Abstract

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The increase in the prevalence of obesity in the United States has been attributed to an environment that promotes a sedentary lifestyle and offers an abundance of energy rich affordable foods. Close examination of historical trends in occupational physical activity and the consumer price index for various food categories do not necessarily support such a view. It is proposed that the increase in the prevalence of obesity in the United States can be attributed to progress in the prevention and the treatment of oral and gastrointestinal disorders which reached a critical mass during the period from 1958 to 1970 prior to the onset of United States obesity epidemic. Time trend analysis shows that the prevalence of dental caries, peptic ulcer and the mortality rate from diarrhea decreased, while the prevalence of gastro-esophageal reflux disease increased prior to or concurrent with the increase in the prevalence of obesity. Furthermore, the number and scope of preventive or treatment measures for dental caries, malocclusion, dentine sensitivity, gastro-esophageal reflux disease and diarrhea increased during the same period. Improvements in the prevention and treatment of dental caries and malocclusion produced a more efficient masticatory apparatus which enabled people to consume more food, while treatment of dentine sensitivity enabled people to consume more sugar containing foods and beverages. Effective suppression of gastric acid enabled people to eat more foods without experiencing heartburn, and better treatment of diarrheal diseases enabled people to absorb more nutrients from the ingested food. The overall improvement in the health and efficiency of the alimentary canal should be considered as a possible alternative explanation for the development of the United States obesity epidemic.

Introduction

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The United States population experienced a dramatic increase in the prevalence of obesity in the latter part of the twentieth century. This increase, which began in 1978 (1,2) and continues to this day, is commonly referred to as the United States obesity epidemic (3). Many theories have been formulated to explain this increase in obesity (4,5). Most of those theories however, explain why some people gain weight while others don’t, without explaining the sudden increase in obesity in the late 1970s that developed into an epidemic. The most widely accepted theory that addresses the epidemic of obesity in the United States attributes the increase in the prevalence of obesity to an environment which promotes a sedentary lifestyle and encourages the consumption of relatively cheap energy dense foods (6,7,3).

The increase in the prevalence of obesity began at a time when the United States experienced a fitness revolution, as evidenced by the popularity of jogging in the 1970s, aerobic exercise in the 1980s, and resistance training in the 1990s. Furthermore, the number of girls and women competing in sports grew exponentially as a result of the passage of the 1972 federal law giving women equal opportunity in sports (8). At the same time, the American public became more aware of the importance of nutrition in health due to the increased attention given in the mass media to the role of lipids and cholesterol in heart disease which led to the proliferation of diet programs (9), and a decline in fat consumption after 1980 (10). The historical context of the United States obesity epidemic therefore, contradicts the environmental theory of obesity which is currently the prevailing opinion concerning obesity in the United States.

The purpose of this communication is to examine critically the environmental theory of obesity and propose an alternative theory which postulates that progress in the prevention and treatment of the disorders of the alimentary canal was responsible for the United States obesity epidemic.

Methods

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General Considerations: Only those diseases or conditions of the alimentary canal that affect a substantial portion of the U.S. population and have a demonstrable effect on body weight or nutrient intake, or their prevention or treatment has an effect on body weight or nutrient intake, were selected for inclusion. All numerical data displayed in tables 1, 2 and 3 came from studies or surveys that were conducted in the United States. Whenever necessary, numerical results were extrapolated from graphs and histograms. Sometimes results from more than one study were combined into a single series, if the age and gender of the populations under study were similar. If the same result was provided separately for men and women such results were combined into averages assuming a one to one ratio of males to females, and provided that those results represented very large samples. Time trends were expressed in terms of the first year of the decade in table 1, or in terms of decades in tables 2 and 3, with each decade usually referring to the span of 0 to 9. Whenever possible a ten year interval was maintained between successive data within the same series, but in some cases the particular data merely represented a year within that decade. If data were available for every year, the middle year of the decade was the usual choice. If not, the middle was created from equidistant years if enough yearly data were available. If data from only one year or segment of a decade was available, then that particular year or the midpoint of that segment represented the decade. In some cases data for a segment of a decade were used to represent single years provided that the single year fell within the segment except in one case where the year in question missed the segment by one year.

Determinants of Energy Balance: The data on the age adjusted prevalence of obesity in the United States were based on the results obtained by the National Health and Nutrition Examination Survey (NHANES) (11). For the purpose of this study, obesity was defined as equivalent to a body mass index (BMI) equal to or greater than 30. Data on caloric intake were also based on results obtained by the NHANES (12). The average annual consumer price index of food items were obtained from data published by the United States Bureau of Labor Statistics (13). The per capita consumption of fruits and vegetables and soft drinks were based on data published by the United States Department of Agriculture (14). Historical trends of television viewing time for children were not available; therefore television viewing times for the general population were used instead (15), assuming that an increase in television viewing or ownership by households is likely to cause a parallel increase in television viewing among children. Data on occupational energy expenditure were based on descriptions in Current Employment Statistics of the Department of Labor (16).

Dental Health: The data for the prevalence of dental caries in the general population were obtained from the NHANES (17,18). The caries status of each person was assessed by the total number of decayed, missing and filled teeth known as the DMFT score. The median age of the groups selected fell in the range from 28 to 29.5 years. (17,18). Water fluoridation data were based on the Fluoridation Census carried out by the Centers for Disease Control (19,20). Data on the number of dental procedures were based on the Survey of Dental Practice and Services Rendered published by the American Dental Association. (21).

Gastro-esophageal Reflux Disease and Peptic Ulcer: The prevalence of Gastro-esophageal reflux disease was based on the number of hospitalizations for white male veterans at all Veterans Administration hospitals throughout the United States obtained from the records of the Department of Veterans Affairs (22). The data for peptic ulcer referred to patient visits to the physicians’ office and antacid therapy referred to the percentage of antacid drugs among all drugs used to treat gastric and other ulcers of unspecified site. Both data were based on statistics from the National Diseases Therapeutic Index compiled by IMS America (23).

