Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ankylosing spondylitis (AS) is a systemic chronic inflammatory disease primarily affecting the axial skeleton. Work disability can be one of the major consequences of AS, and the knowledge about the burden of AS to the patient and society is not well-established yet. The objective of this study was to investigate work disability among patients with AS in the national service and to put forward the related factors and differences among disabled and nondisabled groups. A total of 121 male AS patients were included in the study. Patient demographics and duration of disease were noted, and employment status and disability were questioned. Measures of functionality, axial mobility, health-related quality of life, and depression were used. It was found that 38 patients (31.4%) continued their work lives with no change, 54 patients (44.6%) changed to a lighter job, and 29 patients (24%) were retired due to AS. Differences in age at onset of the disease, time since the diagnosis, C-reactive protein (CRP) levels, and hip involvement were statistically significant. The mean retirement age of the patients was 36 +/- 4.2 years. Frequency of hip involvement was higher in the work-disabled group. Spine was evidently affected more seriously, and CRP values were higher in the work-disabled group. Older age at onset, longer time since the diagnosis, longer diagnosis delay, and some physical impairments like decrease in spinal mobility and hip involvement may preclude AS patients from leading a productive work life.
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PMID:Work disability in ankylosing spondylitis: differences among working and work-disabled patients. 1968 94

Although many studies have found psychological depression associated with higher circulating levels of C-reactive protein (CRP), not all findings are consistent. Since DNA sequence variation in the CRP gene has also been shown to predict plasma CRP levels, we hypothesized that plasma CRP may covary with depressive symptomatology as a function of allelic variation in the CRP gene. We tested this hypothesis in 868 healthy community volunteers of European ancestry. Depressive symptomatology was measured using the Center for Epidemiological Studies-Depression (CESD) scale, and plasma CRP was assayed from whole blood. Three polymorphisms [rs1417938 (A/T), rs1800947 (C/G) and rs1205 (C/T)] were genotyped and three-locus haplotypes were generated. Regression models adjusting for demographic and lifestyle-related covariates showed no direct association of CESD depression scores with CRP. In regression models adjusting for age, gender, education, smoking status and statin use, one CRP haplotype (T-G-C) was associated with CRP level (p=0.014) and a second haplotype (A-G-T) showed marginal association (p=0.064, respectively). Neither haplotype was related to depressive symptoms. However, plasma CRP was predicted by the interaction of A-G-T haplotype with depressive symptomatology (p=0.009). Higher CESD scores were associated positively with CRP levels among individuals with the A-G-T haplotype (p=0.004). In secondary analyses, body mass index was found to partially account for the moderating effects of the A-G-T haplotype on the association of depression with circulating CRP. In conclusion, we found that haplotypic variation in the CRP locus moderates an association of depressive symptoms with circulating CRP, which is partially mediated by BMI.
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PMID:Polymorphisms in the CRP gene moderate an association between depressive symptoms and circulating levels of C-reactive protein. 1979 76

Previous studies have demonstrated increased levels of serum markers of systemic inflammation and immune system function among individuals with depressive symptoms. Despite these observations, the biological mechanisms behind this association remain elusive. The objective of the present analysis was to examine the individual and joint associations of white blood cell counts, platelet counts, and C-reactive protein with depression severity and to determine whether oxidative stress might mediate these associations. We conducted an analysis of 3867 subjects from the 2005-2006 National Health and Nutritional Examination Survey. Ordinal logistic regression was used to assess associations between three levels of depression symptom severity (as measured by the nine-item Patient Health Questionnaire) and serum C-reactive protein, white blood cell counts, platelet counts, and four surrogate markers of oxidative stress. Covariates included sex, age, smoking status, physical activity, education, poverty to income ratio, as well as medication use and medical conditions influencing inflammation levels. In separate models, the risk of moderate to severe depression was significantly greater in the highest quartiles of CRP (OR=1.84. 95 percent confidence interval (CI)=1.35-2.52), WBC (OR=1.70, CI=1.31-2.19), and platelet counts (OR=1.41, CI=1.13-1.76) after adjusting for basic sociodemographic and behavioral factors. After additional adjustment for medication use and oxidative stress surrogate measures, the highest quartile of WBC counts remained associated with depression (OR=1.60, CI=1.23-2.09). Adjustment for oxidative stress measures did not substantially affect estimated associations of inflammation/immunologic markers. In summary, we observed significantly elevated white blood cell counts among subjects with moderate and severe depression, and oxidative stress and a medical history of inflammatory diseases do not appear to mediate this association. Although limited through its use of cross-sectional data, this is the first analysis to simultaneously consider immunologic and oxidative stress markers. Further research is needed to identify the biological basis for this persistent association.
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PMID:Associations between immunologic, inflammatory, and oxidative stress markers with severity of depressive symptoms: an analysis of the 2005-2006 National Health and Nutrition Examination Survey. 1985 25

