Aldesleukin and Weed

{Fulldrug} and Weed

Authored by Pin Ng PhD

Edited by Hugh Soames

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Aldesleukin 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 Aldesleukin. 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 Aldesleukin and Weed.


Mixing Aldesleukin and Weed


Interleukin-2 (IL-2) is an interleukin, a type of cytokine signaling molecule in the immune system. It is a 15.5–16 kDa protein that regulates the activities of white blood cells (leukocytes, often lymphocytes) that are responsible for immunity. IL-2 is part of the body’s natural response to microbial infection, and in discriminating between foreign (“non-self”) and “self”. IL-2 mediates its effects by binding to IL-2 receptors, which are expressed by lymphocytes. The major sources of IL-2 are activated CD4+ T cells and activated CD8 T cells. Put shortly the function of IL-2 is to stimulate the growth of helper, cytotoxic and regulatory T cells.

IL-2 is a member of a cytokine family, each member of which has a four alpha helix bundle; the family also includes IL-4, IL-7, IL-9, IL-15 and IL-21. IL-2 signals through the IL-2 receptor, a complex consisting of three chains, termed alpha (CD25), beta (CD122) and gamma (CD132). The gamma chain is shared by all family members.

The IL-2 receptor (IL-2R) α subunit binds IL-2 with low affinity (Kd~ 10 M). Interaction of IL-2 and CD25 alone does not lead to signal transduction due to its short intracellular chain but has the ability (when bound to the β and γ subunit) to increase the IL-2R affinity 100-fold. Heterodimerization of the β and γ subunits of IL-2R is essential for signalling in T cells. IL-2 can signalize either via intermediate-affinity dimeric CD122/CD132 IL-2R (Kd~ 10 M) or high-affinity trimeric CD25/CD122/CD132 IL-2R (Kd~ 10−11 M). Dimeric IL-2R is expressed by memory CD8+ T cells and NK cells, whereas regulatory T cells and activated T cells express high levels of trimeric IL-2R.

Instructions to express proteins in response to an IL-2 signal (called IL-2 transduction) can take place via 3 different signaling pathways; they are: (1) the JAK-STAT pathway, (2) the PI3K/Akt/mTOR pathway and (3) the MAPK/ERK pathway. The signalling is commenced by IL-2 binding to its receptor, following which cytoplasmatic domains of CD122 and CD132 heterodimerize. This leads to the activation of Janus kinases JAK1 and JAK3 which subsequently phosphorylate T338 on CD122. This phosphorylation recruits STAT transcription factors, predominantly STAT5, which dimerize and migrate to the cell nucleus where they bind to DNA. with an “express other proteins” signal. The proteins expressed by means of the three pathways include bcl-6 (the PI3K/Akt/mTOR pathway), CD25 & prdm-1 (the JAK-STAT pathway) and certain cyclins (the MAPK/ERK pathway).

Gene expression regulation for IL-2 can be on multiple levels or by different ways. One of the checkpoints (in other words one of the things which needs to be done before IL-2 is expressed) is that there must be signaling through a conjunction of a T Cell Receptor (a TCR) and an HLA-peptide complex. As a result of that conjunction a signalling pathway (signalling a cell’s protein making machinery to express or ‘make’ IL-2), a PhosphoLipase-C (PLC) dependent pathway, is set up. PLC activates 3 major transcription factors and their pathways: NFAT, NFkB and AP-1. In addition and after costimulation from CD28 the optimal activation of expression of IL-2 and these pathways is induced. In summary therefore before a cell will make IL-2 in accordance with this pathway there have to be two reactions: TCR+HLA and protein complex on the one hand and CD28 costimulation on the other indeed mere IL-2 ligation to its receptor is too low affinity to enable pathway.

At the same time Oct-1 is expressed. It helps the activation. Oct1 is expressed in T-lymphocytes and Oct2 is induced after cell activation.

NFAT has multiple family members, all of them are located in cytoplasm and signaling goes through calcineurin, NFAT is dephosphorylated and therefore translocated to the nucleus.

AP-1 is a dimer and is composed of c-Jun and c-Fos proteins. It cooperates with other transcription factors including NFkB and Oct.

NFkB is translocated to the nucleus after costimulation through CD28. NFkB is a heterodimer and there are two binding sites on the IL-2 promoter.

