Cannabis research, medicine and use

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Postby Pele'sDaughter » Tue Aug 18, 2009 7:48 pm

Cannabis may prevent osteoporosis

Researchers looking at the effects of cannabis on bones have found its impact varies dramatically with age.

The study found that while the drug may reduce bone strength in the young, it could protect against osteoporosis, a weakening of the bones, in later life.

The results were uncovered by a team at the University of Edinburgh who compared the drug's effects on mice.

Osteoporosis affects up to 30% of women and about 12% of men at some point in their lives.

The group found that cannabis can activate a molecule found naturally in the body that is key to the development of osteoporosis.

When the type 1 cannabinoid receptor (CB1) comes into contact with cannabis, it has an impact on bone regeneration.

However, until now, it was not clear whether the drug had a positive or negative effect.

'Early results'

Researchers, funded by the Arthritis Research Campaign, investigated this using mice which lacked the CB1 receptor.

The scientists then used compounds - similar to those in cannabis - that activated the CB1 receptor.

They found that compounds increased the rate at which bone tissue was destroyed in the young.

Despite this, the study also showed that the same compounds decreased bone loss in older mice and prevented the accumulation of fat in the bones, which is known to occur in humans with osteoporosis.

Stuart Ralston, the Arthritis Research Campaign Professor of Rheumatology at the University of Edinburgh, who led the study, said: "This is an exciting step forward, but we must recognise that these are early results and more tests are needed on the effects of cannabis in humans to determine how the effects differ with age in people.

"We plan to conduct further trials soon and hope the results will help to deliver new treatments that will be of value in the fight against osteoporosis."

The results are published in Cell Metabolism.

http://tinyurl.com/lu36na
(BBC News)
Don't believe anything they say.
And at the same time,
Don't believe that they say anything without a reason.
---Immanuel Kant
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Postby Penguin » Sun Aug 23, 2009 5:30 am

seemslikeadream wrote:Cannabis chemicals may help fight prostate cancer
Wed Aug 19, 2009
By Ben Hirschler

LONDON (Reuters) - Chemicals in cannabis have been found to stop prostate cancer cells from growing in the laboratory, suggesting that cannabis-based medicines could one day help fight the disease, scientists said Wednesday.

After working initially with human cancer cell lines, Ines Diaz-Laviada and colleagues from the University of Alcala in Madrid also tested one compound on mice and discovered it produced a significant reduction in tumor growth.

Their research, published in the British Journal of Cancer, underlines the growing interest in the medical use of active chemicals called cannabinoids, which are found in marijuana.

Experts, however, stressed that the research was still exploratory and many more years of testing would be needed to work out how to apply the findings to the treatment of cancer in humans.

"This is interesting research which opens a new avenue to explore potential drug targets but it is at a very early stage," said Lesley Walker, director of cancer information at Cancer Research UK, which owns the journal.

"It absolutely isn't the case that men might be able to fight prostate cancer by smoking cannabis," she added

The cannabinoids tested by the Spanish team are thought to work against prostate cancer because they block a receptor, or molecular doorway, on the surface of tumour cells. This stops them from dividing.

In effect, the cancer cell receptors can recognize and "talk to" chemicals found in cannabis, said Diaz-Laviada.

"These chemicals can stop the division and growth of prostate cancer cells and could become a target for new research into potential drugs to treat prostate cancer," she said.

Her team's work with two cannabinoids -- called methanandamide and JWH-015 -- is the first demonstration that such cannabis chemicals prevent cancer cells from multiplying.

Some drug companies are already exploring the possibilities of cannabinoids in cancer, including British-based cannabis medicine specialist GW Pharmaceuticals.

It is collaborating with Japan's Otsuka on early-stage research into using cannabis extracts to tackle prostate cancer -- the most commonly diagnosed cancer in men -- as well as breast and brain cancer.

GW has already developed an under-the-tongue spray called Sativex for the relief of some of the symptoms of multiple sclerosis, which it plans to market in Europe with Bayer and Almirall.

Other attempts to exploit the cannibinoid system have met with mixed success. Sanofi-Aventis was forced to withdraw its weight-loss drug Acomplia from the market last year because of links to mental disorders.
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Pregnancy and tobacco, alcohol, cannabis use

Postby Penguin » Wed Oct 21, 2009 5:21 am

New research from University of Cardiff, UK -
Maternal use of tobacco, alcohol and cannabis and their associated effects on the mental health of the baby.

http://bjp.rcpsych.org/cgi/content/abstract/195/4/294
Maternal tobacco, cannabis and alcohol use during pregnancy and risk of adolescent psychotic symptoms in offspring

Background

Adverse effects of maternal substance use during pregnancy on fetal development may increase risk of psychopathology.

Aims

To examine whether maternal use of tobacco, cannabis or alcohol during pregnancy increases risk of offspring psychotic symptoms.

Method

A longitudinal study of 6356 adolescents, age 12, who completed a semi-structured interview for psychotic symptoms in the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort.

Results

Frequency of maternal tobacco use during pregnancy was associated with increased risk of suspected or definite psychotic symptoms (adjusted odds ratio 1.20, 95% CI 1.05–1.37, P = 0.007). Maternal alcohol use showed a non-linear association with psychotic symptoms, with this effect almost exclusively in the offspring of women drinking >21 units weekly. Maternal cannabis use was not associated with psychotic symptoms. Results for paternal smoking during pregnancy and maternal smoking post-pregnancy lend some support for a causal effect of tobacco exposure in utero on development of psychotic experiences.

Conclusions

These findings indicate that risk factors for development of non-clinical psychotic experiences may operate during early development. Future studies of how in utero exposure to tobacco affects cerebral development and function may lead to increased understanding of the pathogenesis of psychotic phenomena.


Full text here:
http://bjp.rcpsych.org/cgi/content/full/195/4/294
PDF: http://bjp.rcpsych.org/cgi/reprint/195/4/294

There were 734 children (11.6% of those interviewed, 95% CI 10.8–12.4%) who were rated as having suspected or definite PILKS, and 300 of these (4.7% of those interviewed) had definite symptoms. A summary of the potential confounders in relation to maternal substance use is presented in Table 1. Individually adjusting for gender, other family history of mental health illness and paternal age made minimal difference to any of the results and these were therefore omitted from the analyses.

Table 1 Descriptive summary of confounders in relation to maternal substance use during pregnancya

Of the children interviewed for PLIKS, there were 6332 with maternal smoking data, 6210 with maternal cannabis use data, and 6245 with maternal alcohol data available. Of these, 1219 (19.3%) of mothers smoked tobacco, 4372 (70.0%) of mothers drank alcohol, and 157 (2.5%) of mothers took cannabis at least once during their pregnancy. There were 4253 adolescents with data available on PLIKS, confounders, and maternal use of tobacco, cannabis and alcohol, and this was the sample used for the main analyses.

Tobacco use during pregnancy
Maternal tobacco use during pregnancy was strongly associated with any suspected or definite PLIKS in the offspring (crude OR for linear trend across four smoking categories 1.33, 95% CI 1.18–1.49), and results were consistent with a dose–response effect (Table 2). This was attenuated only partially after adjusting for confounders (adjusted OR = 1.20, 95% CI 1.05–1.37, P = 0.007). The two confounders that had the greatest effect on attenuating this estimate were paternal smoking and single status of the mother. Further adjusting for gestation, birth weight, 5-minute Apgar score, or age 8 IQ score, as possible mediators for this association, had minimal effects on these results. These estimates were similar for definite PLIKS as an outcome although results were less precise.

