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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

BACKGROUND: Since the introduction of the first atypical antipsychotics in the early 1990s, this class of medication has been increasingly relied upon for the treatment of a variety of patients with psychotic and mood disorders.DATA SOURCES: The following retrospective review was derived from the MEDLINE database using the search terms metabolic syndrome, insulin resistance, obesity, diabetes, severe mental illness, schizophrenia, bipolar disorder, mood disorders, depression, unipolar depression, and prevalence from 1966 to the present. LITERATURE SYNTHESIS: Coincident with the growing usage of these agents, there have been a growing number of literature reports of changes in metabolic homeostasis among patients taking these medications. These changes have led to interest in evaluating whether there is a relationship among these mental illnesses, their psychiatric treatments, and certain physical comorbidities known collectively as the metabolic syndrome. This article reviews the existing literature around the metabolic syndrome in patients with severe mental illnesses. CONCLUSION: Patients with severe mental illnesses, particularly schizophrenia and chronic mood disorders, demonstrate a higher prevalence of metabolic syndrome or its components compared with the general population. Based upon this increased risk in these patients, baseline and periodic medical evaluations should become a standard component in ongoing clinical assessment.
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PMID:The Metabolic Syndrome in Patients With Severe Mental Illnesses. 1536 18

Metabolic syndrome of insulin resistance and depression are both considered important cardiovascular risk factors. The aim of this study was to ascertain a possible association between these conditions in a population sample of 116 subjects (54 males, 62 females, aged 60 +/- 8 and 60 +/- 9 years, respectively). A standard questionnaire-the Hospital Anxiety Depression Scale-was used for the assessment of depressive disorder and clinical definition of insulin resistance, requiring the presence of three or more of the following factors: triglycerides > 1.7 mmol/L; and high-density lipoprotein cholesterol < 1.0 mmol/L; blood pressure >/= 130/85 mm Hg; waist circumference > 102 cm in males and > 88 cm in females; fasting glucose 6.1-7.8 mmol/L. Depressive disorders prevailed significantly more in women than in men (39% and 26%, respectively), and prevalence of depression in subjects with metabolic syndrome of insulin resistance (by definition) was about four times higher than in subjects without depression. Depressive subjects had also higher heart rate, waist circumference, lower high-density lipoprotein cholesterol, higher triglycerides, and higher body mass index. Higher sympathetic nervous activity in insulin-resistant subjects with depression was indicated.
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PMID:Depressive disorders and the metabolic syndrome of insulin resistance. 1547 37

Overproduction of corticotropin-releasing hormone (CRH) and stress system abnormalities are seen in psychiatric diseases such as depression, anxiety, eating disorders, and addiction. Investigations of CRH type 1 receptor (CRHR1) nonpeptide antagonists suggest therapeutic potential for treatment of these and other neuropsychiatric diseases. However, overproduction of CRH in the brain and on its periphery and disruption of the hypothalamic-pituitary-adrenal axis are also found in 'somatic' disorders. Some rare forms of Cushing's disease and related pituitary/adrenal disorders are obvious applications for CRHR1 antagonists. In addition, however, these antagonists may also be effective in treating more common somatic diseases. Patients with obesity and metabolic syndrome who often have subtle, but chronic hypothalamic-pituitary-adrenal hyperactivity, which may reflect central dysregulation of CRH and consequently glucocorticoid hypersecretion, could possibly be treated by administration of CRHR1 antagonists. Hormonal, autonomic, and immune aberrations are also present in chronic inflammatory, autoimmune, and allergic diseases, with considerable evidence linking CRH with the observed abnormalities. Furthermore, autonomic dysregulation is a prominent feature of common gastrointestinal disorders, such as irritable bowel syndrome and peptic ulcer disease. Patients with irritable bowel syndrome and other gastrointestinal disorders frequently develop altered pain perception and affective symptoms. CRH acts peripherally to modulate bowel activity both directly through the autonomic system and centrally by processing viscerosensory and visceromotor neural signals. This review presents clinical and preclinical evidence for the role of CRH in the pathophysiology of these disorders and for potential diagnostic and therapeutic applications of CRHR1 antagonists. Recognition of a dysfunctional stress system in these and other diseases will alter the understanding and treatment of 'psychosomatic' disorders.
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PMID:Nonpeptide corticotropin-releasing hormone receptor type 1 antagonists and their applications in psychosomatic disorders. 1552 86

