BenBurch
Gatekeeper of The Left
One problem with getting old is that I couldn't connect with any even if I wanted to. I know literally nobody who could connect me any more.
Bill Gates, Larry Ellison and Steven Jobs allegedly smoked weed back in the seventies.
Sometimes I wonder if they made anything of their lives. I'll have a look if they're on Facebook and see what I can find out.
, but as we've mentioned several times, it was much milder then.
Heavy Marijuana Use Doesn't Damage Brain
Analysis of Studies Finds Little Effect From Long-Term Use
By Sid Kirchheimer
WebMD Health News
July 1, 2003 -- Long-term and even daily marijuana use doesn't appear to cause permanent brain damage, adding to evidence that it can be a safe and effective treatment for a wide range of diseases, say researchers.
The researchers found only a "very small" impairment in memory and learning among long-term marijuana users. Otherwise, scores on thinking tests were similar to those who don't smoke marijuana, according to a new analysis of 15 previous studies.
Cannabis and the brain
Leslie Iversen
Central effects of cannabinoids include disruption of psychomotor behaviour, short‐term memory impairment, intoxication, stimulation of appetite, antinociceptive actions (particularly against pain of neuropathic origin) and anti‐emetic effects. Although there are signs of mild cognitive impairment in chronic cannabis users there is little evidence that such impairments are irreversible, or that they are accompanied by drug‐induced neuropathology.
And I fail to see how the difference changes that quote, the effect is the same, people just smoke much less for the same desired effect.
Could we please get back to scientific evidence on this thread?
I'm a bit upset that this thread has turned into a discussion of legal-illegal arguments. My main idea on this Science board was to discuss the evidence about brain damage; [...]
[...] I think that I might have introduced legal issues unintentionally by pasting a post from the Social Issues board as my OP (where I opined about what colleges might do to curtail MJ use by students who were wasting private or public money, and possibly contributing to the drug-infused violence in Mexico).
Could we please get back to scientific evidence on this thread?
, but as we've mentioned several times, it was much milder then.
Do you realise you have a psychedelic plant in your avatar?![]()
BTW, Halfcentaur; how do we know that Steve Jobs' pancreatic cancer wasn't caused by smoking MJ back in the 70s?![]()
It's not Morning Glory, it's Bower Vine, (they look similar) which as far as I know, does not have psychedelic properties.
Thank you for all your responses everyone, and attempts to allay my fears about super-weed causing mental illness. The scientific evidence seems inconclusive at this stage, which I think is due to the difficulty of isolating MJ use from other factors, such as pre-disposition and use of other drugs or alcohol.
So until science can devise a better method of reaching the truth, I think I will simply stick with my intuition, which informs me that there is a price to pay for disrupting the body's natural functions which have taken billions of years to evolve.
BTW, Halfcentaur; how do we know that Steve Jobs' pancreatic cancer wasn't caused by smoking MJ back in the 70s?![]()
It's not Morning Glory, it's Bower Vine, [...]
So until science can devise a better method of reaching the truth, I think I will simply stick with my intuition, which informs me [...]
Uh sure, give me the genera and species name would you? It is not pandorea jasminoides, pandorea pandorana, nor the other top five called 'bower vine'. It sure looks like a convolvulaceae.It's not Morning Glory, it's Bower Vine, (they look similar) which as far as I know, does not have psychedelic properties.
No it is not, whether you want to believe it or not there is no increase in mental illness due to marijuana use.Thank you for all your responses everyone, and attempts to allay my fears about super-weed causing mental illness. The scientific evidence seems inconclusive at this stage, which I think is due to the difficulty of isolating MJ use from other factors, such as pre-disposition and use of other drugs or alcohol.
Nope the problem is you do not want to read the data of the extensive epidemiology on the subject.So until science can devise a better method of reaching the truth, I think I will simply stick with my intuition, which informs me that there is a price to pay for disrupting the body's natural functions which have taken billions of years to evolve.
BTW, Halfcentaur; how do we know that Steve Jobs' pancreatic cancer wasn't caused by smoking MJ back in the 70s?![]()
BTW, Halfcentaur; how do we know that Steve Jobs' pancreatic cancer wasn't caused by smoking MJ back in the 70s?![]()
Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells
María Salazar1,2, Arkaitz Carracedo1, Íñigo J. Salanueva1, Sonia Hernández-Tiedra1, Mar Lorente1,2, Ainara Egia1, Patricia Vázquez3, Cristina Blázquez1,2, Sofía Torres1, Stephane García4, Jonathan Nowak4, Gian María Fimia5, Mauro Piacentini5, Francesco Cecconi6, Pier Paolo Pandolfi7, Luis González-Feria8, Juan L. Iovanna4, Manuel Guzmán1,2, Patricia Boya3 and Guillermo Velasco1,2
First published April 1, 2009
Received for publication November 3, 2008, and accepted in revised form February 11, 2009.
