chlorpromazine and Weed
chlorpromazine and Weed
Most people who consume marijuana do so for its mood-altering and relaxing abilities. Weed gives people a high and allows them to relax. However, heavy consumption of weed can cause unwanted results. It can increase the anxiety and depression a person experiences, and it can interact with certain other drugs including chlorpromazine. It is important to remember that interactions do occur with all types of drugs, to a great or lesser extent and this article details the interactions of mixing chlorpromazine and Weed.
Mixing chlorpromazine and Weed
Chlorpromazine (CPZ), marketed under the brand names Thorazine and Largactil among others, is an antipsychotic medication. It is primarily used to treat psychotic disorders such as schizophrenia. Other uses include the treatment of bipolar disorder, severe behavioral problems in children including those with attention deficit hyperactivity disorder, nausea and vomiting, anxiety before surgery, and hiccups that do not improve following other measures. It can be given orally (by mouth), by intramuscular injection (injection into a muscle), or intravenously (injection into a vein).
Chlorpromazine is in the typical antipsychotic class, and, chemically, is one of the phenothiazines. Its mechanism of action is not entirely clear but believed to be related to its ability as a dopamine antagonist. It also has anti-serotonergic and antihistaminergic properties.
Common side effects include movement problems, sleepiness, dry mouth, low blood pressure upon standing, and increased weight. Serious side effects may include the potentially permanent movement disorder tardive dyskinesia, neuroleptic malignant syndrome, severe lowering of the seizure threshold, and low white blood cell levels. In older people with psychosis as a result of dementia it may increase the risk of death. It is unclear if it is safe for use in pregnancy.
Chlorpromazine was developed in 1950 and was the first antipsychotic on the market. It is on the World Health Organization’s List of Essential Medicines. Its introduction has been labeled as one of the great advances in the history of psychiatry. It is available as a generic medication.
Chlorpromazine is used in the treatment of both acute and chronic psychoses, including schizophrenia and the manic phase of bipolar disorder, as well as amphetamine-induced psychosis.
In a 2013 comparison of fifteen antipsychotics in schizophrenia, chlorpromazine demonstrated mild-standard effectiveness. It was 13% more effective than lurasidone and iloperidone, approximately as effective as ziprasidone and asenapine, and 12–16% less effective than haloperidol, quetiapine, and aripiprazole.
A 2014 systematic review carried out by Cochrane included 55 trials that compared the effectiveness of chlorpromazine versus placebo for the treatment of schizophrenia. Compared to the placebo group, patients under chlorpromazine experienced less relapse during 6 months to 2 years follow-up. No difference was found between the two groups beyond two years of follow-up. Patients under chlorpromazine showed a global improvement in symptoms and functioning. The systematic review also highlighted the fact that the side effects of the drug were ‘severe and debilitating’, including sedation, considerable weight gain, a lowering of blood pressure, and an increased risk of acute movement disorders. They also noted that the quality of evidence of the 55 included trials was very low and that 315 trials could not be included in the systematic review due to their poor quality. They called for further research on the subject, as chlorpromazine is a cheap benchmark drug and one of the most used treatments for schizophrenia worldwide.
Chlorpromazine has also been used in porphyria and as part of tetanus treatment. It still is recommended for short-term management of severe anxiety and psychotic aggression. Resistant and severe hiccups, severe nausea/emesis, and preanesthetic conditioning are other uses. Symptoms of delirium in hospitalized AIDS patients have been effectively treated with low doses of chlorpromazine.
Chlorpromazine is occasionally used off-label for treatment of severe migraine. It is often, particularly as palliation, used in small doses to reduce nausea by opioid-treated cancer patients and to intensify and prolong the analgesia of the opioids as well. Efficacy has been shown in treatment of symptomatic hypertensive emergency.
In Germany, chlorpromazine still carries label indications for insomnia, severe pruritus, and preanesthesia.
