Materiały źródłowe

• #1 Obesity in Pediatric Patients – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK570626/

  Childhood obesity, one of the most prevalent chronic conditions in pediatric populations, has escalated into a global epidemic. Many genetic, physiologic, environmental, and socioeconomic factors influence the development of childhood obesity. This condition increases the likelihood of adult obesity and places affected young individuals at risk for serious short- and long-term adverse health outcomes and comorbidities. […] Obesity is multifactorial, originating from a complex interplay between genetic, biological, environmental, socioeconomic, and cultural factors. Genetics and biology are predetermined, while other factors can be modified. Modifiable factors include family behaviors related to eating, sleeping, and exercise, access to healthy food in schools and communities, availability of safe places for physical activity, and adverse childhood experiences.

• #2 Obesity in Children: Background, Etiology and Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/985333-overview

  Obesity predisposes to insulin resistance and type 2 diabetes, hypertension, hyperlipidemia, liver and renal disease, and reproductive dysfunction. This condition also increases the risk of adult-onset obesity and cardiovascular disease. […] Obesity in children is a complex disorder. Its prevalence has increased so significantly in recent years that many consider it a major health concern of the developed world. Many factors, including genetics, environment, metabolism, lifestyle, and eating habits, are believed to play a role in the development of obesity. However, more than 90% of cases are idiopathic; less than 10% are associated with hormonal or genetic causes. […] During childhood and adolescence, excess fat accumulates when total energy intake exceeds total energy expenditure. This energy imbalance can result from excessive energy intake and/or reduced energy expenditure, the latter is usually a consequence of a sedentary lifestyle.

• #3 Obesity in Pediatric Patients – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK570626/

  Weight gain occurs when energy intake, measured in calories, chronically exceeds energy expenditure, eventually leading to obesity. Genetic determinants play a lesser role. Shifting food preferences in recent decades have been influenced by marketing and the availability of high-calorie processed foods like fast food and sugar-sweetened beverages. […] Appetite and satiety are controlled through neuroendocrine feedback mechanisms. Gastrointestinal hormones, such as ghrelin, stimulate appetite, while glucagon-like peptide-1 (GLP-1), Peptide YY, cholecystokinin (CCK), and vagal neural feedback inhibit appetite and promote satiety. […] Adipose tissue contributes to energy balance through adiponectin and leptin, which signal satiety. These hormones provide feedback to the arcuate nucleus in the hypothalamus, which, in turn, sends behavioral and autonomic outputs to the solitary tract nucleus in the brainstem, stimulating gastrointestinal hormone secretion. […] The neuroendocrine interaction between the gut, adipose tissue, and brain maintains the balance between appetite stimulation and adiposity. Mutations in genes involved in the secretion of these hormones are of interest in epigenetic modifications and may represent potential therapeutic targets.

• #3 Genetics and the Pathophysiology of Obesity | Pediatric Research

  https://www.nature.com/articles/pr2003291

  The involvement of genetic factors in the control of body weight is indicated by studies of monozygotic twins showing a high concordance of body composition and response to overfeeding. The genetic susceptibility is in most cases polygenic, with each gene probably contributing a small part, and is rarely the result of a Mendelian gene (monogenic obesity). Whether or not a smaller number of genes with larger phenotypic effects (i.e. major genes) will be discovered in common obese population is still unknown. […] Thus, obesity results from complex genetic and environmental interactions. This renders the search for susceptibility genes in humans extremely difficult.

• #4 New Thoughts on Pediatric Genetic Obesity: Pathogenesis, Clinical Characteristics and Treatment Approach | IntechOpen

  https://www.intechopen.com/chapters/53070

  This increase of knowledge may provide insights into the mechanisms involved in the regulation of body weight and finally lead to specific treatments. […] In these patients, hyperphagia is often a primary phenotypic component. Substantial gaps in understanding the molecular basis of inherited hyperphagia syndromes are present today with a lack of mechanistic targets that can serve as a basis for pharmacologic and behavioral treatments. […] The strongest risk factor for childhood and adolescent obesity is parental obesity. […] The pattern of inheritance of monogenic obesity is different (which may or may not be related to specific syndromes). […] Patients can be affected by monogenic forms, in which obesity is the predominant feature but it is not associated with malformations, or by syndromic obesity: in the latter case, they show also a pattern of clinical features, including developmental delay, dysmorphic features, and/or other developmental abnormalities.

