Definition Essay On Obesity

For the medical journal, see Obesity (journal).

Obesity
Silhouettes and waist circumferences representing optimal, overweight, and obese
SpecialtyEndocrinology
SymptomsIncreased fat[1]
ComplicationsCardiovascular diseases, type 2 diabetes, obstructive sleep apnea, certain types of cancer, osteoarthritis, depression[2][3]
CausesExcessive food, lack of exercise, genetics[1][4]
Diagnostic methodBMI > 7002294199500000000♠30 kg/m2[1]
PreventionSocietal changes, personal choices[1]
TreatmentDiet, exercise, medications, surgery[1][5][6]
PrognosisReduce life expectancy[2]
Frequency700 million / 12% (2015)[7]

[edit on Wikidata]

Obesity is a medical condition in which excess body fat has accumulated to the 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, is over 7002294199500000000♠30 kg/m2, with the range 7002245166250000000♠25–30 kg/m2 defined as overweight.[1] Some East Asian countries use lower values.[8] Obesity increases the likelihood of various diseases and conditions, particularly cardiovascular diseases, type 2 diabetes, obstructive sleep apnea, certain types of cancer, osteoarthritis and depression.[2][3]

Obesity is most commonly caused by a combination of excessive food intake, lack of physical activity, and genetic susceptibility.[1][4] A few cases are caused primarily by genes, endocrine disorders, medications, or mental disorder.[9] The view that obese people eat little yet gain weight due to a slow metabolism is not generally supported.[10] On average, obese people have a greater energy expenditure than their normal counterparts due to the energy required to maintain an increased body mass.[10][11]

Obesity is mostly preventable through a combination of social changes and personal choices.[1] Changes to diet and exercising are the main treatments.[2] Diet quality can be improved by reducing the consumption of energy-dense foods, such as those high in fat and sugars, and by increasing the intake of dietary fiber.[1]Medications may 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][12]

Obesity is a leading preventable cause of death worldwide, with increasing rates in adults and children.[1][13] In 2015, 600 million adults (12%) and 100 million children were obese.[7] Obesity is more common in women than men.[1] Authorities view it as one of the most serious public health problems of the 21st century.[14] 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][15] In 2013, the American Medical Association classified obesity as a disease.[16][17]

Classification

Main article: Classification of obesity

BMI (kg/m2)Classification[18]
fromup to
18.5underweight
18.525.0normal weight
25.030.0overweight
30.035.0class I obesity
35.040.0class II obesity
40.0class III obesity  

Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health.[19] It is defined by body mass index (BMI) and further evaluated in terms of fat distribution via the waist–hip ratio and total cardiovascular risk factors.[20][21] BMI is closely related to both percentage body fat and total body fat.[22] In children, a healthy weight varies with age and sex. Obesity in children and adolescents is defined not as an absolute number but in relation to a historical normal group, such that obesity is a BMI greater than the 95th percentile.[23] The reference data on which these percentiles were based date from 1963 to 1994, and thus have not been affected by the recent increases in weight.[24] BMI is defined as the subject's weight divided by the square of their height and is calculated as follows.

,
where m and h are the subject's weight and height respectively.

BMI is usually expressed in kilograms per square metre, resulting when weight is measured in kilograms and height in metres. To convert from pounds per square inch multiply by 703 (kg/m2)/(lb/sq in).[25]

The most commonly used definitions, established by the World Health Organization (WHO) in 1997 and published in 2000, provide the values listed in the table.[26][27]

Some modifications to the WHO definitions have been made by particular organizations.[28] The surgical literature breaks down class II and III obesity into further categories whose exact values are still disputed.[29]

  • Any BMI ≥ 35 or 40 kg/m2 is severe obesity.
  • A BMI of ≥ 35 kg/m2 and experiencing obesity-related health conditions or ≥40–44.9 kg/m2 is morbid obesity.
  • A BMI of ≥ 45 or 50 kg/m2 is super obesity.

