I finally found the report. Would have been nice if someone had provided the link. (Edit: OK, Alex did, but quite a bit upthread. It's on the
UKAD website, under Rule Violations: UKADvs_TiernanLocke_Decision_341.pdf
As I thought, there is nothing there that supports the conclusion of EPO 10-14 days prior to the sample taken as opposed to a later blood transfusion. In point 4, they say
then jump from that to point 48, where as previously noted here, they say the profile is "consistent with the use of an erythropoietic stimulant which had been discontinued approximately 10 to 14 days before the sample was taken." But as I and others have noted before, it's also consistent with a blood transfusion.
Since the method of manipulation is not relevant to whether JTL would be sanctioned, and if so, for how long (except that it includes the TOB), UKAD did not have to document why they concluded it was EPO. But this is very relevant to any argument about whether JTL stopped doping after the TOB.
The only other evidence noted is the very high but not quite over the limit off-score of about 128 from a sample taken on Sept. 24 at Manchester. This suggests the retics were starting to rise, but it's noted the difference is not significant, and the report says they didn't and couldn't use this evidence in coming to any decision. In any case, a slight rise in retics could be consistent with either EPO taken around TOB or a blood transfusion taken later.
I'll only repeat that the evidence in the literature does not offer strong support for the conclusion that 10-14 days following EPO retics would be severely depressed. It might happen, but a blood transfusion a little later is a much more certain way to get there.
And finally, I'm only jumping into this argument for the sake of the science. Unlike some of you, it doesn't matter to me when JTL doped. I thought some of the arguments in the decision were a little questionable, e.g., they said
This may be correct in a narrow sense, but there is a lot of evidence linking alcohol and reduced reticulocyte synthesis in alcoholics and in folate-deprived patients (the latter was discussed in the decision), and also in vitro. These studies don't prove that acute alcohol may inhibit reticulocyte synthesis in healthy patients, but I would regard this work as evidence for it. I don't have a problem with UKAD dismissing JTL's explanation for lack of strong support, but it's really not out of the question.
As I also pointed out earlier, the decision says he consumed 335 grams of alcohol, or 33 units. But Wiki says in England a unit of alcohol is 7.9 grams, not 10 grams (it is 10 ml). This of course has no bearing on the decision, but to me it's suggestive of sloppiness.