June 19, 2024 By Leah Kuntz

SPECIAL REPORT: ADVANCES IN PSYCHIATRY

Benzodiazepines, a controversial treatment widely prescribed for patients with anxiety and insomnia, carry a considerable risk of abuse. The poster “Mood Over Matter: Literature Review on Benzodiazepine Tapering, Current Practices and Updates on Adjunct Mood Stabilizers,” which was presented at the 2024 APA Annual Meeting, summarized a literature review of current benzodiazepine tapering practices, outpatient detoxification challenges, and potential barriers to discontinuation. The poster presenters also prioritized reviewing literature that highlighted mood stabilizer adjunct use.

Research demonstrates why clinicians should use caution when prescribing benzodiazepines. Results of a recent study revealed that between 2014 and 2016 an estimated 25.3 million (10.4%) adults in the United States reported using benzodiazepines, and approximately 17.2% of these individuals admitted to misuse.

Similarly, the National Institute on Drug Abuse documented that benzodiazepines were implicated in more than 14% of opioid overdose deaths in 2021. Furthermore, a report from the Centers for Disease Control and Prevention pinpointed benzodiazepines as a factor in nearly 7000 overdose deaths across 23 states from January 2019 to June 2020, constituting 17% of all drug overdose deaths. This time frame saw a staggering 520% surge in deaths related to illicit benzodiazepines, and fatalities from prescribed benzodiazepines rose by 22%.

The poster presenters stated that psychiatric and addiction- focused clinicians play an integral role in preventing benzodiazepine misuse and addiction.

To help patients taper benzodiazepines to discontinuation, clinicians must be up-to-date on practices; if clinicians mismanage tapering, sudden withdrawal can prove fatal. Challenges to tapering patients with chronic benzodiazepine use can be found in the Table.

Table. Challenges to Tapering Chronic Benzodiazepine Use

As for tapering strategies, the presenters suggested adjunct mood stabilizers such as carbamazepine and oxcarbazepine. Carbamazepine, when used as an adjunct or prophylactically, can help reduce intense withdrawal symptoms and thus keep patients on track for discontinuation. However, carbamazepine has received criticism regarding its efficacy, and it is well documented to have a series of concerning adverse effects such as skin reactions, agranulocytosis, leukopenia, and significant drug-drug interactions by nature of its metabolism. This makes some clinicians wonder: Are the risks worth the benefit?

Oxcarbazepine has also been proposed as an alternative. Results of some small-scale clinical trials noted moderate efficacy for oxcarbazepine in helping patients with detoxification, and it has fewer adverse effect concerns. The presenters suggested that other mood stabilizers, particularly those with antiepileptic effects, require further research for their potential help with benzodiazepine addiction.

“Through a more current literature review, we hope to increase the tools available to psychiatrists for more success in discontinuation and maintaining sobriety for patients,” the presenters wrote.

In a previous Psychiatric Times article, Steve Adelman, MD, of the University of Massachusetts Medical School in Boston, suggested 8 universal precautions adapted from Gourlay et al for use by psychiatrists who must decide whether to initiate or continue pharmacotherapy with benzodiazepines. They include making a diagnosis with an appropriate differential and creating and ratifying a treatment agreement. However, other clinicians, such as Daniel Morehead, MD, a Psychiatric Times columnist and featured cover author in this issue, suggest that although benzodiazepines carry risks, those risks are exaggerated by government officials, critics, and the public at large.

Source: https://www.psychiatrictimes.com/view/how-to-safely-and-effectively-taper-benzodiazepines

January 3, 2024    |   By Holly Moody-Porter

Source: https://www.umaryland.edu/news/archived-news/december-2023/cannabis-linked-psychiatric-disorders-on-the-rise.php

Polysubstance use—when more than one drug is used or misused over a defined period of time—can occur from either the intentional use of opioids with other drugs or by accident, such as if street drugs are contaminated with synthetic opioids. In the first half of 2018, nearly 63% of opioid overdose deaths in the United States also involved cocaine, methamphetamine, or benzodiazepines, signaling the need to address polysubstance use as part of a comprehensive response to the opioid epidemic. Fentanyl, a highly potent synthetic opioid, has been identified as a driver of overdose deaths involving other opioids, benzodiazepines, alcohol, methamphetamine, and cocaine.

Two classes of drugs are frequently co-used with opioids: depressants and stimulants. Although there are medical uses for some drugs in these classes, they also all have high potential for misuse. Mixing opioids—which are depressants—with other depressants or stimulants, either intentionally or unknowingly, has contributed to the rising number of opioid overdose deaths, which have more than doubled since 2010. Efforts to reduce opioid overdose deaths should incorporate strategies to prevent, mitigate, and treat the use of multiple substances. 

Depressants

Depressants act on the central nervous system to induce relaxation, reduce anxiety, and increase drowsiness. Opioid use concurrent with the use of another sedating drug compounds the respiratory depressant effect of each drug, creating a higher risk for overdose and fatal overdose than when either drug is used alone.

Benzodiazepines

Benzodiazepines are prescribed for medical use as sedatives but are commonly misused for nonmedical purposes and in combination with prescription and illicit opioids. In 2018, just over 9,000 U.S. deaths involved both opioids and benzodiazepines, more than twice the number of 2008 deaths due to such co-use. Moreover, in 2018, nearly half (47.2%) of benzodiazepine overdose deaths involved synthetic opioids (e.g., fentanyl). Fatal overdoses involving both prescription opioids and benzodiazepines nearly tripled from 2004 to 2011.

Alcohol

In 2017, 15% of opioid overdose deaths involved alcohol. From 2012 to 2014, more than 2 million people who misused prescription opioids were also binge drinkers of alcohol (defined as more than five drinks for a man or more than four drinks for a woman within a two-hour period); compared with nondrinkers, binge drinkers were associated with being twice as likely to misuse prescription opioids. Evidence indicates that about 23% of people with an opioid use disorder have a concurrent alcohol use disorder.

Stimulants

Stimulants increase arousal and activity in the brain. In 2017, opioids were involved in more than half of stimulant-involved overdose deaths—about 15,000 total. The co-use of stimulants with synthetic opioids such as fentanyl either intentionally or through drug contamination has increased the number of stimulant-involved overdose deaths. The opposing impacts of increased arousal from stimulants and sedation from opioids on the body can make the outcomes of co-use less predictable and raise the risk of overdose.

Methamphetamine

About 12% of opioid overdose deaths from January to June 2018 involved methamphetamine, an illicit drug. In 2017, opioids were involved in 50% of methamphetamine-involved deaths, and recent data suggests synthetic opioids are driving increases in methamphetamine-involved deaths. One study found that 65% of those seeking opioid treatment had reported a history of methamphetamine use, with more than three-quarters of them indicating that they had used methamphetamines and opioids mostly at the same time or on the same day.

Cocaine

Of the nearly 15,000 cocaine overdose deaths in 2018, nearly 11,000 also involved opioids; this number accounts for about 23% of the total opioid overdose deaths that year. In fact, since 2010 the number of deaths caused by a combination of opioids and cocaine has increased more than fivefold. People who primarily use cocaine but sometimes co-use opioids are at high risk for overdose because of the increasing presence and potency of fentanyl in the drug supply and a lower tolerance for opioids than someone who regularly uses them.

What should be done?

