Atherosclerosis
|
Wobenzym®
also decreased
cholesterol an average of 24% after one month of
therapy. It also lowered the levels of atherogenic
lipoproteins as well as inflammatory markers associated with
atherosclerosis.
It is important to note that in addition to lowering excessive lipids, controlling inflammation in cardiovascular disease is also recognized as an important benefit of systemic enzyme support. One study showed that in patients who had suffered a myocardial infarction, cholesterol dropped 12% and lipoproteins drops 16% after taking 9 Wobenzym® tablets a day for 10 days. A second group in the same study had a 24% drop of cholesterol and 31% drop of lipoproteins within one month at the same dosage. The researched also noted that the immune status of myocardial infarction (MI) patients is significantly impaired and that Wobenzym® had an immunonormalizing affect. A parallel study of myocardial infarction patients and two groups of rabbits reported a “significant decrease of cholesterol level” in both the clinical and the experimental studies. They concluded that “it can be recommended to use Wobenzym in complex treatment of myocardial infarction patients to reduce risk factors of reinfarction.” A 2001 study tracked 52 patients taking Wobenzym® for 6 months. They also noted an improvement lipid levels. They also noted an improvement in cytokine levels, and concluded in postmyocardial infarction patients Wobenzym® helped improve the biochemical and immune abnormalities. It is also notable that patients with autoimmune thyroid disease experienced lower cholesterol and triglyceride levels after being treated with Wobenzym®. Now this may be because their anti-thyroid antibody levels had dropped with Wobenzym® therapy, but it is still notable that cholesterol levels are improved in these patients. I should also point out that improved cholesterol levels are also observed in chronic levier disease patients after they were treated with Wobenzym® From FREQUENTLY ASKED QUESTIONS, with answers by Joseph J Collins, RN, ND Read the special section: : CARVIOVASCULAR AND LYMPHATIC SYSTEMS & WOBENZYM® |
What the literature says about Systemic Enzyme Support and:
Atherosclerosis
The
effect of Wobenzym on the atherogenic potential and inflammatory
factors in postmyocardial infarction patients.
Summary: The effect of systemic enzyme therapy
preparation Wobenzym on the serum atherogenicity and
immunoinflammatory reactions was studied over the period of 6 months
in the postmyocardial infarction patients at the rehabilitation
stage. Inclusion of Wobenzym
into the conventional treatment led to the normalization of an
atherogenic potential and showed a positive effect on inflammatory
process mediators.
Poster Reference Number 26.
The
systemic enzyme therapy in experimental atherosclerosis
Dosenko
V.E., Zakharova V.P., Byc Y.V. The systemic enzyme therapy in
experimental atherosclerosis. Experimental cardiology 2000, No. 5-6,
pp. 87-94. [Russian abstract, Czech abstract]
The etiology and pathogenesis of atherosclerosis
(AS), which is undoubtedly influenced by modified lipoproteins and
damaged arterial wall with altered properties of blood vessel
connective tissue is discussed. The goal of this study was to
estimate the effect of proteolytic enzymes in the treatment and
prophylaxis of AS. The elastolytic system of serum and tissues was
studied.22 adult chinchila rabbits were included into the study. AS
was simulated by means of feeding 0.75% cholesterol diet for 30
days. The animals were divided into three groups: I – controls fed
by a standard diet, II – received only cholesterol diet, III –
received cholesterol diet and Phlogenzym at doses corresponding to
the mean therapeutic dose for men. After 30 days, the animals were
sacrificed. Aortas were homogenized and exploited for biochemical
analysis. Blood was sampled and serum was prepared. The activity of
elastase was determined using a specific chromogenic substrate. The
amount of total cholesterol was assayed. The stripes of aortas were
fixed in HCHO and prepared for histological examination. All data
were statistically evaluated by Student`s t-test.
In the course of AS modeling, a fundamental
impairment of the system elastase-inhibitors was discovered. The
activity of elastase (mM/g of protein or per 1 l of serum resp.),
the content of a2 macroglobulin (a2 M) (mg/g of protein or g/l of
serum resp.), and a1 proteinase inhibitor (mg / g of protein or g/l
of serum resp.) were measured. Changes of the coefficient
inhibitors/elastase, which is a real indicator of elastolytic
system, were studied.
There was no difference in the serum elastase
activity between groups I and II (15.65 ± 0.64 vs. 15.67 ± 3.67),
while there was a statistically significant decrease (7.64 ± 1.08)
in the group III (Phlogenzym). The level of a2 M was statistically
significantly lowered in groups II and III (1.75 ± 0.16; 1.21 ±
0.23) in comparison to the control group (2.61 ± 0.16). The
resulting coefficient of inhibitors/elastase was thus increased in
the Phlogenzym group III (414.9) as compared to the groups I and II
(232.6; 195.9). In other words, a decrease of elastolytic activity
was found in serum of Phlogenzym-treated animals.
The comparison of elastase activity in aorta
homogenates revealed, however, an opposite trend: there was no
difference in elastase activity between groups I and II (2.52 ± 0.19
vs. 1.86 ± 0.44), while there was a statistically significant
increase (5.44 ± 1.15) in the group III (Phlogenzym). The level of
a2 M was statistically significantly lower in the groups II and III
(5.07 ± 1.89; 5.74 ± 1.62) in comparison to the control group (9.72
± 0.74). The coefficient of inhibitors/elastase was thus lowered in
the Phlogenzym group III (1.14) as compared to the groups I and II
(4.20; 3.30). In other words again, an increase of elastolytic
activity was found in the aorta tissue of Phlogenzym-treated
animals.
Histopathological examination revealed
morfological changes of fibrous structures of aorta, lysis of
segments and loosened fibers of elastic membranes in the group II
(cholesterol fed animals). Degeneration of collagen fibers was also
observed. The administration of Phlogenzym had a significant effect
on the elastolytic system of rabbits. The findings in animals
treated by Phlogenzym were less pronounced, collagen and elastic
fibers maintained its structure. The addition of proteolytic enzyme
mixture palliated pathological changes in the course of experimental
atherosclerosis.Elastase is generally considered to cause a
degradation of intercellular proteins only. However, it may have a
protective and prophylactic effect against development of AS.
Elastase operates against decrease of
acetylcholin-induced relaxation and noradrenalin-induced
constriction and it has the ability to lower total cholesterol.
Purified pancreatic elastase (Elaszym) is authorized in Japan and it
is used for prophylaxis and treatment of AS. It contributes to the
decrease of arterial pressure and inhibits aging of arterial blood
vessel tissues. The authors suppose that the strong effect of
elastase against AS is not specific, and the same effect can be
achieved by other proteolytic enzymes administered orally because
they activate the same cell receptors.
Treating AS by a combination polyenzyme
preparation is more advantageous than just elastase monotherapy.