Alcohol, Sleep Deprivation and TV Watching Drive Overeating

Regular readers are well aware that I am more interested in the ‘whys’ of why people eat than in the ‘whats’ of what they eat. Now a paper by Colin Chapman and colleagues from Upsalla University, Sweden, published in the American Journal of Nutrition, looks at the key lifestyle drivers of overeating, with a particular focus on TV watching, sleep deprivation and alcohol consumption as studied in controlled laboratory settings with healthy volunteers. Their search of the literature yielded 8 television studies, 5 sleep studies, and 10 alcohol studies. All three of these factors had significant effects on food intake in the laboratory setting with alcohol having the strongest effect, followed by sleep deprivation and TV viewing. With regards to the possible mechanisms on how these behaviours affect food intake, the authors have the following to offer: Alcohol consumption: “Alcohol is known to induce alterations in circulating ghrelin, a peptide implicated in food reward. In addition, alcohol affects g-aminobutyric acid and opioid systems. The alteration of g-aminobutyric acid signaling in reward centers of the brain stimulates appetite, and opioid signaling has been implicated in regulating the orosensory reward components of eating. These pharmacologic findings are consistent with human studies that showed a greater increase in hunger during the early phase of a test meal after an alcohol preload compared with an energymatched carbohydrate preload. This mimics the pattern of response shown when the palatability of food is enhanced through flavor manipulation.” Sleep Deprivation: “There is similar evidence that links sleep deprivation to an increase in the hedonic value of food. Sleep loss causes a constellation of metabolic and endocrine changes, including an increase in circulating ghrelin. Interestingly, recent studies on sleep deprivation have found that it increases overall brain response to palatable food image. In particular, short sleep increased activation in brain areas involved in reward processing, such as the putamen, nucleus accumbens, thalamus, insula, and anterior cingulate cortex. This strongly suggests that sleep deprivation, like alcohol, leads to deregulation of reward system activation in response to food.” TV Watching: “Several of the studies included in the meta-analysis found that the effect of television viewing on food intake was most pronounced with high-calorie foods, which suggests that television viewing alters the saliency of food reward. Epidemiologic studies have shown a similar trend, in that those who watch more television tend to snack more while watching and to consume more energy-dense… Read More »

Sleep Apnea Limits Response to Obesity Interventions

In follow up to yesterday’s post on the positive impact of CPAP treatment for obstructive sleep apnea (OSA) on weight and cardiometabolic risk factors, here is another study highlighting the importance of diagnosing and managing OSA in obesity patients. This study by Anne-Laure Borel and colleagues from the Institut universitaire de cardiologie et de pneumologie de Québec, Québec, Canada, published in THORAX, the researchers show that OSA attenuates the effects of a lifestyle intervention programme in men with visceral obesity. The authors compare the response of 77 men, selected on the basis of increased waist circumference (≥90 cm) and dyslipidaemia (triglycerides ≥1.69 and/or high-density lipoprotein (HDL) cholesterol <1.03 mmol/litre) to a 1-year healthy eating, physical activity/exercise intervention programme. After the 1-year lifestyle intervention, despite similar compliance to the programme, the 28 men with sleep apnoea syndrome at baseline (ODI ≥10 events/h) showed smaller reductions in body mass index, waist circumference, triglycerides and smaller increases in HDL cholesterol and adiponectin than the 49 men without sleep apnoea. In addition, the higher the baseline ODI and the time spent under 90% oxygen saturation, the lower the reductions in fat mass and visceral adiposity, and the smaller the improvement in glucose/insulin homeostasis indices after 1 year. This finding certainly supports the notion that diagnosis and management of OSA has to be seen as an essential part of obesity management. Here again (according to Helpguide) are the most common symptoms associated with sleep apnea: Major signs and symptoms of sleep apnea Loud and chronic snoring Choking, snorting, or gasping during sleep Long pauses in breathing Daytime sleepiness, no matter how much time you spend in bed Other common signs and symptoms of sleep apnea include: Waking up with a dry mouth or sore throat Morning headaches Restless or fitful sleep Insomnia or nighttime awakenings Going to the bathroom frequently during the night Waking up feeling out of breath Forgetfulness and difficulty concentrating Moodiness, irritability, or depression Signs and symptoms of sleep apnea in children While obstructive sleep apnea can be common in children, it’s not always easy to recognize. In addition to continuous loud snoring, children with sleep apnea may adopt strange sleeping positions and suffer from bedwetting, excessive perspiration at night, or night terrors. Children with sleep apnea may also exhibit changes in their daytime behavior, such as: Hyperactivity or inattention Developmental and growth problems Decrease in school performance Irritable, angry, or hostile… Read More »

CPAP Lowers Body Weight and Improves Metabolic Syndrome in Patients With Sleep Apnea