As Asian populations develop negative health consequences at a lower BMI than Caucasians, some nations have redefined obesity; Japan have defined obesity as any BMI greater than 25 kg/m2[8] while China uses a BMI of greater than 28 kg/m2.[28]

Effects 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][30] As a result, obesity has been found to reduce life expectancy.[2]

Mortality

Obesity is one of the leading preventable causes of death worldwide.[32][33][34] A number of reviews have found that mortality risk is lowest at a BMI of 20–25 kg/m2[35][36][37] in non-smokers and at 24–27 kg/m2 in current smokers, with risk increasing along with changes in either direction.[38][39] This appears to apply in at least four continents.[37] 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).[40] 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.[41] In Asians the risk of negative health effects begins to increase between 22–25 kg/m2.[42] A BMI above 32 kg/m2 has been associated with a doubled mortality rate among women over a 16-year period.[43] In the United States, obesity is estimated to cause 111,909 to 365,000 deaths per year,[2][34] while 1 million (7.7%) of deaths in Europe are attributed to excess weight.[44][45] On average, obesity reduces life expectancy by six to seven years,[2][46] a BMI of 30–35 kg/m2 reduces life expectancy by two to four years,[36] while severe obesity (BMI > 40 kg/m2) reduces life expectancy by ten years.[36]

Morbidity

Main article: Obesity-associated 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.[47]

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.[48]

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][49] Increases in body fat alter the body's response to insulin, potentially leading to insulin resistance. Increased fat also creates a proinflammatory state,[50][51] and a prothrombotic state.[49][52]

Survival paradox

See also: Obesity paradox

Although the negative health consequences of obesity in the general population are well supported by the available evidence, health outcomes in certain subgroups seem to be improved at an increased BMI, a phenomenon known as the obesity survival paradox.[74] The paradox was first described in 1999 in overweight and obese people undergoing hemodialysis,[74] and has subsequently been found in those with heart failure and peripheral artery disease (PAD).[75]

In people with heart failure, those with a BMI between 30.0 and 34.9 had lower mortality than those with a normal weight. This has been attributed to the fact that people often lose weight as they become progressively more ill.[76] Similar findings have been made in other types of heart disease. People with class I obesity and heart disease do not have greater rates of further heart problems than people of normal weight who also have heart disease. In people with greater degrees of obesity, however, the risk of further cardiovascular events is increased.[77][78] Even after cardiac bypass surgery, no increase in mortality is seen in the overweight and obese.[79] One study found that the improved survival could be explained by the more aggressive treatment obese people receive after a cardiac event.[80] Another found that if one takes into account chronic obstructive pulmonary disease (COPD) in those with PAD, the benefit of obesity no longer exists.[75]

Causes

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.[81] A limited number of cases are due primarily to genetics, medical reasons, or psychiatric illness.[9] In contrast, increasing rates of obesity at a societal level are felt to be due to an easily accessible and palatable diet,[82] increased reliance on cars, and mechanized manufacturing.[83][84]

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).[85] While there is evidence supporting the influence of these mechanisms on the increased prevalence of obesity, the evidence is still inconclusive, and the authors state that these are probably less influential than the ones discussed in the previous paragraph.

Diet

Main article: Diet and obesity

A 2016 review supported excess food as the primary factor.[87]Dietary energy supply per capita varies markedly between different regions and countries. It has also changed significantly over time.[86] From the early 1970s to the late 1990s the average food energy available per person per day (the amount of food bought) increased in all parts of the world except Eastern Europe. The United States had the highest availability with 3,654 calories (15,290 kJ) per person in 1996.[86] This increased further in 2003 to 3,754 calories (15,710 kJ).[86] During the late 1990s Europeans had 3,394 calories (14,200 kJ) per person, in the developing areas of Asia there were 2,648 calories (11,080 kJ) per person, and in sub-Saharan Africa people had 2,176 calories (9,100 kJ) per person.[86][88] Total food energy consumption has been found to be related to obesity.[89]