Chlorpromazine and other phenothiazines have been demonstrated to possess antimicrobial properties, but are not currently used for this purpose except for a very small number of cases. For example, Miki et al. 1992 trialed daily doses of chlorpromazine, reversing chloroquine resistance in Plasmodium chabaudi isolates in mice. Weeks et al., 2018 find that it also possesses a wide spectrum anthelmintic effect.
Chlorpromazine is an antagonist of several insect monoamine receptors. It is the most active antagonist known of silk moth (Bombyx mori) octopamine receptor α, intermediate for Bm tyramine receptors 1 & 2, weak for Drosophila octopamine receptor β, high for Drosophila tyramine receptor 1, intermediate for migratory locust (Locusta migratoria) tyramine receptor 1, and high for American cockroach (Periplaneta americana) octopamine receptor α and tyramine receptor 1.
There appears to be a dose-dependent risk for seizures with chlorpromazine treatment. Tardive dyskinesia (involuntary, repetitive body movements) and akathisia (a feeling of inner restlessness and inability to stay still) are less commonly seen with chlorpromazine than they are with high potency typical antipsychotics such as haloperidol or trifluoperazine, and some evidence suggests that, with conservative dosing, the incidence of such effects for chlorpromazine may be comparable to that of newer agents such as risperidone or olanzapine.
Chlorpromazine may deposit in ocular tissues when taken in high dosages for long periods of time.
Absolute contraindications include:
Relative contraindications include:
Very rarely, elongation of the QT interval may occur, increasing the risk of potentially fatal arrhythmias.
Consuming food prior to taking chlorpromazine orally limits its absorption; likewise, cotreatment with benztropine can also reduce chlorpromazine absorption. Alcohol can also reduce chlorpromazine absorption. Antacids slow chlorpromazine absorption. Lithium and chronic treatment with barbiturates can increase chlorpromazine clearance significantly. Tricyclic antidepressants (TCAs) can decrease chlorpromazine clearance and hence increase chlorpromazine exposure. Cotreatment with CYP1A2 inhibitors like ciprofloxacin, fluvoxamine or vemurafenib can reduce chlorpromazine clearance and hence increase exposure and potentially also adverse effects. Chlorpromazine can also potentiate the CNS depressant effects of drugs like barbiturates, benzodiazepines, opioids, lithium and anesthetics and hence increase the potential for adverse effects such as respiratory depression and sedation.
Chlorprozamine is also a moderate inhibitor of CYP2D6 and a substrate for CYP2D6, and hence can inhibit its own metabolism. It can also inhibit the clearance of CYP2D6 substrates such as dextromethorphan, potentiating their effects. Other drugs like codeine and tamoxifen, which require CYP2D6-mediated activation into their respective active metabolites, may have their therapeutic effects attenuated. Likewise, CYP2D6 inhibitors such as paroxetine or fluoxetine can reduce chlorpromazine clearance, increasing serum levels of chlorpromazine and potentially its adverse effects. Chlorpromazine also reduces phenytoin levels and increases valproic acid levels. It also reduces propranolol clearance and antagonizes the therapeutic effects of antidiabetic agents, levodopa (a Parkinson’s medication. This is likely due to the fact that chlorpromazine antagonizes the D2 receptor which is one of the receptors dopamine, a levodopa metabolite, activates), amphetamines and anticoagulants. It may also interact with anticholinergic drugs such as orphenadrine to produce hypoglycaemia (low blood sugar).
Chlorpromazine may also interact with epinephrine (adrenaline) to produce a paradoxical fall in blood pressure. Monoamine oxidase inhibitors (MAOIs) and thiazide diuretics may also accentuate the orthostatic hypotension experienced by those receiving chlorpromazine treatment. Quinidine may interact with chlorpromazine to increase myocardial depression. Likewise, it may also antagonize the effects of clonidine and guanethidine. It also may reduce the seizure threshold and hence a corresponding titration of anticonvulsant treatments should be considered. Prochlorperazine and desferrioxamine may also interact with chlorpromazine to produce transient metabolic encephalopathy.
