Work in progress: Unedited material.
The Rise and Fall of Medical Marijuana
The Compassionate Investigational New Drug program began distributing government-grown marijuana to a handful of medical marijuana patients in 1978. The program still supplies 300 marijuana cigarettes per month to eight surviving patients. In 1992, the program stopped accepting new applications, just as it was about to be inundated by thousands of applicants with AIDS.
Four years later, medical marijuana was legalized in California and Arizona. Because of the medical marijuana initiatives approved in these two states, President Clinton allocated one million dollars to review the existing research. As a result, in 1999, the most respected medical body in the United States, the Institute of Medicine, published Marijuana and Medicine: Assessing the Science Base, in which the authors reported, “The accumulated scientific data indicate a potential therapeutic value for cannabinoid drugs, particularly for pain relief, control of nausea and vomiting, and appetite stimulation.” However they flatly rejected the idea that herbal (usually smoked) cannabis would ever be considered a safe and effective medicine for widespread use.
Despite the fact that the Institute of Medicine concluded after reviewing relevant scientific literature—including dozens of works documenting marijuana’s therapeutic value—that “nausea, appetite loss, pain, and anxiety are all afflictions of wasting, and all can be mitigated by marijuana” and despite the fact that legal access to marijuana for specific medical purposes has been supported by numerous national and state medical organizations, including the American Medical Association-Medical Student Section, the American College of Physicians, the American Psychiatric Association’s Assembly, the American Academy of Addiction Psychiatry, the American Academy of Family Physicians, the California Medical Association, the Medical Society of the State of New York, the Rhode Island Medical Society, the American Academy of HIV Medicine, the HIV Medicine Association, the Canadian Medical Association, the British Medical Association, and the Leukemia and Lymphoma Society, among others (‘Proceedings’ 2008; ‘Medical Marijuana Endorsements’ 2008), indicating a growing acceptability of the therapeutic practice amongst organized medicine groups—a necessary prerequisite for availability of the service, federal agencies who are empowered by Congress make reclassifications based on scientific and medical considerations insist that marijuana “has no currently accepted medical use in treatment in the United States” and that “there is a lack of accepted safety for the use of” marijuana “under medical supervision” as grounds for maintaining its prohibition.
Let’s look at this for a moment…
Cannabis smoke contains many of the same carcinogens as tobacco smoke, including greater concentrations of certain aromatic hydrocarbons such as benzopyrene, prompting fears that chronic marijuana inhalation may be a risk factor for tobacco-use related cancers. Further, those who deny the validity of “medical marijuana,” cite that marijuana smoke contains four fold more tars than tobacco smoke. However, cannabinoids, constituents of marijuana smoke, have been recognized to have potential antitumor properties.
Certain cellular abnormalities in the lungs have been identified more frequently in long-term smokers of cannabis compared to non-smokers. Chronic exposure to cannabis smoke has also been associated with the development of pre-cancerous changes in bronchial and epithelium cells in similar rates to tobacco smokers. Cellular abnormalities were most present in individuals who smoked both tobacco and marijuana, implying that cannabis and tobacco smoke may have an additive adverse effect on airway tissue. The results suggest that long-term exposure to cannabis smoke, particularly when combined with tobacco smoking, is capable of damaging the bronchial system in ways that could one day lead to respiratory cancers.
In a 2005 study, Mia Hashibe and others reviewed two cohort studies and 14 case–control studies with assessment of the association of marijuana use and cancer risk. It was concluded that lung cancer, due to marijuana smoking, was not observed in the cohort studies but increased risks of prostate and cervical cancers among non–tobacco smokers, as well as adult-onset glioma among tobacco and non–tobacco smokers, were observed. The 14 case–control studies included four studies on head and neck cancers, two studies on lung cancer, two studies on non-Hodgkin’s lymphoma, one study on anal cancer, one study on penile cancer, and four studies on childhood cancers with assessment of parental exposures. The results were largely mixed. One case control study reported that marijuana use may increase risk of head and neck cancer, with dose-response relations for both frequency and duration of use. However, another study reported no association between oral cancer and marijuana use in a population-based case–control study. An eightfold increase in risk among marijuana users was observed in a lung cancer study in Tunisia. However, there was no assessment of the dose response, and marijuana may have been mixed with tobacco. Parental marijuana use during gestation was associated with increased risks of childhood leukemia, astrocytoma, and rhabdomyosarcoma, but dose-response relations were not assessed. The researchers concluding, “In summary, sufficient studies are not available to adequately evaluate marijuana impact on cancer risk.”
