Journal articles: 'Metabolic depression'

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Vogelzangs, Nicole, Aartjan T. F. Beekman, Ingrid G. Boelhouwer, Stefania Bandinelli, Yuri Milaneschi, Luigi Ferrucci, and Brenda W. J. H. Penninx. "Metabolic Depression." Journal of Clinical Psychiatry 72, no. 05 (April 5, 2011): 598–604. http://dx.doi.org/10.4088/jcp.10m06559.

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Lamers, F., Y. Milaneschi, P. de Jonge, E. J. Giltay, and B. W. J. H. Penninx. "Metabolic and inflammatory markers: associations with individual depressive symptoms." Psychological Medicine 48, no. 7 (September 11, 2017): 1102–10. http://dx.doi.org/10.1017/s0033291717002483.

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AbstractBackgroundLiterature has shown that obesity, metabolic syndrome and inflammation are associated with depression, however, evidence suggests that these associations are specific to atypical depression. Which of the atypical symptoms are driving associations with obesity-related outcomes and inflammation is unknown. We evaluated associations between individual symptoms of depression (both atypical and non-atypical) and body mass index (BMI), metabolic syndrome components and inflammatory markers.MethodsWe included 808 persons with a current diagnosis of depression participating in the Netherlands Study of Depression and Anxiety (67% female, mean age 41.6 years). Depressive symptoms were derived from the Composite International Diagnostic Interview and the Inventory of Depressive Symptomatology. Univariable and multivariable regression analyses adjusting for sex, age, educational level, depression severity, current smoking, physical activity, anti-inflammatory medication use, and statin use were performed.ResultsIncreased appetite was positively associated with BMI, number of metabolic syndrome components, waist circumference, C-reactive protein and tumor necrosis factor-α. Decreased appetite was negatively associated with BMI and waist circumference. Psychomotor retardation was positively associated with BMI, high-density lipoprotein cholesterol and triglycerides, and insomnia with number of metabolic syndrome components.ConclusionIncreased appetite – in the context of a depressive episode – was the only symptom that was associated with both metabolic as well as inflammatory markers, and could be a key feature of an immuno-metabolic form of depression. This immuno-metabolic depression should be considered in clinical trials evaluating effectiveness of compounds targeting metabolic and inflammatory pathways or lifestyle interventions.

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Fauziyati, Ana, Agus Siswanto, Luthfan Budi Purnomo, and Hemi Sinorita. "Type of psychosocial stressor as risk factor of depressive symptom in metabolic syndrome." Bangladesh Journal of Medical Science 15, no. 2 (August 10, 2016): 262–68. http://dx.doi.org/10.3329/bjms.v15i2.28867.

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Metabolic syndrome and depression are two major diseases over the world, which are increasing in prevalence over time. Depression is a major mental health burden over the world. In long time, depression can lead to metabolic syndrome, while metabolic syndrome is a risk factor for developing depression. Metabolic syndrome is a major risk factor for developing cardiovascular disease. Chronic stress induced by psychosocial stressor leads to the development of both metabolic syndrome and depression. Further research is important to identify which type of psychosocial stressor is the risk factor for depressive symptom in patients with metabolic syndrome. The objective of this study is to identify the type of psychosocial stressor which could be the risk factor for depressive symptom. The study design was case control. The case group consisted of metabolic syndrome patients with depressive symptom, while the control group consisted of metabolic syndrome patients without depressive symptom. Metabolic syndrome was diagnosed based on International Diabetes Federation (IDF) criteria. Depressive symptom was measured by Beck Depression Inventory (BDI). Psychosocial stressors were measured by Stressful Life Events (SLE) questionnaire. Dependent variable was depressive symptom, while independent variables were type of psychosocial stressors (finance, work, social relationship, health and housing). Analysis methods that used in this study were independent t test, Pearson/Spearman correlation analysis, chi square and logistic regression. There were 54 patients in this study, consisted of 24 in case group and 30 in control group. There was no significant difference in most basic characteristics between two groups. There was significant difference of SLE score between two groups. Chi square analysis showed that housing, finance, health, social relationship, and work stressors were risk factors for developing depressive symptom in metabolic syndrome (OR 24.5 (p 0.001); 9.7 (p 0.039); 8.4 (p 0.016); 5.4 (p 0.004); 3.9 (p 0.001), respectively). Demographic factor which also influenced depressive symptom was salary less than 1 million per month (OR 45, p 0.004). According to logistic regression analysis, psychosocial stressors which most influenced the depressive symptom were finance and housing. In conclusion, this study showed that housing, finance, health, social relationship and work stressors were risk factors for developing depressive symptom in metabolic syndrome.Bangladesh Journal of Medical Science Vol.15(2) 2016 p.262-268

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Heiskanen, Tuula H., Leo K. Niskanen, Jukka J. Hintikka, Heli T. Koivumaa-Honkanen, Kirsi M. Honkalampi, Kaisa M. Haatainen, and Heimo T. Viinamäki. "Metabolic Syndrome and Depression." Journal of Clinical Psychiatry 67, no. 09 (September 15, 2006): 1422–27. http://dx.doi.org/10.4088/jcp.v67n0913.

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Heuser, I. "Metabolic syndrome and depression." Journal of Affective Disorders 107 (March 2008): S24—S25. http://dx.doi.org/10.1016/j.jad.2007.12.158.

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Gary, Tiffany L., Kesha Baptiste-Roberts, Rosa M. Crum, Lisa A. Cooper, Daniel E. Ford, and Frederick L. Brancati. "Changes in Depressive Symptoms and Metabolic Control over 3 Years among African Americans with Type 2 Diabetes." International Journal of Psychiatry in Medicine 35, no. 4 (December 2005): 377–82. http://dx.doi.org/10.2190/bq22-4hu0-p6ek-l7yx.

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Objective: It is established that individuals with diabetes have high rates of depression, but the longitudinal relationship between depression and glycemic control has not been well examined, particularly among African Americans. The objective of this study was to evaluate the longitudinal relationship between depressive symptoms and metabolic control. Method: We conducted an earlier cross-sectional study that demonstrated marginal and significant associations between depressive symptoms (using the Center for Epidemiologic Studies Depression Scale [CES-D]) and metabolic control (HbA1c, lipids, blood pressure) among 183 African Americans with type 2 diabetes. In this report, we present data on these individuals, followed for three years, and examine the relationship between change in depressive symptoms and change in metabolic control over that time period. Results: Results showed that that there were no statistically significant associations between baseline or change in depressive symptoms and metabolic control over three years. Limited statistical power may explain this negative finding. Conclusions: This study provides insight into the relationship between depression and metabolic control. Prospective observational studies are needed to further evaluate this relationship.