The widespread availability of nutritional guidelines[90] has done little to address the problems of overeating and poor dietary choice.[91] From 1971 to 2000, obesity rates in the United States increased from 14.5% to 30.9%.[92] During the same period, an increase occurred in the average amount of food energy consumed. For women, the average increase was 335 calories (1,400 kJ) per day (1,542 calories (6,450 kJ) in 1971 and 1,877 calories (7,850 kJ) in 2004), while for men the average increase was 168 calories (700 kJ) per day (2,450 calories (10,300 kJ) in 1971 and 2,618 calories (10,950 kJ) in 2004). Most of this extra food energy came from an increase in carbohydrate consumption rather than fat consumption.[93] The primary sources of these extra carbohydrates are sweetened beverages, which now account for almost 25 percent of daily food energy in young adults in America,[94] and potato chips.[95] Consumption of sweetened drinks such as soft drinks, fruit drinks, iced tea, and energy and vitamin water drinks is believed to be contributing to the rising rates of obesity[96][97] and to an increased risk of metabolic syndrome and type 2 diabetes.[98]Vitamin D deficiency is related to diseases associated with obesity.[99]

As societies become increasingly reliant on energy-dense, big-portions, and fast-food meals, the association between fast-food consumption and obesity becomes more concerning.[100] In the United States consumption of fast-food meals tripled and food energy intake from these meals quadrupled between 1977 and 1995.[101]

Agricultural policy and techniques in the United States and Europe have led to lower food prices. In the United States, subsidization of corn, soy, wheat, and rice through the U.S. farm bill has made the main sources of processed food cheap compared to fruits and vegetables.[102]Calorie count laws and nutrition facts labels attempt to steer people toward making healthier food choices, including awareness of how much food energy is being consumed.

Obese people consistently under-report their food consumption as compared to people of normal weight.[103] This is supported both by tests of people carried out in a calorimeter room[104] and by direct observation.

Sedentary lifestyle

See also: Sedentary lifestyle and Exercise trends

A sedentary lifestyle plays a significant role in obesity.[105] Worldwide there has been a large shift towards less physically demanding work,[106][107][108] and currently at least 30% of the world's population gets insufficient exercise.[107] This is primarily due to increasing use of mechanized transportation and a greater prevalence of labor-saving technology in the home.[106][107][108] In children, there appear to be declines in levels of physical activity due to less walking and physical education.[109] 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[110] found an increase and a study from the United States found leisure-time physical activity has not changed significantly.[111] A 2011 review of physical activity in children found that it may not be a significant contributor.[112]

In both children and adults, there is an association between television viewing time and the risk of obesity.[113][114][115] 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.[116]

Genetics

Main article: Genetics of obesity

Like many other medical conditions, obesity is the result of an interplay between genetic and environmental factors.[118]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.[119] 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.[120] The differences in BMI between people that are due to genetics varies depending on the population examined from 6% to 85%.[121]

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.)[122] 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.[123]

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.[124] Different people exposed to the same environment have different risks of obesity due to their underlying genetics.[125]

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.[126] 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.[127][128]

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,[129] and the eating disorders: 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.[130] The risk of overweight and obesity is higher in patients with psychiatric disorders than in persons without psychiatric disorders.[131]

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

Main article: Social determinants of obesity

While genetic influences are important to understanding obesity, they cannot explain the current dramatic increase seen within specific countries or globally.[132] 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.[133] 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.[134] 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.[135]

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.[134] 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.[136] Stress and perceived low social status appear to increase risk of obesity.[135][137][138]

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.[139] However, changing rates of smoking have had little effect on the overall rates of obesity.[140]

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.[141] This could be partly explained by the fact that having dependent children decreases physical activity in Western parents.[142]

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%.[143]

Malnutrition in early life is believed to play a role in the rising rates of obesity in the developing world.[144] Endocrine changes that occur during periods of malnutrition may promote the storage of fat once more food energy becomes available.[144]

Consistent with cognitive epidemiological data, numerous studies confirm that obesity is associated with cognitive deficits.[145] Whether obesity causes cognitive deficits, or vice versa is unclear at present.