It is critical that state policies addressing the rise in polysubstance use and its link to increased risk of overdose span across prevention, harm reduction, and treatment strategies. To effectively accomplish this, states should:

• Enact policies that increase provider use of prescription drug monitoring programs (PDMPs) to reduce the co-prescription of opioids and benzodiazepines. PDMPs, state-based electronic databases that contain information on controlled substance prescriptions, allow prescribers and pharmacists to monitor patients’ prescription drug use and can promote safer prescribing practices that help prevent overdoses. High rates of benzodiazepine prescribing are correlated with the drug’s involvement in opioid overdose deaths.
• Expand naloxone distribution to reach people who use stimulants. Naloxone reverses the respiratory depression effects of opioids to safeguard against a fatal overdose and remains effective when people use opioids in combination with other drugs. Considering that opioids are frequently implicated in cocaine and methamphetamine overdose deaths, people who primarily use stimulants are recognized as an at-risk population for opioid overdose. Laws that allow for increased community distribution of naloxone can help safeguard against polysubstance use overdoses.
• Amend drug paraphernalia laws to allow possession of fentanyl test strips. Fentanyl test strips can detect the presence of fentanyl in a person’s drug supply when dipped into a solution of a small amount of the drug in water. People who use drugs have indicated that if a test strip found fentanyl in their supply, they would take measures to prevent an overdose, such as injecting at a slower pace or using less of the drug at a time. Fentanyl test strips are mainly used by people who inject opioids but can also be helpful for those who use stimulants and fear fentanyl contamination by preventing unintentional co-use that could lead to a fatal overdose. Amending drug paraphernalia laws to allow the possession of drug-checking devices, including fentanyl test strips, would permit agencies and organizations to distribute test strips to people who use drugs and help to prevent fentanyl-related overdose deaths.
• Prohibit the discharge of patients from publicly funded opioid use disorder (OUD) treatment programs for their continued substance use. Treatment programs often discharge patients from treatment involuntarily because of their continued illicit drug use (a practice commonly called administrative discharge). This practice poses a particular risk for patients being treated for OUD with methadone or buprenorphine who are at high risk for overdose if discharged without medication. Although co-use of other drugs, such as stimulants, with medications for OUD can interfere with treatment, it remains safer for patients to continue medication treatment because of their high risk for overdose from using illicit opioids. People with OUD who use benzodiazepines are particularly at higher risk for overdose when not on medication treatment. Federal guidelines recommend avoiding administrative discharge and instead suggest that treatment programs re-evaluate a patient’s needed level of care if the current treatment plan proves ineffective.

Conclusion

As the increase in opioid use evolves into an increase in polysubstance use, understanding how different substances interact may inform strategies that help prevent overdose. Though some individuals knowingly combine or co-use opioids with stimulants or other depressants, an additional and growing concern is the adulteration of other drug supplies with fentanyl. Strengthening policy efforts across the continuum of prevention, harm reduction, and treatment to address the risks of polysubstance use can slow the rates of drug overdose deaths in the United States.

Source: https://www.pewtrusts.org/en/research-and-analysis/fact-sheets/2020/10/opioid-overdose-crisis-compounded-by-polysubstance-use October 2020

Anybody wondering what happens to the 8 per cent of the skunk-smoking population who develop mental illness should visit any psychiatric hospital in Britain or speak to somebody who has done so What is really needed in dealing with cannabis is a “tobacco moment”, as with cigarettes 50 years ago, when a majority of people became convinced that smoking might give them cancer and kill them. Since then the number of cigarette smokers in Britain has fallen by two-thirds.

A depressing aspect of the present debate about cannabis is that so many proponents of legalisation or decriminalisation have clearly not taken on board that the causal link between cannabis and psychosis has been scientifically proven over the past ten years, just as the connection between cancer and cigarettes was proved in the late 1940s and 1950s.

The proofs have emerged in a series of scientific studies that reach the same grim conclusion: taking cannabis significantly increases the risk of schizophrenia. One study in The Lancet Psychiatry concludes that “the risk of individuals having a psychotic disorder showed a roughly three times increase in users of skunk-like cannabis, compared with those who never used cannabis”. As 94 per cent of cannabis seized by the police today is super-strength skunk, compared to 51 per cent in 2005, almost all those who take the drug today will be vulnerable to this three-fold increase in the likelihood that they will develop psychosis.

Mental health professionals have long had no doubts about the danger. Five years ago, I asked Sir Robin Murray, professor of psychiatric research at the Institute of Psychiatry in London, about them. He said that studies showed that “if the risk of schizophrenia for the general population is about one per cent, the evidence is that, if you take ordinary cannabis, it is two per cent; if you smoke regularly you might push it up to four per cent; and if you smoke ‘skunk’ every day you push it up to eight per cent”.

Anybody wondering what happens to this 8 per cent of the skunk-smoking population should visit any mental hospital in Britain or speak to somebody who has done so. Dr Humphrey Needham-Bennett, medical director and consultant psychiatrist of Cygnet Hospital, Godden Green in Sevenoaks, explained to me that among his patients “cannabis use is so common that I assume that people use or used it. It’s quite surprising when people say ‘no, I don’t use drugs’.”

The connection between schizophrenia and cannabis was long suspected by specialists but it retained its reputation as a relatively benign drug, its image softened by the afterglow of its association with cultural and sexual liberation in the 1960s and 1970s.

This ill-deserved reputation was so widespread that even 20 years ago, the possible toxic side effects of cannabis were barely considered. Zerrin Atakan, formerly head of the National Psychosis Unit at the Maudsley Psychiatric Hospital and later a researcher at the Institute of Psychiatry,

said: “I got interested in cannabis because I was working in the 1980s in an intensive care unit where my patients would be fine after we got them well. We would give them leave and they would celebrate their new found freedom with a joint and come back psychotic a few hours later.”

She did not find it easy to pursue her professional interest in the drug. She recalls: “I was astonished to discover that cannabis, which is the most widely used illicit substance, was hardly researched in the 1990s and there was no research on how it affected the brain.” She and fellow researchers made eight different applications for research grants and had them all turned down, so they were reduced to taking the almost unheard of course of pursuing their research without the support of a grant.

Studies by Dr Atakan and other psychiatrists all showed the connection between cannabis and schizophrenia, yet this is only slowly becoming conventional wisdom. Perhaps this should not be too surprising because in 1960, long after the link between cigarettes and lung cancer had been scientifically established, only a third of US doctors were persuaded that this was the case.

A difficulty is that people are frightened of mental illness and ignorant of its causes in a way that is no longer true of physical illnesses, such as cancer or even HIV. I have always found that three quarters of those I speak to at random about mental health know nothing about psychosis and its causes, and the other quarter know all too much about it because they have a relative or friend who has been affected.

Even those who do have experience of schizophrenia do not talk about it very much because they are frightened of a loved one being stigmatised. They may also be wary of mentioning the role of cannabis because they fear that somebody they love will be dismissed as a junkie who has brought their fate upon themselves.

This fear of being stigmatised affects institutions as well as individuals. Schools and universities are often happy to have a policy about everything from sex to climate change, but steer away from informing their students about the dangers of drugs. A social scientist specialising in drugs policy explained to me that the reason for this is because “they’re frightened that, if they do, everybody will think they have a drugs problem which, of course, they all do”.

The current debate about cannabis – sparked by the confiscation of the cannabis oil needed by Billy Caldwell to treat his epilepsy and by William Hague’s call for the legalisation of the drug – is missing the main point. It is all about the merits and failings of different degrees of prohibition of cannabis when it is obvious that legal restrictions alone will not stop the 2.1 million people who take cannabis from going on doing so. But the legalisation of cannabis legitimises it and sends a message that the government views it as relatively harmless. The very fact of illegality is a powerful disincentive for many potential consumers, regardless of the chances of being punished.

The legalisation of cannabis might take its production and sale out of the hands of criminal gangs, but it would put it into the hands of commercial companies who would want to make a profit, advertise their product and increase the number of their customers. Commercialisation of cannabis has as many dangers as criminalisation.

A new legal market in cannabis might be regulated and the toxicity of super-strength skunk reduced. But the argument of those who want to legalise cannabis is that the authorities are unable to enforce regulations when the drug is illegal, so why should they be more successful in regulating it when its production and sale is no longer against the law?

The problem with these rancorous but sterile arguments for and against legalisation and decriminalisation is that they divert attention from what should and can be done: a sustained campaign to persuade people of all ages that cannabis can send them insane. To a degree people are learning this already from bitter experience. As Professor Murray told me five years ago, the average 19- to 23-year-old probably knows more about the dangers of cannabis than the average doctor “because they have a friend who has gone paranoid. People know a lot more about bad trips than they used to.”

Patrick Cockburn is the co-author of Henry’s Demons: Living With Schizophrenia, A Father and Son’s Story

A depressing aspect of the present debate about cannabis is that so many proponents of legalisation or decriminalisation have clearly not taken on board that the causal link between cannabis and psychosis has been scientifically proven over the past ten years, just as the connection between cancer and cigarettes was proved in the late 1940s and 1950s.