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Flores-Ramos, Mónica, Martín Armando Burrola-Suárez, Rodrigo Guiza-Zayas, J. Miguel Enciso-Araujo, Dannia Islas-Preciado, and Erika Estrada Camarena. "Evaluation of hormonal and metabolic factors related to depression in reproductive age women." Salud mental 43, no. 1 (January 30, 2020): 35–41. http://dx.doi.org/10.17711/sm.0185-3325.2020.006.

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Introduction. Major depressive disorder (MDD) is a prevalent disease affecting women more than men worldwide. Various factors are involved in the genesis of depression, including hormones such as testosterone and certain metabolic factors Objective. To evaluate hormone levels and metabolic variables in women with major depression and healthy controls. Method. A cross-sectional, comparative analytical study was conducted in 40 participants, 23 patients with an MDD diagnosis and 17 controls, all of women in reproductive age between the ages of 18 and 45. Sociodemographic variables, hormonal profile, and metabolic variables were assessed and the 17-item Hamilton Depression Scale was used to evaluate depressive symptoms. Results. No statistically significant differences were observed between the groups in the hormonal and metabolic variables explored. Nevertheless, it was observed that the lower the testosterone levels and the higher the serum glucose levels, the more intense depressive symptoms were. Discussion and conclusion. Testosterone is associated with a lower depressive symptoms score on the Hamilton Depression scale, suggesting a potential antidepressant effect, whereas high glucose levels are associated with a higher score on this scale. We believe that the measurement of hormonal and metabolic variables in women can contribute to a better understanding of the pathophysiology of depression.

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Marijnissen, R. M., N. Vogelzangs, M. E. Mulder, R. H. S. van den Brink, H. C. Comijs, and R. C. Oude Voshaar. "Metabolic dysregulation and late-life depression: a prospective study." Psychological Medicine 47, no. 6 (December 12, 2016): 1041–52. http://dx.doi.org/10.1017/s0033291716003196.

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BackgroundDepression is associated with the metabolic syndrome (MS). We examined whether metabolic dysregulation predicted the 2-year course of clinical depression.MethodA total of 285 older persons (⩾60 years) suffering from depressive disorder according to DSM-IV-TR criteria was followed up for 2 years. Severity of depression was assessed with the Inventory of Depressive Symptomatology (IDS) at 6-month intervals. Metabolic syndrome was defined according the National Cholesterol Education Programme (NCEP-ATP III). We applied logistic regression and linear mixed models adjusted for age, sex, years of education, smoking, alcohol use, physical activity, somatic co-morbidity, cognitive functioning and drug use (antidepressants, anti-inflammatory drugs) and severity of depression at baseline.ResultsMS predicted non-remission at 2 years (odds ratioper component = 1.26, 95% confidence interval 1.00–1.58), p = 0.047), which was driven by the waist circumference and HDL cholesterol. MS was not associated with IDS sum score. Subsequent analyses on its subscales, however, identified an association with the somatic symptom subscale score over time (interaction time × somatic subscale, p = 0.005), driven by higher waist circumference and elevated fasting glucose level.ConclusionsMetabolic dysregulation predicts a poor course of late-life depression. This finding supports the concept of ‘metabolic depression’, recently proposed on population-based findings of a protracted course of depressive symptoms in the presence of metabolic dysregulation. Our findings seem to be driven by abdominal obesity (as indicated by the waist circumference) and HDL cholesterol dysregulation.

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John, George, Mona Asghari, Vipin VP, and Valsamma Eapen. "Depression and Metabolic Syndrome: Two Sides of the Same Coin." Journal of Biomedical and Clinical Research 12, no. 1 (July 1, 2019): 3–9. http://dx.doi.org/10.2478/jbcr-2019-0001.

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Summary This aim of this review was to examine the relationship between metabolic syndrome (MetS) and depression, which is complex and multifaceted with many inter-related factors includinggenetics, lifestylefactors, environmentalfactorsand other psychological factors at play. There is some evidence to suggest that depression may lead to the development of cardiovascular disease through its association with MetS. It has also been suggested that depressive symptoms may be a consequence rather than the cause of the MetS, as obesity and dyslipidemia have been shown as predictive of depressive symptoms. Thus, the relationship between MetS and depression seems to be a two-way street and bi-directional just as the two sides of the same coin.

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Olvera, Rene L., Douglas E. Williamson, Susan P. Fisher-Hoch, Kristina P. Vatcheva, and Joseph B. McCormick. "Depression, Obesity, and Metabolic Syndrome." Journal of Clinical Psychiatry 76, no. 10 (October 21, 2015): e1300-e1305. http://dx.doi.org/10.4088/jcp.14m09118.

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Weber, Bettina, Michael Deuschle, Michael Colla, Florian Lederbogen, and Isabella Heuser. "Major depression and metabolic syndrome." Psychoneuroendocrinology 25 (January 2000): S32. http://dx.doi.org/10.1016/s0306-4530(00)90123-9.

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Marazziti, Donatella, Grazia Rutigliano, Stefano Baroni, Paola Landi, and Liliana Dell'Osso. "Metabolic syndrome and major depression." CNS Spectrums 19, no. 4 (October 8, 2013): 293–304. http://dx.doi.org/10.1017/s1092852913000667.

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Major depression is associated with a 4-fold increased risk for premature death, largely accounted by cardiovascular disease (CVD). The relationship between depression and CVD is thought to be mediated by the so-called metabolic syndrome (MeS). Epidemiological studies have consistently demonstrated a co-occurrence of depression with MeS components, ie, visceral obesity, dyslipidemia, insulin resistance, and hypertension. Although the exact mechanisms linking MeS to depression are unclear, different hypotheses have been put forward. On the one hand, MeS could be the hallmark of the unhealthy lifestyle habits of depressed patients. On the other, MeS and depression might share common alterations of the stress system, including the hypothalamus–pituitary–adrenal (HPA) axis, the autonomic nervous system, the immune system, and platelet and endothelial function. Both the conditions induce a low grade chronic inflammatory state that, in turn, leads to increased oxidative and nitrosative (O&NS) damage of neurons, pancreatic cells, and endothelium. Recently, neurobiological research revealed that peripheral hormones, such as leptin and ghrelin, which are classically involved in homeostatic energy balance, may play a role in mood regulation. Metabolic risk should be routinely assessed in depressed patients and taken into account in therapeutic decisions. Alternative targets should be considered for innovative antidepressant agents, including cytokines and their receptors, intracellular inflammatory mediators, glucocorticoids receptors, O&NS pathways, and peripheral mediators.

