| | Increasing Trends in Incidence of Overweight and Obesity over 5 DecadesAbstract PurposeWe evaluated trends in the incidence of overweight and obesity over the past 50 years. ResultsThe incidences of overweight, obesity, and stage 2 obesity increased across the decades in both sexes (P for trend <.001). For men, the incidence of overweight rose from 21.8% (95% confidence interval [CI], 17.6-26.5) in the 1950s to 35.2% (95% CI, 28.6-42.5) in the 1990s; of obesity from 5.8% (95% CI, 4.4-7.6) to 14.8% (95% CI, 12.2-17.9); and of stage 2 obesity from 0.2% (95% CI, 0.1-0.9) to 5.4% (95% CI, 4.0-7.2). For women, incidence rates of overweight increased from 15.0% (95% CI, 12.3-18.1) to 33.1% (95% CI, 29.0-37.4); of obesity from 3.9% (95% CI, 2.9-5.3) to 14% (95% CI, 11.6-16.7); and of stage 2 obesity from 1.7% (95% CI, 1.1-2.6) to 4.4% (95% CI, 3.2-6.0). Overall, incidence rates of overweight increased 2-fold and that of obesity more than 3-fold over 5 decades, findings that remained robust upon additional adjustment for baseline BMI in each decade. ConclusionsThe incidence of overweight and obesity increased progressively over the last 5 decades, suggesting that the rising trend in prevalence is not a recent phenomenon. The epidemic of obesity in the United States is a major public health problem. Excess adiposity increases risk of diabetes, hypertension, cardiovascular diseases, and certain types of cancers.1, 2, 3, 4 Furthermore, obesity is associated with elevated mortality risks due to cardiovascular disease5 and all-causes.6, 7, 8, 9 Clinical Significance•Incidence rates of overweight increased 2-fold and that of obesity more than 3-fold over the past 5 decades. •The rising trend of excess adiposity is not a recent phenomenon. •Over the 50-year period, there was a decline in the proportion of overweight or obese people who were able to achieve normal or nonobese BMI, respectively. •Long-term data provided by our study can help in estimating the future burden of excess adiposity. The increasing prevalence of overweight and obesity underscores the need to better understand this epidemic. Data from the National Health Examination Survey (NHES I, 1960-1962) and National Health and Nutritional Examination Surveys (NHANES I, 1971-1974; NHANES II, 1976-1980; NHANES III, 1988-1994; NHANES 1999-2000) indicate that the prevalence of obesity (body mass index [BMI] ≥30 kg/m2) in the United States was relatively stable from 1960-1980, at which point rates escalated.10 In comparison, studies have suggested a stable prevalence of overweight (25 ≤ BMI <30 kg/m2) until the 1990s (with the exception of women between the ages of 20 and 29 years in whom overweight prevalence increased before the 1990s).11 In this context, it is important to note that parallel data on temporal trends in the incidence of overweight and obesity in the community are lacking. Such incidence data are critical for understanding reasons underlying rising prevalence trends and for making projections about future burden of obesity. Additionally, an analysis of incidence trends may help clarify the apparent paradox of rising obesity prevalence despite stable overweight prevalence in the 1980s. We examined temporal trends in the incidence of overweight and obesity among Framingham Study participants over a 50-year period from 1950 to 2000. We hypothesized that the current epidemic of obesity was paralleled by an epidemic of overweight, which may have been unapparent in the absence of data on incidence trends. We also postulated that the rising trend of excess adiposity is not a recent phenomenon. Methods  Sample The Framingham Heart Study, a community-based prospective cohort study, began in 1948, with enrollment of 5209 participants (original cohort).12, 13 In 1971, 5124 individuals who were children of the original cohort (and their spouses) were enrolled into the Framingham Offspring Study. Participants in the original cohort are examined biennially, whereas the offspring cohort is evaluated