It is thought that they also feed on blood, because some come out with their heads covered with blood. (How do they know it’s a head? And if they feed on fecal matter by osmosis in those long channels, how and why do they penetrate the intestinal wall and get at the blood?) Volinsky and Gubarev tell us that people with alkaline blood (pH 8-10) are the most susceptible. They helpfully tell us that blood pH can be determined by examining the color of the conjunctiva of the eye: bright pink signifies normal blood pH, bright red means alkaline, and pale means acidic blood. (In case you don’t realize how colossally ridiculous this is, people with a blood pH of 8-10 would not be “susceptible” to anything because they would be dead, and the color of the conjunctiva has nothing whatsoever to do with pH; it becomes redder with infection or inflammation and becomes paler with anemia.)They are call “ropeworms” and the reason I point this out is they are non-existent prior to 2009. These are the specific “pathogens” I am referring to and as you will see, the use of MMS would be counter-intuitive based on size alone. Their very existence defy science as Hall points out. I will have a more thorough take down on this issue in a future posting.
That aside, there is legitimate research and studies being done concerning GI issues and they do appear contradictory if one does not understand how the science or how the peer review process work. (Some take the conservative language used by the writers as evidence of a cover-up forgetting that correlation does not mean causation; it just means there may be a link) :
A [2010] multidisciplinary panel reviewed the medical literature with the aim of generating evidence-based recommendations for diagnostic evaluation and management of gastrointestinal problems in this patient population. The panel concluded that evidence-based recommendations are not yet available. The consensus expert opinion of the panel was that individuals with ASDs deserve the same thoroughness and standard of care in the diagnostic workup and treatment of gastrointestinal concerns as should occur for patients without ASDs.In other words, as Steven Novella notes, "They do not require any special workup, but neither should their GI symptoms be ignored. They further recommend that special intervention may be necessary for the behavioral consequences of GI symptoms when they do occur. When a child with ASD does have a GI disorder, the pain and other symptoms may trigger problem behavior, and therefore special care may need to be taken not only to treat the GI symptoms but to mitigate the negative effect on behavior.
“For professionals and for parents the panel concludes that there are no special diets that have been shown to be of benefit in children with ASD, despite anecdotal reports. Further, children on special diets may be at risk for malnutrition, and therefore nutritional status needs to be assessed.”
In a 2014 study, these same results are mirrored. GI symptoms are present at a higher rate but science doesn’t know why. Science doesn’t know how these GI disturbances may be related to brain function; hence, calling for more research.
Results indicate greater prevalence of GI symptoms among children with ASD compared with control children,,,. Future research must address critical questions about the causes and long-term impact of GI symptoms in ASD. Such analyses will require more systematic research and clinical activities, including improved diagnostic screening, standardized assessment, and exploration of potential moderators (eg, dietary restrictions).That is why research such as this 2013 study are important, as it explores the link between mom’s stress, baby’s gut bacteria and brain development.
,,,Current evidence points to a likely influence of maternal stress experience on the maternal vaginal microbiome,,,. As the neonate’s gut is initially populated by the maternal vaginal microbiome following passage through the birth canal, changes in the vaginal microbiome produced by maternal stress experience would then alter this initial microbe population,,,. From these findings we hypothesize that the vaginal microbiome is modulated by stress through changes in the mucosal immunity, and that these changes in the vaginal microbiome alter the initial population of the offspring’s gut microbiome impacting neurodevelopment.Or this study that also examines the diversity of gut microbiome:
,,,Increasing evidence from recent high-throughput sequencing analyses indicates that disturbances in composition and diversity of gut microbiome are associated with various disease conditions. However, microbiome-level studies on autism are limited and mostly focused on pathogenic bacteria. Therefore, here we aimed to define systemic changes in gut microbiome associated with autism and autism-related GI problems,,,. Unexpectedly, the presence of autistic symptoms, rather than the severity of GI symptoms, was associated with less diverse gut microbiomes,,,. However, multivariate analyses showed that autism-related changes in both overall diversity and individual genus abundances were correlated with the presence of autistic symptoms but not with their diet patterns. Taken together, autism and accompanying GI symptoms were characterized by distinct and less diverse gut microbial compositions with lower levels of Prevotella, Coprococcus, and unclassified Veillonellaceae.What is important to take away from all of the above, none of these studies are saying the subject matter under discussion is the 'cause' of autism; none of the studies suggest that a “cure” has been found. All that was found was GI issues are correlated with autism. A correlation that may have been studied sooner if not for the baggage of the 1998 Wakefield study were he concluded that a persistent measles infection “caused” by the use of MMR led to a “leaky” gut which, in turn, led to autism.
__________
Note: There appears to be a big kafuffle surrounding the 2014 Pediatrics review by McElhanon et al. that I cited above. Not with the study itself but how their findings are being interpreted (by those in the pro and anti vaccine crowds) and the implications.
My purpose in pointing out the Wakefield study is twofold. First, the perceived set back that the ensuing debacle may have caused. Second, as Willingham points out in a subsequent comment, the “cures” (MMS being one example) offered to parents of autistic children can be traced back to the flawed Wakefield study:
And the GI connection in the “autism world” *has* been linked very strongly with DAN quackery and antivax lobbies for precisely the reason that they adhere to Wakefield’s claims and try to blame the gut issues on vaccines–and then have the loudest voices peddling their “cures” to parents. No one “needs” someone to blame for that. There is someone to blame, and it’s not hypocrisy to point that out–it’s called “tracing a path.” A simple google on “autism” and “gut” will make that abundantly clear.Overall, it is an issue that is way beyond what I want to present (the crackpottery surrounding MMS specifically) but an issue that does warrant consideration. Even if Wakefield was right, and there did exist a causal association of ASD and GI issues following MMR, his professional misconduct when performing this study would still warrant the punishment he received.
I may come back and explore this “controversy” as an interesting point has been made or implied in Willingham’s piece and the ensuing comments:
It seems that GI issues are frequently comorbid with neurodevelopmental disorders—not just with ASD–but without any apparent association with MMR: “That in spite of the fact that anxiety is a key feature of autism and that research suggests that autism and anxiety are indeed linked. And that gut conditions like diarrhea and constipation and gut pain are often related to anxiety.Anxiety is a key component in my battle with bipolar and my ensuing agoraphobia.
No comments:
Post a Comment