outcome
Reference | Sham feeding | Rat | Animals are fitted with chronic fistulas to drain liquid food before entering the gastrointestin al tract | Hyperphagia in brief periods of time | No body weight gain | Smith et al. 1989 |
Restriction/Refeedi ng | Rat | access to palatable diet is followed by food deprivation cycle | Rebound hyperphagia of highly palatable food upon refeeding | No body weight gain | Hagan and Moss, 1996 |
Tail pinch | Rat | Pinching a rat’s tail while measuring the rat’s food intake | Increased intake during tail pinching and shortly afterwards | No body weight gain | Rowland and Antelman, 1976 |
Shock stress | Rat | Measurement of food intake after application of an acute 0.6 mA electric shock. | Increased daily consumption of high palatable diet when associated with food restriction | No body weight gain | |
Limited access | Rat/mous e | Limited availability of optional source of dietary fat under non- food-deprived conditions. | Increased high sucrose/fat/mix ed diet at onset of access, and larger fewer sugary meals throughout the access period | Body weight gain/ No body weight gain | ; ; Wojnicki et al. 2008. |
Visible burrow system | Rat | Single housing after 2 weeks exposure to subordination | Hyperphagia from longer meals with longer inter- meal intervals | Body weight gain | |
| | in mixed-sex colonies | occurring in the recovery post- stress phase | | |
Chronic social defeat | Mouse | Single housing after 10 days subordination and protected co-housing with 10 different aggressor mice. | Increased daily food intake, unknown meal pattern occurring in the recovery post- stress phase | Body weight gain | |
Chronic psychosocial stress | Mouse | 4 weeks subordination and protected co-housing with the same aggressor mouse. | Hyperphagia from higher consumption rate and reduced satiety intervals | Body weight gain | Razzoli et al. 2015 |
The sham feeding model is achieved by equipping the animals with chronic fistulas to drain liquid food before entering the gastrointestinal tract therefore producing a defect in satiation. This allows to separate positive oro-sensory feedback, stimulating feeding, from negative intestinal feedback, inhibiting feeding ( Corwin and Buda-Levin, 2004 ; Smith, 2004 ). While this model allows for the exploration of basic mechanisms relevant for binging, it presents limitations for most validity criteria, not reproducing the voluntary elements of food restriction and since animals maintain weight by being fed outside the sham-feeding tests.
Several models have been based upon cycles of dieting and overeating. Restriction/refeeding cycles consist of several days of limited food access followed by a few days of ad libitum access ( Corwin and Buda-Levin, 2004 ; Virts et al. 1992 ). Most commonly body weight diminishes during these protocols, and the increased food intake accomplished with this procedure does not seem to be greater than the amount of food than most animals would eat during a similar time, due to compensatory eating. Nevertheless, some of these studies highlight neural and biological changes that might have importance to binging related disorders ( Colantuoni et al. 2002 , 2001 ; Rada et al. 2005 ).
Another common methodology is based on limited access to fatty food, in particular to an optional source of dietary fat under non-food-deprived conditions over extended period of time. As access to the fat decreases, consumption of the fat increases when it is provided ( Avena et al. 2009 ; Czyzyk et al. 2010 ). Nevertheless, a compensatory eating pattern emerges, as animals overeat on binge days and under eat on non-binge days. This response is very robust as it does not seem to habituate however doesn’t lead to excess body weight or adiposity ( Czyzyk et al. 2010 ). With these limitations in mind, this model presents the advantage of voluntary behaviors that are reliably expressed and of good isomorphic validity, although the binging and non-binging phases seem to correspond to different neurobiological substrates.
