Depression and Bone Metabolism A Review
ABSTRACT There are data to suggest low bone mineral density is disproportionately prevalent among those with psychiatric disorders. This paper aims to review the current evidence on the relationship between depression and bone mineral density, and identify potential mechanisms.
Relevant sources were identified from the Pubmed and Web of Science (ISI) databases from the first relevant publication in 1994 to the present, 2007, using a combination of key words and terms including depression, major depressive disorder, osteoporosis, bone mineral density, hypothalamic-pituitary-adrenal axis, cortisol, cytokines, leptin, antidepressants, selective serotonin reuptake inhibitors, smoking, alcohol, physical activity and diet. Reference lists of chosen articles were further reviewed for associated publications.
The possible association between psychiatric illness, in particular depression, and osteoporosis has been the subject of a growing body of research yielding various findings, although most identify some effect on bone. In addition to medication-related processes and/or modifiable lifestyle factors associated with mood disturbances, endocrine and immune alteration secondary to depression may play a pathogenetic role in bone metabolism.
Additional longitudinal studies, with the advantage of temporal sequencing, remain to be conducted, as well as research into potential mechanisms surrounding the association. Nevertheless, the current findings are of clinical relevance, given the health burden of both depression and osteoporosis.
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ABSTRACT: BACKGROUND: The common mental disorders are potential risk factors for low bone mass as a result of disease and/or medication-related processes. Quantitative heel ultrasound (QUS) is a portable and relatively cheap screening tool for determining fracture risk. Thus, we investigated the association between QUS parameters, mood and anxiety disorders in a population-based sample of 745 men and 897 women. METHODS: Using a clinical interview (SCID-I/NP), mood and anxiety disorders were identified. Bone quality was established using QUS and included the following parameters: Broadband Ultrasound Attenuation (BUA), Speed of Sound (SOS) and Stiffness Index (SI). Anthropometry, socio-economic status (SES), medication use and lifestyle factors were determined. RESULTS: In men, mood and anxiety disorders were associated with lower age-weight- and smoking-adjusted SOS, BUA and SI. In women, age was an effect modifier. Among younger women (≤40yr), mood disorders were associated with lower age-weight- and smoking-adjusted SOS and SI but not BUA. No differences were detected in older women or women with anxiety disorders. These patterns persisted after adjustment for activity, alcohol, calcium intake, SES and medications. LIMITATIONS: Cross-sectional study design, and possible residual or unrecognised confounding. CONCLUSION: Our data suggest that bone quality, as measured by QUS, is reduced among men and younger women with a history of mood disorders. Furthermore, an inverse association between anxiety disorders and bone quality was evident for men. Thus, QUS may be a useful screening tool for determining fracture risk within these populations.Journal of Affective Disorders 10/2012; DOI:10.1016/j.jad.2012.09.025 · 3.71 Impact Factor
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ABSTRACT: Psychiatric disorders may be risk factors for reduced bone mineral density (BMD). Longitudinal evidence is limited and this is yet to be examined among community-dwelling adults with anxiety. We aimed to investigate the cross-sectional and longitudinal relationships between anxiety and depressive symptoms and BMD. This study examined data from the second Nord-Trondelag Health Study (1995-1997; 1194 men and 7842 women) and a follow-up conducted in 2001 (697 men and 2751 women). Symptomatology was ascertained using the Hospital Anxiety and Depression Scale and BMD was measured at the forearm using single-energy X-ray absorptiometry. Information on medication use and lifestyle was self-reported, and these, together with anthropometric measures were tested in multivariate analyses. In men, adjusted BMD was 2.6% lower at the ultradistal forearm for those with depressive symptoms and 2.6% lower at the ultradistal and 2.0% lower at the distal forearm for those with anxiety symptoms. In women, adjusted BMD at the distal and ultradistal forearm was lower for heavier women with depressive symptoms but this relationship diminished with decreasing weight. Forearm BMD was similar for women with or without anxiety symptoms. Longitudinally, neither depressive nor anxiety symptoms were associated with bone loss over 4.6 years. Findings cannot be generalised to other skeletal sites and a longer follow-up period may be necessary to detect differences in bone loss. These results indicate that depressive and anxiety symptoms are cross-sectionally associated with reduced BMD. These findings provide further evidence to support monitoring BMD in individuals diagnosed with psychiatric illness.Journal of Affective Disorders 06/2011; 131(1-3):164-71. DOI:10.1016/j.jad.2010.11.019 · 3.71 Impact Factor
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ABSTRACT: Major depressive disorder is associated with progressive brain changes and is frequently comorbid with cardiovascular disease. There may be shared pathophysiological pathways between cerebral and myocardial dysfunction that impact on apoptosis related proteins. Our aim was to examine behaviour changes of rats with chronic mild stress (CMS), explore the expression of Bax and Bcl-xl in the hippocampus and myocardium, and additionally evaluate the effects of venlafaxine on these molecular mechanisms. Rats were randomly divided into three groups. The behaviour was assessed using the open field and sucrose consumption tests. Gene expression was measured by RT-PCR. In CMS, there was a significant reduction of movements and sucrose consumption, an increased Bax level and a decreased Bcl-xl level in both the hippocampus and myocardium. The venlafaxine group showed an increase in movements and sucrose consumption, as well as upregulated expression of Bcl-xl and downregulated expression of Bax in both the hippocampus and myocardium. These results demonstrate that in CMS, there is an increase in pro-apoptotic pathways that is reversed by venlafaxine. This suggests that there are shared active biochemical pathways that may play a role in the process of neuroprogression that is seen in depression and cardiovascular disorders.Human Psychopharmacology Clinical and Experimental 03/2011; 26(2):95-101. DOI:10.1002/hup.1177 · 1.85 Impact Factor