Diabetes
|
We know that Wobenzym
can increase levels of C-peptide in autoimmune mediated
diabetes, such as type 1 diabetes. In addition to showing
much insulin the pancreas can still make, C-peptide
decreases the progression so the common complications of
diabetes, including the
diabetic nephropathy.
We also note that systemic enzymes can decrease the formation of “advanced glycation end products” (AGEs), which are associated with diabetic nephropathy and other complications of diabetes. IN addition, abnormal cytokines levels are normalized, including transforming growth factor beta-1 (TGF-b1), and interleukin 6. What we have come to realize, is that the complications of diabetes are strongly mediated by the immune system. We see that controlling blood sugar with insulin is not enough to prevent complications such as diabetic nephropathy. The abnormal cytokine levels that occur with diabetes can safely and effectively be normalized with Wobenzym. From FREQUENTLY ASKED QUESTIONS, with answers by Joseph J Collins, RN, ND Read the special section: KIDNEY AND BLADDER CONDITIONS & WOBENZYM® |
What the literature says about Systemic Enzyme Support and:
Diabetes Mellitus
Regular intake of Wobenzym® may prevent late
complications in diabetes mellitus.
Dzivite I.,1 Sochnevs A.,2
Stauder G.,3 Zeibarts M.,4 Lauga U.,4
Ansbergs J.5. Regular intake of Wobenzym® may prevent
late complications in diabetes mellitus. Int. J. Immunotherapy 2001,
Vol. XVII, No. 2/3/4, pp. 143-148- ISSN 0255-9625 218 K/375
(19-05-3)
Summary: In this observational study, the results of a 12-month
treatment of two groups of children, aged 4-18 years, with newly
diagnosed type 1 diabetes were compared. Half of the patients
received insulin preparation only, while the other half was treated
with the combination of a similar insulin preparation and Wobenzym®.
At the start of therapy, the mean values of all laboratory indices
were similar in both groups of children.
A
difference between mean HbA1c levels in both groups was observed at
the first follow-up (p = 0.0179). During treatment, further
differences became highly significant in favor of the enzyme group
(p <0.0001). After 12 months, higher levels of C-peptide were found
in children treated with Wobenzym® (p = 0.0012). At the
start of therapy there were no differences between the groups of
children in the dosage of insulin used. However, from the first
follow-up visit, greater amounts of insulin were used in the control
group.
The
difference between circulating immune complexes (CIC) levels at the
start and end of therapy was also significant in favor of the enzyme
group (p = 0.0018). Enzyme therapy caused no undesirable adverse
effects. Based on the results obtained, Wobenzym® can be
assumed to decrease the activity of the inflammatory process and
support a restitution of pancreatic b-cells. This may explain the
improved metabolic compensation found in patients who received
Wobenzym®.
We
suggest that regular intake of Wobenzym® together with
individually adjusted insulin therapy can prevent the development of
late pathological outcomes in diabetes.
Protease Treatment Delays Diabetes Onset in Diabetes-prone Nonobese
Diabetic (NOD) Mice.
Wiest-Ladenburger U.,1 Richter W.,1
Moeller P.,2 Boehm B. O.1 Protease Treatment
Delays Diabetes Onset in Diabetes-prone Nonobese Diabetic (NOD)
Mice. Inter. Journal of Immunotherapy 1997, Vol. XIII, No. 3/4, pp.
75-78 - ISSN 0255-9625. Inter. Journal of
Tissue Reactions 1997, Vol. XIX, No. 1/2,
abstract 108, pp. 89 - ISSN 0250-0868 SO 112 (4-12-2)
(19-04-2)
Summary: It has recently been demonstrated that proteolytic enzyme
treatment modulates certain immune-mediated diseases. We have,
therefore, studied the effect of administration of a protease
mixture in the NOD mouse, an elegant animal model for autoimmune
insulin-dependent diabetes mellitus (IDDM). Female NOD mice were fed
proteolytic enzymes from age 6 weeks to 10 weeks, within the
subclinical phase of IDDM. Once a week animals received
intragastrically 1 mg Phlogenzym® (n=10 mice) or 0.5 mg Phlogenzym®
(n=10) in 0.5 ml saline or saline only (n=10).
Mice were followed for development of IDDM up to week 23. At week
21, all control animals were diabetic, whereas 25% of the treated
mice were still normoglycemic at the end of the observation period.
No significant appearance of autoantibodies against either isoform
of the important islet cell antigen glutamic acid decarboxylase
(GAD), GAD65 and GAD67, was observed in the mouse sera as determined
by a highly sensitive radioimmunoassay. The histopathological
examination of pancreatic islets showed signs of insulitis in all
mice with a tendency of milder insulitis in the protease-treated
groups.