Stress and binge eating disorders
Stress ( Koolhaas et al. 2011 ; Harris 2015 for a review) has been often applied in developing eating disorder models. During chronic stress and the corresponding hyperactivation of the hypothalamus-pituitary-adrenal (HPA) axis, glucocorticoids and insulin increase craving for calorie-reach meals, a phenomenon explained by the “comfort food” hypothesis ( Dallman et al. 2003 ; Dallman, 2010 ). According to this hypothesis, the preference for palatable food ingestion reduces the negative effects of stress via downregulation of corticotropin releasing factor (CRF) in the amygdala as well as through stimulation the anterior part of the pleasure-associated anterior nucleus accumbens shell that outweighs the contribution of the stress-stimulated posterior, defensive part of this nucleus ( Dallman 2004 , 2003 ; La-Fleur, 2004; Pecoraro, 2004 ; Rebuffe'-Scrive, 1992 ). Additionally, the consumption of palatable foods downregulates the stress response by activating reward pathways through reward-based structural plasticity ( Avena and Bocarsly, 2012 ; Teegarden and Bale, 2008 ). Insulin level, elevated by food overconsumption, are thought to contribute to dampening adrenocorticotropic hormone (ACTH) and glucocorticoid responses to stress, as supported by the negative correlation between the hypothalamic para ventricular nucleus (PVN) CRF mRNA expression and plasma insulin levels ( Dallman et al. 2007 ). As a result, the stress-induced increase in consumption of palatable foods is also associated with reduced behavioral stress indices, such as anxiety-related behaviors, stress-induced learned helplessness, and reactions of pain and distress ( Ulrich-Lai et al. 2015 ).
A variety of stress models have been used to stimulate food intake, differing in nature (physical or psychological), severity, and time of application.
The tail-pinch model has been used to induce hyperphagia, but the effect is short lived and does not set the stage for an increased body weight ( Rowland and Antelman, 1977 ). Furthermore, results from the application of several pharmacological compounds have provided conflicting results, limiting the predictive validity of the model ( Morley et al. 1983 ).
While a similar case can be made for the application of shock stress per se, when combined with food restricting/refeeding protocols shock stress induces binge eating of palatable food ( Hagan et al. 2002 ). Although again the model doesn’t facilitate the development of obesity and has been used to induce bingeing during short durations only, it seems to possess good construct validity and to prove useful for identifying mechanistic predispositions to bingeing. The ability of chronic psychological stress to increase food preferences towards highly palatable food has been related to the intensity of the stress experienced. A milder version of the traditional chronic variable stress in terms of severity and duration/frequency of stress application, resulted in a more modest and short-lived increased preference for palatable foods than in rats stressed in the traditional chronic variable stress ( Thompson et al. 2015 ). These data would suggest that higher intensity paradigms correspond to more pronounced and sustained preference for high palatable foods ( Thompson et al. 2015 ). While the stress relief properties of the consumption of high palatable food may be transitory/temporary during continuous stress exposure, the unresolved hyperactivation of the HPA axis over time can continue to sustain food overconsumption and facilitate obesity, due for example to the permissive effect of glucocorticoids on lipogenesis and fat deposition ( de Guia and Herzig, 2015 ). Nevertheless, palatable food intake blunts acute stress responses both in human and rodent studies, although the mechanisms involved still remain elusive ( Ulrich-Lai et al. 2015 ).
Validity of classical models of binge eating disorders
Most binge eating in humans seems not to be driven by hunger or metabolic demands and most patients are overweight or obese (DSM5; Mathes et al. 2009 ; Mussell et al. 1995 ; Waters et al. 2001 ). Therefore the fact that experimental animals from classical BED models as highlighted above do not show significant increases in body weight/adiposity ( Cao et al. 2014 ; Czyzyk et al. 2010 ) limits their isomorphic validity. Similarly, most stress encountered by human and corresponding with the development of BED are of psychological nature ( Heatherton et al. 1991 ; O’Connor et al., 2008 ), with onset of binge eating being preceded by elevated perceived stress and increased incidence of life stressors ( Pike et al. 2006 ; Striegel-Moore et al. 2007 ).
This again limits the construct validity of some of the traditional models of human BED, particularly if based upon a physical stressor and may only partially target the interested physiology (mechanistic and predictive validity) (Rospond, 2016; add here some of the cits of Rev #3).
Aside from these traditional models of BED recent experimental evidences reviewed below strongly suggest that rodent models of chronic social stress elicit robust changes in eating behavior with high degree of face validity for BED and translational relevance for the human condition ( Table 1 ).
