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פה כמה דברים שאת צריכה להיות מודעת להם כשאת קוראת את החומר המדעי שצורף אינו אותו ): disorder...שם מבאס( -Gender Identity Disorderלמעלה .אחד הוא ש הדבר כמו הרוב המכריע של ההתנהגות שאת מתארת :מדובר פה בהתנהגות שלא כוללת שאופיינית -gender specific/typical behaviourהממצאים של מחקרים בקשר ל את .להומוסקסואלים רבים החברה בכדי שתהיה יכולת בנוסף לכך ,צריך ידע עמוק במתודולוגיה מחקרית של מדעי מחקרים ממוטטת לשפוט את איכות המחקרים .זה נושא ידוע לשמצה כשזה בא לכמות כל כך שגוי כל כך רעוע או בעיבוד ממצאים -research designשהם מוטים ו/או לוקים ב מחקרים שהתוצאות חסרות משמעות לחלוטין (ואני מכירה את זה היטב מהיכרות עמוקה עם בשבילך בנושא ,כולל עיבוד ממצאים עצמאי במסגרת מחקרית) .למזלך ,יש אנשים שעשו בחשבון היא אמינה ולוקחת Baily & Zucker, 1995כבר את העבודה .המטה-אנליזה של רק מחקרים שעומדים בקרייטריונים של אמינות מתודולוגית מדעית .שם נמצא הבדל סטטיסטי משמעותי בין התנהגות ילדותית נשית של ילדים הומוסקסואלים וסטרייטים .הממצאים כמעט כולם מבוססים על דווח רטרוספקטיבי שזאת שיטה קצת וקשה לבדיקה של האובייקטיביות של הדווח .יש רק מחקר אחד פרוספקטיבי בעייתית (Green, 1987).התוצאות שמאשר את נפשיות אצל הורים ובקשר למחקרים שבודקים קורלציה בין הפרעות/בעיות במחלוקת ,ולא מסיבות והומוסקסואליות/התנהגות לא-מגדרית אצל ילדים ,הם מאוד שנויים בתחלית האיסור לקחת אידיאולוגיות אלא בגלל סיבות שקשורות למתודולוגיה .אסור המתודולוגיה ממצאים של מחקרים כאלו כתורה מסיני לפני שנעשתה בדיקה קפדנית של מנסיון .מדובר כמעט תמיד ושל המקורות ונקודות המוצא של החוקרים .ואני אומרת את זה קלאסית עם האמונה באנשים עם ראיית עולם מסויימת/מצומצמת :או פסיכואנליזה ו/או אנשים 'בהתנהגות מגדרית כתוצאה מבעיות התפתחותיות/בעיות עם ההורים וכו שמנסים להראות שדברים כאלו הם כתוצאה מההפרעה כלשהי ולכן הם עצמם מהווים אין בשום פנים ואופן פסול במחקרים של תופעות וממצאים שנוגדים את מה.'הפרעה וכו מה שכן חשוב זה שמחקרים כאלו יעמדו בדרישות של.שאנחנו היינו מעדיפים לחשוב אחוז אפסי של מחקרים כאלו עומדים בקריטריונים.אובייקטיביות ובסיס מדעי חזק מעטים בודקים בציציות של המאמרים לפני שהם מצטטים אותם שוב, לצערי הרב.הללו ושוב, אני, ושוב.ולכן חצאי אמיתות ועוותים למיניהם מקבלים עם הזמן סטטוס של עובדות דבר שאני רואה אותו כפסול ואנטי- מדברת לא מתוך רצון לדחוף אידיאולוגיה מסויימת אלא מתוך רצון לקדם את המדע ע"י הקפדה על מחקר אמין- מדעי. סטטיסטיקה יודע גם שקורלציה אינה שווה ערך לגורם/המבין בשיטות מחקר: בעוד שרבים הגיוני,מגדרית-במידה מנסים להראות שהבעיות של ההורים הם שהובילו להתנהגות הלא חוקרים רבים טוענים. שווה לפחות שהתהליך היה הפוךcausality של כשמדובר במקרה לדעתי צריך לשלוח חוקרים כאלו למחנות ענישה.קורלציה בלבד אבל מי אני בסך הכל? סתם מלכת פורום אחת.מתודולוגים/סטטיסטים. Gender identity refers to an individual’s self perception as male or female, according to the DSM-IV-TR (American Psychiatric Association, 2000). Gender identity is typically consolidated by the age of three to four years and is usually accompanied by gender role behaviour, a behaviour that is consistent with the cultural definition of masculine and feminine roles (Bradley & Zucker, 1997). Gender identity disorder (GID), is defined by the DSM-IV-TR as strong and persistent cross-gender identification, such as fostering behaviour stereotypical of the other sex or the belief that one is of the opposite sex, accompanied by constant discomfort about one’s assigned sex. In addition, to meet criteria for GID diagnosis, the symptoms must not include physical intersex condition and the individual must suffer significant clinical discomfort or impairment in important area of functioning. Transsexualism, a sex reassignment surgery, is considered to be an extreme form of GID, however the prevalence of adults seeking the surgery is low, 1:10,000-30,000 men and 1:30,000100,000 women in Europe and Singapore (American Psychiatric Association, 2000; Cohen-Kettenis & Gooren, 1999). The aetiology of GID is not entirely known at this stage. Research on GID aetiology is focused on biological and psychosocial, mainly familial, factors. Bradley and Zucker (1997) have proposed a