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This article provides a detailed review of the association of major depression with coronary heart disease (CHD), examines the biological variables underpinning the linkage and discusses the clinical implications for treatment. When considering the co-morbidity between major depressive disorder (MDD) and CHD it is important to differentiate between (i) the prevalence and impact of MDD in those with existing CHD and (ii) MDD as a risk factor for the development of CHD. Whether the same biological mechanisms are at play in these two instances remains unknown. Depression is common in patients with CHD. Importantly, depression in these patients increases mortality. There is also consistent evidence that MDD is a risk factor for the development of CHD. The relative risk of developing CHD is proportional to the severity of depression and is independent of smoking, obesity, hypercholesterolaemia, diabetes mellitus and hypertension. There is a clear need to identify the underlying neurochemical mechanisms responsible for MDD and their linkage to the heart and vascular system. Of particular interest are activation of stress pathways, including both the sympathetic nervous system and hypothalamic-pituitary-adrenal axis, and inflammatory-mediated atherogenesis. Elevated sympathetic activity, reduced heart rate variability and increased plasma cortisol levels have been documented in patients with MDD. In addition to direct effects on the heart and vasculature, activation of stress pathways may also be associated with increased release of inflammatory cytokines such as interleukin-6 and tumour necrosis factor-alpha. Elevated levels of C-reactive protein are commonly observed in patients with MDD. The majority of investigations examining treatment of depression following myocardial infarction have focused on safety and efficacy; there is little evidence to indicate that treating depression in these patients improves survival. Given that strategies for preventive therapy remain incompletely formulated, future research should focus on generating a better understanding of the neurobiology of MDD and heart disease as a basis for rational and effective therapy.
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PMID:Cardiovascular abnormalities in patients with major depressive disorder: autonomic mechanisms and implications for treatment. 1955 86

Major depression is associated with medical co-morbidity, such as ischaemic heart disease and diabetes, but the underlying pathophysiological mechanisms remain unclear. The FSL (Flinders Sensitive Line) rat is a genetic animal model of depression exhibiting features similar to those of depressed individuals. The aim of the present study was to compare the myocardial responsiveness to I/R (ischaemia/reperfusion) injury and the effects of IPC (ischaemic preconditioning) in hearts from FSL rats using SD (Sprague-Dawley) rats as controls and to characterize differences in glucose metabolism and insulin sensitivity between FSL and SD rats. Hearts were perfused in a Langendorff model and were subjected or not to IPC before 40 min of global ischaemia, followed by 120 min of reperfusion. Myocardial infarct size was found to be significantly larger in the FSL rats than in the SD rats following I/R injury (62.4+/-4.2 compared with 46.9+/-2.9%; P<0.05). IPC reduced the infarct size (P<0.01) and improved haemodynamic function (P<0.01) in both FSL and SD rats. No significant difference was found in blood glucose levels between the two groups measured after 12 h of fasting, but fasting plasma insulin (70.1+/-8.9 compared with 40.9+/-4.7 pmol/l; P<0.05) and the HOMA (homoeostatic model assessment) index (P<0.01) were significantly higher in FSL rats compared with SD rats. In conclusion, FSL rats had larger infarct sizes following I/R injury and were found to be hyperinsulinaemic compared with SD rats, but appeared to have a maintained cardioprotective mechanism against I/R injury, as IPC reduced infarct size in these rats. This animal model may be useful in future studies when examining the mechanisms that contribute to the cardiovascular complications associated with depression.
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PMID:Evaluation of the relationship between hyperinsulinaemia and myocardial ischaemia/reperfusion injury in a rat model of depression. 1957 93

