AIDS DEFINING ILLNESSES,
THEIR CAUSES AND TREATMENT
Last Update: July 2001
Treatment recommendations based on the works of
Dr. Heinrich Kremer (Hamburg), Prof. Alfred Hässig (Berne), Dr. Stefan
Lanka (Suttgart), Dr. Eleni Papadopulos-Eleopulos et al. (Perth),
Dr. Leonore Herzenberg et al. (Stanford University),
and 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 changes 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
mature predominantly to cells with TH2 cytokine prophile, which migrate
to the bone marrow, where they activate defences against bacteria by
producing antibodies, but only few mature to TH1 cells mesurable in
plasma, which activate the dedection and destruction of fungus and
virus infected cells and of altered cells. If this situation persists,
a higher quantity of proteins of the cytoskeleton and of mitochondria is
released 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), medicaments 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 released through physical exertion on increased exposure to
calcium ions. This affects 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 cotrimoxazol, 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
mitochondria.
- 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 nitricoxyde-molecules, so that ATP production in
mitochondria is not disturbed. An ongoing shortage 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 (cotrimoxazol, 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 radicals) 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 essential
nutrients directly from the myoproteine. By an heightened activity of
reverse transcription the cellnucleus then saves its genotype.
Continuous activation of macrophages leads in this situation to an
ongoing release of messanger substances (Inteleukine 2) which trigger
the release of stress-hormones in the adrenal gland. This hormones
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 continuously 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 decay 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 reactions 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 mitochondrial 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 supported 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 and
sulphur containing moistures or Melaleucae Alternifolia oil as a local
treatment against fungal infection.
- Targeted stress reduction techniques, e.g. autogenic training,
stretching and massages, 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 contact 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 restored.
If limited administration of antibiotics is necessary, this basic
therapy has to be continued. The treatment can be adapted to the
individueal illnesses occuring. Progress achieved by these measures to
bolster the immune system can be monitored by measuring stress hormone
profiles, the T4/T8 cell ratio, macrophage activation (neopterine 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 isolated, photographed or otherwise
properly characterised, as required by the established 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 transcription was then interpreted
as signifying the presence a new virus. A virus-specific enzyme could
not be aprooved according to the established rules. Synthetic protease
inhibitors, which are supposed to inhibit the formation of essential
viral building blocks, over time, cause malaise, diabetes, kidney stones
and liver failure in patients given them. After PIs and nucleoside
analogues are first given, an apparent decline 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 terminators 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.
Study Group for AIDS therapy
c/o Felix A. de Fries
Eglistr. 7 CH-8004 Zürich
Tel./Fax: 0041 1 401 34 24
E-mail: felix.defries@bluewin.ch