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  • Published: 14 April 2004

Obesity: An overview on its current perspectives and treatment options

  • Srinivas Nammi 1 , 3 ,
  • Saisudha Koka 1 ,
  • Krishna M Chinnala 2 &
  • Krishna M Boini 1 , 3  

Nutrition Journal volume  3 , Article number:  3 ( 2004 ) Cite this article

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Obesity is a multi-factorial disorder, which is often associated with many other significant diseases such as diabetes, hypertension and other cardiovascular diseases, osteoarthritis and certain cancers. The management of obesity will therefore require a comprehensive range of strategies focussing on those with existing weight problems and also on those at high risk of developing obesity. Hence, prevention of obesity during childhood should be considered a priority, as there is a risk of persistence to adulthood. This article highlights various preventive aspects and treatment procedures of obesity with special emphasis on the latest research manifolds.

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Introduction

Obesity can be described as the "New World Syndrome". Its prevalence is on continuous rise in all age groups of many of the developed countries in the world. Statistical data reveals that the problem of obesity has increased from 12–20% in men and from 16–25% in women over the last ten years [ 1 ]. Recent studies suggest that nearly 15–20% of the middle aged European population are obese [ 2 ] and that in USA alone it is responsible for as many as 3,00,000 premature deaths each year [ 3 ]. Obese patients have been associated with increased risk of morbidity and mortality relative to those with ideal body weight [ 4 ]. Even modest weight reduction in the range of 5–10% of the initial body weight is associated with significant improvements in a wide range of co-morbid conditions [ 5 – 9 ]. Obesity, which was once viewed as the result of lack of will power, or a lifestyle "choice" – the choice to overeat and under exercise, is now being considered more appropriately by the modern world as a chronic disease, which requires effective strategies for its management.

Obesity, in simple terms, may be defined as a state of imbalance between calories ingested versus calories expended which would lead to excessive or abnormal fat accumulation. Body Mass Index (BMI) is a measure of weight corrected for height and which reflects the total body fat and has been the most accepted parameter for defining over weight [ 10 ].

Optimal BMI increases with age. WHO also classified over weight according to BMI [ 11 ]. There is a very good correlation between BMI and the percentage of body fat in large populations.

Percent Body fat = 1.2 (BMI) + 0.23 (age) - 10.8 (gender) - 5.4

Where gender = '1' for men and '0' for women.

It follows from this equation that for a given height and weight, the percentage of body fat is about 10% higher in women compared to men. The reason for this could be that in women, the excess body fat is usually distributed as subcutaneous fat and is mainly peripheral (thighs, buttocks, breasts) where as in men there is a relative excess of body fat stored in abdominal cavity as abdominal subcutaneous fat.

New classifications of over weight may be based on cut-off points for simple anthropometric measures such as waist hip ratio, total adiposity and intra-abdominal fatness. There exists a correlation between increased BMI, mortality due to allied risks which is depicted in Fig. 1

figure 1

Correlation between increased BMI and risk of mortality

Aetiology of obesity

Obesity is not a single disorder but a heterogeneous group of conditions with multiple causes each of which is ultimately expressed as obese phenotype. Obesity involves complex aetiological links between the genetic, metabolic and neural frameworks on one hand and behavior, food habits, physical activity and socio-cultural factors on the other (Table 1 ).

Genetic considerations

Although obesity had a genetic component, it is not a simple genetic disorder. There is an underlying genetic predisposition to obesity on to which environmental factors are layered. The discovery of 'ob' gene, which was mapped to chromosome 7, has led to a renewed interest in understanding the patho-biological basis of genetic predisposition in obesity. The 'ob' gene codes a hormone called leptin, a 167 amino acid protein and was supposed to be produced in white and brown adipose tissue and placenta [ 12 ]. The leptin receptors are concentrated in hypothalamus and belong to the same class of IL-2 and growth hormone receptors [ 13 ]. Any mutation of 'ob' gene leads to improper coding of leptin, which further results in obesity [ 14 ]. The effects of the 'ob' gene are mediated through effects on both energy intake and energy expenditure. Obesity can also be considered as a "complex trait" as many other genes coding proteins like apolipoprotein B, D, E, β 3 -adrenergic receptor [ 15 ], dopamine D 2 -receptor, tumor necrosis factor (TNF), glucocorticoid receptor etc. are associated with it. So far, 200 genes, gene markers and chromosomal regions have been associated with human obesity [ 16 ].

Neurobiology

Two neurotransmitters neuropeptide Y (NPY) and serotonin (5-HT) are found to play a major role in body weight regulation. NPY is a 36 amino acid peptide, which is concentrated mainly in the hypothalamus; a region crucial to regulation of appetite [ 17 ] has emerged as a possible key neurotransmitter candidate for the regulation of energy homeostasis. Increased NPY activity has been found in the hypothalamus of obese rodents [ 18 ]. NPY increases food in-take through its interaction with a unique Y5 subtype of NPY receptor and hence Y5 receptor antagonists could be effective in the treatment of obesity [ 19 ].

The inhibitory actions of 5-HT on food in-take have been localized to the hypothalamic para ventricular nucleus (PVN), the site at which NPY is most active in inducing feeding behavior [ 20 ]. 5-HT induced reduction in food in-take is mediated by post-synaptic 5-HT IB receptors. The hypophagic actions of 5-HT may be mediated at least partly through the NPY pathway. For example, 5-HT antagonist which stimulates feeding increases NPY concentrations in the arcuate and para ventricular nuclei of the hypothalamus [ 21 ]. Similarly, a 5-HT agonist, which reduces food intake significantly, reduces NPY concentrations in the hypothalamic para ventricular nucleus. Corticotrophin releasing factor (CRF) which also causes weight loss by reducing appetite and act in opposing to NPY on the regulation of energy balances. Cholecystokinin (CCK), a neurotransmitter present in the brain plays a physiological role as a meal termination (satiety) signal between the two receptors such as CCK A and CCK B , CCK acted at CCK A receptors [ 22 ]. Hence, CCK A agonist could also be useful in the treatment of obesity.

Environmental factors

These factors play a critical role in the development of obesity by unmasking genetic or metabolic susceptibilities. Environmental influences act via an increase in energy intake or a decrease in energy expenditure with little physical activity and hence there is increased likelihood of becoming obese. Sedentary behaviors, notably television watching, car ownership also contributes to the risk of obesity. The role of passive over consumption [ 23 ], eating disorders, and preference for high carbohydrate diet also play an important role in increasing the risk of obesity. Other food habits like smoking and alcohol consumption lowers body weight and results in higher BMI respectively.

Psycho-social impact

A number of individual characteristics may place individuals at increased risk of obesity. Restrained eating also plays a role in aetiology of obesity. Restrained eaters report more food carvings and binge eating [ 24 ]. One of the characteristic features of dietary restraints is the tendency towards disinhibited eating in particular circumstances. Restrained eaters may be more susceptible to the availability of highly palatable foods, which act as a stimulus for excess food consumption.

Obesity-associated diseases and risk factors

Cardiovascular diseases (cvd).

Hypertension

Coronary heart disease

Cerebrovascular disease

Varicose veins

Deep venous thrombosis

The increased risk of CVD is 2-fold in women of BMI 25–28.9 kg/m 2 and 3.6 fold for BMI in 29 kg/m 2 or more. In males a 10% increase in body weight increases risk of CVD by 38%, where as 20% weight risk corresponds with 86% increased risk. Blood pressure is increased by 6 mm systole and 4 mm diastole for a 10% gain in body fat. Hyper tension is prevalent in obese adults at a rate of 2.9 fold than non-obese population and weight reduction reduces risk of developing hyper tension [ 25 ].

Respiratory diseases

Sleep apnoea

Hypoventilation syndrome

There are a number of ways in which obesity affects lung function [ 26 ]. An increased amount of fat in the chest wall and abdomen limits respiratory excursion reducing lung volume. As the obesity worsens, so do the apnoeic episodes resulting in frequent awakening and the resultant sleep deprivation produces daytime somnolence.

Metabolic disorders

Hyperlipidemia

Diabetes mellitus

Insulin resistance

Menstrual irregularities

There is a consistent graded relationship between increased BMI and prevalence of NIDDM and insulin resistance [ 27 ]. Over 10 to 15 million Americans with type 2 diabetes are obese [ 28 ]. A mean weight loss of 7% weight reduces risk of developing type 2 diabetes by more than 55% [ 29 ]. BMI above 35 kg/m 2 increases the risk by 93 fold in women and by 42 fold in men. Obesity is associated with lipid disorders in which elevated levels of cholesterol, triglycerides, LDL-cholesterol and low levels of HDL-cholesterol are observed. For every 1 kg of weight loss, there is a corresponding reduction by about 1% in HDL and reduction by 3% of triglycerides. It has been observed that modest weight loss reduces lipid abnormalities [ 30 ] and diabetes mellitus [ 31 ].

Gastrointestinal disorders

Fatty liver and cirrhosis

Haemorrhoids

Colorectal cancer

Gall bladder disease is the most common gastrointestinal disorder in obese individuals. Obese women have a 2.7 fold increase in the prevalence of gall bladder disease. There is an increased risk of gallstones in individuals having BMI of 20 kg/m 2 or more. The mortality rates of cancer of the stomach and pancreas were higher in obese individuals.

Malignancies

Breast cancer

Endometrial Cancer

Prostrate Cancer

Cervical Cancer

Obese women have higher incidence of endometrial, ovarian, cervical and postmenopausal breast cancer, while obese men have incidents of prostrate cancer.

However, it remains to be confirmed whether these malignancies occur as a result of hormonal changes associated with obesity or due to specific dietary pattern.

Miscellaneous

Arthritis and bone mass

Stress is associated with the consumption of high fat foods and leads to weight gain. Obesity is also associated with osteoarthritis of hip and knee although in some cases, mechanical stress associated with obesity leads to osteoarthritis [ 32 ]. Obese women have a higher risk of obstetric complication and have increased risk of caesarean delivery due to variety of foetal size. Recently, an increased risk of neural tube defects especially spinabifida has been reported in women with BMI greater than 29 kg/m 2 .

Prevention of obesity

Obesity is a serious, chronic medical condition, which is associated with a wide range of debilitating and life threatening conditions. The fact that obesity prevalence continues to increase at an alarming rate in almost all regions of the world is of major concern. Hence, an effective control of obesity requires the development of coherent strategies that tackle the main issues related to preventing:

i) The development of over weight in normal weight individuals

ii) The progression of over weight to obesity in those who are already over weight

iii) Weight regain in those who have been over weight or obese in the past but who have since lost weight and

iv) Further worsening of a condition already established.

The prevention of obesity involves action at several levels i) Primary ii) Secondary iii) Tertiary [ 33 ]. Objective of primary prevention is to decrease the number of new cases, secondary prevention is to lower the rate of established cases in the community and tertiary prevention is to stabilize or reduce the amount of disability associated with the disorder. When the attention is focused on the multi-factorial condition such as coronary heart disease (CHD), primary prevention of this involves national programmes to control blood cholesterol levels and secondary prevention deals with reducing CHD risk in those with existing elevated blood cholesterol levels while tertiary action would be associated with preventing re-infarction in those who had a previous heart attack. However, this classification system for prevention of obesity results in a great deal of ambiguity and confusion. To avoid this, the US institute of medicine [ 34 ] has proposed alternative classification of system. The new system separates prevention efforts into 3 levels. Universal (or) public health measures (directed at every one in the population), selective (for a sub-group who may have an above average risk of developing obesity) and indicated (targeted at high risk individuals who may have a detectable amount of excess weight which fore-shadows obesity). However, preventive measures for any disorder may not be helpful in all cases hence, proper management strategies can be integrated along with prevention programmes.

Management of obesity

Management include both weight control or reducing excess body weight and maintaining that weight loss, as well as, initiating other measures to control associated risk factors. Periodic evaluation for obesity should be done by the measurement of BMI, measurement of waist circumference etc., to assess risk factors. Based on the evaluation, appropriate treatment can be suggested. Treatment may consist of modification of diet, increased physical activity, behavioral therapy, and in certain circumstances weight loss medication and surgery.

Dietary therapy

Restrictions of calories represent the first line therapy in all cases except in cases with pregnancy, lactation, terminal illness, anorexia nervosa, cholelithiasis and osteoporosis. Low calorie diets (LCD), which provide 100–1500 kcal/day, resulted in weight loss of 8% of baseline body weight over six months but on long run most of the lost weight is regained [ 35 ].

Very low calories diets (VLCD), which provide 300–800 kcal/day, can be useful in severely obese patients under strict medical supervision. They are found to produce 13% weight loss over six months, i.e. they produce greater initial weight loss than LCDs, however, the long-term (>1 year) weight loss by VLCD's is not found superior to that of the LCDs.

Meal replacement programmes and formula diets can be used as an effective tool in weight management [ 36 ]. Optifast, Medifast are available through physians or hospitals as part of packaged weight-reduction programmes. These products appear to be safe, but maintenance of weight loss over the long term is difficult.

Other over the counter (OTC) variations to formula diets includes Slimfast and Ultra slimfast. The consumer is instructed to drink the formulations and use it to replace one or two meals.

Fat substitutes like Olestra (Olean), which is a non-digestible, non-caloric fat, can be used in food preparations taken by obese patients.

It has been observed that calorie restriction alone has remarkable effects compared to exercise alone [ 37 – 39 ]. A loss of 5% initial weight achieved with diet and exercise is associated with significant improvement in glycylated haemoglobin A IC and that diet control can be useful to treat co morbidities of obesity such as diabetes [ 40 ].

Physical activity

All individuals can benefit from regular exercise [ 41 ]. Physical activity, which increases energy expenditure, has a positive role in reducing fat storage and adjusting energy balance in obese patients. Various exercises preceded and followed by short warm up and cool down sessions help to decrease abdominal fat, prevent loss of muscle mass. Studies revealed that patients who exercise regularly had increased cardio vascular fitness [ 42 , 43 ] along with betterment in their mental and emotional status. Hence a minimum of 30 minutes exercise is recommended for people of all ages [ 44 ] as part of comprehensive weight loss therapy.

Behaviour therapy

Behaviour therapy is a useful adjunct when incorporated into treatment for weight loss and weight maintenance. Patients need to be trained in gaining self-control of their eating habits. Behaviour modification programmes which seek to eliminate improper eating behaviours (eating while watching TV, eating too rapidly, eating when not hungry etc.,) include individual or group counseling of patients.

Self-help groups (weight watchers, Nutri-System) use a program of diet, education and self-monitoring like maintenance of logbook, keeping an account of food intake etc are beneficial.

Pharmacotherapy

Drug treatment is advised only for subjects with BMI > 27 and with associated risk factors or with a BMI > 30 [ 45 ] and thus at medical risk because of their obesity. It should not be used for "cosmetic" weight loss. Weight loss medications should be used only as an adjunct to dietary and exercise regimes coupled with a program of behavioural treatment and nutritional counseling.

Pharmacological approaches in obesity treatment

Most available weight loss medications are "appetite–suppressant" medications. The initial drugs used for appetite suppression were amphetamine [ 46 ], metamphetamine and phenmetrazine (Preludin) and are no longer used in treatment of obesity because of their high potential for abuse.

Inhibitors of 5-hyroxytryptamine (5-HT) reuptake, fenfluramine and dexfenfluramine were licensed for obesity but proved to cause pulmonary hyper tension and increased valvular heart disease [ 47 ] and have been withdrawn from the market. Drugs like phendimetrazine (Plegine), diethylpropion (Tenuate), phentermine (Lonamin) etc., are being marketed but have been classified as controlled substances and are recommended for short-term use only.

The newest agents available for weight loss are sibutramine (Meredia) and orlistat (Xenical). They are the only weight loss medications approved by the US Food and Drug Administration (FDA) for long-term use [ 48 ] in significantly obese patients, although their safety and effectiveness have not been established for use beyond one year.

Sibutramine is the serotonin and norepinephrine re-uptake inhibitor, which induces decreased food intake and increased thermogensis [ 49 – 52 ]. In clinical trials, sibutramine showed a statistical improvement in amount of weight lost versus placebo [ 53 ]. It limits decline of metabolic rate that typically accompanies weight loss [ 54 ]. However, this agent is contraindicated in-patient with known seizure disorders, high blood pressure, congestive heart failure (CHF) a history of myocardial infraction and arrhythmias.

Orlistat is a potent and irreversible inhibitor of gastric, pancreatic lipases. It blocks the digestion of approximately 30% of the ingested dietary triglycerides. Studies proved that it produces 5% more weight loss than in control groups [ 55 ]. It is now available on prescription as Xenical ® (Orlistat-120 mg). The most commonly reported side effects include oily stools, soft stool [ 56 ], and increased defecation and decreased absorption of fat-soluble vitamins (A, D, E and K). Hence, patient may be recommended intake of fat-soluble vitamins [ 57 ] along with it. When used in conjugation with diet it was found to improve glycemic control and cardiovascular disorders [ 58 , 59 ].

In general, monotherapy in obese patients produced sub-optimal weight loss [ 60 ] but the use of more than one weight loss medication at a time (combined drug therapy) is not approved [ 61 ] and hence such an off-label use of combinations of drugs for weight loss is not recommended except as part of a research study.

Drugs under development

There has been a wide search for effective drugs for the treatment of obesity. Some of the promising drug development research areas are mentioned below.

Amylin is a peptide secreted with insulin in response to food intake that shares many other properties with established adiposity signals like insulin and leptin. Its circulating levels can be correlated with body fat. Preclinical studies have shown that amylin complements the effects of insulin in mealtime glucose regulation via several effects, which include a suppression of post meal glucagon secretion, a decrease in gastric emptying, and a decrease in food intake [ 62 ]. The drug pramlintide, a synthetic analogue of amylin is currently in phase III trials.

11β-hydroxysteroid dehydrogenase type-1 (11β-HSD-1) is an enzyme that increases cortisol levels in adipocytes. Studies on mice lacking gene for 11β-HSD-1 suggest that they are resistant to diet induced obesity [ 63 ]. An 11β-HSD-1 inhibitor being developed by Biovitrum is currently in clinical testing.

Stimulation of β 3 adrenoreceptors (β 3 -ARs) by selective agonists improves insulin action and stimulates energy metabolism. In animals, chronic β 3 -AR agonist treatment causes body weight reduction, which is almost entirely due to decrease in body fat [ 64 ]. At least a dozen pharmaceutical companies are in the process of developing β 3 -AR drugs, some of which are already in human testing. AD9677 a β-adrenoceptor agonist is in phase II trails.

The botanical P57 is an extract of steroidal glycosides derived from South African Cactus . The potent appetite suppression may occur via the melanocortin-4 (MCR-4) saponins from the Platycodi radix and Salacia reticulata have been shown to inhibit pancreatic lipase, producing weight loss and reduction of fatty liver in laboratory animals [ 65 ]. Currently, P57 is in Phase II testing and Table 2 summarizes some other important drugs union are under clinical trials for the treatment of obesity.