Diarrhea: Data about diarrheal disease burden was based on the mortality rate for diarrheal diseases among American children published by the Centers for Disease Control (24). Although these data do not represent the actual prevalence of diarrheal diseases in the United States, their change suggests improvements in prevention or treatment of diarrheal diseases in the United States or perhaps in the prevalence of diarrheal diseases. Data about antibiotic and antimicrobial drug use came from the National Prescription Audit (25) which records all antibiotics sold in pharmacies and the National Ambulatory Medical Care Survey (26) which gathers prescription data from practicing physicians. Since the second survey does not cover all prescriptions issued in the United States, the two surveys were treated separately and comparisons were made only within each survey.

Results

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The Environmental Theory of Obesity:  The first part of the environmental theory postulates that the U.S. obesity epidemic was brought about by a shift from an active to a sedentary lifestyle. In adults, this shift was primarily caused by the transition from an industrial to a service based economy (7, 16). As more and more Americans left manufacturing jobs and joined service related jobs, nationwide occupational physical activity declined, causing Americans to spend less energy (16, 6). In support of this theory, a recent comprehensive study (16) showed that both occupational physical activity and occupational energy expenditure declined between 1960 and 2000.  However, time trend comparison of the decrease in occupational energy expenditure with the increase in the prevalence of obesity does not support such a conclusion. While occupational energy expenditure declined at essentially the same rate between 1960 and 1980, (4.3%), and between 1980 and 2000, (4.9%), the increase in the prevalence of obesity between 1980 and 2000 (15.9 extra percentage points) was ten times greater than the increase in the prevalence of obesity between 1960 and 1980 (1.6 extra percentage points) (Table 1). The lack of proportionality between the rate of decrease in occupational energy expenditure and the rate of increase in obesity at different intervals seriously undermines the idea that a decrease in occupational activity is one of the principal causes of the U.S. obesity epidemic. Further evidence against the role of occupational activity comes from studies that have compared obesity and occupation. The prevalence of obesity among employees who engaged in occupations involving low levels of physical activity was found to be only 1.7 percentage points higher than the prevalence of obesity among employees engaged in occupations involving high levels of physical activity(27). Even if we assume that there was a total shift from high to low physical activity occupations in the U.S. work force between 1960 and 2000, this difference would  account for only a fraction of the increase in the prevalence of obesity in the United States in the same period, which amounted to 17.5 percentage points. Results from a study of time trends in the prevalence of obesity among various occupational groups also do not support the role of occupational physical activity in preventing obesity (28). A comparison of trends in the prevalence of obesity among five occupations involving low physical activity ( managers, management related occupations, teachers, sales personnel and financial records keepers) and five other occupations involving high physical activity (farm workers, mechanics, assembly workers, mail carriers, and cleaning workers) between 1986 and 1995, showed that the pooled average annual increase in obesity was 10% higher among men engaged in occupations involving low physical activity than among men engaged in occupations involving high physical activity. In contrast, the pooled average annual increase in obesity was 24% lower among women engaged in occupations involving low physical activity than among women engaged in occupations involving high physical activity. Once again, occupational physical activity did not seem to have an overall protective effect against obesity.  

The prevalence of obesity among children has been attributed to excessive television viewing (4, 29). It has been argued that increased time spent watching television would promote a sedentary lifestyle among children and discourage their participation in physical forms of recreation. Historical studies of trends in television ownership and viewing do not support such a theory. Thus, a 22% increase in television viewing between 1963 and 1980 (15) was accompanied by a 0.4 percentage point increase in the prevalence of obesity among boys and girls between the ages of 12 and 19 (3), whereas a 14.2% increase in television viewing between 1980 and 2000 (Table 1) was accompanied by an 11.1 percentage point increase in the prevalence of obesity in the same group (3). Even though television viewing increased at a lower rate between 1980 and 2000 than it did between 1963 and 1980, it was accompanied by an increase in obesity that was nearly 28 times greater between 1980 and 2000 than it was between 1963 and 1980. While it is conceivable that some parents limited their children’s television viewing, there is no reason to believe that such parental guidance declined suddenly after 1980 when obesity rates increased dramatically. Once again the lack of proportionality in the relationship between television viewing and the prevalence of obesity at two different periods suggests that the two phenomena are not causally related. It should be remembered that television viewing had become widespread long before the onset of the obesity epidemic. The percentage of U.S homes owning a television set increased from 9% in 1950 to 90% in 1962 (30), sixteen years before the onset of the obesity epidemic.

The problem of inactivity among American children is not a new phenomenon. A study of children living in New York in 1940 concluded that 72% of them were inactive (31). Another study published in 1956, observed that suburban high schoolgirls were not physically active (32). Before the advent of television, other forms of sedentary recreation could attract children, such as attending movie theaters, listening to the radio, or reading comic books, yet such forms of recreation did not apparently trigger an epidemic of obesity among American children.

The second part of the environmental theory suggests that the obesity epidemic is the result of increased consumption of relatively cheap calorie dense processed foods. It is argued that since price is a major factor in making purchasing decisions, the sudden increase in the consumer price index for fruits and vegetables that took place in the 1980s may have forced Americans to consume the cheaper calorically dense processed foods and gain weight (7). However, data published by the Department of Agriculture show that the per capita consumption of fruits and vegetables increased in every decade between 1970 and 2000 including the 1980s when the consumer price index for fruits and vegetables showed a sudden increase (Table 1). Furthermore, the increase in the per capita consumption of calories from carbohydrates declined significantly from 5.1 percentage points in the 1980s to 0.9 percentage point in the 1990s, even though the combined consumer price index for sugar and sweets, and cereals and bakery products, which include cakes cookies and pies, registered a smaller increase in the 1990s (29%), than it did in the 1980s (52%) (Table 1). These results suggest that factors other than a sedentary lifestyle and the affordability of calorically dense processed foods may be responsible for the United States obesity epidemic.

