Independent science writer, blogger and infographic designer. In my actual day job I’m a marketing and account manager in a big tech company.

Why do I write a blog? We live in a fantastic, yet confusing time. Going by gut feeling has led me down some not so good paths. I believe that science is a more trustworthy guide in a world that has become too complex for one person to understand. In order to make up my own mind, I obsessively research things in depth. At some point I thought ‘Maybe others might be interested as well?’, so I started to write. Because nothing helps understanding as much as charts and illustrations, I started designing infographics as well.

I love extracting the essence out of complex topics and present them in ways that are easy to understand. Contact me if you want to pay me money for that.

A call for easy bitcoin units

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:

non-intuitive bitcoin denomination

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.

Price of cup of coffee in bitcoin

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:

Bitcoin units table: bitcoin, metric system, abbreviation, nicknames, satoshi

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:

How much will bitcoin be worth in the future

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.

Prices of goods in bitcoin dependent on market capitalization

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”?

Metric units for bitcoin

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.

What if

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

MDMA-assisted Therapy

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.

Can MDMA help veterans suffering from PTSD

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

MDMA-assisted therapy for PTSD study results, MAPSMAPS 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.

How PTSD affects hippocampus, prefrontal cortex and the amygdala 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 classic psychedelics (LSD and psilocybin)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!

 


References

  1. United States: Suicide Injury Deaths and Rates per 100,000. (All Races, Both Sexes, All Ages). 2016. CDC. Retrieved on 2018-03-03 via WISQARS Fatal Injury Reports

  2. National Suicide Data Report. 2016. U.S. Department of Veteran Affairs. 

  3. Rick Doblin. Opening Plenary: Psychedelic Science 2017. 2017. Youtube.  2

  4. A Phase 3 Program of MDMA-Assisted Psychotherapy for the Treatment of Severe Posttraumatic Stress Disorder (PTSD). MAPS. Retrieved 2018-03-01. 

  5. Infographic MDMA-assisted therapy for PTSD. MAPS. Retrieved 2018-03-01. 

  6. Dr. Gabor Maté — New Paradigms, Ayahuasca and Redefining Action. The Tim Ferriss Show. 2018.  2

  7. Psychological trauma. Wikipedia. Retrieved 2017-10-19 

  8. Carhart-Harris RL, Murphy K, Leech R. The Effects of Acutely Administered 3,4-Methylenedioxymethamphetamine on Spontaneous Brain Function in Healthy Volunteers Measured with Arterial Spin Labeling and Blood Oxygen Level-Dependent Resting State Functional Connectivity. Biol Psychiatry. 2015 Oct 15;78(8):554-62. PubMed PMID: 24495461. PMCID: PMC4578244

  9. MDMA – The Movie 2015. Youtube. 

  10. Carbonaro TM, Bradstreet MP, Barrett FS et al. Survey study of challenging experiences after ingesting psilocybin mushrooms: Acute and enduring positive and negative consequences. J Psychopharmacol. 2016 Dec;30(12):1268-1278. Epub 2016 Aug 30. PubMed PMID: 27578767. 

  11. Katie Anderson. MDMA’s impact on romantic relationships. 2016. Youtube. Retrieved 2018-02-28  2 3

  12. Cat McShane. Refinery29: The Couples That Take MDMA To Stay Together. 2017. MAPS.  2

  13. Nutt DJ, King LA, Phillips LD; Independent Scientific Committee on Drugs. Drug harms in the UK: a multicriteria decision analysis. Lancet. 2010 Nov 6;376(9752):1558-65. doi: 10.1016/S0140-6736(10)61462-6. Epub 2010 Oct 29. PubMed PMID: 21036393. 

Microdosing LSD: Smart Drug or Placebo?

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.

Biohackers love microdosing

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. Total Makeover: Microdosing changes image of LSD 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:

James Fadiman's Microdosing Regimen

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.

How does microdosing work

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.

Placebo effect: expectation bias with microdosing

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.

 


References

  1. Leonard A. How LSD Microdosing Became the Hot New Business Trip. Rolling Stone. Nov, 2015. 

  2. Fadiman J, Korb S. Microdosing: The Phenomenon, Research Results, and Startling Surprises. Youtube. Retrieved 2017-08-16.  2

  3. Nichols D. Microdosing with LSD and its Research Potential. Heffter Research Institute. Aug, 2017.  2

  4. Mainen Z. The Science of Serotonin. The 3rd Wave Podcast. May, 2017. 

  5. Carhart-Harris R. LSD with Dr. Robin Carhart-Harris. Smart Drugs Smarts podcast #129. May 20, 2016. 

  6. Van Praag H, Fleshner M, Schwartz MW, et al. Exercise, Energy Intake, Glucose Homeostasis, and the Brain. The Journal of Neuroscience. 2014;34(46):15139-15149. PMCID: PMC4228123

  7. Carhart-Harris RL, Kaelen M, Bolstridge M, et al. The paradoxical psychological effects of lysergic acid diethylamide (LSD). Psychol Med. 2016 May;46(7):1379-90. PubMed PMID: 26847689

  8. Kirsch I, Moore TJ, Scoboria A, et al. 2002. The emperor’s new drugs: an analysis of antidepressant medication data submitted to the US Food and Drug Administration. 2002. Prevent. Treat. 5, 23. 