quadriennially.14, 15 For the present investigation, we chose 2 examinations within each calendar decade from 1950 up to 2000 that were approximately 8 years apart (Figure). The availability of only 2 offspring cohort examinations in the 1970s that were 8 years apart constrained us to using observations from only 2 examinations within each decade. Individuals were eligible if they: were between ages 40 and 55 years at the first of the 2 examinations in a given decade; attended a follow-up examination 8 years later; and were not underweight (BMI <18.5 kg/m2) at the baseline examination. For primary analyses we excluded underweight individuals because such persons may have had illnesses that prevent weight gain. We chose the 40-55 years group because adequate numbers of individuals for this age range were available in each of the 5 decades. All participants gave informed consent and the study protocol was approved by the Institutional Review Board of the Boston Medical Center. Body Mass Index and Risk Factors Measurement At each Framingham study examination, height and weight are measured using standardized protocols.16, 17 BMI was calculated as the weight in kilograms divided by the square of height in meters. Participants underwent assessment of vascular risk factors at each examination.17 Current smoking was defined as regular cigarette smoking in the year preceding the examination. Smoking cessation was defined as a history of quitting smoking subsequent to the baseline examination. A physical activity index18, 19 was calculated based on responses to a physical activity questionnaire for offspring cohort attendees at examinations 2 (1980s) and 4 (1990s). Dietary daily caloric intake was calculated based on 3-day dietary recall information obtained for the offspring cohort in the 1980s and the 1990s.20 BMI on Follow-Up: Definitions of Overweight and Obesity All eligible participants within a given decade were followed for 8 years to assess the development of the BMI outcomes (see below). Categories of BMI were defined according to established guidelines21, 22: normal weight (18.5 to <25 kg/m2), overweight (25 ≤ BMI <30 kg/m2), overweight or more (≥25 kg/m2), obesity (≥30 kg/m2), and stage 2 obesity (≥35 kg/m2). Statistical Methods For each decade from 1950 to 2000, we evaluated the prevalence of BMI categories at the baseline examination in that decade, and assessed trends in prevalence (with generalized estimating equations to account for individuals contributing to more than one decade, 1950s serving as referent). Next, we evaluated the sex-specific 8-year incidence of the following BMI outcomes (eligibility defined by BMI at first examination in each decade): a.Overweight defined as ‘25 ≤ BMI <30 kg/m2’; participants with BMI <25 kg/m2 were eligible for these analyses. Individuals with BMI >30 kg/m2 at follow-up examination were excluded for estimating incidence of overweight alone. b.Overweight or more defined as a BMI ≥25 kg/m2; participants with BMI <25 kg/m2 were eligible for these analyses. c.Obesity defined as a BMI ≥30 kg/m2; participants with BMI <30 kg/m2 were eligible for these analyses. d.Stage 2 obesity defined as a BMI ≥35 kg/m2; participants with BMI <35 kg/m2 were eligible for these analyses. We evaluated trends in incidence of BMI outcomes using sex-specific multivariable pooled logistic regression adjusting for age and smoking cessation, the latter 2 being major confounders. In additional analyses, we adjusted for baseline BMI. The 1950s served as referent. Because individuals who developed an outcome of interest could not contribute to future decades, generalized estimating equations were not necessary for these analyses. We repeated analyses to examine trends in incidence of obesity among nonsmokers; trends in overweight among nonsmokers were not analyzed because there were too few people eligible in the referent decade. We analyzed nonsmokers to determine if our results were influenced by the striking decreases in smoking rates across decades