I have/had ovarian/primary peritoneal cancer. I used thc/cbd oil pills I self made from the start. I am supposedly their “poster child”. I went thru with chemo and surgery. Oh that horror! But when I tried to tell two seperate doctors, the surgeon was all about it, and my oncologist threw a fit and said it was an anecdote. There are more than 100 studies at the NIH govt website.
We gave the highest points to companies that use a CBD distillate for their tinctures. The process of distillation creates an extract that is pure on a molecular level. There are people who think distillate is too pure, and that a full spectrum decarb produces a more effective tincture. But in light of the inconclusive evidence, we prefer a distillate. The process allows for a high degree of control as to the finished product. It’s also odorless and tasteless, so those tinctures tend to taste better.
CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer.[21] In this experimental system, azoxymethane increased premalignant and malignant lesions in the mouse colon. Animals treated with azoxymethane and CBD concurrently were protected from developing premalignant and malignant lesions. In in vitro experiments involving colorectal cancer cell lines, the investigators found that CBD protected DNA from oxidative damage, increased endocannabinoid levels, and reduced cell proliferation. In a subsequent study, the investigators found that the antiproliferative effect of CBD was counteracted by selective CB1 but not CB2 receptor antagonists, suggesting an involvement of CB1 receptors.[22]
In the United States, the public's perception of hemp as marijuana has blocked hemp from becoming a useful crop and product,"[52] in spite of its vital importance prior to World War II.[53] Ideally, according to Britain's Department for Environment, Food and Rural Affairs, the herb should be desiccated and harvested towards the end of flowering. This early cropping reduces the seed yield but improves the fiber yield and quality.[54] In these strains of industrial hemp* the tetrahydrocannabinol (THC) content would have been very low.[52]
Pain management improves a patient’s quality of life throughout all stages of cancer. Through the study of cannabinoid receptors, endocannabinoids, and synthetic agonists and antagonists, the mechanisms of cannabinoid-induced analgesia have been analyzed.[46][Level of evidence:1iC] The CB1 receptor is found in the central nervous system (CNS) and in peripheral nerve terminals.[47] CB2 receptors are located mainly in peripheral tissue and are expressed in only low amounts in the CNS. Whereas only CB1 agonists exert analgesic activity in the CNS, both CB1 and CB2 agonists have analgesic activity in peripheral tissue.[48,49]

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Karl W. Hillig, a graduate student in the laboratory of long-time Cannabis researcher Paul G. Mahlberg[77] at Indiana University, conducted a systematic investigation of genetic, morphological, and chemotaxonomic variation among 157 Cannabis accessions of known geographic origin, including fiber, drug, and feral populations. In 2004, Hillig and Mahlberg published a chemotaxonomic analysis of cannabinoid variation in their Cannabis germplasm collection. They used gas chromatography to determine cannabinoid content and to infer allele frequencies of the gene that controls CBD and THC production within the studied populations, and concluded that the patterns of cannabinoid variation support recognition of C. sativa and C. indica as separate species, but not C. ruderalis.[52] The authors assigned fiber/seed landraces and feral populations from Europe, Central Asia, and Turkey to C. sativa. Narrow-leaflet and wide-leaflet drug accessions, southern and eastern Asian hemp accessions, and feral Himalayan populations were assigned to C. indica. In 2005, Hillig published a genetic analysis of the same set of accessions (this paper was the first in the series, but was delayed in publication), and proposed a three-species classification, recognizing C. sativa, C. indica, and (tentatively) C. ruderalis.[55] In his doctoral dissertation published the same year, Hillig stated that principal components analysis of phenotypic (morphological) traits failed to differentiate the putative species, but that canonical variates analysis resulted in a high degree of discrimination of the putative species and infraspecific taxa.[78] Another paper in the series on chemotaxonomic variation in the terpenoid content of the essential oil of Cannabis revealed that several wide-leaflet drug strains in the collection had relatively high levels of certain sesquiterpene alcohols, including guaiol and isomers of eudesmol, that set them apart from the other putative taxa.[79] Hillig concluded that the patterns of genetic, morphological, and chemotaxonomic variation support recognition of C. sativa and C. indica as separate species. He also concluded there is little support to treat C. ruderalis as a separate species from C. sativa at this time, but more research on wild and weedy populations is needed because they were underrepresented in their collection.
Not until the end of the 20th century was the specific mechanism of action of THC at the neuronal level studied.[citation needed] Researchers have subsequently confirmed that THC exerts its most prominent effects via its actions on two types of cannabinoid receptors, the CB1 receptor and the CB2 receptor, both of which are G protein-coupled receptors.[133] The CB1 receptor is found primarily in the brain as well as in some peripheral tissues, and the CB2 receptor is found primarily in peripheral tissues, but is also expressed in neuroglial cells.[134] THC appears to alter mood and cognition through its agonist actions on the CB1 receptors, which inhibit a secondary messenger system (adenylate cyclase) in a dose-dependent manner. These actions can be blocked by the selective CB1 receptor antagonist rimonabant (SR141716), which has been shown in clinical trials to be an effective treatment for smoking cessation, weight loss, and as a means of controlling or reducing metabolic syndrome risk factors.[135] However, due to the dysphoric effect of CB1 receptor antagonists, this drug is often discontinued due to these side effects.[136]
Content updates feature essential information related to the state’s commercial cannabis regulations and guidelines, the licensing application process, and announcements from the state’s three cannabis licensing authorities and business partners. Links to each state agency’s cannabis information are listed towards to the bottom of the homepage under the “Collaborating State Agencies” header. 
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