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Guppy, M., C. J. Fuery, and J. E. Flanigan. "Biochemical principles of metabolic depression." Comparative Biochemistry and Physiology Part B: Comparative Biochemistry 109, no. 2-3 (October 1994): 175–89. http://dx.doi.org/10.1016/0305-0491(94)90001-9.

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Shaffer, Clare, Christiana Westlin, Susan Whitfield-Gabrieli, and Lisa Feldman Barrett. "Metabolic Classification of Adolescent Depression." Biological Psychiatry 87, no. 9 (May 2020): S414. http://dx.doi.org/10.1016/j.biopsych.2020.02.1056.

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Slater, Natasha, Charlotte Rowley, Rebecca Hayley Venables, Simon White, and Martin Frisher. "Evaluating associations between metabolic health, obesity and depressive symptoms: a prospective analysis of data from the English Longitudinal Study of Ageing (ELSA) with a 2‑year follow‑up." BMJ Open 8, no. 12 (December 2018): e025394. http://dx.doi.org/10.1136/bmjopen-2018-025394.

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ObjectivesConflicting results have been reported when the associations between metabolic health, obesity and depression were examined previously. The primary aim of this study was to determine whether metabolic health or obesity are independently associated with depressive symptoms, among a representative sample of older people living in England. Independent associations between covariates and depression were also examined.DesignProspective study with a 2-year follow-up.SettingThe English Longitudinal Study of Ageing Wave 6 (2012–2013) and Wave 7 (2014–2015).Participants6804 participants aged older than 50 years.Data AnalysisMultivariate models were used to determine whether metabolic health or obesity are independently associated with depressive symptoms at 2-year follow-up. Unadjusted and adjusted ORs with corresponding 95% CI were calculated; the adjusted ORs took account of baseline depression, gender, age, wealth, obesity and poor metabolic health.ResultsBefore adjusting for covariates, poor metabolic health was associated with depressive symptoms at 2-year follow-up (OR 1.24; 95% CI, 1.07 to 1.44, p<0.01). After adjusting for covariates, the association was no longer statistically significant (OR 1.17; 95% CI, 0.99 to 1.38, p=0.07). Similarly, obesity was associated with depressive symptoms at 2-year follow-up before adjusting for covariates (OR 1.54; 95% CI, 1.33 to 1.79, p<0.01). However, after adjusting for covariates the association between obesity and depressive symptoms at 2-year follow-up became statistically insignificant (OR 1.19; 95% CI, 1.00 to 1.41, p=0.06). The strongest predictors for future depression were baseline depression (OR 10.59; 95% CI, 8.90 to 12.53, p<0.01) and lower wealth (OR 3.23; 95% CI, 2.44 to 4.35, p<0.01).ConclusionNeither poor metabolic health nor obesity were associated with a risk of depressive symptoms at 2-year follow-up, after adjusting for covariates. As wealth inequalities continue to rise across England, the risk of depressive symptoms at 2-year follow-up is likely to be elevated in individuals living in the lower wealth quintiles.

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Matić, Tatjana Bošković, Gordana Toncev, Aleksandar Gavrilović, and Dejan Aleksić. "Suffering from cerebral small vessel disease with and without metabolic syndrome." Open Medicine 14, no. 1 (June 11, 2019): 479–84. http://dx.doi.org/10.1515/med-2019-0051.

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AbstractBackgroundCerebral small vessel disease (CSVD) and metabolic syndrome were separately associated with cognitive impairment and depression. However, whether metabolic syndrome adds to cognitive impairment and depression in patients who already have CSVD remained unanswered.ObjectiveThe aim of our study was to investigate the association of metabolic syndrome with cognitive impairment and depression in patients with CSVD who have lacunar lesions or white matter hyperintensities.MethodsThis prospective cohort study was conducted at Neurology Clinic, Clinical Center, Kragujevac, Serbia. Main outcomes of the study were cognitive assessment, and assessment of depression among hospitalized patients with or without CSVD.ResultsThe study included 74 inpatients, 25 of them having lacunary infarctions, 24 with the white matter hyperintensities, and 25 control patients without CSVD. The CSVD was accompanied by impairment of cognition and depression, the patients with lacunary lesions being more cognitively impaired and more depressive than the patients with the white matter hyperintensities. The patients with CSVD who also had metabolic syndrome were more cognitively impaired and depressed than the patients with CSVD alone.ConclusionsIn conclusion, our study showed that metabolic syndrome is associated with further worsening of already impaired cognition and existing depression in patients with CSVD.

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Sharovsky, Lilian Lopes, and Bellkiss Wilma Romano. "Depressive and anxiety symptoms in patients with Metabolic Syndrome." Estudos de Psicologia (Campinas) 30, no. 4 (December 2013): 603–8. http://dx.doi.org/10.1590/s0103-166x2013000400013.

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Depressive symptoms have been associated to the Metabolic Syndrome. Nevertheless, only a few studies have evaluated anxiety and depression concomitantly. The objective of the research was to evaluate the intensity of depressive and anxiety symptoms in patients with Metabolic Syndrome and their relation to demographic variables. A unicenter, transversal study was carried out. A social demographic questionnaire was used. Depressive symptoms were measured with Beck Depression Inventory and anxiety symptoms were measured with Hamilton Anxiety Scale Rate. A total of 103 ambulatory patients, 60 of them men, with mean age 55.4 years (±7,6) with a diagnosis of Metabolic Syndrome were included in the study. Anxiety symptoms of very severe intensity were present in 51.5% (n=53) while severe depressive symptoms in only 5.8% (n=6). Anxiety and depressive symptoms were significantly associated. In this sample, anxiety predominated in relation to the depressive symptoms. The anxiety symptoms were more intense in women and that had low level of education.

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Storey, Kenneth B. "Suspended animation: the molecular basis of metabolic depression." Canadian Journal of Zoology 66, no. 1 (January 1, 1988): 124–32. http://dx.doi.org/10.1139/z88-016.

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An impressive array of organisms is capable of radically depressing basal metabolic rate and entering a hypometabolic state characterized by a marked reduction of many normal physiological functions. Environmental cues are often the trigger: low oxygen, low temperature, or lack of water, for example. Entry into a hypometabolic state does not, apparently, involve major biochemical reorganization but appears, instead, to result from molecular controls operating at a level "above" that of allosteric regulation of enzymes and "below" that of gene expression. The mechanisms involved are widely applicable to the coordinated inactivation of many cellular processes. Studies of anaerobiosis in marine molluscs provide the most complete information on the molecular mechanisms involved in metabolic rate depression. Glycolytic rate depression in the marine whelk involves (i) covalent modification of key regulatory enzymes (e.g., phosphofructokinase, pyruvate kinase) via enzyme phosphorylation to produce less active enzyme forms, (ii) dissociation of enzymes from complexes bound to the subcellular particulate fraction to disrupt pathway flux, and (iii) decreased levels of fructose-2,6-bisphosphate, a potent activator of phosphofructokinase, to help limit the anabolic uses of carbohydrate in the depressed state. Continuing studies are demonstrating the universality of these mechanisms as the basis of metabolic depression, including involvement in mammalian hibernation and anoxia tolerance in goldfish and turtles.

