Obesity is a medical condition in which excess body fat has accumulated to an extent that it may have a negative effect on health.[1] People are generally considered obese when their body mass index (BMI), a measurement obtained by dividing a person’s weight by the square of the person’s height—despite known allometric inaccuracies[a]—is over 30 kg/m2; the range 25–30 kg/m2 is defined as overweight.[1] Some East Asian countries use lower values.[10] Obesity is correlated with various diseases and conditions, particularly cardiovascular diseases, type 2 diabetes, obstructive sleep apnea, certain types of cancer, and osteoarthritis.[2] High BMI is a marker of risk, but not proven to be a direct cause, for diseases caused by diet, physical activity, and environmental factors.[11] A reciprocal link has been found between obesity and depression, with obesity increasing the risk of clinical depression and also depression leading to a higher chance of developing obesity.[3]
Obesity has individual, socioeconomic, and environmental causes, including diet, physical activity, automation, urbanization, genetic susceptibility, medications, mental disorders, economic policies, endocrine disorders, and exposure to endocrine-disrupting chemicals.[1][4][12][13] While a majority of obese individuals at any given time are attempting to lose weight and often successful, research shows that maintaining that weight loss over the long term proves to be rare.[14] The reasons for weight cycling are not fully understood but may include decreased energy expenditure combined with increased biological urge to eat during and after caloric restriction.[14] More studies are needed to determine if weight cycling and yo-yo dieting contribute to inflammation and disease risk in obese individuals.[14]
Effects of Yo yo dieting on health
This kind of diet is associated with extreme food deprivation as a substitute for healthy diet and exercise techniques. As a result, the dieter may experience loss of both muscle and body fat during the initial weight-loss phase (weight-bearing exercise is required to maintain muscle). After completing the diet, the dieter is likely to experience the body’s starvation response, leading to rapid weight gain of only fat. This is a cycle that changes the body’s fat-to-muscle ratio, one of the more important factors in health. A report by the American Psychological Association reviewed thirty-one diet studies and found that after two years of dieting up to a third of dieters weighed more than they did before they began the diet, another third regained the weight they lost, and the last third kept the loss weight off[3] One study in rats showed those made to yo-yo diet were more efficient at gaining weight.[4] However the research compiled by Atkinson et al. (1994)[5] showed that there are “no adverse effects of weight cycling on body composition, resting metabolic rate, body fat distribution, or future successful weight loss”, and that there is not enough evidence to show risk factors for cardiovascular disease being directly dependent on cyclical dieting patterns. A more recent review concluded “…evidence for an adverse effect of weight cycling appears sparse, if it exists at all”.[6]
Since there is “no single definition of weight cycling [that] can be endorsed”, it is almost impossible for research to draw specific conclusions about the actual effects of cyclical dieting, until it becomes more definitely defined.[5]
Effects of Obesity on health
Excessive body weight is associated with various diseases and conditions, particularly cardiovascular diseases, diabetes mellitus type 2, obstructive sleep apnea, certain types of cancer, osteoarthritis,[2] and asthma.[2][36] As a result, obesity has been found to reduce life expectancy.[2]
Mortality
Obesity is one of the leading preventable causes of death worldwide.[38][39][40] A number of reviews have found that mortality risk is lowest at a BMI of 20–25 kg/m2[41][42][43] in non-smokers and at 24–27 kg/m2 in current smokers, with risk increasing along with changes in either direction.[44][45] This appears to apply in at least four continents.[43] In contrast, a 2013 review found that grade 1 obesity (BMI 30–35) was not associated with higher mortality than normal weight, and that overweight (BMI 25–30) was associated with “lower” mortality than was normal weight (BMI 18.5–25).[46] Other evidence suggests that the association of BMI and waist circumference with mortality is U- or J-shaped, while the association between waist-to-hip ratio and waist-to-height ratio with mortality is more positive.[47] In Asians the risk of negative health effects begins to increase between 22–25 kg/m2.[48] A BMI above 32 kg/m2 has been associated with a doubled mortality rate among women over a 16-year period.[49] In the United States, obesity is estimated to cause 111,909 to 365,000 deaths per year,[2][40] while 1 million (7.7%) of deaths in Europe are attributed to excess weight.[50][51] On average, obesity reduces life expectancy by six to seven years,[2][52] a BMI of 30–35 kg/m2 reduces life expectancy by two to four years,[42] while severe obesity (BMI > 40 kg/m2) reduces life expectancy by ten years.[42]