Table 2 Crude and adjusteda odds ratios (OR) and 95% CI for psychosis-like symptoms (PLIKS) by maternal substance use during pregnancy

We further examined possible effects of confounding by studying the effects of paternal smoking during pregnancy and maternal smoking post-pregnancy on risk of PLIKS, to compare these with the effect of maternal smoking during pregnancy (Table 3). Paternal smoking during pregnancy was associated with any suspected or definite PLIKS in the crude analysis, but this was eliminated after adjusting for confounders and maternal smoking (adjusted OR = 1.05, 95% CI 0.95–1.17).

Table 3 Crude and adjusted odds ratios (OR) and 95% CI for any suspected or definite psychosis-like symptoms (PLIKS) in relation to parental tobacco use within and outside the pregnancy period (linear trend across four smoking categories)

Maternal smoking post-pregnancy was also associated with any suspected or definite PLIKS in the crude analysis (Table 3), but again this was eliminated after adjusting for confounders and maternal smoking during pregnancy (adjusted OR = 0.95, 95% CI 0.79–1.14). Maternal smoking during pregnancy and maternal smoking post-pregnancy were quite strongly correlated (Kendall’s {tau}b = 0.76). The standard error for maternal smoking during pregnancy was increased by about 60% when both were included in the same model (Table 3), but that for maternal smoking post-pregnancy was relatively unchanged, indicating that collinearity is unlikely to explain the lack of association for smoking post-pregnancy.32 Note that only 3730 of the 4253 adolescents had additional data on maternal smoking post-pregnancy and therefore results for maternal smoking during pregnancy in Tables 2 and 3 are slightly different as they are based on different data-sets.

We examined whether the effect of maternal tobacco use differed by trimester of exposure. Smoking during any trimester was very correlated with smoking in other trimesters (Kendall’s {tau}b>0.80). The offspring of mothers who used tobacco only in their third trimester had a greater risk of developing any suspected or definite PLIKS than offspring whose mothers smoked only in the first trimester (OR for smoking in third trimester only compared with first trimester only 2.1, 95% CI 0.96–4.59, P = 0.063). There were insufficient numbers of women who only used tobacco in their second trimester to examine specific second trimester effects.

Cannabis use during pregnancy
Maternal cannabis use was not associated with any suspected or definite PLIKS in the crude analysis (OR for linear trend 1.22, 95% CI 0.83–1.79). The odds ratio was reduced after adjusting for confounders (Table 2), with adjustment for maternal tobacco use having the greatest impact on attenuation of this estimate (adjusted OR = 0.94, 95% CI 0.62–1.41, P = 0.755). Of the 157 women with PLIKS data who used cannabis during pregnancy, 51 (32.5%) claimed not to have smoked tobacco during their pregnancy. There were insufficient numbers of women using cannabis to examine trimester-specific effects of cannabis use.

Alcohol use during pregnancy
Although 70% of mothers drank alcohol at least once during their pregnancy, the median number of units of alcohol per week consumed was 0 (range 0 to 102). There was an association between maternal alcohol intake during pregnancy and any suspected or definite PLIKS in the crude analysis (OR per 10-unit increase in alcohol 1.24, 95% CI 1.03–1.50), and this was not substantially altered after adjustment (adjusted OR per 10 units 1.19, 95% CI 0.97–1.45). This was a non-linear effect (likelihood ratio for inclusion of quadratic term in crude model {chi}2 = 7.5, d.f. = 1, P = 0.006). Likelihood ratio test results for the overall effect of alcohol on risk of PLIKS are presented in Table 2. Further adjusting for possible mediators of this association had minimal effects on these results.

The increase in risk of suspected or definite PLIKS was primarily present in the offspring of the 25 mothers (0.6% of the sample) who drank >21 units per week. When omitting this extreme group, as a sensitivity analysis, there was no evidence of a non-linear relationship ({chi}2 = 0.3, d.f. = 1, P = 0.566) and no evidence of association between alcohol use and PLIKS (adjusted OR per 10 units 0.97, 95% CI 0.72–1.31) (Table 2).

We also examined trimester-specific effects of maternal alcohol use. Alcohol intake during the first and third trimesters were correlated, although insufficiently to render collinearity a problem in an analysis with both included in the same model (Pearson’s coefficient 0.54). Within such a model, first trimester alcohol use (adjusted OR per 10 units 1.41, 95% CI 0.95–2.09) but not third trimester use (adjusted OR per 10 units 0.99, 95% CI 0.63–1.55) was associated with increased risk of PLIKS, although the confidence intervals overlapped substantially.

We further examined possible effects of confounding by studying the effects of maternal alcohol use 4 years post-pregnancy on risk of PLIKS in the offspring. The correlation between alcohol use during and post-pregnancy was not very strong (Pearson’s coefficient 0.29). There was no evidence of any association between maternal alcohol use post-pregnancy and any suspected or definite PLIKS either before or after adjusting for alcohol use during pregnancy (LRT for both linear and quadratic terms, {chi}2 = 4.0, d.f. = 2, P = 0.139).

Secondary analyses
There were 165 children (2.6% of those interviewed) with definite, frequent (occurring ≥monthly) PLIKS, and 233 (3.6%) with suspected or definite ‘bizarre’ PILKS. There was no consistent pattern that associations were stronger for either of these outcomes.

Missing data
Results from the multivariable multiple-imputation models were very similar to those using the main data-set, although more precisely estimated, whether we imputed confounders only or outcome measures too.

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Carl Sagans essay on cannabis

Postby Penguin » Wed Oct 21, 2009 5:24 am

Carl Sagan wrote this essay under pseudonym Mr X - after his passing, his identity was revealed according to the wishes of late mr. Sagan,

http://marijuana-uses.com/essays/002.html

This account was written in 1969 for publication in Marihuana Reconsidered (1971). Sagan was in his mid-thirties at that time. He continued to use cannabis for the rest of his life.

It all began about ten years ago. I had reached a considerably more relaxed period in my life - a time when I had come to feel that there was more to living than science, a time of awakening of my social consciousness and amiability, a time when I was open to new experiences. I had become friendly with a group of people who occasionally smoked cannabis, irregularly, but with evident pleasure. Initially I was unwilling to partake, but the apparent euphoria that cannabis produced and the fact that there was no physiological addiction to the plant eventually persuaded me to try. My initial experiences were entirely disappointing; there was no effect at all, and I began to entertain a variety of hypotheses about cannabis being a placebo which worked by expectation and hyperventilation rather than by chemistry. After about five or six unsuccessful attempts, however, it happened. I was lying on my back in a friend's living room idly examining the pattern of shadows on the ceiling cast by a potted plant (not cannabis!). I suddenly realized that I was examining an intricately detailed miniature Volkswagen, distinctly outlined by the shadows. I was very skeptical at this perception, and tried to find inconsistencies between Volkswagens and what I viewed on the ceiling. But it was all there, down to hubcaps, license plate, chrome, and even the small handle used for opening the trunk. When I closed my eyes, I was stunned to find that there was a movie going on the inside of my eyelids. Flash . . . a simple country scene with red farmhouse, a blue sky, white clouds, yellow path meandering over green hills to the horizon. . . Flash . . . same scene, orange house, brown sky, red clouds, yellow path, violet fields . . . Flash . . . Flash . . . Flash. The flashes came about once a heartbeat. Each flash brought the same simple scene into view, but each time with a different set of colors . . . exquisitely deep hues, and astonishingly harmonious in their juxtaposition. Since then I have smoked occasionally and enjoyed it thoroughly. It amplifies torpid sensibilities and produces what to me are even more interesting effects, as I will explain shortly.

