medrol and Weed

{Fulldrug} and Weed

Authored by Pin Ng PhD

Edited by Hugh Soames

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medrol 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 medrol. 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 medrol and Weed.


Mixing medrol and Weed


Methylprednisolone (Depo-Medrol, Medrol, Solu-Medrol) is a synthetic glucocorticoid, primarily prescribed for its anti-inflammatory and immunosuppressive effects. It is either used at low doses for chronic illnesses or used concomitantly at high doses during acute flares. Methylprednisolone and its derivatives can be administered orally or parenterally.

Regardless of route of administration, methylprednisolone integrates systemically as exhibited by its effectiveness to quickly reduce inflammation during acute flares. It is associated with many adverse reactions that require tapering off the drug as soon as the disease is under control. Serious side effects include iatrogenic Cushing’s Syndrome, hypertension, osteoporosis, diabetes, infection, and skin atrophy.

Chemically, methylprednisolone is a synthetic pregnane steroid hormone derived from hydrocortisone and prednisolone. It belongs to a class of synthetic glucocorticoids and more generally, corticosteroids. It acts as a mineralocorticoid and glucocorticoid receptor agonist. In comparison to other exogenous glucocorticoids, methylprednisolone has a higher affinity to glucocorticoid receptors than to mineralocorticoid receptors.

Glucocorticoid’s name was derived after the discovery of their involvement in regulating carbohydrate metabolism. The cellular functions of glucocorticoids, such as methylprednisolone, are now understood to regulate homeostasis, metabolism, development, cognition, and inflammation. They play a critical role in adapting and responding to environmental, physical and emotional stress.

Methylprednisolone was first synthesized and manufactured by The Upjohn Company (now Pfizer) and FDA approved in the United States in October 1957. In 2020, it was the 161st most commonly prescribed medication in the United States, with more than 3 million prescriptions. Methylprednisolone is also on the World Health Organization’s List of Essential Medicines for its effects against lymphoid leukemia.

Methylprednisolone is a synthetic glucocorticoid (GCs) that exhibits pleiotropic effects on a variety of physiological mechanisms. However, they have been prescribed extensively for their effects on inflammation and immunity. The effects of synthetic glucocorticoids, such as methylprednisolone, is dependent on its association with intracellular glucocorticoid receptors (GRs), and to a lesser extent, mineralocorticoid receptors (MRs). GRs are widely distributed in contrast to MRs that show a restricted tissue distribution. By this mechanism, the ligand-bound receptor translocate to the nucleus and modulate gene expression.

In the absence of endogenous or synthetic GCs, monomeric GRs are located in the cytoplasm and form multiprotein complexes with heat shock proteins (HSPs), immunophilins, and other chaperones such as src, and p23. The GR acts in a ligand-dependent manner, with the complex holding the GR in an inactive form with high specificity for the ligand. When methylprednisolone from the plasma or interstitial fluid diffuses passively across the cell membrane, it binds to the GR inducing a conformational change and GC-GR dimerization. It was previously thought that this conformational change was necessary to dissociate the multiprotein complex to allow the ligand bound receptor to translocate to the nucleus. However, recent studies have indicated that chaperones play a role in nuclear import. The now active methylprednisolone-GR complex can either transduce non-genomic changes in the cytoplasm or translocate to the nucleus and regulate transcriptional activity of target genes by direct, tethering or composite mechanisms.

Genomic mechanisms, regardless of which type, elicit responses with a slow onset and a slow dissipation. This is attributed to the duration of mRNA transcription and translation. Glucocorticoids have the ability to regulate roughly 100 to 1000 genes with specificity to cell-type.

Three major mechanisms have described how the MP-GR complex alter gene expression by either binding to DNA or transcription modulators. One mechanism of genomic signaling occurs when the MP-GR complex directly binds to DNA sequences called glucocorticoid response elements (GREs). GREs are located in regulatory regions of target genes and mediate their transactivation or transrepression. For example, the activation of lipocortin 1 (ANAX1) negatively interferes with the production of prostaglandins and leukotrienes, known pro-inflammatory signals. Likewise, negative GREs (nGREs) are responsible for repressing genes involved in immune cell activation.