allostatic load
The term allostatic load is “the wear and tear on the body” which accumulates as an individual is exposed to repeated or chronic stress.[1] It was coined by McEwen and Stellar in 1993.[2]
The term is part of the regulatory model of allostasis, where the predictive regulation or stabilisation of internal sensations in response to stimuli is ascribed to the brain.[3] Allostasis involves the regulation of homeostasis in the body to decrease physiological consequences on the body.[4][5] Predictive regulation refers to the brain’s ability to anticipate needs and prepare to fulfill them before they arise.[3]
Part of efficient regulation is the reduction of uncertainty. Humans naturally do not like feeling as if surprise is inevitable. Because of this, we constantly strive to reduce the uncertainty of future outcomes, and allostasis helps us do this by anticipating needs and planning how to satisfy them ahead of time.[6] But it takes a considerable amount of the brain’s energy to do this, and if it fails to resolve the uncertainty, the situation may become chronic and result in the accumulation of allostatic load.[6]
The concept of allostatic load provides that “the neuroendocrine, cardiovascular, neuroenergetic, and emotional responses become persistently activated so that blood flow turbulences in the coronary and cerebral arteries, high blood pressure, atherogenesis, cognitive dysfunction and depressed mood accelerate disease progression.”[6] All long-standing effects of continuously activated stress responses are referred to as allostatic load. Allostatic load can result in permanently altered brain architecture and systemic pathophysiology.[6]
Allostatic load minimizes an organism’s ability to cope with and reduce uncertainty in the future.[6]
Allostatic load is generally measured through a composite index of indicators of cumulative strain on several organs and tissues, primarily biomarkers associated with the neuroendocrine, cardiovascular, immune and metabolic systems.[12]Indices of allostatic load are diverse across studies and are frequently assessed differently, using different biomarkers and different methods of assembling an allostatic load index. Allostatic load is not unique to humans and may be used to evaluate the physiological effects of chronic or frequent stress in non-human primates as well.[12]In the endocrine system, the increase or repeated levels of stress results in the increased levels of the hormone Corticotropin-Releasing Factor (CRH), which is associated with activation of HPA axis.[5] The Hypothalamic–pituitary–adrenal axis is the central stress response system responsible for modulating inflammatory responses throughout the body. Prolonged stress levels can lead to decreased levels of cortisol in the morning and increased levels in the afternoon, leading to greater daily output of cortisol which in the long term increases blood sugar levels.In the nervous system, structural and functional abnormalities are a result of chronic prolonged stress. The increase of stress levels causes a shortening of dendrites in a neuron. Therefore, the shortening of dendrites causes the decrease in attention.[5] Chronic stress also causes greater response to fear of the unlearned in the nervous system, and fear conditioning.In the immune system, the increase in levels of chronic stress results in the elevation of inflammation. The increase in inflammation levels is caused by the ongoing activation of the sympathetic nervous system.[5] The impairment of cell-mediated acquired immunity is also a factor resulting in the immune system due to chronic stress.[5]
Morbidity
Obesity increases the risk of many physical and mental conditions. These comorbidities are most commonly shown in metabolic syndrome,[2] a combination of medical disorders which includes: diabetes mellitus type 2, high blood pressure, high blood cholesterol, and high triglyceride levels.[53]