  9. Kirsch I, Sapirstein G. Listening to Prozac but hearing placebo: a meta-analysis of antidepressant medication. 1998. Prevent. Treat. 1, 0002a. 

Psychedelics and Mental Health

“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.

Psychedelics effective in mental disorders

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.

Carhart-Harris: Psilocybin in treatment-resistant depression

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.

Placebo control in psychedelic research

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.

Griffiths: psilocybin in end-of-life-anxiety

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

Johnson: effects of psilocybin in tobacco addiction

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

Psychedelic therapy protocol exampleExample 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.

 


References

  1. Watts R, Day C, Krzanowski J, et al. Patients’ Accounts of Increased “Connectedness” and “Acceptance” After Psilocybin for Treatment-Resistant Depression. Journal of Humanistic Psychology. June-19-2017.  2 3 4 5

  2. David Nichols: Breaking the psychedelic research logjam with Dr. David Nichols. Smart Drugs Smarts podcast #176. April 14, 2017. 

  3. Gasser P, Holstein D, Michel Y, et al. Safety and efficacy of lysergic acid diethylamide-assisted psychotherapy for anxiety associated with life-threatening diseases. J Nerv Ment Dis 2014; 202: 513–20. PMID: 24594678 

  4. Grob CS, Danforth AL, Chopra GS, et al. Pilot study of psilocybin treatment for anxiety in patients with advanced-stage cancer. Arch Gen Psychiatry 2011; 68: 71–78. PMID: 20819978 2

  5. Carhart-Harris RL, Bolstridge M, Rucker J, et al. Psilocybin with psychological support for treatment-resistant depression: an open-label feasibility study. Lancet Psychiatry. 2016 Jul;3(7):619-27. PubMed PMID: 2721003 2 3

  6. Osorio Fde L, Sanches RF, Macedo LR, et al. Antidepressant effects of a single dose of ayahuasca in patients with recurrent depression: a preliminary report. Rev Bras Psiquiatr 2015; 37: 13–20. PMID: 25806551 

  7. Moreno FA, Wiegand CB, Taitano EK, Delgado PL. Safety, tolerability, and efficacy of psilocybin in 9 patients with obsessive-compulsive disorder. J Clin Psychiatry 2006; 67: 1735–40. PMID: 17196053 

  8. Johnson MW, Garcia-Romeu A, Cosimano MP, Griffiths RR. Pilot study of the 5-HT2AR agonist psilocybin in the treatment of tobacco addiction. J Psychopharmacol 2014; 28: 983–92. PMID: 25213996  2

  9. Bogenschutz MP, Forcehimes AA, Pommy JA, Wilcox CE, Barbosa P, Strassman RJ. Psilocybin-assisted treatment for alcohol dependence: a proof-of-concept study. J Psychopharmacol 2015; 29: 289–99. PMID: 25586396 

  10. Depression fact Sheet. WHO. 2017. Retrieved 2017-07-28 

  11. Gaynes BN. Identifying difficult-to-treat depression:
differential diagnosis, subtypes, and comorbidities. J Clin Psychiatry 2009; 70 (suppl 6): 10–15. PMID: 19922739 

  12. Griffiths RR, Johnson MW, Carducci MA. Psilocybin produces substantial and sustained decreases in depression and anxiety in patients with life-threatening cancer: A randomized double-blind trial. J Psychopharmacol. 2016 Dec;30(12):1181-1197. PubMed PMID: 27909165  2

  13. Griffiths RR. The science of psilocybin and its use to relieve suffering. YouTube. 2016. Retrieved 2017-04-17. 

  14. National Center for Chronic Disease Prevention and Health Promotion (US) Office on Smoking and Health. The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General. Atlanta (GA): Centers for Disease Control and Prevention (US); 2014. 1, Introduction, Summary, and Conclusions. Available from: https://www.ncbi.nlm.nih.gov/books/NBK294320/ 

  15. Jorenby DE, Hays JT, Rigotti NA, et al. Efficacy of varenicline, an alpha4beta2 nicotinic acetylcholine receptor partial agonist, vs placebo or sustained-release bupropion for smoking cessation: a randomized controlled trial. JAMA. 2006 Jul 5; 296(1):56-63. PubMed PMID: 16820547 

  16. Hall SM, Humfleet GL, Muñoz RF, Reus VI, Robbins JA, Prochaska JJ. Extended treatment of older cigarette smokers. Addiction. 2009 Jun;104(6):1043-52. Epub 2009 Apr 9. Erratum in: Addiction. 2011 Jun;106(6):1204. PubMed PMID: 19392908 

  17. Killen JD, Fortmann SP, Schatzberg AF, et al. Extended cognitive behavior therapy for cigarette smoking cessation. Addiction. 2008 Aug;103(8):1381-90. PubMed PMID: 18855829 

  18. Johnson MW, Garcia-Romeu A, Griffiths RR. Long-term follow-up of psilocybin-facilitated smoking cessation. Am J Drug Alcohol Abuse. 2017 Jan;43(1):55-60. doi: 10.3109/00952990.2016.1170135. Epub 2016 Jul 21. PubMed PMID: 27441452

  19. Carhart-Harris RL, Kaelen M, Bolstridge M, et al. The paradoxical psychological effects of lysergic acid diethylamide (LSD). Psychol Med. 2016 May;46(7):1379-90. PubMed PMID: 26847689

Your Brain on Psychedelic Drugs

“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.

