cymbalta and Weed
cymbalta 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 cymbalta. 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 cymbalta and Weed.
Mixing cymbalta and Weed
Duloxetine, sold under the brand name Cymbalta among others, is a medication used to treat major depressive disorder, generalized anxiety disorder, fibromyalgia, neuropathic pain and central sensitization. It is taken by mouth.
Duloxetine is a serotonin–norepinephrine reuptake inhibitor (SNRI). Similarly to SSRIs and other SNRIs, the precise mechanism for its antidepressant and anxiolytic effects is not known.
Common side effects include dry mouth, nausea, feeling tired, dizziness, agitation, sexual problems, and increased sweating. Severe side effects include an increased risk of suicide, serotonin syndrome, mania, and liver problems. Antidepressant withdrawal syndrome may occur if stopped. There are concerns that use during the later part of pregnancy can harm the developing fetus.
Duloxetine was approved for medical use in the United States and in the European Union in 2004. It is available as a generic medication. In 2020, it was the 27th most commonly prescribed medication in the United States, with more than 22 million prescriptions.
The main uses of duloxetine are in major depressive disorder, generalized anxiety disorder, neuropathic pain, chronic musculoskeletal pain, and fibromyalgia.
Duloxetine is recommended as a first-line agent for the treatment of chemotherapy-induced neuropathy by the American Society of Clinical Oncology, as a first-line therapy for fibromyalgia in the presence of mood disorders by the German Interdisciplinary Association for Pain Therapy, as a Grade B recommendation for the treatment of diabetic neuropathy by the American Association for Neurology and as a level A recommendation in certain neuropathic states by the European Federation of Neurological Societies.
A 2014 Cochrane review concluded that duloxetine is beneficial in the treatment of diabetic neuropathy and fibromyalgia but that more comparative studies with other medicines are needed. The French medical journal Prescrire concluded that duloxetine is no better than other available agents and has a greater risk of side effects.
Duloxetine was approved for the treatment of major depression in 2004. While duloxetine has demonstrated improvement in depression-related symptoms compared to placebo, comparisons of duloxetine to other antidepressant medications have been less successful. A 2012 Cochrane Review did not find greater efficacy of duloxetine compared to SSRIs and newer antidepressants. Additionally, the review found evidence that duloxetine has increased side effects and reduced tolerability compared to other antidepressants. It thus did not recommend duloxetine as a first line treatment for major depressive disorder, given the (then) high cost of duloxetine compared to inexpensive off-patent antidepressants and lack of increased efficacy. Duloxetine appears less tolerable than some other antidepressants. Generic duloxetine became available in 2013.
Duloxetine is more effective than placebo in the treatment of generalized anxiety disorder (GAD). A review from the Annals of Internal Medicine lists duloxetine among the first line drug treatments along with citalopram, escitalopram, sertraline, paroxetine, and venlafaxine.
Duloxetine was approved for the pain associated with diabetic peripheral neuropathy (DPN), based on the positive results of two clinical trials. The average daily pain was measured using an 11-point scale, and duloxetine treatment resulted in an additional 1–1.7 points decrease of pain as compared with placebo. At least 50% pain relief was achieved in 40–45% of the duloxetine patients vs. 20–22% of placebo patients. Pain decreased by more than 90%, in 9–14% of duloxetine patients vs. 2–4% of placebo patients. Most of the response was achieved in the first two weeks on the medication. Duloxetine slightly increased the fasting serum glucose; this effect was deemed to be of “minimal clinical significance”, however.
The comparative efficacy of duloxetine and established pain-relief medications for DPN is unclear. A systematic review noted that tricyclic antidepressants (imipramine and amitriptyline), traditional anticonvulsants and opioids have better efficacy than duloxetine. Duloxetine, tricyclic antidepressants and anticonvulsants have similar tolerability while the opioids caused more side effects. Another review in Prescrire International considered the moderate pain relief achieved with duloxetine to be clinically insignificant and the results of the clinical trials unconvincing. The reviewer saw no reason to prescribe duloxetine in practice. The comparative data collected by reviewers in BMC Neurology indicated that amitriptyline, other tricyclic antidepressants and venlafaxine may be more effective. The authors noted that the evidence in favor of duloxetine is much more solid, however. A Cochrane review concluded that the evidence in support of duloxetine’s efficacy in treating painful diabetic neuropathy was adequate, and that further trials should focus on comparisons with other medications. A crossover trial found that duloxetine, pregabalin, and amitripyline offered similar levels of pain relief. Combination treatment of duloxetine and pregabalin offered additional pain relief for people whose pain is not adequately controlled with one medication, and was safe.
