Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Women who experience violence are significantly more likely to have serious health problems above and beyond any injuries they might incur. The intriguing question is why this is so. In this article, the author describes how three sequelae of violence against women-depression, hostility, and sleep disturbance-can increase the risk of disease. One possible mechanism by which these sequelae increase risk is by elevating levels of pro-inflammatory cytokines. These cytokines have an adaptive function in fighting infection and repairing injured tissues. However, chronically high levels of pro-inflammatory cytokines have been implicated in a wide range of diseases. The author focuses on two illnesses that have not received much attention in the violence against women (VAW) literature: cardiovascular disease and metabolic syndrome, the precursor to type 2 diabetes. Preliminary studies also suggest that treatments that can lower inflammation may be promising adjuncts for survivors of VAW.
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PMID:Inflammation, cardiovascular disease, and metabolic syndrome as sequelae of violence against women: the role of depression, hostility, and sleep disturbance. 1754 69

It has been estimated that up to 1 in 10 adults has at least one adrenocortical nodule up to 1 cm on autopsy; these benign tumors may contribute to metabolic syndrome, hypertension, obesity and abnormalities of the hypothalamic-pituitary-adrenal (HPA) axis that can be linked to other serious disorders such as osteoporosis, depression and late-onset diabetes mellitus. In addition, up to 1 in 1500 of these adrenal "incidentalomas" may hide a carcinoma, which, if diagnosed late or left untreated, is associated with significant morbidity and mortality. Consistent with the theme of this symposium, in the present report, we review the efforts undertaken at the National Institutes of Health (NIH) in the last quarter century to unravel the complex clinical genetics and molecular mechanisms involved in adrenal tumorigenesis. We first proposed that adrenocortical tumors form in a molecular sequence of events similar to that in other organs: as the pathology of the tumor increases towards malignancy, genetic changes accumulate. For example, known genetic associations, like TP53 gene changes, occur during the latest stages of adrenocortical tumorigenesis. At the NIH, significant progress has been made in the understanding of the genetics of primary pigmented adrenocortical disease (PPNAD) and other forms of bilateral adrenocortical hyperplasias. This recently led to the identification of phosphodiesterase 11A ( PDE11A) mutations as a low-penetrance predisposing factor to adrenocortical hyperplasias of both the pigmented and non-pigmented variants.
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PMID:Adrenocortical tumors, primary pigmented adrenocortical disease (PPNAD)/Carney complex, and other bilateral hyperplasias: the NIH studies. 1757 66

The endocannabinoid system (ECS) is an endogenous physiological system composed of two cannabinoid receptors and several endogenous ligands. The ECS is intimately involved in appetite regulation and energy homeostasis, which makes it an intriguing target for pharmacological treatment of obesity, diabetes, and the metabolic syndrome. Rimonabant is the first cannabinoid receptor (CB-1) antagonist being studied and utilized to treat obesity (it is approved in Europe but is currently under review in the United States). Large randomized trials with rimonabant have demonstrated efficacy in treatment of overweight and obese individuals with weight loss significantly greater than a reduced calorie diet alone. In addition, multiple other cardiometabolic parameters were improved in the treatment groups including increased levels of high density lipoprotein cholesterol, reduced triglycerides, reduced waist circumference, improved insulin sensitivity, decreased insulin levels, and in diabetic patients improvement in glycosylated hemoglobin percentage. There was an increase in the adverse effects of depression, anxiety, irritability, and nausea in rimonabant-treated groups. This novel medication may become an important therapeutic option in the fight to reduce cardiovascular disease worldwide through its unique action on cardiometabolic risk.
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PMID:Potential role of the endocannabinoid receptor antagonist rimonabant in the management of cardiometabolic risk: a narrative review of available data. 1758 Jul 28