Complications are either directly caused by obesity or indirectly related through mechanisms sharing a common cause such as a poor diet or a sedentary lifestyle. The strength of the link between obesity and specific conditions varies. One of the strongest is the link with type 2 diabetes. Excess body fat underlies 64% of cases of diabetes in men and 77% of cases in women.[54]
Health consequences fall into two broad categories: those attributable to the effects of increased fat mass (such as osteoarthritis, obstructive sleep apnea, social stigmatization) and those due to the increased number of fat cells (diabetes, cancer, cardiovascular disease, non-alcoholic fatty liver disease).[2][55] Increases in body fat alter the body’s response to insulin, potentially leading to insulin resistance. Increased fat also creates a proinflammatory state,[56][57] and a prothrombotic state.[55][58]
Obesity increases the risk of developing serious illness from coronavirus disease 2019.[59]
Causes of Obesity
At an individual level, a combination of excessive food energy intake and a lack of physical activity is thought to explain most cases of obesity.[88] A limited number of cases are due primarily to genetics, medical reasons, or psychiatric illness.[13] In contrast, increasing rates of obesity at a societal level are felt to be due to an easily accessible and palatable diet,[89] increased reliance on cars, and mechanized manufacturing.[90][91]
A 2006 review identified ten other possible contributors to the recent increase of obesity: (1) insufficient sleep, (2) endocrine disruptors (environmental pollutants that interfere with lipid metabolism), (3) decreased variability in ambient temperature, (4) decreased rates of smoking, because smoking suppresses appetite, (5) increased use of medications that can cause weight gain (e.g., atypical antipsychotics), (6) proportional increases in ethnic and age groups that tend to be heavier, (7) pregnancy at a later age (which may cause susceptibility to obesity in children), (8) epigenetic risk factors passed on generationally, (9) natural selection for higher BMI, and (10) assortative mating leading to increased concentration of obesity risk factors (this would increase the number of obese people by increasing population variance in weight).[92] According to the Endocrine Society, there is “growing evidence suggesting that obesity is a disorder of the energy homeostasis system, rather than simply arising from the passive accumulation of excess weight”.[93]
Sedentary lifestyle
A sedentary lifestyle plays a significant role in obesity.[114] Worldwide there has been a large shift towards less physically demanding work,[115][116][117] and currently at least 30% of the world’s population gets insufficient exercise.[116] This is primarily due to increasing use of mechanized transportation and a greater prevalence of labor-saving technology in the home.[115][116][117] In children, there appear to be declines in levels of physical activity due to less walking and physical education.[118] World trends in active leisure time physical activity are less clear. The World Health Organization indicates people worldwide are taking up less active recreational pursuits, while a study from Finland[119] found an increase and a study from the United States found leisure-time physical activity has not changed significantly.[120] A 2011 review of physical activity in children found that it may not be a significant contributor.[121]
In both children and adults, there is an association between television viewing time and the risk of obesity.[122][123][124] A review found 63 of 73 studies (86%) showed an increased rate of childhood obesity with increased media exposure, with rates increasing proportionally to time spent watching television.[125]
Set point theory of weight
Set point theory, as it pertains to human body weight, states that there is a biological control method in humans that actively regulates weight towards a predetermined set weight for each individual.[1] This may occur through regulation of energy intake (e.g.via increased or decreased appetite) or energy expenditure (e.g. via reduced metabolism or feelings of lethargy).[1][2] Set point theory explains why it is difficult for dieters to maintain weight loss over time, as calorie restriction may become less effective or more difficult to maintain as regulatory mechanisms in the body actively push the body back towards the set point weight.