However, in a later study conducted by Caihua Liang and others (2009) it was shown after adjusting for potential confounders (including smoking and drinking), 10 to 20 years of marijuana use was associated with a significantly reduced risk of head and neck cancers.
In a 2005 study conducted by the University of Colorado it was shown that the pharmacological effects of tobacco and cannabis smoke differ in many ways, mainly because tobacco smoke contains nicotine while cannabis smoke contains tetrahydrocannabinol (THC). Seemingly, the cancer-promoting effects of smoke are increased by nicotine, while they are reduced by THC. Further research has shown that THC and other cannabinoids inhibit the growth of glioma cells both in vitro and in various rodent xenograft models. This anticancer activity is dependent on the modulation of key signaling pathways that trigger cancer cell death as well as other events such as inhibition of tumour angiogenesis, cell proliferation and cell invasion.
In September of 2011, the University of Colorado Cancer Center published a paper which summarized the current status of Marijuana in the United States. The paper summarized that, “There is little direct evidence that THC or other cannabinoids are carcinogenic” and that THC as a compound is not cancer causing. “By contrast, cannabis smoke is carcinogenic in rodents and mutagenic.” However, in humans it has been more difficult to definitively prove.
In January of 2012, a 20-year study of pulmonary function and marijuana exposure concluded that, “Our findings suggest that occasional use (1 joint a day for 7 years or 1 joint/week for 49 years) of marijuana for these or other purposes may not be associated with adverse consequences on pulmonary function. It is more difficult to estimate the potential effects of regular heavy use, because this pattern of use is relatively rare in our study sample; however, our findings do suggest an accelerated decline in pulmonary function with heavy use and a resulting need for caution and moderation when marijuana use is considered.”
Chronic use studies in recreational users in Jamaica, Greece, and Costa Rica in the 1970s-1980s documented minor pulmonary changes without significant neuropsychological or other sequelae (secondary consequence or result). The Chronic Use Study of 4 subjects employing high daily intake of cannabis therapeutically over a long interval in the USA Compassionate Use Investigational New Drug Program similarly demonstrated slight pulmonary function changes, with minimal executive function effects, but no endocrine, immunological, neurophysiological or anatomical changes.
A single New Zealand study published in 2005 showed that cannabis use did increase the risk of lung cancer. In total, 79 cases of lung cancer and 324 controls were included in the study. The risk of lung cancer increased 8% for each joint-yr of cannabis smoking, after adjustment for confounding variables including cigarette smoking, and 7% (95% CI 5–9) for each pack-yr of cigarette smoking, after adjustment for confounding variables including cannabis smoking. However, this study has largely been debunked by several leading international researchers.
In the largest case-control study ever done, Donald Tashkin and others unexpectedly concluded in 2012 that smoking marijuana, even regularly and heavily, does not lead to lung cancer, and there was even a suggestion of some “protective effect” among marijuana smokers who had lower incidences of cancer compared to non-users. The study followed 5,115 regular pot smokers over the course of 20 years.
Tashkin’s group at the David Geffen School of Medicine at UCLA had hypothesized that marijuana would raise the risk of cancer on the basis of earlier small human studies, lab studies of animals, and the fact that marijuana users inhale more deeply and generally hold smoke in their lungs longer than tobacco smokers — exposing them to the dangerous chemicals for a longer time.
While no association between marijuana smoking and cancer was found, the study findings, presented to the American Thoracic Society International Conference, did find a 20-fold increase in lung cancer among people who smoked two or more packs of cigarettes a day.
All research aside, It should be noted that with the development of vaporizers, that use the respiratory route for the delivery of carcinogen- free cannabis vapors, the carcinogenic potential of smoked cannabis has been largely eliminated.
In principle, vaporization offers medical cannabis patients the advantages of inhaled routes of administration: rapid onset, direct delivery into the bloodstream, ease of self-titration and concomitant avoidance of over- and under-dosage, while avoiding the respiratory disadvantages of smoking.
In research conducted by Dale Gieringer et al (2004), vapors from a vaporizer were found to consist overwhelmingly of THC, the major active component in marijuana, whereas combusted smoke contained over 100 other chemicals, including several polynuclear aromatic hydrocarbons (PAHs), carcinogenic toxins that are common in tobacco smoke.
