antabuse and Weed
Edited by Hugh Soames
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antabuse 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 antabuse. 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 antabuse and Weed.
Mixing antabuse and Weed
Disulfiram is a medication used to support the treatment of chronic alcoholism by producing an acute sensitivity to ethanol (drinking alcohol). Disulfiram works by inhibiting the enzyme aldehyde dehydrogenase, causing many of the effects of a hangover to be felt immediately following alcohol consumption. Disulfiram plus alcohol, even small amounts, produces flushing, throbbing in the head and neck, a throbbing headache, respiratory difficulty, nausea, copious vomiting, sweating, thirst, chest pain, palpitation, dyspnea, hyperventilation, fast heart rate, low blood pressure, fainting, marked uneasiness, weakness, vertigo, blurred vision, and confusion. In severe reactions there may be respiratory depression, cardiovascular collapse, abnormal heart rhythms, heart attack, acute congestive heart failure, unconsciousness, convulsions, and death.
In the body, alcohol is converted to acetaldehyde, which is then broken down by acetaldehyde dehydrogenase. When the dehydrogenase enzyme is inhibited, acetaldehyde builds up, causing unpleasant side effects. Disulfiram should be used in conjunction with counseling and support.
Disulfiram is used as a second-line treatment, behind acamprosate and naltrexone, for alcohol dependence.
Under normal metabolism, alcohol is broken down in the liver by the enzyme alcohol dehydrogenase to acetaldehyde, which is then converted by the enzyme acetaldehyde dehydrogenase to a harmless acetic acid derivative (acetyl coenzyme A). Disulfiram blocks this reaction at the intermediate stage by blocking acetaldehyde dehydrogenase. After alcohol intake under the influence of disulfiram, the concentration of acetaldehyde in the blood may be five to 10 times higher than that found during metabolism of the same amount of alcohol alone. As acetaldehyde is one of the major causes of the symptoms of a “hangover”, this produces immediate and severe negative reaction to alcohol intake. About 5 to 10 minutes after alcohol intake, the patient may experience the effects of a severe hangover for a period of 30 minutes up to several hours. Symptoms usually include flushing of the skin, accelerated heart rate, low blood pressure, nausea, and vomiting. Uncommon adverse events include shortness of breath, throbbing headache, visual disturbance, mental confusion, postural syncope, and circulatory collapse.
Disulfiram should not be taken if alcohol has been consumed in the last 12 hours. There is no tolerance to disulfiram: the longer it is taken, the stronger its effects. As disulfiram is absorbed slowly through the digestive tract and eliminated slowly by the body, the effects may last for up to two weeks after the initial intake; consequently, medical ethics dictate that patients must be fully informed about the disulfiram-alcohol reaction.
Disulfiram does not reduce alcohol cravings, so a major problem associated with this drug is extremely poor compliance. Methods to improve compliance include subdermal implants, which release the drug continuously over a period of up to 12 weeks, and supervised administration practices, for example, having the drug regularly administered by one’s spouse.
Although disulfiram remained the most common pharmaceutical treatment of alcohol abuse until the end of the 20th century, today it is often replaced or accompanied with newer drugs, primarily the combination of naltrexone and acamprosate, which directly attempt to address physiological processes in the brain associated with alcohol abuse.
The most common side effects in the absence of alcohol are headache, and a metallic or garlic taste in the mouth, though more severe side effects may occur. Tryptophol, a chemical compound that induces sleep in humans, is formed in the liver after disulfiram treatment. Less common side effects include decrease in libido, liver problems, skin rash, and nerve inflammation. Liver toxicity is an uncommon but potentially serious side effect, and risk groups e.g. those with already impaired liver function should be monitored closely. That said, the rate of disulfiram-induced hepatitis are estimated to be in between 1 per 25,000 to 1 in 30,000, and rarely the primary cause for treatment cessation.
Cases of disulfiram neurotoxicity have also occurred, causing extrapyramidal and other symptoms. Disulfiram can produce neuropathy in daily doses of less than the usually recommended 500 mg. Nerve biopsies showed axonal degeneration and the neuropathy is difficult to distinguish from that associated with ethanol abuse. Disulfiram neuropathy occurs after a variable latent period (mean 5 to 6 months) and progresses steadily. Slow improvement may occur when the drug’s use is stopped; often there is complete recovery eventually.
Disulfiram disrupts metabolism of several other compounds, including paracetamol (acetaminophen), theophylline and caffeine. However, in most cases, this disruption is mild and presents itself as a 20–40% increase in the half-life of the compound at typical dosages of disulfiram.[citation needed]
In medicine, the term “disulfiram effect” refers to an adverse effect of a particular medication in causing an unpleasant hypersensitivity to alcohol, similar to the effect caused by disulfiram administration.
