When we think about vaccine injuries such as autism and epilepsy, we generally consider a direct assault on the brain. But the reality may be far different where injury begins in the gut, leading to brain damage. This article will explore potential mechanisms of gut-brain injuries by vaccination.
As with Parts 1 and 2, we’ll consider individual microbial predisposition as crucial to susceptibility to intestinal injury. The theory is that protective microbes such as Bifidobacteria are why some people appear to escape injury while others are not so fortunate.
Neurodegenerative diseases including multiple sclerosis (MS), Parkinson’s and Alzheimer’s are strongly associated with gut dysbiosis where these problems are now thought to begin in the gut.Diabetes and obesity are associated with brain inflammation. Gut-brain is known to be a two-way street, so diabetes and obesity are improved by reversing brain inflammation. In fact, 90% of fibers in the vagus nerve travel from gut to brain, not brain to gut, surprising and unsettling.
So, to consider vaccine injury as beginning in the gut isn’t such a stretch of the imagination. This connection began the controversy about vaccines and autism proposed by Andrew Wakefield. But the message was lost over the years as people focused on Thimerosal and direct damage to the brain by mercury. Yet the MMR vaccine does not and never did contain mercury. There’s something else going on where vaccines harness the body’s immune system, beginning in the gut, making some individuals their own worst enemy.
Studies have attempted to thwart the idea that vaccine injury begins in the gut. This study refuting the relationship of MMR and inflammatory bowel disease (IBD) leading to autism found “only” 20% of subjects received MMR before the onset of gastrointestinal disturbances leading to autism. That’s quite a large percentage! Such gastrointestinal complaints include constipation associated with low blood levels of serotonin. Given current technology, it would be important to know the microbial balance of these subjects to learn if they were absent or reduced in protective anti-inflammatory microbes such as Bifidobacteria.