Is ketamine going to be Psychedelic Therapy’s opening act? At medium to large doses, Ketamine evokes colorful visions and mystical type experiences that have been linked to positive treatment outcomes. And—unlike other psychedelics—Ketamine has been readily available at clinics worldwide for 50 years.

Psilocybin and MDMA have gotten much attention for their potential efficacy in treating some of the most prevalent psychiatric conditions of our time, such as depression, trauma and anxiety disorders. Phase-3-studies are well underway, effect sizes look promising and therapists around the globe are being trained to bring this new and potentially groundbreaking treatment to the masses. However, clinical approval of psilocybin and MDMA might still be a long way ahead of us. In the meantime, some within the psychedelic community are looking to see whether ketamine may be able to fill the gap.

What is ketamine?

Ketamine is a so-called dissociative anesthetic. Like all good anesthetics, it ensures patients have no body movements, no pain and no memory. What’s more, Ketamine has two important advantages over other anesthetics. First, it doesn’t cause significant drops in blood pressure. And second, it doesn’t cause respiratory depression. These additional features made ketamine the anesthetic of choice for operating under suboptimal conditions, like in the Vietnam War where anesthesiologists, who must monitor vital signs and adjust dosage to keep patients from dying, were rare in the field.

Is ketamine legal?

Yes. Ketamine is legal, dirt cheap and readily available in hospitals everywhere.

However, despite its advantages, clinicians have taken a step back from using ketamine as anesthetic due to its peculiar side effects. Namely, patients have reported bizarre visions and out-of-body experiences on coming out of their anesthesia. Hence the name dissociative anesthetic. These psychoactive properties of ketamine were considered undesirable and as a result, ketamine is used only infrequently as an anesthetic today.

From anesthesia to psychiatry

Starting around the year 2000, ketamine has had a revival in the field of psychiatry. It turns out that, in lower doses, ketamine has distinct antidepressant effects. Ever since, psychiatrists have administered ketamine to patients who suffered from severe depression. The clinical use confirmed what studies had previously shown: for many patients, ketamine could immediately relieve symptoms of depression—even with just one dose. This extremely fast onset closed an important gap in the clinical treatment of depression, because modern antidepressants like SSRIs and SNRIs take about two weeks to come into full effect. Acutely suicidal patients can’t wait that long, thus ketamine has gained popularity again, now as a so-called rapid-acting antidepressant.

Why hasn’t my doctor suggested ketamine to me?

Let’s discuss why ketamine is not without controversy.

- Short-lived duration

About 60-70% of depressed patients respond to ketamine.^{1 2 3 4 5} This is a great result, considering that these patients suffer from a treatment resistant form of depression, meaning that at least two prior treatments have failed. Unfortunately, these effects are short lived. About one week after a single administration of ketamine, the symptoms usually kick back in. ^{1 2 3 4 5}

In clinical practice, patients are started off with a flight of ketamine to lift them out of their depression. At the same time, they are shifted from their old SSRI to a new SSRI. The rationale is that it’s the SSRI that does the long-term stabilization and ketamine is only an add-on to that therapy. Patients who respond to the initial ketamine flight but then relapse may receive a weekly dose of ketamine as maintenance therapy.

- Clinical approval

This is where it gets complicated: Ketamine is approved as anesthetic, but not as an antidepressant. And yet, it’s possible within medical practice to use pharmaceutical drugs for unapproved indications if there is no other treatment available. This is known as off-label use. Ketamine has widely been used off-label in treating treatment-resistant depression. But in order to be formally approved as an indicated treatment it takes a long, complicated and expensive procedure, which typically only pharmaceutical companies can afford. After 20 years of off-label use, the pharma company Johnson & Johnson changed the game. In 2019 they attained FDA approval for a variant of ketamine—Esketamine—which they patented and sell today as a nasal spray called Spravato. Now that there is an approved treatment available, doctors are compelled to use the proprietary nasal spray over regular ketamine. The catch: a single dose of Spravato is priced in the high 3-digits, whereas a dose of regular ketamine costs less than a cup of coffee.

There is little data comparing the efficacy of Esketamine to that of regular ketamine. A small study suggests that Esketamine is not inferior to regular ketamine in treating treatment-resistant depression. ⁶ However, it hasn’t been proven superior either. According to the clinicians that I’m in touch with, regular ketamine is just as good, if not better.

- Abuse potential

Ketamine is a derivative of PCP which some readers may know of as the street drug called Angel Dust. Chemical compounds escaping the lab and being used recreationally is a common theme throughout the history of pharmaceutical drug development. Heroine, cocaine, LSD and various types of methamphetamines were originally developed in pharmaceutical labs for therapeutic purposes. It is because they were so effective that they leaked into the party scene. By their nature, all psychoactive substances that are “fun” will be used recreationally and the same has been true for ketamine. Outside the lab ketamine is sold as Special-K or Vitamin-K in the form of a snortable powder. Ketamine has detrimental side effects if used frequently, it can lead to addiction and—under unfavorable und unsupervised circumstances—can be lethal. More on that later.

Thus, ketamine is not designed for home use, but rather being administered at clinics and by trained medical staff.

Three different ketamine models

What makes ketamine effective? The short answer is: we don’t know for sure. Amongst clinicians, researchers and practitioners we currently find three different hypotheses which—in turn—result in three different treatment models that will be laid out in this section. What’s effective is 1) the pharmaceutical substance, versus 2) the combination with psychotherapy, versus 3) the visions themselves.

Let’s explore what’s behind these three hypotheses and who provides the treatment that comes with them.

1) The medical model

Dosage: 0.5mg/kg
Routes of administration: intravenous drip, nasal spray

The medical model operates with small doses, no visions and higher frequency. With low dosages, psychoactive effects can be kept at bay. On the other hand, low doses need to be administered more often in order to achieve a cumulative effect. As mentioned above, ketamine is used as an add-on treatment to conventional antidepressants. The medical model is the status quo in most larger clinics around the world.

Recently however, a new perspective has emerged amongst experts in the field: what if the psychoactive properties aren’t merely an irritating side effect, but are actually responsible for the efficacy of ketamine?

2) The therapeutic model

Dosage: 0.25-0.75mg/kg
Routes of administration: intravenous drip, intramuscular injection, lozenge

The idea of the therapeutic approach is to use the psychoactive properties of ketamine as lubrication for talk therapy. In other words, to help patients relax and talk about things that are too painful to talk about otherwise. During this approach, patients are fully conscious but feel a bit more disinhibited, which makes it easier for them to open up. ⁷ This approach has been named Ketamine-Assisted Psychotherapy (KAP) and is offered by smaller treatment centers and individual health care providers.

3) The psychedelic model

Dosage: 1-2mg/kg
Routes of administration: intravenous drip, intramuscular injection

In the psychedelic model, the patient is lying down and fully giving in to the psychedelic experience which can involve colorful dream-like visions, meaningful insights and full dissociation which manifests as out-of-body experiences. This is the state that recreational users refer to as being in a k-hole. Psilocybin and LSD Studies from the 1960s until today have shown a correlation between such mystical-type experiences and positive treatment outcomes.⁸ It stands to reason that the same principle could apply to ketamine as well, thus the psychedelic model. But little data has been gathered to confirm this assumption.

Typically it’s the same providers that offer the therapeutic model, that would also offer the psychedelic model. It’s widely agreed however, that this high-dose approach is not appropriate for many patients. ⁷

In our next story we will take a peek inside some of the clinics that offer therapeutic and psychedelic treatment models. Sign up for our mailing list to be notified when the story drops.

 

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References

We—Sapiensoup authors Nadine and Marlene—were taking a long break. Why? We had more babies! Not together obviously, each of us had one more.

Image Credit: Vivek Kumar https://unsplash.com/@vikceo

And while we do believe that Having a Baby Sucks at times, we love them so much that we made more. :heart: The break was good for us and our families. Now, we’re back. Stay tuned for new and fresh stories to be released here on Sapiensoup. The next series will be on Ketamine.

Breastfeeding women have been strongly discouraged from consuming marijuana. This recommendation was primarily based on precaution, rather than data. Now, in April 2018, a new study has been released that provides the most concrete data on THC and breastfeeding in the history of cannabis research. As it turns out, only very small amounts of THC transfer into mothers’ breast milk.

New study, new findings

The researchers Dr. Teresa Baker and Dr. Thomas Hale collected and analyzed breast milk samples of Colorado mothers in 2017. The results were published in the scientific journal Obstetrics & Gynecology on April 6th of 2018.

Here is the rough outline of how the study was conducted:

• 8 mothers who were exclusively breastfeeding
• 2-5 months after giving birth
• Dosage: 23.18 milligrams of THC in a glass pipe. And in case you’re wondering whether such a dose will get you high—yes, yes it will.
• All mothers were regular cannabis users. Most reported occasional use (a few times per week), one mother reported chronic use (daily or multiple times per day).
• 5 samples were analyzed per mother:
  • 1 baseline prior to consumption
  • 4 times after consumption: at 20 minutes, 1 hour, 2 hours and 4 hours

Unfortunately, the original publication is behind a paywall. But here are the two key takeaways from it, put in perspective with what we’ve learned from cannabis research since the 1970s:

1. THC concentration in human breast milk is low

The baby gets on average 2.5% of the maternal THC dose through the breast milk.¹ Only 2.5%—that’s very little. And yet, it’s an apples to oranges comparison if what you really want to know is “How much THC gets into the baby’s system?”. That number would be even lower than 2.5%, and here is why: the mother inhales whereas the baby ingests. This distinction matters, because different consumption modes are associated with different bioavailability rates. And bioavailability rates tell us how much of the consumed substance actually gets absorbed by the body. With inhaled marijuana, the bioavailability is somewhere between 10-35%². When marijuana is ingested, however, the bioavailability drops to 4-12% because of the first pass effect through the liver.² Check out my previous post on The Human Metabolism of THC to learn what exactly causes the lower bioavailability and how THC turns into a different drug when it’s ingested.

This means that the estimated dose for the baby—2.5% of whatever the mother had—is further reduced by the lower bioavailability of THC following ingestion.

2. THC concentration falls off after one hour

The highest concentration of THC in breastmilk occured one hour after cannabis consumption. Below, you can see the amounts of THC in all the analyzed breast milk samples from the present study on a timescale from zero to four hours.

The mean peak concentration was 94 nanograms of THC per milliliter of breast milk (ng/ml) after one hour. Mom number 6 is an outlier with peak values beyond 400 ng/ml which looks dramatic. And yet, regardless of how high the peak THC concentration of each and every mother was, after 4 hours the THC amounts have returned to low levels around 26 ng/ml—even in outlier mom number 6.

How to apply these findings

Okay so what are the practical takeaways for mothers who’d like to make an educated decision about cannabis consumption while nursing? The answer—a stopwatch may be your best friend.

Feed first

Babies have feeding and sleeping rhythms that mothers usually know by heart and they could time their cannabis consumption accordingly. If, for example, a baby drinks at 8pm the last time before it goes down for the night, the mother could consume directly after feeding. In that way, the baby wouldn’t be drinking while the THC concentration is at its peak. If the next feed takes place four hours after the cannabis consumption, baby’s exposure to THC would be rather low. Older babies can even go for 6 to 8 hours without feeding at night. At that point, it’s likely that the milk would contain only residual amounts—if any.

Example of feeding schedule (underlying data from Baker¹, dotted line is my own projection)

The present study tracked THC concentrations over a timeframe of four hours only. Another study is currently in the making that explores a timeframe of 36 hours. Until we have that data, the dotted line in the chart above remains my educated guess.

Pump first

One could further minimize THC exposure by feeding pumped breast milk at the first feeding session after cannabis consumption. In that way, the timespan of non-exposure can be stretched out another 3-4 hours, to a point when THC concentration is minimal and at a 2.5% transfer rate, possibly even non-existent.

Another fall back option could be to replace the first meal with formula instead of pumped breast milk. Personally, I’d be conservative with this option because of the well-established benefits of feeding natural breast milk. A few times might be okay, but I wouldn’t do this on a regular basis. Ironically, withholding natural breast milk from the baby poses its own risks.

Choose your strain

You may want to choose a strain of marijuana that has a higher amount of cannabidiol (CBD). CBD is a natural compound in the cannabis plant that has antibacterial, anti-inflammatory, anti-anxiety and neuroprotective properties.³ Some of the unwanted side-effects of THC—such as alterations in functional brain networks—can be significantly reduced through CBD.⁴ Although CBD doesn’t act on brain-receptors like THC does, it still helps to relax and to relieve anxiety. Hence, going for a well-balanced THC-to-CBD strain, rather than a high-THC strain with low CBD, could help reduce the total THC exposure for the mother and thus, for the baby.

Consider edibles

Another strategy to lower total THC exposure is to choose edibles over inhaling. The chart below compares the total THC exposure between smoking vs. ingesting cannabis. Edibles will produce a decent psychological high (brown) but at considerably lower overall THC levels (green).⁵

Note that the psychological high may differ slightly when using edibles. On the one hand it lasts much longer compared to inhaled cannabis. One the other hand people have reported that they experience a different type of ‘high’. For both reasons, it’s strongly suggested to start with very small amounts and have a trusted friend, babysitter or family member on call who can come and help mother and baby if things go sideways.

Myth debunked: breast milk holds eight times more THC than blood

Remember from our first post on Cannabis and Breastfeeding, how the default statement on the internet is “There is eight times more THC in breast milk than in blood serum”? (Seen here, here, here) What no one mentions however, is that this number is based on one single sample from a heavy-using mother who smoked 7 pipes a day⁶—maybe not the most representative case for new mothers out there. Thanks to the new data we can now lay this controversy to rest. The 8:1-myth is a great tool for scaring breastfeeding women away from cannabis use, when in fact it’s little more than an arbitrary number. It has as much explanatory power as a single temperature measurement is capable of predicting the seasons.

Let me showcase to you why this is. The following chart compares the THC levels in blood serum with the ones in breast milk. Note that the THC dosages aren’t identical. The blood levels were measured in participants who smoked 33.80 milligrams of THC whereas the mothers smoked 23.18 mg of THC. Thus it’s not a perfect comparison, but it’s good enough to convey the point—because after one hour, most of the smoked THC is eliminated from the blood anyway, regardless of how much the initial dose was. Take a look at the THC ratio in milk (green) compared to blood (blue):

Comparison of mean THC levels in breast milk¹ and blood⁷

A little past the first 60 minutes you can see that the ratio between milk and blood in fact is 8:1, meaning there is 8 times as much THC in breast milk than in blood. Rewind 45 minutes, however, and the ratio is 1:1 with the levels in milk and blood being equal. And if you measured the levels at 10 minutes after consumption, you’d find out that the ratio is 1:7, meaning that milk contains only 1/7th of the THC that is found in blood serum.

Quoting a milk-to-blood ratio without giving proper context about the timeline and absolute THC levels is misleading. Compare, for example, the ratios at the 30 minute and 240 minute (4 hour) marks. A ratio of 1:1 sounds less worrisome than 12:1, doesn’t it? Consider, however, that the absolute THC levels at the time of the 12:1 ratio are lower than at the 1:1 ratio. This is how deceptive these numbers can be without the correct context.

In a nutshell, looking at ratio alone is pointless, because

1. The ratio changes all the time, which makes it easy for people to selectively pick the ratio that best pushes their agenda.
2. Absolute levels matter. Even if at 4 hours the ratio is 12:1, meaning that there is 12 times as much THC in breast milk compared to blood, it’s at low overall levels.

My take on mothers who use cannabis

I neither condone nor condemn the use of cannabis while breastfeeding. Above all, I believe we should have more compassion with new mothers. Raising children is hard and the first months and years can be especially challenging. When I had my first child, I remember multiple occasions of me secretly wishing for a joint to help me be more relaxed throughout these exhausting times. On top of that, I’ve come to appreciate cannabis as a catalyst for creativity and lateral, outside-the-box thinking. It has most definitely increased the quality of my work.

Just saying “Don’t use pot, it may harm the baby” falls short of considering the bigger picture. It’s like saying “Don’t drive a car, it may harm the baby”. Do we stop driving cars? No, we use seat belts and drive carefully. Nothing is without risks, the goal is to diligently weigh out risks and benefits.

Mothers should be trusted to make reasonable risk-benefit assessments, since they are the experts for their unique life situation. If they feel that a joint from time to time can meaningfully improve their life quality, I’ll respect that. If they feel that they can be better, calmer and happier mothers by occasionally allowing themselves to use cannabis, I’ll respect that too.

After all, not using cannabis has consequences as well. When the body is stressed, it produces the stress hormone cortisol. Cortisol will temporarily raise energy levels to allow you to deal with the stressor, but chronically elevated cortisol levels have been shown to damage brain cells in the hippocampus and cause premature brain aging.⁸ Stressed mothers not only tend to lash out at their kids more often—what are the long-term effects of that?—but also transfer cortisol through the breast milk. In that way, maternal stress also poses a risk to the baby.

Weighing benefits and risks

I breastfed my first child for almost two years, which is known to be extremely beneficial for a baby’s overall health, immune system and brain development. In contrast, detrimental effects though THC in breast milk are disputed and poorly-researched. Some studies find such effects, others don’t.

Weighing out the benefits of breastfeeding against the risk of THC in breast milk

I believe that two years of mommy’s super-juice will outweigh the occasional joint. Especially, if a mother further mitigated (hypothetical) risks by following smartly timed feeding sessions to absolutely minimize the already low 2.5% transfer rate. Besides, I think it’s exactly this kind of weighing out risks and benefits that qualifies a mother as being responsible. But acting responsibly is only possible if we provide mothers with proper data so that they can make an informed decision in the first place.

Simply saying “Don’t use cannabis while breastfeeding” ignores the fact that 10% of Americans are using cannabis regularly⁴ and that some portion of these 10% are breastfeeding mothers. They are already using. For this reason and those above I’d rather give suggestions how to mitigate risks and support them in making smart choices.

 

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References

Do you have a gut feeling for numbers denominated in bitcoin? I don’t. How much is a coffee? How much is a haircut? How much is a new phone? Obviously, these numbers change all the time with the price of bitcoin. But that’s only one part of what makes thinking in bitcoin so damn difficult.

Disclaimer: there are incredibly smart people working, thinking and writing about bitcoin. I’m not one of them. I’m just a regular user who wants a simple and convenient solution to this problem:

A coffee currently costs 0.00044 bitcoin. Zero, zero … what? Our brains treat a decimal point like the end of a sentence; what’s after the decimal point gets disregarded. Marketing managers have known this for ages, and that’s why a coffee usually costs $2.99 instead of $3.00.

If you want to pay for your coffee in bitcoin—which no one in their sane mind does—here’s the fun you’re getting yourself into.

After the year 2012, when the bitcoin price once and for all left the double digit dollar range, there was never again an easy-to-handle price for your coffee. If you’re struggling with 8 digits after a decimal point—you’re not alone. The alternative, satoshi, isn’t much better either. Satoshis are like the pennies of bitcoin, but where there are 100 pennies to a dollar, there are 100,000,000 satoshis to a bitcoin. This means that denominating prices in satoshis is a little bit like living in country with a hyperinflated national currency. Take for example Vietnam’s dong: one dollar will buy you 22,800 Vietnamese dong. Thus, a $3 cup of coffee would cost 68,400 dong. Not convenient.

Today in bitcoin-land, you have to choose between displaying prices using (a) a very small number denominated bitcoin, or (b) a very large number denominated in satoshis. What’s missing is something in the middle.

The units debate

My vote is to use the metric unit system in increments of thousands. Note that this is in no way original thinking of mine. The terms milli-bitcoin and micro-bitcoin have long been suggested within the bitcoin community, as you can read in the bitcoin wiki. Further shortening a milli-bitcoin to a milli-‘bit’ is something that I’ve seen people do here and there and I think that works just fine. The Bitcoin Improvement Proposal 176 however, suggests calling just micro-bitcoin ‘bit’. Only time will tell what nicknames will be used eventually. Here is what’s on offer today:

I like the metric system because it scales effortlessly. As bitcoin rises in value, prices will move from the mili range into the micro range and eventually into the nano range, at which point it actually becomes practical to denominate prices in satoshis.

You might ask yourself how many decimal places we will actually need and use over time. To answer that question we have to know where the price of bitcoin will settle.

How much will bitcoin be worth?