Self-Reflected by Greg A. DunnThis 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

Griffiths' psilocybin study in healthy volunteers

‘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’.

Neuronal connections and the role of connector hubs in the brain

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.

Comparison of brain's communication pathways after placebo vs. psilocybinCommunication 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.

Drugs and their superpowers

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

The brain's Default Mode Network (DMN) with medial prefrontal cortex (mPFC), posterior cingulate cortex (PCC) and the angular gyrus (AG)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

Neuroscience jargon broken down into simple language

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.

Chemical structure of serotonin, LSD and psilocin

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.

Excitatory vs. inhibitory signaling of neurons

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

How excitatory signals can lead to overall inhibition

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.

Functional selectivity: ligand dependent signaling of the receptor

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 Flexible serotonin molecule compared to big rigid LSD molecule

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

LSD molecule binds to 5-HT2B receptor

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

Lid over LSD molecule in 5-HT2B receptor

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.

 


References

  1. Brooks X. Cary Grant: how 100 acid trips in Tinseltown ‘changed my life’. The Guardian. May, 2017. 

  2. Baer D. How Steve Jobs’ Acid-Fueled Quest For Enlightenment Made Him The Greatest Product Visionary In History. Business Insider. Jan, 2009. 

  3. Griffiths RR, Richards WA, Johnson MW, et al. Mystical-type experiences occasioned by psilocybin mediate the attribution of personal meaning and spiritual significance 14 months later. Journal of psychopharmacology (Oxford, England). 2008;22(6):621-632. PMCID PMC3050654 

  4. Petri G, Expert P, Turkheimer F, et al. Homological scaffolds of brain functional networks. J R Soc Interface. 2014 Dec 6;11(101):20140873. PubMed PMID: 25401177

  5. Carhart-Harris R. [Brain Imaging Studies with Psilocybin and MDMA]. YouTube. 2013. Retrieved 2017-05-38 

  6. Qin P, Northoff G. How is our self related to midline regions and the default-mode network? Neuroimage. 2011 Aug 1;57(3):1221-33. PubMed PMID: 21609772 

  7. Hassabis D, Kumaran D, Maguire EA. Using imagination to understand the neural basis of episodic memory. The Journal of neuroscience: the official journal of the Society for Neuroscience. 2007;27(52):14365-14374. PMCID: PMC2571957 

  8. Buckner RL, Carroll DC. Self-projection and the brain. Trends Cogn Sci. 2007 Feb;11(2):49-57. Epub 2006 Dec 22. Review. PubMed PMID: 17188554 

  9. Fleming SM, Weil RS, Nagy Z, Dolan RJ, Rees G. Relating introspective accuracy to individual differences in brain structure. Science. 2010 Sep 17;329(5998):1541-3. Science. 2012 May 11;336(6082):670. PMCID: PMC317384 

  10. Image modified from: Graner J, Oakes TR, French LM, et. al. Functional MRI in the investigation of blast-related traumatic brain injury. Front Neurol. 2013 Mar 4;4:16.eCollection 2013. PubMed PMID: 23460082 

  11. Carhart-Harris RL, Muthukumaraswamy S, Roseman L, et al. Neural correlates of the LSD experience revealed by multimodal neuroimaging. Proc Natl Acad Sci USA. 2016 Apr 26;113(17):4853-8. PubMed PMID: 27071089  2

  12. Lesser IM, Chung JA. Depression and the Frontal Lobes. In: The Human Frontal Lobes. Miller, Cummings. 2007. 

  13. Cerebral cortex. Wikipedia. Retrieved on 2017-07-21 

  14. Vollenweider FX, Kometer M. The neurobiology of psychedelic drugs: implications for the treatment of mood disorders. Nat Rev Neurosci. 2010 Sep;11(9):642-51. Review. PubMed PMID: 20717121

  15. Nutt D. The Beckley-Imperial Psychedelic Research Program. 2013. YouTube. Retrieved 2017-07-05 

  16. Nichols D. Psychedelic Neuroscience: LSD Gives Up a Secret. 2017. Youtube. Retrieved 2017-05-24 

  17. Nichols DE. Psychedelics. Barker EL, ed. Pharmacological Reviews. 2016;68(2):264-355. PMCID: PMC4813425  2

  18. Illustrations modified from: Wacker D, Wang S, McCorvy JD, et al. Crystal Structure of an LSD-Bound Human Serotonin Receptor. Cell. 2017 Jan 26;168(3):377-389.e12. PubMed PMID: 28129538  2

  19. Passie T, Halpern JH, Stichtenoth DO, et al. The pharmacology of lysergic acid diethylamide: A review. CNS Neuro- sci. Ther. 2008 14, 295–314. 

  20. Merlin MD. Archaeological evidence for the tradition of psychoactive plant use in the old world. Economic Botany. 2003;57:295–323. 

The Psychedelic Experience

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 example 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.

Comparison of Psychedelic Experience of MDMA, LSD, Psilocybin (magic mushrooms) and Ketamine on 5D-ASC scale 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.

Drugs classification by monoamine transporter, G-protein coupled receptors, ionotropic receptors or ion channels 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.

Categorization of psychedelic drugs in empathogen or entactogen, hallucinogen, 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”.

Bad trip with a psychedelic drug from Simpsons 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

Griffiths study results on bad trips from psilocybin 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.