in our cohorts. Likewise, we did not analyze trends in incidence of stage 2 obesity among nonsmokers because there were no events (development of BMI ≥35 kg/m2) observed in the 1950s in nonsmokers. We repeated analyses including individuals who were underweight to see if this altered our incidence estimates. Finally, we studied temporal trends in decade-specific incidence rates of weight loss by examining: a.Overweight individuals who lost weight: proportion of individuals with BMI ≥25 kg/m2 during a decade who subsequently became normal weight (18.5 kg/m2 < BMI <25 kg/m2). b.Obese individuals who lost weight: the proportion of individuals with BMI ≥30 kg/m2 during the decade who subsequently became normal weight or overweight (18.5 kg/m2 < BMI <30 kg/m2). A 2-tailed P value <.05 was considered statistically significant. Results  Baseline Characteristics In our sample, the prevalence of obesity, stage 2 obesity, mean values of height, and weight increased across the decades from the 1950s to 2000 in both sexes (Table 1; P for trend <.001). Over this period, mean BMI increased by about 2.7 kg/m2in men and 1.5 kg/m2 in women. Smoking rates decreased in men more substiantially than in women (P for trend <.001). | ⁎ P-values <.01 for trend across decades in both sexes (with the exception of BMI ≥25 kg/m2 in women); P-values are age-adjusted and based on generalized estimating equations to account for participants contributing to more than one decade. |
Table 2 displays the baseline characteristics of study participants eligible for analyses in each decade. Among eligible individuals from the 1950s to the 1990s, mean weight and height increased, while smoking rates decreased (P <.01). | | |  | | Men | Women |  |
|---|
 | | 1950s | 1960s | 1970s | 1980s | 1990s | 1950s | 1960s | 1970s | 1980s | 1990s |  |
|---|
 | Persons with BMI <30 kg/m2 |  |  | n | 827 | 692 | 887 | 637 | 613 | 1048 | 859 | 1020 | 720 | 731 |  |  | Age, years | 47.2 | 47.5 | 48.3 | 47.1 | 47.4 | 46.8 | 47.6 | 48.3 | 47.0 | 47.3 |  |  | BMI, kg/m2 | 25.5 | 25.7 | 26.1 | 26.0 | 26.1 | 24.5 | 23.9 | 24.2 | 23.9 | 24.0 |  |  | Weight, kg⁎ | 75.7 | 77.2 | 78.6 | 79.8 | 81.5 | 62.2 | 61.1 | 61.5 | 61.7 | 63.8 |  |  | Height, m⁎ | 1.72 | 1.73 | 1.73 | 1.75 | 1.76 | 1.59 | 1.60 | 1.60 | 1.61 | 1.63 |  |  | Smoking, %⁎ | 77.5 | 67.8 | 44.1 | 43.9 | 26.3 | 39.9 | 51.1 | 41.0 | 33.7 | 24.8 |  |  | Persons with BMI <25 kg/m2 |  |  | n | 332 | 269 | 275 | 202 | 182 | 596 | 579 | 656 | 487 | 486 |  |  | Age, years | 46.9 | 47.4 | 48.6 | 46.7 | 47.4 | 46.2 | 47.3 | 48.0 | 46.7 | 46.8 |  |  | BMI, kg/m2 | 22.9 | 23.1 | 23.4 | 23.3 | 23.3 | 22.5 | 22.4 | 22.6 | 22.4 | 22.4 |  |  | Weight, kg⁎ | 68.2 | 69.8 | 70.9 | 72.5 | 73.3 | 57.6 | 57.7 | 58.1 | 58.4 | 59.6 |  |  | Height, m⁎ | 1.72 | 1.74 | 1.74 | 1.76 | 1.77 | 1.60 | 1.60 | 1.60 | 1.61 | 1.63 |  |  | Smoking, %⁎ | 82.8 | 71.8 | 54.7 | 50.0 | 26.9 | 46.0 | 58.2 | 45.5 | 32.9 | 24.1 |  | | | |
| ⁎ P-values <.01 for trend across decades in both sexes; P-values are age-adjusted and based on generalized estimating equations to account for participants contributing to more than 1 decade. |
Among non-overweight offspring study participants, the physical activity index increased from the 1980s to the 1990s (from 36.0 to 37.5 in men, and from 33.9 to 36.8 in women, P <.001 for both) paralleled by increases in reported daily caloric intake (2206 to 2363 kilocalories in men and 1549 to 1676 kilocalories in women, P <.001 for both). Incidence of BMI Outcomes The incidences of overweight, overweight or more, obesity and stage 2 obesity increased from 1950 to 1990 in both sexes (Table 3). In women, the incidence rates of BMI outcomes rose across the 5 decades in a step-wise fashion. In men, incidence rate increases across decades were less graded; rates rose in the 1960s (relative to the 1950s) but then decreased in the 1970s, only to escalate again in the 1980s. | ⁎ Incidence rate per 100 persons. †Individuals with BMI <25 kg/m2 at baseline but with BMI >30 kg/m2 at the follow-up examination were excluded for estimating incidence of overweight alone. |
