How to make Medical Cannabis Oil
Also watch How to Decarboxylate Cannabis: https://youtu.be/nO19GwT1IGs
For this tutorial we used a new induction heating element with temperature control to evaporate the ethanol from the tincture. There’s been a lot of comments from people on our first video that we should not mix olive oil with our extract and that we did not activate the THC. We mix our extract with good quality olive oil because it will be consumed by ingesting it. This is also why we use food grade Ethanol / 96% Alcohol. DON’T USE RUBBING ALCOHOL (isopropyl) USE GRAIN ALCOHOL! If you are going to be ingesting extract and you still have a small amount of solvent left over in your extraction, it is safe to consume small amounts of food grade alcohol. When the extract is diluted with olive oil, the concentration of any remaining alcohol will be microscopic. These extracts are not for combusting. The activation of THC in RAW cannabis is different from activating THC is cured cannabis. We have found that sun drying cannabis for weeks also starts the activation process. Additionally you can preheat the cannabis in an oven for about 24 minutes at 140 C, however you will lose most of the terpenes at this temperature and the synergy of the cannabinoids and terpenoids of whole plant extract will be different. We found that activating THC is most efficiently done during the evaporation process by keeping it between 80C and 100 C for about 30 minutes. After the alcohol has evaporated, heat the extract to 125 C for another 10 minutes making sure the extract keeps moving, not allowing it to burn. There’s a lot of discussion about how to activate THC, we know that our extracts contain on average 50% to 60% THC as these have been testing with thin-layer chromatography and also ingesting the extract and feeling its potency for about 5 hours, mainly from other peoples experiences.
Read More about the subject here: http://mattsands.blogspot.nl/2015/10/…
We advise you to add your own CBD which you can purchase in many places online. Most commercial cannabis contains low levels of CBD When they contain higher levels of CBD, the plant usually has a 1:1 THC/CBD ratio but it probably yields fairly low amounts when extracting the cannabinoids. Therefore we use high THC strains when possible. Good quality CBD extractions are about 50% to 60% pure and cost around $40 for about 1 gram.
According to www.cancer.gov:
Cannabis has been used for medicinal purposes for thousands of years.
By federal law, the possession of Cannabis is illegal in the United States, except within approved research settings; however, a growing number of states, territories, and the District of Columbia have enacted laws to legalize its medical use.
The U.S. Food and Drug Administration has not approved Cannabis as a treatment for cancer or any other medical condition.
Chemical components of Cannabis, called cannabinoids, activate specific receptors throughout the body to produce pharmacologic effects, particularly in the central nervous system and the immune system.
Commercially available cannabinoids, such as dronabinol and nabilone, are approved drugs for the treatment of cancer-related side effects.
Cannabinoids may have benefits in the treatment of cancer-related side effects.
Also According to Cancer.gov:
Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis.[9-12] Two reviews summarize the molecular mechanisms of action of cannabinoids as antitumor agents.[13,14] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. For example, these compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats, while they protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.
The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in HCC. Both agents reduced the viability of HCC cells in vitro and demonstrated antitumor effects in HCC subcutaneous xenografts in nude mice. The investigations documented that the anti-HCC effects are mediated by way of the CB2 receptor. Similar to findings in glioma cells, the cannabinoids were shown to trigger cell death through stimulation of an endoplasmic reticulum stress pathway that activates autophagy and promotes apoptosis. Other investigations have confirmed that CB1 and CB2 receptors may be potential targets in non-small cell lung carcinoma  and breast cancer.
An in vitro study of the effect of CBD on programmed cell death in breast cancer cell lines found that CBD induced programmed cell death, independent of the CB1, CB2, or vanilloid receptors.
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