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Alcohol risks: Quitting Cold Turkey?

Alcohol (ethanol), to the surprise of many, is a drug. Alcohol is a legal drug in many countries and one that is widely accepted. To the point that it’s “weird” when someone is not drinking at a party or social event.

But, does the legality of a substance, plus its social acceptance, qualify alcohol as a safe drug for the consumer?

Stats on Alcohol Emergencies, Economical burden and Deaths, by the NIH:

  • 95,000 people die annually from alcohol-related causes.
  • The rate of all alcohol-related ER visits increased 47% between 2006 and 2014.
  • An estimated 95,000 people (approx. 68,000 men) die from alcohol-related causes annually, making alcohol the third-leading preventable cause of death in the United States.
  • In 2010, alcohol misuse cost the United States $249.0 billion.

In 2011 – 2015, (according to the NIH) leading causes of alcohol-attributable deaths due to chronic conditions in the US were alcohol-associated:

  • Liver disease
  • Heart disease and stroke
  • Unspecified liver cirrhosis
  • Upper aerodigestive tract cancers
  • Liver cancer
  • Supraventricular cardiac dysrhythmia
  • Alcohol use disorder (AUD)
  • Breast cancer
  • Hypertension

How does alcohol affect our brain and why it’s so hard and dangerous for people who drink a lot to stop drinking suddenly?

Alcohol is categorized as a depressant of the nervous system. Alcohol induces sedation and decreases cognitive and motor functions.

You may feel up and excited when you start drinking, but it doesn’t change the fact that alcohol works by enhancing the major inhibitor neurotransmitter, GABA, and by decreasing the activity of a few excitatory neurotransmitters, primarily glutamate.

Chronic use of alcohol has the potential to change levels of mRNA for specific subunits, which suggests that chronic alcohol ingestion can affect gene expression.

Why is abruptly stopping alcohol intake dangerous?

Alcohol inhibits our main glutamate “excitatory” receptor (NMDA neuroreceptors).

Prolonged inhibition of these receptors leads to an increased sensitivity of excitatory receptors, as the brain tries to compensate.

Abrupt cessation of alcohol exposure results in brain hyperexcitability, because receptors previously inhibited by alcohol are no longer inhibited. Brain hyperexcitability manifests clinically as anxiety, irritability, agitation, and tremors. Severe manifestations include alcohol withdrawal seizures and delirium tremens.

Withdrawal seizures:

More common in patients who have a history of multiple episodes of detoxification.

Alcohol withdrawal delirium, or delirium tremens (DTs):

Characterized by clouding of consciousness and delirium. Episodes of DTs have a mortality rate of 1 – 5%. Risk factors:

  • Concurrent acute medical illness
  • Daily heavy alcohol use
  • History of DTs or withdrawal seizures
  • Older age
  • Abnormal liver function
  • Severe withdrawal symptoms on presentation

Summary: Diagnostic Criteria for Alcohol Withdrawal:

I. Cessation of (or reduction in) alcohol use that has been heavy and prolonged.
II. Two (or more) of the following, developing within several hours to a few days after criterion I: (symptoms significantly impair important areas of functioning)

  • Autonomic hyperactivity
  • Increased hand tremor
  • Insomnia
  • Nausea or vomiting
  • Transient visual, tactile, or auditory hallucination s or illusions
  • Psychomotor agitation
  • Anxiety
  • Grand mal seizures

III. The symptoms are not due to a general medical condition and are not better accounted for by another mental disorder.

Alcohol Regulation

Where alcohol is legal it is generally well regulated. This can allow for consumer confidence in the product. During the prohibition era in the U.S., alcoholic products were frequently cut with the dangerous and more toxic methanol (aka. wood alcohol). Methanol poisoning resulted in thousands of deaths. Today, adulteration is common for scheduled drugs purchased from non-official sources. Testing can help identify unregulated drugs. Stay safer, get a drug test kit.

Shop for drug test kits »

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Cocaine Cut: Ephedrine

Ephedrine-Induced PRIAPISM: (Prolonged erected penis)

What is Ephedrine?