Table 4 displays adjusted trends in incidence of BMI outcomes with rates in the 1950s as referent. Overall, incidence rates of overweight increased over 2-fold and that of obesity more than 3-fold over the 5-decade period in both sexes. In models fitting a linear trend across decades, in women there was a 25% (95% confidence interval [CI], 17%-34%) increase in incidence of overweight per decade, a 34% (95% CI, 24%-46%) increase in incidence of obesity per decade, and a 31% (95% CI, 16%-49%) increase in incidence of stage 2 obesity per decade. In men, there was a 20% (95% CI, 10%-32%) increase in incidence of overweight per decade, a 29% (95% CI, 18%-40%) increase in incidence of obesity per decade, and a 97% (95% CI, 63%-138%) increase in incidence of stage 2 obesity per decade. These results remained robust upon additional adjustment for baseline BMI (P = .004 for trend across decades for overweight or more incidence in men; P < .001 for all other BMI outcomes in both sexes). These trends were consistent when we limited our analysis to nonsmokers (Appendix 1). | ⁎ P <.05. †P <.01. ‡P <.001. §Wide 95% CI are the result of the small n in the referent group (2 events in 916 men at risk in 1950s, Table 3). |
Cohort-Specific Incidence Rates in the 1970s In order to investigate if differences in incidence rates across decades were influenced by cohort effects (original cohort contributing data for the 1950s and 1960s, and offspring cohort for 1980s and 1990s), we assessed incidence rates separately for eligible participants in the 2 cohorts in the 1970s (the decade at which individuals between ages 40 and 55 years were available in both cohorts; Appendix 2). The incidence rates of BMI outcomes were similar in the 2 cohorts; whereas point estimates in rates varied for the 2 samples, the 95% CI overlapped. Analyses that included underweight individuals did not materially change incidence rates for overweight, obesity and stage 2 obesity (Appendix 3, Appendix 4). Temporal Trends in Weight Loss The proportions of overweight or more individuals who achieved normal weight status and of obese individuals who became nonobese have steadily decreased over the past 50 years (Table 5, Table 6). | ⁎ Refers to individuals overweight or more (BMI ≥25 kg/m2) during the referent decade who subsequently became normal weight (18.5 kg/m2 <BMI <25 kg/m2). †Refers to those individuals obese or more (BMI ≥30 kg/m2) during the referent decade who subsequently became normal weight or overweight (18.5 kg/m2 <BMI <30 kg/m2). |
| ⁎ Refers to individuals overweight or more (BMI ≥25 kg/m2) during the referent decade who subsequently became normal weight (18.5 kg/m2 < BMI <25 kg/m2). †P <.05. ‡P <.01. §P <.001. ∥Refers to individuals obese or more (BMI ≥30 kg/m2) during the referent decade who subsequently became normal weight or overweight (18.5 kg/m2 < BMI <30 kg/m2). |
Discussion  It is estimated that the lifetime risk of being overweight exceeds 70% and that for obesity it exceeds 35%.23 In the present investigation we assessed if the rising prevalence of overweight and obesity in national cross-sectional surveys was a recent trend or a gradual phenomenon accruing over decades. Our principal findings are 3-fold. First, incidence rates of overweight and obesity increased 2- to more than 3-fold over the last 5 decades in our community-based sample. Second, the incidence rates increased across decades in a fairly monotonic fashion in women. However, incidence rates in men demonstrated a biphasic pattern of increase, with an initial increase in the 1960s and a subsequent one in the 1980s. The reasons for these differing patterns in the 2 sexes are not clear. Third, we noted a striking increase in the prevalence of stage 2 obesity in the 1990s and 2000s, and observed a rising incidence in the 1990s, a matter of great concern. The reasons for the increases in obesity over the past several decades are likely