Binge eating, hyperphagia and metabolic disorders in rodent models of social stress
Metabolic disorders due to psychosocial stress have now been well documented in humans ( Bose, 2009 ; Dallman, 2006 ), non-human primates ( Shively, 2009 ), and rodents ( Bartolomucci et al. 2009 , 2004 ; Coccurello et al. 2009 ; Finger, 2011 ; Kuo et al. 2007 ). Social subordination stress has long been considered ideal to mimic the impact of psychosocial stress on human pathologies ( Bartolomucci et al. 2005 ; Koolhaas et al. 2011 ; Sapolsky, 2005 ; Scott, 2012 ; Razzoli and Bartolomucci, 2016 ) and has been recently presented as a major risk factor for insulin resistance and T2D ( Kelly and Ismail, 2015 ).
Nevertheless limited work addresses the role of subordination stress on meal pattern. In the visible burrow system (VBS) laboratory rats are housed together in a mixed-sex colony for several weeks during which males form a dominance hierarchy through agonistic interactions. Subordinate males present reproducible behavioral, endocrine, physiological, and neurochemical changes consistent with a severe stress phenotype, that is also associated to a profound weight loss due to reduced food intake ( Blanchard et al. 1995 ; Nguyen et al., 2007 ). During recovery from the VBS, subordinate rats immediately become hyperphagic and quickly regain the lost weight primarily as fat, resulting in greater overall and visceral adiposity than dominant and control rats. This effect is further enhanced in rats exposed to a second cycle of VBS stress and recovery. Consistent with increased adiposity, subordinates have elevated plasma leptin and insulin levels ( Tamashiro et al. 2011 , 2006 ). Meal pattern alterations have been observed during VBS housing and correspond to reduced meal size and frequency amounting to a hypophagic response that reflects the behavioral and neuroethological adaptations to the VBS environment. On the other hand, the hyperphagia observed during the VBS recovery is the outcome of larger and longer meals with longer inter-meal intervals ( Melhorn et al. 2010 ).
Similarly to subordinate rats recovering from the VBS, a hyperphagic response has been observed in mice recovering from the chronic sensory contact or social defeat stress (CSD) model ( Kumar et al. 2013 ). In this paradigm a link has been demonstrated between increased hypothalamic expression of the orexigenic neuropeptides NPY and AgRP in subordinate mice. This activation of NPY/AgRP neurons can contribute to the observed increased food intake and body weight and promote the use of carbohydrates as fuel while sparing fat ( Chuang et al. 2010a , 2010b ; Kumar et al. 2013 ). At the endocrine level, leptin production remains suppressed, and ghrelin secretion is increased to induce a potent feeding response that increases available energy stores ( Lutter et al. 2008 ; Chuang et al. 2011 ). Similar to the behavior shown by subordinate in the VBS, in the CSD model hyperphagia results from larger but less frequent meals, considered indicative of a deficit in satiation.
