Monday, December 29, 2008

The Winnowing: John Amory

John Amory MD, is a leading andrologist (male hormone specialist) who testified for Landis in both hearings, arguing the metabolism of testosterone as documented in all reviewed studies does not have divergences between the adiols claimed in the test values.

Amory had served on USADA anti-doping review boards prior to the Landis case. In response to a specific question, he replied, "
I would considering serving on an ADRB again, but part of me is very glad to be focusing on my clinical duties and my research (male contraception, oral testosterone development), and out of the contentious world of doping. "

[Back to the Introduction]

My thoughts about the Landis case are as follows:

1) The results of his IRMS were scientifically indeterminate. There is a nice discussion of this in the article by Berry from Nature which makes this case more eloquently than I can.

2) The criteria for positivity of the IRMS should be standardized between labs based on larger normal samples. For example, the UCLA lab requires the delta of both the 5-alpha-androstanediol and the 5-beta-androstanediol to be significantly elevated, but WADA only requires that a single metabolite be elevated. The latter approach reduces the specificity of the test, thereby increasing the risk of a false positives, which is probably what happened in this case (5-alpha abnormal, 5-beta normal).

3) Testing of the "B" sample should be performed at a centralized reference lab and the results from the B sample should corroborate the results from the "A" sample before a positive result is resulted. Using replicated results from two labs would vastly improve confidence in the results as it is unlikely both labs would be wrong in the same way, and it would defused "the lab is out to get me defense."

4) Only peer-reviewed published literature should be considered as evidence. In the Landis case, the prosecution argued that the 5-alpha/5-beta discrepancy was secondary to the use of testosterone gel by Mr. Landis.

They hypothesized that the use of the gel specifically increased 5-alpha reduced metabolites of testosterone. To support this, they referred to a very small unpublished study that administered testosterone gel in normal men by Schanzer and colleagues. However, in this study only two men had undergone IRMS testing and only one of whom had the isolated elevation in his 5-alpha metabolite. To my knowledge, this study has still not been published, despite that fact that this group has been very active in publishing in this area. Was the original hypothesis correct? Does testosterone gel use selectively increase 5-alpha metabolites? Clearly, it is preferable to use peer-reviewed published papers to try to understand this, and prevent erroneous and premature conclusions from being reached.

John K. Amory MD, MPH
Associate Professor of Medicine
Division of General Internal Medicine
University of Washington


Mike Solberg said...

I have always believed that Amory's testimony was unfairly disregarded by the AAA majority, to the great detriment of fairness in the case. Amory's evidence has always been persuasive to me (persuasive that USADA did not prove its case - not persuasive that Floyd didn't dope, as you can't prove a negative). Add Berry's statistical argument, and ugh, my blood is beginning to boil again!


Cheryl from Maryland said...

I remember being overwhelmed by the clarity of Dr. Armoy's scientific points and his common sense. Reading his post brought out more - WADA's argument (e.g. a last minute attempt to save face) that the lack of proper association between the 5A and 5B values was due to the use of a gel -- a hypothesis only supported by a non-peer reviewed study comprising of one individual using the gel in question. Ugh.

Kudos to Dr. Armory, and best wishes for his future endeavors.