brintellix and Weed

{Fulldrug} and Weed

Authored by Pin Ng PhD

Edited by Hugh Soames

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brintellix 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 brintellix. 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 brintellix and Weed.


Mixing brintellix and Weed


Vortioxetine, sold under the brand names Trintellix and Brintellix among others, is a medication used to treat major depressive disorder. Its effectiveness is viewed as similar to that of other antidepressants. It is taken by mouth.

Common side effects include nausea, vomiting, constipation, and sexual dysfunction. Serious side effects may include suicide in those under the age of 25, serotonin syndrome, bleeding, mania, and SIADH. A withdrawal syndrome may occur if the medication is abruptly stopped or the dose is decreased. Use during pregnancy and breastfeeding is not generally recommended. It is classified as a serotonin modulator and stimulator. How it works is not entirely clear but is believed to be related to increasing serotonin levels and possibly interacting with certain receptors for serotonin.

It was approved for medical use in the United States in 2013. In 2020, it was the 243rd most commonly prescribed medication in the United States, with more than 1 million prescriptions.

Vortioxetine is used as a treatment for major depressive disorder. Effectiveness appears to be similar to other antidepressants and in terms of effect size has been described as modest. Vortioxetine may be used when other treatments have failed. A 2017 Cochrane review on vortioxetine determined that the place for it in the treatment of severe depression is unclear due to low-quality evidence and that more study is needed comparing vortioxetine to selective serotonin reuptake inhibitors (SSRIs) which are typical first-line treatments.

Vortioxetine is also used off-label for anxiety. A 2016 review found it was not useful in generalized anxiety disorder at 2.5, 5, and 10 mg doses (15 and 20 mg doses were not tested). A 2019 meta-analysis found that vortioxetine did not produce statistically significant results over placebo in the symptoms, quality of life and remission rates of generalized anxiety disorder, but it was well-tolerated. However, a 2018 meta-analysis supported use and efficacy of vortioxetine for generalized anxiety disorder, though stated that more research was necessary to strengthen the evidence. A 2021 systematic review and meta-analysis concluded that there was uncertainty about the effectiveness of vortioxetine for anxiety due to existing evidence being very low-quality. In a 2020 network meta-analysis of randomized controlled trials, vortioxetine was associated with among the lowest remission rates for generalized anxiety disorder of the included medications (odds ratio = 1.30 for vortioxetine, range of odds ratios for other agents = 1.13–2.70).

Vortioxetine is contraindicated in those taking monoamine oxidase inhibitors (MAOIs) due to the possibility of serotonin syndrome.

The most common side effects reported with vortioxetine are nausea, vomiting, constipation, and sexual dysfunction, among others. With the exceptions of nausea and sexual dysfunction, these side effects were reported by less than or equal to 10% of study participants given vortioxetine. Significant percentages of placebo-treated participants also report these side effects. Discontinuation of treatment due to adverse effects in clinical trials was 8% with vortioxetine versus 3% with placebo.

Sexual dysfunction, such as decreased libido, abnormal orgasm, delayed ejaculation, and erectile dysfunction, are well-known side effects of SSRIs and serotonin–norepinephrine reuptake inhibitors (SNRIs). In clinical trials, sexual dysfunction occurred more often with vortioxetine than with placebo and appeared to be dose-dependent. The specific incidences[spelling?] of treatment-emergent sexual dysfunction as measured with the Arizona Sexual Experience Scale (ASEX) were 14 to 20% for placebo and 16 to 34% for vortioxetine over a dosage range of 5 to 20 mg/day. The incidence of sexual dysfunction with vortioxetine was similar to that with the SNRI duloxetine, which had an incidence of 26 to 28% at the used dosage of 60 mg/day. However, treatment-emergent sexual dysfunction caused by a prior SSRI was better improved by switching to vortioxetine than by switching to the SSRI escitalopram. In another study, vortioxetine at a dosage of 10 mg/day though not at 20 mg/day produced less sexual dysfunction than the SSRI paroxetine. These findings suggest that although vortioxetine can still cause sexual dysfunction itself, it may cause somewhat less sexual dysfunction than SSRIs and might be a useful alternative option for people experiencing sexual dysfunction with these medications. The rates of voluntarily or spontaneously reported sexual dysfunction with vortioxetine are much lower than with the ASEX, ranging from <1 to 5% for vortioxetine versus <1 to 2% for placebo in clinical trials.