Post translational modifications (PTMs) also contribute to methylprednisolone signaling and can produce genomic and non-genomic effects. The GR has contains several sites for phosphorylation, sumoylation, ubiquitination, and acetylation that primarily occurs after intracellular methylprednisolone binding to the GR. PTMs modulate many functions including nuclear translocation, strength and duration of receptor signaling and cofactor interaction. A specific example is the deacetylation by histone deacetylase 2 (HDACe) was necessary for transrepression of NF-κB.

The mechanisms of non-genomic signaling are distinct from genomic signaling, yet mediate similar pathways and provide therapeutic relevance. These mechanisms are characterized as having a rapid onset (less than 15 minutes), because they do not rely on time-consuming transcription or translation and are not modified by inhibitors of transcription.

Methylprednisolone induced non-genomic signaling is classified by three mechanisms: (1) cytoplasmic glucocorticoid receptor (cGR)-mediated non-genomic effects, (2) membrane-bound glucocorticoid receptor (mGR) non-genomic effects, and (3) physiochemical interactions with cellular membranes (non-specific non-genomic effects).

Proteins that dissociate from the activated GC-cGR complex, initiate intracellular transcription-independent mechanisms. It is evidence that dissociated SRC is responsible for inhibiting the release of arachidonic acid (AA) from cell membrane phospholipids. AA is required for the synthesis of inflammatory mediators (prostaglandins and leukotrienes) and thus AA inhibition mediates several important pathways such as cellular growth, metabolism and inflammation.

Previous studies identified mGRs in lymphoma cells, but it wasn’t until 2004 that mGRs were identified in human peripheral mononuclear cells. The prevalence of mGRs ranges per cell type, with the highest concentration in B lymphocytes at up to 12.3%, up to 9.2% in monocytes, and absent from T lymphocytes. Studies have shown a positive correlation between the mGR-positive cells and disease related activity. There are no proven signaling pathways associated with mGR at this time. Some researchers hypothesize that high disease activity activates mGR expression and upon administering methylprednisolone, creates a negative feedback loop by inducing apoptosis.

High concentrations of methylprednisolone intercalate in plasma and mitochondrial cellular membranes. This association changes physiochemical properties of the membrane; activating membrane proteins, altering cellular functions and ultimately influencing cation transport through the plasma membrane and stimulating the proton leak across the inner mitochondrial membrane. Hindered oxidative phosphorylation compromises ATP production, a major energy source for cellular energy metabolism and immune function. In vivo studies of Con-A stimulated thymocytes (in rats) and human immune cells that were administered high doses of methylprednisolone has been shown to inhibit respiration in a dose-dependent manner, inhibit plasma calcium and sodium uptake, and increase cytoplasmic calcium concentration. The summative process is as follows: Methylprednisolone intercalates in the plasma membrane, causes physiochemical changes, activates membrane proteins that inhibit plasma calcium and sodium uptake (mimicking an energy deficit state). ATP consumption drops (resembled by inhibited respiration), resulting in protein permeability at the inner mitochondrial membrane and uncoupling of oxidative phosphorylation. Of notable importance, DNA/RNA synthesis was not hindered. The dependency of house keeping cells and immune cells on ATP, results in immunosuppression during ATP deficit. Specific immune functions effected by this process are cytokinesis, migration, phagocytosis, antigen processing and presenting, antibody synthesis, cytotoxicity and regulation.

The activation of the hypothalamic-pituitary axis (HPA) stimulates the production of endogenous glucocorticoids within the adrenal cortex. The HPA interprets stimuli (stress, inflammation and circadian cues) and transduces a corresponding physiochemical response. Glucocorticoids released in the blood, serve as a messenger by binding to glucocorticoid receptors in a wide distribution across the body, including the HPA itself. Thus, the physiological range of GCs is monitored by the negative feedback loop GCs exert on any portion of the HPA. Methylprednisolone structurally and functionally mimics endogenous corticoids and will act upon the HPA in a similar fashion.

