J Cleator

Night eating syndrome: implications for severe obesity

Night eating syndrome (NES) was first identified in 1955 by Stunkard, a psychiatrist specialising in eating disorders (ED). Over the last 20 years considerable progress has been made in defining NES as a significant clinical entity in its own right and it has now been accepted for inclusion in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) due for publication in 2013. NES is considered a dysfunction of circadian rhythm with a disassociation between eating and sleeping. Core criteria include a daily pattern of eating with a significantly increased intake in the evening and/or night time, as manifested by one or both of the following: at least 25% of food intake is consumed after the evening meal or at least two episodes of nocturnal eating per week. An important recent addition to core criteria includes the presence of significant distress and/or impairment in functioning. Stunkard’s team recommend further investigation on the pathogenesis of NES, in particular its relationship with traumatic life events, psychiatric comorbidity, the age of onset of NES and course of NES over time. The relationship between NES and other ED also requires further clarification as night-eaters exhibit some features of other ED; previous guidance to separate NES from other ED may have hindered earlier characterisation of NES. Evidence from European and American studies suggests NES features strongly in populations with severe obesity. The complex interplay between depression, impaired sleep and obesity-related comorbidity in severely obese individuals makes understanding NES in this context even more difficult. This review examines evidence to date on the characterisation of NES and concludes by examining the applicability of current NES criteria to individuals with severe obesity.

Effects of peripheral administration of synthetic human glucose-dependent insulinotropic peptide (GIP) on energy expenditure and subjective appetite sensations in healthy normal weight subjects and obese patients with type 2 diabetes

Background  Apart from their role in insulin secretion and glucose homeostasis, the incretin hormones glucagon‐like peptide‐1 (GLP‐1) and glucose‐dependent insulinotropic peptide (GIP) exert a number of extra‐pancreatic effects which in the case of GIP remain largely unknown.

Acute peripheral administration of synthetic human GLP-1 (7–36 amide) decreases circulating IL-6 in obese patients with type 2 diabetes mellitus: A potential role for GLP-1 in modulation of the diabetic pro-inflammatory state?

BACKGROUND To explore the effects of acute administration of GLP-1 and GIP on circulating levels of key adipocyte-derived hormones and gut-brain peptides with established roles in energy and appetite regulation, modulation of insulin sensitivity and inflammation. METHODS Six obese male patients with diet-treated type 2 diabetes (T2DM) and 6 healthy lean subjects were studied. The protocol included 4 experiments for each participant that were carried out in randomised order and comprised: GLP-1 infusion at a rate of 1 pmol/kg/min for 4h, GIP at a rate of 2 pmol/kg/min, GLP-1+GIP and placebo infusion. Plasma leptin, adiponectin, IL-6, insulin, ghrelin and obestatin were measured at baseline, 15, 60, 120, 180 and 240 min following the start of infusion. RESULTS Patients with T2DM had higher baseline IL-6 compared with healthy [day of placebo infusion: T2DM IL-6 mean (SEM) 1.3 (0.3) pg/ml vs 0.3 (0.1)pg/ml, p=0.003]. GLP-1 infusion in T2DM was associated with a significant reduction in circulating IL-6 [baseline IL-6 1.2 pg/ml vs IL-6=0.7 at 120 min, p=0.0001; vs IL-6=0.8 at 180 min, p=0.001]. There was no significant change in leptin, adiponectin, ghrelin or obestatin compared to baseline on all 4 experimental days in both groups. CONCLUSION Short-term infusion of supraphysiological concentrations of GLP-1 in T2DM results in suppression of IL-6, a key inflammatory mediator strongly linked to development of obesity and T2DM-related insulin resistance. It remains to be confirmed whether GLP-1-based diabetes therapies can impact favourably on cardiovascular outcomes.

Obesity and Diabetes.

Obesity increases the risk of developing type 2 diabetes. Jacqueline Cleator and John Wilding describe treatment strategies including diet, activity, pharmacotherapy and surgery. They argue that nurses need to gain a greater understanding of nutritional management and behavioural psychology in order to contribute effectively to treatment.

Ghrelin does not orchestrate the metabolic changes seen in fasting but has significant effects on lipid mobilisation and substrate utilisation

OBJECTIVE Short-term fasting is associated with increased GH pulsatility and mobilisation of fats, but underlying mechanisms are unclear. We studied ghrelins role during fasting and the effects of exogenous ghrelin on lipid mobilisation. DESIGN Randomised placebo-controlled study. METHODS In this study, ten controls (body mass index (BMI) 23.3±3.2), ten morbidly obese subjects (BMI 50.1±10.6) and six post-gastrectomy subjects (BMI 25.2±1.0) were fasted for 36  h undergoing regular blood sampling. On a separate occasion, subjects were infused with either i.v. ghrelin (5  pmol/kg per min) or saline over 270  min. RESULTS Obese and post-gastrectomy subjects had lower ghrelin compared with controls (ANOVA, P=0.02) during the fast. Controls and gastrectomy subjects showed a similar increase in GH pulsatility, circulating non-esterified fatty acids (NEFA) and 3β-hydroxybutyrate (3 HB). Obese subjects had an impaired GH response (P<0.001), reduced excursions of 3 HB (P=0.01) but no change in NEFA excursions (P=0.09) compared with controls. Ghrelin infusion increased GH, NEFA and ketone bodies (ANOVA, P<0.0001) in all the three groups, but GH response was impaired in the obese subjects (P=0.001). Ghrelin also induced a significant (ANOVA, P=0.004) biphasic NEFA response to meals in all the subjects. CONCLUSIONS Despite low circulating ghrelin, gastrectomy subjects maintain a normal metabolic response to fasting, implying that ghrelin plays a minimal role. In contrast, infused ghrelin has significant effects on lipid mobilisation and induces a marked biphasic NEFA response to meals. Hence, ghrelin may play a significant role in meal-related substrate utilisation and metabolic flexibility.