The proofs have emerged in a series of scientific studies that reach the same grim conclusion: taking cannabis significantly increases the risk of schizophrenia. One study in The Lancet Psychiatry concludes that “the risk of individuals having a psychotic disorder showed a roughly three times increase in users of skunk-like cannabis, compared with those who never used cannabis”. As 94 per cent of cannabis seized by the police today is super-strength skunk, compared to 51 per cent in 2005, almost all those who take the drug today will be vulnerable to this three-fold increase in the likelihood that they will develop psychosis.

Home Secretary Sajid Javid: The government will carry out a review of the scheduling of cannabis for medicinal use

Mental health professionals have long had no doubts about the danger. Five years ago, I asked Sir Robin Murray, professor of psychiatric research at the Institute of Psychiatry in London, about them. He said that studies showed that “if the risk of schizophrenia for the general population is about one per cent, the evidence is that, if you take ordinary cannabis, it is two per cent; if you smoke regularly you might push it up to four per cent; and if you smoke ‘skunk’ every day you push it up to eight per cent”.

Those using strong strains of illegal drugs such as cannabis skunk, or the illegal use of prescription drugs are risking their mental health and the lives of others. Suicidal thoughts are not unknown and this letter from a doctor discusses the problems of confidentiality versus life saving – of the patient or others.

To the Clinicians of the Co-Pilot of Germanwings Flight 9525

Dear German Medical Colleagues,

Please bear with me through this rather long letter. There is so much that I have been wondering and worrying about—including you.

I may never know who you are, but if you provided medical or psychiatric care for Andreas Lubitz, co-pilot of Germanwings Flight 9525, we are colleagues. Whether you saw Mr Lubitz years ago or more recently, or whether you saw him privately or as an airline-appointed medical examiner, you had some responsibility for his care.

And you too are his victims, of sorts. I hope your reputation does not suffer unduly. I hope PTSD does not develop as a result of his apparent suicide. If you provided ethical care (ie, competent care), I hope you are not scapegoated. “Monday morning quarterbacking”—an American football saying about reviewing a game the day after it is played—is always so much easier than preventing problems in real time.

After all, if reports of Mr Lubitz taking an injectable antipsychotic during training in 2009 are true, that doesn’t for sure mean that he had an ongoing or intermittent psychosis. Maybe, just maybe, it could have been a short-acting injection for acute agitation due to extreme stress and/or drug abuse. Similarly, treatment back then for an “episode” of “severe” depression could have seemed to be a one-time episode.

On the other hand, there are reports that Lubitz saw psychotherapists “over a long period of time.” Those psychotherapists probably knew the patient best, especially if he had a particular personality disorder or significant traits of concern (eg, undue narcissism, paranoia).

We have not yet heard anything about whether Lubitz had PTSD, but people with this disorder can appear normal. Perhaps the co-pilot dissociated as he crashed the airplane, which would have allowed him to ignore for minutes the passengers’ screams and the banging on the door of the cockpit. That could account for the fact that voice recording picked up no triumphal shouts, only his steady breathing.

This analysis is all speculation, of course. Maybe it’s the kind of “wild analysis” that Freud so deplored.

I do not know how prominent so-called “anti-psychiatrists” are in Germany, but if they are anything like they are here in the US, they are likely to blame psychiatric medication for the co-pilot’s bizarre and tragic behavior. Of course, they could well have a point. Some antidepressants, which can cause visual side effects, were prescribed for Mr Lubitz, agents perhaps, that we don’t in the US.

We know he was concerned about his vision, but speculation so far is that this complaint was psychosomatic. In addition, sudden withdrawal from some antidepressants can lead to increased agitation. Moreover, antidepressants can trigger a (hypo)manic episode, although of course a manic episode can occur that leads to grandiosity and agitation. On the other hand, no one seems to have described such changes in Mr Lubitz before the crash.

Therefore, I hope your medical documentation was good—better than mine usually was. I hope you documented your risk assessment adequately. If you were unsure of what to do, I hope you obtained consultation and/or supervision. If you worked in a system of care, I hope they adequately monitored the quality of care you provided.

I understand that your medical privacy laws are much more stringent than our patchwork of state and national privacy laws are here in the US, both in life and in death. I heard that you can be imprisoned for up to 5 years for not following strict standards of patient confidentiality. Perhaps that prevented you from contacting Lufthansa instead of just giving the patient an unfit-for-work note, which he subsequently tore up. That, and other reasons, may be causing you to bite your tongue to offer further explanation.

I wonder if your stringent privacy laws are a reaction to the breaches of physicians when the Nazis ruled, as well as the subsequent invasion of privacy in East Germany. Are they an overreaction that needs some degree of correction? After all, airline safety is good, and this may have been a perfect confluence of various factors. Further, to exacerbate our existential anxiety, we have the unexplained disappearance of the Malaysian airliner from just about 2 years ago. Was there a copycat aspect to the Germanwings crash?

All medical colleagues must weigh risk to others against the need for patient confidentiality. This can include whether to divulge patient information such as highly contagious diseases like AIDS or Ebola; abuse of a minor or domestic violence; driving while impaired; carrying a gun; running a nuclear power plant; and being responsible for all kinds of public transportation and safety.

Maybe you wish you could talk and give condolences to those who lost family and friends on the doomed airliner. That would be the human thing to do, but perhaps you can’t?

As psychiatrists, suicide and homicide are essentially our only life and death challenges. So when a patient commits suicide and kills 149 others at the same time, what could feel professionally worse?

Yet we all know that we are not particularly successful at predicting actual suicide or homicide. Complicating that, someone troubled who decides that his or her solution is suicide and/or homicide often seems surprisingly well right before the act. He or she is relieved, having decided on the solution to his problems. We must appreciate our limitations.

Everyone wants to know the co-pilot’s motivation. So do I. But nothing is convincing yet about why he would make sure to kill everyone on board. Way back when, I was taught that in general, suicide was motivated by a desire to die, to kill, and/or be killed. This is a rare example of all—a triple play.

We may need system and cultural changes to how we approach some aspects of mental illness, such as the Air Force Suicide Prevention Program in the US. This program has significantly reduced suicide attempts as well as violence to others.

We and our psychiatric patients are stigmatized in many countries. If such stigma can cause inadequate attention to mental health in routine annual check-ups, no wonder mental health examinations are inadequate for airline pilots.

Complicating our work is the denial, lack of insight, and/or loss of memory among some of our patients. The people that we (clinicians and the public) need to fear most (ie, sociopaths) can be the best at hiding the risk they pose. Periodic research about faking psychiatric symptoms in the emergency department indicates how easily we, in our quest to be helpful, can be fooled. We don’t have corroborating lab tests to fall back on, unlike in other areas of medicine.

During my career, I evaluated and treated a fair number of pilots. Almost always, we grappled with the implications of getting treatment and taking medication. What might help their mental problems might, at the same time, cost them their job, and thereby worsen their mental health. No wonder so many pilots hide psychiatric treatment from their employers.

Who knows? Maybe some of you who treated him didn’t even know that Andreas Lubitz was a pilot. We often know little about the real day to day lives of our patients. Maybe we need to know more.

About a century ago, Freud concluded that his was “an impossible profession.” This may well still be so. The burnout rate of physicians and psychiatrists in the US is over 50%. Know that.

I appreciate why we may never hear your side of the story. That may be a shame, for you probably have much to teach us and can transform some of our fantasies into reality.

In terms of our ethical responsibilities to each other, we are indeed our brothers’—and sisters’—keepers. In that regard, let me know if there is anything more I should know or do.