Methylprednisolone is approved for oral and parenteral administration. Methylprednisolone (Medrol) for oral administration is available in a tablet formulation in 2 mg, 4 mg, 8 mg, 16 mg or 32 mg strengths. Both methylprednisolone acetate (Depo-Medrol) and methylprednisolone succinate (Solu-Medrol) are approved for intramuscular injection. Depo-Medrol is additionally approved for intralesional, intra-articular, and soft tissue injections. Depo-Medrol is available as sterile aqueous solution in 20 mg/mL, 40 mg/mL, or 80 mg/mL strengths. Solu-Medrol is the only derivative of methylprednisolone that is approved for intravenous infusion, as the sterile powder is soluble in water and can be mixed with a diluent. Strengths vary from 40 mg to 2g.

Synthetic glucocorticoids are similar to endogenous steroids in metabolism, but differ in affinity for glucocorticoid and mineralocorticoid receptors, affinity for protein-binding, rate of elimination, and metabolic products.

Oral methylprednisolone is readily absorbed from the gastrointestinal tract with a bioavailability of 89.9%. In contrast to endogenous GCs, methylprednisolone does not bind to the glycoprotein transcortin (corticosteroid binding globulin, CBG) but does have moderate protein binding to albumin. Thus, pharmacokinetics of methylprednisolone is linear and show no dose dependency. Patients exhibiting low albumin concentrations are at risk for adverse effects during glucocorticoid therapy. Oral methylprednisolone has a moderate distribution into tissue at 1.38L/kg.

Methylprednisolone is primarily eliminated by hepatic metabolism and renal excretion of metabolites; with renal excretion of unchanged methylprednisolone at only 1.3–9.2%. Methylprednisolone can be interconverted with methylprednisone. Hepatic metabolism is mediated by 11 beta-hydroxysteroid dehydrogenases (11-HSD) and 20-ketosteroid reductases. Methylprednisolone undergoes renal excretion of hydrophilic inactive metabolites, including 20-carboxymelthylprednisolone and 6-hydroxy-20-hydroxymethylprednisolone.

The primary use of methylprednisolone is to suppress inflammatory and immune responses. Methylprednisolone achieves this primarily by regulating the number and function of leukocytes, cytokines and chemokines. Its widespread inflammatory control is conducive in use across multiple disorders regardless of pathology. Methylprednisolone is commonly prescribed as short-term therapy for acute flares, as seen with acute gouty arthritis. It can be prescribed during on-going therapy in lower doses contingent upon monitorization of adverse effects. Dosage strength and formulation are optimized per medical use.

In 2001–2002, 11.4% of patients diagnosed with asthma and seen at an outpatient visit were prescribed oral corticosteroids as a long-term control therapy. The National Asthma Education and Prevention Program (NAEPP) indicates systemic methylprednisolone in both short and long term therapies to quickly control and to suppress persistent asthma, respectively. For exacerbations that result in a visit to the Emergency Department (ED), oral methylprednisolone is preferred over intravenous administration, unless there are issues with adherence or vomiting. Oral methylprednisolone is less invasive and studies have shown that equivalent efficacy compared to intravenous methylprednisolone. Dosage above 60–80 mg/day or 2 mg/kg/day is not recommended as it has not been shown to alter pulmonary function, rate of admission, or length of stay in the hospital compared to lower doses. Following ED discharge, it is advised to prescribed a five-day course of methylprednisolone to decrease the probability of relapse or withdrawal symptoms.

Methylprednisolone is used to treat several rheumatic diseases, such as Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA). Methylprednisolone dosage and administration for these diseases is highly variable due to varied pathophysiology between the diseases and within patients diagnosed with a given disease. In Lupus Nephritis, a common manifestation of SLE, patients are often prescribed methylprednisolone concomitantly with immunosuppressants. Severe manifestations are often treated with Cyclophosphamide or Rituximab and three doses of methylprednisolone IV-pulse treatment (as recommended by ACR guidelines) prior to switching to oral prednisolone and azathioprine for maintenance.

Intra-articular corticosteroid injections (IACI) are a second line therapy to relieve joint pain resulting from rheumatoid arthritis. It is most commonly injected into the joints of the knees and shoulders. Although the injection is local, studies have shown systemic absorption as evidenced by beneficial effects on distant joints. In an attempt to minimize HPA suppression, FDA guidelines have restricted IACIs to three per year, with a minimum of 30 days in between injections.