• #5 Azthena logo with the word Azthena

  https://www.news-medical.net/news/20230406/Pathophysiology-comorbidities-and-interventions-related-to-childhood-obesity.aspx

  Another major biological factor that can contribute to weight gain is the gut microbiome, which is similarly affected by a wide range of factors such as the environment, genetics, lifestyle, diet, gestational age at birth, use of formula during the neonatal and infant stages, feeding practices, age of solid food introduction, and antibiotic use. Dysbiosis, which is defined as an imbalance in the proportion and diversity of gut microbiota, can influence energy dynamics and fat production. […] The genetic factors of obesity can be classified as monogenic or polygenic, the latter of which are more common. Monogenic factors include mutations in specific genes, such as the leptin and tyrosine kinase receptor genes, or genetic disorders such as Prader-Willi Syndrome. […] Polygenic factors involve an interaction between the environment and gene variants that increase an individuals susceptibility to obesity. Behaviors that increase the risk of obesity during the developmental stages include eating larger portions, consumption of high-energy and processed foods, as well as sedentary lifestyles with limited physical exercise, which are also linked to cultural and parenting pressures. […] Obesity is a complex disorder that is influenced by a multitude of biological, genetic, environmental, and lifestyle-associated factors.

• #6 Unexplained Childhood Obesity? Consider Genetic Causes | Children’s Hospital of Philadelphia

  https://www.chop.edu/news/unexplained-childhood-obesity-consider-genetic-causes

  While the major contribution of environmental factors such as consumption of high-energy/high-fat foods, and fast food consumption is well known in the pathogenesis of pediatric obesity, recent studies demonstrate the role of genetic variants in obesity pathogenesis. […] Indeed, genetic disorders associated with obesity are responsible for up to 7% of severe childhood obesity. […] Many genetic diagnoses have been associated with obesity/rapid weight gain. […] The majority are syndromic forms of obesity associated with neurodevelopmental issues, structural birth defects, and/or systemic manifestations as exemplified in James case. […] Among the syndromic forms of obesity, the most common diagnosis in our outpatient clinic is 16p11.2 deletion syndrome. […] Both proximal and distal 16p11.2 deletion syndrome are associated with obesity and neurocognitive impairment.

• #7 Unexplained Childhood Obesity? Consider Genetic Causes | Children’s Hospital of Philadelphia

  https://www.chop.edu/news/unexplained-childhood-obesity-consider-genetic-causes

  Distal 16p11.2 deletion syndrome is due to a 220-kb chromosomal microdeletion of 16p11.2. […] This deletion involves approximately 9 genes including the SH2B1 gene, which is considered to be main driver of the obesity phenotype in this syndrome, because SH2B1 mutant mice demonstrate increased food intake and obesity. […] Other common genetic diagnoses causing syndromic obesity include Down syndrome and Prader-Willi syndrome. […] While these syndromes need to be considered as differential diagnoses for children with obesity, since they tend to cause neonatal problems due to hypotonia and feeding difficulties, the diagnosis of these syndromes tend to be made soon after birth. […] While obese children with syndromic features tend to undergo genetic evaluation, those without syndromic features could have genetic mutations in genes encoding proteins regulating appetites and metabolism.

• #8 Unexplained Childhood Obesity? Consider Genetic Causes | Children’s Hospital of Philadelphia

  https://www.chop.edu/news/unexplained-childhood-obesity-consider-genetic-causes

  These genes include MC4R, LEP, LEPR, PCSK1, and POMC, all belonging to the leptin- melanocortin pathway, which is involved in hunger and energy homeostasis regulation. […] In this class of genetic disorders, treatment with the melanocortin-4 receptor (MC4R) agonist setmelanotide improves hunger and obesity. […] Therefore, identification of pathogenic POMC, PCSK1, and LEPR mutations will have therapeutic implications.

• #9 Obesity in Children: Background, Etiology and Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/985333-overview

  In individuals who are obese, dysfunction in the gut-brain-hypothalamic axis via the ghrelin/leptin hormonal pathway has been suggested to have a role in abnormal appetite control and excess energy intake. […] Studies indicate that dysfunction in this hormonal axis may be the causative factor in as many as 10% of obese subjects, with emphasis particularly on those individuals who appear to manifest familial morbid obesity. […] Despite observations of an etiologic role for genetic and hormonal disorders, these factors alone do not explain the excess weight gain observed in most patients who have obesity and are referred to physicians for evaluation and treatment. […] The accumulation of body fat, particularly in a visceral distribution, reduces the sensitivity to insulin in skeletal muscle, liver tissue, and adipose tissue; this „insulin resistance” predisposes to glucose intolerance and hypertriglyceridemia.

