Subject: The role of
antibiotics in the emergence of AIDS: Conclusion
From: Study group AIDS therapy
felix.defries@bluewin.ch
To those affected,
their doctors and carers
To Media in developed and developping countries
Chemoantibiotics, a principal cause of AIDS defining
illnesses in developed and developing countries
Dear Sir or Madam
Chemoantibiotics (such as Septrime, TMPSMX,
Cotrimoxazole) which are administrated in veneral di-seases and other
infections are a principal cause of AIDS defining illnesses and immune
deficiencies in developing and developed
coundtries.
Chemoantibiotics block the formation and the release
of folic acid and of purine, which are needed for the formation of the
DNA in Mitochondria and exhaust thereby the mitochondrial thiol pool. They
bind to SH-groups of glutathione and cysteine and impair thereby the
activity of mitochondria. (When admi-nistred without control they
also cause the formation of multiresistant strains of
bacteries.) They inhibit by oxydation the transport of oxygen into
the cells (causing
methhaemoglobinaemy) and ex-haust by
oxydation the glutathion molecules in the cells, which are needed for the
reduction of oxygen and the production of ATP in mitochondria. By this they
cause damage to the CD-4 and CD-8 helpercells and induce thereby the
emergence of opportunistic infections (e.g. PCP,
toxoplasmosis,
herpes, Cyto-megalie), that define the AIDS-syndrome. The lack
of glutathion molecules in antigen-presenting cells then induces the
formation of CD-4 cells with the Th-2 cytokine prophile, that activate
the formation of antibodies against external antigens, whereas the
formation of CD-4 helpercells with Th1 cytokine profile, that activate
the dedection and destruction of cells containing viruses,
myccobacteries and fungy, is con-tinuosly inhibited.
The immune deficiencies and the AIDS defining
illnesses induced by this chemoantibiotics have been treated from 1987 on with
nucleosid analog drugs, that have been created for the treatment of
leukemia. Nucleoside analog drugs damage the DNA in mitochondria, effecting
damages to cells in the brain, the muscles, the bone marrow and
internal organs and lasting damage to the CD-4 and CD-8 helpercells and
thereby the emergence of the opportunistic infections, that define
the AIDS syndrome. (Children from mothers, that receive AZT in
their pregnancy, show a far higher risk for a progredient course of
AIDS defining infections than children from pregnant
mothers who did not take AZT (Jour. of AIDS 2000).
In regard of this well documented interactions, that
have been demonstrated in various studies and ani-mal tryals,
the reduction of the administration of chemoantibiotics is the most
important mesure to reduce the emergence of AIDS defining illnesses in
developed and developping countries.
In various articles, that we have sent you earlier, it
was demonstrated, how AIDS defining illnesses can be treated without a
continuous administration of chemoantibiotics and without
nucleoside anlog drugs and how a prevention of infections and immune
deficiencies can be achieved.
If you have questions concerning this articles, don't
hesitate to get back on us by E-mail.
Enclosure: Treatment recommendations
AIDS defining illnesses, their causes and treatment
(Treatment recommendations based on the works of Dr.
Heinrich Kremer, Hamburg, Prof. Alfred Häs-sig, Berne), Dr. Stefan
Lanka (Suttgart) and Eleni Papadopulos-Eleopulos (Royal Hospital, Perth)
available at www.virusmyth.com
and www.continuummagazine.org
and
works of L. A. Herzenberg, J.D. Peterson and S.C. De Rosa (Stanford
University)and of Furchgott and Ignarro avaiable at
www.ncbi.nlm.nih.gov
The many and varied diseases that can define the AIDS
syndrome: fungal infections of the lung, of the mucous membranes, the
brain, and the gut, and the degenerative chan-ges in the endothelial cells
of blood vessels and lymphatic vessels (Kaposi Sarcoma), occur because
of an ongoing heightened production of gaseous nitricoxide and
oxygen radicals in immune cells and other cells. Under these conditions
CD4 helper cells ma-ture predominantly to cells with TH2 cytokine
prophile, which migrate to the bone mar-row, where they activate defences
against bacteria by producing antibodies, but only few mature to TH1 cells
mesurable in plasma, which activate the dedection and destruc-tion
of fungus and virus infected cells and of altered cells. If this
situation per-sists, a higher quantity of proteins of the cytoskeleton and
of mitochondria is relea-sed as en effect of heightened cell decay.