Significant changes in body weight (gain or loss) were not observed with vortioxetine in clinical trials. However reports have come in from users regarding weight gain/loss since the approval of Vortioxetine.

Vortioxetine might cause less emotional blunting than SSRIs and SNRIs based on a couple of preliminary clinical studies.

If vortioxetine is used in combination with other serotonergic drugs like MAOIs or SSRIs, this may result in serotonin syndrome.

Vortioxetine is metabolized primarily by the cytochrome P450 enzyme CYP2D6. Inhibitors and inducers of CYP2D6 may modify the pharmacokinetics of vortioxetine and necessitate dosage adjustments.

Bupropion, a strong CYP2D6 inhibitor, has been found to increase peak levels of vortioxetine by 2.1-fold and total vortioxetine levels by 2.3-fold (bupropion dosed at 300 mg/day and vortioxetine dosed at 10 mg/day). The incidence of side effects with vortioxetine, like nausea, headache, vomiting, and insomnia, was correspondingly increased with the combination. Other strong CYP2D6 inhibitors, like fluoxetine, paroxetine, and quinidine, may have similar influences on the pharmacokinetics of vortioxetine, and it is recommended that the dosage of vortioxetine be reduced by half when it is administered in combination with such medications. Lesser interactions have additionally been identified for vortioxetine with the cytochrome P450 inhibitors ketoconazole and fluconazole.

Rifampicin, a strong and broad cytochrome P450 inducer (though notably not of CYP2D6), has been found to decrease peak levels of vortioxetine by 51% and total levels of vortioxetine by 72% (rifampicin dosed at 600 mg/day and vortioxetine at 20 mg/day). Similar influences on vortioxetine pharmacokinetics may also occur with other strong cytochrome P450 inducers like carbamazepine and phenytoin. As such, it is recommended that increasing vortioxetine dosage be considered when it is given in combination with strong cytochrome P450 inducers. The maximum recommended dose should not exceed three times the original vortioxetine dose.

Vortioxetine and its metabolites show no meaningful interactions with a variety of assessed cytochrome P450 enzymes and transporters (e.g., P-glycoprotein) and hence vortioxetine is not expected to importantly influence the pharmacokinetics of other medications.

The combination of vortioxetine with MAOIs, including other MAOIs like linezolid and intravenous methylene blue, may cause serotonin syndrome and is contraindicated. The risk of serotonin syndrome may also be increased when vortioxetine is combined with other serotonergic drugs, like SSRIs, SNRIs, tricyclic antidepressants (TCAs), triptans, tramadol, tryptophan, buspirone, St John’s wort, fentanyl, and lithium, among others. However, vortioxetine is not considered to be contraindicated with serotonergic medications besides MAOIs.

Vortioxetine increases serotonin concentrations in the brain by inhibiting its reuptake in the synapse, and also modulates (activates or blocks) certain serotonin receptors. This puts it in the class of serotonin modulators and stimulators, which also includes vilazodone. More specifically, vortioxetine is a serotonin reuptake inhibitor, agonist of the serotonin 5-HT1A receptor, partial agonist of the 5-HT1B receptor, and antagonist of the serotonin 5-HT1D, 5-HT3, and 5-HT7 receptors, as well as an apparent ligand of the β1-adrenergic receptor. In terms of functional activity however, vortioxetine appears to be much more potent on serotonin reuptake inhibition and 5-HT3 receptor antagonism than for its interactions with the other serotonin receptors. Whereas vortioxetine has IC50 or EC50 values of 5.4 nM for the SERT and 12 nM for the 5-HT3 receptor, its values are 120 to 450 nM for the 5-HT1A, 5-HT1B, 5-HT1D, and 5-HT7 receptors. This translates to about 22- to 83-fold selectivity for SERT inhibition and 10- to 38-fold selectivity for 5-HT3 antagonism over activities at the other serotonin receptors. 5-HT3 antagonism appears to have a better effect on REM sleep compared to Paroxetine.