model for the aetiology of GID, suggesting that early attachment problems and reactivity to stress together with unstable familial environment increase the anxiety level of the child. The child chooses GID as a relief from anxiety due to factors within the child such as activity level and sensitivity and as parents initially tolerated cross gender behaviour. The present paper critically examines biological and psychosocial evidence for the Bradley and Zucker model and also suggests that factors within the child mentioned by the model include predisposition to GID, such as genetic factors. It also reviews the model shortcomings and briefly presents alternative theories of GID aetiology. Several researches have believed that gender identity might be biologically innate. Evidence for this can be seen in the case of a boy whose sex was reassigned to female in infancy due to damage to his penis. Although raised and treated by parents and the environment as a girl, the child adopted stereotypically male behaviour (Slijper, Drop, Molenaar & de Muinck Keizer-Schrama, 1998). One area of biological research of GID aetiology examines the effects of genetic factors on the development of atypical gender behaviour. Bailey, Dunne and Martin (2000) in a retrospective study of a large sample of an Australian male and female monozygotic (MZ) and dizygotic (DZ) twins population, examined the genetic influences on childhood gender non-conformity and continuous gender identity in adulthood. Childhood gender non-conformity and continuous gender identity measured the preference of children and adults, respectively, for cross sex typical behaviour or feelings, without necessarily meeting the clinical criteria for GID. Bailey et al. (2000) found that childhood gender non-conformity was inherited for both males (.50) and females (.37), however the results for adult continuous gender identity were not significant. A survey of parents responses in a study of 314 MZ and DZ twins from a normal population of children and adolescents, ages 4 – 17 years, Coolidge, Thede and Young (2002) found that the heritability of GID was .62, however the authors emphasised the numbers may be inflated due to a relatively small sample. More recently, Knafo, Iervolino and Plomin (2005) examined, by parents’ ratings, the genetic influences on the development of gender atypical 5,799 three and four years old male and female MZ and DZ twins. Gender atypical boys were the ones rated as relatively more feminine while gender atypical girls were the ones rated as relatively more masculine. Knafo et al. found moderate, yet significant, heritability for boys (.26-.27) and for girls (.42-.50) and large heritability for masculine girls who were also low on femininity (.65-.76). The differences between these findings to the Coolidge et al. (2002) study can be explained by the differences in sample size, participants’ age or the fact that Knafo et al. (2005) did not measure whether their subjects met clinical diagnosis of GID. The genetic studies show at least moderate inheritance for gender non-conformity in children and adolescents, suggesting genetic predisposition to GID for children and adolescents, but not for adults. These findings are consistent with the Bradley and Zucker (1997), which suggested factors within the child contribute to development of GID. It is important to note that the moderate inheritance suggests there are other factors involved in GID aetiology, as mentioned below. Other biological studies hypothesised that excess of prenatal androgens causes masculinity in girls while deficit causes femininity in boys. The immunohormonal theory of GID in boys suggests that women pregnant with male foetus produce antibodies to androgens that pass from the mother to the foetus through the placenta. The antibodies may reduce the androgen’s biological activity and thus compromise the masculinity of the male