Coexisting dysregulations of both the sympathoadrenal system and hypothalamic-pituitary-adrenal-axis in melancholia

Maes, Michaël; Minner, B.; Suy, E.; Vandervorst, C.; Raus, Jef

doi:10.1007/bf01244945

Cited by 39 publications

(16 citation statements)

References 67 publications

(61 reference statements)

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“…Cortisol is a stress hormone, which stimulates glucose production, increases lipolysis and circulating free fatty acids, decreases insulin secretion from beta cells and decreases sensitivity to insulin [24][25][26][27]. It is postulated that a chronically high cortisol level, which is a feature of about 50% of depressed patients, results in obesity, insulin resistance and type 2 diabetes [24,28,29]. Some studies found evidence for this hypothesis [27,28].…”

Section: Discussionmentioning

confidence: 99%

Depression as a risk factor for the onset of type 2 diabetes mellitus. A meta-analysis

et al. 2006

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Aims/hypothesis: Evidence strongly suggests that depression and type 2 diabetes are associated, but the direction of the association is still unclear. Depression may occur as a consequence of having diabetes, but may also be a risk factor for the onset of type 2 diabetes. This study examined the latter association by reviewing the literature and conducting a meta-analysis of longitudinal studies on this topic. Methods: Medline and PsycInfo were searched for articles published up to January 2005. All studies that examined the relationship between depression and the onset of type 2 diabetes were included. Pooled relative risks were calculated using fixed and random effects models. To explore sources of heterogeneity between studies, subgroup analyses and meta-regression analyses were performed. Results: Nine studies met our inclusion criteria for this meta-analysis. The pooled relative risk was 1.26 (1.13-1.39) using the fixed effects model and 1.37(1.14-1.63) using the random effects model. Heterogeneity between studies could not be explained by (1) whether studies controlled for undetected diabetes at baseline; (2) the method of diabetes assessment at followup; (3) the baseline overall risk of diabetes in the study population; and (4) follow-up duration. Conclusions/ interpretation: Depressed adults have a 37% increased risk of developing type 2 diabetes mellitus. The pathophysiological mechanisms underlying this relationship are still unclear and warrant further research. A randomised controlled study is needed to test whether effective prevention or treatment of depression can reduce the incidence of type 2 diabetes and its health consequences.

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Section: Discussionmentioning

confidence: 99%

Depression as a risk factor for the onset of type 2 diabetes mellitus. A meta-analysis

et al. 2006

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“…Some suggest that depression could increase a person's risk of developing type 2 diabetes (13)(14)(15), either by influencing behaviors such as eating and physical activity or via increased sympathoadrenal and hypothalamic-pituitary-adrenal axis activity (16,17). The Diabetes Prevention Program (DPP) offered an opportunity to study depression markers in a population at increased risk for developing type 2 diabetes because they are overweight and have impaired glucose tolerance (IGT).…”

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confidence: 99%

Depression Symptoms and Antidepressant Medicine Use in Diabetes Prevention Program Participants

Rubin

Knowler

et al. 2005

Diabetes Care

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OBJECTIVE -To assess depression markers (symptoms and antidepressant medicine use) in Diabetes Prevention Program (DPP) participants and to determine whether changes in depression markers during the course of the study were associated with treatment arm, weight change, physical activity level, or participant demographic characteristics.RESEARCH DESIGN AND METHODS -DPP participants (n ϭ 3,187) in three treatment arms (intensive lifestyle, metformin, and placebo) completed the Beck Depression Inventory (BDI) and reported on use of antidepressant medicines at randomization and subsequently at each annual visit (average duration in study 3.2 years).RESULTS -On study entry, 10.3% of participants had BDI scores Ն11, which was used as a threshold for mild depression, 5.7% took antidepressant medicines, and 0.9% had both depression markers. During the DPP, the proportion of participants with elevated BDI scores declined (from 10.3% at baseline to 8.4% at year 3), while the proportion taking antidepressant medicines increased (from 5.7% at baseline to 8.7% at year 3), leaving the proportion with either marker unchanged. These time trends were not significantly associated with the DPP treatment arm. Depression markers throughout the study were associated with some participant demographic factors, adjusted for other factors. Men were less likely to have elevated depression scores and less likely to use antidepressant medicine at baseline (9.0% of men and 17.9% of women had at least one marker of depression) and throughout the study (P Ͻ0.0001). Those with more education were less likely to have elevated symptom scores (P ϭ 0.0007) but more likely to be taking antidepressant medicine (P ϭ 0.002). Non-Hispanic white participants were less likely than African Americans to have BDI scores Ն11 (P ϭ 0.03), but white participants were more likely to be taking antidepressant medicine than any other racial/ethnic group (P Ͻ0.0001).CONCLUSIONS -DPP participation was not associated with changes in levels of depression. Countervailing trends in the proportion of DPP participants with elevated depression symptoms and the proportion taking antidepressant medicine resulted in no significant change in the proportion with either marker. The finding that those taking antidepressant medicine often do not have elevated depression symptoms indicates the value of assessing both markers when estimating overall depression rates. Diabetes Care 28:830 -837, 2005D epression is more common among people with diabetes than in the general population (1,2). The causal relationships between depression and glucose metabolism are not well understood, but some associations have been documented. People with diabetes who are depressed have higher HbA 1c levels (3), more diabetes complications (4,5), and much higher general health care costs than people with diabetes who are not depressed (6,7). Treating depression in people with diabetes may be associated with improved glucose control (8,9), but this has not been seen in patients with lower HbA 1c levels (10,1...