It has been claimed that the serotonin transporter (SERT) and 5-HT3 receptor may be primarily occupied at lower clinical doses of vortioxetine and that the 5-HT1B, 5-HT1A, and 5-HT7 receptors may additionally be occupied at higher doses. Occupancy of the serotonin transporter with vortioxetine in young men was found to be highest in the raphe nucleus with median occupancies of 25%, 53%, and 98% after 9 days of administration with 2.5, 10, and 60 mg/day vortioxetine. In another study, serotonin transporter occupancy in men was 50%, 65%, and ≥80% for 5, 10, and 20 mg/day vortioxetine.

Based on its clinical efficacy (e.g., at 5 mg/day), it appears that vortioxetine may produce antidepressant effects at SERT occupancy as low as 50%. This is in apparent contrast to SSRIs and SNRIs, which appear to require a minimum of 70 to 80% occupancy for antidepressant efficacy. These findings are suggestive that the antidepressant effects of vortioxetine may be mediated by serotonin receptor interactions in addition to serotonin reuptake inhibition. A study found no significant occupancy of the 5-HT1A receptor with vortioxetine at 30 mg/day for 9 days, which suggests that at least this specific serotonin receptor may not be involved in the clinical pharmacology of vortioxetine. However, methodological concerns were noted that may limit the interpretability of this result. Occupancy of other serotonin receptors like 5-HT3 and 5-HT7 by vortioxetine in humans does not seem to have been studied. In relation to the preceding, the contribution of serotonin receptor interactions to the antidepressant effects of vortioxetine is unknown and remains to be established. Uncertainties remain about whether vortioxetine is indeed a clinically multimodal antidepressant or whether it is effectively ” another selective serotonin reuptake inhibitor”.

Antagonism of the 5-HT3 receptor has been found to enhance the increase in brain serotonin levels produced by serotonin reuptake inhibition in animal studies. Whether or not the 5-HT3 receptor antagonism of vortioxetine likewise does this in humans or contributes to its clinical antidepressant efficacy is unclear. SSRIs and 5-HT1A receptor agonists often produce nausea as a side effect, whereas 5-HT3 receptor antagonists like ondansetron are antiemetics and have been found to be effective in treating SSRI-induced nausea. It was thought that the 5-HT3 receptor antagonism of vortioxetine would reduce the incidence of nausea relative to SSRIs. However, clinical trials found significant and dose-dependent rates of nausea with vortioxetine that appeared to be comparable to those found with the SNRI duloxetine.

Vortioxetine is well-absorbed when taken orally and has an oral bioavailability of 75%. It is systemically detectable after a single oral dose by 0.781 hours. Peak levels of vortioxetine are reached within 7 to 11 hours post-dose with single or multiple doses. Steady-state levels of vortioxetine are generally reached within 2 weeks of administration, with 90% of individuals reaching 90% of steady state after 12 days of administration. Steady-state peak levels of vortioxetine with doses of 5, 10, and 20 mg/day were 9, 18, and 33 ng/mL, respectively. The accumulation index of vortioxetine (area-under-the-curve levels after a single dose versus at steady state) is 5 to 6. A loading dose given intravenously has been found to achieve steady-state levels more rapidly with oral vortioxetine therapy. The pharmacokinetics of vortioxetine are known to be linear and dose proportional over a range of 2.5 to 75 mg for single doses and 2.5 to 60 mg for multiple doses. Food has no influence on the pharmacokinetics of vortioxetine.

The apparent volume of distribution of vortioxetine is large and ranges from 2,500 to 3,400 L after single or multiple doses of 5 to 20 mg vortioxetine, with extensive extravascular distribution. The plasma protein binding of vortioxetine is approximately 98 or 99%, with about 1.25 ± 0.48% free or unbound.

Vortioxetine is extensively metabolized by oxidation via cytochrome P450 enzymes and subsequent glucuronidation via UDP-glucuronosyltransferase. CYP2D6 is the primary enzyme involved in the metabolism of vortioxetine, but others including CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, and CYP3A4/5 are also involved. It is also metabolized by alcohol dehydrogenase, aldehyde dehydrogenase, and aldehyde oxidase. Six metabolites of vortioxetine have been identified. The major metabolite of vortioxetine (Lu AA34443) is inactive and its minor active metabolite (Lu AA39835) is not thought to cross the blood–brain barrier. The remaining metabolites are glucuronide conjugates. Hence, vortioxetine itself is thought to be primarily responsible for its pharmacological activity.