While considerable research has examined diminished insulin responses within peripheral tissues, comparatively little has been done to examine the effects of this metabolic disruption upon the CNS. The present study employed biochemical and electrophysiological assays of acutely prepared brain slices to determine whether neural insulin resistance is a component of the metabolic syndrome observed within the fructose-fed (FF) hamster. The tyrosine phosphorylation levels of the insulin receptor (IR) and insulin receptor substrate 1 (IRS-1) in response to insulin were significantly reduced within FF hamsters. Also, insulin-mediated phosphorylation of both residues necessary for activation of the serine-threonine kinase Akt/PKB, a key effector of insulin signaling, was markedly decreased. Elevated levels of the protein tyrosine phosphatase 1B, which dephosphorylates the IR and IRS-1, were also observed within the cerebral cortex and hippocampus of FF hamsters. Examination of whether a nutritionally induced compromise of neural insulin signaling altered synaptic function revealed a significant attenuation of insulin-induced long-term depression, but no effect upon either paired-pulse facilitation or electrically induced long-term potentiation. Collectively, our results demonstrate, for the first time, that nutritionally induced insulin resistance significantly affects the neural insulin signaling pathway, and suggest that brain insulin resistance may contribute to cognitive impairment.
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PMID:A biochemical and functional characterization of diet-induced brain insulin resistance. 1593 73

Cytokines mediate and control immune and inflammatory responses. Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis, health, and well-being. Like the stress response, the inflammatory reaction is crucial for survival and is meant to be tailored to the stimulus and time. A full-fledged systemic inflammatory reaction results in stimulation of four major programs: the acute-phase reaction, the sickness syndrome, the pain program, and the stress response, mediated by the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Common human diseases such as atopy/allergy, autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro- versus anti-inflammatory and T helper (Th)1 versus Th2 cytokine balance. Recent evidence also indicates the involvement of pro-inflammatory cytokines in the pathogenesis of atherosclerosis and major depression, and conditions such as visceral-type obesity, metabolic syndrome and sleep disturbances. During inflammation, the activation of the stress system, through induction of a Th2 shift, protects the organism from systemic 'overshooting' with Th1/pro-inflammatory cytokines. Under certain conditions, however, stress hormones may actually facilitate inflammation through induction of interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor-alpha and C-reactive protein production and through activation of the corticotropin-releasing hormone/substance P-histamine axis. Thus, a dysfunctional neuroendocrine-immune interface associated with abnormalities of the 'systemic anti-inflammatory feedback' and/or 'hyperactivity' of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression, and atherosclerosis. These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health. These hypotheses require further investigation, but the answers should provide critical insights into mechanisms underlying a variety of common human immune-related diseases.
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PMID:Cytokine dysregulation, inflammation and well-being. 1616 5

The prevalence of the metabolic syndrome and its sequelae (cardiovascular diseases and diabetes mellitus) is elevated in patients with depression and schizophrenic disorders in comparison with mentally healthy persons. A variety of factors have been proposed to explain this association. These include overlapping pathophysiological mechanisms, an unhealthy lifestyle (poor dietary choices, smoking, lack of exercise), genetic factors and a lack of compliance with therapeutic programs. In addition to this, attention is increasing being focused on the metabolic side effects of (atypical) neuroleptics. Cases of acute ketoacidosis may also be associated with the use of these substances. Since none of the neuroleptics currently commercially available can be guaranteed to be free of metabolic side effects, strict monitoring of depressive or schizophrenic patients receiving such treatment is mandatory.
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PMID:[The metabolic syndrome and mental illness: relevance, risk factors and practical consequences]. 1628 81