foetus (Ellis & Ames, 1987). They also noted that the maternal immune response may develop over several pregnancies. Consistent with the immunohormonal theory, researches found that boys with GID had a later birth order and a larger ratio of brothers to sisters compared to boys without GID (Blanchard, Zucker, Bradley & Hume, 1995; Bradley & Zucker, 1997). However, as discussed later, the birth order and excess number of older brothers relationship with GID can also be explained by the mother’s wish to have a girl after many boys (Blanchard et al., 1995). Support for the theory that prenatal excess of androgen is related to masculinity of girls comes from studies of girls with congenital adrenal hyperplasia (CAH) (Bradley & Zucker, 1997). Chromosomal females with CAH are prenatally exposed to increased levels of adrenal androgens‚ causing various degrees of masculinisation of the genitalia (Slijper et al. 1998). Even with surgically created full female genitalia, girls with CAH appear more masculine, display more masculine behaviour and higher percentage of them have GID than girls from normal population (Dessens, Slijper & Drop, 2005). It is important to note that most girls with CAH do not develop GID and that girls with CAH who were assigned to female gender at birth and treated as females by family and the environment were less likely to be diagnosed with GID and displayed less masculine behaviour than CAH girls who were assigned to female sex later in life (Slijper et al., 1998), suggesting environment factors have also an influence on development of gender identity in CAH girls. The literature also associates with prenatal androgen exposure theory the findings that compare to control groups, boys with GID displayed less rough-andtumble play, lower activity levels and higher sensitivity and girls with GID displayed more rough-and-tumble play and higher activity levels (Bradley & Zucker, 1997), boys with GID were rated as more attractive, with more feminine facial features (Zucker, Wild, Bradley & Lowry, 1993) and girls with GID were rated as less attractive, with less feminine facial features (Fridell, Zucker, Bradley, & Maing, 1996). Post-mortem brain studies showed the size of the bed nucleus of the stria terminalis in male-to-female transsexuals was closer to typical female size than to typical male size (Green, 2000) and the volume and number of neurons of female-tomale transsexuals was closer to that of a typical male (Segal, 2006). The researches linking prenatal androgen exposure with increased masculinity in girls and decreased masculinity or increased femininity in boys suggest predisposition to GID and to cross gender behaviour for males and females, supporting the Bradley and Zucker (1997) model regarding predisposition to GID. Other studies have linked GID with predisposition to stress. Children and adults with GID were found to have other psychiatric disorders, especially internalised disorders such as separation anxiety and depression, in higher rates than normal population (Hepp, Kraemer, Schnyder, Miller & Delsignore, 2005; Zucker, 2005). Zucker, Bradley, & Lowry Sullivan (1996) found that young boys who met full criteria for GID were more likely to suffer separation anxiety than boys who engaged in cross gender behaviour but did not meet full criteria for GID. Coolidge et al. (2002), however, found that more girls and boys with GID suffered comorbid depression but not separation anxiety when compared with normal population. As depression and anxiety suggest predisposition to stress (Tiet et al., 2001), the rates of comorbidity of GID with depression and possibly with separation anxiety support the suggestion of Bradley and Zucker (1997) model that predisposition to stress is a factor in the development of GID. However, the high comorbidity can be attributed to distress of not being accepted by society and parents. Some clinicians claimed that