Ebook Obesity-A practical guide: Part 2

(BQ) Part 2 book Obesity-A practical guide presents the following contents: Obesity and gastrointestinal disorders in children, non-alcoholic fatty liver disease in obesity, polycystic ovary syndrome and obesity, obesity and cancer, obesity and thyroid cancer, depression and obesity, obstetrical risks in obesity,...

Obesity and Gastrointestinal Disorders in Children 12 Uma Padhye Phatak, Madhura Y Phadke, and Dinesh S Pashankar Introduction Obesity in childhood is a major problem facing pediatricians all over the world In the United States, the prevalence of obesity {defined as body mass index (BMI) at or above 95th percentile for age and gender} increased from % before 1980 to 17 % in 2012 among 2-to19-years-old children [1] Similar to the United States, the prevalence of obesity is rising throughout the world [2] It is now a global health issue and affects children in both developed and developing countries [3–5] As in adults, obesity in children can lead to many health-related complications Obesity in children is associated with several co-morbidities including diabetes, hepatic steatosis, hypertension, dyslipidemia, and metabolic syndrome In addition to these diseases, obesity adversely affects the psychosocial well-being and the quality of life of children [6–9] Recent studies in adults and children have reported an association between obesity and a wide range of gastrointestinal disorders [10] The U.P Phatak, MD • M.Y Phadke, MD D.S Pashankar, MD, MRCP (*) Division of Pediatric Gastroenterology, Department of Pediatrics, Yale University School of Medicine, 333 Cedar Street, LMP 4091, New Haven, CT 06520, USA e-mail: uma.phatak@yale.edu; madhura.phadke@yale.edu; dinesh.pashankar@yale.edu common gastrointestinal disorders in children include gastroesophageal reflux (GER), functional gastrointestinal disorders (FGID) such as constipation and irritable bowel syndrome, and organic gastrointestinal disorders such as celiac disease and inflammatory bowel disease (IBD) In this chapter, we discuss association of obesity and these disorders in children We describe prevalence, possible mechanisms, and treatment implications of this association for the practicing physician Obesity and GER Gastroesophageal reflux is a very prevalent problem in adults and children There is convincing evidence in adults that obesity is a risk factor for GER [11], erosive esophagitis, Barrett’s esophagus and esophageal adenocarcinoma [12, 13] (See also Chap 11) In contrast to the abundant literature for adults, the data in pediatrics are limited (Table 12.1) Stordal et al in a study from pediatric clinics in Norway compared GER symptoms in 872 children with asthma and 264 controls [14] They found that being overweight was associated with a higher prevalence of GER symptoms in children of 7–16 years of age with and without asthma (OR 1.8, 95 % CI 1.2–2.6) Following this report, Malaty et al assessed children presenting with diagnosis or symptoms of gastroesophageal reflux disease (GERD) to a pediatric gastroenterology clinic at Texas [15] The authors © Springer International Publishing Switzerland 2016 S.I Ahmad, S.K Imam (eds.), Obesity: A Practical Guide, DOI 10.1007/978-3-319-19821-7_12 149 150 U.P Phatak et al Table 12.1 Pediatric studies on the relationship between obesity and GER References Stordal et al [14] Sample size Study group = 872 (asthmatics) Controls = 264 Design Cross-sectional Questionnaire to assess GERD symptom score Malaty et al [15] Pashankar et al [16] Retrospective study Chart review Cross-sectional Questionnaire to assess GERD symptom score Teitelbaum et al [17] N = 627 No control group Study group = 236 (obese children) Control group = 101 (non-obese) Study group = 757 children Controls = 255 + 1436 children Diagnosis based on clinical history Less commonly on endoscopic/histologic finding Cross-sectional Results Higher prevalence of GER symptoms in overweight than in normal-weight children (OR 1.8, 95 % CI 1.2–2.6) 21.4 % of children with GERD are obese Higher prevalence of GER symptoms in obese children (13.1 %) than controls (2 %) Higher prevalence of obesity in children with GERD compared to control group reported that children with GERD were more likely to be obese with a BMI higher than the BMI reported by the National Health and Nutrition examination survey data We compared the prevalence of GER symptoms between 236 obese children attending obesity clinics and 101 children with normal BMI from the general pediatric clinics from Connecticut, USA [16] In this study, each subject was interviewed using a questionnaire for reflux symptoms and a reflux score was calculated Obesity remained as the only significant predictor for a high reflux symptom score after controlling for variables such as age, sex, race and caffeine exposure Also, the reflux symptom score increased in a linear fashion with their increasing BMI In a group of severely obese children (BMI z-score >2.7), 20 % of children had a positive reflux symptom score [16] Similarly, Teitelbaum et al also found a higher prevalence of obesity amongst children with GER referred to a gastroenterology practice as compared to healthy controls in local and New Jersey control populations [17] of the lower esophageal sphincter [18] Another potential theory is that excess fat in diet could result in a delay in gastric emptying with resultant gastroesophageal reflux Mechanism of Association with Obesity and GER Obesity and Functional Gastrointestinal Disorders (FGIDS) A possible mechanism of obesity inducing GER includes extrinsic gastric compression by surrounding adipose tissue leading to an increase in intra-gastric pressures and subsequent relaxation Obesity and Functional Constipation Clinical Significance It is well known that obesity in childhood often persists up to adulthood In addition, gastroesophageal reflux in childhood is also likely to continue in adulthood Therefore obese children with acid reflux are likely to grow into obese adults with acid reflux and may develop reflux related complications including esophagitis, Barrett’s esophagus and even malignancy Hence early diagnosis and prompt therapy in obese children with GER is crucial to prevent long term morbidity and complications of this condition In adults, decrease in BMI has been shown to improve symptoms of acid reflux While pediatric literature is limited on this topic, weight reduction should be an integral part of management of obese children with gastroesophageal reflux Functional constipation is a common gastrointestinal disorder in adults and children [19] In 12 Obesity and Gastrointestinal Disorders in Children 151 Table 12.2 Pediatric studies on the relationship between obesity and constipation References Fishman et al [22] Sample size Study group = 80 (obese children) No control group Study group = 719 (constipation) Control group = 930 Design Cross-sectional study Questionnaire to assess constipation Retrospective chart review Pashankar et al [23] Misra et al [24] Study group =101 (constipation) Control group = 100 Retrospective chart review Teitelbaum et al [17] Cross-sectional study Phatak et al [25] Study group = 757 (children seen at GI practice) Control group = 255 + 1436 Study group = 450 healthy children adults, large population based studies by Talley et al., and Delgado-Aros et al could not demonstrated any significant association between obesity and constipation [20, 21] In addition, a meta-analysis of ten adult studies also could not find any significant association between increasing BMI and constipation [11] In contrast to the studies on adult subjects, the pediatric literatures suggest a positive relationship between obesity and constipation (Table 12.2) Fishman et al in 2004 administered questionnaires to 80 consecutive children who presented to an obesity clinic in Boston about their bowel movements [22] The authors reported that 23 % of obese children met the criteria for constipation and 15 % reported fecal soiling in this cross-sectional study This prevalence of constipation and encopresis in the obese children was noted to be higher than the historical prevalence reported in the general pediatric population [22] Following these studies, we performed a large retrospective chart review in 2005 comparing 719 children