Note: Descriptions are shown in the official language in which they were submitted.
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USE OF 2-MERCAPTOETHANOLAMINE (2-MEA)
AND RELATED AMINOT~IOL COMPOUNDS AND COPPER(II)-
3,5 DI-ISOPROPYL SALICYLATES AND RELATED COMPOUNDS
IN THE PREVENTION AND TREATMENT OF VARIOUS DISEASES
BACKGROUND OF THE INVENTION
The present invention is directed to new therapeutic compositions and
applications of 2-mercaptoethanolamine (2-MEA) and related aminothiols and
di-isopropyl salicylates, solely or in combination with other factors, agents, or
processes that are physical, chemical and/or biological based, including
precursors, intermediates, end products, catalysts, promoters and/or any factors,
agents, or processes involved directly or indirectly from initial application of the
therapy to the fmal result. More particularly, the present invention is directed to
the use of 2-MEA and related aminothiols and copper(II)-3,5 di-isopropyl
salicylate in the treatment and prevention of AIDS, cancer, autoimmune disease,
microbiological infections, and other diseases where immunological dysfunction
and/or free radical formation function as part of the disease mech~ni~nn
2-MEA has long been used by itself in the treatment of kidney disease,
known as cysteinuria, where it may protect renal function. 2-MEA and related
compounds have also been used as radiation protective agents in various
formulations. This is at least due in part to the powerful antioxidant properties of
these compounds. 2-MEA has also been linked with ulcerogenic plopellies in
animal experiments. 2-MEA has been shown to exert both immunostimulant and
immunomodulant action in in vitro trials. Jeitner et al., Biochimica et Biophysica
Acta 1223:15-22 (1994). Cyst~tnine, a related compound, has demonstrated in
vitro inhibition of HIV. Bergamini et al., J. Clin. Invest. 93:2251-2257 (1994).Other applications of 2-MEA have been in the field of non-specific vitamin
supplementation as a general antioxidant supplement in Swedish Anti-Aging
Formula 223.
SUMMARY OF THE INVENTION
The antioxidant abilities of 2-MEA and related aminothiols make these
compounds a valuable therapeutic adjunct to the treatment of any disease
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condition which directly or indirectly generates or causes the generation of free
radicals. F.~çnti~lly, this includes virtually every known disease condition as
well as other conditions which may not be cornmonly regarded as diseases, as
well as conditions which may be predisposed to or function as pre-cursors to
disease. Although it is contemplated that the present invention include all suchapplications singly or in combination with other traditional therapies, there are
several disease conditions where the application has produced significant results
with the use of 2-MEA singly, or in combination with other factors, agents
and/or processes. These diseases include AIDS, cancer, autoimmllne disease,
microbiological infections, and other diseases where immlln~logical dysfunction
and/or free radical formation function as part of the disease mech~ni~m
In the present invention, 2-ME~ and related aminothiols are used in
cancer prevention and treatment as a general immlln~lstimulant and/or as an
antioxidant to offset some of the toxic sequelae of the disease condition or other
conventional therapies such as chemotherapy and radiotherapy. It is important inthe application of 2-MEA and related arninothiols to either bind the compound toa delivery system which directs its protective action preferentially to healthy cells
and/or time its delivery so as not to interfere with the anticancer activity of the
therapy. A therapy may be beneficial to the body and antagonistic to the diseaseif timed correctly. If antioxidants like 2-MEA, for example, are timed correctlyso as to inhibit or otherwise interfere with agents used in therapy which generate
free radicals, then the previously antagonistic therapy may now protect disease by
interfering with therapy and may now be classified as synergistic.
Application to autoimmune and immunodeficient conditions is indicated
by the immllnoregulating and immunomod~ ting activity demonstrated by
2-MEA. 2-MEA and related aminothiols including penicill~mine andlor
copper(II)-3,5-di-isopropyl salicylate were ~-1mini~t~red to patients as single
agents, or in combination with other factors, agents, or processes which induced,
stimulated, and/or facilitated their efficacy, or inhibited, suppressed or
neutralized their toxic or undesired effects. Some agents and factors may have
dual capabilities.
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Although 2-MEA and related aminothiols may be incorporated in many
uses requiring its antioxidant capabilities of other properties, the present
invention is directed primarily to the medical applications of 2-MEA. The use of2-MEA in the present invention impacts on diseases as varied as AIDS, systemic
lupus erythromatosus, cancer, arthritis, autoimmune diseases, and can be used in~ sunscreens to minimi~t- radiation damage.
Cimetidine, for example, may directly aid in the immunostimulating or
immunomo~ ting action of 2-MEA while inhibiting ulcer formation.
Copper(II)-3,5 di-isopropyl salicylate directly supports the antioxidant ability of
2-MEA while indirectly assisting in the treatment of cancer, for example, by
having its own anti-cancer activity.
A therapeutic composition and method is disclosed for using 2-MEA and
related aminothiols in the treatment and prevention of AIDS, cancer, autoimmune
~lisc~es, and microbiological infections, comprising the step of ~ mini~tPring an
effective dosage of a therapeutic composition comprising 2-MEA or related
aminothiols to a patient having AIDS, cancer, autoimmune disease,
microbiological infections, and other diseases where immunological dysfunction
and/or free radical formation function as part of the disease mech~ni~m The
effective dosage of 2-MEA or related aminothiols for a-lmini~tration to a patient
is between approximately O.Olmg and about SOOmg, at least once daily, up to
four times a day. However, benefits may be achieved with a single dose, a
monthly dose or a weekly dose. However, 2-MEA efficacy is best sustained with
a daily dosage. The therapeutic composition is ~-lminist~red to a patient by a
means selected from the group consisting of oral ~qtlmini~tration, catheter
~lmini~tration, intramuscular ~lministration, intravenous ~lminisfration~
intradermal ~lmini~tration, intradural a~lmini~tration, intravesical ~-lmini~tration,
hllldu~ dl ~lmini.~tration, intrathecal ~(lministration, inhalation, topical
~lmini~tration, sub-cutaneous ~1mini~tration~ and rectal ~(lmini~tration or any
~ other means of ~lministration. The composition is orally ~-lmini.ctered in a form
selected from the group consisting of a capsule, gel cap, liquid, tablet.
In yet another method of the present invention, 2-MEA and related
aminothiols were combined with a living biological delivery system. 2-MEA or
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related aminothiols were incubated with a living biological system to form a
mixture. The mixture was centrifuged to produce a pellet comprising the 2-
MEA, the active ingredient, bound with the living biological system. The pellet
may also include intermediates and/or end products of 2-MEA or related
aminothiols depending on the precursor used. The pellet was ~-~mini~tered as is
or, was re-suspended and washed at least once. The pellet was then ~1mini.~teredto patients.
The living biological system is selected from the group consisting of
yeast, lactic acid cultures, target cells, and other living cells. 2-MEA or related
aminothiols and the living biological system were incubzlte~l between about 6
hours and about 72 hours depending on the type of living biological system. For
example, yeast or yogurt cultures were incubated between about 6 hours and
about 48 hours, lactic acid cultures were incubated between about 24 and about
48 hours, and target cells and other living cells were incubated between about 24
and 72 hours. The centrifuging step was perforrned from about 200 rpm to about
50,000 rpm.
Different centrifugation rates isolate specific components. Ulkacentrifugation
was sometimes employed after Iysis of cell to recover and concentrate organellesand other fractions for use in the invention.
When 2-MEA and related aminothiols are combined with a living
biological delivery system, the pellet can be ~lrnini.~tered to patients in several
ways. First, the pellet can be orally ~-lrnini~tered. The pellet can be suspended
in a yogurt medium and then applied topically to the skin of the patient. Further,
the pellet can be lyophilized and then ~-irnini~tered to the patient.
In another embodiment of the present invention, a therapeutic composition
also called the complex formula is provided comprising therapeutic dosages of 2-MEA or related aminothiols, at least one antioxidant such as BHT, at least one
kansfer factor of the type developed by the inventor and disclosed herein below,and at least one living organism. Copper(II)-3,5 di-isopropyl salicylate may be
included in the complex formulation in place of the 2-MEA or as an additional
component. The 2-MEA or copper compound or the complex formula can
inactivate and stabilize the presentation of the targeted condition, thereby
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minimi7in~ the number of multiphasic steps needed in the neutralization of
anticipated resistance.
