The MMR (Vaccine)-Autism Link
Bill Long 9/11/08
A Sept. 4, 2008 Study
This significant study, jointly done by the Centers for Disease Control and Columbia University (and other) researchers, was an attempt to replicate a 1998 study done by Dr. Andrew Wakefield, an autism researcher who first discovered the presence of measles virus ("MV") RNA in bowel tissue of children with autism spectrum disorders ("ASD") and gastrointenstinal ("GI") disturbances. Wakefield's 1998 study, published in the Lancet, not only demonstrated that a very high percentage of children affected by ASD's also had GI problems, but he posited a mechanism by which these GI problems might lead to autism. To simplify only a little, he argued that a pathway for the genesis of autism could likely be from the MMR vaccine, to the presence of trace amounts of the MV in a child's system, to the seepage of this MV amount through the stomach wall (i.e., the "leaky gut" syndrome) to a combination with other bacteria that would affect the central nervous system to the expression of autistic symptoms. Though this was a hypothetical construct, it was supported by the strong correlation, in Wakefield's study, between ASD and GI disturbance. He thought that the MMR could be a vital causal link in provoking this correlation. Dr. Wakefield has paid a high professional and personal cost for advancing this hypothesis (because some parents decided not to vaccinate their children as a result, which brought the weight of the "disease-control" folks on him, among others), but his thesis remained basically unexamined for a decade. As the Sept. 4 study says,
"Subsequent investigations found no associations between MV exposure and ASD but did not test for the presence of MV RNA in bowel or focus on children with ASD and GI disturbances."
And then, we see the real reason for the study:
"Failure to replicate the original study design may contribute to continued public concern with respect to the safety of the MMR vaccine."
Study and Conclusions In a Nutshell
This study, then, was meant to be a replication of the 1998 study. Like James Adams' 2008 study on mercury in baby hair, which didn't really support Amy Holmes' earlier results on that same issue, this Sept. 4 study couldn't replicate either Wakefield's data nor did it lend any support to his "genesis of autism" thesis. The Sept. 4 study gathered 38 participants, 25 of whom had autism (in this case it was not simply the broader category of ASD's but the "full blown" autism) and GI disturbances and 13 children with GI disturbances alone. The latter were the "controls." Each one of them was to receive a "clinically-indicated ileocolonoscopy," with biopsy of tissue. The number in the sample was rather small (and all the participants were already planning to get a colonoscopy) because it might violate medical ethics to induce a costly, painful and intrusive testing procedure when it was not necessary.
Crucial for the study was to examine the "temporal onset" of GI episodes and autism relative to the timing of the MMR administration. In other words, since Wakefield had advanced the hypothesis of causation, it was important to test whether MMR came first, then came GI disturbance and then came autism. If autism was diagnosed before the MMR was administered, for example, then his theory would not be supported. Of course, it wouldn't necessarily disprove the theory, but it wouldn't make it look good, especially if there were multiple examples where the MMR to GI to autism wasn't happening.
Well, the study found the following. First, it found no differences between case and control groups (i.e., autistic and non-autistic kids) regarding the presence of MV RNA in the ileum and cecum. This is an important finding, for it was directly contrary to Wakefield's conclusion. He had argued there was a high single-digit multiple difference between those autistic children who had traces of MV in their ileum and cecum, and controls. In this case, however, only one subject in the "case" and one in the "control" group still had traces of MV RNA in the ileum and cecum. A second conclusion, however, wasn't as clear-cut for me. The report concluded:
"There were no significant differences in the proportion of cases and controls with MMR before onset of GI episodes: 12 of 25 cases (48%) received MMR before GI episodes as compared with 3 of 13 controls (23%)."
But, at first blush, these numbers do seem significant, don't they? That is, even though there may be little trace of the MV in any of the autistic or "normal" children, almost 1/2 of autistic children, compared to fewer than 1/4 of typical children, received the MMR before the GI episode. Thus, there is a 2:1 ratio of the symptom order: MMR-GI/AUT than MMR-GI-no autism. This would suggest to me that there is something in the autistic children that had a tendency to respond to the MMR in a more severe manner than the "normal" children. What that "something" is ought then to be the subject of lots of further research. Is it a "genetic disposition" or "susceptibility"? Who knows precisely. But this is what we need to discover.
One other conclusion ought to be noted.
"Only 5 of 25 subjects (20%) had received MMR before the onset of GI complaints and had also had onset of GI episodes before the onset of AUT."
Thus, sometimes it was MMR-GI-AUT and sometimes MMR-AUT-GI. This tends to make Wakefield's hypothesis about the pathway leading to autism look very shaky, but it continues to support the notion that something in the MMR vaccine may tend to "trigger" something in a subset of people that leads to a higher rate of autism. Now we know where research should proceed. Wakefield's hypothesis may have been buried by this study, but the question is now all the more urgent. How, indeed, might something in the MMR connect up with something in a subset of kids that might lead the way to autism? You will receive the Nobel Prize if you can answer that question.