Health References

Cannabis Sativa in all of it’s ingestible forms had been made illegal for production and general distribution globally starting in the early 1920’s. Country after country passed legislation banning the production, processing, distribution and use of Cannabis Health Products that had been used extensively for thousands of years.

Interestingly, this is the same period when medical and scientific studies were just getting underway into the positive, healthy uses of many natural substances and compounds. Research subsequent to that period has been well developed for all available pharmaceutical products, all over the counter drugs and most natural botanical health products.

Given the prior illegal status of Marijuana, research proving it’s many health benefits is extremely limited. Scientists have had little available study material to work with. If a research group was able to legally procure a sufficient quantity of medical grade Cannabis product, it was then impossible to complete any double blind, placebo controlled clinical trials on human subjects, as distribution of the test product to the subjects would legally constitute trafficking, punishable by up to life in prison in most jurisdictions and the test subjects would be liable to severe criminal sanctions for possession and consuming a controlled substance for those healthy purposes.In depth research studies have only begun lately with the advent of legal Cannabis Sativa Health Products. The Cannabis health community relies initially on anecdotal information passed down and recorded through the ages.

Cannabis Sativa for Health

Scientific Research Reading Selections…

The following background information on the health benefits of Cannabis Sativa is merely a small sampling of what is available through recent research efforts. Your Doctor or a librarian will be pleased to direct you to literature appropriate to your individual research requirements.

1. Positive effects of low-THC Cannabis oil on Rheumatoid Arthritis

The Effects of GLA on Rheumatoid Arthritis
Janice McColl, B.S.P., M.Sc., M.H.

Many people are looking for a gentler form of treatment that remains effective against arthritic pain and will allow them to reduce their usage of NSAIDs.

Over the last 15 years, researchers have performed several clinical studies that demonstrate the effectiveness of gamma linolenic acid (GLA) on the symptoms of rheumatoid arthritis. Patients appear to be deficient in GLA and many patients respond favorably to treatment with GLA, especially in recent clinical trials where dosages were greater than 1.4 grams of GLA/day. Early studies used relatively low dosages with some success. For example, as early as 1988, researchers confirmed that supplementation with 540 mg of GLA per day could help patients reduce their usage of NSAIDs. Later research showed that higher dosages could achieve still greater results.

In 1993, researchers at the University of Pennsylvania conducted a randomized, double-blind, placebo-controlled, 24-week trial with 37 rheumatoid arthritis patients. Patients in the treatment group received 1.4 grams of GLA per day, and assessed their symptoms on a daily basis. Treatment with GLA reduced the number of tender joints by 36%, the tenderness of the joints by 45%, the number of swollen joints by 28%, and the degree of joint swelling by 41%, whereas the placebo group did not show significant improvement in any measure. The researchers concluded that GLA in the doses used in the study is a well-tolerated and effective treatment for rheumatoid arthritis.

Research has confirmed reductions in the duration of morning stiffness, and reductions in joint swelling and tenderness, and pain. In particular, a recent meta-analysis conducted in April 2000 of six placebo-controlled trials found that the duration of morning stiffness may be reduced by 60 to 70% (eg. two hours of morning stiffness could be reduced to half an hour). Reduction in morning stiffness dramatically improves the quality of life for patients suffering from rheumatoid arthritis.

2. Effect of Omega-3 & Omega-6 rich oils on the immune system and effect on autoimmune diseases.

The following scientific analysis report shows us that Omega-3 (n-3) and Omega-6 (n-6) when used together have a synergistic effect on our immune response, boosting the immune system to allow our bodies to ward off viral and bacterial attacks and to increase the body’s capabilities of combating infection or disease that may already have been introduced.

It is interesting to note that the researchers have here discovered & reported that supplementation with Omega-3 alone- as with their example of using fish oils for these purposes- actually has the effect of degrading the immune system and stimulating any auto-immune diseases that may be effecting the body at that time. This research study highlights the fact that any Omega supplementation must be of the complete Omega Profile, including GLA (Gamma-Linolenic Acid) or very undesirable consequences may result.

The list of auto-immune diseases is unfortunately extensive and it is growing as new discoveries are made. There are close to 100 identified already- all deadly serious. Some of the more common ones are:

• Multiple Sclerosis
• Rheumatoid Arthritis
• Type 1 Diabetes Mellitus
• Fibromyalgia
• Psoriasis
• Thyroid Diseases- hyper and hypo
• Lupus
• Sclerderma
• Celiac Disease

Dietary n-6 and n-3 fatty acids in immunity and autoimmune disease.
Harbige LS., School of Chemical and Life Sciences, University of Greenwich, London, UK.

Clearly there is much evidence to show that under well-controlled laboratory and dietary conditions fatty acid intake can have profound effects on animal models of autoimmune disease. Studies in human autoimmune disease have been less dramatic; however, human trials have been subject to uncontrolled dietary and genetic backgrounds, infection and other environmental influences, and basic trial designs have been inadequate.