Apart from drug treatment, surgery is also indicated when BMI is exceedingly high (>40 kg/m 2 or >30 kg/m 2 with obesity-related medical co-morbidities) and when other treatment modalities have failed [ 66 ]. The most popular surgical procedures used for treatment of severe obesities involve gastric portioning or gastroplasty and gastric by-pass. The gastroplasty procedures create a small gastric pouch, which is drained through a narrow calibrated stoma [ 67 , 68 ]. The intake of solids is therefore considerably limited. Gastric by-pass surgery creates a larger pouch emptied by an anastomosis directly into the jejunum, bypassing the duodenum. It is considered now as the most effective and safe surgery for morbid obesity [ 69 , 70 ]. This technique induces weight loss by combining restricted intake and a moderate degree of malabsorbtion [ 71 ]. Initial loss of weight is greater after this procedure than following gastroplasty [ 72 ].

Gastric and nutritional complications [ 73 ] may be serious implications of the surgery. Nutritional deficiencies and intractable vomiting are frequently associated with surgery. Surgical treatments for obesity resolve most co-morbidities of severe obesity such as hypertension [ 74 , 75 ], serum lipid levels [ 76 ] and diabetes mellitus [ 77 , 78 ].

Obesity is not a social condition but is a rampant disease. Obesity cannot be overviewed as just a matter of overeating and lack of will power but must be considered as a major genetic aetiology modified by environment and should be treated vigorously in the same manner that we now apply to other diseases. A better understanding of the aetiological determinants in individual subjects will provide a basis for more rational intervention to prevent this recalcitrant public health problem. With the increasing awareness and ongoing research in this area there is a considerable reason for optimism that the next coming years will bring better treatment for the obese.

Flegal KM, Carroll MD, Kuczmarski RJ, Johnson CL: Over weight and obesity in the United States: Prevalence and trends, 1960–1994. Int J Obes Relat Metab Disord. 1998, 22: 39-47. 10.1038/sj.ijo.0800541.

Article   CAS   PubMed   Google Scholar  

Bjorntorp P: Obesity. Lancet. 1997, 350: 423-426. 10.1016/S0140-6736(97)04503-0.

US Department of Health and Human Services. Office of the Surgeon General: The surgeon General's call to action to prevent and decrease overweight and obesity. Rockville MD: United States Department of Health and Human Services. 2001

Google Scholar  

Manson JE, Willett WC, Stamfer MJ, Colditz GA, Hunter DJ, Hankinson SE, Hennekens CH, Speizer FE: Body weight and mortality among women. N Eng J Med. 1995, 333: 677-685. 10.1056/NEJM199509143331101.

Article   CAS   Google Scholar  

Blackburn GL: Effect of degree of weight loss on health benefits. Obes Res. 1995, 3: 211s-216s.

Article   PubMed   Google Scholar  

World Health Organization: Obesity: Preventing and managing the global epidemic. World Health Organisation Geneva. 2000

Goldstein DJ: Beneficial health effects of a modest weight loss. Int J Obes Relat Metab Disord. 1992, 16: 397-415.

CAS   PubMed   Google Scholar  

Bosello O, Armellini F, Zamboni M, Fitchet M: The benefits of modest weight loss in type-II diabetes. Int J Obes Relat Metab Disord. 1997, 21: S10-S13.

PubMed   Google Scholar  

Wing RR, Koeske R, Epstein LH, Nowalk MP, Gooding W, Becker D: Long term effects of modest weight loss in type-II diabetic patients. Arch Intern Med. 1987, 147: 1749-1753. 10.1001/archinte.147.10.1749.

Taylor RW, Keil D, Gold EJ, Williams SM, Goulding A: Body mass index, waist girth and waist-to-hip ratio as indexes of total and regional adiposity in women: evaluation using receiver operating characteristic curves. Am J Clin Nutr. 1998, 67: 44-49.

Jacob CS, Katherine MH: Assessing obesity classification and epidemology. Br Med Bull. 1997, 2: 239-

Zhang YY, Proencea R, Maffei M, Barone M, Leopold L, Friedman JM: Positional clone of the mouse obese gene and its human homologue. Nature. 1994, 372: 425-432. 10.1038/372425a0.

Auwerx J, Stales B: Leptin. Lancet. 1998, 351: 732-742. 10.1016/S0140-6736(97)06348-4.

Article   Google Scholar  

Andersson LB: Genes and obesity. Ann Med. 1996, 28: 5-7.

Arner P: The β 3 -adrenergic receptor – a cause & cure of obesity. N Engl J Med. 1995, 333: 382-383. 10.1056/NEJM199508103330612.

Chagnon YC, Perusse L, Weisnagel SJ, Rankinen T, Bouchard C: The human obesity gene map: the 1999 update. Obes Res. 2000, 8: 89-117.

Dryden S, Frankish H, Wang Q, Williams G: Neuropeptide Y and energy balance, one way ahead for the treatment of obesity?. Eur J Clin Invest. 1994, 24: 293-308.

Flier JS, Flier EM: Obesity and the hypothalamus: Novel peptides for new pathways. Cell. 1998, 92: 437-440. 10.1016/S0092-8674(00)80937-X.

Friedman JM: The alphabet of weight control. Nature. 1997, 385: 119-120. 10.1038/385119a0.

Shor Posnar G, Grinker JA, Marinescu C: Hypothalamic serotonin in the control of meal patterns and macronutrient selection. Brain Res Bull. 1986, 17: 663-671. 10.1016/0361-9230(86)90198-X.

Dryden S, Frankish H, Wang Q, Williams G: The serotonin antagonist methysergide increase NPY synthesis and secretion in the hypothalamus of rat. Brain Res. 1995, 699: 12-18. 10.1016/0006-8993(95)00841-D.

Boosalis MG, Gemayel N, Lee A, Bray GA, Laine L, Cohen H: Cholecystokinin and satiety: effect of hypothalamic obesity and gastric bubble insertion. Am J Physiol. 1992, 262: R241-244.

Spiegelman BM, Flier JS: Adipogenesis and obesity: round in out the big picture. Cell. 1996, 87: 377-389. 10.1016/S0092-8674(00)81359-8.

Wadley J: Dietary restraint and binge eating behaviour. Anal Modif. 1980, 4: 647-660.

Tuck ML, Sowers J, Dornfeld L, Kledzik G, Maxwell M: The effect of weight reduction on blood pressure, plasma rennin activity, and plasma aldosterone levels in obese patients. N Engl J Med. 1981, 304: 930-933.

Kolarzyk E, Kiec E, Wiater M: Effect of obesity on the ventilatory capacity of the respiratory system. I. Relation between basic spirometric indicators: vital capacity (VC) and forced expiratory volume (FEV1) and obesity. Med Pr. 1985, 36: 87-95.

Rahilly OS: Non insulin dependent diabetes mellitus: the gathering storm. Br Med J. 1997, 314: 955-960.

Ford ES, Giles WH, Dietz WH: Prevalence of the metabolic syndrome among US adults: findings from the Third National health and Nutrition Examination survey. J Amer Med Assoc. 2002, 287: 356-359. 10.1001/jama.287.3.356.

Franz MJ, Bantle JP, Beebe CA, Brunzell JD, Chiasson JL, Garg A, Holzmeister LA, Hoogwerf B, Mayer_Davis E, Mooradian AD, Purnell JQ, Wheeler M: Evidence based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications. Diabetes care. 2002, 25: 148-198.

Dattilo AM, Kris-Etherton PM: Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis. Am J Clin Nutr. 1992, 56: 320-328.

Anonymous: UK Prospective study on maturity onset diabetes. I. Effect of diet and sulphonylurea, insulin or biguainide therapy on fasting plasma glucose and body weight over one year. Diabetologia. 1983, 24: 404-411.

Davis MA, Neuhaus JM, Ettinger WH, Mueller WH: Body fat distributions and osteoarthritis. Am J Epidemiol. 1990, 132: 701-707.

Timothy PG: Key issues in the prevention of obesity. Br Med Bull. 1997, 53: 359-388.

US Institute of medicine: Reducing risks of mental disorders. Frontiers for preventive intervention research. 1994, Washington, National Academy Press

Wadden TA: Treatment of obesity by moderate and severe caloric restriction results of clinical research tracts. Ann Intern Med. 1993, 119: 688-693.

Ashley JM, St Jeor ST, Schrage JP, Perumean_Chaney SE, Gilbertson MC, McCall NL, Bovee V: Weight control in the physician's office. Arch Intern Med. 2001, 161: 1599-1604. 10.1001/archinte.161.13.1599.

Anderssen S, Holme I, Urdal P, Hjermann I: Diet and exercise intervention have favourable effects on blood pressure in hypertensives: The Oslo Diet and Exercise Study (ODES). Blood Press. 1995, 4: 343-349.

Bertram SR, Venter I, Stewart RI: Weight loss in obese women – exercise vs dietary education. S Afr Med J. 1990, 78: 15-18.

Wood PD, Stefanick ML, Dreon DM, Frey-Hewitt B, Garay SC, Williams PT, Superko HR, Fortman SP, Albers JJ, Vranizan KM, et al: Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise. N Engl J Med. 1988, 319: 1173-1179.

Ditschuneit HH, Flechtner-Mors M, Johnson TD, Adler G: Metabolic and weight loss effects of a long term dietary intervention in obese patients. Am J Clin Nutr. 1999, 69: 198-204.

US Department of Health and Human services: Leading health indicators. Overweight and obesity. Healthy people 2010 (Conference ed. in two volumes). DC. US Department of Health and Human Services, Washington. 2000, 24-45.

Wyatt HR, Wing RR, Hill JO: The National weight control registry. In: Evaluation & Management of obesity. Edited by: Bessesen DH, Kushner RF. 2002, Philadelphia, Hanley & Belfus Inc, 199-224.

Schoeller DA, Shay K, Kushner RF: How much physical activity is needed to minimize weight gain in previously obese women?. Am J Clin Nutr. 1997, 66: 551-556.

Physical Activity and Health: A Report of the surgeon General PA. US Department of Health and Human services. 1996

National Institutes of Health (NHLBI): Clinical guidelines on the identification, evaluation and treatment of overweight and obesity in adults. The evidence report Washington D.C. National Institute of Health, Obese Res. 1998, 6: 51s-201s.

Lessof MH, Myerson A: Benzedrine sulfate as an aid to be the treatment of obesity. N Engl J Med. 1938, 218: 119-205.

Connolly HM, Crary JL, McGoon MD, Hensud DD, Edwards BS, Edwards WD: Valvular heart disease associated with fenfluramine – phentermine. N Engl J Med. 1997, 337: 783-10.1056/NEJM199708283370901.

James WP, Astrup A, Finer N, Hilsted J, Kopelman P, Rossner S, Saris WH, Van Gaal LF: Effect of sibutramine on weight maintenance after weight loss: a randomised trial. STORM Study Group. Sibutramine Trial of Obesity Reduction and Maintenance. Lancet. 2000, 356: 2119-2125. 10.1016/S0140-6736(00)03491-7.

Mun EC, Blackbur GL, Matthews JB: Current status of medical and surgical therapy for obesity. Gastroenterology. 2001, 120: 669-681.

Rolls BJ, Shide DJ, Thorwart ML, Ulbrecht JS: Sibutramine reduces food intake in non-dieting women with obesity. Obes Res. 1998, 6: 1-11.

Hansen DL, Toubro S, Stock MJ, Macdonald IA, Astrup A: Thermogenic effects of sibutramine in humans. Am J Clin Nutr. 1998, 68 : 1180-1186.

Seagle HM, Bessesen DH, Hill JO: Effects of sibutramine on resting metabolic rate and weight loss in over weight women. Obes Res. 1998, 6: 115-121.

Astrup A, Toubro S: When, for whom and how to use sibutramine?. Int J Obes Relat Metab Disord. 2001, 25 (Suppl 4): 52-57. Review

Luque CA: Sibutramine: a serotonin-norepinephrine reuptake inhibitor for the treatment of obesity. Ann Pharmacother. 1999, 33: 968-978. 10.1345/aph.18319.

Sjostrom L, Rissonen A, Andersen T, Boldrin M, Golay A, Koppeschaar HP, Krempf M: Randomised placebo-controlled trial of orlistat for weight loss and prevention of weight in obese patients. European Multicenter Orlistat study group. Lancet. 1998, 352: 167-172. 10.1016/S0140-6736(97)11509-4.

Hill JO, Hauptman J, Anderson JW, Fujioka K, O'Neil PM, Smith DK, Zavoral JH, Aronne LJ: Orlistat, a lipase inhibitor, for weight maintenance after conventional dieting: a 1-year study. Am J Clin Nutr. 1999, 69: 1108-1116.

Mc Duffie JR, Calis KA, Booth SL, Uwaifo GI, Yanovski JA: Effects of orlistat on fat soluble vitamins in obese adolescents. Pharmacotherapy. 2002, 22: 814-822.

Hollander PA, Elbein SC, Hirsch IB, Kelley D, McGill J, Taylor T, Weiss SR, Crockett SE, Kaplan RA, Comstock J, Lucas CP, Lodewick PA, Canovatchel W, Chung J, Hauptman J: Role of orlistat in the treatment of obese patients with type-2 diabetes. A 1-year randomized double blind study. Diabetes care. 1998, 21: 1288-1294.

Davidson MH, Hauptman J, DiGirolamo M, Foreyt JP, Halsted CH, Heber D, Heimburger DC, Lucas CP, Robbins DC, Chung J, Heymsfield SB: Weight control and risk factor reduction in obese subjects treated for 2 years with orlistat: a randomized controlled trial. J Amer Med Assoc. 1999, 281: 235-242. 10.1001/jama.281.3.235.

Wadden TA, Berkowitz RI, Sarwer DB, Prus-Wisniewski R, Steinberg C: Benefits of lifestyle modification in the pharmacologic treatment of obesity: a randomized trial. Arch Intern Med. 2001, 161: 218-227. 10.1001/archinte.161.2.218.

NHLBI: Prescription medication for treatment of obesity. [ http://www.niddk.nih.gov/health/nutrit/nutrit.htm ]

Rushing PA, Hagan MM, Seeley RJ, Lutz TA, Woods SC: Amylin: a novel action in the brain to reduce body weight. Endocrinology. 2000, 141: 850-853. 10.1210/en.141.2.850.

Stewart PM, Tomlinson JW: Cortisol, 11 beta-hydroxysteroid dehydrogenase type 1 and central obesity. Trends Endocrinol Metab. 2002, 13: 94-96. 10.1016/S1043-2760(02)00566-0.

Clapham JC, Arch JRS, Tadayyon M: Anti-obesity drugs: a critical review of current therapies and future opportunities. Pharmacol Ther. 2001, 89: 81-121. 10.1016/S0163-7258(00)00105-4.

Anonymous: P 57 and food intake. obesity Meds and Research News. 2000

Anonymous: NIH Conference. Gastrointestinal surgery for severe obesity. Consensus Development Conference Panel. Ann Intern Med. 1991, 115: 956-961.

Karl JG: Overview of surgical techniques for treating obesity. Am J Clin Nutr. 1992, 55: 552s-555s.

Ashley S, Bird DL, Sugden G, Royston CM: Vertical banded gastroplasty for the treatment of morbid obesity. Br J Surg. 1993, 80: 1421-1423.

Shikora SA, Benotti PN, Forre RA: Surgical Treatment of Obesity. In: Obesity, pathophysiology, psychology and treatment. Edited by: Blackburn GL, Kanders BS. 1994, New York Chapman & Hall, 264-282.

Sagar PM: Surgical treatment of morbid obesity. Br J Surg. 1995, 82: 732-739.

Lonroth H, Dalenback J, Haglind E, Josefsson K, Olbe L, Fagevik Olsen M, Lundell L: Vertical banded gastroplasty by laparoscopic technique in the treatment of morbid obesity. Surg Laparosc Endosc. 1996, 6: 102-107. 10.1097/00019509-199604000-00004.

Salmon PA, McArdle MO: The rationale and results of gastroplasty/gastric by-pass. Obes Surg. 1992, 2: 61-68. 10.1381/096089292765560565.

Seehra H, Macc Dermatt N, Lascelles RG, Taylor TV: Wernicke's encephalapathy after vertical banded gastroplasty for morbid obesity. Br Med J. 1996, 312: 434-

Foley EF, Benotti PN, Borlase BC, Hollingshead J, Blackburn GL: Impact of gastric restrictive surgery on hypertension in the morbidly obese. Am J Surg. 1992, 163: 294-297. 10.1016/0002-9610(92)90005-C.

Carson JL, Ruddy ME, Duff AE, Holmes NJ, Cody RP, Brolin RE: The effect of gastric bypass surgery on hypertension in the morbidity obese patients. Arch Intern Med. 1994, 154: 193-200. 10.1001/archinte.154.2.193.

Olsson SA, Petersson BG, Sorbris R, Nilsson-Ehle P: Effects of weight reduction after gastroplasty on glucose and lipid metabolism. Am J Clin Nutr. 1984, 40: 1273-1280.

Herbst CA, Hughes TA, Gwynne JT, Buckwalter JA: Gastric bariatric operation in insulin treated adults. Surgery. 1984, 95: 209-214.

Pories WJ, Swanson MS, MacDonald KG, Long SB, Morris PG, Brown BM, Barakat HA, deRamon RA, Israel G, Dolezal JM: Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg. 1995, 222: 339-350.

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Nammi, S., Koka, S., Chinnala, K.M. et al. Obesity: An overview on its current perspectives and treatment options. Nutr J 3 , 3 (2004). https://doi.org/10.1186/1475-2891-3-3

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Obesity, Bariatric and Metabolic Surgery pp 3–14 Cite as

Introduction to Obesity

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Obesity is defined as an abnormal or excessive accumulation of fat that may impair health. According to the WHO, any individual with a body mass index (BMI) ≥30 kg/m 2 is obese. A BMI of ≥40 kg/m 2 is defined as severe/class III obesity. This term is also used for individuals with a BMI between 30 and 39.9 kg/m 2 who have significant comorbidities. The rate of severe obesity has increased significantly over the preceding decades with the highest rates reported in Mexico and the United States. The most commonly used measure of adiposity is BMI. Other methods used include bioimpedance analysis, dual-energy x-ray absorptiometry (DEXA), hydrometry, computed tomography (CT), and magnetic resonance imaging (MRI).

Differential distribution of body fat may predispose individuals to conditions such as type 2 diabetes mellitus, cardiovascular diseases, respiratory disorders, infertility, certain forms of cancers, and psychological and social abnormalities. The rates of these conditions increase significantly as BMI increases. Obesity leads to a significant economic burden on the society, both at an individual and the population level. The rise in obesity levels has mirrored the increase in number of bariatric procedures performed worldwide.

  • Weight loss
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World Health Organization. Obesity and overweight [Internet], updated on 1 April 2020. Available at https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight

Revels S, Kumar SA, Ben-Assuli O. Predicting obesity rate and obesity-related healthcare costs using data analytics. Health Policy Technol. 2017;6(2):198–207.

Article   Google Scholar  

Hales CM, Caroll MD, Fryar CD, Ogden CL. Prevalence of obesity and severe obesity among adults: United States, 2017–2018. NCHS Data Brief. 2020;2020(360):8.

