An adoption study of Somatoform Disorders: III. Cross-fostering analysis and genetic relationship to alcoholism and criminality. Archives of General Psychiatry, 41, 872-878

Archives of General Psychiatry (Impact Factor: 14.48). 10/1984; 41(9):872-8. DOI: 10.1001/archpsyc.1984.01790200054007
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The genetic and environmental antecedents of two clinically distinct somatoform disorders were compared in 859 Swedish women adopted at an early age by nonrelatives. The characteristics of both the biological and adoptive parents of high-frequency "somatizers" were different from those of diversiform somatizers. The risk of diversiform somatization was increased in the adopted-away daughters of men treated for male-limited (type 2) alcoholism, but not in daughters of milieu-limited (type 1) alcoholics. In contrast, the biological fathers of high-frequency somatizers often had a history of recurrent convictions for violent crimes since adolescence, but no treatment for alcoholism. Similarly, alcohol abuse by the adoptive father was associated with increased risk of diversiform but not high-frequency somatization. Thus, high-frequency and diversiform somatization are not only clinically distinct, but also have different genetic and environmental backgrounds. The association of diversiform somatization with male-limited alcoholism, and not with milieu-limited alcoholism, also provides independent support for our earlier distinction between these two types of alcoholism.

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Available from: Robert Cloninger, May 21, 2014
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    • "In fact, point prevalence rates of psychiatric disorders among children of depressed parents have been estimated to be 2–5 times above normal (Beardslee et al. 1993, 1998; Weissman et al. 1986). However, heterotypic continuity of psychopathology is also known across generations, such as the consistently reported relationship between parental substance abuse, and antisocial behavior and somatization problems in the daughters (Bohman et al. 1984; Cadoret 1978). There is also a substantial body of research showing that maternal depression and perceived stress are related to disruptive behaviors in offspring (Dumas and Wahler 1985; Ghodsian et al. 1984; Loeber et al. 1998; Zahn-Waxler et al. 1990). "
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    ABSTRACT: Much of the research examining intergenerational continuity of problems from mother to offspring has focused on homotypic continuity (e.g., depression), despite the fact that different types of mental health problems tend to cluster in both adults and children. It remains unclear whether mothers with multiple mental health problems compared to mothers with fewer or no problems are more likely to have daughters with multiple mental health problems during middle childhood (ages 7 to 11). Six waves of maternal and child data from the Pittsburgh Girls Study (n = 2,451) were used to examine the specificity of effects of maternal psychopathology on child adjustment. Child multiple mental health problems comprised disruptive behavior, ADHD symptoms, depressed mood, anxiety symptoms and somatic complaints, while maternal multiple mental health problems consisted of depression, prior conduct problems and somatic complaints. Generalized Estimating Equations (GEE) was used to examine the prospective relationships between mother's single and multiple mental health problems and their daughter's single and multiple mental health problems across the elementary school-aged period (ages 7-11 years). The results show that multiple mental health problems in the mothers predicted multiple mental health problems in the daughters even when earlier mental health problem of the daughters, demographic factors, and childrearing practices were controlled. Maternal low parental warmth and harsh punishment independently contributed to the prediction of multiple mental health problems in their daughter, but mediation analyses showed that the contribution of parenting behaviors to the explanation of girls' mental health problems was small.
    Journal of Abnormal Child Psychology 08/2009; 37(8):1035-48. DOI:10.1007/s10802-009-9337-x · 3.09 Impact Factor
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    • "Type II alcoholism was only demonstrated in males, and with a genetic predisposition there was a nine times increased risk of alcoholism in the adoptees. It could also be demonstrated that females with a genetic predisposition for type II alcoholism had no increased risk of alcoholism or criminality, but instead showed an increased risk of somatisation disorder (Bohman et al. 1984). Later twin and adoption studies have also shown a strong genetic impact on alcoholism in men, whereas the genetic impact on alcoholism in women might be weaker, suggesting gender differences in heritability of alcoholism (McGue et al. 1992; Sigvardsson et al. 1996). "
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    ABSTRACT: The serotonin system is known to play a pivotal role for mood, behaviour and psychic illness as e.g. alcoholism. Alcoholism in both males and females has been associated with polymorphisms in genes encoding for proteins of importance for central serotonergic function. Genotyping of two functional polymorphisms in the promoter region of the serotonin transporter and monoamine oxidase-A, respectively, (5-HTT-LPR and MAOA-VNTR), was performed in a group of women with severe alcohol addiction. A large sample of adolescent females from a normal population was used as controls. A significantly higher frequency of the LL 5-HTT genotype (high activity) was found in female addicts without a known co-morbid psychiatric disorder than in the controls. Genotype of the MAOA-VNTR polymorphism did not differ significantly between addicts and controls. However, within the group of alcoholics, when the patients with known co-morbid psychiatric disorders were excluded, aggressive anti-social behaviour was significantly linked to the presence of the high activity MAOA allele. The pattern of associations between genotypes of 5-HTT-LPR and MAOA-VNTR in women with severe alcoholism differs from most corresponding studies on males.
    Archives of Women s Mental Health 11/2008; 11(5-6):347-55. DOI:10.1007/s00737-008-0033-6 · 2.16 Impact Factor
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    • "Studies of personality characteristics have shown suicidality, affective instability and impulsivity to be heritable (Bouchard, 1994). Impulsive aggression has also been shown clearly to be at least partially heritable as established by both twin (Coccaro et al, 1993) and adoption (Bohman et al, 1984) studies, with suggested heritability estimates from 20-62% (Coccaro et al, 1993). Candidate gene studies provide a window into which specific receptors might be involved in the control of aggression. "
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    ABSTRACT: The neurobiological research that has been the most useful in shedding light on the physiology underlying BPD has examined simpler dimensions of behavior separately, including impulsive aggression and affective instability. Evidence suggests impulsive aggression involves a deficit in serotonergic activity. However, the specific mechanism underlying this remains unknown. It is clear this component of behavior is substantially genetically encoded, and therefore new research has focused on elucidating the specific receptors underlying impulsive aggression through the examination of genes coding for specific receptors. Additional research has focused on the brain regions that underlie aggression, and it is likely that the prefrontal orbital frontal cortex exerts an inhibitory control over aggressive behavior in normal individuals. These regions may be underactive in individuals with impulsive aggression and specifically may not be recruited in these patients in response to a serotonergic activation. Less is understood about the physiology of affective instability in personality disorders, but emerging information suggests it is quite different from the affective instability in primary affective disorder. Preliminary evidence implicates the cholinergic system in the control of affective instability, but more research is required to confirm this. Further elucidation of the physiology of impulsive aggression and affective instability may provide more specific targets in the future for the pharmacologic management of these components of BPD.
    Psychiatric Annals 06/2002; 32(6):329-336. DOI:10.3928/0048-5713-20020601-07 · 0.71 Impact Factor
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