Adiponectin is an adipocyte-specific secretory protein that circulates in serum as three oligomeric complexes known as the high, medium and low molecular weight form (HMW, MMW and LMW). HMW adiponectin has been suggested to be a better predictor of metabolic variables, and it was recently reported that the ratio of HMW to total adiponectin or to LMW, not the absolute amount of plasma adiponectin, might be crucial in determining insulin sensitivity. Insulin resistance (IR) is considered to be a primary component of vascular risk factors. Although the association of depression with atherosclerotic vascular diseases has been well documented, the contribution of IR to the evolution and progression of depression-associated vascular morbidity and mortality remains unknown. The current preliminary study showed that the ratio of HMW to total adiponectin or to LMW, not the absolute amount of plasma adiponectin, was negatively associated with depression severity in healthy elderly subjects without metabolic syndrome. This pilot study supports a promising role of adiponectin multimer distribution for clarifying the pathophysiological mechanism by which depression is associated with increased risk for IR, leading to cardiovascular disease, metabolic syndrome or type 2 diabetes.
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PMID:Adiponectin multimer distribution, not absolute amount of plasma, correlates with depression severity in healthy elderly subjects. 1776 80

Mitochondria are energy-producing organelles that conduct other key cellular tasks. Thus, mitochondrial damage may impair various aspects of tissue functioning. Mitochondria generate oxygen- and nitrogen-derived oxidants, being themselves major oxidation targets. Dysfunctional mitochondria seem to contribute to the pathophysiology of hypertension, cardiac failure, the metabolic syndrome, obesity, diabetes mellitus, renal disease, atherosclerosis, and aging. Mitochondrial proteins and metabolic intermediates participate in various cellular processes, apart from their well-known roles in energy metabolism. This emphasizes the participation of dysfunctional mitochondria in disease, notwithstanding that most evidences supporting this concept come from animal and cultured-cell studies. Mitochondrial oxidant production is altered by several factors related to vascular pathophysiology. Among these, angiotensin-II stimulates mitochondrial oxidant release leading to energy metabolism depression. By lowering mitochondrial oxidant production, angiotensin-II inhibition enhances energy production and protects mitochondrial structure. This seems to be one of the mechanisms underlying the benefits of angiotensin-II inhibition in hypertension, diabetes, and aging rodent models. If some of these findings can be reproduced in humans, they would provide a new perspective on the implications that RAS-blockade can offer as a therapeutic strategy. This review intends to present available information pointing to mitochondria as targets for therapeutic Ang-II blockade in human renal and CV disease.
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PMID:From mitochondria to disease: role of the renin-angiotensin system. 1778 64

This study was designed to test the extent to which depressive symptoms are associated with the presence of the metabolic syndrome (MS) and each of its components, and whether these relationships are gender dependent. Participants were apparently healthy employed men (N=2,355) and women (N=1,525) who underwent a routine health check between the years 2003 and 2005. We used logistic regression analysis, predicting the MS by depressive symptoms, as assessed by the Patient Health Questionnaire, and the following control variables: age, education, smoking status, physical exercise, anxiety, and burnout. As hypothesized, we found that depression among women, but not men, was associated with a 1.94-fold risk of having the MS, and with an elevated risk of having two of its five components: elevated waist circumference (odds ratio, OR=2.23) and elevated glucose levels (OR=2.44). In addition, a positive trend was observed toward an association with the other three components: low high-density lipoprotein, hypertension, and elevated triglycerides. Among men depression was associated with elevated waist circumference only (OR=1.77). These findings suggest that especially among women, the association between depression and cardiovascular diseases might be linked to metabolic processes. If replicated in longitudinal studies, these findings may have important health-care policy implications with regard to depression management interventions.
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PMID:Depression and the metabolic syndrome: gender-dependent associations. 1794 Oct 99