The study used a gas chromatograph mass spectrometer (GCMS) to examine the gas components of the vapor. The analysis showed that vaporized cannabis was remarkably clean, consisting 95% of THC with traces of cannabinol (CBN), another cannabinoid. The remaining 5% consisted of small amounts of three other components: one suspected cannabinoid relative, one suspected PAH (Polycyclic Aromatic Hydrocarbon), and caryophyllene, a fragrant oil in cannabis and other plants. In contrast over 111 different components appeared in the gas of the combusted smoke, including a half dozen known PAHs. Non-cannabinoids accounted for as much as 88% of the total gas content of the smoke.
Another laboratory study found that a vaporisation device provided an efficient and reproducible mode of delivery of THC.A further pilot human laboratory study comparing a vaporiser to smoked cannabis found that the vaporiser was as effective as delivering THC but with little or no increase in carbon monoxide levels, a marker for toxins that may be generated by smoking.
Additionally, medical dispensaries also supply edibles (THC cookies, cake, ice creams etc).
Officially, the US Federal Government’s stance is that cannabis has no medicinal value and therefore lists it as a schedule 1 drug under The Controlled Substances Act. Schedule I drugs are classed as having a high potential for abuse. They have no currently accepted medical use in treatment in the United States, and there is a lack of accepted safety for use of the drug or other substance under medical supervision. Just one other example of a Schedule I drug is heroin.
Odd!? The pharmacology of heroin is virtually identical to that of morphine, other than heroin is a more refined clean form of morphine. Studies comparing the actions of heroin and morphine in cancer patients with severe pain have shown very little difference between the two agents, other than simple potency. Heroin may have a slightly more rapid onset of action than morphine and it is certainly two to three times as potent (presumably due to its greater facility in crossing the blood-brain barrier). The pain relief from both agents is comparable when the doses are adjusted appropriately. At equally effective doses, even the euphoria seen with heroin is virtually identical to that of morphine. From the clinical point of view, there is little difference between one drug and the other. Both are effective analgesics and can be used beneficially in the treatment of severe pain. Heroin is more soluble, which makes it somewhat easier to give large doses by injection, with smaller volumes needed.
In a few countries, most notably the United Kingdom, heroin is used routinely in hospital for acute pain. In The UK diamorphine is the name of the drug, in the rest of the world the chemical name of heroin is diacetylmorphine.
Many countries believe that the international drug conventions prohibit the use of heroin in medical treatment. Furthermore, the International Narcotics Control Board (INCB – who claim to be a neutral UN body) has exerted great pressure on countries to cease prescribing heroin for any medical purpose. Nevertheless, a few countries, including the UK, Belgium, the Netherlands, Iceland, Malta, Canada, and Switzerland, continue to use heroin (diamorphine) for general medical purposes, mostly in hospital settings (usually for severe pain relief).
Contrary to popular belief, Diamorphine is not “crude” or even “bad.” In reality, morphine is crude when compared to heroin. Heroin was made from morphine because, in part, they wanted to have a drug with fewer side effects than morphine or codeine, and heroin does have fewer side effects. The only real problem with heroin, other than addiction, is when it is sold by criminals and administered in non-medical settings. At this point, heroin is cut with all manner of agents, varies greatly in purity and is extremely expensive. The result is drug related crime, inconsistent batch purities, poly drug use (users often topping up with other depressants such as benzodiazepines due to the prohibitive cost of street heroin and as a result greatly increasing the risk of overdose), dirty batches, and needle sharing – leading to blood borne viruses and vein damage – and, of course, overdose.
This said, in spite of all the medical evidence, backed by substantial reviewed research, the US lists heroin as having “no medicinal value”.
So what of cannabis?
The AMA, the largest and oldest U.S. physician based group, in November of 2010 voted to reverse its long held position that marijuana should be retained as a schedule 1 substance with no medical value. The AMA adopted a report drafted by its Council on Science and Public Health (CSAPH) entitled, “Use of Cannabis for Medicinal Purposes,” which affirmed the therapeutic benefits of marijuana and called for further research. The CSAPH report concluded that, “short term controlled trials indicate that smoked cannabis reduces neuropathic pain, improves appetite and caloric intake especially in patients with reduced muscle mass, and may relieve spasticity and pain in patients with multiple sclerosis.” The AMA’s about face on medical marijuana followed an announcement by the Obama Administration discouraging U.S. Attorneys from taking enforcement actions in medical marijuana states. In February 2008, a similar resolution was adopted by the American College of Physicians (ACP), the country’s second largest physician group and the largest organization of doctors of internal medicine.