I can remember another early visual experience with cannabis, in which I viewed a candle flame and discovered in the heart of the flame, standing with magnificent indifference, the black-hatted and -cloaked Spanish gentleman who appears on the label of the Sandeman sherry bottle. Looking at fires when high, by the way, especially through one of those prism kaleidoscopes which image their surroundings, is an extraordinarily moving and beautiful experience.

I want to explain that at no time did I think these things 'really' were out there. I knew there was no Volkswagen on the ceiling and there was no Sandeman salamander man in the flame. I don't feel any contradiction in these experiences. There's a part of me making, creating the perceptions which in everyday life would be bizarre; there's another part of me which is a kind of observer. About half of the pleasure comes from the observer-part appreciating the work of the creator-part. I smile, or sometimes even laugh out loud at the pictures on the insides of my eyelids. In this sense, I suppose cannabis is psychotomimetic, but I find none of the panic or terror that accompanies some psychoses. Possibly this is because I know it's my own trip, and that I can come down rapidly any time I want to.

While my early perceptions were all visual, and curiously lacking in images of human beings, both of these items have changed over the intervening years. I find that today a single joint is enough to get me high. I test whether I'm high by closing my eyes and looking for the flashes. They come long before there are any alterations in my visual or other perceptions. I would guess this is a signal-to-noise problem, the visual noise level being very low with my eyes closed. Another interesting information-theoretical aspects is the prevalence - at least in my flashed images - of cartoons: just the outlines of figures, caricatures, not photographs. I think this is simply a matter of information compression; it would be impossible to grasp the total content of an image with the information content of an ordinary photograph, say 108 bits, in the fraction of a second which a flash occupies. And the flash experience is designed, if I may use that word, for instant appreciation. The artist and viewer are one. This is not to say that the images are not marvelously detailed and complex. I recently had an image in which two people were talking, and the words they were saying would form and disappear in yellow above their heads, at about a sentence per heartbeat. In this way it was possible to follow the conversation. At the same time an occasional word would appear in red letters among the yellows above their heads, perfectly in context with the conversation; but if one remembered these red words, they would enunciate a quite different set of statements, penetratingly critical of the conversation. The entire image set which I've outlined here, with I would say at least 100 yellow words and something like 10 red words, occurred in something under a minute.

The cannabis experience has greatly improved my appreciation for art, a subject which I had never much appreciated before. The understanding of the intent of the artist which I can achieve when high sometimes carries over to when I'm down. This is one of many human frontiers which cannabis has helped me traverse. There also have been some art-related insights - I don't know whether they are true or false, but they were fun to formulate. For example, I have spent some time high looking at the work of the Belgian surrealist Yves Tanguey. Some years later, I emerged from a long swim in the Caribbean and sank exhausted onto a beach formed from the erosion of a nearby coral reef. In idly examining the arcuate pastel-colored coral fragments which made up the beach, I saw before me a vast Tanguey painting. Perhaps Tanguey visited such a beach in his childhood.

A very similar improvement in my appreciation of music has occurred with cannabis. For the first time I have been able to hear the separate parts of a three-part harmony and the richness of the counterpoint. I have since discovered that professional musicians can quite easily keep many separate parts going simultaneously in their heads, but this was the first time for me. Again, the learning experience when high has at least to some extent carried over when I'm down. The enjoyment of food is amplified; tastes and aromas emerge that for some reason we ordinarily seem to be too busy to notice. I am able to give my full attention to the sensation. A potato will have a texture, a body, and taste like that of other potatoes, but much more so. Cannabis also enhances the enjoyment of sex - on the one hand it gives an exquisite sensitivity, but on the other hand it postpones orgasm: in part by distracting me with the profusion of image passing before my eyes. The actual duration of orgasm seems to lengthen greatly, but this may be the usual experience of time expansion which comes with cannabis smoking.

I do not consider myself a religious person in the usual sense, but there is a religious aspect to some highs. The heightened sensitivity in all areas gives me a feeling of communion with my surroundings, both animate and inanimate. Sometimes a kind of existential perception of the absurd comes over me and I see with awful certainty the hypocrisies and posturing of myself and my fellow men. And at other times, there is a different sense of the absurd, a playful and whimsical awareness. Both of these senses of the absurd can be communicated, and some of the most rewarding highs I've had have been in sharing talk and perceptions and humor. Cannabis brings us an awareness that we spend a lifetime being trained to overlook and forget and put out of our minds. A sense of what the world is really like can be maddening; cannabis has brought me some feelings for what it is like to be crazy, and how we use that word 'crazy' to avoid thinking about things that are too painful for us. In the Soviet Union political dissidents are routinely placed in insane asylums. The same kind of thing, a little more subtle perhaps, occurs here: 'did you hear what Lenny Bruce said yesterday? He must be crazy.' When high on cannabis I discovered that there's somebody inside in those people we call mad.

When I'm high I can penetrate into the past, recall childhood memories, friends, relatives, playthings, streets, smells, sounds, and tastes from a vanished era. I can reconstruct the actual occurrences in childhood events only half understood at the time. Many but not all my cannabis trips have somewhere in them a symbolism significant to me which I won't attempt to describe here, a kind of mandala embossed on the high. Free-associating to this mandala, both visually and as plays on words, has produced a very rich array of insights.

There is a myth about such highs: the user has an illusion of great insight, but it does not survive scrutiny in the morning. I am convinced that this is an error, and that the devastating insights achieved when high are real insights; the main problem is putting these insights in a form acceptable to the quite different self that we are when we're down the next day. Some of the hardest work I've ever done has been to put such insights down on tape or in writing. The problem is that ten even more interesting ideas or images have to be lost in the effort of recording one. It is easy to understand why someone might think it's a waste of effort going to all that trouble to set the thought down, a kind of intrusion of the Protestant Ethic. But since I live almost all my life down I've made the effort - successfully, I think. Incidentally, I find that reasonably good insights can be remembered the next day, but only if some effort has been made to set them down another way. If I write the insight down or tell it to someone, then I can remember it with no assistance the following morning; but if I merely say to myself that I must make an effort to remember, I never do.

I find that most of the insights I achieve when high are into social issues, an area of creative scholarship very different from the one I am generally known for. I can remember one occasion, taking a shower with my wife while high, in which I had an idea on the origins and invalidities of racism in terms of gaussian distribution curves. It was a point obvious in a way, but rarely talked about. I drew the curves in soap on the shower wall, and went to write the idea down. One idea led to another, and at the end of about an hour of extremely hard work I found I had written eleven short essays on a wide range of social, political, philosophical, and human biological topics. Because of problems of space, I can't go into the details of these essays, but from all external signs, such as public reactions and expert commentary, they seem to contain valid insights. I have used them in university commencement addresses, public lectures, and in my books.

But let me try to at least give the flavor of such an insight and its accompaniments. One night, high on cannabis, I was delving into my childhood, a little self-analysis, and making what seemed to me to be very good progress. I then paused and thought how extraordinary it was that Sigmund Freud, with no assistance from drugs, had been able to achieve his own remarkable self-analysis. But then it hit me like a thunderclap that this was wrong, that Freud had spent the decade before his self-analysis as an experimenter with and a proselytizer for cocaine; and it seemed to me very apparent that the genuine psychological insights that Freud brought to the world were at least in part derived from his drug experience. I have no idea whether this is in fact true, or whether the historians of Freud would agree with this interpretation, or even if such an idea has been published in the past, but it is an interesting hypothesis and one which passes first scrutiny in the world of the downs.

