Crystal Clear? If you say so.

Good catch, I misread that one. They only draw conclusion based on the results of finding MV genome in the blood. They draw no conclusions on the results of the PMBC PCR results at all.

Unless someone is claiming that looking for MV in the blood is a proxy for gut tissue, then it is crystal clear that this study can’t be compared to Uhlmann. It still leaves them with a flawed hypothesis as well.

That is an entirely accurate and reasonable statement, as far as I can tell. Key words being circulating and antibody levels. No differences. How is that misleading?

If you read their conclusions carefully, they are worded as though they proved the null hypothesis. That would be proving a negative.

“There is no difference between ASD cases and controls in circulating measles
genome or measles antibody levels.”

You can’t make that statement without knowing the rate of false negatives or knowing the efficacy of using PBMCs as a proxy for lingering MV genome.

You’ll note there is no comment on replication of other studies, and I’ve clearly pointed out due to numerous issues (including fundamentally different study groups) in scientifically comparing this study will Uhlmann.

That’s why this whole MMR fiasco is a ridiculously moot issue. Wakefield never found MV in the gut…end of argument.

Just ask Bustin.

I can’t offer any insights concerning the authors’ intentions, but who said anything about proving a negative? The way I read it, they looked for measles and measles antibodies and found no differences between ASD and controls. Failed to replicate or confirm.

Sorry about that last post. Those greater than less than signs always get me.

...

I’m not sure where you got the younger group from? The study group was taken from a cohort born in 1990, 1991. This is corroborrated by the Standard deviation of less than 1. If I remember my stats, that means that greater than 95% of the study group was within 2 years of the mean and 99.7% within 3 years of the mean. Of course, very few details were published in this study making it hard to make any judgements on anything.

The children in the Wakefield study (2000) had a median age of 7 years; range, 3–14. His original study ages were: (4, 9.5, 7, 10, 8, 5, 3, 3.5, 6, 4, 6, 7). All of the study group in the Uhlmann study had ileocolonic lymphonodular hyperplasia.

You stated: “Wakefield has claimed that these kids are chronically infected, not that the infection clears up given enough time.”

Yes, and they studied children with active GI issues. Additionally, they made no definitive claims at all. From their own words, it just raises questions:

“These preliminary studies have focused principally on MV. We have not excluded the presence of alternative infections. Viruses may persist elsewhere, or exert a transient effect not requiring subsequent persistence.
...
Our study raises many questions—most importantly, does MV play an aetiological role in intestinal inflammation in developmental disorder? The study reports for the first time an association between MV infection and ileocolonic lymphonodular hyperplasia and ileocolitis in children with developmental disorder.”

As for PCR, I’ve heard and read so many potential issues and limitations regarding the technique I don’t know what to believe anymore. Don’t mistake my issues with the current study as support for the PCR results of AW’s study (2000), for I am skeptical of those results.

However, that issue does not change the issues with this current study, nor with the invalid attempts to compare the results.

The problem isn’t that you’re dealing with low detection rates, you’re dealing with unknown detection rates.

If you want to prove a negative, you have to know the rate of false negatives.

You also have a string of assumptions here (age of the participants, unknown GI issue status) each of these with unknown probabilities. Since it is a string of assumptions, the probabilities must be multiplied. That usually makes an extremely low probability in the end which would match the result we saw—obviously, there could be any number of other reasons for the null result, including a lack of correlation.

“average age 12, right, but age distribution included children that were much younger and received the MMR more recently. What was the average age of the children in Wakefield’s studies and were there any children that were still measles positive (according to AW) after 10 years?”

I’m not sure where you got the younger group from? The study group was taken from a cohort born in 1990, 1991. This is corroborrated by the Standard deviation of 95% of the study group was