Ephedrine comes from the plant Ephedra sinica, which can be found in Asia. For centuries this herb has been used in China for its medical properties. Famously helpful to break a fever and induce sweating.

Ephedrine is categorized as a stimulant because it is similar structurally to amphetamines. However, the effects of ephedrine are much weaker than amphetamines.

Short History:

Products that contain the herb ephedra have been promoted and used in the United States since the 1980s.

This herb has been advertised as a weight loss aid and enhancer of athletic performance.

However, there is no or very little research backing up these claims. An overwhelming amount of complaints in the 1990s lead to its prohibition.

Legality:

Ephedrine is currently banned by:

  1. Food and Drug Administration (FDA)
  2. National Collegiate Athletic Association (NCAA)
  3. International Olympic Committee (IOC)
  4. National Football League (NFL).

Reports of adverse effects included serious side effects and, in some cases, death. Many of those reports were coming from healthy young customers and professional athletes.

Ephedrine as a stimulant:

The ephedrine alkaloids are stimulants, and so ephedrine can:

  • Increase heart rate
  • Increase blood pressure
  • Relax bronchial tissue
  • Ease shortness of breath
  • Decrease appetite
  • Increase alertness
  • Increase productivity
  • Improve mood
  • Decrease fatigue

At higher doses, it can promote anxiety, restlessness and insomnia.

Ephedrine and Cocaine:

Ephedrine has been commonly used as a cut for cocaine. Is not only cheaper than cocaine, but it also provides a kick of its own. Ephedrine is a stimulant, so, it has the ability to speed up the nervous system. This can lead to serious side effects:

  • High blood pressure
  • Heart attacks
  • Seizures
  • Strokes
  • Irregular heartbeat
  • Death

Cocaine and Ephedrine-Induced PRIAPISM: (Prolonged erected penis)

Drugs that facilitate, potentiate, or mimic the action of sympathetic nerves have been associated with priapism.

Cocaine inhibits norepinephrine (NE) reuptake, in other words, cocaine increases the amount of NE. Ephedrine has a more varied method of action, but it mostly works by increasing the amount of adrenaline and/or norepinephrine (NE).

In theory, ephedrine should not induce priapism. However, in animal and case studies, the combination of ephedrine and cocaine was shown to induce priapism.

More research is needed to reach a concrete answer. However, chronic use of cocaine and ephedrine increases the risk of developing priapism.

Testing Cocaine For Cuts

It is possible to test cocaine for a variety of cuts.

Get your test kit for Ephedrine and other Cocaine Cuts.

You may also like to view cocaine test kits.

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Effects of Mixing Ketamine and Alcohol

The consumption of ketamine and alcohol mixtures (whether deliberately or inadvertently), is relatively common. This combination should genearlly be avoided.

Effects of alcohol on it’s own

In lower doses, alcohol produces effects of relaxedness, a sense of euphoria or giddiness, and it can lower your inhibitions.

In higher doses, alcohol can change your mood, make you more impulsive, slow or slur speech, cause loss of coordination, vomiting and loss of consciousness or gaps in memory, and even kill you.

How ketamine and alcohol interact with the brain?

Ketamine is catalogued as a dissociative analgesic, and alcohol is a depressant. They have the ability to interact with glutamate (the main excitatory neurotransmitter) and GABA (the main inhibitory neurotransmitter).

Alcohol also has the ability to enhance GABA’s receptors activity.

Ketamine and alcohol’s combined effect

Alcohol and ketamine’s combined interaction is complicated. Simply put, when combined, they have an even greater anesthetic effect.

It can become hard to move and talk, and cognitively is hard to process information or be aware of your surroundings.

Their combination is specially dangerous as they can slow down breathing. In high doses it can completely stop breathing.

Ketamine and alcohol have the ability to reduce glutamate activity.

Ketamine and alcohol in the US:

Ketamine was involved in 0.12% of the United States Emergency Department visits involving illicit drugs in 2011.

However, ketamine-related emergency department visits often involved other drugs, with 71.5% of ketamine-related visits in the United States in 2011 involving alcohol.