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Foley, Debra L., Katherine I. Morley, Pamela A. F. Madden, Andrew C. Heath, John B. Whitfield, and Nicholas G. Martin. "Major Depression and the Metabolic Syndrome." Twin Research and Human Genetics 13, no. 4 (August 1, 2010): 347–58. http://dx.doi.org/10.1375/twin.13.4.347.

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AbstractThe aim of this study is to characterize the relationship between major depression and the metabolic syndrome in a large community based sample of Australian men and women aged 26–90 years. A lifetime history of major depression was assessed by telephone interview following the DSM–III-R. A current history of metabolic syndrome was assessed following the United States National Cholesterol Education Program Adult Treatment Panel III (NCEP AP-III) guidelines 1 to 3 years later. Logistic regression was used to estimate the association between depression and the metabolic syndrome, and its component criteria, controlling for age, sex and alcohol dependence. There was no association between a lifetime history of major depression and the presence of the metabolic syndrome. There was a weak association between depression and low high-density lipoprotein cholesterol but not with other component criteria of the metabolic syndrome. Despite calls for interventions directed at depression to reduce the onset of the metabolic syndrome there are important failures to replicate in large samples such as this, no consensus regarding the threshold at which depression may pose a significant risk even allowing for heterogeneity across populations, and no consensus regarding confounders that may explain inter-study differences. The absence of any dosage effect of depression on the associated risk for the metabolic syndrome in other unselected samples does not support a direct causal relationship. The call for intervention studies on the basis of the currently published evidence base is unwarranted.

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Marijnissen, R., N. Vogelzangs, M. Mulder, R. van den Brink, H. Comijs, and R. Oude Voshaar. "Metabolic dysregulation as predictor for the course of late-life depression." European Psychiatry 33, S1 (March 2016): S416. http://dx.doi.org/10.1016/j.eurpsy.2016.01.1504.

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IntroductionDepression is associated with the metabolic syndrome (MS). Recently, the concept of ‘metabolic depression’ has been proposed based on a protracted course of depressive symptoms over time.Objective and aimsWithin the Netherlands study of depression in older persons, we examined whether metabolic dysregulation predicted the two-year course of depression.MethodsA cohort study (n = 285) of depressed persons (≥60 years) with two-year follow up. Depression was classified according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV). Severity of depression was assessed with sum score as well as subscale scores of the Inventory of Depressive Symptomatology (IDS) at six-month intervals. The metabolic syndrome was defined according the National Cholesterol Education Program (NCEP-ATP III). We applied logistic regression and linear mixed models adjusted for a wide range of confounders and severity of depression at baseline.ResultsThe number of MS-components predicted non-remission at two-years (OR = 1.28 [95% CI: 1.00–1.58], P = 0.047), which was driven by waist-circumference, HDL-cholesterol and triglycerides. MS was only associated with the somatic symptom subscale score of the IDS over time, but not with its sum score (interaction time × somatic subscale, P = 0.002). This effect was driven by waist circumference, elevated fasting glucose level and hypertension.ConclusionMetabolic dysregulation predicts the course of late-life depression. This effect seems to be driven by visceral obesity (as indicated by the waist circumference) and lipid dysregulations and with respect to the somatic symptoms of depression.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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Brand, M. D., R. B. Boutilier, J. St-Pierre, and T. Bishop. "Mitochondrial proton leak in metabolic depression." Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 126 (July 2000): S17. http://dx.doi.org/10.1016/s0305-0491(00)80034-6.

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Schwartz, Joseph A. "Late-Life Depression and Metabolic Factors." American Journal of Geriatric Psychiatry 9, no. 3 (June 2001): 315–16. http://dx.doi.org/10.1097/00019442-200108000-00020.

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Haouzi, Philippe, and Andry Van de Louw. "Metabolic and ventilatory depression in rat." Journal of Applied Physiology 113, no. 3 (August 1, 2012): 514. http://dx.doi.org/10.1152/japplphysiol.00615.2012.

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Zach, J., and S. H. Ackerman. "Thyroid function, metabolic regulation, and depression." Psychosomatic Medicine 50, no. 5 (September 1988): 454–68. http://dx.doi.org/10.1097/00006842-198809000-00002.

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Lehto, Soili M., Tuula Heiskanen, Jukka Hintikka, Leo Niskanen, Heli Koivumaa-Honkanen, Tommi Tolmunen, Kirsi Honkalampi, and Heimo Viinamäki. "Metabolic Syndrome—The Impact of Depression." Annals of Epidemiology 18, no. 11 (November 2008): 871. http://dx.doi.org/10.1016/j.annepidem.2008.07.005.

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Kawada, Tomoyuki. "Metabolic syndrome, depression, anxiety and mortality." International Journal of Cardiology 198 (November 2015): 40–41. http://dx.doi.org/10.1016/j.ijcard.2015.06.141.

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Ketola, Tarmo, Janne S. Kotiaho, Dominique Mazzi, and Mikael Puurtinen. "Inbreeding depression in intraspecific metabolic scaling." Animal Biology 63, no. 3 (2013): 357–67. http://dx.doi.org/10.1163/15707563-00002418.

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Metabolic scaling (i.e., the relationship between the size and metabolic rate of organisms) has been suggested to explain a large variety of biological patterns from individual growth to species diversity. However, considerable disagreement remains regarding the underlying causes of metabolic scaling patterns, and what these patterns are. As in all biology, understanding metabolic scaling will require understanding its evolution by natural selection. We searched for evidence of natural selection on metabolic scaling indirectly by manipulating the genetic quality of male and female Drosophila montana flies with induced mutations and inbreeding, building on the notion that mutations and inbreeding will cause predictable changes in characters under directional selection. Irradiation-induced mutations had no effect on the examined traits, most likely because of purging at an early stage. However, inbreeding increased the energy use of larger females, suggesting that selection has favoured low metabolic scaling in females. Inbreeding did not affect metabolic scaling of males. Together, our results suggest that natural selection on metabolic scaling acts differently on the sexes, depending on the relative importance of body size and energetic efficiency to individual fitness. The results call attention to the important notion that size-specific energy use can be an evolutionarily malleable trait.

