Cannabinoid Education

[EDDIEKIRK]

[Vapeit]

Based on this list alone, I would have to choose a strain with the following:



Cannabidiol - 30%

Tetrahydrocannabivarin - 20%

Cannabinol - 20%

Tetrahydrocannabinol - 20%

Cannabichromene - 5%

Cannabigerol - 5%



Gosh I guess this means I'm gonna HAVE to learn something about breeding and testing genetics!

[PiranhasKushBreath]

Based on this list alone, I would have to choose a strain with the following:



Cannabidiol - 30%

Tetrahydrocannabivarin - 20%

Cannabinol - 20%

Tetrahydrocannabinol - 20%

Cannabichromene - 5%

Cannabigerol - 5%



Gosh I guess this means I'm gonna HAVE to learn something about breeding and testing genetics!

There is a company in Portland, Oregon that will test the cannabinoid content of your medicine

[eloquentsolution]

there are more then one.

<blockquote data-ipsquote="" class="ipsQuote" data-ipsquote-contentcommentid="35704" data-ipsquote-contentapp="forums" data-ipsquote-contenttype="forums" data-ipsquote-contentclass="forums_Topic" data-ipsquote-contentid="4459" data-ipsquote-username="Vapeit" data-cite="Vapeit" data-ipsquote-timestamp="1348254600"><div>Based on this list alone, I would have to choose a strain with the following:

Cannabidiol - 30%
Tetrahydrocannabivarin - 20%
Cannabinol - 20%
Tetrahydrocannabinol - 20%
Cannabichromene - 5%
Cannabigerol - 5%

Gosh I guess this means I'm gonna HAVE to learn something about breeding and testing genetics!

There is a company in Portland, Oregon that will test the cannabinoid content of your medicine



</div></blockquote>


skunk pharm believes a more efficient approach is to extract the oil, fractionate the cannabinoids and add them back together in the desired ratios.

[Vapeit]

Thank you both for the info...now all I have to do is figure out a way to get out there lol.

[EDDIEKIRK]

[PiranhasKushBreath]

there are more then one.

Are there in in Benton County you know of?

[drayco_]

http://www.cancer.gov/cancertopics/pdq/c...onal/page4







Cannabinoids
are a group of 21-carboncontaining terpenophenolic
compounds
produced uniquely by
Cannabis
sativaandCannabis indicaspecies.[
1
,
2
] These plant-derived compounds may be referred to as phytocannabinoids. Although delta-9-tetrahydrocannabinol (THC) is the primary psychoactive ingredient, other known compounds with biologic activity are cannabinol, cannabidiol (CBD), cannabichromene, cannabigerol, tetrahydrocannabivarin, and delta-8-THC. CBD, in particular, is thought to have
significant

analgesic
and
anti-inflammatory
activity without the psychoactive effect (high) of delta-9-THC.






Anti-tumor Effects




One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of
tumors
.[
3
] During this 2-year study, groups of mice and rats were given various
doses
of THC by
gavage
. A dose-related decrease in the
incidence
of
hepatic

adenoma
tumors and
hepatocellular carcinoma
was observed in the mice. Decreased incidences of
benign tumors
(
polyps
and adenomas) in other
organs

(mammary gland
,
uterus
, pituitary,
testis
, and
pancreas
) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis
lung

adenocarcinoma

cells

in vitro
and
in vivo
.[
4
] In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.[
5
-
8
]


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
] One review summarizes the molecular mechanisms of action of cannabinoids as antitumor agents.[
13
] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. These compounds have been shown to induce
apoptosis
in
glioma
cells in
culture
and induce
regression
of glioma tumors in mice and rats. Cannabinoids protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1
receptor
.[
14
]


The effects of delta-9-THC and a
synthetic
agonist of the CB2 receptor were investigated in hepatocellular carcinoma (HCC).[
15
] Both agents reduced the viability of hepatocellular carcinoma cellsin vitroand demonstrated antitumor effects in hepatocellular carcinoma 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
[
16
] and breast cancer.[
17
]




Anin vitrostudy 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. CBD inhibited the survival of both
estrogen receptorpositive
and
estrogen receptornegative

breast cancer
cell lines
, inducing apoptosis in a concentration-dependent manner while having little effect on nontumorigenic,
mammary
cells.[
18
]


CBD has also been demonstrated to exert a
chemopreventive
effect in a
mouse model
of
colon cancer
.[
19
] In the
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. Inin vitroexperiments involving
colorectal cancer
cell lines, the investigators found that CBD protected
DNA
from oxidative damage, increased endocannabinoid levels, and reduced
cell proliferation
.


Another investigation into the antitumor effects of CBD examined the role of intercellular adhesion molecule-1 (ICAM-1).[
12
] ICAM-1 expression has been reported to be negatively correlated with cancer
metastasis.
In
lung cancer
cell lines, CBD upregulated ICAM-1, leading to decreased cancer cell invasiveness.


In anin vivomodel using severe combined immunodeficient mice,
subcutaneous
tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines.[
20
] Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had
antiangiogenic
and antiproliferative effects. However, research with immunocompetent murine tumor models has demonstrated immunosuppression and enhanced tumor growth in mice treated with THC.[
21
,
22
]


In addition, both plant-derived and
endogenous
cannabinoids have been studied for anti-
inflammatory
effects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic
inflammation
.[
23
] As a result, a
hypothesis
that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of
colorectal cancer
has been developed.[
24
-
27
]





Appetite Stimulation




Many
animal studies
have previously demonstrated that delta-9-THC and other cannabinoids have a stimulatory effect on
appetite
and increase food intake. It is believed that the endogenous cannabinoid system may serve as a regulator of feeding behavior. The endogenous cannabinoid anandamide potently enhances appetite in mice.[
28
] Moreover, CB1
receptors
in the
hypothalamus
may be involved in the motivational or reward aspects of eating.[
29
]


Analgesia


Understanding the mechanism of cannabinoid-induced
analgesia
has been increased through the study of cannabinoid receptors, endocannabinoids, and
synthetic
agonists and antagonists. The CB1 receptor is found in both the
central nervous system
(CNS) and in peripheral
nerve
terminals. Similar to
opioid
receptors, increased levels of the CB1 receptor are found in regions of the brain that regulate nociceptive processing.[
30
] CB2 receptors, located predominantly in peripheral
tissue
, exist at very low levels in the CNS. With the development of receptor-specific antagonists, additional information about the roles of the receptors and endogenous cannabinoids in the modulation of pain has been obtained.[
31
,
32
]




Cannabinoids may also contribute to pain modulation through an anti-inflammatory mechanism; a CB2 effect with cannabinoids acting on
mast cell
receptors to attenuate the release of inflammatory agents, such as
histamine
and
serotonin
, and on keratinocytes to enhance the release of analgesic
opioids
has been described.[
33
-
35
] One study reported that the efficacy of synthetic CB1- and CB2-receptor agonists were comparable with the efficacy of morphine in a murine model of tumor pain.[
36
]