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

The metabolic syndrome is defined as a constellation of metabolic abnormalities, including glucose intolerance, obesity, dyslipidaemia, and hypertension. It is associated with an elevated risk for cardiovascular disease and type 2 diabetes. Over the past 20 years, a worldwide increase of the metabolic syndrome has taken place. In the USA, 21% to 39% of the general population suffer from metabolic syndrome; in Europe prevalence rates are lower. At the same time, depressive disorders, which are associated with a 1.5 to 2.5 fold risk for cardiovascular events, are increasing. The combination of metabolic syndrome and depression multiplies the risk for severe complications: Due to behavioural, physiological, genetic, and treatment-induced factors, depression stimulates the development of a metabolic syndrome. In reverse, the metabolic syndrome favours development and maintenance of the metabolic syndrome. Consequently, in patients suffering from metabolic syndrome and depression, both disorders must be treated simultaneously. The treatment plan includes weight reduction, physical activity, psychoeducation, family interventions, the patient's subjective explanatory and treatment models, cognitive techniques, and problem solving techniques. Weight, blood pressure, fastening glucose, haemoglobin A1c, and lipids must be controlled in order to monitor treatment progress. Additional drug treatment can be appropriate for hypertension, dyslipidaemia, hyperglycaemia, and depression. Under these conditions, sustained improvements of individual well-being, psychosocial risk-factors, functional limitations, glycemic control, hypertension, and obesity are possible.
 ...
PMID:[Metabolic syndrome and depression]. 1694 96

Sleep has important homeostatic functions, and sleep deprivation is a stressor that has consequences for the brain, as well as many body systems. Whether sleep deprivation is due to anxiety, depression, or a hectic lifestyle, there are consequences of chronic sleep deprivation that impair brain functions and contribute to allostatic load throughout the body. Allostatic load refers to the cumulative wear and tear on body systems caused by too much stress and/or inefficient management of the systems that promote adaptation through allostasis. Chronic sleep deprivation in young healthy volunteers has been reported to increase appetite and energy expenditure, increase levels of proinflammatory cytokines, decrease parasympathetic and increase sympathetic tone, increase blood pressure, increase evening cortisol levels, as well as elevate insulin and blood glucose. Repeated stress in animal models causes brain regions involved in memory and emotions, such as hippocampus, amygdala, and prefrontal cortex, to undergo structural remodeling with the result that memory is impaired and anxiety and aggression are increased. Structural and functional magnetic resonance imaging studies in depression and Cushing's disease, as well as anxiety disorders, provide evidence that the human brain may be similarly affected. Moreover, brain regions such as the hippocampus are sensitive to glucose and insulin, and both type 1 and type 2 diabetes mellitus are associated with cognitive impairment and (for type 2 diabetes mellitus) increased risk for Alzheimer's disease. Animal models of chronic sleep deprivation indicate that memory is impaired along with depletion of glycogen stores and increases in oxidative stress and free radical production. Taken together, these changes in brain and body are further evidence that sleep deprivation is a chronic stressor and that the resulting allostatic load can contribute to cognitive problems, which can, in turn, further exacerbate pathways that lead to disease.
 ...
PMID:Sleep deprivation as a neurobiologic and physiologic stressor: Allostasis and allostatic load. 1697 22

The aim of this study was to identify characteristics of neuropsychological functioning among type 2 diabetic adults with and without major depression. Twenty type 2 diabetics with major depression, 20 non-depressed type 2 diabetics and 34 controls without diabetes or depression were compared. A mixed effects repeated measures analysis of covariance indicated significant differences in overall cognitive functioning between diagnostic groups, specifically depressed diabetics demonstrated greater cognitive dysfunction than controls. Further comparisons indicated that depressed diabetics performed significantly worse than non-depressed diabetics in attention/information processing speed. Relative to controls, depressed diabetics performed significantly worse in attention/information processing speed and executive functioning, while there was a trend for non-depressed diabetics to perform worse in executive functioning. These findings suggest that depression negatively impacts cognitive performance among adults with type 2 diabetes, which may have implications for neural circuitry underlying cognitive and mood changes in diabetic patients.
 ...
PMID:Cognitive function in adults with type 2 diabetes and major depression. 1703 Jan 11