Studies with volunteers recruited at party scenes found that at least 65% of ketamine users also consume alcohol.

Ketamine and alcohol internationally:

Pavarin R.M. et al. (2019) found that alcohol was present in 25% of ketamine recreational misusers admitted to emergency care in Italy.

Darke et al. (2000-2019), found that ethanol (drinking alcohol) was present in over 27.3% of ketamine-related deaths in Australia.

Schifano F (1993-2006), found that alcohol was present in almost 50% of postmortem analyses of ketamine-related deaths in the UK.

Know the signs of trouble:

Keep an eye out for these symptoms, if someone is experiencing them call 911*:

  • Drowsiness
  • Hallucinations
  • Confusion
  • Loss of coordination
  • Trouble breathing
  • Irregular heartbeat
  • Abdominal pain
  • Vomiting
  • Seizures
  • Collapse
  • Pale, clammy skin

*Canada and the US have adopted The Good Samaritan Drug Overdose Act. Which protects you from being charged or convicted for drug possession if you call 911 to report an overdose.

Extra precautions:

  • Test your drugs!
  • Choose a safe setting
  • Don’t use alone
  • Know the risks

Ketamine Test Kits »

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MDMA cut: Synthetic Cathinones “Bath salts”

Where do synthetic cathinones comes from?

Cathinone is a psychoactive compound that comes from the Khat Plant, native to East Africa and the Arabian Peninsula.

Synthetic cathinones are much stronger and dangerous than the natural compound found in the leaves of Khat.

They are ofter referred as “bath salts”, due to being originally marketed as such to avoid regulatory controls.

Synthetic cathinones and MDMA

Synthetic cathinones have been called the “natural amphetamine”, due to sharing similar chemical structures and behavioral effects. Because of this, synthetic cathinones have been claimed to be a safer option to other popular stimulants, like MDMA and cocaine, but this is false.

What have I been taking all this time?

Kalasinsky et al analyzed hair samples of self-reported MDMA takers, to verify if what they’ve been taking is actually MDMA.

Their results showed the presence of various synthetic cathinones in almost 30% of hair samples from club/festival goers who thought they had taken MDMA only. In some hair samples, there was no MDMA at all.

Bath salts make an “excellent” cut for MDMA, they are cheaper to manufacture and they provide similar cognitive and behavioral effects.

Most common synthetic cathinones found in MDMA / sold as MDMA*:

  1. Ethylone
  2.  MDPV (monkey dust)
  3. Mephedrone (4-MMC)
  4. Methylone (bk-MDMA)
  5. Butylone

Why are synthetic cathinones dangerous?

The risks associated with synthetic cathonines are similar to those associated to amphetamines and cocaine. However, as with other substances, what enhances their risks is taking it unknowingly.

Research has suggested that synthetic cathinones have a reduced potential for neurotoxicity (compared to MDMA or Meth), however, they may present a greater threat of overdose.

Why could synthetic cathinones have a greater risk of overdose?

There are many synthetic cathinones available, and new versions are being found in different substances. This leads to a lack of research and misinformation.

Here is one example: MDPV

MDPV, a common synthetic cathinones, interacts with the brain in a similar to cocaine. However, MDPV is 10 times stronger. MDPV is the most common synthetic cathinone found in the blood and urine of patients admitted to emergency departments after taking bath salts.

Main risks of synthetic cathinones

In short, their main risks are based on the fact that most people don’t take bath salts deliberately. Increasing the risk of:

  1. Unexpected stronger doses
  2. Unexpected effects due to the combination of different substances

In extremely rare cases, bath salts can lead to a condition called excited delirium: A state of extreme agitation, aggression, acute distress and sudden death. It usually involves: taking combination of drugs, driving under the influence and pre-existing mental health conditions.

Tips to help stay safe

  1. Don’t take any substance unintentionally.
  2. Know your dosage.
  3. Know the risk.
  4. Test your drugs. The Marquis test is good for differentiating cathinones from MDMA.

MDMA Test Kits »


*Most commonly, but not exclusively an MDMA cut. Cathinones can also be found in cocaine and meth.