Your colleague,
H. Steven Moffic, MD (Steve)

Source: Psychiatric Times psychiatrictimes@email.cmpmedica-usa.com 16^th April 2015

Addiction Science & Clinical Practice

Katherine A Belendiuk1, Lisa L Baldini2 and Marcel O Bonn-Miller345^*

• *Corresponding author: Marcel O Bonn-Miller Marcel.Bonn-Miller@va.gov

Author Affiliations

¹Institute of Human Development, University of California, 1121 Tolman Hall #1690, Berkeley 94720, CA, USA

²Palo Alto University, 1791 Arastradero Road, Palo Alto 94304, CA, USA

³Center of Excellence in Substance Abuse Treatment and Education, Philadelphia VA Medical Center, 3900 Woodland Avenue, Philadelphia 19104, PA, USA

⁴Center for Innovation to Implementation and National Center for PTSD, VA Palo Alto Health Care System, 795 Willow Road (152-MPD), Menlo Park 94025, CA, USA

⁵Department of Psychiatry, University of Pennsylvania Perelman School of Medicine, 3440 Market Street, Philadelphia 19104, PA, USA

For all author emails, please log on.

Addiction Science & Clinical Practice 2015, 10:10 doi:10.1186/s13722-015-0032-7

The electronic version of this article is the complete one and can be found online at:http://www.ascpjournal.org/content/10/1/10

© 2015 Belendiuk et al.; licensee BioMed Central.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Abstract

The present investigation aimed to provide an objective narrative review of the existing literature pertaining to the benefits and harms of marijuana use for the treatment of the most common medical and psychological conditions for which it has been allowed at the state level. Common medical conditions for which marijuana is allowed (i.e., those conditions shared by at least 80 percent of medical marijuana states) were identified as: Alzheimer’s disease, amyotrophic lateral sclerosis, cachexia/wasting syndrome, cancer, Crohn’s disease, epilepsy and seizures, glaucoma, hepatitis C virus, human immunodeficiency virus/acquired immunodeficiency syndrome, multiple sclerosis and muscle spasticity, severe and chronic pain, and severe nausea. Post-traumatic stress disorder was also included in the review, as it is the sole psychological disorder for which medical marijuana has been allowed. Studies for this narrative review were included based on a literature search in PsycINFO, MEDLINE, and Google Scholar. Findings indicate that, for the majority of these conditions, there is insufficient evidence to support the recommendation of medical marijuana at this time. A significant amount of rigorous research is needed to definitively ascertain the potential implications of marijuana for these conditions. It is important for such work to not only examine the effects of smoked marijuana preparations, but also to compare its safety, tolerability, and efficacy in relation to existing pharmacological treatments.

Keywords:

Cannabis; Medical marijuana; Marijuana; Medicine; Treatment; Alzheimer’s disease; ALS; Cachexia; Cancer, Crohn’s disease; Epilepsy; Seizures; Glaucoma; Hepatitis C virus; HCV; HIV; AIDS; Multiple sclerosis; MS; Pain; Nausea; Vomiting; Post-traumatic stress disorder; PTSD

Introduction

National estimates suggest that 5.4 million people in the United States above the age of 12 have used marijuana daily or regularly within the past year [1]. This represents an increase of approximately 74.2 percent since 2006 [1]. Similar increases have also been noted among vulnerable populations in the U.S. (e.g., veterans and adolescents) [2],[3].

Marijuana is currently illegal in every country in the world. In 2012, Uruguay voted to legalize state-controlled marijuana sales but implementation of the law has been postponed until 2015. The policy in the Netherlands is mixed, with permissible retail sale of marijuana at coffee shops, but restrictions on production and possession. Notably, as the concentration of THC in marijuana has increased, Dutch coffee shops have begun to close, as perception of marijuana as a “soft” drug transitions to perceptions of marijuana as a “hard” drug.

Like the Netherlands, the United States currently has a mixed drug policy; marijuana is an illegalSchedule I drug under U.S. Federal law. However, marijuana policies vary by state, with some states (e.g., Colorado and Washington) legalizing the use of recreational marijuana (i.e., allowing the legal possession and use of marijuana under state law), and other states decriminalizing marijuana (i.e., reducing the penalties for possession and/or use of small amounts of marijuana to fines or civil penalties). Furthermore, as of this review, 23 states and the District of Columbia have passed legislation allowing medical marijuana (i.e., individuals can defend themselves against criminal charges related to marijuana possession if a medical need is documented) for the treatment of a variety of medical and psychological conditions. Though the list of conditions for which medical marijuana has been allowed varies at the state level, the majority of states agree on its use for Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), cachexia/wasting syndrome, cancer, Crohn’s disease (CD), epilepsy and seizures, glaucoma, hepatitis C virus (HCV), human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS), multiple sclerosis (MS) and muscle spasticity, severe and chronic pain, severe nausea, and post-traumatic stress disorder (PTSD).

The aim of the present review is to provide a summary of the existing empirical literature regarding the effects of marijuana/cannabinoids on each of the above-noted conditions. Though some recent work has reviewed the adverse effects of marijuana [4] or the efficacy of marijuana for certain conditions (e.g., neurologic) [5], there has yet to be a comprehensive review of the effects of marijuana for each of the medical and psychiatric conditions for which it is currently used.

Methods

The list of all conditions for which medical marijuana is allowed, according to the legislation of each U.S. state for which medical marijuana has been approved, was obtained and examined [6]. From this list, common conditions for which medical marijuana is allowed (i.e., those conditions shared by at least 80 percent of medical marijuana states) were identified as: AD, ALS, cachexia/wasting syndrome, cancer, CD, epilepsy and seizures, glaucoma, HCV, HIV/AIDS, MS and muscle spasticity, severe and chronic pain, and severe nausea. Though not presently a qualifying condition in at least 80 percent of states with medical marijuana laws, PTSD was also included in the review, as it is rapidly gaining attention and recognition as the sole psychological disorder for which medical marijuana is allowed.

Studies for this narrative review were included based on a literature search in the following databases: PsycINFO, MEDLINE, and Google Scholar. Within each database, each combination of the following key marijuana terms and the above-listed conditions were used to conduct a search: cannabis, marijuana, marihuana, cannabinoid, delta-9-tetrahydrocannabinol, THC, cannabidiol, CBD, cannabinol, cannabigerol, Marinol, dronabinol, Sativex, Nabilone, and Nabiximols. References within each obtained article were also examined to assure that no studies were overlooked. Only published, English-language studies were included in this review.

Though the primary focus of this review is on studies of marijuana plant effects, as these are most relevant to recent medical marijuana legislation, synthetic or plant-derived cannabinoids (e.g., dronabinol, Nabilone) were also included due to the general dearth of marijuana plant studies for a number of conditions. Indeed, for purposes of the review, references to oral administrations of marijuana constitute a pharmaceutical grade extraction administered in tablet or liquid form (e.g., dronabinol, Nabilone, Nabiximols), while references to smoked administration of marijuana constitute the inhalation of smoke from burned marijuana leaves and flowers. Finally, the present review is organized alphabetically by condition for which marijuana is allowed, rather than in order of disorder for which it is most to least commonly recommended, or strength of the evidence. We chose this approach as there is currently only state-level data [7]-[9], rather than national, representative data on the primary conditions for which medical marijuana is used or recommended, and the existing literature and state of the evidence for many conditions remains relatively poor.

Results

Alzheimer’s disease

AD, the leading form of dementia in the elderly, is a progressive, age-related disorder characterized by cognitive and memory deterioration [10]. AD has several neuropathological markers, including neuritic plaques and neurofibrillary tangles [11]. Although several researchers have suggested dronabinol and Nabilone may act on these mechanisms to confer therapeutic effects for patients with AD [12],[13], a recent Cochrane systematic review found no evidence that dronabinol was effective in reducing symptoms of dementia [14]. The authors of a placebo-controlled crossover study of 15 patients with AD who were refusing to eat suggest that dronabinol increases weight gain and decreases disturbed behavior [15], but there is insufficient quantitative data to support this conclusion [14], and one study participant had a grand mal seizure following dronabinol administration [15]. Another pilot study of two patients with dementia found that dronabinol reduced nocturnal motor activity [16]. No studies have examined the effects of smoked marijuana in patients with AD. In sum, there is insufficient evidence to recommend marijuana for the treatment of AD. Future directions should include conducting randomized controlled trials (RCTs) comparing both smoked and oral marijuana to placebo and existing treatments, with sample sizes large enough to detect treatment effects and the safety and tolerability of marijuana.