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Robakis, Thalia K., Kathleen Watson-Lin, Tronita E. Wroolie, Alison Myoraku, Carla Nasca, Benedetta Bigio, Bruce McEwen, and Natalie L. Rasgon. "Early life adversity blunts responses to pioglitazone in depressed, overweight adults." European Psychiatry 55 (January 2019): 4–9. http://dx.doi.org/10.1016/j.eurpsy.2018.09.009.

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AbstractPurpose:Early life adversity is associated with both metabolic impairment and depression in adulthood, as well as with poorer responses to antidepressant medications. It is not yet known whether individual differences in sensitivity to antidiabetic medications could also be related to early life adversity. We examined whether a history of early life adversity affected the observed changes in metabolic function and depressive symptoms in a randomized trial of pioglitazone for augmentation of standard treatments for depression.Purpose:Early life adversity is associated with both metabolic impairment and depression in adulthood, as well as with poorer responses to antidepressant medications. It is not yet known whether individual differences in sensitivity to antidiabetic medications could also be related to early life adversity. We examined whether a history of early life adversity affected the observed changes in metabolic function and depressive symptoms in a randomized trial of pioglitazone for augmentation of standard treatments for depression.Findings:We found that early life adversity significantly impaired the metabolic response to pioglitazone. Effects on depressive symptoms did not reach significance, but nonetheless suggested that pioglitazone could mitigate the depressant effects of childhood adversity, only among those insulin resistant at baseline.Conclusions:We conclude that a history of early life adversity may impair the body’s ability to respond to insulin sensitizing pharmacotherapy, and furthermore that its contribution to resistant depression may function in part via the generation of an insulin resistant phenotype.

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Ferreira, Mari Cassol, Camila Piaia, Ana Carolina Cadore, Marinez Amabile Antoniolli, Geni Portela Gamborgi, and Patrícia Pereira de Oliveira. "Clinical variables associated with depression in patients with type 2 diabetes." Revista da Associação Médica Brasileira 61, no. 4 (August 2015): 336–40. http://dx.doi.org/10.1590/1806-9282.61.04.336.

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SummaryBackground:the aim of the study was to evaluate the relationship between type 2 diabetes (T2DM), depression and depressive symptoms and their clinical impact on T2DM.Methods:the authors evaluated 214 outpatients, 105 with diabetes (T2DM group) and 109 non-diabetics (control group), with ages ranging between 50 and 75 years (T2DM group 65.1 ± 5.6 years, control group 63.4 ± 5.8 years). Use of antidepressant treatment or score ≥ 16 on the Beck depression inventory (BDI) was considered depression. Complications of diabetes and total symptom score (TSS) for peripheral neuropathy were reported by patients.Results:diabetes group had a higher frequency of depression (35.2%) compared to controls (21.1%) (p=0,021), with 2.4 times increased risk of depression. The presence of depressive symptoms was also higher in T2DM group (mean BDI 9.5 ± 8.8 versus 6.9 ± 6.2; p=0.039). Symptoms of diabetic neuropathy were higher in depressed subjects. The metabolic control and presence of complications in T2DM group were not associated with depression.Conclusion:T2DM led to an increased risk of depression, but this did not influence the metabolic control or the presence of other complications.

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Fischer, Christina Weide, Nico Liebenberg, Anne Mette Madsen, Heidi Kaastrup Müller, Sten Lund, and Gregers Wegener. "Chronic lipopolysaccharide infusion fails to induce depressive-like behaviour in adult male rats." Acta Neuropsychiatrica 27, no. 3 (February 20, 2015): 189–94. http://dx.doi.org/10.1017/neu.2015.4.

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BackgroundChronic inflammation is implicated in numerous diseases, including major depression and type 2 diabetes mellitus (T2DM). Since depression and T2DM often co-exist, inflammatory pathways are suggested as a possible link. Hence, the establishment of an immune-mediated animal model would shed light on mechanisms possibly linking depression and metabolic alterations.ObjectiveIn this study we investigated a behavioural and metabolic paradigm following chronic infusion with low doses of lipopolysaccharide (LPS) using osmotic minipumps in male rats.MethodsBehavioural testing consisted of evaluating activity level in the open field and depressive-like behaviour in the forced swim test. Metabolic assessment included measurement of body weight, food and water intake, and glucose and insulin levels during an oral glucose tolerance test.ResultsLPS-infused rats showed acute signs of sickness behaviour, but chronic LPS infusion did not induce behavioural or metabolic changes.ConclusionThese results suggest that although inflammation is immediately induced as indicated by acute sickness, 4 weeks of chronic LPS administration via osmotic minipumps did not result in behavioural changes. Therefore, this paradigm may not be a suitable model for studying the underlying mechanisms that link depression and T2DM.

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Seo, Yongseok, Seungyeon Lee, Joung-Sook Ahn, Seongho Min, Min-Hyuk Kim, Jang-Young Kim, Dae Ryong Kang, Sangwon Hwang, Phor Vicheka, and Jinhee Lee. "Association of Metabolically Healthy Obesity and Future Depression: Using National Health Insurance System Data in Korea from 2009–2017." International Journal of Environmental Research and Public Health 18, no. 1 (December 23, 2020): 63. http://dx.doi.org/10.3390/ijerph18010063.

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(1) Background: The health implications associated with the metabolically healthy obese (MHO) phenotype, in particular related to symptoms of depression, are still not clear. the purpose of this study is to check whether depression and metabolic status are relevant by classifying them into four groups in accordance with the MHO diagnostic standard. Other impressions seen were the differences between sexes and the effects of the MHO on the occurrence of depression. (2) Methods: A sample of 3,586,492 adult individuals from the National Health Insurance Database of Korea was classified into four categories by their metabolic status and body mass index: (1) metabolically healthy non-obese (MHN); (2) metabolically healthy obese (MHO); (3) metabolically unhealthy non-obese (MUN); and (4) metabolically unhealthy obese (MUO). Participants were followed for six to eight years for new incidences of depression. The statistical significance of the general characteristics of the four groups, as well as the mean differences in metabolic syndrome risk factors, was assessed with the use of a one-way analysis of variance (ANOVA). (3) Results: The MHN ratio in women was higher than in men (men 39.3%, women 55.2%). In both men and women, depression incidence was the highest among MUO participants (odds ratio (OR) = 1.01 in men; OR = 1.09 in women). It was concluded as well that, among the risk factors of metabolic syndrome, waist circumference was the most related to depression. Among the four groups, the MUO phenotype was the most related to depression. Furthermore, in women participants, MHO is also related to a higher risk of depressive symptoms. These findings indicate that MHO is not a totally benign condition in relation to depression in women. (4) Conclusion: Therefore, reducing metabolic syndrome and obesity patients in Korea will likely reduce the incidence of depression.