Google Scholar  

Abarca-Gómez L, Abdeen ZA, Hamid ZA, Abu-Rmeileh NM, Acosta-Cazares B, Acuin C, Adams RJ, Aekplakorn W, Afsana K, Aguilar-Salinas CA, Agyemang C. Worldwide trends in body-mass index, underweight, overweight, and obesity from 1975 to 2016: a pooled analysis of 2416 population-based measurement studies in 128.9 million children, adolescents, and adults. Lancet. 2017;390(10113):2627–42.

Chooi YC, Ding C, Magkos F. The epidemiology of obesity. Metabolism. 2019;92:6–10.

Article   CAS   Google Scholar  

GBD 2015 Obesity Collaborators. Health effects of overweight and obesity in 195 countries over 25 years. N Engl J Med. 2017;377(1):13–27.

Finkelstein EA, Khavjou OA, Thompson H, Trogdon JG, Pan L, Sherry B, Dietz W. Obesity and severe obesity forecasts through 2030. Am J Prev Med. 2012;42(6):563–70.

Health Survey for England 2018 [NS]. NHS Digital [Internet], cited 12 January 2021. Available from: https://digital.nhs.uk/data-and-information/publications/statistical/health-survey-for-england/2018

Statistics on Obesity, Physical Activity and Diet, England, 2019. NHS Digital [Internet], cited 12 January 2021. Available from: https://digital.nhs.uk/data-and-information/publications/statistical/statistics-on-obesity-physical-activity-and-diet/statistics-on-obesity-physical-activity-and-diet-england-2019

Pischon T, Boeing H, Hoffmann K, Bergmann M, Schulze MB, Overvad K. General and abdominal adiposity and risk of death in Europe. N Engl J Med. 2008;359:2105–20.

Cecchini M, Sassi F, Lauer JA, Lee YY, Guajardo-Barron V, Chisholm D. Tackling of unhealthy diets, physical inactivity, and obesity: health effects and cost-effectiveness. Lancet. 2010;376(9754):1775–84.

Hossain P, Kawar B, El Nahas M. Obesity and diabetes in the developing world – a growing challenge. N Engl J Med. 2007;356(3):213–5.

Ventosa MM. Disentangling effects of socioeconomic status on obesity: a cross-sectional study of the Spanish adult population. Econ Hum Biol. 2016;22:216–24.

Jiwani SS, Carrillo-Larco RM, Hernández-Vásquez A, Barrientos-Gutiérrez T, Basto-Abreu A, Gutierrez L, Irazola V, Nieto-Martínez R, Nunes BP, Parra DC, Miranda JJ. The shift of obesity burden by socioeconomic status between 1998 and 2017 in Latin America and the Caribbean: a cross-sectional series study. Lancet Glob Health. 2019;7(12):e1644–54.

Sigmund E, Badura P, Sigmundová D, Voráčová J, Zacpal J, Kalman M, Pavelka J, Vokacová J, Hamrik Z. Trends and correlates of overweight/obesity in Czech adolescents in relation to family socioeconomic status over a 12-year study period (2002–2014). BMC Public Health. 2018;18(1):122.

Booth HP, Charlton J, Gulliford MC. Socioeconomic inequality in morbid obesity with body mass index more than 40 kg/m 2 in the United States and England. SSM – Popul Health. 2017;3:172–8.

Swinburn BA, Sacks G, Hall KD, McPherson K, Finegood DT, Moodie ML, Gortmaker SL. The global obesity pandemic: shaped by global drivers and local environments. Lancet. 2011;378(9793):804–14.

Kirby JB, Liang L, Chen HJ, Wang Y. Race, place, and obesity: the complex relationships among community racial/ethnic composition, individual race/ethnicity, and obesity in the United States. Am J Public Health. 2012;102(8):1572–8.

Ng M, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980–2013: a systematic analysis for the global burden of disease study 2013. Lancet. 2014;384:766–81.

Neovius K, Rehnberg C, Rasmussen F, Neovius M. Lifetime productivity losses associated with obesity status in early adulthood: a population-based study of Swedish men. Appl Health Econ Health Policy. 2012;10(5):309–17.

Public Health England Guidance – Health matters: obesity and the food environment. Published 31 March 2017.

Castle A. SPICe briefing – obesity in Scotland. Edinburgh: Scottish Parliament; 2015.

Kim DD, Basu A. Estimating the medical care costs of obesity in the United States: systematic review, meta-analysis, and empirical analysis. Value Health. 2016;19(5):602–13.

Wang YC, McPherson K, Marsh T, Gortmaker SL, Brown M. Health and economic burden of the projected obesity trends in the USA and the UK. Lancet. 2011;378(9793):815–25.

Keys A, Fidanza F, Karvonen MJ, Kimura N, Taylor HL. Indices of relative weight and obesity. J Chronic Dis. 1972;25(6):329–43.

Campbell IW, Haslam D. Chapter 1. What is obesity? In: Campbell IW, Haslam D, editors. Your questions answered – obesity. Edinburgh: Churchill Livingstone; 2005. p. 6. ISBN 0433074534.

Rush EC, Goedecke JH, Jennings C, Micklesfield L, Dugas L, Lambert EV, Plank LD. BMI, fat and muscle differences in urban women of five ethnicities from two countries. Int J Obes. 2007;31(8):1232–9.

Camhi SM, Bray GA, Bouchard C, Greenway FL, Johnson WD, Newton RL, Ravussin E, Ryan DH, Smith SR, Katzmarzyk PT. The relationship of waist circumference and BMI to visceral, subcutaneous, and total body fat: sex and race differences. Obesity. 2011;19(2):402–8.

Daniels SR, Khoury PR, Morrison JA. The utility of body mass index as a measure of body fatness in children and adolescents: differences by race and gender. Pediatrics. 1997;99(6):804–7.

Di Angelantonio E, Bhupathiraju SN, Wormser D, Gao P, Kaptoge S, de Gonzalez AB, Cairns BJ, Huxley R, Jackson CL, Joshy G, Lewington S. Body-mass index and all-cause mortality: individual-participant-data meta-analysis of 239 prospective studies in four continents. Lancet. 2016;388(10046):776–86.

Berrington de Gonzalez A, Hartge P, Cerhan JR, Flint AJ, Hannan L, MacInnis RJ, et al. Body-mass index and mortality among 1.46 million white adults. N Engl J Med. 2010;363(23):2211–9.

Harrison GG. Height–weight tables. Ann Intern Med. 1985;103(6 Pt 2):989–94.

Belle SH, Berk PD, Courcoulas AP, Engel S, Flum DR, Gourash W, Horlick M, Hsu JY, Khandelwal S, Mitchell JE, O’Rourke RW. Reporting weight change: standardized reporting accounting for baseline weight. Surg Obes Relat Dis. 2013;9(5):782–9.

Deitel M, Greenstein RJ. Recommendations for reporting weight loss. Obes Surg. 2003;13(2):159–60.

Hatoum IJ, Kaplan LM. Advantages of percent weight loss as a method of reporting weight loss after roux-en-Y gastric bypass. Obesity. 2013;21(8):1519–25.

Health and Social Care Information Center. Statistics on obesity, physical activity and diet – England, 2014 [Internet]. London: Health and Social Care Information Center; 2014. Available from: http://www.hscic.gov.uk/catalogue/PUB13648/Obes-phys-acti-diet-eng-2014-rep.pdf

Dobbelsteyn CJ, Joffres MR, MacLean DR, Flowerdew G. A comparative evaluation of waist circumference, waist-to-hip ratio and body mass index as indicators of cardiovascular risk factors. The Canadian heart health surveys. Int J Obes Relat Metab Disord. 2001;25(5):652–61.

Pouliot MC, Després JP, Lemieux S, Moorjani S, Bouchard C, Tremblay A, Nadeau A, Lupien PJ. Waist circumference and abdominal sagittal diameter: best simple anthropometric indexes of abdominal visceral adipose tissue accumulation and related cardiovascular risk in men and women. Am J Cardiol. 1994;73(7):460–8.

Lean MEJ. Clinical handbook of weight management. London: Martin Dunitz Ltd; 1998.

Dalton M, Cameron AJ, Zimmet PZ, Shaw JE, Jolley D, Dunstan DW, Welborn TA, AusDiab Steering Committee. Waist circumference, waist–hip ratio and body mass index and their correlation with cardiovascular disease risk factors in Australian adults. J Intern Med. 2003;254(6):555–63.

Czernichow S, Kengne AP, Stamatakis E, Hamer M, Batty GD. Body mass index, waist circumference and waist–hip ratio: which is the better discriminator of cardiovascular disease mortality risk? Evidence from an individual-participant meta-analysis of 82 864 participants from nine cohort studies. Obes Rev. 2011;12(9):680–7.

CAS   Google Scholar  

Song X, Jousilahti P, Stehouwer CDA, et al. Comparison of various surrogate obesity indicators as predictors of cardiovascular mortality in four European populations. Eur J Clin Nutr. 2013;67:1298.

Marlowe F, Apicella C, Reed D. Men’s preferences for women’s profile waist-to-hip ratio in two societies. Evol Hum Behav. 2005;26:458–68.

Sun G, French CR, Martin GR, Younghusband B, Green RC, Xie YG, et al. Comparison of multifrequency bioelectrical impedance analysis with dual-energy X-ray absorptiometry for assessment of percentage body fat in a large, healthy population. Am J Clin Nutr. 2005;81(1):74–8.

Völgyi E, Tylavsky FA, Lyytikäinen A, Suominen H, Alén M, Cheng S. Assessing body composition with DXA and bioimpedance: effects of obesity, physical activity, and age. Obesity. 2008;16(3):700–5.

Achamrah N, Colange G, Delay J, Rimbert A, Folope V, Petit A, Grigioni S, Déchelotte P, Coëffier M. Comparison of body composition assessment by DXA and BIA according to the body mass index: a retrospective study on 3655 measures. PLoS One. 2018;13(7):e0200465.

Shepherd JA, Ng BK, Sommer MJ, Heymsfield SB. Body composition by DXA. Bone. 2017;104:101–5.

Rothney MP, Brychta RJ, Schaefer EV, Chen KY, Skarulis MC. Body composition measured by dual-energy X-ray absorptiometry half-body scans in obese adults. Am J Clin Nutr. 1995;61(2):274–8.

Kullberg J, Brandberg J, Angelhed JE, Frimmel H, Bergelin E, Strid L, Ahlstrom H, Johansson L, Lonn L. Whole-body adipose tissue analysis: comparison of MRI, CT and dual energy X-ray absorptiometry. Br J Radiol. 2009;82(974):123–30.

Hu FB. Measurements of adiposity and body composition. In: Hu FB, editor. Obesity epidemiology. New York: Oxford University Press; 2008. p. 53–83.

Chapter   Google Scholar  

Fields D, Hunter G, Goran M. Validation of the BOD POD with hydrostatic weighing: influence of body clothing. Int J Obes. 2000;24:200–5.

Dewit O, Fuller NJ, Fewtrell MS, Elia M, Wells JCK. Whole body air displacement plethysmography compared with hydrodensitometry for body composition analysis. Arch Dis Child. 2000;82(2):159–64.

Kim YJ, Lee SH, Kim TY, Park JY, Choi SH, Kim KG. Body fat assessment method using CT images with separation mask algorithm. J Digit Imaging. 2013;26(2):155–62.

Graffy PM, Sandfort V, Summers RM, Pickhardt PJ. Automated liver fat quantification at nonenhanced abdominal CT for population-based steatosis assessment. Radiology. 2019;293(2):334–42.

Ludwig UA, Klausmann F, Baumann S, et al. Whole-body MRI-based fat quantification: a comparison to air displacement plethysmography. J Magn Reson Imaging. 2014;40(6):1437–44.

Browning LM, Mugridge O, Dixon AK, Aitken SW, Prentice AM, Jebb SA. Measuring abdominal adipose tissue: comparison of simpler methods with MRI. Obes Facts. 2011;4(1):9–15.

Ludescher B, Machann J, Eschweiler GW, Vanhöfen S, Maenz C, Thamer C, et al. Correlation of fat distribution in whole body MRI with generally used anthropometric data. Investig Radiol. 2009;44(11):712–9.

Després J-P, Lemieux I. Abdominal obesity and metabolic syndrome. Nature. 2006;444(7121):881–7.

Matsuzawa Y, Funahashi T, Nakamura T. The concept of metabolic syndrome: contribution of visceral fat accumulation and its molecular mechanism. J Atheroscler Thromb. 2011;18(8):629–39.

Wagenknecht LE, Langefeld CD, Scherzinger AL, Norris JM, Haffner SM, Saad MF, et al. Insulin sensitivity, insulin secretion, and abdominal fat: the insulin resistance atherosclerosis study (IRAS) family study. Diabetes. 2003;52(10):2490–6.

McLaughlin T, Lamendola C, Liu A, Abbasi F. Preferential fat deposition in subcutaneous versus visceral depots is associated with insulin sensitivity. J Clin Endocrinol Metab. 2011;96(11):E1756–60.

Hung CS, Lee JK, Yang CY, Hsieh HR, Ma WY, Lin MS, Liu PH, Shih SR, Liou JM, Chuang LM, Chen MF. Measurement of visceral fat: should we include retroperitoneal fat? PLoS One. 2014;9(11):e112355.

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The authors are grateful to Mr. Imran Alam for their work in producing this chapter in the first edition of the book.

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Lynn, W., Agrawal, S. (2023). Introduction to Obesity. In: Agrawal, S. (eds) Obesity, Bariatric and Metabolic Surgery. Springer, Cham. https://doi.org/10.1007/978-3-030-60596-4_1

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The lived experience of people with obesity: study protocol for a systematic review and synthesis of qualitative studies

  • Emma Farrell   ORCID: orcid.org/0000-0002-7780-9428 1 ,
  • Marta Bustillo 2 ,
  • Carel W. le Roux 3 ,
  • Joe Nadglowski 4 ,
  • Eva Hollmann 1 &
  • Deirdre McGillicuddy 1  

Systematic Reviews volume  10 , Article number:  181 ( 2021 ) Cite this article

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Obesity is a prevalent, complex, progressive and relapsing chronic disease characterised by abnormal or excessive body fat that impairs health and quality of life. It affects more than 650 million adults worldwide and is associated with a range of health complications. Qualitative research plays a key role in understanding patient experiences and the factors that facilitate or hinder the effectiveness of health interventions. This review aims to systematically locate, assess and synthesise qualitative studies in order to develop a more comprehensive understanding of the lived experience of people with obesity.

This is a protocol for a qualitative evidence synthesis of the lived experience of people with obesity. A defined search strategy will be employed in conducting a comprehensive literature search of the following databases: PubMed, Embase, PsycInfo, PsycArticles and Dimensions (from 2011 onwards). Qualitative studies focusing on the lived experience of adults with obesity (BMI >30) will be included. Two reviewers will independently screen all citations, abstracts and full-text articles and abstract data. The quality of included studies will be appraised using the critical appraisal skills programme (CASP) criteria. Thematic synthesis will be conducted on all of the included studies. Confidence in the review findings will be assessed using GRADE CERQual.

The findings from this synthesis will be used to inform the EU Innovative Medicines Initiative (IMI)-funded SOPHIA (Stratification of Obesity Phenotypes to Optimize Future Obesity Therapy) study. The objective of SOPHIA is to optimise future obesity treatment and stimulate a new narrative, understanding and vocabulary around obesity as a set of complex and chronic diseases. The findings will also be useful to health care providers and policy makers who seek to understand the experience of those with obesity.

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PROSPERO CRD42020214560 .

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Obesity is a complex chronic disease in which abnormal or excess body fat (adiposity) impairs health and quality of life, increases the risk of long-term medical complications and reduces lifespan [ 1 ]. Operationally defined in epidemiological and population studies as a body mass index (BMI) greater than or equal to 30, obesity affects more than 650 million adults worldwide [ 2 ]. Its prevalence has almost tripled between 1975 and 2016, and, globally, there are now more people with obesity than people classified as underweight [ 2 ].

Obesity is caused by the complex interplay of multiple genetic, metabolic, behavioural and environmental factors, with the latter thought to be the proximate factor which enabled the substantial rise in the prevalence of obesity in recent decades [ 3 , 4 ]. This increased prevalence has resulted in obesity becoming a major public health issue with a resulting growth in health care and economic costs [ 5 , 6 ]. At a population level, health complications from excess body fat increase as BMI increases [ 7 ]. At the individual level, health complications occur due to a variety of factors such as distribution of adiposity, environment, genetic, biologic and socioeconomic factors [ 8 ]. These health complications include type 2 diabetes [ 9 ], gallbladder disease [ 10 ] and non-alcoholic fatty liver disease [ 11 ]. Excess body fat can also place an individual at increased cardiometabolic and cancer risk [ 12 , 13 , 14 ] with an estimated 20% of all cancers attributed to obesity [ 15 ].

Although first recognised as a disease by the American Medical Association in 2013 [ 16 ], the dominant cultural narrative continues to present obesity as a failure of willpower. People with obesity are positioned as personally responsible for their weight. This, combined with the moralisation of health behaviours and the widespread association between thinness, self-control and success, has resulted in those who fail to live up to this cultural ideal being subject to weight bias, stigma and discrimination [ 17 , 18 , 19 ]. Weight bias, stigma and discrimination have been found to contribute, independent of weight or BMI, to increased morbidity or mortality [ 20 ].

Thomas et al. [ 21 ] highlighted, more than a decade ago, the need to rethink how we approach obesity so as not to perpetuate damaging stereotypes at a societal level. Obesity research then, as now, largely focused on measurable outcomes and quantifiable terms such as body mass index [ 22 , 23 ]. Qualitative research approaches play a key role in understanding patient experiences, how factors facilitate or hinder the effectiveness of interventions and how the processes of interventions are perceived and implemented by users [ 24 ]. Studies adopting qualitative approaches have been shown to deliver a greater depth of understanding of complex and socially mediated diseases such as obesity [ 25 ]. In spite of an increasing recognition of the integral role of patient experience in health research [ 25 , 26 ], the voices of patients remain largely underrepresented in obesity research [ 27 , 28 ].

Systematic reviews and syntheses of qualitative studies are recognised as a useful contribution to evidence and policy development [ 29 ]. To the best of the authors’ knowledge, this will be the first systematic review and synthesis of qualitative studies focusing on the lived experience of people with obesity. While systematic reviews have been carried out on patient experiences of treatments such as behavioural management [ 30 ] and bariatric surgery [ 31 ], this review and synthesis will be the first to focus on the experience of living with obesity rather than patient experiences of particular treatments or interventions. This focus represents a growing awareness that ‘patients have a specific expertise and knowledge derived from lived experience’ and that understanding lived experience can help ‘make healthcare both effective and more efficient’ [ 32 ].

This paper outlines a protocol for the systematic review of qualitative studies based on the lived experience of people with obesity. The findings of this review will be synthesised in order to develop an overview of the lived experience of patients with obesity. It will look, in particular, at patient concerns around the risks of obesity and their aspirations for response to obesity treatment.