I can remember the night that I suddenly realized what it was like to be crazy, or nights when my feelings and perceptions were of a religious nature. I had a very accurate sense that these feelings and perceptions, written down casually, would not stand the usual critical scrutiny that is my stock in trade as a scientist. If I find in the morning a message from myself the night before informing me that there is a world around us which we barely sense, or that we can become one with the universe, or even that certain politicians are desperately frightened men, I may tend to disbelieve; but when I'm high I know about this disbelief. And so I have a tape in which I exhort myself to take such remarks seriously. I say 'Listen closely, you sonofabitch of the morning! This stuff is real!' I try to show that my mind is working clearly; I recall the name of a high school acquaintance I have not thought of in thirty years; I describe the color, typography, and format of a book in another room and these memories do pass critical scrutiny in the morning. I am convinced that there are genuine and valid levels of perception available with cannabis (and probably with other drugs) which are, through the defects of our society and our educational system, unavailable to us without such drugs. Such a remark applies not only to self-awareness and to intellectual pursuits, but also to perceptions of real people, a vastly enhanced sensitivity to facial expression, intonations, and choice of words which sometimes yields a rapport so close it's as if two people are reading each other's minds.

Cannabis enables nonmusicians to know a little about what it is like to be a musician, and nonartists to grasp the joys of art. But I am neither an artist nor a musician. What about my own scientific work? While I find a curious disinclination to think of my professional concerns when high - the attractive intellectual adventures always seem to be in every other area - I have made a conscious effort to think of a few particularly difficult current problems in my field when high. It works, at least to a degree. I find I can bring to bear, for example, a range of relevant experimental facts which appear to be mutually inconsistent. So far, so good. At least the recall works. Then in trying to conceive of a way of reconciling the disparate facts, I was able to come up with a very bizarre possibility, one that I'm sure I would never have thought of down. I've written a paper which mentions this idea in passing. I think it's very unlikely to be true, but it has consequences which are experimentally testable, which is the hallmark of an acceptable theory.

I have mentioned that in the cannabis experience there is a part of your mind that remains a dispassionate observer, who is able to take you down in a hurry if need be. I have on a few occasions been forced to drive in heavy traffic when high. I've negotiated it with no difficult at all, though I did have some thoughts about the marvelous cherry-red color of traffic lights. I find that after the drive I'm not high at all. There are no flashes on the insides of my eyelids. If you're high and your child is calling, you can respond about as capably as you usually do. I don't advocate driving when high on cannabis, but I can tell you from personal experience that it certainly can be done. My high is always reflective, peaceable, intellectually exciting, and sociable, unlike most alcohol highs, and there is never a hangover. Through the years I find that slightly smaller amounts of cannabis suffice to produce the same degree of high, and in one movie theater recently I found I could get high just by inhaling the cannabis smoke which permeated the theater.

There is a very nice self-titering aspect to cannabis. Each puff is a very small dose; the time lag between inhaling a puff and sensing its effect is small; and there is no desire for more after the high is there. I think the ratio, R, of the time to sense the dose taken to the time required to take an excessive dose is an important quantity. R is very large for LSD (which I've never taken) and reasonably short for cannabis. Small values of R should be one measure of the safety of psychedelic drugs. When cannabis is legalized, I hope to see this ratio as one of he parameters printed on the pack. I hope that time isn't too distant; the illegality of cannabis is outrageous, an impediment to full utilization of a drug which helps produce the serenity and insight, sensitivity and fellowship so desperately needed in this increasingly mad and dangerous world.
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Postby Penguin » Wed Oct 21, 2009 5:30 am

Cannabis medicine conference of 2009:
Abstracts of the oral presentations are available as pdf - http://www.cannabis-med.org/meeting/Col ... reader.pdf
48 pages, maybe 30 pages of which are the study abstracts. Recommended reading.

And a short article commenting on the proceedings:
http://www.enewspf.com/index.php?option ... d=88890249

Washington, D.C.--(ENEWSPF)--October 5, 2009. The International Association for Cannabis as Medicine just concluded its 5th Conference on Cannabinoids in Medicine in Cologne, Germany. The conference included significant new evidence that marijuana is a safe, effective medicine for certain conditions, some of which can be found in the conference abstracts, now available online.

Canadian researcher Mark Ware presented results of a yearlong safety study known as the COMPASS study, which compared 215 patients who used marijuana to manage chronic pain with comparable control patients who did not use marijuana. Ware and colleagues report “no difference in serious adverse events” between the two groups, concluding, “Cannabis use for chronic pain over one year is not associated with major changes in lung, endocrine, cognitive function or serious adverse events.”

A much-awaited study came from the University of California, San Francisco, where Donald Abrams and colleagues tested the effects of adding marijuana to the therapeutic regimen of chronic pain patients on long-term morphine or oxycodone therapy. Unfortunately, because the researchers were crunching numbers right up until the conference, the abstract doesn’t include a lot of details. But the study shows that marijuana did indeed add significant pain relief on top of that already provided by the narcotic painkillers. The scientists conclude, “Cannabinoids may augment the analgesic effects of opioids, allowing longer treatment at lower doses with fewer side effects.”

Meanwhile, British researchers added to the body of evidence indicating that marijuana can aid the treatment of multiple sclerosis. Two-hundred and seventy-nine patients received either a standardized cannabis extract, given orally, or a placebo. Patients receiving the extract were twice as likely to experience relief of muscle stiffness, and also reported relief of body pain, spasms, and sleep problems.


I would have pasted all the abstracts here but the formatting was horrible when copied from the pdf, so please grab it yourselves.
Last edited by Penguin on Wed Oct 21, 2009 5:45 am, edited 2 times in total.
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Postby Penguin » Wed Oct 21, 2009 5:33 am

http://www.popsci.com/scitech/article/2 ... -gene-hemp

Publishing in the Journal of Experimental Botany, the researchers note that they specifically targeted the genes responsible for generating the drug-filled hairs highlighted in many a High Times photo spread. By impairing or encouraging the growth of those hairs, scientists could gain precise control over the level of THC in the crop.

From Journal of Experimental Botany - http://jxb.oxfordjournals.org/cgi/reprint/60/13/3715
Identification of candidate genes affecting
D9-tetrahydrocannabinol biosynthesis in Cannabis sativa

----------------------------------------------------------------------

http://www.alternet.org/media/142815/5_ ... t_cannabis

Writing in the journal Science nearly four decades ago, New York State University sociologist Erich Goode documented the media's complicity in maintaining cannabis prohibition.

He observed: "[T]ests and experiments purporting to demonstrate the ravages of marijuana consumption receive enormous attention from the media, and their findings become accepted as fact by the public. But when careful refutations of such research are published, or when later findings contradict the original pathological findings, they tend to be ignored or dismissed."

A glimpse of today's mainstream media landscape indicates that little has changed -- with news outlets continuing to, at best, underreport the publication of scientific studies that undermine the federal government's longstanding pot propaganda and, at worst, ignore them all together.

Here are five recent stories the mainstream media doesn't want you to know about pot:

1. Marijuana Use Is Not Associated With a Rise in Incidences of Schizophrenia

Over the past few years, the worldwide media, as well as federal officials in the United Kingdom, Canada and the U.S. have earnestly promoted the notion that smoking pot induces mental illness.

Perhaps most notably, in 2007 the MSM reported that cannabis "could boost the risk of developing a psychotic illness later in life by about 40 percent" -- a talking point that was also actively promoted by U.S. anti-drug officials.

So, is there any truth to the claim that pot smoking is sparking a dramatic rise in mental illness? Not at all, according to the findings of a study published in July in the journal Schizophrenia Research.

