Longitudinal Relationship of Depressive and Anxiety Symptoms With Dyslipidemia and Abdominal Obesity.

Longitudinal Relationship of Depressive and Anxiety Symptoms With Dyslipidemia and Abdominal Obesity.

Filed under: Depression Treatment

Psychosom Med. 2012 Nov 28;
van Reedt Dortland AK, Giltay EJ, van Veen T, Zitman FG, Penninx BW

ObjectivePrevious research indicates that patients with severe symptoms of depression or anxiety are prone toward the development of dyslipidemia and abdominal obesity. We sought to study these associations longitudinally.MethodsAmong 2126 Netherlands Study of Depression and Anxiety participants, we studied whether severity of depressive (Inventory of Depressive Symptoms) or anxiety (Beck Anxiety Inventory) symptoms at baseline was associated with changes in lipids (i.e., total, high-density lipoprotein [HDL] or low-density lipoprotein cholesterol, and triglycerides) or waist circumference during a 2-year follow-up period. We also examined whether changes in severity of symptoms were associated with changes in lipid or waist circumference levels over these 2 years. Multivariate linear regression analyses were adjusted for age, sex, education, and tobacco consumption.ResultsBaseline symptoms of depression or anxiety predicted a decrease in HDL cholesterol (adjusted ? = -.062 [p = .003] and ? = -.050 [p = .02], respectively) and an increase in waist circumference (adjusted ? = .060 [p = .01] and ? = .053 [p = .02], respectively) for 2 years. Reduction of symptoms of depression or anxiety over time did not coincide with an amelioration of lipid or waist circumference values.ConclusionsPeople with initially severe symptoms of depression or anxiety showed a subsequent decrease in HDL cholesterol levels and an increase in abdominal obesity over time, independent of a potential reduction in symptom severity in this period. Therefore, such people are at elongated and increasing risk for dyslipidemia and obesity, predisposing them to cardiovascular disease.
HubMed – depression

Prospective Examination of Anxiety and Depression Before and During Confirmed and Pseudoexacerbations in Patients With Multiple Sclerosis.

Filed under: Depression Treatment

Psychosom Med. 2012 Nov 28;
Burns MN, Nawacki E, Siddique J, Pelletier D, Mohr DC

ObjectiveThis study was designed to determine whether pseudoexacerbations and confirmed MS exacerbations are preceded by or concurrent with increased anxiety or depressive symptoms.MethodsThis was a secondary analysis of 121 patients with MS who were observed for 48 weeks during a randomized controlled trial. Participants completed monthly self-reports on depressive and anxiety symptoms. Patient-reported exacerbations were assessed through a telephone-administered symptom checklist and neurologic examination.ResultsBoth pseudoexacerbations and confirmed exacerbations were associated with concurrent somatic depressive (? = .16 and ? = .33, respectively; p values < .05), affective depressive (? = .17 [p = .02] and ? = .12 [p = .06]), and anxiety symptoms (? = .24 and ? = .20, p values < .01), controlling for baseline symptoms. Preexisting somatic and affective depressive symptoms predicted amplified relationships between concurrent confirmed exacerbations and these symptoms (? = .19 and ? = .20, respectively; p values < .01). A standard deviation increase in anxiety symptoms relative to baseline predicted subsequent onset of pseudoexacerbations (odds ratio = 1.54, p = .02), whereas increased somatic depressive symptoms predicted confirmed exacerbations (odds ratio = 1.59, p = .01).ConclusionsPatients with MS experiencing pseudoexacerbations or confirmed exacerbations should be assessed and monitored for depressive and anxiety symptoms, and confirmed exacerbations are particularly concerning in patients with a history of depression. The psychological or psychiatric antecedents of MS exacerbations generate new hypotheses on etiologies of confirmed exacerbations and pseudoexacerbations. Trial Registration: clinicaltrials.gov Identifier: NCT00147446. HubMed – depression

Beta Amyloid-Induced Depression of Hippocampal Long-Term Potentiation Is Mediated through the Amylin Receptor.

Filed under: Depression Treatment

J Neurosci. 2012 Nov 28; 32(48): 17401-6
Kimura R, Mactavish D, Yang J, Westaway D, Jhamandas JH

Alzheimer’s disease (AD) is characterized by accumulation of amyloid-? peptide (A?) in the brain regions that subserve memory and cognition. The amylin receptor is a potential target receptor for expression of the deleterious actions of soluble oligomeric A? species. We investigated whether the amylin receptor antagonist, AC253, neutralizes the depressant effects of A?(1-42) and human amylin on hippocampal long-term potentiation (LTP). Furthermore, we examined whether depressed levels of LTP observed in transgenic mice, which overexpress amyloid precursor protein (TgCRND8), could be restored with AC253. In mouse hippocampal brain slices, field EPSPs were recorded from the stratum radiatum layer of the CA1 area (cornu ammonis 1 region of the hippocampus) in response to electrical stimulation of Schaeffer collateral afferents. LTP was induced by 3-theta burst stimulation protocols. A?(1-42) (50 nm) and human amylin (50 nm), but not A?(42-1) (50 nm), depressed LTP evoked using both stimulation protocols. Preapplication of AC253 (250 nm) blocked A?- and human amylin-induced reduction of LTP without affecting baseline transmission or LTP on its own. In contrast to wild-type controls, where robust LTP is observed, 6- to 12-month-old TgCRND8 mice show blunted LTP that is significantly enhanced by application of AC253. Our data demonstrate that the effects of A?(1-42) and human amylin on LTP are expressed via the amylin receptor, and moreover, blockade of this receptor increases LTP in transgenic mice that show increased brain amyloid burden. Amylin receptor antagonists could serve as potentially useful therapeutic agents in AD.
HubMed – depression

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