Vasculitis — new findings and therapy options
Irene Kolbe, Naturopath
1. Introduction Dear colleagues, dear management, dear Mr Sinn and all of the REGUMED employees,
When I got the request to do another speech this year, I was keen to introduce to you a small sensation from the latest findings on the topic of vasculitis, that originated in a very different area of medicine and brought attention to the work of complementary medicine in January 2017.
2. Prof. Haverich’s research work
“A new theory on arteriosclerosis challenges the current doctrine.” So began a headline of a daily newspaper published in Hanover and of the BDH newsletter.
The article was based on a study conducted by Prof. Dr. Axe Haverich from the Medical University of Hanover (MUH department: HTTG surgery). Here is an excerpt from the study, Prof. Haverich:
“It is not fats from the blood, but disruptions in the supply to the arterial wall, that lead to deposits in the inner vascular wall and trigger arterial calcification.”
The doctrine, believed for decades, was based on the idea that sclerosis of the arteries such as, for example, the coronary vessels, was due to fats from the blood accumulating on the internal wall of the blood vessels. As a reaction, the immune system builds up so-called plaque in this area, which can move to the vessel with time.
Professor Dr. Haverich, however, presents a very different theory: “The fat deposits do not come from the blood, but rather from the remains of the dead cells of the vessel wall. “
Therefore, he contradicts the present opinion on the cause of arteriosclerosis being rooted in syndromes affecting metabolic well-being.
An infarction of the arterial wall?
Arteries also need to supply the walls of their vessels with oxygen and nutrients. This happens through tiny supply blood vessels in the exterior wall of the artery, the so-called vasa vasorum. If these shut, the cells die, mainly in the middle wall layer: this leads to an infarction of the artery wall.
The most common trigger of such closures are inflammation reactions that arise through viruses, bacteria and particulates, but also through harmful fat particles.
“The dead cells, including the fat residues, are broken down by the immune system. Through the repair processes with the inflammation factors (dolor, calor, tumor, rubor and functio laesa) by the immune system, the so-called plaque forms, which leads to a thickening of the arteries’ internal wall and can ultimately lead to a closure of the mother vessel.”
Faller/Schunke Anatomy/Physiology 5. Edition Thieme publishing house
Prof. Dr. Haverich first exhibited doubt in the present doctrine, that everything can be attributed to metabolic well-being syndromes, with his observations in the operating theatre.
“During hundreds of bypass operations, we were able to determine that only certain sections of the coronary vessel became sclerotic and closed, while the same vessel was completely pathologically unchanged in other sections”, Prof. Dr. Haverich reports.
Similar observations were made in vessels in the thigh. Common to the areas not affected by arteriosclerosis was that they were surrounded by muscles on the outside. “As all of the small arteries are only seldom affected, doubt must be raised as to whether the process represents a generalised illness that begins on the interior wall”, says Prof. Haverich.
Recent findings have confirmed his theory.
The doubt was nursed by the discovery of new risk factors for arteriosclerosis, such as the observed correlation between an increased rate of heart attacks and the occurrence of flu epidemics with lung inflammations, but also with exposure to particulates.
“These correlations cannot be explained with the current theory of increased fats in the blood alone”, said the scientist.
Old publications could also provide explanations for the recent observations made in the operating theatre.
The new theory on the emergence of arteriosclerosis prepared expanded points for approaching the development of innovative treatment approaches for the illness.
An assumption made by complementary medicine has already been discussed, namely whether these processes are not really transient vasculitis.
Has this not been the case for temporal arteritis, for carotid dissections which have been diagnosed more frequently in the meantime and other transient forms whose triggers cannot be detected with laboratory values alone?
In causal research via testing, patients very often demonstrate correlations that now provide an “intraoperative visual finding” through the research of Prof. Dr. Haverich.
An attempt to confirm vasculitis through laboratory parameters has not yet happened.
Nevertheless, for clarification, the following parameters can be used:
a) Evidence of ANA (Evidence of anti-nuclear antibodies against predominant structures in the cytoplasa but also cell components)
b) Evidence of ANCA (Anti-neutrophile cytoplasmic antibodies against cell components)
As an example, I would like to show you a patient case on this topic.
3. Presentation of patients: Mr D. from Lower Saxony, born 1950
a)
First anamnesis 2014:
Vital parameters: Hypertension 145/90 (under medication) and slight tachycardia arrhythmia
Weight 95 kg at a height of 183 cm
State after repeated bypass OP
E.g. apheresis since 2014
State after EBV infection in 1990 as well as
State after recurrent streptococcus infections
b)
Current condition:
Quickly exhausted, disrupted sleep, cardiac hiccups
Shortness of breath, pressure in the right-hand side upper abdomen and muscle pains
First examination: slightly enlarged liver with soft consistency
c)
Laboratory parameters: (nv = normal value)
Cholinesterase 4877 U/I (nv: 4900-11.900)
Homocysteine 11 ilmo1/1(nv: < 9)
LDL cholesterol 200 mg/dl (nv: < 160.0)
HDL cholesterol 35.0 mg/dl (nv: > 40.0)
Triglycerides 220 mg/dl (nv: < 200.0)
Here is a table of the customary medication
d)
I am listing these medicines because exactly this patient came to me as he was
having to fight against the side effects of these medicines.