Investigators at the Keele University Medical School in Britain compared trends in marijuana use and incidences of schizophrenia in the United Kingdom from 1996 to 2005. Researchers reported that the "incidence and prevalence of schizophrenia and psychoses were either stable or declining" during this period, even the use of cannabis among the general population was rising.

"[T]he expected rise in diagnoses of schizophrenia and psychoses did not occur over a 10-year period," the authors concluded. "This study does not therefore support the specific causal link between cannabis use and incidence of psychotic disorders. … This concurs with other reports indicating that increases in population cannabis use have not been followed by increases in psychotic incidence."

As of this writing, a handful of news wire reports in Australia, Canada, and the U.K. have reported on the Keele University study. Notably, no American media outlets covered the story.

2. Marijuana Smoke Doesn't Damage the Lungs Like Tobacco

Everyone knows that smoking pot is as damaging, if not more damaging, to the lungs than puffing cigarettes, right?

Wrong, according to a team of New Zealand investigators writing in the European Respiratory Journal in August.

Researchers at the University of Otago in New Zealand compared the effects of cannabis and tobacco smoke on lung function in over 1,000 adults.

They reported: "Cumulative cannabis use was associated with higher forced vital capacity [the volume of air that can forcibly be blown out after full inspiration], total lung capacity, functional residual capacity [the volume of air present in the lungs at the end of passive expiration] and residual volume.

"Cannabis was also associated with higher airways resistance but not with forced expiratory volume in one second [the maximum volume of air that can be forcibly blown out in the first second during the FVC test], forced expiratory ratio, or transfer factor. These findings were similar amongst those who did not smoke tobacco. … By contrast, tobacco use was associated with lower forced expiratory volume in one second, lower forced expiratory ratio, lower transfer factor and higher static lung volumes, but not with airways resistance."

They concluded, "Cannabis appears to have different effects on lung function to those of tobacco."

Predictably, the scientists' "inconvenient truth" was not reported in a single media outlet.

3. Cannabis Use Potentially Protects, Rather Than Harms, the Brain

Does smoking pot kill brain cells? Drinking alcohol most certainly does, and many opponents of marijuana-law reform claim that marijuana's adverse effects on the brain are even worse. Are they correct?

Not according to recent findings published this summer in the journal Neurotoxicology and Teratology.

Investigators at the University of California at San Diego examined white matter integrity in adolescents with histories of binge drinking and marijuana use. They reported that binge drinkers (defined as boys who consumed five or more drinks in one sitting, or girls who consumed four or more drinks at one time) showed signs of white matter damage in eight regions of the brain.

By contrast, the binge drinkers who also used marijuana experienced less damage in 7 out of the 8 brain regions.

"Binge drinkers who also use marijuana did not show as consistent a divergence from non-users as did the binge drink-only group," authors concluded. "[It is] possible that marijuana may have some neuroprotective properties in mitigating alcohol-related oxidative stress or excitotoxic cell death."

To date, only a handful of U.S. media outlets -- almost exclusively college newspapers -- have reported the story.

4. Marijuana Is a Terminus, Not a 'Gateway,' to Hard Drug Use

Alarmist claims that experimenting with cannabis will inevitably lead to the use of other illicit drugs persist in the media despite statistical data indicating that the overwhelming majority of those who try pot never go on to use cocaine or heroin.

Moreover, recent research is emerging that indicates that pot may also suppress one's desire to use so-called hard drugs.

In June, Paris researchers writing in the journal Neuropsychopharmacology concluded that the administration of oral THC in animals suppressed sensitivity to opiate dependence.

Also this summer, investigators at the New York State Psychiatric Institute reported in the American Journal on Addictions that drug-treatment subjects who use cannabis intermittently were more likely to adhere to treatment for opioid dependence.

Although a press release for the former study appeared on the Web site physorg.com on July 7, neither study ever gained any traction in the mainstream media.

5. Government's Anti-Pot Ads Encourage, Rather Than Discourage, Marijuana Use

Sure, many of us already knew that the federal government's $2 billion ad campaign targeting pot was failing to dissuade viewers from toking up, but who knew it was this bad?

According to a new study posted online in the journal Health Communication, survey data published by investigators at the Annenberg School for Communication at the University of Pennsylvania found that many of the government's public-service announcements actually encouraged pot use.

Researchers assessed the attitudes of over 600 adolescents, age 12 to 18, after viewing 60 government-funded anti-marijuana television spots.

Specifically, researchers evaluated whether the presence of marijuana-related imagery in the ads (e.g., the handling of marijuana cigarettes or the depiction of marijuana-smoking behavior) were more likely or less likely to discourage viewers' use of cannabis.

Messages that depict teens associating with cannabis are "significantly less effective than others," the researchers found.

"This negative impact of marijuana scenes is not reversed in the presence of strong anti-marijuana arguments in the ads and is mainly present for the group of adolescents who are often targets of such anti-marijuana ads (i.e., high-risk adolescents)," the authors determined. "For this segment of adolescents, including marijuana scenes in anti-marijuana (public-service announcements) may not be a good strategy."

Needless to say, no outlets in the mainstream media -- many of which donated air time to several of the beleaguered ads in question -- have yet to report on the story.
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Postby Pele'sDaughter » Tue Nov 10, 2009 2:40 pm

http://www.commondreams.org/newswire/2009/11/10-1

AMA Calls for Review of Medical Marijuana’s Legal Status
New Policy Marks Historic Shift From Prior Stance
HOUSTON - November 10 - In a move considered historic by supporters of medical marijuana, the American Medical Association's House of Delegates today adopted a new policy position calling for the review of marijuana's status as a Schedule I drug in the federal Controlled Substances Act. The old language in Policy H-95.952 had previously recommended that "marijuana be retained in Schedule I," which groups marijuana with drugs such as heroin, LSD and PCP that are deemed to have no accepted medical uses and to be unsafe for use even under medical supervision.

The revised policy, adopted today, states, "Our AMA urges that marijuana's status as a federal Schedule I controlled substance be reviewed with the goal of facilitating the conduct of clinical research and development of cannabinoid-based medicines, and alternate delivery methods." It goes on to explain that this position should not be construed as an endorsement of state medical marijuana programs.

"This shift, coming from what has historically been America's most cautious and conservative major medical organization, is historic," said Aaron Houston, director of government relations for the Marijuana Policy Project, who attended the AMA meeting. "Marijuana's Schedule I status is not just scientifically untenable, given the wealth of recent data showing it to be both safe and effective for chronic pain and other conditions, but it's been a major obstacle to needed research."

Drugs listed in Schedule II, for which medical use is permitted with strict controls, include cocaine, morphine and methamphetamine. A pill containing THC, the component responsible for marijuana's "high," is classed in Schedule III, whose looser requirements allow phoned-in prescriptions.

###
With more than 26,000 members and 100,000 e-mail subscribers nationwide, the Marijuana Policy Project is the largest marijuana policy reform organization in the United States. MPP believes that the best way to minimize the harm associated with marijuana is to regulate marijuana in a manner similar to alcohol. For more information, please visit http://MarijuanaPolicy.org.
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Postby Pele'sDaughter » Wed Nov 11, 2009 2:39 pm

This looks closely related to studies that were linked in posts on the previous page.

http://www.sciencedaily.com/releases/20 ... 090440.htm

Active Ingredient In Cannabis Eliminates Morphine Dependence In Rats

ScienceDaily (July 15, 2009) — Injections of THC, the active principle of cannabis, eliminate dependence on opiates (morphine, heroin) in rats deprived of their mothers at birth. The findings could lead to therapeutic alternatives to existing substitution treatments.