The review protocol has been registered within the PROSPERO database (registration number: CRD42020214560) and is being reported in accordance with the reporting guidance provided in the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols (PRISMA-P) statement [ 33 , 34 ] (see checklist in Additional file  1 ).

Information sources and search strategy

The primary source of literature will be a structured search of the following electronic databases (from January 2011 onwards—to encompass the increase in research focused on patient experience observed over the last 10 years): PubMed, Embase, PsycInfo, PsycArticles and Dimensions. There is no methodological agreement as to how many search terms or databases out to be searched as part of a ‘good’ qualitative synthesis (Toye et al. [ 35 ]). However, the breadth and depth of the search terms, the inclusion of clinical and personal language and the variety within the selected databases, which cover areas such as medicine, nursing, psychology and sociology, will position this qualitative synthesis as comprehensive. Grey literature will not be included in this study as its purpose is to conduct a comprehensive review of peer-reviewed primary research. The study’s patient advisory board will be consulted at each stage of the review process, and content experts and authors who are prolific in the field will be contacted. The literature searches will be designed and conducted by the review team which includes an experienced university librarian (MB) following the methodological guidance of chapter two of the JBI Manual for Evidence Synthesis [ 36 ]. The search will include a broad range of terms and keywords related to obesity and qualitative research. A full draft search strategy for PubMed is provided in Additional file  2 .

Eligibility criteria

Studies based on primary data generated with adults with obesity (operationally defined as BMI >30) and focusing on their lived experience will be eligible for inclusion in this synthesis (Table  1 ). The context can include any country and all three levels of care provision (primary, secondary and tertiary). Only peer-reviewed, English language, articles will be included. Studies adopting a qualitative design, such as phenomenology, grounded theory or ethnography, and employing qualitative methods of data collection and analysis, such as interviews, focus groups, life histories and thematic analysis, will be included. Publications with a specific focus, for example, patient’s experience of bariatric surgery, will be included, as well as studies adopting a more general view of the experience of obesity.

Screening and study selection process

Search results will be imported to Endnote X9, and duplicate entries will be removed. Covidence [ 38 ] will be used to screen references with two reviewers (EF and EH) removing entries that are clearly unrelated to the research question. Titles and abstracts will then be independently screened by two reviewers (EF and EH) according to the inclusion criteria (Table  1 ). Any disagreements will be resolved through a third reviewer (DMcG). This layer of screening will determine which publications will be eligible for independent full-text review by two reviewers (EF and EH) with disagreements again being resolved by a third reviewer (DMcG).

Data extraction

Data will be extracted independently by two researchers (EF and EH) and combined in table format using the following headings: author, year, title, country, research aims, participant characteristics, method of data collection, method of data analysis, author conclusions and qualitative themes. In the case of insufficient or unclear information in a potentially eligible article, the authors will be contacted by email to obtain or confirm data, and a timeframe of 3 weeks to reply will be offered before article exclusion.

Quality appraisal of included studies

This qualitative synthesis will facilitate the development of a conceptual understanding of obesity and will be used to inform the development of policy and practice. As such, it is important that the studies included are themselves of suitable quality. The methodological quality of all included studies will be assessed using the critical appraisal skills programme (CASP) checklist, and studies that are deemed of insufficient quality will be excluded. The CASP checklist for qualitative research comprises ten questions that cover three main issues: Are the results of the study under review valid? What are the results? Will the results help locally? Two reviewers (EF and EH) will independently evaluate each study using the checklist with a third and fourth reviewer (DMcG and MB) available for consultation in the event of disagreement.

Data synthesis

The data generated through the systematic review outlined above will be synthesised using thematic synthesis as described by Thomas and Harden [ 39 ]. Thematic synthesis enables researchers to stay ‘close’ to the data of primary studies, synthesise them in a transparent way and produce new concepts and hypotheses. This inductive approach is useful for drawing inference based on common themes from studies with different designs and perspectives. Thematic synthesis is made up of a three-step process. Step one consists of line by line coding of the findings of primary studies. The second step involves organising these ‘free codes’ into related areas to construct ‘descriptive’ themes. In step three, the descriptive themes that emerged will be iteratively examined and compared to ‘go beyond’ the descriptive themes and the content of the initial studies. This step will generate analytical themes that will provide new insights related to the topic under review.

Data will be coded using NVivo 12. In order to increase the confirmability of the analysis, studies will be reviewed independently by two reviewers (EF and EH) following the three-step process outlined above. This process will be overseen by a third reviewer (DMcG). In order to increase the credibility of the findings, an overview of the results will be brought to a panel of patient representatives for discussion. Direct quotations from participants in the primary studies will be italicised and indented to distinguish them from author interpretations.

Assessment of confidence in the review findings

Confidence in the evidence generated as a result of this qualitative synthesis will be assessed using the Grading of Recommendations Assessment, Development and Evaluation Confidence in Evidence from Reviews of Qualitative Research (GRADE CERQual) [ 40 ] approach. Four components contribute to the assessment of confidence in the evidence: methodological limitations, relevance, coherence and adequacy of data. The methodological limitations of included studies will be examined using the CASP tool. Relevance assesses the degree to which the evidence from the primary studies applies to the synthesis question while coherence assesses how well the findings are supported by the primary studies. Adequacy of data assesses how much data supports a finding and how rich this data is. Confidence in the evidence will be independently assessed by two reviewers (EF and EH), graded as high, moderate or low, and discussed collectively amongst the research team.

Reflexivity

For the purposes of transparency and reflexivity, it will be important to consider the findings of the qualitative synthesis and how these are reached, in the context of researchers’ worldviews and experiences (Larkin et al, 2019). Authors have backgrounds in health science (EF and EH), education (DMcG and EF), nursing (EH), sociology (DMcG), philosophy (EF) and information science (MB). Prior to conducting the qualitative synthesis, the authors will examine and discuss their preconceptions and beliefs surrounding the subject under study and consider the relevance of these preconceptions during each stage of analysis.

Dissemination of findings

Findings from the qualitative synthesis will be disseminated through publications in peer-reviewed journals, a comprehensive and in-depth project report and presentation at peer-reviewed academic conferences (such as EASO) within the field of obesity research. It is also envisaged that the qualitative synthesis will contribute to the shared value analysis to be undertaken with key stakeholders (including patients, clinicians, payers, policy makers, regulators and industry) within the broader study which seeks to create a new narrative around obesity diagnosis and treatment by foregrounding patient experiences and voice(s). This synthesis will be disseminated to the 29 project partners through oral presentations at management board meetings and at the general assembly. It will also be presented as an educational resource for clinicians to contribute to an improved understanding of patient experience of living with obesity.

Obesity is a complex chronic disease which increases the risk of long-term medical complications and a reduced quality of life. It affects a significant proportion of the world’s population and is a major public health concern. Obesity is the result of a complex interplay of multiple factors including genetic, metabolic, behavioural and environmental factors. In spite of this complexity, obesity is often construed in simple terms as a failure of willpower. People with obesity are subject to weight bias, stigma and discrimination which in themselves result in increased risk of mobility or mortality. Research in the area of obesity has tended towards measurable outcomes and quantitative variables that fail to capture the complexity associated with the experience of obesity. A need to rethink how we approach obesity has been identified—one that represents the voices and experiences of people living with obesity. This paper outlines a protocol for the systematic review of available literature on the lived experience of people with obesity and the synthesis of these findings in order to develop an understanding of patient experiences, their concerns regarding the risks associated with obesity and their aspirations for response to obesity treatment. Its main strengths will be the breadth of its search remit—focusing on the experiences of people with obesity rather than their experience of a particular treatment or intervention. It will also involve people living with obesity and its findings disseminated amongst the 29 international partners SOPHIA research consortium, in peer reviewed journals and at academic conferences. Just as the study’s broad remit is its strength, it is also a potential challenge as it is anticipated that searchers will generate many thousands of results owing to the breadth of the search terms. However, to the best of the authors’ knowledge, this will be the first systematic review and synthesis of its kind, and its findings will contribute to shaping the optimisation of future obesity understanding and treatment.

Availability of data and materials

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Abbreviations

Body mass index

Critical appraisal skills programme

Grading of Recommendations Assessment, Development and Evaluation Confidence in Evidence from Reviews of Qualitative Research

Innovative Medicines Initiative

Medical Subject Headings

Population, phenomenon of interest, context, study type

Stratification of Obesity Phenotypes to Optimize Future Obesity Therapy

Wharton S, Lau DCW, Vallis M, Sharma AM, Biertho L, Campbell-Scherer D, et al. Obesity in adults: a clinical practice guideline. Can Med Assoc J. 2020;192(31):E875–91. https://doi.org/10.1503/cmaj.191707 .

Article   Google Scholar  

World Health Organisation. Fact sheet: obesity and overweight. Geneva: World Health Organisation; 2020.

Google Scholar  

Mechanick J, Hurley D, Garvey W. Adiposity-based chronic disease as a new diagnostic term: the American Association of Clinical Endocrinologists and American College Of Endocrinology position statement. Endocrine Pract. 2017;23(3):372–8. https://doi.org/10.4158/EP161688.PS .

Garvey W, Mechanick J. Proposal for a scientifically correct and medically actionable disease classification system (ICD) for obesity. Obesity. 2020;28(3):484–92. https://doi.org/10.1002/oby.22727 .

Article   PubMed   Google Scholar  

Biener A, Cawley J, Meyerhoefer C. The high and rising costs of obesity to the US health care system. J Gen Intern Med. 2017;32(Suppl 1):6–8. https://doi.org/10.1007/s11606-016-3968-8 .

Article   PubMed   PubMed Central   Google Scholar  

Department of Health and Social Care. Healthy lives, healthy people: a call to action on obesity in England. London: Department of Health and Social Care; 2011.

Di Angelantonio E, Bhupathiraju SN, Wormser D, Gao P, Kaptoge S, de Gonzalez AB, et al. Body-mass index and all-cause mortality: individual-participant-data meta-analysis of 239 prospective studies in four continents. Lancet. 2016;388(10046):776–86. https://doi.org/10.1016/S0140-6736(16)30175-1 .

Sharma AM. M, M, M & M: a mnemonic for assessing obesity. Obesity Reviews. 2010;11(11):808–9. https://doi.org/10.1111/j.1467-789X.2010.00766.x .

Article   PubMed   CAS   Google Scholar  

Asnawi A, Peeters A, de Courten M, Stoelwinder J. The magnitude of association between overweight and obesity and the risk of diabetes: a meta-analysis of prospective cohort studies. Diabetes Res Clin Pract 2010;89:309-19. Diab Res Clin Pract. 2010;89:309–19.

Dagfinn A, Teresa N, Lars JV. Body mass index, abdominal fatness and the risk of gallbladder disease. 2015;30(9):1009.

Longo M, Zatterale F, Naderi J, Parrillo L, Formisano P, Raciti GA, et al. Adipose tissue dysfunction as determinant of obesity-associated metabolic complications. Int J Mol Sci. 2019;20(9).

Fontaine KR, Redden DT, Wang C, Westfall AO, Allison DB. Years of life lost due to obesity. 2003;289(2):187-193.

Grover SA, Kaouache M, Rempel P, Joseph L, Dawes M, Lau DCW, et al. Years of life lost and healthy life-years lost from diabetes and cardiovascular disease in overweight and obese people: a modelling study. 2015;3(2):114-122.

Ackerman S, Blackburn O, Marchildon F, Cohen P. Insights into the link between obesity and cancer. Curr Obes Rep. 2017;6(2):195–203. https://doi.org/10.1007/s13679-017-0263-x .

Wolin K, Carson K, Colditz G. Obesity and cancer. Oncol. 2010;15(6):556–65. https://doi.org/10.1634/theoncologist.2009-0285 .

Resolution 420: Recognition of obesity as a disease [press release]. 05/16/13 2013.

Brownell KD. Personal responsibility and control over our bodies: when expectation exceeds reality. 1991;10(5):303-10.

Puhl RM, Latner JD, O'Brien K, Luedicke J, Danielsdottir S, Forhan M. A multinational examination of weight bias: predictors of anti-fat attitudes across four countries. 2015;39(7):1166-1173.

Browne NT. Weight bias, stigmatization, and bullying of obese youth. 2012;7(3):107-15.

Sutin AR, Stephan Y, Terracciano A. Weight discrimination and risk of mortality. 2015;26(11):1803-11.

Thomas SL, Hyde J, Karunaratne A, Herbert D, Komesaroff PA. Being “fat” in today’s world: a qualitative study of the lived experiences of people with obesity in Australia. 2008;11(4):321-30.

Ogden K, Barr J, Rossetto G, Mercer J. A “messy ball of wool”: a qualitative study of the dimensions of the lived experience of obesity. 2020;8(1):1-14.

Ueland V, Furnes B, Dysvik E, R¯rtveit K. Living with obesity-existential experiences. 2019;14(1):1-12.

Avenell A, Robertson C, Skea Z, Jacobsen E, Boyers D, Cooper D, et al. Bariatric surgery, lifestyle interventions and orlistat for severe obesity: the REBALANCE mixed-methods systematic review and economic evaluation. 2018;22(68).

The PLoS Medicine Editors. Qualitative research: understanding patients’ needs and experiences. Plos Med. 2007;4(8):1283–4.

Boulton M, Fitzpatrick R. Qualitative methods for assessing health care doi:10.1136/qshc.3.2.107. Qual Health Care. 1994;3:107–13.

Johnstone J, Herredsberg C, Lacy L, Bayles P, Dierking L, Houck A, et al. What I wish my doctor really knew: the voices of patients with obesity. Ann Fam Med. 2020;18(2):169–71. https://doi.org/10.1370/afm.2494 .

Brown I, Thompson J, Tod A, Jones G. Primary care support for tackling obesity: a qualitative study of the perceptions of obese patients. Br J Gen Pract. 2006;56(530):666–72.

PubMed   PubMed Central   Google Scholar  

Brown I, Gould J. Qualitative studies of obesity: a review of methodology. Health. 2013;5(8A3):69–80.

Garip G, Yardley L. A synthesis of qualitative research on overweight and obese people’s views and experiences of weight management. Clin Obes. 2011;1(2-3):10–126.

Coulman K, MacKichan F, Blazeby J, Owen-Smith A. Patient experiences of outcomes of bariatric surgery: a systematic review and qualitative synthesis. Obes Rev. 2017;18(5):547–59. https://doi.org/10.1111/obr.12518 .

European Patients’ Forum. “Patients’ Perceptions of Quality in Healthcare”: Report of a survey conducted by EPF in 2016 Brussels: European Patients’ Forum; 2017.

Moher D, Shamseer L, Clarke M, Ghersi D, Liberati A, Petticrew M, et al. Preferred reporting items for systematic review and meta-analysis protocols (PRISMA-P) 2015 statement. Syst Rev. 2015;4(1):1. https://doi.org/10.1186/2046-4053-4-1 .

Shamseer L, Moher D, Clarke M, Ghersi D, Liberati A, Petticrew M, et al. Preferred reporting items for systematic review and meta-analysis protocols (PRISMA-P) 2015: elaboration and explanation. BMJ. 2015;349(jan02 1):g7647. https://doi.org/10.1136/bmj.g7647 .

Toye F, et al. Meta-ethnography 25 years on: challenges and insights for synthesising a large number of qualitative studies. BMC Med Res Methodol. 2014;14(80).

Lockwood C, Porrit K, Munn Z, Rittenmeyer L, Salmond S, Bjerrum M, et al. Chapter 2: Systematic reviews of qualitative evidence. In: Aromataris E, Munn Z, editors. JBI Manual for Evidence Synthesis: JBI; 2020, doi: https://doi.org/10.46658/JBIMES-20-03 .

Methley AM, et al. PICO, PICOS and SPIDER: a comparison study of spcificity and sensitivity in three search tools for qualitative systematic reviews. BMC Health Services Res. 2014;14.

Covidence. Cochrane Community; 2020. Available from: https://www.covidence.org .

Thomas J, Harden A. Methods for the thematic synthesis of qualitative research in systematic reviews. BMC Med Res Methodol. 2008;8(1):45. https://doi.org/10.1186/1471-2288-8-45 .

Lewin S, Booth A, Glenton C, Munthe-Kaas H, Rashidian A, Wainwright M, et al. Applying GRADE-CERQual to qualitative evidence synthesis findings: introduction to the series. Implement Sci. 2018;13(1):2. https://doi.org/10.1186/s13012-017-0688-3 .

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Acknowledgements

Any amendments made to this protocol when conducting the study will be outlined in PROSPERO and reported in the final manuscript.

This project has received funding from the Innovative Medicines Initiative 2 Joint Undertaking (JU) under grant agreement No 875534. The JU receives support from the European Union’s Horizon 2020 research and innovation programme and EFPIA and T1D Exchange, JDRF and Obesity Action Coalition. The funding body had no role in the design of the study and will not have a role in collection, analysis and interpretation of data or in writing the manuscript.

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EF conceptualised and designed the protocol with input from DMcG and MB. EF drafted the initial manuscript. EF and MB defined the concepts and search items with input from DmcG, CleR and JN. MB and EF designed and executed the search strategy. DMcG, CleR, JN and EH provided critical insights and reviewed and revised the protocol. All authors have approved and contributed to the final written manuscript.

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Additional file 1:..

PRISMA-P (Preferred Reporting Items for Systematic review and Meta-Analysis Protocols) 2015 checklist: recommended items to address in a systematic review protocol*.

Additional file 2: Table 1

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Farrell, E., Bustillo, M., le Roux, C.W. et al. The lived experience of people with obesity: study protocol for a systematic review and synthesis of qualitative studies. Syst Rev 10 , 181 (2021). https://doi.org/10.1186/s13643-021-01706-5

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  • Published: June 2007

Obesity in Childhood: Introduction and General Considerations

  • Charles H Hennekens 1 , 2 , 4 ,
  • Wendy R Schneider 1 &
  • E Joan Barice 1 , 3 , 4  

Pediatric Research volume  61 ,  pages 634–635 ( 2007 ) Cite this article

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Obesity in childhood is perhaps the most major clinical and public health problem in the United States and most developed countries and is rapidly becoming so in developing countries. The National Health and Nutrition Examination Survey (NHANES) is a federally funded periodic survey of a random sample of the U.S. population. In NHANES data over the past several decades, there is a 3-fold increase in the prevalence of obesity in childhood ( 1 – 4 ). These data are alarming but, perhaps not surprising.

The landmark Framingham Heart Study, which enrolled and followed over 5000 residents of a single community in Massachusetts for over 40 years, has demonstrated that in middle age the average American gains about seven pounds per decade of life. Thus, for these and other cogent reasons, it appears that, at present, the adult population of the U.S. is the fattest society in the world and likely to be the fattest in the history of the world ( 5 ). Further, there are even more alarming trends in obesity in childhood in developing countries ( 6 , 7 ). Thus, the epidemic of obesity in childhood in the United States and most developed countries is now becoming a pandemic.