Set point theory differentiates between active compensation and passive compensation. In active compensation, a regulatory mechanism in the body effects energy expenditure or intake. In passive compensation, a decrease in body fat levels leads to a decrease in energy compensation even without a regulatory mechanism as there is less weight to be carried. Set point theory posits active compensation in addition to passive compensation.[3]
Set point theory can be construed as implying weight regulation in a wide or tight range around the set point,[4] in a symmetric or in an asymmetric manner (i.e. treating weight gain and loss either the same or differently),[4] and may apply to regulation of body fat levels specifically (in a multi-compartment model) or to overall body weight.[5]
Set point theory applies to both downward and upward adjustment of weight.[2][5] This return to the pre-change weight occurs faster than would be expected if individuals simply returned to their normal caloric intake and energy expenditure even after accounting for lower energy needs after weight loss, indicating an active response by the body encouraging weight gain.[3] While the set point applies to both deviations driven by weight loss and weight gain, the set point response driving a person to regain weight to regain the set point is stronger than the response to lose weight after gaining weight above the set point,[5] implying that it may be easier to gain than to lose weight.
Genetics
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A 1680 painting by Juan Carreno de Miranda of a girl presumed to have Prader–Willi syndrome[126]
Like many other medical conditions, obesity is the result of an interplay between genetic and environmental factors.[127] Polymorphisms in various genes controlling appetite and metabolism predispose to obesity when sufficient food energy is present. As of 2006, more than 41 of these sites on the human genome have been linked to the development of obesity when a favorable environment is present.[128] People with two copies of the FTO gene (fat mass and obesity associated gene) have been found on average to weigh 3–4 kg more and have a 1.67-fold greater risk of obesity compared with those without the risk allele.[129] The differences in BMI between people that are due to genetics varies depending on the population examined from 6% to 85%.[130]
Obesity is a major feature in several syndromes, such as Prader–Willi syndrome, Bardet–Biedl syndrome, Cohen syndrome, and MOMO syndrome. (The term “non-syndromic obesity” is sometimes used to exclude these conditions.)[131] In people with early-onset severe obesity (defined by an onset before 10 years of age and body mass index over three standard deviations above normal), 7% harbor a single point DNA mutation.[132]
Studies that have focused on inheritance patterns rather than on specific genes have found that 80% of the offspring of two obese parents were also obese, in contrast to less than 10% of the offspring of two parents who were of normal weight.[133] Different people exposed to the same environment have different risks of obesity due to their underlying genetics.[134]
The thrifty gene hypothesis postulates that, due to dietary scarcity during human evolution, people are prone to obesity. Their ability to take advantage of rare periods of abundance by storing energy as fat would be advantageous during times of varying food availability, and individuals with greater adipose reserves would be more likely to survive famine. This tendency to store fat, however, would be maladaptive in societies with stable food supplies.[135] This theory has received various criticisms, and other evolutionarily-based theories such as the drifty gene hypothesis and the thrifty phenotype hypothesis have also been proposed.[136][137]
Other illnesses
Certain physical and mental illnesses and the pharmaceutical substances used to treat them can increase risk of obesity. Medical illnesses that increase obesity risk include several rare genetic syndromes (listed above) as well as some congenital or acquired conditions: hypothyroidism, Cushing’s syndrome, growth hormone deficiency,[138] and some eating disorders such as binge eating disorder and night eating syndrome.[2] However, obesity is not regarded as a psychiatric disorder, and therefore is not listed in the DSM-IVR as a psychiatric illness.[139] The risk of overweight and obesity is higher in patients with psychiatric disorders than in persons without psychiatric disorders.[140]
Certain medications may cause weight gain or changes in body composition; these include insulin, sulfonylureas, thiazolidinediones, atypical antipsychotics, antidepressants, steroids, certain anticonvulsants (phenytoin and valproate), pizotifen, and some forms of hormonal contraception.[2]
Social determinants
The disease scroll (Yamai no soshi, late 12th century) depicts a woman moneylender with obesity, considered a disease of the rich.
Obesity in developed countries is correlated with economic inequality
While genetic influences are important to understanding obesity, they cannot explain the current dramatic increase seen within specific countries or globally.[141] Though it is accepted that energy consumption in excess of energy expenditure leads to obesity on an individual basis, the cause of the shifts in these two factors on the societal scale is much debated. There are a number of theories as to the cause but most believe it is a combination of various factors.
