scholarly journals Castelli risk indexes 1 and 2 are higher in major depression but other characteristics of the metabolic syndrome are not specific to mood disorders

Life Sciences ◽  
2014 ◽  
Vol 102 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Heber Odebrecht Vargas ◽  
Sandra Odebrecht Vargas Nunes ◽  
Décio Sabbatini Barbosa ◽  
Mateus Mendonca Vargas ◽  
Ariane Cestari ◽  
...  
2007 ◽  
Vol 30 (4) ◽  
pp. 95
Author(s):  
Valerie Taylor ◽  
Glenda M. MacQueen

Bipolar disorder and major depression are life-shortening illnesses. Unnatural causes such as suicide and accidents account for only a portion of this premature mortality1 Research is beginning to identify that mood disordered patients have a higher incidence of metabolic syndrome, an illness characterized by dyslipidemia, impaired glucose tolerance, hypertension and obesity.2 Metabolic syndrome is associated with an increased risk for a variety of physical illnesses. Hypothesis: Never treated patients with mood disorders have preexisting elevations in the prevalence of the component variables of metabolic syndrome. Central obesity will be especially elevated, predicting increased premature mortality. Methods: We assessed never treated patients with mood disorders for metabolic syndrome and its component variables. Patients were assessed at baseline and followed up at 6-month intervals. All psychiatric pharmacotherapy was documented. Body mass index (BMI) was also obtained and the percentage of deaths attributable to overweight and obesity was calculated using the population attributable risk (PAR). [PAR= ∑[P (RR-1)/RR] Results: Prior to the initiation of treatment, patients did not differ from population norms with respect to metabolic syndrome or BMI. At 2-year follow-up, BMI had increased for unipolar patients 2.02 points and 1.92 points for bipolar patients. (p < .001) This increase in BMI predicted an increase in mortality of 19.4%. Conclusion: An increase in visceral obesity is often the first component of metabolic syndrome to appear and may indicate the initiation of this disease process prematurely in this group. The increase in BMI places patients with mood disorders at risk for premature mortality and indicates a need for early intervention. References 1.Osby U, Brandt L, Correia N, Ekbom A & Sparen P. Excess mortability in bipolar and Unipolar disorder rin Sweden. Archives of General Psychiatry, 2001;58: 844-850 2.Toalson P, Saeeduddin A, Hardy T & Kabinoff G. The metabolic syndrome in patients with severe mental illness. Journal of Clinical Psychiatry, 2004; 6(4): 152-158


2006 ◽  
Vol 47 (6) ◽  
pp. 491-497 ◽  
Author(s):  
Richard A. Bermudes ◽  
Paul E. Keck ◽  
Jeffrey A. Welge

2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Amir H. Sam ◽  
Victoria Salem ◽  
Mohammad A. Ghatei

Endocannabinoid antagonism as a treatment for obesity and the metabolic syndrome became a hugely anticipated area of pharmacology at the start of the century. The CB1 receptor antagonist Rimonabant entered the European mass market on the back of several trials showing weight loss benefits alongside improvements in numerous other elements of the metabolic syndrome. However, the drug was quickly withdrawn due to the emergence of significant side effects—notably severe mood disorders. This paper provides a brief overview of the Rimonabant story and places the recent spate of FDA rejections of other centrally acting weight loss drugs entering Phase 3 trials in this context.


2009 ◽  
Vol 71 (3) ◽  
pp. 266-272 ◽  
Author(s):  
Edie M. Goldbacher ◽  
Joyce Bromberger ◽  
Karen A. Matthews

2011 ◽  
Vol 262 (4) ◽  
pp. 313-320 ◽  
Author(s):  
Kai G. Kahl ◽  
Wiebke Greggersen ◽  
Ulrich Schweiger ◽  
Joachim Cordes ◽  
Chakrapani Balijepalli ◽  
...  

CNS Spectrums ◽  
2001 ◽  
Vol 6 (7) ◽  
pp. 581-589 ◽  
Author(s):  
Baiju C. Gohil ◽  
Leonard A. Rosenblum ◽  
Jeremy D. Coplan ◽  
John G. Kral

AbstractObesity has negative health consequences related to fat distribution, particularly the central or visceral accumulation of fat. The major complications associated with visceral obesity, termed the “Metabolic Syndrome of Obesity,” or “Syndrome X,” are type II diabetes, hypertension, and dyslipidemia. As with certain mood disorders, the syndrome may be a consequence of neuroendocrine perturbations typically associated with chronic stress. Our work with bonnet macaque monkeys provides an animal model for the relationship between early stress, behavioral and hypothalamic-pituitary-adrenal (HPA) axis dysregulation, and Syndrome X. During their infant's first half-year, mothers face a variable foraging demand (VFD), in which ample food varies unpredictably in the difficulty of its acquisition, and the offspring show persistent abnormalities in systems known to modulate stress and affective regulation. Early work on the bonnet macaque noted the emergence of a sample of spontaneously obese subjects as they matured. Using the VFD model, the current study showed that there was a clear relationship between early cerebrospinal fluid corticotropin-releasing factor levels and subsequently measured body mass index, supporting the hypotheses regarding the interactive roles of early experience and HPA axis dysregulation in the ontogeny of both metabolic and mood disorders.


Author(s):  
Luiz Gustavo Piccoli de Melo ◽  
Sandra Odebrecht Vargas Nunes ◽  
George Anderson ◽  
Heber Odebrecht Vargas ◽  
Décio Sabbattini Barbosa ◽  
...  

2014 ◽  
Vol 36 (5) ◽  
pp. 509-515 ◽  
Author(s):  
Floriana S. Luppino ◽  
Paul F. Bouvy ◽  
Erik J. Giltay ◽  
Brenda W.J.H. Penninx ◽  
Frans G. Zitman

2015 ◽  
Vol 179 ◽  
pp. 148-155 ◽  
Author(s):  
Chiara Cristina Bortolasci ◽  
Heber Odebrecht Vargas ◽  
Sandra Odebrecht Vargas Nunes ◽  
Luiz Gustavo Piccoli de Melo ◽  
Márcia Regina Pizzo de Castro ◽  
...  

2010 ◽  
Vol 13 (4) ◽  
pp. 347-358 ◽  
Author(s):  
Debra L. Foley ◽  
Katherine I. Morley ◽  
Pamela A. F. Madden ◽  
Andrew C. Heath ◽  
John B. Whitfield ◽  
...  

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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