Butrans and Weed
Butrans 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 Butrans. 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 Butrans and Weed.
Mixing Butrans and Weed
Buprenorphine, sold under the brand name Subutex among others, is an opioid used to treat opioid use disorder, acute pain, and chronic pain. It can be used under the tongue (sublingual), in the cheek (buccal), by injection (intravenous and subcutaneous), as a skin patch (transdermal), or as an implant. For opioid use disorder, it is typically started when withdrawal symptoms have begun and for the first two days of treatment under direct observation of a health-care provider.
In the United States, the combination formulation of buprenorphine/naloxone (Suboxone) is usually prescribed to discourage misuse by injection. However, more recently the efficacy of naloxone in preventing misuse has been brought into question, and preparations of buprenorphine combined with naloxone could potentially be less safe than buprenorphine alone. Maximum pain relief is generally within an hour with effects up to 24 hours. Buprenorphine affects different types of opioid receptors in different ways. Depending on the type of receptor, it may be an agonist, partial agonist, or antagonist. Buprenorphine’s activity as an agonist/antagonist is important in the treatment of opioid use disorder: it relieves withdrawal symptoms from other opioids and induces some euphoria, but also blocks the ability for many other opioids, including heroin, to cause an effect. Unlike full agonists like heroin or methadone, buprenorphine has a ceiling effect, such that taking more medicine past a certain point will not increase the effects of the drug.
Side effects may include respiratory depression (decreased breathing), sleepiness, adrenal insufficiency, QT prolongation, low blood pressure, allergic reactions, constipation, and opioid addiction. Among those with a history of seizures, a risk exists of further seizures. Opioid withdrawal following stopping buprenorphine is generally less severe than with other opioids. Whether use during pregnancy is safe is unclear, but use while breastfeeding is probably safe, since the dose the infant receives is 1-2% that of the maternal dose, on a weight basis.
Buprenorphine was patented in 1965, and approved for medical use in the United States in 1981. It is on the World Health Organization’s List of Essential Medicines. In addition to prescription as an analgesic it is a common medication used to treat opioid use disorders, such as addiction to heroin. In 2020, it was the 186th most commonly prescribed medication in the United States, with more than 2.8 million prescriptions. Buprenorphine may also be used recreationally for the high it can produce. In the United States, buprenorphine is a schedule III controlled substance.
Buprenorphine is used to treat people with opioid use disorder. In the U.S., the combination formulation of buprenorphine/naloxone is generally prescribed to deter injection, since naloxone, an opioid antagonist, is believed to cause acute withdrawal if the formulation is crushed and injected.: 99 Taken orally, the naloxone has virtually no effect, due to the drug’s extremely high first-pass metabolism and low bioavailability (2%). However, the efficacy of naloxone in preventing misuse by injection has more recently been brought into question and preparations including naloxone could even be less safe than preparations containing solely buprenorphine. Anecdotally, posters on drug-related online forums have stated that they were able to attain a high by injecting preparations of buprenorphine despite being combined with naloxone.
Before starting buprenorphine, individuals are generally advised to wait long enough after their last dose of opioid until they have some withdrawal symptoms to allow for the medication to bind the receptors, since if taken too soon, buprenorphine can displace other opioids bound to the receptors and precipitate an acute withdrawal. The dose of buprenorphine is then adjusted until symptoms improve, and individuals remain on a maintenance dose of 8–16 mg.: 99–100 Because withdrawal is uncomfortable and a deterrent for many patients, many have begun to call for different means of treatment initiation. Some providers have begun to use the Bernese method, also known as microdosing, in which very small doses of buprenorphine are given while patients are still using street opioids, and without precipitating withdrawal, with medicine levels slowly titrated upward.