The correlation between social class and BMI varies globally. A review in 1989 found that in developed countries women of a high social class were less likely to be obese. No significant differences were seen among men of different social classes. In the developing world, women, men, and children from high social classes had greater rates of obesity.[142] An update of this review carried out in 2007 found the same relationships, but they were weaker. The decrease in strength of correlation was felt to be due to the effects of globalization.[143] Among developed countries, levels of adult obesity, and percentage of teenage children who are overweight, are correlated with income inequality. A similar relationship is seen among US states: more adults, even in higher social classes, are obese in more unequal states.[144]
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Many explanations have been put forth for associations between BMI and social class. It is thought that in developed countries, the wealthy are able to afford more nutritious food, they are under greater social pressure to remain slim, and have more opportunities along with greater expectations for physical fitness. In undeveloped countries the ability to afford food, high energy expenditure with physical labor, and cultural values favoring a larger body size are believed to contribute to the observed patterns.[143] Attitudes toward body weight held by people in one’s life may also play a role in obesity. A correlation in BMI changes over time has been found among friends, siblings, and spouses.[145] Stress and perceived low social status appear to increase risk of obesity.[144][146][147]
Smoking has a significant effect on an individual’s weight. Those who quit smoking gain an average of 4.4 kilograms (9.7 lb) for men and 5.0 kilograms (11.0 lb) for women over ten years.[148] However, changing rates of smoking have had little effect on the overall rates of obesity.[149]
In the United States the number of children a person has is related to their risk of obesity. A woman’s risk increases by 7% per child, while a man’s risk increases by 4% per child.[150] This could be partly explained by the fact that having dependent children decreases physical activity in Western parents.[151]
In the developing world urbanization is playing a role in increasing rate of obesity. In China overall rates of obesity are below 5%; however, in some cities rates of obesity are greater than 20%.[152]
Malnutrition in early life is believed to play a role in the rising rates of obesity in the developing world.[153] Endocrine changes that occur during periods of malnutrition may promote the storage of fat once more food energy becomes available.[153]
Consistent with cognitive epidemiological data, numerous studies confirm that obesity is associated with cognitive deficits.[154][155]
Whether obesity causes cognitive deficits, or vice versa is unclear at present.
Public health
Obesity prevention requires a complex approach, including interventions at community, family, and individual levels.[1][11] Changes to diet and exercising are the main treatments recommended by health professionals.[2] Diet quality can be improved by reducing the consumption of energy-dense foods, such as those high in fat or sugars, and by increasing the intake of dietary fiber.[1] However, large-scale analyses have found an inverse relationship between energy density and energy cost of foods in developed nations.[15] Low-income populations are more likely to live in neighborhoods that are considered “food deserts” or “food swamps” where nutritional groceries are less available.[16] Medications can be used, along with a suitable diet, to reduce appetite or decrease fat absorption.[5] If diet, exercise, and medication are not effective, a gastric balloon or surgery may be performed to reduce stomach volume or length of the intestines, leading to feeling full earlier or a reduced ability to absorb nutrients from food.[6][17]
Obesity is a leading preventable cause of death worldwide, with increasing rates in adults and children.[1][18] In 2015, 600 million adults (12%) and 100 million children were obese in 195 countries.[7] Obesity is more common in women than in men.[1] Authorities view it as one of the most serious public health problems of the 21st century.[19] Obesity is stigmatized in much of the modern world (particularly in the Western world), though it was seen as a symbol of wealth and fertility at other times in history and still is in some parts of the world.[2][20] In 2013, several medical societies, including the American Medical Association and the American Heart Association, classified obesity as a disease.[21][22][23]
The World Health Organization (WHO) predicts that overweight and obesity may soon replace more traditional public health concerns such as undernutrition and infectious diseases as the most significant cause of poor health.[169] Obesity is a public health and policy problem because of its prevalence, costs, and health effects.[170] The United States Preventive Services Task Force recommends screening for all adults followed by behavioral interventions in those who are obese.[171] Public health efforts seek to understand and correct the environmental factors responsible for the increasing prevalence of obesity in the population. Solutions look at changing the factors that cause excess food energy consumption and inhibit physical activity. Efforts include federally reimbursed meal programs in schools, limiting direct junk food marketing to children,[172] and decreasing access to sugar-sweetened beverages in schools.[173] The World Health Organization recommends the taxing of sugary drinks.[174] When constructing urban environments, efforts have been made to increase access to parks and to develop pedestrian routes.[175] There is low quality evidence that nutritional labelling with energy information on menus can help to reduce energy intake while dining in restaurants.[176]
stress
Stress eating is consuming food in response to stress, especially when you are not hungry. Similarly, emotional eating is eating in response to feeling. Emotional eating means that your emotions—not your body—dictate when and how much you eat.