IL-2 has essential roles in key functions of the immune system, tolerance and immunity, primarily via its direct effects on T cells. In the thymus, where T cells mature, it prevents autoimmune diseases by promoting the differentiation of certain immature T cells into regulatory T cells, which suppress other T cells that are otherwise primed to attack normal healthy cells in the body. IL-2 enhances activation-induced cell death (AICD). IL-2 also promotes the differentiation of T cells into effector T cells and into memory T cells when the initial T cell is also stimulated by an antigen, thus helping the body fight off infections. Together with other polarizing cytokines, IL-2 stimulates naive CD4 T cell differentiation into Th1 and Th2 lymphocytes while it impedes differentiation into Th17 and folicular Th lymphocytes.

IL-2 increases the cell killing activity of both natural killer cells and cytotoxic T cells.

Its expression and secretion is tightly regulated and functions as part of both transient positive and negative feedback loops in mounting and dampening immune responses. Through its role in the development of T cell immunologic memory, which depends upon the expansion of the number and function of antigen-selected T cell clones, it plays a key role in enduring cell-mediated immunity.

IL-2 has been discovered in all classes of jawed vertebrates, including sharks, at a similar genomic location. In fish, IL-2 shares a single receptor alpha chain with its related cytokines IL-15 and IL-15-like (IL-15L). This “IL-15Rα” receptor chain is similar to mammalian IL-15Rα, and in tetrapod evolution a duplication of its coding gene plus further diversification created mammalian IL-2Rα. Sequences, and structural analysis of grass carp IL-2, suggest that fish IL-2 binds IL-15Rα in a manner reminiscent of how mammalian IL-15 binds to IL-15Rα.

Despite fish IL-2 and IL-15 sharing the same IL-15Rα chain, the stability of fish IL-2 is independent of it whereas IL-15 and especially IL-15L depend on binding to (co-presentation with) IL-15Rα for their stability and function. This suggests that, like in mammals, fish IL-2, in contrast to fish IL-15 and IL-15L, is not relying on “in trans” presentation by its receptor alpha chain. As a free cytokine, mammalian IL-2 that is secreted by activated T cells is important for a negative feedback loop by the stimulation of regulatory T cells, the latter being the cells with the highest constitutive IL-2Rα (aka CD25) expression. Besides this negative feedback loop, mammalian IL-2 also participates in a positive feedback loop because activated T cells enhance their own IL-2Rα expression. As in mammals, fish IL-2 also stimulates T cell proliferation and appears to preferentially stimulate regulatory T cells. Fish IL-2 induces the expression of cytokines of both type 1 (Th1) and type 2 (Th2) immunity.

As has been found in some studies on mammalian IL-2, data suggest that fish IL-2 can form homodimers and that this is an ancient property of the IL-2/15/15L-family cytokines.

Homologues of IL-2 have not been reported for jawless fish (hagfish and lamprey) or invertebrates.

While the causes of itchiness are poorly understood, some evidence indicates that IL-2 is involved in itchy psoriasis.

Aldesleukin is a form of recombinant interleukin-2. It is manufactured using recombinant DNA technology and is marketed as a protein therapeutic and branded as Proleukin. It has been approved by the Food and Drug Administration (FDA) and in several European countries for the treatment of cancers (malignant melanoma, renal cell cancer) in large intermittent doses and has been extensively used in continuous doses.

Interking is a recombinant IL-2 with a serine at residue 125, sold by Shenzhen Neptunus.

Neoleukin 2/15 is a computationally designed mimic of IL-2 that was designed to avoid common side effects. However, clinical trials into this candidate were discontinued.

Various dosages of IL-2 across the United States and across the world are used. The efficacy and side effects of different dosages is often a point of disagreement.

The commercial interest in local IL-2 therapy has been very low. Because only a very low dose IL-2 is used, treatment of a patient would cost about $ 500 commercial value of the patented IL-2. The commercial return on investment is too low to stimulate additional clinical studies for the registration of intratumoral IL-2 therapy.

Usually, in the U.S., the higher dosage option is used, affected by cancer type, response to treatment and general patient health. Patients are typically treated for five consecutive days, three times a day, for fifteen minutes. The following approximately 10 days help the patient to recover between treatments. IL-2 is delivered intravenously on an inpatient basis to enable proper monitoring of side effects.

