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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several studies have investigated a connection between diabetes and major depressive disorder (MDD). Whether these associations are mediated by changes in insulin is not known. Insulin seems to play a role in violent behaviour. To further elucidate the role of insulin in MDD and violent, aggressive, or impulsive behaviour, we measured insulin in cerebrospinal fluid (CSF) in 74 patients with a recent suicide attempt. Patients were divided into those with and without MDD, and they were also subgrouped by whether the suicide attempt was considered to be violent or not. It was found that patients with a violent suicide attempt had significantly higher CSF-insulin (5.9+/-1.0 pmol/l) than those with a nonviolent attempt (5.3+/-0.7 pmol/l). In contrast, there were no significant differences in CSF-insulin between patients with MDD and patients without. Our findings support the hypothesis that CSF-insulin is involved in violent behaviour, but not connected to MDD as such.
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PMID:High CSF-insulin in violent suicide attempters. 1566 18

Major depressive disorder (MDD) is a highly prevalent disease, frequently characterized by recurrent or chronic course, and by comorbidity with other medical illnesses. The lifetime prevalence of MDD ranges up to 17% in the general population, and it almost doubles in patients with diabetes (9-27%), stroke (22-50%), or cancer (18-39%). Moreover, MDD worsens the prognosis, quality of life, and treatment compliance of patients with comorbid medical illnesses. Similar to what is observed with other comorbid illnesses, MDD worsens the outcome of kidney disease patients by increasing both morbidity and mortality. Treatment of depressive symptoms in renal failure patients increases medication acceptability and therefore potentially improves the overall patient outcome. The issue of the safety of antidepressant treatment in subjects with renal failure is frequently counterbalanced by the risks associated with depression comorbidity, provided that antidepressants with a low volume of distribution and low protein binding are prescribed, and most important, at low initial doses. Screening for CYP isoenzyme interactions with current medications is also recommended before starting antidepressant treatment.
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PMID:Depression and renal disease. 1577 49

The high incidence of depression in end-stage renal disease (ESRD) patients is well documented. Our group and others have estimated that 20-30% of ESRD patients experience major depression. Several recent studies have emphasized the relationship between depressive symptoms and mortality and morbidity in both hemodialysis (HD) and peritoneal dialysis (PD) patients. We screened 380 PD patients for depression using the Beck Depression Inventory (BDI). The mean patient age was 59.9 +/- 14.1 (SD) years, 55% were Caucasian, 51% were male, and 39% had diabetes. The mean BDI score was 12.1 +/- 7.7; 49% had a score of 11 or greater. Fifty-five percent refused further assessment to confirm the diagnosis of major depression, while 45% of patients eligible for treatment agreed to further assessment. Their mean BDI was 18.8 +/- 6.2. Eighty-four percent were diagnosed with major depression on direct interviews and offered pharmacologic treatment, 16% did not meet the criteria for a diagnosis of depression, and 50% successfully completed 12 weeks of pharmacologic treatment. The BDI score of these patients at the start of treatment was 17.4 +/- 6.6, and at completion of treatment it was 8.4 +/- 3.0. Thirty-eight percent of treatment failures were in those who were also diagnosed with a DSM-IV personality disorder. Major depression is common in PD patients, and is potentially treatable with pharmacologic therapy. However, there are major problems providing a depression assessment and treatment program to such patients. Problems include refusal to complete depression assessment and patients with axis 2 personality disorders who have difficulty complying with treatment. Although depression treatment can improve depressive symptoms, it is unclear whether such therapy will improve medical outcomes.
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PMID:The identification and treatment of depression in patients maintained on dialysis. 1577 59

The objective of this study was to investigate the relative impact of brain white matter hyperintensities (WMHs), cardiovascular risk factors and elements of the one-carbon cycle metabolism (including serum folate, vitamin B12 and homocysteine levels) on the outcome of antidepressant treatment in non-elderly subjects with major depressive disorder (MDD). Fifty MDD subjects were administered brain magnetic resonance imaging (MRI) scans at 1.5 T to detect T2 WMHs. The severity of brain WMHs was classified with the Fazekas scale (range=0-3). We assessed cardiovascular risk factors in all MDD subjects (age, gender, smoking, diabetes, family history, hypertension, cholesterol). MDD patients also had serum folate, vitamin B12 and homocysteine levels measured. All MDD subjects received treatment with fluoxetine 20 mg/day for 8 weeks. In a logistic regression, the severity of subcortical WMHs and the presence of hypofolatemia were independent predictors of lack of clinical response to antidepressant treatment. Separately, hypofolatemia also predicted lack of remission to antidepressant treatment. These associations were independent of the presence of smoking, diabetes, family history, hypercholesterolemia, hyperhomocysteinemia and low B12 levels. Although preliminary, the results of the present work suggest that subcortical brain WMHs and hypofolatemia may have an independent negative impact on the likelihood of responding to antidepressant treatment in non-geriatric subjects with MDD.
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PMID:Brain MRI white matter hyperintensities and one-carbon cycle metabolism in non-geriatric outpatients with major depressive disorder (Part II). 1629 3