High levels of pro-inflammatory biomarkers have been reported in depression. In the present study, five pro-inflammatory biomarkers were measured in the blood of patients with major depressive disorder (MDD). Biomarker levels were compared to age- and sex-matched healthy subjects. Patients with MDD had significantly higher baseline levels of tumour necrosis factor-alpha (TNFalpha, P=0.04), interleukin-1beta (IL1beta, P=0.03), and monocyte chemotactic protein-1 (MCP-1; P=0.02) compared to controls. There were no differences between groups in levels of cell determinant-40 ligand (CD40L) and C-reactive protein (CRP). A subset of the MDD patients consented to undergo treatment with venlafaxine (an SNRI: at lower doses a selective serotonin reuptake inhibitor; at higher doses also a norepinephrine reuptake inhibitor) for 8 weeks. By week 8, all treatment completers had responded therapeutically. However, levels of TNFalpha, IL1beta, and MCP-1 remained elevated. A concave quadratic equation described the associations between plasma venlafaxine concentrations and IL1beta (P=0.03), TNFalpha (P=0.09), and MCP-1 (P=0.02), suggesting that these biomarkers may have become selectively lowered in the serotonergic dose range of venlafaxine. This is the first report of venlafaxine's possible effect on pro-inflammatory biomarkers.
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PMID:Pro-inflammatory biomakers in depression: treatment with venlafaxine. 1992 73

Physiological changes during gestation and after delivery are associated with postpartum thyroid dysfunction, which is due to thyroid autoimmunity in some cases. Postpartum thyroid dysfunction, in turn, has been associated with postpartum depression (PPD). The aim of the present study was to evaluate whether thyroid function immediately after delivery can predict postpartum depression at 8 weeks and 32 weeks after delivery. This study examined 1053 postpartum Spanish women without a previous history of depression. We evaluated depressive symptoms at 48h, 8 weeks and 32 weeks postpartum and used a diagnostic interview to confirm major depression for all probable cases. Free thyroxin (fT4), thyroid-stimulating hormone (TSH), thyroid peroxidase antibodies (TPOAb) and C-reactive protein (CRP) were assayed at 48h postpartum. Binary and multivariate logistic regression analyses were performed to determine independent risk factors for PPD. Although 152 women (14.4%) had high TPOAb (>27IU/mL) and slightly elevated TSH concentrations with normal fT4, we did not find any association between thyroid function and PPD. This thyroid dysfunction was not associated with CRP concentrations that were outside of the normal range (>3mg/L). We conclude that thyroid function at 48h after delivery does not predict PPD susceptibility.
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PMID:Thyroid function 48h after delivery as a marker for subsequent postpartum depression. 1993 74

Depression is associated with dysregulated hypothalamic-pituitary-adrenal (HPA) axis function, overactivity of the sympathoadrenal system, and increased levels of inflammation markers. It is not known whether these biological processes are disproportionately elevated in response to acute negative emotional arousal by mental stress (MS). The present study investigates responses of neurohormones and inflammatory markers to MS in 14 clinically depressed (age: 42+/-10 years; 50% female) and 14 non-depressed control (age: 39+/-6 years; 50% female) participants. Heightened acute MS reactivity was documented in depressed participants (adrenocorticotropic hormone, rho=0.001; norepinephrine, rho=0.042; epinephrine, rho=0.039), and a delayed increase in cortisol was observed (rho=0.002). Inflammation markers increased more strongly in depressed versus non-depressed participants (IL-6, rho=0.027; tumor necrosis factor-alpha, rho=0.050; and recovery C-reactive protein, rho=0.003). It is concluded that depressed individuals display hyper-reactivity of neuroimmunological markers in response to acute negative emotions. This hyper-reactivity may serve a pathologic role in the elevated morbidity and mortality risk associated with depression.
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PMID:Neurohormonal and inflammatory hyper-responsiveness to acute mental stress in depression. 2011 67