Other drugs that prolong the QT interval, such as quinidine, verapamil, amiodarone, sotalol and methadone, may also interact with chlorpromazine to produce additive QT interval prolongation.
The British National Formulary recommends a gradual withdrawal when discontinuing antipsychotics to avoid acute withdrawal syndrome or rapid relapse. Symptoms of withdrawal commonly include nausea, vomiting, and loss of appetite. Other symptoms may include restlessness, increased sweating, and trouble sleeping. Less commonly, there may be a feeling of the world spinning, numbness, or muscle pains. Symptoms generally resolve after a short period of time.
There is tentative evidence that discontinuation of antipsychotics can result in psychosis. It may also result in reoccurrence of the condition that is being treated. Rarely, tardive dyskinesia can occur when the medication is stopped.
Chlorpromazine is classified as a low-potency typical antipsychotic. Low-potency antipsychotics have more anticholinergic side effects, such as dry mouth, sedation, and constipation, and lower rates of extrapyramidal side effects, while high-potency antipsychotics (such as haloperidol) have the reverse profile.
Chlorpromazine is a very effective antagonist of D2 dopamine receptors and similar receptors, such as D3 and D5. Unlike most other drugs of this genre, it also has a high affinity for D1 receptors. Blocking these receptors causes diminished neurotransmitter binding in the forebrain, resulting in many different effects. Dopamine, unable to bind with a receptor, causes a feedback loop that causes dopaminergic neurons to release more dopamine. Therefore, upon first taking the drug, patients will experience an increase in dopaminergic neural activity. Eventually, dopamine production of the neurons will drop substantially and dopamine will be removed from the synaptic cleft. At this point, neural activity decreases greatly; the continual blockade of receptors only compounds this effect.
Chlorpromazine acts as an antagonist (blocking agent) on different postsynaptic and presynaptic receptors:
The presumed effectiveness of the antipsychotic drugs relied on their ability to block dopamine receptors. This assumption arose from the dopamine hypothesis that maintains that both schizophrenia and bipolar disorder are a result of excessive dopamine activity. Furthermore, psychomotor stimulants like cocaine that increase dopamine levels can cause psychotic symptoms if taken in excess.
Chlorpromazine and other typical antipsychotics are primarily blockers of D2 receptors. In fact an almost perfect correlation exists between the therapeutic dose of a typical antipsychotic and the drug’s affinity for the D2 receptor. Therefore, a larger dose is required if the drug’s affinity for the D2 receptor is relatively weak. A correlation exists between average clinical potency and affinity of the antipsychotics for dopamine receptors.
Chlorpromazine tends to have greater effect at serotonin receptors than at D2 receptors, which is notably the opposite effect of the other typical antipsychotics. Therefore, chlorpromazine with respect to its effects on dopamine and serotonin receptors is more similar to the atypical antipsychotics than to the typical antipsychotics.
Chlorpromazine and other antipsychotics with sedative properties such as promazine and thioridazine are among the most potent agents at α-adrenergic receptors. Furthermore, they are also among the most potent antipsychotics at histamine H1 receptors. This finding is in agreement with the pharmaceutical development of chlorpromazine and other antipsychotics as anti-histamine agents. Furthermore, the brain has a higher density of histamine H1 receptors than any body organ examined which may account for why chlorpromazine and other phenothiazine antipsychotics are as potent at these sites as the most potent classical antihistamines.
In addition to influencing the neurotransmitters dopamine, serotonin, epinephrine, norepinephrine, and acetylcholine it has been reported that antipsychotic drugs could achieve glutamatergic effects. This mechanism involves direct effects on antipsychotic drugs on glutamate receptors. By using the technique of functional neurochemical assay chlorpromazine and phenothiazine derivatives have been shown to have inhibitory effects on NMDA receptors that appeared to be mediated by action at the Zn site. It was found that there is an increase of NMDA activity at low concentrations and suppression at high concentrations of the drug. No significant difference in glutamate and glycine activity from the effects of chlorpromazine were reported. Further work will be necessary to determine if the influence in NMDA receptors by antipsychotic drugs contributes to their effectiveness.
