4. American Diabetes Association Position Statement. Diabetes Care 2002;25(1):202-212. 5. Taubes G. Epidemiology Faces It’s Limits. …
Feeding
Risk Factor Frenzy
Jon Robison, PhD, MS
The article in the August 25th issue of the Journal of The American Medical
Association, Sugar-Sweetened Beverages, Weight Gain, and Incidence of Type
2 Diabetes in Young and Middle-Aged Women, adds yet another chapter to the
feeding frenzy that drives our nations love affair with epidemiological
risk factorology This article is a textbook case study in the misuse of
epidemiological research for the development of health recommendations for
the public
The article is strewn with misleading and sometimes inaccurate
statements and enough statistical hocus pocus to make all but the most
adept junk-science sleuth dizzy Perhaps the most glaring problem with this
article, however, is the blatant blurring of the distinction between
correlation or association and causation A correlation describes the
strength of a relationship between two factors It turns out, for instance,
that there is a correlation between baldness in men and heart disease This
simply means that there is some relationship between baldness and heart
disease If we observe a
large group of men over a period of years, those
who are bald are statistically more likely to have a heart attack than are
those with a full head of hair We say that the correlation or association
between these two variables is positive, and that baldness is a risk factor
for heart disease in men 1
Despite the evidence that bald men have an increased risk of heart
disease, however, certainly no one would claim that giving a bald man a
toupee would decrease his risk This is because baldness does not have any
influence on heart health, but is simply a factor that happens to be found
more often in men with heart disease Therefore, when we say that any two
factors such as baldness and heart disease are positively correlated, we
are saying nothing about whether one causes or even affects the other
Heres how the same problem occurs, as it does in this article, with
nutrition research In a certain population being studied, a particular
disease is found to be positively correlated with eating a specific food
This means that people who ate this food were more likely to develop the
disease in question than people who didnt eat the food It is then
reported that eating this food
incrreased the risk of getting this disease
If the report garners enough attention health professionals may well begin
to make recommendations for changes in peoples eating habits based on the
reported findings
In this particular article, the diseases in question are obesity and
diabetes and the food involved is the much-maligned sugar in sweetened
beverages The problem is that the identification of this food as a risk
factor in this study may or may not mean there is a causal link with the
diseases in question It is entirely possible that subsequent studies will
not find an association between this food and these diseases In fact,
previous studies have actually suggested the opposite association between
sugar consumption and obesity,2,3 and after reviewing the relevant
research, The American Diabetes Association concluded in a recent Position
Statement that intake of sucrose and sucrose containing foods does not
need to be restricted because of concern about aggravating hyperglycemia
4
In a discussion on the limitations of epidemiological research in the
prestigious journal Science, Leading UCLA epidemiologist Sander Greenland
summed up the complexities involved
with obscuring the differences between
correlation and causation by saying,
There is nothing sinful about going out and getting evidencenothing
sinful about seeing if that evidence correlatesthe sin comes in
believing a causal hypothesis is true because your study came up with
a positive result 5
Unfortunately, this sin is committed numerous times in this article, as
the critical distinction between correlation and causation falls by the
wayside In setting up their argument in the very first paragraph, the
authors state recent evidence suggests an association between the intake
of sugar-sweetened soft drinks and the risk of obesity in children In
the very next sentence they make the unwarranted jump to causation saying,
besides contributing to obesity, sugar-sweetened drinks might So, in
fact, they have already concluded that half of their hypothesis is correct,
before even presenting the evidence
Even more blatantly, in their closing comments the authors conclude,
because of the observational nature of the study, we cannot prove that the
observed associations are causal Yet this does not stop them from making
the jump to causation in the next
paragraph by recommending that, Public
Health Strategies to prevent diabetes and type 2 diabetes should focus on
reducing sugar-sweetened beverage consumption
Interestingly, a closer look at the findings shows that even the
proposed associations between the variables are questionably weak at best
After correcting for confounding factors, the relative risk of developing
diabetes in women drinking the greatest vs the least amount of sugar-
sweetened beverages was 132 Epidemiologists generally agree that relative
risks less than 2 should be ignored or at least viewed with extreme
skepticism, particularly when there is conflicting research available 5
Applying epidemiological research in this fashion is simply bad
science It tends to scare and confuse people and it greatly oversimplifies
the complicated etiology of the types of chronic conditions in question A
number of leading scientists involved in conducting this type of research
have acknowledged the significance of this problem Perhaps those who have
not should heed the warning of Dimitrios Trichopoulos, head of the
epidemiology department at Harvard School of Public Health:
We are fast becoming a nuisance to
societyPeople dont take us
seriously anymore, and when they do take us seriously, we may
unintentionally do more harm than good 5
References
1 Lotutu PA, Chae CU, Ajani VA, Hennekens CH, Manson JE Male Pattern
Baldness and Coronary Heart Disease Arch Intern Med 2000:160:165-171
2 Gibney, M, Siman-Grant, M, Stanton, J, Keast, D Consumption of
Sugars
American Journal of Clinical Nutrition 621 suppl:178S-193S
3 Ruxton, C, Garceau, F, Cottrell R Guidelines for Sugar Consumption
in Europe: Is a quantitative approach justified? European Journal of
Clinical Nutrition 1999;537:503-513
4 American Diabetes Association Position Statement Evidence-Based
Nutrition Principles and Recommendations for the Treatment and
Prevention of Diabetes and Related Complications Diabetes Care
2002;251:202-212
5 Taubes G Epidemiology Faces Its Limits Science 1995;269:164-169
Source:jonrobison.net