• #10 Childhood Obesity | IntechOpen

  https://www.intechopen.com/chapters/52778

  Hormonal disorders associated with childhood obesity include growth hormone deficiency, growth hormone resistance, hypothyroidism, leptin deficiency or resistance to leptin action, glucocorticoid excess (Cushing syndrome), precocious puberty, polycystic ovary syndrome (PCOS), prolactin-secreting tumors. […] Furthermore, in obese individuals, dysfunction in the gut-brain hypothalamic axis and ghrelin/leptin hormonal pathway has been proposed to have a role in excess energy intake and abnormal appetite control.

• #11 Childhood Obesity: Pathogenesis, Prevention And Treatment

  https://www.prepladder.com/neet-ss-pediatrics/nutrition-and-nutritional-disorders-in-children/childhood-obesity-the-pathogenesis-prevention-and-treatment

  The pathogenesis of childhood obesity consists of a complex interplay of factors that are related to diet and nutrition, lifestyle and environmental factors, neural and endocrine factors, and genetic mutations and syndromes. […] Low levels of Adiponectin have been linked in certain studies to an increased risk of childhood obesity and type 2 diabetes mellitus. Adiponectin lowers the risk factors for obesity and is also involved in glycaemic management in youngsters. […] The drugs which are related to the high risk of obesity are corticosteroids, valproate, lithium, carbamazepine, olanzapine, gabapentin, cyproheptadine, and propranolol. […] The co-morbidities that are associated with the risk factor for obesity include dyslipidaemia, hypertension, non-alcoholic fatty liver disease (NAFLD), metabolic syndrome, PCOD, pseudotumor cerebri, Blount disease, slipped capital femoral epiphysis, asthma, and obstructive sleep apnoea.

• #12 Children and adolescents’ obesity is the 21st century health problem – Bocharova – Kazan medical journal

  https://kazanmedjournal.ru/kazanmedj/article/view/20709

  There is evidence that changes in the intestinal microbiota may contribute to the pathogenesis of obesity and the development of metabolic disorders associated with obesity, including DM2, nonalcoholic fatty liver disease, metabolic syndrome, and cardiovascular diseases. […] The etiology of obesity has been linked to various factors, such as dietary, environmental, educational, and genetic. However, these factors do not fully explain the global gradual increase in the incidence of obesity, and it has recently been shown that the characteristics of microbiota play a causative role in obesity. […] One of the potential indicators that can contribute to the development of obesity is a gastrointestinal microbiome, which has a significant effect on the metabolism of the whole organism and the development of obesity.

• #13 Children and adolescents’ obesity is the 21st century health problem – Bocharova – Kazan medical journal

  https://kazanmedjournal.ru/kazanmedj/article/view/20709

  The action of antibiotics has an overwhelming effect on the intestinal microbiota. […] It was demonstrated that the content of short-chain fatty acids, the end products of fermentation of dietary fiber by anaerobic intestinal microbiota, is higher in obese children, which indicates intestinal dysbacteriosis and its exacerbation; therefore, intestinal fermentation should be considered as one of the factors affecting the etiology of obesity in children. […] Personalized nutrition, the use of prebiotics, probiotics, postbiotics, and synbiotics, transplantation of fecal microbiota, dietary education, and physical activity are the main approaches aimed at using the intestinal microbiota as a therapeutic target for obesity in children. […] The cumulative severity and obesity severity are recognized as primary mediators of worsening cardiovascular and metabolic outcomes. […] Treatment of obesity in the early stages before the onset of concomitant diseases can prevent its development into serious clinical and psychosocial problems.

• #14 The Genetic Basis of Childhood Obesity: A Systematic Review

  https://www.mdpi.com/2072-6643/15/6/1416

  Genetic variations include single-nucleotide polymorphisms (SNPs), copy number variants (CNVs), and small insertions and deletions, each contributing to the development of obesity according to either the common-disease–common-variant hypothesis or the opposing, rare-variant hypothesis. […] The obese state is characterized by a complex metabolic imbalance, associated with major changes in metabolic processes, including the central and peripheral nervous system regulation of energy balance, glucose, lipid, and adipose tissue homeostasis, as well as their interactions. […] In metabolically healthy obesity, new, small adipocytes are formed (hyperplasia), while in impaired adipogenesis, the existing adipocytes become hypertrophic, which is a state associated with metabolic disorders of obesity favoring stress-induced hypoxia, low-grade inflammation, and insulin resistance.