This study examines relationships between patient reported outcomes (PROs) and clinical outcomes in Type 2 diabetes mellitus (T2DM). Patients at the outpatient clinics of a university hospital completed measures of generic health status (SF-12), diabetes-specific quality of life (Audit of Diabetes Dependent Quality of Life - ADDQoL), and depressive symptoms (Center for Epidemiologic Studies Depression - CES-D). Patient reported data were merged with a retrospective collection of clinical and utilization data, including HbA1C, from electronic medical records. A Charlson comorbidity score, diabetes complications score, BMI, and total number of ER and hospital visits were calculated. Usable response rate was 44.3% (n = 385). Patients were dichotomized into glycemic control levels based on the ADA recommended A1C level < 7.0, vs. >or= 7.0. The ADDQoL, PCS-12, and MCS-12 scores were separately examined as dependent variables using hierarchical regression models, with glycemic control as the primary explanatory variable, and controlling for demographics and clinical variables including comorbidities and complications. Glycemic control was not a significant predictor in any regression model. Obesity was a significant predictor leading to poorer PCS-12 and MCS-12 scores, while depressive symptoms significantly resulted in lower PCS-12, MCS-12 and ADDQoL scores. These and other factors related to self-management behaviors may contribute to a greater understanding of how to intervene with patients with T2DM. The use of such PROs alongside biomedical measures such as A1C is recommended.
 ...
PMID:Quality of life, health status and clinical outcomes in Type 2 diabetes patients. 1703 3

Type 2 diabetes and major depression are disorders that are mutual risk factors and may share similar pathophysiological mechanisms. To further understand these shared mechanisms, the purpose of our study was to examine the biochemical basis of depression in patients with type 2 diabetes using proton MRS. Patients with type 2 diabetes and major depression (n=20) were scanned along with patients with diabetes alone (n=24) and healthy controls (n=21) on a 1.5 T MRI/MRS scanner. Voxels were placed bilaterally in dorsolateral white matter and the subcortical nuclei region, both areas important in the circuitry of late-life depression. Absolute values of myo-inositol, creatine, N-acetyl aspartate, glutamate, glutamine, and choline corrected for CSF were measured using the LC-Model algorithm. Glutamine and glutamate concentrations in depressed diabetic patients were significantly lower (p<0.001) in the subcortical regions as compared to healthy and diabetic control subjects. Myo-inositol concentrations were significantly increased (p<0.05) in diabetic control subjects and depressed diabetic patients in frontal white matter as compared to healthy controls. These findings have broad implications and suggest that alterations in glutamate and glutamine levels in subcortical regions along with white matter changes in myo-inositol provide important neurobiological substrates of mood disorders.
 ...
PMID:Measurement of brain metabolites in patients with type 2 diabetes and major depression using proton magnetic resonance spectroscopy. 1718 Jan 24

Depression affects millions of people in the United States. Drugs used to treat depression can lead to weight gain, which could predispose a person to type 2 diabetes. Also, certain medications that may be used to treat depression with psychotic features can lead to metabolic syndrome and new-onset diabetes. Diabetes is another chronic health care condition that affects millions of people in the United States. Diabetes is the leading cause of nontraumatic amputations and a leading cause of blindness. Both conditions can result in a lower quality of life. Clinicians face challenges in treating either condition, but can face greater ones when the conditions occur together. This article reviews the literature concerning depression and diabetes.
 ...
PMID:Diabetes and depression: a review of the literature. 1727 May 91

The objective of the present study was to establish the frequency of psychiatric comorbidity in a sample of diabetic patients with symmetric distal polyneuropathy (SDPN). Sixty-five patients with type 2 diabetes mellitus were selected consecutively to participate in the study at Instituto Estadual de Diabetes e Endocrinologia. All patients were submitted to a complete clinical and psychiatric evaluation, including the Portuguese version of the structured clinical interview for DSM-IV, the Beck Depression Inventory, the Neuropathy Symptom Score, and Neuropathy Disability Score. SDPN was identified in 22 subjects (33.8%). Patients with and without SDPN did not differ significantly regarding sociodemographic characteristics. However, a trend toward a worse glycemic control was found in patients with SDPN in comparison to patients without SDPN (HbA1c = 8.43 +/- 1.97 vs 7.48 +/- 1.95; P = 0.08). Patients with SDPN exhibited axis I psychiatric disorders significantly more often than those without SDPN (especially anxiety disorders, in general (81.8 vs 60.0%; P = 0.01), and major depression--current episode, in particular (18.2 vs 7.7%; P = 0.04)). The severity of the depressive symptoms correlated positively with the severity of SDPN symptoms (r = 0.38; P = 0.006), but not with the severity of SDPN signs (r = 0.07; P = 0.56). In conclusion, the presence of SDPN seems to be associated with a trend toward glycemic control. The diagnosis of SDPN in diabetic subjects seems also to be associated with relevant psychiatric comorbidity, including anxiety and current mood disorders.
 ...
PMID:Comorbidity of psychiatric disorders and symmetric distal polyneuropathy among type II diabetic outpatients. 1727 65