In the chronic psychosocial stress model, subordinate mice develop a hyperphagia-dependent insulin resistance which, associated to high fat diet feeding, leads to MetS and obesity ( Bartolomucci et al. 2009 , 2005 ; Dadomo et al. 2011 ; Razzoli et al. 2015a ; Sanghez et al. 2016 , 2013 ). Similarly to the CSD, the chronic psychosocial stress model is also based on the exploitation of a naturalistic valid construct of social disparity, the difference between the two being the instability (the former) versus the stability (the latter) of the social hierarchy ( Razzoli and Bartolomucci, 2016 ). In the chronic psychosocial stress model, the subordinate animals exhibit a complex behavioral and metabolic syndrome characterized by up-regulated HPA axis functioning, behavioral depression-like disorders and autonomic and immune-endocrine changes ( Bartolomucci, 2007 ; Bartolomucci et al. 2010 , 2005 ; Dadomo et al. 2011 ). Hyperphagia arises and persists spontaneously in subordinate mice ( Bartolomucci et al., 2010 , 2009 , 2004 ; Dadomo et al. 2011 ; Patterson et al. 2013 ; Sanghez et al. 2013 ). Furthermore, hyperphagia is not a compensatory response since, in mice housed at room temperature, it develops in absence of increased energy expenditure ( Moles et al. 2006 ; Sanghez et al. 2013 ) and in presence of depression of locomotor activity ( Bartolomucci et al. 2010 , 2009 ; Dadomo et al. 2011 ; Razzoli et al. 2014 ). The overstimulation of food intake that leads to obesity occurs in concert with stress induced elevations of circulating corticosterone, glucose, and ghrelin, and hypothalamic expression of AGRP and NPY mRNA ( Bartolomucci 2007 ; Bartolomucci et al. 2010 , 2005 ; Dadomo et al. 2011 ; Razzoli et al. 2015, 2014 ; Patterson et al. 2013 ). In the subordinate mouse, the presence of an altered inhibitory feedback of the HPA axis suggested by elevated corticosterone levels, downregulated expression of hippocampal GR and dexametasone resistance ( Bartolomucci et al. 2004 , 2003 ; Razzoli et al. 2014 ) could contribute over time to sustain hyperphagia, while it is known that interruption of ghrelin signaling can blunt hyperphagia and its anabolic consequences ( Patterson et al. 2013 ). On the other hand, lower levels of ghrelin receptors in the hypothalamic PVN have been associated with increased consumption of fat rich foods ( Patterson and Abizaid, 2013 ).
An in depth analysis of subordinate meal pattern assigned a strong validity for modeling human BED associated with obesity (Razzoli et al. 2015): subordinate mice ingest more food at higher rate and with reduced satiety ratio than control mice, suggesting an impaired satiety ( Strubbe and Woods, 2004 ), and a heightened stress reactivity ( Harb et al. 1985 ; Krebs et al. 1997 ). Interestingly, this phenomenon does not reach a ceiling effect, since hyperphagia can increase further in response to an acute stress (Razzoli et al. 2015). The microstructure of subordinate hyperphagia changes over time, evolving from longer and more frequent meals to a paroxystic eating, consisting of an exaggerated amount of food consumed over much shorter meal times. Altogether, these features make the case for considering chronic subordination stress a valid model of BED since the majority of the diagnostic criteria are captured ( Corwin and Buda-Levin, 2004 ) ( Table 1 ): 1) The behavior occurs repeatedly over an extended period of time; 2) Bingeing animals consume more food in brief, discrete, periods of time than controls do under similar circumstances. 3) If compensatory behavior is present, it should be initiated by the animal rather than imposed by the investigator.
The association of subordination induced bingeing with the propensity to obesity and MetS as part of the subordinate metabolic phenotype is also very remarkable ( Sanghez et al. 2016 , 2013 ). When subordinate mice are fed standard diet, their hyperphagia is associated with dyslipidemia but normal glucose tolerance in presence of increased body weight ( Sanghez et al. 2013 ). Conversely, glucose intolerance, insulin resistance, and obesity develop due to the synergistic effect of high fat diet and subordination stress induced hyperphagia ( Bartolomucci et al. 2009 ; Dadomo et al. 2011 ; Sanghez et al. 2013 ). Among the endocrine and metabolic changes induced in subordinate mice, increased glucocorticoid and free fatty acid levels might be considered crucial contributors for the development of insulin resistance through the downregulation of the insulin signaling pathway ( Kahn, 1994 ; Sanghez et al. 2013 ; Shpilberg et al. 2012 ; Stumvoll, 2005 ; Taniguchi et al. 2006 ). Subordination stress is able to induce a molecular signature of insulin resistance in skeletal muscle and liver which is larger in magnitude to the effect of high fat diet per se ( Sanghez et al. 2016 ). Decreased IRS1/2 appears to be the key molecular node critically downregulated in the signaling pathway of subordinate mice. Interestingly, the adipose tissue is found to remain insulin sensitive possibly to help repartitioning of nutrients to the fat organ ( Sanghez et al. 2016 ).