Add to this, that it’s somewhat paradoxical that the US Federal Government claims that cannabis has “no medicinal value”, when Marinol (active, Dronabinol, a synthetic THC) was approved by the FDA in 1985 to treat nausea and vomiting associated with cancer chemotherapy in patients who have failed to respond adequately to conventional treatments.
The FDA also approved MARINOL® to treat appetite loss associated with weight loss in people with AIDS. In clinical trials, it was shown that the appetite stimulant effect of Marinol Capsules in the treatment of AIDS related anorexia resulted in improved body weight and mood, and decreases in nausea.
Yet another synthetic Cannaboid product, Nabiximols (trade name Sativex) is registered and prescribed in several countries. Sativex is a cannabinoid oromucosal mouth spray developed by the UK company GW Pharmaceuticals for multiple sclerosis (MS) patients, who can use it to alleviate neuropathic pain. spasticity, overactive bladder, and other symptoms. Sativex is also being developed in Phase III trials as a potential treatment to alleviate pain due to cancer.
In June 2010, the Medicines and Healthcare products Regulatory Agency of the United Kingdom licensed Sativex as a prescription-only medicine for the treatment of spasticity due to multiple sclerosis.
Sativex was also approved in Spain for MS spasticity in the second half of 2010 and was launched in that country in March 2011. It was approved in the Czech Republic in April 2011, in Germany in May 2011 and in Denmark in June 2011. It has also been recommended for approval in Italy, Sweden and Austria.
In Canada, Sativex has been approved for the treatment of MS spasticity. It has also received a licence with conditions for two additional uses: for treatment for the symptomatic relief of neuropathic pain in multiple sclerosis,and also for pain due to cancer.
Additionally, Cannabinoid medicines such as Sativex have been proposed as promising medicines for the treatment of Parkinson’s disease (PD), Huntington’s disease (HD) and other brain neuron related motor function diseases.
In spite of this, in 2006 the Food and Drug Administration (FDA) issued an advisory against smoked medical cannabis stating that, “marijuana has a high potential for abuse, has no currently accepted medical use in treatment in the United States, and has a lack of accepted safety for use under medical supervision. Furthermore, there is currently sound evidence that smoked marijuana is harmful.” In 2011,The National Institute on Drug Abuse (NIDA) stated that “Marijuana itself is an unlikely medication candidate for several reasons: (1) it is an unpurified plant containing numerous chemicals with unknown health effects; (2) it is typically consumed by smoking further contributing to potential adverse effects; and (3) its cognitive impairing effects may limit its utility”.
Let’s address their points. “(1) it is an unpurified plant containing numerous chemicals with unknown health effects.”
True, the jury is still out on factors such as addiction and mental illness – particularly among vulnerable young people and those predisposed to mental illness. For instance, it is claimed that marijuana is addictive for about 9% of adults who use it (compared with about 15% who use alcohol and 15% who use cocaine), according to federal data. Because it is the most widely used illegal substance in the country, marijuana dependence is more common than addiction to either cocaine or heroin despite its lower addiction potential. But then again, the same bodies (NIDA and the FDA) have authorized drugs such as barbiturates, benzodiazepines, opiate pain relievers, amphetamines and stimulants where there is a known and well-documented propensity to addiction and negative “health effects.”
Just two examples…
Opioid pain relievers (OPR) can be deadly, with too high a dose or when taken with other CNS depressants, like alcohol. Brand names include, Vicodin, OxyContin, and Percocet.