Maintaining weight loss after bariatric surgery: when the spectator role is no longer enough

Bariatric (weight loss) surgery is the gold standard treatment for severe obesity. Concern exists that patients are regaining weight in the longer term. Success and cost‐effectiveness of surgery are threatened due to the re‐emergence of related conditions such as diabetes. This exploratory qualitative study investigates patients’ expectations and experiences of weight regain (WR) 2 years or more after Roux‐en‐Y gastric bypass (RYGB). Ten participants (two men and eight women) who experienced WR were interviewed between 2 and 6 years following surgery. Findings highlight that participants reacted to initial weight loss as passive spectators and were unprepared for subsequent WR. Their tolerability of WR reduced as the amount of regain increased, suggesting a ‘line of tolerance’ for WR. WR was influenced by a new vulnerability arising from weight loss over time, and participants struggled to manage their own weight actively as surgical effects waned. They considered self‐management skills, and carer and professional support to be limited at the time when WR was most likely to occur. Degrees of tolerability are noted in individuals regaining weight after RYGB. More studies are needed to further understand these problems. Pre‐ and post‐operative support and teaching patients self‐management skills may be helpful to minimize WR.

Characteristics and perspectives of night-eating behaviour in a severely obese population.

What is already known about this subject Night‐eating syndrome (NES) can be a feature of severe obesity. NES is a dysfunction of circadian rhythm and is associated with impaired sleep. What this study adds Night eaters with severe obesity are more likely to be low in mood and unemployed compared with non‐night eaters. Night eaters with severe obesity describe compulsive and uncontrolled eating.

Correlations between night eating, sleep quality, and excessive daytime sleepiness in a severely obese UK population

OBJECTIVE The relationships between night eating, poor sleep quality, and obesity-related comorbidity in a severely obese UK clinic population is unknown. We used validated tools to identify prevalence and to explore this relationship. METHODS Consecutive consenting clinic attendees completed the Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Score (ESS), and Night Eating Questionnaire (NEQ) to identify sleep quality, excessive daytime sleepiness (EDS) (a surrogate marker for suspected obstructive sleep apnea [OSA]), and night eating, respectively. Proportions of individuals above and below tool cutoff points were compared. Pearson product moment correlation coefficients examined relationships between total scores. RESULTS Reported prevalence from 144 participants (mean body mass index [BMI] 46.9 [9.5] kg/m(2); age 44.6 [12.1]years; 68% women) had poor sleep quality (73.0%), suspected OSA (30.8%), and night-eating behavior (2.8%). The strongest correlation between PSQI and NEQ scores (r=0.54; P<.001) was undiminished after controlling for EDS. Although significantly correlated, PSQI and ESS scores (r=0.31; P<.001) reduced after controlling for night eating (r=0.21; P=.02). Correlation between NEQ and ESS scores (r=0.26; P=.002) was smaller and nonsignificant after controlling for sleep quality (r=0.12; P=.18). CONCLUSIONS Poor sleep quality is common in severe obesity, though night eating is rare. The association between poor sleep quality and night eating is not influenced by the presence of EDS.

An assessment of the UK inpatient care for heart failure patients with diabetes

Background: Diabetes is a common co-morbidity for patients with heart failure. Diabetes as a co-morbidity means that inpatient care should focus on both conditions to maximize the treatment regimen. However, this pressing issue is not widely researched and so it is unclear whether the acute care management needs of these patients are being met. Aims: (1) To assess the differences in the number of hospital readmissions between patients with heart failure and patients with heart failure–diabetes; (2) to assess the use of integrated care approach for patients with heart failure–diabetes during the index heart failure-related admission; (3) to explore patient experiences of admissions. Methods: A mixed methods design was used: we identified heart failure-related admissions between 1 April 2011 and 31 March 2012 in two hospitals, then reviewed medical records and interviewed 14 patients. Results: Over a 12 month period patients with heart failure–diabetes (n=172) had more heart failure-related Accident and Emergency attendance episodes (incident rate ratio 1.24, p<0.01) and hospital readmissions (incident rate ratio 1.23, p=0.01) than patients with heart failure (n=370). We reviewed 72 medical records which met inclusion criteria (adults with heart failure–diabetes, ejection fraction <45%): during admission most of them were reviewed by heart failure specialists but less than one-third were reviewed by diabetes specialists. The interview respondents addressed the need for better integration and co-ordination of care. Conclusions: This is one of the first UK studies to assess the integration of inpatient care for those with heart failure and multi-morbidities. The findings suggest that maximal care management during admission should be explored as a way of reducing the frequent readmissions and improving patient outcomes.