I really don't want to start a Daily Mail style "cure for T1?" thread, but I noticed some stuff the other day about trials Dr Denise Faustman is running with the good old fashioned BCG injections, and was wondering whether any docs/techy people have any thoughts about it.
I know nothing about medicine so can't express a view but am wondering what other people think. is it just an interesting bit of research or is she on to something?
A lot of people scoffed at Banting coming from left-field in the way he did, so who knows, how crazy would it be if a few BCG injections were sitting there staring us in the face and no-one had noticed?
Her theory is that BCG injections selectively kills off rogue T cells and allows remaining beta cells to regenerate even in longer terms T1s.
She doesn't seem like a snake-oil merchant: Director of the Immunobiology Laboratory at the Massachusetts General Hospital (MGH) and an Associate Professor of Medicine at Harvard Medical School. Bill and Melinda Gates and Lee Iacocca are funding her.
From her faqs page: http://www.faustmanlab.org/research/faq.html
The phase 1 report is here:http://www.faustmanlab.org/docs/academic/JournalPone0041756.pdf
I know nothing about medicine so can't express a view but am wondering what other people think. is it just an interesting bit of research or is she on to something?
A lot of people scoffed at Banting coming from left-field in the way he did, so who knows, how crazy would it be if a few BCG injections were sitting there staring us in the face and no-one had noticed?
Her theory is that BCG injections selectively kills off rogue T cells and allows remaining beta cells to regenerate even in longer terms T1s.
She doesn't seem like a snake-oil merchant: Director of the Immunobiology Laboratory at the Massachusetts General Hospital (MGH) and an Associate Professor of Medicine at Harvard Medical School. Bill and Melinda Gates and Lee Iacocca are funding her.
From her faqs page: http://www.faustmanlab.org/research/faq.html
"5. What were the results of the Phase I trial?
In the Phase I human study, BCG was administered to adults who had been living with type 1 diabetes for an average of 15 years. This treatment not only helped eliminate the defective T cells that mistakenly attack and destroy the insulin-producing cells of the pancreas, it also temporarily restored the ability of the pancreas to produce small amounts of insulin. The results were published in 2012. The next step, a Phase II study, is currently being underway, with the goal of identifying the drug dose and schedule that will put advanced type 1 diabetes into remission."
In the Phase I human study, BCG was administered to adults who had been living with type 1 diabetes for an average of 15 years. This treatment not only helped eliminate the defective T cells that mistakenly attack and destroy the insulin-producing cells of the pancreas, it also temporarily restored the ability of the pancreas to produce small amounts of insulin. The results were published in 2012. The next step, a Phase II study, is currently being underway, with the goal of identifying the drug dose and schedule that will put advanced type 1 diabetes into remission."
The phase 1 report is here:http://www.faustmanlab.org/docs/academic/JournalPone0041756.pdf
"We also found
that BCG vaccination and an unexpected EBV infection in a
placebo-treated diabetic subject, both known triggers of innate
immunity, caused rapid increases in circulating insulin-autoreac-
tive T cells that were mostly dead. The rapid release of dead
insulin-autoreactive T cells supports the hypothesis, first demon-
strated in the NOD-mouse model of autoimmune diabetes, that
BCG ameliorates the advanced autoimmune process underlying
type 1 diabetes by stimulating TNF, which selectively kills only
disease-causing cells and, further, permits pancreas regeneration
[7,8] as evidenced by the transient increase in C-peptide secretion
we observed using an ultrasensitive C-peptide assay."
that BCG vaccination and an unexpected EBV infection in a
placebo-treated diabetic subject, both known triggers of innate
immunity, caused rapid increases in circulating insulin-autoreac-
tive T cells that were mostly dead. The rapid release of dead
insulin-autoreactive T cells supports the hypothesis, first demon-
strated in the NOD-mouse model of autoimmune diabetes, that
BCG ameliorates the advanced autoimmune process underlying
type 1 diabetes by stimulating TNF, which selectively kills only
disease-causing cells and, further, permits pancreas regeneration
[7,8] as evidenced by the transient increase in C-peptide secretion
we observed using an ultrasensitive C-peptide assay."