In 2008, drug overdoses in the United States caused 36,450 deaths. OPR were involved in 14,800 deaths (73.8%) of the 20,044 prescription drug overdose deaths. Death rates varied fivefold by state. States with lower death rates had lower rates of nonmedical use of OPR and OPR sales. During 1999–2008, overdose death rates, sales, and substance abuse treatment admissions related to OPR all increased substantially. Prescription drugs are now killing far more people than illegal drugs, and while most major causes of preventable deaths are declining, those from prescription drugs are drastically increasing. Data from the U.S. Centers for Disease Control and Prevention in 2009, showed for the first time ever in the US, more people were killed by prescription drugs than motor vehicle accidents which were previously the number one cause of accidental deaths in the United States. By 2010, enough OPR were sold to medicate every American adult with a typical dose of 5 mg of hydrocodone every 4 hours for 1 month. OxyContin is the brand name of a time-release formula of oxycodone produced by the pharmaceutical company Purdue Pharma. It was approved by the U.S. Food and Drug Administration in 1995 and first introduced to the U.S. market in 1996.By 2001, OxyContin was the best-selling non-generic narcotic pain reliever in the U.S; 2008 sales in the U.S. totaled $2.5 billion.
Nearly half of all pharmaceutical drugs within the United States were not only produced overseas, but an alarming number of 81% of the 3,765 foreign factories have never been inspected by the Food and Drug Administration (FDA). Of these factories, many are unregulated and stationed in China. Additionally, the percentage climbs even higher when looking at the active ingredients for pharmaceuticals. About 80%of these active ingredients are created overseas. Inspections of foreign drug manufacturers are an important element of the FDA’s oversight of the supply chain, but the U.S Government Accountability Office (GAO) showed that FDA conducts relatively few such inspections. In 2008, GAO reported that in fiscal year 2007 FDA inspected 8 percent of foreign establishments subject to inspection and estimated that, at that rate, it would take the FDA about 13 years to inspect all such establishments. Additionally, In contrast to domestic inspections which are conducted without prior notice, the FDA contacts foreign manufacturers prior to inspection to ensure that the appropriate personnel are present and that the establishment is manufacturing its product during the time of the inspection. In some cases, the FDA must obtain permission from the foreign government of the country in which an establishment is located in order to conduct an inspection. FDA officials report that inspections may be conducted several months after an establishment has been notified of FDA’s intent to conduct an inspection due to the need to obtain visas and other delays. As a result of such advance notice, FDA staff conducting the inspections may not observe an accurate picture of the manufacturer’s day-to-day operations.
The “war on drugs” has focused nearly exclusively on the illegal trafficking of drugs like cocaine, methamphetamine, heroin, and marijuana, while the most powerful drug dealers of all — the pharmaceutical companies — are allowed to expand their businesses with the U.S Government’s approval. But then with the millions of dollars that various politicians take in donations and backroom golden handshakes from pharmaceutical companies this is hardly surprising.
The Pharmaceutical Research and Manufacturers of America, also known as PhRMA, is one of the largest and most influential lobbying organizations in Washington.Representing 48 pharmaceutical companies, PhRMA has 20 registered lobbyists on staffand has contracted with dozens of lobby and PR firms. In 2010, PhRMA spent $21,740,000 on lobbying costs.
Then there is the “American Legislative Exchange Council” (ALEC.) ALEC is not a lobbyist group – it is much more powerful than that. With more than 2,000 members, ALEC is the nation’s largest, non-partisan, individual public-private membership association of state legislators. Through ALEC, behind closed doors, corporations hand state legislators the changes to the law they desire that directly benefit their bottom line. Along with legislators, corporations have membership in ALEC. Corporations sit on all nine ALEC task forces and vote with legislators to approve “model” bills. They have their own corporate governing board which meets jointly with the legislative board. (ALEC says that corporations do not vote on the board.) They fund almost all of ALEC’s operations. Elected legislators who are active in ALEC, overwhelmingly right-wing politicians, then bring those proposals home and introduce them in statehouses without disclosing that corporations crafted and voted on the bills.
Soon after Wisconsin Governor Scott Walker came into office, Walker and GOP state legislators pushed for the adoption of Wisconsin Act 2, an ALEC-influenced bill that benefitted the bottom line of PhRMA members. The bill seeks to implement “tort reform” by “limiting the ability to hold corporations accountable for causing injury or death” and “make it easier for corporations like pharmaceutical manufacturers to escape liability for manufacturing dangerous products or products with insufficient warnings about hazards.” The legislation drew heavily from ALEC Model bills on tort reform, including the “Constitutional Guidelines for Punitive Damages Act” and the “Product Liability Act.” On January 27, 2011, the bill was signed into law. Republicans also sought to pass LRB 2890, a bill introduced in October 2011 that is based on ALEC’s “Drug Liability Act.” The bill “gives drug and medical device manufacturers complete immunity from lawsuits based on strict liability if the product was approved by the Food and Drug Administration.”