This emerging pandemic results from genetic and environmental factors, chiefly increased caloric intake and physical inactivity ( 3 , 6 , 8 – 12 ). Further, and also not surprisingly, childhood obesity has contributed to marked increases in metabolic syndrome and type 2 diabetes in U.S. children ( 13 – 15 ). The increasing prevalence of metabolic syndrome and type 2 diabetes in childhood has also been well documented in developing countries, including China ( 16 , 17 ).

Among most middle-aged adult populations, smokers tend to be thinner due to the effects of smoking on decreasing appetite and increasing basal metabolic rate. Among adolescents in both developed and developing countries, the rise in cigarette consumption is associated with increasing obesity perhaps due, at least in part, to increasing levels of physical inactivity ( 12 , 18 – 20 ).

At present, most of the remarkable decline in mortality from coronary heart disease in the United States over the past several decades is currently due to diagnosis and treatment rather than primary prevention. Further, the rate of decline is decreasing and coronary heart disease will increase as the current generation of U.S. children and adolescents reach middle age ( 18 ). For all these reasons, cardiovascular disease (CVD) is and will remain the leading killer in the United States and most developed countries. Thus, the long-term consequences of childhood obesity could cause our current generation of children to become the first in the history of the United States to have a decreased life expectancy than their parents ( 13 , 21 ). In addition, however, the alarming increases in obesity and tobacco consumption in developing countries has led the World Health Organization to estimate that CVD will rise from number 5 to number 1, the leading killer in the entire world after another decade ( 6 , 7 ).

There is increasing evidence that atherosclerosis begins in childhood. In the Bogalusa Heart Study, autopsy studies of children showed a clear relationship between the number and severity of risk factors, principally obesity, with atherosclerosis in both the aorta and coronary arteries ( 14 , 22 ). Thus, the need for primary prevention of cardiovascular disease beginning in childhood is clear (7,13–15,23), but there is no consensus regarding the best approach that includes therapeutic lifestyle changes as well as pharmacologic therapies. While further research is certainly warranted, so too are clinical and health policy measures ( 24 – 29 ).

In this issue of the journal, new predictors of metabolic syndrome in children, epidemiology of childhood obesity, and the relation to subsequent cardiovascular disease are addressed. All these issues underscore the crucial need for primary prevention of obesity in children throughout the world.

Ogden CL, Carroll MD, Curtin LR, McDowell MA, Tabak CJ, Flegal KM 2006 Prevalence of overweight and obesity in the United States, 1999–2004. JAMA 295 : 1549–1555

Article   CAS   Google Scholar  

Ogden CL, Flegal KM, Carroll MD, Johnson CL 2002 Prevalence and trends in overweight among US children and adolescents, 1999–2000. JAMA 288 : 1728–1732

Article   Google Scholar  

Nader PR, O'Brien M, Houts R, Bradley R, Belsky J, Crosnoe R, Friedman S, Mei Z, Susman EJ 2006 Identifying risk for obesity in early childhood. Pediatrics 118 : 594–601

Lissau I, Overpeck MD, Ruan WJ, Due P, Holstein BE, Hediger ML, the Health Behaviour in School-aged Children Obesity Working Group 2004 Body mass index and overweight in adolescents in 13 European countries, Israel and the United States. Arch Pediatr Adolesc Med 158 : 27–33

Kolata G 1998 Obesity's link to early death found less than suspected. The New York Times (January 1, 1998)

World Health Organization 2000 WHO Technical Report Series 894: Obesity: Preventing and Managing the Global Epidemic. A report of a WHO consultation, Geneva Available at: http://www.iotf.org/policy.asp Accessed on 1/7/07

Caterson ID, Hubbard V, Bray GA, Grunstein R, Hansen BC, Hong Y, Labarthe D, Seidell JC, Smith SC Jr 2004 Prevention conference VII: obesity, a worldwide epidemic related to heart disease and stroke: Group III: worldwide comorbidities of obesity. Circulation 110 : 476–483

US Department of Health and Human Services 2001 The Surgeon General's call to action to prevent and decrease overweight and obesity. Public Health Service, Office of the Surgeon General, Rockville, MD Available at: http://www.surgeongeneral.gov/topics/obesity/calltoaction/CalltoAction.pdf Accessed on 1/7/07

Faith MS 2005 Development and modification of child food preferences and eating patterns: behavior genetics strategies. Int J Obes 29 : 549–556

Faith MS, Berkowitz RI, Stallings VA, Kerns J, Storey M, Stunkard AJ 2004 Parental feeding attitudes and styles and child body mass index: prospective analysis of a gene-environment interaction. Pediatrics 114 : 429–436

Mulvihill C, Németh A, Vereecken C 2004 Body image, weight control and body weight. In: Currie C, Roberts C, Morgan A, Smith R, Settertobulte W, Samdal O, Rassmussen, VB (eds.) Young people's health in context: international report from the HBSC 2001/02 survey . WHO Policy Series: Health policy for children and adolescents No. 4, WHO Regional Office for Europe, Copenhagen, pp 120–129 Available at: http://www.hbsc.org/publications/reports.html . Accessed on 1/7/07

Google Scholar  

Janssen I, Katzmarzyk P, Boyce W, Vereecken C, Mulvihill C, Roberts C, Currie C, Pickett W 2005 Comparison of overweight and obesity prevalence in school-aged youth from 34 countries and their relationships with physical activity and dietary patterns. Obes Rev 6 : 123–132

van Dam RM, Willett WC, Manson JE, Hu FB 2006 The relationship between overweight in adolescence and premature death in women. Ann Intern Med 145 : 91–97

Freedman DS, Khan LK, Dietz WH, Srinivasan SR, Berenson GS 2001 Relationship of childhood overweight to coronary heart disease risk factors in adulthood: The Bogalusa Heart Study. Pediatrics 108 : 712–718

Liu J, Wade TJ, Tan H 2007 Cardiovascular risk factors and anthropometric measurements of adolescent body composition: a cross-sectional analysis of the Third National Health and Nutrition Examination Survey. Int J Obes 31 : 59–64

Fu J-F, Liang L, Zou C-C, Hong F, Wang C-L, Wang X-M, Zhao Z-Y 2007 Prevalence of the metabolic syndrome in Zhejiang Chinese obese children and adolescents and the effect of metformin combined with lifestyle intervention. Int J Obes 31 : 15–22

Chu N-F 2001 Prevalence and trends of obesity among school children in Taiwan–the Taipei Children Heart Study. Int J Obes 25 : 170–176

Hennekens CH 1998 Increasing burden of cardiovascular disease: current knowledge and future directions for research on risk factors. Circulation 97 : 1095–1102

Samdal O, Tynja J, Roberts C, Sallis JF, Villberg J, Wold B 2006 Trends in vigorous physical activity and TV watching of adolescents from 1986 to 2002 in seven European countries. Eur J Public Health Oct 28; [Epub ahead of print]. Available at: http://eurpub.oxfordjournals.org/cgi/content/abstract/ckl245v1 . Accessed on 1/7/07

Hublet A, De Bacquer D, Valimaa R, Godeau E, Schmid H, Rahav G, Maes L 2006 Smoking trends among adolescents from 1990 to 2002 in ten European countries and Canada. BMC Public Health 6 : 280 Available at: http://www.biomedcentral.com/1471-2458/6/280 . Accessed on 1/7/07

Robert Wood Johnson Foundation/AHA/American Stroke Association 2005 A nation at risk: obesity in the United States, statistical sourcebook. AHA National Center, Dallas, TX, p 3. Available at: http://www.americanheart.org/presenter.jhtml?identifier=3030570 . Accessed on 1/4/07

Freedman DS, Dietz WH, Srinivasan SR, Berenson GS 1999 The relation of overweight to cardiovascular risk factors among children and adolescents: The Bogalusa Heart Study. Pediatrics 103 : 1175–1182

Singhal A 2006 Early nutrition and long-term cardiovascular health. Nutr Rev 64 : S44–S49

Inge TH, Xanthakos SA, Zeller MH 2007 Bariatric surgery for pediatric extreme obesity: now or later?. Int J Obes 31 : 1–14

Cassady D, Vogt R, Oto-Kent D, Mosiey R, Lincoin R 2006 The power of policy: a case study of healthy eating among children. Am J Public Health 96 : 1570–1571

Barlow SE, Trowbridge FL, Klish WJ, Dietz WH 2002 Treatment of child and adolescent obesity: reports from pediatricians, pediatric nurse practitioners, and registered dietitians. Pediatrics 110 : 229–235

PubMed   Google Scholar  

Wojcjcki JM, Heyman MB 2006 Healthier choices and increased participation in a middle school lunch program: effects of nutrition policy changes in San Francisco. Am J Public Health 96 : 1542–1547

Harrell JS, McMurray RG, Gansky SA, Bangdiwala SL, Bradley CB 1999 A public health vs a risk-based intervention to improve cardiovascular health in elementary school children: The Cardiovascular Health in Children Study. Am J Public Health 89 : 1529–1535

Harper MG 2006 Childhood obesity strategies for prevention. Fam Community Health 29 : 288–298

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Department of Biomedical Science, Center of Excellence, FL Atlantic University, Boca Raton, 33431, FL

Charles H Hennekens, Wendy R Schneider & E Joan Barice

Departments of Medicine & Epidemiology and Public Health, University of Miami Miller School of Medicine, Miami, 33136, FL

Charles H Hennekens

Psychiatry and Behavioral Science, University of Miami Miller School of Medicine, Miami, 33136, FL

E Joan Barice

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Charles H Hennekens & E Joan Barice

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Hennekens, C., Schneider, W. & Barice, E. Obesity in Childhood: Introduction and General Considerations. Pediatr Res 61 , 634–635 (2007). https://doi.org/10.1203/PDR.0b013e3180686cf1

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obesity introduction research paper

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Obesity has increasingly been identified as a critical global public health concern. This focus on obesity as a health priority raises complex bioethical issues. These include how obesity is defined and categorized, the implications of the centrality of personal responsibility in medical and public health approaches, how competing ethical frames impact social justice concerns, and the growing “moral panic” concerning obesity. A critical examination of how obesity is defined as a medical problem suggests that ethical approaches could be more productive if obesity were addressed as a social problem with medical consequences, rather than emphasizing it as a medical problem with social consequences.

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There has been a dramatic rise in the prevalence of obesity globally in the last three decades, and the World Health Organization (WHO) estimates around 11 % of the world’s total population is obese (WHO 2012). Obesity is seen as a major public health concern because it is widely recognized as a precipitating factor in the parallel emergence of chronic diseases as a primary cause of death in many countries. Obesity is often reported as a major drain on medical systems, and the growing obesity rates in developing countries are often cited as especially worrying in this regard. From a bioethics perspective, the focus on obesity as a health priority raises complex issues. This entry highlights inter-related and key bioethical dimensions of contemporary concerns around and approaches to obesity, including the means by which people are categorized as obese or not, the medicalization of obesity as a disease that needs to be treated, implications of the centrality of individual responsibility in medical and public health approaches, obesity as a social justice issue, and media and growing “moral panic.”

Obesity is most simply defined as an excess of adipose (fat) tissue, usually with negative health effects. However, this definition is problematic. Medically, as discussed below, the science of obesity is increasingly suggesting that many people can be both obese and healthy. However, “obese” and “obesity” are terms that have also entered everyday media and other public discourses in ways that are mostly negative and imply ill-health and disease. The growing assumption that obesity is defined as a negative characteristic is historically and culturally particular, in marked contrast to cross-cultural records that describe plump bodies as powerful, sexy, social, abundant, fertile, and certainly healthy (Brewis 2011a).

Ethical Dimensions

The Categorization of Obesity. A definition of obesity based upon the notion of excess body fat requires measurement against a standard of what constitutes “normal.” Given that human bodies are highly ecologically flexible and vary in averages across populations, the imposition of a single standard for classification as obese raises some complex bioethical issues. The most widely employed means to classify people as obese, and then assess variation in population levels of obesity, is through use of body mass index (BMI).

BMI does not directly measure body fat; rather, it is a proxy measure using the ratio of mass (weight) relative to height. Using statistical methods and prescriptive and risk models, four basic categories of weight (underweight, normal, overweight, obese) have been identified and are now widely applied, from the doctor’s office to large public health interventions. These standard categories are arbitrarily defined through cutoff points related to morbidity and mortality rates found in large-scale epidemiological studies, with obesity normally set at a BMI of 30 or higher.

While BMI as a measure of obesity is sometimes useful, particularly in clinical studies, because of both individual and population variation, this mapping of weight to health risk is not precise or even especially predictive. For example, there is growing evidence that many people clinically defined as obese prove to be metabolically healthy even as they are advised by doctors they need to lose weight, and that the level of obesity at which conditions like diabetes and heart disease become more prevalent differs across populations. Moreover, BMI does not discriminate between muscle mass, bone, connective tissue, and amount types of adipose tissue, obscuring accurate measurement of total body fat. As a result, people with highly-developed musculature are labeled obese by the measure, even when they have low levels of actual body fat. Further, some populations have greater bone density on average or shorter leg bone length resulting in falsely high BMI scores (Hruschka et al. 2013). For example, for decades there has been a public health concern focused on very high obesity risk in Pacific Island populations, but more recent studies have shown that the disease correlates of obesity emerge at higher levels of adiposity in comparison to other groups. Hence, the common standard for categorizing obesity probably misassigns a significant number of people and accordingly implies health risks where none may exist (and vice versa). Additionally, women have a higher percentage of body fat than men, and weight tends to increase in both genders as individuals age. Attempts to address the weaknesses in BMI classifications have resulted in alternative methods that more accurately measure the amount and distribution of body fat, but these use technologies or expertise that are difficult to implement in real-world settings.

Defining Obesity as a Disease. Defining obesity against a set standard of what is a normal or healthy level of body fat leads to an emphasis on prevention and cure, and underscores obesity as (1) a problem, with (2) an identifiable cause (diagnosis), and that (3) requires evaluation, intervention, management, and control. The central bioethical issue is this: regardless of how people are classified into an obese category, once so categorized it is generally assumed that labeling a person as unhealthy is warranted and medical or other intervention is necessary. Certainly, obesity has become increasingly identified as a major factor and index of ill-health over the last two decades. This culminated in the formal recognition of obesity as a disease by the American Medical Association in 2013, even in the absence of other risk factors or clinical symptoms. The growing medicalization of obesity as a condition explains why highly invasive and often risky medical treatments for obesity, such as bariatric surgery, are on the rise. The emphasis on excess weight as a health problem also negatively impacts how people view and relate to their own and others’ bodies and in ways that create emotional and social distress related to failing to meet social prescriptions for an ideal or acceptable body size.

Levels of Analyses and Ultimate Causation. Current scientific evidence on the causes of obesity can be analyzed at different levels, often working iteratively and in feedback with each other. At the genetic level, some individuals have a predisposition toward higher weights, weight gain, and difficulty in weight loss, related to genetic variants in appetite, metabolism, and activity. At the individual level, obesity is the result of excess calorie intake over calories expended through physical activity, but individual-level factors such as income, education level, ethnicity, age, and gender also predict differential risks of being obese, as does use of certain medications or comorbidities such as depression. Institutional factors such as health care access also matter.

At the community, neighborhood, or regional level, obesity risk accrues differently based solely on where people live. One factor in this pattern is the rapid urbanization of the world’s population: urbanization is associated with higher rates of obesity, and an increasing majority of humans live in cities. This correlation is due, in part, to the low cost of high density foods, changes in activity with the move to urban settings and structural and economic barriers to healthier lifestyles (Metzl and Hansen 2014). Further, within those cities, specific locales and their inhabitants’ lifestyles vary based upon social, spatial, and economic factors. The built environment of a particular locale is one example of how the physical expression of social, spatial, and economic factors relates to obesity prevalence: walkability, public transportation, access to fresh foods, safety, parks, light and shade, access to healthcare, and density all help shape obesity risk. For example, barriers in transportation and distance may make it difficult for residents to access healthy foods, while the perception by residents that the place they live in is unsafe or of poor quality may limit opportunities to be physically active. Social and economic factors also influence residential effects, including social exclusion, discrimination, and diminished economic infrastructure. Efforts to address residential effects often evoke stakeholder objections, as these efforts may inhibit personal choice, stigmatize neighborhood residents, or create changes that conflict with personal lifestyles and cultural values (ten Have et al. 2011).

Education and wealth, and most especially poverty, are also implicated in obesity risk. The relationship between income and obesity is complex and varies depending on the economic development of the resident country. Most nations, even the poorest, demonstrate some level of obesity, even in the presence of food shortages and undernutrition. The combination of under and over nutrition increases the likelihood of obesity and has significant implications in terms of health risks and negative health effects. As poorer nations become increasingly urbanized and industrialized, these problems are exacerbated, particularly as low income countries have fewer healthcare resources to meet the challenges posed by chronic conditions associated with obesity. This “dual burden” is also evident in middle-income countries: as economic changes at both the household and national level occur, families with a dual burden of having overweight and underweight individuals become increasingly prevalent.

Evidence suggests that income and obesity also rise together as inexpensive food becomes easily accessible. However, this trend reverses at the point where the apparent social costs of obesity outweigh the advantages. In middle to high-income countries, obesity tends to be inversely correlated with socioeconomic status, meaning that the highest obesity rates are found in those populations with the lowest incomes and with the lowest levels of educational achievement (Brewis 2011a). At a national level, BMI appears to rise in the early and accelerated phases of economic development due to a complex set of factors including urban migration, a shift from traditional occupations, and increased technology. At the individual level, poverty is contextual, demonstrating a complex residential pattern, with both rural and urban poverty linked to lower education and higher obesity.

While there have been some efforts to develop community-level interventions in line with increasing recognition of these upstream causes of obesity risk, medical and public health interventions continue to give the most attention to individual behavior change. The standard treatment model, often shared by clinicians and patients alike, is that the individual must lose excess weight by eating less and/or exercising more. This is despite decades of evidence that most such behavioral change strategies eventually fail to result in weight lost, and often serve to promote weight regain (Brewis 2011a).

Obesity and Social Justice Considerations. The role of proximate and ultimate factors discussed above means that obesity can be framed as a social justice issue, not solely a medical one. This suggests a very different course, emphasis, and pathway for public health interventions. Policies that seek to restrict behavior (passively or actively) can disproportionately affect the poor, the rural, and the malnourished. Of critical importance is who designs, implements, and evaluates these efforts. How do these interventions ethically impact personal physical health while promoting equality and maintaining individual autonomy? If population-level interventions are not necessarily individually beneficial and may in fact have psychosocial and cultural costs with their own negative health consequences, should public health entities intervene at all? These are some of the ethical issues that arise when the focus moves away from considering obesity fundamentally a medical problem to thinking about obesity at the aggregate level.

The challenge is to consider both the ultimate (structural) as well as the proximate factors (nutrition, activity, and medical conditions) that shape obesity risk when developing obesity policy and interventions. Identifying the causes of obesity, when coupled with how it is defined, becomes important in the ethical frame used to intervene. To date, there have been multiple framings in approaches to combat the rise of obesity. These ethical frames are not mutually exclusive and often coexist within a particular approach. Understanding the ethical platform from which programs spring will enable better understanding of the consequences (intentional or unintentional), successes, and failures. Identifying obesity as a health problem is more than defining disease, biomedical risk, and treatment; assigning responsibility – individual or otherwise – becomes part of the equation. The increasing prevalence of obesity on a global scale is accompanied by concerns that society is harmed in some way. This sense of harm in turn is linked to the notion of blame. How responsibility and blame are assigned varies with different ethical frames.