manifold. Our data demonstrate a decrease in incidence rates of weight loss among both overweight and obese individuals over the past 50 years. Smoking cessation among adults has been related to an increased prevalence of overweight.24 Indeed, smoking rates decreased considerably in our study cohort over the past 50 years. However, adjusting for smoking cessation did not significantly alter the incidence trends in our investigation. Increased mean energy intake among adults between 1970 and 2000 has also been implicated as a potential cause for the growing obesity epidemic.25, 26 Such increases in energy intake have been attributed to increases in mean food and beverage portion sizes,27 and consumption of energy-dense fast foods.28 Consistent with these data, the self-reported mean energy intake in our cohort increased between the 1980s and the 1990s. Decreased physical activity in the United States population has been suggested as a causal factor for greater obesity prevalence. Data from the Behavioral Risk Factor Surveillance System (BRFSS), as well as from our cohort indicate that self-reported physical activity has actually increased moderately from the 1980s into the 2000s.29, 30 One explanation for the rising incidence in obesity in the face of higher physical activity may be that increases in caloric intake may have been greater relative to increases in physical activity. An alternative explanation is that the physical activity questionnaire in BFRSS and our study may not have captured adequately overall increases in sedentary lifestyle among adults. Factors contributing to a sedentary lifestyle include less physically demanding occupations,31 changing land-use patterns (eg, urban sprawl32), and increased automotive travel.33 Temporal Trends in BMI Prevalence and Incidence: Comparison with Published Literature The baseline prevalence of overweight (or more), obesity, and stage 2 obesity in our sample in each decade closely resembles that for corresponding age groups in the NHANES data.10, 11, 34, 35 However, our estimates of prevalence of overweight (or more) and obesity were higher in the 1990s and 2000s than those reported for comparable age groups in BRFSS.36, 37, 38 Lower prevalence estimates in BRFSS may be due to self-reported height and weight ascertainment. Previous studies of self-reported weight and height report that overweight participants tend to underestimate their true weight, whereas most participants overestimate their height.39, 40 Also, inaccurate height reporting increases after age 45 years.40 Previous longitudinal studies of BMI and weight categories41, 42, 43, 44, 45 have not focused on temporal trends in incidence of overweight and obesity during the past 5 decades; therefore, we are unable to compare our results with other studies. Our incidence data complement available information on the prevalence of overweight and obesity from national surveys. The substantial incidence rates of overweight, obesity, and stage 2 obesity in our study population in the 1990s are consistent with a parallel increase in the prevalence of obesity nationwide. Overall, our longitudinal observations over 50 years suggest that the increase in prevalence of overweight and obesity was accompanied by increasing incidence rates for both. Strengths and Limitations The strengths of our investigation include the use of prospectively collected data over a 50-year period in a community-based study, and the standardized measurements of BMI over this period. Nonetheless, several limitations should be acknowledged. We evaluated only participants aged 40-55 years (an unavoidable constraint of studying BMI trends for participants in a similar age range over 5 decades) that limits the generalizability of our results to persons older or younger, and limits the comparison of our findings with observations in the NHANES samples. Our sample consisted of 2 separate cohorts—original cohort participants contributed observations in the earlier decades (1950s and 1960s), whereas