The Weed America Loves to Hate
Beth McCauley, a 57-year-old Los Angeles business executive, had a vicious case of trigeminal neuralgia, a facial pain condition so excruciatingly painful it’s often called “the suicide disease.” “It feels like my entire face is on a greasy griddle at 350 degrees, with someone pushing my face down on it,” McCauley told me. She tried Buddha-like acceptance of her fate, which helped somewhat. Biofeedback, which also helped. And a pain medication that helped until its side effects made her cut her dose drastically.1 Finally, in desperation, she tried marijuana, or, more correctly, cannabis, which comes from the plant Cannabis sativa.
“It was the most amazing thing,” she said. Now when she gets breakthrough pain, she takes a puff or two of a joint. “The pain stays there, but it moves about a foot and a half off my face. All of a sudden, I can just breathe,” said McCauley, who has formed a company that tests the purity of cannabis. She can completely forget about the pain and go about her business, with relief coming in less than a minute. “I don’t even think about my face anymore,” she told me. “I can keep going. It changed my life.”
Cannabis has changed Marcy Duda’s life, too. Duda, 50, a skinny, blond Massachusetts grandmother of two, told me marijuana is the only thing that touches her migraines, which she describes as “hot, hot ice picks” in the left side of her head.2 Duda has had migraines her whole life. But they got much worse a decade or so ago after she had two operations to remove aneurysms, weak areas in the blood vessels in her brain that could have ruptured—fatally—at any moment. She survived the surgeries but was left with chronic pain all down her left side, as if her body were cut in half. Doctors gave her drugs, but nothing really worked. Then she tried cannabis, which she smokes—researchers prefer the term “inhales”—through a vaporizer. Her experience is much like McCauley’s. “It doesn’t miraculously wipe the headaches away,” Duda said, “but it’s better than any other drug.” And unlike drugs that must pass through the digestive system, she has found, inhaled marijuana gives her instant relief.
Beth McCauley and Marcy Duda are among the countless Americans—nobody knows the actual number—who use marijuana for a variety of medical problems, including pain. But lost in the headlines about unscrupulous marijuana smugglers and teenage abusers is what scientific research says about how marijuana works in the body.
In this chapter, we’ll explore what that evidence does—or does not— show about medical marijuana’s safety and effectiveness. We’ll see how marijuana interacts with pain circuits in the brain. How effectively it may combat pain. How serious the side effects are, and for whom.
And of course, what the risks of dependence and addiction are. Whether marijuana creates tolerance (the need to keep increasing doses to get the same effect). And whether the government-approved, single-ingredient pills are as effective as inhaling the real stuff with all the components nature concocted. (We will not get into the distracting issue of dangerous synthetic cannabinoids such as “Spice,” “K2,” and “Aroma,” which should not be confused with medical marijuana.3, 4, 5, 6) At the end of the chapter, we will, of course, address the legal and political issues surrounding marijuana, and offer one solution.7
But first, a startling contrast. In the United States, the federal government still seems to see marijuana, even medical marijuana, as dangerous and seductive.8 In spite of significant evidence that marijuana is remarkably safe. Put bluntly, people do not die from marijuana. There are simply no deaths—zero—attributable to marijuana, according to the government’s own statistics, from the federal Centers for Disease Control and Prevention, as well as from other studies.9, 10 In stark contrast, government figures show that 443,000 American adults die every year from cigarette smoking, and more than 80,000 die annually from excessive alcohol use.11, 12 Even nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen are more dangerous than marijuana—they kill an estimated 7,000 to 10,000 American adults a year.13
The main reason marijuana is so nonlethal is that, unlike opioids, it does not cause respiratory depression. This means it is unlikely to cause a person to stop breathing. With marijuana, overdosing is extremely rare and is usually accompanied by the use of other drugs, such as alcohol, as McGill University researchers noted in a 2005 review.14 In fact, they add, a lethal dose of tetrahydrocannabinol (THC) has never been reported. Two other large studies support this, showing no increase in the death rate attributable to cannabis.15 Even the National Institute on Drug Abuse acknowledges the nonlethality of cannabis.
“Marijuana does not kill directly,” acknowledged Steven Gust, special assistant to the director of National Institute on Drug Abuse (NIDA), though it can contribute to risky behavior, such as driving while stoned and drunk.16 This safety profile has held true for decades, as even an administrative law judge for the Drug Enforcement Administration noted in 1988 in an official finding of fact: “There is no record in the extensive medical literature describing a proven, documented cannabis-induced fatality.” (By contrast, the judge noted, aspirin causes hundreds of deaths a year.)17
So what is this plant that is causing such controversy? Cannabis (and scientists prefer this term to marijuana) is a psychoactive plant with significant healing properties that has been around for millennia. It is believed to contain hundreds of different chemicals. Usually smoked as a cigarette, it’s the most commonly used illegal substance in America, according to NIDA.18 In 2010, 17.4 million Americans were current users of marijuana, up from 14.4 million in 2007.19
But cannabis is also one of the most potent natural herbal medicines in the world, a staple of traditional Chinese medicine. Indeed, flowers from the female cannabis plant were found in the 2,700-year-old tomb of a medicine man in Northern China. From China, the medicinal use of marijuana spread to India. There, a British surgeon “discovered” its healing properties and introduced it into Western medicine in the 1840s. (There’s even a story—false, as it turns out—that Queen Victoria used cannabis for menstrual cramps.20, 21, 22)
Among other uses, cannabis was used as a treatment for migraines in many ancient cultures, not just the Chinese and Indian, but Egyptian, Assyrian, Greek, and Roman as well.23, 24 By the early 1900s, it wasn’t just ancient cultures that appreciated cannabis. Americans were catching on, too, including pharmaceutical companies, which saw the promise of marijuana and began creating their own preparations, according to cannabis researcher Donald Abrams, an AIDS and cancer specialist at the University of California, San Francisco.25 This placid state of affairs continued until 1937, when a prominent Prohibitionist, Harry J. Anslinger, who later became the head of the Federal Narcotics Bureau, got Congress to pass the Marijuana Tax Act. He tried to describe marijuana “in so repulsive and terrible terms that people wouldn’t even be tempted to try it,” noted the late Yale University drug historian David Musto.26
Even back in Anslinger’s day, there was no evidence that cannabis was demonic. In fact, the American Medical Association opposed the Marijuana Tax Act out of fear that the act would impede future research. (Which it did.) In 1942, the La Guardia Commission in New York likewise concluded that marijuana, despite allegations to the contrary, would not lead to crime or mental illness. Nonetheless, that same year, amid growing anti-pot fervor, cannabis was removed from the US Pharmacopeia, the nonprofit, nongovernmental public health organization that sets standards for medicines and food.27