A review of duloxetine found that it reduced pain and fatigue, and improved physical and mental performance compared to placebo.
The U.S. Food and Drug Administration (FDA) approved the drug for the treatment of fibromyalgia in June 2008.
It may be useful for chronic pain from osteoarthritis.
On 4 November 2010, the U.S. Food and Drug Administration (FDA) approved duloxetine to treat chronic musculoskeletal pain, including discomfort from osteoarthritis and chronic lower back pain.
Duloxetine failed to receive US approval for stress urinary incontinence amid concerns over liver toxicity and suicidal events; it was approved for this use in the UK, however, where it is recommended as an add-on medication in stress urinary incontinence instead of surgery.
The safety and utility of duloxetine in the treatment of incontinence has been evaluated in a series of meta analyses and practice guidelines.
The following contraindications are listed by the manufacturer:
In addition, the FDA has reported on life-threatening drug interactions that may be possible when co-administered with triptans and other drugs acting on serotonin pathways leading to increased risk for serotonin syndrome.
Nausea, somnolence, insomnia, and dizziness are the main side effects, reported by about 10% to 20% of patients.
In a trial for major depressive disorder (MDD), the most commonly reported treatment-emergent adverse events among duloxetine-treated patients were nausea (34.7%), dry mouth (22.7%), headache (20.0%) and dizziness (18.7%), and except for headache, these were reported significantly more often than in the placebo group. In a long-term study of fibromyalgia patients receiving duloxetine, frequency and type of adverse effects was similar to that reported in the MDD trial above. Side effects tended to be mild-to-moderate, and tended to decrease in intensity over time.
In four clinical trials of duloxetine for the treatment of MDD, sexual dysfunction occurred significantly more frequently in patients treated with duloxetine than those treated with placebo, and this difference occurred only in men. Specifically, common side effects include difficulty becoming aroused, lack of interest in sex, and anorgasmia (trouble achieving orgasm). Loss of or decreased response to sexual stimuli and ejaculatory anhedonia are also reported. Frequency of treatment-emergent sexual dysfunction were similar for duloxetine and SSRIs when compared in a 6-month observational study in depressed patients. Rates of sexual dysfunction in MDD patients treated with duloxetine vs escitalopram did not differ significantly at 4, 8, and 12 weeks of treatment, although the trend favored duloxetine (33.3% of duloxetine patients experienced sexual side effects compared to 43.6% of those receiving escitalopram and 25% of those receiving placebo).
During marketing of other SSRIs and SNRIs, there have been spontaneous reports of adverse events occurring upon discontinuation of these drugs, particularly when abrupt, including the following: dysphoric mood, irritability, agitation, dizziness, sensory disturbances (e.g., paresthesias such as brain zap electric shock sensations), anxiety, confusion, headache, lethargy, emotional lability, insomnia, hypomania, tinnitus, and seizures. The withdrawal syndrome from duloxetine resembles the SSRI discontinuation syndrome.
When discontinuing treatment with duloxetine, the manufacturer recommends a gradual reduction in the dose, rather than abrupt cessation, whenever possible. If intolerable symptoms occur following a decrease in the dose or upon discontinuation of treatment, then resuming the previously prescribed dose may be considered. Subsequently, the physician may continue decreasing the dose but at a more gradual rate.
In placebo-controlled clinical trials of up to nine weeks’ duration of patients with MDD, a systematic evaluation of discontinuation symptoms in patients taking duloxetine following abrupt discontinuation found the following symptoms occurring at a rate greater than or equal to 2% and at a significantly higher rate in duloxetine-treated patients compared to those discontinuing from placebo: dizziness, nausea, headache, paresthesia, vomiting, irritability, and nightmare.
