DEA Administrator Michele Leonhart filed paperwork today announcing that the agency is seeking to increase its marijuana production quota for the year 2015 by nearly three-fold.
Federal regulations permit a farm at the University of Mississippi to cultivate set quantities of cannabis for use in federally approved clinical trials. Regulators at the DEA, the US Food and Drug Administration, PHS (Public Health Service), and the US National Institute on Drug Abuse must approve any clinical protocol seeking to study the plant’s effects in human subjects.
The agency says that the increased production is necessary because “research and product development involving cannabidiol is increasing beyond that previously anticipated.” The agency further acknowledges having received increased requests from NIDA “to provide for ongoing and anticipated research efforts involving marijuana.”
The administration of the non-psychotropic cannabinoid cannabidiol (CBD) leads to improvement in bone fracture healing, according to preclinical data published online ahead of print in the Journal of Bone and Mineral Research.
Investigators at the Hebrew University Bone Laboratory in Israel assessed the ability of CBD administration to promote healing in rats with mid-femoral fractures. Researchers reported, “CBD markedly enhanced the biomechanical properties of the healing femora after 8 weeks.”
Authors also evaluated the administration of THC and CBD together, but reported that this combined preparation was “not advantageous” over CBD alone — indicating that the plant’s potential bone-stimulating properties are primarily specific to cannabidiol.
They concluded: “CBD alone is sufficiently effective in enhancing fracture healing. … Multiple experimental and clinical trials have portrayed CBD as a safe agent suggesting further studies in humans to assess its usefulness for improving fracture healing.”
Researchers have previously acknowledged that endogenous cannabinoids stimulate bone formation and inhibit bone loss, potentially paving the way for the future use of cannabinoid drugs for combating osteoporosis.
On Monday, I published a rebuttal of these claims in a commentary published on the website Alternet.org — an excerpt of which appears below.
Debunking the Latest Pathetic Fear Smear Campaign Against Marijuana
[excerpt] [N]umerous (though far less publicized) studies have come to light downplaying the likelihood that cannabis use is a direct cause of psychiatric disorders like schizophrenia. Specifically, a 2009 paper in the journal Schizophrenia Research compared trends in marijuana use and incidences of schizophrenia in the United Kingdom from 1996 to 2005. Authors reported that “incidence and prevalence of schizophrenia and psychoses were either stable or declining” during this period, even though pot use among the general population was rising. They 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.”
Similarly, a 2010 review paper published by a pair of British scientists in the journal Addiction reported that clinical evidence indicating that use of he herb may be casually linked to incidences of schizophrenia or other psychological harms is not persuasive. Authors wrote: “We continue to take the view that the evidence that cannabis use causes schizophrenia is neither very new, nor by normal criteria, particularly compelling. … For example, our recent modeling suggests that we would need to prevent between 3000 and 5000 cases of heavy cannabis use among young men and women to prevent one case of schizophrenia, and that four or five times more young people would need to avoid light cannabis use to prevent a single schizophrenia case. … We conclude that the strongest evidence of a possible causal relation between cannabis use and schizophrenia emerged more than 20 years ago and that the strength of more recent evidence may have been overstated.”
More recently, researchers at Harvard University released a study further rebutting this allegation. Writing in 2013 in Schizophrenia Research, investigators compared the family histories of 108 schizophrenia patients and 171 individuals without schizophrenia to assess whether youth cannabis consumption was an independent factor in developing the disorder. Researchers reported that a family history of schizophrenia increased the risk of developing the disease, regardless of whether or not subjects consumed weed as adolescents. They concluded: “The results of the current study, both when analyzed using morbid risk and family frequency calculations, suggest that having an increased familial risk for schizophrenia is the underlying basis for schizophrenia in these samples and not the cannabis use. While cannabis may have an effect on the age of onset of schizophrenia it is unlikely to be the cause of illness.”
In fact, some researchers speculate that specific cannabinoids, such as cannabidiol (CBD), may even be efficacious in treating symptoms of psychosis. According to a review published in the January 2014 issue of the journal Neuropsychopharmacology: “CBD has some potential as an antipsychotic treatment. … Given the high tolerability and superior cost-effectiveness, CBD may prove to be an attractive alternative to current antipsychotic treatment.” Specifically, a 2012 double-blind, randomized placebo-controlled trial assessing the administration of CBD versus the prescription anti-psychotic drug amisulpride in 42 subjects with schizophrenia and acute paranoia concluded that two substances provided similar levels of improvement, but that cannabidiol did so with far fewer adverse side effects.
Case reports in the scientific literature also indicate that some patients turn to cannabis for subjective benefits, though other studies indicate that pot use may exacerbate certain symptoms in patients with psychiatric disorders. Nonetheless, even a recent paper summarizing the “adverse health effects of recreational cannabis use” acknowledges, “It is difficult to decide whether cannabis use has had any effects on psychosis incidence, because even if a relationship were to be causal, cannabis use would produce a very modest increase in incidence.”
You can read my full commentary here.
You can also watch my discussion with Thom Hartmann of The Big Picture (air date: February 23) here.