Then, in 1970, Congress enacted the Controlled Substance Act, which classified marijuana, like heroin, as a Schedule I drug, the “worst” category. A substance in this category is deemed to have a high potential for abuse and no accepted medical use. The result is what Time magazine in 2010 called a “flawless bureaucratic catch-22…. Pot is listed as Schedule I because science hasn’t found an accepted medical use for it, but science can’t find a medical use for it because it’s listed as Schedule I.”28 (Actually, even the government may not be so sure marijuana is medically useless. In October 2003, the Department of Health and Human Services took out a patent on cannabinoids for potential use as antioxidants and neuroprotectants.29)
Until the 1970 act, laws in all states that prohibited marijuana allowed exceptions for using marijuana as a medicine, according to Michael Cutler, a Massachusetts lawyer who works on reforming marijuana laws.30 On the plus side, the 1970 law also called for a study on marijuana, which was duly performed by a national group, the Shafer Commission.31 In 1972, the commission recommended a medical exemption for marijuana, as well as decriminalization. But once again, Congress was not buying. It rejected this idea, and antidrug sentiment continued to grow.32 In 1986, President Reagan signed the Anti-Drug Abuse Act, which ordered mandatory sentences without parole for those convicted of possession or sale of all illegal drugs, including stiff sentences for cannabis.33
* * *
Today, in the Orwellian world of the federal bureaucracy, it is extremely difficult for American scientists to obtain legal marijuana to study, although a handful of California researchers have managed to do it. For research on any controlled substance provided by the government, three things have to happen. The researcher must get investigational new drug (IND) approval from the Federal Drug Administration (FDA). The researcher must also get the appropriate registration from the Drug Enforcement Administration (DEA). And the protocol for the proposed study must be deemed to have scientific merit by one of three processes—a grant review from the National Institutes of Health, an ad hoc review by NIDA, or, in the case of marijuana, a Public Health Service (PHS) committee review for studies that are funded by nongovernment sources.34
In 1999, the Public Health Service established a special process for evaluating proposed studies of marijuana that would involve use of government-provided marijuana. Not surprisingly, advocates of research on marijuana see this as the government singling out marijuana as forbidden territory for study.35, 36, 37, 38 As a practical matter, what all this means is that in order to conduct a clinical study of cannabis, a scientist has to pass muster with the FDA, the DEA, and the PHS, at which point NIDA then may give the scientist federally grown marijuana to study.
And therein lies a problem. NIDA’s stated goal is to study marijuana to look for evidence of harm, not to find potential benefits. It is “not NIDA’s mission to study the medicinal use of marijuana or to advocate for the establishment of facilities to support this research,” NIDA director Nora Volkow told the Boston Globe in 2006.39 And, as Steven Gust, told me, “NIDA is in the business of studying, for the most part, the detrimental effects of drugs.”40 But the real catch is that the only legal source of marijuana is that grown by the government itself on a single, 12-acre farm run by the National Center for Natural Products Research (NCNPR) at the University of Mississippi.41, 42 That farm is overseen by NIDA.
“We are the farmer,” as NIDA’s Gust put it. It is misleading, he says, to view NIDA as the obstacle or gatekeeper for research on marijuana: “If a study has been approved by the DEA, the FDA and the PHS, if all those agencies say yes, once those three boxes are checked, we will send the marijuana.”43
But that’s not how would-be marijuana researchers see it. They see NIDA as having a de facto monopoly on all the carefully cultivated, standardized strains of cannabis that they would like to study. (Scientists could, of course, study black market marijuana, but not only would this be illegal, it would be bad science: Strains of marijuana sold on the street vary widely in potency and constituents.)
The government justifies this de facto monopoly in part on the basis of an international treaty called the Single Convention on Narcotic Drugs of 1961, which the government interprets as saying the United States may have only one source of cannabis.44 Others dispute this interpretation, among them, Mary Ellen Bittner, a DEA administrative law judge. In a finding in 2007, she recommended ending the government’s monopoly on medical marijuana research.45
A number of legitimate researchers have been stymied by the government’s reluctance to part with its marijuana. In the mid-1990s, Donald Abrams, the California AIDS researcher mentioned earlier, got FDA approval to study cannabis’s potential benefits for AIDS/HIV patients. With the FDA’s approval in hand, he then petitioned NIDA for the federally grown cannabis he needed for the study. He was turned down. Abrams was frustrated.
“I must tell you that dealing with your Institute has been the worst experience of my career,” Abrams wrote to NIDA. He eventually reworded his proposal to appeal to what NIDA wanted—that is, to look for harms. This time, he was approved, and he got $1 million to boot.46, 47 To be sure, some professional medical associations—most notably, the American Society of Addiction Medicine—approve of this restricted state of affairs.48 But other medical groups lament the obstacles facing scientists trying to grow marijuana in order to study it, among them the American College of Physicians and the American Medical Association.49, 50
Among the most frustrated scientists is Lyle Craker. Craker is a friendly, white-haired crop physiologist and professor of plant and soil sciences at the University of Massachusetts. In 2001, he applied to the DEA for a license to cultivate cannabis for use in clinical trials by medical doctors. The research was to be privately funded, so he wasn’t even looking for federal money. He is still waiting for the DEA’s answer, despite an administrative judge’s ruling that it is in the public interest for Craker to be granted a license.
Craker is hardly a wild-eyed pothead. “He’s the Rosa Parks of medical marijuana,” Rick Doblin told me. Doblin holds a PhD in public policy from Harvard’s Kennedy School of Government and founded an advocacy group called MAPS in 1986.51, 52 “Craker is “perfect. He doesn’t smoke, he’s not an advocate for legalization. He’s a senior faculty member. He can’t be intimidated. He’s simply saying there should be more research.”
Craker is a patient man. But three years after he filed his initial application for a license and got no response from the DEA, he sued. His suit was supported by the American Civil Liberties Union (ACLU), the late US Senator Edward Kennedy, and numerous medical, patient, and advocacy groups.
In a sense, Craker’s initial lawsuit was partially successful. The Court of Appeals in the District of Columbia ordered the administration to stop stalling and respond.53 The DEA did respond—by rejecting Craker’s petition. It argued that the Single Convention treaty requires the government to maintain only one source of marijuana and that allowing Craker to run a facility at UMass would violate government policy. Judge Bittner disagreed.54 In a final ruling in February 2007, she recommended that Craker be allowed to grow research cannabis. Finally, thought Craker.