• #15 Early Immune Disorders Induced By Childhood Obesity – The Free Obesity eBook

  https://ebook.ecog-obesity.eu/chapter-biology/early-immune-disorders-induced-childhood-obesity/

  Childhood obesity is increasing at epidemic proportions and is a massive public health concern. Obesity is associated with chronic inflammation and alteration in immune responses. This chronic low grade sterile or cold inflammation has been proposed to underpin the development of obesity related co-morbidites including insulin resistance, type 2 diabetes mellitus and cardiovascular disease. […] Research determining the inflammatory environment and immune function in childhood obesity is essential to determine early mechanistic links between obesity and the development of complications, so as to permit prevention, early detection and intervention. […] The increased incidence of metabolic, autoimmune and inflammatory conditions in obese youth indicates how early the adverse effects of obesity on immune regulation can occur. Metabolic conditions such as insulin resistance (IR) and Type-2 Diabetes Mellitus are steadily increasing in childhood obesity, with metabolic syndrome occurring in up to 50% of obese children in the United States. Macrophages have been proposed as the primary immune population in the development of IR. Adipose tissue macrophages (ATM) change to a pro-inflammatory state (M1) in obesity and subsequently secrete excessive pro-inflammatory cytokines which perpetuate hyperinsulinism. The risk of developing autoimmune Type 1 Diabetes Mellitus is also increased in children who are obese or have a higher body mass index, though the mechanism behind this is not fully understood.

• #16 The Genetic Basis of Childhood Obesity: A Systematic Review

  https://www.mdpi.com/2072-6643/15/6/1416

  A cross-talk between adipose tissue and the immune system takes place, with multiple genes associated with obesity encoding immune-cell-related proteins. […] An excess in macronutrients intake leads to obesity and creates a chronic low-grade aseptic systemic inflammation. […] The proinflammatory state of obesity is also characterized by an anti-inflammatory adaptive response, characterized by changes in T-cell subpopulations in the adipose tissue. […] Finally, microbial agents, such as viruses and viral-like agents, also play an important role in the pathogenesis of obesity, a phenomenon referred to as “infectobesity.”

• #17 Childhood Obesity | IntechOpen

  https://www.intechopen.com/chapters/52778

  Almost all obesity in children is strongly influenced by environmental factors, caused by a sedentary lifestyle or a caloric intake that is greater than needs. […] Insulin resistance is defined as a decreased response of tissue to the action of insulin, and due to lowering of the capacity of insulin to stimulate glucose utilization by muscle cells and fat cells and to suppress hepatic glucose production, and insulin resistance in the protein and lipid metabolism. […] The association of obesity with insulin resistance is well-known: the factors and the mechanism by which the insulin resistance compensation is produced by beta islet cells and those that lead to the „failure” of the pancreatic beta cells in obese patients. […] The metabolic syndrome (central obesity, hypertension, glucose intolerance and hyperlipidemia) increases risk for cardiovascular morbidity and mortality.

• #18 Obesity in Children: Background, Etiology and Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/985333-overview

  In a study by DAdamo et al that evaluated the role of fatty liver in the alteration of insulin sensitivity and -cell function in obese patients, the investigators concluded that fatty liver, independent of visceral fat and intramyocellular lipid content (ICML), has a central role in insulin resistance in obese adolescents. […] The increasing prevalence of obesity in childhood and adolescence, accompanied by insulin resistance, appears to explain the increasing incidence of type 2 diabetes in adolescents, particularly in minority populations.

• #19 Insulin Resistance in Youth May Inform Type 2 Diabetes Prevention | Newswise

  https://www.newswise.com/articles/insulin-resistance-in-youth-may-inform-type-2-diabetes-prevention

  In adolescents who were insulin-resistant, insulin was unable to inhibit the breakdown of fat, largely because insulin failed to activate the main enzyme regulating fat breakdown in adipose tissue. […] As a result, excess fatty acids continued to flow into other tissues, which may help explain why some adolescents with obesity develop type 2 diabetes. […] We are seeing a well-characterized mechanism respond differently in two distinct populations of children with obesity. […] The team hopes their identification of this altered mechanism can help researchers better understand how to therapeutically intervene. […] I want to stop the onset of type 2 diabetes—that’s our goal. […] Then, we can hopefully design a strategy to make these youth more sensitive to insulin signaling and mitigate negative downstream consequences.

