Leveraging risk communication science across US federal agencies.

Many US federal agencies apply principles from risk communication science across a wide variety of hazards. In so doing, they identify key research and practice gaps that, if addressed, could help better serve the nation’s communities and greatly enhance practice, research, and policy development.

No Impaired Glucose Tolerance in Primary Insomnia Patients with Normal Results of Polysomnography.

Background: According to recent studies, sleep restriction and disruption both have a prominent negative influence on glucose metabolism. This could also be shown in sleep disorders, such as sleep apnea and the restless legs syndrome. However, similar studies regarding insomnia have not been that consistent, yet.

Impaired glucose tolerance in sleep disorders.

Background: Recent epidemiological and experimental data suggest a negative influence of shortened or disturbed night sleep on glucose tolerance. Due to the high prevalence of sleep disorders this might be a major health issue. However, no comparative studies of carbohydrate metabolism have been conducted in clinical sleep disorders.

The Munich vulnerability study on affective disorders: microstructure of sleep in high-risk subjects.

Vulnerability markers for affective disorders have focused on stress hormone regulation and sleep. Among rapid eye movement (REM) sleep, increased REM pressure and elevated REM density are promising candidates for vulnerability markers. Regarding nonREM sleep, a deficit in amount of and latency until slow wave sleep during the first half of the night is a characteristic for depression.

Dex/CRH-test response and sleep in depressed patients and healthy controls with and without vulnerability for affective disorders.

Sleep electroencephalographic (EEG) abnormalities and increased hypothalamo-pituitary-adrenal (HPA) axis activity are the most prominent neurobiological findings in depression and were suggested as potential biomarker for depression. In particular, increased rapid eye movement sleep (REM) density, deficit in slow wave sleep and excessive stress hormone response are associated with an unfavorable long-term outcome of depression. Recent studies indicate that the sleep and endocrine parameters are related to each other.

Acute cortisol administration increases sleep depth and growth hormone release in patients with major depression.

Acute administration of cortisol increases non-rapid-eye movement (non-REM) sleep, suppresses rapid-eye movement (REM) sleep and stimulates growth hormone (GH) release in healthy subjects. This study investigates whether cortisol has similar endocrine and electrophysiological effects in patients with depression who typically show a pathological overactivity of the hypothalamus-pituitary-adrenal (HPA) system. Fifteen depressed inpatients underwent the combined dexamethasone/corticotropin-releasing hormone test followed by three consecutive sleep EEG recordings in which the patients received placebo (saline) and hourly injections of cortisol (1mg/KG BW).

Rapid eye movement (REM) sleep: an endophenotype for depression.

Disturbed sleep is one of the hallmark signs of depression. After successful treatment, many of these signs disappear; however, changes in rapid eye movement (REM) sleep may persist and even predict recurrence of depression. High-risk studies have established these alterations to be not only biological scars but true endophenotypes for depression.

Immune-endocrine host response to endotoxin in major depression.

Objective: An impaired hypothalamic-pituitary-adrenocortical (HPA) function is a well-established finding in major depression (MD), but it is still unclear how this dysfunction affects immune responses in this disorder.

Method: To further examine the relationship between immune and endocrine responses in MD, 0.4ng/kg body weight endotoxin [LPS] or 100mug hCRH were sequentially applied to 12 patients with MD and to 12 age- and gender-matched healthy controls after pre-treatment with 1.

The dopaminergic midbrain participates in human episodic memory formation: evidence from genetic imaging.

Recent data from animal studies raise the possibility that dopaminergic neuromodulation promotes the encoding of novel stimuli. We investigated a possible role for the dopaminergic midbrain in human episodic memory by measuring how polymorphisms in dopamine clearance pathways affect encoding-related brain activity (functional magnetic resonance imaging) in an episodic memory task. In 51 young, healthy adults, successful episodic encoding was associated with activation of the substantia nigra.

The Munich vulnerability study on affective disorders: premorbid polysomnographic profile of affected high-risk probands.

Background: The most characteristic alterations in the sleep electroencephalogram (EEG) during major depression are a shortened latency to rapid eye movement (REM) sleep and an elevated REM density. Because these changes persist in remission, they might represent vulnerability markers. To identify vulnerability markers, we investigated premorbid sleep EEG parameters in healthy high-risk probands (HRPs) with a positive family history of affective disorders.

The Munich vulnerability study on affective disorders: premorbid neuroendocrine profile of affected high-risk probands.

One of the most characteristic alterations in depression is a disturbed regulation of the hypothalamic-pituitary-adrenocortical (HPA) system. A function test combining the pre-treatment of 1.5 mg dexamethasone (DEX) with a challenge of 100 microg corticotropin-releasing hormone (CRH) reveals a pathological increase in the adrenocorticotropin and cortisol release in patients with major depression.

Activation of midbrain structures by associative novelty and the formation of explicit memory in humans.

Recent evidence suggests a close functional relationship between memory formation in the hippocampus and dopaminergic neuromodulation originating in the ventral tegmental area and medial substantia nigra of the midbrain. Here we report midbrain activation in two functional MRI studies of visual memory in healthy young adults. In the first study, participants distinguished between familiar and novel configurations of pairs of items which had been studied together by either learning the location or the identity of the items.

The Munich vulnerability study on affective disorders: premorbid psychometric profile of affected individuals.