In yet another embodiment of the present invention, a therapeutic
composition and method is disclosed for using copper(II)-3,5 di-isopropyl
salicylate in the treatment and prevention of AIDS, cancer, autoimmune diseases,- and microbiological infections, comprising the step of z~ mini~t~ring an effective
dosage of a therapeutic composition comprising copper(II)-3~5 di-isopropyl
salicylate to a patient having AIDS, cancer, autoimmune disease, microbiologicalinfections, and other diseases where immunological dysfunction and/or free
radical formation function as part of the disease mech~ni~m The effective
dosage of copper(II)-3,5 di-isopropyl salicylate for ~r1mini~tration to a patient is
between approximately lOmg and about SOOmg, three times a day.
Administration of the composition to a patient is accomplished in the same ways
as previously described for 2-MEA, and is orally ~lmini~tf red in the same formsas 2-MEA.
Like 2-MEA, copper(II)-3,5 di-isopropyl salicylate was combined with a
living biological delivery system using the same method steps and same living
biological systems as described for 2-MEA. Copper(II)-3,5 di-isopropyl
salicylate and the living biological system were incubated between about 6 hoursand about 72 hours depending on the type of living biological system. The pelletfurther included intermediates and/or end products of copper(II)-3,5 di-isopropyl
salicylate. The centrifuging step was performed from about 200 rpm to about
50,000 rpm. Different centrifugation rates isolate specific components.
Ultracentrifugation was sometimes employed after lysis of cell to recover and
concentrate organelles and other fractions for use in the invention. The pellet
was a-1mini~tered orally to the patient, suspended in a yogurt medium and applied
topically to the skin of the patient, or Iyophilized and then ~lnnini~tered to the
patient.
The therapeutic composition compri~in~ an effective dosage of 2-MEA
further includes an effective dosage of at~tast one antioxidant, wherein at least
one antioxidant is selected from the group consisting of BHT, BHA. ethoxyquin,
TBHQ, nordihydroguaracetic acid, lipoic acid, and vitamin C. The effective
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dosage of BHT for ~lmini~tration ranges between about 0.01 and about 2% of
the dietary intake by patient weight.
The therapeutic composition comprising 2-MEA may further include an
effective amount of at least one transfer factor in type and/or target. The
effective dosage of the transfer factor for ~1mini~ration purposes ranges between
about lmg and about Sg per day. The transfer factor is selected from the group
c~n.~i~ting of transfer factor of resistance, transfer factor of synergy, and transfer
factor of anticipation.
The therapeutic composition may further include an effective dosage of
living microor~ni~m~ selected from the group consisting of acidophilus,
theophilus, thermophilus, lactobacillus bulgaricus, lactobacillus plantarur7z, yeas~,
kef r and rhizopus. One yeast that was used in the present invention was
saccharomyces cerevisiae.
DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS
The present invention is directed to the use of 2-MEA and related
aminothiols and copper(II)-3,5 di-isopropyl salicylate in the treatment of
individuals with AIDS, cancer, microbiological infections and other immllne
deficient conditions as an adjunct to chemotherapy or radiotherapy, as a broad
spectrum antioxidant substance for life extension, in combination with other
compounds, or by itself. The effects of 2-MEA and copper(II)-3,5 di-isopropyl
salicylate may be enhanced in combination with other compounds which function
in one of several ways: 1) augment the effect of the compounds; 2) neutralize
their side-effects; and/or 3) alter the targeted condition directly. ~or example,
use of 2-MEA in combination with cimetidine (Tagamet'~9) or other comparable
stomach pain relievers reduces the likelihood of ulcers commonly associated withthe use of 2-MEA, an ulcerogenic compound. 2-MEA was also combined with
certain antibiotics to neutralize the ulcerogenic side-effects of 2-MEA.
Vaccination and antibiotics against heliobacter pylori and other ulcer-related
organisms may be combined with 2-MEA to minimi7f ulcerogenic potential.
In augmenting the efficacy of 2-MEA, a wide range of antioxidants was
used including but not limited to vitamins C and E, beta-carotene, supplements
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such as pycnogenol, selenium, germanium, nordihydroguaracetic acid, dimethyl
sulfoxide, other natural or artificial antioxidants such as copper(II)-3,5 di-
isopropyl salicylate, butylated hydroxytoluene (BHT), butylated hydroxyanisole
(BHA), ethoxyquin, TBHQ, oxygen peroxide, folic acid or any antioxidant. The
S antioxidants helped to elimin:~lte the free radicals, which are directly or indirectly
generated by a number of disease conditions. These compounds in combination
with 2-MEA and related aminothiols including penicillamine augmented the
efficacy of 2-MEA in disease conditions, for example, AIDS, where 2-MEA and
antioxidant activity was desired. In AIDS, part of the virus' generation is
predicated on the virus using oxidized co-factors. Upon entering the cell, 2-MEAinhibits the co-factors from being oxidized, thereby preventing the virus from
~imil~ting. Other antioxidants as listed above were found to enhance the
effects of 2-MEA by enhancing its antioxidant effect.
Other factors that were found to augment 2-MEA's efficacy include
intermediates and end products of 2-MEA and related aminothiols. The 2-MEA
acts on cells, and then the intermediates were extracted from the cells. The 2-
MEA was also added to target cells like skin cells, immune cells, etc. and then
extracted from the target cells, thereby carrying the intermediates, activating
factors, co-factors and other components which were activated by 2-MEA. 2-
MEA has many functions, including one as an immune stimulator. A preferred
method for using 2-MEA in a way that will enhance its immune functions upon
lmini~tration to a patient is to use 2-MEA as well as its extracts from target
cells. The extracts include genetic changes, enzymatic changes as well as
activation factors. In other words, the present invention provides a method by
which induced and amplified changes by 2-MEA are used to enhance the
immunological and the antioxidant capacity of 2-MEA upon arlmini.ctration in
vivo or in vitro to a patient or desired host system including :~nim~
The 2-MEA and related aminothiols including penicill~mine were
~rlmini~tered at all stages of the disease conditions tested at a dosage betweenabout 0.01mg and about 500mg, at least daily up to ~ times daily. Depending on
whether the activated target cells were human or animal origin and if you extract
by injection or orally, 2-MEA dosages varied widely. When the 2-MEA acted on
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the target cells, the cells then produced genetic information for cellular
multiplication and expansion. For example, O.lmg to about lOOmg or more of
the transfer factor exkacted from the activated target cells was an adequate daily
dose to give patients.
It was also found that white blood cells removed from a patient and
incubated with 2-MEA caused cellular multiplication. The incubated cells were
then injected back into the patient. The combination of the white blood cells and
the 2-MEA produced a variety of extracts, kansfer factors, precursors, etc. All of
these products were capable of being ~rlmini.~tered back into the respective
patients for keatment purposes. In the alternative, each of these products were
broken down chemically, physically or biologically and the extracts therefrom
were ~lmini.~t~red to the patients.
2-MEA may cause genetic, enzymatic, and other changes in the imml-ne
cells, which angment their efficacy and numbers. At the same time, 2-MEA may
inhibit mutation and resistance in the targeted condition, for example, inhibition
of viral replication in HIV.
Sparing function is unique to pharmacology, and is defined by the
inventor as the optimal bioavailability and efficacy of a compound being
facilitated by induction of secondary changes stimulated by the compound prior
to its ~riministration. To exemplify this, 2-MEA will induce cellular
multiplication and changes on various levels of cellular function. A fraction ofthe sl~lminictered dose is used in the induction of these changes, leaving less of
the 2-MEA to carry out its primary and other functions in its original form.
Similarly, copper{II}-3,5 di-isopropyl salicylate will induce the formation of
superoxide dismutase amongst other cellular changes. A fraction of the
copper(II)complex will be used up in this induction, leaving less of the original
form to carry out its primary antioxidant and other functions. Generation or
creation of the in(luce~l change by supplementation of induced factors or their
induction by genetic codes or factors such as kansfer factors will minimi7~ the
amount of precursor eg.,2-MEA,
,
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copper(II)-3,5 di-isopropyl salicylate to be used in this manner and, thus have a
sparing effect. Compounds may then mzlintzlin greater concentration and durationof action.