Chlorpromazine does also act as a FIASMA (functional inhibitor of acid sphingomyelinase).
Chlorpromazine is an antagonist to H1 receptors (provoking antiallergic effects), H2 receptors (reduction of forming of gastric juice), M1 and M2 receptors (dry mouth, reduction in forming of gastric juice) and some 5-HT receptors (different anti-allergic/gastrointestinal actions).
Because it acts on so many receptors, chlorpromazine is often referred to as a “dirty drug”.
In 1933, the French pharmaceutical company Laboratoires Rhône-Poulenc began to search for new anti-histamines. In 1947, it synthesized promethazine, a phenothiazine derivative, which was found to have more pronounced sedative and antihistaminic effects than earlier drugs.: 77 A year later, the French surgeon Pierre Huguenard used promethazine together with pethidine as part of a cocktail to induce relaxation and indifference in surgical patients. Another surgeon, Henri Laborit, believed the compound stabilized the central nervous system by causing “artificial hibernation”, and described this state as “sedation without narcosis”. He suggested to Rhône-Poulenc that they develop a compound with better stabilizing properties. In December 1950, the chemist Paul Charpentier produced a series of compounds that included RP4560 or chlorpromazine.
Chlorpromazine was distributed for testing to physicians between April and August 1951. Laborit trialled the medicine on at the Val-de-Grâce military hospital in Paris, using it as an anaesthetic booster in intravenous doses of 50 to 100 mg on surgery patients and confirming it as the best drug to date in calming and reducing shock, with patients reporting improved well being afterwards. He also noted its hypothermic effect and suggested it may induce artificial hibernation. Laborit thought this would allow the body to better tolerate major surgery by reducing shock, a novel idea at the time. Known colloquially as “Laborit’s drug”, chlorpromazine was released onto the market in 1953 by Rhône-Poulenc and given the trade name Largactil, derived from large “broad” and acti* “activity”.
Following on, Laborit considered whether chlorpromazine may have a role in managing patients with severe burns, Raynaud’s phenomenon, or psychiatric disorders. At the Villejuif Mental Hospital in November 1951, he and Montassut administered an intravenous dose to psychiatrist Cornelia Quarti who was acting as a volunteer. Quarti noted the indifference, but fainted upon getting up to go to the toilet, and so further testing was discontinued (orthostatic hypotension is a known side effect of chlorpromazine). Despite this, Laborit continued to push for testing in psychiatric patients during early 1952. Psychiatrists were reluctant initially, but on 19 January 1952, it was administered (alongside pethidine, pentothal and ECT) to Jacques Lh. a 24-year-old manic patient, who responded dramatically, and was discharged after three weeks having received 855 mg of the drug in total.
Pierre Deniker had heard about Laborit’s work from his brother-in-law, who was a surgeon, and ordered chlorpromazine for a clinical trial at the Sainte-Anne Hospital Center in Paris where he was Men’s Service Chief. Together with the Director of the hospital, Jean Delay, they published their first clinical trial in 1952, in which they treated 38 psychotic patients with daily injections of chlorpromazine without the use of other sedating agents. The response was dramatic; treatment with chlorpromazine went beyond simple sedation with patients showing improvements in thinking and emotional behaviour. They also found that doses higher than those used by Laborit were required, giving patients 75–100 mg daily.
Deniker then visited America, where the publication of their work alerted the American psychiatric community that the new treatment might represent a real breakthrough. Heinz Lehmann of the Verdun Protestant Hospital in Montreal trialled it in 70 patients and also noted its striking effects, with patients’ symptoms resolving after many years of unrelenting psychosis. By 1954, chlorpromazine was being used in the United States to treat schizophrenia, mania, psychomotor excitement, and other psychotic disorders.