Because obesity is a major risk factor for the development of the MetS and type 2 diabetes ( Björntorp and Rosmond, 2000 ; Després and Lemieux, 2006 ; Eckel et al. 2005 ; Haslam and James, 2005 ; Zimmet et al. 2001 ) a food restriction regimen promoting weight loss should normalize the MetS as well ( Aude et al. 2004 ; Kastorini et al. 2011 ). Preventing hyperphagia using a pair feeding protocol in subordinate mice abrogated body weight gain and visceral adiposity compared to subordinate mice that were fed ad libitum, without normalizing glucose homeostasis, potentially due to an exaggerated hunger stress sensitivity as demonstrated by the exacerbated hypercorticosteronemia induced by fasting (Razzoli et al. 2015). Additional studies are warranted to evaluate if the limited food availability in pair fed animals could have the potential to stimulate food intake as suggested by increased craving induced by deprivation protocols in humans as well as bingeing as a consequence of limited access models in rodents ( Berner et al., 2008 ; Polivy et al. 2005 ). Still, the prevention of subordination-induced obesity by precluding hyperphagia maintains clear translational implications for therapeutic interventions ( McElroy et al. 2004 ) offering the potential of treating obesity with non-pharmacological interventions effective for binge eating and acting in a faster way (drugs are often effective after several weeks of treatment).
Concluding Remarks and Future Perspectives
The treatment of eating and metabolic disorders has proven challenging. While obesity, T2D, and metabolic disorders have become pandemic, there are still unmet needs in spite of the available pharmacological, surgical, and behavioral therapeutic strategies. One critical issue is that obesity is typically viewed as a homogenous condition, but there may be important and discrete etiopathologies – including, for example, binge-eating. This indirectly underscores the role played by external factors such as low socio-economic status and psychosocial stress as predispositions for the development of a broad spectrum of eating and obesity-associated conditions. So far, an increasing scientific scrutiny has contributed to identify several endocrine players in the dynamic regulation of metabolic function in response to stress, both at the central and peripheral level. A strong need remains to develop valid preclinical models of stress-related metabolic disorders. Evidences reviewed here suggest that the development and validation of a preclinical model in which binge-eating is associated with obesity is critical to disentangling underlying molecular mechanisms, generating testable predictions of innovative drug candidates, and translating preclinical observations into clinical settings. This is particularly poignant since the available classical models of BED do not recapitulate most of the diagnostic criteria and lacki construct validity. Conversely, chronic subordination stress models offer several advantages in linking stress to binging and obesity to ultimately facilitate the identification of the neurobiological basis of BED-related obesity.
- Eating disorders and obesity are prevalent and can associate with psychological stress.
- Human studies link bingeing and stress exposure.
- Most classic preclinical models of binge eating involve food deprivation and acute stress.
- Mouse subordination stress causes bingeing and metabolic disorder similarly to humans.
Acknowledgments
AB is supported by NIH/NIDDK R01DK102496, NIH/NIA R01AG043972. SC is supported by NIDDK/NIH P30DK50456, and CP is supported by NIMH/NIHT32082761
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- Patient Care & Health Information
- Diseases & Conditions
- Childhood obesity
Childhood obesity is a serious medical condition that affects children and adolescents. It's particularly troubling because the extra pounds often start children on the path to health problems that were once considered adult problems — diabetes, high blood pressure and high cholesterol. Childhood obesity can also lead to poor self-esteem and depression.
One of the best strategies to reduce childhood obesity is to improve the eating and exercise habits of your entire family. Treating and preventing childhood obesity helps protect your child's health now and in the future.
Not all children carrying extra pounds are overweight. Some children have larger than average body frames. And children normally carry different amounts of body fat at the various stages of development. So you might not know by how your child looks if weight is a health concern.
The body mass index (BMI), which provides a guideline of weight in relation to height, is the accepted measure of overweight and obesity. Your child's doctor can use growth charts, the BMI and, if necessary, other tests to help you figure out if your child's weight could pose health problems.
When to see a doctor
If you're worried that your child is putting on too much weight, talk to his or her doctor. The doctor will consider your child's history of growth and development, your family's weight-for-height history, and where your child lands on the growth charts. This can help determine if your child's weight is in an unhealthy range.