In 2012 The Institute for Safe Medical Practices (ISMP) published a report: “Duloxetine and Serious Withdrawal Symptoms”. The report highlights early clinical studies which found “abrupt discontinuation showed that withdrawal effects occurred in 40-50% of patients, that 10% of those were severe and approximately half were not resolved when side effects monitoring had ended after one or two weeks”.
Withdrawal symptoms listed in 48 case reports (in the first quarter of 2012) included anger, crying, dizziness and suicidal ideation.
The report concluded there was insufficient information and a lack of clear warnings about the effects of discontinuing Duloxetine and that in many cases withdrawal symptoms may be “severe, persistent, or both”, adding “the prescribing information for physicians and pharmacists does not provide realistic schedules for tapering or a clear picture of the likely incidence of these reactions”.
In the United States all antidepressants, including duloxetine carry a black box warning stating that antidepressants may increase the risk of suicide in persons younger than 25. This warning is based on statistical analyses conducted by two independent groups of the FDA experts that found a 2-fold increase of the suicidal ideation and behavior in children and adolescents, and 1.5-fold increase of suicidality in the 18–24 age group.
To obtain statistically significant results the FDA combined the results of 295 trials of 11 antidepressants for psychiatric indications. As suicidal ideation and behavior in clinical trials are rare, the results for any drug taken separately usually do not reach statistical significance.
In 2005, the United States FDA released a public health advisory noting that there had been eleven reports of suicide attempts and three reports of suicidality within the mostly middle-aged women participating in the open label extension trials of duloxetine for the treatment of stress urinary incontinence (SUI). The FDA described the potential role of confounding social stressors “unclear”. The suicide attempt rate in the SUI study population (based on 9,400 patients) was calculated to be 400 per 100,000 person years. This rate is greater than the suicide attempt rate among middle-aged U.S. women that has been reported in published studies, i.e., 150 to 160 per 100,000 person years. In addition, one death from suicide was reported in a Cymbalta clinical pharmacology study in a healthy female volunteer without SUI. No increase in suicidality was reported in controlled trials of Cymbalta for depression or diabetic neuropathic pain.
Reported adverse events that were temporally correlated to duloxetine therapy include rash, reported rarely, and the following adverse events, reported very rarely: alanine aminotransferase increased, alkaline phosphatase increased, anaphylactic reaction, angioneurotic edema, aspartate aminotransferase increased, bilirubin increased, glaucoma, hepatotoxicity, hyponatremia, jaundice, orthostatic hypotension (especially at the initiation of treatment), Stevens–Johnson syndrome, syncope (especially at initiation of treatment), and urticaria.
Duloxetine inhibits the reuptake of serotonin and norepinephrine (NE) in the central nervous system. Duloxetine increases dopamine (DA) specifically in the prefrontal cortex, where there are few DA reuptake pumps, via the inhibition of NE reuptake pumps (NET), which is believed to mediate reuptake of DA and NE. Duloxetine has no significant affinity for dopaminergic, cholinergic, histaminergic, opioid, glutamate, and GABA reuptake transporters, however, and can therefore be considered to be a selective reuptake inhibitor at the 5-HT and NE transporters. Duloxetine undergoes extensive metabolism, but the major circulating metabolites do not contribute significantly to the pharmacologic activity.
In vitro binding studies using synaptosomal preparations isolated from rat cerebral cortex indicated that duloxetine was approximately 3 fold more potent at inhibiting serotonin uptake than norepinephrine uptake.
Major depressive disorder is believed to be due in part to an increase in pro-inflammatory cytokines within the central nervous system. Antidepressants including ones with a similar mechanism of action as duloxetine, i.e. serotonin metabolism inhibition, cause a decrease in proinflammatory cytokine activity and an increase in anti-inflammatory cytokines; this mechanism may apply to duloxetine in its effect on depression but research on cytokines specific to duloxetine therapy is lacking.
The analgesic properties of duloxetine in the treatment of diabetic neuropathy and central pain syndromes such as fibromyalgia are believed to be due to sodium ion channel blockade.
