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Studies in psychiatric patients described an association between lower serum cholesterol concentrations, suicidality, depression, impulsivity, and aggression which is not entirely attributable to depression-related malnutrition and weight-loss. Several lines of evidence suggest that a serotonergic deficit in the prefrontal cortex may predispose vulnerable subjects to impulsive, autoaggressive, and suicidal behaviour in stressful life-events. In-vitro studies, animal experiments, and human in-vivo studies support the hypothesis that cholesterol reduction may contribute to the serotonergic abnormalities which have been postulated in suicidal subjects. Recently it was hypothesized that decreased consumption of polyunsaturated fatty acids, especially omega-3 fatty acids, may be a risk factor for depression and suicide. Data from human studies in healthy volunteers suggest that increasing the dietary intake of omega-3 fatty acids may increase central serotonergic activity and reduce impulsive and aggressive behaviours. Earlier epidemiological studies showed an association between low cholesterol concentrations and increased suicide risk. Recent epidemiological studies with greater samples and longer follow-up periods, however, even showed a positive correlation between cholesterol concentrations and suicide risk after controlling for potential confounding variables. Large trials of statins (simvastatin, lovastatin, pravastatin) did not show an increase of suicide mortality.

Studies in postmortem brain tissue from suicide victims show a presynaptic serotonergic deficit resulting in compensatory upregulation of postsynaptic 5-HT2 receptors in the prefrontal cortex. Reduced levels of cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid, the major serotonin metabolite, are associated with violent suicide attempts independent of psychiatric diagnosis and predict future suicide attempts and suicide completion, consistent with the notion of a biochemical trait. Neuroendocrine challenge tests, platelet studies and a polymorphism in the gene for tryptophan hydroxylase, the rate-limiting enzyme in the biosynthesis of serotonin, suggest that serotonergic activity may be reduced. This serotonergic abnormality might be related to the vulnerability or diathesis for suicidal behaviour by predisposing individuals to impulsive and autoaggressive behaviour. The hypothesis of hyperactivity of the hypothalamic pituitary adrenal axis (HPA) is supported by the postmortem findings of increased CSF corticotropin releasing hormone (CRH) concentrations and reduced CRH receptor binding sites in the frontal cortex of suicide victims (interpreted as downregulation following CRH hypersecretion) and dexamethasone nonsuppression in suicide attempters. Animal studies and in vitro experiments indicate that the HPA system modulates serotonergic activity. It is hypothesized that the serotonergic alterations potentially result from dysregulation of the HPA system. Data from epidemiological and clinical studies demonstrate that low levels of cholesterol are associated with increased suicide risk. In neuronal membranes cholesterol modulates presynaptic and postsynaptic serotonergic neurotransmission. In monkeys dietary cholesterol lowering inhibits central serotonergic activity and predisposes the animals to impulsive and aggressive behaviour. It is speculated that dysregulation of the HPA system and disordered cholesterol metabolism could enhance the serotonergic deficit, thus contributing to a neurobiological vulnerability or diathesis for impulsive and autoaggressive behaviour.

This article reviews recent research results on posttraumatic stress disorder (PTSD). Epidemiological studies show that PTSD is a common disorder within the normal population with a high degree of chronic courses. Degree of severity as well as dissociative symptoms during the traumatic event seem to have an impact on course and outcome of PTSD. A genetic disposition, familial psychopathology and premorbid personality traits as background variables seem to have an influence on the development of PTSD whereas coping strategies, as well as social support, modify the course of the disease. The investigation of biological parameters refers to the hypothalamic-pituitary-adrenal-axis system, provocation studies, psychophysiological studies, and studies of the endogenous opiate system. In regard to therapy studies only those with a randomised allocation to two different therapies as well as with a control group without therapy or a waiting list group are considered, using the DSM-III or DSM-III-R diagnostic criteria for PtSD. Five pharmacological studies could show a positive effect by antidepressants. Six behaviour therapy studies (two systematic desensitisation and four flioding) produced an improvement of PTSD symptomatology. The pathogenetic models discussed here are memory imprinting, kindling, dysregulation of the opioid neuromodulation, classical conditioning and disturbed cognitive schemas, which reflect as single models only a facet of the pathogenesis.