Lifestyle issues — too little activity and too many calories from food and drinks — are the main contributors to childhood obesity. But genetic and hormonal factors might play a role as well.
More Information
- Mayo Clinic Minute: Out of shape kids and diabetes
Risk factors
Many factors — usually working in combination — increase your child's risk of becoming overweight:
- Diet. Regularly eating high-calorie foods, such as fast foods, baked goods and vending machine snacks, can cause your child to gain weight. Candy and desserts also can cause weight gain, and more and more evidence points to sugary drinks, including fruit juices and sports drinks, as culprits in obesity in some people.
- Lack of exercise. Children who don't exercise much are more likely to gain weight because they don't burn as many calories. Too much time spent in sedentary activities, such as watching television or playing video games, also contributes to the problem. TV shows also often feature ads for unhealthy foods.
- Family factors. If your child comes from a family of overweight people, he or she may be more likely to put on weight. This is especially true in an environment where high-calorie foods are always available and physical activity isn't encouraged.
- Psychological factors. Personal, parental and family stress can increase a child's risk of obesity. Some children overeat to cope with problems or to deal with emotions, such as stress, or to fight boredom. Their parents might have similar tendencies.
- Socioeconomic factors. People in some communities have limited resources and limited access to supermarkets. As a result, they might buy convenience foods that don't spoil quickly, such as frozen meals, crackers and cookies. Also, people who live in lower income neighborhoods might not have access to a safe place to exercise.
- Certain medications. Some prescription drugs can increase the risk of developing obesity. They include prednisone, lithium, amitriptyline, paroxetine (Paxil), gabapentin (Neurontin, Gralise, Horizant) and propranolol (Inderal, Hemangeol).
Complications
Childhood obesity often causes complications in a child's physical, social and emotional well-being.
Physical complications
Physical complications of childhood obesity may include:
- Type 2 diabetes. This chronic condition affects the way your child's body uses sugar (glucose). Obesity and a sedentary lifestyle increase the risk of type 2 diabetes.
- High cholesterol and high blood pressure. A poor diet can cause your child to develop one or both of these conditions. These factors can contribute to the buildup of plaques in the arteries, which can cause arteries to narrow and harden, possibly leading to a heart attack or stroke later in life.
- Joint pain. Extra weight causes extra stress on hips and knees. Childhood obesity can cause pain and sometimes injuries in the hips, knees and back.
- Breathing problems. Asthma is more common in children who are overweight. These children are also more likely to develop obstructive sleep apnea, a potentially serious disorder in which a child's breathing repeatedly stops and starts during sleep.
- Nonalcoholic fatty liver disease (NAFLD). This disorder, which usually causes no symptoms, causes fatty deposits to build up in the liver. NAFLD can lead to scarring and liver damage.
Social and emotional complications
Children who have obesity may experience teasing or bullying by their peers. This can result in a loss of self-esteem and an increased risk of depression and anxiety.
To help prevent excess weight gain in your child, you can:
- Set a good example. Make healthy eating and regular physical activity a family affair. Everyone will benefit and no one will feel singled out.
- Have healthy snacks available. Options include air-popped popcorn without butter, fruits with low-fat yogurt, baby carrots with hummus, or whole-grain cereal with low-fat milk.
- Offer new foods multiple times. Don't be discouraged if your child doesn't immediately like a new food. It usually takes multiple exposures to a food to gain acceptance.
- Choose nonfood rewards. Promising candy for good behavior is a bad idea.
- Be sure your child gets enough sleep. Some studies indicate that too little sleep may increase the risk of obesity. Sleep deprivation can cause hormonal imbalances that lead to increased appetite.
Also, be sure your child sees the doctor for well-child checkups at least once a year. During this visit, the doctor measures your child's height and weight and calculates his or her BMI . A significant increase in your child's BMI percentile rank over one year may be a possible sign that your child is at risk of becoming overweight.
- Helping your child who is overweight. National Institute of Diabetes and Digestive and Kidney Diseases. https://www.niddk.nih.gov/health-information/weight-management/helping-your-child-who-is-overweight. Oct. 14, 2020.
