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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- "Musculoskeletal and gastrointestinal disorders tended to be associated with mood disorders, although we speculate that the heterogeneous groupings we employed may have diluted associations in our sample population. Mood disorders and symptomology have previously been shown to be associated with low BMD and subsequent fracture, where both biological and medication related processes are thought to play a role . Similarly, mood disorders have been shown to be associated with gastrointestinal disorders in both clinical and population-based samples [72-74]. "
ABSTRACT: Background The mind-body nexus has been a topic of growing interest. Further data are however required to understand the specific relationship between mood and anxiety disorders and individual physical health conditions, and to verify whether these psychiatric disorders are linked to overall medical burden. Methods This study examined data collected from 942 men, 20 to 97 years old, participating in the Geelong Osteoporosis Study. A lifetime history of mood and anxiety disorders was identified using the Structured Clinical Interview for DSM-IV-TR Research Version, Non-patient edition (SCID-I/NP). The presence of medical conditions (lifetime) was self-reported and confirmed by medical records, medication use or clinical data. Anthropometric measurements and socioeconomic status (SES) were determined and information on medication use and lifestyle was obtained via questionnaire. Logistic regression models were used to test the associations. Results After adjustment for age, socioeconomic status, and health risk factors (body mass index, physical activity and smoking), mood disorders were associated with gastro oesophageal reflux disease (GORD), recurrent headaches, blackouts and/or epilepsy, liver disorders and pulmonary disease in older people, whilst anxiety disorders were significantly associated with thyroid, GORD and other gastrointestinal disorders, and psoriasis. Increased odds of high medical burden were associated with both mood and anxiety disorders. Conclusions Our study provides further population-based evidence supporting the link between mental and physical illness in men. Understanding these associations is not only necessary for individual management, but also to inform the delivery of health promotion messages and health care.BMC Medicine 04/2013; 11(1):110. DOI:10.1186/1741-7015-11-110 · 7.25 Impact Factor
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- "As such, both mood and anxiety disorders as well osteoporosis have been recognised as national health priorities in many countries. With few exceptions, an inverse relationship exists between mood disorders, symptoms and bone metabolism (Williams et al., 2009). A recent research synthesis with meta-analyses concluded that mood disorders should be considered a risk factor for osteoporosis , based on aggregated data showing an association with low bone density (Cizza et al., 2010). "
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; 146(3). DOI:10.1016/j.jad.2012.09.025 · 3.38 Impact Factor
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- "Many different medical disorders and conditions, which are associated with immuno-inflammatory and O&NS pathways, show a high comorbidity with depression: a) medical disorders, such as chronic obstructive pulmonary disease (COPD), cardiovascular disorder (CVD), chronic fatigue syndrome, obesity and the metabolic syndrome, rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD), psoriasis, osteoporosis, and diabetes type 1 and 2; b) neurodegenerative or neuroinflammatory disorders, such as Alzheimer's (AD), PD and Huntington's disease, multiple sclerosis (MS) and stroke; and c) conditions, such as hemodialysis, IFNα-based immunotherapy, and the postnatal period [25,163]. We have argued that these disorders/conditions are all accompanied by activation of immuno-inflammatory and O&NS pathways and therefore may cause the basic immune/inflammatory state which may lead to comorbid depression . "
ABSTRACT: It is of considerable translational importance whether depression is a form or a consequence of sickness behavior. Sickness behavior is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation. There are considerable phenomenological similarities between sickness behavior and depression, for example, behavioral inhibition, anorexia and weight loss, and melancholic (anhedonia), physio-somatic (fatigue, hyperalgesia, malaise), anxiety and neurocognitive symptoms. In clinical depression, however, a transition occurs to sensitization of immuno-inflammatory pathways, progressive damage by oxidative and nitrosative stress to lipids, proteins, and DNA, and autoimmune responses directed against self-epitopes. The latter mechanisms are the substrate of a neuroprogressive process, whereby multiple depressive episodes cause neural tissue damage and consequent functional and cognitive sequelae. Thus, shared immuno-inflammatory pathways underpin the physiology of sickness behavior and the pathophysiology of clinical depression explaining their partially overlapping phenomenology. Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, clinical depression, a lifelong disorder with positive feedback loops between (neuro)inflammation and (neuro)degenerative processes following less well defined triggers.BMC Medicine 06/2012; 10(1):66. DOI:10.1186/1741-7015-10-66 · 7.25 Impact Factor