Some emotional eaters binge when they are sad or confused. For others, eating can be a way of avoiding thinking about problems or taking the action required to solve them.
So why do we eat when we are stressed? Because for most of us, food offers comfort. And unfortunately, the least healthy foods usually offer the most comfort.
If we reached for veggies in times of emotional discomfort, we’d be OK. But how many people turn to carrot sticks when they’re feeling stressed? It’s the high-fat, high-calorie foods we love that make us feel better. The more fattening, sweeter or the saltier the food, the better we seem to feel.
Management of Obesity
The main treatment for obesity consists of weight loss via calorie restricted dieting and physical exercise.[21][88][183][184] Dieting, as part of a lifestyle change, produces sustained weight loss, despite slow weight regain over time.[21][185][186][187] Although 87% of participants in the National Weight Control Registry were able to maintain 10% body weight loss for 10 years,[188] the most appropriate dietary approach for long term weight loss maintenance is still unknown.[189] Intensive behavioral interventions combining both dietary changes and exercise are recommended.[21][183][190] Intermittent fasting has no additional benefit of weight loss compared to continuous energy restriction.[189] Adherence is a more important factor in weight loss success than whatever kind of diet an individual undertakes.[189][191]
Several hypo-caloric diets are effective.[21] In the short-term low carbohydrate diets appear better than low fat diets for weight loss.[192] In the long term, however, all types of low-carbohydrate and low-fat diets appear equally beneficial.[192][193] A 2014 review found that the heart disease and diabetes risks associated with different diets appear to be similar.[194] Promotion of the Mediterranean diets among the obese may lower the risk of heart disease.[192] Decreased intake of sweet drinks is also related to weight-loss.[192] Success rates of long-term weight loss maintenance with lifestyle changes are low, ranging from 2–20%.[195] Dietary and lifestyle changes are effective in limiting excessive weight gain in pregnancy and improve outcomes for both the mother and the child.[196] Intensive behavioral counseling is recommended in those who are both obese and have other risk factors for heart disease.[197]
Medical interventions
The most effective treatment for obesity is bariatric surgery.[6][21] The types of procedures include laparoscopic adjustable gastric banding, Roux-en-Y gastric bypass, vertical-sleeve gastrectomy, and biliopancreatic diversion.[198] Surgery for severe obesity is associated with long-term weight loss, improvement in obesity-related conditions,[203] and decreased overall mortality, however, improved metabolic health results from the weight loss, not the surgery.[204] One study found a weight loss of between 14% and 25% (depending on the type of procedure performed) at 10 years, and a 29% reduction in all cause mortality when compared to standard weight loss measures.[205] Complications occur in about 17% of cases and reoperation is needed in 7% of cases.[203] Due to its cost and risks, researchers are searching for other effective yet less invasive treatments including devices that occupy space in the stomach.[206] For adults who have not responded to behavioral treatments with or without medication, the US guidelines on obesity recommend informing them about bariatric surgery.[183]
How Cognitive Behavioral Therapy Can Help Treat Food Addiction
If you have difficulty with overeating, you may wonder whether cognitive behavioral therapy (CBT) can help you stop your problem behaviors and food addiction. This example puts you in the place of a fictitious person who has characteristics and circumstances often seen in people who come for treatment for food addiction. This can show you what happens in CBT and how it can help people stop overeating.