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Smoking Too Much Weed? Here’s Some Info & Tips

Cannabis can be physically and psychologically addictive. If don’t like how much you’re smoking, or resent the feeling of “needing” to smoke, there are some steps you can take.

Seeking Treatment for Cannabis Addiction

Adults are less likely to seek treatment for cannabis abuse when compared to other drugs. Possibly because cannabis users believe their products are less dangerous, and/or less habit forming than “harder” drugs. According to recent studies, an adult seeking treatment is usually someone who on average, has used cannabis on a regular basis for more than 10 years, and has seriously attempted to quit more than 6 times.

Each year in the U.S., over 300,000 people enter treatment for cannabis use disorders.

The type of treatment may depend on whether or not the person has any comorbidities, such as psychiatric problems or addiction to other substances.

Treatments for Cannabis Addiction

1. Rehabilitation or detoxification centers: Not very common, but they can be helpful for people who have poor social functioning or comorbid psychiatric disorders, such as other addiction(s).

2. Outpatient therapy: These programs involve working with a psychotherapist or other mental health provider and attending sessions consistently.

3. Support groups: In-person or online support groups can help individuals connect with others going through the same and, thus, help each other.

Tips For Quitting

Withdrawal symptoms will differ depending on usage. Meaning for how long has the person used and how frequent. For someone who uses daily, slowly reducing might be easier than abruptly stopping. However, for someone who uses occasionally, completely stoping might not be so difficult.

Tips:

  • Try eating healthy food, like fruits and vegetables. Sugar and junk food can make you feel worse.
  • Don’t forget to drink water and try avoiding caffeinated beverages.
  • Sleep and rest are very important. If sleeping well has become difficult, exercising daily will definitely help.
  • Surround yourself with supportive friends and family, you don’t have to go through this alone. Supportive groups are also an option, don’t isolate yourself.
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Is Cannabis Addictive?

Short answer, yes. Cannabis can be addictive, physically and psychologically. Recent studies suggest that about 9% of cannabis smokers will become dependent. The addiction rate would likely increase to 17%, if the consumer started in their teens.

Unlike other substances, cannabis is not a highly addictive drug. It requires heavy and frequent use to create dependence. Lopez-Quintero et al. found that the cumulative probability estimate of transition to dependence was 67.5% for nicotine users, 22.7% for alcohol users, 20.9% for cocaine users, and 8.9% for cannabis users.

Signs of Cannabis Addiction:

  1. Wanting and trying to quit/reduce consumption but failing
  2. Using more cannabis than intended
  3. Craving cannabis
  4. Spending a lot of time trying to get weed/going out of your way to getting weed
  5. Continuing use, even if consumption is affecting social relationships, work and/or essential activities
  6. Needing higher concentrations/consuming more to obtain the same high
  7. There is research, however, still inconclusive, suggesting problems with memory, attention and learning in the longterm
  8. Experiencing withdrawal symptoms

Why do we experience cannabis withdrawal symptoms?

After frequent use, your body has to adjust to not having that regular supply of delta-9 tetrahydrocannabinol (THC), the primary psychoactive in cannabis. The more you smoke, the more your brain will be accustomed to this steady supply. Once the supply stops, withdrawal symptoms may appear, which is basically your brain asking for more THC.

Withdrawal symptoms usually peak within the first week after quitting and last up to 2 weeks.

Cannabis Withdrawal Symptoms Include:

  • Diminished appetite
  • Mood changes
  • Irritability
  • Sleep difficulties, including insomnia
  • Headaches
  • Loss of focus
  • Cravings
  • Sweating, including cold sweats
  • Chills
  • Increased feelings of depression
  • Stomach problems

Compared to other drugs (Like heroin or alcohol), cannabis withdrawal symptoms are not as severe, as they are not physically life-threatening.

THC Levels on the Rise

In the 1990s, the average THC content in confiscated cannabis samples was less than 4%. In 2018, it was more than 15%. The increasing potency of weed, combined with the use of high-THC concentrates, raises concerns that the consequences of cannabis use today could be more detrimental than in the past, particularly among those who are new to cannabis use and in young people, whose brains are still developing.