Gut bacteria

See also: Infectobesity

The study of the effect of infectious agents on metabolism is still in its early stages. Gut flora has been shown to differ between lean and obese humans. There is an indication that gut flora in obese and lean individuals can affect the metabolic potential. This apparent alteration of the metabolic potential is believed to confer a greater capacity to harvest energy contributing to obesity. Whether these differences are the direct cause or the result of obesity has yet to be determined unequivocally.[146]

An association between viruses and obesity has been found in humans and several different animal species. The amount that these associations may have contributed to the rising rate of obesity is yet to be determined.[147]

Pathophysiology

Main article: Pathophysiology of obesity

There are many possible pathophysiological mechanisms involved in the development and maintenance of obesity.[148] This field of research had been almost unapproached until the leptin gene was discovered in 1994 by J. M. Friedman's laboratory.[149] While leptin and ghrelin are produced peripherally, they control appetite through their actions on the central nervous system. In particular, they and other appetite-related hormones act on the hypothalamus, a region of the brain central to the regulation of food intake and energy expenditure. There are several circuits within the hypothalamus that contribute to its role in integrating appetite, the melanocortin pathway being the most well understood.[148] The circuit begins with an area of the hypothalamus, the arcuate nucleus, that has outputs to the lateral hypothalamus (LH) and ventromedial hypothalamus (VMH), the brain's feeding and satiety centers, respectively.[150]

The arcuate nucleus contains two distinct groups of neurons.[148] The first group coexpresses neuropeptide Y (NPY) and agouti-related peptide (AgRP) and has stimulatory inputs to the LH and inhibitory inputs to the VMH. The second group coexpresses pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) and has stimulatory inputs to the VMH and inhibitory inputs to the LH. Consequently, NPY/AgRP neurons stimulate feeding and inhibit satiety, while POMC/CART neurons stimulate satiety and inhibit feeding. Both groups of arcuate nucleus neurons are regulated in part by leptin. Leptin inhibits the NPY/AgRP group while stimulating the POMC/CART group. Thus a deficiency in leptin signaling, either via leptin deficiency or leptin resistance, leads to overfeeding and may account for some genetic and acquired forms of obesity.[148]

Public health

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.[151] Obesity is a public health and policy problem because of its prevalence, costs, and health effects.[152] The United States Preventive Services Task Force recommends screening for all adults followed by behavioral interventions in those who are obese.[153] 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 junkfood marketing to children,[154] and decreasing access to sugar-sweetened beverages in schools.[155] The World Health Organization recommends the taxing of sugary drinks.[156] When constructing urban environments, efforts have been made to increase access to parks and to develop pedestrian routes.[157]

Reports

Many organizations have published reports pertaining to obesity. In 1998, the first US Federal guidelines were published, titled "Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report".[158] In 2006 the Canadian Obesity Network published the "Canadian Clinical Practice Guidelines (CPG) on the Management and Prevention of Obesity in Adults and Children". This is a comprehensive evidence-based guideline to address the management and prevention of overweight and obesity in adults and children.[81]

In 2004, the United Kingdom Royal College of Physicians, the Faculty of Public Health and the Royal College of Paediatrics and Child Health released the report "Storing up Problems", which highlighted the growing problem of obesity in the UK.[159] The same year, the House of CommonsHealth Select Committee published its "most comprehensive inquiry [...] ever undertaken" into the impact of obesity on health and society in the UK and possible approaches to the problem.[160] In 2006, the National Institute for Health and Clinical Excellence (NICE) issued a guideline on the diagnosis and management of obesity, as well as policy implications for non-healthcare organizations such as local councils.[161] A 2007 report produced by Derek Wanless for the King's Fund warned that unless further action was taken, obesity had the capacity to cripple the National Health Service financially.[162]

Comprehensive approaches are being looked at to address the rising rates of obesity. The Obesity Policy Action (OPA) framework divides measure into 'upstream' policies, 'midstream' policies, 'downstream' policies. 'Upstream' policies look at changing society, 'midstream' policies try to alter individuals' behavior to prevent obesity, and 'downstream' policies try to treat currently afflicted people.[163]

Management

Main article: Management of obesity

The main treatment for obesity consists of dieting and physical exercise.[81] Diet programs may produce weight loss over the short term,[164] but maintaining this weight loss is frequently difficult and often requires making exercise and a lower food energy diet a permanent part of a person's lifestyle.[165][166]