The Relationship between Obesity and Disorders of the Alimentary Canal:  Results from historical studies of public health have led to the conclusion that a mutual relationship exists between health and body weight (33). Many diseases such as tuberculosis, anemia and peptic ulcer were found to be associated with lower BMI(34,35). Other diseases such as bronchitis, emphysema and asthma showed a U shaped relationship with body weight where the prevalence of the disease was higher at both ends of the BMI spectrum (35). Improved health due to eradication or treatment of such diseases would be associated with increased body weight (7). Consequently, inductees to the United States Armed Forces during World War II were found to be heavier than inductees during World War I (36). However, weight gain associated with recovery from such diseases was likely to be modest, since many of those diseases had a U shaped relationship with body weight and/or did not involve the alimentary canal. In contrast, the eradication and treatment of the diseases of the alimentary canal are likely to have a more profound effect on body weight, because in addition to restoring well being, they can improve the function of the alimentary canal in processing, digesting and absorbing food. Among the disorders of the alimentary canal that are likely to have such an impact on body weight are dental caries, malocclusion, dentine sensitivity, gastro-esophageal reflux disease, peptic ulcer and diarrhea.

Dental health and body weight: For most people, solid food represents the principal source of caloric intake. Before being swallowed, solid food needs to be shredded by mastication. For optimum masticatory performance, an individual needs a full complement of intact teeth and a functionally stable occlusion (37). Having decayed or missing teeth and an unstable occlusion, undermine one’s ability to chew food properly and may result in diminished caloric intake (38) and lower body weight (39). Dentine sensitivity, on the other hand could affect one’s ability to enjoy sugar containing foods and beverages.

Dental caries and body weight: Dental caries is the most common cause of tooth loss (40). Those with fewer or decayed teeth possess lower bite force (41, 42) and experience chewing disability (43, 44) and oral pain (45, 43) during eating. Furthermore, tooth loss can result in reduced total energy intake (46) and dietary restriction (44, 47). In children, severe dental caries is associated with lower body weight (48, 49, 50), whereas accelerated dental development (50), or dental rehabilitation is associated with subsequent weight gain (49, 51). Such findings suggest that a reduction in the prevalence of dental caries would result in better mastication, greater food consumption, and subsequent weight gain.

Several advances in the prevention and treatment of dental caries in the second half of the twentieth century helped reduce the prevalence of dental caries in the United States. Until the 1940s, tooth extraction was a popular form of treatment due to the widespread acceptance of the theory of focal infection (52). Subsequent improvements in the diagnosis and treatment of dental caries reduced the need for tooth extraction. The use of preventive procedures, such as periodic check ups, plaque removal and topical fluoride application, had a significant impact on the dental health of the U.S. public. Preventive dentistry, which began to increase in the 1950s, became so popular that by 1976, 45% of all U.S. dentists reported employing dental hygienists (53). However, the greatest advance in the prevention of dental caries was achieved by fluoridation of the drinking water. The anti cavity property of fluoride, which was confirmed from epidemiological evidence gathered in the 1930s and 1940s (19), led to the idea that fluoridation of drinking water could help prevent tooth decay. Fluoridation of drinking water in the United States began in 1945. By 1975, almost half of the U.S. population was exposed to fluoridated drinking water (19) (Table 3). The combined effect of these advances in prevention and treatment of dental caries was evident in epidemiological surveys (17, 18) that showed that the dental health status of the U.S. population as measured by the number of decayed, missing and filled teeth had improved parallel to the increase in the prevalence of obesity in the United States (Table 2).

Malocclusion and body weight: A proper intercuspal relationship which leads to a functionally stable occlusion between the upper and lower molars is important for the optimal performance of the masticatory apparatus (54). An improper or abnormal intercuspal relationship can give rise to malocclusion.  According to a recent survey, only 35% of the adult U.S. population has optimal occlusion (55). Malocclusion, especially in severe cases, can affect one’s ability to break down and swallow food (54). Subjects with malocclusion have poorer masticatory performance than subjects with normal occlusion (56). They perform more irregular and inconsistent strokes during mastication (57), and execute more masticatory cycles, and take longer to eat the same amount of food than those with normal occlusion (58), possibly as an adaptive response to compensate for the smaller occlusal contact area that they possess (59). Furthermore, malocclusion is associated with a greater risk for temporomandibular dysfunction, (60) a disease which impairs masticatory function (61) and dietary intake (62).

Since malocclusion impedes masticatory function and masticatory function is related to body weight (63, 64) it would be expected that there would be a negative relationship between malocclusion and body weight. There are no large scale studies that have addressed this relationship, but some studies suggest that such a relationship may exist. One study has found that the prevalence of overweight is 5% less and the prevalence of underweight 2.5% more among adolescents with dental crowding (65). Another study has shown that the occurrence of two or more malocclusion traits was significantly higher among premature babies (66), who are known to achieve lower BMI later in life (67). Finally, obstructive sleep apnea patients who were obese had less craniofacial abnormalities including class II malocclusion than those who were not obese (68).

A negative association between malocclusion and body weight would imply a downward trend in the prevalence of malocclusion parallel to the upward trend in the prevalence of obesity. A recent survey has shown that the prevalence of overbite in the United States declined between 1966 and 1988 (69). This progress can be attributed to the six fold increase in the popularity of orthodontic treatment between 1959 and 1979 (Table 3). Orthodontic treatment reduces the number of occlusal interferences (70), improves mastication (71), reduces the incidence of temporomandibular disease (72) and leads to increased body weight (73).

Dentin Sensitivity and Body Weight: Dentin sensitivity is a condition that is characterized by sharp pain arising from external stimuli such as dietary sugar, in otherwise intact or normal teeth. It is estimated that it affects 15-20% of the adult U.S. population (74). Nerve sensitization due to occlusal or other trauma (75) can make the dental pulp vulnerable to osmotic shock caused by high concentrations of sugar found in certain foods and drinks. Soft drinks and fruit juices are particularly harmful to sensitive teeth (76), since they contain citric acid and sugar in high concentrations. The citric acid exposes the dental pulp by opening the dentinal tubules, and the sugar delivers the osmotic shock. Those who suffer from dentine sensitivity cannot enjoy soft drinks unless they receive treatment for dentine sensitivity.