 


References

  1. The Mushroom/LSD Experience Explained & Explored Retrieved 2017-06-20. 

  2. The resource erowid, reports a common dose to be at around 100 micrograms of LSD. LSD Dosage Retrieved 2017-06-20. 

  3. Dittrich A. The standardized psychometric assessment of altered states of consciousness (ASCs) in humans. Pharmacopsychiatry. 1998 Jul;31 Suppl 2:80-4. Review. PubMed PMID: 9754838 

  4. Some titles were modified for better understanding. Data from Studerus E, Gamma A, Vollenweider FX. Psychometric Evaluation of the Altered States of Consciousness Rating Scale (OAV). Bell V, ed. PLoS ONE. 2010;5(8):e12412. PMCID: PMC2930851 and Carhart-Harris RL, Muthukumaraswamy S, Roseman L. Neural correlates of the LSD experience revealed by multimodal neuroimaging. Proc Natl Acad Sci U S A. 2016 Apr 26;113(17):4853-8. PubMed PMID: 27071089  2

  5. What’s not displayed in the chart are the two remaining dimensions acoustic alterations and altered vigilance. 

  6. Vollenweider FX, Kometer M. The neurobiology of psychedelic drugs: implications for the treatment of mood disorders. Nat Rev Neurosci. 2010 Sep;11(9):642-51. Epub 2010 Aug 18. Review. PubMed PMID: 20717121

  7. Psychedelic drug. Wikipedia. Retrieved 2017-06-20 

  8. Lüscher C, Ungless MA. The Mechanistic Classification of Addictive Drugs. PLoS Medicine. 2006;3(11):e437. PMCID: PMC1635740 

  9. Turner DM. 1994. The Essential Psychedelic Guide. Panther Press  2 3 4 5

  10. NMDA receptor. Wikipedia. Retrieved 2017-06-20 

  11. Bear M, Connors BW, Paradiso MA. Neuroscience. Exploring the Brain. 4th edition. Wolters Kluwer. 

  12. Carbonaro TM, Bradstreet MP, Barrett FS et al. Survey study of challenging experiences after ingesting psilocybin mushrooms: Acute and enduring positive and negative consequences. J Psychopharmacol. 2016 Dec;30(12):1268-1278. Epub 2016 Aug 30. PubMed PMID: 27578767 2 3

  13. McMains V quotes Griffiths RR. 2017. Study explores the enduring positive, negative consequences of ingesting ‘magic mushrooms’ on HUB. Retrieved 2017-06-14 

  14. Hartogsohn I. The American Trip: Set, Setting, and Psychedelics in 20th Century Psychology. MAPS Bulletin Special Edition. Spring 2013. Retrieved 2017-06-07  2

  15. Strongly recommended read: Kotler S, Wheal J. 2017. Stealing Fire. Dey Street Books. 

Eat yourself happy

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.

nutrients in food influence happiness through serotonin in brain

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.

How do you call an amino acid with an attitude? A-mean-oh-acidImage 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 biosynthesisSerotonin 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.

 


References

  1. Tryptophan. Wikipedia. Retrieved on 2017-05-22. 

  2. Amino acids such as tyrosine, phenylalanine, leucine, isoleucine and valine3 

  3. Bear M, Connors BW, Paradiso MA. Neuroscience. Exploring the Brain. 4th edition. Wolters Kluwer.  2 3

  4. Møller SE. Serotonin, carbohydrates, and atypical depression. Pharmacol Toxicol. 1992;71 Suppl 1:61-71. Review. PubMed PMID: 1480561 

  5. Original work with skeletal structures from Wikimedia Commons by NEUROtiker 

  6. Wurtman RJ, Hefti F, Melamed E. Precursor control of neurotransmitter synthesis. Pharmacol Rev. 1980 Dec;32(4):315-35. PubMed PMID: 6115400 

  7. Blomstrand E, Hassmén P, Ekblom B, et al. Administration of branched-chain amino acids during sustained exercise–effects on performance and on plasma concentration of some amino acids. Eur J Appl Physiol Occup Physiol. 1991;63(2):83-8. PubMed PMID: 1748109

Psychedelic Drugs and the Serotonergic System

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:

You can't understand psychedelic drugs and antidepressants without understanding the serotonergic system in the brain first

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.

Neuron with its soma, dendrites, axon and axon terminals. Electrical vs. chemical signal at the synapse.

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, serotonin, adrenaline and oxytocin. A simplistic view: Neurotransmitters dopamine, serotonin, adrenaline, oxytocin and their functions 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, others speak adrenaline 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 brainSerotonergic 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. Chemical communication at the synapse between presynaptic and postsynaptic membrane

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.

Lifecycle of serotonin at the synapse: synthesis, storage, release, receptor activation and clearing, reuptake and metabolismSignaling 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

Serotonin transporters SERT on the presynaptic membrane

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.

Protection against overstimulation of neurons

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-HT2A receptors, since they are the target of hallucinogenic drugs like LSD and psilocybin.

Serotonin 5-HT receptor subtypes

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-HT2A 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. Comparison of chemical skeletal structure of serotonin and LSDChemical 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.

How SSRIs block serotonin reuptake of serotonin transporters SERT

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.

How MDMA works in brain at synapse and how MDMA affects serotonin transporters SERT and vesicle transporters VMAT2

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-HT2A receptor—to which they bind directly, thereby activating it. The 5-HT2A 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 psilocybin (magic mushrooms) and placebo. Homological scaffoldsCommunication 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.