offspring cohort members provided information during the later decades (1980s and 1990s). Birth cohort effects have been described with later birth cohorts demonstrating a greater propensity for obesity.41 We found no clear-cut evidence of cohort-related differences in incidence of overweight and obesity. Our study cohort is overwhelmingly white, and our results may not be generalizable to nonwhites. Physical activity and dietary caloric intake measurements were available only for recent decades; consequently, we were unable to assess the contributions of these factors to the rising incidences of obesity. We did not account for temporal changes in the incidence of chronic diseases (like cancer) that may influence BMI trends. Lastly, we were unable to examine trends in the incidence of central adiposity because waist measurements were not obtained at early examinations. NHANES data suggest that the prevalence of abdominal adiposity has increased from 1960-1962 to 1999-2000.46 Implications To our knowledge, the present investigation is the first systematic analysis of the incidence of overweight, obesity, and stage 2 obesity over 5 decades in a community-based sample in the United States. Increased incidences of overweight and obesity over the last 50 years suggests that the rising trend of excess adiposity is not a recent phenomenon, although rates have escalated in the last decade. If these patterns of rising incidence continue unabated, the community burden of overweight and obesity may continue to increase over the next decade. Data provided by our study can help in the estimation of the future burden of excess adiposity combining the trajectory of incidence rates over 50 years (average increase per decade of 20%-30% for overweight and 30%-35% for obesity) with the incidence rates observed in the last decade. Appendix  | ⁎ Incidence rate per 100 persons. |
References  1. 1Calle EE, Thun MJ, Petrelli JM, Rodriguez C, Heath CW. Body-mass index and mortality in a prospective cohort of U.S.adults. N Engl J Med. 1999;341:1097–1105. MEDLINE |
CrossRef
2. 2Wilson PW, D’Agostino RB, Sullivan L, Parise H, Kannel WB. Overweight and obesity as determinants of cardiovascular risk: the Framingham experience. Arch Intern Med. 2002;162:1867–1872. MEDLINE |
CrossRef
3. 3Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med. 2003;348:1625–1638.
CrossRef
4. 4Krauss RM, Winston M, Fletcher RN, Grundy SM. Obesity: impact of cardiovascular disease. Circulation. 1998;98:1472–1476. MEDLINE 5. 5Caterson ID, Hubbard V, Bray GA, et al. Prevention Conference VII: obesity, a worldwide epidemic related to heart disease and stroke: Group III: worldwide comorbidities of obesity. Circulation. 2004;110:e476–e483.
CrossRef
6. 6Allison DB, Fontaine KR, Manson JE, Stevens J, VanItallie TB. Annual deaths attributable to obesity in the United States. JAMA. 1999;282:1530–1538. MEDLINE |
CrossRef
7. 7Flegal KM, Graubard BI, Williamson DF, Gail MH. Excess deaths associated with underweight, overweight, and obesity. JAMA. 2005;293:1861–1867.
CrossRef
8. 8Mokdad AH, Marks JS, Stroup DF, Gerberding JL. Actual causes of death in the United States, 2000. JAMA. 2004;291:1238–1245.
CrossRef
9. 9Mokdad AH, Marks JS, Stroup DF, Gerberding JL. Correction: actual causes of death in the United States, 2000. JAMA. 2005;293:293–294.
CrossRef
10. 10Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trends in obesity among US adults, 1999-2000. JAMA. 2002;288:1723–1727. MEDLINE |
CrossRef
11. 11Flegal KM, Carroll MD, Kuczmarski RJ, Johnson CL. Overweight and obesity in the United States: prevalence and trends, 1960-1994. Int J Obes Relat Metab Disord. 1998;22:39–47. MEDLINE 12. 12Dawber TR, Meadors GF, Moore FE. Epidemiological approaches to heart disease: the Framingham Study. Am J Public Health. 1951;41:279–281. 13. 13Dawber TR, Kannel WB. An approach to longitudinal studies in a community: the Framingham Study. Ann N Y Acad Sci. 1963;107:539–556. MEDLINE |
CrossRef
