Understanding How THC Kills Cancer in Humans by Dennis Hill

Understanding How THC Kills Cancer in Humans

First let’s look at what keeps cancer cells alive, then we will come back and examine
how THC unravels cancer’s aliveness.
In every cell there is a family of interconvertible sphingolipids that specically manage the life and death of that cell. is pro le of factors is called the “Sphingolipid Rheostat.” If ceramide (a signaling metabolite of sphingosine-1-phosphate) is high, then cell death (apoptosis) is imminent. If ceramide is low, the cell is strong in its aliveness.
Very simply, when THC connects to the CB1 or CB2 cannabinoid receptor site on the
cancer cell, it causes an increase in ceramide synthesis which drives cell death. A normal healthy cell does not produce ceramide in the presence of THC, thus is not affected by the cannabinoid.
The cancer cell dies, not because of cytotoxic chemicals, but because of a tiny little shift in the mitochondria. Within most cells there is a cell nucleus, numerous
mitochondria (hundreds to thousands), and various other organelles in the cytoplasm. The purpose of the mitochondria is to produce energy (ATP) for cell use. As ceramide starts to accumulate, turning up the Sphingolipid Rheostat, it increases the mitochondrial membrane pore permeability to cytochrome c, a critical protein in energy synthesis. Cytochrome c is pushed out of the mitochondria, killing the source of energy for the cell.
Ceramide also causes genotoxic stress in the cancer cell nucleus generating a protein
called p53, whose job it is to disrupt calcium metabolism in the mitochondria. If this weren’t enough, ceramide disrupts the cellular lysosome, the cell’s digestive system that provides nutrients for all cell functions. Ceramide, and other sphingolipids, actively inhibit pro-survival pathways in the cell leaving no possibility at all of cancer cell survival.
The key to this process is the accumulation of ceramide in the system. is means
taking therapeutic amounts of THC, steadily, over a period of time, keeping metabolic
pressure on this cancer cell death pathway.
How did this pathway come to be? Why is it that the body can take a simple plant
enzyme and use it for profound healing in many di erent physiological systems? is
endocannabinoid system exists in all animals of creation, just waiting for it’s matched exocannabinoid activator.
This is amazing. Our own endocannabinoid system covers all cells and nerves; it is the messenger of information owing between our immune system and the central nervous
system (CNS). It is responsible for neuroprotection, and micro-manages the immune
system. is is the primary control system that maintains homeostasis; our well being.
Just out of curiosity, how does the work get done at the cellular level, and where does the body make the endocannabinoids? Here we see that endocannabinoids have their origin in nerve cells right at the synapse. When the body is compromised through illness or injury it calls desperately to the endocannabinoid system and directs the immune system to bring healing. If these homeostatic systems are weakened, it should be no surprise that exocannabinoids are therapeutic. It helps the body in the most natural way possible.
To see how this works we visualize the cannabinoid as a three dimensional molecule,
where one part of the molecule is configured to fit the nerve or immune cell receptor site just like a key in a lock. There are at least two types of cannabinoid receptor sites, CB1 (CNS) and CB2 (immune). In general CB1 gives us the buzz, and CB2 activates the immune system, but it’s much more complex than this. Both THC and anandamide activate both receptor sites. Other cannabinoids activate one or the other receptor sites. Among the strains of Cannabis, C. sativa tends toward the CB1 receptor, and C. indica tends toward CB2. So sativa is better for buzz, and indica is better for healing. Another factor here is that sativa is dominated by THC cannabinoids, and indica is predominately CBD (cannabidiol).
It is said that THC and CBD are biomimetic to anandamide, that is, the body can use
both interchangeably. Thus, when stress, injury, or illness demand more from endogenous anandamide than can be produced by the body, its mimetic exocannabinoids can rush to the rescue. If the stress is transitory, then the treatment can be transitory. If the demand is sustained, such as in cancer, then treatment needs to provide sustained pressure of the modulating agent on the homeostatic systems.
Typically CBD gravitates to the densely packed CB2 receptors in the spleen, home to
the body’s immune system. From there, immune cells seek out and destroy cancer cells.
Interestingly, it has been shown that THC and CBD cannabinoids have the ability to kill cancer cells directly without going through immune intermediaries. THC and CBD hijack the lipoxygenase pathway to directly inhibit tumor growth. As a side note, it has been discovered that CBD inhibits anandamide reuptake. is means that cannabidiol helps the body preserve its own natural endocannabinoid by inhibiting the enzyme that breaks down anandamide.
This brief survey touches lightly on a few essential concepts. Mostly I would like to
leave you in complete amazement that nature has designed the perfect medicine that ts
exactly with our own immune system of receptors and signaling metabolites to provide
perfect health all the time. It is my hope that my own prostate cancer dies out quickly in the face of intensive cannabis extract treatment currently in progress. The C-T Scan will tell the story next month.

~Dennis Hill
Legal in California


Bibliography

1. http://cancerres.aacrjournals.org/content/65/5/1635.abstract
Sami Sarfaraz, Farrukh Afaq, Vaqar M. Adhami, and Hasan Mukhtar + Author
Affiliations. Department of Dermatology, University of Wisconsin, Madison,
Wisconsin

2. http://www.ncbi.nlm.nih.gov/sites/pubmed
J Neuroimmunol. 2007 Mar;184(1-2):127-35. Epub 2006 Dec 28.
Immune control by endocannabinoids - new mechanisms of neuroprotection?
Ullrich O, Merker K, Timm J, Tauber S.
Institute of Immunology, Medical Faculty, Otto-von-Guericke-University
Magdeburg, Leipziger Str. 44, 39120 Magdeburg, Germany.
oliver.ullrich@medizine.uni-magdeburg.de

3. http://en.wikipedia.org/wiki/Endocannabinoid_system
Endocannabinoid synthesis & release.

4. http://en.wikipedia.org/wiki/Cannabinoids
Cannabinoid receptor type 1.

5. http://www3.interscience.wiley.com/journal/121381780/abstract?
CRETRY=1&SRETRY=0
Journal of Neurochemistry, Volume 104 Issue 4, Pages 1091 - 1100
Published Online: 18 Aug 2008

6. http://leavesofgrass.info/info/Non-Psychoactive-Cannabinoids.pdf
Non-psychotropic plant cannabinoids: new therapeutic opportunities from an
ancient herb.
Angelo A. Izzo, Francesca Borrelli, Raffaele Capasso, Vincenzo Di Marzo, and
Raphael Mechoulam. Department of Experimental Pharmacology, University
of Naples Federico II, Naples, Italy. Institute of Biomolecular Chemistry,
National Research Council, Pozzuoli (NA), Italy. Department of Medicinal
Chemistry and Natural Products, Hebrew University Medical Faculty,
Jerusalem, Israel, Endocannabinoid Research Group, Italy

7. http://sciencenews.org/view/feature/id/59872/title/Not_just_a_high
Scientists test medicinal marijuana against MS, inflammation and cancer
By Nathan Seppa June 19th, 2010; Vol.177 #13 (p. 16)

8. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1766198/?tool=pmcentrez
A house divided: ceramide, sphingosine, and sphingosine-1-phosphate in
programmed cell death.

Tarek A. Taha, Thomas D. Mullen, and Lina M. Obeid
Division of General Internal Medicine, Ralph H. Johnson Veterans
Administration Hospital, Charleston, South Carolina 29401; and Department
of Medicine, Medical University of South Carolina, Charleston, South Carolina
29425