No
strict, product-specific studies are yet available for MED
MARIJUANA™ products. To present background
information on the health benefits of our Cannabis
Sativa supplements, we are pleased to make
available to the public a sampling of the reference material
compiled by MED MARIJUANA™
on the health benefits of low-THC Cannabis and the component
make-up of their oils.
For
a complete review of the available literature please CONTACT
us to arrange a personal information session with
one of our local distributors.
1.
Positive effects of low-THC Cannabis oil on Rheumatoid Arthritis
One of the primary components of our oil is Gamma-Linolenic
Acid(GLA). GLA is an essential building block of
life and is not easily found in nature. In addition to our oils
it is found from two other plant sources but in one of those sources
the amount of GLA found would require the daily ingestion of gallons
of the plant oil to achieve an effective supplementation level.
The other source has toxic components bound to the GLA, preventing
adequate ingestion levels without poisoning the entire body.
MED MARIJUANA™ select their Cannabis
plant stock for high GLA production levels; grow their
plants in an environment which will allow the plants to fully
develop their GLA potential and process the plants in a manner
to best preserve these delicate properties.
This medical report is one small example of the positive Natural
Health Benefits to be found in MED
MARIJUANA™ products.
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
MED
MARIJUANA™ Cannabis Sativa Oils
contain the complete Omega profile in a balanced blend to perfectly
meet our body’s needs and uptake abilities.
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
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 matter 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
extracts containing no THC whatsoever, as well had anti-tumor
effects, which as you may read, they do.
By
presenting this information we are in no way claiming that MED
MARIJUANA™ products will have the same benefits.
No one knows. Research into that field has just begun and will
carry on for many years to come. This information is presented
to highlight the fact that Cannabis
Sativa , whether full-strength THC or low-THC
such as MED MARIJUANA™
is, has a multitude of health uses which have not yet been fully
researched and documented.
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
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