Treatment of dentine sensitivity first gained scientific basis in the early 1940s when a preparation of sodium fluoride paste applied topically proved to be effective in clinical trials (77). As a result, office treatment of dentine sensitivity with fluoride paste increased across the United States in the following decades (Table 3). Eventually, office treatment of dentine sensitivity branched into other methods such as dentine coating and laser treatment with longer lasting effects (78). In home treatment of dentine sensitivity began in 1961 with the launching of Sensodyne, the first desensitizing toothpaste (77). It was followed by other forms of do it yourself treatments such as mouth washes and chewing gum (79).

At present, there are no studies of time trends in the prevalence of dentine sensitivity in the United States. However, there is reason to believe that a decline in the prevalence of dentine sensitivity may have occurred, because the prevalence of many dental disorders which contribute to the development of dentine sensitivity, such as malocclusion, (75) dental caries, large restorations (80) and tooth loss (81) have all declined in recent decades (69) (Table 2). The prevention and treatment of dentine sensitivity, can in the long run, enable more people to consume sugar containing foods and beverages without suffering adverse consequences. Consequently, the consumption of sugar containing soft drinks, which are considered to be a contributing factor to the obesity epidemic (82), increased by 60% from 22.2 gallons per person per year in 1970 to 35.6 gallons in 1990 (Table 1).

Gastro-esophageal reflux disease and body weight: Gastro-esophageal reflux disease or heartburn is a common disorder that affects almost 25% to 40% of the U.S. population (83, 84).  Several studies have shown that it is positively associated with obesity (85, 86). This association can be explained by the findings that both obesity (87, 82) and reflux disease (88, 89, 90, and 84) are caused by the same type of diet that consists of soft drinks and foods that are high in fat and carbohydrates and low in fiber. It is therefore not surprising that the prevalence of obesity and gastro-esophageal reflux disease increased in tandem between 1970s and 1990s (Table 2). People with heartburn often learn how to avoid foods and beverages that cause heartburn (84). However, successful treatment of heartburn could free some individuals to consume such offending foods and beverages and gain weight, or free others who are already overweight from changing their eating habits and losing weight. The findings that long term use of proton pump inhibitors is associated with undesired weight gain (91), and that overweight people are more likely to use proton pump inhibitors than people of normal weight (92), lend support to such an argument.

Progress in antacid therapy began shortly before the obesity epidemic. Until the early 1950s antacid therapy consisted mainly of a milk diet and alkaline powders (93, 94). Modern antacid therapy began in the early 1960s with the use of Aluminum/Magnesium antacid tablets (93) which neutralize excess gastric acid. Subsequent research into the mechanism of acid secretion yielded pharmacological antacids in the form of Histamine-2 receptor antagonists in the 1970s and proton pump inhibitors in the 1980s (94), which are more effective than chemical antacids because they act in a more sustained fashion by preventing acid production (94). The improvement in the effectiveness of acid suppression was accompanied by a dramatic increase in the use of antacids for the treatment of gastric ulcer between the1970s and the 1990s (table 30). A temporal relationship between the increase in obesity on one hand and the prevalence of reflux disease (Table 2) and antacid therapy (Table 3) on the other, gives additional support for the role of antacids in the development of the obesity epidemic.

Helicobacter pylori and body weight: Helicobacter pylori is a common pathogen that plays an etiologic role in the development of gastritis and peptic ulcer (95). The prevalence of infection with H. pylori in the United States was estimated to be 30% in 1960 but declined to about 20% in 1990 (96). There was a parallel decline in the prevalence of peptic ulcer between the 1960s and the 1990s (Table 2). The decrease in the prevalence of infection with H. pylori could be attributed, at least in part, to its unintentional eradication through the large scale use of antibiotics (95) and antacids which increased before and during the obesity epidemic (Table 3).

Numerous clinical studies have consistently shown that eradication of H. pylori results in weight gain (97, 98), suggesting that there could be a negative relationship between H. pylori infection status and body weight. However, epidemiological studies have failed to show such a relationship in the general population (99). One explanation for the lack of an association between H. pylori infection and lower body weight could lie in a recent study which has shown that the success rate for H. pylori eradication is significantly lower among overweight individuals than among individuals of normal weight (100). Therefore, the unintentional eradication of H. Pylori through the use of antibiotics between the 1960s and 1990s may have been more successful among individuals of lower body weight, thus erasing any association between H. pylori infection and lower body weight. Such a scenario leaves open the possibility that unintentional eradication of H. pylori may have contributed to the U.S. obesity epidemic.

Diarrhea and Body Weight: Diarrhea is an important cause of morbidity and mortality worldwide. In the 1950s, diarrhea represented 16% of all illnesses reported for children in the United States (101), whereas among adults, diarrhea represented 1.5% of all hospitalizations between 1979 and 1995 (102). Diarrhea affects body weight through its detrimental effect on nutritional absorption, causing a loss of 500 calories per day (103). An episode of diarrhea of more than a few days’ duration can cause significant weight loss (103). Therefore it would be reasonable to suggest that there would be a negative relationship between diarrhea and body weight and that eradication and treatment of diarrhea could lead to weight gain in the general population. Early advances in the fight against diarrhea came through public health measures such as sewage disposal, water treatment and food safety (104). Nevertheless, diarrhea remained a serious problem because treatment of diarrheal diseases lacked scientific basis. Withholding food and intestinal purge, which exacerbated nutrient loss, were often part of the treatment in the early part of the twentieth century (105). The use of oral antibiotics in the 1950s was effective in improving symptoms and reducing the excretion of pathogens into the environment (106). Therefore, the increase in the use of antibiotics between the 1960s and the 1970s, as well as between the 1980s and the 1990s (Table 3) may have had a role in curtailing the incidence of diarrheal diseases in the United States. Improved knowledge of electrolyte physiology and glucose transport in the 1950s and 1960s led to the development of oral rehydration therapy which reversed nutritional loss associated with diarrhea (107). The treatment of diarrhea gained another modality in the 1960s with the use of anti motility drugs which inhibited excessive bowel motility and promoted fluid and salt absorption (105). As a result of such advances in the prevention and treatment of diarrhea the childhood mortality rate improved significantly between the 1960s and 1990s (Table 2), while the number of hospitalizations for gastroenteritis among adults declined by 20% between 1979 and 1995 (102).