Objective: We conducted a longitudinal high-risk study to identify psychometric vulnerability markers for affective disorders.

Method: We examined 82 healthy subjects [high-risk probands (HRPs)] with at least one first-degree relative suffering from an affective disorder. The premorbid psychometric profile of 20 HRPs who developed a psychiatric disorder during follow-up was compared with the profile of control subjects without personal and family history of psychiatric disorders matched for age and gender.

Sleep in eating disorders.

Sleep research on eating disorders has addressed two major questions: (1) the effects of chronic starvation in anorexia nervosa and of rapidly fluctuating eating patterns in bulimia nervosa on the sleep regulating processes and (2) the search for a significant neurobiological relationship between eating disorders and major depression. At present, the latter question appears to be resolved, since most of the available evidences clearly underline the notion that eating disorders (such as anorexia and bulimia nervosa) and affective disorders are two distinct entities. Regarding the effects of starvation on sleep regulation, recent research in healthy humans and in animals demonstrates that such a condition results in a fragmentation of sleep and a reduction of slow wave sleep.

The Munich Vulnerability Study on Affective Disorders: risk factors for unipolarity versus bipolarity.

Background: An individual with a high genetic load for psychiatric disorders is subject to a considerable risk factor for an affective illness. Family studies usually try to distinguish between bipolar and unipolar disorders since it was suggested that they might show different modes of inheritance. The aim of this study was to differentiate between healthy members of unipolar and bipolar families without a previous history of any psychiatric disorder according to the neurobiological and psychometric findings.

The Munich Vulnerability Study on Affective Disorders: stability of polysomnographic findings over time.

Background: Some of the sleep abnormalities found in depression also persist in remission, suggesting that these parameters could represent trait or vulnerability markers. In a previous study, we found that about one third of a group of high-risk probands (HRPs) showed sleep patterns that were comparable to those of depressed patients. In the present study, we re-investigated a subsample of these HRPs to evaluate the stability of these findings over time.

Patterns of response to repeated total sleep deprivations in depression.

Background: Patterns of response and nonresponse in repeated sleep deprivation (SD) are of both clinical and scientific interest; as yet, studies have yielded inconsistent results.

Methods: Eighteen inpatients suffering from a major depression were subjected to a series of six scheduled total sleep deprivations within 3 weeks; 12 of them completed the whole protocol. All were under a constant antidepressant medication with amitriptyline.

Neuroendocrine, polysomnographic and psychometric observations in healthy subjects at high familial risk for affective disorders: the current state of the 'Munich vulnerability study'.

The present article summarizes the main results of the cross-sectional part of the 'Munich Vulnerability Study' in which healthy first-degree relatives of patients with an affective disorder were investigated by assessing their neuroendocrine, polysomnographic and psychometric status. As patients with an acute episode of a major depression, the group of the healthy relatives exhibited signs of a hyperactive hypothalamic-pituitary-adrenocortical system verified by the combined dexamethasone corticotropin-releasing hormone (DEX/CRH) test, as well as a slow wave sleep deficit in the first sleep cycle and an increased amount of rapid eye movements during REM sleep. The psychometric profile of the healthy relatives was characterised by elevated scores on the scales measuring 'Rigidity' and 'Autonomic Lability'.

Schizophrenia: glutathione deficit in cerebrospinal fluid and prefrontal cortex in vivo.

Schizophrenia is a major psychiatric disease, which affects the centre of the personality, with severe problems of perception, cognition as well as affective and social behaviour. In cerebrospinal fluid of drug-free schizophrenic patients, a significant decrease in the level of total glutathione (GSH) by 27% (P<0.05) was observed as compared to controls, in keeping with the reported reduced level of its metabolite gamma-glutamylglutamine.

Neuropsychological assessments before and after treatment in patients with anorexia nervosa and bulimia nervosa.

In psychiatric patients the identification of cognitive deficits which predict a poor clinical outcome is important for the development of specific treatment strategies aimed at the amelioration of these impaired cognitive functions to increase the likelihood of full clinical remission. However, such attempts are absent in bulimia nervosa (BU), are scarce in anorexia nervosa (AN) and, furthermore, provide conflicting results. In the present prospective study we investigated the neuropsychological demands in 12 patients with AN and in 14 patients with BU before, during, and after a treatment period.

The pre-morbid psychometric profile is stable over time in subjects at high familial risk for affective disorders.

Background: The pre-morbid personality profile 'autonomic lability' (e.g. elevated neuroticism, frequent somatic complaints and increased interpersonal sensitivity) is suggested to be an antecedent of major depression.

The Munich vulnerability study on affective disorders: overview of the cross-sectional observations at index investigation.

Background: An altered nocturnal sleep pattern and a dysfunction of the hypothalamic-pituitary-adrenocortical system are neurobiological abnormalities typical for depression. A persistence of these neurobiological alterations during remission has been shown to be associated with an increased risk for a relapse. However, it remains unclear whether these persisting abnormalities are trait markers indicative of an increased vulnerability for affective disorders or only represent 'biological scars' acquired during past episodes.

[The Munich Vulnerability Study of Affective Disorders. Overview of the results at index study].

The neurobiological alterations commonly found in affective disorders (e.g., alterations in the nocturnal sleep profile, dysfunction of the hypothalamic-pituitary-adrenocortical system) gradually recover with improvement of the depressive syndrome.