with chronic functional constipation with 930 age- and gender- matched controls from pediatric clinics in Iowa, USA [23] We found that the overall prevalence of obesity in both boys Cross-sectional study Questionnaire to assess constipation per ROME III criteria Results Higher prevalence of constipation in obese children (23 %) Higher prevalence of obesity in children with constipation (22.4 %) than control group (11.7 %) Higher prevalence of overweight in children with constipation than control group (43 % vs 30 %) Higher prevalence of obesity in children with constipation than control group Higher prevalence of constipation in obese/ overweight children (23 %) than normal-weight children (14 %) and girls was significantly higher in the constipated group (22.4 %) compared with the control group (11.7 %) Another retrospective chart review by Misra et al reported a similar finding that children with constipation were more likely to be overweight when compared with controls [24] The authors also noted that among the children with chronic constipation, the group of overweight children was male predominant (70.45 % vs 47.36 %), had increased incidence of psychological/behavioral disorders (45.45 % vs 22.8 %) and was more likely to fail treatment (40.9 % vs 21.05 %) More recently two large cross sectional studies by Teitelbaum et al and our’s have found a positive association between obesity and constipation [17, 25] We interviewed 450 children who presented for routine annual physical examinations and immunizations to pediatric clinics in Connecticut A diagnosis of functional constipation was made using a questionnaire based on the Rome III criteria We found that healthy obese/overweight children had a significantly higher prevalence of constipation than their healthy normal-weight counterparts (23 % vs 14 %) [25] Hence, all pediatric data thus far report a significant association between obesity and constipation 152 Obesity and Irritable Bowel Syndrome In adults, the available data on the association between obesity and irritable bowel syndrome (IBS) are conflicting A study of 43 morbidly obese adults referred for surgical consultation for gastric bypass surgery were found to have increased prevalence of symptoms of IBS as compared to normal weight controls [26] Similarly, a large epidemiologic study in USA found a positive relationship between diarrhea and BMI [21] In contrast, a large cohort study in New Zealand did not find a statistically significant relationship between obesity and IBS in adults [20] In children, there are two studies that have explored this association Teitelbaum et al found a significantly higher prevalence of obesity in children with IBS as compared to local and statewide controls in New Jersey, USA [17] In our study from Connecticut, we found an increased prevalence of IBS in obese/overweight children (16.1 %) as compared with normal-weight children (6.9 %) [25] We also found that the statistical significance was maintained when obese and overweight children were compared independently with normal-weight children; thus both pediatric studies have noted a positive relationship between obesity and IBS Mechanism Behind Association of Obesity and FGIDS Overall, the exact mechanism of association between obesity and FGIDs remains unclear Based on the present data, it remains to be elucidated whether the association between obesity and FGIDs is spurious or whether there is a mechanistic link between the two Several different theories including the role of an unhealthy diet, alterations in the levels of neuropeptides and psychosocial factors have been implicated as potential mechanisms for the association between obesity and FGIDs Obese and overweight children often have a diet low in natural fiber and high in sugar and fat U.P Phatak et al One potential theory for this association is that a diet low in natural fiber (fruits and vegetables) could result in increased prevalence of constipation in obese children Some obese children often consume diet containing excess sugars such as fructose corn syrup present in fruit juices and carbonated beverages It is thought that a diet high in such sugars may result in an osmotic effect with resultant pain, bloating and diarrhea Alterations in psychosocial functioning with resultant depression, anxiety, and poor selfesteem are often present in obese children [6–9] There is also an association between these factors and FGIDs [27] It is however unclear at present whether these factors are causes or effects of association between obesity and gastrointestinal disorders Another area that is of great interest in obesity is the role of brain-gut neuropeptides such as leptin, ghrelin, cholecystokinin, and glucagonlike peptide-1 [28] Even minor alterations in the levels of these neuropeptides have been implicated in altered eating behaviors, hunger, satiety and changes in gastrointestinal motility One potential explanation is that these neuropeptides may be the missing link between obesity and FGIDs It has been shown that normal-weight individuals have higher levels of ghrelin than obese-individuals [28] In addition, GI neuropeptides such as ghrelin accelerate colonic and small intestinal transit and have strong pro-kinetic actions Benninga et al in a cross-sectional study evaluated the role of delayed colonic motility in 19 obese children with constipation [29] The authors reported a high frequency of constipation in obese children but were unable to find a significant relationship between delayed colonic transit time and constipation in these obese children Although the authors found that the colonic motility was delayed only in a minority of obese children, this possible mechanism needs to be further explored in larger groups of children [29] Clinical Significance The recently reported association of obesity with FGIDs in children has clinical implications 12 Obesity and Gastrointestinal Disorders in Children 153 In our study, 47 % of the obese/overweight children had at least one FGID as compared with 27 % of the normal-weight children Interestingly, only 36 % of the children with a FGID sought medical attention for their symptoms [25] These results underscore the need for better awareness of this association amongst health care providers and the need to explore for gastrointestinal symptoms in obese/overweight children In a prospective cohort study, Bonilla et al evaluated the possible effect of obesity on the outcome of 188 treated children with abdominalpain related FGIDs The authors found that obese children were more likely to have significantly higher intensity and frequency of pain, school absenteeism and disruption of daily activities at 12–15 months follow-up than non-obese children [30] This study first highlighted the poor longterm prognosis of obese children with abdominalpain related FGIDs and the need for prompt diagnosis and aggressive management Similarly, obese children with constipation were more likely to fail therapy compared to non-obese children with constipation in another study by Misra et al [24] In addition, the authors also found that the obese children with constipation were more likely to have psychological and behavioral problems as compared to the control group Therefore, awareness of this association and prompt therapy may prevent both physical and psychological morbidity in this group of children In addition to standard therapy, dietary intervention in form of high fiber diet is strongly recommended in these children as it is beneficial to both obesity and constipation at diagnosis of celiac disease Tucker et al in their study cohort of 187 adults diagnosed with celiac disease between 1999 and 2009, found that 44 % were overweight, 13 % were obese and only % of subjects were underweight at the time of diagnosis of celiac disease [31] Recent pediatric studies report prevalence rates of overweight/obesity ranging from to 19 % at the time of diagnosis of celiac disease (Table 12.3) [32– 37] It is interesting that these prevalence rates are higher than the prevalence rates of being underweight in most of these studies As obesity is increasing in the general population, it is not surprising that certain patients with celiac disease are obese at the time of their diagnosis The treatment for celiac disease is implementation of