Dennis Hill: Understanding and Preventing cancer with Cannabinoids & the Endocannabinoid System

Concise and clear,Dennis.

Patients for Medical Cannabis

We have answered the question, What cures all cancer?… Cannabis therapeutics.
Now I have another question; What is the cause of all cancer? Show me the science.
Today we know the cause of all cancer… sugar.  And today we have the science.

Scientists reveal the relationship between sugar, cancer
A nine-year joint research project has led to a crucial breakthrough in cancer research. Scientists have clarified how the Warburg effect, a phenomenon in which cancer cells rapidly break down sugars, stimulates tumor growth. This discovery provides evidence for a positive correlation between sugar and cancer, which may have far-reaching impacts on tailor-made diets for cancer patients. 

We are talking about the cause within the cell; not the external causes like Glyphosate, sunlight, testosterone, etc. Within the cell there is one cause of accelerated growth: sugar.

How It Works

There is a plentiful supply of research articles and personal testaments that…

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Update on medical marijuana trial

My last post on 12/11/14 was written one month after I started a marijuana medication protocol to treat my prostate cancer, staged as Gleason 9(5+4) after an unsuccessful radical  prostatectomy, which itself was followed by an equally unsuccessful course of salvage radiation treatment.

I posted a graphic display of these treatment failures on my Facebook page, using commonly accepted standards for the scientific analysis of PSA kinetics, particulrly a metric termed “Specific Growth Rate” (SGR) which quantifies changes in the rate of change during a course of treatment. You can read about this research methodology by accessing an article published  on-line by Dr Glenn Tisman ( Google his name and ” psa variability”).

Before treatment my SGR indicated that my cance was growing at a rate of 26% per month. Another indicator of growth rate is “doubling time” and this metric indicated that it took roughly 2.6 months for my cancer to increase in size by 100%. this lead to the gecisionfor surgical removal of the prostate to reduce the risk for lethality associated with such an aggressive cancer.

Unfortunately, the SGR immediately after surgery was still very high ( 13% increase per month) but imaging studies suggested that that the cancer might still be confined to the prostate bed and therefore might be treated successfully by salvage radiation to that area.

The failure of that approach to treatment was documented by a return of the cancer’s SGR to 26% per month during the first 4 months after treatment, the same rate present before surgery.

Tisman suggests in his article that cancer’s may display a particular  SGR which is their characteristic signature. Clearly, neithwr of these treatments had altered this aspect of my prostate cancer.

I am very pleased to report that my cancer’s current SGR ,  calculated on the basis of 4 PSA test  results obtained since I completed the intensive phase of the treatment protocol 2 months ago, indicates that the progression of the cancer( as indexed by this surrogate measure of tumor activity) has been dramtically stopped in its tracks. PSA values actually decresed during that interval ( from 7.73 ng/mL to 7.29 ng/mL), an SGR of

-.04% per month.

A visual inspection of the graphic results plotted using a semi- log,celeration charting format, and assisted by the use of a Process Behavior Control Chart that helps to identify signals in noisy data suggest that these most recent test results most likely reflect ransom fluctuations about a stable mean value of roughly 8 ng/mL. However, this graphic format provides very precise criteria to be used in evaluating any subsequent changes to determine how long this period of stability will be maintained or if there is new evidence that the size of the underlying tumor has actually shrunk.

In addition to relying to these  PSA kinetics as indirect measures of tumor activity, a recent imaging study detected the location of the surviving tumor, and a repeat study in 6 months will provide the basis for a  direct measurement of any changes produced by the medical marijuana trial.

I am writting up these results for submission to an on-line publication- “The Journal of Patient Experience” which accepts case studies of this nature.

I will also submit them to a more “scientific journal” but the medical community is still not very receptive to the possiblilty that such results are even possible, let alone routinely encountered.

To the best of my knowledge, no equivalent study has yet been published using this degree of experimental control and accepted quantitative data analytic techniques.

I welcome feedback from readers of rhis blog, particularly regrading other quantitative studies that I might have overlooked.

Thanks to Dennis among others for encouragement and advice during this arduous journey.

I am continuing to take a maintenance dose of a THC/CBD preparation that I can obtain from a licensed dispensary in NYCity that is similar to the one I used in the induction phase of the study, except that this is administered sub- lingually as a tincture. The daily dose is adjusted according to my conflicting desires to continue to bombard  my tumor with the chemical solution that stymies its ability to reproduce while at the same time allowing me to function more or less”normally” during the day.

i think I mentioned previously that the resting level of THC in my system was a staggeringly high 766 ng/mL, which rendered me stoned but functional for 2 and 1/2 months – a small proce to pay for the positive outcomes I have experienced  so far.

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The perfect is …

The perfect is the enemy of the good

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