We compared chronic care utilization in four major health systems in the U.S.: the military health system (TRICARE), the Department of Veterans Affairs (VA), Medicaid, and employer-sponsored commercial plans. Prevalence rates and key performance indicators were constructed from administrative data in federal fiscal year 2003 for eight chronic conditions: hypertension, major depression, diabetes, tobacco dependence, ischemic heart disease, severe mental illness, persistent asthma, and stroke. Continuously enrolled beneficiaries under 65 years old were studied: TRICARE (N = 2,963,987), VA (N = 2,114,739), Medicaid enrollees in five states (N = 5,554,974), and commercial insurance (N = 5,212,833). Condition-specific adjusted prevalence rates and measures were compared using the standardized rate ratio. For the majority of the conditions, the estimated prevalence rates were highest in the VA and Medicaid populations. Prevalence rates were generally lower in TRICARE and commercial plans. Medicaid beneficiaries had the highest hospitalization rates in four of the six conditions where hospitalization rates were measured. These results provide empirical evidence of differences in chronically ill patient populations in several of the major U.S. health insurance systems.
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PMID:A four-system comparison of patients with chronic illness: the Military Health System, Veterans Health Administration, Medicaid, and commercial plans. 1978 Mar 68

Worldwide, diabetes and depression are highly prevalent conditions that are independently-associated with increased healthcare costs, disability, lost productivity, and premature mortality. Approximately 10% of individuals with diabetes have major depression and 30% have both major and minor depression. Individuals with diabetes have two-fold increased odds of having depression compared with individuals without diabetes. Although, there are effective treatments for depression, studies have shown that only 50% of adults with depression are recognized in primary care and that treatment for depression is less than ideal in this setting. The epidemiology, treatment and costs of depression in adults with Type 2 diabetes are reviewed and an expert opinion on the best treatments for depression, and future clinical and research directions in this field of research are offered.
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PMID:Epidemiology, treatment and costs of depression in adults with Type 2 diabetes. 1980 73

Impaired glucose tolerance and diabetes have been associated with depression, and antidepressant treatment is assumed to improve impaired glucose tolerance. However, antidepressant treatment is also considered as a risk factor for the development of diabetes. Reports about glucose tolerance under antidepressant treatment frequently lack appropriate control groups. We conducted the oral glucose tolerance test (OGTT) in 10 healthy controls selected from an epidemiological sample with a negative lifetime history of mental Axis I disorder. Controls were carefully matched to a sample of inpatients with major depression that participated in an OGTT before and after antidepressant treatment with mirtazapine. All participants underwent a standard OGTT protocol. In patients, a second (after 2 weeks) and a third (after 4-6 weeks) OGTT was performed under treatment with mirtazapine. Compared to healthy controls, we observed significantly impaired glucose tolerance in acutely depressed patients. Effect size calculation indicated a moderate to large effects on glucose and insulin concentrations in response to an OGTT. Although glucose tolerance improved under mirtazapine treatment, insulin sensitivity was still impaired and remained significantly lower in patients compared to controls.
Exp Clin Endocrinol Diabetes 2010 Feb
PMID:Glucose tolerance in depressed inpatients, under treatment with mirtazapine and in healthy controls. 1983 72

The circulating level of brain-derived neurotrophic factor (BDNF) is reduced in patients with major depression and type-2 diabetes. Because acute exercise increases BDNF production in the hippocampus and cerebral cortex, we hypothesized that endurance training would enhance the release of BDNF from the human brain as detected from arterial and internal jugular venous blood samples. In a randomized controlled study, 12 healthy sedentary males carried out 3 mo of endurance training (n = 7) or served as controls (n = 5). Before and after the intervention, blood samples were obtained at rest and during exercise. At baseline, the training group (58 + or - 106 ng x 100 g(-1) x min(-1), means + or - SD) and the control group (12 + or - 17 ng x 100 g(-1) x min(-1)) had a similar release of BDNF from the brain at rest. Three months of endurance training enhanced the resting release of BDNF to 206 + or - 108 ng x 100 g(-1) x min(-1) (P < 0.05), with no significant change in the control subjects, but there was no training-induced increase in the release of BDNF during exercise. Additionally, eight mice completed a 5-wk treadmill running training protocol that increased the BDNF mRNA expression in the hippocampus (4.5 + or - 1.6 vs. 1.4 + or - 1.1 mRNA/ssDNA; P < 0.05), but not in the cerebral cortex (4.0 + or - 1.4 vs. 4.6 + or - 1.4 mRNA/ssDNA) compared with untrained mice. The increased BDNF expression in the hippocampus and the enhanced release of BDNF from the human brain following training suggest that endurance training promotes brain health.
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PMID:Endurance training enhances BDNF release from the human brain. 1992 61