Advances in the understanding of lactose intolerance, were also helpful in reducing the incidence of diarrhea in the United States. Lactose intolerance, which is caused by the reduced activity of the enzyme lactase (108), is found in over two thirds of Blacks, Hispanics, Native Americans, Jews and Orientals, and in about 5-15% of Northern European Americans (109). It is an important cause of non infectious diarrhea, particularly among children (110,103). Adolescents who suffer from lactose intolerance have lower BMI than those who do not (111). Treatment of lactose intolerance in children by elimination of lactose from the diet results in significant weight gain (110). Lactose free formulas and lactase tablets which were developed in the 1970s (112) can also prevent lactose induced diarrhea.

Discussion

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The combined effects of advances in the prevention and treatment of dental caries, malocclusion, dentine sensitivity, gastro-esophageal reflux disease and diarrhea may have contributed to the obesity epidemic by enabling Americans to ingest a greater variety of foods and beverages and absorb more nutrients, with the least likelihood of experiencing adverse consequences.

Table 4 presents the advances in the prevention and treatment of oral and gastrointestinal disorders in chronological order. Such progress, which began several decades before the obesity epidemic, reached a critical mass in the period between 1958 and 1970. It is conceivable that this critical mass may have triggered the obesity epidemic which began eight years later in 1978. The effect of this critical mass may have been delayed because many of those advances would have required time to transform into practical treatments and gain widespread acceptance. Furthermore, the effects of some treatments are likely to be slow due to the sporadic (e.g. diarrhea) or gradual (e.g. dental caries) nature of the disease. Over the ensuing decades, the combined effects of those advances may have contributed to the increase in the prevalence of obesity by decreasing the prevalence and duration of oral and gastrointestinal disorders.

If the proposed theory is valid, a slowdown in the rate of increase in the prevalence of obesity should take place, because progress in the prevention and treatment of oral and gastrointestinal diseases has also slowed down (Table 4). The prevalence of a few existing measures such as water fluoridation and antacid therapy have already reached a plateau. (Table 3) As the prevalence of those and other measures reaches saturation point, their impact on the prevalence of obesity is likely to diminish. A recent meta-analysis has concluded that the worldwide epidemic of obesity, including that of the United States has leveled off since 1999 (120). The prevalence of obesity in the United States in 2010 was 35.7%, (121) which represented a 4.8 percentage point increase since 2000. (Table 1) Such increase was considerably less than the increase in the prevalence of obesity between 1990 and 2000 which was 7.7 percentage points (Table 1). These findings lend further support to the theory that progress in the prevention and treatment of oral and gastrointestinal diseases has contributed to the United States obesity epidemic.

The present theory does not contradict the basic concept that excess energy can cause weight gain. Nor does it exclude other possible factors that may have contributed to the obesity epidemic. Rather, it explains how the American public was able to consume and absorb more caloric nutrients as a result of advances in the prevention and treatment of oral and gastrointestinal disorders.

Abbreviations

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BMI: Body Mass Index
DMFT: Decayed, Missing, and Filled Teeth
NHANES: National Health and Nutrition Examination Survey

