@ Tom, mms in oil?

[Guest guest]

Evening

Tom,

I

have a question for you. while researching a cancer protocol for one of

our blacksalve list pooches I came across information on the now extinct

GrouppeK site (I made a mirror of the whole site) about oil vs water soluble

for cancer treatment. Dr. Steve passed on last August and his sister

removed the blog about a week ago.

From

the below, and I’m no scientist, chemist et all…but I wondered.

Since chlorine dioxide according to this site…

http://www.btcproducts.co.za/generators_applications.asp

Chlorine

Dioxide is hugely more soluble in oil (hydrocarbons)

My

question would be would there be benefits to putting mms in something like say

coconut milk or any oil for that matter. See part in bold below to

explain my ‘I wonder’…

Xxx

rose

YUCKKO™

AND QUERCUR™ TREATMENT PROTOCOLS

There is no

perfect treatment protocol for any disease, least of all cancer. Some cancer

respond very well to gentle treatment protocols that emphasize death by

programmed cell death, while other, more virulent, aggressive forms of cancer

can only be killed by necrosis. Radiation and chemotherapy kill primarily by

inducing massive necrosis in tumor masses, which makes them, to date, the most

effective forms of cancer treatment. Unfortunately, chemotherapy and radiation

are non-selective killers. They kill ALL routinely growing cells, such as those

in the bone marrow, skin, gastrointestinal tract, hair follicle, and the cells

attempting to repopulate tissue wounds.

The natural

medicines in YUCKKO™ and QUERCUR™ have no or very low toxicity

towards normal cells, yet, under certain circumstances, they interfere

significantly with the growth pathways of cancer cells, resulting in their

death by programmed cell death or necrosis. When some of these natural medicines

are additionally combined with commonly available supplements, they become

extremely powerful treatment modalities. The secret, which we are now publicly

disclosing to the world, is how we get these substances into the body in

sufficient concentrations to have a therapeutic effect.

Coconut

milk!!!

We

know…sounds stupid, simplistic and ridiculous. Coconut milk is the

“magic” delivery vehicle for introduction of these extremely

powerful natural medicines into the body? In a word, YES! Coconut milk is a combination

of coconut water and coconut, homogenized into a milk of sorts. It is 50%

saturated fat, but the saturated fat contains a very high concentration of

lauric acid, a medium chain fatty acid that is a wonderful food and an enhancer

of programmed cell death in cancer cells. Coconuts are the only dietary source

of lauric acid; it doesn’t exist in other foods to any meaningful extent.

Coconut oil was used by theatres in the US to flavor popcorn until the US

cereal grain industry lobbied to have this “dangerous” saturated

fat replaced with cereal grain oils. Coconut oil is very healthy, because the

lauric acid, a 12 carbon fatty acid, is too short to be incorporated into

arteries. In fact, the reverse is true. Lauric acid is a wonderful source of

energy, as are all fatty acids, at least in comparison to sugars and proteins,

and is an anti-cancer natural molecule as well. So you decide…politics

and corporate greed or scientific reality. It shouldn’t be a difficult

decision.

Many natural

medicines, such as quercetin and curcumin, exist in two basic biochemical

forms. One form, called a glycoside, has a sugar attached to it. This molecular

modification makes the compound soluble in water and theoretically

bioavailable. Unfortunately, glycosides have little biological activity. The

non-glycoside versions of natural molecules like quercetin and curcumin have

full biological activity but poor solubility in water. They are, in fact,

lipophilic or lipid (fat) loving. So we dissolved them in a fat, coconut milk,

and introduced them into the body via the lymphatic system, which is how fats

enter the body.

Orally

ingested molecules enter the body in two ways. Peptides, sugars, and other

molecules, such as natural medicines (flavonoids, flavones, etc.) enter the

body via the portal system. This is the classic method of entry into the body

via the blood. Entry into the blood via the intestines is a complicated

process. First, the molecules have to be actually absorbed by the cells in the

intestines. If they enter the intestinal cells, they can be immediately

modified by the cells and released back into the lumen of the intestines in a

“swinging door” fashion and excreted. Assuming a molecule like

quercetin makes it past this first step, it can be further modified or destroyed

by the liver. This is called the first pass phenomenon and it’s the

“pox on the butt” of the entire pharmaceutical and biotech

industry. The liver is a wonderful organ that protects us against strange

foreign molecules, including therapeutically beneficial molecules like modern

drugs and natural medicines, such as quercetin and curcumin. Sometimes, the

liver, in its “ignorance”, works against us.