Framing Obesity Solutions

Emphasis on Individual Responsibility. The notion of individual responsibility has dominated the discourse surrounding the obesity crisis and efforts to contain the problem. Individual responsibility is rooted in notions of individual autonomy based within a moralistic theory of personal determination. Morality frames emphasize the threat to social values and economic stability by focusing on personal choice and the impact these choices have on society (Boero 2012). A morality frame advances notions of normal, ideal, virtue, right, and wrong. In this frame, obesity is related to personal failings – a lack of self-discipline, restraint, rationality, and moral failings attributed to poor life choices (gluttony, sloth, and a lack of adherence to personal improvement). Obesity, therefore, is self-induced and harm is self-inflicted. Because the individual is responsible for their health and body, blame is personal and can take the form of value imperatives about who is obese or overweight and who is responsible. Interventions and public health campaigns using this frame focus on problem awareness, promote better individual health behaviors, and encourage personal responsibility. Interventions range from educational efforts to weight loss programs, “fat taxes” (on calorie or fat dense foods), and increased insurance rates for individuals with high BMIs. This type of framing, when used in conjunction with a medical definition of obesity, places the focus of the intervention on achieving a physical ideal body weight and ignores the psychosocial dimensions of health, even as it places responsibility upon the individual (as psychologically weak or morally lax). Stigmatization, discrimination, and negative self-image are the result, which have their own negative health consequences (Sagay 2013; Puhl and Heuer 2010).

Biomedical and Public Health Frames. The biomedical frame uses the language of risk to intervene and regulate the body in order to promote health or, more usually, decrease illness or disease. Obesity in this frame is seen as pathologic – a biological condition to be monitored, treated, and cured. The body is understood to be the recipient of treatment, a somewhat passive vessel that needs management by healthcare professionals (Sagay 2013). De-emphasizing personal responsibility can be helpful in decreasing stigma, but medicalization also promotes stigmatization by labeling obese bodies as sick. Framing obesity in terms of mortality and morbidity imparts urgency and authority to the issue. The locus for intervention is on proximate factors and responsibility remains with the individual-aspatient, though the medical system is a crucial partner in terms of defining the problem and determining and managing treatment. Generally individual and small-scale interventions focused on dietary choice, activity, and medical/surgical interventions are utilized in this context. However, the biomedical frame informs larger policy issues resulting in industry and governmental regulations generally rooted in economic analyses, such as differential insurance rates for individuals based upon weight, corporate programs to incentivize weight reduction or dietary choice, bans or taxes on sugar-sweetened beverages, and regulation of nutritional information on food products.

A public health frame assigns responsibility to the government (local, state, and federal). Public health entities are most often located within governments and are charged with setting standards, regulating and protecting public safety and promoting health, and minimizing or preventing public harm while at the same time ensuring individual liberty, privacy, and public access to needed resources. This equation differs internationally as notions of individual and public health are culturally constituted. In general, obesity is seen as a threat to public health and the approach taken is to reduce the threat, generally combining individual and systemic approaches to address the issue. Ethical approaches in this frame deal with the differential distribution of obesity across groups and subpopulations as prevalence and risk manifest variably within cultural groups, gender, socioeconomic status, etc. Financial triggers (incentives & disincentives), built environment changes that alter lifestyle options (slowing elevators, car-free zoning, food banning), and informational campaigns are often used or suggested within a public health intervention. Issues of justice and fairness can be particularly problematic in this framing as the dual focus of public health creates a tension between liberty and protection. Obesity at the individual level includes social and economic disparities as well as discrimination and psychological stress from weight bias. Addressing these issues within the systemic frames of government, business, and infrastructure (including larger social forces) can contribute to stigmatization, discrimination, and differential opportunities and access.

Thus, in practice, there is a smorgasbord of antiobesity efforts, structured within multiple framings – moralistic, biomedical, and public health – that tend to be disconnected from each other. Even assuming a universal definition of obesity and its determinants exists, the ethics of policy interventions still needs to be addressed. At the heart of the ethics, debate is concerned over individual choice, autonomy, and the exacerbation of stigma and discrimination. Rephrasing the two previous ethical questions might then ask: What are the individual’s essential rights and responsibilities concerning weight? Secondly, what is the responsibility of the government in providing healthy, safe environments for its citizens?

This tension between rights and responsibilities (individual, societal, and governmental) plays out differently globally. The body (and body size) is understood as a “domain of liberty and autonomy” (Tirosh 2014, p. 1801), but the expression of these values is differentially understood across societies. When seen as a lifestyle issue, obesity remains focused at the individual and local levels, to be dealt with through small-scale interventions in select populations to encourage individuals to control their weight and make healthier choices (moralistic frame). These types of interventions tend to ignore the complexity of factors (and responsibilities) underlying obesity and keep responsibility (and blame) with the individual. Growing public discourse has revolved around policy changes to combat the “rising epidemic” of obesity. Public health officials have supported this groundswell of opinion through campaigns to promote the adoption of a healthy lifestyle, emphasizing a diet high in fruits, vegetables, complex carbohydrates, and lean proteins and sufficient exercise – efforts that highlight personal choice and responsibility. Much of the work on prevention and intervention at this level has had mixed results. Even among public health practitioners who seek to address structural components underlying obesity, the political weight of the morality frame leads them to use “code language” such as “make the healthy choice, the easy choice.” Essentially structural changes are presented as changes enabling personal choice.

At a governmental level, rising healthcare costs in conjunction with rising obesity rates globally and concerns over the efficacy of individual-level interventions are frequently cited as an impetus for governmental strategies and policies to guide widespread interventions, primarily through legislation. Governmental interventions are influenced by the culture, political system, economics, and traditions of the nations involved, resulting in a spectrum of policies and programs globally. Efforts range from health education to restrictive taxes on unhealthy foods and beverages, with a goal of shaping behavior by restricting or coercing individual choice. In the European Union (EU), a concerted effort is being made to encourage voluntary action on the part of industry partners to alter nutrition and activity environments. Voluntary efforts to support decision-making through evidence-based information, self-regulation of product claims (labeling, advertisements) through the proposed establishment of an industry code of conduct, food redistribution (surplus fruits/vegetables) focused on children 4–12 years old, reformulation of foods to decrease sugar, fat, and salt, and sustainable urban transportation facilities to promote physical activity/ public infrastructure (Commission of the European Communities 2007) are examples of this type of intervention. In the USA, taxation of SSBs and calorie-dense foods has been implemented (or attempted), most notably in New York City and the Navajo Nation. China, Britain, and Mexico have all passed or attempted to enact legislation that aims to regulate behavior with an eye to reducing the economic burden of healthcare. Often, particular populations are targeted for interventions, as evidence indicates that obesity is more prevalent in these groups. Unfortunately, these efforts can take the form of value imperatives about who is obese or overweight and who is responsible, encouraging the spread of stigmatization and victimization (Puhl and Heuer 2010).

Some initiatives have sought to create structural or environmental changes to address the inequities, disparities, and deficits implicated in obesity (public health framing with social justice focus). Policies attempting to reduce the unequal distribution of resources, barriers to healthy foods and activities, and social and economic inequities can be found in new regulations requiring enhanced visibility and simplified nutritional labeling; limitations on commercial advertising of high density, low-nutrient foods to children; venue-specific banning of “unhealthy items” such as high-fat items in restaurants or SSBs in school vending machines; and limiting the proximity of fast-food restaurants to schools (Kass et al. 2014; ten Have et al. 2011). These types of initiatives still impact personal choice and liberty and have resulted in public debates regarding the role of government in regulating health. Impacting broader economic and social structures is more challenging from the local level, though increasingly tools like health impact assessments and health in all policies are being used to provide more equity in land use decisions, and have even been used to evaluate local minimum wage, affordable housing, and supplemental nutrition policies. Criticisms of obesity policies have ranged from concerns over the inhibition of individual autonomy, the expansion of the paternalistic “nanny” state (and subsequent economic burden), and the inequitable treatment and stigmatization of low-income populations.

Ethical discussions concerning interventions that limit choice or coerce behavior tend to be centered on arguments about legitimacy and utility. Legitimacy focuses on the value to society in instituting a particular policy or practice. Generally, the discussion revolves around the role of paternalism (soft or hard) in promoting the general welfare of the individual. Paternalism is best viewed as a sliding scale that ranges from promoting informed choice (information campaigns) through implementation of incentives (free or reduced costs, tax benefits, etc.) and ultimately various forms of coercion (bans, taxation). Utility looks at the cost-benefit ratio: is a policy or intervention likely to succeed and does it offer enough benefit to offset the reduction in choice, liberty, or privacy. Because there is little cohesion in how data is collected internationally, making evidence based comparisons of the effectiveness of different types of interventions is difficult. In general, arguments made for coercive policies are rooted in the premise that obesity is associated with higher morbidity and attendant higher costs of treatment. As previously noted, this is by no means a validated conclusion and therefore the utility of such efforts is suspect.

An example of this trade-off is the call for school districts to restrict soft drinks on school campuses. This type of intervention may have the unintended consequence of reducing the school’s revenue stream, resulting in less money available for student education or extra-curricular activities. Obesity prevalence is associated with poverty and disadvantage, disproportionately impacting precisely those communities whose schools need funding the most. Reduced funding may lead to a reduction in programming and healthy food options, elimination of physical education or play equipment, poor food quality to reduce costs, increased sedentism, and reduced educational opportunities (Crooks 2003). The result may be an environmental trade-off of biological costs for social benefits – poorer nutritional quality in order to provide education for all students and thus hopefully propel the students out of poverty.

Another example is the call to use social pressure tactics, similar to antismoking campaigns, to leverage public opinion toward acceptance of stringent governmental regulations. The trade-off here is to focus on increased legitimacy at the expense of utility. This type of intervention operates at the individual, acute, and proximate level and does not address any of the underlying structural conditions. Couched as “stigmatization lite” the argument is that overweight and obese individuals do not recognize their “problem” and need to be awakened to reality. Unfortunately increasing stigmatization of the individual has not been demonstrated to positively impact behavior change; rather, it produces the opposite impact. Discrimination is implicated in stress induced physiological responses associated with obesity that not only negatively impact health but also discourage potential participation in health-related activities. Beyond this, how is the level of stigma “titrated?” Increasing antiobesity thinking may contribute to the moral panic over the rise in obesity rates (Campos et al. 2006).

Stigmatization And Moral Panic

Obesity and Weight-related Stigma. Any discussion on bioethics needs to address the issue of stigmatization (and resulting victimization and discrimination) of obese individuals. Placing the responsibility for one’s weight on the individual has led to sanctioned discrimination in the form of diminished access to goods, services, and employment opportunities and higher healthcare costs for obese individuals. Obesity has even been used as evidence in child abuse cases and other legal interventions. Despite multiple framings of obesity as a medical and public health problem, the persistent focus on individual responsibility and autonomy continues to direct the understanding of obesity through the lens of morality – a platform for value imperatives and subsequent stigmatization.

Obesity stigma must be addressed within the social and structural conditions that produce it. That is, there must be recognition that even a focus on ultimate factors (zoning laws, bans, taxation, urban renewal) can have unintended consequences resulting in increased discrimination. In the past, public health concerns were often the result of an external agent (bacterial or viral agent, poor sanitation, cigarettes, etc.), allowing the focus of interventions to remain external to the body/self. However, weight (and excess weight) is rooted in the body itself – it is a domain of the self. Eating and movement are necessary components of life and are seen as highly personal, as one chooses what, when, and how to eat, move, and function bodily within personal environments. Because these activities are necessary (one cannot stop eating, for example), efforts have focused on changing personal decisions related to eating and activity. Attempts to alter these bodily functions with an external agent (medication, surgery) have had mixed results, but as long as eating and activity are categorized as personal choices, stigmatization will remain a factor.

Media and Corporate Roles. The “moral panic” that has resulted from the framing of obesity as an epidemic has produced a media onslaught. This begs the question of whether the media is reflecting this panic or creating it. Popular media promotes a thin ideal body size (particularly for women), while continuing to also promote the sale of obesogenic products. Fast food and junk food advertisements, product placement in movies, casting of thin ideal body types, and disparaging characterizations of obese characters are prevalent throughout multiple media formats. Visual representations of obese bodies that employ “de-evolution tropes” (which portray the human species as degenerating from more fit ancestors) are common. Media use (screen time) is certainly associated with increased snacking and requests for caloriedense foods and decreased activity and altered sleep patterns (American Academy of Pediatrics 2011).

The increasing documentation of these negative social and physical impacts of media treatment of obesity has led to a mishmash of corporate efforts and legislative calls to action. For example, the Disney Corporation has announced that it will no longer advertise “junk foods” on its television channel. However, Disney continues to promote thin body ideals in its movie and cartoon heroines. McDonald’s has been criticized for targeting children with “toy” gifts in their high fat and sugar Happy Meals. Several European Union countries have instituted restrictions on food advertising aimed at very young children. The impacts of the media on obesity risk and stigma bring to the fore the ongoing ethical conundrum concerning the extent to which governments should have control over media that promote unhealthy behaviors or stigmatization. Issues of free speech, government regulation, and equal access to opportunity and goods have all been cited as deterrents to government regulation of advertising and media. Combining this with a moralistic frame that castigates large bodies as personal failures and the bioethical landscape is messy indeed.

Obesity arises through individual behaviors shaped within varied epigenetic, cognitive, sociocultural, physical, material, political, and other institutional structures and environments. Bioethically, based on the discussion above, this entry suggests that obesity is perhaps more productively addressed as a social problem with medical consequences rather than a medical problem with social consequences. Competing frames of obesity, whether medically or otherwise problematized or not (moralistic, medical/ healthcare, public health, governmental), are rooted in concerns about the ethical behavior of members within the group, not about the larger social, economic, and political domains. Social justice models for obesity intervention rightly focus on the role of the built environment, but rarely tackle the ultimate determinants like poverty, education, and discrimination. Many complex bioethical questions remain: Is it possible to account for acute and chronic dimensions as well as proximate and ultimate factors and mitigate some of the unintended, negative consequences of interventions? How can health policies and interventions ethical approaches be constructed to take into account the very real social dimensions of weight and the body? If health is a public good, what are the ethical implications of not intervening?

Ultimately, being obese is both a private and public matter. While an individual’s weight is the result of multiple individual and biosocial components, the individual’s body is subject to public scrutiny and – increasingly – public regulation. The consequences of public efforts, both intended and unintended, need to be critically examined within the context of how obesity is defined as a problem, the frame used to address the problem as defined, and then how, with whom, and at what level various prevention and intervention efforts are implemented.

Bibliography :

  • American Academy of Pediatrics. (2011). Policy statement – children, adolescents, obesity, and the media. Pediatrics, 128(1), 201–208.
  • Boero, N. (2012). Killer fat: Media, medicine, and morals in the American “Obesity Epidemic.” New Brunswick: Rutgers University Press.
  • Brewis, A. (2011a). Obesity: Cultural and biocultural perspectives. New Brunswick: Rutgers University Press.
  • Campos, P., Saguy, A., Ernsberger, P., Oliver, E., & Gaesser, G. (2006). The epidemiology of overweight and obesity: Public health crisis or moral panic? International Journal of Epidemiology, 35, 55–60.
  • Commission of the European Communities. (2007). A strategy for Europe on nutrition, overweight and obesity related health issues. Brussels, SEC. 706–7.
  • Crooks, D. (2003). Nutrition and the sale of snack foods. Medical Anthropology Quarterly, 17(2), 182–199.
  • Hruschka, D. J., Rush, E., & Brewis, A. (2013). Population differences in the relationship between height, weight, and adiposity: An application of Burton’s model. American Journal of Physical Anthropology, 151, 68–76.
  • Kass, N., Hecht, K., Paul, A., & Birnbach, K. (2014). Ethics and obesity prevention: Ethical considerations in 3 approaches to reducing consumption of sugar-sweetened beverages. Public Health Ethics, 104(5), 787–795.
  • Metzl, J., & Hansen, H. (2014). Structural competency: Theorizing a new medical engagement with stigma and inequality. Social Science & Medicine, 103, 126–133.
  • Puhl, R., & Heuer, C. (2010). Obesity stigma: Important considerations for public health. Framing Health Matters, 100(6), 1019–1028.
  • Sagay, A. (2013). What’s wrong with fat? Oxford: Oxford University Press.
  • ten Have, M., de Beaufort, I. D., Teixera, P. J., Mackenbach, J. P., & van der Heide, A. (2011). Ethics and prevention of overweight and obesity: An inventory. Obesity Reviews, 12, 669–679.
  • Tirosh, Y. (2014). Three comments on paternalism in public health. Connecticut Law Review, 46(5), 1795–1816.
  • World Health Organization. (2012). Obesity and overweight: fact sheets. World Health Organization. Retrieved from https://www.who.int/en/news-room/fact-sheets/detail/obesity-and-overweight
  • Brewis, A. (2011b). Obesity: Cultural and biocultural perspectives. New Brunswick: Rutgers University Press.
  • Puhl, R. M., & Heuer, C. A. (2009). The stigma of obesity: A review and update. Obesity, 17(5), 941–964.
  • Saguy, A. (2012). What’s wrong with fat? Oxford: Oxford University Press.

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Introduction

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  • What is obesity?

Obesity is a chronic condition defined by an excess amount of body fat. It indicates a weight greater than what is considered healthy. 

Obesity has been more precisely defined by the National Institutes of Health (the NIH) as a BMI (Body Mass Index) of 30 and above. (A BMI of 30 is about 30 pounds overweight.) The BMI, a key index for relating body weight to height, is a person's weight in kilograms (kg) divided by their height in meters (m) squared.

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  • What Causes Obesity?
  • Health Risks Linked to Obesity
  • Childhood Obesity
  • Treatments for Obesity

The balance between calorie intake and energy expenditure determines a person's weight. If a person eats more calories than he or she burns (metabolizes), the person gains weight (the body will store the excess energy as fat). If a person eats fewer calories than he or she metabolizes, he or she will lose weight. Therefore, the most common causes of obesity are overeating and physical inactivity. Ultimately, body weight is the result of genetics, metabolism, environment, behavior, and culture.