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Christian, Keith A., Gavin S. Bedford, and Timothy J. Schultz. "Energetic consequences of metabolic depression in tropical and temperate-zone lizards." Australian Journal of Zoology 47, no. 2 (1999): 133. http://dx.doi.org/10.1071/zo98061.

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One response of ectothermic animals to periods of inactivity is inverse acclimation, or metabolic depression, which results in the conservation of energy. Most studies of metabolic depression and acclimation have involved temperate-zone species, and the information from tropical species has been largely restricted to laboratory studies that failed to demonstrate thermal acclimation of metabolism. Recently, metabolic depression has been shown in several species of reptiles from the wet-dry tropics of northern Australia during the dry season. We review existing data on the energy budgets of temperate and tropical species during periods of inactivity and make calculations of energy saved due to metabolic depression across a range of temperatures. Because tropical species experience relatively high temperatures during periods of inactivity, they have a greater potential for energy savings, any enhancement of their metabolic depression is disproportionately advantageous with respect to energy savings, and in some species metabolic depression is probably essential for survival. Thus, we would expect metabolic depression to be well developed in some tropical reptiles. The lack of thermal acclimation in laboratory studies indicates that environmental parameters other than temperature (such as food or water) may initiate metabolic depression in tropical species. Higher temperatures, however, magnify the energy savings accomplished by metabolic depression.

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Kim, Yunmi, and Hyun-Young Kim. "Association Between Depression and Metabolic Syndrome in Korean Adults: Data From the 2014 and 2016 Korea National Health and Nutrition Examination Survey." Asia Pacific Journal of Public Health 31, no. 1 (November 23, 2018): 18–29. http://dx.doi.org/10.1177/1010539518813704.

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This study aimed to examine the association of depression with metabolic syndrome and to investigate levels of awareness and treatment of depression in Korean adults. We analyzed data extracted from the Korea National Health and Nutrition Examination Survey (2014 and 2016) using the Patient Health Questionnaire-9 depression screening instrument. Among the survey participants, 10 459 were selected for data analysis. Of them, 7.2% had depression, 24.4% had metabolic syndrome, and 10.0% had both depression and metabolic syndrome. Among those with depression, 33.1% were aware of their condition and 25.7% received treatment, with significant differences found between those with and without metabolic syndrome. The mean Patient Health Questionnaire-9 scores significantly increased with the number of metabolic syndrome components ( F = 6.06, P = <.001). In logistic regression analysis, the odds ratio (OR) for depression with metabolic syndrome was 1.41 (95% confidence interval [CI] = 1.12-1.76). For the number of metabolic syndrome components, having 2 (OR = 1.37, 95% CI = 1.01-1.86), 3 (OR = 1.57, 95% CI = 1.12-2.21), 4 (OR = 1.95, 95% CI = 1.32-2.87), and 5 (OR = 2.18, 95% CI = 1.38-3.46) conditions significantly increased the OR for depression. Including depression in the management of metabolic syndrome could help make people with depression more aware of their condition.

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Vancampfort, D., C. U. Correll, M. Wampers, P. Sienaert, A. J. Mitchell, A. De Herdt, M. Probst, T. W. Scheewe, and M. De Hert. "Metabolic syndrome and metabolic abnormalities in patients with major depressive disorder: a meta-analysis of prevalences and moderating variables." Psychological Medicine 44, no. 10 (November 21, 2013): 2017–28. http://dx.doi.org/10.1017/s0033291713002778.

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BackgroundIndividuals with depression have an elevated risk of cardiovascular disease (CVD) and metabolic syndrome (MetS) is an important risk factor for CVD. We aimed to clarify the prevalence and correlates of MetS in persons with robustly defined major depressive disorder (MDD).MethodWe searched Medline, PsycINFO, EMBASE and CINAHL up until June 2013 for studies reporting MetS prevalences in individuals with MDD. Medical subject headings ‘metabolic’ OR ‘diabetes’ or ‘cardiovascular’ or ‘blood pressure’ or ‘glucose’ or ‘lipid’ AND ‘depression’ OR ‘depressive’ were used in the title, abstract or index term fields. Manual searches were conducted using reference lists from identified articles.ResultsThe initial electronic database search resulted in 91 valid hits. From candidate publications following exclusions, our search generated 18 studies with interview-defined depression (n = 5531, 38.9% male, mean age = 45.5 years). The overall proportion with MetS was 30.5% [95% confidence interval (CI) 26.3–35.1] using any standardized MetS criteria. Compared with age- and gender-matched control groups, individuals with MDD had a higher MetS prevalence [odds ratio (OR) 1.54, 95% CI 1.21–1.97, p = 0.001]. They also had a higher risk for hyperglycemia (OR 1.33, 95% CI 1.03–1.73, p = 0.03) and hypertriglyceridemia (OR 1.17, 95% CI 1.04–1.30, p = 0.008). Antipsychotic use (p < 0.05) significantly explained higher MetS prevalence estimates in MDD. Differences in MetS prevalences were not moderated by age, gender, geographical area, smoking, antidepressant use, presence of psychiatric co-morbidity, and median year of data collection.ConclusionsThe present findings strongly indicate that persons with MDD are a high-risk group for MetS and related cardiovascular morbidity and mortality. MetS risk may be highest in those prescribed antipsychotics.

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Martinac, M., D. Babić, and M. Pavlović. "Type D personality and metabolic syndrome in patients with depression." European Psychiatry 41, S1 (April 2017): S533. http://dx.doi.org/10.1016/j.eurpsy.2017.01.726.

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IntroductionPathogenesis of metabolic syndrome (MS) and depression (MDD) is complex and insufficiently explored. In addition to chronic stress, psychotrauma, hypercortisolemia and immunological factors, some personality features may have an impact. Type D personality, most influential personality type in psychosomatic medicine, consists of two dimensions: negative affect (NA) and social inhibition (SI). Individuals with type D personality are more anxious, irritable and depressed and they do not share these emotions with others because of their fear of rejection. Type D personality was proven to be a risk factor for some MS components, as well as for the occurrence of depressive symptoms in cardiac patients.AimTo investigate the association of type D personality with MS and its components in MDD patients.MethodsCross-sectional study was conducted on the sample of 80 patients with depression and 40 healthy subjects as the control group. Mini International Neuropsychiatric Interview (MINI questionnaire) and Hamilton Rating Scale for Depression (HDRS-17) were used for the diagnosis of depression. Type D personality was determined by DS14 questionnaire. The MS diagnosis was made according to ATP III criteria.ResultsThe presence of type D personality did not significantly contribute to the probability of developing MS in patients with depression. NA was associated with abdominal obesity, low HDL-cholesterol and hypertension.ConclusionNegative affect was proven to be an independent risk factor in the pathogenesis of obesity, hypertension, and reduced level of HDL-cholesterol, while type D personality in general did not have predictive value for the MS development.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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Jääskeläinen, Tuija, Paul Knekt, Jaana Suvisaari, Satu Männistö, Timo Partonen, Katri Sääksjärvi, Niina E. Kaartinen, Noora Kanerva, and Olavi Lindfors. "Higher serum 25-hydroxyvitamin D concentrations are related to a reduced risk of depression." British Journal of Nutrition 113, no. 9 (April 2, 2015): 1418–26. http://dx.doi.org/10.1017/s0007114515000689.