Next off the block… ADHD drugs, or “Speed” for kiddies.
Legalized amphetamines, or stimulants, are most commonly prescribed for attention deficit/hyperactivity disorder (ADHD) and today are dolled out like lollies to millions of children and others worldwide. Brand names include, Concerta, Dexedrine, and Ritalin.
Over the past 15 years doctors have been prescribing stimulants for a rapidly rising number of patients, who also increasingly take the drugs for many years. With the expanded and extended use of stimulants comes mounting concern that the drugs might wreak silent havoc on the brain over the long term. Some recent studies, most of them involving animals, hint that stimulants could alter the structure and function of the brain in ways that may depress mood, boost anxiety and, in sharp contrast to their short-term effects, lead to cognitive problems.
Before 1970, the diagnosis of ADHD was relatively rare for schoolchildren and almost nonexistent for adolescents and adults. Between 1980 and 2007, there was an almost 8-fold increase of ADHD prevalence in the United States compared with rates of 40 years ago. Considering the prevalence of school-administered stimulants as synonymous with the prevalence of ADHD, it is estimated the prevalence of ADHD in American schoolchildren as 1% in the 1970s, 3% to 5% in the 1980s, and 4% to 5% in the mid to late 1990s. In 2007, using data from the National Survey of Children’s Health, Visser and colleagues reported that 7.8% of youths aged 4 to 17 years had a diagnosis of ADHD and 4.3% reported current use of a medication for the disorder; although it is definitely known that there are rare occurrences of cardiovascular adverse events associated with medications used in the treatment of ADHD, including methylphenidate, amphetamine products, and atomoxetine.
In 1997, Congress passed the FDA Modernization Act, which encouraged the pharmaceutical industry to develop and test drugs for children by extending patent exclusivity. This resulted in a dramatic increase in randomized controlled trials in children that involved stimulant compounds for ADHD and further supported an evidence-based rationale for medication intervention in ADHD. As a result, the prescribing of stimulants for children with ADHD increased 4-fold between 1987 and 1996, with a further increase of 9.5% between 2000 and 2005. Currently, slightly more than 4% of children and adolescents in the United States use ADHD medications. The long-term benefits and risks of stimulant treatment are not known definitively.
A DEA report from 1996 states that, “ medical experts agree that these drugs do help the small percentage of children who need them. But there is also strong evidence that the drugs have been greatly over-prescribed in some parts of the country as a panacea for behavior problems. These drugs have been over-promoted, over-marketed and over-sold, resulting in profits of some $450 million annually. This constitutes a potential health threat to many children and has also created a new source of drug abuse and illicit traffic. The data shows that there has been a 1,000 percent increase in drug abuse injury reports involving methylphenidate for children in the 10 to 14 age group. This now equals or exceeds reports for the same age group involving cocaine. The reported numbers are still small but experts feel that this is only the “tip of the iceberg.”
In a 2006 study, researchers investigated the characteristics of use, misuse, and abuse of stimulant medication among students at a northeastern US university. Researchers sent an invitation to take an Internet survey to student e-mail addresses and passed 150 paper surveys in undergraduate classes, analyzing 1,025 (975 electronically) returned surveys. Sixteen percent of respondents reported abusing or misusing stimulant medication. Ninety-six percent of respondents who specified a medication preferred to abuse or misuse Ritalin. Men and women reported similar use patterns. Most respondents who abused or misused stimulant medication swallowed pills; 40% used intranasally. Reasons for abusing or misusing stimulant medication included improving attention, partying, reducing hyperactivity, and improving grades. Consistent with previous studies, results suggest that abuse of stimulant medication is a concern on college campuses.
Health risks related to stimulant abuse include increased heart and respiratory rates, excessive sweating, vomiting, tremors, anxiety, hostility and aggression, and in severe abuse, suicidal/homicidal tendencies, convulsions, and cardiovascular collapse. Amphetamine-based drugs for ADHD, such as Adderall and Dexedrine, now come with a new, expanded ‘black box’ warning for an increased risk of sudden death in patients with heart problems.
