Summary

This document covers the multifaceted aspects of obesity. It analyses the impact of obesity on various health issues, including increased cancer risks, hepatobiliary disorders, and reproductive problems. The document also explores the etiology or causes of obesity, such as genetics, environmental factors, and metabolic imbalances.

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Obesity increases cancer risk Females Males Endometrium Prostate Ovary Pancreas Cervix Breast (postmenopausal) Oesophagus Females & Males colon, gallbladder, kidney, liver Obesity and hepatobiliary disorders Abdominal obesity ↑ risk of non-alcoholic fatty liver disease (NAFLD) ◦ Steatos...

Obesity increases cancer risk Females Males Endometrium Prostate Ovary Pancreas Cervix Breast (postmenopausal) Oesophagus Females & Males colon, gallbladder, kidney, liver Obesity and hepatobiliary disorders Abdominal obesity ↑ risk of non-alcoholic fatty liver disease (NAFLD) ◦ Steatosis  steatohepatitis  cirrhosis  liver failure Obesity ↑ risk of gallstones (cholelithiasis) ◦ Prevalence of gallstones >3X in BMI >30 compared to healthy BMI (NHANES III) ◦ More related to abdominal obesity, more in women than men ◦ Risk is also increased with rapid weight loss Obesity and reproductive disorders Males: ◦ Reduced testoterone, increased estrogens levels ◦ Gynecomastia Females: ◦ Polycystic ovary syndrome (PCOS) in 5-10% of women of reproductive age:  irregular cycles, acne, excess body hair, infertility ◦ During pregnancy: ↑ risk gestational diabetes, preeclampsia (high blood pressure), labor and delivery complications, fetal and maternal death. 4. Etiology of obesity oEnergy balance oAppetite and body weight regulation oGenes oEnvironmental factors oMedical conditions and medications oOther factors Obesity is a complex illness Heredity Education Inactivity Nutrition Socioeconomic Status Psychology Culture An ancient metabolism in a modern world… Our genes and metabolism evolved in a context of starvation, to conserve and store energy: critical to survival  not adapted to face food abundance and sedentary lifestyles Mismatch between our physiology and the environment Energy balance Body fat Energy intake Energy expenditure First law of thermodynamics Energy balance Body fat Energy intake Energy expenditure High fat, energy-dense foods Palatable, low cost, available foods Large portion sizes Sedentary behavior ↓ Work-related physical activity ↓ Ac vi es of daily living Obesogenic environment Metabolism in obesity Energy Expenditure Components 3000 kcal/d 2500 2000 1500 15-30% Physical Activity Energy (PAE) 5-10% Thermic Effect of Feeding (TEF) 60-75% Resting Energy Expenditure (REE) 1000 500 0 lightly to moderately active individuals Energy Expenditure Components 3000 kcal/d 2500 2000 1500 40-50% 15-30% 5-10% 5-10% 60-75% 50-60% 1000 500 0 lightly to moderately active Active Energy Expenditure Components 3000 kcal/d 2500 2000 40-50% 15-30% 1500 5-10% 15-20% 5-10% 5-10% 1000 60-75% 500 0 lightly/moderately active 50-60% Active 70-80% Sedentary obese Higher REE bc need more mass to walk/etc. bc heavier (extra load) —> the same walk for somebody active vs active will take more energy for somebody OB than active bc of extra load Regulation of appetite: Definitions Hunger: physical sensation indicating need or intense desire for food Satiety: feeling of fullness after eating feeling full now Satiation: state of being satisfactorily full associated with length of time between meals feeling full for a longer period of time Appetite: desire to eat (greek “orexis”) ◦ Homeostatic control (hypothalamus) nobody would eat more than what they need if only hypothalamus ◦ Hedonic control (mesolimbic): influence of environmental factors, emotional, social on pleasure and reward from eating (dopaminergic pathways) based on pleasure of transport of dopamine: reward, desire eating everything explaining that figure is in paper « The Defence of Body Weight » Regulation of food intake (homeostasis) Projections from ARC (arcuate nucleus) to other regions of hypothalamus: PVN: hunger suppressing hormones Lateral hypothalamus: hunger stimulating hormones stimulate appetite Central PVN PUMC: down regulates appetite POMC Peripheral reflect energy balance Signal reflecting energy balance: leptin produce but adipose tissue (the more adipose tissue there is, the more leptin there is, which means stop eating —> not really what we are seeing, ppl prone to OB less sensible to leptin) Peptides hormones produced by gut: when there’s food, these are secreted (Sumithran and Proietto, Clin Sci 2013) Need to be able to recognize them (be able to tell if anorexigenic or orexigenic) in midterm Peptides and hormones involved in central regulation of appetite