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Vitamin D has been suggested to protect against depression, but epidemiological evidence is scarce. The present study investigated the relationship of serum 25-hydroxyvitamin D (25(OH)D) with the prevalence of depressive and anxiety disorders. The study population consisted of a representative sample of Finnish men and women aged 30–79 years from the Health 2000 Survey. The sample included 5371 individuals, of which 354 were diagnosed with depressive disorder and 222 with anxiety disorder. Serum 25(OH)D concentration was determined from frozen samples. In a cross-sectional study, a total of four indicators of depression and one indicator of anxiety were used as dependent variables. Serum 25(OH)D was the risk factor of interest, and logistic models used further included sociodemographic and lifestyle variables as well as indicators of metabolic health as confounding and/or effect-modifying factors. The population attributable fraction (PAF) was estimated. Individuals with higher serum 25(OH)D concentrations showed a reduced risk of depression. The relative odds between the highest and lowest quartiles was 0·65 (95 % CI 0·46, 0·93;Pfor trend = 0·006) after adjustment for sociodemographic, lifestyle and metabolic factors. Higher serum 25(OH)D concentrations were associated with a lower prevalence of depressive disorder especially among men, younger, divorced and those who had an unhealthy lifestyle or suffered from the metabolic syndrome. The PAF was estimated to be 19 % for depression when serum 25(OH)D concentration was at least 50 nmol/l. These results support the hypothesis that higher serum 25(OH)D concentrations protect against depression even after adjustment for a large number of sociodemographic, lifestyle and metabolic factors. Large-scale prospective studies are needed to confirm this finding.

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Lamers, F., Y. Milaneschi, and B. Penninx. "S.02.01 Immune-metabolic depression: evidence for a subtype of depression." European Neuropsychopharmacology 29 (December 2019): S2. http://dx.doi.org/10.1016/j.euroneuro.2019.09.022.

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Ali, Mazen Khalil, and Haitham Ali Jahrami. "Prevalence of Metabolic Syndrome and Metabolic Abnormalities among Patients with Depression." Bahrain Medical Bulletin 40, no. 2 (June 2018): 86–89. http://dx.doi.org/10.12816/0047555.

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Brooks, Steven D., Stanley M. Hileman, Paul D. Chantler, Samantha A. Milde, Kent A. Lemaster, Stephanie J. Frisbee, J. Kevin Shoemaker, Dwayne N. Jackson, and Jefferson C. Frisbee. "Protection from chronic stress- and depressive symptom-induced vascular endothelial dysfunction in female rats is abolished by preexisting metabolic disease." American Journal of Physiology-Heart and Circulatory Physiology 314, no. 5 (May 1, 2018): H1085—H1097. http://dx.doi.org/10.1152/ajpheart.00648.2017.

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While it is known that chronic stress and clinical depression are powerful predictors of poor cardiovascular outcomes, recent clinical evidence has identified correlations between the development of metabolic disease and depressive symptoms, creating a combined condition of severely elevated cardiovascular disease risk. In this study, we used the obese Zucker rat (OZRs) and the unpredictable chronic mild stress (UCMS) model to determine the impact of preexisting metabolic disease on the relationship between chronic stress/depressive symptoms and vascular function. Additionally, we determined the impact of metabolic syndrome on sex-based protection from chronic stress/depressive effects on vascular function in female lean Zucker rats (LZRs). In general, vasodilator reactivity was attenuated under control conditions in OZRs compared with LZRs. Although still impaired, conduit arterial and resistance arteriolar dilator reactivity under control conditions in female OZRs was superior to that in male or ovariectomized (OVX) female OZRs, largely because of better maintenance of vascular nitric oxide and prostacyclin levels. However, imposition of metabolic syndrome in combination with UCMS in OZRs further impaired dilator reactivity in both vessel subtypes to a similarly severe extent and abolished any protective effect in female rats compared with male or OVX female rats. The loss of vascular protection in female OZRs with UCMS was reflected in vasodilator metabolite levels, which closely matched those in male and OVX female OZRs subjected to UCMS. These results suggest that presentation of metabolic disease in combination with depressive symptoms can overwhelm the vasoprotection identified in female rats and, thereby, may reflect a severe impairment to normal endothelial function. NEW & NOTEWORTHY This study addresses the protection from chronic stress- and depression-induced vascular dysfunction identified in female compared with male or ovariectomized female rats. We determined the impact of preexisting metabolic disease, a frequent comorbidity of clinical depression in humans, on that vascular protection. With preexisting metabolic syndrome, female rats lost all protection from chronic stress/depressive symptoms and became phenotypically similar to male and ovariectomized female rats, with comparably poor vasoactive dilator metabolite profiles.

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Mannie, Zola N., Clare Williams, Jonathan Diesch, Andrew Steptoe, Paul Leeson, and Philip J. Cowen. "Cardiovascular and metabolic risk profile in young people at familial risk of depression." British Journal of Psychiatry 203, no. 1 (July 2013): 18–23. http://dx.doi.org/10.1192/bjp.bp.113.126987.

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BackgroundDepression is associated with increased risk of several general medical conditions, including diabetes and cardiovascular disease. The nature of the association is complex and may involve bidirectional causation or a common pathophysiology.AimsTo determine whether young people without depression but at increased familial risk have altered metabolic and blood pressure markers relative to matched controls.MethodWe studied young people (n = 85), who had a parent with depression but no personal history of depressive illness (FH+) and healthy controls (n = 69). Cardiovascular risk profile was assessed by a fasting blood sample to measure insulin, glucose, lipids and high-sensitivity C-reactive protein (CRP) and blood pressure was measured centrally and peripherally. Arterial stiffness and waking cortisol concentration were also measured.ResultsCompared with controls, the FH+ group demonstrated increased peripheral and central systolic blood pressure, increased arterial stiffness and diminished insulin sensitivity but they did not differ from controls in measures of lipids, CRP or waking cortisol.ConclusionsOur data suggest that young people at increased familial risk of depression show evidence of altered cardiovascular risk profile in young adulthood even in the absence of depressive symptoms. It is possible therefore that vulnerability to conditions such as hypertension and diabetes may precede the onset of major depression and may share common risk factors.