You are a binge eater who binges on candy, cookies, and chocolate several times a day. Your overeating started in childhood when you would eat candy in secret at night. You describe your binges as emotional eating because you eat when you felt upset.
You do everything you can to prevent weight gain, including skipping regular meals, exercising for hours, using laxatives to “clear yourself out,” and occasionally, making yourself vomit. Your family doctor became concerned that you were developing problems with incontinence from laxative overuse, and she referred you to CBT to help you stop overeating.
Overeating Due to Emotional Reasoning
Your cognitive-behavioral therapist guides you in recording the thoughts and feelings you experience before, during and after bingeing on sweet food. By analyzing the thoughts and feelings you have around food, you and your therapist come to understand that you are emotional eating and possibly even binge eating in response to negative emotions due to faulty thinking (cognitive distortions).
For example, if someone pushed in front of you in line, you would feel that this must mean you are a worthless person, and you would immediately buy a bar of chocolate to eat and make yourself feel better. One day, a colleague didn’t respond when you said “Good morning,” and you reasoned this was because your colleague disliked you.
Each time a minor disappointment of this sort occurred, which was almost daily, you would go to your secret stash of chocolate or head to the grocery store for a binge. In spite of this well-established pattern of behavior, although you wanted to stop overeating, you just did not know another way to handle your uncomfortable feelings of worthlessness.
The CBT therapist explains to you that your binge eating is based on emotional reasoning and, although eating might make you feel temporarily comforted, would not help you feel better about yourself. In fact, overeating was having the opposite effect and was actually making you feel worse about yourself, which would then worsen your overeating.
CBT for Children
Childhood OBESITY
The healthy BMI range varies with the age and sex of the child. Obesity in children and adolescents is defined as a BMI greater than the 95th percentile.[29] The reference data that these percentiles are based on is from 1963 to 1994 and thus has not been affected by the recent increases in rates of obesity.[30] Childhood obesity has reached epidemic proportions in the 21st century, with rising rates in both the developed and the developing world. Rates of obesity in Canadian boys have increased from 11% in the 1980s to over 30% in the 1990s, while during this same time period rates increased from 4 to 14% in Brazilian children.[256] In the UK, there were 60% more obese children in 2005 compared to 1989.[257] In the US, the percentage of overweight and obese children increased to 16% in 2008, a 300% increase over the prior 30 years.[258]
As with obesity in adults, many factors contribute to the rising rates of childhood obesity. Changing diet and decreasing physical activity are believed to be the two most important causes for the recent increase in the incidence of child obesity.[259] Antibiotics in the first 6 months of life have been associated with excess weight at age seven to twelve years of age.[158] Because childhood obesity often persists into adulthood and is associated with numerous chronic illnesses, children who are obese are often tested for hypertension, diabetes, hyperlipidemia, and fatty liver disease.[88] Treatments used in children are primarily lifestyle interventions and behavioral techniques, although efforts to increase activity in children have had little success.[260] In the United States, medications are not FDA approved for use in this age group.[256] Multi-component behaviour change interventions that include changes to dietary and physical activity may reduce BMI in the short term in children aged 6 to 11 years, although the benefits are small and quality of evidence is low.[261]
Other animals
Obesity in pets is common in many countries. In the United States, 23–41% of dogs are overweight, and about 5.1% are obese.[262] The rate of obesity in cats was slightly higher at 6.4%.[262] In Australia the rate of obesity among dogs in a veterinary setting has been found to be 7.6%.[263] The risk of obesity in dogs is related to whether or not their owners are obese; however, there is no similar correlation between cats and their owners.[264]
