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      The association between smoking prevalence and eating disorders: a systematic review and meta-analysis : Smoking in eating disorders

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          Emotion regulation model in binge eating disorder and obesity--a systematic review.

          Deficits in emotion regulation processes are a common and widely used explanation for the development and maintenance of binge eating disorder (BED). It is assumed that BED patients - as they have difficulty regulating their negative emotions - use binge eating to cope with these emotions and to find relief. However, the number of experimental studies investigating this assumption is scarce and the differentiation of obese individuals with and without BED regarding the emotion regulation model is not verified. We reviewed literature for experimental studies investigating the emotion regulation model in obese patients (OB) with and without BED. Our search resulted in 18 experimental studies examining the triggering effect of negative emotions for binge eating or its effects on subsequent relief. We found evidence indicating that negative emotion serves as a trigger for binge eating in the BED group unlike the obese group without BED. Considering the small number of studies, we found evidence for a (short-term) improvement of mood through food intake, irrespective of group.
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            Binge eating disorder and obesity.

            M de Zwaan (2001)
            Binge eating disorder (BED) was included in the DSM IV as a proposed diagnostic category for further study and as an example for an eating disorder not otherwise specified (EDNOS). BED is characterized by recurrent episodes of binge eating in the absence of regular compensatory behavior such as vomiting or laxative abuse. Related features include eating until uncomfortably full, eating when not physically hungry, eating alone and feelings of depression or guilt. BED is associated with increased psychopathology including depression and personality disorders. Although BED is not limited to obese individuals, it is most common in this group and those who seek help do so for treatment of overweight rather than for binge eating. In community samples, the prevalence of BED has been found to be 2-5%, in individuals who seek weight control treatment the prevalence is 30%. BED is more equal in gender ratio than bulimia nervosa. Eating disorder treatments such as cognitive behavior therapy (CBT) or interpersonal psychotherapy (IPT) improve binge eating with abstinence rates of about 50%. Antidepressants are also effective in reducing binge eating, though less so than psychotherapy. Standard weight loss treatments including bariatric surgery do not seem to exacerbate binge eating problems. Thus, both eating disorder and obesity treatments seem to be beneficial in BED. However, it is recommended today that treatment should first be directed at the disordered eating and associated psychopathology.
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              Association of mitochondrial DNA levels with frailty and all-cause mortality.

              Mitochondrial function is altered with age and variants in mitochondrial DNA (mtDNA) modulate risk for several age-related disease states. However, the association of mtDNA copy number, a readily available marker which reflects mitochondrial depletion, energy reserves, and oxidative stress, on aging and mortality in the general population has not been addressed. To assess the association between mtDNA copy number and two primary outcomes--prevalent frailty and all-cause mortality--we utilize data from participants who were from two multicenter, multiethnic, community-based, prospective studies--the Cardiovascular Health Study (CHS) (1989-2006) and the Atherosclerosis Risk in Communities (ARIC) study (1987-2013). A total of 4892 participants (43.3% men) from CHS and 11,509 participants (44.9% men) from ARIC self-identifying as white or black were included in the analysis. mtDNA copy number, the trait of interest, was measured using a qPCR-based method in CHS and an array-based method in ARIC from DNA isolated from whole blood in participants from both cohorts. In race-stratified meta-analyses, we observe a significant inverse association of mtDNA copy number with age and higher mtDNA copy number in women relative to men. Lower mtDNA copy number was also significantly associated with prevalent frailty in white participants from CHS (OR 0.91, 95% CI 0.85-0.97). Additionally, mtDNA copy number was a strong independent predictor of all-cause mortality in an age- and sex-adjusted, race-stratified analysis of 16,401 participants from both cohorts with a pooled hazard ratio of 1.47 (95% CI 1.33-1.62) for the lowest quintile of mtDNA copy number relative to the highest quintile. Key messages: Mitochondrial DNA (mtDNA) copy number is associated with age and sex. Lower mtDNA copy number is also associated with prevalent frailty. mtDNA copy number is a significant predictor of all-cause mortality in a multiethnic population.
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                Author and article information

                Journal
                Addiction
                Addiction
                Wiley
                09652140
                November 2016
                November 2016
                July 18 2016
                : 111
                : 11
                : 1914-1922
                Affiliations
                [1 ]Department of Neurosciences; University of Padova; Padova Italy
                [2 ]Local Health Unit ULSS 17; Mental Health Department; Monselice Padova Italy
                [3 ]Institute of Clinical Research; and Education in Medicine (IREM); Padova Italy
                [4 ]Department of Medicine, DIMED; University of Padua; Padova Italy
                [5 ]Department of Pathology and Diagnostics; Verona University and Hospital Trust; Verona Italy
                [6 ]University of Leuven; KU Leuven Department of Rehabilitation Sciences; Leuven Belgium
                [7 ]University of Leuven-KU Leuven, University Psychiatric Centre; Kortenberg- Leuven Belgium
                [8 ]The Zucker Hillside Hospital, Psychiatry Research; Northwell Health System; Glen Oaks New York USA
                [9 ]Hofstra Northwell School of Medicine; Hempstead New York USA
                [10 ]The Feinstein Institute for Medical Research; Manhasset New York USA
                [11 ]Albert Einstein College of Medicine; Bronx New York USA
                [12 ]Population Health Research Institute; St George's University of London; London UK
                [13 ]KaskiSewa Hospital and Research Centre; Pokhara Nepal
                [14 ]New York Psychiatric Institute; Columbia University; NYC USA
                [15 ]Physiotherapy Department; South London and Maudsley NHS Foundation Trust; Denmark Hill London SE5 8AZ UK
                [16 ]Health Service and Population Research Department; Institute of Psychiatry, King's College, London; De Crespigny Park London UK
                Article
                10.1111/add.13457
                27206671
                1143a083-645f-4b39-a1c5-5efb8593f56a
                © 2016

                http://doi.wiley.com/10.1002/tdm_license_1.1

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