• #20 PEDIATRIC OBESITY‚ Etiology‚ Pathogenesis and Treatment

  https://www.berri.es/libreria_medica/PEDIATRIC-OBESITY_-Etiology_-Pathogenesis-and-Treatment/Freemark/9781603278737/334380/cod=334380&dir_volver=1&cat=LM24&numpags=600

  Childhood obesity and its co-morbidities — including type 2 diabetes, hypertension, dyslipidemia, sleep apnea, and fatty liver disease — have seen striking increases in recent years. […] Despite a wealth of investigation, there is considerable controversy regarding the etiology of childhood obesity and the optimal approaches for prevention and treatment. […] The distinguished authors re-assess the roles of genetic and environmental factors in the pathogenesis of childhood obesity and critically review new studies of the effects of lifestyle, pharmacologic, and surgical interventions. […] The role of diet: Laura Johnson and Susan Jebb […] Pathogenesis of insulin resistance and glucose intolerance in childhood obesity: Ram Weiss and Sonia Caprio […] Pathogenesis and management of dyslipidemia in obese children: Brian McCrindle […] Pathogenesis of hypertension and renal disease in obesity: Tracy Hunley and Valentina Kon […] Pathogenesis and treatment of hypothalamic obesity: Robert Lustig.

• #21 Paediatric obesity: a systematic review and pathway mapping of metabolic alterations underlying early disease processes | Molecular Medicine | Full Text

  https://molmed.biomedcentral.com/articles/10.1186/s10020-021-00394-0

  The present global eminence of childhood obesity and associated early onset of asymptomatic complications, has not escaped the awareness of metabolomics research. […] The complex synergistic intertwining of such influencing variables is vital. […] The significant metabolites that were extracted from included studies were reviewed in light of their potential value as early-stage hallmarks of future metabolically unhealthy phenotypes together with in-depth interpretation of disturbances observed in their associated metabolic pathways. […] The central carbon metabolism was shifted towards hypoxic conditions in children with obesity as high pyruvate, lactate and alanine served as markers of disrupted metabolism occurring early in life. […] The BCAAs leucine and isoleucine have been related to the PI3KAKTmTOR pivotal nutrient-sensitive signaling pathway that is implied in -cell growth and proliferation as well as its downstream effector functions including glucose uptake by GLUT4 in insulin sensitive tissues, i.e. liver, muscle and adipose tissue. […] In this regard, a reduced level of arginine, which forms a substrate for nitric oxide synthase, has been related to increased production of ROS and nitric oxide, especially in the mitochondria of the liver.

• #22 Childhood obesity – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/childhood-obesity/symptoms-causes/syc-20354827

  Childhood obesity is a complex condition. Various factors can play a part in causing it. These include: […] Genetic and hormonal factors. […] Some other factors for childhood obesity may be out of a parent’s ability to control. They include the following: […] Sometimes, changes to certain genes can play a part in childhood obesity. So can conditions linked with hormones and many other processes that happen inside the body. […] Personal stress and family stress can raise a child’s risk of obesity. Ongoing stress can cause the body to make high amounts of hormones such as cortisol. High levels of these hormones can cause feelings of increased hunger. They also can trigger cravings for foods that have lots of fat and added sugar. […] Certain medicines can raise the risk of obesity.

• #23 Azthena logo with the word Azthena

  https://www.news-medical.net/news/20230920/Obesity-pathogenesis-Unanswered-questions-and-future-directions.aspx

  Prof. John Speakman from the Shenzhen Institute of Advanced Technology (SIAT) of the Chinese Academy of Sciences, alongside Prof. Kevin Hall from the National Institutes of Health (U.S.), Prof. Thorkild Sorensen from the University of Copenhagen and Prof. David Allison from Indiana University (U.S.), has published a perspective article on potential mechanisms of obesity pathogenesis. […] Recent advances in obesity research have been significant. Leptin, a hormone produced by fat cells, plays a pivotal role in regulating food consumption by triggering brain signals. The traditional view of adipose tissue as a passive storage unit has shifted to recognizing its active role in producing hormones that impact the entire body. […] How is body weight and adiposity regulated, and what factors influence this regulation? The intricate mechanisms behind powerful regulatory signals and their vulnerability remain unclear.

• #24 Causative Mechanisms of Childhood and Adolescent Obesity Leading to Adult Cardiometabolic Disease: A Literature Review

  https://www.mdpi.com/2076-3417/11/23/11565

  The mechanisms that lead from weight excess to pathology are discussed within each level of this approach, firstly regarding the general distribution of surface fat describing the mechanisms behind sexual dimorphism in the android versus gynoid fat disposition, as well as their link to obesity-related disease by correlating to a major culprit of cardiometabolic risk, which is central obesity. The physiopathological pathways explaining the connection between central obesity and cardiometabolic risk are discussed in the perspective of the possible role of increased lipolytic activity of visceral adipose tissue altering hepatic and general metabolism. Further on, the particular role of excess fat localized in the proximity of specific organs is presented. Excess perihepatic fat and the flawed intracellular deposition of triglycerides in hepatocytes linked to non-alcoholic fatty liver disease are presented. Epicardial, perivascular, and perirenal excess adipose tissue disposition and their detrimental effect on hemodynamics and metabolism are discussed subsequently.