a strict gluten-free diet Typically, a gluten-free diet leads to symptomatic improvement in patients including improvement in growth parameters Recent studies have reported a trend towards obesity on a gluten-free diet In a study of 679 adults with celiac disease from Boston, 15.8 % of patients with normal to low BMI became overweight on a gluten-free diet [35] In children the effects of a gluten-free diet on the BMI z-scores are mixed Some studies have noted an increase in BMI z-scores [32, 34] whereas others have reported a decrease in BMI z-scores [33, 36, 37] on a gluten-free diet In their cohort of 142 children with celiac disease, Reilly et al noted that compliance to a gluten free diet was an important factor to prevent obesity on a gluten-free diet [33] Thus recent studies show that children with celiac disease can be obese at presentation and also have a risk of developing obesity on a gluten-free diet Obesity and Organic Gastrointestinal Disorders Obesity and Celiac Disease Celiac disease is an autoimmune disease triggered by exposure to gluten-containing foods in genetically predisposed individuals The classic manifestations of celiac disease include symptoms of malabsorption including diarrhea, malnutrition and failure to thrive However, more recently, obesity is being increasingly recognized Obesity and Inflammatory Bowel Disease Inflammatory bowel disease includes chronic conditions such as Crohn’s disease, and Ulcerative colitis Traditionally, weight loss and poor growth were common presenting symptoms at the time of diagnosis of IBD Contrary to these classic presenting symptoms, recent studies in adults and children have suggested a rise in 154 U.P Phatak et al Table 12.3 Prevalence of obesity at diagnosis of celiac disease and inflammatory bowel disease (IBD) References Norsa et al [32] Reilly et al [33] Valletta et al [34] Brambilla et al [36] Venkatasubramani et al [37] Kugathasan et al [39] Sample size 114 142 149 150 143 783 Disorder Celiac Celiac Celiac Celiac Celiac IBD Long et al [40] 1598 IBD prevalence of obesity at the time of diagnosis of IBD Moran et al conducted a time-trend analysis of 40 randomized controlled adult trials from 1991 to 2008 to include a total of 10,282 patients with Crohn’s disease [38] They found a significant increase in weight and BMI at the time of diagnosis over this time period In a multicenter pediatric study, Kugathasan et al evaluated 783 children with newly diagnosed IBD from USA [39] Although majority of these children were normal weight, 10 % of children with Crohn’s disease and up to 30 % of children with ulcerative colitis had a BMI diagnosis consistent with overweight Long et al., in a cross-sectional study design of 1598 children, found that the prevalence of overweight/obesity in their cohort of children was 20.0 % for Crohn’s disease and 30.1 % for ulcerative colitis and indeterminate colitis [40] African American race and Medicaid insurance were positively associated with overweight/obese status in their study cohort Hence presence of obesity is not an uncommon finding at the time of diagnosis of IBD in children Mechanisms of Association of Obesity and Organic Gastrointestinal Disorders Overweight/obese at presentation 14.1 % 19 % 14 % 12 % 5% 10 % Crohn’s disease, up to 30 % Ulcerative colitis 20 % children with Crohn’s disease and 30 % children with ulcerative colitis were overweight or obese prompt work-up have helped in diagnosing these children early before growth failure sets in It appears that children with celiac disease are likely to be overweight or obese if their diagnostic work up was initiated based on positive screening tests rather than clinical features [41] It is unclear at present whether there is a cause-effect relationship between obesity and IBD The current adult data are mixed and no pediatric studies have been conducted to date to explore the nature of this association Chan et al reported a lack of association between obesity and development of incident IBD [42], however, Khalili et al reported that adiposity was associated with an increased risk of Crohn’s disease in a large cohort of US women [43] Obesity has been linked to elevated levels of pro-inflammatory cytokines such as TNF-alpha and IL-6 [44] Obese individuals have also been shown to have high levels of inflammation in the gastrointestinal tract as measured by fecal calprotectin [45] It is possible that the elevations in the proinflammatory cytokines may be a link between obesity and IBD Hence, it appears that the association between obesity and IBD is evolving and larger studies are needed to explore this association further Clinical Significance It may be that this increase in prevalence of obesity at the time of diagnosis of organic diseases such as celiac disease and IBD is merely mirroring the increasing prevalence of obesity in the general population Increased awareness and Celiac disease and inflammatory bowel disease are organic gastrointestinal disorders in children and historically were associated with failure to thrive at presentation Recent reports indicate 12 Obesity and Gastrointestinal Disorders in Children 155 rising prevalence of obesity in children with these disorders at presentation Interestingly, more children with celiac disease diagnosed at present are likely to be overweight or obese than being underweight [32–37] So practitioners should consider these diagnoses in appropriate settings despite presence of obesity In children with celiac disease, gluten-free diet can lead to rapid increase in weight and put children at increased health risks associated with obesity Close nutritional monitoring of children on gluten-free diet is recommended to avoid this problem Obesity can adversely affect the course of IBD in adults and children In a large retrospective analysis of 2065 adult patients with Crohn’s disease from a gastroenterology clinic in Paris, Blain et al reported that obese patients had increased morbidity, worse disease activity and more frequent perianal complications [46] Two studies in adults report dose escalation of biologic therapy due to severity of disease in obese adults with IBD [47, 48] Krane et al found that operative time and blood loss were significantly longer in the overweight and obese adults undergoing surgery for IBD as compared to normalweight adults [49] In children, Long et al found that high BMI was associated with previous IBD related surgery suggesting that these children may have a more severe disease course [40] This finding is in contrast to the pediatric study by Zwintscher et al who reviewed the 2009 inpatient database from Washington State for all IBD admissions [50] No significant association was noted between obesity and IBD disease severity and the rate of surgical intervention after review of 12,465 inpatient pediatric admissions As obesity may adversely affect the course of IBD, nutritional counseling and weight management should be an integral part of the management strategy in these patients celiac disease and inflammatory bowel disease which used to be associated with growth failure in the past Obesity can adversely affect outcome of these gastrointestinal disorders It is important for practicing physicians to be aware of this association and its significance so that they can provide appropriate care to children such as weight reduction measures which can improve the symptoms of gastrointestinal disorders Conclusion In summary, recent pediatric studies show that there is an association between obesity and gastrointestinal disorders such as 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inflammation as measured by fecal calprotectin: a link between lifestyle factors and colorectal cancer risk Cancer Epidemiol Biomarkers Prev 2004;13:279–84 46 Blain A, Cattan S, Beaugerie L, et al Crohn’s disease clinical course and severity in obese patients Clin Nutr 2002;21:51–7 47 Bultman E, De Haar C, Liere-Baron V, et al Predictors of dose escalation of adalimumab in a prospective cohort of Crohn’s disease patients Aliment Pharmacol Ther 2012;35:335–41 48 Harper J, Sinanan M, Zisman T Increased body mass index is associated with earlier time to loss of response to infliximab in patients with inflammatory bowel disease Inflamm Bowel Dis 2013;19:2118–24 12 Obesity and Gastrointestinal Disorders