Prior research has demonstrated that shortly after the 1991 Gulf War (Gulf War I), chronic multisymptom illness (CMI) was more common among deployed veterans than among nondeployed veterans. The aims of the current study were to determine the prevalence of CMI among deployed and nondeployed veterans 10 years after Gulf War I, compare the distribution of comorbid conditions, and identify prewar factors associated with CMI. Cross-sectional data collected from 1,061 deployed veterans and 1,128 nondeployed veterans examined between 1999 and 2001 were analyzed. CMI prevalence was 28.9% among deployed veterans and 15.8% among nondeployed veterans (odds ratio = 2.16, 95% confidence interval: 1.61, 2.90). Deployed and nondeployed veterans with CMI had similarly poorer quality-of-life measures and higher prevalences of symptom-based medical conditions, metabolic syndrome, and psychiatric disorders. Diagnoses of prewar anxiety disorders (not related to post-traumatic stress disorder) and depression were associated with CMI among both deployed and nondeployed veterans. Nicotine dependence and veteran-reported physician-diagnosed infectious mononucleosis were associated with CMI among deployed veterans, and migraine headaches and gastritis were associated with CMI among nondeployed veterans. CMI continues to be substantially more prevalent among deployed veterans than among nondeployed veterans 10 years after Gulf War I, but it manifests similarly in both groups. It is likely to be a common, persistent problem among veterans returning from the current Gulf War.
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PMID:Chronic multisymptom illness complex in Gulf War I veterans 10 years later. 1694 67

Well over 80 years ago Philip Smith described the beneficial clinical effects of adrenocortical extracts in animal models of adrenal insufficiency. In the ensuing years, scientists across the globe have sought to understand the mechanisms by which adrenal hormones and their synthetic analogues produce their complex and varied actions. Particular attention has focused on the glucocorticoids, partly because they have a vital place in the treatment of inflammatory and autoimmune disorders but also because dysregulation of the secretion and/or activity of endogenous glucocorticoids is increasingly implicated in a number of common disorders that pose a growing clinical burden, such as obesity, type II diabetes, the metabolic syndrome, hypertension and depression. This review considers some of the key advances that have been made in our understanding of the physiology, pathology and pharmacology of the glucocorticoids. Emphasis is placed on the molecular mechanisms of glucocorticoid signalling and the complex mechanisms that regulate the access of steroids in the systemic circulation to their receptors in their various target cells and tissues. In addition, consideration is given to the irreversible 'organisational' actions of glucocorticoids in perinatal life and to the potential role of the steroids in the aetiology of disease.
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PMID:Glucocorticoids: exemplars of multi-tasking. 1640 12

This article boldly challenges the dynamic psychiatrist to engage directly and vigorously into a matter that many would prefer to regard somewhat passively. That passivity is no longer acceptable. The metabolic syndrome has become a central medical concern because of the epidemic of obesity. It causes cardiovascular disease, diabetes, some cancers, sleep apnea, sexual dysfunction, and infertility. Obesity leads to depression, anxiety, and osteoarthritis. Some atypical antipsychotic medicines contribute to the metabolic syndrome, but the epidemic is widespread independent of atypicals. Practical steps by psychiatrists to monitor metabolic parameters are not as simple as they appear to be. Yet this is an area of clinical practice that cannot be ignored. Psychodynamic therapists need to awaken to the health of patients because the metabolic syndrome is more life-threatening than self-mutilation and many other self-destructive behaviors. The article discusses countertransference and transference issues stirred up when physicians begin to take responsibility for the total health of their patients. Freud oriented us to focus on both sides of the mind body relationship. Recent research on obesity, hypertension, diabetes, sleep, anxiety,depression, exercise and dyslipidemia is reviewed from the viewpoint of how it impinges on the office practice of a dynamic psychiatrist.
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PMID:A psychodynamic approach to screening for the metabolic syndrome. 1701 91

Considerable knowledge has accumulated in recent decades concerning the significance of physical activity in the treatment of a number of diseases, including diseases that do not primarily manifest as disorders of the locomotive apparatus. In this review we present the evidence for prescribing exercise therapy in the treatment of metabolic syndrome-related disorders (insulin resistance, type 2 diabetes, dyslipidemia, hypertension, obesity), heart and pulmonary diseases (chronic obstructive pulmonary disease, coronary heart disease, chronic heart failure, intermittent claudication), muscle, bone and joint diseases (osteoarthritis, rheumatoid arthritis, osteoporosis, fibromyalgia, chronic fatigue syndrome) and cancer, depression, asthma and type 1 diabetes. For each disease, we review the effect of exercise therapy on disease pathogenesis, on symptoms specific to the diagnosis, on physical fitness or strength and on quality of life. The possible mechanisms of action are briefly examined and the principles for prescribing exercise therapy are discussed, focusing on the type and amount of exercise and possible contraindications.
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PMID:Evidence for prescribing exercise as therapy in chronic disease. 1664 91


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