Amyotrophic lateral sclerosis

ALS is a fatal neurological disease with symptoms that include weakness, spasticity, and respiratory difficulties. Cannabinoids are hypothesized to act in the regions of established pathophysiology for ALS [17] and could be used for symptom management (e.g., pain, spasticity, wasting, respiratory failure, dysphagia, negative mood, and dysautonomia) [18]. Although there is limited evidence from a survey of patients with ALS that marijuana consumed in a variety of forms (i.e., oral, smoked, vaporized, and eaten) improves speech and swallowing [19], the anti-salivatory components of marijuana may reduce the risk of aspiration pneumonia, while also increasing patient comfort [18],[19]. These survey findings indicate that up to 10 percent of patients use marijuana for symptom management, and these self-reports suggest efficacy in increasing appetite and mood and decreasing pain, spasticity, and drooling. However, as is consistent with the half-life of smoked marijuana, the beneficial effects of marijuana on symptoms of ALS were fewer than 3 hours in duration [19]. The only randomized, double-blind, placebo-controlled crossover trial of marijuana in patients with ALS has a small sample size (N = 27) and indicates that while 5 mg of dronabinol is well-tolerated, there was no effect on number or intensity of cramps, quality of life, appetite, sleep, or mood [20]. There is currently insufficient clinical evidence in humans with ALS to recommend cannabinoids as primary or adjunctive therapy.

Cachexia/wasting syndrome

Cachexia is the general wasting and malnutrition that occurs in the context of chronic diseases such as HIV/AIDS and cancer. In patients with HIV or cancer, smoked marijuana and dronabinol have been shown to increase weight gain [21],[22] and food intake [22],[23] compared to placebo. In a within-subject, double-blind, staggered, double-dummy study of nine individuals with muscle mass loss, dronabinol resulted in significantly greater calorie consumption than smoked marijuana [24]. A within-subject, double-blind, placebo-controlled trial with seven HIV-positive marijuana smokers taking antiretroviral medications found that compared to placebo, dronabinol increased caloric intake [25]. Additional studies indicate that dronabinol administration increases appetite, decreases nausea, and protects against weight loss [26], with effects on appetite and weight stability enduring in long-term follow-up [27].

Both dronabinol and smoked marijuana increase the number of eating occasions [22],[25], and smoked marijuana may also affect weight gain and calorie intake by modulating appetite hormones [28]. Importantly, weight gain in one study was greater than would have been expected based on increased calorie consumption alone [23], which may be particularly relevant for those who have impaired food intake and/or nausea. These studies demonstrate that marijuana has positive effects on cachexia resulting from a medical condition, but are largely limited by small sample sizes. Additionally, studies comparing THC to FDA-approved medication (i.e., megestrol) indicate that THC is less effective in promoting appetite and weight gain [29]. In sum, there is moderate support for the use of cannabinoids for cachexia/wasting, and dronabinol has been FDA-approved for anorexia associated with weight loss in individuals with AIDS. Additional studies with larger sample sizes that examine the efficacy of marijuana compared to nutritional support/calorie augmentation in the treatment of cachexia are indicated.

Cancer

Cancer is a qualifying medical condition in every state that has approved marijuana for medical use [30]. The majority of clinical research examining the relation between THC and cancer has evaluated the effect of smoked THC on the risk for cancer, or the palliative effects of THC on chemotherapy-related nausea and emesis, chronic pain, and wasting (reviewed in respective sections); few studies have studied the effect of marijuana in any form on the treatment of primary cancer pathology. In vitro and in vivo research suggests that cannabinoids inhibit tumor growth [30] via several proposed mechanisms (e.g., suppression of cell proliferation, reduced cell migration, increased apoptosis) [31]; however, in vitro and in vivo studies also have shown that THC increases tumor growth due to reduced immune response to cancer [32]. The only clinical trial of THC on cancer examined intracranial administration of THC to nine patients with recurrent glioblastoma multiforme who had failed surgical- and radiotherapy, and results indicated that THC decreased tumor growth, while being well-tolerated with few psychotropic effects [33]. This study is limited by lack of generalizability, and clinical trials with larger representative samples that examine oral or smoked administration of THC are essential to elucidate the effects on cancer pathology. There is currently insufficient evidence to recommend marijuana for the treatment of cancer, but there may be secondary treatment effects on appetite and pain.

Crohn’s disease

CD is an inflammatory bowel disease (IBD) that has no cure; treatment targets include reducing inflammation and secondary symptoms. Between 16 percent and 50 percent of patients use marijuana to relieve symptoms of IBD [34]-[36], and patients using marijuana for 6 months or longer are five times more likely to have had surgery for their IBD [34]; whether marijuana exacerbates disease progression or more severe disease results in self-medication is unclear. Only one placebo-controlled study of the effects of marijuana in patients with CD has been conducted[37]. This study found that there was no difference between placebo and smoked marijuana on CD remission (defined as a CD Activity Index (CDAI) of less than 100), and that marijuana was superior to placebo in promoting clinical response (a decrease in CDAI score greater than 100), reducing steroid use, and improving sleep and appetite [37]. Importantly, this study did not include objective measurement of inflammatory activity, and there was no significant difference in placebo and treatment groups 2 weeks after treatment cessation [37]. Until clinical trials with objective measurement of treatment effects over an extended period of time are conducted to examine the safety and efficacy of marijuana for the treatment of IBD, there is insufficient evidence for the use of marijuana for the treatment of IBD.

Epilepsy and seizures

The known effects of cannabinoids on epilepsy and seizures are largely from animal studies, surveys, and case studies. Several animal studies indicate that marijuana and its constituents exhibit anticonvulsant effects [38]-[41] and reduce seizure-related mortality [39], but there is also evidence that cannabinoids can lower the threshold for seizures [42], and THC withdrawal increases susceptibility for convulsions [42]. Cross-sectional surveys indicate that 16–21 percent of patients with epilepsy smoke marijuana [43],[44], with some reporting positive effects (e.g., spasm reduction) and a belief that marijuana is an effective therapy [44], and others reporting increased seizure frequency and intensity [43]. Based on a Cochrane review, the few RCTs that have been conducted in humans include a total of 48 participants [45] and only examine treatment with cannabidiol. These trials exhibited heterogeneity of effects: some indicated a reduction in seizure frequency [46],[47], while others demonstrated no effect compared to placebo [48]. In addition, none of the studies examined response at greater than 6-month follow-up [45]. Systematic reviews of the literature have concluded that there is insufficient clinical data to support or refute the use of cannabinoids for the treatment of epilepsy and seizures [5],[45].

Glaucoma

Glaucoma is a neurodegenerative eye disease that can cause blindness by damaging retinal ganglion cells and axons of the optic nerve. Intraocular pressure (IOP) can influence both onset and progression of glaucoma and is often a target for intervention. Small samples have demonstrated reduced IOP following smoked marijuana [49],[50], but the effect is only present in 60–65 percent of individuals [51] and lasts for 3–4 hours, requiring repeated dosing throughout the day [52]. Furthermore, patients discontinue marijuana use due to side effects (e.g., dizziness, anxiety, dry mouth, sedation, depression, confusion, weight gain, and distortion of perception[53]), and this treatment discontinuity may exacerbate optic nerve damage and obviate the benefits of reduced IOP [54]. Limited research and documented toxicity have resulted in the American Glaucoma Society [54], Canadian Opthalmological Society [55], and the American Academy of Ophthalmology’s Complementary Therapies Task Force [52] determining that there is insufficient evidence to indicate that marijuana is safer or more effective than existing pharmacotherapy or surgery for the reduction of IOP. Development of eye drops for topical application of THC would minimize psychoactive and other side effects but is complicated by the high lipophilicity and low water solubility of cannabinoids [52],[56]. Additionally, the distance from the application site to the retina may be too great to afford neuroprotective benefits [52], given that only 5 percent of an applied dose penetrates the cornea to the intraocular space [56].

Hepatitis C virus

There have been no RCTs examining the use of cannabinoids on HCV infection. Of the studies that have been conducted, one longitudinal study demonstrates that smoked marijuana has no effect on HCV progression in individuals with HIV [57]. In contrast, individuals with HCV who smoke marijuana have a higher fibrosis progression rate [58] and more severe steatosis [59], with daily smokers having a more rapid rate of progression and greater severity [60] than occasional marijuana users [58],[59]. Marijuana may have independent negative effects on steatosis [59], but because none of these findings were in the context of a clinical trial, these correlations are not causal and it is possible that individuals who use marijuana do so to manage greater symptom severity [60].