Abstract Background. High levels of high-sensitivity C-reactive protein (hs-CRP) are associated with depressed mood, but the causal relationships are not known. Therefore, we examined the relationships between hs-CRP and incident depressed mood among the elderly. Methods. Altogether 764 (69%) individuals out of a representative sample of subjects aged 70 years or older (N = 1113) were screened with the Short Zung Self Rating Depression Scale (SZSRDS), and serum hs-CRP determinations were done at the same time. After a two-and-a-half-year follow-up, the SZSRDS examinations were repeated among those who were free of depressed mood (SZSRDS score >or=28 or use of an anti-depressant drug) at the baseline (N = 404). Analysis of covariance (ANCOVA) and logistic regression were used to analyse the relationship between the baseline hs-CRP (<1, 1 < 3, 3 <10 mg/L) and the follow-up SZSRDS scores (10-40) and depressed mood. Results. Baseline hs-CRP was not associated with an increasing trend in SZSRDS scores and depressed mood in the total study population, but there was a significant gender interaction. Among the men, elevated hs-CRP was associated with an increasing trend in the SZSRDS score and depressed mood. Conclusions. High hs-CRP predicts a higher incident SZSRDS score and depressed mood among older men, suggesting a possible inflammatory etiology for depression.
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PMID:The relationships between high-sensitivity C-reactive protein and incident depressed mood among older adults. 2017 Feb 91

To identify genetic factors that interact with social environments to impact human health, we used a bioinformatic strategy that couples expression array-based detection of environmentally responsive transcription factors with in silico discovery of regulatory polymorphisms to predict genetic loci that modulate transcriptional responses to stressful environments. Tests of one predicted interaction locus in the human IL6 promoter (SNP rs1800795) verified that it modulates transcriptional response to beta-adrenergic activation of the GATA1 transcription factor in vitro. In vivo validation studies confirmed links between adverse social conditions and increased transcription of GATA1 target genes in primary neural, immune, and cancer cells. Epidemiologic analyses verified the health significance of those molecular interactions by documenting increased 10-year mortality risk associated with late-life depressive symptoms that occurred solely for homozygous carriers of the GATA1-sensitive G allele of rs1800795. Gating of depression-related mortality risk by IL6 genotype pertained only to inflammation-related causes of death and was associated with increased chronic inflammation as indexed by plasma C-reactive protein. Computational modeling of molecular interactions, in vitro biochemical analyses, in vivo animal modeling, and human molecular epidemiologic analyses thus converge in identifying beta-adrenergic activation of GATA1 as a molecular pathway by which social adversity can alter human health risk selectively depending on individual genetic status at the IL6 locus.
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PMID:Computational identification of gene-social environment interaction at the human IL6 locus. 2017 30

Anxiety confers increased risk for inflammatory diseases, and elevated inflammatory activity in anxious individuals may contribute to this increased risk. One complication, however, is that anxiety could be associated with inflammatory activity either through a specific anxiety pathway or through a more general negative emotionality pathway. To investigate, we measured levels of the stress hormone cortisol, the pro-inflammatory cytokine interleukin-6 (IL-6), and the systemic inflammatory marker C-reactive protein (CRP), as well as depression and neuroticism, in clinically anxious and non-anxious adults. Compared with non-anxious participants, clinically anxious participants exhibited significantly lower levels of morning cortisol and significantly higher levels of IL-6, independent of age, sex, and depressive symptoms. These group differences were robust when controlling for neuroticism. Conversely, the groups had equivalent levels of CRP in all analyses. Results are indicative of anxiety-specific effects on inflammatory activity, and highlight a pathway by which anxiety may increase risk for inflammatory diseases.
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PMID:Clinical anxiety, cortisol and interleukin-6: evidence for specificity in emotion-biology relationships. 2022 85

Obesity and related metabolic conditions are of epidemic proportions in most of the world, affecting both adults and children. The accumulation of lipids in the body in the form of white adipose tissue in the abdomen is now known to activate innate immune mechanisms. Lipid accumulation causes adipocytes to directly secrete the cytokines interleukin (IL) 6 and tumor necrosis factor alpha (TNFalpha), but also monocyte chemoattractant protein 1 (MCP-1), which results in the accumulation of leukocytes in fat tissue. This sets up a chronic inflammatory state which is known to mediate the association between obesity and conditions such as cardiovascular disease, type 2 diabetes, and cancer. There is also a substantial literature linking inflammation with risk for depression. This includes the observations that: (1) people with inflammatory diseases such as multiple sclerosis, cardiovascular disease, and psoriasis have elevated rates of depression; (2) many people administered inflammatory cytokines such as interferon alpha develop depression that is indistinguishable from depression in non-medically ill populations; (3) a significant proportion of depressed persons show upregulation of inflammatory factors such as IL-6, C-reactive protein, and TNFalpha; (4) inflammatory cytokines can interact with virtually every pathophysiologic domain relevant to depression, including neurotransmitter metabolism, neuroendocrine function, and synaptic plasticity. While many factors may contribute to the association between inflammatory mediators and depression, we hypothesize that increased adiposity may be one causal pathway. Mediational analysis suggests a bi-directional association between adiposity and depression, with inflammation possibly playing an intermediary role.
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PMID:Eating ourselves to death (and despair): the contribution of adiposity and inflammation to depression. 2041 47


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