (cross-sectional) (Levine, Murnen, Smith, & Groesz, 2007, in preparation) Longitudinal Prospective (Field et al., 1999, 2001; Harrison et al., in press; McKnight Investigators, 2003) Experimental (Stice, Spangler, & Agras, 2001) Experimental prevention (see Levine & Smolak, 2006, chapter 13) I’ll add a couple of other longitudinal studies re: media and body image/internalization/wt concerns (I think the Fields et al study, e.g., looks at media separately; I have to look).I’ll add a couple of other longitudinal studies re: media and body image/internalization/wt concerns (I think the Fields et al study, e.g., looks at media separately; I have to look).

    16. Meta-Analytic Data for Females: Murnen, Levine, Groesz, & Smith (2007)

    17. Evidentiary Bases for a Sociocultural Perspective: Mass Media Meta-analysis of correlational research shows moderate effect size for fashion magazine exposure and internalization of thin ideal (d = .21) and weight concerns (d = .18) with smaller effect sizes for TV exposure. (ethnicity may be a moderator) Meta-analysis of experimental research shows moderate effect size (d = .31) of viewing thin media images on body image with prior history of body dissatisfaction an important moderator (d = .50) Recent research: mediators & moderators include activation of appearance-focused schema, internalization of thin ideal social comparison

    18. Evidentiary Bases for a Sociocultural Perspective: Mass Media Prospective, Longitudinal Studies McKnight investigators (2003): Over a 3-year period, media modeling was part of a multidimensional factor that predicted the onset of bulimia nervosa, subclinical bulimia nervosa, or binge eating disorder in adolescent girls. Field et al. (1999, 2001): Over a 1-year-period, and independent of age and BMI, trying to look like “same-sex figures in the media” was a predictor of the development of weight concerns, chronic dieting, and monthly purging (girls only) in large samples of boys and girls ages 9 through 14.

    19. Evidentiary Bases for a Sociocultural Perspective: Mass Media Prospective, Longitudinal Studies Harrison et al. (2006): Over a 1-year period, television exposure (but not magazine exposure) predicted significant increases in disordered eating and in endorsement of a thin(ner) future body ideal for girls in 2nd – 4th grade (mean age = 8-9) BUT Studies with older children and young adolescents (e.g., McCabe and Ricciardelli (2005) and with older adolescents (e.g., Presnell et al., 2004; Stice (1998) found that perceived media influence and “media modeling” were not significant predictors of a variety of body dissatisfaction and variety of risky eating and unhealthy weight/shape management behaviors, whereas, in general parental influences and same-sex peer influences were.

    20. Reinforces the need for well-articulated models, careful attention to methodology (including outcome variables), and an evidentiary basis Emphasizies the “disorder” in eating disorders and the importance of “specificity” in risk factors and outcomes Emphasizes the fact that some families and thus some individuals are at high risk due to genetic vulnerability (whatever that may turn out to mean in term of gene-environment interactions and transactions) Reinforces the importance of selective and targeted prevention for those at high risk Reinforces a contention at the heart of feminist and community-oriented approaches to research and prevention: Perspective, power, politics are always in play in defining, researching, and treating a “disorder”. . . . Conclusions and Implications: A Critique [Including Appreciation] of The Bio-psychiatric Critique

    21. Advancement of the field in recognized and “legitimate” ways Effective understanding, treatment, and prevention of eating disorders – equifinality and equipotentiality (and the challenges of [non]specificity and co-morbidity) Prevention or modulation of those variable factors (whether they be latent genes, or “shared” or “unshared” environments) that constitute and/or activate various forms of individual—and sociocultural—vulnerability Conclusions and Implications: A Critique [Including Appreciation] of The Bio-psychiatric Critique

    22. Conclusions and Implications: A Critique of The Biopsychiatric Critique Point 1: “Research on the etiology of eating disorders has lagged behind other areas of psychiatry due to the imminent plausibility of sociocultural theories about the illness. . . Point 2: [sociocultural explanations] have hindered recognition of the seriousness of eating disorders” Point 3: “The sheer convenient believability of sociocultural explanations has influenced research directions”

    23. Point 3: “The sheer convenient believability of sociocultural explanations has influenced research directions. . . .” We can’t ignore, as is the case for depression and for alcohol abuse and dependence, what is believable and apparent based on lived experiences of patients, professionals, and people in general The sociocultural perspective and specific models (e.g., Thompson et al.’s “Tripartite Model” or Stice’s “Dual Pathway Model” or Ricciardelli & McCabe’s “Biopsychosocial Model”) are not based on “believability” or “convenience” or “face validity” – They are based on a very scientific and compelling blend of theory, methodology, and, for the most part replicable (robust) convergent findings that point to small-to-moderate effects for sociocultural factors (Stice, 2002) The sociocultural perspective has a theoretical and empirical foundation that is at least as strong, if not much stronger, than the biopsychiatric perspective and its emphasis on very limited behavior genetic models (see Jacobi et al.’s, 2004, review) and on a model of temperament which has little or no connection with developmental psychology or developmental psychopathology Conclusions and Implications: A Critique of The Bio-psychiatric Critique

    24. It’s Fine to Accuse Me of Ignoring or Being Unable to Comprehend the “Science of Genetics” Or Their Links to, e.g., Serotonin or Temperament? But Let Us, Together: Think very carefully about what taking genetics into consideration means -- theoretically -- methodologically -- practically Equalize the burden of proof – Genes –> neurotransmitter systems –> neurological systems and temperament (or OCPD) ? response to or creation of environments ? ED Can’t just present correlations and claim you have the upper hand. . . .