But it turned out that the ultimate decision wasn’t hers to make. It was DEA acting administrator Michele Leonhart’s. In January 2009, just as President George W. Bush was leaving office and six days before President Barack Obama was to be inaugurated, Leonhart, a Bush appointee, rejected Bittner’s recommendations and ruled against Craker. To the surprise of many people who had believed Obama’s pro-medical marijuana campaign statements in 2008, Obama went on to reappoint Leonhart, who was confirmed as head of the DEA in 2010.
During his presidential campaign, Obama had told the editorial page editor for the Mail Tribune, a southern Oregon newspaper, that he took a “practical” view of medical marijuana, adding that “there is really no difference” between a doctor prescribing medical marijuana as a treatment for glaucoma or as a cancer treatment “and a doctor prescribing morphine or anything else.” Obama went on to say in that interview that he would not “punish doctors” for prescribing cannabis in an appropriate way, even though “that may require some changes in federal law.”55, 56
His administration did keep that promise—for a while. When asked during a press conference on February 25, 2009, if recent raids on medical marijuana providers in California represented American policy going forward, his attorney general, Eric Holder, said, “No. What the president said during the campaign, you’ll be surprised to know, will be consistent with what we’ll be doing in law enforcement.” In October 2009, David Odgen, a deputy attorney general, also seemed to hew to the Obama campaign rhetoric. Ogden wrote a memo saying that while the Department of Justice remains committed to prosecuting significant traffickers of illegal drugs, including marijuana, the government should not focus federal resources on individuals who are in clear compliance with state laws on medical marijuana.57 Ogden added that it would not be an efficient use of limited federal resources to prosecute people with cancer or other serious illnesses who use marijuana as part of a recommended treatment regimen.
But something snapped in Washington. On June 29, 2011, a different deputy attorney general, James M. Cole, changed the administration’s tune.58, 59 In his memo, Cole noted a big increase in large-scale, commercial cultivation and sale of medical marijuana. From now on, the Cole memo said, people in the marijuana cultivation business “are in violation of the Controlled Substances Act, regardless of state law.”60, 61 Today, more than a decade after he first applied for a license to cultivate marijuana, Craker’s case is still tied up in court. In May 2012, Craker’s legal team once again presented their case against the DEA, in federal court.62 So far, there has been no resolution.63
Craker is not the only cannabis researcher to run afoul of the government’s obsessive fear of marijuana. Ethan Russo is a neurologist who treated migraine patients for a quarter of a century in Missoula, Montana. He now lives on an island off Seattle. The author of several historical reviews of cannabis, Russo tried for more than 15 years to study herbal cannabis for migraine. His first proposed study was turned down at NIDA in 1997. He tried again in 1998. Same result. “I thought it was a good protocol, but politics entered into this, I’m afraid,” he told me.64 His hopes rose briefly in 1999, when the prestigious Institute of Medicine acknowledged the promise of medicinal marijuana.65 Suddenly, the FDA did accept his application and approved his study.
But then he bumped into that old catch-22. He couldn’t proceed until he got an additional review from the Public Health Service. His migraine study was rejected. Although Russo arguably knows more about the biology of cannabis than any other scientist on the planet, he gave up fighting the government.66 He now consults for a UK company called GW Pharmaceuticals that makes Sativex, an oral-mucosal spray made from extracts of two standardized cannabis strains that are mixed to give fixed doses of THC and cannibidiol (CBD). (Sativex is approved in several countries, but not in the United States, although it is now in an FDA-approved trial for cancer pain.)
To be sure, there have been a few scientists who have scored government marijuana to study. They are a team of researchers led by Igor Grant, Thomas Coates, and J. H. Atkinson, physicians who run the Center for Medicinal Cannabis Research at the University of California, San Diego. In 2001, they received $8.1 million from the state of California for cannabis research—and somehow got NIDA to part with enough government-grown marijuana from Mississippi to sponsor 14 studies, including the first clinical trials of inhaled marijuana in more than two decades.67, 68 It wasn’t easy.
Many scientists “are just not going to go through this kind of effort,” Atkinson acknowledged. But the California team’s persistence did pay off in research showing that cannabis is indeed a promising therapy, especially since its mechanisms of action are different from those of standard treatments.69 That’s the good news. The bad is that the center has now spent all its money. It is still a resource for other scientists, but it won’t fund any new research projects. Meanwhile, as Craker, Russo, and the California scientists were fighting to study cannabis, an entirely separate effort has also being going on, this one spearheaded by Jon Gettman.
As leader of the Coalition for Rescheduling Cannabis (CRC), Gettman filed a petition in 1995 and again in 2002 to get marijuana taken out of Schedule I, arguing that there is enough evidence of its medical usefulness that the government should not claim it has none.70, 71 He suggested that marijuana be regulated as a Schedule III, IV, or V (over-the-counter) substance or simply be regulated like alcohol or tobacco. In June 2011, the Global Commission on Drug Policy, an august, nonpartisan group, also recommended the rescheduling of certain drugs—cannabis, coca leaf, and MDMA—because the current scheduling has “obvious anomalies.”72
Remarkably, Gettman’s petition cited 87 healthcare or state government entities supporting medical marijuana use, including the American Academy of Family Physicians, the American Public Health Association, the National Association of [state] Attorneys General, the National Institute of Medicine, and many others. After years of government inaction, Gettman went to court to compel the DEA to respond to his petition. On July 8, 2011, nine years after the second petition, the DEA finally did rule—it denied Gettman’s petition.73, 74
Although Gettman’s coalition had argued that cannabis is less likely to lead to dependence than other Schedule I or II drugs, that argument didn’t fly. The DEA insisted that long-term, regular use of marijuana “can lead to physical dependence and withdrawal following discontinuation as well as psychic addiction or dependence.” The government also reiterated its standard line, saying that it would not reschedule marijuana because it “has a high potential for abuse, has no accepted medical use in the United States, and lacks an acceptable level of safety for use even under medical supervision.” Strikingly, while referencing studies on potential health risks of marijuana, the DEA made no mention of other studies showing medical efficacy. It also failed to note its own role in blocking studies that the FDA had already approved.75, 76
Advocates for medical marijuana howled. “The federal government is making no bones about its aggressive policy to undermine medical marijuana,” complained Americans for Safe Access, one of the groups supporting the Gettman petition.77
It’s been known since 1964 that the primary psychoactive ingredient in marijuana is THC, or delta-9-tetrahydrocanninbol, a substance first isolated by Raphael Mechoulam, an Israeli chemist.78 But it was not until decades later that scientists stumbled upon something even more interesting.