In yet another therapeutic approach to treating disease conditions like
S AIDS, cancer etc., 2-MEA was used in combination with other traditional
medical therapies. Viral inhibitors dideoxyinosine (DDI), AZT, protease
inhibitors, etc. and other agents combine effectively with 2-MEA as it affects
viral replication at different sites. 2-MEA exhibited a very powerful
multiplication, immunostimulating and immunomodlll7ttin~; activity. As a result,much greater efficacy against the virus was achieved with 2-MEA, leading to a
rapid rise and norm~li7~tion of T-cell parameters accompanied by a sustained
drop in PCR. Lower dosages of drugs like AZT were required and much less
toxicity occurred. Further, a much greater duration in the efficacy of the othertherapeutic agents occurred in the presence of 2-MEA.
In the present invention, 2-MEA was combined with ozone, an oxidant.
When ozone is at its maximum peak, 2-MEA is not; when 2-MEA is at its
maximum peak, ozone is not. The rationale for the combination 2-MEA and
ozone therapy is to have 2-MEA inactivate the intracellular virus so that the virus
and the cells are prevented from dividing. Ozone, on the other hand, kills viruses
in the bloodstream. The ozone is pulsed for a specific time period ranging from
hours to days apart followed by 2-MEA therapy. Improvement was still
observed when the modalities were used simultaneously, but interference also
occurred. Each therapy is alternated so that 2-MEA is s~-lmini~tered one day andthe ozone therapy is given the following day. Ozone was ~mini.~tered by IV,
orally, intramuscularly, by enema, etc. Blood tests were given at selected time
periods to measure 2-MEA levels and oxidation levels. 2-MEA acts by entering
the patient's cells and preventing the ozone from activating the virus. Viruses
need oxidized components to grow inside cells. Ozone kills viruses in the blood.Ozone is capable of killing viruses outside the cells. The general idea with this
combination therapy was to have an agent enter the cell while another agent
killed the viruses in the bloodstream. This was achieved in several ways.
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First, medical equipment like infusion pumps pump blood into a chamber
where it is ozonized, and then returned back into the patient's body. The
inventor found that it did not matter how much 2-MEA was in the body, if you
blast it with ozone, the viruses were killed. Ozone therapy and 2-MEA can also
S be combined and then pulsed into the body. Ozone therapy is currently one of
the most common AIDS therapies. The ozone itself is inexpensive, but the
procedure and equipment are quite costly. Moreover, ozone is effective for only
a short period of time because of its toxicity. Almost everything that damages
the body occurs when large amounts of free radicals are released. Ozone acts
locally and spontaneously, so when the cells are protected by 2-MEA in the
body, ozone produces ~ m~gin~ effects against the targeted disease without
~1~m~gin~ the patient's normal cells.
In another embodiment of the present invention, the inventor developed a
therapeutic kit, which combines a therapeutically effective dosage of 2-MEA in
any form with an ozone preparation and a vaccine preparation. The 2-MEA
offsets the ozone's ~ m~ging effect on the cells. 2-MEA augments the ozone
~l~m~ging effect against the targeted disease. 2-MEA functions by augmenting
the ozone effect not only against HIV, but also against other viral and microbial
infections. 2-MEA amplifies the immune response which ozone by itself cannot
achieve. While ozone may cause problems with vaccines by restricting some
portion of the immune response and thereby damage the vaccine, adding 2-MEA
to the vaccine protected it against the ozone's deleterious effects.
The addition of 2-MEA was found to augment the human immune
response to the AIDS vaccine and, therefore, serves as a potential adjunct to
immunotherapy for any viral or microbial disease. Injection of 2-MEA produced
a more immediate and systemic effect~ and caused less problems for individuals
with ulcers by not passing through the stomach.
With chemotherapy, for example, the genetic information either protected
white blood cells and the enzymatic information from the intermediates, and end
products of the healthy white blood cells, can be used to selectively protect them,
as opposed to 2-MEA which also protects the cancer cells. If amplified genetics
are used, you might be able to protect the white blood cells without necessarily
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protecting the cancer cells because the genetic information would be translated by
the cancer cells.
Transfer Factors and 2-MEA
Some transfer factors mentioned below and transformation factor are
terms coined by the inventor. Transfer factors cause the activation of T-cells to
attack the HIV. By raising a transfer factor against HIV in an animal system,
that animal produces a simple transfer factor which causes the T-cells to increase
in number and attack the HIV. Transfer factor can be raised against live HIV
and trigger the immune system to attack the live virus. A transient increase in T-
cells occurs and when they die, a drop in the T-cells occurs.
When 2-MEA is used in the patient, the viral structure will appear to
change. You want to use a transfer factor of resistance or anticipation or
transformation factors. Transfer factor of resistance involves taking a transferfactor, for example, from a horse which is resistant to AIDS, and add it to a test
tube cont:~inin~ about 10,000 human or the patient's own T-cells. The AIDS
virus is then added to the test tube. Of those approximate 10,000 T-cells which
accept the transfer factor, most will attack the AIDS virus and die. However,
some of the T-cells will accept a special part of the transfer factor of resistance,
attack the AIDS virus and not die. Procedurally, incubate the surviving human
T-cells having the transfer factor from the resistant animal with general human T-
cells or even with the patient's own T-cells. Then culture the surviving T-cellsbecause these cells have developed resistance to HIV. This step can be
performed in one of two ways. One approach is to obtain more T-cells from the
patient, incubate them with the transfer factor of resistance, and then ~1mini.~t~r
them back into the patient. In the alternative, remove T-cells from pooled humanblood, incubate them with the transfer factor of resistance, and then ~ ministerthem to the preselected patients. In yet another approach, inject the transfer
factor of resistance into an animal, and allow the animal to amplify the transfer
factor. Next, extract the transfer factor from the animal's blood, and then
~lmini~ter the transfer factor into the patient.
A second type of transfer factor is transfer factor of synergy, and refers to
the time period during which T-cells and PCR loads both rise in the patient's
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body. Over a period of about 2-3 months, the PCR load and T-cells counts were
examined by the inventor on a daily basis. Although prior to the present
invention, it was believed that as AIDS patients started to deteriorate, T-cellswent down and the viral load increased, the inventor found otherwise. In fact, in
quite a number of conditions and several days a month, the relationship was justthe opposite. In fact, the T-cells were found to increase as well as the PCR load.
Similarly, the T-cells also decreased as well as the PCR load. Sometimes, the
PCR decreased and the T-cells increased, or the PCR increased and the T-cells
decreased. At times, studies showed the rise between T-cell counts and PCR
counts almost parallel.
There were other times during the testing when the HIV virus and the
immune system were both stimulated together. There were other periods when,
despite viral stimulation, the immune system was not broken down. There was a
phase during which synergy existed between the immune system and HIV.
Certain infections caused the T-cell count to rise and the PCR load increase.
These included certain colds and flus. There were influences that made the T-
cells resistant to viral amplification's fl~m~ging effects. The virus would still
grow in the T-cells but was unable to kill them.
A vaccine was duplicated which made the T-cells and the PCR increase
together. Doubling of PCR would accompany similar increases in T-cell counts
with certain staphylococcal extract vaccines. Certain phages of sfaphylococci
could cause the T-cells to increase with variable effects on PCR. At the same
time that the virus was growing, and when the T-cells and the PCR increased,
these T-cells possessed a transfer factor of synergy. When this transfer factor of
synergy was extracted out of the T-cells and incubated with the HIV virus or if a
vaccine was used to raise them both together and incubated them with HIV, HIV
still grew in those cells, but did not kill them.
A transfer factor of resistance does not allow for the amplification of the
virus, so in vitro you do not get viral growth. On the other hand, transfer factor
of synergy allows the virus to grow in harmony with the T-cells. The virus can
divide in two ways. First, it can grow in the cell and cause it to explode.
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Secondly, it is believed that the HIV virus divides by budding off the T-cell
membrane. The second option is compatible with cell survival.
A third transfer factor is transfer factor of provirus (TFP). In an
experiment, T-cells from an AIDS patient were removed, amplified in a horse or
chicken, and then re~-lmini~tered to the patient when his supply became depleted.