Methylprednisolone is not typically recommended for primary or secondary adrenocortical insufficiency compared to other corticosteroids which have a higher affinity for mineralocorticoid receptor and salt retaining properties.

The labeled indications below are categorized by route of administration then by medical discipline.

Some of the off-label indications of methylprednisolone include acute spinal cord injury, acute respiratory distress syndrome, alcoholic hepatitis, hormonal resuscitation in cadaveric organ recovery, and chronic obstructive pulmonary disease.


Signifies varying strengths of available forms. Is not indicative of frequency nor daily cumulative dose; varies per patient and condition.

Benzyl alcohol should not to be used on neonates

Preservative free formulation

Methylprednisolone should not be taken orally by people who have systemic fungal infections, with the exception of Depo-Medrol when administered as an intra-articular injection for localized joint conditions. Methylprednisolone is contraindicated in those with known hypersensitivity to methylprednisolone or its components Steroids should be used with caution in patients with ulcerative colitis, heart disease or hypertension, peptic ulcer, renal insufficiency, osteoporosis, myasthenia gravis, glaucoma, and diabetes. Psychic manifestations may appear while taking methylprednisolone, ranging from euphoria, insomnia, personality changes to depression. Caution is required for patients with predisposed psychoses, as psychotic tendencies may be exacerbated while taking corticosteroids.

Solu-Medrol 40 mg dosage contains lactose monohydrate produced from cow’s milk; It should not be taken by anyone with known hypersensitivity to dairy products or its components. Severe medical events have been associated with epidural administration of Solu-Medrol and Depo-Medrol, including spinal cord infarction, paraplegia, quadriplegia, cortical blindness and stroke. Intramuscular injections should not be administered to those with idiopathic thrombocytopenic purpura. Formulations of Solu-Medrol and Depo-Medrol containing benzyl alcohol are contraindicated for use in premature infants. Exposure of neural tissue to excessive amounts of benzyl alcohol has been associated with toxicity and in rare events has resulted in death.

Adverse reactions may overshadow the therapeutic effects of methylprednisolone.

There is minimal clinical diagnostic criteria to define the psychic adverse effects (PAE) associated with methylprednisolone use in patients with systemic lupus erythematosus (SLE). The prevalence varies from 1.3 to 62% of adult treated patients. The type and severity of neuropsychiatric symptoms also varies significantly between patients, with 33% of patients reporting mild to moderate PAE and 5-10% reporting severe PAE. Methylprednisolone dose and duration have been implicated in PAE development. 20 mg/day of prednisone (16 mg/day of methylprednisolone) is the threshold dosage for PAE development agreed upon by many studies. Short-term pulse IV therapy at high doses is associated with rapid onset of manic and hypomanic symptoms, whereas long term therapy gives rise to depressive symptoms (suicide attempts infrequent). PAE are reversible with treatment reduction or discontinuation.

Iatrogenic Cushing’s Syndrome is a direct complication of glucocorticoid therapy, and the most common cause of exogenous Cushing’s Syndrome. Clinical features of Cushing’s Syndrome is inclusive of many adverse effects in glucocorticoid therapy. Traditional symptoms include weight gain, myopathy, osteoporosis, increased risk of infection, hypertension and psychological effect. Fat deposition is centralized on the trunk, in between shoulders (“buffalo hump”), and on the face (“moon face”). Patient education and provider monitoring is the first step in recognizing and diagnosing Iatrogenic Cushing’s Syndrome. Exogenous glucocorticoids suppress adrenocorticotropic hormone (ATCH) production, which can be verified by AM biochemical analysis. The onset of side effects varies; neuropsychiatric symptoms can arise within a few hours, while osteoporosis would take months to develop.

The metabolic effects of taking methylprednisolone involve the continuous breakdown of proteins for gluconeogenesis increase necessity for insulin. This results in hyperlipidemia, weight gain, myopathy that may prompt a patient to cease treatment.

The Immunodeficiency section tabulates known pathogens of concern in glucocorticoid induced immunodeficiency.