Nobody knows. Really. Nobody. As of now, it’s all hypothetical models and best guesses. One way to think about the future value of bitcoin is to select a traditional value category, such as the world’s gold reserves or the world’s total money supply and then divide the market capitalization of that value category by 21 million—the total number of bitcoin that will ever exist. That’ll present you with a certain price per bitcoin. The Money Project published a brilliantly visualized comparison of such value categories which we will use as a basis for our hypothetical calculation. Let’s consider gold, narrow money and broad money:

If bitcoin only ever reached the market capitalization of gold, i.e. $7.7 trillion, each bitcoin would be worth $366,667. If it replaced the global money supply, that number would reach millions of dollars.

I want to be clear that this is a quick and dirty calculation, based on unrealistic assumptions like total market adoption and is oblivious to forever lost bitcoins. The actual bitcoin price will almost certainly turn out differently. Having said that, I do believe that cryptocurrencies are the future of money. There are good reasons why bitcoin is superior to gold or ordinary banknotes. If you’d like to know what those reasons are, I recommend reading The Bullish Case for Bitcoin.

So don’t consider the above calculation financial advice. Rather, it’s a necessary assumption to answer our original question: how many decimal places does a good bitcoin unit system need to accommodate?

Let’s take a look at future prices of goods. I projected the price of a coffee ($3), a Tesla Model S ($71,000) and a 2-bedroom home in Manhattan, NYC ($1,800,000) onto these three different scenarios.

Even in the broad money scenario we’d end up with relatively bulky numbers if prices were denominated exclusively in bitcoin and satoshis. The metric unit system, however, offers an at-max 3-digit denomination for any price, regardless what the bitcoin market capitalization will turn out to be.

Problem solved. Now what?

Merely having a solution, doesn’t equal the adoption of a solution. In order for the metric approach to become the prevalent unit system in bitcoin, people have to actually use it. Some bitcoin wallets have started offering metric denominations, but one rarely hears ‘milli-bitcoin’ used in everyday language.

So, why aren’t people using it?

I think the reason is that bitcoin has been more commonly used in written language than in spoken language. Reading “0.00044 BTC” poses less of a challenge to the human brain than hearing “zero point zero zero zero four four bitcoin” in conversation.

Today, most people use bitcoin either as a store of value or for trading. Hardly anyone uses bitcoin to pay for coffee. I believe that will change in the future, though, and as we see more and more prices denominated in bitcoin, the demand for an easy unit system will increase. No one can really predict which terms will make it into popular language. Maybe it’ll be millies and mikes and maybe it won’t. After all, who would’ve predicted that we’d ever have words like “selfie”, “hangry” or “swag”?

Nakamoto, why…?

What really gets me is this: why on earth would bitcoin’s creator make 1 bitcoin equal 100 million satoshis in the first place?! If Satoshi Nakamoto had given it just one more decimal place, making 1 bitcoin equal to 1 billion satoshis, bitcoin would have been metric-friendly out of the box: we would have had perfect milli, micro and nano divisions.

I don’t get it. Maybe the failure to design for metric-system friendliness is the best proof yet that Satoshi Nakamoto was an American.

My 3 favorite reads on bitcoin

I’m just a lay user sharing her thoughts. If you want to hear actual experts talking about bitcoin, you might want to check out the following links.

Bitcoin basics: Bitcoin Explained by Upfolio

Understanding the price of bitcoin: Speculative Bitcoin Adoption/Price Theory by Michael B. Casey

Why bitcoin is the better money: The Bullish Case for Bitcoin by Vijay Boyapati

Every day, 120 Americans commit suicide; 20 of them are war veterans.^{1 2} “I know without a doubt: MDMA saved my life.” said one war veteran who was suffering from post-traumatic stress disorder (PTSD), a mental condition which is hard to cure and may lead to further disorders such as anxiety, depression and addiction.

More than 868,000 US war veterans suffer from PTSD and their families suffer with them.³ Living with a partner or parent with PTSD means living with their elevated levels of anger or irritability which are often paired with feelings of hopelessness, guilt or depression and all too frequently accompanied with substance abuse. At best, this poses a challenging family life, at worst it can lead to suicide. As dark as this situation may be, a new ray of hope is emerging from—of all things—MDMA: a substance currently deemed an illegal party drug. MDMA-assisted therapy has proven to be far more effective than any other PTSD treatment available today. The Food and Drug Administration (FDA) has approved a roadmap to legalize the substance for medical use by 2021.

MDMA is currently being researched for its efficacy in social anxiety, end-of-life distress, couples therapy and most pressingly: PTSD. Consider that more US troops die from suicide than in combat. Besides the emotional costs of such a condition, an estimated $17 billion are spent on disability compensation for veterans suffering from PTSD each year.³

Unlike common psychiatric medicine, that has to be taken on a daily basis and potentially for the rest of one’s life, MDMA is only administered a few times. According to the latest study by MAPS, after only three sessions of MDMA-assisted therapy, 61% of patients no longer suffered from PTSD.⁴ The effects are immediate and long-lasting; an earlier study showed that even after four years later the patients did not tend to relapse.⁵

MAPS study results. Snippet from MAPS infographic on PTSD

What these numbers don’t reflect are the dramatic stories of the war veterans, rape survivors and victims of childhood abuse behind these statistics. For years, they had lived with chronic anxiety, depression and panic attacks until they finally underwent MDMA-assisted therapy. Scott, who served in Afghanistan and Iraq and had seen three of his comrades commit suicide, said “I know without a doubt: MDMA saved my life.” Watch some of the study participants tell their story in their own words. You might want to keep a tissue handy.

What is trauma?

“Trauma is not a divorce, your mother’s depression, your father’s alcoholism or physical abuse.” explains Dr. Gabor Maté, psychiatrist and expert in trauma, addiction and ADD. While such experiences may be traumatic, they’re not the trauma itself. He emphasizes that “Trauma is not what happens to you, trauma is what happens inside you.”⁶ And what may happen inside of you as a result of a traumatic event is that you get disconnected from your emotions and your body. This in turn makes it increasingly difficult for you to be present in the moment. You develop a negative view of the world, of yourself and you develop a defensive attitude towards other people. ⁶

“Trauma isn’t what happens to you, it’s what happens inside you.”

And indeed, people suffering from PTSD often find it difficult to regulate their emotions and navigate relationships. The typical clinical symptoms of PTSD are insomnia, anxiety, nightmares, emotional distress or panic attacks. ⁷

Post-traumatic stress disorder in the brain

How does PTSD manifest in the brain? People who suffer from PTSD show a decreased activity in the hippocampus and the prefrontal cortex—areas associated with learning, rational thinking and decision making. At the same time, a brain area called the amygdala—responsible for emotions, fear conditioning and fight-or-flight responses— shows increased activity levels. The amygdala is the commander-in-chief of your survival instincts. When she speaks, everybody listens.

Snippet from MAPS infographic on PTSD

Now, when a PTSD patient is reminded of a traumatic experience—through subtle cues like sounds, smells or fabrics—their amygdala takes over and shuts down the higher order functions of their brain, like the prefrontal cortex. The individual is left with a seemingly irrational fear response that can manifest as stress, panic or aggression. People who suffer from PTSD have the hardest time processing their trauma rationally, because whenever they’re confronted with their traumatic experience, the rational areas of their brains are simply not accessible.

MDMA helps navigating trauma

MDMA can help patients with PTSD to revisit their traumatic experiences without being overwhelmed by negative emotions. MDMA decreases activity in the amygdala⁸ and leaves the prefrontal cortex online, enabling patients to analyze and reflect on their experiences, which in turn gives them the chance to integrate these experiences into their lives.

A rape survivor described it as “It was like I got to do brain surgery on myself. I could go into my mind and see the thought patterns and the belief systems that had calcified in there and rewire them.”⁹

The right dose of MDMA puts patients in a so-called optimal arousal zone. That’s a state in which the patient is positive and calm while at the same time being motivated to engage in a therapeutic process and open to connect. Usually, patients suffering from PTSD struggle to be any of the above. They tend instead to be hypervigilant, closed up and reluctant to talk about their experience. For all these reasons, MDMA-assisted therapy is beginning to look like a fast lane to healing trauma.

Integration, integration, integration

MDMA alone doesn’t cure patients of their PTSD, it’s the combination of the substance and psychotherapy. The leading research organization in this field, MAPS (Multidisciplinary Association for Psychedelic Studies), uses a 12-week treatment protocol that distinguishes between three kinds of sessions: (1) preparation sessions, (2) dosing sessions and (3) integrative psychotherapy sessions.

Treatment rooms have a cosy, living-room style atmosphere

It’s of the utmost importance that patients feel safe and at home with their therapist. Not having a trusted ‘sitter’ was found to be one of the strongest predictors of a so-called bad trip.¹⁰ During preparation sessions, patient and therapist get to know one another and get comfortable with the setting. The dosing sessions usually include two therapists: ideally one male and one female. The star therapist-team in the MAPS studies were psychiatrist Michael Mithoefer and psychiatric nurse Ann Mithoefer, who is Michael’s wife. They are professionals with years of experience and training in special techniques such as Holotropic Breathwork, which Stanislav Grof developed based on decades of learnings from LSD-assisted therapy.

Michael and Annie Mithoefer, therapists at MAPS

During an MDMA dosing session, people are capable of accessing subconscious content that would usually be filtered or blocked out by their normal waking state of consciousness. When this door opens, patients can go through intense outbursts of emotions like sadness, desire or fear and often have meaningful insights. After the acute effects of the substance have tapered off, the therapist helps the patient to integrate their experience. This means helping the patient to acknowledge and allow their feelings, and as a next step, reflect on them in a self-compassionate way. If, as Dr. Gabor Maté proposes, trauma is the disconnection from one’s body and emotions, then integration is one’s re-connection to them.

Integration is one’s re-connection with their body and emotions.

Can MDMA fix your relationship?

Relationships are hard. The daily grind of bills, chores and raising children takes a toll on most every couple. Over time, misunderstandings and communication pitfalls turn into negative behavior patterns and—fast forward ten or twenty years—what used to be love may have turned into mere (dys)functional co-habitation.

For many couples this ends in either a loveless marriage or divorce. Preliminary studies have shown that MDMA-assisted therapy can help couples quickly get to the bottom of their problems and work through them. This is what we know so far:

MDMA helps the couple remember their initial feelings of love and deep connection to one another and thereby creates a safe space in which “you can say anything” as one study participant described.¹¹ In an environment where one can be vulnerable, couples begin to talk openly about their sexual fantasies, their insecurities, their needs and desires. One woman even confessed that she had cheated on her husband. In their exceptionally open and accepting state, the couple managed to deal with her affair in a compassionate way which eventually resulted in strengthening their bond.¹¹

With fear, defensiveness and resentment out of the way, couples are afforded a “nice clean slate” from which they can tackle their problems.¹¹

To be clear, the idea is not to use MDMA regularly to be in a better mood with your partner. But a few strategically placed sessions can create enough momentum to permanently change relationship dynamics. A couple from another study stated that their MDMA sessions have torn down the barriers between them so they can talk more freely when sober.¹² MDMA doesn’t fix your relationship. “It’s not a magic bullet. It’s how you integrate what you learn into your life.” explained a male participant from the same study. When he and his wife get into a conflict nowadays, rather than mindlessly arguing they ask “What is this really about?”.¹²

I’ve personally interviewed a number of couples who have used MDMA to work through tough phases in their relationships. What I’ve heard over and over again was “I don’t know if we’d still be together if it weren’t for MDMA”.

MDMA-assisted couples therapy

When couples seek out professional help they’re usually on a hair-trigger with one another, quite possibly already considering divorce. The clock is ticking, and what they need is immediate relief.

A few intentionally placed MDMA-assisted therapy sessions can be exactly the kind of drastic intervention that’s necessary. Several couples have told me “if done well, such a session can be like years of counseling”.

Currently, the focus of MDMA-assisted research lies in the treatment of trauma. The use of MDMA for couples therapy is an under-researched field and to my knowledge is practiced only in the underground or on a couple’s own accord, without the supervision of a therapist. While the lack of a therapist is certainly not ideal, the much bigger problem is the health risk associated with the use of an unregulated substance. Whereas a correctly measured dose of pure MDMA is relatively safe and has a lower toxicity profile that legal drugs like alcohol or cigarettes¹³—acquired from the black market, the user has no gauge of purity, correct dosage or possible contamination with harmful additives. The danger comes not with the use, but with the criminalization of MDMA.

Currently, our society is operating on a double standard. Have you ever been to a Christmas party without a bar? We allow alcohol as a means to bond with our co-workers. But we forbid MDMA as a means to mend our personal relationships.

The medical case for MDMA is strong and over the coming years, we will see country after country legalize the substance for therapeutic use. I can see a future in which therapists might add MDMA-assisted marriage counseling or MDMA-assisted family reconciliation to their portfolio. Personally, I’d certainly take advantage of such an offering.

This is the final article in my 7-part series on psychedelic drugs.

Medical Benefits of Psychedelic Drugs
Psychedelic Drugs and the Serotonergic System
The Psychedelic Experience
Your Brain on Psychedelic Drugs
Psychedelics and Mental Health
Microdosing LSD: Smart Drug or Placebo?
MDMA-assisted Therapy

Final Thoughts

The research I’ve done while writing this series has convinced me that psychedelic substances will fundamentally transform our approach to mental health. Some of the most reputable universities in the world—Imperial College London, Johns Hopkins, NYU—are leading modern research in psychedelics. They have produced staggering results which have encouraged yet further institutions to engage in this re-emerging field of research. For the first time, we see more publications on psychedelics today than we saw in the 1960s.

Number of scientific articles on PubMed. Medline trend ©Alexandru Dan Corlan

But it’s more than data and science. I’ve now met many of the people behind this so-called psychedelic renaissance and I’ve found them to be incredibly smart, caring and passionate. Indeed, their work has inspired me to make my own contribution. In May 2017, I founded the Psychedelic Society Vienna to start an evidence-based conversation about the true risks and benefits of psychedelic substances. We run events, workshops and integration circles and work towards bringing psychedelic research to Austria. Our community is growing rapidly and has brought many wonderful people and meaningful friendships into my life. Thank you all!

 

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References

Microdosing LSD promises to act like a mix of Adderall and Prozac but without the side effects. Sounds too good to be true; is it? Some swear by microdosing while others call it a placebo effect. We researched the scientific explanations why microdosing might actually work, the risks involved and evaluated the evidence as of today. Here is what we found.

Microdosing gained currency in Silicon Valley in late 2015 and is spreading like wildfire across the rest of the world. Software developers microdose to enhance their problem-solving capabilities. Biohackers microdose to boost their productivity. People with mood disorders microdose to alleviate symptoms of depression and anxiety.

Stories of young professionals taking tiny doses of acid before going to the office have been making headlines all throughout the media with The New York Times, The Guardian, BBC, CNN, Forbes, Wired, Rolling Stone and Vice picking up on the trend. Search Google for ‘microdosing’ and you’ll find books, podcasts, subreddits and even a new online course on microdosing. Microdosing caters to the needs of a modern society: being highly effective, thinking out of the box and being happy in a fast and competitive world. By doing so, it gives LSD a total image makeover. Today, it’s not ‘smelly hippies’ who use LSD; it’s übersmart twenty-somethings¹, tech-entrepreneurs and high-achievers.

How does microdosing LSD work?

The concept is simple: take a sub-perceptual dose of LSD every few days. Why not every day? The body quickly builds up a tolerance against LSD, and taking a dose every day would diminish the effects. Currently, James Fadiman’s microdosing protocol is considered the gold standard of microdosing:

Unlike the recreational use of LSD, with microdosing you’re not supposed to feel any psychedelic effects. “If you’re taking a microdose and you’re feeling a little high, you’ve been taking a little too much.” says Fadiman.² The goal is to stay under the perceptual threshold. If a full recreational dose of LSD is 100 micrograms, a good first shot for a microdose is 10 micrograms. From there, the dose can be tweaked until the user has found their personal optimum.

LSD is usually distributed on so-called blotters, small strips of paper onto which LSD has been applied in its previously liquid form. Let’s say one blotter holds 100 micrograms of LSD. Because cutting such a tiny blotter into 10 even tinier pieces poses a challenge to most people’s fine motor skills, the easier method is dissolving the blotter in distilled water.

Dissolving a blotter containing 100 micrograms of LSD in 10 millilitres of water, leaves you with a simple ratio of 1 milliliter water = 10 micrograms of LSD. Medical syringes are convenient tools for withdrawing precise amounts of liquid from a bigger container.

The Third Wave, a website dedicated to microdosing, suggests that microdosing leads to increased creative output, more physical energy, improved emotional balance and heightened spiritual awareness. Now, what does the evidence say?

Evidence

Let’s distinguish between two kinds of evidence: (1) anecdotal evidence, which is the report about an isolated use case. And (2) scientific evidence, which rests on the scientific method and is therefore considered the highest quality of evidence.

1. Anecdotal evidence

The internet is full of microdosing user reports. The overwhelming majority of these reports are positive. Users state that microdosing indeed increases their focus, overall life-satisfaction and helps them with depression and menstrual nuisances like cramping and PMS (premenstrual syndrome). Note however that there are examples to the contrary as well: some users report irritability, mood swings and anxiety after they had started their microdose regimen. This was what I experienced. On dosing days I was fine but on non-dosing days I felt anxious and depressed to an extent that made me quit my self-experiment after 22 days.

2. Scientific evidence

In short: there is none.

The closest thing to scientific evidence is James Fadiman’s research project in which he systematically analysed the self-reports of 418 microdosing individuals.² Undoubtedly this is an interesting analysis, but it’s in no way scientific proof. Why? For many reasons. The most important one is that he didn’t have a control group in place. Without a proper control group, there is no way of knowing how much of the observed effects stem from placebo and how much from the actual substance.

The kind of evidence that we’d like to see is a double-blind, placebo controlled study. That means that neither the participant nor the researcher knows if the participant is receiving LSD or a placebo. Currently, there are no such studies.

Why microdosing might work

Despite the lack of scientific evidence, let’s look at possible explanations why microdosing might in fact work.

Stimulant

It’s well-documented that LSD can have stimulant effects in the brain. LSD binds to the serotonin 2A receptor, which in turn can increase the production of dopamine, the neurotransmitter associated with reward. Drugs like cocaine, amphetamine and Adderall all stimulate dopamine receptors. What’s the minimum effective dose for LSD to induce such a stimulating effect? We don’t know.

“It is at least theoretically possible that low doses of LSD could enhance the biosynthesis of dopamine” states Dr. David Nichols, professor of pharmacology at Purdue University. “One consequence could be a mild stimulation that would be reminiscent of a low dose of methylphenidate (Ritalin) or modafinil (Provigil), drugs that are used to treat ADHD or improve vigilance.”³

This explanation is appealing because microdosers frequently report needing less coffee and yet being able to maintain an effortless focus. However, appealing doesn’t equal true. We’ll need to wait for actual evidence before we can state that very small doses of LSD have the described stimulating effect.

Neuroplasticity

Another explanation why microdosing might work is because it may enhance neuroplasticity. Neuroplasticity is the brain’s ability to form new neuronal connections and by doing so, learning new things. Important side note: losing neuronal connections is just as important as building them. Why? Because in order to change a certain behavior, you first have to let go of your current behavior.

Animal studies have shown that the neurotransmitter serotonin plays a key role in losing neuronal connections and hence enabling behavioral change.⁴. It’s possible that psychedelic drugs enhance neuroplasticity too because they activate some of the same serotonin receptors.

In a nutshell: psychedelic substances may increase the flexibility of your current thinking, making it easier for you to abandon old patterns and learning new things. Studies in animals have shown enhanced neuroplasticity even long after the drug has worn off.⁵

Does that mean that LSD makes you smarter? No. Reading books makes you smarter. But LSD may help you retain and apply new knowledge.

Read this before you advocate LSD for brain growth

Even though it’s intriguing to state “LSD enhances neuroplasticity”, I find it important to be transparent about the limitations of this argument. First, psychedelic drugs are not the only way to increase neuroplasticity. Simple things like exercise or fasting increase cognitive performance as well⁶—and this has been proven in humans and not just in animals. Second, we don’t know how much of a psychedelic substance is needed to increase neuroplasticity. It may very well be the case that a 30-minute jog followed by a cold shower is more effective than an LSD trip toward this end. And third, the animal studies mentioned above were conducted with regular to high doses of LSD, not with microdoses. We don’t know the threshold at which LSD may enhance neuroplasticity. Thus, microdosing may or may not have a positive effect on neuroplasticity. We simply don’t know.

For a great review of the current state of scientific research regarding neuroplasticity and neurogenesis, check out the article Do psychedelics trigger neurogenesis? Here’s what we know on Psymposia.