By taking these medicines, the coenzyme 010, amongst others, was completely “robbed”.
Along with the causal treatment, I relied on these as an alternative
ArmoLipid® with fermented red rice, coenzyme 010, astaxanthin and folic
acid. (MEDA Pharma)
An article by Dr. med. Volker Schmiedel (former chief physician at the Habichtswald hospital in Kassel) describes this: “… the use of lipid reducers for high levels of cholesterol alone is extremely marginal. Only in connection with pre-existing vessel damage would this application be justified in traditional medicine, if at all.”
He continues: “Administering natural fish oil in high doses would be a real alternative. However, a consequent relevant reduction in LDL cholesterol is often not, or barely, achieved.”
What is so interesting and special about fermented red rice?
Red rice is a common white rice that is fermented with the help of the fungi, monascus purpueus (red rice mould). During this process, not only the red colour appears, but also a substance called Monacolin K.
Monacolin K is nothing other than a natural statine. It has the same chemical structure as synthetic statines and affects the same mechanism in the human body.
Dr. Schmiedel asked the question: “If it is now developed like the synthetic structure, then surely it also has all the same side effects?”
In response, there have been numerous studies that correspond to the traditional medicine “gold standard” (controlled by placebo groups, randomised, double-blind) and they do not exhibit the side effects of synthetic statines.
Patients, especially those that suffer from the side effects of conventional statines, e. g. liver and muscle damage, therefore discontinue intake, obtaining a quantifiable reduction of LDL cholesterol through the fermented red rice.
It is, however, not just about a “laboratory cosmetic”, but a measurable limitation of risks.
This was also used:
2. ACIDUM TARTARICUM, the tartaric acid processed in potency grades D6, D12, D30 and D200 as we also know these from other carboxylic acids.The tartaric acids are able to block enzymatic processes (e. g. inflammation in the vessels) and improve the flow characteristics of the blood at the same time, which represents the problem, especially for vasculitides in the capillary area.
This is how I treated these patients, on theone hand, for the side effects of statines and on the other hand, for the bloods’ flow system.
Subsequently, bioresonance is employed at this point:
With the following question for programme search function:
1. Bacterial/viral contamination
2. State of the tissue
3. Circulation, especially capillaries
4. Change in the capillaries – internal scars
5. Liver gall system
4. Treatment with BICOM BICOM optima®
Basic programme
Programmes in alternation according to testing in groups Pathogen with respective ampoules: EBV and streptococcus
978.1 contamination through pathogens
996.0 virus treatment
978.2 reaction to pathogens
3013.0 contamination through pathogens
Blockages in tissue
3040.0 tissue regeneration
951.1 blockages in the tissue — cell regeneration
3036.0 poisoning
Circulation
3032.0 circulation
3031.0 circulation
Scar tissue balancing
900.2/910.5 internal scars
910.3/927.3/341.4 scar treatment
Liver programmes
310.9 liver acute
311.1 liver chronic
3063.0 liver poisoning (alternative: 430.2)
3064.0 liver gall regeneration
Final examination 2015
Current relevant laboratory parameters
Cholinesterase 5580 U/I (nv: 4900-11.900)
Homocysteine 9 vmo1/1(nv: < 9)
LDL cholesterol 155 mg/dl (nv: 40.0)
Triglycerides 189 mg/di (nv: < 200.0)
Physical examination
Vital parameters: Hypertension135/80
Improvement of heart rhythm
Weight 89 kg at a height of 183 cm
Stability of coronary vessels (heart catheter monitor)
Apheresis has been suspended for the time being
Current condition
Improved fitness
No breathing difficulties when under duress
No pressure in the upper right abdomen (liver size normal upon palpation)
5. In conclusion, some images from the first anamnesis in the dark field
These images were taken of the patient in a sober status and are all images of fresh blood, directly after being taken.
© HP Irene Kolbe
Intracellular: Contamination of erythrocytes with anisocytosis (generally viral, bacterial contamination)
© HP Irene Kolbe
Intracellular contamination of erythrocytes with thickened cell membranes
© HP Irene Kolbe
Impaired flow characteristics visible in thrombocyte-symplasts
Impaired flow charecteristics visible in thrombocyte-smplasts, erythrocytes near symplasts changed form and signs of toxin contamination.
Thank you for your attention!
Thank you to Prof. Dr. Haverich, who, through his research, has opened up a new idea, or even confirmed an assumption, for therapists in natural medicine.
Salutogenesis has been taken into consideration.
Literature
Prof. Dr. Axel Haverich “View on the Pathogenesis of Atherosclerosis” January 16, 2017 German translation in excerpts
Dr. med. Volker Schmiedel 2016-07 Naturopath: “Red rice flour for good blood lipids”
A. Kracke: “Threatment with physiological carboxylic acid preparations by the company SANUM-Kehlbeck” SANUM Post No. 101/2012, Semmelweis publishing house