There is a

way around this problem, which the pharmaceutical industry has been busy trying

to exploit for years. Fats, as in oils of any kind, do not enter the blood from

the intestines. They directly enter the lymphatic system, the system of ducts

that bathes all the tissues of the body. The lymph fluid originates from the

blood but it is a completely different circulatory system in the body. The

clear liquid that moves from the blood to the tissues bathes all the tissues in

the body with nutrients, drugs, and oxygen. It also removes waste products.

This liquid is collected in lymphatic ducts and returned to the blood where

waste products are removed by the liver and kidneys. If you can target the

lymphatic system with a drug or natural medicine, thereby bypassing initial

contact with the blood circulatory system, you can substantially enhance the

introduction of biologically active substances into the body.

Introducing

medicines directly into the lymphatic system is especially important if you are

attempting to treat an immunological disease, such as lymphoma, or a viral disease

such as HIV. These diseases exist, so to speak, in the lymphatic system. But

this same argument applies to carcinoma and sarcoma cancers as well. Growth

factors for endothelial cells (blood vessels) such as VEGF (vascular

endothelial growth factor) are secreted from established tumors under a variety

of conditions, including reduced oxygen tension. VEGF not only stimulates the

growth of new blood vessels into tumors, it also stimulates established blood

vessels to “leak”, as in to release enhanced amounts of lymphatic

fluid, protein, nutrients, and oxygen from the blood into the tissue spaces.

Contrary to current medical dogma and scientific models, the requirement for

blood vessel growth into tumors depends largely on the geometry of the tumor

mass. Tumors with a large surface area, like ’s open chest tumor,

“wept” massive amounts of lymph fluid, but didn’t bleed.

There were no or few blood vessels feeding the cancer growth. The growth of the

tumors and the spread of metastatic cells were promoted by lymph fluid and its

vascular system. Therefore, introducing medicines directly into the lymphatic

system is an attractive alternative to IV injections or blood targeted oral

formulations.

GLUCOCORTICOIDS

AND CANCER

Glucocorticoids

do not cause cancer, but they can protect cancer cells from dying of suicide or

programmed cell death, thereby perpetuating their existence and spread

throughout the body. Although glucocorticoids, such as prednisone and

dexamethasone, are frequently used in the treatment of lymphomas and leukemias,

they should never be used to treat non-lymphoid cancers. Presently,

dexamethasone is used in conjunction with chemotherapy to prevent chemo-induced

nausea, edema and other problems. Unfortunately, the use of glucocorticoids

like dexamethasone in the treatment of non-lymphoid cancers, for whatever

reason, is seriously counterproductive.

During a

stress response, glucocorticoids induce programmed cell death in unnecessary or

extraneous lymphoid cells. Immune cells that have been activated by antigen and

immune hormones are resistant to the apoptosis inducing effects of elevated

glucocorticoid concentrations. However, and this is a point largely forgotten

or ignored by many in the medical profession, glucocorticoids stabilize virtually

all other cells in the body against damage during an acute stress response.

Glucocorticoids accomplish this by inhibiting the ability of cells, whether

they are brain, liver, kidney, skin, breast, prostate, or whatever, from

committing suicide via programmed cell death in the face of an equilibrium

disruptive event, such as a temporary lack of oxygen. The ability of

glucocorticoids to stabilize the cells of the body is absolutely critical to

survival and the maintenance of homeostasis.

The ability

of glucocorticoids to stabilize the cells of the body during normal stress has

certain drawbacks when cancer is involved. One of the first biochemical events

that occur during a cells progression to becoming fully malignant is an

increase in the number of glucocorticoid receptors within the cell. In addition

to an increased number of hormone receptors, glucocorticoid receptors can be

activated inappropriately by a process called nitration. The nitration of

proteins occurs when a particular amino acid, such as tyrosine, is covalently

modified by a nitrate group. In most cases, this form of modification inhibits

the activity of the protein. Glucocorticoid receptors are actually activated by

this process. The major donor of nitrate groups is a highly chemically reactive

molecule called peroxynitrite. Peroxynitrite is involved in many diseases

processes and is almost always associated with inflammation.

In addition

to genetic changes to the glucocorticoid receptor and chemical modifications to

the receptor, psychological stress, characterized by an increase in the level

of glucocorticoids and epinephrine in the blood, also contributes to the growth

and spread of cancer cells throughout the body. It is well established that the

five year survival rate after successful cancer therapy is heavily influenced

by the psychological status of the patient. Patients who experience severe

anxiety or feelings of helplessness have a greater incidence of cancer

reoccurrence. In a very real sense, the fear of cancer reoccurrence is a participating

factor in the actual rate of reoccurrence.