14. 14Feinleib M, Kannel WB, Garrison RJ, McNamara PM, Castelli WP. The Framingham Offspring Study (Design and preliminary data). Prev Med. 1975;4:518–525. MEDLINE |
CrossRef
15. 15Kannel WB, Feinleib M, McNamara PM, Garrison RJ, Castelli WP. An investigation of coronary heart disease in families (The Framingham offspring study). Am J Epidemiol. 1979;110:281–290. MEDLINE 16. 16World Health Organization. Physical Status: The Use and Interpretation of Anthropometry (Report of a WHO Expert Committee). Geneva, Switzerland: World Health Organization; 1995;. 17. 17Cupples LA, D’Agastino RB. Some risk factors related to the annual incidence of cardiovascular disease and death using pooled repeated biennial measurements: Framingham Study, 30-year follow-up. In: Kannel WB, Wolf PA, Garrison RJ editor. The Framingham Heart Study: an Epidemiologic Investigation of Cardiovascular Disease. Washington, DC: NIH Publication; 1987;p. 87–203. 18. 18Sherman SE, D’Agostino RB, Cobb JL, Kannel WB. Physical activity and mortality in women in the Framingham Heart Study. Am Heart J. 1994;128:879–884. MEDLINE |
CrossRef
19. 19Sherman SE, D’Agostino RB, Silbershatz H, Kannel WB. Comparison of past versus recent physical activity in the prevention of premature death and coronary artery disease. Am Heart J. 1999;138:900–907. Abstract | Full Text |
Full-Text PDF (234 KB)
|
CrossRef
20. 20Millen BE, Quatromoni PA, Franz MM, et al. Population nutrient intake approaches dietary recommendations: 1991 to 1995 Framingham Nutrition Studies. J Am Diet Assoc. 1997;97:742–749. Abstract | Full Text |
Full-Text PDF (956 KB)
|
CrossRef
21. 21National Institutes of Health. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults—The Evidence Report. Obes Res. 1998;6(Suppl 2):51S–209S. 22. 22WHO Consultation on Obesity. Obesity: Preventing and Managing the Global Epidemic. Geneva, Switzerland: World Health Organization; 2000;. 23. 23Vasan RS, Pencina MJ, Cobain M, Freiberg MS, D’Agostino RB. Estimated risks for developing obesity in the Framingham Heart Study. Ann Intern Med. 2005;143:473–480. 24. 24Flegal KM, Troiano RP, Pamuk ER, Kuczmarski RJ, Campbell SM. The influence of smoking cessation on the prevalence of overweight in the United States. N Engl J Med. 1995;333:1165–1170. MEDLINE |
CrossRef
25. 25Briefel RR, Johnson CL. Secular trends in dietary intake in the United States. Annu Rev Nutr. 2004;24:401–431. MEDLINE |
CrossRef
26. 26Trends in intake of energy and macronutrients—United States, 1971-2000. MMWR Morb Mortal Wkly Rep. 2004;53:80–82. 27. 27Nielsen SJ, Popkin BM. Patterns and trends in food portion sizes, 1977-1998. JAMA. 2003;289:450–453. MEDLINE |
CrossRef
28. 28Paeratakul S, Ferdinand DP, Champagne CM, Ryan DH, Bray GA. Fast-food consumption among US adults and children: dietary and nutrient intake profile. J Am Diet Assoc. 2003;103:1332–1338. Abstract | Full Text |
Full-Text PDF (87 KB)
|
CrossRef
29. 29Prevalence of no leisure-time physical activity—35 States and the District of Columbia, 1988-2002. MMWR Morb Mortal Wkly Rep. 2004;53:82–86. 30. 30Simpson ME, Serdula M, Galuska DA, et al. Walking trends among U.S. adults: the Behavioral Risk Factor Surveillance System, 1987-2000. Am J Prev Med. 2003;25:95–100. Abstract | Full Text |
Full-Text PDF (125 KB)
|
CrossRef
31. 31King GA, Fitzhugh EC, Bassett DR, et al. Relationship of leisure-time physical activity and occupational activity to the prevalence of obesity. Int J Obes Relat Metab Disord. 2001;25:606–612. MEDLINE |
CrossRef
32. 32Ewing R, Schmid T, Killingsworth R, Zlot A, Raudenbush S. Relationship between urban sprawl and physical activity, obesity, and morbidity. Am J Health Promot. 2003;18:47–57. MEDLINE 33. 33Brownson RC, Boehmer TK, Luke DA. Declining rates of physical activity in the United States: what are the contributors?. Annu Rev Public Health. 2005;26:421–443. MEDLINE |
CrossRef
34. 34Gregg EW, Cheng YJ, Cadwell BL, et al. Secular trends in cardiovascular disease risk factors according to body mass index in US adults. JAMA. 2005;293:1868–1874.
