To the Editor: The Centers for Disease Control and Prevention(CDC) recommends using the body-mass index (BMI) for age asa marker in assessing patients between the ages of 2 and 20years for obesity.1 In the article by Bibbins-Domingo et al.(Dec. 6 issue),2 weight alone was used as a marker for obesityin adolescents, which may not reflect the true underlying value.Was this approach justified? Furthermore, the assumption thata high BMI does not directly increase the risk of coronary heartdisease (CHD) may be unwarranted, since there is enough evidenceto the contrary.3
Hari K.V.S. Kumar, M.D. Kirti D. Modi, M.D., D.M. Saroj K. Patnaik, M.D. Medwin Hospitals Hyderabad 500001, India hariendo{at}rediffmail.com
References
Kuczmarski RJ, Ogden CL, Guo SS, et al. 2000 CDC growth charts for the United States: methods and development. Vital and health statistics. Series 11. No. 246. Hyattsville, MD: National Center for Health Statistics, May 2002. (DHHS publication no. (PHS) 2002-1696.)
Bibbins-Domingo K, Coxson P, Pletcher MJ, Lightwood J, Goldman L. Adolescent overweight and future adult coronary heart disease. N Engl J Med 2007;357:2371-2379. [Free Full Text]
Lawlor DA, Leon DA. Association of body mass index and obesity measured in early childhood with risk of coronary heart disease and stroke in middle age: findings from the Aberdeen children of the 1950s prospective cohort study. Circulation 2005;111:1891-1896. [Free Full Text]
To the Editor: The results of the study by Bibbins-Domingo etal. are consistent with our recent analyses of trends in CHDin the United States.1,2 Between 1980 and 2000, the age-adjustedrate of death from coronary heart disease was halved, with 341,745fewer such deaths in 2000. Approximately 47% of the decreasewas attributable to treatments and approximately 44% to changesin major risk factors. Crucially, these gains were offset byincreases in diabetes and obesity. Between 1980 and 2000, BMI(defined as the weight in kilograms divided by the square ofthe height in meters) increased from 25.5 to 28.2, accountingfor approximately 25,900 additional deaths.2
Our model used the large random-effects meta-analysis (witha total of 302,296 subjects) by Bogers et al.3 A five-unit increasein BMI generated a 29% increase in deaths from coronary heartdisease, or, crucially, a 16% increase after adjustment forcholesterol level and blood pressure.3 Might Bibbins-Domingoet al. have underestimated the mortality effects?
Trends toward increased mortality from coronary heart diseaseare already detectable in the U.S. population.4 From 1997 through2002, the mortality rate leveled off among men who were 35 to44 years of age and actually increased by 1.3% annually amongwomen in the same age group.4 Perhaps the party is already over.
Simon Capewell, M.D. University of Liverpool Liverpool L69 3GB, United Kingdom capewell{at}liverpool.ac.uk
Julia A. Critchley, D.Phil. University of Newcastle Newcastle NE2 2JH, United Kingdom
References
Unal B, Critchley JA, Capewell S. Small changes in United Kingdom cardiovascular risk factors could halve coronary heart disease mortality. J Clin Epidemiol 2005;58:733-740. [CrossRef][ISI][Medline]
Ford ES, Ajani UA, Croft JB, et al. Explaining the decrease in U.S. deaths from coronary disease, 1980-2000. N Engl J Med 2007;356:2388-2398. [Free Full Text]
Bogers RP, Bemelmans WJ, Hoogenveen RT, et al. Association of overweight with increased risk of coronary heart disease partly independent of blood pressure and cholesterol levels: a meta-analysis of 21 cohort studies including more than 300 000 persons. Arch Intern Med 2007;167:1720-1728. [Free Full Text]
Ford ES, Capewell S. Coronary heart disease mortality among young adults in the U.S. from 1980 through 2002: concealed leveling of mortality rates. J Am Coll Cardiol 2007;50:2128-2132. [Free Full Text]
The authors reply: Kumar et al. incorrectly state that we usedweight alone as a marker for obesity. Our article states thatwe used BMI for adults and CDC growth charts for adolescents.Contrary to the suggestion by Kumar et al. and by Capewell andCritchley that an elevated BMI is an established independentrisk factor for CHD, we find the evidence mixed and the possibleindependent relationship of BMI with the risk of CHD controversial.Bogers et al., cited by Capewell and Critchley, showed thathalf of the effect of obesity on CHD was attributable to cholesteroland hypertension but that study did not adjust for changes inglucose metabolism; the authors themselves acknowledged thatthe residual risk may be due to diabetes. Lawler et al., thestudy cited by Kumar et al. as evidence that obesity has a directeffect on CHD, actually concluded that childhood BMI was notassociated with the subsequent risk of CHD. We modeled the well-establishedassociation of increases in BMI with changes in diastolic bloodpressure, changes in levels of high-density lipoprotein (HDL)and low-density lipoprotein (LDL) cholesterol, and diabetes.We did not model an independent association of BMI with therisk of CHD after accounting for these measured factors on thebasis of our analysis of Framingham data and observations thatthe relationship between BMI and the risk of CHD is substantiallydiluted after blood pressure, cholesterol levels, and the presenceor absence of diabetes are considered.1,2 In fact, we couldnot find data confirming an independent relationship betweenBMI and the risk of CHD after adjusting for measured blood pressure,measured HDL and LDL cholesterol, and confirmed presence orabsence of diabetes.
Capewell and Critchley and their colleagues,3 like our group,4used epidemiologic data to explain previous trends in deathfrom CHD, and they have recently presented data showing a slowingof the declines in mortality from CHD among men between theages of 35 and 54 years and an insignificant increase amongwomen in the same age group.5 By comparison, our recent analysisestimated future CHD. Even if, as we acknowledge in our article,we may have underestimated the effect of obesity to avoid overstatingthe case, we agree that obesity-induced changes in risk factorsfor CHD represent a potential time bomb that could offset muchof the progress made over the past four decades.
Kirsten Bibbins-Domingo, Ph.D., M.D. University of California at San Francisco San Francisco, CA 94143 bibbinsk{at}medicine.ucsf.edu
Lee Goldman, M.D., M.P.H. Columbia University College of Physicians and Surgeons New York, NY 10032
References
Jee SH, Sull JW, Park J, et al. Body-mass index and mortality in Korean men and women. N Engl J Med 2006;355:779-787. [Free Full Text]
McTigue K, Larson JC, Valoski A, et al. Mortality and cardiac and vascular outcomes in extremely obese women. JAMA 2006;296:79-86. [Free Full Text]
Ford ES, Ajani UA, Croft JB, et al. Explaining the decrease in U.S. deaths from coronary disease, 1980-2000. N Engl J Med 2007;356:2388-2398. [Free Full Text]
Hunink MG, Goldman L, Tosteson AN, et al. The recent decline in mortality from coronary heart disease, 1980-1990: the effect of secular trends in risk factors and treatment. JAMA 1997;277:535-542. [Abstract]
Ford ES, Capewell S. Coronary heart disease mortality among young adults in the U.S. from 1980 through 2002: concealed leveling of mortality rates. J Am Coll Cardiol 2007;50:2128-2132. [Free Full Text]
Previous