Health Risks

Recall that LSD’s principal target in the brain is the serotonin 2A receptor. The activation of this specific receptor gives users a psychedelic experience and has furthermore been associated with increased cognitive flexibility.⁷ Not too bad so far. However, LSD activates an array of other receptors as well. One of them is the serotonin 2B receptor.

Activation of the serotonin 2B receptor stimulates the growth of cardiac ventricular and valve tissue.³ Long-term activation of this receptor may lead to Valvular Heart Disease which means that the heart’s valves don’t work like they should.

Some of you may remember fenfluramine, or “Fen-Phen”, a weight-loss drug that was pulled off the market because some patients had developed a heart disease after using it. Fenfluramine activates the serotonin 2B receptor with a similar potency as LSD does, thus the concern regarding an ongoing use of LSD.

Microdosing advocates argue that an LSD microdose is several thousand times smaller than a typical dose of fenfluramine. Hence, microdosing has nowhere near the heart disease risk associated with fenfluramine. Nevertheless, they advise to limit microdosing regimens to a maximum of 90 days. On the other side, sceptics like Dr. David Nichols argue that even low doses could be problematic because—unlike normal serotonin—an LSD molecule can get trapped in the receptor for up to 8 hours, thus constantly stimulating it.

Another potential health risk stems from the criminalization of LSD. Because users can’t buy the substance from an official, quality-assured vendor, there is little transparency as to what substance they actually hold in their hands. In other words, there is a risk that they are not using LSD but some other unknown substance with an unknown risk profile.

Is microdosing just placebo?

Never underestimate the power of placebo. Numerous studies have demonstrated strong placebo effects in chronic pain and mood disorders. For example, in antidepressant drug trials, the placebo response makes up for 75% of the positive effect of the antidepressant. ^{8 9}

How we experience reality is heavily biased by our expectations. With microdosing, I believe we’re dealing with a strong positive expectation bias and therefore a strong placebo effect. Think about it like this: would you expose yourself to the risk of being convicted and maybe even losing your job if you didn’t expect a big reward on the other side of the equation? At least that’s how I thought when I first tried it. I really wanted microdosing to work.

The Beckley Foundation has proposed a placebo-controlled study in order to investigate the effects of microdosing LSD at 10, 20 and 50 micrograms. During the experiment, participants will undergo a series of tests like playing Go against a computer, questionnaires and brain scans. If you want this study to be carried out, please support the researchers by donating to the project.

If microdosing indeed turned out to be effective—and more importantly—effective at a lower risk profile than common antidepressants and stimulants, that’d be good news.

And if it turned out to be a placebo effect? In fact, I believe that’d be good news too. Why? Because it would reinforce the idea that a mind can heal itself: alleviating pain, stabilizing moods and enjoying life more. If so, our challenge wouldn’t be to find the right pharmacological fix, but rather to identify strategies how we can activate these apparent self-healing pathways on our own.

On a related but different kind of self-healing process will be our next and final story in the 7-part-series on psychedelic drugs: MDMA-assisted therapy. You can sign up for our newsletter and get notified when we publish it.

Medical Benefits of Psychedelic Drugs
Psychedelic Drugs and the Serotonergic System
The Psychedelic Experience
Your Brain on Psychedelic Drugs
Psychedelics and Mental Health
Microdosing LSD: Smart Drug or Placebo? (You’ve just read it)
MDMA-assisted Therapy

If you are located in the Vienna area, we invite you to join the Psychedelic Society Vienna, where we regularly discuss the latest research and developments in the world of psychedelia.

 

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References

“When you take psilocybin, it’s like taking onboard your own psychotherapist.” said a study participant about his psychedelic experience.¹ A widespread belief about psychedelic drugs is that they can turn users mentally ill; what the data shows, however, is that psychedelics can achieve quite the opposite effect: they afford patients a relief of symptoms. Indeed, a growing body of evidence supports that psychedelic drugs may be extraordinarily effective in treating mood disorder and addiction.

Depression. Anxiety. Addiction. Most everyone of us knows somebody who is battling such a condition. Talk therapies may help, but sometimes they don’t. Antidepressants may help, but sometimes they don’t. Some patients are of the opinion that antidepressants are like “Band-Aids” in the way that they never really tackle the underlying issues of their problems.¹

I haven’t yet heard psychedelics getting described as “Band-Aids”. What I have heard from users is that psychedelics do something like the opposite: they confront you with your greatest vulnerabilities and help you come to peace with them.

“We’re looking at a new paradigm for the way these [mental disorders] can be treated”² says pharmacologist Dr. David Nichols, president and co-founder of the Heffter Research Institute. In this post we’ll look at the latest results from psychedelic research and how they may revolutionize our approach to mental health.

Treating mental disorders

Recent studies have found psychedelics to reduce symptoms of anxiety,^{3 4} depression,^{5 4 6} and obsessive-compulsive disorder⁷ as well as addiction.^{8 9} The effects often lasted for several months after just one or two exposures to the drug.⁵

The results of these recent studies are frankly mind-blowing. I’d like to present to you three of them, all carried out by reputable research teams across the U.S. and Europe.

1. Treatment-resistant depression

The World Health Organization estimates that more than 300 million people suffer from depression.¹⁰ Antidepressants and psychotherapy can offer some relief, but 20 percent of patients are treatment-resistant, meaning they don’t respond to any intervention whatsoever.¹¹

In a recent pilot study performed in the U.K., Dr. Carhart-Harris and his team studied the effects of psilocybin in exactly these kinds of treatment-resistant patients.⁵ The participants had suffered from moderate to severe depression for, on average, 18 years of their lives. All of them had previously tried psychiatric drugs and therapy or counselling, but with no success.

The chart below shows the individual depression assessments of the twelve participants. One week after the dose, 67 percent were free from depression. And three months after the dose, 42 percent remained in remission.

And the long-term effects? Six months after the experiment, 30 percent of the initially treatment-resistant patients remained entirely free from depression. For 75 percent, the psychedelic experience brought some degree of reduction in depressive symptoms.¹

Note that this was an open-label study with a small number of participants and no control group. A lack of controls is usually a red flag and tells you that the study shouldn’t be taken at face value. In this case however, the study at hand was a pilot for larger randomized controlled trials. Research is expensive and just like engineers build a prototype before they roll out large-scale production, researchers do pilot studies before they run full-blown trials. With dramatic results like these, it’s reasonable to expect fully randomized, double-blind, placebo-controlled studies in the near future. And speaking of placebo-controlled studies…

How do you fake a trip?

Controlling for the placebo effect poses a real challenge in psychedelic research. With a psychoactive substance, it’s easy for participants to know whether they have received the placebo or the active substance, and this can render the controls ineffective.

So what can be done? Some researchers use active placebos. Instead of giving the participant a do-nothing pill, they’re given either a very mild dose of the tested drug or an entirely different psychoactive substance. This approach obviously comes with its own challenges, but given the limited options it might be the better bet.

2. End-of-life anxiety

How would you feel if you were diagnosed with life-threatening cancer? Not surprisingly, facing one’s own mortality can unleash strong emotions. Up to 40 percent of cancer patients develop a mood disorder which in turn interferes with their chances of recovery.¹² Psychedelic drugs certainly can’t heal cancer, but it appears they can mitigate the accompanying psychological distress.

Lead researcher Roland Griffiths and his team at Johns Hopkins University School of Medicine tested this hypothesis with 51 cancer patients. One group received a high dose of psilocybin, whereas the control group received an active placebo, which in this case was a very low dose of psilocybin that had no detectable behavioral effects. In this way, all participants were told they were taking psilocybin and this controlled for expectancy.

Five weeks after the treatment with high-dose psilocybin, 92 percent of depressed patients and 76 percent of anxious patients showed significant improvements in symptoms. These positive results were not only immediate, but also long-lasting. Six months after their psychedelic experience, the patients suffering from depression were still going strong with improvement rates of 79 percent. Regarding end-of-life anxiety, the improvement rate further increased from 76 percent five weeks after the treatment to 83 percent six months after the treatment. What’s more, half a year after the psilocybin session, over 80 percent of all participants stated that the experience had increased their well-being and/or life satisfaction.¹²

“Such a substantial and enduring effect after one dose is unprecedented in the field of psychiatry.” says Roland Griffiths, professor of neuroscience and psychiatry at Johns Hopkins.¹³

“Such a substantial and enduring effect after one dose is unprecedented in the field of psychiatry.”

3. Nicotine addiction

Smoking causes almost half a million deaths in the U.S. every year and is related to annual health care expenditures of $170 billion.¹⁴ Overcoming nicotine addiction poses a real challenge to smokers. Smoking cessation programs such as the popular Quit for Life program achieve abstinence rates of only 17.2 percent at six months. If supported with medication and weekly counseling meetings, the success rate can rise to 35 percent, dependent on the medication used.¹⁵ The highest success rates were seen in programs containing extensive cognitive-behavioral therapy, plus pharmaceuticals, plus nicotine replacements. Such comprehensive programs show abstinence rates of 45 to 59 percent at six months.^{16 17}

Matthew Johnson, expert in drug dependence at Johns Hopkins, wanted to see if psilocybin could help smokers to quit their addiction. In an open-label pilot study, 15 nicotine-dependent smokers were guided through a 15-week smoking cessation protocol which provided high levels of psychological support, but no pharmaceuticals or nicotine replacements. The participants had smoked on average 19 cigarettes per day for 31 years and had attempted to quit smoking six times before. After the program, which included up to three psilocybin sessions, 80 percent of the participants were smoke free at the six-month mark.⁸

At 12 months after the quitting date, 67 percent of participants were smoke free, and 87 percent rated their psilocybin sessions amongst the five most personally meaningful and spiritually significant experiences of their lives. Even at around 2.5 years after the quitting date, a solid 60 percent of study participants remained smoke-free.¹⁸

The numbers produced by these three studies are impressive to say the least. Equally impressive is hearing what the participants have to say about these treatment experiences.

Real people, real experiences

Recall the treatment-resistant depression study from above. Six months after the single psilocybin session, the research team followed up with the participants and interviewed them about their session experience and their life ever since.¹

“It was like the light switch being turned on in a dark house.”

Almost half of participants reported major lifestyle changes during the months following the psilocybin session. Frequent changes involved improvements to diet, exercise, and cutting down on drinking alcohol. “I lost a lot of weight just purely because I didn’t want to eat badly and that went on for some months. I couldn’t eat what I knew wasn’t good for me.” Some changed their social circles, went out more, got new jobs, learned to drive, built a new kitchen, volunteered with refugees, travelled or picked up acting, comedy or dance classes.

Across all the stories, researchers identified two major themes of inner change. First, a change from disconnection to connection and second, a change from emotional avoidance to acceptance.

Disconnection to connection

Depression can feel as if you’re in a “mental prison” where you’ve gotten stuck in your thoughts. It “robs you of your confidence in yourself” and makes you increasingly less able to engage with your environment. The result is isolation, and whether it’s a perceived or actual isolation, depression is a lonely condition.

About the time following the psilocybin session, participants reported how they “had the mental agility to overcome problems”. They noticed a boost in self-worth, how they were able to adopt fresh perspectives and how they rekindled previous interests. “[My wife and I] went for dinner for the first time in 6 years: we were like a couple of teenagers.” told one participant. Another shared “I went past a bike shop and went in off the street and said ‘can I hang out and help out?’ I went there for 6 months and helped renovate his shop.”

Some described it as reconnecting to “who they had been” before the depression had developed. Their self-perception changed. Nearly half of the group described realizations of “being a good person” and feelings of self-compassion and self-worth. They felt not only more connected to their surrounding but also more connected to themselves.

Avoidance to acceptance

Boys don’t cry. A common root of depression is the inability or unwillingness to deal with certain emotions. “My whole life I’ve self-medicated to try to make emotions more bearable, sometimes with food, cigarettes, painkillers.”

One participant saw “emotions as weakness” because he had been raised in an environment where he learned to “put his feelings in a box because you can’t be upset, you’re a man”. Others had gone through traumatic events in their past. Regardless the origin, when participants came face-to-face with their emotions during the psilocybin sessions—which happened regularly—it triggered intense yet cathartic experiences. Powerful bouts of sobbing were observed throughout the sessions, which participants later described as “purification”.

After the session, participants noticed a fresh openness to experiencing emotions, a change that was often long-lasting. One participant described it as “a rebooting of the mind”, another noting that “it reconfigures you somehow.”

All participants said they preferred psilocybin over conventional treatments. To many of them, antidepressants and talk therapies seemed as if they were reinforcing disconnection and emotional avoidance. Some participants explained that their past therapists were trying to motivate them from the ‘outside’. Psilocybin, however, helped them to access an ‘inner voice’ which they said felt immensely powerful and highly motivating. “It’s almost as if when you take the capsules it’s like taking onboard your own psychotherapist.” With psilocybin, they had an empowered experience of self-reflection, which previous therapy attempts did not provide.

Rosalind Watts, the lead researcher of this study, proposes that with psilocybin “patients and clinicians may be granted a broader palette of treatment options in the future, affording them an opportunity to select a treatment that best suits the specific needs and/or desires of a given patient.”

“Patients and clinicians may be granted a broader palette of treatment options in the future.

A new approach to mental health

Why are psychedelics so fundamentally different from regular antidepressants? Antidepressants work by increasing the overall levels of serotonin in the synapse, which in turn, leads to more frequent activation of serotonin receptors. Psychedelics activate serotonin receptors too, but in a more targeted way than antidepressants. They activate only certain subtypes of serotonin receptors which are understood to increase cognitive flexibility.¹⁹ Like one of the study participants stated above, psilocybin gave him “the mental agility to overcome problems” and that is precisely what’s required to achieve long-lasting results.

In a nutshell: do psychedelics alone cure mental disorders? No. Rather, psychedelics may serve as a catalyst for patients adopting new perspectives and making important lifestyle changes. Hence, kicking off a treatment protocol with strategically planned dosing session may substantially increase the overall effectiveness of the treatment.¹

Example of a structured treatment protocol involving psychedelic drugs

Given the growing body of evidence supporting the safety and efficacy of psychedelic drugs, I believe it’s a matter of time until jurisdictions around the globe will approve psychedelics for medical use. Organizations like MAPS, Beckley Foundation and Heffter Research Institute play a key role in advancing psychedelic research and driving drug-policy reforms in a peaceful and sensible manner.

In the meantime, a phenomenon called microdosing has become popular in Silicon Valley and beyond. Our next post will take a closer look at microdosing LSD for the purpose of enhancing cognitive performance. You can sign up for our newsletter and get notified when we publish it.

Medical Benefits of Psychedelic Drugs
Psychedelic Drugs and the Serotonergic System
The Psychedelic Experience
Your Brain on Psychedelic Drugs
Psychedelics and Mental Health (You’ve just read it)
Microdosing LSD: Smart Drug or Placebo?
MDMA-assisted Therapy

If you are located in the Vienna area, we invite you to join the Psychedelic Society Vienna Meetup, where we’ll discuss the latest research and developments in the field.

 

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References

“During my LSD sessions, I would learn a great deal” said Cary Grant about the 100 acid trips he dropped in the search of his true self. “And the result was a rebirth. I finally got where I wanted to go”.¹ Steve Jobs described taking LSD as “a profound experience, one of the most important things in my life”.² How is it that we never hear such grand endorsements about heroin, alcohol or cigarettes? What is it about psychedelics that has the power to change lives for the better? The answer might lie in the unique ways that psychedelics interact with the brain. In this post we’ll go deep on the molecular level—in a fun way.

This and more stunning artwork is available on gregadunn.com

The experiences of Cary Grant and Steve Jobs are in no way isolated cases. In a recent experiment at Johns Hopkins University School of Medicine, 36 healthy volunteers were given a high dose of the hallucinogen psilocybin (the active ingredient in so-called ‘magic mushrooms’). Two thirds of participants rated it amongst “the five most meaningful and spiritually significant events of my life”. They reported increased well-being and positive behavior changes even 14 months after the psychedelic experience with no additional uses of the substance. ³

‘Higher’ state of consciousness?

In this post, when I say ‘psychedelic drugs’ I’m referring to the classic psychedelics namely LSD, psilocybin, DMT, ayahuasca and peyote. Users of these drugs often report experiencing a ‘higher state of consciousness’ in which their perception seems enriched.

When researchers first scanned a human brain under the influence of these drugs, they expected to measure an increase in brain activity. To their surprise, most of the brain remained at the same level of activity except for a few areas. In those few areas the activity didn’t increase as expected, but rather decreased. What’s more, the participants experiencing the most intense psychedelic effects also showed the strongest decreases of activity in those particular areas. In other words, the lesser the activity, the stronger the trip.

Now, how does that make sense? Psychedelic drugs leave your brain’s executive functions intact: you can move, think, speak, know when to use the bathroom and other useful things. What they shut down however are certain connector hubs in the brain.

To understand the role of these connector hubs, think of traffic in a big city. When you shut down a major highway, drivers have to deviate from their normal routes and often find themselves in unfamiliar territory. Because a big city has an abundance of streets, drivers can still get to their destination, but only after a more lengthy and perhaps interesting ‘trip’.

Something similar happens when psychedelics shut down certain connector hubs in the brain. All of a sudden, there is a lot more cross-talk between areas which usually wouldn’t communicate.

The visualization below compares the brain’s communication pathways during (a) a regular state, with all the connector hubs intact. And (b) the psychedelic state, with the connector hubs shut down, leading to an abundance of novel communication pathways between brain areas.

Communication pathways after (a) placebo and (b) psilocybin⁴

By this time, you may be asking yourself ‘What are these mysterious connector hubs and what do they do in the first place?’ The following section is all about these hubs and how they make up the so-called default mode network in your brain. This network is a relatively new discovery and turns out to play a key role in understanding the effects of psychedelics.

The Default Mode Network

Whenever your mind is not engaged in a specific task, it switches into a kind of “autopilot” mode referred to as the default mode network or DMN for short. One way to think about the DMN is as an integration center, where information is collected and organized in ways that makes it coherent with regard to the rest of your cognition.⁵ The DMN is like a librarian who—when not handling immediate customer requests—indexes and categorizes books to keep the library neatly organized.

Another way to think about the DMN is as the center of the self. It’s engaged in self-reflection and metacognition, i.e. thinking about thinking. It allows you to mentally travel back and forth in time, pondering autobiographical events or future problems.^{6 7 8 9}

¹⁰The brain’s default mode network (DMN) consists of the posterior cingulate cortex (PCC), medial prefrontal cortex (mPFC) and the angular gyrus (AG)

These important functions make the DMN a vital connector hub in the human brain and part of what distinguishes us from other species. However, an overactive DMN is associated with people being neurotic, depressed or anxious.

Disrupting the default mode network

When psychedelic drugs shut off certain connector hubs, they also reduce the stability of the networks that exist on top of these hubs, in our case: the default mode network.¹¹ So, if you were to disrupt your DMN—for example through the use of psychedelic drugs—how would it change the way you think and act?

When the usual DMN connectivity is not available and signals therefore travel on different routes, you experience reality in a different way. This is why the psychedelic state is often called an altered state of consciousness. ‘Seeing with your eyes shut’ and a disintegration of the self as you know it are two typical characteristics of such a state.¹¹ To learn more, check out The Psychedelic Experience post with a side-by-side comparison of how different drugs change your perception.

Particularly in people suffering from mood disorders, psychedelics frequently show another interesting effect: their condition improves. Mental disorders such as depression, anxiety and obsessive compulsive disorders (OCD) are often associated with a hyperactive DMN.¹² If you disrupt the DMN, you often see substantial and long-lasting reductions in symptoms. We’ll talk more about concrete study results in a follow-up article next week.

Psychedelics are unique in how they can modulate the DMN. How they work in the brain is endlessly fascinating—and unfortunately—pretty complicated. And yet, I’ll have a try in explaining it in simple terms:

Your brain on psychedelic drugs

Right. Let’s break that down into normal language:

I. Receptor binding

Psychedelics interact with the serotonergic system in the brain, meaning they can bind to serotonin receptors. Why? Because serotonin, LSD and psilocin—the psychoactive metabolite of psilocybin—look very similar on a molecular basis.

But whereas serotonin binds to about a dozen different subtypes of serotonin receptors, psychedelic drugs bind to a very specific subtype, the so-called serotonin 2A receptor. LSD additionally binds to a few other subtypes of serotonin and dopamine receptors, but to a lesser degree. Most relevant for the psychedelic experience is the serotonin 2A receptor.