Examples:
The synthesis of disulfiram, originally known as tetraethylthiuram disulfide, was first reported in 1881. By around 1900, it was introduced to the industrial process of sulfur vulcanization of rubber and became widely used. In 1937
a plant physician in the American rubber industry described adverse reactions to alcohol in workers exposed to tetramethylthiuram monosulfide and disulfide, and proposed that this effect of disulfiram and related compounds might lead to ”the cure for alcoholism”; the effect was also noticed in workers at a Swedish rubber boot factory.
In the early 1940s it had been tested as a treatment for scabies, a parasitic skin infection, as well as intestinal worms.
Around that time, during the German occupation of Denmark, Erik Jacobsen and Jens Hald at the Danish drug company Medicinalco picked up on that research and began exploring the use of disulfiram to treat intestinal parasites. The company had a group of enthusiastic self-experimenters that called itself the “Death Battalion”, and in the course of testing the drug on themselves, accidentally discovered that drinking alcohol while the drug was still in their bodies made them mildly sick.
They made that discovery in 1945, and did nothing with it until two years later, when Jacobsen gave an impromptu talk and mentioned that work, which was discussed afterwards in newspapers at the time, leading them to further explore the use of the drug for that purpose. That work included small clinical trials with Oluf Martensen-Larsen, a doctor who worked with alcoholics. They published their work starting in 1948.
The chemists at Medicinalco discovered a new form of disulfiram while trying to purify a batch that had been contaminated with copper. This form turned out to have better pharmacological properties, and the company patented it and used that form for the product that was introduced as Antabus (later anglicized to Antabuse).
This work led to renewed study of the human metabolism of ethanol. It was already known that ethanol was mostly metabolized in the liver, with it being converted first to acetaldehyde and then acetaldehyde to acetic acid and carbon dioxide, but the enzymes involved were not known. By 1950 the work led to the knowledge that ethanol is oxidized to acetaldehyde by alcohol dehydrogenase and acetaldehyde is oxidized to acetic acid by aldehyde dehydrogenase (ALDH), and that disulfiram works by inhibiting ALDH, leading to a buildup of acetaldehyde, which is what causes the negative effects in the body.
The drug was first marketed in Denmark and as of 2008, Denmark is the country where it is most widely prescribed. It was approved by the FDA in 1951. The FDA later approved other drugs for treatment of alcoholism, namely naltrexone in 1994 and acamprosate in 2004.
Though the Occupational Safety and Health Administration (OSHA) in the US has not set a permissible exposure limit (PEL) for disulfiram in the workplace, the National Institute for Occupational Safety and Health has set a recommended exposure limit (REL) of 2 mg/m and recommended that workers avoid concurrent exposure to ethylene dibromide.
Disulfiram has been studied as a possible treatment for cancer, parasitic infections, anxiety disorder, and latent HIV infection.
Disulfiram has shown reversing of retinitis pigmentosa in rats.
When disulfiram creates complexes with metals (dithiocarbamate complexes), it is a proteasome inhibitor and as of 2016 it had been studied in in vitro experiments, model animals, and small clinical trials as a possible treatment for liver metastasis, metastatic melanoma, glioblastoma, non-small cell lung cancer, and prostate cancer. Various clinical trials of copper depletion agents have been carried out.
In the body, disulfiram is rapidly metabolized to diethyldithiocarbamate (ditiocarb), which binds to metal ions such as zinc or copper to form zinc or copper diethyldithiocarbamate (zinc or copper ditiocarb). The zinc diethyldithiocarbamate (zinc-ditiocarb) metabolite of disulfiram is extremely potent against the diarrhea and liver abscess-causing parasite Entamoeba histolytica and might be active against other deadly parasites.
Disulfiram has also been identified by systematic high-throughput screening as a potential HIV latency reversing agent (LRA). Reactivation of latent HIV infection in patients is part of an investigational strategy known as “shock and kill” which may be able to reduce or eliminate the HIV reservoir. Recent phase II dose-escalation studies in patients with HIV who are controlled on antiretroviral therapy have observed an increase in cell-associated unspliced HIV RNA with increasing exposure to disulfiram and its metabolites. Disulfiram is also being investigated in combination with vorinostat, another investigational latency reversing agent, to treat HIV.
Disulfiram has been shown to inhibit the papain-like proteases of MERS-CoV and SARS-CoV. It has been examined in a small inconclusive retrospective observational study for its effects on COVID-19 symptoms and is currently in Phase 2 clinical trials.
Research has found that anxiety is one of the leading symptoms created by marijuana in users, and that there is a correlation between antabuse and Weed and an increase in anxiety.
Anyone mixing antabuse and weed is likely to experience side effects. This happens with all medications whether weed or antabuse is mixed with them. Side effects can be harmful when mixing antabuse and weed. Doctors are likely to refuse a patient a antabuse 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 antabuse 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 antabuse 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 antabuse. 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, antabuse and Weed, dol not interact is wrong. There will always be an interaction between antabuse 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 antabuse and Weed is Scromiting. This condition, reportedly caused by mixing antabuse 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 antabuse 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 antabuse and weed can cause health issues the more a person consumes it.