Joseph Biederman, a high-profile doctor who is largely responsible for the explosion of children on psychiatric drugs, first for attention deficit hyperactivity disorder (ADHD) and then for bipolar disorder, in 2008 was called to task by congressional investigators for taking $1.6 million from drug makers from 2000 to 2007 and failing to report most of these earnings to his university, Harvard – a major conflict of interest on the part of an academic researcher. In 2007, Biederman was ranked as the second highest producer of high-impact papers in psychiatry overall throughout the world with 235 papers cited a total of 7048 times over the past 10 years as determined by the Institute for Scientific Information (ISI).The same organization ranked Biederman at number one in terms of total citations to his papers published on ADD/ADHD in the past decade After being called to task by investigators, as part of this legal proceeding, Biederman was forced to provide documents relating to his interactions with Johnson & Johnson, the giant pharmaceutical company. These documents included presentations he made over several years summarizing the work of his center financed by Johnson & Johnson. On March 20, 2009, the New York Times reported that Biederman pitched Johnson & Johnson that his proposed research studies on its antipsychotic drug Risperdal would turn out favorably for Johnson & Johnson — and then Biederman delivered the goods.
The Times also reported that in 2005 Biederman proposed a study on adolescents using the ADHD-drug Concerta, manufactured by Johnson & Johnson, and he assured the company that his study would “extend to adolescents positive findings with Concerta.” And in 2006, Biederman was co-author of a study showing that children given Concerta for a prolonged period did not have reduced growth, allaying a significant concern about the medicine — but in contradiction to what has now been established.
Lets for a moment compare legal drug deaths to cannabis (it will only take moment and the picture is more than clear – except for where the US Federal Government is concerned).
Prescription Drug Deaths in the US in 2010 total 82,724
Tobacco related deaths in the US total 443,000 deaths per year, and an estimated 49,000 of these smoking-related deaths are the result of secondhand smoke exposure
Alcohol related deaths in the US is estimated to be at 75,000 per year
Cannabis related deaths in the US in 2010 – not a single death is recorded where cannabis is the primary drug. I.e. In The Substance Abuse and Mental Health Services Administration’s (SAMHSA) 2003 report Mortality Data from the Drug Abuse Warning Network, 2001 stated, “Marijuana is rarely the only drug involved in a drug abuse death. Thus … the proportion of marijuana-induced cases labeled as ‘One drug’ (i.e., marijuana only) will be zero or nearly zero.”
Cannaboids and Research
The cannabinoid Δ9-tetrahydrocannabinol (THC) was characterised in the 1960s, but for the next 20 years, it was unclear how THC exerted its effect on the brain. In 1988, endogenous THC-binding receptors were reported. Soon after, a naturally occurring cannabinoid (termed an ‘endogenous cannabinoid’, or an ‘endocannabinoid’) was identified in the brain—anandamide. Since then, several other endocannabinoids have been discovered.
The naturally occurring cannaboids in cannabis activate specific receptors found throughout the body to produce pharmacologic effects, particularly in the central nervous system and the immune system.
Cannabis sativa L. is a rich source of a variety of compounds, including classes such as cannabinoids, terpenoids and flavonoids. To date, approximately 68 different cannabinoids have been identified in the plant.
The rising prominence of phytocannabinoid-rich botanicals in health care is actually a rediscovery and not a novel medical practice since the medicinal use of dried, resinproducing pistillate inflorescences of Cannabis sativa has an extensive ancient history cross-culturally, with the oldest documented references known today in the Chinesepharmacopoeia of Emperor Shen-Nung dated to 2737 BCE in the oral tradition, but written down in the first century CE (Earlywine 2002, p.26; Abel 1980). The medical use of cannabis in the modern period was common in the USA from the mid-1850s to the early 1940s due to its introduction into Western medicine as ‘Indian Hemp’ by Calcutta Medical College co-founder and professor, Dr. W.B. O’Shaughnessy.
Cannabinoids and opioids share several pharmacologic properties, including antinociception, hypothermia, sedation, hypotension and inhibition of intestinal mobility and locomotor activity. Data suggest the existence of independent but related analgesic pathways for cannabinoids and opioids such that the two may be synergistic. Cannabinoids may also ameliorate opioid side effects, particularly nausea and vomiting.
Cannabinoids, along with other bioactive compounds, have many distinct pharmacologic properties, including analgesic, antiemetic, antispasmodic, antioxidative, neuroprotective, antidepressant, anxiolytic, and anti-inflammatory properties, as well as glial cell modulation and tumor growth regulation. Their application in pain treatment is especially promising as cannabinoids inhibit pain in “virtually every experimental pain paradigm” insupraspinal, spinal, and peripheral regions and have no risk, unlike opiates, of accidental lethal overdose.