  • Genetics. A person is more likely to develop obesity if one or both parents are obese. Genetics also affect hormones involved in fat regulation. 
  • Overeating. Overeating leads to weight gain, especially if the diet is high in fat. 
  • A diet high in simple carbohydrates. The role of carbohydrates in weight gain is not clear. Carbohydrates increase blood glucose levels, which in turn stimulate insulin release by the pancreas, and insulin promotes the growth of fat tissue and can cause weight gain. 
  • Frequency of eating. The relationship between frequency of eating (how often you eat) and weight is somewhat controversial. There are many reports of overweight people eating less often than people with normal weight. Scientists have observed that people who eat small meals four or five times daily, have lower cholesterol   levels and lower and/or more stable blood sugar levels than people who eat less frequently. One possible explanation is that small frequent meals produce stable insulin levels, whereas large meals cause large spikes of insulin after meals.
  • Physical inactivity. Sedentary people burn fewer calories than people who are active. The National Health and Nutrition Examination Survey (NHANES) showed a strong correlations between physical inactivity and weight gain in both sexes.
  • Medications. Medications associated with weight gain include certain antidepressants, anticonvulsants, some diabetes   medications, certain hormones such as oral   contraceptives, and most corticosteroids. Some high blood pressure medications and antihistamines cause weight gain. 
  • Psychological factors. For some people, emotions influence eating habits. Many people eat excessively in response to emotions such as boredom, sadness, stress, or anger. 
  • Diseases such as hypothyroidism, insulin resistance, polycystic ovary syndrome, and Cushing's syndrome are also contributors to obesity.

Excess weight may increase the risk for many health problems, including

  • type 2 diabetes
  • high blood pressure
  • heart disease and strokes
  • certain types of cancer
  • sleep apnea
  • osteoarthritis
  • fatty liver disease
  • kidney disease
  • pregnancy problems, such as high blood sugar during pregnancy, high blood pressure, and increased risk for cesarean delivery (C-section)

National Institute of Diabetes ad Digestive Kidney Diseases

In the United States, the percentage of children and adolescents affected by obesity has more than tripled since the 1970s. Data from 2015-2016 show that nearly 1 in 5 school age children and young people (6 to 19 years) in the United States has obesity.

Many factors contribute to childhood obesity, including:

  • Metabolism—how your body changes food and oxygen into energy it can use.
  • Eating and physical activity behaviors.
  • Community and neighborhood design and safety.
  • Short sleep duration.
  • Negative childhood events

Genetic factors are difficult to change. However, people and places can play a role in helping children achieve and maintain a healthy weight. Changes in the environments where young people spend their time—like homes, schools, and community settings—can make it easier for youth to access nutritious foods and be physically active. Schools can adopt policies and practices that help young people eat more fruits and vegetables, eat fewer foods and beverages that are high in added sugars or solid fats, and increase daily minutes of physical activity.  These kinds of school-based and after-school programs and policies can be cost-effective and even cost-saving.

Centers for Disease Control and Prevention

There are countless weight-loss strategies available but many are ineffective and short-term, particularly for those who are morbidly obese. Among the morbidly obese, less than 5 percent succeed in losing a significant amount of weight and maintaining the weight loss with non-surgical programs — usually a combination of dieting, behavior modification therapy and exercise.

People do lose weight without surgery, however, particularly when they work with a certified health care professional to develop an effective and safe weight-loss program. Most health insurance companies don't cover weight-loss surgery unless you first make a serious effort to lose weight using non-surgical approaches.

Many people participate in a combination of the following therapies:

1. Dietary Modification

2. Behavior Modification

3. Exercise

4. Medications

USFC Health

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The Endocrine Society

This site serves as the one-stop clearinghouse for the general public seeking information on the key scientific trends and advancements that may one day lead to a slimmer, fitter America.

  Mayo Clinic

Complications of Obesity

Obesity Society

Research. Education. Action.

The State of Obesity

National School Breakfast and Lunch Program: 70th Anniversary

  World Health Organization

General information on obesity and childhood obesity, including global strategy on diet, physical activity and health.

Academy of Nutritionist and Dietetics

  • Time to Act on Obesity

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How To Write A Strong Obesity Research Paper?

Jessica Nita

Table of Contents

obesity introduction research paper

Obesity is such a disease when the percent of body fat has negative effects on a person’s health. The topic is very serious as obesity poisons the lives of many teens, adults and even children around the whole world.

Can you imagine that according to WHO (World Health Organization) there were 650 million obese adults and 13% of all 18-year-olds were also obese in 2016? And scientists claim that the number of them is continually growing.

There are many reasons behind the problem, but no matter what they are, lots of people suffer from the wide spectrum of consequences of obesity.

Basic guidelines on obesity research paper

Writing any research paper requires sticking to an open-and-shut structure. It has three basic parts: Introduction, Main Body, and Conclusion.

According to the general rules, you start with the introduction where you provide your reader with some background information and give brief definitions of terms used in the text. Next goes the thesis of your paper.

The thesis is the main idea of all the research you’ve done written in a precise and simple manner, usually in one sentence.

The main body is where you present the statements and ideas which disclose the topic of your research.

In conclusion, you sum up all the text and make a derivation.

How to write an obesity thesis statement?

As I’ve already noted, the thesis is the main idea of your work. What is your position? What do you think about the issue? What is that you want to prove in your essay?

Answer one of those questions briefly and precisely.

Here are some examples of how to write a thesis statement for an obesity research paper:

  • The main cause of obesity is determined to be surfeit and unhealthy diet.
  • Obesity can be prevented no matter what genetic penchants are.
  • Except for being a problem itself, obesity may result in diabetes, cancers, cardiovascular diseases, and many others.
  • Obesity is a result of fast-growing civilization development.
  • Not only do obese people have health issues but also they have troubles when it comes to socialization.

obesity introduction research paper

20 top-notch obesity research paper topics

Since the problem of obesity is very multifaceted and has a lot of aspects to discover, you have to define a topic you want to cover in your essay.

How about writing a fast food and obesity research paper or composing a topic in a sphere of fast food? Those issues gain more and more popularity nowadays.

A couple of other decent ideas at your service.

  • The consequences of obesity.
  • Obesity as a mental problem.
  • Obesity and social standards: the problem of proper self-fulfilment.
  • Overweight vs obesity: the use of BMI (Body Mass Index).
  • The problem of obesity in your country.
  • Methods of prevention the obesity.
  • Is lack of self-control a principal factor of becoming obese?
  • The least obvious reasons for obesity.
  • Obesity: the history of the disease.
  • The effect of mass media in augmentation of the obesity level.
  • The connection between depression and obesity.
  • The societal stigma of obese people.
  • The role of legislation in reducing the level of obesity.
  • Obesity and cultural aspect.
  • Who has the biggest part of the responsibility for obesity: persons themselves, local authorities, government, mass media or somebody else?
  • Why are obesity rates constantly growing?
  • Who is more prone to obesity, men or women? Why?
  • Correlation between obesity and life expectancy.
  • The problem of discrimination of the obese people at the workplace.
  • Could it be claimed that such movements as body-positive and feminism encourage obesity to a certain extent?

Best sample of obesity research paper outline

An outline is a table of contents which is made at the very beginning of your writing. It helps structurize your thoughts and create a plan for the whole piece in advance.

…Need a sample?

Here is one! It fits the paper on obesity in the U.S.

Introduction

  • Hook sentence.
  • Thesis statement.
  • Transition to Main Body.
  • America’s modern plague: obesity.
  • Statistics and obesity rates in America.
  • Main reasons of obesity in America.
  • Social, cultural and other aspects involved in the problem of obesity.
  • Methods of preventing and treating obesity in America.
  • Transition to Conclusion.
  • Unexpected twist or a final argument.
  • Food for thought.

Specifics of childhood obesity research paper

obesity introduction research paper

A separate question in the problem of obesity is overweight children.

It is singled out since there are quite a lot of differences in clinical pictures, reasons and ways of treatment of an obese adult and an obese child.

Writing a child obesity research paper requires a more attentive approach to the analysis of its causes and examination of family issues. There’s a need to consider issues like eating habits, daily routine, predispositions and other.

Top 20 childhood obesity research paper topics

We’ve gathered the best ideas for your paper on childhood obesity. Take one of those to complete your best research!

  • What are the main causes of childhood obesity in your country?
  • Does obesity in childhood increase the chance of obesity in adulthood?
  • Examine whether a child’s obesity affects academic performance.
  • Are parents always guilty if their child is obese?
  • What methods of preventing childhood obesity are used in your school?
  • What measures the government can take to prevent children’s obesity?
  • Examine how childhood obesity can result in premature development of chronic diseases.
  • Are obese or overweight parents more prone to have an obese child?
  • Why childhood obesity rates are constantly growing around the whole world?
  • How to encourage children to lead a healthy style of life?
  • Are there more junk and fast food options for children nowadays? How is that related to childhood obesity rates?
  • What is medical treatment for obese children?
  • Should fast food chains have age limits for their visitors?
  • How should parents bring up their child in order to prevent obesity?
  • The problem of socializing in obese children.
  • Examine the importance of a proper healthy menu in schools’ cafeterias.
  • Should the compulsory treatment of obese children be started up?
  • Excess of care as the reason for childhood obesity.
  • How can parents understand that their child is obese?
  • How can the level of wealth impact the chance of a child’s obesity?

Childhood obesity outline example

As the question of childhood obesity is a specific one, it would differ from the outline on obesity we presented previously.

Here is a sample you might need. The topic covers general research on child obesity.

  • The problem of childhood obesity.
  • World’s childhood obesity rates.
  • How to diagnose the disease.
  • Predisposition and other causes of child obesity.
  • Methods of treatment for obese children.
  • Preventive measures to avoid a child’s obesity.

On balance…

The topic of obesity is a long-standing one. It has numerous aspects to discuss, sides to examine, and data to analyze.

Any topic you choose might result in brilliant work.

How can you achieve that?

Follow the basic requirements, plan the content beforehand, and be genuinely interested in the topic.

Option 2. Choose free time over struggle on the paper. We’ve got dozens of professional writers ready to help you out. Order your best paper within several seconds and enjoy your free time. We’ll cover you up!

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obesity introduction research paper

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Childhood and Adolescent Obesity in the United States: A Public Health Concern

Adekunle sanyaolu.

1 Federal Ministry of Health, Abuja, Nigeria

Chuku Okorie

2 Essex County College, Newark, NJ, USA

3 Saint James School of Medicine, Anguilla, British West Indies

Jennifer Locke

Saif rehman.

Childhood and adolescent obesity have reached epidemic levels in the United States. Currently, about 17% of US children are presenting with obesity. Obesity can affect all aspects of the children including their psychological as well as cardiovascular health; also, their overall physical health is affected. The association between obesity and other conditions makes it a public health concern for children and adolescents. Due to the increase in the prevalence of obesity among children, a variety of research studies have been conducted to discover what associations and risk factors increase the probability that a child will present with obesity. While a complete picture of all the risk factors associated with obesity remains elusive, the combination of diet, exercise, physiological factors, and psychological factors is important in the control and prevention of childhood obesity; thus, all researchers agree that prevention is the key strategy for controlling the current problem. Primary prevention methods are aimed at educating the child and family, as well as encouraging appropriate diet and exercise from a young age through adulthood, while secondary prevention is targeted at lessening the effect of childhood obesity to prevent the child from continuing the unhealthy habits and obesity into adulthood. A combination of both primary and secondary prevention is necessary to achieve the best results. This review article highlights the health implications including physiological and psychological factors comorbidities, as well as the epidemiology, risk factors, prevention, and control of childhood and adolescent obesity in the United States.

Introduction

Childhood and adolescent obesity have reached epidemic levels in the United States, affecting the lives of millions of people. In the past 3 decades, the prevalence of childhood obesity has more than doubled in children and tripled in adolescents. 1 The latest data from the National Health and Nutrition Examination Survey show that the prevalence of obesity among US children and adolescents was 18.5% in 2015-2016. Overall, the prevalence of obesity among adolescents (12-19 years; 20.6%) and school-aged children (6-11 years; 18.4%) was higher than among preschool-aged children (2-5 years; 13.9%). School-aged boys (20.4%) had a higher prevalence of obesity than preschool-aged boys (14.3%). Adolescent girls (20.9%) had a higher prevalence of obesity than preschool-aged girls (13.5%; Figure 1 ). 1 Moreover, the rates of obesity have been steadily rising from 1999-2000 through 2015-2016 ( Figure 2 ). 1 According to Ahmad et al, 80% of adolescents aged 10 to 14 years, 25% of children younger than the age of 5 years, and 50% of children aged 6 to 9 years with obesity are at risk of remaining adults with obesity. 2

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Prevalence of obesity among children and adolescents aged 2 to 19 years, by sex and age: the United States, 2015-2016.

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Object name is 10.1177_2333794X19891305-fig2.jpg

Trends in obesity prevalence among children and adolescents aged 2 to 19 years: the United States, 1999-2000 through 2015-2016.

Obesity can affect all aspects of children and adolescents including but not limited to their psychological health and cardiovascular health and also their overall physical health. 3 The association between obesity and morbid outcomes makes it a public health concern for children and adolescents. 4 Obesity has an enormous impact on both physical and psychological health. Consequently, it is associated with several comorbidity conditions such as hypertension, hyperlipidemia, diabetes, sleep apnea, poor self-esteem, and even serious forms of depression. 5 In addition, children with obesity who were followed-up to adulthood were much more likely to suffer from cardiovascular and digestive diseases. 3 The increase in body fat also exposes the children to increase in the risk of numerous forms of cancers, such as breast, colon, esophageal, kidney, and pancreatic cancers. 6

Due to its public health significance, the increasing trend in childhood obesity needs to be closely monitored. 7 However, these trends have proved to be challenging to quantify and compare. While there are many factors and areas to consider when discussing obesity in children and adolescents, there are a few trends that are evident in recent studies. For example, the prevalence of obesity varies among ethnic groups, age, sex, education levels, and socioeconomic status. A report published by the National Center for Health Statistics using data from the National Health and Nutrition Examination Survey provides the most recent national estimates from 2015 to 2016 on obesity prevalence by sex, age, race, and overall estimates from 1999-2000 through 2015-2016. 1 Prevalence of obesity among non-Hispanic black (22.0%) and Hispanic (25.8%) children and adolescents aged 2 to 19 years was higher than among both non-Hispanic white (14.1%) and non-Hispanic Asian (11.0%) children and adolescents. There were no significant differences in the prevalence of obesity between non-Hispanic white and non-Hispanic Asian children and adolescents or between non-Hispanic black and Hispanic children and adolescents. The pattern among girls was similar to the pattern in all children and adolescents. The prevalence of obesity was 25.1% in non-Hispanic black, 23.6% in Hispanic, 13.5% in non-Hispanic white, and 10.1% in non-Hispanic Asian girls. The pattern among boys was similar to the pattern in all children and adolescents except that Hispanic boys (28.0%) had a higher prevalence of obesity than non-Hispanic black boys (19.0%; Figure 3 ). 1 This review article is aimed at studying the health implications including physical and psychological factors and comorbidities, as well as the epidemiology, risk factors, prevention, and control of childhood and adolescent obesity in the United States.

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Object name is 10.1177_2333794X19891305-fig3.jpg

Prevalence of obesity among children and adolescents aged 2 to 19 years, by sex and race and Hispanic origin: the United States, 2015-2016.

Methodology

We performed a literature search using online electronic databases (PubMed, MedlinePlus, Mendeley, Google Scholar, Research Gate, Global Health, and Scopus) using the keywords “childhood,” “adolescents,” “obesity,” “BMI,” and “overweight.” Articles were retrieved and selected based on relevance to the research question.

Ethical Approval and Informed Consent

Ethics approval and informed consent were not required for this narrative review.

Definition of Childhood Obesity

Defining obesity requires a suitable measurement of body fat and an appropriate cutoff range. 8 Body mass index (BMI) was calculated as weight in kilograms divided by height in meters squared, rounded to 1 decimal place. Obesity in children and adolescents was defined as a BMI of greater than or equal to the age- and sex-specific 95th percentile and overweight with a BMI between the 85th and 95th percentiles of the 2000 Centers for Disease Control and Prevention (CDC) growth charts. 9

However, the use of the BMI percentile according to the age/sex of the CDC growth charts for very high BMIs can result in estimates that differ substantially from those that are observed, 10 , 11 and this constrains the maximum BMI that is attainable at given sex and age. 12 , 13 These limitations have resulted in the classification of severe obesity as a BMI ≥120% of the 95th percentile rather than a percentile greater than the 95th percentile. 11 , 14 A BMI of 120% of the 95th percentile corresponds to a BMI of ~35 among 16 to 18 year olds.

Physiology of Energy Regulation and Obesity

Obesity is a chronic multifactorial disease, characterized by an excessive accumulation of adipose tissue, commonly as a result of excessive food intake and/or low energy expenditure. Obesity can be triggered by genetic, psychological, lifestyle, nutritional, environmental, and hormonal factors. 15

Obesity is found in individuals that are susceptible genetically and involves the biological defense of an elevated body fat mass, the mechanism of which could be explained in part by interactions between brain reward and homeostatic circuits, inflammatory signaling, accumulation of lipid metabolites, or other mechanisms that impair hypothalamic neurons. 16

Normal energy regulation physiology is under tight neurohormonal control. The neurohormonal control is performed in the central nervous system through neuroendocrine connections, in which circulating peripheral hormones, such as leptin and insulin, provide signals to specialized neurons of the hypothalamus reflecting body fat stores and induces appropriate responses to maintain the stability of these stores. The hypothalamic region is where the center of the regulation of hunger and satiety is located. Some of them target the activity of endogenous peptides, such as ghrelin, pancreatic polypeptide, 17 peptide YY, and neuropeptide Y, 18 as well as their receptors.

The physiology of energy regulation may result in obesity in susceptible people when it goes awry from genetic and environmental modulators. There is strong evidence of the majority of obesity cases that are associated with central resistance to both leptin and insulin actions. 19 , 20 The environmental modulators equally play critical roles in obesity. Changes in the circadian clock are associated with temporal alterations in feeding behavior and increased weight gain. 21 Stress interferes with cognitive processes such as executive function and self-regulation. Second, stress can affect behavior by inducing overeating and consumption of foods that are high in calories, fat, or sugar; by decreasing physical activity; and by shortening sleep. Third, stress triggers physiological changes in the hypothalamic-pituitary-adrenal axis, reward processing in the brain, and possibly the gut microbiome. Finally, stress can stimulate the production of biochemical hormones and peptides such as leptin, ghrelin, and neuropeptide Y. 17

The lateral hypothalamus (LH) plays a fundamental role in regulating feeding and reward-related behaviors; however, the contributions of neuronal subpopulations in the LH are yet to be identified thoroughly. 22 The LH has also been associated with other aspects of body weight regulation, such as physical activity and thermogenesis. 23 The LH contains a heterogeneous assembly of neuronal cell populations, in which γ-aminobutyric acid (GABA) neurons predominate. 23 LH GABA neurons are known to mediate multiple behaviors important for body weight regulation, thus altering energy expenditure. 23

Etiology and Risk Factors

Excess body fat is a major health concern in childhood and adolescent populations. The dramatic increase in childhood obesity foreshadows the serious health consequences of their adult life. As obesity begins from childhood and spans through adult life, it becomes increasingly more difficult to treat successfully. Being able to identify the risk factors and potential causes of childhood obesity is one of the best strategies for preventing the epidemic. 24

According to the Morbidity and Mortality Weekly Report released in 2011, there is an acceptance that there is no single cause of childhood obesity and that energy imbalance is just a part of the numerous factors. 25 Many children have a discrepancy between what is taken in and what is expended. 26 For example, children with obesity consume approximately 1000 calories more than what is necessary for their body to function healthily and to be able to participate in regular physical activities. Over 10 years, there will be an excess of 57 pounds of unnecessary weight. With excessive caloric intake, as well as sedentary lifestyles, childhood obesity will continue to rise if no changes are implemented. Adding daily physical activity, better sleep patterns, as well as dietary changes can help decrease the number of excess calories and help with obesity-related problems in the future.