The effect was very short-term. In yet another method, the TFP from these same
white blood cells was amplified in an animal, and then rç~t1mini~tered to the
patient. When transfer factor is amplified, it is not known what type of transfer
factor is produced as the end result. When the transfer factor was amplified andadded to the patient's white blood cells in a test tube, the T-cells grew.
Secondary amplification can then take place in vivo or in vitro.
Two things that are needed to cause a virus to go into a dormant state.
One is for the virus to want to go into a dormant state, and the other is for the
cell to force the virus to go into a dorrnant state. Viral specific factors can be
isolated and cell specific factors can be isolated for a provirus state. A transfer
factor was removed from the white blood cells and then amplified in an animal
in vivo. The amplified transfer factor was then added to the animal's provirus T-
cells in vitro. Transfer factor of provirus was added to non-infected T-cells along
with HIV, and then cultured together. The inventor found that the T-cell count
did not drop over 24-48 hours, and the HIV count did not increase or amplify
either. Why is it that a transfer factor of provirus was involved rather than
another type of transfer factor? When the white blood cells were stressed, the
provirus becarne activated into a live virus and the mixture not only showed a
high yield of HIV, but was also infective to other white blood cells.
There are three different but potent transfer factors, each of which can be
used in combination with 2-MEA. For every beneficial transfer factor, there is
an equal and opposite transfer factor (increased susceptibility, increased
resistance, active viral phase). For every transfer that can help the human body" and be actively safe, there is a transfer factor that can cause damage. An
antiserum to the non-beneficial transfer factor would help to neutralize its
~ negative effects.
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A transfer factor extracted from a cell that is actively dying, for exarnple,
is a transfer factor of disease rather than a transfer factor of resi~t~nce. If 100
cells are infected with AIDS and most die, they release transfer factors of
sensitivity, not transfer factor of resistance. If 100 cells become infected with
AIDS and most survive, a transfer factor of resistance has been produced.
Transfer factor of sensitivity is used because one can alter the cells of the
patient with transfer factor of sensitivity in vitro, then vaccinate the patientagainst that so that the cells never get a chance to multiply, expand or put outtheir transfer factor which will influence other cells. The sensitive part of the
system can be stopped from being amplified. For every transfer factor that is
good, there is a transfer factor that is deleterious. The idea is to isolate thenegative transfer factor only to prevent it from generating and spreading to other
cells.
Another type of transfer factor is curative transfer factor, which is transfer
factor extracted from ~nim~l~ Transfer factor from a horse is used because a
horse is not susceptible to AIDS or HIV. If you vaccinate the horse against the
targeted disease, remove the transfer factor and treat the patient with the horse
transfer factor, the transfer factor will activate the patient's T-cells just the same
way they did the horse, but the horse's T-cells are resistant to HIV and the
human ones are not. They will attack the virus and die. The only way to make
the transfer factor of the prior art viable is to use with the transfer factor of
activity a transfer factor of resistance. One has to find the cells that will accept,
not only increased activity from the horse, but also increased resistance from the
horse. Unless cells are given arnplified transfer factor of re~ tzmce, they will succumb to the infection.
Animal cells may resist HIV infection by virtue of superior irnmune
function to human and/or by the lack of receptors to which HIV may attach and
enter cells. As the second of these options gives animal cells inherent resistance
not found in hurnan cells, simple use of transfer factor from activated animal
cells will induce greater anti-viral attack by vulnerable human Iymphocytes and
result in greater incidence of cellular infection. One way of preventing this
outcome is by using transfer factor of resistance.
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Another approach is to look for another cell type other than the targeted
response cell, the T-cell. It is assumed that because the T-cells attack HIV, the
T-cells need to be stimulated against HIV. But, :~nim~l.s do not have a first
response against HIV with T-cells. Instead, their first response is with
neutrophils. So whether we talk about AIDS or cancer, there is an initial
response by an animal injected with neutrophils. Even in cases involving ~nim~l.s
which do not respond with neutrophils, they can respond with other cells almost
as effectively as humans do with T-cells. The further away one moves on the
evolutionary scale from the human, the more varied the response against HIV.
The lower you go on the animal scale and the further removed from the human
being, the less likely you are to get anti-HIV activity of T-cells and the more
likely you are to get neutrophils or T-cells, or whatever the animal's or fish'smain immune response is. Even sharks have an effective anti-HIV system. The
further the species gap, the less likely you are to respond immunologically in the
same way. That is a bonus because it means that if you go to a chicken, for
example, you will not stimulate its T-cells. Tn~tç~l you stim~ te neutrophils orB-cells and antibody-generating mech~ni~m~ A totally new immune response
can, thus, be activated in the patient.
AIDS patients have many neutrophils. They individuals have a large
amount of neutrophils because the neutrophils are not attacked by HIV, and
neutrophils are resistant to HIV. If you vaccinate an animal with HIV and it
responds with a neutrophil attack, the transfer factor from the neutrophils can
then be used to arrn human neutrophils against HIV. What has been done is that
part of the imrnune system is armed against the HIV virus that has not been seenbefore. But now that the transfer factor was used to activate it, the virus can be
attacked by a part of the immune system that cannot succumb to the virus.
These transfer factors are called curative transfer factors.
In carrying out the method of producing transfer factor and activating the
immune system, a large amount of transfer factors were isolated from a horse
against cancer cells, simply by injecting the horse with cancer cells. The immune
response occurred with neutrophils within 3 hours following the injection.
Extraction was usually performed within 2-3 weeks following the injection.
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However, if you wait this long, you actually miss the most effective transfer
factor, which is produced about 3-6 hours after the first injection.
The isolated transfer factor can be used in several ways. First, you can
activate the part of the human immllne system designed to respond to HIV and, ifyou activate that part, you have to use a transfer factor of resistance to make sure
that your new response is also rçci.~t~nt. In the alternative, you proceed to a part
of the immune system that is not designed in the human to attack HIV, learn how
to activate that part of the immune system in an animal, and isolate the animal's
transfer factor.
A third option is to take a mixture of transfer factors of resistance,
anticipation, provirus, synergy, neutrophils, T-cells, of early, intermediate and late
response etc. from all the white blood cells in an animal and expose it to mixedwhite blood cells from humans or, even better, from the patient. If you add a
mixture of transfer factors to the patient's blood from the animal and, instead of
activating the T-cells, you activate the patient's blood cells, the patient's
neutrophils will now attack the virus. Upon amplification of the transfer factorfrom the neutrophils, you produce an autogenous transfer factor which will causea resistance of the cells that attack the virus. In yet another approach,
transfer factors from all of the different cell types of are isolated and then
exposed to different types of cells. Look for the cells which are not usually
involved in the anti-AIDS process to develop anti-AIDS activity. There are threeadvantages of activating human white blood cells: 1) there are a lot more
neutrophils than there are T-cells; 2) the neutrophil pool has not already been
depleted by HIV; and 3) the pool is resistant to HIV.
Standard transfer factor mz~nllf~cturing processes may be augmented by
physical, chemical or biochemical stimulation of white blood cell division priorto the extraction process. Phages may cause amplification both before the
extraction process and afterwards by at least stimulating division of responsivetarget cells. Phages stim~ te amplification of the target cells, and will uptakeand amplify the transfer factor. Phages may also extend the target cell beyond
the Hayflick limit.
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Transformation factors work differently than transfer factors. For
example, you can produce transformation factors which are like a transfer factorfrom neutrophils which are capable of transforming T-cells into resistant parts of
the immune system against HIV. In contrast to transfer factors, transformation
factors are factors extracted out of one cell type that are capable of causing achange in another cell type. Neutrophils were used to extract transformation
factors. Transformation factors will also transform target cells into resistant cells.
In the present invention, transformation factor was isolated from white blood
cells and used to activate red blood cells and from neutrophils to activate
lymphocytes. Unlike transfer factors, transformation factors also have a strong
capacity for being curative. The further down the specie level you descend from
the human system, the more likely that transformation factors are being used
instead of transfer factors, and the less likely one will encounter human analogs
in the :~nims~l~ specie. In other words. the more primitive the animal~ the morelikely that a transformation factor is involved.