In the short-term low carbohydrate diets appear better than low fat diets for weight loss.[167] In the long term; however, all types of low-carbohydrate and low-fat diets appear equally beneficial.[167][168] A 2014 review found that the heart disease and diabetes risks associated with different diets appear to be similar.[169] Promotion of the Mediterranean diets among the obese may lower the risk of heart disease.[167] Decreased intake of sweet drinks is also related to weight-loss.[167] Success rates of long-term weight loss maintenance with lifestyle changes are low, ranging from 2–20%.[170] Dietary and lifestyle changes are effective in limiting excessive weight gain in pregnancy and improve outcomes for both the mother and the child.[171] Intensive behavioral counseling is recommended in those who are both obese and have other risk factors for heart disease.[172]

Five medications have evidence for long-term use orlistat, lorcaserin, liraglutide, phentermine–topiramate, and naltrexone–bupropion.[173] They result in weight loss after one year ranged from 3.0 to 6.7 kg over placebo.[173] Orlistat, liraglutide, and naltrexone–bupropion are available in both the United States and Europe, whereas lorcaserin and phentermine–topiramate are available only in the United States.[174] European regulatory authorities rejected the latter two drugs in part because of associations of heart valve problems with lorcaserin and more general heart and blood vessel problems with phentermine–topiramate.[174] Orlistat use is associated with high rates of gastrointestinal side effects[175] and concerns have been raised about negative effects on the kidneys.[176] There is no information on how these drugs affect longer-term complications of obesity such as cardiovascular disease or death.[5]

The most effective treatment for obesity is bariatric surgery

A "super obese" male with a BMI of 53 kg/m2: weight 182 kg (400 lb), height 185 cm (6 ft 1 in). He presents with stretch marks and enlarged breasts

Relative risk of death over 10 years for white men (left) and women (right) who have never smoked in the United States by BMI.[31]

1961

2001–03

Map of dietary energy availability per person per day in 1961 (left) and 2001–2003 (right)[86] Calories per person per day (kilojoules per person per day)

  no data

  <1,600 (<6,700)

  1,600–1,800 (6,700–7,500)

  1,800–2,000 (7,500–8,400)

  2,000–2,200 (8,400–9,200)

  2,200–2,400 (9,200–10,000)

  2,400–2,600 (10,000–10,900)

  2,600–2,800 (10,900–11,700)

  2,800–3,000 (11,700–12,600)

  3,000–3,200 (12,600–13,400)

  3,200–3,400 (13,400–14,200)

  3,400–3,600 (14,200–15,100)

  >3,600 (>15,100)

Average per capita energy consumption of the world from 1961 to 2002[86]
The disease scroll (Yamai no soshi, late 12th century) depicts a woman moneylender with obesity, considered a disease of the rich.
A comparison of a mouse unable to produce leptin thus resulting in obesity (left) and a normal mouse (right)

It has long been debated whether obesity is a relative measure and should not be used as a stigma to label overweight people. However, the fact is, when the weight of a person significantly exceeds a certain norm for their age and gender, the health and well-being of a person tends to generally decrease in quality. Obesity might not be a serious disease in the commonly established meaning of this term, since it is not contagious like the flu, irreversible like AIDs, or deadly like cancer. Yet it has been proven there are numerous links to a higher probability of heart-related diseases, depression and passiveness, diabetes, and premature aging of the body as a whole and the brain in particular. Moreover, obesity decreases the general quality of life, since it becomes difficult for an obese person to enjoy simple activities, stay energetic and active, succeed in sports, and enjoy a full-range diet. Thus, when talking about obesity in a country like America, where the problem is especially acute and critical, we need to consider the most probable causes and factors of obesity in order to come up with an effective health program to deal with this issue in the United States.

Obesity can be argued to be genetically predisposed and there is little governments and NGOs can do about this fact. It is true that some people are born with a higher probability of being overweight and eventually obese than others (Porps 73). However, such predisposition cannot be considered a purely “American problem” since it is almost equally spread amongst different races and ethnicities. Statistically, around 20% of people in the world suffer from obesity. However, this number is significantly higher for the US population. Thus, we need to look at those factors that could explain why the problem of obesity is more serious in America than in, for example, Germany, Russia, or Brazil. One of such factors is the factor of eating habits.