The impact of dietary fatty acids on animal autoimmune disease models appears to depend on the animal model and the type and amount of fatty acids fed. Diets low in fat, essential fatty acid-deficient, or high in n-3 fatty acids from fish oils increase the survival and reduce disease severity in spontaneous autoantibody-mediated disease, whilst linoleic acid-rich diets appear to increase disease severity. In experimentally-induced T-cell-mediated autoimmune disease, essential fatty acid-deficient diets or diets supplemented with n-3 fatty acids appear to augment disease, whereas n-6 fatty acids prevent or reduce the severity. In contrast, in both T-cell and antibody-mediated auto-immune disease the desaturated and elongated metabolites of linoleic acid are protective.

Suppression of autoantibody and T lymphocyte proliferation, apoptosis of autoreactive lymphocytes, and reduced pro-inflammatory cytokine production by high-dose fish oils are all likely mechanisms by which n-3 fatty acids ameliorate autoimmune disease. However, these could be undesirable long-term effects of high-dose fish oil which may compromise host immunity. The protective mechanism(s) of n-6 fatty acids in T-cell- mediated autoimmune disease are less clear, but may include dihomo-gamma-linolenic acid- and arachidonic acid-sensitive immunoregulatory circuits such as Th1 responses, TGF beta 1-mediated effects and Th3-like responses.

It is often claimed that n-6 fatty acids promote autoimmune and inflammatory disease based on results obtained with linoleic acid only. It should be appreciated that linoleic acid does not reflect the functions of dihomo-gamma-linolenic and arachidonic acid, and that the endogenous rate of conversion of linoleic to arachidonic acid is slow (Hassam et al. 1975, 1977; Phylactos et al. 1994; Harbige et al. 1995).

In addition to effects of dietary fatty acids on immunoregulation, inflammation as a consequence of immune activation in autoimmune disease may also be an important mechanism of action whereby dietary fatty acids modulate disease activity. In conclusion, regulation of gene expression, signal transduction pathways, production of eicosanoids and cytokines, and the action of antioxidant enzymes are all mechanisms by which dietary n-6 and n-3 fatty acids may exert effects on the immune system and autoimmune disease. Probably the most significant of these mechanisms in relation to our current understanding of immunoregulation and inflammation would appear to be via fatty acid effects on cytokines.

The amount, type and balance of dietary fatty acids and associated antioxidant nutrients appear to impact on the immune system to produce immune-deviation or immunosuppressive effects, and to reduce immune-mediated inflammation which will in turn affect the susceptibility to, or severity of, autoimmune disease.

3. Cancer Tumor shrinking abilities of non-psychoactive Cannabis.

 

A series of scientific studies has been undertaken around the world to investigate anecdotal information that Cannabis Sativa could shrink and eliminate certain cancerous tumors. The studies centered on Glioma’s, which are very aggressive brain cancers. The researchers wished to use the most lethal and difficult to treat subject area available. The tumors shrunk and/or disappeared with use of the tested substance.

Initial trials involved full strength THC Cannabis. The work in the study below was undertaken to determine if Cannabis Sativa extracts containing no THC whatsoever, as well had anti-tumor effects.

Antitumor effects of ajulemic acid (CT3), a synthetic non-psychoactive cannabinoid.
Recht LD, Salmonsen R, Rosetti R, Jang T, Pipia G, Kubiatowski T,
Karim P, Ross AH, Zurier R, Litofsky NS, Burstein S.
Department of Neurology, University of Massachusetts Medical School
55 Lake Avenue North, Worcester, MA 01655, USA.

In preclinical studies, AJA has been found to be a potent anti-inflammatory agent without psychoactive properties. Based on recent reports suggesting antitumor effects of cannabinoids (CBs), we assessed the potential of AJA as an antitumor agent. AJA proved to be approximately one-half as potent as THC in inhibiting tumor growth in vitro against a variety of neoplastic cell lines. However, its in vitro effects lasted longer. The antitumor effect was stereospecific, suggesting receptor mediation.

Unlike THC, however, whose effect was blocked by both CB(1) and CB(2) receptor antagonists, the effect of AJA was inhibited by only the CB(2) antagonist. Additionally, incubation of C6 glioma cells with AJA resulted in the formation of lipid droplets, the number of which increased over time; this effect was noted to a much greater extent after AJA than after THC and was not seen in WI-38 cells, a human normal fibroblast cell line. Analysis of incorporation of radiolabeled fatty acids revealed a marked accumulation of triglycerides in AJA-treated cells at concentrations that produced tumor growth inhibition. Finally, AJA, administered p.o. to nude mice at a dosage several orders of magnitude below that which produces toxicity, inhibited the growth of subcutaneously implanted U87 human glioma cells modestly but significantly.

We conclude that AJA acts to produce significant antitumor activity and effects its actions primarily via CB(2) receptors. Its very favorable toxicity profile, including lack of psychoactivity, makes it suitable for chronic usage. Further studies are warranted to determine its optimal role as an antitumor agent.

PMID: 11551521
Biochem J 2001 Aug 15;358(Pt 1):249-55