Teleoanalysis: combining data from different types of study

Epidemiological
studies are useful for creating new hypotheses about disease causation. However,
to prove that a statistical association is causal demands experimentation,
because even the strongest association may be secondary to the real cause.

     To bypass this elementary principle, Professor
Wald and Dr. Morris, representatives for a new branch in the medical sciences
named aetiological epidemiology, have invented a statistical instrument to
synthesise different categories of evidence.¹ By teleoanalysis as
they call it, it is possible to measure the extent to which a disease can be
prevented, for instance how much ischaemic heart disease that can be avoided by
reducing dietary saturated fat. They admit that the crucial experiments, the
dietary trials, have failed, but as we “know” that saturated fat intake
increases the risk of heart disease, we can use a surrogate outcome, the
intermediate factor cholesterol as evidence, implying that we also “know”
that high cholesterol increases the risk. Say Law and Morris, the latter has
been shown in epidemiological cohort studies and in trials of cholesterol
lowering drugs.

     These assumptions are false, however. The
allegation that patients with heart disease have eaten more animal fat than
healthy individuals has been falsified by at least 21 cohort studies and six
case-control studies including more than 150.000 individuals,² and
other types of epidemiological studies have been just as unsuccessful. For
instance, dynamic population studies, including data from more than 100 time
periods in 35 countries, have found no association between changes of saturated
fat consumption and changes of coronary mortality, and in four cohort studies no
association was found between degree of atherosclerosis at autopsy and dietary
intake of saturated fat.²

     The evidence from the cholesterol lowering drug
trials are just as invalid. Cholesterol lowering had no effect on heart
mortality before the statin era,³ and the effect of the statins is
most likely due to other, more beneficial effects on the cardiovascular system.
Dose-response has been claimed, but only by comparing mean values from the trials.
In all clinical and angiographic trials, where dose-response was calculated from
individual data, the effect was independent on the degree of cholesterol
lowering, a strong argument against causality.^4,5

     According to Wald and Morris the name
teleoanalysis was chosen to indicate thoroughness and completeness. It is
difficult to find a more misleading term considering that I have only mentioned
a few of the studies that contradict the diet-heart idea. There are many, many
more.^4-7 

1. Wald
   NJ, Morris JK. Teleoanalysis:
   combining data from different types of study.BMJ
   2003; 327: 616-618. [Full
   text][PDF]
2. Ravnskov
   U. The questionable role of saturated and polyunsaturated fatty acids in
   cardiovascular disease. J Clin Epidemiol 1998;51:443-460. [Abstract]
3. Ravnskov
   U. Cholesterol lowering trials in coronary heart disease: frequency of
   citation and outcome. BMJ 1992;305: 15-19. [Abstract]
4. Ravnskov
   U. A hypothesis out-of-date: The diet-heart idea. J Clin Epidemiol. 2002:1057-1063.
   [Abstract]
5. Ravnskov
   U. Is atherosclerosis caused by high cholesterol? QJM 2002; 95: 397-403.
6. THINCS,
   The International Network of Cholesterol Skeptics; www.thincs.org
7. Ravnskov
   U. The Cholesterol Myths. Washington DC: New
   Trends Publishing, 2000.