There is increasing evidence that methyl jasmonate, a plant stress hormone, may be the ultimate stand alone treatment for ALL cancers and leukemias. The original research on MJ as a treatment for cancer began in Israel, but now scientists in other countries, including the US and Japan, have begun their own research programs on the anti-cancer properties of this simple compound.
MJ is a simple compound that in crude form is used to prevent the infection of plants by bacteria. In pure form, it is used by cosmetics companies as a scent. Now we know that MJ is a viable treatment for cancer and different forms of leukemia. Eventually, the Israeli scientists who discovered the anti-cancer properties of MJ will receive the Nobel Prize.
The ultimate anti-cancer compound is toxic to cancer but not normal cells. Preferably there would be no side effects such as vomiting and hair loss. Also, it would be nice if this compound was relatively inexpensive and easy to administer. Naturally, this is all wishful thinking. No such compound exists.
Or does it?
We all know that damage to the outer mitochondrial membrane is a primary signal for programmed cell death. However, the initiation of apoptosis AKA programmed cell is a complicated process. It requires the activation of many genes and the inactivation of others. Genetic defects in key gene activity can block the initiation of apoptosis. For example, during periods of oxidative stress or DNA damage the universal tumor suppressor p53 is activated. This protein promotes programmed cell death, thereby inhibiting the development of cancers. Unfortunately, over 50% of all cancers harbor genetic defects in the p53 gene rendering it ineffective in promoting cancer cell death.
Methyl jasmonate selectively kills cancer cells by binding to their mitochondria membranes and inducing damage. This damage initiates apoptosis, BUT it bypasses the normal complicated biochemical steps involved classical programmed cell death. MJ induced cell death is direct. It does not depend on the activation of other genes or the p53 status of the cancer cell.
We now know why MJ is so effective in killing cancer and leukemia cells.
First, a small technical review is in order.
It is well established that cancer cells are capable of using aerobic glycolysis to promote their growth and survival. The average cancer cell uses a combination of both glycolysis and respiration in its metabolism. The high aerobic glycolysis metabolism is critically important for cancer cells because it produces a rapid source of ATP. In addition, the glycolytic pathway activates the pentose monophosphate shunt. This shunt provides compounds that regenerate glutathione, the major anti-oxidant in cells, while producing precursors for the biosynthesis of nucleic acid, phospholipids, fatty acids, cholesterol, and porphyrins. Clearly high levels of aerobic glycolysis are absolutely necessary for the growth and survival of cancer and leukemia cells.
Over the last few years it has become clear that the enzyme hexokinase 2 (HK2), the first step in the metabolism of glucose, is over expressed in cancer cells. This enzyme, in order to be active, MUST bind the outer membrane of the mitochondria. Recent reports have found that the docking protein for HK2 on the mitochondrial membrane is VDAC, voltage dependent anion channel. The presence of VDAC on the mitochondrial membrane, the overexpression of the HK2 enzyme and the binding of HK2 to VDAC are fundamental aspects of the Warburg Effect, the aerobic glycolytic metabolism of cancer cells.
VDAC is a very interesting protein. It is the most prevalent protein in the mitochondrial outer membrane. This pore protein transports ADP and inorganic phosphate into the mitochondria for the production of ATP, the energy source of all cells. It also transports ATP out of the mitochondria into the cytoplasm of the cell. If VDAC activity is inhibited, apoptosis occurs.
In order for HK2 to promote aerobic glycolysis, it is dependent on the VDAC mediated transport of ATP to the bound HK2 enzyme.
HK2 binds VDAC after it is phosphorylated by enzymes such as AKT. AKT is a known cell growth and survival factor for cancer cells.
The binding of HK2 to VDAC apparently stabilizes VDAC and prevents its inactivity. As long as VDAC remains active, apoptosis is prevented.
A number of VDAC inhibitors are now known to induce apoptosis. But this is only part of the story.
The release of cytochrome C, normally bound to the inner mitochondrial membrane, initiates the complex biochemical pathways associated with apoptosis. When HK2 is dislodged from the VDAC complex, cytochrome C is released into the cytoplasm. However, this effect is probably indirect. The inner mitochondrial membrane contains a protein called the permeability transition pore (PTP). Disruption of the functioning of this pore causes depolarization, membrane swelling, and the release of cytochrome C from its membrane binding site.
Hexokinase 2 detachment from the VDAC complex promotes the inactivation of both the VDAC and PTP pore complexes. This results in an inhibition of ATP synthesis and the promotion of cell death by necrosis, apoptosis and autophagy.
VDAC is not simply a binding site for HK2. The binding of HK2 to VDAC stabilizes the pore complex and prevents apoptosis.
A few months ago a study was published showing that methyl jasmonate binds directly to hexokinase and detaches it from VDAC. This results in an inactivation of VDAC and glycolysis, while promoting mitochondrial membrane swelling, and the release of cytochrome C into the cytoplasm. Cellular death rapidly follows.
In addition to promoting apoptosis, methyl jasmonate also promotes necrosis. MJ promoted necrosis occurs in at least two different ways. First, it damages the mitochondria and promotes ATP depletion. Second, it promotes the expression of the tumor necrosis factor receptor in the membrane of cancer cells. TNF is the single most potent anti-cancer immune hormone yet identified.
Methyl jasmonate is administered in two different ways.
As an aerosol MJ is added to distilled water in a small personal steamer such as that manufactured by Vicks. It is sold by Amazon.com and large drug stores. 2 grams (2 milliliters) of MJ is added to the surface of the water where it will float as a light oil. The steamer is turned to high and the steam/MJ is inhaled into the lung. Breathe through the mask for 15-20 minutes. This is done every six days. I see no reason why it could not be done more often.
Topically 10 grams of MJ is added to 4 ounces of 70% DMSO gel. http://www.herbalremedies.com sells the gel that we prefer. It is made by Clinic Service Company.
This gel is applied up the nose for the treatment of brain cancer and onto the scrotum for the treatment of prostate cancer. As a more general method of delivery, the gel is applied to the arm pits. The arm pit area contains a high concentration of lymph nodes and lymphatic fluid. This is an excellent portal of topical entry into the circulation. The hair follicles in the arm pits are literally holes in the skin where MJ can be intoduced into the body. But first the hair follicles must be thoroughly washed with a detergent shampoo like Selsen Blue. This shampoo cleans out the crap clogging the follicle shafts. The topical formulations can be applied daily, although I would be careful sticking too much MJ at once up the nose.
Methyl jasmonate is used by Grouppe Kurosawa for our skin cream SkinAlive(R). We will sell 10 grams to others in the US for $180 including priority mail shipping. The total cost is $200 for shipping to Europe. Shipping costs vary for other parts of the world.
Payment is made by PayPal to smartin@grouppekurosawa.net.
It is my opinion that methyl jasmonate is the ONLY stand alone treatment for cancer and leukemia. Unlike other promising anti-cancer products which cannot be obtained by the general public, MJ is made by different manufacturers for sale to the cosmetics industry. It is a tad expensive, but a little goes a long way.
Stay tuned...
Grouppe Kurosawa, Medicine in the Public Interest
http://www.grouppekurosawa.com
