Cannabis and the myriad of compounds found inside the plant have been successfully utilised for the treatment of nausea and vomiting from chemotherapy and have also potentiated the effects of opioid pain medications in treating cancer pain. Cannabinoids have been shown to help encourage sleep, stimulate appetite, reduce depression and anxiety, and lift the spirits of patients undergoing cancer treatment, all of which can contribute greatly to quality of life.  Cancer treatment often attracts dubious claimants who extend hope to those desperate for it, resulting in claims of cancer cures; for which there is only promising anecdotal evidence. For more information, see our article on CBD for nausea and vomiting and cannabis for cancer appetite loss and cachexia, along with CBD for depression, and CBD for anxiety.
Cannabis products rich in cannabinoids shouldn’t be replaced for more conventional cancer treatments, but informed oncologists are usually in support of its use as a co-treatment with conventional regimens. Animal studies of plant cannabinoids have shown that they’re capable of decreasing tumor growth and metastasis (migration of cells). Alongside this, fairly limited human studies (though increasing), have shown that plant cannabinoids could be safe and effective antitumor compounds, but that they aren’t effective for all cancer types and some cannabinoids could, in certain cancers, increase the growth of tumors. 
Using cannabis products to successfully treat the major symptoms of cancer is not controversial. In a review of the available evidence on the uses of medicinal cannabis, there was strong scientific evidence for its use in cancer, chemotherapy-induced nausea (CIN) and vomiting, identified pain, appetite stimulation/weight gain, and sleep, as being supported by varied but credible scientific literature.  There are high quality randomized controlled clinical trials to support the treatment of pain, and controlled trials of weaker quality that support the treatment of insomnia, CIN, and appetite/weight loss.  Medical cannabis has also been found to be of great value for relieving, reducing, preventing, or distracting from both neuropathic (nerve) and visceral (organ) pain.       The great benefit of medicinal cannabis for chemotherapy-induced nausea, and in countering the loss of appetite, has also been extensively studied: Cannabis is an established treatment, and it is unique in that it also may stimulate appetite.      
Quality of life issues are other areas where cannabis could be of value, as cannabidiol (CBD) has shown itself to be an effective non-psychoactive treatment for a myriad of conditions, such as anxiety, chronic pain, depression, sleep issues, and more. A low dose of tetrahydrocannabinol is also understdood to provide a vehicle to lift mood. Cannabis can be of great value for patients with cancer who could understandably be anxious and/or depressed from their cancer diagnosis, and the resulting complications of its treatment: weakness, fatigue, hair loss, loss of vocation, insomnia, isolation, and in some cases, poverty. We are awaiting further clinical studies looking at cannabis use in treating anxiety among cancer patients, although a series of case reports discovered a lower incidence of anxiety among cancer patients who used cannabis. 
The extremely complicated mechanisms of the antitumor action of cannabinoids has been described in the literature.     The evidence is clear that CBD and THC have very different antitumor mechanisms of action, and seem to have additive activity. Thus, CBD and THC are better at killing cancer cells together than each on their own, and seem to sensitize cancers to the killing effects of radiation or chemotherapy.  In a couple of open-source papers, researchers describe the actions of cannabinoids that seem to reveal their potential as antitumor medications.  
Cancer-cell studies that are preclinical in nature, have shown that botanical and synthetic cannabinoids possess antitumor activity, by promoting cancer cell death, inhibiting cell proliferation and invasiveness, reducing the growth of the new blood supply needed for tumor growth, and reducing metastasis. Several studies with tetrahydrocannabinol, however, have shown the biphasic, dose dependent nature of cannabinoids, with protumor effects both in cell-line cultures of breast, prostate, hepatoma, bronchial, and lung cancers and in two experimental animal studies.    In addition to this, in the same cell-line culture models, different cannabinoids can have opposite effects; with THC stimulating cell growth, and other cannabinoids inhibiting cell growth. 
In the 1950s, the Royal Brompton Hospital in London created and administered the “Brompton cocktail” for intractable cancer pain. This combination of morphine, cocaine, chloroform, and cannabis with cherry syrup was used for 70 years until it fell out of favor and was replaced by next-generation opioids. Cannabis has been utilized to help with the side effects of cancer chemotherapy since the late 1970s, however it gained more recognition in the 1990s. Cannabis use among chemotherapy patients is widely responsible for medical cannabis laws being passed in many states.