Location Hypothalamus Anorexigenic Orexigenic POMC Nesfatin-1 TRH CRH Oxytocin Serotonin Histamine Urocortin Neuropeptide Y (NPY) AgRP Orexins MCH Endocannabicoids Opioids (Sumithran and Proietto, Clin Sci 2013) Peptides and hormones involved in central regulation of appetite Location GI tract Pancreas Anorexigenic Orexigenic Cholecystokinin (CCK) Glucagon-like peptide (GLP-1) Peptide YY (PYY) Oxyntomodulin Enterostatin Bombesin Uroguanylin Amylin Insulin Pancreatic peptide (PP) Ghrelin Adipocytes Leptin (Sumithran and Proietto, Clin Sci 2013) Genetic factors oRare congenital causes (see Table 12.4) oObesity is a polygenic disease: multiple genes having relatively small effect on predisposition vs. environment oGenes may affect several aspects: regulation of appetite, metabolism, distribution of body fat, … The onset of the obesity epidemic has occurred recently  not primarily a result of genetic factors not bc of a change in our genetic Susceptibility to obesity is genetically and epigenetically determined interaction of genes with environnment (toxins, nutrients, etc.) —> affects how the gene expressed itself Cultural transmission, environmental factors to take into consideration too Genes in obesity Types of evidence of genetic influence oFamily studies o Adoption studies: adult BMI of an adopted child more related to BMI of biologic (than adoptive) parents factors can override the o Twins raised apart: 50-80% of BMI explained by genetic environmental genes oOverfeeding identical twins: similar weight gain will use energy in a similar way oCandidate genes oGenome wide association studies (GWAS) don’t need to memorize these (SNIPS) ◦ Leptin receptor (LEPR), proopiomelanocortin (POMC), pro-hormone convertase 1 (PC1), brain derived neurotropic factor (BDNF),… ◦ Fat mass and obesity-associated gene (FTO) and melanocortin-4 receptor (MCR4) genes are the major contributors (6%) of cases Don’t have to memorize them Medical conditions and pharmacological agents Hypothyroidism: have to replace hormone = tx common after pregnancy can cause weight gain bc of water retention no the endogenous insulin that predisposes to OB need to inject more insulin —> weight gain sulfonylureas stimulates insulin secretion (Nelms, Table 12.4) Environmental factors Obesogenic environment = physical, social, cultural and economic factors that promote weight gain and are barriers to weight loss Neighbourhood, workplace, school, transport, screen time, … that promote sedentary lifestyle All-time accessibility to food, low cost, large portions, energy-dense foods (↑ kcal/g) See Nelms, boxes 12.6 and 12.7 Other factors associated with obesity sleep deprived: less physical activity, hormone influence (high cortisol), more time to eat oSleep deprivation associated with OB in children and young adults high and oPre-natal exposures: low birth weight, high maternal BMI and pregnancy weight gain high OB oBreast-feeding might be protective against Breastfeed during 6 months oSmoking cessation smoking accelerates BMR —> lowers metabolic rate + ppl eat more oViruses (AD-36) Adenovirus-36 oToxins (endocrine disrupting chemicals, e.g. bisphenol A) oMicrobiota Definition - The Obesity Society 2018 Position Statement Obesity is a multi-causal chronic disease recognized across the life-span resulting from long-term positive energy balance with development of excess adiposity that over time leads to structural abnormalities, physiological derangements, and functional impairments. The disease of obesity increases the risk of developing other chronic diseases and is associated with premature mortality. As with other chronic diseases, obesity is distinguished by multiple phenotypes, clinical presentations, and treatment responses. Jastreboff AM et al. Obesity 27:7-9, 2019 Definition – Obesity Canada 2020 Clinical Practice Guidelines Obesity is a prevalent, complex, progressive and relapsing chronic disease, characterized by abnormal or excessive body fat (adiposity), that impairs health. At the population level, health complications from excess body fat increase as BMI increases. At the individual level, complications occur because of excess adiposity, location and distribution of adiposity and many other factors, including environmental, genetic, biologic and socioeconomic factors. no mention of BMI here People living with obesity face substantial bias and stigma, which contribute to increased morbidity and mortality independent of weight CMAJ 2020;192:E875-91 or BMI. 5. Assessment Should be holistic to identify root causes: o o o o Dietary history and habits Physical activity Medical, psychosocial, cultural aspects Behavioral aspects Dietary history and habits oWeight history, previous diets if a lot of failed diets, may be difficult to do