Type 2 diabetes mellitus (DM2) is a common metabolic disorder. DM2 is associated with cognitive impairments, and with depressive symptoms, which occur in about one third of patients. In the current study we compared the cognitive profile and psychological well-being of 119 patients with DM2 (mean age: 66 +/- 6; mean duration: 9 +/- 6 years) with 55 age and education matched-control participants. Groups were compared on cognitive performance in five major cognitive domains, psychological wellbeing [assessed by Symptom Checklist (SCL)-90-R and the Beck Depression Inventory (BDI-II)] and abnormalities on brain MRI. We hypothesized an interrelationship between cognition, MRI abnormalities, and psychological well-being. DM2 patients performed significantly worse than controls on cognitive tasks, especially on tasks that required more mental efficiency, although the differences were modest (effect sizes Cohen d < .6). We speculate that DM2 patients have a diminished ability to efficiently process unstructured information. Patients with DM2 had significantly higher scores on the SCL-90-R (p < .001) and on the BDI-II (p < .001) and worse MRI ratings than controls, but psychological distress did not correlate with cognition, MRI ratings or biomedical characteristics. Contrary to our hypothesis, cognitive disturbances and psychological distress thus seem independent symptoms of the same disease.
 ...
PMID:A detailed profile of cognitive dysfunction and its relation to psychological distress in patients with type 2 diabetes mellitus. 1728 86

The aim of the investigation was to study the significance of the functional condition of endothelium for the evaluation of ischemic episodes in patients with type 2 diabetes mellitus (DM2). Ninety-three patients (52 men; 41 women; mean age 58.3+/-4.8 years) were examined. Group 1 consisted of 47 patients with coronary heart disease (CHD) and CD2; group 2 consisted of 46 CAD patients without carbohydrate exchange disorder. Both groups were comparable by gender, age, and the main risk factors. The patients were examined using Holter monitoring, physical load test, EchoCG, reactive hyperemia test (ultrasound evaluation of the endothelium-dependent brachial artery dilation). The number of painless ischemic episodes (PIE), the total duration of ischemia, the maximum degree of ST depression prevailed in group 1 patients. Correlation analysis demonstrated a significant negative correlation between endothelial dysfunction, one the one part, and the number and duration of PIE and the time between the ischemic ST depression and pain syndrome, on the other, in group 1 patients.
 ...
PMID:[Clinicofunctional evaluation of ischemic episodes and vascular endothelium in patients with type 2 diabetes]. 1729 80

We have previously shown that type 2 diabetes (T2D) in the mouse is associated with increased responsivity to innate immune challenge. Here we demonstrate that in a mouse model of type 1 diabetes (T1D) LPS-dependent suppression of social exploration (SE) is augmented and dependent on hyperglycemia. T1D was induced in mice with intraperitoneal (i.p.) streptozotocin (STZ). After 4d, STZ treated mice had blood glucose levels of 417+/-34mg/dl compared to 160+/-11mg/dl in non-STZ treated mice. When these diabetic mice were challenged with i.p. lipopolysaccharide (LPS), LPS-induced depression of SE was nearly 2.7-fold greater in diabetic mice at 2h than in non-diabetic mice. Examination of peritoneal proinflammatory cytokine levels 2h after LPS administration showed that diabetic mice had 4-, 2.5- and 3.6-fold greater concentrations of IL-1beta, IL-6 and TNF-alpha, respectively, when compared to non-diabetic mice. Control of blood glucose levels with injected insulin in diabetic mice improved 2h post LPS-induced loss of SE by 3.9-fold. Interestingly, insulin given intracerebroventricularly to diabetic mice did not impact LPS-induced loss of SE but did increase basal SE 8, 12 and 24h later. Finally, administration of STZ to hyperglycemic/hyperinsulinemic db/db mice did not alter LPS-induced loss of SE. Taken together these findings indicate that mice with T1D have augmented loss of SE in response to LPS and this is due to hyperglycemia and not to insulin.
 ...
PMID:LPS-dependent suppression of social exploration is augmented in type 1 diabetic mice. 1732 Nov 7


<< Previous 1 2 3 4 5 6 7 8 9 10