smokinheavy79
New Member
you need to go by the trichs not the pistils. if they are cloudy it will be a good heady high, if they are like 30-35% its more body, couchlock
*true, you'll find Ed stating that in his book(s).. but he didnt do the research that led to that scientific tid-bit ..terpenes-flavanoids-bioflavanoids-etc-unknown-etc, so much more left to discoverI have read that Ed Rosenthal recently has claimed that terpenes, the stuff responsible for the smell and taste, may also play a role in the quality and type of high.
yeah, theres SO MUCH stuff in cannabis. we are only beginning to discover things about it. imagine when we know about every cannabanoid, and what it does to the body in relation to others. THC by itself will make you go crazy, but combined with CBD and some CBN, u feel good. so those other cannabanoids may have special abilities when combined with other cannabanoids, or other substances, at ratios that are not naturally found in the plant. there may be advantages to cannabanoids that the plant could never(very unlikely) produce*true, you'll find Ed stating that in his book(s).. but he didnt do the research that led to that scientific tid-bit ..terpenes-flavanoids-bioflavanoids-etc-unknown-etc, so much more left to discover
--cheers
that is useful. thanks.
During the later stages, when flower production has slowed, THC is degrading to other related chemicals such as CBD.
what is cbd?
No, if you see those colors you have waited to long to harvest and have lost THC allowing it to degrade into mildly psychoactive CBN, the primary waste product of oxidized THC.u can also look through a microscope an if ur crystals have a brown or tan tint to it or if they are brown or tan then ur shit is ready to be dryed out an cured.THEN U ENJOY.
That is an old out of date incorrect trichome color chart made when less was known about cannabinoids and peak potency levels.is it just me or is that 50/50 pic lacking half amber?
THC by itself will make you go crazy, but combined with CBD and some CBN, u feel good.
I have read that Ed Rosenthal recently has claimed that terpenes, the stuff responsible for the smell and taste, may also play a role in the quality and type of high.
From Amazon - $39.95 Veho VMS-001 x20-x200 Magnification Discovery Digital USB Microscope with Alloy StandHairs can be bad indicators. Some turn early, some never turn and a lot depends on the strain. The radio shack scope for trichs is a bit of a pain, but a better read then hairs. Those USB scopes have come down in price ($35-$40). I'm eager to try one.
This is true for smokers. I'm not a real smoker. Just when I need to sleep. For my pain I want CBD's I want the earthy feel of my body the slight mesmerizing feel as I walk around but don't want the couch lock. I hate feeling stupid. There is so much more to this plant then studied. It's the stoners that say THC is all they want and that gives us med pat. A bad name. We need more real studies on other things then THC and CBD. How about CBA CBC CBN and the mixture of the noids within the plant we call weed?I feel like this CBD vs THC argument goes to far, I mean if you want to get couch locked pick a strain that does that and let it get ripe. If you want a clear head high get a strain that does that and let it get ripe. I guess if you only have one strain it could make sense to harvest at different times so you can have slightly different batches but I would rather just get another strain for my desired effects.
For me its pretty simple , you would only ever pick ripe fruits , so same applies to weedAntitumor Effects
One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors. 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.
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. One review summarizes the molecular mechanisms of action of cannabinoids as antitumor agents. 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 gliomacells 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.
The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in HCC. 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 and breast cancer.
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 receptorpositive and estrogen receptornegative breast cancercell lines, inducing apoptosis in a concentration-dependent manner while having little effect on nontumorigenic, mammary cells.
CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer. 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). ICAM-1 expression has been reported to be negatively correlated with cancermetastasis. 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.
In addition, both plant-derived and endogenous cannabinoids have been studied for anti-inflammatoryeffects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation. As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of colorectal cancer has been developed.
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. 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.