In order to study psychiatric disorders, neurobiologists use animal models, especially maternal deprivation models. Depriving rats of their mothers for several hours a day after their birth leads to a lack of care and to early stress. The lack of care, which takes place during a period of intense neuronal development, is liable to cause lasting brain dysfunction.

The study was carried out by Valérie Daugé and her team at the Laboratory for Physiopathology of Diseases of the Central Nervous System (UPMC / CNRS / INSERM).

Valérie Daugé's team at the Laboratory for Physiopathology of Diseases of the Central Nervous System (UPMC / CNRS / Inserm) analyzed the effects of maternal deprivation combined with injections of tetrahydrocannabinol, or THC, the main active principle in cannabis, on behavior with regard to opiates.

Previously, Daugé and her colleagues had shown that rats deprived of their mothers at birth become hypersensitive to the rewarding effect of morphine and heroin (substances belonging to the opiate family), and rapidly become dependent. In addition, there is a correlation between such behavioral disturbances linked to dependence, and hypoactivity of the enkephalinergic system, the endogenous opioid system.

To these rats, placed under stress from birth, the researchers intermittently administered increasingly high doses of THC (5 or 10 mg/kg) during the period corresponding to their adolescence (between 35 and 48 days after birth). By measuring their consumption of morphine in adulthood, they observed that, unlike results previously obtained, the rats no longer developed typical morphine-dependent behavior. Moreover, biochemical and molecular biological data corroborate these findings. In the striatum, a region of the brain involved in drug dependence, the production of endogenous enkephalins was restored under THC, whereas it diminished in rats stressed from birth which had not received THC.

Such animal models are validated for understanding the neurobiological and behavioral effects of postnatal conditions in humans. In this context, the findings point to the development of new treatments that could relieve withdrawal effects and suppress drug dependence.

The enkephalinergic system produces endogenous enkephalins, which are neurotransmitters that bind to the same receptors as opiates and inhibit pain messages to the brain.
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Postby tron » Thu Dec 24, 2009 1:06 pm

crosspost from another topic feel free to add



also in the uk we have to contend with weed sprayed with allsorts of nasty stuff

guy in this forum thinks its the government

http://lem.localinet.co.uk/phpBB2/viewt ... 964211d331

http://www.gritweed.co.uk/

Chances are you have stumbled accross this website because you have either heard rumours about the existence of a new type of contaminated cannabis (grit weed) or you have been unfortunate enough to acquire some and are wondering whether to smoke it or not.

'Grit Weed' has become the colloquial name for a general form of contaminated herbal cannabis that has been treated with a variety of unknown sand / grit like substances which appear to have been added to the plant prior to harvest in order to increase the weight of the plant’s yield.

The purpose of this website is to attempt to raise awareness of the issue amongst regular cannabis users as well as the UK health and police authorities. Whilst we do not condone the use of any illegal drugs we feel that recreational cannabis users have a right to be kept informed about the potentially serious health implications relating to this recent wave of contamination.

Please feel free to email us with any information that you may have in relation to gritweed contamination in the UK - we will gladly publish any new findings.

To read more about out gritweed awareness campaign, click here. For further information about grit weed, including a summary of the common varieties, please click here.

http://www.youtube.com/watch?v=wfhKUY2MPjU

there are more videos at youtube......i was specifically trying to find one where a guy mixes the weed in water and something ends up undissolved but in suspension in the water like some form of clay, they basically spray crap on to make a few more $$ per kilo the government know this well and do nothing to protect the people other than to say "its illegal its your own fault"

another annoying thing is the veitnamese mafia who grow most of the weed in this country and sell it unripe and wet wankers

sorry for offtopic rant

should have made a new topic cause its kinda important


...also soapbar http://www.ukcia.org/activism/soapbar.php

this is the resin the uk government refer to as being safer than the high strength sinsemillia ,most of the time it doesnt even contain cannabis, people who i know smoke this stuff even though they know whats in it
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Re: Carl Sagans essay on cannabis

Postby Perelandra » Sat Dec 26, 2009 3:07 am

Penguin wrote:Carl Sagan wrote this essay under pseudonym Mr X - after his passing, his identity was revealed according to the wishes of late mr. Sagan,

http://marijuana-uses.com/essays/002.html
That Sagan essay was excellent, thank you Pengs.

Wow, tron. Never heard of such stuff.
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Re: Cannabis research, medicine and use

Postby Penguin » Wed Jan 13, 2010 6:12 am

http://www3.interscience.wiley.com/jour ... 1/abstract

Cannabis and crime: findings from a longitudinal study
Willy Pedersen 1 & Torbjørn Skardhamar 2
1 Department of Sociology and Human Geography, University of Oslo and Norwegian Institute for Alcohol and Drug Research, Oslo, Norway and 2 Statistics Norway, Oslo, Norway
Correspondence to Willy Pedersen, Department of Sociology and Human Geography, University of Oslo, Box 1096, 0317 Oslo, Norway. E-mail: willy.pedersen@sosiologi.uio.no
Copyright Journal compilation © 2010 Society for the Study of Addiction
KEYWORDS
Alcohol • cannabis • crime • illegal drugs • longitudinal • marijuana
ABSTRACT

Aim To examine the association between cannabis use during adolescence and young adulthood, and subsequent criminal charges.

Methods Data were obtained from the Young in Norway Longitudinal Study. A population-based sample (n = 1353) was followed from 13 to 27 years of age. Data were gathered on cannabis use, alcohol consumption and alcohol problems, and use of other illegal substances such as amphetamines, cocaine and opiates. In addition, extensive information on socio-demographic, family and personal factors was collected. This data set was linked to individual-level information from official Norwegian crime statistics.

Findings We found robust associations between cannabis use and later registered criminal charges, both in adolescence and in young adulthood. These associations were adjusted for a range of confounding factors, such as family socio-economic background, parental support and monitoring, educational achievement and career, previous criminal charges, conduct problems and history of cohabitation and marriage. In separate models, we controlled for alcohol measures and for use of other illegal substances. After adjustment, we still found strong associations between cannabis use and later criminal charges. However, when eliminating all types of drug-specific charges from our models, we no longer observed any significant association with cannabis use.

Conclusions The study suggests that cannabis use in adolescence and early adulthood may be associated with subsequent involvement in criminal activity. However, the bulk of this involvement seems to be related to various types of drug-specific crime. Thus, the association seems to rest on the fact that use, possession and distribution of drugs such as cannabis is illegal. The study strengthens concerns about the laws relating to the use, possession and distribution of cannabis.

Submitted 9 February 2009; initial review completed 2 March 2009; final version accepted 19 June 2009


http://www.heretohelp.bc.ca/publications/cannabis/bck/7
Cannabis, Tobacco and Alcohol Use in Canada
Comparing risks of harm and costs to society

........
In terms of social costs, the vast majority of the social costs of cannabis are enforcement-related while the vast majority of tobacco costs are health-related. The social costs of alcohol are about evenly distributed between health care and enforcement.

