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Referral to Slimming World in UK Stop Smoking Services (SWISSS) versus stop smoking support alone on body weight in quitters: results of a randomised controlled trial.
Lycett, D, Aveyard, P, Farmer, A, Lewis, A, Munafò, M
BMJ open. 2020;10(1):e032271
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Weight gain is a well-known consequence of smoking cessation. The aim of this study was to compare standard stop smoking behavioural support with an intervention that, in addition to providing standard stop smoking support, included personalised weight management support, provided by Slimming World. This study is a parallel group, individually randomised controlled trial. Participants were randomised (1:1) to usual care or Slimming World with usual care. Stop smoking advisors were unaware of the randomisation sequence. Results showed that referral to the Slimming World programme plus usual stop smoking support achieved significantly less weight gain than usual stop smoking support alone. Furthermore, percentage quit was no worse in the treatment than the control group. Authors conclude that referral to a behavioural weight loss programme may be a pragmatic option within stop smoking clinics.
Abstract
INTRODUCTION Most people who stop smoking gain weight. Dietary modification may seem an obvious solution, but food restriction may increase cigarette craving and smoking relapse. TRIAL DESIGN An unblinded parallel randomised controlled trial. METHODS Participants were adult smokers with a body mass index greater or equal to 23 kg/m2. Setting was National Health Service commissioned Stop Smoking Services, interventions were referral to a commercial weight management programme, plus stop smoking support (treatment group), compared with stop smoking support alone (control group). Objective was to compare weight change between interventions in smoking abstainers and not abstinent rates in all. Primary outcome was change in weight (kg) at 12 weeks. Randomisation sequence was computer generated and concealed until allocation. RESULTS Seventy-six participants were recruited, 37 were randomised to the treatment group and 39 to the control group. Change in weight was analysed in long-term abstainers (13 treatment, 14 control) only because the aim was to prevent weight gain associated with smoking cessation. Abstinence was analysed on an intention-to-treat basis (37 treatment, 39 control). At 12 weeks weight gain was less in the treatment than the control group with an adjusted mean difference of -2.3 kg 95% CI (-4.4 to -0.1). Craving scores were lower (Mood and Physical Symptoms Scale craving domain -1.6 (-2.7 to -0.5)) and quit rates were higher in the treatment than the control group (32% vs 21%), although the trial was not powered to superiority in cravings and quit rates. No adverse events or side effects were reported. CONCLUSION In people who are obese and want to quit smoking, these data provide modest encouragement that providing weight management at the time of quitting may be helpful. Those who are not obese, but who are informed about potential weight gain during their quit attempt, were uninterested in a weight management programme. TRIAL REGISTRATION NUMBER ISRCTN65705512.
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Brain-Behavior-Immune Interaction: Serum Cytokines and Growth Factors in Patients with Eating Disorders at Extremes of the Body Mass Index (BMI) Spectrum.
Caroleo, M, Carbone, EA, Greco, M, Corigliano, DM, Arcidiacono, B, Fazia, G, Rania, M, Aloi, M, Gallelli, L, Segura-Garcia, C, et al
Nutrients. 2019;11(9)
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Eating disorders such as anorexia, binge eating and night-time eating cause great fluctuations in body mass and have also been shown to alter the immune system, and more specifically markers of inflammation called cytokines. In this observational study of 90 patients with known eating disorders, the researchers tried to identify how much BMI, ‘underweightness’ and malnutrition influenced the body’s pro-inflammatory response and upset the normal immune response. They found that many inflammatory cytokines were elevated in the blood samples taken, a likely response to the conditions of stress in the body. These cytokines are known to interact with the nervous system and were also influenced by other common symptoms such as depression. They were able to group the differences in cytokines for anorexia nervosa, binge-eating disorder, post-dinner eating, night-eating, sweet-eating and fasting. These markers of dysfunctional eating behaviours may help form part of a therapeutic approach to treating eating disorders based on supporting the immune response and reducing inflammation to stabilise metabolic processes. Future studies in a larger population of patients is necessary to determine the relevance of these findings.
Abstract
Alterations of the immune system are known in eating disorders (EDs), however the importance of cytokine balance in this context has not been clarified. We compared cytokines and growth factors at opposite ends of BMI ranges, in 90 patients classified in relation to BMI, depressive and EDs comorbidities. Serum concentrations of interleukin (IL)-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), vascular endothelial growth factor (VEGF), and epidermal growth factor (EGF) were determined by a biochip analyzer (Randox Labs). Differences were calculated through ANOVA. Possible predictors of higher cytokine levels were evaluated through regression analysis. IL-1α, IL-10, EGF, and IFN-γ were altered individuals with anorexia nervosa (AN) and binge eating disorder (BED). Night-eating was associated with IL-8 and EGF levels, IL-10 concentrations with post-dinner eating and negatively with sweet-eating, long fasting with higher IFN-γ levels. IL-2 increase was not linked to EDs, but to the interaction of depression and BMI. Altogether, for the first time, IL-1α, IL-10, EGF, and IFN-γ were shown to differ between AN and HCs, and between AN and individuals with obesity with or without BED. Only IL-2 was influenced by depression. Dysfunctional eating behaviors predicted abnormal concentrations of IL-10, EGF, IL-8 and IFN-γ.