The estimated total clearance of vortioxetine ranges from 30 to 41 L/h. The elimination half-life of vortioxetine is 66 hours, with a range of 59 to 69 hours after single or multiple doses. Elimination of vortioxetine is almost entirely via the liver (99%) rather than the kidneys (<1%). Approximately 85% of vortioxetine was recovered in a single-dose excretion study after 15 days, with 59% in urine and 26% in feces.

Genetic variations in cytochrome P450 enzymes can influence exposure to vortioxetine. CYP2D6 extensive metabolizers have approximately 2-fold higher clearance of vortioxetine than CYP2D6 poor metabolizers. The estimated clearance rates were 52.9, 34.1, 26.6, and 18.1 L/h for CYP2D6 ultra-rapid metabolizers, extensive metabolizers, intermediate metabolizers, and poor metabolizers. Area-under-the-curve levels of vortioxetine were 35.5% lower in CYP2D6 ultra-rapid metabolizers than in extensive metabolizers, though with significant overlap due to interindividual variability. Dosage adjustment for CYP2D6 ultra-rapid metabolizers is considered to not be necessary. Vortioxetine exposure in CYP2D6 poor metabolizers is expected to be approximately twice as high as in extensive metabolizers. Depending on the individual response, dosage adjustment may be considered for CYP2D6 poor metabolizers, with a maximum recommended dosage of 10 mg/day for known such individuals. In addition to CYP2D6, CYP2C19 extensive metabolizers have 1.4-fold higher clearance of vortioxetine than poor metabolizers. However, this is not considered to be clinically important and dose adjustment is not considered to be necessary based on CYP2C19 status.

Vortioxetine (1-[2-(2,4-dimethylphenylsulfanyl)phenyl]piperazine) is a bis-aryl-sulfanyl amine as well as piperazine derivative. The acid dissociation constant (pKa) values for vortioxetine hydrobromide were determined to be 9.1 (± 0.1) and 3.0 (± 0.2) according to an Australian Public Assessment Report.

Vortioxetine was discovered by scientists at Lundbeck who reported the rationale and synthesis for the drug (then called Lu AA21004) in a 2011 paper.

In 2007, the compound was in Phase II clinical trials, and Lundbeck and Takeda entered into a partnership in which Takeda paid Lundbeck $40 million up-front, with promises of up to $345 million in milestone payments, and Takeda agreed to pay most of the remaining cost of developing the drug. The companies agreed to co-promote the drug in the US and Japan, and that Lundbeck would receive a royalty on all such sales. The deal included another drug candidate, tedatioxetine (Lu AA24530), and could be expanded to include two other Lundbeck compounds.

Vortioxetine was approved by the U.S. Food and Drug Administration (FDA) for the treatment of major depressive disorder (MDD) in adults in September 2013, and it was approved in the European Union later that year.

It is made by the pharmaceutical companies Lundbeck and Takeda.

Vortioxetine was previously sold under the brand name Brintellix in the United States, but in May 2016, the US Food and Drug Administration (FDA) approved a name change to Trintellix in order to avoid confusion with the blood-thinning medication Brilinta (ticagrelor). In India, it is sold under the name Vantaxa.

Vortioxetine was under development for the treatment of generalized anxiety disorder and attention-deficit hyperactivity disorder (ADHD) but development for these indications was discontinued. As of August 2021, vortioxetine remains in development for the treatment of anxiety disorders, binge-eating disorder, and bipolar disorder. It is in phase II clinical trials for these indications. There is also interest in vortioxetine for the potential treatment of social phobia, neuropathic pain, and for cognitive enhancement in major depression.


Research has found that anxiety is one of the leading symptoms created by marijuana in users, and that there is a correlation between brintellix and Weed and an increase in anxiety.


Anyone mixing brintellix and weed is likely to experience side effects. This happens with all medications whether weed or brintellix is mixed with them. Side effects can be harmful when mixing brintellix and weed. Doctors are likely to refuse a patient a brintellix 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 brintellix 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 brintellix 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 brintellix. 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, brintellix and Weed, dol not interact is wrong. There will always be an interaction between brintellix 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


One of the milder side effects of mixing brintellix and Weed is Scromiting. This condition, reportedly caused by mixing brintellix 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 brintellix 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 brintellix and weed can cause health issues the more a person consumes it.