In terms of costs per user: tobacco-related health costs are over $800 per user, alcohol-related health costs are much lower at $165 per user, and cannabis-related health costs are the lowest at $20 per user. On the enforcement side, costs for cannabis are the highest at $328 per user—94% of social costs for cannabis are linked to enforcement. Enforcement costs per user for alcohol are about half those for cannabis ($153), while enforcement costs for tobacco are very low.
Conclusion

The harms, risks and social costs of alcohol, cannabis and tobacco vary greatly. A lot has to do with how the substances are handled legally. Alcohol and tobacco are legal substances, which explain their low enforcement costs relative to cannabis. On the other hand, the health costs per user of tobacco and alcohol are much higher than for cannabis. This may indicate that cannabis use involves fewer health risks than alcohol or tobacco. These variations in risk, harms and costs need to
be taken into account as we think about further efforts to deal with the use of these three substances in Canada. Efforts to reduce social costs related to cannabis, for example, will likely involve shifting its legal status by decriminalizing casual use, to reduce the high enforcement costs. Such a shift may be warranted given the apparent lower health risk associated with most cannabis use.


http://www.sciencedaily.com/releases/20 ... 101538.htm
Minimal Relationship Between Cannabis And Schizophrenia Or Psychosis, Suggested By New Study
ScienceDaily (Oct. 22, 2009) — Last year the UK government reclassified cannabis from a class C to a class B drug, partly out of concerns that cannabis, especially the more potent varieties, may increase the risk of schizophrenia in young people. But the evidence for the relationship between cannabis and schizophrenia or psychosis remains controversial. A new study has determined that it may be necessary to stop thousands of cannabis users in order to prevent a single case of schizophrenia.

Scientists from Bristol, Cambridge and the London School of Hygiene and Tropical Medicine took the latest information on numbers of cannabis users, the risk of developing schizophrenia, and the risk that cannabis use causes schizophrenia to estimate how many cannabis users may need to be stopped to prevent one case of schizophrenia. The study found it would be necessary to stop 2800 heavy cannabis users in young men and over 5000 heavy cannabis users in young women to prevent a single case of schizophrenia. Among light cannabis users, those numbers rise to over 10,000 young men and nearly 30,000 young women to prevent one case of schizophrenia.

That's just part of the story. Interventions to prevent cannabis use typically do not succeed for every person who is treated. Depending on how effective an intervention is at preventing cannabis use, it would be necessary to treat even higher numbers of users to achieve the thousands of successful results necessary to prevent a very few cases of schizophrenia.

Matt Hickman, one of the authors of the report recently published in the journal Addiction, said that "preventing cannabis use is important for many reasons -- including reducing tobacco and drug dependence and improving school performance. But our evidence suggests that focusing on schizophrenia may have been misguided. Our research cannot resolve the question whether cannabis causes schizophrenia, but does show that many people need to give up cannabis in order to have an impact on the number of people with schizophrenia. The likely impact of re-classifying cannabis in the UK on schizophrenia or psychosis incidence is very uncertain."

Journal Reference:

1. Hickman et al. If cannabis caused schizophrenia-how many cannabis users may need to be prevented in order to prevent one case of schizophrenia? England and Wales calculations. Addiction, 2009; 104 (11): 1856 DOI: 10.1111/j.1360-0443.2009.02736.x
http://dx.doi.org/10.1111/j.1360-0443.2009.02736.x


Related earlier study from Denmark-
http://archpsyc.ama-assn.org/cgi/conten ... 65/11/1269
Context Cannabis-induced psychosis is considered a distinct clinical entity in the existing psychiatric diagnostic systems. However, the validity of the diagnosis is uncertain.

Objectives To establish rate ratios of developing cannabis-induced psychosis associated with predisposition to psychosis and other psychiatric disorders in a first-degree relative and to compare them with the corresponding rate ratios for developing schizophrenia spectrum disorders.

Design A population-based cohort was retrieved from the Danish Psychiatric Central Register and linked with the Danish Civil Registration System. History of treatment of psychiatric disorder in family members was used as an indicator of predisposition to psychiatric disorder. Rate ratios of cannabis-induced psychosis and schizophrenia associated with predisposition to psychiatric disorders were compared using competing risk analyses.

Setting Nationwide population-based sample of all individuals born in Denmark between January 1,1955, and July 1, 1990 (N = 2 276 309).

Patients During the 21.9 million person-years of follow-up between 1994 and 2005, 609 individuals received treatment of a cannabis-induced psychosis and 6476 received treatment of a schizophrenia spectrum disorder.

Results In general, the rate ratios of developing cannabis-induced psychosis and schizophrenia spectrum disorder associated with predisposition to schizophrenia spectrum disorder, other psychoses, and other psychiatric disorders in first-degree relatives were of similar magnitude. However, children with a mother with schizophrenia were at a 5-fold increased risk of developing schizophrenia and a 2.5-fold increased risk of developing cannabis-induced psychosis. The risk of a schizophrenia spectrum disorder following a cannabis-induced psychosis and the timing of onset were unrelated to familial predisposition.

Conclusions Predisposition to both psychiatric disorders in general and psychotic disorders specifically contributes equally to the risk of later treatment because of schizophrenia and cannabis-induced psychoses. Cannabis-induced psychosis could be an early sign of schizophrenia rather than a distinct clinical entity.


http://www.emaxhealth.com/1275/39/34876 ... sease.html
Compounds found in cannabis (marijuana) may help relieve symptoms of inflammatory bowel disease. The two compounds, cannabinoids THC and cannabidiol, have an impact on the body system that controls the function of the intestinal tract.

Inflammatory bowel diseases include ulcerative colitis and Crohn’s disease, which together affect more than 1 million people in the United States. Although these diseases are related and both involve chronic inflammation of the intestinal tract, along with abdominal cramps, bloody diarrhea, and fever, they are not the same. One main difference is that ulcerative colitis can be cured with surgery, but Crohn’s disease cannot.

Inflammatory bowel disease most often develops in people between the ages of 10 and 30, although a smaller peak has been seen in people ages 50 to 60. The cause is unknown, although experts believe both genetic and environmental factors are involved. More specifically, it is proposed that a genetic susceptibility is triggered by factors such as stress, diet, or bacteria, which then leads to a dysfunctional immune response and inflammation.

Treatment of inflammatory bowel disease involves symptom relief. In this new study, the results of which were presented at The British Pharmacological Society’s winter meeting in London, researchers noted that the body produces its own cannabinoid molecules, which are called endocannabinoids. These molecules increase the permeability of the protective lining of the intestines during inflammation, which allows bacteria to escape into the intestinal tract. This suggests that overproduction of these molecules is harmful to the gut.

The researchers also found, however, that they could reverse this process when they introduced cannabinoids derived from marijuana. These plant-extracted compounds “appeared to allow the epithelial cells to form tighter bond with each other and restore the membrane barrier,” noted Dr. Karen Wright, the study’s lead author and the Peel Trust Lecturer in Biomedicine at Lancaster University.

So far the research on the marijuana compounds against inflammatory bowel disease has been limited to cell cultures, but the investigators are encouraged by the results thus far. Dr. Wright also noted that “while THC has psychoactive properties,” cannabidiol does not, and it has proven to be effective in restoring membrane integrity in their research on inflammatory bowel disease.

SOURCES:
American College of Gastroenterology
Lancaster University news release
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Re: Cannabis research, medicine and use

Postby Gnomad » Tue Nov 01, 2011 8:04 am

Could cannabis actually lower chance of infant mortality?
From this thread:
viewtopic.php?p=432524#p432524

I only could get the abstract, but unless I am reading this wrong somehow, it is a total mind-blower! (And it ain't easy to blow Granny's mind! amim.smiley.gif )

http://pediatrics.aappublications.org/c ... type=HWCIT

PEDIATRICS Vol. 100 No. 1 July 1997, pp. 79-83
Mortality Within the First 2 Years in Infants Exposed to Cocaine, Opiate, or Cannabinoid During Gestation


Received Jul 26, 1996; accepted Nov 14, 1996.

Enrique M. Ostrea Jr*, Anthony R. Ostrea*, and Pippa M. Simpson From the * Department of Pediatrics, Hutzel Hospital, Children's Hospital of Michigan and Wayne State University, Detroit, Michigan.