References

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1. Kuczmarski RJ, Flegal KM, Campbell SM, Johnson CL. Increasing prevalence of overweight among US adults. JAMA 1994; 272:205-10.
2. Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trends in obesity among US adults. JAMA 2002; 288:1723-7.
3. Wang Y, Beydoun MA. The obesity epidemic in the United States--Gender, age, socioeconomic/ethnic, and geographic characteristics: A systematic review and meta-regression analysis. Epidemiol Rev 2007; 29:6-28.
4. Keith SW, Redden DT, Katzmarzyk PT et al. Putative contributors to the secular increase in obesity: exploring the roads less traveled. Int J Obes 2006; 30:1585-94.
5. Zinn AR, Palmer BF. Unconventional wisdom about the obesity epidemic. Am J Med Sci 2010; 340:481-91?
6. Hill JO, Peters JC. Environmental contributions to the obesity epidemic. Science 1998; 280:1371-4.
7. Finkelstein EA, Ruhm CJ, Kosa KM. Economic causes and consequences of obesity. Annu Rev Public Health 2005; 26:329-57.
8. Hattery A. Title IX at 40: More work needs to be done. USA Today 2012; June 21:p7A.
9. Helm J. Myth-busting: Our take on the diet book craze. Chicago Tribune 2007; March 7; Section 7: p3.
10. Willet WC. Is dietary fat a major determinant of body fat? Am J Clin Nutr 1998; 67(Suppl):556S-62S.
11. Centers for Disease Control and Prevention. Prevalence of overweight, obesity and extreme obesity among adults: United States, trends 1960-62 through 2005-2006. www.cdc.gov/nchs/data/hestat/overweight/overweight_adult.htm
12. Wright JD, Kennedy-Stephenson MS, Wang CY, McDowell MA, Johnson CL. Trends in intake of energy and macronutrients—United States, 1971-2000. MMRW 2004; 53:80-2.
13. United States Department of Labor. Bureau of Labor Statistics. Consumer price index for all urban consumers (CPI-U). www.bls.gov/cpi/cpid.
14. United States Department of Agriculture. Economic Research Service. Fruits and vegetables (fresh weight equivalent): per capita availability, 1970-2000. www.ers.usda.gov/data-products/food-availability-(per-capita)-data-system.aspx
15. Brownson RC, Boehmer TK, Luke DA. Declining rates of activity in the United States: What are the contributors? Annu Rev Public Health 2005; 26:421-43.
16. Church TS, Thomas DM, Tudor-Locke C et al. Trends over 5 decades in U.S. occupation-related physical activity and their associations with obesity. PLoS One 2011; 6:e19657.
17. Graves RC, Stamm JW. Decline of dental caries. What occurred and will it continue? J Canad  Dent Assn 1985;51:693-9.
18. Beltran-Aguilar ED, Barker LK, Canto MT et al. Surveillance for dental caries, dental sealants, tooth retention, edentulism, and enamel fluorosis---United States, 1988-1994 and 1999-2002. MMWR 2005;54:1-44.
19. Horowitz HS. The effectiveness of community water fluoridation in the United States. J Pub Health Dent 1996;56:253-258.
20. Centers for Disease Control. National Oral Health Surveillance system. Fluoridation growth. www.cdc.gov/nohss/FSGrowth _text.htm
21. American dental association. The 1990 survey of dental services rendered. June 1994.
22. El-Serag HB, Sonnenberg A. Opposing time trends of peptic ulcer and reflux disease. Gut 1998;43:327-333.
23. Munnangi S, Sonnenberg A. Time trends of physician visits and treatment patterns of peptic ulcer disease in the United States. Arch Intern Med 1997;157:1489-94.
24. Kilgore PE, Holman RC, Clarke MJ, Glass RI. Trends of diarrheal disease-associated mortality in US children, 1968 through 1991. JAMA 1995;274:1143-51.
25. Finkel MJ. Magnitude of antibiotic use. Ann Intern Med 1978;89:791-2.
26. McCaig LF, Hughes JM. Trends in antimicrobial drug prescribing among office-based physicians in the United States. JAMA 1995;273:214-9.
27. King GA, Fitzhugh EC, Bassett DR et al. Relationship of leisure-time activity and occupational activity to the prevalence of obesity. Int J Obes 2001;25:606-12.
28. Caban AJ, Lee DJ, Fleming LE, Gomez-Marin O, Leblanc W, Pitman T. Obesity in US workers: The national health interview survey, 1986 to 2002. Am J Pub Health 2005;95:1614-22.
29. Dietz WH, Gortmaker SL. Do we fatten our children at the television set? Obesity and television viewing in children and adolescents. Pediatrics 1985;75:807-12.
30. Baughman JL. Television comes to America. Illinois History March 1993. www.lib.niu.edu/1993/ihy930341.html
31. Bruch H. Obesity in childhood. Am J Dis Child 1940;60:1082-109.
32. Johnson ML, Burke BS, Mayer J. Relative importance of inactivity and overeating in the energy balance of obese high school girls. Am J Clin Nutr 1956;4:37-44.
33. Costa DL, Steckel RH. Long term trends in U.S. health, welfare, and economic growth. In health and welfare during industrialization. Steckel RH, Flood R, eds. 1997;pp:47-89. Chicago, University of Chicago Press.
34. Tverdal A. Height, weight and incidence of tuberculosis. Bull Intern Union Against Tuberculosis and Lung Dis 1988;63:16-8.
35. Negri E, Pagano R, Decarli A, La Vecchia C. Body weight and the prevalence of chronic diseases. J Epidem Comm Health 1988;42:24-9.
36. Karpinos BD. Height and weight of selective service registrants processed for military service during World War II. Hum Biol  1958;30:292-321.
37. Sassouni V, Dahar P. Introduction. In Orthodontics in Dental Practice, Sassouni V et al eds. 1971; pp:xi-xvi.
38. Gordon SR, Kelley SL, Sybyl JR, Mill M, Kramer A, Jahnigen DW. Relationship in very elderly veterans of nutritional status, self-perceived chewing ability, dental status, and social isolation. I Am Geriatr Soc 1985;33:334-9.
39. de Morais Turelli MC, de Souza Barbosa T, Gaviao MB. Associations of masticatory performance with body and dental variables in children. Pediatr Dent 2010;32:283-8.
40. Liss J, Evenson P, Loewy S, Ayer WA. Changes in the prevalence of dental disease. JADA 1982;105:75-9.
41. Helkimo E, Carlsson GE, Helkimo M. Bite force and state of dentition. Acta Odontol Scand 1977;35:297-303.
42. Kampe T, Haraldson T, Hannerz H, Carlsson GE. Occlusal perception and bite force in young subjects with and without dental fillings. Acta Odontol Scand 1987;45:101-7.
43. Singh KA, Brennan DS. Chewing disability in older adults attributable to tooth loss and other oral conditions. Gerodontology 2012;29:106-10.