Anticipatory Transfer Factor
Anticipatory transfer factor has never been considered in the prior art to
the knowledge of the inventor. It is useful because, for example, if you vaccinate
a child against measles, mumps, or other childhood diseases, you have the risk of
the child succumbing to a long-term side effect of the vaccine itself. The childmay develop sub-acute sclerosing panencephalitis for example. Pretreating the
patient with an anticipatory transfer factor against the vaccine will most likely
achieve the following: a) minimi7~o the time needed to develop immunity
because of the prior exposure; b) may obviate the need for a living vaccine
because the living vaccines are dangerous {you can use a killed vaccine if you
amplify the immune response with transfer factor}; c) may even obviate the use
of vaccines. The best anticipatory transfer factor is made of the patient's own
cells. The best way to vaccinate someone with minim~l risk is to remove their
blood, expose it to the targeted agent, and then isolate the transfer factor from the
mixture and re-~rlmini~ter it to the patient or mix autogenous blood with transfer
factor and re-introduce into the patient.
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While one may not be able to duplicate exactly what is going to happen to
the patient by conducting in vitro studies, one may use an ~plo~liate animal
system to raise the transfer factor of anticipation. One problem is that z~nim~l.s
do not become infected with the HIV to produce AIDS. A preferred system is to
use the patient's own cells in vivo where they are exposed in a short burst to 2-
MEA, the changed virus is isolated, and the transfer factor and transformation
factors raised against the changed virus. The transfer factor is then ~lmini~tf~red
back to the patient after about 1-2 days when the 2-MEA has washed out of his
system. The result is vaccinating the patient against how the virus is going to
look when 2-MEA is reintroduced into his system. Use the transfer factor and
vaccine that was raised against the transformed virus for about 2-3 weeks when
the immune response is adequate. Then start the patient on the 2-MEA.
To determine what the virus is going to look like, one could perform
similar animal studies by ~ministcring 2-MEA to the animal, and then injecting
it with normal HIV from the patient or from food. The problem, however, is that
the virus will not enter the animal cells and will not create analogous changes.This applies equally well to other therapeutic compounds such as DDI, AZT, etc.
As a better alternative, one can anticipate the changes that are going to be made
in a patient by exposing the patient to short bursts of 2-MEA or the desired
therapeutic composition or performing in vifro studies, vaccinate and raise
transformation factor against the changes, stop the patient from taking the
medication for a time period. vaccinate him against the changes, and then re-start
the medication. The trouble with AZT and protein inhibitors is that you cannot
start and stop them in this manner because it may induce viral changes, mutations
or rçsi~tz~nce. Furthermore, these drugs are not innocuous agents; they have their
own side effects. A better approach is to keep these drugs in reserve and start
treatment with an innocuous agent like 2-MEA first. After you elicit the
m~ iml~m immunological response from 2-MEA and related aminothiols, and
then s~lmini~ster 2-MEA in combination with AZT, then 2-MEA, AZT plus DDI,
singly or in combination, to maximize the length of time of the anticipatory
changes and the initiating therapy.
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With 2-MEA, it is harder to induce a change because 2-MEA does not
affect the virus directly like most other agents. 2-MEA affects the virus
indirectly by optimal intracellular antioxidation of the cytoplasm, which prevents
the membrane or outer wall of the virus from being built because viruses need
oxidized co-factors. 2-MEA, therefore, affects the host cell more so than the
virus itself, and the virus would have to adapt to a change in its environment to
its host cell rather than to a direct attack. Viruses can respond better to a direct
attack than to a change in the cell environment. The change in the environment
also means that 2-MEA may not be able to prevent the insertion of virus into a
cell, but it can prevent its proper replication in a cell. so 2-MEA exhibits a good
preventative function.
There a number of ways in which to augment this effect by stopping the
binding of the virus to the T-cell or whatever kind of cell. AL721 (lecithin
extract) is one agent which makes the T-cell membranes more fluid. By itself,
lS AL721 has not been useful because there is no such thing as a complete blockage
so the virus can still bypass, enter and multiply in the cell. However, upon theaddition of AL721 to 2-MEA, you have a blockage of entry and the blockage of
multiplication upon entry. A combination of AL721, AZT,and 2-MEA provided
a blockage of entry, a blockage of reverse transfer into the nucleus, and a
blockage of multiplication. In essence, the more agents added, the more sites
that were blocked effectively.
Therapeutic agents which offset the ulcerogenic effects of 2-MEA
Copper(II)-3,5 diisopropyl salicylate exhibits anti-ulcerogenic activity. It
is a compound that can be used in an effective dosage of between approximately
lOmg and about 500mg, three times a day. Copper(II)-3,5 diisopropyl salicylate
is a compound which has dual efficacy having both an anti-infl~mm~tory and
some immune simulation capabilities. Generally, copper(II)-3,5 diisopropyl
salicylate raises the level of superoxide dismutase, an intracellular enzyme which
inhibits oxidation from taking place in the cell and may indeed function like 2-MEA. Copper(II)-3,5 diisopropyl salicylate has been largely researched for its
infl~mm~tory activity. The inventor found that copper(II)-3,5 di-isopropyl
salicylate preverits the 2-MEA from being able to cause ulcers, and ~llgment~ the
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intracellular antioxidation effect directly by raising the superoxide ~ mllt~ee
levels intracellularly. When using this compound in a preparation, a preferred
method is to raise a transformation factor in anticipation of the changes in theformula with 2-MEA and other compounds.
Copper(II)-3,5 diisopropyl salicylate was used to treat an auto-immune
disease where infl~mm~tion was a problem, starting with about 30mg daily,
divided into three doses of 10mg. The capsule comprised about 10mg
copper(II)-3,5 diisopropyl salicylate, 200g 2-MEA, 100mg transfer factor, 100mg
BHT, and about 100-150mg of AL721. Copper(II)-3,5 diisopropyl salicylate may
be used by itself, in place of 2-MEA, in combination with traditional
pharmaceuticals like AZT, BBI, DDC, etc., and as an adjunct to all other
therapies for infl~mm~tory ~ e~ces m~lign~nt ~ e~ces7 infectious ~ e~ces, etc.
Penicillamine is used to pull out excess iron from the body. There are
prescription items only, whereas 2-MEA is probably available in the stores.
Mutation inhibition factors and reactivation inhibition factors are defined
as any factor which prevents a virus from mutating. By definition, this includesmost of the above except that conventional therapies actually promote viral
mutation. One way the virus mutates is by marriage with and cannibalism of
cellular structures, microorganism structures, and perhaps other viral structures in
the system. Two things can occur if a major virus like herpes or shingles gets
into the system. The herpes virus may either be reactivated by it or it may be
mutated by it. One way to avoid this is to use a broad spectrum of preservativesantiseptic antibiotics. BHT has a large LD50, has been be used for a long time,
and is generally considered a safe product. BHT augmented the antioxidant
capacity of 2-MEA intracellularly and prevented additional infections, several
microbial and viral infections, which would in turn control the infection that
would mutate or activate the virus. To o~Li~ c BHT's activity, BHT should be
combined with other microorgzlnicm~ or a living biological system. This is
essentially a mixture of microorg~ni~m~ that cannot colonize the patient's
intestine but prevent infections from coming in. These microorg~ni~m.~ can also
be inhaled to protect your lungs and others may be rubbed onto the skin. Having
a known set of microorg~ni~m~ colonizing the body or monopolizing the body
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makes it harder for the virus to mutate in a form that you can anticipate. A
range of microorg~ni~m~ will colonize and stabilize the microflora and prevent
antigens from activating the virus through the draining of the immune function or
super added infection and prevent a mutation of the virus.
The changes in transfer factor of synergy are not just changes that happen
to the cell. The changes occur to the virus too. Two closely related viruses will
always interfere strongly with each other. For example, you cannot infect
bacteria with a phage and then infect it with a similar phage. One way to protect
T-cells against a mutated HIV is to actually infect those T-cells with a pro-virus
form of HIV. If you extract out the virus from the patient when it was not
breaking up his T-cells, and then inject it back into him when it is breaking uphis T-cells, his own mutants of virus will compete with each other for the T-
cells.
One way to slow down the T-cell breakdown is to re-infect the patient
with the original strain which he was coping well with. The original strain willcompete with the mutant strain for the receptors on the cell. Once the old strain
attaches to the cell, the antibodies formed wi11 be able to destroy it. It is a way
of therapeutic insertion or of constantly keeping the virus competing with its old
form. It is a way of reversing the tide of mutation.