All human beings, and indeed other mammals, birds, fish and even reptiles, are born with the ability to make both marijuana-like chemicals called cannabinoids and the cannabinoid receptors into which they fit. Cannabinoid receptors can be triggered not only by these endogenous cannabinoids, but also by externally obtained cannabinoids like THC and CBD from the marijuana plant itself and by synthetic cannabinoids made in the lab. In fact, to scientists’ surprise, cannabinoid receptors turn out to be all over the place, among the most abundant receptors in our bodies.79
Why on earth would our nervous systems be so full of cannabinoid receptors? So that our caveman ancestors might someday stumble upon a marijuana plant and smoke it to get high? Probably not. More likely, evolution favored us with all these cannabinoid receptors for a more practical reason, like dampening pain. And perhaps to give us that “runner’s high,” which is fueled, it turns out, not just by endorphins but by endogenous cannabinoids as well.80, 81
Two of the most important endogenous cannabinoids are anandamide and 2-arachidonyl-glycerol, or 2-AG, lipids that have a wide range of biological functions, including pain processing.82 Basically, they make us “relax, eat, sleep, forget and protect.”83, 84
When people are deficient in endocannabinoids, they may be more susceptible to certain pain conditions, including migraine, fibromyalgia, and irritable bowel syndrome.85, 86 Italian researchers, for instance, have shown that cannabinoid levels are too low in migraine sufferers. Certain mutations in the receptor for anandamide can also raise the risk of migraine.87 On the other hand, boosting levels of endocannabinoids— in part by blocking substances that break them down—is a promising a new approach to reducing pain.88 In fact, some pain drugs that we already use, such as NSAIDs, or nonsteroidal anti-inflammatory drugs, seem to work in part by stopping this breakdown of endocannabinoids.89
The two most important cannabinoid receptors are CB1 and CB2. The CB1 receptors reside mostly in the central nervous system and on peripheral nerves, while CB2 receptors are mostly in immune cells, including microglia and, to a lesser extent, in the central nervous system.90, 91 These receptors are clearly vital to survival. Mice genetically engineered to lack CB1 receptors show increased anxiety and susceptibility to depression.92 They don’t respond normally to reward stimuli.93 And they eat less and lose weight.94 CB1 receptors also seem to play a role in the placebo response.95
THC triggers its high when it lands on CB1 receptors.96 The other cannabinoid, CBD, doesn’t bind strongly to either CB1 or CB2 receptors, though it does seem to partially block the binding of THC to CB1.97 When CB2 receptors are activated, the main effect is reduced inflammation and activity in spinal cord pain relay centers, as well as protection of nerves from oxidative damage.98, 99, 100
The holy grail of marijuana pain research is to unravel the mysteries of the two cannabinoid receptors and the two major cannabinoids from plants, THC and CBD. In theory, teasing apart this biochemistry will allow the creation of fine-tuned marijuana strains that decrease the psychoactive effects of marijuana—the high—and increase pain-relieving effects.
There’s a catch in this theory, though. It may be that a little of the psychoactive effect from smoking marijuana is what helps pain patients like Marcy Duda and Beth McCauley dissociate emotionally from their pain, even though the physical pain is still there. A 2013 study from Oxford University showed that cannabis does indeed make pain less unpleasant, at least in healthy volunteers studied in a pain lab.101 Using fMRI brain scanning, the researchers found that while THC did not reduce the intensity of pain, it did reduce the emotional impact. In other words, the CB1 effect from the plant itself may be unwanted in the eyes of people opposed to marijuana, but its very “mood-altering effect may be an important part of the overall therapeutic response” note McGill University researchers Mark Ware and Vivianna Tawfik.102
And of course, it’s the high from THC that recreational marijuana users and abusers seek. In recent years, precisely because it does not trigger a high, CBD has actually been bred out of marijuana strains sold illegally.103 With any cannabis on the black market in North America, “the CBD just isn’t there. The black market cannabis is virtually all high-THC strains,” Ethan Russo told me.104
Back in the early 1970s, there was a perfect balance of THC and CBD in natural cannabis plants from Afghanistan. This balance produced a modulatory effect. The CBD blocked the intoxication, rapid heartbeat, and sedation of THC alone, but also boosted the good effects—pain control and reduced inflammation.105 Drug companies have been trying to come up with man-made equivalents. Several have tested CB2-only drugs, but so far, the results have been disappointing.106, 107, 108, 109 As for the two synthetic cannabis medications on the US market, the jury is out. Both drugs act on both CB1 and CB2 receptors, and Marinol, which contains THC, can produce a high if the dose is sufficient. So far, both Marinol (dronabinol) and Cesamet (nabilone) are approved only for anorexia and nausea, though they can be used “off label” for pain, as well as for improving sleep.110
In truth, nothing man-made appears to be as effective—or as quick— for pain relief as smoking or inhaling the cannabis plant itself.111, 112 Cesamet is perceived to produce more undesirable side effects, to take a long time to work, and to be more expensive than smoked cannabis.113 Marinol has shown efficacy as an add-on to opioid therapy in some people with chronic pain.114 But it can be hard for people to find the right dose because of individual variations in how their digestive systems absorb the drug.115
There’s a downside to smoking the real plant itself, though. Even one puff of high-potency cannabis may overshoot what you need for pain control.116 That’s because smoked cannabis has a narrow therapeutic index—a small gap between symptom control and side effects. The overshoot problem typically occurs, however, chiefly with people who have not used marijuana much; experienced users become quite good at getting their doses right. By contrast, the marijuana extract Sativex, which contains both THC and CBD, seems to have a wider therapeutic index. This suggests that people may be able to spray just enough into their mouths to control pain without producing unwanted side effects. Sativex is used in Canada, Great Britain, Spain, and Germany for neuropathic pain, cancer pain, and multiple sclerosis, though its effectiveness for multiple sclerosis is questionable.117, 118, 119, 120, 121 It also appears mildly effective in people with rheumatoid arthritis pain, according to company-sponsored trials.122 It is not approved in the United States, but a 2012 international, randomized, double-blind, placebo-controlled trial for poorly controlled pain in 263 people with advanced cancer was promising, showing both efficacy and safety at low and medium doses.123
Since the focus of this book is chronic pain, we’ll concentrate here on marijuana as a pain reliever, not on its other medical effects, such as reducing nausea and anorexia. But just for the record, it’s worth noting that there have been two major reviews in recent years of more than 100 randomized, double-blind, placebo-controlled clinical trials involving more than 6,100 patients with a variety of medical conditions.124, 125
These and other studies show that marijuana is effective at combating nausea, vomiting, appetite loss, glaucoma, irritable bowel disease, muscle spasticity in multiple sclerosis, muscle spasms, Tourette’s syndrome, epilepsy, and symptoms of amyotrophic lateral sclerosis (ALS, or Lou Gehrig’s disease).126, 127, 128, 129, 130 There may be another benefit as well. In animals, at least, there’s preliminary evidence that marijuana can block the growth of tumors, according to a 2003 review by Spanish researchers.131 Specifically, cannabinoids seem to fight tumors by blocking inflammation, cell proliferation, and cell survival, other research shows.132, 133 It may also be possible to block cancers that start in immune cells by targeting CB2 receptors on those cells, though this is very preliminary.134
But pain is the point here. And, to put it bluntly, marijuana works. Not dazzlingly, but about as well as opioids. That is, it can reduce chronic pain by more than 30 percent.135, 136 And with fewer serious side effects. To be sure, some researchers think it’s too soon to declare marijuana and synthetic cannabinoids a first-line treatment for pain, arguing that other drugs should be tried first.137 But that may be too cautious a view.