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Lin, Kuan Pin, Tien Li Liang, I. Chen Liao, and Shiow Luan Tsay. "Associations Among Depression, Obesity, and Metabolic Syndrome in Young Adult Females." Biological Research For Nursing 16, no. 3 (September 19, 2013): 327–34. http://dx.doi.org/10.1177/1099800413500138.

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Depression may be a risk factor for obesity or metabolic syndrome. The aims of this study were to determine the relationships among depression, obesity, and metabolic syndrome in young adult females as well as the role of depression in the components of metabolic syndrome. A cross-sectional study was conducted on 323 young adult females. Demographic characteristics, anthropometric measurements, and laboratory values were collected. The criteria of the Bureau of Health Promotion, Department of Health, Taiwan, were used to define metabolic syndrome. Depression was measured using the Center for Epidemiologic Studies Depression scale. The prevalence of depression in the sample was 17%, that of overweight and obesity was 17%, and that of metabolic syndrome was 6.8%. Depression showed significant associations with high body mass index (BMI), increased waist circumference and blood pressure (BP), and overweight and obesity (β = 0.15, odds ratio [OR] = 1.17, 95% confidence interval [CI] = [1.11, 1.23], p < .001). No associations were observed between depression and metabolic syndrome (β = −0.01, OR = 0.99, 95% CI = [0.92, 1.06], p = .69) or any of its individual components after adjustment for BMI and demographic variables. The findings show that depression was associated with increasing odds of overweight and obesity in young adult females and may also have increased the physiological risk associated with metabolic syndrome. Early detection of depression and obesity as part of metabolic syndrome is important in the health management of young adult females for decreasing the risks of cardiovascular disease and diabetes.

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Chan, Kenny L., Flurin Cathomas, and Scott J. Russo. "Central and Peripheral Inflammation Link Metabolic Syndrome and Major Depressive Disorder." Physiology 34, no. 2 (March 1, 2019): 123–33. http://dx.doi.org/10.1152/physiol.00047.2018.

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Metabolic syndrome and major depression are two of the most common and debilitating disorders worldwide, occurring with significant rates of comorbidity. Recent studies have uncovered that each of these conditions is associated with chronic, low-grade inflammation. This is characterized by increased circulating pro-inflammatory cytokines, altered leukocyte population frequencies in blood, accumulation of immune cells in tissues including the brain, and activation of these immune cells. Cytokines that become elevated during obesity can contribute to the progression of metabolic syndrome by directly causing insulin resistance. During chronic stress, there is evidence that these cytokines promote depression-like behavior by disrupting neurotransmitter synthesis and signal transduction. Animal models of obesity and depression have revealed a bi-directional relationship whereby high-fat feeding and chronic stress synergize and exacerbate metabolic dysregulation and behavioral abnormalities. Although far from conclusive, emerging evidence suggests that inflammation in the central and peripheral immune system may link metabolic syndrome to major depressive disorder. In this review, we will synthesize available data supporting this view and identify critical areas for future investigation.

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Rethorst, Chad D., Ira Bernstein, and Madhukar H. Trivedi. "Inflammation, Obesity, and Metabolic Syndrome in Depression." Journal of Clinical Psychiatry 75, no. 12 (December 24, 2014): e1428-e1432. http://dx.doi.org/10.4088/jcp.14m09009.

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Virtanen, Marianna, Jane E. Ferrie, Tasnime Akbaraly, Adam Tabak, Markus Jokela, Klaus P. Ebmeier, Archana Singh-Manoux, and Mika Kivimäki. "Metabolic Syndrome and Symptom Resolution in Depression." Journal of Clinical Psychiatry 78, no. 01 (January 25, 2017): e1-e7. http://dx.doi.org/10.4088/jcp.15m10399.

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Caroli, A., M. Lorenzi, C. Geroldi, F. Nobili, B. Paghera, M. Bonetti, M. Cotelli, and G. B. Frisoni. "Metabolic Compensation and Depression in Alzheimer’s Disease." Dementia and Geriatric Cognitive Disorders 29, no. 1 (2010): 37–45. http://dx.doi.org/10.1159/000257761.

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Smith, K., and P. Kontari. "Metabolic Factors in Cognitive Impairment and Depression." Innovation in Aging 2, suppl_1 (November 1, 2018): 771. http://dx.doi.org/10.1093/geroni/igy023.2853.

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Pineda Olvera, Anna E., Sunita M. Stewart, Linda Galindo, and Jacqualene Stephens. "Diabetes, depression, and metabolic control in Latinas." Cultural Diversity and Ethnic Minority Psychology 13, no. 3 (July 2007): 225–31. http://dx.doi.org/10.1037/1099-9809.13.3.225.

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Vaccarino, Viola, Candace McClure, B. Delia Johnson, David S. Sheps, Vera Bittner, Thomas Rutledge, Leslee J. Shaw, et al. "Depression, the Metabolic Syndrome and Cardiovascular Risk." Psychosomatic Medicine 70, no. 1 (January 2008): 40–48. http://dx.doi.org/10.1097/psy.0b013e31815c1b85.

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Kayes, Sara M., Rebecca L. Cramp, and Craig E. Franklin. "Metabolic depression during aestivation in Cyclorana alboguttata." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 154, no. 4 (December 2009): 557–63. http://dx.doi.org/10.1016/j.cbpa.2009.09.001.

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Pakay, Julian L., Philip C. Withers, Andrew A. Hobbs, and Michael Guppy. "In vivo downregulation of protein synthesis in the snailHelix apersaduring estivation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 1 (July 1, 2002): R197—R204. http://dx.doi.org/10.1152/ajpregu.00636.2001.

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Protein synthesis is downregulated during metabolic depression in a number of systems where the metabolic depression is effected by obvious extrinsic cues. The metabolic depression of the estivating land snail Helix apersa occurs in the absence of any obvious physiological stress and has an intrinsic component independent of temperature, pH, O2status, or osmolality. We show that this metabolic depression is accompanied by a downregulation of protein synthesis in vivo. The rate of protein synthesis decreases in two major tissues during estivation: to 23% and 53% of the awake rate in hepatopancreas and foot muscle, respectively. We show from calculations of the theoretical contribution of protein synthesis to total O2consumption that the depression of protein synthesis must be a significant, obligate, in vivo component of metabolic depression in H. aspersa.

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Journal articles on the topic 'Metabolic depression'

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