Hi, all.
Concerning gluten, it should be noted that a person can be intolerant to gluten and casein and not produce antibodies to them.
The following explanation is from Prof. Richard Deth, who has been active for several years in autism research:
"Gluten and casein-derived opiate peptides inhibit uptake of
cysteine by GI epithelial cells, making more available to gut organisms,
potentially shifting the flora toward cysteine-requiring organisms and strains.
Skin and IgE testing of gluten and casein does not reveal their GI effect to
inhibit cysteine uptake. The latter may promote IgE in some individuals, but
gluten and casein intolerance is not necessarily allergic.
There are digestive enzyme products containing the proline-directed dipeptidase
DPPIV, which breaks down the opiate peptides and may ameliorate their effects."
I think that it's likely that this mechanism can help to lead to a couple of other features that
are important in ME/CFS: glutathione depletion and production of hydrogen sulfide.
Cysteine is usually the rate-limiting amino acid for the production of glutathione, so
if its absorption by the gut is inhibited, that could help to deplete glutathione.
Dr. de Meirleir has identified the production of hydrogen sulfide by dysbiotic bacteria
as an important mechanism in ME/CFS. Some bacteria are capable of producing
hydrogen sulfide from cysteine.
The bottom line is that if a person has glutathione depletion, gut problems, and a positive hydrogen sulfide urine test, and if they have not tried a gluten-free, casein-free diet, they should strongly consider it.
Best regards,
Rich
Concerning gluten, it should be noted that a person can be intolerant to gluten and casein and not produce antibodies to them.
The following explanation is from Prof. Richard Deth, who has been active for several years in autism research:
"Gluten and casein-derived opiate peptides inhibit uptake of
cysteine by GI epithelial cells, making more available to gut organisms,
potentially shifting the flora toward cysteine-requiring organisms and strains.
Skin and IgE testing of gluten and casein does not reveal their GI effect to
inhibit cysteine uptake. The latter may promote IgE in some individuals, but
gluten and casein intolerance is not necessarily allergic.
There are digestive enzyme products containing the proline-directed dipeptidase
DPPIV, which breaks down the opiate peptides and may ameliorate their effects."
I think that it's likely that this mechanism can help to lead to a couple of other features that
are important in ME/CFS: glutathione depletion and production of hydrogen sulfide.
Cysteine is usually the rate-limiting amino acid for the production of glutathione, so
if its absorption by the gut is inhibited, that could help to deplete glutathione.
Dr. de Meirleir has identified the production of hydrogen sulfide by dysbiotic bacteria
as an important mechanism in ME/CFS. Some bacteria are capable of producing
hydrogen sulfide from cysteine.
The bottom line is that if a person has glutathione depletion, gut problems, and a positive hydrogen sulfide urine test, and if they have not tried a gluten-free, casein-free diet, they should strongly consider it.
Best regards,
Rich
I am pleased to see that you have begun to mention hydrogen sulfide in your posts. It is satisfying to see that my conceptual model demonstrating the potential connection between hydrogen sulfide and CFS is becoming accepted by prominent scientists. When I wrote my hypothesis, I was told that it could take thirty years before my ideas would be understood by the medical community, but already I can see aspects of my work being tested in a number of places. As I noted in my poster at the last IACFS/ME conference, dairy actually produces hydrogen sulfide, as do wine, sugar, and eggs, to name a few. Yeast and mold produce also H2S. And the story continues, from bacteria to the mitochondria. Perhaps we have the makings of a unifying theory, in that it potentially has the ability to explain so many of the findings in CFS (even glutathione depletion through the transsulfuration pathway!).
One thing puzzled me in your post. Dr. DeMeirleir appears to have embraced my theory as though it was his own, but has he actually demonstrated the production of H2S as an important mechanism in CFS? He said at the 2009 ME/CFS London conference that the results of his H2S tests shown on his slides would be published shortly thereafter, but I have not seen such a publication. Do you (or anyone else reading this blog) know where I can find it? I think it is important that all test results which underlie public statements be published and subjected to critical scrutiny of peer review and random trials if we are to make meaningful medical progress.
All the best,
Marian Lemle