symptoms of comorbidity as well as GID symptoms were reduced with increased acceptance of oneself and parents (Pickstone-Taylor, 2003; Rosenberg, 2002), suggesting environmental influences on the development of GID. Several researches found non-shared environment influences on atypical gender behaviour and GID in childhood, adolescence and adulthood for both male and female, ranging from .50 - .69 (Bailey et al., 2000; Coolidge et al., 2002). Others found shared environment effects on atypical gender behaviour in three and four year old boys and girls ranging from .33 - .57, but not for girls who were low in femininity as well as high on masculinity (Knafo et al., 2005). These studies suggest environment effects play an important role in the development of GID. Research was done to examine what are the environmental factors associated with the development of GID. Bradley and Zucker (1997) suggested that parents of children who later developed GID, initially tolerated the cross gender behaviour. Further more, they suggested that GID and cross gender behaviour of boys are linked to mother’s encouragement of feminine behaviour and discouragement of masculine behaviour. Some support for that theory may come from Zucker et al. (1994) who found that mothers’ wish for having a girl increased with the number of only male children they had and from Blanchard et al. (1995) who found that boys with GID and cross-gender behaviour had relatively higher number of older brothers than control boys. Combined together it is possible that mothers wish for a girl after having already several boys causes the mother to encourage feminine behaviour and discourage masculine behaviour, and subsequently the development of GID. This theory, however, is yet to be empirically tested. Parents of GID children were found to have higher levels of psychopathology than parents of normal children (Cohen-Kettenis & Gooren, 1999). Mothers to children with GID suffered more depression, borderline and other psychiatric problems and fathers suffered more substance abuse compared to control (Bradley & Zucker, 1997). Boys with GID tended to have atypically close mothers and distant fathers while girls with GID tended to have two distant parents (Segal, 2006). The parents’ distance suggests attachment problems while the high psychopathology of parents suggests unstable familial environment, both supporting the Bradley and Zucker (1997) that links attachment problems and insecure environment with GID. However, a direct connection between parenting style and GID is yet to be established and it may be that the parental distance from GID children is influenced by parents’ frustration of the child’s atypical behaviour. Another important factor in the understanding of GID is the differences between referral rates of boys and girls with GID to clinical treatment versus the prevalence of GID in the general population. Coolidge et al. (2002) found that the .7% of boys and 3.7% of girls in general population met clinical diagnosis for GID but the boys to girls ratio of referral to clinical treatment was 6.6:1 (Zucker, Bradley & Sanikhani, 1997). An explanation for the higher referral of boys is offered by the social constuctionist approach (Gottschalk, 2003) suggesting that GID is basically a social construct, stems from society’s assumed roles for males and females. Social constuctionism claims that adults and children who engage in cross gender behaviour simply express a valid preference. The difference in referral rates, according to social constructionism, simply reflects that cross gender behaviour is more tolerated by society in females than in males. Bradley and Zucker (1997) model does not offer an explanation for the different referral rates. Another aspect of GID that is not explained by Bradley and Zucker (1997) model is that only 20% of children with GID continue to display gender dysphoria in