Dr. Robin S Goland a co-director of the Naomi Berrie Diabetes Center at Columbia University in NY may be left with a non white population as the pale Type 1 diabetics in Manhattan flock to Boston to take advantage of the teachings of Dr. Denise L Faustman.
The
book we recently put together has now been officially published (it is
geared toward researchers & is focused on BCG and TNF in various
forms of autoimmunity) http://www.reuters.com/article/2014/04/22/ma-bcg-autoimmunity-grp-idUSnBw226373a+100+BSW20140422
PLoS One. 2012;7(8):e41756. doi: 10.1371/journal.pone.0041756. Epub 2012 Aug 8.
Proof-of-concept, randomized, controlled clinical trial of Bacillus-Calmette-Guerin for treatment of long-term type 1 diabetes.
Faustman DL1, Wang L, Okubo Y, Burger D, Ban L, Man G, Zheng H, Schoenfeld D, Pompei R, Avruch J, Nathan DM.
Abstract
BACKGROUND:
No targeted immunotherapies reverse type 1 diabetes in humans. However, in a rodent model of type 1 diabetes, Bacillus Calmette-Guerin (BCG) reverses disease by restoring insulin secretion. Specifically, it stimulates innate immunity by inducing the host to produce tumor necrosis factor (TNF), which, in turn, kills disease-causing autoimmune cells and restores pancreatic beta-cell function through regeneration.METHODOLOGY/PRINCIPAL FINDINGS:
Translating these findings to humans, we administered BCG, a generic vaccine, in a proof-of-principle, double-blind, placebo-controlled trial of adults with long-term type 1 diabetes (mean: 15.3 years) at one clinical center in North America. Six subjects were randomly assigned to BCG or placebo and compared to self, healthy paired controls (n = 6) or reference subjects with (n = 57) or without (n = 16) type 1 diabetes, depending upon the outcome measure. We monitored weekly blood samples for 20 weeks for insulin-autoreactive T cells, regulatory T cells (Tregs), glutamic acid decarboxylase (GAD) and other autoantibodies, and C-peptide, a marker of insulin secretion. BCG-treated patients and one placebo-treated patient who, after enrollment, unexpectedly developed acute Epstein-Barr virus infection, a known TNF inducer, exclusively showed increases in dead insulin-autoreactive T cells and induction of Tregs. C-peptide levels (pmol/L) significantly rose transiently in two BCG-treated subjects (means: 3.49 pmol/L [95% CI 2.95-3.8], 2.57 [95% CI 1.65-3.49]) and the EBV-infected subject (3.16 [95% CI 2.54-3.69]) vs.1.65 [95% CI 1.55-3.2] in reference diabetic subjects. BCG-treated subjects each had more than 50% of their C-peptide values above the 95(th) percentile of the reference subjects. The EBV-infected subject had 18% of C-peptide values above this level.CONCLUSIONS/SIGNIFICANCE:
We conclude that BCG treatment or EBV infection transiently modified the autoimmunity that underlies type 1 diabetes by stimulating the host innate immune response. This suggests that BCG or other stimulators of host innate immunity may have value in the treatment of long-term diabetes.TRIAL REGISTRATION:
ClinicalTrials.gov NCT00607230.Comment in
Targeting innate immunity to treat long-term type 1 diabetes. [Regen Med. 2012]The Italians in New York who suffer from MS are already on the plane to Rome to take advantage of the work of Ristori.
Ristori
G, Romano S, Cannoni S, Visconti A, Tinelli E, Mendozzi L, Cecconi P,
Lanzillo R, Quarantelli M, Buttinelli C, Gasperini C, Frontoni M,
Coarelli G, Caputo D, Bresciamorra V, Vanacore N, Pozzilli C, Salvetti
M.
Neurology. 2014 Jan 7;82(1):41-8. doi: 10.1212/01.wnl.0000438216.93319.ab. Epub 2013 Dec 4.