Autophagy can promote cell survival or cell death, but the molecular basis underlying its dual role in cancer remains obscure. Here we demonstrate that Δ9-tetrahydrocannabinol (THC), the main active component of marijuana, induces human glioma cell death through stimulation of autophagy. Our data indicate that THC induced ceramide accumulation and eukaryotic translation initiation factor 2α (eIF2α) phosphorylation and thereby activated an ER stress response that promoted autophagy via tribbles homolog 3–dependent (TRB3-dependent) inhibition of the Akt/mammalian target of rapamycin complex 1 (mTORC1) axis. We also showed that autophagy is upstream of apoptosis in cannabinoid-induced human and mouse cancer cell death and that activation of this pathway was necessary for the antitumor action of cannabinoids in vivo. These findings describe a mechanism by which THC can promote the autophagic death of human and mouse cancer cells and provide evidence that cannabinoid administration may be an effective therapeutic strategy for targeting human cancers.
http://cancerres.aacrjournals.org/content/66/13/6748.abstractCannabinoids Induce Apoptosis of Pancreatic Tumor Cells via Endoplasmic Reticulum Stress–Related Genes
Pancreatic adenocarcinomas are among the most malignant forms of cancer and, therefore, it is of especial interest to set new strategies aimed at improving the prognostic of this deadly disease. The present study was undertaken to investigate the action of cannabinoids, a new family of potential antitumoral agents, in pancreatic cancer. We show that cannabinoid receptors are expressed in human pancreatic tumor cell lines and tumor biopsies at much higher levels than in normal pancreatic tissue. Studies conducted with MiaPaCa2 and Panc1 cell lines showed that cannabinoid administration (a) induced apoptosis, (b) increased ceramide levels, and (c) up-regulated mRNA levels of the stress protein p8. These effects were prevented by blockade of the CB2 cannabinoid receptor or by pharmacologic inhibition of ceramide synthesis de novo. Knockdown experiments using selective small interfering RNAs showed the involvement of p8 via its downstream endoplasmic reticulum stress–related targets activating transcription factor 4 (ATF-4) and TRB3 in Δ9-tetrahydrocannabinol–induced apoptosis. Cannabinoids also reduced the growth of tumor cells in two animal models of pancreatic cancer. In addition, cannabinoid treatment inhibited the spreading of pancreatic tumor cells. Moreover, cannabinoid administration selectively increased apoptosis and TRB3 expression in pancreatic tumor cells but not in normal tissue. In conclusion, results presented here show that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB2 receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress–related genes ATF-4 and TRB3. These findings may contribute to set the basis for a new therapeutic approach for the treatment of pancreatic cancer. (Cancer Res 2006; 66(13): 6748-55)
http://www.jci.org/articles/view/37948 and Emet:
Cannabinoids Induce Apoptosis of Pancreatic Tumor Cells via Endoplasmic Reticulum Stress–Related Genes
Pancreatic adenocarcinomas are among the most malignant forms of cancer and, therefore, it is of especial interest to set new strategies aimed at improving the prognostic of this deadly disease. The present study was undertaken to investigate the action of cannabinoids, a new family of potential antitumoral agents, in pancreatic cancer. We show that cannabinoid receptors are expressed in human pancreatic tumor cell lines and tumor biopsies at much higher levels than in normal pancreatic tissue. Studies conducted with MiaPaCa2 and Panc1 cell lines showed that cannabinoid administration (a) induced apoptosis, (b) increased ceramide levels, and (c) up-regulated mRNA levels of the stress protein p8. These effects were prevented by blockade of the CB2 cannabinoid receptor or by pharmacologic inhibition of ceramide synthesis de novo. Knockdown experiments using selective small interfering RNAs showed the involvement of p8 via its downstream endoplasmic reticulum stress–related targets activating transcription factor 4 (ATF-4) and TRB3 in Δ9-tetrahydrocannabinol–induced apoptosis. Cannabinoids also reduced the growth of tumor cells in two animal models of pancreatic cancer. In addition, cannabinoid treatment inhibited the spreading of pancreatic tumor cells. Moreover, cannabinoid administration selectively increased apoptosis and TRB3 expression in pancreatic tumor cells but not in normal tissue. In conclusion, results presented here show that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB2 receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress–related genes ATF-4 and TRB3. These findings may contribute to set the basis for a new therapeutic approach for the treatment of pancreatic cancer. (Cancer Res 2006; 66(13): 6748-55)
The Bower Vine pictured in my avatar was bought from Home Depot a few years ago, clearly labelled, and is now growing in my garden. It is a perennial, as opposed to Morning Glory which is an annual plant, dying off in the winter.