Title: Gluten sensitivity and infections that break barriers
Abstract:
Gluten sensitivity is caused by infections that can barrier cross the intestine or the blood brain barrier. These infections break the tight junctions between cells allowing them to cross over into the body. The holes they make are large enough that the macromolecule gluten can cross the intestinal barrier behind them. Once inside the body gluten directly stimulates macrophages to make TNF. TNF promotes the inflammatory response.
Introduction:
Since the Dutch famine of 1944 we have understood that gluten can be detrimental to health. When bread was scarce less deaths occurred from celiac disease. Celiacs were recommended to avoid breads, to avoid gluten. Gluten sensitivity is now recognized to exist without celiac disease. Multiple diseases have been associated with gluten sensitivity: Schizophrenia, Pandas, Autism, IBS, and psoriasis. What do all these diseases have in common that would trigger gluten sensitivity? The infections they are linked to are very different and these specific diseases are rarely overlapping and are not considered to be related in cause. ( T.gondii, strep, sutterella, e.coli, and mycobacterias ) What these diseases have in common are infections with a shared trait, a shared ability of crossing the tight junctions of the intestinal or brain barrier.
Hypothesis:
An infection capable of breaking through the tight junctions of the intestinal lumen will trigger gluten sensitivity because when they tear through they create the hole that allows gluten to cross over. When gluten crosses over two things happen: the inflammation is magnified when gluten stimulates macrophages and gluten is seen as an intruder with the infection. Imagine your body taking a picture of the crime scene using antibodies. Gigantic gluten is foreign just as the infection is.
Evaluation of Hypothesis
This paper will look at the infections associated with each gluten sensitive disease and demonstrate that they all have the ability to break tight junctions and it will look at the current research of gluten stimulation of macrophages.
*** this paper is still being written
Abstract:
Gluten sensitivity is caused by infections that can barrier cross the intestine or the blood brain barrier. These infections break the tight junctions between cells allowing them to cross over into the body. The holes they make are large enough that the macromolecule gluten can cross the intestinal barrier behind them. Once inside the body gluten directly stimulates macrophages to make TNF. TNF promotes the inflammatory response.
Introduction:
Since the Dutch famine of 1944 we have understood that gluten can be detrimental to health. When bread was scarce less deaths occurred from celiac disease. Celiacs were recommended to avoid breads, to avoid gluten. Gluten sensitivity is now recognized to exist without celiac disease. Multiple diseases have been associated with gluten sensitivity: Schizophrenia, Pandas, Autism, IBS, and psoriasis. What do all these diseases have in common that would trigger gluten sensitivity? The infections they are linked to are very different and these specific diseases are rarely overlapping and are not considered to be related in cause. ( T.gondii, strep, sutterella, e.coli, and mycobacterias ) What these diseases have in common are infections with a shared trait, a shared ability of crossing the tight junctions of the intestinal or brain barrier.
Hypothesis:
An infection capable of breaking through the tight junctions of the intestinal lumen will trigger gluten sensitivity because when they tear through they create the hole that allows gluten to cross over. When gluten crosses over two things happen: the inflammation is magnified when gluten stimulates macrophages and gluten is seen as an intruder with the infection. Imagine your body taking a picture of the crime scene using antibodies. Gigantic gluten is foreign just as the infection is.
Evaluation of Hypothesis
This paper will look at the infections associated with each gluten sensitive disease and demonstrate that they all have the ability to break tight junctions and it will look at the current research of gluten stimulation of macrophages.
*** this paper is still being written
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