Review: Depression. An Important Comorbidity with Metabolic Syndrome in a General Population
The reviewed article is ‘Depression: An important comorbidity with metabolic syndrome in a general population’ by Dunbar and colleagues from 2008 and freely available here. In the abstract the authors conclude that
‘Metabolic syndrome was associated with depression but not psychological distress or anxiety‘
So is it possible on the basis of this study to draw the above conclusions. The researchers completed three cross-sectional studies in rural Australia. The first thing to say is that as the study was conducted in rural Australia the findings might be specific for this population. It seems more likely that this should be generalisable. However if we consider urban versus rural settings for instance a number of other factors come into play ranging from the structure of health service provision through to social networks and lifestyle which might influence either metabolic syndrome or depression or both. Men and women ‘aged 25 to 84 years were selected from the electoral roll’ by a random sampling method. I couldn’t find a reference to the type of random sampling method that was used but it is reasonable to suppose that there was no obvious selection bias as a result other than the self-selection that results from participation. The authors do note however that the study did not include those that had left the region and this is relevant in the context of the above point about urban versus rural settings. The researchers identify a number of outcome measures including psychosocial factors and factors relevant to the diagnosis of metabolic syndrome such as fasting glucose and waist and hip circumference. The criteria for metabolic syndrome were clearly identified. The researchers also used the Hospital Anxiety and Depression Scale, a commonly used scale which aids the assessment of depression in the hospital population. However the authors also used the ‘Kessler 10 measure’ which I wasn’t familiar with and describe it as a five-point likert scale where cumulative scores result in categorisation into low and moderate-high levels of ‘psychological distress’ in the last 4-weeks. The internal consistency values for K10 and the HADS subcomponents were provided ranging from 0.79 to 0.87. The primary outcome measures (or at least I presume they were the primary outcome measures) were clearly stated and the author examined the relationship between anxiety, depression and the metabolic syndrome. The statistical analysis of other relationships between the many variables that were used in the study was also clearly stated. 409 subjects met the criteria for the metabolic syndrome and a comparison was then made between those with and without the metabolic syndrome. I didn’t particularly understand the following within the results section
‘Participants with the metabolic syndrome were more likely to have moderate to severe depression (10 vs 6.9%, p = 0.069)‘
In the remainder of the sentence the authors write that with regards to another measure there was no statistical significance. However the p value above would not be significant either (at the 5% level). However the researchers did find a significant difference between metabolic syndrome and the diagnosis of depression (i.e. without reference to specific subtypes such as moderate or severe) and this time the difference reached a significance of 0.013 and depression scores were 3.41 versus 2.95. Thus there is a mean difference of roughly 1.5 points on the HADS depression subscale (I presume that it was this subscale although not stated explicitly in the sentence) at the group level.
So the relationship appears significant but the direction of this relationship is unclear as it was a cross-sectional study. A longitudinal study might be able to shed light on the directionality of the relationship. The authors speculate that an inflammatory pathway might mediate the link between depression and the metabolic syndrome.
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Review: Valproate and Neuroprotection
The article reviewed here is ‘Valproate and Neuroprotection Effects for Bipolar Disorder’ by Murad Atmaca. This is a brief review looking at the potential neuroprotective effects of Valproate in Bipolar Disorder (BPaD). There is no stated methodology for this review. The author considers the evidence for BPaD as a neurodegenerative process by focusing briefly on one study showing a reduction in glial cells in area 9. There is then a look at Proton Magnetic Resonance Spectroscopy imaging studies which allow visualisation of cell components (e.g. choline-containing compounds which are found in neurons and glial cells). Atmaca then focuses on one of these compounds – N-acetylsaspartate (which is found in neurons alone) and builds the argument for suggesting that this may not primarily be a proxy marker for neuronal structural integrity one of the assumptions made in the literature as there is a reversibility in lowered NAA levels. However in order to progress, a decision has to be made about what NAA does represent and Atmaca seems to settle on the conclusion that lowered levels of NAA are equivalent to a loss of neurons or related losses (e.g. loss of axonal function). Using this assumption, Atmaca then looks at some of the MRS research in BPaD and notes that in one study the ratio NAA/CHO was lower in controls compared to those on a combination of Quetiapine and Valproate. There is then further indirect evidence of a protective effect of valproate against excitoxicity. A number of cellular mechanisms are then considered – effectively Atmaca attempts to outline some possible pathways through which any such effects might occur before finishing with a look at some evidence of reduced brain volume reduction with Valproate. Although cellular mechanisms would be expected to form the basis for drug effects, the more convincing evidence for drug effects come from sufficiently powered longitudinal randomised-controlled trials preferably over a reasonably long time period. However, this paper is concise and Atmaca puts some pieces of the jigsaw puzzle together although time and further evidence will tell if these are the right pieces.
References
Atmaca M. Valproate and neuroprotective effects for bipolar disorder. International Review of Psychiatry. August 2009. 21(4). 410-413.
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The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.