When you extract out virus from a pro-virus stage, cells synergize with
the virus and have difficulty being destroyed by more aggressive forms of the
virus because the virus already in them is protecting them against the more
aggressive one.
Levamisole, illlelr~lon, interleukin or any immune stim~ nts can all work
in this formulation. Once there is the transfer factor of anticipation, use can
begin on the conventional therapies for AIDS which include immune stimulants
which include all the other agents because, in the past, immune stimulants only
caused a temporary and transient change that would pass and leave the patients in
a worse state. You could use interferon and interleukin to stimulate the AIDS
patient, have the T-cells show greater numbers, and then the person dies becausehe used up his reserves. With transfer factors of anticipation, resistance and
transformation factors, when you stimulate the immlln~ system, it will be a
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different system, one that is resistant to the disease and one that can anticipate
the damages. You can now start using immune stim~ nt~ as well, and thesc will
all fit into the formulation. The preferred composition of this invention is thecombination of 2-MEA, transfer factor, BHT, and living org~ni~m.~ in a single
dosage.
Penicillin and penicill~mine also have short-term activity against HIV.
Very high dosages of penicillin may actually help in the treatment of AIDS
patients temporarily. The preferred culture techniques are techniques where
or~ni~m~ are made to compete for nutrients and/or one or more org~ni~m~ are
forced to use other org~ni~m~ in culture for nutrition and/or when such nutrition
is deficient in the medium and/or where one or more of the org~nicmc is selectedfor by provision of its optimal needs. These can be used to develop
microorg~ni~m~ whole, part, or extract thereof with specific activity against
targeted condition or organism. It is, therefor, possible to produce a penicillin
with strong anti-HIV activity. Anticipatory vaccines against other infections
which occur with AIDS can also be added to this formula. Preferred culture
techniques include living cells such as human and/or autogenous Iymphocytes,
fibroblasts, etc. which may be used in whole, part or extracts thereof.
Other immunostimulating, immunomodulating, inductors/augmentors of
normal cellular function
Coenzyme Q10 is a powerful antioxidant, a mitochondrial antioxidant and
entrocytoplasmic, which enables it to synergize with 2-MEA and copper(II)-3,5
diisopropyl salicylate and BHT. Coenzyme Q10 is also an immune stimulant.
Reishi mushrooms or shitake mushrooms from health food stores all have
some immune stimulatory function. The anticipatory, mutation inhibition factor
and antioxidant ability mixed with 2-MEA should be part of the invention. All
major vitamins and minerals, transformation factor, methionine. selenium,
chromium picolonate, growth hormones should be added amongst many other
factors.
Micrococcus extract is very powerful against AIDS. Living org~ni~m~ are
biological enhancement factors.
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T-8 cell is the suppressive cell; T-4 cell is the helper cell. T-8 counts
usually raise very high in AIDS patients; the T-4 counts plummet. T-8:T-4 ratio
should be a little above 1 in normal conditions.
If the therapy is given within proximity of the radiotherapy and
S chemotherapy, it may negate the effects of the chemotherapy and radiotherapybecause it is a powerful antioxidant. Time for ~lmini~tration would be 2 weeks
after the chemo is given; 2-3 weeks after radiation is given. It may also raise the
tolerance level of the body so you can use more chemotherapy and radiation. 2-
MEA and other powerful antioxidants and other anti-cancer agents such as
bleomycin are more active in reduced oxidized state. The chemo goes into the
body, oxidizes, kills the cells, and then the 2-MEA pushes it back into reduced
state, so it becomes toxic again. Parts of this formula may aggravate some
chemotherapy toxicity. Smaller doses of chemo can be given by constantly
reactivating it. Instead of giving bleomycin in huge doses that cause hair to fall
out, you give 2-MEA and it will reactivate the bleomycin originally given.
Living biological system is a mixture of org~ni~m.~ isolated from food, but
which coexist together which can synergize together and which can come into a
steady state of harmony. So all of these go into the stomach and grow into an
ecosystem, which is a living biological system. This is part of the 2-MEA
formula or the microbial environmental stability factor. You know what the
microbes will be. Living biological systems alone have an interference action
with HIV and HIV co-factors and are good stimulants. They are part of the
formula yet need to stand on their own. They would also help prevent ulcer
formation. Lactic acid bacteria (acidophilus), kefir, and rhizopus are safe, non-
pathologenic org~ni~m.~ in a mixture whereby each, as a unit or in combination,
donate beneficial features to the whole host and/or where they exist in an
ecosystem which prevents superadded infection to the infiltration of the host bypathogenic org~ni~m~. The orp~ni~m~ and strains chosen for this living
biological system have specific capacity for me~ tin~; anti-cancer activity and
cholesterol lowering activity, as well as organism maintenance activity. The
- difference between living biological systems and prior art, where prior art is the
~-lmini.~tration of several strains of acidophilus, for example~ or mixtures of up to
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6-10 different org~nicmC, is that a living biological system by its source and
nature generally comprises more than 30 org~nicnn~. In fact, the more org~nicmc
involved in the living biological system is usually the greater stability and
duration of action and the greater spectrum of activity. Being isolated from food
sources, natural kefir, for example, can compose thousands of or~ni.cm.C, and a
living biological system, in its optimum state, would combine several hundreds of
org~ni~m.c to best offset infection and to function best as a community.
Prior art consists of acidophilus, for example, in capsules, chosen for its
purity and color, whereas in nature nothing exists like that. Living biological
systems described here are unique in a) the combination; b) the number of
org~ni~mC; c) the location of the org~ni.cmc There is no other therapy which
seeks to occupy structures other than the intçstines, for example, of living
biological systems. These can also be inserted as a nasal spray for nasal sinuses
and lungs, where a living biological system can comprise viruses, bacteria, fungi,
etc. For example, in the immune compromised state, phages for various bacteria
can be assembled as a living biological system and inhaled on a daily or weekly
basis to prevent infection with said bacteria. The living biological system as
described herein may be defined by its constituents or may be defined by the
activity of the constituents. For example, a virus, bacteria, fungus and yeast
which carry anti-cancer activity could be combined into an anti-cancer living
biological system. Living biological systems may exist whole or processed such
that they are Iysed so that whatever internal enzymatic factors may be released
into the system. They can also be form~ te(l to target specific sources and their
internal nutrients can do the same, and a living biological system can be formedwhich would be a constant producer of by-products. For example, org~ni.cm.c
which are capable of manufacturing vitamin C can be orally zl-lmini.ct~red once a
month and would continue to produce the said vitamin in body for the duration
of the month. Living biological systems make it possible to insert replicating
forms of enzymes so that it is taken only once a month or once a year.
Living biological systems may be used as mutation imagery factors and
reactivation inhibitory factors. One of the most powerful vaccines is the insertion
of a dead feline panleukopenia virus into the blood stream of an AIDS patient. It
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may be because HIV functions as a hybrid of feline panleukopenia virus and
hepatitis. HIV will function like a mixture of these two viruses. If you
vaccinate against the function that is composed of two different things, and youupset the equilibrium by adding more of one, you disrupt the structure. HIV
does not look like a simple hepatitis fused, but the theory is there. It is similar to
~ disruption or vaccinating against something against the mech~ni.~m Feline
p~nleukopenia virus causes destruction of leukemia of white blood cells, as doesAIDS. Vaccinating against feline panleukopenia virus somehow also vaccinates
against its destructive capacity, and it is similar to the AIDS destructive capacity.
Once you have vaccinated the body against one, the other also follows. There
are a line of vaccines which are developed which do not attack the cause, but the
mech~ni~m Smallpox and vaccinia are similar viruses so you can use one to
irnmunize against the other. Bacterial phages and HIV are in no way similar,
except that they can attack a cell, insert themselves into it, and cause the cell to
die. You can use phages to vaccinate against AIDS. You can use feline
panleukopenia virus, which can affect the white blood cells and kill it, againstAIDS. An AIDS infected immune system will still act against feline
panleukopenia virus, and it induce cell death in only a certain number of ways,
and there is an overlap between what is used by the FPLV and the HIV. You
can push the HIV into a dormant state to stop it from killing the cells by
vaccinating against PLPV. The thing they have in common is the release of the
death sequence, so that by vaccinating against one, you prevent the formation ofdeath sequence which prevents the other from functioning.