Osteoporosis is a type of bone disease characterized by a loss of bone density, mass and architecture that leaves a patient susceptible to fractures. The World Health Organization (WHO) defines osteoporosis in caucasian postmenopausal women as a bone mineral density (BMD) and a T-score of -2.5 or less. The prevalence of osteoporosis in patients with SLE varies geographically and some attribute it to BMD and T-score diagnostic appropriateness. British 10.3%, Chinese 21.7%The Canadian Clinical Practice Guidelines and The American College of Rheumatology have switched to using a Z-score as a diagnostic marker for osteoporosis but have failed to find a clinical diagnostic threshold. Additionally, a UK-based study showed that BMD may underrepresent a patient with SLE, as their risk for fractures is 22% higher than the healthy individual.

Exogenous corticosteroids induce osteoporosis by increasing bone resorption and reducing bone formation. Bone loss can be pronounced within the first few months of initiating methylprednisolone with a steady decrease with chronic use. Trabecular bone loss in the lumbar spine precedes cortical bone loss in the femoral neck.

Allergic: allergic or hypersensitivity reactions, anaphylactoid reaction, anaphylaxis, and urticaria.

Cardiovascular: hypertension, congestive heart failure in susceptible patients, premature atherosclerotic disease, arrhythmias, and possible hyperlipidemia.

Dermatologic: impaired wound healing, petechiae and ecchymoses, thinning of the skin, facial erythema, and increased sweating.

Endocrine: Cushingoid features, growth suppression in children, secondary adrenocortical and pituitary unresponsiveness, menstrual irregularities, decreased carbohydrate intolerance, and latent diabetes mellitus. In patients with diabetes, increased requirements of insulin or oral hypoglycemic agents.

Fluid and electrolyte disturbances: sodium retention, fluid retention, potassium loss, hypokalemic alkalosis, or congestive heart failure in susceptible patients.

Gastrointestinal: peptic ulcer, pancreatitis, abdominal distention, and ulcerative esophagitis.

Metabolic: protein catabolism which causes negative nitrogen balance.

Musculoskeletal: muscle weakness, loss of muscle mass, steroid myopathy, osteoporosis, tendon rupture (especially Achilles), vertebral compression fractures, aseptic necrosis of femoral and humeral heads, and pathologic fracture of long bones.

Neurological: increased intracranial pressure with papilledema, convulsions, vertigo, and headache.

Ophthalmic: posterior sub-capsular cataracts, increased intraocular pressure, glaucoma, and exophthalmos.

Feedback of the exogenous glucocorticoids at the hypothalamic–pituitary–adrenal (HPA) axis inhibits the secretion of the corticotropin-releasing hormone (CRH) and the adrenocorticotropic hormone (ATCH) at the hypothalamus and pituitary glands, respectively. Prolonged suppression leads to inadequate responses to physical and emotional stresses, such as illness and trauma. Suppression of ATCH may result in adrenal hypoplasia or secondary adrenal gland atrophy within 6 weeks of methylprednisolone therapy, leaving a patient at risk for developing life-threatening adrenal insufficiency crisis. Factors that contribute to the extent of HPA axis suppression include steroid hormone potency (type of compound and route of administration), cumulative dose, duration of treatment and concomitant drug use. Any individual who has taken steroid hormones for 2+ weeks is at risk for developing HPA axis suppression. Systemic methylprednisolone risk has been marked as moderate within the class of synthetic glucocorticoids.

Consult with your physician prior to discontinuing methylprednisolone for any reason. Abrupt termination of the drug commonly causes transient non-specific symptoms such as loss of appetite, upset stomach, vomiting, drowsiness, confusion, headache, fever, joint and muscle pain, peeling skin, and weight loss. These symptoms can be attributed to steroid withdrawal syndrome, adrenal insufficiency or disease relapse. Those who have been taking methylprednisolone as a long-term treatment may be gradually be tapered off to minimize withdrawal symptoms and potential for relapse. If symptoms are exacerbated, temporarily increasing methylprednisolone dosage has shown clinical relevancy. Studies retesting patients upon methylprednisolone withdrawal, showed persistent adrenal insufficiency, with one study showing 15% after 3 years. However, there was a wide range of prevalence and lack of uniformity in the follow-up timeline.

Caution is advised when taking methylprednisolone concurrently with the medications described below.