Overall, marijuana and its prescription cousins show a significant analgesic effect compared to placebo in people with all sorts of chronic, non-cancer pain, according to a 2011 review of 15 high-quality studies.138 And one of the huge advantages may be that marijuana can allow people in severe pain to take lower doses of opioids. While doctors often shy away from prescribing opioids to patients who also use marijuana, this may be backward: There’s evidence that marijuana can make opioids more effective and allow patients to take less of them.139, 140, 141 In general, marijuana seems to work best, ironically enough, for people with the most intractable pain. It is less effective for acute pain, such as pain after surgery.142, 143 And it has only mixed efficacy against acute pain intentionally induced in the lab.144
Some conditions in particular—neuropathic pain, fibromyalgia, and pain from multiple sclerosis—seem amenable to the pain-reducing effects of cannabis and its synthetic cousins. There is less research on other problems, such as migraine and cancer pain, in part because of the US government’s restrictive access policies. With neuropathic pain, which affects 1 to 2 percent of the population, cannabis is quite a promising treatment, according to a report from the San Diego–based Center for Medicinal Cannabis Research.145 Research from the Canadian Consortium for the Investigation of Cannabinoids has come to the same conclusion.146 And, as Beth McCauley and Marcy Duda discovered on their own, most of the reduction in pain comes from the first marijuana cigarette, with subsequent doses not adding significantly to the effect.147 In other words, you don’t have to get stoned out of your mind to get pain relief.
In fact, a steady drumbeat of studies has confirmed the effectiveness of cannabis for neuropathic pain relief. In a 2008 UC Davis study, 38 patients rated their neuropathic pain after inhaling cannabis or placebo: Smoking cannabis clearly reduced their daily pain.148 In 2009, other researchers followed 28 patients who puffed away—under direct observation in a hospital. Again, cannabis yielded significant pain relief, as well as improvements in mood and daily functioning.149
In 2010, a different study set researchers buzzing at the annual meeting of the International Association for the Study of Pain. The study was done by Mark Ware, a McGill University anesthesiologist with a big smile and a passion for scientific rigor. Ware looked at 21 neuropathic pain patients and found that one puff through a pipe three times a day for five days yielded significant pain relief, as well as better sleep. And patients smoking marijuana with the highest concentrations of THC got the most benefit.150, 151
As a Canadian researcher, Ware isn’t caught up in cannabis politics the way American scientists are. Scientists “should study herbal cannabis the same as any other substance,” he told me one day in his Montreal office overlooking the St. Lawrence River. “We should establish its safety profile, its efficacy, etc. If it’s as good as everyone says it is, it could be considered as rational medical therapy.”152
People with fibromyalgia seem to be helped by marijuana or the synthetics, too. A 2008 randomized, double-blind, placebo-controlled Canadian study in 40 fibromyalgia patients found that the patients getting Cesamet got pain relief but also complained of side effects such as drowsiness, dry mouth, vertigo, confusion, and dissociation.153 A 2011 Spanish study compared 28 fibromyalgia patients who inhaled cannabis or consumed it orally to 28 nonusers. The cannabis users had less pain and stiffness, were more relaxed, and had increased feelings of well-being. They also scored higher on a questionnaire for mental health.154
For multiple sclerosis (MS) pain, the prescription Sativex spray seems to work, reducing pain and sleep problems more than placebo.155 As for migraines, American scientists, as we’ve seen, have had trouble getting legal marijuana from the federal government to study. In theory, though, marijuana should work for migraines because it can activate CB1 receptors.156, 157, 158
Remember those syllogisms they used to teach in college logic classes? “John is a human. All humans have legs. Therefore John has legs.” My version goes like this: Marijuana, like alcohol, caffeine, and opioids, is a drug. All drugs have risks. Therefore marijuana has risks.
That said, the evidence shows that marijuana has a remarkably safe profile. And this is in spite of the fact that the US government has lopsidedly supported studies of risks rather than benefits. But because anti-marijuana politics has focused so much on the risks, we’ll address them one by one, and see what the research shows.
One of the most often alleged risks of marijuana is that it is a “gateway” drug that leads to other illegal drug use. This is only partly true. Because it is the most widely used illicit drug, marijuana is predictably the first illicit drug most people encounter, acknowledged a 1999 review by the Institute of Medicine, an arm of the National Academy of Sciences.159 “Not surprisingly,” the report said, “most users of other illicit drugs have used marijuana first.” But here’s the catch. Most drug users begin their drug using with the legal drugs alcohol and nicotine. Because underage smoking and alcohol use typically precede marijuana use, the report said, marijuana is not the most common, and is rarely the first, “gateway” to illicit drug use.
Assessing the medical risks of marijuana is tricky, in part because most research has been done in young, recreational users. In general, adolescents and young adults who use cannabis recreationally tend to be heavier users, while older people who use cannabis medicinally tend to use smaller doses for symptom relief.160 When researchers look at medicinal use, they don’t find much harm. In a review of 23 randomized controlled trials and eight observational studies of medicinal use, McGill University researchers Tongtong Wang and Mark Ware found that the overall risk of adverse events for short-term (two-week) use of cannabinoids and cannabis extracts was minor.161 The most common problem was dizziness. But by and large, the rates of serious adverse events did not differ between people taking medicinal cannabis and controls. And, as would be predicted from the biology of marijuana itself, the risks that do exist are lower when people take formulations that include both THC and CBD rather than THC alone.162 So, let’s take a look at the medical risks one by one—dependence and addiction, cancer, schizophrenia and other forms of psychosis, other psychiatric problems, cognitive problems, respiratory damage and cardiac issues.
