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      Special considerations for the child with obesity: An Obesity Medicine Association (OMA) clinical practice statement (CPS) 2024

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          Abstract

          Background

          This Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) details assessment and management of the child with overweight or obesity. The term “child” is defined as the child between 2 and 12 years of age. Because children are in a continual state of development during this age range, we will specify when our discussion applies to subsets within this age range. For the purposes of this CPS, we will use the following definitions: overweight in the child is a body mass index (BMI) ≥ 85th and <95th percentile, obesity in the child is a BMI ≥95th percentile, and severe obesity is a BMI ≥120% of the 95th percentile.

          Methods

          The information and clinical guidance in this doi 10.13039/100006091, OMA; Clinical Practice Statement are based on scientific evidence, supported by medical literature, and derived from the clinical perspectives of the authors.

          Results

          This OMA Clinical Practice Statement provides an overview of prevalence of disease in this population, reviews precocious puberty in the child with obesity, discusses the current and evolving landscape of the use of anti-obesity medications in children in this age range, discusses the child with obesity and special health care needs, and reviews hypothalamic obesity in the child.

          Conclusions

          This OMA Clinical Practice Statement on the child with obesity is an evidence based review of the literature and an overview of current recommendations. This CPS is intended to provide a roadmap to the improvement of the health of children with obesity, especially those with metabolic, physiological, psychological complications and/or special healthcare needs. This CPS addresses treatment recommendations and is designed to help the clinician with clinical decision making.

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          Most cited references146

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          Childhood obesity: causes and consequences

          Childhood obesity has reached epidemic levels in developed as well as in developing countries. Overweight and obesity in childhood are known to have significant impact on both physical and psychological health. Overweight and obese children are likely to stay obese into adulthood and more likely to develop non-communicable diseases like diabetes and cardiovascular diseases at a younger age. The mechanism of obesity development is not fully understood and it is believed to be a disorder with multiple causes. Environmental factors, lifestyle preferences, and cultural environment play pivotal roles in the rising prevalence of obesity worldwide. In general, overweight and obesity are assumed to be the results of an increase in caloric and fat intake. On the other hand, there are supporting evidence that excessive sugar intake by soft drink, increased portion size, and steady decline in physical activity have been playing major roles in the rising rates of obesity all around the world. Childhood obesity can profoundly affect children's physical health, social, and emotional well-being, and self esteem. It is also associated with poor academic performance and a lower quality of life experienced by the child. Many co-morbid conditions like metabolic, cardiovascular, orthopedic, neurological, hepatic, pulmonary, and renal disorders are also seen in association with childhood obesity.
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            Obesity and Its Metabolic Complications: The Role of Adipokines and the Relationship between Obesity, Inflammation, Insulin Resistance, Dyslipidemia and Nonalcoholic Fatty Liver Disease

            Accumulating evidence indicates that obesity is closely associated with an increased risk of metabolic diseases such as insulin resistance, type 2 diabetes, dyslipidemia and nonalcoholic fatty liver disease. Obesity results from an imbalance between food intake and energy expenditure, which leads to an excessive accumulation of adipose tissue. Adipose tissue is now recognized not only as a main site of storage of excess energy derived from food intake but also as an endocrine organ. The expansion of adipose tissue produces a number of bioactive substances, known as adipocytokines or adipokines, which trigger chronic low-grade inflammation and interact with a range of processes in many different organs. Although the precise mechanisms are still unclear, dysregulated production or secretion of these adipokines caused by excess adipose tissue and adipose tissue dysfunction can contribute to the development of obesity-related metabolic diseases. In this review, we focus on the role of several adipokines associated with obesity and the potential impact on obesity-related metabolic diseases. Multiple lines evidence provides valuable insights into the roles of adipokines in the development of obesity and its metabolic complications. Further research is still required to fully understand the mechanisms underlying the metabolic actions of a few newly identified adipokines.
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              Prevalence of impaired glucose tolerance among children and adolescents with marked obesity.

