EGAA 2 – Allergies / AIDS

Contents:

Plant extract (hops (humulon), procyanidine from cocoa) 47,04 %
Zeolithe 22,76 %
Seaweed powder 22,76 %
Silicon dioxide 7,44 %

Boosting effect by quantum dots :
1:16 for humulone
1:51 for procyanidine

The reason of AIDS is still unknown
After a quarter of a century we know, AIDS is a cellular (TH1-modulated) immune deficiency or even a complete lack of it. As a consequence, there is no protection against viral diseases (and infections with mycobacteria, like tuberculosis and leprosy) and cancer cells. This may end in death.

Egaa 2 - Pic 1 (Englisch)From the beginning it was guessed, it could be a viral infection of the immune system. The virus however (a retro virus is assumed) is not identified according to classical microbiological criteria. On the other hand, just as little, it is not proved that the virus does not exist.

Just as well, virus identification by PCR only, has to be distrusted. A PCR gives me a very good fingerprint, but, „there is no use of a fingerprint for the detective if he has no suspect” (freely quoted from Karin Mullis who invented PCR).

A cell count of T-helper cells (with CD4+-marker) in peripheral blood is as questionable. It does not differentiate between TH1 and TH2 and there are other cells bearing the same marker. We well know that a lack of one type of immune response is often compensated by a high activity of the other type. Therefore an increasing CD4+-cell count does not indicate an increase in cellular immune response. From trials in pigs suffering from PMWS we know, that TH-cell count in peripheral blood does not correlate with cell counts in lymph nodes. In one of the biggest studies on antiviral medication of AIDS (Lederberg et al. 2006) over 10 years with 22000 patients from 811 physicians and 22 countries only a mean increase of CD4+-cell counts from 170 to 200/µl by antiretroviral treatment resulted (standard value 400-1500/µl). In the summary this small increase was related to mortalities: ”Virological response after starting HAART improved over calendar years, but such improvement has not translated into a decrease in mortality”. More clearly: the treatment improved laboratory parameters but not health.

In spite of these analytical doubts virus load and CD4+-cell counts had been used in the following trials. They are parameters therapists are familiar with. If a new disease appears, accompanied by a virus (like AIDS 25 years ago) two hypotheses result:
§ The virus can develop, because there is a lack of cellular immune response
§ The virus (in TH1-cells as hosts) causes the lack of cellular immune response

Depending on which of these hypotheses is right, two diametrically opposed treatments result. In the first case cellular immune response should be restored, and by promoting TH1-cells the virus should be eliminated.

In the second case the virus has to be attacked. It is not possible to kill a virus (in physiological conditions) for the simple reason that it is without its own metabolism and is not really living. It is necessary therefore to kill the host cell. This is performed by substances causing a termination of DNA like NRTI and NNRTI, while the third part of a triple therapy, a proteinase inhibitor, unfortunately kills mitochondria if used in the usual concentrations

For another cellular immune deficiency, occurring together with a (identified) circo virus in piglets, PMWS (Post Weaning Multisystemic Wasting) we developed a way (Gradl 2004) to switch the balance between TH1 and TH2 in favour of TH1. By humulone, the bitter of hops as quantum dot (Gradl 2008), prostaglandin formation is inhibited and TH2 is reduced. By this way TH1-cells are promoted. Using procyanidines as quantum dots effector cells of cellular immunity are improved. In addition we used a guluronan complex from alginic acid, improving oxygen transfer to cells significantly (Gradl, Maurer 2000). This mixture had been completed by extracts from cloves and nutmeg (both inhibit prostaglandin formation), lemon skin (anti-oxidant) and thyme (adaptogen). Used in feed, in piglets suffering from PMWS it was possible to increase daily weight gain by 13.8 %, feed conversion by 16 % and to reduce losses significantly. These are nearly values that can be expected in piglets without PMWS. In this case the second hypothesis proofed to be right. After restoring cellular immunity the animals could cope with the virus. TH1-cells increased from 9.3 to 21.5 % of CD4+-cells.

Trail 1
Encouraged by these results, we tried to use the same preparation in HIV-infections and full blown AIDS. We could not find a therapist neither in Europe nor in North America. Therefore we started with so-called patients beyond treatment in East Africa (Gradl 2011) using EGAA-2.

40 patients (women and men aged between 19 and 48 years) in Kampala (Uganda), suffering from full blown AIDS received orally EGAA-2 daily for 90 days. On days 0, 45 and 90 bodyweight, CD4+-counts, virus load, general health status and additional diseases had been recorded.