Cannabinoids have been shown to induce their biological effects mainly by binding to specific cannabinoid receptors. Presently, two main subtypes of cannabinoid receptors have been identified, designated cannabinoid receptor 1 (CB1) and cannabinoid receptor 2 (CB2). Although, CB1 is predominantly expressed in the brain (central nervous system, CNS), it has also been detected in the periphery. CB1 receptors appear to be responsible for the euphoric and anticonvulsive effects of cannabis. Conversely, CB2 receptor appears to be the principal form of cannabinoid receptor within the immune system, with no quantifiable expression in the brain. CB2 receptors appear to be responsible for the anti-inflammatory and possibly other therapeutic effects of cannabis.
In a recent study the effects of two synthetic cannabinoids – Methanandamide (MET) and JWH-015 – were tested to treat prostate cancer. The researchers tested the chemicals on different human prostate cancer cell lines grown in the lab, and found that they could slow down their growth and trigger cell death.
By using drugs that block either one receptor or the other, or a genetic technique called RNA interference to ‘knock out’ CB1 or CB2 in turn, the scientists found that the anti-cancer effects of MET and JWH-015 were brought about by CB2.
The Californian Fiasco
In 1997, the US Federal Government began a campaign to arrest and prosecute medical cannabis patients and their providers. These raids resulted in two Supreme Court Cases, OCBC (United States v. Oakland Cannabis Buyers’ Cooperative, May 14, 2001) and Gonzales v. Raich (2005). In each of these cases the Justices found that the federal law and state law can exist in conflict and that the US Federal Government could continue their campaign against medical marijuana patients at their discretion However, the Justices questioned “the wisdom’ of going after patients and their providers and called on Congress to change the current laws to allow for medical use. The US Federal Government chose to ignore these callings and as a result a legal dichotomy between the med states and the federal government exists.
According to the DEA, California is responsible for more than a third of the cannabis harvest, with an estimated production of $13.8 billion that exceeds the value of the state’s grapes, vegetables and hay combined.
California contains 13.25% of annual marijuana users in the United States according to the National Survey on Drug Use and Health but also accounts for 38.68% of the marijuana produced in the United States, a ratio of production to use of 2.92. On this basis California is considered a major export state in which marijuana is produced both for instate use and export to other areas. According to the HIDTA (High Intensity Drug Trafficking Area), California may supply as much as 3/4 of the cannabis consumed in the US.
In 2006 US authorities eradicated 2,642,352 plants in California. In 2007 there were 4,961,313 marijuana plants seized. During 2008, there were 5,432,053 plants eradicated and in 2009 the total eradication was 7,519,580 plants, nearly a 300 percent increase in 4 years.
Putting this into context, there were 1,489,643 kilograms of cannabis seized during 2009 at the U.S.-Mexico border. This amounts to 1,486 Metric Tons of cannabis, about 1/3rd of what was eradicated in California in the same year.
During 2009 law enforcement agencies reported to the Drug Enforcement Administration Domestic Cannabis Suppression and Eradication Program (DC/SEP) that they seized 10.3 million marijuana plants from indoor and outdoor grow sites. According to the UNODC 10-20% of illegal cannabis is located and seized. Using the figure of 15% would mean that 49,104,576 plants were grown, in 2009, in California alone.
In line with these figures, marijuana arrests in California increased in 2008 to their highest level since possession was decriminalized in 1976, according to data from the Cal DOJ Bureau of Criminal Statistics. California reported 17,126 felony arrests in 2008, up from 16,124 in 2007, while misdemeanor marijuana possession arrests jumped from 57,995 to 61,366. According to data from the Bureau of Criminal Statistics, California reported nearly the same number of marijuana arrests in 2009 (17,008 felony and 61,164 misdemeanor marijuana arrests, for a total of 78,172).
Possession arrests have soared 127 percent since 1990, a time period when arrests for other crimes plummeted by an average of 40 percent, according to the Center on Juvenile and Criminal Justice in San Francisco.
The number of marijuana prisoners has held more or less steady in California since the height of the drug war in the late 1980s, despite the passage of Prop. 215. There are now over 14 times as many marijuana prisoners in California as in 1980. This does not account for federal prisoners, all of whom are serving mandatory minimums of at least five years for medical marijuana related offences.
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