Medical cannabis

See ((marijuana)

Medical cannabis, or medical marijuana  are prescribed by physicians.

Evidence suggests that cannabis can reduce nausea and vomiting during chemotherapy, improve appetite in people with HIV/AIDS, reduces chronic pain and muscle spasms and treats severe forms of epilepsy.

Its short-term use increases the risk of minor and major adverse effects.


Its  ommon side effects include dizziness, feeling tired, vomiting, and hallucinations.

Long-term effects of cannabis have not been established.


Concerns include memory, cognition problems, risk of addiction, schizophrenia in young people, and the risk of children taking it by accident.

It can  be administered through  capsules, lozenges, tinctures, dermal patches, oral or dermal sprays, cannabis edibles, and vaporizing or smoking dried buds. 

Synthetic cannabinoids are available for prescription use, such as dronabinol and nabilone. 

In the United States, 33 states and the District of Columbia have legalized cannabis for medical purposes.

beginning with the passage of California’s Proposition 215 in 1996.[12]

A Cannabis plant includes more than 400 different chemicals, of which about 70 are cannabinoids.

The variations in ratio of CBD-to-THC in botanical and pharmaceutical preparations determines the therapeutic vs psychoactive effects.

CBD attenuates THC’s psychoactive effects of cannabis.

Is medical cannabis useful treatment for any condition: 

Evidence is moderate that it helps in chronic pain and muscle spasms.

Low quality evidence suggests its use for reducing chemotherapy- induced nausea, improving appetite in HIV/AIDS, improving sleep, and improving tics in Tourette syndrome.

Its use be stopped in pregnancy.

It is somewhat effective in chemotherapy-induced nausea and vomiting.

Long-term cannabis use may cause nausea and vomiting, the cannabinoid hyperemesis syndrome.

Cannabinoids use in treating chemotherapy-induced nausea in children, has a high side-effect profile of drowsiness, dizziness, altered moods, increased appetite, ocular problems, orthostatic hypotension, muscle twitching, pruritus, vagueness, hallucinations, lightheadedness and dry mouth.

Evidence is lacking for both efficacy and safety in treating patients with HIV/AIDS or for anorexia associated with AIDS. 

There is only limited evidence for the effectiveness of cannabis in relieving chronic pain.

A review found tentative evidence for use of cannabis in treating peripheral neuropathy, but little evidence of benefit for other types of long term pain.

When cannabis is inhaled to relieve pain, blood levels of cannabinoids rise faster than when oral products are used.

Inhaled cannabis peaks  within three minutes and attaining an analgesic effect in seven minutes.

There is limited and weak evidence that smoked cannabis is effective for chronic non-cancer pain.

There is limited evidence that medical cannabis is effective for neuropathic pain.

It considered to be generally safe, and it appears safer than opioids in palliative care.

Cannabis’ efficacy is not clear in treating neurological problems, including multiple sclerosis (MS) and movement problems.

The combination of Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) extracts give subjective relief of spasticity, though objective post-treatment assessments do not reveal significant changes.

Oral cannabis extract is effective for reducing patient-centered measures of spasticity.

Cannabidiol, has been approved for treating two severe forms of epilepsy, Lennox-Gastaut syndrome and Dravet syndrome.

There is no evidence that medical cannabis is effective for treating posttraumatic stress disorder.

Adverse effects of medical cannabis use are not serious.

Adverse effects include: tiredness, dizziness, increased appetite, and cardiovascular,psychoactive effects, short-term memory impairment, impaired motor coordination, altered judgment, and paranoia or psychosis at high doses.

These adverse effects resolve over a period of days or weeks, as tolerance increases.

Medicinal cannabis is not believed to cause any permanent cognitive impairment in adults.

Long-term effects  in adolescents is not known.

The ability to drive vehicles or to operate machinery may be impaired until a tolerance is developed.

Acute effects of medical cannabis may include anxiety and panic, impaired attention, and memory, an increased risk of psychotic symptoms, and possibly accidents.