2 patients died and two dropped out (could not be examined again) for unknown reasons. On day 90 28 (74% of 38) patients could be found to be below the limits of full blown AIDS due to CD4+-counts and virus load. Diarrhoea stopped in all of these cases and body weight became normal. In the remaining 10 cases in 8 people health status as well as CD4+-counts and virus load improved significantly. 6 months after the start of the trial 19 patients were able to go to work regularly again.

Egaa 2 - Pic 2 (Englisch)Fig.: Shift of immune response in full blown AIDS. Number of virus copies.

Egaa 2 - Pic 3 (Englisch)Fig.: Shift of immune response in full blown AIDS: Increase in T-helper cells (CD4+)

Trial 2
21 patients in Nairobi, Kenya, suffering from HIV/AIDS were given EGAA-2 daily for 3 months. One of them died after two weeks. One patient left Nairobi and could not be contacted again. 19 patients could be evaluated (4 male and 15 female patients).

Age:
The age was between 29 and 58 years (an average of 40.7 years). They were tested HIV-positive between 3 month and 8 years (an average of 5.6 years).

CD4+-count: At the start of the trial CD4+-count was between 52/µl and 453/µl (an average of 209/µl) and 265/µl to 920/µl (an average of 565/µl) three month later. CD4+-counts increased in all cases, in one case even from 52/µl to 532/µl and in another from 58/µl to 485/µl.
Tuberculosis: 5 patients suffered from tuberculosis, which improved in all cases. After three months three of them were free of tuberculosis, starting from a very severe state. In two cases the health of tuberculosis patients had improved significantly.
Body weight: In all cases body weight increased, starting with 35 to 85 kg (an average of 52.2 kg) to 46 to 100 kg (an average of 65.0 kg). In one case body weight increased from 37 kg to 60 kg.

Egaa 2 - Pic 4 (Englisch)Fig.: Shift of immune response in full blown AIDS: Increase in T-helper cells (CD4+)

Symptoms were recorded only for some patients. It can be assumed that the others did not show these symptoms
§ Night sweats: Disappeared. In the remaining case it decreased significantly.
§ Fever: disappeared in 2 out of 2 cases.
§ Diarrhoea: disappeared in 6 out of 6 cases.
§ Headache: disappeared in 11 out of 11 cases.
§ Pneumonia: disappeared in 4 out of 4 cases.
§ General weakness: in 10 out of 11 cases patients recovered completely. In the remaining case health improved significantly.
§ Skin thrash: disappeared in 3 out of 3 cases.
§ Mental status: improved to normal in 4 out of 5 cases and significantly in the remaining case.
§ Respiratory problems: disappeared in 2 out of 2 cases.
§ Lipodystrophy, abscess, swelling of the ankles, paralysis, joint pain, herpes, white coated tongue and very dry skin became significantly better or disappeared in single individual cases.

Egaa 2 - Pic 5 (Englisch)Fig.: Shift of immune response in full blown AIDS: increase in body weight

These trials in Africa showed that in full blown AIDS cellular immunity can be restored by EGAA-2. Since health also in terminal cases could be restored it can be assumed that there was a cellular immune deficiency based on which the virus could develop. Due to the questionable virus determination it makes no sense to speculate whether in Africa there are other subtypes of the virus that can be treated easier.

Allergy
AllergyHay fever
The trial had been performed together with 17 physicians and health practitioners, starting December 2006. Due to an extremely warm winter hazel, alder, birch and willow flowered end of February. Assessment was 28.02. In some unclear cases the patients had been contacted by phone. No reaction of a patient with known allergy was taken as positive.

24 patients were assessed end of April again. 11 patients finished the trial, 10 of them because they were free of symptoms.

From 35 cases 6 were free of symptoms, 15 were significantly improved and 8 slightly. A verification after pollen count of birch showed an improvement of even 84% (55% significantly better and 32% free of symptoms). In 4 cases out of 5 cases of chronic allergic asthma (3-27 years duration) an improvement could be seen (2 cases free of symptoms (1 case of them chronic since 11 years)).

Egaa 2 - Pic 6 (Englisch)Fig.: Allergy trial Regensburg

Allergy 2
Previous trials with horses suffering from allergic summer eczema resulted in promising improvements in therapy as well as in prophylaxis. The horses received orally a combination of phase transfer catalysts (from brown algae) together with nanocarriers (loaded with humulone) and cocoa (containing procyanidine).

The same product was administered for six weeks to 14 patients suffering from hay fever using a dose of three tablets (450 mg each) a day.
Egaa 2 - Pic 7 (Englisch)

In 79% of all cases hay fever symptoms improved. 57% were significantly better or without symptoms.