Both buprenorphine and methadone are medications used for detoxification and opioid replacement therapy, and appear to have similar effectiveness based on limited data. Both are safe for pregnant women with opioid use disorder, although preliminary evidence suggests that methadone is more likely to cause neonatal abstinence syndrome. In the US and European Union, only designated clinics can prescribe methadone for opioid use disorder, requiring patients to travel to the clinic daily. If patients are drug free for a period they may be permitted to receive “take home doses,” reducing their visits to as little as once a week. Alternatively, up to a month’s supply of buprenorphine has been able to be prescribed by clinicians in the US or Europe who have completed a basic training (8–24 hours in the US) and received a waiver/licence allowing prescription of the medicine. In France, buprenorphine prescription for opioid use disorder has been permitted without any special training or restrictions since 1995, resulting in treatment of approximately ten times more patients per year with buprenorphine than with methadone in the following decade. In 2021, seeking to address record levels of opioid overdose, the United States also removed the requirement for a special waiver for prescribing physicians. Whether this change will be sufficient to impact prescription is unclear, since even before the change as many as half of physicians with a waiver permitting them to prescribe buprenorphine did not do so, and one third of non-waivered physicians reported that nothing would induce them to prescribe buprenorphine for opioid use disorder.
A transdermal patch is available for the treatment of chronic pain. These patches are not indicated for use in acute pain, pain that is expected to last only for a short period of time, or pain after surgery, nor are they recommended for opioid addiction.
With respect to equianalgesic dosing, when used sublingually, the potency of buprenorphine is about 40 to 70 times that of morphine. When used as a transdermal patch, the potency of buprenorphine may be 100 to 115 times that of morphine.
Common adverse drug reactions associated with the use of buprenorphine, similar to those of other opioids, include nausea and vomiting, drowsiness, dizziness, headache, memory loss, cognitive and neural inhibition, perspiration, itchiness, dry mouth, shrinking of the pupils of the eyes (miosis), orthostatic hypotension, male ejaculatory difficulty, decreased libido, and urinary retention. Constipation and central nervous system (CNS) effects are seen less frequently than with morphine. Central sleep apnea has also been reported as a side effect of long-term buprenorphine use.
The most severe side effect associated with buprenorphine is respiratory depression (insufficient breathing). It occurs more often in those who are also taking benzodiazepines or alcohol, or have underlying lung disease. The usual reversal agents for opioids, such as naloxone, may be only partially effective, and additional efforts to support breathing may be required. Respiratory depression may be less than with other opioids, particularly with chronic use. In the setting of acute pain management, though, buprenorphine appears to cause the same rate of respiratory depression as other opioids such as morphine. Central sleep apnea is possible with long-term use, possibly resolving with dose reduction.
Buprenorphine treatment carries the risk of causing psychological or physiological (physical) dependencies. It has a slow onset of activity, with a long duration of action, and a long half-life of 24 to 60 hours. Once a patient has stabilised on the (buprenorphine) medication and programme, three options remain – continual use (buprenorphine-only medication), switching to a buprenorphine/naloxone combination, or a medically supervised withdrawal.
Achieving acute opioid analgesia is difficult in persons using buprenorphine for pain management. However, a systematic review found no clear benefit to bridging or stopping buprenorphine when used in opioid substitution therapy to facilitate perioperative pain management, but failure to restart it was found to pose concerns for relapse. Therefore, it is recommended that buprenophine opioid substitution therapy is continued in the perioperative period when possible. In addition preoperative pain management in patients taking buprenorphine should use an interdisciplinary approach with multimodal analgesia.
Buprenorphine has been reported to possess these following pharmacological activities:
In simplified terms, buprenorphine can essentially be thought of as a nonselective, mixed agonist–antagonist opioid receptor modulator, acting as an unusually high affinity, weak partial agonist of the MOR, a high affinity antagonist of the KOR and DOR, and a relatively low affinity, very weak partial agonist of the ORL-1/NOP.
Although buprenorphine is a partial agonist of the MOR, human studies have found that it acts like a full agonist with respect to analgesia in opioid-intolerant individuals. Conversely, buprenorphine behaves like a partial agonist of the MOR with respect to respiratory depression.
Buprenorphine is also known to bind to with high affinity and antagonize the putative ε-opioid receptor.
Full analgesic efficacy of buprenorphine requires both exon 11- and exon 1-associated μ-opioid receptor splice variants.
The active metabolites of buprenorphine are not thought to be clinically important in its CNS effects.