one oFood intake (24-h recall or other method) small change in food can change a lot (ex: diet soda vs soda) oPatterns of meals: at what time food is consumed, where, with whom, that when you eat later it’s not good, it’s more that if you don’t eat all day, you’ll eat for what reason, … not more in the evening where ? usually eat less with ppl, eat more in front of TV, etc. oAbility to cook, access to food, budget more takeout, microwave dinner limit them in their choices, so may opt for a less varied oAllergies, intolerances, beliefs about foods may diet that can be more calorie dense see for deficiency, might oUse of vitamin/mineral supplements, herbs, natural products can flight something out of the oMedications o Emotional eating, mindless eating, knowledge deficit what is their relationship with food in general ordinary (unregulated supplement that can harm them) Physical activity assessment want to see their energy balance From interview, questionnaires or filling log sheets to get an idea of all their daily activities, not only Detail types of activities + time spent for each: want gym bc underestimation ◦ Daily activities: type of work (standing/sitting/physically demanding), mode of transportation, house chores (inside/outside), stair climbing, leisure activities ◦ Time spent sitting, standing, sleeping ◦ Formal exercise habits (walking, running, cycling, swimming, weight lifting, all others sports) Does not capture fidgeting and intensity of PA Physical activity assessment Pedometers: step count can be a tool to promote somebody to do more physical activity Accelerometers: energy spent for PA and total/day ◦ Belt device, bracelet, arm band, watch, … ◦ May include: step count, time sleeping, estimated REE,… ◦ Tri-axial are more accurate Apps on cell phones not precise but gives overall picture Understanding the language o Physical activity = ALL leisure & non-leisure body movement resulting in a substantial increase in EE. o Exercise = a form of leisure time PA that is planned, structured, and repetitive. Its main objective is to improve or maintain physical fitness. o Physical fitness = a set of attributes that are either health or performance (skill) related. The ability to carry out daily tasks with vigor and alertness, without undue fatigue, and with ample energy to enjoy leisure time the body do daily tasks easily (not bc you can lift a lot pursuits and to meet unforeseen emergencies. can of weights like bodybuilder that you are physically fit) o Active living = when physical activities are an integral part of daily living. Physical Activity Level (PAL) Description PAL Bed or chair bound 1.2 Seated work with little movement; little or no leisure activity 1.3 – 1.5 Low 1.3 Seated work with requirements to move; little strenuous activity 1.5 – 1.7 Moderate 1.5 Standing work or very active 1.8 – 1.9 High 1.8 Strenuous work or highly active 2.0 – 2.4* 30-60 min of strenuous leisure activity 4-5 times/wk * Difficult to maintain over long periods of time Moderate Physical Activities need to consider intensity + time of the physical activity METs need more information to do it: how much time did they spend doing this or that Metabolic equivalent task: energy cost of physical activities 1 MET = 3.5 mL O2 uptake/kg BW/minute 100 kg that sleeps for 1hour —> 1 1 MET = 1 kcal/kg BW/hour (sitting or lying quietly) ex: METs x 100 kg x 1 hour = 100 kcal 1 hour swimming —> 7 METs x 100 kg x 1 ◦ Sleeping = 0.9 METs hour = 700 kcal Ppl with higher weight will spend more ◦ Walking slowly = 2.5 METs energy ◦ Vacuuming = 3.5 METs ◦ Swimming = 7.0 METs ◦ More in Nelms, Table 3.13 and Compendium of Physical Activities METs of common daily activities Medical, psychosocial, cultural aspects oPhysical examination, blood pressure, lab tests oPresence of uncommon causal disease (e.g., hypothyroidism) oComplications of obesity oAge < 16, pregnancy, lactation oPsychological disorder, especially eating disorders, anxiety, depression oSociocultural practices and beliefs oPrevious approaches to weight control, to help assess the persons judgment oPatient’s readiness (“Stage of Change” model may be used) Behavioral aspects Readiness to change ◦ Assess readiness to long-term commitment ◦ Family, friend or social support ◦ Right timing ◦ Identify barriers to make long-term changes Use Stages of Change theory (next slide) Stages of Change Model Precontemplation No intention on changing behavior Contemplation Relapse Fall back into old patterns of behaviors Aware a problem exists but no commitment to action Maintenance Preparation Sustained changes, new behaviors replace old Intent of taking action to address the problem Action Active modification of behavior

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