Against these proteins a higher rate of the antibodies are formed. This
antibodies and antibodies that occure in hepatitis and due to toxic
pollution are detected by the HIV-antibody tests. Once a certain,
arbitrary level is reached, the patient is declared "HIV
positive".
A elevated level of nitricoxide and oxygen radicals
comes about as a result of:
- ongoing contact with antigens (e.g. from repeated or
chronic infections, injuries, operations and dirty water).
- repeated contact of foreign proteins to the plasma
(from coagulation proteins in blood preparations and from semen liquid
in unprotected anal intercourse)
- contact to toxic substances in food (e.g.
aphlatoxines in wet cereals), medica-ments and from environment pollution,
toxic decomposition products from modern chemicals (heavy
metals (e.g. carrier substances in hepatitis B-vaccines, amalgan fillings)
- inhalation of nitrites ("poppers") which
are stored in cells as NO2. They are re-leased through physical exertion on
increased exposure to calcium ions. This af-fects the endothelial cells of
blood vessels and lymphatic vessels with a small capillary diameter, and
leads thereby to degenerative changes (swollen lymph nodes and finally
to Kaposi Sarcoma).
- impairment of the mitochondria, the single cell
energy suppliers, which synthesize the energy-carrying-molecule ATP,
used for all functions of the organism
The causes of chronic mitochondrial damage are:
- damage of the mitochondrial DNA due to antibiotics
(e.g. sulpha compounds such as Septrime, TMPSMX) which block the
synthetisation of folic acid and purine, and lead thereby to the
exhaustion of the mitochondrial thiol-pool. Likely effects are caused by
heavy metals and by cytostatics like AZT. All this substances bind the
SH-groups of glutathione and cysteine and impair thereby the
activity of mitochon-dria.
- reduced glutathione produced resulting from liver
damage, e.g. chronic hepatitis (occuring frequently in gay men,
hemophiliacs and intravenuous drug consumers), excessive alcohol consumption, or
through shortage of nutritional cysteine, esp. in developing countries.
Glutathion molecules reduce oxygen- and nitricoxydemole-cules, so that ATP
production in mitochondria is not disturbed. An ongoing shorta-ge of
glutathione means that phagozyte poison themselves attacking fungi and
virus containing cells by means of NO.
- reduced oxygen transport in cells because of
oxidation (methhaemoglobinaemia) which exceeds the reductive
capacity of glutathione. This comes about because of the strongly
oxidising effect of nitrites (poppers), antibiotics (Septrime, TMPSMX)
and insecticides (e.g. Lindan in moistures against crab louse),
nucleoside analogues (e.g. AZT), heavy metals and chemicals.
- lack of plant antioxidants which bind to toxic
degradation products (oxygen
radi-cals) and thereby reduce inflammation and stressreactions.
On prolonged impairment of mitochondria, they dissolve
their symbiosis with the host ("Warburg Phenomenon"). Cells
then increasingly switch over to producing energy by anaerobic fermentation,
which results in excess lactic acid production, and the growth of fungi
and opportunists, and ultimately to wasting, at which point cells obtain
es-sential nutrients directly from the myoproteine. By an
heightened activity of reverse transcription the cellnucleus then saves its
genotype.
Continuous activation of macro-phages leads in this
situation to an ongoing release of messanger substances (Inteleu-kine
2) which trigger the release of stress-hormones in the adrenal gland.
This hormo-nes induce the formation of TH2 CD-4 cells, that activate
the formation of antibodies in the bone marrow, whereas cellular immune
reactions induced by TH1 cells are conti-nuously suppressed.
By means of:
- A supply of sulphur compounds in sea salt, mineral
water and algal products, and of cysteine and methionine containing
protein mixtures, (Cysteine,
N-acetyl-cysteine and arginin, (3-8 gramme
daily)also in curd and whey) and folic acid (300 miligramme daily) can
stimulate glutathione formation in the liver. Glutathione must
be administered in the mean time intravenously (600 milligramme daily)
untill its formation in the liver works sufficiently again.
- Plant antioxidants, e.g. PADMA 28 (2-3 times 2
tabletts daily) or artemisia annua in UWEMBA pastilles (available from
www.nusag.com) which bind to toxic oxygen de-cay products, and natural
protease inhibitors (heparine and heparinoids in agar, algae or cartilage
preparations), which activate the body's own anti-proteases and bind
to cations that attack the cell walls, slow down chronic inflammatory
reacti-ons going allong with increased cell division.