In positron emission tomography (PET) imaging studies, buprenorphine was found to decrease whole-brain MOR availability due to receptor occupancy by 41% (i.e., 59% availability) at 2 mg, 80% (i.e., 20% availability) at 16 mg, and 84% (i.e., 16% availability) at 32 mg.
Unlike some other opioids and opioid antagonists, buprenorphine binds only weakly to and possesses little if any activity at the sigma receptor.
Buprenorphine also blocks voltage-gated sodium channels via the local anesthetic binding site, and this underlies its potent local anesthetic properties.
Similarly to various other opioids, buprenorphine has also been found to act as an agonist of the toll-like receptor 4, albeit with very low affinity.
Buprenorphine is metabolized by the liver, via CYP3A4 (also CYP2C8 seems to be involved) isozymes of the cytochrome P450 enzyme system, into norbuprenorphine (by N-dealkylation). The glucuronidation of buprenorphine is primarily carried out by UGT1A1 and UGT2B7, and that of norbuprenorphine by UGT1A1 and UGT1A3. These glucuronides are then eliminated mainly through excretion into bile. The elimination half-life of buprenorphine is 20 to 73 hours (mean 37 hours). Due to the mainly hepatic elimination, no risk of accumulation exists in people with renal impairment.
One of the major active metabolites of buprenorphine is norbuprenorphine, which, in contrast to buprenorphine itself, is a full agonist of the MOR, DOR, and ORL-1, and a partial agonist at the KOR. However, relative to buprenorphine, norbuprenorphine has extremely little antinociceptive potency (1/50th that of buprenorphine), but markedly depresses respiration (10-fold more than buprenorphine). This may be explained by very poor brain penetration of norbuprenorphine due to a high affinity of the compound for P-glycoprotein. In contrast to norbuprenorphine, buprenorphine and its glucuronide metabolites are negligibly transported by P-glycoprotein.
The glucuronides of buprenorphine and norbuprenorphine are also biologically active, and represent major active metabolites of buprenorphine. Buprenorphine-3-glucuronide has affinity for the MOR (Ki = 4.9 pM), DOR (Ki = 270 nM) and ORL-1 (Ki = 36 μM), and no affinity for the KOR. It has a small antinociceptive effect and no effect on respiration. Norbuprenorphine-3-glucuronide has no affinity for the MOR or DOR, but does bind to the KOR (Ki = 300 nM) and ORL-1 (Ki = 18 μM). It has a sedative effect but no effect on respiration.
Buprenorphine is a semisynthetic derivative of thebaine, and is fairly soluble in water, as its hydrochloride salt. It degrades in the presence of light.
Buprenorphine and norbuprenorphine may be quantified in blood or urine to monitor use or non-medical recreational use, confirm a diagnosis of poisoning, or assist in a medicolegal investigation. A significant overlap of drug concentrations exists in body fluids within the possible spectrum of physiological reactions ranging from asymptomatic to comatose. Therefore, having knowledge of both the route of administration of the drug and the level of tolerance to opioids of the individual is critical when results are interpreted.
In 1969, researchers at Reckitt and Colman (now Reckitt Benckiser) had spent 10 years attempting to synthesize an opioid compound “with structures substantially more complex than morphine could retain the desirable actions whilst shedding the undesirable side effects”. Physical dependence and withdrawal from buprenorphine itself remain important issues, since buprenorphine is a long-acting opioid. Reckitt found success when researchers synthesized RX6029 which had showed success in reducing dependence in test animals. RX6029 was named buprenorphine and began trials on humans in 1971. By 1978, buprenorphine was first launched in the UK as an injection to treat severe pain, with a sublingual formulation released in 1982.
In the United States, buprenorphine and buprenorphine with naloxone were approved for opioid use disorder by the Food and Drug Administration in October 2002. The DEA rescheduled buprenorphine from a schedule V drug to a schedule III drug just before approval. The ACSCN for buprenorphine is 9064, and being a schedule III substance, it does not have an annual manufacturing quota imposed by the DEA. The salt in use is the hydrochloride, which has a free-base conversion ratio of 0.928.