• #25 Causative Mechanisms of Childhood and Adolescent Obesity Leading to Adult Cardiometabolic Disease: A Literature Review

  https://www.mdpi.com/2076-3417/11/23/11565

  The information in Section 4 emphasizes the need for more refined methods to assess obesity by considering adipose tissue disposition. […] Section 8 (Mechanisms of obesity-related cardiometabolic disease) aims to describe the mechanisms behind these associations. These two sections mostly refer to cardiovascular and metabolic diseases and the mechanisms incriminated in their development in obese patients, i.e., arterial hypertension, ventricular hypertrophy, heart failure, atherosclerotic vascular diseases (ischemic heart disease, cerebrovascular disease, and peripheral artery disease), type 2 diabetes, and dyslipidemia. […] The physio-pathological pathways leading from obesity to cardiovascular disease involve both direct and indirect mechanisms with both local and systemic action. From a hemodynamic standpoint, the adaptive changes of the cardiovascular system are due to the structural and functional alterations imposed by the increase in circulating volume and metabolic strain attributable to excess adipose tissue. This generates a hyperdynamic cardiovascular system constrained to adapt the cardiac output by increasing stroke volume and heart rate. Peripheral vascular resistance increases due to sympathetic hyperreactivity and the systemic proinflammatory status associated with obesity. The most direct consequence of these modifications is an increase in blood pressure, which partly explains the causation behind the higher prevalence of arterial hypertension in obese patients.

• #26 Obesity and hypertension in children and adolescents | Clinical Hypertension | Full Text

  https://clinicalhypertension.biomedcentral.com/articles/10.1186/s40885-024-00278-5

  Overweight and obesity affect BP in many ways, and adiposity and weight gain are essential contributors to primary hypertension. The development of hypertension in obesity is influenced by several factors, including increased sympathetic nervous system (SNS) activity, activation of the renin-angiotensin-aldosterone system (RAAS), and compression of the kidneys due to fat accumulation, resulting in increased renal sodium reabsorption and impaired pressure natriuresis. […] Increased SNS is thought to play an essential role as a mechanism for hypertension in obesity. In a study showing that weight gain itself increases SNS, 12 healthy men were made to gain 5 kg of weight by overeating, and when comparing before and after, there was a significant increase in total fat and abdominal fat and a substantial increase in muscle SNS and SBP, suggesting a relationship between obesity and hypertension.

• #27

  https://journals.lww.com/jaaosglobal/fulltext/2019/05000/the_role_of_obesity_in_pediatric_orthopedics.2.aspx

  Pediatric obesity has become a worldwide epidemic and leads to notable effects on the developing skeleton that can have lifelong implications. Obesity in the pediatric population alters bone metabolism, increasing the risk for fracture. […] Obesity plays a strong role in altering this normal accrual because increased body fat has a negative effect on attaining peak bone mass. […] Obesity plays a strong role in bone physiology, especially through the metabolic syndrome which is a well-known condition related to abdominal obesity, altered glucose metabolism, dyslipidemia, and hypertension. […] Elevated leptin levels accelerate bone resorption and decreases bone formation through increased RANKLA expression and decreased Receptor Activator of Nuclear factor Kappa-B Ligand (RANKL) inhibition.

• #28

  https://journals.lww.com/jaaosglobal/fulltext/2019/05000/the_role_of_obesity_in_pediatric_orthopedics.2.aspx

  Vitamin D deficiency has been found in 29% of overweight children, 34% of obese children, and 49% of severely obese children. […] Obese children have poorer balance than normal weight age-matched controls and lower bone mineral content to size ratio. […] Obesity has an effect on both the pattern and severity of orthopaedic injuries. […] The fact that obese children are more likely to sustain severe injury patterns has been supported by others. […] These studies support the idea that as body mass increases, so does the force generated from a comparable mechanism of injury, thus leading obese children to sustain more severe injury patterns than their nonobese peers. […] Challenges created by obesity during fracture care are well documented in the adult orthopaedic literature. […] Obesity markedly alters the physiologic and mechanical forces in pediatric patients. This is a modifiable factor that can be positively altered, leading to decreased postoperative complication risk and improved patient health and safety.

