Archive | September, 2016

No, Wakefield’s Autistic Enterocolitis Does Not Exist

2 Sep

Listen to Andrew Wakefield talk for a while and he will tell you his work has been replicated. Usually claiming replicated multiple times and around the world. Since he says it, it gets repeated by his supporters in online discussions.

For those who get dragged into those discussions, here is another paper to reference. This one takes on the idea that there is a bowel disease specific to autism. Wakefield’s “autistic enterocolitis”

People have looked and, guess what, it isn’t there. Yes, autistics get bowel disease. Being autistic doesn’t prevent bowel disease. The fact that some do, indeed, get bowel disease isn’t what Wakefield claimed. He claimed a “new syndrome”.

It doesn’t exist.

Here’s the abstract. The group is reputable and, in fact, has expressed sympathetic views towards Wakefield.

Evaluation of Intestinal Function in Children With Autism and Gastrointestinal Symptoms.

OBJECTIVE:
Alterations in intestinal function, often characterized as a “leaky gut,” have been attributed to children who are on the autism spectrum. Disaccharidase activity, intestinal inflammation, and permeability were analyzed in 61 children with autism and 50 nonautistic individuals with gastrointestinal symptoms.

METHODS:
All patients had duodenal biopsies assayed for lactase, sucrase, maltase, and palatinase activity. Intestinal permeability was evaluated by rhamnose/lactulose test and measured by high-performance liquid chromatography-mass spectrometry. Intestinal inflammation was evaluated by fecal calprotectin and lactoferrin levels using enzyme-linked immunosorbent assay and histology.

RESULTS:
Some children with autism had mild levels of mucosal inflammation on intestinal biopsy. Disaccharidase activity was not different in autistic and nonautistic individuals. Fecal calprotectin and lactoferrin were similar in both groups. Differences between lactulose and rhamnose recovery and lactulose/rhamnose ratio in urine were not statistically different in patients with and without autism.

CONCLUSIONS:
The present study supports the observation that children with autism who have symptoms of gastrointestinal disorders have objective findings similar to children without autism. Neither noninvasive testing nor endoscopic findings identify gastrointestinal pathology specific to autism, but may be of benefit in identifying children with autism who have atypical symptoms.

If you are getting ready to write, “but they might not have seen enough kids to find one with autistic enterocolitis”, according to Wakefield, most of the kids his team tested had his “new syndrome”. If that were true, this team would have found it.

Add this to “MMR causes autism” as one of the failed ideas of Andrew Wakefield. Not that he will ever admit it.


By Matt Carey