A lower dose regimen involves injection of IL-2 under the skin typically on an outpatient basis. It may alternatively be given on an inpatient basis over 1–3 days, similar to and often including the delivery of chemotherapy.

Intralesional IL-2 is commonly used to treat in-transit melanoma metastases and has a high complete response rate.

In preclinical and early clinical studies, local application of IL-2 in the tumor has been shown to be clinically more effective in anticancer therapy than systemic IL-2 therapy, over a broad range of doses, without serious side effects.

Tumour blood vessels are more vulnerable than normal blood vessels to the actions of IL-2. When injected inside a tumor, i.e. local application, a process mechanistically similar to the vascular leakage syndrome, occurs in tumor tissue only. Disruption of the blood flow inside of the tumor effectively destroys tumor tissue.

In local application, the systemic dose of IL-2 is too low to cause side effects, since the total dose is about 100 to 1000 fold lower. Clinical studies showed painful injections at the site of radiation as the most important side effect, reported by patients. In the case of irradiation of nasopharyngeal carcinoma the five-year disease-free survival increased from 8% to 63% by local IL-2 therapy

Systemic IL-2 has a narrow therapeutic window, and the level of dosing usually determines the severity of the side effects. In the case of local IL-2 application, the therapeutic window spans several orders of magnitude.

Some common side effects:

More serious and dangerous side effects sometimes are seen, such as breathing problems, serious infections, seizures, allergic reactions, heart problems, kidney failure or a variety of other possible complications. The most common adverse effect of high-dose IL-2 therapy is vascular leak syndrome (VLS; also termed capillary leak syndrome). It is caused by lung endothelial cells expressing high-affinity IL-2R. These cells, as a result of IL-2 binding, causes increased vascular permeability. Thus, intravascular fluid extravasate into organs, predominantly lungs, which leads to life-threatening pulmonary or brain oedema.

Other drawbacks of IL-2 cancer immunotherapy are its short half-life in circulation and its ability to predominantly expand regulatory T cells at high doses.

Intralesional IL-2 used to treat in-transit melanoma metastases is generally well tolerated. This is also the case for intralesional IL-2 in other forms of cancer, like nasopharyngeal carcinoma.

Eisai markets a drug called denileukin diftitox (trade name Ontak), which is a recombinant fusion protein of the human IL-2 ligand and the diphtheria toxin. This drug binds to IL-2 receptors and introduces the diphtheria toxin into cells that express those receptors, killing the cells. In some leukemias and lymphomas, malignant cells express the IL-2 receptor, so denileukin diftitox can kill them. In 1999 Ontak was approved by the U.S. Food and Drug Administration (FDA) for treatment of cutaneous T cell lymphoma (CTCL).

IL-2 does not follow the classical dose-response curve of chemotherapeutics. The immunological activity of high and low dose IL-2 show sharp contrast. This might be related to different distribution of IL-2 receptors (CD25, CD122, CD132) on different cell populations, resulting in different cells that are activated by high and low dose IL-2. In general high doses are immune suppressive, while low doses can stimulate type 1 immunity. Low-dose IL-2 has been reported to reduce hepatitis C and B infection.

IL-2 has been used in clinical trials for the treatment of chronic viral infections and as a booster (adjuvant) for vaccines. The use of large doses of IL-2 given every 6–8 weeks in HIV therapy, similar to its use in cancer therapy, was found to be ineffective in preventing progression to an AIDS diagnosis in two large clinical trials published in 2009.

More recently low dose IL-2 has shown early success in modulating the immune system in disease like type 1 diabetes and vasculitis. There are also promising studies looking to use low dose IL-2 in ischaemic heart disease.

IL-2 cannot accomplish its role as a promising immunotherapeutic agent due to significant drawbacks which are listed above. Some of the issues can be overcome using IL-2 ic. They are composed of IL-2 and some of its monoclonal antibody (mAb) and can potentiate biologic activity of IL-2 in vivo. The main mechanism of this phenomenon in vivo is due to the prolongation of the cytokine half-life in circulation. Depending on the clone of IL-2 mAb, IL-2 ic can selectively stimulate either CD25 (IL-2/JES6-1 complexes), or CD122high cells (IL-2/S4B6). IL-2/S4B6 immune complexes have high stimulatory activity for NK cells and memory CD8 T cells and they could thus replace the conventional IL-2 in cancer immunotherapy. On the other hand, IL-2/JES6-1 highly selectively stimulate regulatory T cells and they could be potentially useful for transplantations and in treatment of autoimmune diseases.