There may be secondary effects of cannabinoids on HCV treatment side effects: dronabinol and Nabilone stabilized treatment-induced weight-loss [61]; and dronabinol, Nabilone, and marijuana procured from a marijuana club (dose and method of administration unspecified) increased HCV treatment duration and reduced post-treatment virological relapse [61],[62]. However, there is also a potential drug-drug interaction between ribavirin, a traditional HCV treatment, and marijuana due to shared cytochrome 450 metabolism [63]. Because 90 percent of HCV infections are the result of injection drug use [64], treatment of symptoms with marijuana may be contraindicated for this subpopulation, particularly because marijuana use in the context of other substance use (i.e., alcohol) has multiplicative effects on the odds of fibrosis severity [60]. Given that newer treatments for HCV (e.g., sofosbuvir) are replacing ribavirin, there will likely be less need for use of marijuana in management of treatment-related side effects. In sum, there is currently insufficient empirical support to recommend marijuana for the treatment of HCV.

HIV/AIDS

Marijuana use in HIV-infected patients is typically for the management of side effects (e.g., nausea) of older antiretroviral treatments and AIDS-related symptoms, including weight-loss and HIV-associated neuropathy (covered in cachexia and pain sections, respectively). Survey studies indicate that 23 percent of patients with HIV/AIDS smoked marijuana in the past month and do so largely to improve mood and appetite and reduce pain [65]; these patients may exhibit tolerance and need higher doses of THC than are currently approved by the FDA for use in clinical trials [25] to experience treatment effects. The few RCTs that have been conducted in a small number of patients with HIV/AIDS largely examined the effects of marijuana (synthetic or natural marijuana that is smoked or ingested) on symptoms (e.g., nausea and appetite) over a short treatment window (21–84 days; see [66] for systematic review). Studies examining the effects of marijuana on the pharmacokinetics of antiretroviral medication demonstrated that neither smoked marijuana nor dronabinol affects short-term clinical outcomes (e.g., viral load, CD4 and CD8 counts [67]), influences the efficacy of antiretroviral medication [68], or indicates that dose adjustments for protease inhibitors are necessary [21]. However, individuals who are dependent on marijuana have demonstrated poorer medication adherence and greater HIV symptoms and side effects than nonusers and nondependent users [69]. Furthermore, while some studies have no participant withdrawal due to adverse events [21],[70],[71], others reported treatment-limiting adverse events [26],[72],[73]. Finally, because drug use is a risk factor for HIV infection [74], treatment of symptoms with marijuana may be contraindicated for this subpopulation. In sum, there is variability in short-term outcomes and insufficient long-term data addressing the safety and efficacy of marijuana when used to manage symptoms of HIV/AIDS and its role in those also using newer, better-tolerated antiretroviral agents.

Multiple sclerosis and muscle spasticity

Muscle spasticity, a common feature of MS, is disordered sensorimotor control that leads to involuntary muscle activation [75] that results in pain, sleep disturbance, and increased morbidity[76]. The majority of studies examining spasticity have compared oral or sublingual forms of cannabinoids to placebo and found reduced spasm severity [77]-[84], with symptom improvement enduring at long-term follow-up [85]-[87], and also reduced spasm frequency and spasm-related pain and sleep disturbances [77],[88],[89]. With regard to smoked marijuana, one study found reductions in muscle spasticity [90]; however, another study showed that smoking marijuana impaired posture and balance in individuals with spasticity [91], so there is currently insufficient evidence to determine the efficacy of smoked marijuana on spasticity [5].

Surveys of patient populations show that between 14 and 16 percent of patients with MS report using marijuana for symptom management [92],[93] and that compared to non-marijuana-using individuals with MS, marijuana-using individuals with MS have decreased cognitive functioning[90],[94],[95]. Because cognitive dysfunction is present in 40–60 percent of individuals with MS before marijuana administration [96], marijuana use may further compromise impaired cerebral functioning in a neurologically vulnerable population. Additionally, future studies should carefully consider outcome assessment. The primary methods of measuring spasticity, the Ashworth Scale and patient self-report, may not be appropriate measures because antispastic drugs do not decrease Ashworth ratings, and patient-reported spasticity severity may be poorly correlated with patient functioning (i.e., a patient whose spasticity compensated for motor weakness may be unable to ambulate with reduced spasticity) [97]. Importantly for both MS and other neurological disorders, the American Academy of Neurology does not advocate the use of marijuana for the treatment of neurological disorders, due to insufficient evidence regarding treatment efficacy [98].

Post-traumatic stress disorder

There has been a recent emergence of empirical studies of the effects of marijuana on symptoms of PTSD, borne primarily out of the observation that individuals with PTSD report using marijuana to cope with PTSD symptoms; specifically, hyperarousal, negative affect, and sleep disturbances[99]-[101]. Empirical work has consistently demonstrated that the endocannabinoid system plays a significant role in the etiology of PTSD, with greater availability of cannabinoid type 1 receptors documented among those with PTSD than in trauma-exposed or healthy controls [102],[103]. Though the use of marijuana and oral THC [104],[105] have been implicated as a potential mechanism for the mitigation of many PTSD symptoms by way of their effects on the endocannabinoid system, some researchers caution that endocannabinoid activation with plant-based extracts over extended periods may lead to a number of deleterious consequences, including receptor downregulation and addiction [102].

There have been no RCTs of marijuana for the treatment of PTSD, though there has been one small RCT of Nabilone that showed promise for reducing nightmares associated with PTSD [106]. One unpublished pilot study of 29 Israeli combat veterans showed reductions in PTSD symptoms following the administration of smoked marijuana, with effects seen up to one year post-treatment[107]. Remaining studies have been primarily observational in nature, documenting that PTSD is associated with greater odds of a cannabis use disorder diagnosis [108] and greater marijuana craving and withdrawal immediately prior to a marijuana cessation attempt [109]. Indeed, sleep difficulties (a hallmark of PTSD) have been associated with poor marijuana cessation outcomes[110],[111], while cannabis use disorders have been associated with poorer PTSD treatment outcomes [112]. Given the lack of RCTs studying marijuana as a treatment for PTSD, there is insufficient scientific evidence for its use at this time.

Severe and chronic pain

Clinical trials have examined smoked and oral administration of cannabinoids on different types of pain (e.g., neuropathic, post-operative, experimentally induced) in multiple patient populations (e.g., HIV, cancer, and fibromyalgia). Two meta-analyses have been conducted examining the association between marijuana and pain. In the first, 18 RCTs demonstrated that any marijuana preparation containing THC, applied by any route of administration, significantly decreased pain scores from baseline compared to placebo [113]. The second examined 19 RCTs of smoked marijuana in individuals with HIV, which also indicated greater efficacy in reducing pain (i.e., sensory neuropathy) compared to placebo [114]. Importantly, the first meta-analysis showed that marijuana increased the odds of altered perception, motor function, and cognition by 4 to 5 times[113], and the second study did not recommend marijuana as routine therapy [114]. Dosage is an important factor to consider for administration of cannabinoids for pain management, as some studies have found that higher doses of smoked marijuana are associated with improved analgesia[115], whereas other studies show that higher doses of smoked marijuana increase pain response[116]. Because the analgesic effects of marijuana are comparable to those of traditional pain medications [117], future research should aim to identify which analgesics provide the lowest risk profile for the management of severe and chronic pain. Although there is preliminary support to suggest that marijuana may have analgesic effects, there is insufficient research on dosing and side effect profile, which precludes recommending marijuana for the management of severe and chronic pain.

Severe nausea

The majority of research related to the effects of marijuana on severe nausea has involved oral administration of marijuana to individuals with chemotherapy-induced nausea and vomiting (CINV). Oral marijuana (i.e., THC suspension in sesame oil and gelatin) has been shown to be more effective in reducing CINV than placebo [118], including the number and volume of vomiting episodes, and the severity and duration of nausea [119]. When compared to traditional anti-emetics, some meta-analytic reviews indicate that oral THC is more effective in reducing CINV[120]-[123], others find no significant difference [122],[124]-[126], and another suggests that combining both is the most effective at reducing the duration and severity of CINV than either alone [127]. Recent advances in both anti-emetic agents and the mechanisms of cannabinoid administration (i.e., sublingual application) warrant future research.

