Moderators: Elvis, DrVolin, Jeff
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.
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.
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.
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.
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.
That Sagan essay was excellent, thank you Pengs.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
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
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.
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
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.
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
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
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.
"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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