• #29 Skin and obesity in childhood: an update

  https://www.aimspress.com/article/doi/10.3934/medsci.2021026?viewType=HTML

  Overweight and obesity have grown in children in the last decades and are now an epidemic, leading to significant public health issues in developed and underdeveloped nations. Obese children have a higher prevalence of skin lesions than normal weight children. […] The most frequent obesity-associated dermatological complications in children are acanthosis nigricans and acrochordons, atopic dermatitis, skin infections, and endocrinological changes including hyperinsulinism and hyperandrogenism. Other common skin manifestations associated with obesity are striae distensae and plantar hyperkeratosis. […] Although the causes of the majority of the skin lesions associated with obesity are not known, the larger mass of adipose tissue and the secretion of peptides (cytokines, hormones, etc.) from enlarged fat cells due to obesity could lead to skin lesions. Therefore, the prevention of obesity is essential to avoid most skin-associated lesions.

• #30 Child and adolescent obesity | Nature Reviews Disease Primers

  https://www.nature.com/articles/s41572-023-00435-4

  The prevalence of child and adolescent obesity has plateaued at high levels in most high-income countries and is increasing in many low-income and middle-income countries. Obesity arises when a mix of genetic and epigenetic factors, behavioural risk patterns and broader environmental and sociocultural influences affect the two body weight regulation systems: energy homeostasis, including leptin and gastrointestinal tract signals, operating predominantly at an unconscious level, and cognitive-emotional control that is regulated by higher brain centres, operating at a conscious level. […] Comorbidities of obesity, including type 2 diabetes mellitus, fatty liver disease and depression, are more likely in adolescents and in those with severe obesity. […] Development and implementation of interventions to prevent paediatric obesity in children should focus on interventions that are feasible, effective and likely to reduce gaps in health inequalities.

• #31 pfm :: Precision and Future Medicine

  https://www.pfmjournal.org/m/journal/view.php?number=165

  The consequences of obesity in children are multifold for both individual health and public healthcare systems. At the individual level, childhood obesity is associated with concurrent short-term comorbidities in all organ systems, including hypertension, dyslipidemia, fatty liver disease, gastroesophageal reflux, polycystic ovarian syndrome, pubertal disorders, intracranial hypertension, asthma, obstructive sleep apnea, skeletal and muscular acute injuries, and slipped capital femoral epiphysis. […] However, cardiometabolic risk factors and the metabolic syndrome are clearly associated with the degree of obesity, with adjusted odds ratios for meeting the International Diabetes Federation criteria for the metabolic syndrome increasing sequentially from 54.2 to 283.3 to 950.3 for overweight, class I, and class II/III obesity respectively.

• #32 Childhood Obesity: Causes & Problems

  https://my.clevelandclinic.org/health/diseases/9467-obesity-in-children

  Social determinants of health (SDoHs) are the conditions in the environments where you’re born, live, learn, work and play that can affect your health. […] Advertising for fast food restaurants and unhealthy foods and beverages can contribute to childhood obesity. […] Rarely, other health conditions may be a contributing factor to childhood obesity. […] Hormonal imbalances that can contribute to childhood obesity include: hypothyroidism, hypothalamic tumor, growth hormone deficiency, Cushing syndrome. […] Your child’s healthcare provider will determine if your child’s health is at risk due to their weight. […] Comprehensive obesity treatment typically includes: providing intensive, long-term treatment, evaluating and monitoring your child for obesity-related medical and psychological complications, identifying and addressing social drivers of health (like access to affordable healthy foods), using non-stigmatizing approaches to treatment that consider your child and family’s unique qualities and situation, using motivational interviewing that addresses nutrition, physical activity and health behavior change, setting holistic treatment goals, integrating intensive health behavior and lifestyle treatment (IHBLT) with weight loss medications and/or metabolic and bariatric surgery if necessary, adjusting treatment to the ongoing and changing needs of your child and family. […] Experts in childhood obesity highly recommend the use of intensive health behavior and lifestyle treatment (IHBLT).

• #33 Potential mechanisms in childhood obesity: causes and prevention – Energy Balance and Obesity – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK565802/

  Experiences during early life stages (including prenatal factors, such as exposures that women experience, and postnatal factors, such as infant and young child feeding) can have important, long-term impacts on future health, including risk of obesity. […] Family environment is important for children’s health behaviours and outcomes. The relationship between family socioeconomic status and obesity is complex, has changed over time, and varies between population groups and between countries. […] The global childhood obesity epidemic demands a population-based, multisectoral, multidisciplinary, and culturally relevant approach. Children need assistance and special efforts to help them develop healthy eating patterns and physical activity behaviours and maintain an optimal body weight. […] To prevent obesity, it is recommended that children should: (i) increase consumption of fruits and vegetables, legumes, whole grains, and nuts; (ii) limit energy intake; (iii) limit the intake of high-energy-density foods, such as fried foods, fast foods, processed foods, and sugars, as well as sugar-sweetened beverages; and (iv) be physically active and reduce sedentary behaviours (accumulate at least 60 minutes of moderate to vigorous activity each day, and limit screen time).