in Children 157 49 Krane M, Allaix M, Zoccali M, et al Does morbid obesity change outcomes after laparoscopic surgery for inflammatory bowel disease? Review of 626 consecutive cases J Am Coll Surg 2013;216:986–96 50 Zwintscher N, Horton J, Steele S Obesity has minimal impact on clinical outcomes in children with inflammatory bowel disease J Pediatr Surg 2014; 49:265–8 Non-alcoholic Fatty Liver Disease in Obesity 13 Silvia M Ferolla Introduction Nonalcoholic fatty liver disease (NAFLD) is defined as the presence of excessive lipid accumulation in the liver (at least in % of the hepatocytes) of individuals without significant alcohol consumption and/or other known causes of steatosis, such as use of steatogenic medications and prior gastric or jejunoileal bypass NAFLD encompasses a spectrum of clinicopathological conditions that ranges from simple hepatic steatosis (nonalcoholic fatty liver [NAFL]) to hepatic steatosis associated with necroinflammatory lesions (nonalcoholic steatohepatitis [NASH]), which may progress to hepatic fibrosis and cirrhosis and even to hepatocellular carcinoma (HCC) [1] NAFL and NASH have different histological features, natural history and clinical evolution NAFL is characterized by the presence of hepatic steatosis without any evidence of hepatocellular injury Otherwise, NASH is defined as the presence of hepatic steatosis and inflammation with hepatocyte injury associated or not with fibrosis [1] Patients with NAFL have very slow if any histological progression, while NASH can exhibit S.M Ferolla Departmento de Clinica Medica, Faculdade de Medicina, Universidade Federal de Minas Gerais, Belo Horizonte 30130-100, Brazil e-mail: contato@silviaferolla.com.br histological progression to cirrhotic-stage disease [2] In a long-term follow-up study, 10 % of the patients with NASH developed end-stage liver disease in a period of 13 years Progression of liver fibrosis was associated with more pronounced insulin resistance (IR) and significant weight gain Survival of patients with NASH was reduced; they often died from cardiovascular or liver-related causes [3] The differences in the natural history of NAFLD are believed to be related to host characteristics, and associated risk factors NAFLD is usually associated with the metabolic syndrome (MS) [4], which is characterized by numerous interrelated risk factors for cardiovascular disease such as obesity, IR, type-2 diabetes and arterial hypertension Obesity and diabetes are predictors of advanced liver fibrosis and cirrhosis in NAFLD patients [5] The global incidence of NAFLD is unknown since it depends on the population studied and on the methods used to diagnose this condition (e.g., liver biopsy, magnetic resonance spectroscopy and/or ultrasound) In spite of these limitations, the prevalence of NAFLD and NASH in the general population in the Western Countries is estimated to reach 20–30 % and 1–3 %, respectively [3, 6–8] Furthermore, some data indicate that NAFLD has become the most common cause of chronic liver disease in young adults and children [9] Evidence suggests that obesity and IR are the major factors that lead to the development of NAFLD [10] Because the prevalence of MS and © Springer International Publishing Switzerland 2016 S.I Ahmad, S.K Imam (eds.), Obesity: A Practical Guide, DOI 10.1007/978-3-319-19821-7_13 159 27 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 Obesity Prevention in Young Children Rev 2012:13(4):299–315 doi:10.1111/j.1467-789X 2011.00950.x Reger B, Wootan MG, Booth-Butterfield S Using mass media to promote healthy eating: a communitybased demonstration project Prev Med 1999;29(5): 414–21 World Health Organization Population- based approaches to childhood obesity prevention Geneva: WHO Press; 2012 Matsudo V The role of partnerships in promoting physical activity: the experience of Agita Sao Paulo Health Place 2012;18(1):121–2 Gamez R, Parra D, Pratt M, Schmid TL Muevete Bogota: promoting physical activity with a network of partner companies Promot Educ 2006;13(2): 138–43, 64–9 Natale R, Uhlhorn S, Lopez-Mitnik G, Camejo S, Delamater A, Messiah S Caregiver’s country of birth is a significant determinant of accurate perception of preschool-age children’s weight Health Education and Behavior 2015: pii:1090198115599395 [Epub ahead of print] Coleman G Eating right is basic 3rd ed East Lansing: Michigan State University Bulletin Office; 1995 Oakley CB, Bomba AK, Knight KB, Byrd SH Evaluation of menus planned in Mississippi childcare centers participating in the Child and Adult Care Food Program J Am Diet Assoc 1995;95(7):765–8 Ball SC, Benjamin SE, Ward DS Dietary intakes in North Carolina child-care centers: are children meeting current recommendations? 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Appetite 2008; 50(2–3):477–85 114 Haycraft E, Blissett J Eating disorder symptoms and parenting styles Appetite 2010;54(1):221–4 115 Krebs NF, Jacobson MS Prevention of pediatric overweight and obesity Pediatrics 2003;112(2):424–30 27 Obesity Prevention in Young Children 116 Gidding SS, Dennison BA, Birch LL, Daniels SR, Gillman MW, Lichtenstein AH, et al Dietary recommendations for children and adolescents: a guide for practitioners Pediatrics 2006;117(2): 544–59 117 Hoelscher DM, Kirk S, Ritchie L, CunninghamSabo L Position of the Academy of Nutrition and Dietetics: interventions for the prevention and treatment of pediatric overweight and obesity J Acad Nutr Diet 2013;113(10):1375–94 118 Pomeranz JL, Miller DP Policies to promote healthy portion sizes for children Appetite 2015;88:50–8 doi:10.1016/j.appet.2014.12.003 119 U.S Department of Education, Office of Special Education Programs, Individuals with Disabilities Education Act (IDEA) database, retrieved October 3, 2014, from https://inventory.data.gov/dataset/ 8715a3e8-bf48-4eef-9deb-fd9bb76a196e/resource/ a68a23f3-3981-47db-ac75-98a167b65259 120 Chen AY, Kim SE, Houtrow AJ, Newacheck PW Prevalence of obesity among children with chronic conditions Obesity 2010;18(1):210–3 121 De S, Small J, Baur LA Overweight and obesity among children with developmental disabilities J Intellect Dev Disabil 2008;33(1):43–7 122 Rimmer J, Yamaki K, Lowry B, Wang E, Vogel L Obesity and obesity‐related secondary conditions in adolescents with intellectual/developmental disabilities J Intellect Disabil Res 2010;54(9): 787–94 123 Curtin C, Anderson SE, Must A, Bandini L The prevalence of obesity in children with autism: a secondary data analysis using nationally representative data from the National Survey of Children’s Health BMC Pediatr 2010;10(1):11 349 124 Emond A, Emmett P, Steer C, Golding J Feeding symptoms, dietary patterns, and growth in young children with autism spectrum disorders Pediatrics 2010;126(2):e337–42 doi:10.1542/peds.2009-2391 125 Ho HH, Eaves LC, Peabody D Nutrient intake and obesity in children with autism Focus Autism Other Dev Disabl 1997;12(3):187–92 126 Rimmer JH, Marques AC Physical activity for people with disabilities Lancet 2012;380(9838): 193–5 127 Natale R, Camejo S, Asfour LS, Uhlhorn SB, Delamater A, Messiah SE Promoting healthy weight among children with developmental disabilities Journal of Early Intervention, 2015 128 Curtin C, Bandini LG, Perrin EC, Tybor DJ, Must A Prevalence of overweight in children and adolescents with attention deficit hyperactivity disorder and autism spectrum disorders: a chart review BMC Pediatr 2005;5(1):48 129 Ogden CL, Carroll MD, Kit BK, Flegal KM Prevalence of childhood and adult obesity in the United States, 2011–2012 JAMA 2014;311(8): 806–14 130 Lindsay AC, Sussner KM, Kim J, Gortmaker SL The role of parents in preventing childhood obesity Future Child 2006;16(1):169–86 131 McBean LD, Miller GD Enhancing the nutrition of America’s youth J Am Coll Nutr 1999;18(6): 563–71 132 Centers for Disease Control Division of Human Development ad Disability People with disabilities Healthy weight and obesity prevention in schools 2013 Retrieved from www.cdc.gov/ncbddd/ disabilityandhealth/documents/pd_healthywt_obesity_schools.pdf Index A ACE See Angiotensin-converting enzyme (ACE) ACSM See American College of Sports Medicine (ACSM) Activated protein kinase (AMPK) adiponectin, leptin, 49 malonyl-CoA decarboxylase, 35 Adenosine triphosphate (ATP), 15, 18, 19, 35, 59, 72, 73, 108, 124, 160 Adipocyte trypsin (ADIPSIN), 2, Adiponectin, 124, 202 antiatherogenic properties, bloodstream, fatty acid oxidation, 281 HDL, 4–5 IL-6 and TNF-α, insulin resistance, insulin sensitivity, 281 and leptin, metabolic effects, myocardial infarction (MI), nuclear factor B pathway, plasma, Adipose tissue adiponectin, 281 BAT (see Brown adipose tissue (BAT)) leptin, 281 pro-inflammatory cytokines, 281 WAT (see White adipose tissue (WAT)) Adipose triglyceride lipase (ATGL), 18 ADIPSIN See Adipocyte trypsin (ADIPSIN) Adrenocorticotrophic hormone (ACTH), 188 Adult stem cells (ASCs), 24–25 American College of Sports Medicine (ACSM), 323 AMPK See Activated protein kinase (AMPK) Anaplastic thyroid cancers (ATCs), 222 Angiotensin-converting enzyme (ACE), 7, 92, 188 Anti-reflux surgery, 144 Apnea-hypopnea index (AHI), 133 Arabidopsis thaliana, 39 ASCs See Adult stem cells (ASCs) ATCs See Anaplastic thyroid cancers (ATCs) ATGL See Adipose triglyceride lipase (ATGL) ATP See Adenosine triphosphate (ATP) Attention deficit hyperactivity disorder (ADHD), 343 Autism spectrum disorder (ASD), 343 B BA See Bile acids (BA) Bariatric surgery adipose tissue, 281 body weight loss, 286 eating behavior, 286–287 enterohormones, 280 ghrelin, 280 GIP, 281 GLP-1, 280–281 GORD LAGB, 145 LRYGB, 145 LSG, 145 pathophysiologic mechanism, 144 procedures, 144–145 surgical management, 145 gut microbiota, 291 historical procedures, 276 malabsorptive operations, 278 NIH, 275 physiological mechanisms, 285 restrictive operations laparoscopic adjustable gastric banding, 277 laparoscopic sleeve gastrectomy, 277–278 vertical banded gastroplasty, 276–277 robotics, 281–282 RYGB (see Roux-en-Y gastric bypass (RYGB)) VBG, 275 World Health Organization’s projections, 275 BAT See Brown adipose tissue (BAT) BDNF polymorphisms See Brain-derived neurotrophic factor (BDNF) polymorphisms BED See Binge eating disorder (BED) BES See Binge eating scale (BES) Bile acids (BA), 290–291 Biliopancreatic diversion-duodenal switch (BPD-DS), 278 © Springer International Publishing Switzerland 2016 S.I Ahmad, S.K Imam (eds.), Obesity: A Practical Guide, DOI 10.1007/978-3-319-19821-7 351 352 Binge eating disorder (BED) considerations and clinical relevance, 310 diagnostic category, 310 LOC, 310 Binge eating scale (BES), 311 Blount’s disease, 250 BMI See Body mass index (BMI) BMP See Bone morphogenetic protein (BMP) Body mass index (BMI) abnormal maternal, offspring health delivery, 270 neonatal, 270–271 pregnancy, 269–270 CVD, 108 GER, 150 NAFLD, 160 OSA, 132–133 pregnancy, 268–269 variance, missing heritability, 93 Bone morphogenetic protein (BMP), 16, 18 Brain-derived neurotrophic factor (BDNF) polymorphisms depression and bipolar disorder, 238 hippocampus, 238 Met-carrier and exposure, children, 238 MRI techniques, 238 nutrition and microbiota, 239 Breast cancer CLS, 218–219 estimation, 218 estrogen, 218 gene methylation, 219 insulin resistance, 218 Breastfeeding experimental research, 298–299 formula, 297 longitudinal cohort studies, 297 mechanisms, 298 observational studies balancing confounders, 299 cross-population studies, 299 systematic reviews, 299 study designs, 298 Brown adipose tissue (BAT) anatomical locations anterior abdominal wall and inguinal area, 15 children, 15 men and women, 15 sexual dimorphism, 15 subcutaneous, 15 temperature, 16 anti-obesity effects, 15 brite/beige, 13, 15 CCS, 21–22 cell-based therapies, 25 characteristics, 14 cytoplasmatic composition and morphology, 14 endocrine organ, 13 FDG, 13 Index food intake and energy expenditure, 14 HD, 22–23 heat, 13 hyper-adrenergic stimulation, 13 metabolic disorders, 15 mitochondria, 14 MSL, 22 obesity-related diseases, 20–21 origin and differentiation, 16–18 PCOS, 205 SNS, 15 thermogenesis, 18–20 UCP1, 15 C Cancer breast, 218 CRC, 216–217 endometrial, 211 esophageal, 217 HCC (see Hepatocellular carcinoma (HCC)) insulin resistance, 212, 213 leptin and adiponectin, 212, 214 lipid accumulation, 212 metaflammation, 212 pancreatic, 217–218 thyroid (see Thyroid cancer) Cancer cachexia syndrome (CCS), 21–22 CARDIA See Coronary artery risk development in young adults (CARDIA) Carnitine palmitoyl transferase (CPT1), 33, 35 CCS See Cancer cachexia syndrome (CCS) Celiac disease, 153 Central nervous system (CNS) hypothalamus, 60 IL-6 levels, LepRs, 46 leptin, NPY, 238 RYGB, eating-inhibitory effects, 291–292 Central sleep apnea (CSA), 131 Childhood obesity prevention behavior management, 336 caregivers, 336 dietary and physical activities, 335 etiology, 344 kindergarten children, 336 literature, 344–345 meta-analysis, 336 national and international policy, 344 nutritional (see Nutritional gatekeepers) physical activity, 344 portion control disabilities, 343–344 family style, 343 food preferences and eating behaviors, 343 marketing, 342 parenting practices, 343 Index self-regulation, 342 sizes, 342 preschool settings, 336 prevention effects, 335, 336 statistics, 335 Chronic kidney disease (CKD) and CVD, 184–185 and ESRD, 183 and GFR, 183 HTN and DM, 183 metaflammation and insulin resistance adiponectin, 190–191 D-lactate, 191 ESRD, 192 fatty acids and Fetuin-A, 190, 191 LPS and cytokine production, 191 peripheral adipose tissue, 192 podocytes, 192 ROS, 191 SIBO, 191 MHO and MAO populations, 183 systolic and diastolic blood pressure, 183 CKD See Chronic kidney disease (CKD) CLS See Crown-like structures (CLS) CNS See Central nervous system (CNS) CNVs See Copy number variations (CNVs) cOCP See Combined oral contraceptive pill (cOCP) Colorectal cancer (CRC) advanced stage, 216 factors, 216 gut microbiota, 216–217 risk of, 216 Combined oral contraceptive pill (cOCP), 204 Complementary feeding breastfeeding research, 301 fat, 303 longitudinal cohorts, 302 macronutrients, 302 protein, 302 recommendations, 301 solid foods, 301 summing up, 303 systematic reviews, 302 Copy number variations (CNVs), 94–95 Coronary artery risk development in young adults (CARDIA), 70 Coronary heart disease adipocytes, 109 adipokines, 110 atherosclerosis, 108 BMI and threshold, waist circumference, 108 body mass index, 107 CVD, 107 FATE study, 109 NHANES, 107 non-ectopic fat, 109 Nurses Health Study, 107 obesity and atherosclerosis, 109 PDAY, 108 353 percutaneous treatment cardiac catheterization, 111 obesity paradox, 111 pharmacotherapy, 112–113 surgical revascularization, 112 Syntax/Syntax II Scores, 112 stratification strategies, 110–111 visceral fat depots, 110 CPT1 See Carnitine palmitoyl transferase (CPT1) CRC See Colorectal cancer (CRC) Crown-like structures (CLS), 218–219 D DEBQ See Dutch eating behavior questionnaire (DEBQ) Depression and obesity antidepressants, 235 BDNF polymorphisms and brain volumes, 238–239 behavioral and sociocultural factors, 235–236 carbohydrates, 237–238 CCK release, 238 gastrin-releasing peptide, 238 glucocorticoids elevation, 237 hyperglycemia, 236 leptin levels, 237 metabolic dysfunction, 236 MetS, 235, 241 mood and chronic social stress, 238 morphometric feature/change, 237 NPY, 238 nutrition activation, 237 pioglitazone, 237 RAGEs, 236 risk factors, 235, 240 SAGEs, 236 sideeffects, 235 SSRIs, 235 treatments antidepressant drugs, 239 anti-obese properties, 239 brain function, 239–240 metformin, 239 psychotherapy and exercise programs, 239 Diabetes (DM) childhood malnutrition, 117 consequences, 119–120 non-obese person, 118 prevalence data collection, 118 GULF News, 118–119 MENA region, 118 types, 118 risk factors, 119 sign and symptoms, 119 T2DM, 117–118 types, 117 Diabetic neuropathy, 321, 324 Diagnostic and statistical manual of mental disorders (DSM-5), 314 354 Differentiated thyroid cancers (DTCs), 221, 222 Digital health adoption, 258 functionalities, 258 health-related technology, 258 internet weight loss programs, 258 lifestyle choices, 258 traditional behavioral weight loss treatments, 258 Disordered eating bariatric surgery, 311 BED, 310 BES, 311 binge eating, 310 characterization, 309 children and adolescents, 309 DEBQ, 311 EDDS, 311 emotional eating, 315–316 factors, 309 grazing, 312–313 LOC, 310 NES, 313–315 QEWP5, 311 semi-structured clinical interview, 311 subjective experience, 311 TFEQ, 312 treatment, 312 World Health Organization, 309 DM See Diabetes (DM) DSM-5 See Diagnostic and statistical manual of mental disorders (DSM-5) DTCs See Differentiated thyroid cancers (DTCs) Dutch eating behavior questionnaire (DEBQ), 311 E Eating disorder diagnostic scale (EDDS), 311 Eating-inhibitory effects, 291–292 Ecological momentary assessment (EMA) behavior sampling technique, 263 clinical recommendations, 263 diverse populations, 263 ecological momentary systems, 263 electronic devices, 263 evidence-based strategy, 264 factors, 263 retrospective designs, 263 Ecological momentary interventions (EMI) See Ecological momentary assessment (EMA) EDDS See Eating disorder diagnostic scale (EDDS) Electron spin resonance (ESR), 68 EMA See Ecological momentary assessment (EMA) Emotional eating adults, prevalence, 315 assessment, 316 associated features and clinical relevance, 315 characterization, 315 treatment, 316 Index Endoplasmic reticulum (ER) chronic stress, 126 complicaions governmental and international levels, 128 parental levels, 127 personal level, 127 social level, 127–128 endogenous and exogenous stressors, 126 unfolded and misfolded proteins, 126 Enterohormones, 280 ER associated degradation (ERAD), 126 Esophageal cancer, 217 Expanded Food and Nutrition Education Program (EFNEP)., 340 F FAS See Fatty-acid synthase (FAS) Fat mass and obesity-associated gene (FTO), 200 Fatty-acid synthase (FAS), 212, 213 Female metabolic syndrome, 206 FFAs See Free fatty acids (FFAs) 18 F-fluorodeoxyglucose (FDG), 13 FGIDS See Functional gastrointestinal disorders (FGIDS) Fibronectin type III domain containing protein (FNDC5), 24 FNDC5 See Fibronectin type III domain containing protein (FNDC5) Focal segmental glomerulosclerosis (FSGS), 184 Follicular thyroid carcinomas (FTCs), 222 Free fatty acids (FFAs) hepatic influx, 163 lipolysis, 124 metabolic pathways, 160 obesity-related insulin resistance, β-oxidation, 18 serine phosphorylation, 124 whole body glucose homeostasis, 124 FTCs See Follicular thyroid carcinomas (FTCs) FTO See Fat mass and obesity-associated gene (FTO) Functional gastrointestinal disorders (FGIDS) clinical implications, 152–153 constipation, 150–151 IBS, 152 mechanisms, 152 G Gaming, 261–262 Gastroesophageal reflux (GER) acid, 150 BMI, 150 diagnosis, 150 mechanism of obesity, 139, 149, 150 prevalence, 150 symptoms, 149 Gastrointestinal disorders BMI, 149 Index FGIDS (see Functional gastrointestinal disorders (FGIDS)) obesity and GER, 149–150 organic (see Organic gastrointestinal disorders) Gastrointestinal hormones gut hormones, 289, 290 RYGB surgery, 289–290 Gastro-oesophageal junction (GOJ ), 141–142, 145 Gastro-oesophageal reflux disease (GORD) abdominal obesity, 140 anatomical and physiological factors, 140 anti-reflux surgery, 144 bariatric surgery, 144–145 Barrett’s oesophagus, 139, 140 body fat distribution, 140 Bristol Helicobacter project, 140 conservative treatment vs surgical management, 144 definition, 139 diagnosis, 143 epithelial factors, 142 GOJ and LOS, 141, 142 heartburn and regurgitation, 140 hormonal changes, 142 24-h pH monitoring, 143 multivariate survival analysis, 140 oesophagitis, 139 overweight, 139 prevalence, 139–140 symptoms, 143 tissue resistance, 142 TLOSRs, 142 weight loss, 143 Genetic Investigation of ANthropometric Traits (GIANT), 91–92 Genetics, human obesity agriculture development, 87 DNA sequence variants, 87–88 epigenetic process, 88 genetic factors, 87 hypothesis, 87 lifestyle factors bariatric surgery, 98–99 drug-genotype interaction, 98 gene-gene interaction (epistasis), 96–97 gut microbiota, 99–101 nutrition and genomics, 97 physical activity and genomics, 97–98 obesogenic environment, 88 predisposition heritability BMI, 88 candidate gene studies, 90 genes associated, 91 heterogeneous condition, 88 linkage analysis, 90 monogenic forms, 88 next-generation sequencing, 89–90 pathogenesis, 88 phenotypic variations, 88 sex-specific effect, 88 355 Genome-wide association studies (GWAS), 91 GER See Gastroesophageal reflux (GER) Ghrelin, 124, 280 GIANT See Genetic Investigation of ANthropometric Traits (GIANT) GLP-1 See Glucagon-like peptide-1 (GLP-1) Glucagon-like peptide-1 (GLP-1), 280–281 Glucose-dependent insulinotropic polypeptide (GIP), 281 Glucose metabolism and insulin sensitivity, 323 GOJ See Gastro-oesophageal junction (GOJ ) GORD See Gastro-oesophageal reflux disease (GORD) Grazing assessment, 313 considerations and clinical relevance, 313 intentionally fractionating, 312 nomenclatures, 312 treatment, 313 Gut hormones glucose metabolism, 290 potential mechanisms, 290 RYGB, 289 Gut microbiota, 99–101, 291 H hASCs See Human adipose-derived stem cells (hASCs) HCC See Hepatocellular carcinoma (HCC) HD See Huntington’s disease (HD) Healthy inside-healthy outside (HI-HO), 338–339 Hepatocellular carcinoma (HCC) death rates, 211, 214 ER-stress and ROS, 216 incidence and mortality risk, 214 NASH and NAFLD, 214–216 High-density lipoprotein (HDL), 4–5 glucose/insulin ratio, 70 metabolic syndrome, 21 triglyceride levels, 183 HI-HO See Healthy inside-healthy outside (HI-HO) Human adipose-derived stem cells (hASCs), 25 Huntington’s disease (HD), 22–23 I IBS See Irritable bowel syndrome (IBS) ICAM-1 See Intracellular adhesion molecule (ICAM-1) Inducible pluripotent stem (iPS) cells, 25 Infant nutrition breastfeeding, 297–303 complementary feeding, 301–303 evidence, 297 health outcomes, 297 interventions, 304 obesogenic behaviors, 304 parenting and food, 303–304 probit trial, 300 protein and amino acids, 300 taste and flavor exposures, 303 356 Insulin resistance hyperinsulinemia, 212 NAFLD, 215–216 PCOS adverse effects, 201 luteinising hormone (LH), 201 ovarian effects, 201 PI3-kinase and MAP kinase pathways, 201 T2DM mechanism, 125 obesity, 125–126 Insulin signalling pathway adiponectin, 124 brown adipose tissue, 124 glucagon, 125 glucose uptake, 123 GLUT-4, 123 IRS phosphorylation, 123 leptin, 124 plasminogen activator inhibitor-1, 125 white adipose tissue, 123–124 Intracellular adhesion molecule (ICAM-1), 8–9 iPS cells See Inducible pluripotent stem (iPS) cells Irritable bowel syndrome (IBS) Crohn’s disease, 153 prevalence, 153–154 proinflammatory cytokines, 154 surgery, 152 ulcerative colitis, 153 USA, 152 L Laparoscopic adjustable gastric banding (LAGB), 145, 277, 278, 280 Laparoscopic Roux en-Y gastric bypass (LRYGB), 144, 145 Laparoscopic sleeve gastrectomy (LSG), 144, 145 BPD-DS, 277, 278 malabsorptive operation, 277 procedure’s growth, 278 Lateral hypothalamic area (LHA), 50–51, 60, 61 LC n-3 PUFA See Long-chain omega-3 polyunsaturated fatty acids (LC n-3 PUFA) LepRs See Leptin receptor (LepRs) Leptin adipokines, 45 AMPK, 49 chronic diseases, 45 deficiency, 46, 47 energy and metabolic homeostasis, 49, 50 energy expenditure, 45, 51 food intake, 49–51 FoxO1, 49 gene and structure, 45 glucose and lipid metabolism, 51 IRS/PI3K, 49 JAK2/STAT3, 48 JAK2/STAT5, 48 neuroendocrine function, 51–52 production and regulation, 46 receptor, 46 SHP2/ERK, 48–49 Index signalling, 47 Leptin receptor (LepRs), 46 LHA See Lateral hypothalamic area (LHA) Lifestyle intervention, 76, 170, 321, 325 Lipid accumulation FAS and SREBP, 212, 213 insulin resistance, 212 NAFLD, 215, 216 Long-chain omega-3 polyunsaturated fatty acids (LC n-3 PUFA) adipose tissue inflammation, 36–37 adiposity reduction, 34 aetiology, 29 animal evidence body weight and adiposity, 33 brown fat mass, 33 carbohydrate types, 33 diets modulate adiposity and body weight, 33 metabolic effects, 33 obesity-promotion, 33 POP, 33–34 arachidonic acid, 30 calorific intake and expenditure, 29 cardiovascular homeostasis, 30, 31 enzyme-mediated induced synthesis, 31 EPA and DHA, 37–38 erythrocyte levels, 32 fat oxidation, 33, 35 Health Professional Follow-Up Study, 32 insulin sensitivity, 35 lack of consistency, 32 linoleic and α-linoleic acid, 29, 30 measurement, 32 metabolic syndromes, 29 metabolism, 30, 31 muscle blood flow, 35–36 Nurses’ Health Study, 32 osteoarthritis and cancers, 29 RCT, 31–32 ROS, 29 satiety, 35 supply and demand, 38–39 suppression, fat synthesis, 35 LOS See Lower oesophageal sphincter (LOS) Loss of control (LOC) over eating, 310, 311, 313 Lower oesophageal sphincter (LOS), 141, 142 LRYGB See Laparoscopic Roux en-Y gastric bypass (LRYGB) LSG See Laparoscopic sleeve gastrectomy (LSG) M MAMS See Mitochondrial associated membranes (MAMS) MAP kinase pathways See Mitogen-activated protein kinase (MAP kinase) pathways Maternal obesity, 271–272 MCH See Melanin-concentrating hormone (MCH) Mediterranean diet, 76, 97 MEDs See