Disclaimer: the information contained in this article is to be used for informational purposes only and does not consitute medical advice. People wishing to make changes to their lifestyle or treatment plan, including using medical marijuana, should always seek the advice of medical professionals experienced in the use of medical marijuana. Although news of the benefits of medical marijuana and cannabidiol products products is quickly spreading, it's important to find common ground with your doctor when discussing using these products. As with all medical marijuana use, start low and slow, titrate the dose appropriately, and contact your licenced medical practitioner for support, regardless of whether you're based in the united states or New Zealand.
While the antitumor action of cannabinoids is generally accepted as plausible, there could be a credible explanation for the pro-tumor effects of THC in some types of cancer. Immune suppression can be a risk factor for the emergence, worsening, of malignancies, as we know well from AIDS. The potential activation of the immunosuppressant CB2 receptor could reduce the immune response that ordinarily controls growth or spreads of certain cancers.  Compared to normal tissues, there are many more CB1 and CB2 receptors on the cells of some cancers; breast, prostate, leukemia, melanoma, colorectal, thyroid, and hepatocellular malignancies; and in some cases, this “overexpression” (more numerous than normal) of receptors correlates with tumor aggressiveness. The secondary cannabinoid receptors, TRPV1 and GPR-55, also may be overexpressed. Why these receptors are overexpressed is not known, but parallels from drug studies suggest that the tissues are “hungry” for cannabinoids to attach to their receptors – so they make more receptors. In fact, when endocannabinoid levels are measured in animal models or patients with malignancies, they can be elevated, and fatty acid amide hydrolase (FAAH), the enzyme that breaks down anandamide, may be depressed. While these data are generally interpreted to indicate that overexpression of the receptors suggests an attempt by the body to kill or inhibit tumor activity, in some cases it may be associated with protumor activity, and may indicate either a better or worse prognosis. 
Endocannabinoids are produced by the body’s own endogenous cannabinoid system (ECS), which is now considered to be the most important system of physiology inside the body, responsible for maintaining order and balance across every major bodily system; from the reproductive and cardiovascular, to the circulatory and respiratory. The ECS has receptors throughout the body that work like lock and key for cannabinoids, called CB1 and CB2. What’s more, this “ghost in the machine” can become dysfunctional from too many demands placed upon it. In other words, too much stress (emotional and/or physical) can overwhelm the ECS leading to states of disease and dysfunction in the body. Many autoimmune conditions are now linked to a dysfunctional ECS, along with many states that prevent the body’s immune system from detecting and destroying cancerous rogue cells. It could be said that all illness starts and ends with the ECS. It’s important to note then, that plant cannabinoids from cannabis / hemp have the ability to support and nourish the ECS, restoring it back to normal functioning and pulling it out of a state of disorder. However, the body’s repair systems are limited, and if the organism is too far out of balance, the body may struggle to heal while efforts are directed at other stresses and issues at hand. Depending on the state of imbalance and “unhealth” in the body, will largely determine whether the person or organism has past a “point of no return” where other measures may need to be taken in order to work alongside the ECS in helping to restore health and healing. For more information, read The Endocannabinoid System Explained.
THC activation of the CB1 receptor in hormone-sensitive breast cancer cells produces different antitumor cellular effects from those caused by THC in HER2+ cancer cells.  In the case of HER2+ cells, it is activation of the CB2 receptor that has the anticancer effects.  The terpene beta-caryophyllene activates CB2. In a preclinical trial, tetrahydrocannabinol has been shown to upregulate the estrogen receptor, beta.  While THC and selective CB1 and CB2 activators have been studied most, a considerable volume of preclinical data has pointed to the viability of cannabidiol (CBD)  and CBDA  against breast cancer. Preclinical studies show that cannabis flower or infused products with roughly balanced ratios of CBD and THC (1:1 or similar) may be valuable adjunctive therapy with conventional chemotherapy. 
Malignant glioma (brain cancer) studies showed that cannabinoids (a variety of CBD, THC, and various synthetic drugs were used) inhibited tumor growth, growth of new blood vessels, metastasis, and, in all but one study, selectively killed cancerous cells without affecting normal cells.  Another study showed a dramatic synergistic effect of radiation and low dose of THC plus CBD (approximately 1:1) in glioma, and hypothesized that cannabinoids prime tumors to respond to radiation and impair the ability of the cancer to repair DNA damage from radiation. 
A pilot study,  published in 2006, involved nine patients with recurrent glioblastoma multiforme that had shown tumor progression, despite application of all conventional treatments. A catheter was inserted into the tumor itself and a THC solution of 5 ng was injected daily, increasing the dose for a dosing cycle of about 10 days. The initial dose was very small, about 20 to 40 mcg and was titrated to 80 to 180 mcg. Three of the nine patients improved clinically, and two of them lived approximately one year; an utterly extraordinary survival for recurrent glioblastoma that has failed “rescue” therapy.