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“…Therefore, it has been hypothesized that, in major depression, hypofunctional · 2 -ARs and, consequently, an impaired negative feedback on the presynaptic neuron, could produce a disinhibition of noradrenergic output and exaggerated noradrenaline release in response to any activation of the catecholaminergic system [6]. In major depression, signs of hypofunctional · 2 -ARs are accompanied by indications of increased catecholaminergic turnover [5,[24][25][26][27][28] It may be hypotesized that changes in the affinity of · 2 -ARs may play a role in the biophysiology of fibromyalgia. Indeed, there is now some evidence that central as well as peripheral · 2 -ARs mediate nociception, analgesia, causalgia and tactile hyperesthesia [29,30].…”

Section: Discussionmentioning

confidence: 99%

“…Because of the symptomatic similarities between depression and fibromyalgia, measurements of biochemical markers of depression in patients with fibromyalgia are useful [3]. It has been suggested that changes in sympathetic activity may occur both in major depression [4][5][6] as well as in fibromyalgia. Bennett et al [7] found that the inceased sympathetic tone Maes/Libbrecht/Delmeire/Lin/De Clerck/ Scharpe/Janca in fibromyalgia was correlated with an increased density of platelet · 2 -adrenoceptor (· 2 -AR) binding sites.…”

Section: Introductionmentioning

confidence: 99%

Changes in Platelet Alpha-2-Adrenoceptors in Fibromyalgia: Effects of Treatment with Antidepressants

Maes

Libbrecht²,

Delmeire³

et al. 1999

Neuropsychobiology

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The aim of this study was to determine platelet α₂-adrenergic receptor (α₂-AR) binding sites in fibromyalgia both before and after treatment with sertraline or placebo. The maximum number of binding sites (B_max) and their affinity (K_d) for [³H]rauwolscine, a selective α₂-AR antagonist, were measured in 13 normal volunteers and 22 fibromyalgia patients. Severity of illness was evaluated by means of the Hamilton Depression Rating Scale (HDRS) and dolorimetric assessments of tenderness at tender points. Fibromyalgia patients had repeated measurements of [³H]rauwolscine binding characteristics both before and after subchronic treatment with sertraline or placebo for 12 weeks. [³H]rauwolscine binding K_d values were significantly higher in fibromyalgia patients than in normal volunteers. There were significant inverse correlations between [³H]rauwolscine binding K_d values and duration of illness, age and lower energy. Significantly higher [³H]rauwolscine binding K_d values were found in fibromyalgia patients in an early phase of illness (<3 years) than in fibromyalgia patients with a protracted illness (>3 years). Repeated administration of sertraline had no significant effects on [³H]rauwolscine binding B_max or K_d values. The results suggest that fibromyalgia and, in particular, fibromyalgia in an early phase of illness, is accompanied by lowered affinity of platelet α₂-ARs.

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Coexisting dysregulations of both the sympathoadrenal system and hypothalamic-pituitary-adrenal-axis in melancholia

Cited by 39 publications

References 67 publications

Depression as a risk factor for the onset of type 2 diabetes mellitus. A meta-analysis

Depression as a risk factor for the onset of type 2 diabetes mellitus. A meta-analysis

Depression Symptoms and Antidepressant Medicine Use in Diabetes Prevention Program Participants

Changes in Platelet Alpha-2-Adrenoceptors in Fibromyalgia: Effects of Treatment with Antidepressants

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