Cannabis and Sleep
Many people are using cannabis as a sleeping medication but does it really work?
Posted Nov 06, 2012
Mental health clinicians are aware that many psychiatric patients use cannabis. It also appears that many patients suffering with insomnia also use it. Although it remains illegal and many people are arrested for possession annually, it does not seem that anyone wanting to use it has difficulty obtaining it and more states are providing for medicinal use of it. Connecticut is the most recent state to decriminalize possession of small amounts of cannabis and to provide for medical marijuana.
This is a timely issue as there are two states that have ballot initiatives for today that could result in legalization of medical marijuana (Massachusetts and Arkansas) and two others (Washington and Colorado) will be considering essentially legalizing adult possession with regulation and taxation similar to that used with alcohol. This could lead to further conflict between state and federal law enforcement.
Cannabis has been used for thousands of years for its psychoactive and purported medicinal qualities. Cannabis has often been classified as a hallucinogen and regarded as a minor psychedelic although more recently it is being seen as a unique and complex drug with many different effects, some of which may be of medical value. It can be classified in a number of ways such as a hallucinogen, a psychedelic, or as a drug that causes an altered state of consciousness with mild euphoria, relaxation, perceptual alterations and enhanced sensory experiences (see references below). It can also cause distressing and unpleasant effects as well, such as intense anxiety that is often described as “paranoia”.
Culturally, cannabis has had a somewhat different role in society than other drugs that may be abused, often being associated with the counterculture or the subculture represented in movies such as “Up in Smoke”, “The Pineapple Express” or any of the Harold and Kumar movies. In recent years research has been increasing with regard to psychedelics and related drugs such as ketamine for the first time since the early 1970s. Research regarding psychedelics and marijuana is being spearheaded by organizations such as MAPS (Multidisciplinary Association for Psychedelic Studies), and new knowledge about the potential therapeutic uses of these agents is increasing.
But what evidence do we have regarding cannabis and its effects on sleep? Not much. Most of the research on cannabis and sleep was conducted in the 1970s and is discussed below. Currently research on the medicinal use of cannabis is restricted due to the legal status of marijuana.
As it turns out cannabis is an exceedingly complex drug preparation and its effects depend on the variety of the plant, the composition of the chemicals in any given sample, the route of administration, the setting in which it is used and the psychological set of the user.
Cannabis is a plant with three different strains that reportedly have different psychoactive characteristics depending on the specific chemical make up of the plants. Cannabis sativa is generally the most commonly used strain and is considered the most psychoactive. In recent years selective breeding in both the underground production system and by those working in the medical marijuana field has modified it to increase its psychoactivity or enhance various putative medicinal effects. For example, some samples may be extremely psychedelic while are others are more sedating.
These drug effects are caused by the action of chemicals known as cannabinoids that activate cannabinoid receptors in the central nervous system. The primary cannabinoids responsible for the characteristic psychological effects of marijuana are THC (tetrahydocannabinol) and CBD (cannabidiol). THC is the only cannabinoid found in marijuana that has direct psychological effects but its effects may be modified by the action of cannabidiol and perhaps other cannabinoids as well. In small doses THC tends to be a sedative, in moderate doses to be a stimulant, in large doses it is psychedelic, and in very large doses may cause psychotic-like symptoms.
While cannabis is sometimes eaten in foods such as brownies, it is most often smoked. This allows users to more carefully titrate the dose by checking the subjective effects before taking another puff. Medical marijuana patients are now using vaporizers to absorb THC while avoiding the inhalation of smoke. Eating marijuana may result in extremely powerful effects that become apparent only some time after consumption with no way of reducing the dose. The setting in which it is used will also affect the user’s experience. A quiet and supportive environment is less likely to result in anxiety. It should also be noted that some people are much more sensitive to the effects of cannabis and may have strong reactions to even fairly small doses.
As noted above, although the psychoactive effects of cannabis are primarily due to THC, the effects of using complex plant material is not the same as if pure THC were to be used alone. THC can cause anxiety reactions but higher concentrations of cannabidiol may be effective in decreasing this effect by increasing relaxation. To date two receptors for cannabinoids have been found. CB1receptors are primarily located in the central nervous system and CB2 receptors are primarily found in the periphery of the body, especially in the immune system. CB1 receptors are located in diverse areas of the brain and are activated by endocannabinoids that are produced naturally in the nervous system and function to regulate various nervous system processes.