Kids are natural born scientists

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-HT2A receptors has astounding effects on brain circuitries that are involved in the sense of self and consciousness. You can think of the 5-HT2A 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.

 


References

  1. David E. Nichols. LSD Neuroscience. 2013. Youtube. Retrieved 2017-05-25.  2

  2. Nichols DE. Serotonin, and the Past and Future of LSD. MAPS Bulletin Spring 2013. Retrieved 2017-05-26.  2 3 4 5

  3. Mann JJ. Role of the serotonergic system in the pathogenesis of major depression and suicidal behavior. Neuropsychopharmacology. 1999 Aug;21(2 Suppl):99S-105S. Review. PubMed PMID: 10432495 

  4. Sodhi MS, Sanders-Bush E. Serotonin and brain development. Int. Rev. Neurobiol. 2004;59:111–74. PubMed PMID: 15006487 

  5. Illustration from Wikimedia Commons. Modified from Paradiso MA, Bear MF, Connors BW. Neuroscience: exploring the brain. 2007. Hagerstwon, MD: Lippincott Williams & Wilkins 

  6. Bear M, Connors BW, Paradiso MA. Neuroscience. Exploring the Brain. 4th edition. Wolters Kluwer.  2 3

  7. Zafeiriou D., Ververi A, Vargiami E. The Serotonergic System: Its Role in Pathogenesis and Early Developmental Treatment of Autism. Current Neuropharmacology. 2009;7(2):150-157. PMC2730007 

  8. Serotonin transporter. Wikipedia. Retrieved on 2017-05-22. 

  9. Reneman L, Endert E, de Bruin K. The acute and chronic effects of MDMA (“ecstasy”) on cortical 5-HT2A receptors in rat and human brain. Neuropsychopharmacology. 2002 Mar;26(3):387-96. PubMed PMID: 11850153. 

  10. 5-HT receptor. Wikipedia. Retrieved on 2017-05-22. 

  11. Refrigerator mother theory. Wikipedia. Retrieved on 2017-05-26. 

  12. Whitaker-Azmitia PM. The discovery of serotonin and its role in neuroscience. Neuropsychopharmacology. 1999 Aug;21(2 Suppl):2S-8S. PubMed PMID: 10432482 

  13. Eiden LE, Weihe E. VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse. Annals of the New York Academy of Sciences. 2011;1216:86-98. PMCID: PMC4183197 

  14. MDMA Basics. Erowid. Retrieved on 2017-05-22. 

  15. Dopamine. Wikipedia. Retrieved on 2017-05-22. 

  16. David Nutt. Psychedelic Research, From Brain Imaging to Policy Reform. 2017. Youtube. Retrieved 2017-05-29. 

  17. Carhart-Harris RL, Muthukumaraswamy S, Roseman L, et al. Neural correlates of the LSD experience revealed by multimodal neuroimaging. Proc Natl Acad Sci U S A. 2016 Apr 26;113(17):4853-8. PubMed PMID: 27071089

  18. Petri G, Expert P, Turkheimer F, et al. Homological scaffolds of brain functional networks. J R Soc Interface. 2014 Dec 6;11(101):20140873. PubMed PMID: 25401177

Medical benefits of psychedelic drugs

“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 proven effective against mental disorders like depression

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.

David Nutt's harm assessment of 20 popular drugs from The Lancet, 2010Drug 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.

risk of overdose and dependency of legal and illegal drugs including psychedelic drugs such as MDMA, LSD, psilocybin, ketamineSafety 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.

Made up example of a treatment protocol with psychedelic drugsHypothetical 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.

medical benefits of psychedelic drugs related to mood, life satisfaction, creativity, PTSD, anxiety, OCD, depression and more

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.

 


References

  1. Jacobson R. Turn On, Tune In, Get Better: Psychedelic Drugs Hold Medical Promise. 2014. Scientific American 

  2. Any Mental Illness (AMI) Among U.S. Adults. 2015. National Institute of Mental Health. 

  3. Olesen J, Gustavsson A, Svensson M. The economic cost of brain disorders in Europe. Eur J Neurol. 2012 Jan;19(1):155-62. PubMed PMID: 22175760

  4. Office for National Statistics. Estimate of the number of days of sickness absence taken: by reason, UK, 2013 to 2015. 2016. 

  5. American Society of Addiction Medicine. Opioid Addiction 2016 Facts & Figures. - Data from: Center for Behavioral Health Statistics and Quality. (2016). Key substance use and mental health indicators in the United States: Results from the 2015 National Survey on Drug Use and Health (HHS Publication No. SMA 16-4984, NSDUH Series H-51). Retrieved from http://www.samhsa.gov/data/  2

  6. Katz J. You Draw It: Just How Bad Is the Drug Overdose Epidemic?. 2014. New York Times. 

  7. Costs of Substance Abuse. 2010. National Institute on Drug Abuse. 

  8. Rick Doblin. Psychedelic Science 2017. 2017. Youtube.  2

  9. Kirsch I. Antidepressants and the Placebo Effect. Zeitschrift Fur Psychologie. 2014;222(3):128-134. PMCID: PMC4172306 

  10. By User:Tesseract2. Wikimedia Commons with layout modifications by Sapiensoup - data from Nutt DJ, King LA, Phillips LD; Independent Scientific Committee on Drugs. Drug harms in the UK: a multicriteria decision analysis. Lancet. 2010 Nov 6;376(9752):1558-65. doi: 10.1016/S0140-6736(10)61462-6. Epub 2010 Oct 29. PubMed PMID: 21036393. CC BY-SA 3.0, 

