Correspondence
Letter Regarding Article by Christou et al,
“Fatness Is a Better Predictor of Cardiovascular
Disease Risk Factor Profile Than Aerobic Fitness
in Healthy Men”
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Macera CA. Changes in physical fitness and all-cause mortality: a prospective study of healthy and unhealthy men. JAMA. 1995;273:
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To the Editor:
Christou et al1 postulated that fatness is a better predictor of
cardiovascular disease (CVD) risk factors than aerobic fitness.
The interpretations of the data may be misleading. Theoretically, 2 risk factors can be (1) independently associated with
a disease or (2) may be different steps along the same causal
pathway. In a chain of causation in which one factor affects
another factor, which eventually leads to disease, we must
interpret the analyses with caution. An example could be
fatness leading to atherosclerosis, which could lead to CVD. If
we adjust for the intermediate factor (atherosclerosis), then
the effect of fatness disappears completely if the effect of
fatness is mediated entirely through this factor. If the effect of
fatness was mediated through mechanisms other than atherosclerosis as well, only part of the association between fatness
and CVD would disappear.2 The fact that the 6 figures in the
article showing the association between fatness and the risk
factors with and without adjustment did not change when
adjusted for fitness strongly supports the hypothesis that
fatness is an intermediate factor closer to the end point in a
causal chain from fitness to the risk factor; however, the
authors came to the opposite conclusion.
Another concern with the study is a mean fitness level of 42
mL · min⫺1 · kg⫺1, with few subjects below 30 mL · min⫺1 ·
kg⫺1. The association between fitness and CVD risk factors is
not linear, but risk increases steeply when fitness decreases
below 30 to 35 mL · min⫺1 · kg⫺1.3 Because individuals with
elevated risk factor levels were excluded, they also excluded
individuals for whom the effect of physical fitness was
apparent.
Accordingly, the 3 implications the authors mentioned should
be altered. (1) “First, men who are overweight or obese should be
encouraged to reduce body fatness, regardless of their aerobic
fitness.” Low fitness may be the principal cause of fatness,
mediated through insulin resistance. (2) “Second, weight management and prevention of excess adiposity should be a primary
cardiovascular health goal for men.” We would add that this
could be done by staying active and insulin sensitive. (3) “Third,
in lean trained men, the cardioprotective influence of habitual
physical activity may be mediated in part through the maintenance of optimal body weight and fatness.” Studies analyzing
changes in physical activity or fitness in relation to CVD risk or
mortality have shown a lower CVD rate among subjects who
increase levels of activity or fitness that is independent of weight
change.4,5
In conclusion, low fitness and fatness may both be important
predictors of CVD risk factors.
Response
Andersen and colleagues make several statements regarding
our article published in Circulation,1 and we would like to
address each point separately.
First, the authors state that we “postulated” that fatness is a
better predictor of cardiovascular disease (CVD) risk factors than
aerobic fitness. This is an inaccurate précis of our article. We
stated no such hypothesis. Rather, our stated purpose was to
determine which of these putative influences better predicts
traditional CVD risk factors in healthy men. We took no a priori
position on this question.
Second, the authors state that the interpretation of our data
may be misleading because 2 risk factors can either be independently associated with a disease or be different steps of the same
causal pathway. Our analysis was designed to examine the
independent association of fitness (or fatness) with CVD risk
factors, while partialling out the effects of fatness (or fitness) and
age. Our study design did not allow determination of the
sequence of events in a causal pathway, as suggested by
Andersen and colleagues.
Third, the authors state that the mean V̇O2max of 42 mL ·
min⫺1 · kg⫺1 is of concern. Our subject cohort included men
with a broad fitness range, including highly trained competitive athletes. As such, a mean V̇O2max of 42 mL · min⫺1 · kg⫺1
is not remarkable. The authors also state that few subjects had
a V̇O2max below 30 mL · min⫺1 · kg⫺1 and that risk increases
steeply below 30 to 35 mL · min⫺1 · kg⫺1. In fact, 15% of our
participants had a V̇O2max below 30 mL · min⫺1 · kg⫺1, and
almost 40% of the subjects led sedentary lifestyles. The
statement by Andersen and colleagues that risk increases
steeply below a V̇O2max of 30 to 35 mL · min⫺1 · kg⫺1 also is
misleading. This conclusion is drawn from a study2 conducted
on adolescent boys and girls in which body fatness was not
measured, and both V̇O2max (from submaximal exercise heart
rates) and risk factors (from questionnaires or field tests) were
estimated.
Fourth, the authors state that “[b]ecause individuals with
elevated risk factor levels were excluded, they also excluded
individuals for whom the effect of physical fitness was
apparent,” inferring that our analysis may have been biased by
subject exclusion criteria. Again, our analysis included subjects with a broad range of fitness levels and a large
proportion of sedentary men. In addition, we clearly stated the
limitation that our findings should be restricted to healthy men
(top of page 1913).
Finally, Andersen and colleagues advise that we change our
conclusion on the basis of their interpretation of our data. In
particular, they emphasize the need to include information
about the insulin-sensitizing effect of physical activity. However, on page 1911 of our article under the subheading
“Aerobic Fitness and CVD Risk Factor Profile,” we discuss
this issue and state, “These observations support the need for
regular aerobic exercise as an important strategy to promote
optimal insulin sensitivity.”
Lars Bo Andersen, DMSc, PhD
Sigmund A. Anderssen, PhD
Department of Sports Medicine
Norwegian School of Sport Sciences
Oslo, Norway
Bengt Saltin, MD, PhD
Copenhagen Muscle Research Center
Rigshospitalet
Copenhagen, Denmark
1. Christou DD, Gentile CL, DeSouza CA, Seals DR, Gates PE. Fatness is
a better predictor of cardiovascular disease risk factor profile than aerobic
fitness in healthy men. Circulation. 2005;111:1904 –1914.
e253
e254
Correspondence
Overall, it appears that a central underlying concern of
Andersen and colleagues is that the conclusions of our study
underestimate and/or underemphasize the importance of physical
activity/aerobic fitness in controlling CVD risk factors. This is
not the case. The primary take-home message from our article is
not that habitual physical activity and fitness are unimportant, but
rather that body fatness should not be ignored as a key determinant of the CVD risk factor profile.
Demetra D. Christou, PhD
Christopher L. Gentile, MS
Christopher A. DeSouza, PhD
Douglas R. Seals, PhD
Phillip E. Gates, PhD
Department of Integrative Physiology
University of Colorado
Boulder, Colo
1. Christou DD, Gentile CL, DeSouza CA, Seals DR, Gates PE. Fatness is
a better predictor of cardiovascular disease risk factor profile than aerobic
fitness in healthy men. Circulation. 2005;111:1904 –1914.
2. Andersen LB. Blood pressure, physical fitness and physical activity in
17-year-old Danish adolescents. J Intern Med. 1994;236:323–329.
Downloaded from http://circ.ahajournals.org/ by guest on June 14, 2017
Letter Regarding Article by Christou et al, ''Fatness Is a Better Predictor of
Cardiovascular Disease Risk Factor Profile Than Aerobic Fitness in Healthy Men''
Lars Bo Andersen, Sigmund A. Anderssen and Bengt Saltin
Downloaded from http://circ.ahajournals.org/ by guest on June 14, 2017
Circulation. 2005;112:e253-e254
doi: 10.1161/CIRCULATIONAHA.105.565572
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