Absorption: Duloxetine is acid labile, and is formulated with enteric coating to prevent degradation in the stomach. Duloxetine has good oral bioavailability, averaging 50% after one 60 mg dose. There is an average 2-hour lag until absorption begins with maximum plasma concentrations occurring about 6 hours post dose. Food does not affect the Cmax of duloxetine, but delays the time to reach peak concentration from 6 to 10 hours.
Distribution: Duloxetine is highly bound (>90%) to proteins in human plasma, binding primarily to albumin and α1-acid glycoprotein. Volume of distribution is 1640L.
Metabolism: Duloxetine undergoes predominately hepatic metabolism via two cytochrome P450 isozymes, CYP2D6 and CYP1A2. Circulating metabolites are pharmacologically inactive. Duloxetine is a moderate CYP2D6 inhibitor.
Elimination: Administered in healthy young male subjects at doses between 20 and 40 mg twice a day, had a half-life of 12.5 hours and its pharmacokinetics are dose proportional over the therapeutic range. Steady-state is usually achieved after 3 days. Only trace amounts (<1%) of unchanged duloxetine are present in the urine and most of the dose (approx. 70%) appears in the urine as metabolites of duloxetine with about 20% excreted in the feces.
Smoking is associated with a decrease in duloxetine concentration.
Duloxetine was created by Eli Lilly and Company researchers. David Robertson; David Wong, a co-discoverer of fluoxetine; and Joseph Krushinski are listed as inventors on the patent application filed in 1986 and granted in 1990. The first publication on the discovery of the racemic form of duloxetine known as LY227942, was made in 1988. The (+)-enantiomer, assigned LY248686, was chosen for further studies, because it inhibited serotonin reuptake in rat synaptosomes to twice the degree of the (–)-enantiomer. This molecule was subsequently named duloxetine.
In 2001, Lilly filed a New Drug Application (NDA) for duloxetine with the US Food and Drug Administration. In 2003, however, the FDA “recommended this application as not approvable from the manufacturing and control standpoint” because of “significant cGMP (current Good Manufacturing Practice) violations at the finished product manufacturing facility” of Eli Lilly in Indianapolis. Additionally, “potential liver toxicity” and QTc interval prolongation appeared as a concern. The FDA experts concluded that “duloxetine can cause hepatotoxicity in the form of transaminase elevations. It may also be a factor in causing more severe liver injury, but there are no cases in the NDA database that clearly demonstrate this. Use of duloxetine in the presence of ethanol may potentiate the deleterious effect of ethanol on the liver.” The FDA also recommended “routine blood pressure monitoring”, since there was a dose-dependant increase in elevated blood pressure readings, including at the new highest recommended dose of 120 mg “where 24% of patients had one or more blood pressure readings of 140/90 vs. 9% of placebo patients.”
After the manufacturing issues were resolved, the liver toxicity warning included in the prescribing information, and the follow-up studies showed that duloxetine does not cause QTc interval prolongation, duloxetine was approved by the FDA for depression and diabetic neuropathy in 2004. In 2007, Health Canada approved duloxetine for the treatment of depression and diabetic peripheral neuropathic pain.
Duloxetine was approved for use of stress urinary incontinence (SUI) in the EU in 2004. In 2005, Lilly withdrew the duloxetine application for stress urinary incontinence (SUI) in the U.S., stating that discussions with the FDA indicated “the agency is not prepared at this time to grant approval … based on the data package submitted.” A year later Lilly abandoned the pursuit of this indication in the U.S. market.
The FDA approved duloxetine for the treatment of generalized anxiety disorder in February 2007.
Cymbalta generated sales of nearly US$5 billion in 2012, with US$4 billion of that in the U.S., but its patent protection terminated 1 January 2014. Lilly received a six-month extension beyond 30 June 2013, after testing for the treatment of depression in adolescents, which may produce US$1.5 billion in added sales.
The first generic duloxetine was marketed by Indian pharmaceutical company Dr. Reddy’s Laboratories.
Research has found that anxiety is one of the leading symptoms created by marijuana in users, and that there is a correlation between cymbalta and Weed and an increase in anxiety.