Mobile electronic devices (MEDs) Medullary thyroid cancers (MTCs), 222 Melanin-concentrating hormone (MCH), 50, 51 Melatonin (MEL), 24–25 Index MENA See Middle East and North Africa (MENA) Metabolically healthy obesity (MHO) vs metabolically abnormal obesity (MAO) definition, 181 HOMA-IR, 182 measurement, 182 NAFL and CKD, 182 NWMA, 182 NWMH, 181 obese females, 182 OWMA, 181 OWMH, 181 Metabolic syndrome (MetS), 235, 241 MHO vs MAO See Metabolically healthy obesity (MHO) vs metabolically abnormal obesity (MAO) Middle East and North Africa (MENA), 118 Missing heritability, human obesity BMI variance, 93 CNVs, 94–95 epigenetic factors, 95–96 FTO gene, 93 SNPs, 93–94 Mitochondrial associated membranes (MAMS), 126 Mitogen-activated protein kinase (MAP kinase) pathways, 201 Mobile electronic devices (MEDs) heterogeneity, 260 Keep It Off study, 260 literature, 260 materials, 259 PDAs, 259 promoting health behaviors, 259 SMS technology, 259, 260 MSL See Multiple symmetric lipomatosis (MSL) MTCs See Medullary thyroid cancers (MTCs) Multiple symmetric lipomatosis (MSL), 22 N NAFLD See Non-alcoholic fatty lidisease (NAFLD) NASH See Non-alcoholic steatohepatitis (NASH) National Health and Nutrition Examination Survey (NHANES), 70, 107, 140, 150 National Institute of Health (NIH), 275 NES See Night eating syndrome (NES) Neuro-endocrine system energy and life, 59 energy cycle body mass and obesity, 59–60 gastrointestinal hormones and neuron systems, 60–61 ghrelin, 61–62 satiety and body weight, 60–61 Neuropathy, diabetic, 321, 324 Neuropeptide Y (NPY), 50, 61, 62, 238, 240 New-technology devices behavioral treatments, 258 development, 257 digital health, 258–259 EMA and EMI, 262–264 gaming, 261–262 health information, 257 357 heterogeneity, 257 MEDs, 259–260 mobile phone(s), 257 non-internet users, 257 virtual reality (VR) technology, 262 web-based tools, 260–261 Next generation sequencing (NGS), 90, 91 NGS See Next generation sequencing (NGS) NHANES See National Health and Nutrition Examination Survey (NHANES) Night eating syndrome (NES) assessment, 314–315 characterization, 313 clinical features, 314 DSM-5, 314 features, 314 treatment, 315 NIH See National Institute of Health (NIH) Non-alcoholic fatty liver disease (NAFLD) adipokines, 162 antioxidants, 169 bariatric surgery, 167 BMI, 160 clinicopathological conditions, 159 development, 160 diagnosis alanine aminotransferase ratio, 165 aspartate aminotransferase, 165 circulating levels, cytokeratin-18, 165 CT and MRI, 165 fibrosis score, 165 hepatic steatosis, 164 HFE gene, 164 invasive and morbimortality approach, 165 serum ferritin and transferrin saturation, 164 transient elastography, 165 ultrasonography, 165 dietary patterns, 164, 166 excessive lipid accumulation, 159 gut and adipose tissue-derived factors, 161 gut-microbial alternation and TLR stimulation, 163–164 hepatic and plasma lipoprotein triglyceride, 160 hepatic steatosis and inflammation, 214 hypolipidemic medications, 168–169 IL-1a and IL-1b, 163 insulin resistance, 161–162, 215–216 insulin-sensitizing medications, 167–168 lipid accumulation, 215 macrophages, 163 metabolic pathways, 160–161 and NASH, 159 necroinflammation and fibrosis, 160 omega-3 PUFA, 169 oxidative stress, 160 peroxisome proliferator-activated receptors, 162–163 physical exercise, 166 prevalence, 159–160, 214 probiotics, 169–170 proinflammatory cytokines, 160, 162 risk factors, 159 weight loss medications, 167 358 Non-alcoholic steatohepatitis (NASH) cytokine CXCL10, 214 development, 215 hepatic cirrhosis, 214 oxidative stress, 216 prevalence, 215 NPY See Neuropeptide Y (NPY) Nutritional gatekeepers community based programs, 338 description, 336–337 eating habits, 337 eight right, 339–340 ethnicity and culture, 340–341 family childcare homes vs centres, 340 health start project, 339 HI-HO, 338–339 hip-hop to health junior, 339 mother’s self-efficacy, 337 perception of overweight, 341–342 SCT, 337 SEM, 337–338 O Obesity consequences, 121 cost of controlling, 122 definition, 245 and diabetes, 121–122 and gastrointestinal disorders, 149–155 global increament, 120–121 and GORD (see Gastro-oesophageal reflux disease (GORD)) leptin deficiency, 52 leptin resistance, 52 measurement, 120 overlapping biochemistry, 122–123 and overweight, 120 and PCOS (see Polycystic ovary syndrome (PCOS)) prevalence, 120 SBD (see Sleep-related breathing disorder (SBD)) and thyroid cancer, 221–229 treatment beige/brite fat, 23 cold-induced energy expenditure, 24 energy intake and energy expenditure, 23 irisin and BMP7, 24 MEL, 24–25 pharmacological strategies, 23 weight loss, 52–53 Obesity hypoventilation syndrome (OHS) characteristics, 133 clinical features, 134 diagnosis, 133 pathogenesis, 133 prevalence, 133 relationship, OSA, 134 Index Obesity related glomerulopathy (ORG) chronic inflammatory state, 184 FSGS, 184 mechanisms, 184 metaflammation, 185 Obesity related kidney disease fatty liver accumulation, 186 FFA, FETUIN-A and TLR-4, 185–186 gastrointestinal microbiome in adults, 186 Bacteriodetes, 187 bifidobacteria, 187 germ-free mice, 187 TLR-4 and CD14 receptors, 187 metainflammation, 184 nutritional FFA, 185 treament dietary intervention, 193 glycemic control, 192 IKK and JNK pathways, 193 lipid accumulation, 193 oxidative/inflammatory pathways, 193 RAAS, 192 therapeutic intervention, 192 Obesogenic behaviors, 304 Obestatin, 124–125 Obstetrical risks abnormal nutritional status, 267 global health crisis, 267 offspring health, abnormal maternal BMI delivery, 270 neonatal, 270–271 pregnancy, 269–270 pregnancy, 268–269 prevalence, 267 young adulthood, 271–272 Obstructive sleep apnoea (OSA) AHI, 133 BMI, 132–133 characteristics, 132 diagnosis, 135 PCOS, 199–200, 204 relationship, OHS, 134 risk factors, 132 treatment options, 135–136 upper airway collapsibility, 133 Oesophagogastroduodenoscopy (OGD), 143 OHS See Obesity hypoventilation syndrome (OHS) Omega-3 polyunsaturated fatty acid supplementation, 169 Organic gastrointestinal disorders clinical significance, 154–155 IBD, 153–154 mechanisms, 154 obesity and celiac disease, 153 Index Orthopaedics and trauma adipokines, 246 cast immobilization, 251 categories of patients, 245 in children brain trauma, 249 elective surgery, 250 femur fractures, 249 paediatric fractures, 249 recommendations, 250 and teenagers, 249 complication rates, 248, 251 financial impact, 247 fracture types, 250–251 global population, estimation, 246–247 high-calorie foods and sedentary lifestyle, 246 hip surgery, 252–253 imaging evaluation, 251 incisions, 249 knee surgery, 253 lower limb surgery, 251–252 materials, 248 medical imaging, 247–248 multivariate analysis, 246 patient position, 249 pro-and anti-inflammatory agents, 246 retrograde nailing, 251 surgical procedure, information, 248 thromboembolism, 249 upper limb surgery, 251 OSA See Obstructive sleep apnoea (OSA) Oxidative stress antioxidant, 66, 71 biomarkers, 68, 69 damage, 66 ER stress, 73 free radical, 66 glycolytic metabolites, pathways, 73 hyperglycaemia, 73 impaired glucose tolerance, 74 newborns, 71 nutritional intervention aerobic and resistance exercise, 75 lipoic acid (LA), 77 mediterranean diet, 76 oxidant/antioxidant balance, 75 polyphenol-gut microbiota, 78 retrospective analysis, 75 vitamin deficiency, 77 western diets, 76 obesity and diseases relationship, 78, 79 pathogenic factors, 74, 75 physiological effects, 66 plasma antioxidant profiles, 68 PON1 catalytic activity, 70 potential mechanisms, 71, 72 redox state, 68 RNS, 66 359 ROS, 65, 66 spatial and temporal regulation, 66–67 systemic oxidative stress, 65 TOS, 68 tumour suppressor genes, 75 P PA See Physical activity (PA) PAI-1 See Plasminogen activator inhibitor-1 (PAI-1) Pancreatic cancer, 217–218 Papillary thyroid carcinomas (PTCs), 221–222 Parenting styles, infant nutrition, 303–304 Pathobiological determinants of atherosclerosis in youth (PDAY), 108 PCOS See Polycystic ovary syndrome (PCOS) PDAs See Personal digital assistants (PDAs) PDAY See Pathobiological determinants of atherosclerosis in youth (PDAY) Persistent organic pollutants (POP), 33–34 Personal digital assistants (PDAs), 259 Phosphatidylinositol 3-kinase (PI3-kinase) pathways, 201 Physical activity (PA) adherence, 330 advantages, 330 arthritis, 321 blood pressure, 324 body composition and weight loss, 322–325 cardiovascular markers, 324 