THC Cannabinoid In Marijuana

Discussion in 'Medicinal Marijuana' started by ScrogBetty, Jun 7, 2012.

  1. ScrogBetty

    ScrogBetty Admin Staff Member

    Tetrahydrocannabinol – or what most medical marijuana patients commonly call THC, is mixture over 80 different cannabinoids (THC, CBD, CBG, CBC, CBGa, CGCa, THCa, CBDa ...etc). THC is primarily known as the highly sought after psychoactive compound in the marijuana plant that you find on your shelves at your collectives today.
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    A High THC% is primarily the byproduct of well a grown marijuana plant - that produces rich colas, heavy and resinous, with fat swollen glandular trichomes. The male plant of the marijuana species is considered to be useless; from a getting “high” standpoint, as it's THC content is far below that of its female counterparts. Other important items of note, when you do notice males within your cultivated area, one must make sure to eliminate their presence long before they have dropped their pollen sacs. Or else you will have pollinated flower which obviously leads to a seed rich crop, and no one wants that.

    The sticky and resinous pistils are more correctly known as Trichomes, and the risen rich glands often tend to develop on the flower, at its height of budding, just before harvest. As the marijuana plant progresses throughout its development cycle, in either your indoor grow room, or towards November, if you're outdoors. The pistils and glands swell with resin and stored water, as the stored nutrient rich water converts and develops into THC glands –these THC glands under close microscopic observation tend to resemble the human brain receptors.
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    Primarily - THC is found within the Cannabis Indica strains and Cannabis Sativa strains. There is an additional strain of cannabis, the once thought to be “blacksheep” of the cannabis family… you know, useless. Cannabis ruderalis contains next to no THC, thereby making it useless for any medicinal application. That being said cannabis ruderalis is an extremely hardy and fast growing , low grade marijuana plant, that can flourish in the toughest of soil conditions, much better than her cousins cannabis indica, or cannabis sativa. It is just because of this hardiness that many subtropical marijuana growers in arid regions often prefer to crossbreed their higher THC cannabis Indica, with the lower percentage THC cannabis ruderalis in order to create a durable, drought resistant, genetic strain with a relatively high THC content.
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    The THC content in cannabis Indica tends to be extremely high; as that is what this strain was genetically bred for. The plants themselves are relatively stocky in nature. A short, stout, bush with wide, deep green leafs. Under normal conditions, your average Indica marijuana plant will finish flowering within eight - ten weeks of the first sign of its sex (I like to switch nutes: from grow to flower July 1). At completion of flowering, provided it has been properly feed and been given all of the needed micro nutrients it desires, you should end up with sticky dense bud and a very favorable you yield.
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    That Indica “elevation” is a much more physical high, than a cerebral state of mind. Which is to say that, the Indica THC content is wonderful for reducing stress in those moments during your day when you just need to take a timeout. The THC content and Indica is also used as a wonderful means of mitigating those daily aches and pains in the lower back, knees and hips. While some might complain that these strains are too heavy and leaves you glued to the yoga mat, I personally find it to be one that lifts the mind to the heavens.
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    Sativa tends to be a gentler and less potent THC content. The THC percentage in today's average sativa flower, which we find on the many of the dispensary shelves in California today, is guaranteed to be an elevating and energetic high. I tend to refer to see you Sativa as a “working man's” strain, as it allows me to be creative while still being productive. When I become mentally locked up and struggle for ideas - if allowed, stepping out and medicating for just a few minutes with a nice N.Y. City Diesel strain; I can feel the mental damn break, as the ideas begin to flow back into the conscious mind.
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  2. Xander420

    Xander420 New Member

    Great post!
     
    2 people like this.
  3. Steve Cool

    Steve Cool Tokemaster General Staff Member

    Cannabinoids are a group of 21-carbon–containing terpenophenolic compounds produced uniquely by Cannabis sativa and Cannabis indica species.[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.

    Antitumor 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 (HCC) 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 HCC.[15] Both agents reduced the viability of HCC cells in vitro and demonstrated antitumor effects in HCC 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]

    An in vitro study 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 receptor–positive and estrogen receptor–negative 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. 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.

    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 an in vivo model 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]

    CBD may also enhance uptake of cytotoxic drugs into malignant cells. Activation of the transient receptor potential vanilloid type 2 (TRPV2) has been shown to inhibit proliferation of human glioblastoma multiforme cells and overcome resistance to the chemotherapy agent carmustine.[28] In an in vitro model, CBD increased TRPV2 activation and increased uptake of cytotoxic drugs, leading to apoptosis of glioma cells without affecting normal human astrocytes. This suggests that coadministration of CBD with cytotoxic agents may increase drug uptake and potentiate cell death in human glioma cells.

    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.[29] Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.[30]

    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.[31] 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.[32,33]

    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.[34-36] 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.

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