II. Long axons

Serotonin 2A receptors sit on specific types of neurons which have long axons that span across the brain, as opposed to neurons with short axons that only connect to other cells in their close vicinity. These large neurons have axons that leave the cortex and run down into areas below the prefrontal cortex.¹³ Doing so, they have top-down control over the regions they connect to, and in this case it’s areas associated with emotions and stress responses.¹⁴

III. Excitatory neurons

Neurons can be either excitatory or inhibitory. Think of training a dog.

Both, “speak” and “quiet” are signals that produce a certain reaction. An excitatory signal tells the neuron to “fire”, whereas an inhibitory signal says “don’t fire”. Remember, psychedelics stimulate serotonin 2A receptors, and those are located on excitatory neurons, meaning causing the neuron to fire. Logically, one would think that taking a psychedelic drug would lead to more firing in the brain. Paradoxically, the opposite is the case. How does that make sense?

When activation leads to inaction

LSD binds to the serotonin 2A receptor and causes the neuron to fire off an excitatory signal. When these neurons fire, they also stimulate nearby, inhibitory neurons called fast spiking interneurons, which have serotonin 2A receptors as well. So what happens is a massive firing and an even greater inhibition at the same time. Eventually, the inhibitory signaling is stronger than the excitatory and you’re left with a net decrease in activity.¹⁵

IV. Unique signaling

Just because serotonin and psychedelic drugs bind to the same serotonin 2A receptor doesn’t mean that they produce the same signal. For a long time, scientists believed that receptors worked like light switches, meaning that they are either on or off. According to this theory, psychedelics and serotonin must have had the exact same effect: either binding to the receptor and activating it, or clearing the receptor and deactivating it. But today we know that each molecule interacts with a receptor in its own unique way, causing a unique signal within the cell. How does that work? When a molecule binds to a receptor, the receptor has to physically accommodate the molecule’s unique shape. And by doing so it activates certain signaling pathways within the neuron.¹⁶ The jargon for this principle is functional selectivity, in case you wish to go deeper.

Ok, so an LSD molecule doesn’t actually look like a rainbow. Rather, it’s a big, rigid molecule which takes up a lot more space within the receptor than the smaller, more flexible serotonin molecule.¹⁷

And receptors don’t look like sticks but more like funny party streamers being tied together at the ends with a thin thread. So, when LSD binds to a receptor, it looks a little something like this:¹⁸

You can see how the party streamers give way to the big LSD molecule and thereby trigger a distinct signaling pathway within the cell. Tip: if you ever talk to a biochemist about this, don’t call it a party streamer—call it a helix.

As of today, it remains unknown which signaling pathway is most relevant for the psychedelic experience.¹⁷ What we do know is that it’s a different pathway than the one activated by serotonin.

Why an acid trip lasts so long

Serotonin molecules clear receptors a split second after binding to them. In contrast, when LSD binds to a receptor, the receptor collapses over the molecule and forms a lid, preventing the LSD from clearing.¹⁸

As long as the LSD molecule is trapped within the receptor, it causes the receptor to send off signals—for a few hours and sometimes longer. That’s why mere micrograms of LSD can make users ‘trip’ for 6-15 hours.¹⁹

Drugs as tools

You can probably see now that psychedelics work like no other molecule in the brain. Fossil evidence supports that humans have made use of psychoactive plants for as much as 10,000 years during ritual ceremonies.²⁰ Ancient societies regarded psychedelic drugs as tools; will modern society adopt this perspective once again? Personally, I see a number of persuasive reasons why we should:

First, psychedelic drugs are remarkably safe. There is not one single documented case of an overdose from LSD or psilocybin in humans. What makes them unsafe is acquiring them from strangers on the street with no transparency regarding additives and purity.

Second, they don’t cause addiction. If a user were to take psychedelics with high frequency, they lose their effects. The body quickly builds up a tolerance which can’t be overcome by stronger doses. It takes a refractory period of at least a few days until the desired effect can be reproduced. In that way, it’s really a drug for ‘special occasions’.

Third, there is a ton of anecdotal evidence that psychedelics are useful tools for personal growth. And a growing body of scientific evidence supports that psychedelics may be extraordinarily effective in treating mood disorders and addiction.

In our next post we’ll talk more about psychedelics and mental disorders. You can sign up for our newsletter and get notified when we publish it.

Medical Benefits of Psychedelic Drugs
Psychedelic Drugs and the Serotonergic System
The Psychedelic Experience
Your Brain on Psychedelic Drugs (You’ve just read it)
Psychedelics and Mental Health
Microdosing LSD: Smart Drug or Placebo?
MDMA-assisted Therapy

If you are located in the Vienna area, we invite you to join the Psychedelic Society Vienna Meetup, where we’ll discuss the latest research and developments in the field.

 

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References

For someone who has never taken a psychedelic drug it can be difficult to imagine what it’s like. You’ve probably heard of melting walls, tasting colors or kaleidoscopic vision.¹ Such pronounced hallucinations are typically the outcome of high doses of LSD or psilocybin. In moderate doses, however, the effects are more subtle. Colors appear more vivid and patterns may morph slightly, but users usually don’t see things that aren’t actually there.

On TV and in movies, psychedelic experiences are often misrepresented or exaggerated. Looking for more realistic examples of common dose effects² I found this photo depicting what someone might see while looking at an otherwise normal patch of grass.

Hallucinogenic vision by Chelsea Morgan

It’s still grass, but the colors are amplified and the individual blades of grass seem to compose geometric shapes, maybe you can even detect objects or faces.

The higher the dose, the more intense the hallucinations. The following image demonstrates a visual experience one may get from a slightly higher dose of LSD:

Visual acuity enhancement by StingrayZ

In any case, visual effects are just one aspect of the psychedelic experience. Psychedelic drugs create an altered state of consciousness that I like to describe as interpreting reality in a different way. Others have described it as seeing the world through the unbiased eyes of a child. But if you ask ten other people, you’ll get ten other answers. So, let’s hold the subjective descriptions aside for a moment and look at a quantified model of altered states of consciousness.

Measuring altered states of consciousness

In order to measure psychedelic experiences, researchers use a model called the five-dimensional altered states of consciousness rating scale (5D-ASC).³ Each psychedelic drug creates a unique signature on that scale. In the chart below I’ve combined data from several 5D-ASC studies⁴ in order to compare the psychedelic experience of MDMA, LSD, psilocybin and ketamine.

The psychedelic experience according to the 5D-ASC scale.⁴

Just three of the five⁵ dimensions are displayed above. Let’s take a closer look at what they mean:

1. Perception

Imagery & sound

The degree of hallucinations is dependent on (1) the type of drug and (2) the amount taken. Of the four drugs charted above, MDMA has little potential for producing audiovisual hallucinations, while LSD is the most reliable for creating some sort of changed imagery. The imagery can be elementary: seeing patterns or lights behind closed eyes, or complex: seeing entire scenes behind closed eyes or having an extremely vivid imagination. A different study, using psilocybin, showed that a high dose is twice as likely to produce visual hallucinations than a low dose.⁶

Changed Meaning

The things you hear and see might change their meaning under the influence of a psychedelic drug. Think of a glass of water: under normal circumstances you might think ‘I drink water when I’m thirsty’. But when consuming a psychedelic substance you might think ’water is the essence of life’. In a recreational drug use context, this change of meaning could make for a few fun stories. In a therapeutic context, however, changing meaning is an important step in order to change thinking and eventually, changing behavior. Think of something that would usually scare you to death, say: spiders. Imagine you took a psychedelic substance and then a spider crawled up next to you. Instead of writhing with disgust, you might think ‘What a peculiar yet fascinating creature’ and pursue its movements with childlike wonder.

Disrupting negative thought patterns is a key element of psychotherapy and can be a lengthy process. Though psychedelic substances present themselves as powerful tools to profoundly and instantaneously change an individual’s perspective, more research has to be done in order to prove their safety.

2. Self-disintegration

Disembodiment & losing control

Who isn’t worried about losing control over their body? This fear is what makes the dimension of self-disintegration so frightening for many of us. It includes feelings of floating, detaching the mind from the body, no longer having a body or one’s own will, having difficulties distinguishing the important from the unimportant or making decisions. Some of that sounds scary, agreed. At the same time, certain practices such as meditation and sensory deprivation tanks aim for creating some of the exact same experiences.

Ketamine scores particularly high in this dimension. LSD, psilocybin and MDMA produce fewer disembodiment experiences.

Anxiety

Note how all four psychedelic drugs score very low on anxiety. That means that even in combination with a possibly daunting out-of-body experience or visual hallucination, users don’t feel anxious about their experience. So-called bad trips more often than not result from a bad choice regarding set and setting, which we’ll discuss in just a moment.

3. Oceanic boundlessness

If the previous section was about the negative side of self-disintegration, this section is about the positive side of it. ‘What’s positive about the disintegration of the self’ you ask? Well, let me ask you in return: do you ever struggle with your self? Most of us experience feelings of anxiety, perfectionism, compulsion, stress, inferiority or guilt. Putting one’s self on hold at times can offer a great deal of relief.

Oceanic boundlessness is a blissful state of contentedness. People experience a deep connection with the world around them. Some describe it as connecting to something “larger” than the self, others talk about having spiritual experiences. LSD and psilocybin score higher than ketamine and MDMA in this dimension. The exception is the blissful state category, where MDMA is ahead by comparison. That makes sense, if you recall how MDMA floods the brain with serotonin, the happiness inducing neurotransmitter.

Different drugs, different experiences

Why do MDMA, LSD, psilocybin and ketamine produce distinctly different experiences? They are all called ‘psychedelics’ because they induce an altered state of consciousness.⁷ But biochemically, they create their effects by interacting with different elements within the central nervous system.

Mechanistic classification of drugs⁸

Within that model, you can further categorize psychedelic drugs according to their subgroups, medical use cases and effects in the brain. MDMA is an empathogen or entactogen, LSD and psilocybin are hallucinogens and ketamine is a dissociative anesthetic.

If you struggle to understand the drug’s effects in the brain, read the explanatory primer on the Serotonergic System. With plenty of illustrations and infographics it’ll take you step by step from knowing nothing about neurotransmitters and synaptic receptors to knowing more than most people.

User stories

How does the theory translate into real experiences of real individuals? What follows are some colorfully described user stories.

MDMA

“When ecstasy is coming on it feels fantastically exhilarating. Users report feeling blissed out, energetic, and emotionally opened and loving.”⁹
How MDMA works in the brain.

LSD

“Ecstatic feelings of love and happiness, affinity for other people, feeling of being at home with one’s self and the universe, flowing visions with more intricacy, beauty, and color than anything found in nature, sound which one can taste and feel with heart and soul, a sense of suspension in time and feeling akin with eternity and infinity, a brilliantly lucid mind able to see itself from vast and novel perspectives, an overwhelming tide of emotions…”⁹

Psilocybin

Mushrooms produce effects similar to those of LSD but with a different signature. Users frequently describe their experience to be unpredictable and more mysterious. With magic mushrooms “I’ve often felt that I’m in the presence of an ancient teacher, whereas with LSD, it can feel like I’m simply traversing my own mental pathways.”⁹

Ketamine

Ketamine functions very differently than the other drugs discussed in this series. While most psychedelics interact with the serotonergic system, ketamine interacts with the glutamatergic system. Glutamate is the most abundant neurotransmitter in the brain and plays a vital role in controlling synaptic plasticity, learning and memory¹⁰.

Ketamine’s psychoactive effects derive from blocking a certain type of glutamate receptor, specifically the NMDA receptor.¹¹ Being a dissociative anesthetic, the ketamine-induced psychedelic experience has pronounced out-of-body elements including at times even loss of bodily control. At low doses, ketamine puts users in a dreamy, mildly psychedelic state. At high doses, some find it terrifying and some call it “the most intense, bizarre, and enjoyable psychedelic”⁹. One experienced user described it like this: “As the high is coming on there is a break in the continuity of consciousness. […] Frequently there is no recollection of ever having been myself, been born, had a personality or body, or even known of planet earth. The experience is one of being in total orgasm with the universe. I feel like I’m in hyperspace, simultaneously connected to all things.”⁹

Bad trips

What about bad trips? Do they exist? Yes, they do. The research team around Roland Griffiths at Johns Hopkins University performed an online survey in which they asked psilocybin users to share details about their worst “bad trip”.

Inspired by Darrik May who used this image for his talk at the Psychedelic Science 2017 conference

62 percent of respondents rated their worst bad trip to be amongst the ten most psychologically difficult or challenging experiences of their lives. What’s surprising is that about the same percentage of users also considered it amongst the ten most meaningful experiences of their lives.¹² “A difficult experience, sometimes described as catharsis, often results in positive personal meaning or spiritual significance.” says Griffths.¹³

How 2,000 psilocybin users rated their worst bad trip¹²

Challenges may eventually lead to personal growth. 76 percent of participants reported that their difficult experience led to increases in current well-being and life satisfaction.¹² This suggests that a “bad trip” might not be so bad after all.

And what triggered these difficult experiences in the first place? Dosage, set and setting were significantly related to the degree of difficulty and duration of the unpleasant experience.

The importance of ‘Set and Setting’

The individual psychedelic experience depends on a number of things. Obviously, it depends on the dose and type of drug the user is consuming. But it also depends on the user’s body composition, gender, genes, their sensitivity to certain drugs or drug interactions with other pharmaceuticals the user is taking, such as contraception or psychiatric meds. And as if all that wasn’t enough variability already, the experience depends greatly on what is called set and setting. Set refers to the individual’s mindset and experience, whereas setting refers to the surrounding and atmosphere.

Taking MDMA during a couples therapy session has entirely different effects than taking MDMA at an electronic dance festival. The psychedelic experience is a function of the mindset as well as the physical and social environment.

The influence of set and setting may explain the staggering variance within early psychedelic research. When LSD was first distributed in the 1950s, it was marketed as a psychosis-inducing drug and was used in clinical psychiatry. Experiments usually took place in highly impersonal surroundings—think stark hospital rooms—and the subjects were often psychiatric in-patients or from socially disadvantaged populations, such as prisoners or drug addicts. In some cases, they had little choice but to participate in these experiments. Now imagine such a subject being tied down to a hospital bed, harsh lighting, rude staff and doctors looking for signs that the administered substance has made the subject become psychotic. Anyone would have a difficult time in such a setting—with or without the drug.

Less than a decade later, LSD became popular amongst college students as a substance that would expand consciousness and enhance creative thinking. Participants joined the studies voluntarily because they were anticipating a meaningful experience. The experiments were often carried out in lovingly furnished rooms with interesting art, flowers and music for the volunteers to enjoy while they waited for the drug to kick in. The researchers would respond to the participant’s personal needs and treat them with kindness and respect.¹⁴ Sounds as if someone is about to have a good time—with or without the drug.

Throughout the 1950s and 1960s, various interest groups evaluated LSD’s suitability for serving their particular causes. Those efforts resulted in no less than nine different main conceptions of LSD, among them LSD as a psychotomimetic, a psychotherapeutic tool, a creativity enhancer, a spiritual sacrament, a mind control tool (by the CIA), a battlefield weapon (by the U.S. Chemical Corps), and a revolutionary molecule (by groups such as the Yippies and The Weathermen).¹⁴

This all goes to show that set and setting profoundly influence actual psychedelic experiences. Through continued research, however, we’ve been able to pin down a few common denominators of all psychedelic experiences, such as timelessness, selflessness and effortlessness¹⁵. In the next story, we’ll look at how these common denominators manifest in the brain. Or to put it another way: what exactly happens in the brain when people lose their sense of time and self?

This was part 3 of our series on psychedelic drugs.

Medical Benefits of Psychedelic Drugs
Psychedelic Drugs and the Serotonergic System
The Psychedelic Experience (You’ve just read it)
Your Brain on Psychedelic Drugs
Psychedelics and Mental Health
Microdosing LSD: Smart Drug or Placebo?
MDMA-assisted Therapy

You can sign up and get notified when we publish our next story.

If you are located in the Vienna area, we invite you to join the Psychedelic Society Vienna meetup, where we’ll discuss the latest research and developments in the field.

 

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References

The neurotransmitter serotonin is deeply involved in regulating mood and anxiety. If your brain is low on serotonin, you might feel depressed or irritable. So, what can you do to keep up a steady supply of serotonin? Step number one: eat right.

Well over 90 percent of serotonin in our body is made in our gut. But since serotonin can’t cross the blood-brain barrier, it has to be produced in the brain from scratch.

How the brain makes serotonin

Neurons need two things to create serotonin: (1) tryptophan and (2) a couple of enzymes.

1. Tryptophan 

Tryptophan is an essential amino acid which we get from our diet. The average western diet is rich in tryptophan. It is particularly plentiful in proteins such as eggs, meats, soybeans and dairy products. Carbohydrates like chocolate, oats, rice or quinoa contain less tryptophan but are still considered good sources.¹

But eating a protein rich diet doesn’t guarantee a sufficient tryptophan supply. Paradoxically, quite the opposite is the case. The problem with a protein rich diet is amino acid competition. What does that mean? Proteins contain not only tryptophan, but a number of other amino acids² which are better at crossing the blood-brain barrier. So, when tryptophan and its amino acid friends come knocking at the blood-brain barrier’s door, tryptophan doesn’t get in.

Image from Asap Science

With carbohydrates, the situation is reversed because carbohydrates—unlike proteins—raise insulin levels in the blood. Insulin, in turn, decreases the blood levels of the other amino acids but doesn’t affect tryptophan. You could say that insulin removes some competition in favor of tryptophan and thus helps tryptophan cross the blood-brain barrier.³

And indeed, people suffering from seasonal affective disorder (SAD) or premenstrual syndrome (PMS)—which are both expressed through depressed moods—often report carbohydrate cravings, almost as an attempt of self-medication.⁴ Eating carbohydrate meals which contain some protein might be a good compromise to ensure a steady supply of brain tryptophan.

Carbohydrate meals which contain some protein might help maintaining steady supply of serotonin in your brain.

2. Enzymes

Once tryptophan has crossed the blood-brain barrier, the first enzyme (tryptophan hydroxylase) turns tryptophan into 5-HTP and the second enzyme (decarboxylase) turns 5-HTP into serotonin.

Serotonin biosynthesis⁵

The brain has plenty of these enzymes in stock. What usually causes the bottleneck in serotonin production is the availability of tryptophan.³

Tryptophan supplements

There is some evidence that nutritional supplements containing purified tryptophan raise brain tryptophan levels more efficiently than nutrition. That would make sense, since the supplement doesn’t contain any of the competing amino acids.⁶

Exercise

Another way to facilitate tryptophan’s entry in the brain is through exercise. When your muscles work hard, they are hungry for amino acids. That works in your favor, because exercise only decreases blood levels of amino acids other than tryptophan.⁷ Consequently, tryptophan experiences an easier uptake at the blood-brain barrier.

Learn more

Tryptophan plays a role in regulating serotonin levels in the brain, but that’s only one piece of the puzzle. The larger serotonergic system is complex and mysterious. If you want to understand how it works, check out our story on Psychedelic Drugs and the Serotonergic System.

 

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References

Most of us know someone who has taken antidepressants. But psychedelic drugs? Not so much. Many people believe they are illegitimate and dangerous. You might be surprised to hear that psychedelic drugs like MDMA and LSD have a lot in common with antidepressants. They both work with the same neurotransmitter in the brain: serotonin.

And indeed, antidepressants and psychedelic drugs promise to heal similar mental illnesses and can also have similar side effects. Do you know how they work in the brain? No? Good! That’s exactly what this article is about. Before we can talk about your brain on these drugs, though, it’s important to have a basic understanding of the brain and its serotonergic system. Don’t worry, it’s super fascinating stuff, and easy as 1-2-3:

1. Brain basics

Below, we’ll talk about neurotransmitters, synapses and chemical signaling. If these things are even vaguely familiar to you, then read on. If not, I recommend reading part 2 of Tim Urban’s fantastic—and highly entertaining—Neuralink and the Brain’s Magical Future story on the Wait But Why blog. You’ll learn everything from brain anatomy to neural networks in just 15 minutes.

How neurons communicate

When a neuron fires, the cell body (soma) sends an electrical signal down its axon to its axon terminals. This is where one neuron connects to the dendrites of the next neuron. In between is the synapse. From the axon terminals, a chemical signal activates the dendrites and sends a message to the soma of the next neuron. The soma collects the messages and once a threshold is exceeded, it fires off an electrical signal down its own axon and the process repeats.

Chemical signals are made from neurotransmitters. How they are produced, sent and received is the key to understanding the interactions between drugs and the serotonergic system.