              Childhood obesity, epidemic in the United States, has been accompanied by an increase in the prevalence of type 2 diabetes among children and adolescents. We determined the prevalence of impaired glucose tolerance in a multiethnic cohort of 167 obese children and adolescents. All subjects underwent a two-hour oral glucose-tolerance test (1.75 g [DOSAGE ERROR CORRECTED] of glucose per kilogram of body weight), and glucose, insulin, and C-peptide levels were measured. Fasting levels of proinsulin were obtained, and the ratio of proinsulin to insulin was calculated. Insulin resistance was estimated by homeostatic model assessment, and beta-cell function was estimated by calculating the ratio between the changes in the insulin level and the glucose level during the first 30 minutes after the ingestion of glucose. Impaired glucose tolerance was detected in 25 percent of the 55 obese children (4 to 10 years of age) and 21 percent of the 112 obese adolescents (11 to 18 years of age); silent type 2 diabetes was identified in 4 percent of the obese adolescents. Insulin and C-peptide levels were markedly elevated after the glucose-tolerance test in subjects with impaired glucose tolerance but not in adolescents with diabetes, who had a reduced ratio of the 30-minute change in the insulin level to the 30-minute change in the glucose level. After the body-mass index had been controlled for, insulin resistance was greater in the affected cohort and was the best predictor of impaired glucose tolerance. Impaired glucose tolerance is highly prevalent among children and adolescents with severe obesity, irrespective of ethnic group. Impaired oral glucose tolerance was associated with insulin resistance while beta-cell function was still relatively preserved. Overt type 2 diabetes was linked to beta-cell failure.
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                Author and article information

                Contributors
                Journal
                Obes Pillars
                Obes Pillars
                Obesity Pillars
                Elsevier
                2667-3681
                23 May 2024
                September 2024
                23 May 2024
                : 11
                : 100113
                Affiliations
                [1]Alamo City Healthy Kids and Families, 1919 Oakwell Farms Parkway, Ste 145, San Antonio, TX, 78218, USA
                [2]Division of Pediatric Endocrinology, Department of Pediatrics, New York Presbyterian Hospital, Weill Cornell Medicine, 525 East 68th Street, Box 103, New York, NY, 10021, USA
                [3]Division of Weight & Wellness, 41 Donald B Dean Drive, Maine Medical Center, South Portland, ME, 04106, USA
                [4]St. Elizabeth Physicians Group, Medical Weight Management Center, Erlanger, KY, 41018, USA
                [5]Department of Pediatrics, University of Cincinnati College of Medicine, Center for Better Health & Nutrition, The Heart Institute, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH, 45229, USA
                [6]Division of Pediatric Endocrinology, Barbara Bush Children's Hospital, Division of Weight and Wellness, Maine Medical Center, 41 Donald B Dean Drive, South Portland, ME, 04106, USA
                [7]Children's Mercy Kansas City Center for Children's Healthy Lifestyles & Nutrition Medical, Weight Management, Department of General Academic Pediatrics Internal Medicine-Pediatrics, University of Missouri Kansas City, 2401 Gillham Road, Kansas City, MO, 64108, USA
                [8]Children's Mercy Kansas City Center for Children's Healthy Lifestyles & Nutrition Department of Academic Pediatrics, University of Missouri Kansas City School of Medicine, 2401 Gillham Road, Kansas City, MO, 64108, USA
                [9]Children's Mercy Kansas City Center for Children's Healthy Lifestyles & Nutrition Department of Pediatrics, Division of Developmental & Behavioral Health/Weight Management University of Missouri Kansas City School of Medicine, 2401 Gillham Road, Kansas City, MO, 64108, USA
                [10]Allen F. Browne, LLC, Falmouth, ME, USA
                Author notes
                [* ]Corresponding author. PPCNP-BC, FAANP, FAAN, 25 Andrews Avenue, Falmouth, ME, 04105, USA. nancytkacz@ 123456sbcglobal.net
                Article
                S2667-3681(24)00015-9 100113
                10.1016/j.obpill.2024.100113
                11216014
                38953014
                19e97697-8cf2-4faa-9c66-e77f96b52bbd
                © 2024 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 16 May 2024
                : 21 May 2024
                : 22 May 2024
                Categories
                Review: Clinical Practice Statement

                child,obesity,special health care needs,precocious puberty,anti-obesity medications,ho/rohhad,rapid-onset obesity,hypoventilation,hypothalamic dysfunction,autonomic dysregulation

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