- PMID:
- 24306002
- [PubMed - indexed for MEDLINE]
2.
Paolillo A, Buzzi MG, Giugni E, Sabatini U, Bastianello S, Pozzilli C, Salvetti M, Ristori G.
J Neurol. 2003 Feb;250(2):247-8. No abstract available.
- PMID:
- 12622098
- [PubMed - indexed for MEDLINE]
3.
Rook GA, Ristori G, Salvetti M, Giovannoni G, Thompson EJ, Stanford JL.
Immunol Today. 2000 Oct;21(10):503-8. Review. No abstract available.
- PMID:
- 11071529
- [PubMed - indexed for MEDLINE]
New York, NY, full of the good and the bad and those who read and write and think and those who think that the Naomi Berrie Diabetes Center at Columbia University is unable and/or unwilling to learn from the work of Dr. Denise L Faustman.
The Tuskeegee Airman support shooting the white boy with BCG to see if BCG will indeed treat Type 1 diabetes and other autoimmune diseases.
Recent arrivals in New York laugh at NY MD's who are unfamiliar with BCG.
Study Reveals Sizable Increase in Diabetes Among Children
For years doctors have warned of a rising epidemic of diabetes among children. Yet there has been surprisingly little firm data on the extent of this disease among younger Americans.
Now a nationally representative study has confirmed that from 2001 to 2009 the incidence of Type 1 and Type 2 diabetes drastically increased among children and adolescents across racial groups.
The prevalence of Type 1 diabetes
increased 21 percent among children up to age 19, the study found. The
prevalence of Type 2 diabetes among those ages 10 to 19 rose 30 percent
during the period.
Those
are “big numbers,” said Dr. Robin S. Goland, a co-director of the Naomi
Berrie Diabetes Center at Columbia University Medical Center in New
York, who has been in practice for about 25 years. “In my career, Type 1
diabetes was a rare disease in children, and Type 2 disease didn’t
exist. And I’m not that old.”
The
analysis, published on Saturday in JAMA, the journal of the American
Medical Association, includes data from more than three million children
younger than 20 in five states — California, Colorado, Ohio, South
Carolina and Washington — as well as from selected American Indian
reservations.
The
research was funded by the Centers for Disease Control and Prevention
and the National Institutes of Health and is part of a continuing study,
Search for Diabetes in Youth, examining the condition among children.
In Type 1 diabetes, a patient’s immune system attacks cells in the pancreas that make insulin, a hormone required to control blood sugar levels. Historically, children affected by the disease were more often white.
But
the new report found the prevalence also has increased among black and
Hispanic youths. The greatest increase occurred among 15- to
19-year-olds.
“I
don’t understand the basis for an increase,” said Dr. Goland, who was
not involved in the research. “There are a few possibilities, but we
need to figure it out if it’s something in the environment or something
in our genes.”
Some
minority youths are far less likely to control their high blood sugar,
and more likely to have complications like eye disease, kidney disease,
heart disease and amputations, said Dr. Dana Dabelea, the lead author of
the new study and a professor of epidemiology and pediatrics at the
Colorado School of Public Health. She called the increase in Type 1
diabetes among these children “particularly worrisome.”
Type
2 diabetes used to be called “adult-onset” diabetes because it was so
unusual in children. It is thought to be brought on by a genetic
predisposition to poor insulin action and secretion, often exacerbated
by obesity
and inactivity. The new analysis reported increases among black, white
and Hispanic children, but not among Asian-Pacific Islander and American
Indian children.
The
study’s authors speculated that the uptick in Type 2 diabetes may
result from “minority population growth, obesity, exposure to diabetes
in utero and perhaps endocrine-disrupting chemicals.”
The
increase will have public health consequences, the researchers said.
More children will enter adulthood at increased risk of early
complications, and diabetes is harder to treat in children than in adults. Younger patients also still have reproductive years ahead of them.
“Diabetes in pregnancy is a risk factor for diabetes in the next generation,” Dr. Dabelea said.
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