Rhône-Poulenc licensed chlorpromazine to Smith Kline & French (today’s GlaxoSmithKline) in 1953. In 1955 it was approved in the United States for the treatment of emesis (vomiting). The effect of this drug in emptying psychiatric hospitals has been compared to that of penicillin and infectious diseases. But the popularity of the drug fell from the late 1960s as newer drugs came on the scene. From chlorpromazine a number of other similar antipsychotics were developed. It also led to the discovery of antidepressants.
Chlorpromazine largely replaced electroconvulsive therapy, hydrotherapy, psychosurgery, and insulin shock therapy. By 1964, about 50 million people worldwide had taken it. Chlorpromazine, in widespread use for 50 years, remains a “benchmark” drug in the treatment of schizophrenia, an effective drug although not a perfect one.
Brand names include Thorazine, Largactil, Hibernal, and Megaphen (sold by Bayer in West-Germany since July 1953).)
Chlorpromazine has tentative benefit in animals infected with Naegleria fowleri, and shows antifungal and antibacterial activity in vitro.
The veterinary use of chlorpromazine has generally been superseded by use of acepromazine.
Chlorpromazine may be used as an antiemetic in dogs and cats, or, less often, as sedative before anesthesia. In horses, it often causes ataxia and lethargy, and is therefore seldom used.
It is commonly used to decrease nausea in animals that are too young for other common anti-emetics. It is also sometimes used as a preanesthetic and muscle relaxant in cattle, swine, sheep, and goats.
The use of chlorpromazine in food-producing animals is not permitted in the EU, as a maximum residue limit could not be determined following assessment by the European Medicines Agency.
Research has found that anxiety is one of the leading symptoms created by marijuana in users, and that there is a correlation between chlorpromazine and Weed and an increase in anxiety.
Anyone mixing chlorpromazine and weed is likely to experience side effects. This happens with all medications whether weed or chlorpromazine is mixed with them. Side effects can be harmful when mixing chlorpromazine and weed. Doctors are likely to refuse a patient a chlorpromazine prescription if the individual is a weed smoker or user. Of course, this could be due to the lack of studies and research completed on the mixing of chlorpromazine and Weed.
Heavy, long-term weed use is harmful for people. It alters the brain’s functions and structure, and all pharmaceuticals and drugs including chlorpromazine are designed to have an impact on the brain. There is a misplaced belief that pharmaceuticals and medication work by treating only the parts of the body affected yet this is obviously not the case in terms of chlorpromazine. For example, simple painkiller medication does not heal the injury, it simply interrupts the brains functions to receive the pain cause by the injury. To say then that two drugs, chlorpromazine and Weed, dol not interact is wrong. There will always be an interaction between chlorpromazine and Weed in the brain11.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678684/.
One of the milder side effects of mixing chlorpromazine and Weed is Scromiting. This condition, reportedly caused by mixing chlorpromazine and Weed, describes a marijuana-induced condition where the user experiences episodes of violent vomiting, which are often so severe and painful that they cause the person to scream. The medical term for Scromiting by mixing chlorpromazine and Weed is cannabinoid hyperemesis syndrome, or CHS. For these reasons, some people choose to quit smoking weed.
It was first included in scientific reports in 2004. Since then, researchers have determined that Scromiting is the result of ongoing, long-term use of marijuana—particularly when the drug contains high levels of THC, marijuana’s main psychoactive ingredient. Some experts believe that the receptors in the gut become overstimulated by THC, thus causing the repeated cycles of vomiting.
In the long run, a person can become even more depressed. There is a belief that marijuana is all-natural and not harmful to a person’s health. This is not true and chlorpromazine and weed can cause health issues the more a person consumes it.
How does Weed effect the potency of chlorpromazine?
The way in which the body absorbs and process chlorpromazine may be affected by weed. Therefore, the potency of the chlorpromazine may be less effective. Marijuana inhibits the metabolization of chlorpromazine. Not having the right potency of chlorpromazine means a person may either have a delay in the relief of their underlying symptoms.