Anyone mixing cymbalta and weed is likely to experience side effects. This happens with all medications whether weed or cymbalta is mixed with them. Side effects can be harmful when mixing cymbalta and weed. Doctors are likely to refuse a patient a cymbalta 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 cymbalta 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 cymbalta 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 cymbalta. 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, cymbalta and Weed, dol not interact is wrong. There will always be an interaction between cymbalta 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 cymbalta and Weed is Scromiting. This condition, reportedly caused by mixing cymbalta 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 cymbalta 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 cymbalta and weed can cause health issues the more a person consumes it.
How does Weed effect the potency of cymbalta?
The way in which the body absorbs and process cymbalta may be affected by weed. Therefore, the potency of the cymbalta may be less effective. Marijuana inhibits the metabolization of cymbalta. Not having the right potency of cymbalta means a person may either have a delay in the relief of their underlying symptoms.
A person seeking cymbalta 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 cymbalta 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 cymbalta and Weed
Many individuals may not realize that there are side effects and consequences to mixing cymbalta 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 cymbalta and Weed due to the chances of mild, moderate and severe side effects. If you are having an adverse reaction from mixing cymbalta and Weed it’s imperative that you head to your local emergency room. Even mixing a small amount of cymbalta and Weed is not recommended.
Taking cymbalta and Weed together
People who take cymbalta and Weed together will experience the effects of both substances. Technically, the specific effects and reactions that occur due to frequent use of cymbalta and weed depend on whether you consume more weed in relation to cymbalta or more cymbalta in relation to weed.
The use of significantly more weed and cymbalta 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 cymbalta may experience effects such as:
- reduced motor reflexes from cymbalta and Weed
- dizziness from Weed and cymbalta
- nausea and vomiting due to cymbalta and Weed
Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and cymbalta leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.
Mixing weed and cymbalta
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 cymbalta this primary effect is exaggerated, increasing the strain on the body with unpredictable results.
Weed and cymbalta affects dopamine levels in the brain, causing the body both mental and physical distress. Larger amounts of cymbalta and weed have a greater adverse effect yet leading medical recommendation is that smaller does of cymbalta can be just as harmful and there is no way of knowing exactly how cymbalta and weed is going to affect an individual before they take it.
Taking cymbalta and weed together
People who take cymbalta and weed together will experience the effects of both substances. The use of significantly more cymbalta 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 cymbalta may experience effects such as:
- reduced motor reflexes from cymbalta and weed
- dizziness from weed and cymbalta
- nausea and vomiting of the cymbalta
Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and cymbalta leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.
Weed Vs cymbalta
Taking cymbalta in sufficient quantities increases the risk of a heart failure. Additionally, people under the influence of cymbalta and weed may have difficulty forming new memories. With weed vs cymbalta in an individual’s system they become confused and do not understand their environment. Due to the synergistic properties of cymbalta when mixed with weed it can lead to confusion, anxiety, depression and other mental disorders. Chronic use of cymbalta 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/.
cymbalta Vs Weed
Studies investigating the effects of drugs such as cymbalta and weed have shown that the potential for parasomnia (performing tasks in sleep) is dramatically increased when cymbalta 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 cymbalta together.
When a small to medium amount of weed is combined with cymbalta, 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 cymbalta.
How long after taking cymbalta can I smoke weed or take edibles?
To avoid any residual toxicity it is advisable to wait until the cymbalta has totally cleared your system before taking weed, even in small quantities.
Overdose on cymbalta and weed
In the case of Overdose on cymbalta or if you are worried after mixing cymbalta 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 cymbalta or mixed weed with cymbalta 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 cymbalta and weed in their system.
Mixing cymbalta and weed and antidepressants
Weed users feeling depressed and anxious may be prescribed antidepressant medication. There are some antidepressant users who also use cymbalta and weed. These individuals may not realize that there are side effects and consequences to consuming both cymbalta, marijuana and a range of antidepressants.
Studies on weed, cymbalta 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 cymbalta
A lot of people suffer from depression caused by weed and cymbalta. 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 cymbalta and weed
Quitting weed to take cymbalta
Medical professionals say an individual prescribed or taking cymbalta 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 cymbalta.
A person beginning to use cymbalta 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 cymbalta can affect a person in various ways. Different types of marijuana produce different side effects. Side effects of weed and cymbalta 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 cymbalta 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 cymbalta 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 cymbalta 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 cymbalta.
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/