The current focus on identifying genes which predispose to psychiatric illness sharpens the need to identify environmental factors which interact with genetic predisposition and thus contribute to the multifactorial causation of these disorders. One such factor may be early parental loss (EPL). The putative relationship between early environmental stressors such as parental loss and psychopathology in adult life has intrigued psychiatrists for most of this century. We report a case control study in which rates of EPL, due to parental death or permanent separation before the age of 17 years were evaluated in patients with major depression (MD), bipolar disorder (BPD) and schizophrenia (SCZ), compared to individually matched, healthy control subjects (MD-Control, 79 pairs; BPD-Control, 79 pairs; SCZ-Control, 76 pairs). Loss of parent during childhood significantly increased the likelihood of developing MD during adult life (OR = 3.8, P = 0.001). The effect of loss due to permanent separation (P = 0.008) was more striking than loss due to death, as was loss before the age of 9 years (OR = 11.0, P = 0.003) compared to later childhood and adolescence. The overall rate of EPL was also increased in BPD (OR = 2.6, P = 0.048) but there were no significant findings in any of the subcategories of loss. A significantly increased rate of EPL was observed in schizophrenia patients (OR = 3.8, P = 0.01), particularly before the age of 9 years (OR = 4.3, P = 0.01). Comparison of psychosocial, medical and clinical characteristics of subjects with and without a history of EPL, within the larger patient groups from which the matched samples were drawn (MD, n = 136; BPD, n = 107; SCZ, n = 160), yielded few significant findings. Among the controls (n = 170), however, subjects who had experienced EPL, reported lower incomes, had been divorced more frequently, were more likely to be living alone, were more likely to smoke or have smoked cigarettes and reported more physical illness (P = 0.03-0.001). Long term neurobiological consequences of early environmental stressors such as maternal deprivation have been extensively studied in many animal species. Recently, enduring changes in hypothalamic-pituitary-adrenal axis function, including corticotrophin releasing factor gene expression, have received particular attention. Analogous processes may be implicated in the effect of EPL on human vulnerability to psychopathology, via alterations in responsiveness to stress. Genetic predisposition may influence the degree of susceptibility of the individual to the effects of early environmental stress and may also determine the psychopathological entity to which the individual is rendered vulnerable as a consequence of the stress.
Background and Purpose-The association between ischemic childhood stroke and thrombophilia has been debated. We studied the prevalence of thrombophilia risk factors in 65 unrelated children with ischemic stroke compared with 145 control subjects. Methods-Patients and control subjects were tested for antithrombin protein C and protein S deficiencies, the presence of antiphospholipid antibodies (APLA), factor V Leiden (FVL), G20210A polymorphism of factor II gene (FII G20210A), and C677T polymorphism of 5,10-methylenetetrahydrofolate reductase gene (C677T MTHFR). Results-Of 65 children, 7 had a stroke in the neonatal/perinatal period and therefore were analyzed separately. Thirty-one of the remaining 58 patients with pediatric stroke (53.4%) were found to have at least 1 thrombophilia marker compared with only 25.5% of control subjects. None of the patients or control subjects had protein S or antithrombin III deficiency. The prevalence of protein C deficiency was higher among pediatric stroke patients than among control subjects, but the difference was not statistically significant (ORϭ7, 95% CI 0.75 to 65.1). Heterozygous FII G20210A and homozygous MTHFR 677T were not associated with an increased risk for stroke (ORϭ1.29, 95% CI 0.2 to 8.2; and ORϭ1.06, 95% CI 0.4 to 2.7, respectively). In contrast, the presence of APLA was associated with a Ͼ6-fold risk of stroke (ORϭ6.08, 95% CI 1.5 to 24.3), and the heterozygosity for FVL increased the risk of stroke by almost 5-fold (ORϭ4.82, 95% CI 1.4 to 16.5). Five patients with pediatric stroke had a combination of Ն2 thrombophilia markers, whereas none of the control subjects had a combination of the markers. Most of the patients with neonatal/perinatal stroke were found to have at least 1 thrombophilia marker. Conclusions-These data suggest that the prevalence of thrombophilia markers is increased in children with stroke compared with control subjects and, specifically, that FVL and APLA contribute significantly to stroke occurrence.
ITAMAR RAZ, MD FOR THE ISRAEL DIABETES RESEARCH GROUP (IDRG) INVESTIGATORS*OBJECTIVE -Erectile dysfunction is frequently observed in diabetes. The current study aims to assess the association of a comprehensive set of clinical, socioeconomic, and lifestyle parameters with erectile dysfunction in diabetic men. 1-7). Hyperlipidemia, hypertension, and cardiovascular disease (CVD), which frequently complicate diabetes, and drugs that are commonly given to diabetic patients (i.e., antihypertension agents) are associated with higher frequency of erectile dysfunction (1,5,8 -10). RESEARCH DESIGN AND METHODSThe prevalence of erectile dysfunction is expected to double by the year 2025, and the growing global epidemic of diabetes contributes to this forecast (11). Despite being associated with poor quality of life, erectile dysfunction is seldom addressed by primary-care physicians and specialists (12). The current study aims to define, from a comprehensive set of socioeconomic, lifestyle, and clinical characteristics reported to be associated with erectile dysfunction in population studies, attributes that are significantly and independently associated with greater risk for erectile dysfunction in diabetic men. This will allow physicians to identify patients at increased risk for erectile dysfunction who could benefit from preventive measures and timely treatment. RESEARCH DESIGN AND METHODS -The study participants included diabetic men treated in ambulatory secondary and tertiary diabetes care clinics in Israel.A random sample of calendar days was obtained for each clinic participating in the study. During these days, all scheduled visits of diabetic male patients (age Ͼ18 years) were registered. Patients with comorbidities that might have caused erectile dysfunction regardless of diabetes (i.e., congenital or acquired spinal, pelvic, or penile malformations and injuries; prostate cancer; alcohol or drug abuse; depression; and schizophrenia) were excluded. Eligible patients were included in the study after obtaining their informed consent. The study protocol was approved by the local ethics committees.Participants completed a questionnaire containing information on sociodemographic and lifestyle characteristics.
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