  11. Fentanyl. Wikipedia. Retrieved on 2017-04-27. 

  12. By User:Thundermaker. Wikimedia Commons layout modifications by Sapiensoup – data from Gable RS. (2006). Acute toxicity of drugs versus regulatory status. In Drugs and Society: U.S. Public Policy. Lanham, Maryland: Rowman & Littlefield. pp. 149–62; Table 7.1 Safety Ratio and Dependence Potential of Psychoactive Drugs. CC BY-SA 3.0 

  13. Nielson L. Hallucinogen in ‘magic mushrooms’ helps longtime smokers quit in Hopkins trial. 2014. Hub, Johns Hopkins  2

  14. The Medical History of Psychedelic Drugs. 2007. Dissertation presented to the University of Cambridge. 

  15. Griffiths RR, Johnson MW, Carducci MA. Psilocybin produces substantial and sustained decreases in depression and anxiety in patients with life-threatening cancer: A randomized double-blind trial. J Psychopharmacol. 2016 Dec;30(12):1181-1197. PubMed PMID: 27909165

  16. Robin Carhart-Harris at TED. 2016. Psychedelics: Lifting the veil. Youtube. 

  17. Strongly recommended read: Kotler S, Wheal J. 2017. Stealing Fire.. Dey Street Books. 

  18. Fink E. 2015. When Silicon Valley takes LSD. CNN tech. 

Kalbfreundliche Milch aus Österreich

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.

Kühe haben enge Beziehung zu ihrem Kalb

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.

Mutterkuhhaltung: Kalbfreundliche Milch aus muttergebundener Kälberaufzucht ist derzeit weder im Supermarkt noch im Biomarkt in Österreich zu kaufen

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.

Kühe in Österreich sind 70% Milchvieh und 30% Mastvieh

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.

 


Referenzen

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

  1. Siehe EU-Bio-Verordnung 889/2008 

  2. Quelle: Bundesanstalt für Agrarökonomik 

  3. Sambraus HH. 1991. Nutztierkunde: Biologie, Verhalten, Leistung und Tierschutz. UTB für Wissenschaft: Agrarwissenschaften, Veterinärmedizin, Zoologie. Ulmer. 

Having a baby sucks

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

baby doesn't stop crying

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.

relative loss of happiness after child birth, unemployment, divorce of death of partner

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.

how happiness will decrease after baby is born

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.

Generations names of 20th century and historic events

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.

how your baby will bring happiness and personal growth to your life

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.

a baby constrains and upgrades the parent's life at the same time

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.

stop whitewashing early parenthood or parents will think they are doing it wrong

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.

 


References

  1. Disclaimer: While most stories on Sapiensoup Blog are science-based, this one is primarily based on the personal opinions and experiences of the author. 

  2. Margolis R, Myrskylä M. Parental Well-being Surrounding First Birth as a Determinant of Further Parity Progression. Demography. 2015. 52: 1147. 

  3. This affects primarily stay-at-home-moms. Social isolation and some of the other challenges I address in this article might not concern working moms. They’ll have different challenges to face though. 

  4. According to this generations chart 

  5. Swain JE, Kim P, Ho SS. Neuroendocrinology of Parental Response to Baby-Cry. Journal of neuroendocrinology. 2011;23(11):1036-1041.  2

The Skeptic's Guide to Embracing Homeopathy

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.

argument if homeopathy works

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

fight about efficacy of homeopathy

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.

efficacy of placebo effect in depression, migraine, pain

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.

use homeopathy as placebo

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:

dilution in homeopathy

[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.

 


References

  1. Shang A, Huwiler-Müntener K, Nartey L. Are the clinical effects of homoeopathy placebo effects? Comparative study of placebo-controlled trials of homoeopathy and allopathy. Lancet. 2005 Aug 27-Sep 2;366(9487):726-32. PubMed PMID: 16125589. 

  2. Moffet HH. Sham acupuncture may be as efficacious as true acupuncture: a systematic review of clinical trials. J Altern Complement Med. 2009 Mar;15(3):213-6. Review. PubMed PMID: 19250001. 

  3. Pinch B. More Than Just a Sugar Pill: Why the placebo effect is real. Harvard University Blog. 

  4. de la Fuente-Fernández R, Lidstone S, Stoessl AJ. Placebo effect and dopamine release. J Neural Transm Suppl. 2006;(70):415-8. Review. PubMed PMID: 17017561. 

  5. Moseley JB, O’Malley K, Petersen NJ. A Controlled Trial of Arthroscopic Surgery for Osteoarthritis of the Knee. N Engl J Med 2002; 347:81-88July 11, 2002 

  6. Miller FG, Colloca L, Kaptchuk TJ. The placebo effect: illness and interpersonal healing. Perspectives in biology and medicine. 2009;52(4):518. PMCID: PMC2814126 

  7. Freakonomics Podcast: Bad Medicine. Episode 1: 98.6. ; Episode 2: drug trials. ; Episode 3: death diagnosis. 

  8. Who prescribes homeopathy might be subject to national medical practices. Here in Austria, most general practitioners have some sort of expertise in complementary medicine. 