In the years before buprenorphine/naloxone was approved, Reckitt Benckiser had lobbied Congress to help craft the Drug Addiction Treatment Act of 2000, which gave authority to the Secretary of Health and Human Services to grant a waiver to physicians with certain training to prescribe and administer schedule III, IV, or V narcotic drugs for the treatment of addiction or detoxification. Before this law was passed, such treatment was permitted only in clinics designed specifically for drug addiction.
The waiver, which can be granted after the completion of an eight-hour course, was required for outpatient treatment of opioid addiction with buprenorphine from 2000 to 2021. Initially, the number of people each approved physician could treat was limited to 10. This was eventually modified to allow approved physicians to treat up to 100 people with buprenorphine for opioid addiction in an outpatient setting. This limit was increased by the Obama administration, raising the number of patients to which doctors can prescribe to 275. On 14 January 2021, the US Department of Health and Human Services announced that the waiver would no longer be required to prescribe buprenorphine to treat up to 30 people concurrently.
New Jersey authorized paramedics to give buprenorphine to people at the scene after they have recovered from an overdose.
In the European Union, Subutex and Suboxone, buprenorphine’s high-dose sublingual tablet preparations, were approved for opioid use disorder treatment in September 2006. In the Netherlands, buprenorphine is a list II drug of the Opium Law, though special rules and guidelines apply to its prescription and dispensation. In France, where buprenorphine prescription by general practitioners and dispensed by pharmacies has been permitted since the mid-1990s as a response to HIV and overdose risk. Deaths caused by heroin overdose were reduced by four-fifths between 1994 and 2002, and incidence of AIDS among people who inject drugs in France fell from 25% in the mid-1990s to 6% in 2010.
Buprenorphine is available under the trade names Cizdol, Brixadi (approved in the US by FDA for addiction treatment in 2023), Suboxone (with naloxone), Subutex (typically used for opioid use disorder), Zubsolv, Bunavail, Buvidal (approved in the UK, Europe and Australia for addiction treatment in 2018), Sublocade (approved in the US in 2018), Probuphine, Temgesic (sublingual tablets for moderate to severe pain), Buprenex (solutions for injection often used for acute pain in primary-care settings), Norspan, and Butrans (transdermal preparations used for chronic pain). In Poland buprenorphine is available under the trade names Bunondol (for pain treatment, when morphine is too little; amounts of 0.2mg and 0.4mg) and Bunorfin (for addicts substitution in amount of 2 and 8mg).
Some evidence supports the use of buprenorphine for depression. Buprenorphine/samidorphan, a combination product of buprenorphine and samidorphan (a preferential μ-opioid receptor antagonist), appears useful for treatment-resistant depression.
In combination with samidorphan or naltrexone (μ-opioid receptor antagonists), buprenorphine is under investigation for the treatment of cocaine dependence, and recently demonstrated effectiveness for this indication in a large-scale (n = 302) clinical trial (at a high buprenorphine dose of 16 mg, but not a low dose of 4 mg).
Buprenorphine has been used in the treatment of the neonatal abstinence syndrome, a condition in which newborns exposed to opioids during pregnancy demonstrate signs of withdrawal. In the United States, use currently is limited to infants enrolled in a clinical trial conducted under an FDA-approved investigational new drug (IND) application. Preliminary research suggests that buprenorphine is associated with shorter time in hospital for neonates, compared to methadone. An ethanolic formulation used in neonates is stable at room temperature for at least 30 days.
In one study, buprenorphine was found to be effective in a subset of individuals with treatment-refractory obsessive–compulsive disorder.
Veterinarians administer buprenorphine for perioperative pain, particularly in cats, where its effects are similar to morphine. The drug’s legal status and lower potential for human abuse makes it an attractive alternative to other opioids.
It has veterinary medical use for treatment of pain in dogs and cats, as well as other animals.
Research has found that anxiety is one of the leading symptoms created by marijuana in users, and that there is a correlation between Butrans and Weed and an increase in anxiety.
