Impaired Carbohydrate Digestion, Bacterial Dysbiosis and Autism…the Unfinished Story
I have to say, I really hate it when a really exciting bit of research is just dropped. It’s like having a TV show you like cancelled mid-season…and you’re just kind of left hanging…forever….
As it’s Thursday, I thought I’d to a TBT, and tell you about a paper that I have been brooding about for 7 years now. In 2011, some of the major researchers in autism from Columbia University, Harvard, etc. did a small study (22 children), comparing the intestines of typically-developing children with gastrointestinal disease to those of children with gastrointestinal disease and autism.[i] They made several major discoveries:
- The small intestines of more than 93% of children on the autism spectrum had decreased levels of the enzymes necessary to break down carbohydrates.
- In order for nutrients to get from your intestine into your blood stream, the cells on the villi of the small intestine (enterocytes) have what amount to specialized doorways that “fit” various nutrients. These are called transporters. The front door, the one on the side of the intestine, that transports glucose (the sugar molecule that feeds every cell in your body) into the enterocyte is called SGLT1 (sodium-dependent glucose co-transporter, for all you technically-minded people), and the one on the back door, that allows glucose (and galactose and fructose – all your single molecule sugars) to pass from the cell into the blood stream is called GLUT2 (glucose transporter 2). The researchers found “a significant decrease” in the number of these transporters, meaning that the kids on the spectrum have a hard time clearing their intestines of sugars…thus, feeding bacterial overgrowth. (These two findings (low carbohydrate enzymes and transporters) of course provides at least some explanation as to why the Specific Carbohydrate Diet is so amazingly effective in kids with autism.)
- And yes, a bacterial overgrowth is exactly what they found. The inability to digest and absorb carbohydrates leaves them sitting in the intestine feeding bacteria, resulting in “…significant and specific compositional changes in the microbiota” of the children with autism
Briefly, a few more important items of note in this paper:
- The altered gut flora showed an increase in the family of bacteria that include Clostridia. See my post about Dr. Derrick MacFabe, and his work on this.
- “The onset of GI symptoms was reported to occur before or at the same time as the development of autism in 67% of the [children]” and these symptoms were associated with the increased levels of various bacterial species including Clostridia.
- “…our data show that at least some children with autism have a distinct intestinal profile that is linked to deficient expression of disaccharidases and hexose transporters, potentially promoting maldigestion, malabsorption, and multicomponent, composition dysbiosis…” which sets the stage for “…further research aimed at defining the epidemiology, diagnosis, and informed treatment of GI symptoms in autism.”
So yeah…it’s been 7 years, and I’m still waiting for that further research. There has never been an explanation for the alteration in the transport system or a reason given for the low levels of carbohydrate enzymes. (By the way, that finding actually dates back to the late 1990s and the work of Dr. Horvath at the University of Maryland…which I can describe in a further post if anyone is interested. Just let me know!) Alterations in the biome are accepted now as a leading cause of autism, so why there has never been a sequel to this research is inexplicable.
Maybe the first one was a box office flop?
[i] Williams, BL, Hornig, M, Buie, T, Bauman, HL, Paik, MC, Wick, I, Bennett, A, Jabado, O, Hirschberg, DL, Lipkin, WI. Impaired carbohydrate digestion and transport and mucosal dysbiosis in the intestines of children with autism and gastrointestinal disturbances. PLoS One. 2011. 6;9:e23585.