 n this Special Topics interview, correspondent Gary Taubes talks
with Dr. William Dietz of the Centers for Disease Control and
Prevention (CDC) about his highly cited work in obesity research. The
recent Special Topics analysis of obesity research in the past decade
ranks Dr. Dietz among the top 25 researchers in this specialized area,
with 47 papers cited a total of 1,532 times. Dr. Dietz’s most-cited
paper, "Long-term morbidity and mortality of overweight
adolescents—a follow-up of the Harvard Growth Study of 1992 to
1935," (New England
Journal of Medicine 327 [19]: 1350-5, 5 November 1992), was cited
302 times at the time of the analysis, and, according to the ISI
Essential
Science Indicators
Web product, currently
has 348 citations. Dr. Dietz is a member of the Division of Nutrition
and Physical Activity, which is part of the National Center for
Chronic Disease Prevention and Health Promotion at the CDC.
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 What inspired you to study 60-year-old data for the effects of
adolescent obesity, and how did you even know of the Harvard Growth
Study?
Actually this data set fell into our laps. The Harvard Growth Study
was initiated by the Harvard School of Education in 1922 to examine
the relationship of growth to academic performance. I didn't know
about it until a dentist called me up one day and asked me if I knew
about this study and would I be interested in getting access to the
records. He knew that the University of Pennsylvania anthropology
department had all the original records of children and adolescents
who had been studied from the time they entered school until the time
they graduated. And it was a fairly sizable group of children. The
study represented an unparalleled opportunity to begin to look at the
impact of early growth on later health outcomes. So the way we got
that data was completely serendipitous.
How did you use the data for the study?
At the time Aviva Must was a graduate student with me. She began
looking into these data and linking them to what are called, somewhat
morbidly, the death tapes. These are a compendium of reported causes
of death linked to names. The death tapes allowed us to do a follow-up
of people based on their names and causes of death. In addition, there
had been another survey linked to this data by anthropologists, if I
remember correctly, who were mostly interested in breast cancer. They
had gone back and followed up on a number of these children when they
were about 50 years of age. They asked questions about cigarette
smoking, but they also asked about their body weight at mid-life, when
the group was in their 50’s. That survey enabled us to look at the
effect of early childhood growth and, more specifically, adolescent
weight on both adult morbidity and mortality, while controlling for
mid-life weight. We could separate out the influence of adolescent
weight and adult weight on morbidity and mortality. So, for example,
we could see if the main impact of adolescent weight was to make
somebody overweight as an adult and therefore more susceptible to the
complications of obesity. On the other hand, we could also control for
adult weight and just look at the influence of adolescent weight on
morbidity and mortality. When we did so, we still found a significant
influence of adolescent obesity on adult morbidity and mortality.
What was your interpretation of that finding?
It implies that there is something going on during adolescence that
makes an individual more susceptible to the complications of obesity
as an adult. One potential candidate is the disposition of visceral
fat. We know that adolescence is a time when the sex-linked fat
distribution develops. Adolescent boys develop central body fat; girls
develop gluteal fat. One possibility is that adult morbidity and
mortality is mediated by those differences in fat distribution, which
are accentuated by obesity present in adolescence. The second
possibility is that simply the duration of the added weight may have
an impact. The first explanation is my preference.
Why do you think the paper had such impact?
One reason is that it's a unique study. Fifty-year follow-up
studies with careful childhood measurements are pretty rare in the
literature. Secondly, I think the other potential factor that makes
this such an influential paper is it was possible to control
observations for mid-life weight, which enabled us to refine further
observations we made. Thirdly, it didn't hurt that it was published in
the New England Journal of Medicine.
Did you follow up on the original observation in later research?
I don’t know any easy way we could reprise that paper. We have
looked at some implications. For example, I published a paper that
argued that there were critical periods in the development of obesity.
The Harvard Growth Study influenced my thinking. I argued that there
were three critical periods: the NEJM article emphasized
adolescents, but there is subsequent literature on birth weight—high
birth weight infants are more likely to go on to become obese—and
another period of so-called adiposity rebound. There are also other
factors, like breast-feeding or television viewing, that can mediate
development of obesity during these three intervals .
What is the connection with breast-feeding?
Children who are breast-fed have lower risk of obesity. I just
wrote an editorial for JAMA on this subject. The behavioral
theory behind this is that when the mother is breast-feeding, it's
really only the infant's satiety cues that prompt her to terminate the
feeding episode. However, if the child is being fed formula out of a
bottle, the gauge of whether the infant had enough to eat depends on
how much of the bottle the infant has finished. The physiological
explanation may have to do with the increase of insulin levels in the
infant responding to formula feeding. A much higher insulin response
to formula may influence growth factors and prompt weight gain in
formula-fed infants.
Do you have one question you would like to see answered more than
any other on the subject of adolescent obesity?
Yes. What nutritional factors are driving the epidemic? Let me
clarify that. There have been lots of changes in the U.S. diet over
the last 20 to 30 years, which is the period of time that adolescent
obesity has increased most rapidly. These include an increased
proportion of the family food budget spent on food consumed outside
the home, increased soda and sugared beverage consumption, a reduction
in family meals, an increase in variety of foods consumed, an increase
in portion size, and an increase in meal skipping. But none of these
factors have been conclusively linked to the increased risk of
obesity. Preliminary data links each one of those to increased risk,
but none have been linked tightly enough to allow us argue that these
are things all Americans should do or should avoid.
What is the single biggest challenge to finding the answers?
It's an analytic one. And there are two elements to that:
traditional dietary analyses have relied on caloric intake or fat
intake or percentage of calories from fat, rather than looking at
dietary patterns, which are what I just relayed to you. The other is
an absence of prospective or longitudinal studies that allow us to
link those behaviors to the development of obesity. We must do more
prospective studies that look at dietary intakes or patterns of intake
and their influence on subsequent fatness in children and teenagers.
What do you feel you've accomplished in your research?
I think we put this problem on the map. Twenty years ago, I was one
of half a dozen people interested in childhood obesity or concerned
about it as a problem. Today, obesity is widely recognized as a major
health problem in the United States. And I hope that some of the work
we've done is ultimately going to lead to solutions to prevent this
problem or to effectively treat it.
Are you optimistic?
Yes and no. Do we have an effective way of preventing and treating
obesity? No. But I think the awareness of obesity is similar to the
awareness about smoking in the 1950s. The decline in smoking rates
began with increased awareness of the consequences of smoking, in
particular the Surgeon General's report linking lung cancer with
smoking and the withdrawal of advertisements for smoking. That led to
a plateau in cigarette consumption. Subsequently, with the advent of
non-smokers' rights campaign, there's been a decline in cigarette
consumption. The challenge is to find the equivalent of a non-smokers'
rights campaign with respect to obesity. I don't think we have an
answer to that as yet. But I think the increased awareness of the
problem is a start.
Dr. William Dietz
National Center for Chronic Disease Prevention and Health Promotion
Division of Nutrition and Physical Activity
Centers for Disease Control and Prevention
Atlanta, GA, USA
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ESI Special Topics,
April 2002
Citing URL - http://www.esi-topics.com/obesity/interviews/DrWilliamDietz.html
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