- Co-enzyme Q10 and NADH and high doses of Vitamin C
and E can improve electron transport in the respiratory chain of cells.
Folic acid (300 milligramme daily), thiols L-carnitin and low doses of
selenium, (e.g. brewers'yeast), and zinc can support the
synthetisation of ATP in mitochondria and the repair of damage to
mi-tochondrial DNA.
- Opportunistic infections (fungy, PCP and others can
be treated by omega-3 fatty acids in fishoil (3 tablespoons daily)
In dificult cases gamma globulin, selective cyclo-oxygenese-2 inhibitors
and difluoromethylornithine as a polyamine inhibitor can
be administrated.
The activity of killer cells and neutrophillia can be
sup-ported by the administration of glutamine (40 grammes daily) and
L-Arginin (20-30 grammes daily).
- DHEAS (200 milligrammes daily) can diminish ongoing
stress reactions in the immune system (TH1-TH2-switch) caused by the
release of stresshormones (cortisol) in the adrenal gland.
- Essential fatty acids in linseed oil, thistle oil,
soya oil and omega-3 fatty acid in fish oil mixed with curd, which
enhighten the uptake of oxygen in cells
- Carduus marianus or Aloe vera to support the liver
and partly fermented beverages that can restore the gut flora
- Ethereal oils, rubbed on to the chest and in the
armpits serve to stimulate the immune system through the ground
substance (matrix)
- Extract of grape fruit kernels, gargling with
honey/vinegar andsulphur containing moistures or Melaleucae
Alternifolia oil as a local treatment against fungal
in-fection.
- Targeted stress reduction techniques, e.g. autogenic
training, stretching and mas-sages, and refraining from excesive
physical exercise (using perfomance-enhancing drugs, e.g. coffee,
alcohol, nicotine, amphetamines (X-tasy), cocaine, heroin and poppers.)
- avoiding inflammatory reactions and infections by
avoiding injuries and the con-tact of foreing proteins to the plasma
(e.g. by protection in anal intercourse).
- of a nourishment poor in sugar amd acid but rich in
roughage and bases, with much high-value carbohydrates and
potatoe,
plant antioxidants, e.g. vegetables, fruit, herbal and green
teas, cold-pressed oils, partly fermented dairyproducts,
algae, soya beans, and fish but not iron-rich red meat............a flexible resistance in people with AIDS
defining illnesses can be resto-red.
If limited administration of antibiotics is necessary,
this basic therapy has to be continued. The treatment can be
adapted to the individueal illnesses occuring. Pro-gress achieved by
these measures to bolster the immune system can be monitored by
mea-suring stress hormone profiles, the T4/T8 cell ratio, macrophage activation
(neopteri-ne test) and cutaneous anergy, the glutathione level in plasma
and in T-4 helper cells.
HIV, which is held to be responsible for causing 30
different AIDS-defining diseases, has never been shown to be
transmissible nor self-reproducing; it has never been iso-lated,
photographed or otherwise properly
characterised, as required by the
esta-blished rules of virology. The original experimental technique of Gallo
and Montagnier in 1984 on which the HIV-antibody-tests were constructed,
involved culturing cells from AIDS patients with leucaemic
cells and embryonal cells, that show a high activity of reverse
transcription. This effect of an artificially amplified reverse transcrip-tion
was then interpreted as signifying the presence a new virus. A
virus-specific en-zyme could not be aprooved according to the established rules.
Synthetic protease in-hibitors, which are supposed to inhibit the
formation of essential viral building blocks, over time, cause malaise,
diabetes, kidney stones and liver failure in pati-ents given them. After PIs
and nucleoside analogues are first given, an apparent de-cline in
inflammatroy reactions and „virus production" may be
observed, but it then rises again, which is attributed to resistance developping.
Nucleoside analog drugs, that destroy for a limited time through
cytostatic effects bacteries and fungy, are only ever 1% incorporated
into the cell nucleus, where they should work as DNA termi-nators
against HIV. As it has been demonstrated by animal trials since 1990 they
cause irreversible damage to the mitochondrial DNA and
thereby damage to the brain, the bone marrow, the muscles and internal
organs and a lasting decrease of CD-4 and CD-8 cells causing opportunistic
infections (cytomegalie, herpes simplex, PCP and hepatitis
non-A-non-B) that define the AIDS-syndrome.