    25. NOT a fixed determination of the overall effect of genes on a trait, to the exclusion of environment NOT a statement, or a proof, that “genes cause the behavior or disorder in question” – correlation does not equal causality The Heritability “Coefficient” is: “a descriptive statistic that gives an estimate of the effect size for a latent trait of genetic influence based upon a particular population measured in a particular way at a particular moment in time. It provides a statistical indicator that speaks to the confidence that one might have in inferring that genetic differences among individuals account for more than zero of the reliable variance in a trait. . .” -- Rende, 2004, p. 117 It’s Fine to Accuse Me of Ignoring Genetics, Or Their Links to, e.g., Serotonin or Temperament? But Let Us, Together, Remember that Heritability:

    26. Let Us Together Be Careful and Sensible Consider the following imaginary example (From Lerner, 2002, p. 253): A long-standing law dictates that only men can hold positions of leadership in a society. 10,000 people are chosen at random from the society. People could be classified into two groups: Those with absolutely no chance at being elected to a position of leadership and those with some meaningful chance. All the difference in eligibility between the two groups can be summarized, i.e., accounted for, by genetic difference. The heritability of eligibility for elected office is thus 100%. -- High heritability does not mean that characteristics are fixed, unchangeable, or unresponsive to environmental change -- “Behavior genetics is concerned with the ‘what is’ rather than the ‘what could be’ or the ‘what should be” – Richard Rende

    27. Let Us, Together Remember the Complexity of the Task Confronting Behavior Genetics and the Parsing [Analyzing] of Variation Phenotypic variation is a function of genotype (all forms of genetic variability) + shared environment (e.g., family differences) + non-shared environment (unique experiences and unique interpretations of similar experiences) + gene-environment interaction + gene-environment correlation + Passive Evocative Active error and chance (e.g., measurement, chance) – which inflates estimates of non-shared environment

    28. Type of Twin Lifetime AN Status MZ DZ Neither has AN 1,802 2,375 Discordant 14 33 Concordant 1 1 Pairwise Concordance .07 .03 Proband-wise Concordance .125 .057 Tetrachoric r .56 .36 Let Us Together Be Careful and Sensible: Let’s Not Get Carried Away: Bulik et al. (2006) – Archives of General Psychiatry

    29. Let’s Not Get Carried Away: Bulik et al. (2006) – Archives of General Psychiatry Type of Twin Lifetime AN Status MZ DZ Neither 1,802 2,375 Discordant 14 33 Concordant 1 1 Pairwise Concordance .07 .03 Proband-wise Concordance .125 .057 Tetrachoric r .56 .36

    30. Sensible Conclusions - I It does not make any sense from a theoretical or empirical position to claim that “All instances of real disordered eating are genetic” or that “eating disorders are a genetic illness” There are no, or precious few, data to support the claim that “eating disorders are caused primarily by genetics” In polygenic conditions, genes don’t “cause” anything, they contribute to liability “drive for thinness” and “fear of fat” – let alone sexual abus and objectification-- are not reducible to a set of genes creating proteins and neurotransmitters . . . . And in most psychiatric disorders that the majority of variation examined in twin studies is attributable to non-genetic effects and that “shared” as well as environmental effects have been shown to operate in areas of “disorder” related to “socialization” such as drug abuse and criminality

    31. Conclusions and Implications: The Bio-psychiatric Critique Reinforcing the need for well-articulated models, careful attention to methodology (including outcome variables), and an evidentiary basis Emphasizing the fact that individual differences in genetic constitution contributes to individual differences in liability for a spectrum of disordered eating – and that some families and thus some individuals are at particularly high risk due to genetic vulnerability (whatever that may turn out to mean in term of gene-environment interactions and transactions)

    32. Conclusions and Implications: Potential Common Ground Advancement of the field in recognized and “legitimate” ways Rich understanding of the ways in which genes, proteins, neurotransmitters, neuronal functioning, brain organization, experience, families, subcultures, and so forth interact in both directions – in an epigenetic, reciprocally determined fashion – to influence normal and abnormal development Prevention or modulation of those variable factors (whether they be “shared” or “unshared” environments) that constitute and/or activate various forms of individual—and sociocultural—vulnerability

    33. “I’m Beggin’ You, Don’t Bring Me Down” “Studying important human behaviors scientifically is vexing. The field of behavior genetics repre-sents an incomplete attempt. Similar limitations apply to psychobiology and to environmentally oriented social science. If everyone were frank about the limitations of their chosen field, we might all be more able to appreciate the valid contributions of others, enabling us to commence work on the prodigious task of formulating a solid scientific basis for the human sciences” (p. 152) Turkheimer, Goldsmith, & Gottesman (1995)

    34. Beware of Solutions that Seem Obvious A Simplified Look at the Rose Paradox (Austin, 2001; Rose, 1995) Number Risk % - Disorder N___ 10,000 High 12 1200 90,000 Lower 2 1800 100,000 total Low-mod? 3 3000 Selective-Targeted Prevention is not the only answer!

    35. Prevention, Knowledge, and Research “If you want to truly understand something, try to change it” - Kurt Lewin (1890-1947) (no date/source, as quoted in APA Policy and Planning Board. (2007). Who cares about APA policy and does it have an impact? American Psychologist, 62, 491-503.)

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