Neurotransmitters

You have probably heard of the neurotransmitters dopamine and serotonin. A simplistic view would be that dopamine regulates feelings of reward and serotonin regulates feelings of happiness. Yes, it’s more complex than this, but we’re just getting started.

We have more than 100 different types of neurotransmitters in our brain and their job is facilitating the communication between neurons. Think of a neurotransmitter as a language: some neurons speak dopamine, others speak serotonin and so on. While some neurons are multilingual, let’s say fluent in serotonin and dopamine, most of them speak just one language. All neurons which speak serotonin make up the serotonergic system.

2. The serotonergic system

The serotonergic system is amongst the oldest neurotransmitter systems in the brain. It might be as old as 750 million years; even single-celled organisms carry serotonin receptors.^{1 2} In humans, those neurons originate from the raphe nuclei in the brainstem and form a network spanning every corner of the brain and influencing nearly every aspect of our lives. It plays a key role in regulating mood, sexual behavior, aggression, impulsivity, cognitive function, appetite, pain, thermoregulation, circadian rhythm, sleep and memory. ^{3 4}

Serotonergic pathways in the brain⁵ With all of these control functions, it makes sense that many prescription drugs—and most antidepressants—target the serotonergic system. What might not be so obvious, however, is that psychedelic drugs like MDMA (aka. molly, ecstasy), LSD (aka. acid) and psilocybin (aka. magic mushrooms) also stimulate the serotonergic system to create their unique effects.

All those substances do essentially one thing: they raise the serotonergic activity in the brain. Why? Because raising serotonergic activity makes you happy, social and active; whereas lowering serotonergic activity makes you depressed, irritable and more prone to mental illnesses.

Serotonin in the synapse

This is where it gets really interesting. Before we dive into the life of a serotonin molecule, let’s make sure we’re all on the same page. Take another look at the more detailed version of how communication happens at the synapse. On the top is the axon terminal of the “sender-neuron” which is often referred to as the presynaptic neuron. On the bottom is the “receiver-neuron”—the postsynaptic neuron. The skin of the neurons is the membrane; and the little gap in between is called the synaptic cleft. What gets sent from the sender to the receiver? A chemical signal, otherwise known as neurotransmitter; and in the case of a serotonergic neuron the neurotransmitter is serotonin.

Now we get to the nitty gritty. The following graphic illustrates the lifecycle of a serotonin molecule. Follow the orange dots from one to seven and check out the explanation below.

Signaling in chemical synapses

1 Synthesis

Well over 90 percent of the serotonin in our body is made in our gut. But since serotonin can’t cross the blood-brain barrier, it has to be synthesized in the brain from scratch. What does cross the blood-brain barrier however is tryptophan, the fundamental building block of serotonin.⁶ Within the neuron, enzymes turn tryptophan into 5-HT which is the chemical name for serotonin.⁷

How does our body get tryptophan in the first place? Tryptophan is contained in certain foods, particularly proteins. You may have heard that turkey is rich in tryptophan—so is every other kind of meat, as well as cheese, dairy products and eggs. Paradoxically, eating a protein rich diet is not necessary useful for a steady tryptophan supply in the brain. Why? Read my story about amino acid competition at the blood-brain barrier.

2 Storage

Serotonin is stored in tiny bubbles—only 50 nanometers in diameter—called vesicles. How does it get in there? Initially, the serotonin floats in the cytosol, the fluid within the neuron. A transport protein called VMAT2 fishes the serotonin out of the cytosol and channels it into one of the vesicles. The vesicles then travel closer towards the synaptic cleft and wait for their signal.

3 Release

When signalled, the vesicles meld with the cell membrane in a process called exocytosis. The serotonin gets released into the synaptic cleft.

4 Receptor activation

When serotonin binds to the receptors of the postsynaptic neuron, each receptor sends off a signal to the cell body of the neuron. When enough of these signals accumulate, the postsynaptic neuron fires, causing an electrical signal to travel down its axon to its own axon terminals, in turn causing a release of serotonin that stimulates the next neuron. This chain reaction cascades through any number of neurons….

5 Receptor clearing

Where does a serotonin molecule go after it has activated a receptor? There are a few options: (a) it may get taken back up into the presynaptic neuron; (b) it may get taken up by a neighboring glial cell (glial cells are the most abundant cells in the brain—they don’t transmit signals but they do help keep everything neat and tidy); or (c) it may get diffused away from the synaptic cleft via extracellular fluid.⁶

6 Reuptake

Along the presynaptic membrane are serotonin transporters (SERT) that pull serotonin back into the cell in a process called reuptake. These transporters are basically groups of proteins that act like a gate: one in—one out. One molecule binds to the transporter on the outside of the membrane and changes the transporter’s configuration. Consequently, another molecule drops off, but on the inside of the membrane.⁸

Back in the presynaptic neuron, some of the serotonin gets reloaded into vesicles and will be reused. Producing serotonin from scratch is a complex process and takes time. Therefore, recycling helps the brain maintain a steady supply.

7 Metabolism

Any remaining serotonin gets broken down by the enzyme MAO (monoamine oxidase) and excreted from the cell as the metabolite 5-HIAA (5-Hydroxyindoleacetic acid).

How serotonin neurons avoid overstimulation

The brain can’t produce large quantities of serotonin at once, therefore it doesn’t release large quantities of serotonin at once either. In fact, serotonergic neurons have multiple ways of up- and downregulating their serotonin response in order to maintain balance and protect themselves from overstimulation.

Follow the orange dots below to see a few examples of these protection strategies.

If there is (1) a high concentration of serotonin outside the neuron, the neuron reacts with

(2a) Reducing receptor density

Amazingly, a neuron can cause its receptors to retract behind the synaptic membrane, putting them out of reach of being activated by over-abundant serotonin. With fewer receptors available, fewer activations occur, and the neuron is in turn less likely to fire off a signal.⁹

(2b) Feedback via autoreceptors

Receptors are not only found on the postsynaptic membrane. Some are located on the axon terminals or even directly on the soma of a neuron. If too much serotonin is floating around in the brain and these autoreceptors get activated, they send an inhibitory signal to the presynaptic neuron that causes it to (3) throttle the release of serotonin.⁶

The versatility of serotonin receptors

Do you recall from the beginning how serotonin regulates mood, sexual behavior, cognitive function, sleep, memory and so on? How does it accomplish all that? Well, in reality there isn’t just one single type of serotonin receptor—there are 14. They are numbered from 1 to 7 and further categorized into A, B, C, etc. Remember, the chemical name for serotonin is 5-HT. Going forward we’ll talk a lot about 5-HT_2A receptors, since they are the target of hallucinogenic drugs like LSD and psilocybin.

All 5-HT subtypes possess special qualities in how they regulate mood, anxiety, impulsivity, aggression, migraines, etc. Some of these subtypes act as regular receptors at the postsynaptic membrane, while others act as autoreceptors on the axon terminals, dendrites or directly on the cell body. The 5-HT_2A receptor, for example, is a receptor on the postsynaptic membrane and regulates mood, anxiety and schizophrenia.¹⁰ Wikipedia offers a fantastic overview of 5-HT receptor subtypes if you wish to go deeper.

3. How antidepressants & psychedelic drugs stimulate the serotonergic system

Now that you know how serotonin acts in the synaptic cleft it will be easy for you to understand the mechanisms of antidepressants like SSRIs and MAOIs as well as psychedelic drugs like LSD, psilocybin and MDMA. Each of these substances stimulate serotonergic neurons, but each in different ways.

Antidepressants

Before 1950 it was believed that mental illnesses like schizophrenia or autism were caused by “refrigerator mothers”—mothers who were emotionally distanced and cold with their offspring.¹¹ The psychiatric community had no idea that behaviour patterns, such as schizophrenic or autistic behaviour, might arise from neurochemical events in the brain.¹

In the late 1930s, serotonin was first discovered in the gut where it played a role in muscle contraction. It took another 15 years before it was detected in the brain—which was in 1953—but still only in the context of muscle contraction. One year later, in 1954 two scientists noticed the chemical similarity between serotonin and LSD. Chemical structure of LSD and serotonin²

They had already known that LSD had peculiar effects on mind and behavior, because Sandoz Laboratories had marketed LSD as a psychiatric drug since 1947. Putting one and one together, these two scientists suggested that serotonin might play an important role in mental illness.¹²

“If neuroscience can be said to have a beginning, one could argue that it occurred in 1954, with the idea that the action of LSD might be related to its effects on the brain serotonin system.”²

After it became obvious, that serotonin was deeply involved in mental sanity it quickly became the center of attention of pharmaceutical companies. Understanding the mechanism by which mood is regulated allowed pharmacologists to experiment with ways to influence it. One result has been the creation of many antidepressant drugs. Here is how they work.

SSRIs: Blocking serotonin reuptake

Selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed antidepressant drugs today. You’ve probably heard of Prozac, Celexa, Lexapro, Seroxat or Zoloft. They are all SSRIs.

SSRIs bind to serotonin transporters (SERT) on the presynaptic membrane and block them. This means serotonin can’t get taken back up into the presynaptic neuron. More serotonin remains in the synaptic cleft where it continues to bind to receptors and activates them.

MAOIs: Blocking metabolism

Monoamine Oxidase Inhibitors (MAOI) are older antidepressants, which are still in use, but not commonly prescribed because of their potentially lethal effects. MAOIs keep serotonin from being metabolized and excreted from the neuron, which in turn increases its availability.

Psychedelic drugs

Antidepressants ultimately raise serotonin levels, so does MDMA.

MDMA

MDMA is a sneaky bastard. Insidiously it takes control of the infrastructure and turns the whole system upside down. How does it do that? First, MDMA enters the neuron via the serotonin transporters (SERT). Once inside the neuron, it inhibits the vesicular transporters (VMAT2) which means that serotonin is not neatly packed within the vesicles anymore, but now accumulates within the cytosol. Then, MDMA reverses the direction of the SERT, meaning instead of transporting serotonin into the neuron, they now release it into the cleft and deny its reuptake.¹³ The result is a dramatic increase of serotonin levels in the synaptic cleft which makes the receptors on the postsynaptic membrane go haywire for a few hours.

Moreover, MDMA increases dopamine and norepinephrine (i.e. noradrenaline) levels, which gives it its ecstatic properties. This temporary overstimulation of the serotonergic system leaves the neurons depleted of serotonin and needing to recover after the drug use.

Why it doesn’t cause addiction

What if MDMA is taken daily to keep up colossal serotonin levels? The short answer is: doesn’t work; the effect of MDMA is capped by the available serotonin. If the brain is depleted from serotonin, MDMA has no material to work with and therefore the effects would be rather disappointing for the user. The brain needs time to replenish its supply before the drug could achieve the desired effects once more. Many users feel irritable and depressed after using MDMA.¹⁴ But when using again is not an option, there isn’t much of an addiction loop they could tap into. With this built-in mandatory refractory period, the physical addiction potential of psychedelic drugs is limited.

With a built-in, mandatory refractory period, the physical addiction potential of psychedelic drugs is quite limited.

Remember how the brain usually doesn’t release large quantities of serotonin at once? Other neurotransmitter systems in the brain are more suitable for this task: dopamine for example. The dopaminergic system does react well to repeated stimulation and is therefore frequently involved in addiction. Drugs which target the dopaminergic system are cocaine, amphetamine, methamphetamine, but also Adderall and Ritalin.¹⁵

LSD, psilocybin and other hallucinogens

Unlike MDMA, hallucinogens don’t flood the brain with serotonin. They target a specific subtype of serotonin receptor—the 5-HT_2A receptor—to which they bind directly, thereby activating it. The 5-HT_2A receptor is known to play a key role in regulating mood, anxiety, schizophrenia and consciousness.

There is so much to say about how hallucinogens affect the brain. The initial hypothesis—that hallucinogens increase the activity in certain areas of the brain—was recently abandoned. In fact, hallucinogens temporarily shut down some major connecting hubs.¹⁶

Why does this stir a researcher’s blood? Because if you want to know what a certain area in the brain does, it helps to observe what goes missing if you shut it off. Turned out, shutting off those connector hubs led to the interruption of the brain’s default mode network (DMN).¹⁷ You can think of the DMN as something like a screensaver which randomly shuffles through images of your past, your future, your to-do list, the super size menu that you shouldn’t have eaten, the sad face of a person you hurt and so on. Interrupting the DMN has very interesting consequences which we will—at length—cover in a future post. It’s a phenomenally interesting topic that deserves its own post (and requires a couple of thousands more words to explain).

Also, when breaking up the regular communication pathways, the brain starts to communicate in brand new ways. This visualization shows brain regions communicating which one another in (a) a normal state or (b) after administering psilocybin. On the left you can see that the color-coded regions communicate mostly amongst themselves, i.e. the dots of the purple region talk to other dots within the purple region. But under the influence of an hallucinogenic drug the purple dots start talking to all kinds of other brain regions.

Communication pathways in the brain after (a) placebo and (b) psilocybin¹⁸

These novel communication pathways might be able to explain the creativity-enhancing and problem-solving qualities that are often attributed to hallucinogenic drugs.

The problem with criminalization

What’s the essential nature of science? (1) You find an interesting thing, (2) you test and observe how the thing behaves under different conditions and (3) you come up with a hypothesis.

Psychedelic drugs and the serotonergic system are deeply intertwined. Not only was LSD involved in the initial discovery of the serotonergic system which later revolutionized psychiatry.² Today, psychedelic research could yet again revolutionize our understanding of the human brain. Manipulating 5-HT_2A receptors has astounding effects on brain circuitries that are involved in the sense of self and consciousness. You can think of the 5-HT_2A receptor as the little kid’s basket and hallucinogens as a potent tool to test it. Psychedelic drugs might be nothing less than our key to deciphering consciousness.

With brand-new imaging technology, we could now watch the brain as it loses its sense of time and space. We could observe which regions fall out of sync when it dissolves its sense of self. We could literally watch the brain as it changes its state of consciousness. The problem is, we’re not allowed to. The current drug legislation makes psychedelic research so difficult and so expensive, that only very few research teams manage to get approval and funding for their studies.

Criminalization of psychedelic drugs stands between science and the exploration of consciousness.

A mighty and mysterious system

Having discovered the serotonergic system less than 70 years ago, there is much that remains unknown about this mighty and mysterious network of neurons. We know that it is crucial for a lot of processes, but the ins and outs are not well understood even today. It will be a long time before we’ll figure out the exact mechanisms of this versatile system.²

In the meantime, every new study on psychedelics reveals fascinating new insights about consciousness, the brain’s default mode network and mental disorders. Over the next posts in our Psychedelic Drugs series we’ll cover the outcome of those recent studies.

Medical Benefits of Psychedelic Drugs
Psychedelic Drugs and the Serotonergic System (You’ve just read it)
The Psychedelic Experience
Your Brain on Psychedelic Drugs
Psychedelics and Mental Health
Microdosing LSD: Smart Drug or Placebo?
MDMA-assisted Therapy

Wow, that was a lot of information to take in. But you did it! Now you know more about the serotonergic system than any of your friends (except if your friends are neuroscientists). Since you seem to be really interested in the topic you might want to get notified when we publish our next story.

If you are located in the Vienna area, we invite you to join the Psychedelic Society Vienna meetup, where we’ll discuss the latest research and developments in the field.

 

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References

“Psychedelic drugs are poised to be the next major breakthrough in mental health care” writes Scientific American.¹ Dropping acid to treat depression—seriously…?!

Psychedelic drugs can seem pretty scary at first. At some point in your life, you’ve probably heard stories about LSD causing schizophrenia, triggering flashbacks, or even making people jump out of windows because they think they can fly.

Some of these stories contain a kernel of truth, while others are simply urban legends. I’ll go into detail about these concerns in later posts—including what the latest scientific research tells us about them.

But for now, try to set aside any horror stories you may have heard. A large and growing body of evidence supports that psychedelic drugs have an acceptable risk-benefit ratio and are worth a closer look.

Drop acid, save taxes

Mental disorders are doubly destructive: first in the suffering they cause for the afflicted, second in how expensive and time-consuming they are to treat. New research is demonstrating that certain psychedelic drugs are extraordinarily effective in treating mental health issues like depression, post-traumatic stress disorder (PTSD) and addiction.

The benefits for individual patients are dramatic on their own, but equally compelling are the economic effects of lowering the costs of treating these illnesses. When patients get faster and more effective relief, health care systems and their taxpayers do too.

Here are a few quick facts that give a sense of just how big—and expensive—a problem we’re dealing with:

• One in five U.S. adults experience a mental illness.²
• Depression is the most costly mental disorder in Europe.³
• Depression is the number one reason for absenteeism from the workplace in the U.K. after minor illnesses.⁴
• The U.S. is facing an opioid addiction epidemic: two million are addicted to prescription opioids and another 591,000 to heroin. ⁵ More Americans die from drug overdoses than from car accidents and gun homicides combined.⁶
• Tobacco and alcohol abuse in the U.S. causes total annual costs of $500 billion.⁷
• 868,000 U.S. veterans are suffering from post-traumatic stress disorder (PTSD). With an estimated annual cost of $20,000 per veteran this adds up to $17 billion of PTSD disability payments. ⁸

Currently, patients are being prescribed expensive drugs and are going through years of psychotherapy. But how much does that actually help? Take depression for example: patients must take their medication on a daily basis, it takes at minimum two weeks before the pills are effective and they come with serious, undesirable side effects. Meanwhile, they are only slightly more effective than a placebo pill.⁹ I’d shop for a better deal.

Antidepressants are expensive, but barely more effective than a placebo pill.

Psychedelic drugs have repeatedly demonstrated high rates of efficacy—much higher than common antidepressants—after just a couple administrations of the drug. The effects are immediate, long lasting, show little side effects and don’t require indefinite daily medication.

Purposefully used, psychedelic drugs could relieve pressure on our health care systems and thus on taxpayers. More importantly, it could help millions of people who are stuck with mental disorders move on with their lives.

This is the first in a series of blog posts, where I will investigate the medical benefits of psychedelic drugs, namely LSD (aka acid), psilocybin (aka magic mushrooms), MDMA (aka ecstasy) and ketamine.

Are psychedelic drugs dangerous?

Psychedelic drugs are heavily stigmatized. In most countries they are subject to the most restrictive drug laws. Governments consider them to have (1) a high potential for abuse and (2) no currently accepted medical applications. Those assumptions have been proven wrong by countless studies. But drug legislation hasn’t caught up with the facts yet. Consequently, medical use of psychedelic drugs remains illegal.

In 2010 David Nutt, Ph.D., former president of the European College of Neuropsychopharmacology and advisor to the British government on the misuse of drugs, presented a rational analysis of the 20 most popular illegal drugs. He analyzed the individual and social harm of the drugs.

Drug harms in the UK (Nutt)¹⁰

Besides the more obvious, immediate physical harm to the user (in light blue) every drug implies a certain degree of social harm (in dark blue), such as damage to families or cost of health care and police. Nutt found that heroin, crack cocaine and methamphetamine (aka crystal meth) were most damaging to the user. Alcohol was the most damaging to others because it causes loss of relationships and tangibles, injuries to others (including fights, domestic violence, traffic accidents) and economic costs. Put bluntly: society pays the price of addiction.

Psychedelic drugs (highlighted in yellow) scored very low on the overall ranking (no. 11, 17, 18 and 20) and imposed practically no damage to others.

Drug abuse and toxicity

Drug addiction is a serious problem. It’s important to note however, that the legal status of a drug does not necessarily correlate with its potential for abuse. Cannabis, for example, is still a Schedule 1 drug in the U.S. but its physical addiction potential is comparably low. Furthermore—due to its extremely low toxicity—deaths from overdosing cannabis are unheard of.

Examples to the contrary are commonly prescribed opioids. Legal narcotic drugs like oxycodone (e.g. OxyContin) or fentanyl, which is 50 times more potent than morphine¹¹, possess highly addictive and toxic properties. Opioid abuse is skyrocketing in the U.S.. More Americans die from overdosing a prescription pain reliever than overdosing from heroin.⁵ Opioid prescription drugs would be located in the top right corner on the chart below despite being classified only as a Schedule 2 drug: high potential for abuse but with accepted medical use.

Safety ratio and dependency (Gable)¹²

The chart shows the dependency potential on the y-axis and the safety ratio on the x-axis: the lower the ratio, the safer the drug. A value of 0.1 means that consuming ten times the active dose of a drug is lethal. A value of 0.01 would require a consumption of 100 times the active dose for it to be lethal. For marijuana, LSD and psilocybin it would require 1000 times the active dose to be lethal. And indeed, there is not one documented case of a lethal overdose of those substances in humans ever.