44. Sheiham A, Steele J. Does the condition of the mouth and teeth affect the ability to eat certain foods, nutrient and dietary intake and nutritional status amongst older people? Public Health Nutr 2001;4:797-803.
45. Reid BC, Chenette R, Macek MD. Prevalence and predictors of untreated caries and oral pain among Special Olympic athletes. Spec Care Dentist 2003;23:139-42.
46. Suzuki K, Nomura T, Sakurai M, Sugihara N, Yamanaka S, Matsukubo T. Relationship between number of present teeth and nutritional intake in institutionalized elderly. Bull Tokyo dent Coll 2005;46:135-43.
47. Chauncey HH, Muench ME, Kapur KK, Wayler AH. The effect of the loss of teeth on diet and nutrition. Int Dent J 1984;34:98-104.
48. Pinto A, Kim S, Wadenya R, Rosenberg H. Is there an association between weight and dental caries among pediatric patients in an urban dental school? A correlation study. J Dent Educ 2007;71:1435-40.
49. Sheiham A. Dental caries affects body weight, growth and quality of life in preschool children. Br Dent J 2006;201:625-6.
50. Hilgers KK, Akridge M, Scheetz JP, Kinane DE. Childhood obesity and dental development. Pediatr Dent 2006;28:18-22.
51. Thomas CW, Primosch RE Changes in incremental weight and well-being of children with rampant caries following complete dental rehabilitation. Pediatr Dent 2002;24:109-13.
52. Burt BA. Influences for change in the dental health status of populations: An historical perspective. J Public Health Dent 1978;38:272-88.
53. Burt BA, Warner KE. Prevention of oral disease. In Reducing the cost of dental care, Kudrle RT, Meskin L, eds 1983;pp:132-161.
54. Proffit WR, Fields HW. Malocclusion and dentofacial deformity in contemporary society. In Contemporay orthodontics 2^nd ed. Proffit WR, Fields HW, eds. 1993;pp2-16.
55. Proffit WR, Fields HW, Moray LJ. Prevalence of malocclusion and orthodontic treatment need in the United states: estimates from the NHANES III survey. Int J Adult Orthodon Orthognath Surg 1998;13:97-106.
56. Magalhaes IB, Pereira LJ, Marques LS, Gameiro GH. The influence of malocclusion on masticatory performance. Angle Orthodontist 2010;80:981-7.
57. Ahlgren J. Pattern of chewing and malocclusion of teeth. Acta Odontol Scand 1967;25:3-13.
58. Ingervall B, Carlsson GE. Masticatory muscle activity before and after elimination of balancing side interference. J Oral Rehabil 1982;9:183-192.
59. Lepley CR, Throckmorton GS, Ceen RF, Buschang PH. Relative contributions of occlusion, maximum bite force, and chewing cycle kinematics to masticatory performance. Am J Orthod Dentofacial Orthop 2011;139:606-13.
60. Simmons HC, Oxford DE, Hill MD. The prevalence of skeletal Class II patients found in a consecutive population presenting for TMD treatment compared to the national average. J Tenn Dent Assoc 2008;88:16-8.
61. Hansdottir R, Bakke M. Joint tenderness, jaw opening, chewing velocity, and bite force in patients with temporomandibular joint pain and matched healthy control subjects. J Orofac Pain 2004;18:108-13.
62. Irving J, Wood GD, Hackett AF. Does temporomandibular disorder pain dysfunction syndrome affect dietary intake? Dent Update 1999;26:405-7.
63. Braun S, Bantleon H-P, Hnat WP, Freudenthaler JW, Marcotte MR, Johnson BE. A study of bite force, part 1: Relationship to various physical characteristics. Angle Orthod 1995;65:367-72.
64. Ikebe K, Matsuda K, Morii K, Nokubi T, Ettinger RL. The relationship between oral function and body mass index among independently living older Japanese people. Int J Prosthodont 2006;19:539-46.
65. Thomaz EBAF, Cangussu MCT, da Silva AAM, Assis AMO. Is malnutrition associated with crowding in permanent dentition. Int J Environ Res Public Health 2010;8:3531-44.
66. Paulsson L, Soderfeldt, B, Bondemark L. Malocclusion traits and orthodontic treatment needs in prematurely born children. Angle Orthod 2008;78:786-92.a
67. Fewtrell MS, Lucas A, Cole TJ, Wells JC. Prematurity and reduced body fatness at 8-12 y of age. Am J Clin Nutr 2004;80:436-40.
68. Ferguson KA, Ono T, Lowe AA, Ryan F, Fleetham JA. The relationship between obesity and craniofacial structure in obstructive sleep apnea. Chest 1995;108:375-81.
69. Brunelle JA, Bhat M, Lipton JA. Prevalence and distribution of selected occlusal characteristics in the US population, 1988-1991. J Dent Res 1996;75(Spec No):706-13.
70. Henrikson T, Nilner M, Kurol J. Signs of temporomandibular disorders in girls receiving orthodontic treatment. S prospective and longitudinal comparison with untreated Class II malocclusions and normal occlusion subjects. Europ J Orthodont 2000;22:271-81.
71. Tome W, Yashiro K, Takada K. Orthodontic treatment of malocclusion improves impaired skillfulness of masicatory jaw movements. Angle Orthod 2009;79:1078-83.
72. Egermark I, Thilander B. Craniomandibular disorders with special reference to orthodontic treatment: An evaluation from childhood to adulthood. Am J Orthod Dentofac Ortop 1992;101:28-34.
73. Castelo PM, Gaviao MB, Pereira LJ, Bonjardim LR. Evaluation of changes in muscle thickness, bite force and facial symmetry during early treatment of functional posterior crossbite. J Clin Pediatr Dent 2010;34:369-74.
74. Cummins D. Dentin hypersensitivity: from diagnosis to a breakthrough therapy for everyday sensitivity relief. J Clin dent 2009;20:1-9.
75. Ikeda T, Nakano M, Bando E, Suzuki A. The effect of light premature occlusal contact on tooth pain threshold in humans. J Oral Rehabil 1998;25:589-95.
76. Clark DC, Woo G, Silver JG, Woo G, Grisdale JC. The influence of frequent ingestion of acids in the diet on treatment of dentin sensitivity. J Can Dent Assoc 1990;56:1101-3.
77. Rosenthal MW. Historic review of the management of tooth sensitivity. Dent Clin N Amer 1990;34:403-27.
78. Al-Sabbagh M, Brown A, Thomas MV. In-Office treatment of dentinal sensitivity. Dent Clin N Amer 2009;53:47-60.
79. Orchardson R, Gillam DG. Managing dentin hypersensitivity. JADA 2006;137:990-8.
80. Chabanski MB, Gillam DG. Aetiology, prevalence and clinical features of cervical dentine sensitivity. J Oral Rehabil 1997;24:15-9.
81. Addy M. Etiology and clinical implications of dentine hypersensitivity. Dent Clin N Amer 1990;34:503-14.