Egaa 2 - Pic 8 (Englisch)Fig.: Case study hay fever

Mechanism of action
The aim of the immune system is to differentiate between self and not-self to eliminate foreign substances like bacteria, virus or other intruders. There are four main types of immune reactions:
Egaa 2 - Pic 9 (Englisch)Fig.: Ways of immune response

Innate immunity:
In most cases the intruder is processed in an unspecific way by macrophages being eliminated by natural killer cells (NK-cells) a sort of lymphocytes.

Three reactions are specific to a specific antigen (normally molecules on the surface of bacteria and virus or foreign protein etc.). After being presented to T-helper cells (TH, a sort of lymphocytes) they activate three different ways of immune response:
§ Humoral response (TH2 mediated): TH2-cells process the antigen and present it to B-lymphocytes which transform into plasma cells, producing antibodies specific to the specific antigen. Reacting with the antigen an antigen-antibody-complex is formed that can be eliminated by macrophages or attach to mast cells starting an inflammatory reaction. Antibodies are effective against most bacteria and intestinal parasites.
§ Cellular response (TH1 mediated): TH1-cells present the antigen to specific T-killer cells that can eliminate the intruder mainly via nitric oxide (NO).This response is effective against virus, mycobacteria but also in eliminating the body’s own cancer cells.
§ Immunosuppression by Treg cells: Not in all cases an immune response is positive. During pregnancy e.g. a cellular immune response to the (semi-foreign) embryo may result in abortion. Like most reactions immune reactions tend to overreact and have to be regulated down. This is performed by so called Treg cells. It would be helpful to find a way to stimulate Treg cells specifically to regulate down autoimmune diseases.

Differentiation of TH1- and TH2-cells: The balance of TH1- and TH2-cells is critical sometimes. Allergies of immediate type are an overreaction of humoral response (TH2 mediated). In some cases (PMWS in piglets; full blown AIDS in human), TH1-mediated response lacks completely (Maurer, Gradl 2002). Both cases are over-compensated by high antibody titres.

After the decision to start a TH1 mediated immune response (or vice versa) the other type is suppressed by cytokines (IL-10, IL-4, IL-5 or INF-γ, Fig. 9).The suppression of TH2 may increase TH1-mediated response

Egaa 2 - Pic 10 (Englisch)Fig.: Differentiation of TH1 and TH2

TH2 cells are promoted by prostaglandin-2 which is formed from arachidonic acid from cell walls by cyclo-oxygenase-2 (COX2). This enzyme can effectively be inhibited by humulone, the bitter of hops. If applied orally, the necessary quantity however is much too bitter. By using quantum dot-technology the same effect can be obtained by only 3.6 mg per day. This means that using this small amount a mainly humoral immune response can be turned into a cellular response. The effect can even be enhanced by procyanidines (as quantum dots) acting on T-killer cells (Fig. 10) (Appelton, Tomlinson, Wikoughby 1996).

Egaa 2 - Pic 11 (Englisch)Fig.: Shift of immune response by humulone and procyanidines

Annex

Use of EGAA-2 in vitro

Human leucocytes (buffy coat) were washed twice in TC 199 and made up in TC 199 to 4 x 106 cells/ml.
10 concentrations of EGAA-2 in TC 199 in 8 replicates were added in micro titre plates (50 µl to 150 µl cell suspension). 2x 8 rows served as controls. After incubation of 48 hours (36°C) INF-γ, IL-2, IL-4, and IL-10 were determined by Elisa in the supernatants. Mean changes in percent in comparison to the controls are used as results.
For human dose a body weight of 70 kg and a blood volume of 6 l were assumed.

Egaa 2 - Annex 1
In further trials concentrations between 1 and 0.02 mg/kg bodyweight (0.75-75 mg/70 kg) were used:

Use of EGAA-2 in vivo

50 mice NMRI (20 g) received daily for 5 days a concentrations series of IS in 1 ml of water (tube feeding). After 5 days blood was gained by heart puncture. In serum INF-γ and IL-10 were determined by ELISA. Mean values of changes in percent of cytokines in comparison to controls were calculated.
Egaa 2 - Annex 2
In further trials a dose of 20-75 mg/70 kg was used.

Basic tables in vitro

Egaa 2 - Annex 3

Egaa 2 - Annex 4

Egaa 2 - Annex 5

Egaa 2 - Annex 6

Egaa 2 - Annex 7

Egaa 2 - Annex 8

Egaa 2 - Annex 9

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