According to an immunology textbook: “IL-2 is particularly important historically, as it is the first type I cytokine that was cloned, the first type I cytokine for which a receptor component was cloned, and was the first short-chain type I cytokine whose receptor structure was solved. Many general principles have been derived from studies of this cytokine including its being the first cytokine demonstrated to act in a growth factor–like fashion through specific high-affinity receptors, analogous to the growth factors being studied by endocrinologists and biochemists”.: 712 

In the mid-1960s, studies reported “activities” in leukocyte-conditioned media that promoted lymphocyte proliferation.: 16  In the mid-1970s, it was discovered that T-cells could be selectively proliferated when normal human bone marrow cells were cultured in conditioned medium obtained from phytohemagglutinin-stimulated normal human lymphocytes.: 712  The key factor was isolated from cultured mouse cells in 1979 and from cultured human cells in 1980. The gene for human IL-2 was cloned in 1982 after an intense competition.

Commercial activity to bring an IL-2 drug to market was intense in the 1980s and ’90s. By 1983, Cetus Corporation had created a proprietary recombinant version of IL-2 (Aldesleukin, later branded as Proleukin), with the alanine removed from its N-terminal and residue 125 replaced with serine.: 76–77 : 201  Amgen later entered the field with its own proprietary, mutated, recombinant protein and Cetus and Amgen were soon competing scientifically and in the courts; Cetus won the legal battles and forced Amgen out of the field. By 1990 Cetus had gotten aldesleukin approved in nine European countries but in that year, the U.S. Food and Drug Administration (FDA) refused to approve Cetus’ application to market IL-2. The failure led to the collapse of Cetus, and in 1991 the company was sold to Chiron Corporation. Chiron continued the development of IL-2, which was finally approved by the FDA as Proleukin for metastatic renal carcinoma in 1992.

By 1993 aldesleukin was the only approved version of IL-2, but Roche was also developing a proprietary, modified, recombinant IL-2 called teceleukin, with a methionine added at is N-terminal, and Glaxo was developing a version called bioleukin, with a methionine added at is N-terminal and residue 125 replaced with alanine. Dozens of clinical trials had been conducted of recombinant or purified IL-2, alone, in combination with other drugs, or using cell therapies, in which cells were taken from patients, activated with IL-2, then reinfused. Novartis acquired Chiron in 2006 and licensed the US aldesleukin business to Prometheus Laboratories in 2010 before global rights to Proleukin were subsequently acquired by Clinigen in 2018 and 2019.


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


Anyone mixing Aldesleukin and weed is likely to experience side effects. This happens with all medications whether weed or Aldesleukin is mixed with them. Side effects can be harmful when mixing Aldesleukin and weed. Doctors are likely to refuse a patient a Aldesleukin 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 Aldesleukin 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 Aldesleukin 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 Aldesleukin. 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, Aldesleukin and Weed, dol not interact is wrong. There will always be an interaction between Aldesleukin 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 Aldesleukin and Weed is Scromiting. This condition, reportedly caused by mixing Aldesleukin 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 Aldesleukin 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 Aldesleukin and weed can cause health issues the more a person consumes it.


How does Weed effect the potency of Aldesleukin?


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


A person seeking Aldesleukin 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 Aldesleukin 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 Aldesleukin and Weed


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


Taking Aldesleukin and Weed together


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


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


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


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

Mixing weed and Aldesleukin


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


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


Taking Aldesleukin and weed together


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


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


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

Weed Vs Aldesleukin


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


Aldesleukin Vs Weed


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


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


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


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


Overdose on Aldesleukin and weed


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


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


Studies on weed, Aldesleukin 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 Aldesleukin


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


Quitting weed to take Aldesleukin


Medical professionals say an individual prescribed or taking Aldesleukin 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 Aldesleukin.


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


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


Aldesleukin and Weed

Aldesleukin 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