Americans have a tendency towards substantial fast food and soft drink consumption. Eating french fries, pizza, cheeseburgers, and drinking Coca-Cola are the top metabolism inhibitors in modern American society. By consuming such foods and drinks regularly, American teenagers, adults, and children slow down their metabolism by up to 12 times, as research has proven (Henrix 122). This means the same amount of food will be digested and absorbed 12 times slower by an American teen than by a healthy-eating Russian or African child. Moreover, numerous health issues such as ulcers, dysbacteriosis, cholecystitis, and diabetes, which are also directly related to one’s eating habits, have a negative influence on a person’s weight and the amount of fat in a body. Hence, when working towards decreasing obesity rates, we need to start from completely changing our dietary habits and refraining from eating fast foods or drinking soft drinks.

Another point to consider when talking about American dieting habits is the lack of fresh fruits and vegetables in their everyday ration. We seem to think a glass of orange juice, watered down from concentrate and flavored with artificial sweeteners, or a few grapes on top of a cupcake for dessert, or a bowl of spinach salad for dinner, does the trick and provides the necessary amount of vitamins, microelements, and minerals for our body and mind. However, this is far from being true, as dietitians inform. Five different fruits and five different vegetables a day is the minimum requirement for healthy development (Parker 56). The key is to eat in variety and to eat fresh, garden-grown products. In the United States, there are few places where fresh, recently-picked, and naturally-grown fruits and vegetables are sold at local markets. In the majority of cases, it is the supermarket chains which distribute such products to Americans across the country. Fruit and vegetables from a supermarket, like Wallmart or Safeway, do not supply us with even half of the valuable nutrients compared to fruits and vegetables from one’s own garden, picked right before consumption and grown without using pesticides and fertilizers.

Unfortunately, keeping our own gardens and growing our own fruits and vegetables is not an act most Americans are able or willing to do. Then, is there a solution? Organic food, which many consider to be rather pricy, is in fact much healthier than what we are offered in the regular chain supermarkets. When it comes to health, prevention and precaution are less expensive than the treatment afterwards. The solution that is most suitable for an average American family is to shop organic, fresh, and healthy, choosing vegetables and fruits over unhealthy calorie-booster snacks like chips, pretzels, and donuts (Open 43).

One more important factor we often forget about when investigating the reasons for high obesity rates in the United States is the factor of portion size. Comparative studies have often proven the size of an average serving portion in America is many times higher than in the majority of other countries. For instance, one portion of pasta in an average American middle-class restaurant can be split into 3.6 Japanese portions, 3.2 Chinese portions, 3.1 French portions, 2.8 Russian portions, 2.3 Polish portions and 2.2 Italian portions (Kin 21). Do Americans need to eat this much? We are not the tallest or the most active nation in the world, but for some reason, we consume twice as much as the Dutch, who ride bicycles while we drive cars, or the Russians, who walk by foot an average of 2.9 miles a day while we barely do half a mile. Americans are getting used to eating more than their body needs since early childhood. Next time we go to a restaurant to order a full bowl of salad followed by a huge plate of spaghetti and a glass of ice tea, we need to remind ourselves how our stomachs are only the size of an average man’s fist normally, but not if you stuff it with loads of food.

Whether we like to admit it or not, obesity is a problem for Americans. The quality of life and the state of health of Americans is much lower than it should be. Some may argue they try to live an active life, doing sports and participate in community activities, but they still have weight problems. This is the case for many Americans who forget that along with changing their lifestyle, going to a gym and running in the mornings, they need to cardinally change their eating habits, consume more fresh and healthy natural foods, stop eating junk food, lessen their portions by half and start eating smart.

References

Porps, Brain. Genetic Basis of Obesity. Cambridge: Cambridge Press, 2011. Print.

Henrix, William. Soft Drinks and Metabolism. Seattle: Rain City Press, 2010. Print.

Parker, Jones. The Five Secrets to Food. Connecticut: Bridge Publishing, 2009. Print.

Open, Rimpa. How to Shop Organic in a Non-Organic Society . London: Ioatolla Press, 2008. Print.

Kin, Richard. Portions of Mind and Stomach. New York: Boulevard Publishing, 2009. Print.

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