Closely timed, repeated intake of psychedelic substances do not produce satisfying effects in the user. Therefore the potential for abuse is limited. It’s widely understood that psychedelic drugs do not lead to physical addiction. In fact, studies have shown that they might facilitate coming off an alcohol or nicotine addiction.¹³

Therapeutic potential

Many glowing results of early psychedelic research during the 1950s and 60s were a consequence of overzealous researchers reporting what they wanted to see. The research was poorly conducted and lacked patient follow-up for documenting long-term results. Many of the miraculous results could not be reproduced when proper scientific controls were in place.¹⁴

Science has changed a lot over the past 70 years and most of the early psychedelic research does not meet the rigorous standards of scientific research today.

And while all of that remains true, you don’t want to throw out the baby with the bath water. Recent studies with rigorously applied scientific standards have shown promising therapeutic effects in patients suffering from all kinds of psychological disorders.

Psychedelics might not be a miraculous cure on their own. But combined with—for example—psychotherapy we might look at a treatment protocol which is far more effective than the (expensive) status quo.

Hypothetical example of a treatment protocol

Who is driving research on psychedelic drugs?

Psychedelic drugs were declared illegal by the mid 1960s and thus early psychedelic research came to a standstill. For more than four decades, it was virtually impossible to conduct further research. Over the last 15 years however, research on psychedelics has experienced a renaissance.

Today, psychedelic drugs are not the north star of a young political counterculture. It’s renowned scientists and non-profit pharmaceutical companies who carry out studies and work with government legislators. No riots, no orgies, no festivals, no cult.

Prestigious research teams across the world run fully randomized, double-blind, placebo controlled trials—the gold standard of modern research—to explore the therapeutic properties of psychedelic drugs. And reputable science journals and newspapers like The New York Times, The Washington Post, The Guardian or Wired publish the findings. Why? Because the results are literally mind-altering.

The organizations gathering these findings are amongst the most prestigious in the world:

Researchers at Johns Hopkins University School of Medicine have found that a single high dose of psilocybin decreased depression and anxiety in 92 percent of patients with life-threatening cancer.¹⁵ In another study, psilocybin helped smokers overcome their nicotine addiction. At six months 80 percent were still abstinent. Compare that to an otherwise typical success rate of 15 to 30 percent.¹³

A research group from Imperial College London looked at patients who suffered from treatment-resistant depression and found that only two doses of psilocybin could stop or decrease their symptoms of depression for months.¹⁶

The Multidisciplinary Association for Psychedelic Studies (MAPS) achieved groundbreaking results applying MDMA-assisted therapy to patients suffering from treatment-resistant PTSD. After only three sessions of MDMA, 61 percent of patients no longer met the criteria for PTSD. And the benefits even increased over time. ⁸

Scientists present their studies on psychedelics at TED conferences. New York Times bestselling authors are writing about a revolution in states of consciousness.¹⁷ Silicon Valley connoisseur Tim Ferriss states “The billionaires I know, almost without exception, use hallucinogens on a regular basis.”¹⁸ And the rest of the valley follows: microdosing LSD is trending for its alleged performance-enhancing and problem-solving properties. The stigma on psychedelics is eroding in front of our eyes.  

The stigma on psychedelic drugs is eroding in front of our eyes.

Who is not driving research? —Big pharma. Drugs which are administered only once or twice are not good for business. Therefore, research is driven predominantly by universities and nonprofit organizations.

Psychedelic drugs series

Throughout the coming chapters, I’ll share some of the most fascinating insights from current research: What exactly does LSD do to the brain? Why does ketamine lead to instant relief from depression? How does MDMA conquer fear in traumatized patients? Why are a growing number of technologists in Silicon Valley microdosing LSD? Does LSD really trigger psychoses and so-called flashbacks?

And for those of you who wonder “How does it actually feel taking a psychedelic drug?” —science has an answer for you too.

That’s a lot of ground to cover, and that’s why this is the first in a series of blog posts:

Medical Benefits of Psychedelic Drugs (You’ve just read it)
Psychedelic Drugs and the Serotonergic System
The Psychedelic Experience
Your Brain on Psychedelic Drugs
Psychedelics and Mental Health
Microdosing LSD: Smart Drug or Placebo?
MDMA-assisted Therapy

You can sign up and get notified when we publish our next story.

If you are located in the Vienna area, we invite you to join the Psychedelic Society Vienna meetup, where we’ll discuss the latest research and developments in the field.

 

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References

Was Milchproduzenten verschweigen: Kälber werden nach der Geburt von der Mutterkuh getrennt.

Egal ob Biobauernhof oder konventionelle Viehhaltung: Kälber von Milchkühen werden innerhalb der ersten Lebenswoche von ihrer Mutter getrennt, häufig innerhalb weniger Stunden nach der Geburt.

Die Milchkuh wird jedes Jahr wieder geschwängert damit ihre Milchproduktion nicht nachlässt. Auch jedes weitere Kalb wird ihr weggenommen.

Die wenigsten Konsumenten wissen, dass ihre Milch aus nicht-kalbfreundlicher Herkunft stammt. Wer seine Milch im Supermarkt oder sogar im Bioladen kauft, muss mit an Sicherheit grenzender Wahrscheinlichkeit davon ausgehen, dass der Milchkuh ihr Kalb nach der Geburt weggenommen wurde.

Warum ist das so?

Die Milch der Mutterkuh ist für die Milchwirtschaft bestimmt. Damit das Kalb die Milch nicht „wegtrinkt“, wird es von der Mutter getrennt.

Auch am Biobauernhof?

Ja. In Biobetrieben muss das Kalb zwar anfangs mit „natürlicher“ Milch ernährt werden, diese trinkt es allerdings aus einem Kübel/Eimer.¹ Bei der Mutter darf es nicht säugen und wird deshalb räumlich getrennt.

Aber ich sehe oft Kälber die bei ihren Müttern trinken…?!

Das sind keine Milchkühe, sondern Kühe die für die Fleischproduktion vorgesehen sind. In der Mastviehhaltung wird die Milch der Kühe im Regelfall nicht kommerziell verwertet. Deshalb dürfen diese Kälber bei der Mutterkuh bleiben und säugen.

In Österreich sind 70 Prozent der Kühe für die Milchproduktion vorgesehen (Milchvieh) und 30 Prozent für die Fleischproduktion (Mastvieh). In reinen Biobetrieben sind etwas mehr als die Hälfte der Kühe Milchkühe.²

Was hat die Trennung für Konsequenzen?

Kühe sind hingebungsvolle Mütter. Sie lecken ihre Kälber trocken, säugen und beschützen sie. Binnen kürzester Zeit erkennen sich Mutter und Kalb an Geruch und Stimme. Werden sie getrennt, schreit die Kuh tage-, manchmal wochenlang nach ihrem Kalb. Das Kalb ist ohne das Saugen von Muttermilch anfälliger für Krankheiten und entwickelt Verhaltensanomalien, wie z.B. gegenseitiges Besaugen mit anderen Kälbern.³

Warum gibt es im Supermarkt keine kalbfreundliche Milch?

Gute Frage! Kaum ein/e KonsumentIn weiß, dass selbst die beste Bio-Heumilch nicht aus kalbfreundlicher Haltung stammt. Würden die Kunden vermehrt nach kalbfreundlicher Milch verlangen, dann würden Bio- und Supermärkte womöglich eine solche auch anbieten.

Kalbfreundliche Milch ist teurer in der Produktion. Solange es keine Nachfrage vom Markt gibt, können es sich Kleinbetriebe nicht leisten, kalbfreundliche Milch separat abzufüllen.

Was kann ich tun?

Bewusstsein schaffen

Ich vermute dass viele KonsumentInnen—vor allem jene die heute schon Bio kaufen—Milch aus kalbfreundlicher Herkunft bevorzugen würden.

Es fehlt das Bewusstsein, dass Bio-Milch nicht automatisch schon kalbfreundlich ist.

Erzähle ich es weiter, reagieren die meisten Menschen betroffen. Sie wären gerne dazu bereit einen Euro mehr für kalbfreundliche Milch auszugeben.

Anreiz für Nahversorger setzen

Verlange in Bio- und Supermärkten immer wieder nach kalbfreundlicher Milch. Der Fachbegriff dafür lautet Milch aus muttergebundener Kälberaufzucht, oder auch Milch aus Mutterkuhhaltung. Wenn jeden Tag ein/e KundIn nachfragt, dann nimmt der Markt womöglich kalbfreundliche Milch in sein Sortiment auf und die Produktion wird für Kleinbetriebe rentabel.

(Meine persönliche Erfahrung ist, dass man den VerkäuferInnen fast immer erklären muss, was man mit kalbfreundlicher Milch meint. Mir wurde schon in einem Bio-Bauernladen fälschlicherweise Rohmilch als kalbfreundliche Milch verkauft. Als ich direkt beim Bauernhof nachfragte stellte sich heraus, dass es ganz normale Bio-Rohmilch war, die nicht aus muttergebundener Kälberaufzucht stammte.)

Adressen für kalbfreundliche Milch

Ich habe bei BIO AUSTRIA und der Landwirtschaftskammer nachgefragt. Es gibt noch kaum Betriebe in Österreich die sich muttergebundener Kälberaufzucht in der Milchwirtschaft verschrieben haben. Hier eine Adressen-Sammlung. Unser Ziel ist es, diese Liste stetig zu erweitern.

Weinkirnhof, NÖ

Bonnleiten 7a, 3073 Stössing (30 Minuten von Wien entfernt)

Der Weinkirnhof ist ein kleiner Biobauernhof in Niederösterreich mit rund 20 Kühen, auf dem muttergebundene Kälberaufzucht gelebt wird. Man kann kalbfreundliche Milch frisch ab Hof kaufen.

Ich habe den Betrieb im April 2017 besichtigt. Gabriela Schöffl ist die Jung-Bäuerin, die muttergebundene Kälberaufzucht am Hof eingeführt hat. Sie erzählt: „Vor einigen Jahren gab es eine Kuh die gerade ihr erstes Kalb bekommen hatte. Sie war eine besonders gute Mutter und hat stundenlang ihrem neugeborenen Kalb beim Schlafen zugesehen. Als man ihr das Kalb wegnahm, hat sie sehr gelitten. Ich habe damals entschieden, dass ich das den Tieren nicht antun möchte.“ Seitdem dürfen am Weinkirnhof die Kälber bei der Mutterkuh bleiben.

Gabriela und ihr Mann Bernhard bieten regelmäßig Besichtigungen und Events auf ihrem Hof an. Für Gruppen und Schulklassen gibt es ein geführtes Programm „Schule am Bauernhof“.

Rainer Bergbauer, VBG

Auf der Egg 183, 6867 Schwarzenberg

Der Hof von Rainer Bergbauer und seiner Frau Manuela ist ein Demeter zertifizierter Biobauernhof in der Nähe von Bregenz und Dornbirn in Vorarlberg. Seit fünf Jahren praktizieren sie reine muttergebundene Aufzucht bei allen ihren Tieren, sprich Kühe, Schafe, Schweine und Hühner.

Manuela erzählt: “Unsere Produkte stellen wir alle selber her und vermarkten diese auf den Wochenmärkten in Dornbirn und Bregenz und in unserem Hoflädele am Schwarzenberg. Wir sind stolz darauf einen Weg gefunden zu haben, wie unsere Tiere bei der eigenen Mutter groß werden dürfen.”

Aus muttergebundener Aufzucht kann man dort nicht nur Milch sondern auch Joghurt, Topfen und Käse sowie verschiedene Fleischprodukte erwerben.

 

Kennst du weitere Betriebe, von denen man kalbfreundliche Milch beziehen kann? Bitte hinterlasse uns eine Notiz im Kommentar-Feld.

 

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Referenzen

Danke Wikimedia Commons (User: Uberpruster) für das Foto unter 3.0. license

I’m dead serious—you’re signing up for two years of misery. And nobody is talking about it. Here is my story.¹

Having a baby is worse than the death of your spouse?

Imagine your spouse or partner, the most important person in the world died. Horrible, right? Well, according to a 2015 study² having a baby is worse. In numbers, it’s 50 percent worse than the death of your partner or being unemployed. The birth of your first child is almost three times as bad as a divorce.

There you have it: Having a baby sucks.

When you hold your baby for the first time it is the moment: peak awesomeness. But within a few weeks of baby’s birth, your happiness will fall off a cliff. Your life will become so shitty, that you’ll find yourself breaking down in tears on the bathroom floor. You will wonder if you have just completely ruined your life. You will snap at your partner. You will come face to face with the most disgusting side of your personality. You will want to give the child back.

What makes it so bad exactly?

Both parents suffer. For the mother it’s the hardest, hands down. You’ll witness the metamorphosis of a lovely butterfly into a tired, snarky, miserable bitch with dark circles under her eyes, vomit on her shoulder, wet stains from leaking nipples and smelly hair tied back into a ponytail. This is the new baseline.

Whatever the woman did so far to be a happy and confident individual will be pulled out from under her feet. No more pursuing her intellectual interests, Sunday brunch, yoga, CrossFit, spa weekends, dinner parties—gone! Everything which made her what she is: her job, her expertise, her friends, her passion, her calling—gone!

Ladies, I’m talking about a total disintegration of your identity. You’ll be a slave to this dependent and demanding little human being. Your baby will be unreasonable and unfair. There will be no end to its needs nor to your tasks. You’ll beg to go back to your stressful 60-hour-job because now you’re on duty 24/7. No weekends, no evenings, no coffee breaks. Hell—you won’t even have time to take a dump.

And worst of all there’s the social isolation. Unless you have family or friends with kids living next door, you’ll be alone with your baby most of the time.³

Don’t be so foolish to think you’ll go places with a small child. First, you’ll find it impossible to get out of the door. The moment you put the baby down in order to perform, say, the most basic personal hygiene, the baby will cry. Also, don’t underestimate the sheer amount of stuff you need to pack when you go out with a baby: diapers, wet wipes, changing pad, diaper cream, plastic bag for dirty diaper, burp cloths, pacifier, tissues, blanket, spare clothes, nursing pads, sunscreen…

If you actually do manage to leave the house, be prepared that it’ll take twice as long to get anywhere because your baby’s crying will make you stop every couple of minutes. You’ll be a sweaty mess when you finally arrive at the coffee shop to meet your friend for lunch. Then, rocking, feeding and burping the baby will make it virtually impossible to maintain a conversation. And get used to gulping your food down cold since babies reliably start crying the moment a meal gets served. Am I scaring you off yet? Did I mention the social awkwardness of breastfeeding in public? Picture yourself sitting in a packed restaurant with your breast hanging out for 20 minutes. I hope you don’t have any inhibitions.

People are polite enough, but no one enjoys the presence of a screaming baby. Good luck dealing with your guilt at constantly ruining other people’s lunch breaks, meetings or commutes.

Now, was all that hassle worth leaving the house in the first place? Hardly. Sooner or later you’ll become like other parents and leave the house only when absolutely necessary. And if you think now that “Being home is not the end of the world. I can read a book, binge on my favorite TV show or check my Instagram.”—trust me: you won’t be able to do any of that. Before I had a baby, I didn’t know that you could be busy all day and bored out of your mind at the same time.

Being at home with a baby feels like solitary confinement.

The nail in your relationship’s coffin

You and your partner will fight a lot. About everything. Constantly. Think about it like this: whatever bugs you about your partner now, will make you want to tear their heads off once the baby is born. There is a reason why sleep deprivation is classified as a form of torture. You quickly lose your kindness, patience, sense of humor, your sanity.

If you think a baby will fix your relationship—think again.

You might wonder “People have had kids forever and if it was truly that awful they would have said so.” While this sounds logical, consider how the definition of awful changes in relation to the other awful things you have experienced in your life.

Hardship is relative

If you were born in Europe in the early 1900s, you lived through the terror of two world wars and the great depression. Having a baby back then was probably not the biggest stressor in your life.

The post-war generations were brought up under difficult circumstances by authoritarian—and often violent—caregivers.

If you’re reading this, you’re probably a member of the Generation Y (1976-1990) or the so-called Millennials (1991-2005)⁴. If you were also born and raised in the western hemisphere, you were lucky to grow up in a safe and comfortable environment. Your parents—Baby Boomers and Generation X—had already taken a stand for gender equality, countered racism and superseded the authoritarian approach to parenting. This means that—as a group—you’ve experienced a lot less shitty stuff in your life.

The worst events of your lifetime were perhaps 9/11 (the majority followed on TV) and the financial crisis of 2008. The financial crisis certainly took its toll on the early members of Generation Y. But most of us were either still in school—thus financially supported by our parents—or had just started out a career with an underpaid job and a cheap rent. Because we didn’t have a lot to lose, the crisis only affected us peripherally.

There is no shame in living a protected life, it’s a privilege. It’s important to acknowledge the fact however, that not having experienced war, political suppression, famine or poverty—our younger generations’ experience of hardship has been limited. Therefore…

Having a baby is likely going to be the worst experience of your life.

Two years. And then…?

At around two years, your child can walk, has acquired basic communication skills and develops an attitude if their own. While the latter can often present a challenge, the whole package starts to look like fun for the parents. In the long run, you’ll come to see that the “worst experience of your life” was just a dip in your overall happiness curve.

After two years you will have adjusted to the new situation. You will have grown as a person and have made a number of adjustments and optimizations to your life that will change it for the better. Sometimes extreme pressure is just what it takes to form a diamond.

My daughter mercilessly eliminated baggage I was carrying for reasons of courtesy, guilt or compensation. I quit meeting people half-heartedly, stopped pointless internet surfing, I abandoned all non-essential home improvement projects. I stopped obsessing about looks and went with natural nails, low-maintenance haircuts, functional clothing, threw out all my high heel shoes, and the list goes on. My child forced me to set priorities like nothing else I’ve ever experienced. In fact, my life has gotten an upgrade.

Natural dopamine hits

Of course, having a baby doesn’t suck entirely. For example, the baby will get you high on dopamine and oxytocin a lot of the time.⁵ Those are two of the many neurotransmitters which make you experience a form of happiness.

A little wave of happiness hits you every time your child smiles or masters a new skill.

Interestingly, mothers also show a dopamine response to a crying baby.⁵ And indeed, those countless little dopamine and oxytocin highs every day feel wonderful and can bring a lot of joy into a parent’s life.

Like a phoenix from the ashes

After the disintegration of your identity, chances are that you’ll come out the other side a better version of yourself. Athletes train under adverse conditions so that they can perform better under regular conditions. It’s the same principle applied to your personality and relationship. What doesn’t kill it makes it stronger. Children are the kind of hardship that can make you come to terms with your deepest issues and resolve them.

Stop whitewashing early parenthood

We have to be honest with new parents—particularly the mothers—or they’ll think they’re doing it wrong. Take this as an analogy: people who sign up for a marathon usually know beforehand how brutal it is going to be. If they only found out halfway into the race, they’d be overwhelmed and might want to give up.

In the same way we should be honest about just how tough those first years are going to be. We can’t spare new parents the stress of sleep deprivation, domestic isolation or relationship glitches—those things are inevitable. But we can spare them the additional pain of thinking that the stress they are experiencing is due to their personal shortcomings. If I had known that having a baby sucks, I wouldn’t have felt like such an idiot.

Despite all my ranting, I wholeheartedly recommend motherhood. I recommend it the same way I recommend traveling the world on a shoestring. It shapes character.

As things naturally relax after the first two years, parents quickly forget the early hardships—just like the pain of giving birth—and remember the good times. What they say then is “Your life changes completely, but I wouldn’t have it any other way” or “Children are a gift”. While this might be true once you’ve gotten some perspective, this is not how it feels in the moment. So, my advice for soon-to-be parents is: expect the biggest challenge of your life.

 

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References

You know homeopathy is bogus; but your child doesn’t! The Power of Placebo: How you and your family can get a great deal out of homeopathy without actually believing in it.

My mom and I have had this conversation a gazillion times. Then, last Christmas, we got into a full-blown fight.

Study after study shows, that homeopathy has no effect beyond placebo.¹ Same is true for acupuncture, cupping and some other types of so called complementary medicine.² The placebo effect however is powerful and worth further investigation.

How the placebo effect works

Brain-imaging studies have confirmed that patients don’t just imagine placebo responses. Placebos trigger real biochemical responses in the body.³

Placebos cause measurable changes in neurobiological signaling pathways.