Importantly, patients receiving cannabinoids for severe nausea reported toxicities, including paranoid delusions (5%), hallucinations (6%), and dysphoria (13%) [122]. Additionally, cannabinoid hyperemesis syndrome has been documented, in which persistent and regular marijuana use (i.e., daily or weekly use for more than 1 year) is associated with cyclic vomiting (i.e., episodic nausea and vomiting) [128] and nonresponse to treatment for cyclic vomiting [129]. Dronabinol has been FDA-approved for CINV in individuals who have not shown a treatment response to traditional anti-emetics, but in line with recommendations from the American Society of Clinical Oncology [130] and the European Society for Medical Oncology [131], cannabinoids should not be utilized as a first-line treatment for nausea and vomiting.

Conclusions

The reviewed literature highlights the dearth of rigorous research on the effects of marijuana for the most common conditions for which it is currently recommended. It is paramount that well-designed RCTs with larger sample sizes be conducted to determine the actual medical benefits and adverse effects of marijuana for each of the above conditions. Indeed, recent reviews [4],[132] comprehensively discuss adverse events associated with marijuana use, and while it is beyond the scope of the current paper to review these effects in-depth, they are important to consider when evaluating whether or not to recommend marijuana for a medical or psychiatric disorder in place of other existing treatment options.

Given the extensive literature speaking to the harms associated with marijuana use, research on the comparative safety, tolerability, efficacy, and risk of marijuana compared to existing pharmacological agents is needed. The present literature also illuminates the need for research into the effects of isolated cannabinoids (e.g., THC, CBD) as well as species of smoked marijuana (e.g., indica and sativa), as the majority of medical marijuana users ingest marijuana by smoking the marijuana plant [133],[134], which contains a wide variety of phytocannabinoids at varying potencies [135],[136]. Furthermore, improved and objective measurement of clinical outcomes should be implemented in clinical trials to determine treatment efficacy. Finally, little research has considered the issues of dose, duration, and potency. If research identifies a therapeutic effect of marijuana for medical or psychiatric conditions, there will need to be revisions in marijuana policy to increase quality control so that dose and potency are valid and reliable. Additionally, risk of abuse and diversion can be decreased by developing prescribing practices with continued supervision of a medical professional, creating prescription monitoring programs to reduce the risk of “doctor shopping”, and identifying provisions for the safe disposal of unused cannabinoids. In sum, the current literature does not adequately support the widespread adoption and use of marijuana for medical and psychiatric conditions at this time.

Source: :http://www.ascpjournal.org/content/10/1/10 21^st April 2015

Abbreviations

THC: Δ⁹-tetrahydrocannabinol

HIV: Human immunodeficiency virus

AIDS: Acquired immunodeficiency syndrome

RCTs: Randomized controlled trials

IOP: Intraocular pressure

MS: Multiple sclerosis

CINV: Chemotherapy-induced nausea and vomiting

HCV: Hepatitis C virus

ALS: Amyotrophic lateral sclerosis

CD: Crohn’s disease

IBD: Inflammatory bowel disease

AD: Alzheimer’s disease

PTSD: Post-traumatic stress disorder

CB1: Cannabinoid type 1

CBD: Cannabidiol

Competing interests

Dr. Belendiuk holds stock in Shire Pharmaceuticals.

Authors’ contributions

Dr. KAB synthesized the literature and authored sections of the manuscript. Ms. LLB assisted with the literature search and synthesis. Dr. MOB-M conceived the review, assisted in the search and synthesis of existing literature, and authored sections of the manuscript. All authors read and approved the final manuscript.

Acknowledgements

Dr. Belendiuk’s salary was supported by National Institute of Mental Health R01 MH40564.

Dr. Bonn-Miller’s salary was supported by the VA Center of Excellence for Substance Abuse Treatment and Education.

Literature review and synthesis was supported by a grant from the VA Substance Use Disorder Quality Enhancement Research Initiative (SUDQ-LIP1410).

The above funding agencies played no role in the writing of the manuscript or decision to submit the manuscript for publication. The expressed views do not necessarily represent those of the Department of Veterans Affairs.

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“Even at normal doses, taking psychiatric drugs can produce suicidal thinking, violent behavior,  aggressiveness, extreme anger,  hostility, irritability, loss of ability to control impulses, rage reactions, hallucinations, mania, acute psychotic episodes, akathisia, and bizarre, grandiose, highly elaborated destructive plans, including mass murder.

“Withdrawal from psychiatric drugs can cause agitation, severe depression, hallucinations, aggressiveness, hypomania, akathisia, fear, terror, panic, fear of insanity, failing self-confidence, restlessness, irritability, aggression, an urge to destroy and, in the worst cases, an urge to kill.” -  From “Drug Studies Connecting Psychotropic Drugs with Acts of Violence” – unpublished.

My previous article on Global Research discussed the frustration of large numbers of aware observers around the world that were certain that Andreas Lubitz, the suicidal mass murderer of 149 passengers and crewmembers of the of the Lufthansa airliner crash, was under the intoxicating influence of brain-disabling, brain-altering, psychotropic medicines that had been prescribed for him by his German psychiatrists and/or neurologists who were known to have been prescribing for him.

These inquiring folks wanted and needed to know precisely what drugs he had been taking or withdrawing from so that the event could become a teachable moment that would help explain what had really happened and then possibly prevent other “irrational” acts from happening in the future. For the first week after the crash, the “authorities” were closed mouthed about the specifics, but most folks were willing to wait a bit to find out the truth.

However, another week has gone by, and there has still been no revelations from the “authorities” as to the exact medications, exact doses, exact combinations of drugs, who were the prescribing clinics and physicians and what was the rationale for the drugs having been  prescribed. Inquiring minds want to know and they deserve to be informed.

There are probably plenty of reasons why the information is not being revealed. There are big toes that could be stepped on, especially the giant pharmaceutical industries. There are medico-legal implications for the physicians and clinics that did the prescribing and there are serious implications for the airline corporations because their industry is at high risk of losing consumer confidence in their products if the truth isn’t adequately covered up. And the loss of consumer confidence is a great concern for both the pharmaceutical industry and its indoctrinated medical providers.

It looks like heavily drugged German society is dealing with the situation the same way the heavily drugged United States has dealt with psychiatric drug-induced suicidality and drug-induced mass murders (such as have been known to be in a cause and effect relationship in the American epidemic of school shootings – see www.ssristories.net).

The Traffickers of Illicit Drugs That Cause Dangerous and Irrational Behaviors Such as Murders and Suicides are Punished. Why not Legal Drug Traffickers as Well?

But there is a myth out there that illegal brain-altering drugs are dangerous but prescribed brain-altering drugs are safe. But anyone who knows the molecular structure and understands the molecular biology of these drugs and has seen the horrific adverse effects of usage or withdrawal of legal psychotropic drugs knows that the myth is false, and that there is a double standard being applied, thanks to the cunning advertising campaigns from Big Pharma.

But there is an epidemic of legal drug-related deaths in America, so I submit a few questions that people – as well as journalists and lawyers who are representing drug-injured plaintiffs – need to have answered, if only for educational and preventive practice purposes:

1) What cocktail of 9 different VA-prescribed psych drugs was “American Sniper” Chris Kyle’s Marine Corps killer taking after he was discharged from his psychiatric hospital the week before the infamous murder?

2) What were the psych drugs that Robin Williams got from Hazelden just before he hung himself?

3) What were the myriad of psych drugs, tranquilizers, opioids, etc that caused the overdose deaths of Philip Seymour Hoffman, Michael Jackson, Whitney Houston, Heath Ledger, Anna Nicole Smith, etc, etc, etc (not to mention Jimi Hendrix, Bruce Lee, Elvis Presley and Marilyn Monroe) – and who were the “pushers” of those drugs?

4) What was the cocktail of psychiatric and neurologic brain-altering drugs that Andreas Lubitz was taking before he intentionally crashed the passenger jet in the French Alps – and who were the prescribers?