Comorbidity is the rule with anxiety and depressive disorders. Anxiety and major depressive disorder are often comorbid with each other; these disorders are commonly associated with other psychiatric disorders; and they are frequently found coexisting with long-standing chronic medical conditions such as cardiovascular disease and diabetes mellitus. The comorbidity of major depressive and anxiety disorders is associated with barriers to treatment and worse psychiatric outcomes, including treatment resistance, increased risk for suicide, greater chance for recurrence, and greater utilization of medical resources. Effective recognition and treatment of anxiety and depression may be associated with functional improvement in the medical disorders (eg, lower HbA1c level in patients with diabetes). Paying careful attention to the development of anxiety and depression may also positively impact the economic burden of these disorders. To help primary care physicians better understand the comorbidity of depression and anxiety and medical disorders, the authors describe three case scenarios.
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PMID:Understanding comorbidity with depression and anxiety disorders. 1673 13

Depression generally begins before Type II diabetes and coronary artery disease; however, no data are available on whether asthma or major depressive disorder (MDD) have an earlier onset. The age at onset of asthma and depression were collected from 85 adult asthma patients with current MDD. The mean ages at onset of asthma and MDD were 21.0 years and 28.8 years, respectively. Asthma preceded MDD in 62% of cases; MDD preceded asthma onset in 24% of cases; and asthma and MDD had a concurrent onset in 14% of the cases. In asthma patients, unlike patients with Type II diabetes and coronary artery disease, depression appears generally to occur after the onset of asthma.
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PMID:Age at onset of major depression in inner-city adults with asthma. 1684 92

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.
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PMID:Cognitive function in adults with type 2 diabetes and major depression. 1703 Jan 11

Among polyunsaturated omega-3 fatty acids, ALA (alpha-linolenic acid) provided the first coherent multidisciplinary experimental demonstration of the effect of diet (one of its major macronutrient) on the structure, the biochemistry, the physiology and thus the function of the brain. In fact, DHA (docosahexaenoic acid) is one for the major building structures of membrane phospholipids of brain and absolute necessary of neuronal function. It was first demonstrated that the differentiation and functioning of cultured brain cells requires not only ALA, but also the very long polyunsaturated omega-3 (DHA) and omega-6 carbon chains. Then, it was found that ALA acid deficiency alters the course of brain development, perturbs the composition of brain cell membranes, neurones, oligodendrocytes and astrocytes, as well as sub cellular particles such as myelin, nerve endings (synaptosomes) and mitochondria. These alterations induce physicochemical modifications in membranes, lead to biochemical and physiological perturbations, and results in neurosensory and behavioural upset. Consequently, the nature of polyunsaturated fatty acids (in particular omega-3, ALA and DHA) present in formula milks for infants (premature and term) conditions the visual, neurological and cerebral abilities, including intellectual. Dietary omega-3 fatty acids are involved in the prevention of some aspects of ischemic cardiovascular disease (including at the level of cerebral vascularization), and in some neuropsychiatric disorders, particularly depression, as well as in dementia, including Alzheimer's disease and vascular dementia. The implication of omega-3 fatty acids in major depression and bipolar disorder (manic-depressive illness) is under evaluation. Their dietary deficiency (and altered hepatic metabolism) can prevent the renewal of membranes and consequently accelerate cerebral ageing; nonetheless, the respective roles of the vascular component on one hand and the cerebral parenchyma itself on the other have not yet been clearly elucidated. Low fat diet may have adverse effects on mood. The nature of the amino acid composition of dietary proteins contributes to cerebral function; taking into account that tryptophan plays a special role. In fact, some indispensable amino acids present in dietary proteins participate to elaborate neurotransmitters (and neuromodulators). The regulation of glycaemia (thanks to the ingestion of food with a low glycaemic index ensuring a low insulin level) improves the quality and duration of intellectual performance, if only because at rest the brain consumes more than 50% of dietary carbohydrates, approximately 80% of which are used only for energy purpose. In infants, adults and aged, as well as in diabetes, poorer glycaemic control is associated with lower performances, for instance on tests of memory. At all ages, and more specifically in aged people, some cognitive functions appear sensitive to short term variations in glucose availability. The presence of dietary fibbers is associated with higher alertness ratings and ensures less perceived stress. Although an increasing number of genetic factors that may affect the risk of neurodegenerative disorders are being identified, number of findings show that dietary factors play major roles in determining whether the brain age successfully of experiences neurodegenerative disorders. Effects of micronutrients have been examined in the accompanying paper.
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PMID:Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 2 : macronutrients. 1706 10

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.
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PMID:Measurement of brain metabolites in patients with type 2 diabetes and major depression using proton magnetic resonance spectroscopy. 1718 Jan 24

The multifactorial nature of depression resembles that of other complex disorders such as diabetes mellitus or coronary artery disease. However, while for the latter disorders predisposing and risk factors have been identified, such knowledge is still scarce in depression. In this review we propose to use diabetes mellitus, for which characteristic milestones have been condensed to obesity-hyperinsulinaemia-insulin resistance-diabetes mellitus, as a conceptual analogical model. Based on this model we hypothesize that depression develops according to a similar pattern: prolonged psychological stress-hyperserotonism-serotonin resistance-major depression. We review extensive supporting evidence from human studies and animal models of depression, including stress involvement in the aetiology of depression, evidence for increased synaptic serotonin and decreased 5-HT1A receptor activity. Conceptualizing the pathogenesis of depression as a multi-step process may inspire new concepts, which will eventually lead to delineation of additional preventive and therapeutic interventions similar to those currently practised in diabetes.
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PMID:Major depression as a disorder of serotonin resistance: inference from diabetes mellitus type II. 1725 Jul 76


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