JAMA. 2005 Apr 20;293(15)--for free

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http://jama.ama-assn.org/cgi/content/full/293/15/1861

Maco

Message: 7

Date: Tue, 19 Apr 2005 16:51:02 -0700 (PDT)

From: Al Pater <old542000@...>

Subject: JAMA. 2005 Apr 20;293(15)

Hi All,

The below pretty much summarizes the pdf-available papers of possible

interest in

JAMA this week.

The JAMA issue is not yet in Medline.

This Week in JAMA

JAMA. 2005 Apr 20;293(15):1829.

BMI, Death, and Cardiovascular Risk

Trends in weight-related morbidity and mortality are the focus of 2 articles

in

this issue of JAMA. First, Flegal and colleagues (SEE ARTICLE) used nationally

representative data from NHANES I, II, and III and follow-up data collected

through

2000 to estimate the number of excess deaths in 2000 associated with body mass

index

(BMI), categorized as underweight, normal weight, and obese. They found that

compared with normal weight, both underweight and obesity were associated with

increased mortality, and the risk associated with obesity declined over time. In

the

second article describing 40-year trends in cardiovascular disease risk factors

by

BMI categories, Gregg and colleagues (SEE ARTICLE) report that the prevalence of

high cholesterol levels, hypertension, and current smoking have declined,

particularly among overweight and obese persons. Diabetes was the only risk

factor

found to have a stable prevalence over the 40 years. In an editorial, (SEE

ARTICLE)

Mark discusses challenges in assessing obesity-related health risks.

Editorials

Deaths Attributable to Obesity

H. Mark

JAMA. 2005 Apr 20;293(15)::1918-1919.

In this issue of JAMA, 2 studies1-2 present new analyses on the subject of

obesity. The study by Flegal et al1 is likely to generate interest because it

provides an estimate for deaths attributable to obesity that appears to strongly

contradict prior estimates published in JAMA. Flegal et al1 estimate that there

were

about 112 000 obesity-attributable deaths in the United States in 2000, far

lower

than the 414 000 estimated by Mokdad et al3-4 for the same year and the 280 000

estimated by et al.5 for 1991. The magnitude of the differences cries

out

for explanation of the reasons behind these differences. Some might wonder: If

well-intentioned efforts to calculate this number can result in such widely

varying

estimates, is it worth trying to do at all?

The underlying methods of all these studies involve the concept of

population-attributable fraction. Population-attributable fraction (or

attributable

fraction or etiologic fraction) is the proportion of morbidity or mortality in a

population that can be attributed to a particular cause or risk factor and is

one of

the empowering concepts of the public health perspective on health. The

attributable

fraction focuses attention not on a particular disease or risk of disease in the

individual but on the health of populations. In its most basic equation, this

quantity shows that the burden of disease caused by any risk factor is a

function of

the prevalence of that risk factor and the magnitude of its causal association

with

disease, usually expressed as relative risk. The greater the prevalence of the

risk

factor and the greater the relative risk, the greater the

population-attributable

fraction. The calculation offers a perspective on health that crosses

disciplines

and specialties and attempts to focus attention on causes of disease that are

most

responsible for death and illness. Over the past 40 years, cigarette smoking, a

common habit with highly elevated relative risks for several different causes of

death, has always risen to the top of the list. The attention paid to the

problem of

cigarette smoking as a major cause of disease and death has been in part a

result of

the information and perspective provided by population-attributable fraction

calculations.

Thus, it is natural, almost imperative, for public health care practitioners

to

apply this perspective to obesity, an issue perceived to be a growing public

health

problem. There is no doubt that the prevalence of obesity is increasing in the

United States. However, for many reasons it is much more difficult to estimate

the

burden of disease due to obesity. Although weight is an easily measured

characteristic, at a conceptual level attributing deaths to obesity requires

many

assumptions that are often not fully spelled out in most studies.

Consideration of the causal pathways through which obesity increases

mortality is

important. Body mass index itself is affected by dietary intake and physical

activity levels, which may affect health in ways mediated by body mass index or

independent of it. According to the most recent clinical guidelines for

cardiovascular risk reduction, most of the risk of cardiovascular disease caused

by

obesity is thought to be mediated through traditional risk factors such as

diabetes,

cholesterol, and hypertension.6 Thus, the guidelines do not incorporate obesity

as

an independent factor in which to estimate risk of cardiovascular disease.