At issue is whether a rational basis exists for the government’s contention that cannabis is properly designated as a schedule I substance — defined as possessing a “high potential for abuse,” “no currently accepted medical use in treatment,” and “a lack of accepted safety … under medical supervision.” A federal court has not heard evidence on the matter since the early 1970s.
Lawyers for the federal government argue that it is rational for the government to maintain the plant’s prohibitive status as long as there remains any dispute among experts in regard to its safety and efficacy. Defense counsel — attorneys Zenia Gilg and Heather Burke of the NORML Legal Committee — contend that the federal law prohibiting Justice Department officials from interfering with the facilitation of the regulated distribution of cannabis in over 20 US states can not be reconciled with the government’s continued insistence that the plant is deserving of its Schedule I status under federal law.
In October, defense counsel and experts presented evidence over a five-day period arguing that the scientific literature is not supportive of the plant’s present categorization. “Numerous clinical trials have been conducted using whole plant marijuana and have concluded the evidence strongly suggests therapeutic value,” defense counsel affirmed in a written brief filed with the court last month. “Physicians in 23 states and the District of Columbia have been recommending whole plant cannabis for treatment of a myriad of medical conditions. The United States, through SAMHSA (Substance Abuse Mental Health Services Administration, a branch of HHS), holds a patent [on the therapeutic utility of the plant.]”
“… It is unimaginable to believe that if heroin, cocaine, methamphetamine, or even over-the-counter medications were being distributed in 23 states and the District of Columbia, Congress and the President would abdicate all regulatory authority to those jurisdictions, and then cut off all funds … to intervene in related distribution activities. … Even the most vivid imagination would be hard pressed to reconcile such action with a ‘rational belief’ that marijuana is one of the most dangerous drugs in the nation.”
In a brief filed with the court by the federal government, it contends: “Congress’ decision to treat marijuana as a controlled substance was and remains well within the broad range of permissible legislative choices. Defendants appear to argue that Congress was wrong or incorrectly weighed the evidence. Although they failed to prove even that much, it would be insufficient. Rational basis review does not permit the Court’s to ‘second guess’ Congress’ conclusions, but only to enjoin decisions that are totally irrational or without an ‘imaginable’ basis.”
They add: “Congress is not required to be ‘right,’ nor does it matter if the basis on which Congress made its decision turns out to be ‘wrong.’ All that is required is that Congress could rationally have believed that its action — banning the production and distribution of marijuana — would advance its indisputably legitimate interests in promoting public health and welfare. Because qualified experts disagree, it is not for the Courts to decide the issue and the statute must be upheld.”
The Judge is anticipated to rule on defense’s motion within 30 days.
Legal briefs in the case, United States v. Pickard, et. al., No. 2:11-CR-0449-KJM, are available online here.
It was less than a year ago when the mainstream media was chock-full of headlines like this one: ‘Brain changes associated with casual marijuana use in young adults, study finds.’ The alarmist headlines were in response to a controversial paper published by researchers at Harvard University in Boston and Northwestern University in Chicago which alleged to have found differences in brain morphology in a cohort of 20 college-age marijuana users as compared to 20 non-users. The study’s investigators attributed the differences to subjects’ cannabis use.
But a funny thing happened when a team of scientists from the University of Colorado and the University of Kentucky tried to replicate these results in a separate, larger sample (158 participants) of subjects after rigorously controlling for both groups’ use of alcohol.
Writing in the January 28 edition of The Journal of Neuroscience, authors summarized:
“[T]his retrospective study examined brain morphology in a sample of adult daily marijuana users (n = 29) versus nonusers (n = 29) and a sample of adolescent daily users (n = 50) versus nonusers (n = 50). Groups were matched on a critical confounding variable, alcohol use, to a far greater degree than in previously published studies.
We acquired high-resolution MRI scans, and investigated group differences in gray matter using voxel-based morphometry, surface-based morphometry, and shape analysis in structures suggested to be associated with marijuana use, as follows: the nucleus accumbens, amygdala, hippocampus, and cerebellum.
No statistically significant differences were found between daily users and nonusers on volume or shape in the regions of interest. Effect sizes suggest that the failure to find differences was not due to a lack of statistical power, but rather was due to the lack of even a modest effect.”
Why the contradictory results? Investigators speculated that previously reported imaging studies failed to adequately control for the impact of alcohol, a substance that “unlike marijuana, … has been unequivocally associated with deleterious effects on brain morphology and cognition in both adults and adolescents.” In other words, researchers theorized that previously reported differences in the brain images of marijuana consumers as compared to non-users were likely because of subjects consumption of booze, not cannabis.
They concluded, “In sum, the results indicate that, when carefully controlling for alcohol use, gender, age, and other variables, there is no association between marijuana use and standard volumetric or shape measurements of subcortical structures. … [I]t seems unlikely that marijuana use has the same level of long-term deleterious effects on brain morphology as other drugs like alcohol. The press may not cite studies that do not find sensational effects, but these studies are still extremely important.”
An abstract of the study, “Daily Marijuana Use Is Not Associated with Brain Morphometric Measures in Adolescents or Adults,” is online here.