Here is how it works: when you are in pain and your doctor prescribes a pain medication, your prefrontal cortex forms an expectation of something positive. Reward pathways in the brain get activated and cause the release of endorphins. Endorphins make you feel good and—more importantly—bind to opioid receptors (much like morphine) and therefore act like a natural pain killer.

Dopamine is another neurotransmitter which is released from gleeful anticipation. Patients suffering from Parkinson’s disease or depression experience a symptoms relief from a placebo; all because of their own dopamine response.⁴

Placebo effects are even known in surgery. The outcomes of actual arthroscopic knee surgery for arthritis has proven to be no better than sham surgery.⁵ Both types of surgery produced the same positive results in patients.

Human factor

The degree of personal care a patient receives, correlates with the success of the therapy. When a doctor listens empathically, patients get better almost immediately. The placebo effect is amplified even more if the patient is educated about exactly how and when the medication will come into effect.⁶

The more information is shared about the effects of the pretended medicine, the stronger the placebo effect.

No effects without side effects

Generally, an organism gravitates towards health. Meaning, that most minor health issues like stress, pain, fatigue, cough, muscle tension, inflammation and the like are temporary and will get better on their own.

Bouncing back to normal can be accelerated or at least less debilitating thanks to drugs. But that comes at the costs of side effects. Pain meds stress the stomach. Antidepressants kill your libido. Coffee makes you sweat.

Prescription drugs come with effects and side effects.

The chasm is actually much deeper. You would think that medical procedures are based on evidence and the scientific method. They’re not. The history of western medicine is studded with treatments which were based on anecdotes and bits of evidence at best. What mattered most of all was the esteemed authority of the doctor. Examples of ineffective and often torturous treatments are blood letting, lobotomies or the overuse of mercury. And despite major improvements, 15 percent of all medical practices get reversed even today.⁷

Furthermore, clinical trials for a new drug are often biased or even manipulated. I highly recommend listening to the three-part series Bad Medicine on Freakonomics Radio if you want to learn more about modern medicine. And believe me, you do!

My personal credo is, that if I can abstain from medication, I will. Here’s where homeopathy comes in.

Homeopathy: a powerful placebo without side effects

Homeopathy checks all boxes for being a powerful placebo:

• Recommended by doctors⁸
• Sold in pharmacies
• Look & feel of ordinary pharmaceuticals
• Has complicated Latin names like Arconitum Compositum
• Is socially accepted
• Short intervals of intake

At the same time, homeopathy has no side effects. Why? Because the high dilution effectively eliminates all active ingredients. Richard Dawkins drew a catchy comparison: for a commonly prescribed 30C dilution, it’s like taking one molecule of the active ingredient and diluting it with all the atoms of the solar system.⁹ Justin Cooke from The Sunlight Experiment did a beautiful job illustrating the dilution process. Click to enlarge:

[Update] Hyland’s scandal 2017

No side effects is only true if the original substance is diluted to the point of inefficacy. The scandal around Hyland’s teething tablets shows how substandard manufacturing practices can pose a real threat to consumers. Inconsistent amounts of atropa belladonna aka deadly nightshade were found in the tablets, possibly harming hundreds of babies. They might even be linked to the death of eight babies over the past 10 years.

This scandals makes me reconsider my choice of placebo. Fortunately some pharmacies produce non-homeopathic placebo pills, which don’t contain any active ingredient, not even theoretically. Personally I’ll go with those in the future. Let me know what you use as placebo.

Placebo works best in children

In my estimation, placebo can be useful for all kinds of minor aliments like headache, cough, runny nose, anxiety, etc. Eventually children would bounce back to normal on their own, but with a powerful placebo I have experienced that I can speed up the process.

As a parent you have superpowers. Your child sees you as all-knowing and almighty. If you tell them that this medicine will heal their boo-boo, the placebo effect will rise to its fullest effect.

With the best of intentions we lie about Santa Claus. Why not lie about medicine too?

If my child suffered from depression and I had a 60 percent chance to mitigate the symptoms by using nothing else than a sugar pill—I’d give it a shot.¹⁰

My daughter is a young toddler. Together we’ve been through multiple colds, infections, teething and all kinds of children’s diseases. I know when I can get away using a placebo and when it’s time for real medicine. For example: I wouldn’t treat an acute ear infection with a placebo, but a mild to moderate cold—no problem! Generally, my goal is to go for as long as possible without actual medication.

Is prescribing a placebo ethical?

Intentionally deceiving patients would go against most doctor’s ethics. But in a doctor-parent-child relationship this is of no concern. The physician gives full disclosure to the parent who makes an informed decision about their child’s treatment.

Maximizing the placebo effect

As a parent, this is what you can do to max out the power of the placebo effect:

• Connect with your child and make sure to get their full attention.
• Ask specific questions: where, when, how long and how does it hurt? Listen closely to your child and repeat what they have said. (e.g. “I hear you have a sore throat and it hurts pretty bad. It’s especially painful in the morning, and drinking and eating hurts too. And when you talk it gets worse. But after lunch it’s always better.”)
• Explain to your child that this medicine will help them heal. Explain precisely what it will do and when. The more (age appropriate) information you give your child the better they can form expectations.
• Create a ritual. Children love rituals and let them play an active role in the administration of the pills. You could—for example—chant a magic spell and when the pills are swallowed make your child clap three times to seal the spell.
• Repeat the ritual multiple times per day.

My daughter barely understands the concept of medicine yet. But when I pull out the pills and drops, she knows magic is about to happen. Hokus Pokus Fidibus, Abra Kadabra! She loves it.

 

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References

How much THC makes it into breast milk? Can it get a baby “high”? What are the long-term effects on the child?

Update: also check out our latest post on this topic: Only small amounts of THC transfer into breast milk, that includes most recent scientific findings from April, 2018.

I nursed my daughter for almost two years. You bet, I had a glass of wine from time to time. I knew how long it would take my body to clear the alcohol so that—after a couple of hours—I could feed again without exposing my child to any risk. But with cannabis, nursing mothers are pretty much groping in the dark.

With cannabis, nursing mothers are pretty much groping in the dark.

Marijuana is legal in half of the States in the US and legal-ish in 16 other countries around the world. And mothers out there are wondering under which circumstances medical or recreational cannabis use is safe while breastfeeding.

The official guideline is that breastfeeding women should not use cannabis. This is because not enough is known about the topic to state “safe amounts” to mothers. I wasn’t satisfied with that answer, so I kept on digging. Here, I’ll present an overview of the scientific facts, so that you can make up your own mind.

Let’s break the topic down into two questions:

I. How much THC makes it into breast milk?
II. What are the effects on the child?

I recommend reading my post on the Human Metabolism of THC. Knowing about how THC—the main active ingredient in cannabis—is metabolized will increase your understanding of the topic. For those in a hurry: at minimum check the infographic and use it as a cheat sheet.

We will deal with very small numbers. A quick refresher on the notation and conversion of grams, milligrams and nanograms:

g = gram	1 g = 1,000 mg
mg = milligram	1 mg = 1,000,000 ng
ng = nanogram	1 ng = 0.000000001 g

I. How much THC makes it into breast milk?

“It is generally accepted that all medications transfer into human milk to some degree, although it is almost always quite low. Only rarely does the amount transferred into milk produce clinically relevant doses in the infant.” reads the introduction to the reference book Medication and Mothers’ Milk.¹ It is widely used in American hospitals to determine contraindications of drugs for breastfeeding mothers. The chapter on THC is short and doesn’t contain original research. Yet.

Dark Age of Data

There is little data published on THC levels in mother’s milk. Most data is from the 1970s and 80s. A study from the 70s found that in monkeys only 0.2% of the ingested THC by the mother gets into the breast milk.²

How about humans?
Hard to believe, but there is only one study (!) in which two samples (!) of human breast milk were analyzed.³ The two mothers were heavy users and their milk showed THC levels of 105ng/ml and 340ng/ml.⁴

Those two data points are interesting, but don’t answer the question how much THC makes it into breast milk because:

• We don’t know how much marijuana was initially consumed.
• We don’t know how long since the last marijuana consumption.
• With a one-time measurement we don’t see how the THC concentration in breast milk behaves over 24 hours.
• Both mothers were heavy users who were consuming marijuana on a daily basis. With regular use, THC accumulates in the body over time, especially in fat. And there is a lot of fat in breast milk. We don’t know which part of the detected THC is due to accumulation and which part is recently consumed THC.
• A sample size of two isn’t representative for a larger population.

True? There is eight times more THC in breast milk than in blood?

This 8:1 ratio has spread across the internet. Beware every author who quotes that number as if it were a fact—they’ve got the story wrong. Here is what actually happened:

Once upon a time in 1982³, there was one cannabis smoking mother who agreed to have her blood and breast milk analyzed simultaneously for THC. She was a heavy user, smoking marijuana out of a pipe seven times per day. About one hour after her last consumption the researchers took a sample of her blood and breast milk. It turned out, THC levels in her breast milk were eight times higher than in her blood.

But one sample is not representative for a larger population, nor was it the goal of the study. The study’s goal was to find out if THC was present in human breast milk at all and if so, whether it was going to be metabolized in the child. (The answer to both questions is yes.)

The 8:1 ratio was solely an observation regarding that particular case of the heavy using mother. In my eyes, those researchers are heroes for collecting and sharing that data. But they would surely not approve people quoting that 8:1 ratio out of context.

In short: that study did not find that the THC concentration in milk is 8:1 compared to blood. This ratio was true for one case and one case only.

Here are the claims actually supported by science:

1. THC blood levels have proven to be highly variable across subjects.
2. THC blood levels drop soon after consumption because THC is rapidly taken up by fat tissue. It’s plausible therefore that THC levels would be higher in milk because of its high fat content.
3. Recreational users clear their systems faster.

Quick-and-dirty math

Don’t you want to know how high that baby above got from the THC infused breast milk? I was curious and did the math. Turned out, in one feeding baby experienced about 1.1 percent of what an adult would experience if he ate a weed cookie. In other words:

The baby experienced the equivalent of a space cookie’s crumb.

Why didn’t I compare it to the mom’s marijuana pipe? Because (1) the data doesn’t exist and (2) eating cannabis is very different to smoking it. Hence, I believe it’s a more accurate comparison if we stick to the same metabolic pathway through the stomach. From another study⁵ we know that 20mg of ingested THC produce a decent psychological effect in an adult man. I compared that to a 3 months old baby. The results vary according to how you set the parameters.⁶ Other authors came close but arrive at slightly different conclusions, e.g. Bennett who landed at a baby’s dose of 0.8 percent of the maternal intake of one joint (per feeding).⁷

Be that as it may—half a crumb or three—you get an idea about the magnitude we’re operating at. Keep in mind however, that a new crumb is added to the pile every time the baby feeds. The crumbs are getting smaller but we don’t know how fast. To my knowledge there is no study examining the rate of THC elimination from breast milk and that’s precisely the problem.

Not knowing how fast THC clears from breast milk is what’s keeping responsible mothers from a responsible use of cannabis.

II. What are the effects on the child?

The entire academic discussion revolves around two studies which present inconsistent results:

One study⁸ from 1985 found no effects. The other identified slightly reduced motor development in kids of frequent users.⁹ That was only true if the mother consumed cannabis in the first month after birth and more frequently than 15 days per month. At one year old, those kids scored more poorly than the kids of non-users.¹⁰ However, those results can’t be distinguished from cannabis use during pregnancy; 84% of the mothers who used cannabis while breastfeeding had done so during pregnancy too.¹¹

Ironically, the kids whose mothers used cannabis less than 15 days per month scored higher than the kids of non-users. The narrow lead wasn’t statistically significant though, which means that there was no difference between kids of occasional users and non-users. Furthermore, no differences in mental development were detected amongst any of the three groups.

Summary

Very little amounts of THC get transferred into breast milk. Scientific publications give examples of 0.8 percent of the maternal intake of one joint per feeding⁷ or a total daily intake of 0.01 to 0.1 milligrams of THC through breastmilk if the mother smokes 1 or 2 cannabis cigarettes per day.¹² The particular circumstances under which those numbers were gathered should be kept in mind though:

Potency of marijuana

Over the past 35 years, marijuana has evolved. The study³ most authors refer to was conducted in the early 80s, when the average concentration of THC was at 3.2 percent. Until 2008, it had risen to 8.5 percent.¹³ In Colorado the average potency of flower (i.e. buds) in 2015 was at 17.1 percent THC.¹⁴

Occasional vs. regular use

The few samples analyzed all came from mothers who smoked on a daily basis. With regular use, THC accumulates in fat deposits, from where it is slowly released back into the bloodstream. That’s why the half-life of THC is longer in regular users. Recreational users show lower THC levels in blood and urine and clear it faster from their systems. How fast THC is cleared from specifically breast milk has not been researched yet.

Potential risk for child

Whether the transferred THC has adverse effects on the child is controversial. (Thin) evidence supports both sides of the argument. Heavy cannabis use in the first month of life might result in inferior motor skills at one year old. But that could also be a result of regular cannabis exposure during the preceding pregnancy.

Weighed against benefits of breastfeeding

On the other hand, the benefits of breastfeeding for mother and child are well documented: optimal nourishment, protection against infections, increased IQ, less obesity, reduced risk of ovarian and breast cancer, the list goes on.¹⁵

Traditionally, nursing mothers were advised to stop breastfeeding if they wanted to consume cannabis. In recent years, however this position has weakened. The strong health benefits of breastfeeding have led many lactation professionals towards a more moderate benefit/risk calculation.¹⁶ Especially with moderate or occasional use, evidence of detrimental effects of cannabis for the child has yet to be presented. Some doctors even go as far as to say that occasional or low regular use while breastfeeding will probably not be of relevance to the child’s development.¹⁷

My take on the topic

Don’t judge

I believe the reasons why a nursing mother would decide to consume cannabis are personal and complex. Furthermore, I believe that most mothers care deeply for their baby and wouldn’t make such a decision lightly.

Personally, I was scared of consuming marijuana while breastfeeding and refrained from even taking an aspirin. But also, I didn’t have the information I have today. Maybe today my decision would be different.

Rather, provide information

I’m not a doctor and this isn’t medical advice. Having said that, here is what I personally found to be useful from studying scientific literature:

Eating vs. smoking. Ingesting cannabis produces a similar high but at a considerably lower THC exposure. Start small.

Side stream smoke. Side stream smoke poses a risk to anyone, including you and your baby. Besides THC it holds carcinogens and other toxins.

Backstop. Have someone sober around who can take over with the child if needed. With varying potency of product, effects can be unpredictable. Especially casual users can experience paranoia or impaired judgement. Caring for a child in such a case can be difficult.

Timing matters. During pregnancy and the first three months of life, a baby’s developing organism is most vulnerable. During that time keep exposure to a minimum.

Minimum effective dose (MED). The less, the better – true for almost anything.

 

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References

It’s widely-known that Tetrahydrocannabinol (THC) is the active ingredient in cannabis and the reason people experience a psychological high. Less widely-known, however, is what happens to THC in the body and how that impacts the psychological high.

This post presents a summary of scientific research on the human metabolism of THC—visualized and explained in simple language.

Originally, my goal was to write on the effect of cannabis in breast milk (update: which I now did) but as I got deeper into the subject matter I became fascinated with the metabolic pathway of THC and what that means for its psychological effect. I learned why—also on a molecular level—cannabis turns into a different kind of drug when it is eaten vs. smoked, why it has such a long half-life in the body and how inhalation technique greatly impacts bioavailability. I spent two months reading my way through scientific papers not freely available to the public, analyzing original data and making sense of it all. The majority of sources for this post are from scientific journals and occasionally from Wikipedia for definition purposes.

I was surprised that I couldn’t find any infographics on the subject. So after collecting all this data, I decided to create an infographic myself that sums up the human metabolism of THC. Enjoy and feel free to share it. I encourage you however, to read the post as well, since it contains additional information that goes beyond the infographic.

To understand the pathway of THC in the human body, you must first understand what THC does when it hits your body. You might find the biochemistry part at the beginning challenging. I certainly did when I started applying myself to the topic. Believe me, it’s worth it—I promise the reading gets easier and incredibly interesting further on.

A bit of biochemistry

When cannabis is consumed, the liver breaks down the main psychoactive ingredient delta-9-THC into other molecules. First, enzymes turn delta-9-THC into 11-OH-THC (which is also psychoactive) and then into 11-COOH-THC which is not psychoactive.¹

You’ll find different versions of naming those molecules across the internet. If you end up as confused as I was, check the following table for clarification:

Name used here	Pronunciation	Molecular notation	Also known as
delta-9-THC	“delta 9 THC”	Δ9-THC	THC
11-OH-THC	“hydroxy THC”	11-OH-Δ9-THC	11-hydroxy-THC
11-COOH-THC	“carboxy THC”	11-COOH-Δ9-THC	11-nor-9-carboxy-THC, 9-carboxy-THC, THC-COOH

THC = Tetrahydrocannabinol

Again, in the liver, delta-9-THC turns into 11-OH-THC which turns into 11-COOH-THC. You’ll need to remember this as I will now explain how THC travels through the human body.

Note: The three THC molecules have different properties. For the sake of clarity I’ll call them by their full names—delta-9-THC, 11-OH-THC, 11-COOH-THC—unless I mean THC in general.

Metabolic pathway of THC

Whether one inhales or ingests cannabis makes a big difference in terms of the metabolic pathway that THC takes through the body. And as we will see in the sections to follow, that pathway will impact the efficacy of THC.

Inhalation

When cannabis is smoked or vaporized, delta-9-THC enters the bloodstream via absorption through the lungs. Once in the bloodstream, the delta-9-THC travels straight to the heart, and the heart then pumps it through the entire body—including the brain—allowing it to bind to cannabinoid receptors. The psychologically experienced high kicks in as the THC molecules pass the blood-brain barrier and bind to receptors in the brain.

There are two kinds of cannabinoid receptors:

1. CB1 receptors, which are activated by delta-9-THC and 11-OH-THC and found primarily in the brain and central nervous system; and
2. CB2 receptors, which are activated by cannabinol and found primarily in the tonsils, spleen and white blood cells.

Each time the blood circulates through the body, a certain portion of it passes through the liver. There, psychoactive delta-9-THC is metabolized into psychoactive 11-OH-THC and non-psychoactive 11-COOH-THC. Afterward, these two metabolites travel along with delta-9-THC to the heart and from there throughout the body. Like delta-9-THC, 11-OH-THC also binds to CB1 receptors in the brain.

The biological pathway through the lungs typically results in a steep increase of delta-9-THC in the bloodstream within 10 minutes of consumption. 11-OH-THC peaks slightly later, at around 15 minutes. After that, levels of both psychoactive molecules decrease sharply until, after 12 hours, their concentration falls under the detectable limit of 0.5 ng/ml. The second and non-psychoactive metabolite 11-COOH-THC peaks more than one hour after consumption and circulates in the bloodstream for a long time. In the quoted study it took 168 hours, i.e. 7 days, to fall under the detectable limit.²

Ingestion

When ingested, delta-9-THC enters the bloodstream through the walls of the stomach and intestines. Tests with radiolabeled delta-9-THC molecules show this process to be highly effective, with 90-95% of delta-9-THC molecules being absorbed, depending on the carrier medium.³ When absorbed gastrointestinally, delta-9-THC travels first to the liver where most of it is eliminated or metabolized before it has ever had a chance to activate a receptor. After this first pass through the liver, the remaining delta-9-THC and both its metabolites get to the heart and from there into circulation. Delta-9-THC and 11-OH-THC reach the brain simultaneously.

Bioavailability

How much of the consumed THC actually makes it into the bloodstream? There is no easy answer. The fact is that bioavailability fluctuates wildly.

Inhalation

In an experiment, six test subjects smoked the exact same amount of delta-9-THC. Test subject Mr. Burns exhibited almost three times as much delta-9-THC in his bloodstream compared to Homer who showed the lowest concentration. For all test subjects the peak was within 6 to 10 minutes after inhalation.²

What influences bioavailability? Two main factors are (1) method of inhalation, e.g. vaping or smoking, smoking in a joint or pipe, and (2) whether the test subject is an infrequent or regular user. Technique matters, as depth of inhalation, puff duration and breath hold increase bioavailability³; regular users inhale more efficiently and therefore show a 50-70% higher bioavailability of delta-9-THC.^{4 5}

Across all users, light and heavy, the bioavailability for inhaled delta-9-THC is between 10-35%.³

Ingestion

For ingested delta-9-THC, bioavailability is only between 4-12%. In contrast to inhalation, the user has little influence on the degree of bioavailability, with the exception of choosing a more optimal carrier medium. In many studies the choice was sesame oil or a similar high-fat carrier. After oral use, high variability was observed not only in the absolute levels of THC but also in the timing when users show peak concentration. Concretely, person A can exhibit peak concentration after one hour of ingestion whereas person B can exhibit peak concentration after six hours. Multiple peaks have been reported as well.³

Which produces stronger effects, inhalation or ingestion?