• #34 pfm :: Precision and Future Medicine

  https://www.pfmjournal.org/m/journal/view.php?number=165

  Severe obesity, an increasing problem in recent years, is associated with an increased number of comorbid cardiometabolic conditions. […] Childhood obesity eventually tracks into obesity in 55% of adolescents, with 80% of obese adolescents remaining obese in adulthood. […] The most recent clinical guidelines for the evaluation and treatment of overweight and obesity in children and adolescents were published by the American Academy of Pediatrics (AAP) in 2023. […] Intensive health behavior modification and lifestyle interventions are central to childhood obesity treatment, with a focus on healthy eating habits and increased physical activity. […] Although healthy eating and physical activity form the basis of successful obesity treatment, there are limitations in the extent and maintenance of weight loss with lifestyle modifications alone.

• #35 pfm :: Precision and Future Medicine

  https://www.pfmjournal.org/m/journal/view.php?number=165

  In the recent AAP guidelines, offering obesity pharmacotherapy in adjunction with intensive health behavior lifestyle treatment in children aged 12 years or older has been regarded as a paradigm shift that will hopefully improve outcomes in pediatric obesity. […] The past few years have brought about the approval of several medications for the adolescent population that could be effective adjuncts to lifestyle modifications for sustained weight loss. […] The medications reviewed were orlistat, phentermine monotherapy, glucagon-like peptide-1 (GLP-1) receptor agonists (liraglutide and semaglutide), and phentermine/topiramate, with a focus on efficacy, adverse effects, and practical information regarding the usage of each of these medications in children and adolescents. […] Obesity in children is a chronic and complex disease associated with numerous comorbidities that persist into adulthood. While intensive health behaviors and lifestyle interventions are fundamental to weight loss, lifestyle modifications alone may be insufficient to effectively lose and maintain weight in children and adolescents. The addition of obesity pharmacotherapy may especially benefit children and adolescents who have proven unsuccessful in intensive behavioral and lifestyle interventions, remain above certain thresholds of BMI, with or without comorbid conditions. […] The recent approval of anti-obesity medications for children and adolescents and guidelines that stress the importance of offering pharmacotherapy adjunct to behavior and lifestyle treatment may improve weight loss outcomes and consequently decrease cardiovascular risk.

• #36 Children and adolescents’ obesity is the 21st century health problem – Bocharova – Kazan medical journal

  https://kazanmedjournal.ru/kazanmedj/article/view/20709

  The article presents a literature review which devotes to one of the major issues of healthcare today obesity in children and adolescents. The consequences of childhood obesity, methods of determination and pathophysiology of obesity are described in detail. […] It was considered the influence of genetic factors in the formation of obesity, the effect of intestinal microbiota in the pathogenesis of obesity. […] Understanding the multifactorial mechanisms involved in the formation of obesity in children and adolescents provides opportunities for the early prevention of obesity and its complications. […] Obesity can result from a prolonged energy imbalance between nutrient intake and activity, with physical activity and a sedentary lifestyle affecting the latter. […] However, obesity results from a complex interaction between genetic, epigenetic, environmental, and behavioral factors.

• #37 Novel Genetic Loci Identified for the Pathophysiology of Childhood Obesity in the Hispanic Population | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0051954

  Genetic variants responsible for susceptibility to obesity and its comorbidities among Hispanic children have not been identified. […] Unprecedented phenotyping and high-density SNP genotyping enabled localization of novel genetic loci associated with the pathophysiology of childhood obesity. […] Identification of genes underlying these distinct patterns of association also may unravel important biological pathways involved in the pathophysiology of childhood obesity. […] Our unprecedented phenotypes represent not only adiposity, but also biological processes underlying the development of childhood obesity. […] Identified genome-wide significant loci: 1) corroborated genes implicated in other studies (MTNR1B, ZNF259/APOA5, XPA/FOXE1 (TTF-2), DARC, CCR3, ABO); 2) localized novel genes in plausible biological pathways (PCSK2, ARHGAP11A, CHRNA3); and 3) revealed novel genes with unknown function in obesity pathogenesis (MATK, COL4A1). […] Characterization of the underlying functional genetic variants contributing to this serious public health problem in Hispanic children will involve additional study.

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