In addition

to inhibiting programmed cell death in cancer cells, glucocorticoids are well

established anti-inflammatory agents. Although most, if not all cancers begin

at sites of chronic inflammation, the inflammation associated with cancer is

chronic, and weak, rather than acute and strong. The presence of a weak

inflammatory environment may be due to excessive binding of glucocorticoids

within the tumor mass. Stress, resulting in an increase in glucocorticoid

synthesis and release, is also a factor in protecting cancer cells from PCD.

A good

example of the difference between chronic and acute inflammation is the analogy

of bacteria growing in nutrient rich warm water. As long as the temperature is

not too high, the bacteria will grow rapidly. However, if the temperature is

increased, the bacteria rapidly die. This is very similar to what happens in a

cancer lesion. The inflammatory hormones are growth promoting in low

concentrations, but deadly when elevated beyond a certain concentration. In a

very real sense, it you want to kill cancer cells, especially those associated

with a tumor mass, you MUST induce an acute, deadly inflammatory response

against the tumor. No other treatment protocol will work. This is exactly what

occurs when tumors are treated with chemotherapy and radiation. Radiation and

chemotherapy drugs induce a massive inflammatory response within the tumor

mass, resulting in their death from both PCD and necrosis, primarily the latter.

Although a radiation beam can be targeted, chemotherapeutic drugs cannot. They

will kill any growing cells, normal or carcinogenic, hence the death of hair

follicles, bone marrow failure, damage to the gastrointestinal tract resulting

in vomiting, and skin lesions. Chemotherapy drugs also cause what some people

called “brain freeze”, a state of confusion that takes a long time

to go away. In stark contrast to radiation and chemotherapy, the natural

medicines in the Kurosawa kocktail protocols kill only cancer cells with very

discomfort to the patient.

After an

acute inflammatory response is induced against the tumor, resulting in necrosis

and increased inflammation, the inflammation should be allowed to

“ride” so the lesion heals properly by the migration of new tissues

into the wound. There are two fundamental phases of inflammation at work here.

The first is destruction of the cancer cells and the second, equally important,

is the healing of the wound. Both phases of inflammation are dependent on the

systematic release of pro-inflammatory immune hormones, hormones whose

synthesis and/or release is inhibited by glucocorticoids.

Another

factor worthy of mention is the immune response against cancer cells. Although

some scientists have attempted to activate the immune response against tumor

masses, these attempts have always failed. Cancer cells secrete a number of

factors, such as prostaglandins, histamine and reactive molecules like

peroxynitrite that inhibit the ability of white blood cells to recognize and

destroy cancer cells. Immunotherapy is an interesting concept, but it fails to

recognize the harsh conditions under which most advanced cancers survive in.

Cancer cells have adapted to these conditions but normal white blood cells have

not. Even if a T lymphocyte could recognize a particular cancer cell, the

factors secreted by the cancer cells would prevent the activation of the T

lymphocyte and subsequent death of the cancer.

In summary,

glucocorticoids affect non-lymphoid tumors in four fundamental ways. First and

foremost, they protect, as in prevent, cancer cells from dying of programmed

cell death. Second, they inhibit the biochemical pathways necessary for

mounting an acute, destructive inflammatory response against the tumor mass.

Third, they inhibit the biochemical pathways involved in new cell migration

into the lesion and the secretion of collagen, the polymer or scaffold upon

which most cells rest. Fourth, they inhibit the activities of both specific

(activated T lymphocytes) and non-specific (natural killer cells and

macrophages) immune responses against the cancer cells.

In the

Grouppe Kurosawa model of cancer treatment, it is necessary to partially block

the synthesis of hydrocortisone in the adrenal glands, and to curtail

hydrocortisone binding to cancer cells. This will release cancer cells from the

protective shield provided by enhanced hydrocortisone binding. This is step one

in our treatment protocol and it can be accomplished with the simple,

inexpensive natural sleep hormone melatonin. We like to call this step

“releasing the parking brake”. Melatonin is one of God’s most

remarkable natural drugs. More about melatonin later.

THE

PI3K/AKT BIOCHEMICAL PATHWAY

The PI3K

(phosphatidylinositol 3-kinase)/ AKT (protein kinase biochemical pathway is

fundamental to the survival of cells after activation by growth factors

(epidermal growth factor, platelet derived growth factor, insulin, insulin-like

growth factor, vascular endothelial growth factor, HER growth factors, etc) and

cytokines (immune hormones such as interleukin-3 and interleukin-6, etc.). If

activation of the PI3K/AKT (henceforth PIA) pathway is blocked, the cellular

activation signal initiated by a growth factor or cytokine will result in the

death of the cell by PCD.