How does Weed effect the potency of brintellix?


The way in which the body absorbs and process brintellix may be affected by weed. Therefore, the potency of the brintellix may be less effective. Marijuana inhibits the metabolization of brintellix. Not having the right potency of brintellix means a person may either have a delay in the relief of their underlying symptoms.


A person seeking brintellix 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 brintellix 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 brintellix and Weed


Many individuals may not realize that there are side effects and consequences to mixing brintellix 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 brintellix and Weed due to the chances of mild, moderate and severe side effects. If you are having an adverse reaction from mixing brintellix and Weed it’s imperative that you head to your local emergency room. Even mixing a small amount of brintellix and Weed is not recommended.


Taking brintellix and Weed together


People who take brintellix and Weed together will experience the effects of both substances. Technically, the specific effects and reactions that occur due to frequent use of brintellix and weed depend on whether you consume more weed in relation to brintellix or more brintellix in relation to weed.


The use of significantly more weed and brintellix 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 brintellix may experience effects such as:


  • reduced motor reflexes from brintellix and Weed
  • dizziness from Weed and brintellix
  • nausea and vomiting due to brintellix and Weed


Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and brintellix leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.

Mixing weed and brintellix


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 brintellix this primary effect is exaggerated, increasing the strain on the body with unpredictable results.


Weed and brintellix affects dopamine levels in the brain, causing the body both mental and physical distress. Larger amounts of brintellix and weed have a greater adverse effect yet leading medical recommendation is that smaller does of brintellix can be just as harmful and there is no way of knowing exactly how brintellix and weed is going to affect an individual before they take it.


Taking brintellix and weed together


People who take brintellix and weed together will experience the effects of both substances. The use of significantly more brintellix 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 brintellix may experience effects such as:


  • reduced motor reflexes from brintellix and weed
  • dizziness from weed and brintellix
  • nausea and vomiting of the brintellix


Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and brintellix leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.

Weed Vs brintellix


Taking brintellix in sufficient quantities increases the risk of a heart failure. Additionally, people under the influence of brintellix and weed may have difficulty forming new memories. With weed vs brintellix in an individual’s system they become confused and do not understand their environment. Due to the synergistic properties of brintellix when mixed with weed it can lead to confusion, anxiety, depression and other mental disorders. Chronic use of brintellix 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


brintellix Vs Weed


Studies investigating the effects of drugs such as brintellix and weed have shown that the potential for parasomnia (performing tasks in sleep) is dramatically increased when brintellix 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 brintellix together.


When a small to medium amount of weed is combined with brintellix, 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 brintellix.


How long after taking brintellix can I smoke weed or take edibles?


To avoid any residual toxicity it is advisable to wait until the brintellix has totally cleared your system before taking weed, even in small quantities.


Overdose on brintellix and weed


In the case of Overdose on brintellix or if you are worried after mixing brintellix 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 brintellix or mixed weed with brintellix 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 brintellix 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 brintellix and weed and antidepressants


Weed users feeling depressed and anxious may be prescribed antidepressant medication. There are some antidepressant users who also use brintellix and weed. These individuals may not realize that there are side effects and consequences to consuming both brintellix, marijuana and a range of antidepressants.


Studies on weed, brintellix 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 brintellix


A lot of people suffer from depression caused by weed and brintellix. 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 brintellix and weed


Quitting weed to take brintellix


Medical professionals say an individual prescribed or taking brintellix 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 brintellix.


A person beginning to use brintellix 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 brintellix can affect a person in various ways. Different types of marijuana produce different side effects. Side effects of weed and brintellix 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 brintellix 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 brintellix 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 brintellix 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 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 brintellix.


If you take brintellix, and also drink Alcohol or MDMA, you can research the effects of brintellix and Alcohol , brintellix and Cocaine as well as brintellix 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.


brintellix and Weed

brintellix and Weed

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  • 1
    1.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
  • 2
    2.G. Lafaye, L. Karila, L. Blecha and A. Benyamina, Cannabis, cannabinoids, and health – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from
  • 3
    3.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