82. Malik VS, Schulze MB, Hu FB. Intake of sugar-sweetened beverages and weight gain: a systematic review. Am J Clin Nutr 2006;84:274-88.
83. Modlin I, Kidd M. GERD 2003: issues from the past and a consensus for the future. Drugs Today 2004;40(Suppl A):3-8.
84. Feldman M, Barnett C. Relationships between the acidity and osmolality of popular beverages and reported postprandial heartburn. Gastroenterology 1995;108:125-31.
85. Corley DA, Kubo A. Body mass index and gastroesophageal reflux disease: a systematic review and meta-analysis. Am J Gastroenterol 2006;101:2619-28.
86. Jacobson BC, Somers SC, Fuchs CS, Kelly CP, Camargo CA. Body-mass index and symptoms of gastroesophageal reflux in women. N Eng J Med 2006;354:2340-8.
87. Hill JO. Understanding and addressing the epidemic of obesity: an energy balance perspective. Endocr Rev 2006;27:750-61.
88. El-Serag HB, Satia JA, Rabeneck L. Dietary intake and the risk of gastro-oesophageal reflux disease: a cross sectional study in volunteers. Gut 2005;54:11-7.
89. Sutphen JL, Dillard VL. Dietary caloric density and osmolality influence gastroesophageal reflux in infants. Gastroenterology 1989;97:601-4.
90. Austin GL, Thiny MT, Westman EC, Yancy WS, Shaheen NJ. A very low-carbohydrate diet improves gastroesophageal reflux and its symptoms. Dig Dis Sci 2006;51:1307-12.
91. Yoshikawa I, Nagato M, Yamasaki M, Kummel K, Osaka M. Long-term treatment with proton pump inhibitor is associated with undesired weight gain. World J Gastroenterol 2009;15:4794-8.
92. Kit BK, Ogden CL, Flegal KM. Prescription medication use among normal weight, overweight, and obese adults, United States, 3005-2008. Ann Epidemiol 2012;22:112-9.
93. Bonnevie O. Developments in the treatment of peptic ulcer. Scand J Gastroent 1987;22(Suppl 127):51-4.
94. Diaz-Rubio M. Historical perspective of gastric acid inhibition. Drugs 2005;65 Suppl 1:1-6.
95. Genta RM. Review article: after gastritis – an imaginary journey into a Helicobacter-free world. Aliment Pharmacology Ther 2002;16(Suppl 4):89-94.
96. Rupnow MFT, Shachterr RD, Owens DK, Parsonnet J. A dynamic transmission model for predicting trends in Helicobacter pylori and associated diseases in the United States. Emerge Inf Dis 2000;6:228-37.
97. Francois F, Roper J, Joseph N, et al. The effect of H. pylori eradication on meal-associated changes in plasma ghrelin and leptin. BMC Gastroenterol 2011;11:37.
98. Lane JA, Murray LJ, Harvey IM, Donovan JL, Nair P, Harvey RF. Randomized clinical trial: Helicobacter pylori eradication is associated with a significantly increased body mass index in a placebo-controlled study. Aliment Pharmacol Ther 2011;33:922-9.
99. Ioannou GN, Weiss NS, Kearney DJ. Is Helicobacter pylori seropositivity related to body mass index in the United States? Aliment Pharmacol Ther 2005;21:765-7.
100. Abdullahi M, Annibale B, Cappocia D, et al. The eradication of Helicobacter pylori is affected by body mass index (BMI). Obes Surg 2008;18:1450-4.
101. Glass RI, Lew JF, Gangarosa RE, LeBaron CW, Ho M-S. Estimates of morbidity and mortality rates for diarrheal diseases in American children. J Pediatr 1991;118:S27-33.
102. Mounts AW, Holman RC, Clarke MJ, Bresee JS, Glass RI. Trends in hospitalizations associated with gastroenteritis among adults in the United States, 179-1995. Epidemiol Infect 1999;123:1-8.
103. Rosenberg IH, Solomons NW, Schneider RE. Malbsorption associated with diarrhea and intestinal infections. Am J Clin Nutr 1977;30:1248-1253.
104. Centers for Disease Control, National Center for Environmental Health. Achievements in public health, 1900-1999: control of infectious diseases. MMWR 1999;48:621-9.
105. McMahan ZH, Dupont HL. Review article: the history of acute infectious diarrhoea management – from poorly focused empiricism to fluid therapy and modern pharmacotherapy. Aliment Pharmacol Ther 2007;25:759-69.
106. Levine MM. Antimicrobial therapy for infectious diarrhea. Rev Inf Dis 1986;8(Suppl 2):S207-16.
107. Hirschhorn N. The treatment of acute diarrhea in children. An historical and physiological perspective. Am J Clin Nutr 1980;33:637-63.
108. Sahi T. Hypolactasia and lactase persistence. Historical review and terminology. Scand J Gastroenterol 1994;29 (Suppl 202):1-6.
109. Bayless TM, Rothfield B, Massa C, Wise L, Paige D, Bedine MS. Lactose and milk intolerance: clinical implications. New Eng J Med1975;292:1156-9.
110. Gracey M, Burke V. Sugar-induced diarrhoea in children. Arch Dis Child 1973;48:331-6.
111. Landau DA, Goldberg A, Levi Z, Levy Y, Niv Y, Bar-Dayan Y. The prevalence of gastrointestinal diseases in Israeli adolescents and its association with body mass index, gender, and Jewish ethnicity. J Clin Gastroenterol 2008;42:903-9.
112. Carper S. A quick history of lactose intolerance. 2011 http://planetlactose.blogspot.com/2011/quick- history- of-lactose-intolerance.html
113. Murray J. Fluoridation studies and dental caries. Br Dent J 1970;129:467-70.
114. Hemphill FM. Trends of diarrheal disease mortality in the United States 1941 to 1946, inclusive. Public Health Reports 1948;63:1699-711.
115. Centers for Disease Control. Division of Oral health. Achievements in public health, 1900-1999: fluoridation of drinking water to prevent dental caries. JAMA 2000;283:1283-6.
116. Hinman AR, Orenstein WA, Papania MJ. Evolution of measles elimination strategies in the United States. J Infect Dis 2004;189(Suppl 1):S17-22.
117. Abbott Nutrition. About us. http://abbottnutrition.com/about-us/our-history.aspx
118. Warner CW, McIsaac RL. The evolution of peptic ulcer therapy. A role for temporal control of drug delivery. Ann NY Acad Sci 1991;618:504-16.
119. Stern WR. Summary of the 34^th meeting of the Food and Drug administration Gastrointestinal Drugs advisory Committee March 15and 16, 1989. Am J Gastroenterol1989;84:1351-5.
120. Rokholm B, Baker JL, Sorenson TIA. The leveling off of the obesity epidemic since the year 1999 – a review of evidence and perspectives. Obes Rev 2010;11:835-46.
121.Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of obesity in the United States, 2009-2010. NCHS data brief, no 82. Hyattsville, MD: National Center for Health Statistics. 2012.

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