  9. Richard Dawkins on Youtube. Homeopathy - Con or Cure. 

  10. Weimer K, Gulewitsch MD, Schlarb AA. Placebo effects in children: a review. Pediatr Res. 2013 Jul;74(1):96-102. PubMed PMID: 23598811. 

Cannabis and Breastfeeding. The Facts.

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

I nursed my daughter for more than 1.5 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.

does THC belong to 99% or 1%

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.

math on how high baby gets from THC infused breastmilk

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.

Better times ahead

Dr. Thomas Hale—clinical pharmacologist and professor of pediatrics—is the author of the earlier mentioned reference book Medications and Mothers’ Milk. In the book, he currently discourages cannabis use due to the lack of data.

In 2017, Dr. Hale and a team of other researchers started to collect breastmilk samples of Colorado moms to gain a better understanding of how much THC actually transfers into human milk. The study was published in the scientific journal Obstetrics & Gynecology last week (April 2018) and we’ll shortly publish a follow up post here on Sapiensoup to share the findings with you.

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.

motor development scores at one year old

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.

 


References

  1. Hale TW, Rowe HE. 2016. Medications & Mothers’ Milk 2017. 17th edition. Springer Publishing Company. 

  2. Chao FC, Green DE, Forrest IS, et al. The passage of 14C-delta-9-tetrahydrocannabinol into the milk of lactating squirrel monkeys. Res Commun Chem Pathol Pharmacol. 1976 Oct;15(2):303-17. PubMed PMID: 824699. 

  3. Perez-Reyes M, Wall ME. Presence of delta9-tetrahydrocannabinol in human milk. N Engl J Med. 1982 Sep 23;307(13):819-20. PubMed PMID: 6287261.  2 3

  4. Mother 1: 105 ng/ml and negative for metabolites. Mother 2: 340 ng/ml, 11-OH-THC 4 ng/ml, no 11-COOH-THC 

  5. Hollister LE, Gillespie HK, Ohlsson A, Lindgren JE, Wahlen A, Agurell S. Do plasma concentrations of delta 9-tetrahydrocannabinol reflect the degree of intoxication? J Clin Pharmacol. 1981 Aug-Sep;21(8-9 Suppl):171S-177S. PubMed PMID: 6271822. 

  6. Results may differ according to assumed parameters such as volume of milk intake, weight of baby, weight of man and amount of THC in cookie. My assumptions were: (1) Breastmilk contains 170 nanograms of THC per milliliter (i.e. average of the three measurements from the 1982 study: 60.3 ng/ml, 105 ng/ml and 340 ng/ml). (2) a daily intake of 700 milliliters (33.7 fl oz). (3) divided over 7 feeding sessions. (4) baby’s weight: 6 kilograms (13.2 lbs). (5) the adult man’s weight: 80 kg (176.4 lbs) which was the average when the study was run. (6) THC in cookie: 20 mg (20 mg of THC per cookie may be considered “mild” nowadays. The potency of cannabis has multiplied since the 1980s and off-the-shelf edibles often come generously dosed.) 

  7. Bennett PN. Cannabis. Bennett PN and the WHO Working Group, editors. Drugs and human lactation. 2nd ed. 1997.  2

  8. Tennes K, Avitable N, Blackard C, et al. Marijuana: prenatal and postnatal exposure in the human. NIDA Res Monogr. 1985;59:48-60. PubMed PMID: 3929132. 

  9. Astley SJ, Little RE. Maternal marijuana use during lactation and infant development at one year. Neurotoxicol Teratol. 1990 Mar-Apr;12(2):161-8. PubMed PMID: 2333069. 

  10. Average scores: kids of mothers consuming cannabis more than 15 days per month (90), less than 15 days per months (106), no cannabis at all (102) 

  11. Metz TD, Stickrath EH. Marijuana use in pregnancy and lactation: a review of the evidence. Am J Obstet Gynecol. 2015 Dec;213(6):761-78. PubMed PMID: 25986032 

  12. Grotenhermen F. Clinical Pharmacokinetics of Cannabinoids. Journal of Cannabis Therapeutics, Vol. 3(1) 2003. Link to PDF 

  13. National Center for Natural Products Research. Quarterly report: Potency Monitoring Project, Report 104, December 16, 2008, thru March 15, 2009. Link to PDF 

  14. Orens A. Light M. RowberryJ. Et al. Marijuana Equivalency in Portion and Dosage. Colorado Department of Revenue. August 10, 2015 Link to PDF 

  15. WHO on breastfeeding 

  16. Bergeria CL, Heil SH. Surveying Lactation Professionals Regarding Marijuana Use and Breastfeeding. Breastfeeding Medicine. 2015;10(7):377-380. PMCID: PMC4692106 

  17. FAQ with Dr. Franjo Grotenhermen 

Human Metabolism of THC

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.

Thumbnail-Infographic-Human-Metabolism-THC

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.

Metabolites-of-THC
Metabolites of delta-9-THC

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.

Metabolic pathway of THC after inhalation
Metabolic pathway of THC after inhalation

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.

Metabolic-Pathway-Stomach
Metabolic pathway of THC after ingestion

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

Distribution of THC in the body over time.

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.”