- Childhood obesity causes and consequences. Centers for Disease Control and Prevention. https://www.cdc.gov/obesity/childhood/causes.html. Accessed Oct. 14, 2020.
- Kliegman RM, et al. Overweight and obesity. In: Nelson Textbook of Pediatrics. 21st ed. Elsevier; 2020. https://www.clinicalkey.com. Accessed Oct. 14, 2020.
- Hay WW, et al., eds. Normal childhood nutrition and its disorders. In: Current Diagnosis & Treatment: Pediatrics. 25th ed. McGraw Hill; 2020. https://accessmedicine.mhmedical.com. Accessed Oct. 20, 2020.
- Skelton JA. Management of childhood obesity in the primary care setting. https://www.uptodate.com/contents/search. Accessed Oct. 14, 2020.
- Klish WJ, et al. Definition, epidemiology and etiology of obesity in children and adolescents. https://www.uptodate.com/contents/search. Accessed Oct. 14, 2020.
- Polfuss ML, et al. Childhood obesity: Evidence-based guidelines for clinical practice — Part one. Journal of Pediatric Health Care. 2020; doi:10.1016/j.pedhc.2019.12.003.
- Davis RL, et al. Childhood obesity: Evidence-based guidelines for clinical practice — Part two. Journal of Pediatric Health Care. 2020; doi:10.1016/j.pedhc.2020.07.011.
- Mayo Clinic Children's Center Pediatric Weight Management Clinic
- Mayo Clinic Minute: Weight loss surgery for kids
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Essay on obesity! Find high quality essays on 'Obesity' especially written for school, college, science and medical students. These essays will also guide you to learn about the causes, factors, treatment, management and complications related to obesity. Obesity is a chronic health condition in which the body fat reaches abnormal level.
Besides health complications, obesity causes an array of psychological effects, including inferiority complex among victims. Obese people suffer from depression, emanating from negative self-esteem and societal rejection. In some cases, people who become obese lose their friends and may get disapproval from teachers and other personalities ...
Obesity has become a global epidemic and is one of today's most public health problems worldwide. Obesity poses a major risk for a variety of serious diseases including diabetes mellitus, non-alcoholic liver disease (NAFLD), cardiovascular disease, hypertension and stroke, and certain forms of cancer (Bluher, 2019).Obesity is mainly caused by imbalanced energy intake and expenditure due to a ...
This essay will explore the various causes of obesity and their effects on individuals and society as a whole. One of the primary causes of obesity is dietary habits and nutritional intake. The consumption of high-calorie, low-nutrient foods, such as fast food, sugary beverages, and processed snacks, has become increasingly prevalent in modern ...
Introduction. Obesity is an increasing, global public health issue. Patients with obesity are at major risk for developing a range of comorbid conditions, including cardiovascular disease (CVD), gastrointestinal disorders, type 2 diabetes (T2D), joint and muscular disorders, respiratory problems, and psychological issues, which may significantly affect their daily lives as well as increasing ...
Obesity is a growing concern in many parts of the world, with rates on the rise. According to the World Health Organization (WHO), obesity has more than doubled globally since 1980. This essay will examine the causes of obesity, including dietary habits, sedentary lifestyles, and genetic factors, and explore the significant effects it has on individuals and society as a whole.
Being overweight or obese can have a serious impact on health. Carrying extra fat leads to serious health consequences such as cardiovascular disease (mainly heart disease and stroke), type 2 diabetes, musculoskeletal disorders like osteoarthritis, and some cancers (endometrial, breast and colon). These conditions cause premature death and ...
Obesity can also cause respiratory problems, sleep apnea, and osteoarthritis. Obesity is linked to various psychological problems such as depression, anxiety, and low self-esteem. The stigma associated with obesity can lead to social rejection, discrimination, and negative body image. These psychological problems can reduce the quality of life ...
The health risks caused by overweight and obesity are increasingly well documented and understood. In 2019, higher-than-optimal BMI caused an estimated 5 million deaths from noncommunicable diseases (NCDs) such as cardiovascular diseases, diabetes, cancers, neurological disorders, chronic respiratory diseases, and digestive disorders (1).