The third observation is that a living feline panleukopenia virus may not
have any greater effect than a dead feline panleukopenia virus. The reason is
that the living one may cause some harm to the immune system and can
overcome it. Whereas a dead one will only be reactivated at the site of viral
activity. If you put in a fragmented virus where a virus is actively growing, even
if it is another virus, a dead virus can use the first virus's growth mech~ni~m~ to
reassemble itself. If you inject feline panleukopenia virus into a body that is
infected with AIDS, only the cells infected with AIDS, which have a system for
growing and structuring viruses, can absorb the feline panleukopenia dead and
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reassemble it. Now the virus shows up in every AIDS-infected cell -- and only
in every AIDS-infected cell. The body can identify that and can attack it and
destroy it. Particularly if the virus being used to reactivate has foreign graftantigens from the same species or different species. The AIDS-infected cell now
looks like a foreign cell from another source. Furthermore, specif1c antisera may
be used against the reactivated virus and the complex that it forms.
Once reactivated, 2-MEA can hold that reactivated virus, so you can
vaccinate against it, raise transfer factors against the reactivated virus, use 2-
MEA to hold the situation as status quo until the immune system can build up
and attack it.
2-MEA can be delivered by cell targets, by liposome and by agents to be
uptaken by the target. For example, in the case of leukemia, if you want to place
the 2-MEA in the normal cells but not leukemia cells, you would incubate the 2-
MEA in culture with a bacteria which your body is likely to attacl;. Kill the
bacteria and inject it into the membrane which is saturated with 2-MEA into the
body. The normal white blood cells would attack it and absorb the 2-MEA.
whereas the cancerous white blood cells would not respond to it. This will get 2-
MEA specifically into a site where you want it. You can use any of the various
ingredients.
Clinical Examples of Efficacy
An AIDS Patient - 28-vear-old Male
Lethargy, low T-cell count - 200
T4/T8 ratio - 0.24
Following 4 weeks on 2-MEA at 200mg three times daily orally. Moderate
increase in energy levels; T-cell count - 350. T4/T8 ratio was 0.5.
An AIDS Patient - 48-vear-old Male
Diarrhea, pneumonia (pneumocystis)
T-cell count - 8
Treated with 2-MEA at 200mg TDS
Copper(II)2,3.5-di-isopropyl salicylate was a/lmini.~tered 10mg daily.
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BHT was ~1ministçred 600mg per day. Living biological culture systems/cell
extracts at a dose of lOg TDS - membrane/enzyme and other living biological
system components from org~nisms (non-pathogenic) found in food and from
org~ni~ms that include lactobacilli, acidophilus, bulgaricus, bifidus, thermophilus
as well as kefir and various rhizopii, at 300 million org~nism.s per mg. After
three days of treatment, there was resolution of the diarrhea. The pneumonia
subsided in 1 week (patient was also on antibiotic therapy). The patient's T-cell
count after 4 weeks was 60.
An AIDS Pa~ient - 59-year-old Male
Patient presented with Kaposi's Sarcoma involving both extremities which was
very painful. The T-cell count was 120 and the T4/T8 ration was 0.6. The
patient was treated with 2-MEA, 200mg TDS. The patient was also given
copper(II)-3,5-di-isopropyl salicylate, lOmg TDS; BHT at 600mg daily; living
biological system as in the previously mentioned case; Also micrococcus sp and
extracts were used. ATP/UTP/GTP - lOmg each orally daily; multiple
nutritional supplement base including enzymes, antioxidants natural and artificial,
etc.; KREBS cycle nutrients; enzymes; and cofactors. Following treatment, the
pain disappeared in 2 days. Energy levels increased within 24 hours. Within 3
weeks, the T-cell count was 400 and T4/T8 ratio was 1.2. Further, shrinkage of
Kaposi's lesions was observed.
Prostate Cancer with Bone Metastasis in 69-year-old Male
Complex formula as in previous case involving a 59 year old male was used.
Pain decreased within 6 hours. Immunological parameters also improved within
3 weeks.
Complex formulation suspended during radiotherapy. It is theoretically possible
for this therapy to interfere with chemotherapy/radiotherapy or any other
treatment which acts at least in part by the generation of free radicals. By useof specificity and targeting patent technology by the same inventor, benefits ofthe formulation such as antioxidant ability, could be directed to healthy cells, for
example, and away from diseased cells, without use of that technology, however,
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or selective delivery of precursors, int~rmetli~tc~ or end-products, then one needs
to observe the caution mentioned. This, however, covers the use of any or all ofthe ingredients in the recovery from toxic effects of treatment including those of
chemotherapy and radiotherapy. As previously mentioned, unless precise
targeting is available, it is better to use the antioxidant part of the formulation
following the toxic therapy and not simultaneously. Living biological systems
as complicated as those mentioned here and as simple as those of acidophilus andother yogurt cultures are being patented here for use solely or in combination
with other factors, agents and products thereof in the prophylaxis and treatmentof the side-effects of chemotherapy and radiotherapy. It is easy to see how
living systems such as those can prevent bowel flora imh~l~nce as can be caused
by such therapy and how this ability, as well as the ability to prevent
opportunistic bowel infections which may follow diarrhea and/or
immunosuppression precipitated by the therapy, may be beneficial. There are
other mech~nisms at play here, including immunostimulant properties and other
anti-disease factors inherent in or inducible by the appropriate living biological
systems.
Post radiotherapy, the patient was recommenced on the l~lcl~ldtion. All
malaise and nausea resolved in three days. White blood cell counts which had
dropped below half normal to normal levels in four days.
Ten patients were ~flmini~tered the complex formulation as above at one-
third the normal dose, and were matched for age/sex and stage of disease. The
supplemented group tolerated chemotherapy and radiotherapy with minim:~l side
effects. Superior response and clinical condition of supplemented group was not
only evident subjectively but objectively, also in that the control group repeatedly
demonstrated lower immnn~logical parameters, required more transfusions and
almost double the number of days hospitalization as the group receiving the
supplementation over a two-year follow-up.
There were eight deaths in the control group to only four in the
supplemented group.
Twenty AIDS patients with T-cell counts 400-500 were divided into two
groups. Ten patients were supplemented, the other ten availed themselves of
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whatever therapy they had available. After a 6-year follow-up, all
unsupplemented group had died; six of the ten supplemented were still alive.
Improvements have been noted in multiple other conditions including
arthritis, multiple sclerosis, cardiovascular disease, asthma, chronic fatigue
S syndrome, systemic lupus erytheromatosis, autoimml-ne disease, acute and
degenerative diseases, infections, among others.
There are multiple applications relating to the immunopotenti~ting,
antioxidant and ulcerogenic activities of 2-MEA and related aminothiols that maybe of use. This invention covers the use of such compounds in any condition
where neutralization of free radicals may play a beneficial role. This patent also
covers the use of anti-ulcer and preventive medication/compounds/therapies in
combination with 2-MEA. Use of 2-MEA and related aminothiols in
combination with copper(II)-2~3-di-isopropyl salicylate could fulfill the
requirements of an ulcerogenic with the added benefits bestowed by the anti-
cancer, antiviral, antioxidant and other properties of copper(II)-2,3-di-isopropyl
salicylate.
BIOPHARMACEUTICALS
A new line of therapeutic/preventative and supplemental products where a
pharmaceutical agent is bound to an infection with affinity for target
organism/cell where the biological agent or fragment thereof is used for specific
delivery to target; to optimize concentration of agent at target; to process theagent so as to produce useful precursors intermediates and end-products; and to
augment directly or indirectly the effect required. Biological delivery
mech~ni.~m~ may also be used to minimi7e irritant or other side effects of
therapeutic agents.
1) MINIMIZING SIDE EFFECTS
2-MEA and copper(II)-3,5 di-isopropyl salicylate can both cause local
irritant effects in therapeutic levels. 2=MEA has been known to cause ulcer
formation. Copper(II)-3,5 di-isopropyl salicylate is topically irritant. When
placed into a biological carrier (inert such as liposomes benefit may be obtained
from improved efficiency of absorption and perhaps preferential distribution;
binding to targeting agents has been in prior art largely reserved to the use of
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monoclonal antibodies; the problem here has always been one of disassociation
of antibody-ph:~rm~eutical complex and of the targeting mechanism being
restricted to the delivery of agent at the superficial membrane site.