As we previously

discussed, cell growth is a precarious process. The fragile nature of cell

growth was built into “the nature” of a cell as a fail-safe

mechanism. When a growth factor/cytokine stimulates biochemical pathways that

activate a cell to divide, they also activate the PIA pathway to protect the

cells from self-destruction along the way. The PIA pathway accomplishes this

critical task in numerous different ways.

First, an

abbreviated overview of the complicated PIA pathway is in order.

When a

growth factor/cytokine (henceforth GFC) stimulates its receptor on the outer

membrane of a cell, it causes the receptor to undergo a conformational change.

This conformational change allows the receptor protein to bind the PIA enzyme

and localize it to the inner membrane of the cell. PIA is an enzyme that

phosphorylates, or adds a phosphate group to the lipid phosphatidylinositol.

These newly phosphorylated lipids draw other molecules to the inner surface of

the membrane, thereby setting off a chain reaction of biochemical activity. The

phosphorylation reaction mediated by PIA can be reversed by a molecule called

PTEN, a phosphatase that removes the phosphate associated with the 3 position

on the phosphatidylinositol molecule. If the PTEN molecule is inactive, as it

is in the majority of cancers, the PIA biochemical pathway can proceed largely

unabated by feedback inhibition.

One of the

molecules that bind PIP3, the phosphorylated phosphatidylinositol lipid, is

PDK1, a kinase. This enzyme adds a phosphate group to the AKT enzyme, among

others, thereby activating it. AKT (protein kinase , in turn, activates and

deactivates a host of other proteins involved in cell proliferation and cell

survival. PDK1 is a very important enzyme because it activates numerous other

protein kinases from the AGC group (PKA, PKG and PKC).

PTEN is

considered a tumor suppressor gene, because the introduction of an active PTEN

gene into almost any cancer will cause it to stop growing and die. Although

PTEN can inhibit other biochemical pathways, such as RAS/RAF/MEK/ERK and FAK,

the pathway involved in cytoskeletal rearrangement, its inhibition of the

biochemical pathways “downstream” of PI3K activation are of

paramount importance.

In the

laboratory, we can inhibit the activation of specific biochemical pathways with

pin point precision. This isn’t possible in the real world of the body.

Fortunately, nature has smiled on us and provided us with natural, non-toxic

inhibitors of the PI3K pathway. Although these natural inhibitors kill tumor cells,

they do not kill normal cells, quite unlike radiation and chemotherapy.

HIF-1 AND

CANCER

All oxygen

dependent organisms, from bacteria to humans, must be able to sequester oxygen

in their environment in order to live. Hypoxia refers to a reduction in the supply

of adequate amounts of oxygen, resulting in a failure to generate enough ATP to

survive. Hypoxia can occur for many reasons. Climbing a tall mountain can cause

hypoxia and so-called oxygen sickness. Disease states such as arteriosclerosis

restrict blood flow hereby depriving cells of oxygen, and predisposing people

to heart attacks. Massive bleeding, whether due to an operation or injury, can

also cause hypoxia. Hypoxia is a stress-inducing situation which, under certain

circumstances, can induce programmed cell death (PCD) in cells. Obviously, it

would not be in our survival interests to have a large number of our cells die,

and our organs fail, if they were temporarily deprived of oxygen. This is where

the protein HIF-1, hypoxia-inducible factor 1, plays an important role in

maintaining the homeostatic balance of the body.

HIF-1 is

induced by a reduction in the level of oxygen experienced by the body. When

expressed, HIF-1 blocks PCD, and regulates the activity of literally hundreds

of enzymes and proteins in the body in an effort to cope with the reduced

oxygen tension. While some enzymes and proteins are turned on, others are

turned off. Genes that regulate the uptake and metabolism of glucose are

powerfully activated by HIF-1. This makes perfect sense since enhanced glucose

uptake and its metabolism via glycolysis is the fastest way to generate ATP and

to correct the metabolic imbalance caused by a reduction in available oxygen.

Although the metabolism of sugars, fats and proteins via respiration requires

oxygen, the rapid metabolism of glucose via glycolysis does not. The rapid

metabolism of glucose in the presence of oxygen is called aerobic glycolysis

and it is a fundamental characteristic of the metabolism of cancer cells.

, Ph.D

Chief Scientist, Grouppe Kurosawa