Testing THC and CBD Levels in Cannabis

It’s possible to test THC and CBD levels in cannabis products such as buds and infusions. You can test your own products with one of our cannabis test kits.

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MDMA (Molly) Dosage

Oral dosage range is from 30 mg to 200 mg.

Oral Doses: (for pure or uncut MDMA)

  • Minimum amount for effect (threshold): 30 mg
  • Light dose: 40-75 mg
  • Common dose for sensitive people: 60 -90 mg
  • Average dose: 75 – 125 mg
  • Common dose for less sensitive people: 110 – 150 mg
  • Strong: 150 – 200 mg
  • Heavy: 200 mg (+)

*Research suggests that women tend to be more sensitive to larger doses than men.

Metabolizing MDMA

The drug is broken down metabolically, mainly in the liver, where an enzyme designated CYP2D6 is chiefly responsible. However, enzymes involved in its breaking down slow down at relatively low concentrations of the drug. If the dose is increased, higher affinity enzymes become saturated, and there is a significant increase in the drug’s concentration in the blood and brain.

If you want to re-dose, wait for at least 2 hours! If you need to re-dose frequently, it means that tolerance is building up and it may be a sign to reduce consumption. MDMA consumption can lead to neurotoxicity.

MDMA Testing

Although you bought MDMA, it’s common to find MDMA mixed with caffeine, Methamphetamine, Amphetamines (speed), DXM, Pseudo/Ephedrine, Ketamine, Benzodiazepines and TFMPP.

Always test your drugs. Otherwise, your dose could include undesirable effects and its potency might be unreliable.

MDMA (Molly) Test Kit – Package »

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Microdosing

James Fadiman’s Protocol (Beginners Protocol)

What’s micro-dosing?

Micro-dosing involves taking a tiny dose of psychedelic hallucinogens or other drugs. Most popularly, people use magic mushrooms (psilocybin) or LSD (acid), but you could potentially micro-dose on any substance. Also, when taking a micro-dose, you should not experience sensory or cognitive distortion. If you do, decrease the dose!

What are the benefits of micro-dosing?

Most data collected indicating potential health benefits of micro-dosing were collected through self-reporting, which is not the most reliable way. However, more and more studies are investigating their direct effect. Another issue, is that we don’t really know the long-term effects of micro-dosing.

A study in Harm Reduction Journal categorized several possible benefits from reports by microdosers. These benefits include:

  1. Improved focus, concentration, and mindfulness
  2. Improved energy, wakefulness, and stimulation
  3. Cognitive benefits, such as enhanced problem solving
  4. Social benefits
  5. Reduced anxiety
  6. Creativity
  7. Reduced symptoms, such as stress
  8. Improved mood, optimism, and life appreciation
  9. Improved body functioning
  10. Self-efficacy, including improved ambition, productivity, and motivation

Microdosing Protocols

There are different protocols that can help guide you through this journey. All of them include a resting period of 2-4 weeks after finishing a cycle of 4-8 weeks of micro-dosing. This is an essential step to avoid building tolerance and maintain the beneficial effects.

  1. Fadiman Protocol
  2. Micro-dosing Institute Protocol
  3. MDI
  4. Stamet’s Protocol
  5. Nightcap Protocol
  6. Intuitive micro-dosing

James Fadiman’s Protocol

The most well-known micro-dosing protocol is named after Dr. James Fadiman. He created this protocol to observe the effects of micro-dosing by clearly distinguishing between micro-dosing days and non-microdosing days.

Cycle:

  • DAY 1: 1st micro-dosing day
  • DAY 2: transition day (after glow effect)
  • DAY 3: normal day
  • DAY 4: 2nd micro-dosing day

CYCLE: Continue this cycle for four to eight weeks
RESET: Two to four weeks of rest

Micro-dosing recommendations:

  • Be conservative when it comes about dosage and days between doses. Dr. Fadiman recommends something like one-tenth of a normal dose. For LSD, a normal dose could be between 100-120 micrograms (mcg), so a micro-dose should be between 6 and 12 mcg. However, you are your own expert, listen to your body!
  • Follow your nomal patters: make sure you eat as normal, drink water, take your medication, have restful sleep, and any normal activity you follow.
  • Be discreet about who you tell about your experience.
  • Test your substance! No benefit will come from a laced substance.