Suicidality under extreme life circumstances is a poorly researched area. However, suicidal behaviour could be better understood by looking at extreme conditions such as the life of internees in German concentration camps. Former inmates of different German concentration camps reported on a low suicide rate in contrast to a high rate of suicide ideas. Reasons for such a low suicide rate are discussed.

Beginning with the eighties, a paradigm-change concerning anxiety disorders has taken place in considerable parts of psychiatry. Anxiety disorders are no longer regarded as consequences of conflicts and ineffective defences or as concomitants of other psychiatric disorders but rather as disorders of their own. This resulted in a modified outlook on anxiety disorders focusing on the acute panic attack (Panic disorder) instead of focusing on chronic anxiety (Anxiety neurosis). This paper reviews recent empirical studies concerning classification, pathogenesis, and therapy of anxiety disorders, i.e. after introduction of the concept of Panic disorder. Epidemiological studies could demonstrate that in western countries anxiety disorders account for the most frequent psychiatric disorders with prevalence rates of 2.0% to 4.7%. Panic disorders show prevalence rates of 0.4% to 1.1%. Results of recent follow-up studies indicate a favorable course for outpatients and an unfavorable course for inpatients with anxiety disorders. Family studies reported on positive familial loading for Panic disorder but not for Agoraphobia and Generalized anxiety disorder. A twin study found higher concordance rates for panic attacks and Agoraphobias in monozygotic twins than in dizygotic twins. Pharmacological provocation studies with lactate infusion, CO2-inhalation, and administration of Caffeine, Yohimbine, Isoproterenol showed a higher vulnerability of patients with Panic Disorder as compared to healthy controls. However, all studies display methodological short-comings and could be interpreted differently as to the concept of a biologically determined vulnerability. Provocation studies using inverse Benzodiazepine-agonists dealt only with healthy probands. Whereas life events play a rather unimportant role für the pathogenesis of anxiety disorders, recent studies point to the influence of cognitive processes and personality variables for the pathogenesis of anxiety disorders. Concerning treatment of anxiety disorders and especially of panic disorders, pharmacological studies as well as studies of behavioural therapy indicate very good results for acute treatment and good results for behavioural therapy with respect to one to four year follow-up studies. Recently, combined drug and psychotherapy gains growing interest. Conclusions are drawn with respect to the usefulness of the new classification, i.e. after the introduction of Panic disorder as a diagnostic category, and references are given for further research strategies.

The article surveys empirical studies on the relation between alcohol addiction and depression. For a better understanding and interpretation of the results of these empirical since the end of the 'sixties, the author presents first of all a brief historical abstract of the development of classification of depressive disorders and of the definition of alcoholism. In this article, the author restricts his comments to studies conducted since the end of the 'sixties, as self-rating scales or observers-rating scales or standardised interviews have been employed from that time for characterising the pattern of signs and symptoms and for diagnosis, and now widely used diagnostic schemas also became available (ICD-8, Feighner's criteria, DSM-II). For further clarification studies on genetic studies in the patients' families and on the premorbid personality of alcoholics and depressives are utilised for assessment. The results of these empirical studies are interpreted from the "diagnostic viewpoint" of the 'eighties (i.e. from the viewpoint of ICD-9 and DSM III). Suggestions for further research approach are given. The survey shows that depressive moods appear with greater frequency in patients with alcohol abuse or alcoholism who are under inpatient or outpatient treatment. However, such depressions are usually not very intensive; they will mostly subside towards the end of the treatment course. "Primary depression" and "secondary depression" are seen with an incidence rate far beyond the value expected if two diseases would merely coincide at random, in patient populations whenever alcoholism is involved. On the other hand, no increased prevalence rate for alcoholism was seen in first-degree relations of patients with "major depression" and "Bipolar I disorder", compared with a random sample of a healthy population and first-degree relations of such a random sample. To date we can say that a considerably increased incidence of alcohol abuse, but not of alcohol addiction, is definitely present in clinical populations of patients with bipolar disorders. However, because of the lack of studies which differentiate by means of operationalised criteria between manias and hypomanias and between alcohol addiction and alcohol abuse, it has not been clarified to the present time whether alcohol abuse found in these studies is mainly linked to manic/hypomanic or depressive phases, or whether the alcohol abuse is independent of these phases.(ABSTRACT TRUNCATED AT 400 WORDS)