Regular readers will be well aware of the rather strong association between obstructive sleep apnea (OSA) and excess weight. This is often a two-way street, with OSA leading to poor sleep and sleep cycle disruption, which in turn can affect daytime activity levels and (most likely) eating behaviour. In addition, the intermittent hypoxia associated with OSA has been implicated in hypertension and poor metabolic control. A recent study by Surendra Sharma (no relation) from the All India Institute of Medical Sciences, New Delhi India, published in the New England Journal of Medicine, demonstrates the positive impact of treating OSA with CPAP on body weight and metabolic syndrome. Sharma and colleagues, studied 86 patients, 75 (87%) of whom had the metabolic syndrome, in a double-blind, placebo-controlled trial, in which they randomly assigned patients with OSA to 3 months of therapeutic CPAP followed by 3 months of sham CPAP, or vice versa, with a washout period of 1 month in between. CPAP treatment (vs. sham CPAP) was associated with small but significant mean decreases in blood pressure, cholesterol and triglyceride levels, as well as Hba1C levels. Metabolic syndrome status was reversed in 13% under CPAP vs. 1% under sham treatment. I was quite interested in seeing that there was also a small, but statistically significant reduction in body weight, BMI, and waist circumference. Thus, as the authors note, “We demonstrated a significant decrease in BMI and abdominal fat, by using CT, in association with CPAP therapy. These findings could be secondary to a decrease in daytime somnolence and a consequent increase in physical activity after CPAP use at night.” Moreover, “Weight loss could also be a mechanism for improvement in components of the metabolic syndrome in this study, as suggested by the correlation of the metabolic syndrome with a change in BMI. However, baseline BMI was not a determinant of response to therapy.” The latter finding comes as no surprise given that there is a rather poor relationship between BMI and cardiometabolic risk factors (which is exactly why we came up with the Edmonton Obesity Staging System). Overall, the findings certainly support the notion that patients presenting with excess weight and cardiometabolic risk factors should be routinely screened for OSA and that they stand to substantially benefit from its treatment. AMS Edmonton, Alberta Sharma SK, Agrawal S, Damodaran D, Sreenivas V, Kadhiravan T, Lakshmy R, Jagia P, & Kumar A (2011). CPAP… Read More »

Sleep Restriction Activates Brain Centres That Regulate Appetite

Regular readers will be well aware of the emerging evidence that quality and amount of sleep can have profound effects on eating behaviour and may well be an important factor in the development of obesity. A study by Marie-Pierre St-Onge and colleagues from Columbia University, New York, in a paper published in the American Journal of Clinical Nutrition, used functional Magnetic Resonance Imaging (fMRI) to examine the effect of sleep restriction on brain regions sensitive to food stimuli. The researchers studied 30 healthy, normal-weight men and women for a 2-phase inpatient crossover study in which they spent either 4 h/night (restricted sleep) or 9 h/night (habitual sleep) in bed. Overall neuronal activity in response to food stimuli was significantly greater after restricted sleep than after habitual sleep, particularly in areas associated with reward, cognitive processing, decision-making, and self-control, including the putamen, nucleus accumbens, thalamus, insula, and prefrontal cortex. The findings of this study link restricted sleep and susceptibility to food stimuli and are consistent with the notion that reduced sleep may lead to greater propensity to overeat. “These changes associated with reduced sleep apparently affect brain regions known to be linked to motivation and desire and may indicate an increased propensity to seek food in individuals who are not getting enough sleep. These actions, in a world where food is readily accessible, would promote weight gain. Overall, these findings suggest that changes in neuronal activity in response to food stimuli after insufficient sleep are precursors to energy balance regulation mechanisms in the brain.” Certainly more evidence that lack of sleep may be driving those cravings and impulsive eating that could be contributing to weight gain. AMS Edmonton, Alberta St-Onge MP, McReynolds A, Trivedi ZB, Roberts AL, Sy M, & Hirsch J (2012). Sleep restriction leads to increased activation of brain regions sensitive to food stimuli. The American journal of clinical nutrition PMID: 22357722 .

Clinical Assessment: Dysglycemia, Dyslipidemia, Hypertension, Obstructive Sleep Apnea

Today’s post is another excerpt from “Best Weight: A Practical Guide to Office-Based Weight Management“, recently published by the Canadian Obesity Network. This guide is meant for health professionals dealing with obese clients and is NOT a self-management tool or weight-loss program. However, I assume that even general readers may find some of this material of interest. Dysglycemia Patients who develop type 2 diabetes experience a progressive deterioration of glucose tolerance over time, from normoglycemia to impaired fasting glucose or impaired glucose tolerance, to overt diabetes. Most patients with type 2 diabetes are obese, and abdominal obesity has been recognized as a significant risk factor for the development of type 2 diabetes. With the exception of metformin, the pharmacological treatment of diabetes generally promotes weight gain. This includes sulphonylureas, thiazolidinediones, and most insulins. Newer hypoglycemic agents including insulins (e.g., detemir), long-acting insulin analogues (e.g., insulin, glargine, detemir), and DPP-IV inhibitors (e.g., sitagliptin, vildagliptin) may have a lower risk for weight gain. A new class of GLP-1 agonists (e.g., exenatide, liraglutide) may induce modest weight loss. Dyslipidemia Obesity-associated dyslipidemia has been shown to be atherogenic. Abdominal obesity is associated with increases in plasma triglycerides and decreases in HDL cholesterol. The effect of obesity on LDL cholesterol is less clear, but obese individuals have increased atherogenic small, dense LDL particles and elevated levels of apolipoprotein B (Apo B). Increased levels of lipoprotein a (Lpa) are also commonly seen in patients with abdominal obesity. Hypertension Hypertension is closely related to abdominal obesity, particularly in younger individuals. Obesity-related hypertension is characterized by sodium retention, increased sympathetic activity and activation of the renin-angiotensin-aldosterone system (RAAS). Obstructive Sleep Apnea The presence of obstructive sleep apnea is an important cause of “resistant” hypertension in obese patients and should be formally ruled out in all obese hypertensive patients. Screening for sleep apnea is covered in Chapter 5. Smoking Status Smoking cessation is a major goal for cardiopulmonary risk management. It is important to recognize that smoking is commonly used as a weight-control measure, particularly in younger women. The fear of weight gain should be acknowledged as a significant obstacle to smoking cessation, but it is less likely to produce negative health consequences than continued smoking. © Copyright 2010 by Dr. Arya M. Sharma and Dr. Yoni Freedhoff. All rights reserved. The opinions in this book are those of the authors and do not represent those of the Canadian… Read More »