The following chart compares the delta-9-THC exposure of three different methods of intake: inhalation, ingestion and injection. In practice, delta-9-THC is usually not injected, but was done so in this study as a control for determining the bioavailability of different routes. The same study suggests a mean bioavailability of 18% for inhalation and 6% for ingestion.⁶

Looking at this chart I was tempted to conclude that inhalation produces a stronger psychoactive effect than ingestion but there are a number of problems with this assumption.

First is that with bioavailability fluctuating wildly between users, it’s difficult to determine the right dose for a fair comparison. Should you compare smoking 13 milligrams to eating 20? Or should you compare it to eating 40 milligrams, considering the much lower bioavailability of delta-9-THC when ingested?

Second—and more importantly—THC blood levels are a terrible indicator for the magnitude of a psychological high.

THC blood levels are a terrible indicator for the magnitude of a psychological high.

Blood transports the THC but it’s the destination that matters:

• Psychoactive THC binds to CB1 receptors in the brain. That’s why a few minutes after inhalation we already see higher THC concentrations in the brain than in the blood.

• THC is highly fat-soluble. THC is rapidly taken up by fat tissue, where it likes to accumulate and sit for many days. From these fat deposits, it is slowly released back into the bloodstream.⁷

As you can see in the chart above,⁷ after smoking THC there is a time lag between concentrations in the blood and brain. That’s why high THC levels in the bloodstream don’t mean that the user experiences a psychological high at the same time.

Finally, THC is not just THC. Some studies suggest, that the psychological high correlates better with the blood levels of the metabolite 11-OH-THC whose absolute representation would be much lower than the one of delta-9-THC.⁸ More on this in the next and final sections.

Psychological high

Just around the time when THC concentration is at a high point in the brain, psychoactive effects start to manifest. In the study described below, users were asked to rate the intensity of their experience over time on a scale from 1 to 10 in both inhalation and ingestion scenarios.

Inhalation

In the “smoking” chart below, you see the typical spike of delta-9-THC levels at the beginning, followed by 11-OH-THC peaking a few minutes later (the study at hand does not display 11-OH-THC levels). The subjectively rated effect achieves the highest level around 10 minutes after the delta-9-THC peak.⁹

Ingestion

The second tab above shows the same data for ingestion of 20 milligrams of delta-9-THC. Note that the time axis contains different values. Gastrointestinal absorption happens more slowly and usually results in a continuous rise and fall of blood levels and psychological high. Keep in mind that the values represent only averages. While person A experiences a “3”, person B might experience a “9”. Therefore the chart has to be taken with a grain of salt.

Comparing the psychological high over a timescale from 15 minutes to 360 minutes (i.e. 6 hours) reveals the potency of delta-9-THC via the pathway through the stomach.

The study at hand shows comparably small psychological effects for oral consumption. I’ve seen a second dataset which documented a much stronger psychological high which lasted almost twice as long as in the above study (with the same dose).^{8 9}

Many users claim that edibles produce a stronger and more “psychedelic” effect when compared to smoking. Unfortunately, there aren’t many studies that have assessed the quality of psychological effects across different methods of intake. Based on the data I’ve found, I can neither support nor dismiss such a claim.

An insight the data does provide, however, is that the ratio of delta-9-THC to 11-OH-THC impacts the intensity of the psychological high. And this ratio depends directly on the method of intake.

The ‘first-pass effect’ through the liver drastically changes the ratio of the two psychoactive cannabinoids.

When cannabis is inhaled, blood tests show a 10:1 ratio between delta-9-THC and 11-OH-THC. When cannabis is ingested, however, blood tests show this same ratio being 1:1.⁸

11-OH-THC passes the blood-brain-barrier more easily than delta-9-THC. Moreover, in animal tests 11-OH-THC has shown to be three to seven times more potent than delta-9-THC, i.e. three to seven times more capable of binding to the CB1 receptors in the brain.³

Altogether, this means that the lower bioavailability of delta-9-THC when ingested seems to get balanced out by the larger occurrence of 11-OH-THC and its higher potency in the brain.

The conclusion is that 11-OH-THC gets you a ‘better bind for the buck’.

What I’ve learned

There aren’t many studies which investigate the correlation of psychological high to THC concentration in blood serum. But the ones who did, pointed to a better correlation of 11-OH-THC with the psychological high state. That’s interesting news for the notorious optimizer in me, because it lets you achieve more with less.

I don’t want to get caught up in a discussion about drugs being good or bad. I respect individuals making decisions about how they want to think, feel and live. And as long as they don’t hurt anybody else, I think people should be free to use drugs—legal or illegal—as tools to attain their desired state of consciousness.

Having said that, it’s also a fact that drugs have desired effects and undesired side effects. And for the sake of maintaining good health over a lifetime, minimizing exposure to drugs is worth striving for.

Ergo, if I had the opportunity to enjoy the well-documented benefits of cannabis at a fraction of the associated exposure, that’s hitting a sweet spot. Especially for folks who are interested in achieving mild, enduring effects which blend in smoothly with their everyday lives.

Lightly-dosed edibles may be a ‘sweet spot’ for health-conscious folks looking for mild and enduring effects at low levels of exposure.

Minimum effective dose

Coming up with the right minimum effective dose (MED) is a matter of trial and error. Bioavailability fluctuates wildly across individuals and gender. The enzymes in the liver of a man and a woman work differently, which leads to a lower rate of blood plasma clearing in women,¹⁰ something to take into account too.

So, where to start? Some edibles sold in US states, which have legalized marijuana, contain astronomical doses of 100 milligrams and more. I haven’t encountered studies with oral doses of less than 20 milligrams, but 20 milligrams resulted in a medium to strong effect across the board which makes me believe the MED is significantly lower than that. The US state Colorado mandates a restriction of 10 milligrams of THC per edible, which is also the state’s recommended dose per “serving”. If one THC infused gummy bear contained 10 milligrams of THC, I’d consider just eating the feet.¹¹

Smoker’s paranoia

Another—quite useful—lesson I learned researching the metabolism of delta-9-THC is about dealing with smoker’s paranoia. Most of us have been there: you, a friend, a first timer, an excessive dose or simply a bad day. Happens to the best. Next time I see somebody freaking out I’ll say something along the lines of “Yes, you’re super baked. That’s because you have peak THC concentration in your brain right now. Hang in there buddy, science taught us the peak doesn’t last very long. In just a few minutes it’ll be a smooth ride down the other end.”

 

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Ich esse gerne Rindfleisch. Bilder von industrieller Tierhaltung fahren mir aber durch Mark und Bein. Deswegen verbringe ich gefühlte Stunden vor dem Kühlregal im Supermarkt und vergleiche Etiketten auf Frischfleisch.

Wenn ich im Schnitt 70%¹ mehr Geld für Bio-Rindfleisch ausgebe, möchte ich zwei Dinge wissen: erstens, auf welche Bio-Siegel kann ich mich verlassen? Und zweitens, ist eine Bio-Kuh auch wirklich glücklich?

I. Auf welche Bio Siegel kann man sich verlassen?

Produkte mit der Kennzeichnung „aus natürlicher Landwirtschaft” oder „aus kontrolliertem Anbau” wirken wie Bio-Produkte, sind es aber oft nicht. Die Vielzahl an Bio-Kennzeichnungen ist verwirrend. Es gibt allerdings eine einfache Hilfe um sich zurecht zu finden: das Bio-Siegel der Europäischen Union. Denn als Faustregel gilt: wenn “Bio” oder „ökologisch” draufsteht dann gelten mindestens die Auflagen der EU. Und die Bestätigung dafür, ist das grüne Logo auf der Verpackung.

Die EU regelt die Produktion und Verarbeitung von Bio-Erzeugnissen² und bildet damit die Grundlage für alle weiteren nationalen und regionalen Bio-Siegel.

Das EU-Bio-Siegel zeigt dem Konsumenten, dass das Produkt “weitgehend” aus biologischer Landwirtschaft stammt.

Um eine Idee davon zu bekommen, was in dieser Verordnung vorgeschrieben ist, hier ein kleiner Auszug:

Die EU-Bio-Verordnung sieht z.B. vor, dass 95% der Rohstoffe aus biologischem Anbau stammen müssen. Gentechnik ist verboten und auch synthetische Dünge- sowie Pflanzenschutzmittel sind untersagt.

Die Gabe von Hormonen oder der präventive Einsatz von Antibiotika ist verboten. Erkrankt ein Tier, muss zuerst eine Therapie mit Pflanzenextrakten oder homöopathischen Mitteln angestrebt werden. Sollte diese zu keinem Behandlungserfolg führen, so kann ein Tierarzt auch synthetische Medikamente und Antibiotika einsetzen. Werden einem Tier Antibiotika verabreicht, so verdoppelt sich die Wartezeit zur kommerziellen Vermarktung und auch die Milch darf während dieser Zeit nicht als Bio-Milch vertrieben werden. Werden häufiger als drei Mal pro Jahr synthetische Medikamente oder Antibiotika verabreicht, so ist das Tier nicht mehr „Bio” und muss konventionell vermarktet werden.

AMA-Austria und BIO AUSTRIA

Zusätzlich gibt es in Österreich noch andere Gütesiegel wie z.B. das AMA Biosiegel oder das BIO AUSTRIA Logo. Beide stützen sich auf die EU Verordnung und setzen weitere, noch strengere Richtlinien oben auf. Sie regeln hauptsächlich Hygiene, Herkunft und Qualitätskontrolle.

Der Unterschied zwischen dem schwarz-weissen und dem roten AMA Biosiegel liegt darin, dass für das rote Siegel sämtliche Rohstoffe aus Österreich stammen müssen.

II. Steht Bio Haltung für glückliche Kühe?

Schwierige Frage. „Glück” ist schon bei uns Homo Sapiens schwer zu messen – wie misst man „Glück” bei einer Kuh? Interpretiert man Glück als die Abwesenheit von Stress, so könnte man den Stress (d.h. Cortisol-Levels) von Bio-Kuh und konventionel gehaltener Kuh messen und vergleichen. Bei meiner Recherche habe ich zu wenig Datenmaterial gefunden um so eine Hypothese weiter zu verfolgen.

Daher habe ich entschieden das „Glück” der Kühe auf fünf Kategorien herunterzubrechen:

Auslauf

In der konventionellen Viehhaltung besteht keine Pflicht die Tiere auf die Weide zu lassen. Hier macht das Wörtchen „Bio” einen großen Unterschied. Die EU-Bio-Verordnung schreibt vor:

• ständigen Zugang zu Freigelände. Diese Auslaufflächen müssen so gestaltet sein, dass die Tiere Schutz vor Regen, Sonne, Kälte oder Hitze finden. Die Größe der Auslauffläche richtet sich nach dem Gewicht des Tieres. Für ein beispielsweise 400kg schweres junges Mastrind sind es 3,7m² Mindestfläche, für eine Milchkuh sind es 4,5m² pro Tier und bei Zuchtstieren sind es 30m² pro Tier
• Zugang zu Weideland, wann immer der Zustand des Bodens und die Witterungsbedingungen dies zulassen – mindestens aber 180 Tage pro Jahr. Die Größe des Weidelandes soll in etwa 1 ha pro ausgewachsener Kuh betragen.³

Futter

Das Futter muss zu mindestens 60% aus Gras, Heu und Stroh aus biologischem (vorzugsweise Eigen-) Anbau bestehen. Bio-Kraftfutter darf bis zu einem Anteil von 40% verzehrt werden,⁴ Tiermehl ist untersagt. Kälber müssen mit natürlicher Milch gefüttert werden, vorzugsweise mit der Milch der Mutterkuh.

Um das BIO AUSTRIA Logo ausweisen zu dürfen muss der Raufutteranteil mindestens 85% betragen.

Stall

Im Stall ist der Platz pro Tier abhängig von seinem Gewicht. Beispielsweise hat ein 400kg schweres, junges Mastrind zumindest 5m² Platz im Stall. Für seine Milchkuh-Kolleginnen sind 6m² pro Tier reserviert. Das klingt nach mehr, läuft allerdings bei dem durchschnittlichen Gewicht von 600kg einer Milchkuh auf ein ähnliches Verhältnis von Gewicht zu Quadratmeter hinaus. Für die Tiere sind bequeme, saubere, trockene Ruhe- bzw. Liegeflächen mit ganztägiger Tränkmöglichkeit bereitzustellen.

Herdengröße

Unter natürlichen Bedingungen besteht eine Rinderherde aus etwa 20-30 Kühen mit ihren Jungtieren. Ich vergleiche diese Herdengröße mit dem Viehbestand der österreichischen Bio-Bauern.

Von den insgesamt 379.895 Rindern aus Bio-Landwirtschaftsbetrieben in Österreich werden die meisten in kleinen Betrieben gehalten. 30% der Bio-Rinder teilen sich beispielsweise auf 22% der Bio-Betriebe auf. Man sieht auch, dass fast die Hälfte der Bio-Betriebe relativ kleine Herden von weniger als 19 Tieren hält. Knapp zwei Drittel haben weniger als 30 Kühe am Hof. Das sind 37% aller Bio-Rinder in Österreich. Zwei Drittel der Bio-Rinder werden in Größen von maximal 50 Tieren gehalten.⁵

Österreich ist im europäischen Vergleich Spitzenreiter in der Bio-Rinderhaltung. Der Bio-Anteil in EU-27 lag in 2010 im Durchschnitt bei unter 3%.⁶ In Österreich kamen in 2013 mehr als 19% aller Rinder aus biologischer Haltung, Tendenz steigend.

Auch die oben beschriebene kleine Herdengröße ist eher unüblich im europäischen Vergleich. Eine Auswahl der Top 5 Bio-Produzenten plus Deutschland und Frankreich zeigt, wie Rinder bei unseren EU-Nachbarn gehalten werden (ohne Trennung von biologischer und konventioneller Haltung).

In den Vergleichsländern werden über zwei Drittel der Rinder in Großbetrieben von über 100 Rinder pro Betrieb gehalten. In Österreich werden nur 14% so gehalten und innerhalb der biologischen Landwirtschaft sind es sogar nur 7%. Die kleineren Herdengrößen in Österreich sprechen – stark vereinfacht – für bessere Bedingungen für die Kühe.

Sozialverhalten

Rinder haben ein ausgeprägtes Sozialverhalten. Es gibt eine Rangordnung und klare Regeln innerhalb einer Herde. Kälber haben eine enge Beziehung zur Mutterkuh: wenn eine Kuh ein Kalb gebärt, leckt sie es trocken und säugt es mehrmals täglich. Die Milch der ersten Tage ist besonders reichhaltig und wichtig für das Immunsystem der Kälber. Nach kurzer Zeit erkennt die Kuh ihr Kalb am Geruch, nach wenigen Tagen kennen sie gegenseitig ihre Stimmen. Rund sechs Monate säugt das Kalb am Euter seiner Mutter.

In der Milchviehhaltung werden die Kälber binnen der ersten Lebenswoche, oft schon nach wenigen Stunden oder Tagen, von der Mutter getrennt. Die Kuh ruft noch tagelang nach ihrem Jungen. Früh getrennte Kälber zeigen häufig Verhaltensauffälligkeiten wie gegenseitiges Besaugen.

Auch Bio-Kälber werden von ihrer Mutter getrennt

Warum werden Mutterkuh und Kalb eigentlich getrennt? Muttertiere produzieren grundsätzlich so viel Milch wie ihre Nachkommen benötigen. Um mehr Milch zu erwirtschaften als das Kalb benötigt, muss man in der Milchproduktion tricksen:

1. Die Milchkuh bekommt zusätzlich Kraftfutter. Eine österreichische Milchkuh erzielt eine jährliche Milchleistung von durchschnittlich 6.580 Liter pro Jahr,⁷ das ist mehr als doppelt so viel als sie für die Ernährung ihres Kalbs benötigen würde.⁸ Raufutter – sprich Gras, Heu, Stroh – hat einen relativ niedrigen Energiewert und reicht nicht aus, um diesen erhöhten Energiebedarf zu decken. Daher wird mit sogenanntem „Kraftfutter” zugefüttert. Dieses besteht bei einem Bio-Milchbauern zumeist aus geschroteten Getreidesorten und Eiweißfrüchten (z.B. Soja, Erbsen) aus Bio-Anbau.
2. Milchkühe werden jedes Jahr geschwängert, denn ohne Kalb – keine Milch.
3. Auch bei der Herstellung von Biomilch, werden die Kälber bald nach der Geburt von der Mutterkuh getrennt. Die Kälber müssen zwar laut EU-Bio-Verordnung „natürliche Milch” zu trinken bekommen – das kann Frischmilch oder auch Milchpulver⁹ sein – allerdings bekommen sie diese aus mechanischen Trinkvorrichtungen verabreicht. Am Euter der Mutter dürfen die Kälber nicht trinken. Die vorgeschriebene Gruppenhaltung ab dem Alter von einer Woche soll dem Kalb ein Leben im Sozialverband bieten. Dieser Verband ist meist eine Gruppe von Kälbern und bedeutet nicht, dass das das Tier mit seiner Mutter beisammen sein darf um seinem natürlichen Sozialverhalten – Säugen und Ablecken – nachzugehen. Milch aus echter „Mutterkuhhaltung” sucht man in österreichischen Supermärkten vergebens.

„Aber ich sehe oft Kühe mit ihren Jungen auf der Wiese grasen, wie kann das sein wenn die Tiere getrennt werden?”

Mutterkuhhaltung gibt es natürlich schon, aber nicht bei Milchkühen.

Ein kleiner Exkurs in die konventionelle Rindviehhaltung macht das verständlicher: in der Rindviehhaltung unterscheidet man zwischen Milchvieh, für die Milchproduktion und Mastvieh, für die Fleischproduktion. In Österreich werden über zwei Drittel der Kühe als Milchvieh gehalten und rund ein Drittel als Mastvieh.¹⁰ Da die Milch des Mastviehs nicht kommerziell verwertet wird, kann das Kalb bei der Mutterkuh bleiben und säugen.

Im Klartext bedeutet das: wer nicht möchte dass Kalb und Mutter getrennt werden, darf keine Milch aus dem Supermarkt kaufen, egal ob Bio-Milch oder konventionelle Milch.

Wer nicht möchte, dass Kalb und Mutter getrennt werden, darf keine Milch kaufen.

Auch die strengen, österreichischen Bio-Richtlinien von AMA-Austria oder BIO AUSTRIA schreiben keine Muttergebundene Kälberaufzucht für Milchvieh vor.

Wo gibt es Milch aus Muttergebundener Kälberaufzucht in Österreich zu kaufen?

Ich habe viel herumgefragt und konnte selbst in dezidierten Bauernläden in Wien keine solche Milch finden. Sie wird meist nur direkt am Bauernhof zum Eigenbedarf getrunken und stammt von Mütterkühen (sprich von Mastvieh), nicht von Milchkühen.

Das Problem scheint zu sein, dass Milchproduktion eine sehr arbeitsintensive Form der Landwirtschaft ist. Durch Muttergebundene Kälberaufzucht erhöht sich der Arbeitsaufwand und verringert sich der Milchoutput – keine sonderlich attraktive Nische, nicht einmal für Kleinbetriebe.

In meinem Folgeartikel Kalbfreundliche Milch aus Österreich liste ich Bezugsquellen für Milch aus muttergebundener Kälberaufzucht auf.

Macht der Kauf von Bio-Produkten dann überhaupt Sinn?

Absolut! Auch wenn outputorientierte Nutztierhaltung immer einen Kompromiss für die artgerechte Form der Tierhaltung darstellt, so sind die Bedingungen in der Bio-Haltung doch merklich besser als in der konventionellen Haltung.

Noch viel wichtiger ist “Bio” allerdings für die Nachhaltigkeit in der Landwirtschaft:

• Nährstoffe im Boden bleiben erhalten. Durch abwechslungsreiche Fruchtfolgen und regelmäßige Pausen können sich die Böden erholen.
• Grundwasser wird nicht mit Kunstdüngern belastet.
• Da der Biobauer keine künstlichen Pflanzenschutzmittel einsetzen darf, ist eine hohe Biodiversität in seinem Eigeninteresse.

Biologische Landwirtschaft schont Böden und Gewässer und hilft damit uns und zukünftigen Generationen.

 

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