Enzyme inducers

All drugs that fall within the class of enzyme inducers increase the clearance and decrease the half-life of methylprednisolone when co-administered. Phenobarbital, phenytoin, rifampin, carbamazepine and barbiturates, increase hepatic enzymes and rate of elimination, thus reducing the immunosuppressive effect of methylprednisolone. Increased dosages may be required to achieve desired effect of methylprednisolone.

Cytochrome P450 (CYP) 3A4 inhibitors

Troleandomycin, ketoconazole, and Clarithromycin inhibit metabolism; and may decrease rate of elimination and increase half-life of methylprednisolone. Dosages should be decreased accordingly to avoid side effects. Another CYP 3A4 inhibitor, grapefruit juice, prolongs half-life of oral methylprednisolone.

Oral contraceptives

Oral contraceptives inhibit oxidative processes, as highlighted by its ability to decrease methylprednisolone clearance.

P-glycoprotein inhibitors

Methylprednisolone is shown to be a substrate of P-glycoprotein; its inhibition is thought to increase methylprednisone absorption and distribution. No clinical relevance has been linked.

Ciclosporin, tacrolimus, sirolimus (Rapamycin)

Methylprednisolone and cyclosporin inhibit metabolism and therefore increase the likelihood of experiencing side effects associated with either of the individual drugs. In addition to known individual side effects, convulsions have been reported.

Cox1 inhibitors

Methylprednisolone may increase rate of elimination with chronic high dose aspirin. Patients are susceptible to increased salicylate serum levels or salicylate toxicity upon termination of methylprednisolone. Excessive caution should be taken when prescribing methylprednisolone and aspirin to patients with hypoprothrombinemia.


Anticoagulants exhibit variable interactions; monitoring coagulation indices is recommended to achieve the desired effect.

Oral methylprednisolone (Medrol) and its derivatives are a white, odorless crystalline powder. Its solubility ranges from practically insoluble in water, very slightly soluble in ether, slightly soluble in acetone and chloroform to sparingly soluble in alcohol, dioxane and methanol. Methylprednisolone acetate suspension (Depo-Medrol) is a 6-methyl derivative of prednisolone that melts at 215 degrees Celsius with some decomposition. Methylprednisolone sodium succinate (Solu-Medrol) is the sodium succinate ester of methylprednisolone. Contrary to the solubilities above, methylprednisolone sodium succinate is soluble in water and alcohol, slightly soluble in acetone and insoluble in chloroform

Methylprednisolone, or 6α-methylprednisolone, also known as 11β,17,21-trihydroxy-6α-methylpregna-1,4-diene-3,20-dione, is a synthetic pregnane steroid and a derivative of hydrocortisone (11β,17α,21-trihydroxypregn-4-ene-3,20-dione) and prednisolone (11β,17α,21-trihydroxypregn-1,4-diene-3,20-dione). A variety of methylprednisolone esters with differing characteristics exist and have been marketed for medical use. They include methylprednisolone aceponate (Advantan), methylprednisolone acetate (Depo-Medrol), methylprednisolone succinate (Solu-Medrol), and methylprednisolone suleptanate (Medrosol, Promedrol).

Synthetic steroids are synthesized from cholic acid and sapogenins obtained from cattle and plants, respectively.

Methylprednisolone was first synthesized and manufactured by The Upjohn Company (now Pfizer) and Food and Drug Administration (FDA) approved in the United States on 2 October 1957. The patent has since expired, and generics are now available. In 2020, it was the 161st most commonly prescribed medication in the United States, with more than 3 million prescriptions. Methylprednisolone has been a prescribed therapy amidst the COVID-19 pandemic, but there is no evidence it is either safe or effective for this purpose.

Methylprednisolone has been a prescribed therapy amidst the COVID-19 pandemic, but there is no evidence it is either safe or effective for this purpose.


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


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


How does Weed effect the potency of medrol?


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


A person seeking medrol 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 medrol 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 medrol and Weed


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


Taking medrol and Weed together


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


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


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


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

Mixing weed and medrol


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


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


Taking medrol and weed together


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


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


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

Weed Vs medrol


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


medrol Vs Weed


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


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


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


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


Overdose on medrol and weed


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


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


Studies on weed, medrol 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 medrol


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


Quitting weed to take medrol


Medical professionals say an individual prescribed or taking medrol 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 medrol.


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


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


medrol and Weed

medrol 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