How does Weed effect the potency of antabuse?
The way in which the body absorbs and process antabuse may be affected by weed. Therefore, the potency of the antabuse may be less effective. Marijuana inhibits the metabolization of antabuse. Not having the right potency of antabuse means a person may either have a delay in the relief of their underlying symptoms.
A person seeking antabuse 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 antabuse 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 antabuse and Weed
Many individuals may not realize that there are side effects and consequences to mixing antabuse and Weed such as:
- Dizziness
- Sluggishness
- Drowsiness
- Shortness of breath
- Itching
- Hives
- Palpitations
- Respiratory Depression
- Cardiac Arrest
- Coma
- Seizures
- Death
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 antabuse and Weed due to the chances of mild, moderate and severe side effects. If you are having an adverse reaction from mixing antabuse and Weed it’s imperative that you head to your local emergency room. Even mixing a small amount of antabuse and Weed is not recommended.
Taking antabuse and Weed together
People who take antabuse and Weed together will experience the effects of both substances. Technically, the specific effects and reactions that occur due to frequent use of antabuse and weed depend on whether you consume more weed in relation to antabuse or more antabuse in relation to weed.
The use of significantly more weed and antabuse 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 antabuse may experience effects such as:
- reduced motor reflexes from antabuse and Weed
- dizziness from Weed and antabuse
- nausea and vomiting due to antabuse and Weed
Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and antabuse leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.
Mixing weed and antabuse
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 antabuse this primary effect is exaggerated, increasing the strain on the body with unpredictable results.
Weed and antabuse affects dopamine levels in the brain, causing the body both mental and physical distress. Larger amounts of antabuse and weed have a greater adverse effect yet leading medical recommendation is that smaller does of antabuse can be just as harmful and there is no way of knowing exactly how antabuse and weed is going to affect an individual before they take it.
Taking antabuse and weed together
People who take antabuse and weed together will experience the effects of both substances. The use of significantly more antabuse 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 antabuse may experience effects such as:
- reduced motor reflexes from antabuse and weed
- dizziness from weed and antabuse
- nausea and vomiting of the antabuse
Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and antabuse leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.
Weed Vs antabuse
Taking antabuse in sufficient quantities increases the risk of a heart failure. Additionally, people under the influence of antabuse and weed may have difficulty forming new memories. With weed vs antabuse in an individual’s system they become confused and do not understand their environment. Due to the synergistic properties of antabuse when mixed with weed it can lead to confusion, anxiety, depression and other mental disorders. Chronic use of antabuse 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/.
antabuse Vs Weed
Studies investigating the effects of drugs such as antabuse and weed have shown that the potential for parasomnia (performing tasks in sleep) is dramatically increased when antabuse 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 antabuse together.
When a small to medium amount of weed is combined with antabuse, 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 antabuse.
How long after taking antabuse can I smoke weed or take edibles?
To avoid any residual toxicity it is advisable to wait until the antabuse has totally cleared your system before taking weed, even in small quantities.
Overdose on antabuse and weed
In the case of Overdose on antabuse or if you are worried after mixing antabuse 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 antabuse or mixed weed with antabuse 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 antabuse and weed in their system.
Excessive Weed intake and result in scromiting, chs, and anxiety disorder. It is advisable to quit vaping weed if you are feeling these symptoms.
Mixing antabuse and weed and antidepressants
Weed users feeling depressed and anxious may be prescribed antidepressant medication. There are some antidepressant users who also use antabuse and weed. These individuals may not realize that there are side effects and consequences to consuming both antabuse, marijuana and a range of antidepressants.
Studies on weed, antabuse 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 antabuse
A lot of people suffer from depression caused by weed and antabuse. 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 antabuse and weed
Quitting weed to take antabuse
Medical professionals say an individual prescribed or taking antabuse 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 antabuse.
A person beginning to use antabuse 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 antabuse can affect a person in various ways. Different types of marijuana produce different side effects. Side effects of weed and antabuse may include:
- loss of motor skills
- poor or lack of coordination
- lowered blood pressure
- short-term memory loss
- increased heart rate
- increased blood pressure
- anxiety
- paranoia
- increased energy
- increased motivation
Mixing antabuse 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 antabuse 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 antabuse 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 antabuse.
If you take antabuse, and also drink Alcohol or MDMA, you can research the effects of antabuse and Alcohol , antabuse and Cocaine as well as antabuse and MDMA here.
To find the effects of other drugs and weed refer to our Weed and Other Drugs Index A to L or our Weed and Other Drugs Index M-Z.
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.
antabuse and Weed
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