Psychotic episodes typically resolve within minutes or hours.

There were 455,000 emergency room visits associated with cannabis use in 2011. 

Chronic use side effects include: 

bronchitis, a cannabis dependence syndrome, and subtle impairments of attention and memory. 

Compared to non-smokers, people who smoked cannabis regularly in adolescence exhibit reduced connectivity in specific brain regions associated with memory, learning, alertness, and executive function.

A study suggested that sustained heavy, daily, adolescent onset marijuana  use over decades is associated with a decline in IQ by age 38.

No effects found in those who initiated cannabis use later in life, or who 

ceased use earlier in adulthood.

Some suggest that the  IQ deficit may be a precursor, rather than result, of cannabis use.

Chronic heavy marijuana smoking is associated with coughing, production of sputum, wheezing, coughing, and other symptoms of chronic bronchitis.

Regular cannabis use has not been shown to cause significant abnormalities in lung function.

Its smoke contains thousands of organic and inorganic chemical compounds. 

Cannabis’s tar is chemically similar to that found in tobacco smoke, and  contains over fifty known carcinogens.

Carcinogens identified in cannabis smoke, include nitrosamines, reactive aldehydes, and polycyclic hydrocarbons, including benzapyrene.

Light and moderate use of cannabis is not associated with a increase risk of lung or upper airway cancer. 

Combustion products are not present when consuming THC in pill form, or consuming cannabis edibles.

Cannabis rarely can aggravate  arteritis.

Other serious cardiovascular events including myocardial infarction, stroke, sudden cardiac death, and cardiomyopathy have been reported to be associated with cannabis use. 

Its usually causes no tolerance or withdrawal symptoms except in heavy users. 

In heavy users 42% experience withdrawal symptoms when they tried to quit marijuana: craving, irritability, boredom, anxiety and sleep disturbances.

About 9% of those who experiment with marijuana eventually become dependent. 

The dependence rate increases to one in six among those who begin use as adolescents, and one-quarter to one-half of those who use it daily.

The highest risk of cannabis dependence is found in those with: a poor academic achievement, deviant behavior in childhood and adolescence, rebelliousness, poor parental relationships, or a parental history of drug and alcohol problems.

Exposure to marijuana has biologically-based physical, mental, behavioral and social health consequences.

Exposure to marijuana is associated with diseases of the liver, particularly hepatitis C, lungs, heart, and vasculature.

THC intoxication impairs cognitive functioning on an acute basis, including the ability to plan, organize, solve problems, make decisions, and control impulses, especially in new users.

Patients habituated to high-level ingestion may have reduced cognition during withdrawal. 

Long-term effect studies on cognition have conflicting results, with some studies finding no difference between long-term abstainers and never-users and others finding long-term deficits. 

A systematic review focused on neuroimaging studies found little evidence supporting an effect of cannabis use on brain structure and function.

A  meta-analysis concluded that any long-term cognitive effects were relatively modest in magnitude and limited to certain aspects of learning and memory.

THC can cause acute transient psychotic symptoms in healthy individuals and people with schizophrenia.

A  meta analysis concluded that cannabis use reduced the average age of onset of psychosis by 2.7 years relative to non-cannabis use.

A  meta analysis concluded that adolescent use of cannabis increases the risk of psychosis, and that the risk is dose-related.

Studies find elevated levels of apolipoprotein C-III (apoC-III) in chronic smokers: An increase in apoC-III levels induces the development of hypertriglyceridemia.

Cannabis contains more than 460 compounds; at least 80 of these are cannabinoids.

The most psychoactive cannabinoid found in the cannabis plant is tetrahydrocannabinol (or delta-9-tetrahydrocannabinol, commonly known as THC).

Other cannabinoids include delta-8-tetrahydrocannabinol, cannabidiol (CBD), cannabinol (CBN), cannabicyclol (CBL), cannabichromene (CBC) and cannabigerol (CBG).

These other cannabinoids 

 have less psychotropic effects than THC, but may play a role in the overall effect of cannabis.