Dependence is a physical adaptation that leads to withdrawal symptoms if a drug is stopped, especially if it’s stopped abruptly. Addiction is different—it’s a neurobiological condition characterized by impaired control over drug use, compulsive use, continued use despite harm, and craving. But many people, including doctors, researchers, and federal agencies, confuse the two terms. With marijuana, there are reports of withdrawal symptoms in both adults and adolescents, especially among heavy users.163 But even when mild physiological withdrawal does occur in heavy users, the symptoms are not as impairing as those caused by alcohol.164 NIDA insists, though, that marijuana users run the risk of both dependence and addiction.165, 166, 167
And that’s slightly true. But the research shows that cannabis has a lower rate of dependence/addiction than alcohol, cocaine, heroin, or tobacco, although the risk increases with dose.168 Among users of tobacco, for instance, 32 percent become addicted, Susan Weiss, acting director of the office of science policy and communications at NIDA, told me. For heroin, it’s 23 percent, for cocaine, 17 percent, for alcohol, 15 percent—and for marijuana, 9 percent.169, 170
Historically, one of the big fears about smoking marijuana was that it might raise the risk of cancer. This does not appear to be the case. A 2009 study by researchers at the University of Leicester in England did find that cannabis smoke can damage DNA, raising the theoretical possibility that the damaged DNA could produce cancer.171
But the bulk of the evidence points the other way. In fact, as we noted earlier, a 2003 review by Spanish researchers suggested that marijuana may actually block the growth of tumors, at least in animals.172 In human studies, it appears that once the effect of smoking tobacco is accounted for, there’s no extra risk from smoking marijuana, as a landmark 2006 California study showed. In this research, scientists from France, the University of Michigan, the Albert Einstein College of Medicine, UCLA, and other medical centers pooled their efforts to study 1,212 people with lung and oral cancers and 1,040 people without.173
The team asked all the participants about marijuana habits, using a standardized questionnaire. When the researchers controlled for tobacco smoking, there was no positive association of the cancers and marijuana. The researchers had hypothesized that long-term heavy use of marijuana would increase the risk of lung and head and neck cancers. But after controlling for cigarette smoking, they found no evidence of that.174
In 2009, many of the same researchers looked more specifically at head and neck cancers. They pooled data from other studies involving more than 4,000 people with these cancers and more than 5,000 people without and asked them about marijuana use.175 Once again, there was no elevated risk of the cancers from marijuana. Even NIDA, on its website, acknowledges that studies have not found an increased risk of lung cancer in marijuana smokers.176
Another concern is whether marijuana raises the risk of psychosis, especially schizophrenia. This is not a big concern for older people who use marijuana medically, but it may be for adolescent and young adult recreational users whose brains are still developing and who are at the age when schizophrenia is most likely to develop. In 2002, British researchers analyzed data on more than 50,000 people (97 percent of all males aged 18–20) who had been drafted in 1969–1970 into the Swedish army.177 The study, published in the British Medical Journal, found that cannabis use was linked to a higher risk of schizophrenia, and the more the men smoked, the higher the risk. The link could not be explained away by the use of other drugs or personality traits. In that same issue of the journal, other British researchers studying 759 New Zealanders also found that early adolescent use of cannabis was a risk factor for schizophrenia, with use at age 15 carrying more risk than use after age 18.178
That same year (2002), yet another team, this time a group of Dutch, British, and French researchers, came to similar conclusions.179 These researchers looked at more than 4,000 psychosis-free people and 59 others who been diagnosed with a psychotic disorder. They tracked all the subjects’ marijuana use for three years. They found that smoking marijuana increased the risk both of a person becoming newly psychotic and of faring poorly if the person already had a diagnosis of psychosis. In 2004, a different Dutch team reviewed five other studies and found that cannabis use seems to raise the risk of schizophrenia, especially in vulnerable people.180 In 2007, a meta-analysis of data pooled from 35 other studies further strengthened the link. If a person smokes cannabis during his or her youth, this analysis found, there’s a significantly increased the risk of psychosis later in life.181
Other studies hammer this home. In 2010, Australian researchers found that teenagers who started using cannabis early, around age 15, and kept smoking for six years until they were 20 had more than twice the normal risk of psychosis.182 In 2011, Australian researchers who analyzed pooled data from 83 studies concluded that cannabis users who develop psychosis do so at an earlier age (by about two years) than nonusers.183 You might think, then, that it’s an open-and-shut case for the link between adolescent marijuana use and schizophrenia. But it’s not that simple. If marijuana use really does increase the risk of schizophrenia, this should show up in large populations as marijuana use has increased over the years.
It doesn’t.