adulthood. One possibility is that GID is simply an early manifestation of homosexuality (Blanchard et al., 1995). Support to that approach is found in clinical reports that symptoms of GID in male adolescents reduced once they assumed a homosexual sexual orientation (Rosenberg, 2002) and by the DSM-IV-TR description that by adulthood 75% of boys with GID become homosexuals or bisexuals without GID and that almost all adult females with GID are sexually attracted to females (American Psychiatric Association, 2000). The view that GID is early manifestation of homosexuality does not take into account that in adulthood only half of males with GID are sexually attracted males while the other half is sexually attracted to females. The later group tends to have later onset of GID than the former (Zucker et al., 1996), which might suggest different aetiology for the two groups. Further study is required to explore that possibility. Conclusion The Bradley and Zucker model suggests that the aetiology of GID involves predisposition to GID, high reactivity to stress and early attachment problems together with stressful familial environment and initial tolerance of cross gender behaviour by parents. The literature supports the model with a range of biological and psychosocial evidence found to be associated with the development of GID. The biological evidence, genetic and prenatal androgen exposure, are consistent with factors within the child or predisposition to GID, suggested by Bradley and Zucker model. The high comorbidity of GID with internalised disorders suggests high reactivity to stress. The psychosocial factors that found to be associated with GID are stressful familial environment, possibly caused by parents high psychopathology and early attachments problems with distant father for boys and two parents for girls are also consistent with the model. The Bradley and Zucker model fails to explain the low prevalence of adult GID compare to childhood GID, the different referral rates of boys and girls and the two different types of male GID, sexual attraction to males and sexual attraction to females. The aetiology of adult GID and the different types of sexual attractions among adult males with GID are worthy of further study. References American Psychiatric Association (2000). Diagnostic and statistical manual of mental disorders (DSM-IV-TR) (4th ed. Revised). Washington, DC: Author. Bailey, J. M., Dunne, M. P., & Martin, N. G. (2000). Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample. Journal of Personality and Social Psychology, 78, 524-536. Blanchard, R., Zucker, K. J., Bradley, S. J., & Hume, C. S. (1995). Birth order and sibling sex ratio in homosexual male adolescents and probably prehomosexual feminine boys. Developmental Psychology, 31, 22-30. Bradley, S. J., & Zucker, K. J. (1997). Gender identity disorder: A review of the past 10 years. Journal of the American Academy of Child & Adolescent Psychiatry, 36, 872-880. Cohen-Kettenis, P. T., & Gooren, L. J. G. (1999). Transsexualism: A review of etiology, diagnosis, and treatment. Journal of Psychosomatic Research, 46, 315-333. Coolidge, F. L., Thede, L. L., & Young, S. E. (2002). The Heritability of Gender Identity Disorder in a Child and Adolescent Twin Sample. Behavior Genetics, 32, 251-257. Dessens, A. B., Slijper, F. M. E., & Drop, S. L. S. (2005). Gender Dysphoria and Gender Change in Chromosomal Females with Congenital Adrenal Hyperplasia. Archives of Sexual Behavior, 34, 389-397. Ellis, L., & Ames, M. A. (1987). Neurohormonal functioning and sexual orientation: A theory of homosexuality-heterosexuality. Psychological Bulletin, 10, 233258. Fridell, S. R., Zucker, K. J., Bradley, S. J., & Maing, D. M. (1996). Physical attractiveness of girls with gender identity disorder. Archives of Sexual Behavior,l 25, 17-31. Gottschalk, L. (2003). Same-sex sexuality and childhood gender non-conformity: A spurious