Infographic-Human-Metabolism-THC

 


  1. Wikipedia on Tetrahydrocannabinol 

  2. Huestis MA, Henningfield JE, Cone EJ. Blood cannabinoids. I. Absorption of THC and formation of 11-OH-THC and THCCOOH during and after smoking marijuana. J Anal Toxicol. 1992 Sep-Oct;16(5):276-82. PubMed PMID: 1338215.  2

  3. Grotenhermen F. Pharmacokinetics and pharmacodynamics of cannabinoids. Clin Pharmacokinet. 2003;42(4):327-60. Review. PubMed PMID: 12648025.  2 3 4 5

  4. Lindgren JE, Ohlsson A, Agurell S, et al. Clinical effects and plasma levels of delta 9-tetrahydrocannabinol (delta 9-THC) in heavy and light users of cannabis. Psychopharmacology (Berl). 1981;74(3):208-12. PubMed PMID: 6267648. 

  5. Ohlsson A, Lindgren JE, Wahlen A, et al. Single dose kinetics of deuterium labelled delta 1-tetrahydrocannabinol in heavy and light cannabis users. Biomed Mass Spectrom. 1982 Jan;9(1):6-10. PubMed PMID: 6277407. 

  6. Ohlsson A, Lindgren JE, Wahlen A, et al. Plasma delta-9 tetrahydrocannabinol concentrations and clinical effects after oral and intravenous administration and smoking. Clin Pharmacol Ther. 1980 Sep;28(3):409-16. PubMed PMID: 6250760. 

  7. Nahas GG. Marijuana: toxicity and tolerance. In Medical Aspects of Drug Abuse. 1975. Republished in Ashton CH. Pharmacology and effects of cannabis: a brief review. Br J Psychiatry. 2001 Feb;178:101-6. Review. PubMed PMID: 11157422.  2

  8. Wall ME, Perez-Reyes M. The metabolism of delta 9-tetrahydrocannabinol and related cannabinoids in man. J Clin Pharmacol. 1981 Aug-Sep;21(8-9 Suppl):178S-189S. PubMed PMID: 6271823.  2 3

  9. Hollister LE, Gillespie HK, Ohlsson A, et al. Do plasma concentrations of delta 9-tetrahydrocannabinol reflect the degree of intoxication? J Clin Pharmacol. 1981 Aug-Sep;21(8-9 Suppl):171S-177S. PubMed PMID: 6271822.  2

  10. Sharma P, Murthy P, Bharath MMS. Chemistry, Metabolism, and Toxicology of Cannabis: Clinical Implications. Iranian Journal of Psychiatry. 2012;7(4):149-156. PMCID: PMC3570572 

  11. Helpful suggestion found in the Stranger

Sind Bio-Kühe glücklich?

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?

Bio Logos Österreich

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.

EU Bio-Logo
EU Bio-Logo

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.

Vergleich: EU-Bio Logo mit AMA Bio und AMA AUSTRIA
Vergleich: EU-Bio Logo mit AMA Bio und AMA AUSTRIA

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.

Rinder Futter
Was Kühe fressen

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.

Bio-Rinderhaltung in Österreich: Vergleich der Strukturdaten Herdengröße und Anzahl der Betriebe
Vergleich der Strukturdaten Bio-Rinderhaltung in Österreich: Herdengröße und Anzahl der Betriebe

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.

EU Vergleich Anteil Bio-Landwirtschaft
EU Vergleich: Anteil Bio-Landwirtschaft, Eurostat 2013

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).

Strukturdaten Rinderhaltung in EU: Herdengröße und Anzahl der Betriebe
Vergleich der Strukturdaten Rinderhaltung in EU: Herdengröße und Anzahl der Betriebe, EuroStat 2013

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.

Anteil Milch- vs. Mutterkuh im Vergleich biologische vs. konventionelle Rinderhaltung in Österreich
Vergleich Bio-Rinderhaltung vs. Rinderhaltung gesamt in Österreich, Bundesanstalt für Agrarökonomik, 2015

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.

Anteil von Viehtyp am Gesamt-Rinderbestand in Österreich, Bundesanstalt für Agrarökonomik, 2015
Viehhaltung Österreich Rinder 2015: Rinderbestand gesamt

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.

Fazit

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.

 


  1. Eigene Berechnung: Verschiedene Rindfleischteile (Hüftsteak, Gulasch, Schnitzel, Faschiertes) im Preisvergleich zwischen Bio und konventioneller Herkunft. Verglichen wurden Proben von drei Einzelhandelsketten in Österreich: Spar, Billa und Hofer am 25.10.2016. 

  2. EU-Bio-Verordnung 834/2007 und 889/2008 

  3. Tatsächlich ist die Berechnung der Größe des Weidelandes von vielen Faktoren abhängig. Wer sich hierfür genauer interessiert, dem empfehle ich direkt in der Bio-Verordnung 889/2008 – Artikel 14 nachzulesen. 

  4. Während der Laktationsperiode darf das Verhältnis von Rau- und Kraftfutter 50:50 betragen. 

  5. Daten aus “Struktur der Rinderhaltenden Betriebe in Österreich zum Stichtag 1.12.2015”, Bundesanstalt für Agrarökonomik, BMLFUW 

  6. Facts and figures on organic agriculture in the European Union, 2013 

  7. Statistik Austria 

  8. Wikipedia 

  9. laut tel. Auskunft von BIO AUSTRIA ist Bio-Milchpulver verhältnismäßig teuer und wird nur in Notfällen eingesetzt 

  10. laut Bundesanstalt für Agrarökonomik