Also, during childhood, excess fat accumulates when the increase in caloric intake exceeds the total energy expenditure. 26 Furthermore, children living in the United States today compared with children living in the 1900s are participating in more than 6 hours per day activities on social media. This includes but is not limited to traditional television, video gaming, and blogging/Facebook activities. An additional economic rationalization for the increase in childhood obesity is technology. In other words, Americans can now eat more in less time.

In a study, Cutler et al found that an increase in consumption of food tends to be related to technology innovation in food production and transportation. Technology has thus made it increasingly possible for firms to mass prepare food and ship to consumers for ready consumption, thereby taking advantage of scale economies in food preparation. The result of this change has been a significant reduction in the time costs for food production. These lower time costs have led to increased food consumption and, ultimately, increased weights. 27 Eliminating the time cost of food preparation disproportionately increases consumption for hyperbolic discounters because time delay is a particularly important mechanism for discouraging those individuals from consuming. 27 Society today prefers immediate satisfaction with regard to food and convenience over the long-term goals of living a long, healthy life. The availability of high-caloric, less-expensive food coupled with the extensive advertisement and easy accessibility of these foods has contributed immensely to the rising trend of obesity. 28 For example, there have been reductions in the price of McDonalds and Coca-Cola (5.44% and 34.89%, respectively) between 1990 and 2007, while there was about a 17% increase in the price of fruits and vegetables between 1997 and 2003. 29

Likewise, only 16% of children walk or bike to school today as compared with 42% in the late 1960s. However, the distance, convenience, weather, scanty sidewalks, and anxiety about crimes against children could all contribute to this difference. Furthermore, with elementary, middle, and high school combined, only 13.8% of these schools provide adequate daily physical education classes for at least 4 hours a week. 30

Some other potential risk factors have been reported through research studies that involve issues that affect the child in utero and childhood. Table 1 represents potential risk factors and confounders of childhood obesity. 31

Potential Risk Factors of Childhood Obesity.

Abbreviations: BMI, body mass index; SES, socioeconomic status.

Catalano et al argues that maternal BMI before conception, independent of maternal glucose status or birth weight, is a strong predictor of childhood obesity. 32 Infants at the highest quarter for weight at 8 and 18 months are more likely to become children with obesity at age 7, than children in the lower quarters. Certain behaviors have been linked to childhood obesity and overweight; these are a lack of physical activity and unhealthy eating patterns (eating more food away from home, drinking more sugar-sweetened drinks, and snacking more frequently), resulting in excess energy intake. 22 , 31 In addition, when one parent presents with obesity, there is an increased potential for the child to become obese over the years. Naturally, the risk is higher for the children when both parents present with obesity. Furthermore, a study that followed children over time observed that children who got less sleep <10.5 hours at age 3 were 45% more likely to be children with obesity at the age of 7, than children who got greater than 12 hours of sleep during their first 3 years of life. 33 , 34

While all the above-mentioned factors are informative, there is still the need for further research concerning childhood and adolescent obesity and obesity in general. Risk factors for obesity in childhood are still somewhat uncertain, and evidence-based research for preventative strategies is lacking. Moreover, effective action to prevent the childhood obesity epidemic requires evidence-based on early life risk factors, and this evidence, unfortunately, is still incomplete. Furthermore, a research study has attempted to capture the complete picture of childhood obesity early life course risk factors. In the study, they identified that parental BMI and gestational weight gain among other factors should be considered in prevention programs. 35

Health Effects of Childhood Obesity

Childhood obesity is known to have a significant impact on both physical and psychological health. Sahoo et al stated that “childhood obesity can profoundly affect children’s physical health, social and emotional well-being, as well as self-esteem.” They associated poor academic performance and a lower quality of life experienced by the child with childhood obesity. They also stated that “metabolic, cardiovascular, orthopedic, neurological, hepatic, pulmonary, and menstrual disorders among others are consequences of childhood obesity.” 36 There are many health consequences of childhood obesity, and three of the more common ones are sleep apnea, diabetes, and cardiovascular diseases. 36

Psychological Consequences of Obesity

Several studies related to childhood and adolescent obesity have focused primarily on physiological consequences. Other studies have been conducted regarding the association between psychiatric disorders and obesity; these have resulted in conflict due to obesity being found to be an insignificant factor for psychopathology. However, a comparative study by Britz et al found that high rates of mood, anxiety, somatoform, and eating disorders were detected among children with obesity. The study also observed that most psychiatric disorders began after the onset of obesity. In this large population-based study, it was found that a staggering 60% of females and 35% of males reported that they have engaged in binge eating and expressed a lack of control over their diet. 37

Goldfield et al conducted a study among 1400 adolescents with obesity, overweight, and normal weight in grades 7 to 12. Their BMIs, as determined by the International Obesity Task Force, were the criteria used to define each group. Each participant completed a questionnaire on body images, eating behaviors, and moods. Adolescents with obesity reported significantly higher body dissatisfaction, social isolation, depression symptoms, anhedonia, and negative self-esteem than those of normal weight. 38 There is widespread stigmatization of people with obesity that causes harm rather than the intention to motivate people to lose weight. Stigma contributes to behaviors such as binge eating, social isolation, avoidance of health care services, decreased physical activity, and increased weight gain, which worsens obesity and creates additional barriers to healthy behavior change. 39 Weight-based bullying in youth is considered a common, serious problem in many countries. 40 In a study conducted by O’Brien et al, to test whether the association between weight stigma experiences and disordered eating behaviors, that is, emotional eating, uncontrolled eating, and loss-of-control eating, are mediated by weight bias internalization and psychological distress among 634 undergraduate university students, and results of statistical analyses showed that weight stigma was significantly associated with all measures of disordered eating, and with weight bias internalization and psychological distress. 41

Asthma and Obesity

There is mounting evidence that childhood obesity is a risk factor for the development of asthma. 42 A research study was conducted by Belamarich et al to investigate 1322 children aged 4 to 9 years with asthma. Obesity, as defined by the CDC, is the BMI, with weight and height being greater than the 95th percentile. This was the criteria used to identify the 249 children with obesity, while the BMI between the 5th and 95th percentile identified the children who were not obese. After a baseline assessment was done, the 9-month study found that the children with obesity had a higher number of days of wheezing over 2 weeks (4.0 vs 3.4) and as well had more unscheduled emergency hospital visits (39% vs 31%). 42

Obesity directly correlates with the severity of asthma, as well as poor response to corticosteroids. 43 In fact, children with obesity who also have a history of asthma are more challenging to control and linked to worse quality of life. 44 A prospective trial found that weight loss in patients with obesity and a history of asthma can significantly aid them to control the asthma attacks. 43

Chronic Inflammation and Childhood Obesity

Lumeng and Saltiel reported that obesity in children affects multiple organ systems and predisposes them to diseases. The effect of obesity on the tissue can manifest in the development of insulin-resistant type 2 diabetes, the risk of cancer, and pulmonary diseases. 45

The inflammatory response to obesity triggers pathogens, systematic increases in circulatory inflammatory cytokines, and acute-phase reactants (eg, C-reactive proteins), which inflames the tissues. This is often caused by the activation of tissue leukocytes. Chronic inflammation in children with obesity can induce meta-inflammation that is unique when compared with other inflammatory paradigms (eg, infection, autoimmune diseases). 45 Researchers have reported that children with obesity are at risk of lifelong meta-inflammation. In these children, the inflammatory markers are elevated as early as in the third year of life. 45 , 46 This has been linked to heart disease later in life. 19 The long-term consequences of such findings can cause cumulative vascular damage that correlates with the increased weight status. 47

The short-term and long-term effects of obesity on the health of children is a significant concern because of the negative psychological and health consequences. 46 The potential negative psychological outcomes are depressive symptoms, poor body image, low self-esteem, a risk for eating disorders, and behavior and learning problems. Additional negative health consequences include insulin resistance, type 2 diabetes, asthma, hypertension, high total, and low-density lipoprotein cholesterol and triglyceride levels in the blood, low high-density lipoprotein cholesterol levels in the blood, sleep apnea, early puberty, orthopedic problems, and nonalcoholic steatohepatitis 46 , 47 ( Figure 4 ). Children with obesity are more likely to become adults with obesity, thus increasing their risk for several diseases before they even reach their teen years. 48

An external file that holds a picture, illustration, etc.
Object name is 10.1177_2333794X19891305-fig4.jpg

Comorbidities and potential health consequences of childhood obesity. 47

Prevention and Control

There are two primary components to the prevention and control of childhood obesity.

The first is to educate parents on proper nutritional requirements for their children and the second is to implement the learned information. Educating parents on proper nutrition and dietary caloric intake requirements for their children is at the forefront for the prevention of obesity; however, the way the information is disseminated may affect the usefulness of the information. For example, one of the main limitations to the education of parents about childhood obesity is that typically written information is used as the conduit to health information and disease prevention. 49 The Growing Right Onto Wellness (GROW) trial used a systematic assessment of patient education material that was used for the prevention of childhood obesity in the low health literate population. 49 Results suggest that the average readability is of grade 6 level (SMOG [Simple Measure of Gobbledygook] Index 5.63 ± 0.76 and Fry graph 6.0 ± 0.85) and that adjustment of education material must be done for low health literate populations to adequately comprehend educational material and maintain motivation on the prevention of childhood obesity. 49 A similar study was conducted to further support this improvement when using color-coordinated diagrams to help parents visualize instead of trying to comprehend with numbers and words. It proved to be successful as parents were able to see where they were going wrong and make the necessary changes in their children’s diet. 49

Similarly, the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development conducted a study on 744 adolescents and parents, and analyzed data to determine if parental (maternal and paternal, individually) reactions to children’s behavior was related to childhood obesity. 50 The study concluded that informing parents that their attitude toward their children’s behaviors will play a prominent role in preventing childhood obesity. 50 Parental education on nutrition, health, and the involvement of politicians, physicians, and school personnel are key for the prevention of childhood obesity. However, community and educational institutions have begun legislating and incorporating programs such as providing healthy foods at schools and also health information sessions directed toward young individuals, aimed at preventing childhood obesity in the United States and Canada. 51

Another effective prevention measure against childhood obesity is the awareness of parents on the meal and snack portion sizes. In a systematic review conducted on the effects of portion size manipulation with children and portion education/training interventions on dietary intake with parents, it was determined that the ability of adults to accurately estimate portion size improved following education/training. 52 Education of parents and children on diet requirements has its limitations in that the information must be easy to understand and be easily accessible in order to be practical. Making the available education materials easier to understand from just tables and numbers to more relatable aspects such as colors or figures, parents were able to visualize the changes they need to make whether it is with regard to portion sizes or even seeing how much childhood obesity is present in their family. Although much of the literature provided to parents is targeted to help those with lower numeracy skills, many parents benefited from the information being comparative from right/wrong and good/bad with regard to dieting. 49

The study recommended that proper educational materials, including useful and understandable literature, be used to control meal portion sizes and to help parents identify when children are at risk of obesity. Similarly, healthy eating practices should be taught by schools as a mandatory and essential method in the prevention of childhood obesity. 52

The implementation of healthy eating practices and adequate exercise regimes are essential in the prevention and control of childhood obesity. For example, information from systematic reviews, randomized controlled trials, and well-designed observational studies indicate that evidence-based prevention and control of childhood obesity can be accomplished with the collaboration of community/school, primary health care, and home-based/family-based interventions that involve both physical activity and dietary component. 53 In particular, the control of children with obesity is of significant value, as is the prevention of obesity. Two randomized control trials of 182 families were conducted from November 2005 to September 2007, and they studied the efficacy of US pediatric obesity treatment guidelines in children aged 4 to 9 years with a standardized BMI (ZBMI) greater than the 85 percentile. 54 Briefly, Trial 1 studied the impact on ZBMI by reducing snack foods and sugar-sweetened beverages and increasing fruits, vegetables, and low-fat dairy. 54 Trial 2 studied the impact on ZBMI by decreasing sugar-sweetened beverages and increasing physical activity and increasing low-fat milk consumption and reducing television watching. In Trial 1, the resulting ZBMI reduced within 6 months, and this was maintained through to the 12th month (ΔZBMI 0-12 months = −0.12 ± 0.22). 53 In Trial 2, the resulting ZBMI reduced within 6 months and continued to improve till the 12 months (ΔZBMI 0-12 months = −0.16 ± 0.31). 50

A similar cluster-randomized trial in England studied the effects of the reduction of carbonated beverages on the number of children with obesity in 29 classes (644 children). 51 Results indicate that a decrease of 0.6 glasses of carbonated drinks (250 mL) over three days per week decreased the number of children with obesity by 0.2%, while the control group increased by 7.5% (mean difference = 7.7%, 2.2% to 13.1%) at 12 months. However, diet control is only one component of the control and prevention of childhood obesity, while adequate exercise is another. 55

A systematic review and meta-analyses of the impact of diet and exercise programs (single or combined) was done on their effects on metabolic risk reduction in the pediatric population. 56 Analyses indicated that the addition of exercise to dietary intervention led to greater improvements in the levels of high-density lipoprotein cholesterol (3.86 mg/dL; 95% confidence interval [CI] = 2.70 to 4.63), fasting glucose (−2.16 mg/dL; 95% CI = −3.78 to −0.72), and fasting insulin (−2.75 µIU/mL; 95% CI = −4.50 to −1.00) over 6 months. 56 Diet and exercise are both important factors in the control and prevention of childhood obesity. It is our recommendation that parents and community (teachers and doctors) should be involved in identifying children at risk based on their BMI and participate in implementing practices such as good diet control through the reduction of sugary drinks, fatty foods, and also encouraging safe exercise programs to prevent and control childhood obesity in the society. 56

While all of the previous data express the more obvious prevention methods with regard to childhood obesity, it is imperative to note that ensuring that the whole family is involved in the intervention will yield the greatest results. 2 All current studies indicate that families must be included in childhood treatment of obesity. However, for the success of the child’s weight loss program, it is vital that the parents understand that the causes of obesity are often a mixture of four factors: genetic causes, parental habits, overeating, and poor exercise habits. Thus, instilling some responsibility on the parents and informing them that controlled food preparation, diet control, and family participation in physical activities will all assist in the treatment and control of obesity in their children. 2

Childhood obesity has increased significantly in recent decades and has quickly become a public health crisis in the United States and all over the world. Its increase in prevalence has provoked widespread research efforts to identify the factors that contributed to these changes. 57 Obesity starts with an imbalance between caloric intake and caloric expenditure. 58 Children with obesity are at greater risk of adult obesity; therefore, if we can educate and improve the health habits of families even before they start having children, this can help reduce the increasing rate of childhood obesity in the United States. Parents and caregivers with proper education on the causes and consequences of childhood obesity can help prevent childhood obesity by providing healthy meals and snacks, daily physical activity, and nutrition education to their family members. 59 Families need to take the approach of not adapting to their family being on a diet but more of a healthy lifestyle. A family’s home environment can influence children at a young age; therefore, making changes starting in the household early can educate and influence them to grow up healthy. Although prevention programs may be more expensive in the short term, the long-term benefits acquired through prevention are much more likely to save an even greater amount of health care costs. Not only will the children have a better childhood and self-esteem, but prevention programs can also decrease the incidence of cardiovascular diseases, diabetes, stroke, and possibly cancers in adulthood. 60 The overall need to decrease the obesity rate will help children and their families in the generations to come by building a healthy lifestyle and environment. In order to tackle the climbing obesity rate, overall health and lifestyle needs to be a priority as they balance one with the other. 49 While effective interventions to thwart childhood obesity still remain elusive, the sustainability of the interventions already in place will enable children and their families to adopt these important health behaviors as lifelong practices and improve their health. 58

Treatment of Obesity and the Physiology of Energy Regulation

As discussed previously, a variety of mechanisms participate in weight regulation and the development of obesity in children, including genetics, developmental influences (“metabolic programming” or epigenetics), individual and family health behaviors, and environmental factors. Among these potential mechanisms, only environmental factors are potentially modifiable during childhood and adolescence.

Unfortunately, despite intensive lifestyle modifications and support for healthy practices within the children’s environment, some children will continue to struggle with extreme excess weight and associated comorbidities. 61 , 62 Therefore, a combination of pharmacotherapy and lifestyle modification can be considered. 61 Overweight children should not be treated with medications unless significant, severe comorbidities persist despite lifestyle modification. The use of pharmacotherapy should also be considered in overweight children with a strong family history of type 2 diabetes or cardiovascular risk factors. Constant bidirectional communication between the brain and the gastrointestinal tract, as well as the brain and other relevant tissues (ie, adipose tissue, pancreas, and liver), ensures that the brain constantly perceives and responds accordingly to the energy status/needs of the body. This elegant biological system is subject to disruption by a toxic obesogenic environment, leading to syndromes such as leptin and insulin resistance, and ultimately further exposing individuals who are obese to further weight gain and type 2 diabetes mellitus. Currently, the only Food and Drug Administration–approved prescription drug indicated for the treatment of pediatric obesity is orlistat (Xenical; Genentech USA, Inc, South San Francisco, CA). 63 Orlistat works by inhibiting gastric and pancreatic lipases, the enzymes that break down triglycerides in the intestine. Moreover, imaging studies in humans are beginning to examine the influence that higher- order/hedonic brain regions have on homeostatic areas, as well as their responsiveness to homeostatic peripheral signals. With a greater understanding of these mechanisms, the field moves closer to understanding and eventually treating the casualties of obesity.

The number of children with obesity in the United States has increased substantially over the years; due to its public health significance, the increasing trends need to be closely monitored. While a complete picture of all the risk factors associated with obesity remains elusive, many of the studies agreed that prevention is the key strategy for controlling the current problem. Since the combination of diet, exercise, and physiological and psychological factors are all important factors in the control and prevention of childhood obesity, primary prevention methods should be aimed at educating the child and family and encouraging appropriate diet and exercise from a young age through adulthood while secondary prevention should be targeted at lessening the effect of childhood obesity by preventing the child from continuing unhealthy habits and obesity into adulthood. A combination of primary and secondary prevention is necessary to achieve the best results. Thus, a combined implementation of both types of preventions can significantly help lower the current prevalence of childhood and adolescent obesity in the United States. Failure to take appropriate actions could lead to serious public health consequences.

Author Contributions: AS: Contributed to conception and design; drafted manuscript; gave final approval; agrees to be accountable for all aspects of work ensuring integrity and accuracy.

XQ: Contributed to the acquisition, analysis, and interpretation.

JL: Contributed to the acquisition, analysis, and interpretation.

SR: Contributed to the acquisition, analysis, and interpretation.

Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.

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