A person seeking chlorpromazine medication that uses weed should speak to their doctor. It is important the doctor knows about a patient’s weed use, so they can prescribe the right chlorpromazine medication and strength. Or depending on level of interactions they may opt to prescribe a totally different medication. It is important for the doctor to know about their patient’s marijuana use. Weed is being legalized around the US, so doctors should be open to speaking about a patient’s use of it.
Sideffects of chlorpromazine and Weed
Many individuals may not realize that there are side effects and consequences to mixing chlorpromazine and Weed such as:
- Shortness of breath
- Respiratory Depression
- Cardiac Arrest
Interestingly, it is impossible to tell what effect mixing this substance with Weed will have on an individual due to their own unique genetic make up and tolerance. It is never advisable to mix chlorpromazine and Weed due to the chances of mild, moderate and severe side effects. If you are having an adverse reaction from mixing chlorpromazine and Weed it’s imperative that you head to your local emergency room. Even mixing a small amount of chlorpromazine and Weed is not recommended.
Taking chlorpromazine and Weed together
People who take chlorpromazine and Weed together will experience the effects of both substances. Technically, the specific effects and reactions that occur due to frequent use of chlorpromazine and weed depend on whether you consume more weed in relation to chlorpromazine or more chlorpromazine in relation to weed.
The use of significantly more weed and chlorpromazine will lead to sedation and lethargy, as well as the synergistic effects resulting from a mixture of the two medications.
People who take both weed and chlorpromazine may experience effects such as:
- reduced motor reflexes from chlorpromazine and Weed
- dizziness from Weed and chlorpromazine
- nausea and vomiting due to chlorpromazine and Weed
Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and chlorpromazine leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.
Mixing weed and chlorpromazine
The primary effect of weed is influenced by an increase in the concentration of the inhibitory neurotransmitter GABA, which is found in the spinal cord and brain stem, and by a reduction in its effect on neuronal transmitters. When weed is combined with chlorpromazine this primary effect is exaggerated, increasing the strain on the body with unpredictable results.
Weed and chlorpromazine affects dopamine levels in the brain, causing the body both mental and physical distress. Larger amounts of chlorpromazine and weed have a greater adverse effect yet leading medical recommendation is that smaller does of chlorpromazine can be just as harmful and there is no way of knowing exactly how chlorpromazine and weed is going to affect an individual before they take it.
Taking chlorpromazine and weed together
People who take chlorpromazine and weed together will experience the effects of both substances. The use of significantly more chlorpromazine with weed will lead to sedation and lethargy, as well as the synergistic effects resulting from a mixture of the two medications.
People who take both weed and chlorpromazine may experience effects such as:
- reduced motor reflexes from chlorpromazine and weed
- dizziness from weed and chlorpromazine
- nausea and vomiting of the chlorpromazine
Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and chlorpromazine leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.
Weed Vs chlorpromazine
Taking chlorpromazine in sufficient quantities increases the risk of a heart failure. Additionally, people under the influence of chlorpromazine and weed may have difficulty forming new memories. With weed vs chlorpromazine in an individual’s system they become confused and do not understand their environment. Due to the synergistic properties of chlorpromazine when mixed with weed it can lead to confusion, anxiety, depression and other mental disorders. Chronic use of chlorpromazine and weed can lead to permanent changes in the brain22.G. Lafaye, L. Karila, L. Blecha and A. Benyamina, Cannabis, cannabinoids, and health – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5741114/.
chlorpromazine Vs Weed
Studies investigating the effects of drugs such as chlorpromazine and weed have shown that the potential for parasomnia (performing tasks in sleep) is dramatically increased when chlorpromazine and weed are combined. Severe and dangerous side effects can occur when medications are mixed in the system, and sleep disorders are a common side effect of taking weed and chlorpromazine together.