Anyone mixing Butrans and weed is likely to experience side effects. This happens with all medications whether weed or Butrans is mixed with them. Side effects can be harmful when mixing Butrans and weed. Doctors are likely to refuse a patient a Butrans 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 Butrans 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 Butrans 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 Butrans. 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, Butrans and Weed, dol not interact is wrong. There will always be an interaction between Butrans 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 Butrans and Weed is Scromiting. This condition, reportedly caused by mixing Butrans 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 Butrans 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 Butrans and weed can cause health issues the more a person consumes it.
How does Weed effect the potency of Butrans?
The way in which the body absorbs and process Butrans may be affected by weed. Therefore, the potency of the Butrans may be less effective. Marijuana inhibits the metabolization of Butrans. Not having the right potency of Butrans means a person may either have a delay in the relief of their underlying symptoms.
A person seeking Butrans 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 Butrans 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 Butrans and Weed
Many individuals may not realize that there are side effects and consequences to mixing Butrans 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 Butrans and Weed due to the chances of mild, moderate and severe side effects. If you are having an adverse reaction from mixing Butrans and Weed it’s imperative that you head to your local emergency room. Even mixing a small amount of Butrans and Weed is not recommended.
Taking Butrans and Weed together
People who take Butrans and Weed together will experience the effects of both substances. Technically, the specific effects and reactions that occur due to frequent use of Butrans and weed depend on whether you consume more weed in relation to Butrans or more Butrans in relation to weed.
The use of significantly more weed and Butrans 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 Butrans may experience effects such as:
- reduced motor reflexes from Butrans and Weed
- dizziness from Weed and Butrans
- nausea and vomiting due to Butrans and Weed
Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and Butrans leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.
Mixing weed and Butrans
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 Butrans this primary effect is exaggerated, increasing the strain on the body with unpredictable results.
Weed and Butrans affects dopamine levels in the brain, causing the body both mental and physical distress. Larger amounts of Butrans and weed have a greater adverse effect yet leading medical recommendation is that smaller does of Butrans can be just as harmful and there is no way of knowing exactly how Butrans and weed is going to affect an individual before they take it.
Taking Butrans and weed together
People who take Butrans and weed together will experience the effects of both substances. The use of significantly more Butrans 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 Butrans may experience effects such as:
- reduced motor reflexes from Butrans and weed
- dizziness from weed and Butrans
- nausea and vomiting of the Butrans
Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and Butrans leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.
Weed Vs Butrans
Taking Butrans in sufficient quantities increases the risk of a heart failure. Additionally, people under the influence of Butrans and weed may have difficulty forming new memories. With weed vs Butrans in an individual’s system they become confused and do not understand their environment. Due to the synergistic properties of Butrans when mixed with weed it can lead to confusion, anxiety, depression and other mental disorders. Chronic use of Butrans 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/.
Butrans Vs Weed
Studies investigating the effects of drugs such as Butrans and weed have shown that the potential for parasomnia (performing tasks in sleep) is dramatically increased when Butrans 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 Butrans together.
When a small to medium amount of weed is combined with Butrans, 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 Butrans.
How long after taking Butrans can I smoke weed or take edibles?
To avoid any residual toxicity it is advisable to wait until the Butrans has totally cleared your system before taking weed, even in small quantities.
Overdose on Butrans and weed
In the case of Overdose on Butrans or if you are worried after mixing Butrans 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 Butrans or mixed weed with Butrans 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 Butrans and weed in their system.
Mixing Butrans and weed and antidepressants
Weed users feeling depressed and anxious may be prescribed antidepressant medication. There are some antidepressant users who also use Butrans and weed. These individuals may not realize that there are side effects and consequences to consuming both Butrans, marijuana and a range of antidepressants.
Studies on weed, Butrans 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 Butrans
A lot of people suffer from depression caused by weed and Butrans. 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 Butrans and weed
Quitting weed to take Butrans
Medical professionals say an individual prescribed or taking Butrans 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 Butrans.
A person beginning to use Butrans 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 Butrans can affect a person in various ways. Different types of marijuana produce different side effects. Side effects of weed and Butrans 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 Butrans 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 Butrans 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 Butrans 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 Butrans.
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/