Many phenotypes of public health importance (e.g., diabetes, coronary artery disease, major depression, obesity, and addictions to alcohol and nicotine) involve complex pathways of action. Interactions between genetic variants or between genetic variants and environmental factors likely play important roles in the functioning of these pathways. Unfortunately, complex interacting systems are likely to have important interacting factors that may not readily reveal themselves to univariate analyses. Instead, detecting the role of some of these factors may require analyses that are sensitive to interaction effects.In this study, we evaluate the sensitivity and specificity of the restricted partition method (RPM) to detect signals related to coronary artery disease in the Genetic Analysis Workshop 16 Problem 3 data using the 50,000 k candidate gene single-nucleotide polymorphism set. Power and false-positive rates were evaluated using the first 100 replicate datasets. This included an exploration of the utility of using of all genotyped family members compared with selecting one member per family.
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PMID:Power and false-positive rates for the restricted partition method (RPM) in a large candidate gene data set. 2001 69

Evidence indicates rates of depressive disorders are higher among adults with diabetes than in the general population. The instrument most frequently utilized in primary care to screen for major depression is The Patient Health Questionnaire (PHQ-9). Its use can have a dramatic impact on the initial diagnosis and ongoing treatment of patients with diabetes and depression.
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PMID:Detecting and managing depression in type II diabetes: PHQ-9 is the answer! 2033 82

Bipolar disorder shares depressive symptoms with unipolar major depressive disorder but is defined by episodes of mania or hypomania. Bipolar disorder in its broadest sense has a community lifetime prevalence of 4% and is a severely impairing illness that impacts several aspects of patients' lives. Race, ethnicity, and gender have no effect on prevalence rates, but women are more likely to experience rapid cycling, mixed states, depressive episodes, and bipolar II disorder than men. Patients with bipolar disorder have high rates of disability and higher rates of mortality than individuals without bipolar disorder. Natural causes such as cardiovascular disease and diabetes, as well as suicide and other "unnatural" causes are key contributors to the high mortality rate. The costs associated with bipolar disorder include not only the direct costs of treatment, but also the much greater indirect costs of decreased productivity, excess unemployment, and excess mortality.
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PMID:Diagnostic features, prevalence, and impact of bipolar disorder. 2057 24

The purpose of this study was to examine the effect of type 2 diabetes with major depression on cortical gray matter using magnetic resonance imaging and cortical pattern matching techniques. We hypothesized that diabetic subjects and depressed diabetic subjects would demonstrate decreased cortical gray matter thickness in prefrontal areas as compared to healthy control subjects. Patients with type 2 diabetes (n=26) and patients with diabetes and major depression (n=26) were compared with healthy controls (n=20). Gray matter thickness across the entire cortex was measured using cortical pattern matching methods. All subjects with diabetes demonstrated decreased cortical gray matter thickness in the left anterior cingulate region. Additionally, depressed diabetic subjects showed significant cortical gray matter decreases in bilateral prefrontal areas compared with healthy controls. Correlations between clinical variables and cortical gray matter thickness revealed a significant negative relationship with cerebrovascular risk factors across all three groups, most consistently in the left dorsomedial prefrontal cortex. A significant positive relationship between performance on attention and executive function tasks and cortical gray matter thickness predominantly in left hemisphere regions was also seen across all subjects. Depression and diabetes are associated with significant cortical gray matter thinning in medial prefrontal areas.
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PMID:Regional cortical gray matter thickness differences associated with type 2 diabetes and major depression. 2083 54


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