Product placement: LSD Test Kits »

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Cocaine Cut: Levamisole (Livestock Dewormer)

What’s Levamisole?

Levamisole was first synthesized in 1966. It was intended to be use as an anthelminthic (anti-parasitic drugs) and as an immunomodulatory agent for inflammatory conditions. However, in 2000, it was withdrawn from the US market due to side effects and is currently used only for veterinary purposes.
Over the last decade, levamisole has been increasingly encountered as an additive in both powder and crack cocaine.

What’s Levamisole role in Cocaine?

Levamisole has become an “excellent” cut for cocaine, as its cheaper for producers and it resembles to cocaine physically and chemically.

Levisamole once consumed is metabolized to aminorex, a compound with amphetamine-like psychostimulatory properties and a long half-life. These characteristics permits levamisole to enhance the effects of cocaine.

Still, a much higher dose of levamisole is required to affect monoamine reuptake in a way similar to cocaine. Users of drugs containing a high levamisole-to-cocaine ratio are likely to consume significant amounts in order to achieve the desired effects, putting them at higher risks of severe side effects from the adulterant.

Effects of Levamisole:

As use of cocaine cut with levamisole becomes more prevalent, complications directly attributable to the chemical are increasingly being recognized.

Levamisole use can present with a number of adverse effects:

  • Nausea and vomiting
  • Headache
  • Fatigue
  • Fever
  • Diarrhea
  • Myalgia
  • Dizziness
  • Confusion
  • Rash

Serious complications include:

  • Agranulocytosis
  • Leukopenia
  • Thrombocytopenia
  • Vasculopathy and vasculitis
  • Dermal necrosis
  • Leukoencephalopathy
  • Psychosis
  • Pulmonary hypertension and hemorrhage
  • Glomerulonephritis
  • Emboli
  • Arthritis
  • CAD
  • Collapse

Product Placement: Levamisole and other cuts can be detected with our Cocaine Cuts Test Kit.

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Combining Psilocybin Mushrooms & Antidepressants

If you’re thinking about taking magic mushrooms with antidepressants, read this post.

What is Psilocybin?

Psilocybin is the main psychoactive component of psychedelic mushrooms. Once ingested, psilocybin is converted to psilocin, which has the ability to cross the blood-brain barrier. Psilocin works by bringing a partial agonist effect on mainly the 5-HT 1A receptors.

Psilocin has the ability to activate serotonergic receptors, which causes a flow of excitatory activity in the brain. This wave spreads throughout the main perceptual centers of the brain and can alter normal waking consciousness.

Reported effects:

  1. Unusual and colourful visuals with eyes open or closed
  2. Disintegration of ‘self’ or ‘ego’
  3. Unconstrained explorative thinking, cognitive, affective and perceptual changes
  4. Sense of connectedness to self, others and the world

Therapeutic benefits of psilocybin

There’s more and more research indicating the positive benefits of psilocybin in a therapeutic context. Psilocybin has been shown to significantly reduce symptoms in people suffering from severe depression. Also, psilocybin seems to prolong these positive effects more than typical treatments, especially when combined with therapeutic integration programs.

In addition to depression, psilocybin has been shown to reduce symptoms of anxiety, PTSD, substance abuse and end-of-life distress (people struggling with terminal diseases).

Can you take psilocybin while on antidepressants?

Like psilocybin, most typical antidepressants work on the serotonergic system . Mixing antidepressants and psilocybin could lead to an overstimulation of serotonin, known as the serotonin syndrome.

Serotonin is a natural chemical that helps regulate many different functions, such as: mood, sleep, digestion, sexual desire, among others. Depression has been linked to an imbalance of serotonin in the brain, but too much serotonin is no good either.

