Clamped Corticosterone (B) Reveals the Effect of Endogenous B on Both Facilitated Responsivity to Acute Restraint and Metabolic Responses to Chronic Stress

To determine the effects of both corticosterone (B) and chronic stressors on acute ACTH responses to restraint, young male rats were exposed to streptozotocin-induced diabetes, cold (5-7 degreesC) or intracerebroventricular (icv) neuropeptide Y (NPY) for 5 d and then exposed to restraint within 2 h after lights on. Two groups of rats were studied: intact and adrenalectomized replaced with B pellets that maintained plasma B in the normal mean 24-h range of intact rats. In addition to ACTH and B responses to restraint on d 5, body weight, food intake, fat depots, glucose and other hormones were measured to determine the role of stress-induced elevations in B on energy balance. ACTH responses to restraint were normal in intact rats subjected to diabetes or cold. By contrast, there was no ACTH or B response to restraint in NPY-infused intact rats. All 3 groups of chronically stimulated adrenalectomized rats with clamped B had facilitated ACTH responses to restraint compared to their treatment controls. Overall food intake increased in all groups of stressed rats; however, augmented intake occurred only during the light in intact rats and equally in the light and dark in B-clamped rats. White adipose depot weights were decreased by both diabetes and cold and increased by NPY in intact rats; the decreases with cold and increases with NPY were both blunted and changes in fat stores were not significant in adrenalectomized, B-clamped rats. We conclude that: 1. diabetes- and cold-induced facilitation of restraint-induced afferent input to hypothalamic control of the hypothalamo-pituitary-adrenal (HPA) axis is opposed in intact rats by the elevated feedback signal of B secretion; 2. NPY does not induce facilitation of afferent stress pathways; 3. chronic stimulation of the HPA axis induces acute hyperresponsiveness of hypothalamic neurons to restraint provided that the afferent input of this acute stimulus is not prevented by B feedback; 4. stimulus-induced elevations in B secretion result in day-time feeding; 5. insensitivity of both caloric efficiency and white fat stores to chronic stress in adrenalectomized, B-clamped rats results from loss of normally variable B levels.     

The nature of environmental influences on weight and obesity: a behavior genetic analysis.

The nature of environmental influences on individual differences in weight and obesity is presently unclear. To resolve this issue, behavior genetic studies are reviewed for their relevance to environmental influences on weight and obesity. Results are consistent in suggesting that environmental experiences are important for weight and obesity, although they account for much less variation than do the effects of genes. Furthermore, only environmental experiences that are not shared among family members appear to be important. In contrast, experiences that are shared among family members appear largely irrelevant in determining individual differences in weight and obesity. These conclusions are consistent with a growing body of evidence on the relative unimportance of such shared experiences for many psychological characteristics.     

Standards for the Reporting of Genetic Counseling Interventions in Research and Other Studies (GCIRS): an NSGC Task Force Report

As the demand for evidence to support the value of genetic counseling increases, it is critical that reporting of genetic counseling interventions in research and other types of studies (e.g. process improvement or service evaluation studies) adopt greater rigor. As in other areas of healthcare, the appraisal, synthesis, and translation of research findings into genetic counseling practice are likely to be improved if clear specifications of genetic counseling interventions are reported when studies involving genetic counseling are published. To help improve reporting practices, the National Society of Genetic Counselors (NSGC) convened a task force in 2015 to develop consensus standards for the reporting of genetic counseling interventions. Following review by the NSGC Board of Directors, the NSGC Practice Guidelines Committee and the editorial board of the Journal of Genetic Counseling, 23 items across 8 domains were proposed as standards for the reporting of genetic counseling interventions in the published literature (GCIRS: Genetic Counseling Intervention Reporting Standards). The authors recommend adoption of these standards by authors and journals when reporting studies involving genetic counseling interventions.     

Development of social functioning in preschizophrenia children and adolescents: a systematic review

Schizophrenia is associated with severe deficits in social functioning. Similar deficits may be present prior to psychosis onset, in childhood and adolescence. If so, then prepsychosis social deficits could provide clues to the development of pathological processes in preschizophrenia children and could potentially improve early identification of the disorder and suggest targets for intervention. Evidence is reviewed from birth cohort, case- control, and familial high-risk studies within distinct periods of development to clarify the nature, timing, and specificity of social deficits in preschizophrenia children and adolescents. The results indicate that poor social functioning does differentiate preschizophrenia children and adolescents from their peers and can be a sensitive and potentially specific predictor of schizophrenia, not just psychopathology in general. Furthermore, age (but not sex) appears to be an important moderator of the strength and specificity of the association between particular social deficits (e.g., externalizing, internalizing) and later schizophrenia. Results are discussed in the context of current developmental theories of timing and pathophysiology of schizophrenia involving hypothalamic- pituitary-adrenal dysregulation. Implications for the early identification and treatment of preschizophrenia individuals are also considered.     

The nature of schizotypy among multigenerational multiplex schizophrenia families

Identification of endophenotypes (Gottesman & Gould, 2003; Gottesman & Shields, 1972) that genetically correlate with schizophrenia and are genetically homogeneous is an important strategy for detecting genes that affect schizophrenia risk. Symptoms of schizotypy may familially correlate with schizophrenia; however, there are critical limitations of the current literature concerning this association. The present study examined the genetic architecture and genetic associations between schizotypy and schizophrenia among multigenerational, multiplex schizophrenia families. Genetic schizotypy factor scales were developed that genetically correlated with schizophrenia, although some relations were unexpected in direction suggesting minimization of "psychotic-like" symptoms. These genetic schizotypy factor scales did not genetically correlate with major depressive disorder or substance dependence indicating specificity to schizophrenia. The results highlight the possibility of significant response bias in schizophrenia families, particularly among close relatives, and suggest an important consideration when acquiring self-report information. This is a topic that deserves future study as the origins of this putative bias in relatives are unclear. In addition, the results support the identification of genetic schizotypy factors as a promising technique for maximizing genetic correlation of endophenotypes with schizophrenia.