- 11:26 pm - Tue, Aug 19, 2014

Q: Re: MCV. You missed the point here. Dehydration (from alcohol) might cause changes in MCV (hyperosmolarity of plasma when fluid is lost, thus smaller red cells). EPO influence on MCV not discussed in the case.

Anonymous
right but follow along here for a bit

the heart of the case is the probability of doping given the ABP values estimated with Bayesian statistics.

for simplicity and because the actual ABP software is a bit of a black box consider walking through the argument in terms of Bayes theorem.

the probability of doping given the ABP results equals the prior probability of doping times the probability of the ABP results given doping divided by the probability of the ABP results.

P(doping/ABP) = P(doping)*P(ABP/doping) / P(ABP)

UKAD basically argued that the probability of doping was astronomically high because the probability of the results were astronomically low

**^P(doping/ABP)** = P(doping)*P(ABP/doping) / **vP(ABP)**

JTL’s side argued that dehydration was likely so the probability of the ABP results was actually high and therefore the probability of doping low

**vP(doping/ABP)** = P(doping)*P(ABP/doping) / ^**P(ABP)**

UKAD countered and said that since the MCV was normal then the probability of dehydration was so low as to be negligible

**^P(doping/ABP)** = P(doping)*P(ABP/doping) / **vP(ABP)**

the issue is that if you argue that MCV is good enough to rule out dehydration (which its not) then you can argue that its certainly good enough to rule out high dose EPO (which again it is not) AND since the results can not be explained by micro dose EPO then EPO can be ruled out all together.

that last part is a MAJOR issue for UKAD had JTL’s side been savvy enough to pick up on it.

since the entire argument revolves around a Bayesian estimate of probability as soon as UKAD introduced evidence of a normal MCV and also insisted on no dehydration then this evidence must be used to update the Bayesian estimate. (I understand this is not how the legal system works as you seem to get to coast through if your opponent is weak but it is how stats/science/reality works)

so with this evidence (if its good enough for UKAD then its good enough for this blog for the sake of discussion) we can populate the equation with some numbers to see how ruling out EPO changes the probability.

UKAD calculated P(doping/ABP) at 99.9999%

a conservative estimate of the prior probability of doping p(doping) might be 15%

plugging these values in

.999999 = .15*P(ABP/doping) / P(ABP)

6.6666 = P(ABP/doping) / P(ABP)

in terms of oxygen vector doping EPO likely accounts for the majority of doping and we’ll use 65% here as a reasonable example

taking EPO out of the equation means that your prior probability of doping is no longer 15% but now 5.25%

ie

**vP(doping/ABP)** = **vP(doping)***P(ABP/doping) / P(ABP)

or solving for the probability of doping given the values

P(doping/ABP) = .0525 * 6.6666

P(doping/ABP) = .350

probability of JTL doping = 35%

JTL not guilty

the values were more likely a lab or physiological anomaly

now this is a bit of an oversimplification but had JTL’s side picked up on the above then this case would likely not have played out as such a clear slam dunk decision

on the other hand

if UKAD had said fine there could be dehydration they could have then gone on to point out that the MCV must have come down from an elevated value making high dose EPO all the more likely given the extremely low retic and a still high for even a dehydrated state in season Hgb concentration

…

for those wondering what MCV has to do with EPO

when EPO stimulates red cell production the new cells tend to be larger in size so that the mean corpuscular volume MCV tends to get elevated. after coming off of EPO the MCV drifts back down as the cells age. MCV has in the past been proposed as an indirect marker for EPO use. MCV can also be affected by blood storage conditions so could potentially have some utility in picking up transfusions as well.