In 2009, United Kingdom researchers from Keele University looked at the medical records of almost 600,000 people, more than 2 percent of the entire UK population aged 16 to 44. They studied the years from 1996 to 2005, when there was a substantial rise in cannabis use. They found no evidence of increasing schizophrenia or psychoses in this time period.184 If there is an increased risk, then, perhaps it occurs in people genetically susceptible to psychosis.185 But that raises the question of what a biochemical link between cannabis and schizophrenia might be, and the data on that are inconclusive.186, 187
Bottom line? There is only equivocal evidence for the hypothesis that cannabis can cause schizophrenia.188 Young, recreational users should probably be cautious, McGill University researchers concluded, but older people using marijuana medically probably need not worry.189
Research on potential links between cannabis and anxiety or depression is inconclusive. In 2002, Australian researchers reported that teenage girls who inhaled marijuana at least once a week were twice as likely as less frequent users to experience depression or anxiety over the next seven years.190 But other research shows that, while anxiety, paranoia, and disorientation do occur in new cannabis users, these problems are uncommon in regular users. Indeed, a systematic review of the data does not find a strong association between chronic cannabis use in young people and psychosocial harm.191
Cognitive problems attributed to marijuana have also been a concern, but again, the jury is still out. In 2002, researchers from Harvard’s McLean Hospital studied 122 long-term, heavy cannabis users and 87 people who had minimal cannabis exposure, and subjected them all to a number of cognitive tests. As hypothesized, the people who started using cannabis earlier in adolescence did do more poorly on cognitive tests. But it’s not clear how to interpret this. The heavy cannabis users may have been on a bad track to begin with. As the authors put it delicately in this and a subsequent study, these people may already have “eschewed academics and diverged from the mainstream culture.”192, 193 In 2008, Australian researchers used magnetic imaging (MRIs) to scan the brains of 15 men in their late 30s who had inhaled more than five joints a day for an average of almost 20 years. The men had not used other drugs or had any neurological problems. They were compared to 16 similar men who had not used cannabis. The brains of the marijuana group showed reduced volume in two areas key to emotional and cognitive functioning, the amygdala and the hippocampus, suggesting possible damage.194
In 2009, a different group of Australian and Irish researchers used fMRI scans and also documented changes. They found that several brain regions, particularly the anterior cingulate cortex and right insula, were underactive in chronic cannabis users.195 This is troubling, to be sure, as was a 2010 study from McLean Hospital in which researchers looked at 33 chronic marijuana users and 26 nonusers and put them all through neurocognitive tests and brain scans to assess the ability to plan and do abstract thinking.196 The McLean team found that age of initial heavy use of marijuana was crucial. People who started before age 16 made twice as many mistakes on the tests, a pattern that got worse the more the teenagers smoked. Even when told they had made errors, the marijuana users kept making mistakes and had more trouble following rules and maintaining focus. In 2012, researchers from Duke University’s Center for Child and Family Policy analyzed data on 1,037 people from birth to age 38 and found that those who were diagnosed with marijuana dependency as teenagers and who continued to use it had cognitive declines.197
Pretty worrisome stuff, to be sure. But other data suggest that once a person stops using marijuana, some cognitive changes like memory bounce back to normal.198, 199 And when San Diego researchers pooled data from a dozen studies on 704 cannabis users and 484 nonusers, they found that while chronic marijuana users sometimes showed a decreased ability to remember new information, other cognitive functions weren’t affected at all.200
Since the main way marijuana is taken in to the body is by inhalation, one of the persistent concerns has been whether smoked cannabis causes respiratory damage. In many ways, smoking is not an ideal “drug-delivery system” because of respiratory risk. (The flip side of this is that inhalation of any drug—whether marijuana or inhaled analgesia—is great if the goal is to get the drug to the brain quickly.) The challenge for researchers has been to tease apart the potential respiratory damage from smoking marijuana from that due to smoking tobacco because the same people often do both. In 2007, New Zealand researchers did just that. They recruited 339 people from four different groups—those who smoked only cannabis, those who smoked only tobacco, those who smoked both, and those who smoked neither.201 They found that smoking one marijuana joint had similar adverse effects—in terms of airflow obstruction—as 2.5 to 5 cigarettes, although inhaled marijuana was not linked to chronic obstructive pulmonary disease (COPD), as cigarettes are.202
In a 2012 American study of more than 5,000 men and women in four cities, researchers found that occasional and low cumulative marijuana use was not associated with adverse effects on pulmonary function.203 In a more high-tech study, Canadian researchers used smoking machines to compare the ingredients in smoke from both tobacco and marijuana.204 They found that ammonia was 20 times more prevalent in marijuana smoke, as were other substances, but different potentially harmful ingredients were less prevalent. In yet another study, a different Canadian team, McGill’s Mark Ware and Vivianne Tawfik, scoured 79 research papers on adverse effects of cannabis published from 1966 through 2004. Long-term, heavy cannabis smokers did get more bronchitis, they found. And inhaled marijuana did contain many of the same constituents as tobacco smoke, as well as higher concentrations of polyaromatic hydrocarbons, which are known carcinogens.205
But—and here’s the surprise—the researchers couldn’t find any lung damage in long–term users, nor any link between smoking pot and the cancers typically associated with tobacco smoking. Moreover, whatever respiratory risk there may be from smoking marijuana can be at least partially offset by vaporizing (inhaling marijuana smoke through a gadget that delivers just the vapor). This allows the active ingredient of marijuana, THC, to get into the bloodstream without toxic carbon monoxide, a constituent of both marijuana and tobacco smoke. Vaporizing heats the cannabis to between 180 and 200 degrees Celsius. This releases the cannabinoids on the surface of cannabis flowers and leaves, but avoids the combustion (which happens at 230 degrees Celsius or higher) that yields smoke toxins. In a pivotal 2007 study, California scientist Donald Abrams asked 18 healthy subjects to inhale standardized marijuana for six days and measured the carbon monoxide (CO) in their expirations. When the subjects used vaporizers, he found little if any increase in CO.206 Researchers from the State University of New York at Albany confirmed the benefits of vaporizing in a 2010 study.207
Overall, the cardiac risk from marijuana appears small. Marijuana can increase heart rate and blood pressure and can increase the risk of heart attack in the first hour after smoking, which suggests that people with uncontrolled hypertension or active heart disease should be cautious about marijuana use. Marijuana also lowers the resistance in blood vessel walls, meaning that if a person stands up suddenly, there can be a sudden drop in blood pressure. There have also been a few reports of minor strokes (transient ischemic attacks) right after marijuana use. But by and large, there appears to be no link between marijuana use and hospitalization or death from cardiovascular disease.208, 209, 210
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After analyzing all these potential risks, the conclusion is inescapable. It’s a dumb idea to drive if you’re high on marijuana.211 And it’s probably prudent for anyone at risk of schizophrenia, especially teenagers and young adults, to steer clear of it.
But aside from that, marijuana is a valuable option for pain control. “To reject the therapeutic potential of cannabis and cannabinoids on the grounds of toxicity and potential abuse is to throw the baby out with the bathwater,” as Mark Ware, the McGill anesthesiologist and marijuana researcher put it.212
Marijuana is simply not the dangerous drug that the federal government claims it is. In fact, it meets the standard criteria for any good drug—it is both safe and effective.
Frankly, I didn’t start out researching this chapter as a proponent of the legalization of marijuana. I don’t even like the stuff. But I have slowly become an advocate, which puts me in some rather unexpected company—like that of evangelical leader Pat Robertson. “I really believe we should treat marijuana the way we treat beverage alcohol,” Robertson told the New York Times in March 2012. “I’ve never used marijuana and I don’t intend to, but it’s just one of those things that I think: this war on drugs just hasn’t succeeded.”213
More and more Americans agree.214, 215 A Gallup survey in October 2011 showed that a record-high 50 percent of Americans now say the use of marijuana should be legalized, up from 46 percent last year.216 This attitude has been growing steadily since Gallup first asked the question in 1969, when only 12 percent of Americans favored legalization. Among the supporters is California’s lieutenant governor, Gavin Newsom.217
Even the presidents of key Latin American countries—Costa Rica, Guatemala, El Salvador, Colombia, and Mexico—now say they want to discuss the option of legalizing drugs because of the violence associated with the failing drug war.218, 219 In fact, the momentum for legalization in Latin America seems to grow almost daily. In 2012, Uruguay’s president Jose Mujica called for the regulated and controlled legalization of marijuana. Across Latin America, leaders appalled by the spread of drug-related violence are mulling policies that would once have been inconceivable, the New York Times reported in July 2012.220 Indeed, the Times noted, if Uruguay completely legalizes marijuana, it would go beyond the Netherlands and Portugal, which have had lenient marijuana policies for years. No other country has seriously considered creating a completely legal state-managed monopoly for marijuana or any other substance prohibited by the 1961 United Nations Single Convention on Narcotic Drugs. Even Sanjay Gupta, CNN’s chief medical correspondent, has publicly renounced his opposition to marijuana (http://www.cnn.com/2013/08/08/health/gupta-changed-mind-marijuana), arguing the government is wrong to say marijuana has no medical use and has high abuse potential.