Polycystic ovarian syndrome (PCOS) is extremely common among reproductive-aged women, but often goes undiagnosed. PCOS is associated with the metabolic syndrome and carries a greatly increased risk of impaired glucose tolerance and type 2 diabetes mellitus, and cardiovascular risks. Treatment of PCOS may provide relief of cosmetic problems and depression by improving patient self-esteem. In addition, because of its association with the metabolic syndrome, type 2 diabetes mellitus, and cardiovascular disease, its recognition and treatment can potentially be life saving. This article reviews the impact, pathophysiology, and associated risks of obesity and the metabolic syndrome in PCOS.
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PMID:Obesity and the polycystic ovary syndrome. 1796 14

Psoriasis is a chronic and debilitating inflammatory disease associated with serious comorbidities. Psoriasis can have a significant impact on a patient's quality of life and is associated with loss of productivity, depression, and an increased prevalence of malignancy. Emerging comorbidities of psoriasis include cardiovascular disease and metabolic syndrome. Psoriasis patients have an increased prevalence of the core components of metabolic syndrome, including obesity, dyslipidemia, and insulin resistance. The relationship between psoriasis and comorbidities such as metabolic syndrome and cardiovascular disease is likely linked to the underlying chronic inflammatory nature of psoriasis. The molecular mechanisms involved in psoriasis-associated dysregulation of metabolic function are believed to be due, in large part, to the action of increased levels of proinflammatory factors, such as tumor necrosis factor-alpha, that are central to the pathogenesis of psoriasis. Recent studies investigating the effects of tumor necrosis factor antagonists on the treatment of cardiovascular disease and metabolic syndrome support this concept.
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PMID:Psoriasis comorbidities. 1827 20

The many similarities between the metabolic syndrome and Cushing's syndrome led to the hypothesis that excess glucocorticoids (GC) are part of the pathogenesis linking their features. We review recent work that confirms the initial similarities (obesity, glucose intolerance, hypertension, and hyperlipidemia) and extends them to associated features of both syndromes (osteopenia, hypogonadism, leukocytosis, depression, and muscle weakness). Recent studies report that these features also occur in subclinical Cushing's syndrome, hypercortisolemic depression, and the transgenic overexpression of 11beta-hydoxysteroid dehydrogenase type 1 (11beta-HSD1) in mouse models of excess GC in adipose tissue. Reducing excess GC--in the clinical syndromes and in the mouse model-reverses many of these features. Because local tissue excess GC may have a central role in the pathogenesis of the metabolic syndrome, selective 11beta-HSD1 inhibitors are under active development by several pharmaceutical companies.
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PMID:Adrenal steroids and the metabolic syndrome. 1836 16

The aging process depends on genetic stability, metabolic control, and resistance to stress; longevity in particular seems related to resistance to stress. Responses to stress anticipate adaptation to an unacceptable disparity between real or imagined personal experience and expectation, including adaptive stress, anxiety, and depression. However, if stress persists, it may lead to chronic diseases, ranging from inflammation and cancer to degenerative diseases. For some time, only remarkable stress was acknowledged to induce immune and vascular alterations, such as infection or hypertension. Now it is known that moderate stress independent of conventional risk factors can induce a potent alteration of health conditions and consequently shorten life quality and lifespan. Inflammation is a critical defense mechanism, that, uncontrolled, contributes to chronic conditions with inflammatory pathogenesis. Stressful life conditions turn out to induce a diffuse (systemic) pro-inflammatory status. Subclinical chronic inflammation is an important pathogenic factor in the development of metabolic syndrome, a cluster of common pathologies, including cardiovascular disease. Markers include mediators associated with endothelial activation and dysfunction. This work reports the in vitro and in vivo effects of the monoterpene AISA 5203-L on human vascular endothelial cells in reversing replicative senescence in preventing and alleviating nonpathological stress, as assessed by a functional observational battery (FOB) of 44 tests, addressing behavioral, neurological, and physiological criteria.
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PMID:Anti-inflammatory senescence actives 5203-L molecule to promote healthy aging and prolongation of lifespan. 1837 Jun 5


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