On-time delivery! Obesity is a factor that increases the risk of many other internal human diseases. The World Health Organization, in a 2020 report, warns that obesity causes respiratory and heart failure, coronary heart disease, hypertension, and arthritis and can lead to the development of diabetes and some cancers.
250 Words Essay on Obesity Introduction. Obesity represents a significant public health issue worldwide, posing detrimental effects to physical health and psychological well-being. It is a complex disorder involving an excessive amount of body fat, often resulting from a combination of genetic, behavioral, and environmental factors. Causes of ...
Cardiovascular system. In people with obesity, the heart needs to work harder to pump blood around the body. This leads to high blood pressure, or hypertension. High blood pressure is the leading ...
Breathing problems, such as asthma and sleep apnea. Joint problems such as osteoarthritis and musculoskeletal discomfort. Gallstones and gallbladder disease. Childhood obesity is also associated with: 4,5,6. Psychological problems such as anxiety and depression. Low self-esteem and lower self-reported quality of life.
In the United States, overweight and obesity are chronic diseases that contribute to excess morbidity and mortality. Despite public health efforts, these disorders are on the rise, and their consequences are burgeoning. 1 The Centers for Disease Control and Prevention report that during 2017 to 2018, the prevalence of obesity in the United States was 42.4%, which was increased from the ...
Adult obesity [body mass index (BMI) >30 kg/m 2] was estimated to affect 10.8% of men (266 million) and 14.9% of women (375 million) worldwide in 2014. This has more than doubled when compared with worldwide figures in 1975 where 3.2% of men and 6.4% of women were obese. If this trend persists, by 2025, 18% of men and 21% of women will be obese ...
Being obese can lead to other serious health problems such as type 2 diabetes, asthma, liver and kidney disease, high blood pressure, heart diseases, different types of cancers such as breast and bowel cancer and it can even lead to a stroke. Obesity can affect an induvial daily activities as they will get shortness of breath often, excessively ...
Argumentative Essay on Obesity. Obesity is a growing epidemic that has plagued societies around the world. With the rise of fast food chains, sedentary lifestyles, and a lack of education on proper nutrition, obesity rates have skyrocketed in recent years. While some argue that obesity is a personal choice and should not be seen as a public ...
Overweight and obesity may raise your risk of developing certain types of cancer. Men with overweight or obesity are at a higher risk for developing cancers of the colon, rectum, and prostate. 10 Among women with overweight or obesity, cancers of the breast, lining of the uterus, and gallbladder are more common.
Obesity is the major cause of type 2 diabetes. It can cause resistance to insulin, the hormone that controls blood sugar. When obesity causes insulin resistance, blood sugar becomes higher than normal. Joint problems, such as osteoarthritis. Obesity can affect the knees and hips because of the stress placed on the joints by extra weight.
Obesity in childhood is the most challenging public health issue in the twenty-first century. It has emerged as a pandemic health problem worldwide. The children who are obese tend to stay obese in adulthood and prone to increased risk for diabetes and cardiac problems at a younger age. Childhood obesity is associated with increased morbidity and premature death.[1] Prevention of obesity in ...
Some genetic and lifestyle factors affect an individual's likelihood of adult obesity; thus, the significant clusters of obesity observed in specific geographical regions and contexts also signal the impact of socioeconomic and environmental factors in "obesogenic" environments [13].Understanding the causes and determinants of obesity is a critical step toward creating effective policy and ...
Eating disorders and obesity are prevalent and can associate with psychological stress. Human studies link bingeing and stress exposure. Most classic preclinical models of binge eating involve food deprivation and acute stress. Mouse subordination stress causes bingeing and metabolic disorder similarly to humans.
Regularly eating high-calorie foods, such as fast foods, baked goods and vending machine snacks, can cause your child to gain weight. Candy and desserts also can cause weight gain, and more and more evidence points to sugary drinks, including fruit juices and sports drinks, as culprits in obesity in some people. Lack of exercise.