Objective. To determine the mortality rate, during the first 2 years of life, in infants who were exposed to cocaine, opiate, or cannabinoid during gestation.

Methods. For a period of 11 months, a large group of infants were enrolled and screened at birth for exposure to cocaine, opiate, or cannabinoid by meconium analysis. Death outcome, within the first 2 years after birth, was determined in this group of infants using the death registry of the Michigan Department of Public Health.

Results. A total of 2964 infants was studied. At birth, 44% of the infants tested positive for drugs: 30.5% positive for cocaine, 20.2% for opiate, and 11.4% for cannabinoids. Compared to the drug negative group, a significantly higher percentage (P < .05) of the drug positive infants had lower weight and smaller head circumference and length at birth and a higher percent of their mothers were single, multigravid, multiparous, and had little to no prenatal care. Within the first 2 years of life, 44 infants died: 26 were drug negative (15.7 deaths per 1000 live births) and 18 were drug positive (13.7 deaths per 1000 live births). The mortality rate among cocaine, opiate, or cannabinoid positive infants were 17.7, 18.4, and 8.9 per 1000 live births, respectively. (emphasis mine- Granny) Among infants with birth weight http://pediatrics.aappublications.org/m ... le.gif2500 g, infants who were positive for both cocaine and morphine had a higher mortality rate (odds ratio = 5.9, confidence interval [CI] = 1.4 to 24) than drug negative infants. Eleven infants died from the sudden infant death syndrome (SIDS); 58% were positive for drugs, predominantly cocaine. The odds ratio for SIDS among drug positive infants was 1.5 (CI = 0.46 to 5.01) and 1.9 (CI = 0.58 to 6.2) among cocaine positive infants.

Conclusion. We conclude that prenatal drug exposure in infants, although associated with a high perinatal morbidity, is not associated with an overall increase in their mortality rate or incidence of SIDS during the first 2 years of life. However, a significantly higher mortality rate was observed among low birth weight infants (http://pediatrics.aappublications.org/m ... le.gif2500 g) who were positive for both cocaine and opiate.




OK, folks, here's the nitty-gritty- deaths per 1,000.

Total deaths -.............. 44

Drug negative deaths- ... 26....... 15.7 deaths per 1000 live births

All drug positive deaths-.. 18....... 13.7 deaths per 1000 live births

Cocaine positive deaths-.. __ .......17.7 deaths per 1000 live births

Opiate positive deaths-..... __ .......18.4 deaths per 1000 live births

Cannabinoid positive deaths-.__..... 8.9 deaths per 1000 live births


The only reason that the "drug baby" group had a lower mortality rate than the "drug free" babies, was the cannabis group! Opiate and cocaine deaths were higher than the "drug free" group- as you would expect. :frown: But look at cannabis! Almost a 50% reduction in mortality compared to the "drug free" babies! So, do you think that using cannabis might actually be good for your baby's survival?

Think of the children!

(It's just so cool when you can turn a prohib "war cry" against them! :frown: )


Granny :)
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Re: Cannabis research, medicine and use

Postby Gnomad » Tue Nov 01, 2011 8:21 am

Something from the "Captain Obvious" department:

Neurophysiological functioning of occasional and heavy cannabis users during THC intoxication.
http://www.ncbi.nlm.nih.gov/pubmed/21975580

Theunissen EL, Kauert GF, Toennes SW, Moeller MR, Sambeth A, Blanchard MM, Ramaekers JG.
Source
Department of Neuropsychology and Psychopharmacology, Faculty of Psychology and Neuroscience, Maastricht University, P.O. Box 616, 6200MD, Maastricht, The Netherlands, e.theunissen@maastrichtuniversity.nl.
Abstract
RATIONALE:
Experienced cannabis users demonstrate tolerance to some of the impairing acute effects of cannabis.

OBJECTIVES:
The present study investigates whether event-related potentials (ERPs) differ between occasional and heavy cannabis users after acute Δ(9)-tetrahydrocannabinol (THC) administration, as a result of tolerance.

METHODS:
Twelve occasional and 12 heavy cannabis users participated in a double-blind, placebo-controlled, crossover study. On two separate days, they smoked a joint containing 0 or 500 μg/kg body weight THC. ERPs were measured while subjects performed a divided attention task (DAT) and stop signal task (SST).

RESULTS:
In the DAT, THC significantly decreased P100 amplitude in occasional but not in heavy cannabis users. P300 amplitude in the DAT was significantly decreased by THC in both groups. The N200 peak in the SST was not affected by treatment in neither of the groups. Performance in the SST was impaired in both groups after THC treatment, whereas performance in the DAT was impaired by THC only in the occasional users group.

CONCLUSIONS:
The present study confirms that heavy cannabis users develop tolerance to some of the impairing behavioral effects of cannabis. This tolerance was also evident in the underlying ERPs, suggesting that tolerance demonstrated on performance level is not (completely) due to behavioral compensation.


NORML reports on the same study-
http://norml.org/news/2011/10/27/experi ... study-says

And another new study, concerning Crohn's disease sufferers:
http://norml.org/news/2011/09/22/study- ... tion-drugs
( http://www.ncbi.nlm.nih.gov/pubmed/21910367 )

"All patients stated that consuming cannabis had a positive effect on their disease activity"

Tel Aviv, Israel: Cannabis use is associated with a reduction in Crohn's disease (CD) activity and disease-related surgeries, according to the results of a retrospective observational study published in the August issue of the Journal of the Israeli Medical Association.

Investigators at the Meir Medical Center, Institute of Gastroenterology and Hepatology assessed 'disease activity, use of medication, need for surgery, and hospitalization' before and after cannabis use in 30 patients with CD.

Authors reported, "All patients stated that consuming cannabis had a positive effect on their disease activity" and documented "significant improvement" in 21 subjects.

Specifically, researchers found that subjects who consumed cannabis "significantly reduced" their need for other medications. Participants in the trial also reported requiring fewer surgeries following their use of cannabis.

"Fifteen of the patients had 19 surgeries during an average period of nine years before cannabis use, but only two required surgery during an average period of three years of cannabis use," authors reported.

They concluded: "The results indicate that cannabis may have a positive effect on disease activity, as reflected by a reduction in disease activity index and in the need for other drugs and surgery. Prospective placebo-controlled studies are warranted to fully evaluate the efficacy and side effects of cannabis in CD."

Researchers at the Meir Medical Center are presently evaluating the safety and efficacy of inhaled cannabis for patients with CD and Ulcerative Colitis in a double-blind, placebo-controlled trial.

Crohn's disease and Ulcerative Colitis are inflammatory bowel diseases. According to survey data published earlier this year in the European Journal of Gastroenterology and Hepatology, an estimated one-third of patients with colitis and one-half of subjects with CD acknowledge having used cannabis to mitigate their disease symptoms.

For more information, please contact Paul Armentano, NORML Deputy Director, at: paul@norml.org. Full text of the study, "Treatment of Crohn's disease with cannabis: an observational study," appears in the Journal of the Israeli Medical Association. The study also appears online here: http://www.ima.org.il/imaj/ar11aug-01.pdf.
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Re: Cannabis research, medicine and use

Postby wordspeak2 » Thu Jan 05, 2012 11:12 am

Sorry to youtube you, but this just in- RAW cannabis has particular and unparalleled medical value: http://www.youtube.com/watch?v=z0VUsak2o9E
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Re: Cannabis research, medicine and use

Postby Laodicean » Thu Jan 05, 2012 12:00 pm

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