CrossRef
35. 35Hedley AA, Ogden CL, Johnson CL, et al. Prevalence of overweight and obesity among US children, adolescents, and adults, 1999-2002. JAMA. 2004;291:2847–2850.
CrossRef
36. 36Ahluwalia IB, Mack KA, Murphy W, Mokdad AH, Bales VS. State-specific prevalence of selected chronic disease-related characteristics—Behavioral Risk Factor Surveillance System, 2001. MMWR Surveill Summ. 2003;52:1–80. MEDLINE 37. 37Mokdad AH, Serdula MK, Dietz WH, et al. The spread of the obesity epidemic in the United States, 1991-1998. JAMA. 1999;282:1519–1522. MEDLINE |
CrossRef
38. 38Mokdad AH, Ford ES, Bowman BA, et al. Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001. JAMA. 2003;289:76–79. MEDLINE |
CrossRef
39. 39Palta M, Prineas RJ, Berman R, Hannan P. Comparison of self-reported and measured height and weight. Am J Epidemiol. 1982;115:223–230. MEDLINE 40. 40Rowland ML. Self-reported weight and height. Am J Clin Nutr. 1990;52:1125–1133. MEDLINE 41. 41McTigue KM, Garrett JM, Popkin BM. The natural history of the development of obesity in a cohort of young U.S.adults between 1981 and 1998. Ann Intern Med. 2002;136:857–864. 42. 42Stevens J, Knapp RG, Keil JE, Verdugo RR. Changes in body weight and girths in black and white adults studied over a 25 year interval. Int J Obes. 1991;15:803–808. MEDLINE 43. 43Kahn HS, Williamson DF, Stevens JA. Race and weight change in US women: the roles of socioeconomic and marital status. Am J Public Health. 1991;81:319–323. MEDLINE |
CrossRef
44. 44Burke GL, Bild DE, Hilner JE, et al. Differences in weight gain in relation to race, gender, age and education in young adults: the CARDIA Study (Coronary Artery Risk Development in Young Adults). Ethn Health. 1996;1:327–335. MEDLINE |
CrossRef
45. 45Sheehan TJ, DuBrava S, DeChello LM, Fang Z. Rates of weight change for black and white Americans over a twenty year period. Int J Obes Relat Metab Disord. 2003;27:498–504. MEDLINE |
CrossRef
46. 46Okosun IS, Chandra KM, Boev A, et al. Abdominal adiposity in U.S. adults: prevalence and trends, 1960-2000. Prev Med. 2004;39:197–206. MEDLINE |
CrossRef
a Framingham Heart Study, Framingham, Mass b Division of Cardiology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Mass c Department of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass d National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md e Department of Mathematics and Statistics, Boston University, Boston, Mass f Preventive Medicine and Cardiology Sections, Boston Medical Center, Boston University School of Medicine, Boston, Mass. Requests for reprints should be addressed to Ramachandran S. Vasan, MD, Framingham Heart Study, 73 Mount Wayte Avenue, Suite 2, Framingham, MA 01702-5803.
Supported by a National Institutes of Health/National Heart, Lung, and Blood Institute, contract N01-HC-25195, and research grants 2K24HL04334 (R.S.V.), and K23HL074077 (T.J.W.). The funding sources had no role in the design/conduct of the study, management, analysis, and interpretation of data, or the preparation of the manuscript. The National Heart Lung Blood Institute funded the collection of data on height and weight (NO1-HC-25195) used in this investigation, and approved the manuscript. Dr. Vasan had full access to all of the data in the study and takes responsibility for the integrity of and the accuracy of the data analysis. PII: S0002-9343(06)00674-7 doi:10.1016/j.amjmed.2006.06.004 © 2007 Elsevier Inc. All rights reserved. | |
|