definition, 321 exercise program, 327 fitness, 322 general safety tips, 328 glucose metabolism and insulin sensitivity, 323 guidelines, 331 individual’s health conditions, 327 lifestyle interventions, 321–322 neuropathy, 321, 324 osteoarthritis, 328 positive effects, 322 precautions absolute contraindications, 329 diabetic complications, 329–330 medications, obese and diabetic person, 328–329 non-optimal glucose levels, 329 prescriptions aerobic training and resistance training mode, 325 glycemic control, 326 lifestyle behaviors, 327 meta-analysis, 325–326 recommendations, 325, 326 regular exercise, 327 sedentary behavior, 321, 322 PI3-kinase pathways See Phosphatidylinositol 3-kinase (PI3-kinase) pathways Plasminogen activator inhibitor-1 (PAI-1), 2, 7–9, 125 360 Polycystic ovary syndrome (PCOS) cardinal characteristics, 199 cardio-metabolic risk factors, 202–203 development, 205–206 diagnosis, 199 epidemiological data, 200 fat adipokines, 201–202 imaging techniques, 204 and insulin resistance, 201 magnetic resonance (MR), 204 steroids, 201–202 visceral adipose tissue, 203–204 female metabolic syndrome, 206 management, 206 OSA, 199–200 prevalence, 199 T2DM and FTO, 200 treatment, obese women BAT and WAT, 205 medical sticking plaster, 204 menstrual cyclicity, 204 metabolic panacea, 205 metformin, 205 pathogenic mechanisms, 204 weight gain and obesity, 204–205 POP See Persistent organic pollutants (POP) Positive regulatory domain containing 16 (PRDM16), 16 Pregnancy benefits, 269 biologic processes, 268 characterization, 269 extreme obesity, 269 maternal hyperglycemia, 268 metabolic changes, 268 reproductive outcomes, 268 risks, 269–270 Pro-opiomelancortin (POMC) pathway., 189 PTCs See Papillary thyroid carcinomas (PTCs) Q Questionnaire on eating and weight patterns-5 (QEWP5), 311 R RAAS See Renin-angiotensin-aldosterone system (RAAS) Randomized controlled trials (RCT), 31–32 RAS See Renin angiotensin system (RAS) RCT See Randomized controlled trials (RCT) Reactive nitrogen species (RNS) biochemical characteristics, 66, 67 endogenous antioxidant compounds, 67 Reactive oxygen species (ROS) antioxidant supplements, 77 biochemical characteristics, 66, 67 endogenous antioxidant compounds, 67 Index endothelial dysfunction, 73 genetic variants, 74 metabolic syndrome, 74 mononuclear cells, 68 redox sensitive transcription factors, 72 Receptor for advanced glycation end products (RAGEs), 236 Renin-angiotensin-aldosterone system (RAAS) abdominal visceral fat, 190 angiotensinogen, 188 calorie intake and inactivity, 188 cytokines, 189 hypertension, 189 insulin-stimulated NO synthesis, 188 JG cells, 188 obesity and metabolic syndrome, 189 perirenal fat, 191 renal blood flow, 190 sodium reabsorption, 189 sympathetic nervous system, 189 type I receptor, 188 Renin angiotensin system (RAS), 7–8, 225 Retinol binding protein-4 (RBP4), 125 RNS See Reactive nitrogen species (RNS) Robotics, 281–282 ROS See Reactive oxygen species (ROS) Roux-en-Y gastric bypass (RYGB) alimentary limb, 279 BA, 290–291 central nervous system, 291–292 conditioned taste aversion, 288 energy expenditure, 287–288 food intake and meal pattern, 286–287 food reward, 288–289 gastrointestinal hormones, 289–290 gold standard operation, 280 progressive ratio test, 288 restrictive gastrojejunal anastomosis, 279 taste and food preference, 288 RYGB See Roux-en-Y gastric bypass (RYGB) S SBD See Sleep-related breathing disorder (SBD) Selective serotonin reuptake inhibitors (SSRIs), 235, 237 SEM See Socio-ecological model (SEM) Serum advanced glycation endproducts (SAGEs), 236 Sex hormone binding globulin (SHBG), 201 SHBG See Sex hormone binding globulin (SHBG) Single nucleotide polymorphisms (SNPs) chromosome 16q12, 91 redox balance, 74 Single-photon emission tomography (SPECT), 110 Sleep-related breathing disorder (SBD) acute and chronic medical conditions, 131 CSA, 131 diagnosis, 135 effects, obesity Index adipose tissues, 132 CNS, 132 structural defects, 132 upper airway obstruction, 131–132 morbidity and mortality, 135 OHS, 133–134 OSA, 132–133 repeated airway collapse, 131 risk, 131 treatment options, 135–136 Small intestinal bacterial overgrowth (SIBO), 191 SNS See Sympathetic nervous system (SNS) Social cognitive theory (SCT), 337 Socio-ecological model (SEM) drink and snack policy, 338 individual-level behaviors, 337 institutions and community, 337 phycial activity, 338 screen time policy, 338 SPECT See Single-photon emission tomography (SPECT) SSRIs See Selective serotonin reuptake inhibitors (SSRIs) Sterol regulatory element-binding protein-1 (SREBP-1), 34, 35 Sterol regulatory element-binding protein (SREBP), 212, 213 Sympathetic nervous system (SNS), 15, 18, 21 T T2DM See Type diabetes mellitus (T2DM) TFEQ See Three-factor eating questionnaire (TFEQ) THA See Total hip arthroplasty (THA) Thiazolidinediones (TZDs), 5–7 Three-factor eating questionnaire (TFEQ), 312 Thyroid cancer ATCs, 222 DTCs, 221, 222 excessive weight, 221 exposure, 222 FTCs, 222 MTCs, 222 neck palpation, 222 neoplasms, 221 and obesity 1990–2000, 222–223 2001–2010, 223 2011–2012, 223–224 2014, 224 adiponectin, 227 cytokines, 225–226 hormones, 225 leptin, 227–228 resistin, 228–229 TNF-α, 226 occurrence and progression, 221 papillary, 221–222 361 TKA See Total knee arthroplasty (TKA) TLOSRs See Transient lower oesophageal sphincter relaxations (TLOSRs) TNF-α See Tumour necrosis factor-alpha (TNF-α) TOS See Total oxidant status (TOS) Total hip arthroplasty (THA), 252–253 Total knee arthroplasty (TKA), 248, 252, 253 Total oxidant status (TOS), 68 Transient lower oesophageal sphincter relaxations (TLOSRs), 142 Tumour necrosis factor-alpha (TNF-α) FFA, 185 and IL-6, adiponectin, 4, NAFLD, 163, 164, 167 thyroid cancer, 226 WAT, 5, 123 Type 1A diabetes mellitus (T1DM), 117 Type diabetes mellitus (T2DM), 59, 117 and cardiovascular disease, 211 development, 206 and ER (see Endoplasmic reticulum (ER)) FTO, 200 hyperglycaemia, 122 meta-analysis, 119 metabolic syndromes, 122 nuclear Kappa B, 124 obesity and diabetes, 121 OSA, 199–200, 204 PAI-1 and visfatin, 125 TZDs See Thiazolidinediones (TZDs) U UCP1 See Uncoupling protein (UCP1) UDCA See Ursodeoxycholic acid (UDCA) Uncoupling protein (UCP1), 15 anti-obesity effects, 15 brown adipocytes, lipids, 18 multilocular morphology, 15 Ursodeoxycholic acid (UDCA), 170 V Vascular cell adhesion molecule (VCAM-1), 8–9 VBG See tical banded gastroplasty (VBG) VCAM-1 See Vascular cell adhesion molecule (VCAM-1) Vertical banded gastroplasty (VBG) complications, 277 gastric volume reduction, 276 narrow gastric pouch, 276 Virtual reality (VR) technology, 262 Visfatin, 8, 124, 202 VR technology See Virtual reality (VR) technology W WAT See White adipose tissue (WAT) Web-based tools, 260–261 362 Weight loss and PA ACSM recommendations, 323 aerobic exercises, 323 Diabetes Prevention Program, 324 diet and weight management, 324 lifestyle interventions, 325 obese individuals, 322–323 obesity epidemic, 322 risk of weight gain, 322 surgery/caloric restriction, 324, 325 White adipose tissue (WAT) adipokines and atherosclerosis, 8–9 adiponectin, 3–5 ADIPSIN, autocrine, paracrine and endocrine effects, brown adipose fat cells, corticosteroids, free fatty acids, interleukin (IL)-6, 5–6 leptin, 2–3 lipid, low-grade inflammatory state, mitochondria, Index neuroendocrine functions, nucleus, obesity, PAI-1, PCOS, 205 pink adipocytes, pregnancy and lactation, RAS, 7–8 resistin, 6–7 skin, T2DM, 123–124 TNF-α, unilocular adipocytes, Y Young adulthood, maternal obesity in utero nutrition, 271 interventions strategies, 271–272 maternal body weight, 271 pregnancy, 271 weight gain, 271 Young children, obesity prevention See Childhood obesity prevention ... supplements for non-alcoholic S.M Ferolla 20 7 20 8 20 9 21 0 21 1 21 2 21 3 21 4 21 5 21 6 21 7 21 8 fatty liver disease and/or steatohepatitis Cochrane Database Syst Rev 20 07;1:CD004996 Nobili V, Manco M, Devito... strain GG in pediatric obesity-related liver 179 22 6 22 7 22 8 22 9 23 0 23 1 disease J Pediatr Gastroenterol Nutr 20 11; 52: 740–3 doi:10.1097/MPG.0b013e31 821 f9b85 Ma YY, Li L, Yu CH, Shen Z, Chen LH, Li... Hepatology 20 09;49:1017–44 doi:10.10 02/ hep .22 7 42 174 91 Lall CG, Aisen AM, Bansal N, Sandrasegaran K Nonalcoholic fatty liver disease AJR Am J Roentgenol 20 08;190:993–10 02 doi:10 .22 14/AJR.07 .20 52 92