Calculating obesity-related deaths without accounting for other cardiovascular

risk

factors, as has been done in previous studies,3-5 assumes a consistent

relationship

between obesity and these mediating risk factors. However, in the study by Gregg

et

al2 in this issue of JAMA, analysis of representative samples of Americans show

that

the association of obesity and other cardiovascular risk factors has changed

over

the past 40 years. Obese persons now smoke less and have lower cholesterol

levels

and lower blood pressure. Although mortality outcomes are not evaluated in the

study

by Gregg et al,2 because of interactions between risk factors, this

across-the-board

decrease in risk factors across all weight groups could translate to a lowering

of

the elevated risk of death associated with obesity.

However, other gaps in current knowledge about health risks of obesity might

temper this possibility. Most deaths occur among older persons, whose weight

during

old age may or may not reflect weight throughout their entire lifetime. Studies

evaluating risks of obesity usually assess weight at a single point in time

rather

than throughout life. Knowledge is not complete regarding the health effects of

differing lifetime trajectories of body weight. Many studies have shown that

obesity

among children and adolescents is increasing.7 Younger age of onset of obesity

may

result in a longer duration of obesity throughout life, which may increase

obesity-related mortality. Many other issues complicate the assessment of

obesity-related disease, including choice of statistical techniques and choice

of

study populations in which to calculate mortality risks, to name a few issues.

Complicating the task even further is the basic issue of numerical

uncertainty,

caused by the need to estimate many numbers from so many different data sources.

An

important and possibly overlooked contribution by the study by Flegal et al1 is

the

formal calculation of confidence intervals around the estimate of

obesity-related

deaths. When relative risk estimates are only modestly elevated, as in the case

of

obesity, very small changes in the relative risk translate to large differences

in

the population-attributable fraction.8 Thus, it should come as no surprise that

the

95% confidence interval around the estimate of 112 000 deaths ranges from 54 000

to

170 000, greater than a 3-fold difference reflected within the range. Although

the

other studies3, 5 that previously estimated obesity-attributable death did not

include confidence intervals, the estimates from those studies should be assumed

to

have underlying uncertainty at least as great.

These studies and their disparate findings highlight the importance of

continuing

to develop more rigorous approaches for estimating obesity-attributable deaths.

Ultimately, though, it may be possible to gain a better and more realistic

understanding of the preventable disease burden caused by obesity by evaluating

public health and individual programs designed to both prevent and treat

obesity,

such as diet and exercise programs. Such programs should also be evaluated for

their

ability to reduce disease and morbidity in addition to effects on body weight,

for

there may be additional benefits (or possible risks). With sufficient knowledge

of

the effectiveness and required resources of these programs, it will be possible

to

make rational decisions regarding the best way to maintain and improve the

health of

the public.

REFERENCES

1. Flegal KM, Graubard BI, on DF, Gail MH. Excess deaths associated with

underweight, overweight, and obesity. JAMA. 2005;293:1861-1867.

2. Gregg 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.

3. Mokdad AH, Marks JS, Stroup DF, Gerberding JL. Actual causes of death in the

United States, 2000 [published correction appears in JAMA. 2005;293:298]. JAMA.

2004;291:1238-1245.

4. Mokdad AH, Marks JS, Stroup DF, Geberding JL. Correction: actual causes of

death

in the United States, 2000. JAMA. 2005;293:293-294.

5. DB, Fontaine KR, Manson JE, et al. Annual deaths attributable to

obesity

in the United States. JAMA. 1999;282:1530-1538.

6. National Cholesterol Education Program (NCEP) Expert Panel on Detection.

Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment

Panel

III). Third Report of the National Cholesterol Education Program (NCEP) Expert

Panel

on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults

(Adult

Treatment Panel III) final report. Circulation. 2002;106:3143-3421. FULL TEXT

7. Ogden CL, Flegal KM, Carroll MD, et al. Prevalence and trends in overweight

among

US children and adolescents, 1999-2000. JAMA. 2002;288:1728-1732.

8. Flegal KM, on DF, Pamuk ER, Rosenberg HM. Estimating deaths

attributable

to obesity in the United States. Am J Public Health. 2004;94:1486-1489.