In regards to lung cancer, more review of the medical literature has found that both CBD and THC act upon the CB1 and CB2 receptors of the endocannabinoid system, plus a broad range of other important receptors and molecular pathways in lung cancer cells (including the prostaglandin system through cyclooxygenase 2 upregulation) in studies using human cell-line cultures and rodent disease models.    CBD and THC have shown major antitumor mechanisms in all areas: increased cell death, reduced tumor growth, metastasis, and angiogenesis, even in studies of treatment-resistant non-small-cell cancer cells. Cannabinoids could be considered for adjunctive therapy and very much should be included as palliative therapy to potentiate a slowing of the progression of lung cancers.
In addition, there are some preclinical studies of cannabinoids and intestinal cancer. Some reviews of the evidence are encouraging, showing that activation of CB1, CB2, and TRPV1 receptors reduce tumor growth and protect mice from induction of colon cancer experimentally.   CBD and plant-based CBD products, in particular, have shown promising results in reducing carcinogenesis and inhibiting cancer cell growth.   The intensity of CB2 expression in biopsy specimens from 175 colorectal cancer patients correlated with tumor progression.   Although potent, non-physiologic doses of cannabinoid activators are antiproliferative and proapoptotic, low doses consistent with physiologic endocannabinoid levels pro-proliferative.  Cannabidiol, which not a direct agonist of either the CB1 or CB2 receptor, has shown consistently antiproliferative and anticarcinogenic activity, with a whole-plant extract of cannabinoids (including moderate amounts of THC) enriched with plant-based CBD performing better than pharmaceutical CBD and THC. 
Prostate cancer is covered in cell-line studies   noting a potential role for CB1 and CB2 agonists in reducing prostate cancer cell growth, although a higher-dose related increase in proliferation was noted in some studies with THC, anandamide, and 2-AG.  An extensive, definitive prostate cancer cell-line and mouse-model study of 12 non-THC cannabinoids concluded that CBD administered in an extract of “biologic drug substances” (BDS) from raw cannabis products, was the most successful in inhibiting prostate cancer cells. When dosed in a mouse model, the CBD-BDS concoction potentiated the effects of the cancer chemotherapeutic agents, docetaxel and bicaltamide.  CBD did not act through the cannabinoid or TRPV receptors, suggesting that additive effects with THC may be possible.
In summarising, medicinal cannabis is well established as an effective treatment for symptoms of cancer and chemotherapy, but unfortunately no clinical trials exist to guide its use in the treatment of malignancies.
Utilising medicinal cannabis to treat the actual cancer, as opposed to its symptoms, only makes sense in the following circumstances, due to the nature that there is no reliable medical evidence to support the use of medical cannabis as the sole treatment for cancers of any type:
Normal cells divide to form new cells as the body needs them, and they mature into distinct cell types with specific functions. When they grow old or become damaged, they undergo programmed cell death (apoptosis). In cancers, this orderly process breaks down. Given the central role that the endocannabinoid system plays in the normal life cycle of cells, it is thought that there is opportunity for new cannabinoid-based cancer therapies.
Chemotherapy and radiation regimens not only affect cancer cells, they damage normal cells as well, while cannabinoids offer the unusual advantage of killing only cancer cells, leaving normal cells unharmed. In this way, cannabinoids function like targeted chemotherapy (treatments that affect the dysfunctional programming unique to cancer cells), in that they specifically attack tumor cells to induce cell death, inhibit growth of tumor blood vessels, and reduce tumor growth of metastasis without damage to normal cells.
Cannabis products can be effectively taken sublingually and swallowed, but sublingual has a faster onset and is more predictable. Swallowed medicines tend to provide longer-lasting effects, analgesia, and provide some advantages for nausea and vomiting, given they are taken two to three hours before a chemotherapy session.
Vaporizing cannabis products can be effective and dose titration is more easily achieved. Inhaled THC can be of value for those with both acute and anticipatory nausea.
Almost all varieties and strains of cannabis can address the adverse effects stemming from cancer treatments. In particular, the strains Cannatonic/ACDC for their high-CBD content; and Grand Daddy Purple, OG Kush, Bubba Kush, and Pincher Creek for their THC and terpene content. For more information, see our Ultimate Guide to Terpenes.
For more information, see our other article on CBD for cancer.
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