Interestingly, CB receptors do not function in the standard way that we were taught neurons work in our high school and college biology classes. In the standard model, a pre-synaptic cell releases a chemical called a neurotransmitter that crosses the gap (synapse) between the cells and affects the downstream (postsynaptic) cell by changing the probability that the downstream cell will fire (depolarize). Some neurotransmitters such as dopamine and serotonin have modulating effects on downstream neurons. Other neurotransmitters are either excitatory and increase the probability that downstream cells will fire or inhibitory and decrease the probability of firing. The primary inhibitory neurotransmitter in the central nervous system is GABA and a primary excitatory neurotransmitter is glutamate. Cells affected by GABA are targeted by the major prescription sleeping medications and this is how they work to produce drowsiness.
Endocannabinoids, however, act on CB1 receptors through a process known as retrograde signaling. In other words, it is the postsynaptic cell that releases the cannabinoid that travels against the usual flow of neurotransmitters and affects the pre-synaptic cell. This allows postsynaptic cells to control incoming activity. If pre-synaptic cells are releasing GABA, endocannabinoids will decrease their output thus increasing the excitability of the postsynaptic cell. If the pre-synaptic cells are releasing gultamate the effect will be to decrease excitability of the postsynaptic cell.
THC is an exogenous plant derived cannabinoid that affects the functioning of the CB1 and CB2 receptors. THC’s psychoactive effects are produced by its interaction with the CB1 receptors. The complex possibilities presented by the way in which it can increase or decrease excitation gives some indication of how complex its effects can be, especially given that CB1 receptors are widespread throughout the central nervous system. THC is a unique, naturally occurring drug that causes its psychoactive effects in a much different fashion than the classical psychedelics such as LSD and DMT that are 5HT 2A (serotonin subtype) receptor agonists.
Many sleeping medications, such as the benzodiazepines, convert deep sleep into lighter sleep, so that while the total amount of sleep may be modestly increased, it may not be of optimal quality. Certainly anyone who has used alcohol to help sleep knows that in the long run, it really doesn’t. In fact, while alcohol initially can make you drowsy and even increases deep sleep, it later causes sleep to be light and fragmented. People who have had the misfortune of over-indulging in alcoholic beverages and have awakened with a terrible hangover know this all too well. However sleepy the hung over person feels, it is impossible to get comfortable and fall back asleep. This is why, for purposes of good sleep hygiene, we recommend limiting daily intake of alcohol to no more than 1 or 2 standard doses (4 – 6 oz of wine, 12 oz of beer or 1.5 oz of liquor) and not drinking after dinner so that the alcohol has time to get out of your system before trying to sleep.
The studies on cannabis and sleep that were conducted in the 1970’s (see Roehrs and Roth, 2011), give some information about the possible affects of cannabis on sleep. Low doses of THC (4 to 20 mg) mildly decreased REM sleep in both regular users and nonusers. Interestingly, deep sleep was increased when cannabis was initially used but this effect disappeared after repeated use. With high doses of THC (50 to 210 mg) REM sleep was decreased in both regular users and nonusers. Total sleep time was not affected but deep sleep was decreased. When THC was stopped some rebound in REM sleep was found with reduced sleep time and increased time to fall asleep.
Some people do have withdrawal symptoms when stopping prolonged and heavy use of cannabis and this can adversely affect sleep.
Clearly, many people are using cannabis as a sleeping agent and further research is needed, if a way can be found to do this despite the current legal difficulties to conducting marijuana research. Whether or not cannabis use helps or hurts sleep is not clear from the limited evidence reviewed above. Some advocates believe that it can be very beneficial but at this point, I think the best advice is that natural sleep remains the most optimal. It’s best to use any sleeping medication, whether prescribed, OTC, or obtained from joints, brownies, or bongs, as little as possible.
Glennon, R. A. (2008). Neurobiology of hallucinogens in Galanter, M. & Kleber, H. D. (Eds) Textbook of Substance Abuse Treatment 4rd Edition. Washington, D.C.: American Psychiatric Publishing.
Martin, B. R. (2000). Neurobiology of marijuana in Galanter, M. & Kleber, H. D. (Eds) Textbook of Substance Abuse Treatment 3rd Edition. Washington, D.C.: American Psychiatric Publishing.
Roehrs, T. & Roth, T. (2011). Medication and Substance Abuse in Kryger, M. H., Roth, T. & Dement, W. C. Principles and Practice of Sleep Medicine 5th Edition. St. Louis, Missouri: Elsevier Saunders.
Weaver, M. F. & Schnoll, S. H. (2008). Hallucinogens and Club Drugs in Galanter, M. & Kleber, H. D. (Eds) Textbook of Substance Abuse Treatment 4rd Edition. Washington, D.C.: American Psychiatric Publishing.