The  most studied cannabinoids are THC, CBD and CBN.

CB1 and CB2 are the primary cannabinoid receptors.

CB1 and CB2 receptors are 

responsible for several of the effects of cannabinoids.

Both CB1 and CB2 belong  to a group of receptors called G protein-coupled receptors (GPCRs). 

G-Protein-coupled receptors CB1 are found in very high levels in the brain.

CB1 receptors are thought to be responsible for psychoactive effects.

CB2 receptors are found peripherally throughout the body and are thought to modulate pain and inflammation.

Inhaled and vaporized THC have a bioavailability ranging from 10-35%,  similar to absorption profiles of smoked THC.

Oral administration has the lowest bioavailability of approximately 6%.

Oral administration variable absorption has the longest time to peak plasma levels of 2-6 hours compared to smoked or vaporized THC.

CBD also has poor oral bioavailability, of approximately 6%. 

The low bioavailability of oral cannabis is attributed to significant first-pass metabolism in the liver and erratic absorption from the gastrointestinal tract. 

Oral  administration of CBD has a faster time to peak concentrations (2 hours) than THC.

Cannabinoid distribution is dependent on route of administration. 

Smoking and inhalation of cannabis have better absorption than do other routes of administration, and therefore also have more predictable distribution.

THC is highly protein bound upon absorbtion.

Only 3% of THC is found unbound in the plasma. 

THC is distributed  rapidly to highly vascularized organs such as the heart, lungs, liver, spleen, and kidneys, and to various glands. 

Low levels can be detected in the brain, testes, and unborn fetuses.

THC further distributes into fatty tissues a few days after administration due to its high lipophilicity.

Delta-9-THC is the primary molecule responsible for the effects of cannabis. 

Delta-9-THC is metabolized in the liver and turns into 11-OH-THC.

Both Delta-9-THC and 11-OH-THC are psychoactive. 

11-OH-THC is metabolized in the liver into 11-COOH-THC, which is the second metabolic product of THC.

Ingestion of cannabis products lead to a slower onset of effect than the inhalation : THC travels to the liver first through the blood before it travels to the rest of the body. 

Inhaled cannabis can result in THC going directly to the brain, where it then travels from the brain back to the liver in recirculation for metabolism.

Both routes of metabolism result in the metabolism of psychoactive THC to inactive 11-COOH-THC.

THC and CBD, their metabolites are excreted mostly via feces, rather than by urine.

After delta-9-THC is hydroxylated into 11-OH-THC via CYP2C9, CYP2C19, and CYP3A4, it undergoes metabolism into more than 30 metabolites, a majority of which are products of glucuronidation. 

Approximately 65% of THC is excreted in feces and 25% in the urine, while the remaining 10% is excreted by other means.

The terminal half-life of THC is 25 to 36 hours, and for CBD it is 18 to 32 hours.

CBD is hydroxylated by P450 liver enzymes into 7-OH-CBD. 

Its metabolites are products of primarily CYP2C19 and CYP3A4 activity.

The majority of CBD is excreted in feces and some in the urine.

Smoking has been the means of administration of cannabis for many users, but it is not suitable as a medicine.

Smoking is the most common method of medical cannabis consumption in the US.

The potential for adverse effects from smoke inhalation makes smoking a less viable option than oral preparations.

Cannabinoid medicines are available in pill form: dronabinol and nabilone and liquid extracts formulated into an oromucosal spray as nabiximols.

Oral preparations of cannabinoids are  taken into  fatty tissue, from which they are released slowly, and the significant first-pass liver metabolism, which breaks down Δ9THC and contributes further to the variability of plasma concentrations.

The US Food and Drug Administration has not approved smoked cannabis for any condition or disease:  evidence is lacking concerning safety and efficacy.

Marijuana has a high potential for abuse, has no currently accepted medical use in treatment in the United States, and has a lack of accepted safety for use under medical supervision.


The legalization of medical marijuana is associated with a lower rate of opioid dispensing and pain related hospital events.

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