5) What are the correctly prescribed drugs that annually kill over 100,000 hospitalized Americans per year and are estimated to kill twice that number of out-patients?

(See http://www.collective-evolution.com/2013/05/07/death-by-prescription-drugs-is-a-growing-problem/)

Because the giant pharmaceutical companies want these serious matters hushed up until the news cycle blows over (so that they can get on with business as usual), and because many prescribing physicians seem to be innocently unaware that any combination of two or more brain-altering psychiatric drugs have never been tested for safety (either short or long-term), even in the rat labs, future celebrities and millions of other patient-victims will continue dying – or just be sickened from a deadly but highly preventable reality.

But what about “patient confidentiality”, a common excuse for withholding specific information about patients (even if crimes such as mass murder are involved)? It turns out that what is actually being protected by that assertion are the drug providers and manufacturers. Common sense demands that such information should not be withheld in a criminal situation.

America’s corporate controlled media makes a lot of money from its relationships with its wealthy and influential corporate sponsors, contributors, advertisers, political action committees and politicians, but, tragically, the media has been clearly abandoning its historically-important investigative journalistic responsibilities (that are guaranteed and protected by the Constitution). It is obvious that the media has allied itself with the corporate “authorities” that withhold, any way they can, the important information that forensic psychiatrists (and everybody else) needs to know.

We should be calling out and condemning the authorities that are withholding the information about the reported “plethora of drugs” that is known to have been prescribed for Lubitz by his treating “neurologists and psychiatrists”, drugs that were found in his apartment on the day of the crash and identified by those same authorities who have not revealed the information to the people who need to know. Two weeks into the story and there still has been no further information given, or as far as I can ascertain, or asked for by journalists.

So, since the facts are being withheld by the authorities, I submit some useful lists of common adverse effects of commonly prescribed crazy-making psych drugs that Lubitz may have been taking. Also included are a number of withdrawal symptoms that are routinely  and conveniently mis-diagnosed as symptoms of a mental illness of unknown cause.

And at the end of the column are some excerpts from the FAA on psych drug use for American pilots. I do not know how different are the rules in Germany, but certainly both nations have to rely on voluntary information from the pilots.

1) Common Adverse Symptoms of Antidepressant Drug Use

Agitation, akathisia (severe restlessness, often resulting in suicidality), anxiety, bizarre dreams, confusion, delusions, emotional numbing, hallucinations, headache, heart attacks  hostility, hypomania (abnormal excitement), impotence, indifference (an “I don’t give a damn attitude”), insomnia, loss of appetite, mania, memory lapses, nausea, panic attacks, paranoia, psychotic episodes, restlessness, seizures, sexual dysfunction, suicidal thoughts or behaviors, violent behavior, weight loss, withdrawal symptoms (including deeper depression)

2) Common Adverse Psychological Symptoms of Antidepressant Drug Withdrawal

Depressed mood, low energy, crying uncontrollably, anxiety, insomnia, irritability, agitation, impulsivity, hallucinations or suicidal and violent urges. The physical symptoms of antidepressant withdrawal include disabling dizziness, imbalance, nausea, vomiting, flu-like aches and pains, sweating, headaches, tremors, burning sensations or electric shock-like zaps in the brain

3) Common Symptoms of Minor Tranquilizer Drug Withdrawal

Abdominal pains and cramps, agoraphobia , anxiety, blurred vision, changes in perception (faces distorting and inanimate objects moving), depression, dizziness, extreme lethargy, fears, feelings of unreality, heavy limbs, heart palpitations, hypersensitivity to light, insomnia, irritability, lack of concentration, lack of co-ordination, loss of balance, loss of memory, nightmares, panic attacks, rapid mood changes, restlessness, severe headaches, shaking, sweating, tightness in the chest, tight-headedness

4) Common (Usually Late Onset) Adverse Psychological Symptoms From Anti-Psychotic Drug Use

Blurred vision, breast enlargement/breast milk flow,  constipation, decreased sweating, dizziness, low blood pressure, imbalance and falls, drowsiness, dry mouth, headache, hyperprolactinemia (pituitary gland dysfunction), increased skin-sensitivity to sunlight, lightheadedness, menstrual irregularity (or absence of menstruation), sexual difficulty, (decline in libido, anorgasmia, genital pain).

The lethal adverse effects of antipsychotic drugs include Catatonic decline, Neuroleptic Malignant Syndrome (NMS, a condition marked by muscle stiffness or rigidity, dark urine, fast heartbeat or irregular pulse, increased sweating, high fever, and high or low blood pressure); Torsades de Pointes (a condition that affects the heart rhythm and can lead to sudden cardiac arrest”; Sudden death

5) Late and Persistent Adverse Effects of Antipsychotic Drug Use  (Some of these symptoms may even start when tapering down or discontinuing the drug!)

Aggression, akathisia (inner restlessness, often intolerable and leading to suicidality), brain atrophy (shrinkage), caffeine or other psychostimulant addiction, cataracts, creativity decline, depression, diabetes, difficulty urinating, difficulty talking, difficulty swallowing, fatigue and tiredness, hypercholesterolemia, hypothyroidism, intellectual decline (loss of IQ points), obesity, pituitary tumors, premature death, smoking – often heavy – (nicotine addiction), tardive dyskinesia (involuntary, disfiguring movement disorder), tongue edge “snaking” (early sign of movement disorder), jerky movements of head, face, mouth or neck, muscle spasms of face, neck or back, twisting the neck muscles, restlessness – physical and mental (resulting in sleep difficulty), restless legs syndrome, drooling, seizure threshold lowered, skin rashes (itching, discoloration), sore throat, staring, stiffness of arms or legs, swelling of feet, trembling of hands, uncontrollable chewing movements, uncontrollable lip movements, puckering of the mouth, uncontrollable movements of arms and legs, unusual twisting movements of body, weight gain, liver toxicity

6) Common Symptoms of Antipsychotic Drug Withdrawal

Nausea and vomiting, diarrhea, rhinorrhea (runny nose), heavy sweating, muscle pains, odd sensations such as burning, tingling, numbness,  anxiety, hypersexuality, agitation, mania, insomnia, tremor, voice-hearing

FAA Medical Certification Requirements for Psychotropic Medications

https://www.leftseat.com/psychotropic.htm

Pilots can only take one of four antidepressant drugs – Celexa (Citalopram), Lexapro (Escitalopram), Prozac (Fluoxetine) and Zoloft (Sertraline).

Most psychiatric drugs are not approved under any circumstances.

These include but are not limited to:

• Abilify (Aripiprazole)
• Effexor (Venlafaxine)
• Elavil (Amitriptyline)
• Luvox (Fluvoxamine Maleate)
• Monoamine Oxidase Inhibitors
• Paxil (Paroxetine)
• Remeron (Mirtazapine)
• Serzone (Nefazodone)
• Sinequan (Doxepin)
• Tofranil (Imipramine)
• Trazodone
• Tricyclic Antidepressants
• Wellbutrin (Bupropion)

To assure favorable FAA consideration, the treating physician should establish that you do not need psychotropic medication. The medication should be discontinued and the condition and circumstances should be evaluated after you have been off medication for at least 60 and in most cases 90 days.

Should your physician believe you are an ideal candidate, you may be considered by the FAA on a case by case basis only. Applicants may be considered after extensive testing and evidence of successful use for one year without adverse effects. Medications used for psychiatric conditions are rarely approved by the FAA. The FAA has approved less than fifty (50) airmen under the FAA’s SSRI protocol.

After discontinuing the medication, a detailed psychiatric evaluation should be obtained. Resolved issues and stability off the medication are usually the primary factors for approval.

Dr Kohls is a retired physician who practiced holistic mental health care for the last decade of his family practice career. He writes a weekly column on various topics for the Reader Weekly, an alternative newsweekly published in Duluth, Minnesota, USA. Many of Dr Kohls’ weekly columns are archived at http://duluthreader.com/articles/categories/200_Duty_to_Warn.

Source:  http://www.globalresearch.ca/the-connections-between-psychotropic-drugs-and-irrational-acts-of-violence/5441484  April 08, 2015