connection. Journal of Gender Studies, 12, 35-50. Hepp, U., Kraemer, B., Schnyder, U., Miller, N., & Delsignore, A. (2005). Psychiatric comorbidity in gender identity disorder. Journal of Psychosomatic Research, 58, 259-261. Knafo, A., Iervolino, A. C., & Plomin, R. (2005). Masculine Girls and Feminine Boys: Genetic and Environmental Contributions to Atypical Gender Development in Early Childhood. Journal of Personality and Social Psychology, 88, 400-412. Pickstone-Taylor, S. (2003). Children with gender nonconformity – criticises Bradley and Zucker. Journal of the American Academy of Child & Adolescent Psychiatry, 42, 266. Rosenberg, M. (2002). Children with gender identity issues and their parents in individual and group treatment. Journal of the American Academy of Child & Adolescent Psychiatry, 41, 619-621. Segal, N. L. (2006). Two Monozygotic Twin Pairs Discordant for Female-to-Male Transsexualism. Archives of Sexual Behavior, 35, 347-358. Slijper, F. M. E., Drop, S. L. S., Molenaar, J. C., & de Muinck Keizer-Schrama, S. M. P. F. (1998). Long-term psychological evaluation of intersex children. Archives of Sexual Behavior, 27, 125-144. Tiet, Q. Q., Bird, H. R., Hoven, C. W., Moore, R., Wu, P., Wicks, J. et al. (2001). Relationship between specific adverse life events and psychiatric disorders. Journal of Abnormal Child Psychology, 29, 153-164. Zucker, K. J., Bradley, S. J., & Lowry Sullivan, C. B. (1996). Traits of separation anxiety in boys with gender identity disorder. Journal of the American Academy of Child & Adolescent Psychiatry, 35, 791-798. Zucker, K. J., Bradley, S. J., & Sanikhani, M. (1997). Sex differences in referral rates of children with gender identity disorder: Some hypotheses. Journal of Abnormal Child Psychology, 25, 217-227. Zucker, K. J., Green, R., Garofano, C., Bradley, S. J., et al. (1994). Prenatal gender preference of mothers of feminine and masculine boys: Relation to sibling sex composition and birth order. Journal of Abnormal Child Psychology, 22, 1-13. Zucker, K. J. (2005). Gender identity disorder in children and adolescents. Annual Reviews of Clinical Psychology, 1, 467-492. Zucker, K. J., Wild, J., Bradley, S. J., & Lowry, C. B. (1993). Physical attractiveness of boys with gender identity disorder. Archives of Sexual Behavior, 22, 1993, 23-36. הנושא שלGENDER IDENTITY DISORDER ויש שם,לשנה שלישית באוניברסיטה אני מצרפת את המאמר והנה תקציר בעברית.הרבה חומר שרלוונטי לשאלה שלך: 70% מצד.מהבנים שמגלים התנהגות אופיינית בד"כ לבנות יגדלו להיות הומואים שני לא כל. יחס דומה לא קיים אצל בנות.ההומואים גילו התנהגות כזאת בילדות בנות שמגלות,התנהגות שיותר אופיינית לבנים לא בהכרח יגדלו להיות כלומר ההסבר שמקובל על.החוקרים הוא שהתנהגות 'גברית' אצל בנות יותר לסביות נשית' אצל בנים ולכן יותר בנות מאפשרות ' מקובלת על ידי החברה מאשר התנהגות שני המבוגרים נוטים לא לעשות לעצמן לשחק במשחקים גבריים מצד אחד ומצד .מזה עניין גדול אצל בנות שמופנים לטיפול הם בנים אבל במדגמים שנעשו על באותו נושא ,רוב הילדים התנהגות 'גברית' מאשר בנים שמתנהגים אוכלוסיה כללית יש יותר בנות שמגלות '.בצורה 'נשית כמו שציינת למעלה .הבעיות עשויות להתעורר לא בגלל אין ממש טיפול להתנהגות תגובות הילדים מסביב ובמיוחד ההורים .מאד חשוב הנטייה עצמה לוורוד אלא בגלל עליו להשתנות .הלחץ יכול להביא להקצנה של לקבל את הילד כפי שהוא ולא ללחוץ .ההתנהגות במקום לירידה -GENDERקטן של בעיות הורמונליות שיכולות להיות קשורות ל יש אחוז .שאין לך אינפומציה כזאת לגבי הילד אבל אני מניחה IDENTITY, להיות מבוגרים שמרוצים מה עוד עובדה חשובה היא שרוב הילדים גדליםאו ימשיכו לרצות שלהם .אחוז ממש מזערי יגיע לעשות ניתוח לשינוי מין GENDER .להיות בן המין השני חברתי בלבד ורק החברה מחליטה מה הוא GENDERיש שטוענים שכל הנושא של משחק כזה או אחר .מצד שני יש אופייני לבנים או לבנות ,ואין נטייה טבעית לסוג של אופיינית לשני המינים .מחקרים שמראים הורמונים משחקים תפקיד בהתנהגות .כלומר ,יש עוד הרבה שלא ידוע בנושא שיחקתי יותר עם בנים עד כיתה ג' ולא זוכרת ששיחקתי בבובות אני באופן אישי .לא לנטייה המינית היום ,לא יודעת יותר מדי ,אם זה קשור או