Symptoms of serotonin syndrome:

Serotonin syndrome symptoms usually occur within several hours of taking a new drug or increasing the dose of a drug you’re already taking.

Symptoms:

  1. Agitation or restlessness
  2. Insomnia
  3. Confusion
  4. Rapid heart rate and high blood pressure
  5. Dilated pupils
  6. Loss of muscle coordination or twitching muscles
  7. High blood pressure
  8. Muscle rigidity
  9. Heavy sweating
  10. Diarrhea
  11. Headache
  12. Shivering
  13. Goose bumps

Severe serotonin syndrome can be life-threatening.

Severe Symptoms:

  1. High fever
  2. Tremor
  3. Seizures
  4. Irregular heartbeat
  5. Unconsciousness

Treatment:
Serotonin syndrome generally doesn’t cause any problems once serotonin levels are back to their original levels. It often resolves within 24 hours of discontinuing the serotonergic agent. Attention with drugs with long half-lives or active metabolites as they may cause symptoms to persist. Irreversible monoamine oxidase inhibitors (MAOIs) carry the greatest risk, and symptoms can persist for several days.

SSRI & Psilocybin:

Selective Serotonin Reuptake Inhibitors (SSRIs) are the most commonly prescribed medications for depression, OCD, PTSD, and other anxiety disorders. Some of the most well-known SSRIs include:

  • Citalopram (Celexa, Cipramil)
  • Escitalopram (Lexapro, Cipralex)
  • Fluoxetine (Prozac, Sarafem)
  • Fluvoxamine (Luvox, Faverin)
  • Paroxetine (Paxil, Seroxat)
  • Sertraline (Zoloft, Lustral)

While in rare cases, it has been hypothesized that this can lead to serotonin syndrome. With proper dosage, guidance and supervision, such risks can be mitigated. Treatment programs tend to accepts individuals on SSRIs, usually taking into account their medical history, and other factors.

SNRI & Psilocybin:

Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) boost both serotonin and norepinephrine levels in the brain. Some typically prescribed SNRIs are:

  • Desvenlafaxine (Pristiq, Khedezla)
  • Duloxetine (Cymbalta)
  • Levomilnacipran (Fetzima)
  • Milnacipran (Ixel, Savella)
  • Venlafaxine (Effexor XR)

Just like with SSRIs, we would expect SNRIs to overlap with the effects of psilocybin. However, there are no reports of serious adverse effects of combining the two. There’s data suggesting that SNRIs actually reduce the effect of psychedelics.

MAOIs & Psilocybin:

Monoamine Oxidase Inhibitors (MAOIs) work by preventing the breakdown of monoamine neurotransmitters (dopamine, serotonin, and norepinephrine) and thus, boosting their levels.
Common MAOI medications include:

  • Bifemelane (Alnert, Celeport)
  • Caroxazone (Surodil, Timostenil)
  • Isocarboxazid (Marplan)
  • Metralindole (Inkazan)
  • Moclobemide (Aurorix, Manerix)

There is the small possibility of serotonin syndrome if MAOIs are combined with psilocybin. It is advised to avoid taking large doses of psilocybin if you are taking MAOIs. However, some people have reported that combining MAOIs with classic psychedelics reduces the effect of the psychedelic. As always, it is recommended to start with small doses.

*Attention! Mixing MAOIs with MDMA has potentially fatal effects as the risk of serotonin syndrome is much higher. Do not mix MAOIs with MDMA.

Least Common Medication Combined with Psilocybin for Depression:

TCA/TeCA: Data suggest that they can cause death by their effects on the heart. Is not recommended to mix these with psilocybin.

NRI/NDRI: There’s not enough research to know what the interaction would be between psilocybin and NRIs/NDRIs, thus, is better not to combine them.

SMS/SAR: work on the serotonin system in a potentially less predictable way than SSRIs (activating and deactivating specific receptors). Thus, is not recommended to mix these substances.

Lithium: Its mode of action is not completely understood, but there is research indicating that Lithium is a dangerous substance to combine with psychedelics. It has been reported to cause seizures, heart failure, and even death.