In the United States, medical marijuana is currently legal, albeit still controversial, in the District of Columbia and in 18 states, with the biggest use—and biggest ongoing battles—in California and Colorado.221 As of the 2012 election, marijuana is also legal for recreational use in Colorado and Washington.222
Some people oppose this trend, among them Kansas physician Eric Voth of the Institute on Globe Drug Policy, who derides what he calls the “medical excuse movement.” Ballot initiatives and legislative initiatives are “not the way we bring medicines to market. We bring them to market through the FDA” he told PBS in August 2011.223
Gil Kerlikowske, the White House “drug czar,” has sounded a similar theme. Responding to a petition to legalize marijuana, he insisted that marijuana use is “not a benign drug.”224 (Of course, neither is tobacco or alcohol, both of which are legal.)
The groundswell for outright legalization is clearly growing. In the summer of 2011, congressmen Barney Frank (D-MA) and Ron Paul (R-TX) filed one bipartisan bill to end prohibition of marijuana at the federal level and another to remove marijuana from Schedule I or II in the federal categorization of controlled substances.225 Initially, the bills went nowhere. But by early 2012, several more bills had been filed in Congress. The bills would have the federal government regulate marijuana the way it regulates alcohol, and oversight of marijuana would be removed from the Drug Enforcement Administration and given to a newly renamed Bureau of Alcohol, Tobacco, Marijuana, and Firearms.226
Even Obama, who has acknowledged using marijuana as a teenager, has begun changing his tune. After the 2012 election, he told ABC-TV’s Barbara Walters that prosecuting recreational users in states that have made marijuana legal should not be a “top priority.”227 Obama called the marijuana issue “a tough problem, because Congress has not yet changed the law…. How do you reconcile a federal law that still says marijuana is a federal offense and state laws that say it’s legal?”
Suppose we did make marijuana legal? What might happen? Among other things, it would make economic sense. Harvard University economist Jeffrey A. Miron calculates that legalizing marijuana could save $7.7 billion per year in enforcement of marijuana prohibition, most of which would accrue to budget-strapped states, but some to the federal government as well. Beyond that, taxing legal marijuana would yield $2.4 billion, Miron calculates, if it were taxed like all other goods. And a whopping $6.2 billion if it were taxed comparably to alcohol and tobacco.228
Maine now allows qualified patients—with a doctor’s approval—to buy marijuana from small growers and nonprofit centers, a move that has created jobs and turned underground businesses into taxpaying operations, according to a 2012 Boston Globe analysis.229 The growers collect a 5 percent sales tax and pay tax on their own income as well.
Frankly, in an ideal world, I would like to see marijuana not just legalized and taxed, but treated as a dietary supplement. This would make it subject to postmarketing surveillance by the US Food and Drug Administration. Recategorizing marijuana as a dietary supplement wouldn’t be easy.230, 231, 232 But if it were a supplement, and if a given product were linked with harm when used as directed on the label, producers could be forced to withdraw that brand from the market. Wouldn’t it be nice to be able to go into any health food store and buy a packet of marijuana with an accurate, informative label showing how much psychoactive THC and how much nonpsychoactive CBD that product contained? Right now, there is no way for consumers to know whether what they’re buying is pure and produced by licensed, reliable growers. There’s no easy way to know whether your marijuana was grown, dried, and packaged safely, without molds such as aspergillus, pesticides, formaldehyde, or other toxins. Consumers have a right to know such things, and manufacturers, a duty to inform.
To me, the argument for legalization boils down to this. Marijuana is not the “gateway” drug for illicit drug use that opponents of legalization say it is. Underage drinking and smoking are the real culprits. Marijuana is quite safe—far safer, mortality data show, than NSAIDs, acetaminophen, alcohol, and cigarettes, not to mention illegal drugs like heroin and cocaine. Marijuana is a reasonably effective pain reliever, on a par with opioids. Moreover, when used with opioids, it can reduce the amount of opioids needed to control pain.
Beyond those arguments, though, there’s a practical one: The war against marijuana has failed. Why not bow to scientific, social and economic reality? If we made marijuana legal, we could focus law enforcement efforts on real criminals. Not on responsible adults and people in pain.
No one has put this better than Gustin L. Reichbach, a pancreatic cancer patient and justice of the State Supreme Court in Brooklyn. In May, 2012, Reichbach wrote an op-ed piece in the New York Times. He noted that he did not “foresee that, after having dedicated myself for 40 years to a life of the law, including more than two decades as a New York State judge, my quest for ameliorative and palliative care would lead me to marijuana.”
Despite ongoing mainstream treatment, “nausea and pain are constant companions,” the judge wrote. “Every drug prescribed to treat one problem leads to one or more drugs to offset its side effects. Pain medication leads to loss of appetite and constipation. Anti-nausea medication raises glucose levels, a serious problem for me with my pancreas so compromised. Sleep, which might bring respite from the miseries of the day, becomes increasingly elusive.”
To his surprise, Reichbach found that “inhaled marijuana is the only medicine that gives me some relief from nausea, stimulates my appetite and makes it easier to fall asleep. The oral synthetic substitute, Marinol, prescribed by my doctors, was useless…. I find a few puffs of marijuana before dinner gives me ammunition in the battle to eat. A few puffs more at bedtime permits desperately needed sleep.”
“This is not a law and order issue; it is a medical and a human rights issue,” the judge went on. “Because criminalizing an effective medical technique affects the fair administration of justice, I feel obliged to speak out as both a judge and a cancer patient suffering with a fatal disease.” He concluded his piece poignantly: “Medical science has not yet found a cure, but it is barbaric to deny us access to one substance that has proved to ameliorate our suffering.”233
Judge Reichbach died two months later.234