When a small to medium amount of weed is combined with chlorpromazine, sleep disorders such as sleep apnea can occur. According to the latest data from the US Centers for Disease Control and Prevention (CDC) most ER visits and hospitalizations caused by too much weed were associated with other substances such as chlorpromazine.
How long after taking chlorpromazine can I smoke weed or take edibles?
To avoid any residual toxicity it is advisable to wait until the chlorpromazine has totally cleared your system before taking weed, even in small quantities.
Overdose on chlorpromazine and weed
In the case of Overdose on chlorpromazine or if you are worried after mixing chlorpromazine and weed, call a first responder or proceed to the nearest Emergency Room immediately.
If you are worried about someone who has taken too much chlorpromazine or mixed weed with chlorpromazine then call a first responder or take them to get immediate medical help. The best place for you or someone you care about in the case of a medical emergency is under medical supervision. Be sure to tell the medical team that there is a mix of chlorpromazine and weed in their system.
Mixing chlorpromazine and weed and antidepressants
Weed users feeling depressed and anxious may be prescribed antidepressant medication. There are some antidepressant users who also use chlorpromazine and weed. These individuals may not realize that there are side effects and consequences to consuming both chlorpromazine, marijuana and a range of antidepressants.
Studies on weed, chlorpromazine and antidepressants is almost nil. The reason for so little information on the side effects of the two is mostly down to marijuana being illegal in most places – although a number of states in the United States have legalized the drug.
Self-medicating with Weed and chlorpromazine
A lot of people suffer from depression caused by weed and chlorpromazine. How many? According to Anxiety and Depression Association of America (ADAA), in any given year, it is estimated that nearly 16 million adults experience depression. Unfortunately, that number is likely to be wrong due to under reporting. Many people do not report suffering from depression because they do not want to be looked at as suffering from a mental illness. The stigmas around mental health continue and people do not want to be labeled as depressed.
Potential side effects from mixing chlorpromazine and weed
Quitting weed to take chlorpromazine
Medical professionals say an individual prescribed or taking chlorpromazine should not stop using weed cold turkey. Withdrawal symptoms can be significant. Heavy pot users should especially avoid going cold turkey. The side effects of withdrawal from weed include anxiety, irritability, loss of sleep, change of appetite, and depression by quitting weed cold turkey and starting to take chlorpromazine.
A person beginning to use chlorpromazine should cut back on weed slowly. While reducing the amount of weed use, combine it with mindfulness techniques and/or yoga. Experts stress that non-medication can greatly improve a person’s mood.
Weed and chlorpromazine can affect a person in various ways. Different types of marijuana produce different side effects. Side effects of weed and chlorpromazine may include:
- loss of motor skills
- poor or lack of coordination
- lowered blood pressure
- short-term memory loss
- increased heart rate
- increased blood pressure
- increased energy
- increased motivation
Mixing chlorpromazine and weed can also produce hallucinations in users. This makes marijuana a hallucinogenic for some users. Weed creates different side effects in different people, making it a very potent drug. Now, mixing chlorpromazine or other mental health drugs with weed can cause even more unwanted side effects.
Mixing drugs and weed conclusion
Long-term weed use can make depression and anxiety worse. In addition, using marijuana can prevent chlorpromazine from working to their full potential33.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678684/. Weed consumption should be reduced gradually to get the most out of prescription medication. Marijuana is a drug and it is harmful to individual’s long-term health. Weed has many side effects and the consequences are different to each person who uses it, especially when mixed with chlorpromazine.
Or you could find what you are looking for in our Alcohol and Interactions with Other Drugs index A to L or Alcohol and Interactions with Other Drugs index M to Z , Cocaine and Interactions with Other Drugs index A to L or Cocaine and Interactions with Other Drugs index M to Z or our MDMA and Interactions with Other Drugs Index A to L or MDMA and Interactions with Other Drugs Index M to Z.
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- 11.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678684/
- 22.G. Lafaye, L. Karila, L. Blecha and A. Benyamina, Cannabis, cannabinoids, and health – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5741114/
- 33.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678684/