Whereas the concept of biopharmaceuticals includes the use of
monoclonal antibodies to deliver not only therapeutic but also preventative and
other agents to the target tissue (prior art covers delivery to diseased tissue);
current art provides for delivery of protective and other desirable agents to
healthy tissue and/or to ~ e~es other than cancer which is the centerpiece of
prior art.
A major variation on prior art in the use of biological mech~ni~m~ is not
restricted to biological amplification and processing pathways but involved the
use of antigens rather than antibodies in the preferential delivery mech~ni~m
2) ANTIGEN DELIVERY MECHANISM
Various antigens have the capacity to bind directly to the target cell or
tissue either by affinity or by virtue of prevailing conditions within the vicinity
and structure of the tissue to be targeted, e.g., Iymphopoietic tissue may be
targeted b viruses such as mumps virus or feline panleukopenia virus. Any
biological/chemical or physical agent incorporated in this living system or partthereof will automatically be carried to target. Chemotherapeutic agents may be
carried to tumor masses including the use of anaerobic or microaerophilic
org~ni~m~ to deliver chemotherapeutic agents in high concentration to the centerof tumor masses. An example to be outlined serves to demonstrate this
amplification technique as relates to immunostimulants.
Prior art in vaccination relates to the use of non-specific adjuvants such as
that of Freunds along with vaccine to be given or the use of interferon,
interleukin, etc. Prior art does not include direct targeting or amplification
technology.
An antibody needs to go after receptors whereas biopharmaceuticals go
after prevailing conditions. An antibody to cancer needs the cancer cell to
express the antigen. Biopharmaceuticals may go after a condition ie., lack of
oxygen in the center of a cancer mass. If an organism is anaerobic or
microaerophilic and you saturate it with a ph~rm~ce~ltical, or supplement or a
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genetic sequence, then the organism will go to where there is no oxygen and
deliver its payload. An example of the mechanism of action of
biopharmaceuticals is presented below.
A microaerophilic or aerophilic organism in 500cc of trypticated soy broth
in the presence of a radioactive isotope, Il3'. Incubation and fermentation
occurred over a 2-3 day period. The org~ni~m~ were filtered through a filter
membrane, for example a 0.2 micron filter. The filtrate was re-suspended and
washed in normal saline. The filtered fraction was re-constituted to a
concentration of 10 million org~ni~m~ per 1 cc. 1 ml was injected into a rate
bearing Morris TC hepatoma. Following 24 hours, radiation was detected at the
tumor site. After 48-72 hours, necrosis was seen at the tumor site.
In other experiments, staphylococcus aureus is incubated in a medium of
trypticated sov broth for 24 hours. Medium also includes 5mm of 2-MEA.
Identical preparation is made without the 2-MEA. 100cc of inoculated broth is
then passed through a 0.2 micron filter. Pellets deposited on the filter are
resuspended in 10cc of normal saline then refiltered and resuspended. Both a
suspended in 10cc of normal saline and 5mm of 2-MEA and the full 10cc are
injected into each of two horses. White blood cell are collected at 3 hours, 24
hours and 14 days. Crude transfer factor extract was prepared by freezing,
thawing and 0.2 micron filtration of 100cc of white blood cells suspended in
normal saline at concentration of ten million cells per cc.
One cc of transfer factor was fed to Balb C mice every day for 10 days
followed by bacterial cell challenge. One cc contz~ininp~ 10 million orp~ni.~m~ of
the original staphylococcus lethargy was noted for 1-3 days but no abscesses
developed. Control group of 10 mice was inoculated intramuscularly. These
were evaluated after 10 days. Six of the mice developed abscesses locally. All
demonstrated lethargy for several days after inoculation.
The suggestion that the transfer factor was more effective from the horse
treated with the 2-MEA suggested a specific stimulation of appropriate cellular
response. When 2-MEA was combined in solution with the bacterial p~ ,aldlion
immediately prior to inoculation of horse, transfer factor demonstrated no marked
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increase in efficacy, although transfer factor yield may have been greater than the
control yield.
Incorporation of 2-MEA and other immunostimlllant~ into the cells or
org~ni~m~ to be targeted or against which an immune response needs elicitation
including bacterial, viral and m~ n~nt cells among others may lead to superior
vaccines.
An extension of this invention is the feeding of transfer factor in culture
plel,alaLion of vaccine and/or provision concomitantly to increase efficacy of
therapy.
Copper di-isopropyl salicylate can induce production of superoxide
dismutase. Preincubation with a biological delivery system such as living
human/animal cells or various microorg~ni~m.~ such as yeast will enable not onlytargeted delivery of the compound but can also generate superoxide f~ m~lt~e
and/or other antioxidant enzymes as active factors. Biological active factors may
be amplified by exposure to an oxidant such as 2% peroxide. Following
generation of antioxidant enzymes, the peroxide may be neutralized by
antioxidants such as vitamin C. In all the above cases, targeting complex may beused whole or in part, living or inactivated by physical, chemical or biologicalagents such as ultrasound, phenol or enzymatic degradation.
Use of biological delivery mech~ni.~m~ also enables the topical application
of such products for cosmetic, protective and other effects. One modality of
application involves the absorption~ activation and application of 2-MEA and
copper di-isopropyl salicylate into target cells such as yeast or lactobacilli or
human cells with 2-MEA and grown into a culture. Human cells and/or
autogenous cells of skin, blood or other source may be cultured i~ vitro and
suspended live or killed in a cosmetic base or yogurt base. Culture techniques
may dedifferentiate cell types and/or may be used to stress the cells or
manipulate in other ways to produce antioxidant and other beneficial enzymes
and factors. Manipulation of temperature will yield to factors protective against
heat and cold, as well as moisture loss, if that is made a condition of culture.Following stress, cells may be returned to friendly antioxidized environment to
reduce free radicals. Cells are then disrupted or fixed so as to m~int~in all
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beneficial factors and not allow for their return to original parameters. In living
or dead state, such cells will m~int~in genetic and other response modalities
which may prove beneficial as therapy/prevention/
supplementation or topical application to recipient. Various donor systems may
yield beneficial properties but autogenous cells which have been manipulated or
augmented in a physical/chemical or biological manner enable greater interactionand protection of recipient.
Cells suffer radiation damage, for example, when exposed to frequencies
that are absorbed by vital cellular fractions such as the DNA and those structure
are damaged. It is possible to evaluate the sites most frequently damaged and
prepare a topical concentrate of the same or similar structures to shield the body.
It is also possible to anticipate the exposure and make preparations from cells
that service such exposure to confer protection and it is possible to use the whole
cell, genetic fractions or other fractions to confer the resistance. Autogenous
cells, however, provide the best matching of DNA and other susceptible
fractions. Addition of 2-MEA to the culture media can increase their re~i~t~nce
to radiation and other factors, thus providing for greater shielding. Copper(II)3,5 di-isopropyl salicylate and other antioxidants may also similarly be used.
Autogenous cosmetics can also include immllne cell amplification from
blood used a cosmetic to combat pimples. Again, this invention covers the
concept of the use of living systems or fragments thereof to provide shielding or
protection against particular challenge or disorder. Autogenous cells ensure
minim~l allergic responses, improved efficacy and bioavailability. Use of 2-
MEA and related aminothiols and/or copper(II) 3,5 di-isopropyl salicylate and
other di-isopropyl salicylates, as well as other factors, may amplify and augment
efficacy.
The use of such preparations particularly autogenous may shield normal
cells from radiotherapy by coating the outside of the body with counterparts
which have been augmented and/or amplified to receive harmful frequencies,
whether on the body or fixed in a shield/filter between the beam source and the
- body. Normal structures should be spared at least some damage and optimal
damage to disease-specific structures achieved. With biopharmaceuticals, the
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agent can be processed and presented to the body in a more effective form such
as precursors, intermediates and end products.
Certain modifications and improvements will occur to those skilled in the
art upon a reading of the foregoing description. It should be understood that all
S such modifications and improvements have been deleted herein for the sake of
conciseness and readability but are properly within the scope of the following
claims.
34
