In May of this year, when I relocated to NYC for a few months, I started an experiment with an undefined end date: I made a commitment to create conscious, intentional distance between myself and all expressions of current events and mainstream media.

If a newspaper ends up in front of me, I toss it in the nearest recycling bin. If CNN blares at the airport, I turn my back and put in headphones. I no longer subscribe to any list referencing current events or outrage. I walk away from banal conversations or force a change in subject and delete the random videos people send me without watching them.

I cannot tell you what the weather forecast is without sticking my hand out the window. I don’t know who is throwing their hat in the ring for presidential nominations. When I found out about the Maui wildfires—on an instagram account dedicated to good news—my heart sank at the sight of it all, and still I immediately unfollowed.

There was a time when I thought that being up to date on current events is part of what made you a good citizen. Whether it was my uppity liberal arts education or my uppity liberal arts friends, I don’t know, but manufacturing my own interest in the world’s chaos felt like a duty I was obliged to perform. Perhaps, back when information was handed out in digestible bits through letters that took weeks to arrive and journalism that only delivered the news once a day, an overview of national and global happenings wasn’t so detrimental. A forty-five minute newspaper read was tempered by twenty three hours of distance. Gossip spread around town and provided for idle chatter, sure, but everyone was more or less getting the same information so I imagine there was only so much to say. And without the ability to tweet about whatever issue pissed people off, the incendiary nature of it all likely didn’t have enough oxygen to really catch fire. This allowed for the most collectively important issues rise above, leading to vast societal changes like the Renaissance, Women’s Rights Movement, and Civil Rights Movement.

My embargo exists to see what sort of movements I might experience within myself absent of noise imposed upon me. After all, can we really say that the life of someone who chooses to spend their time marveling at the beauty of a tree is any less meaningful than the person who spends their time picketing outside the Supreme Court?

The changes I’ve felt within myself have been profound in the most surprising and delightful ways. With so much mental and energetic space cleared up, I’ve been learning and creating at an unprecedented rate. Everything everywhere is art. The food I’m cooking for work has become bold, ambitious, and unapologetic—an adjective that might not seem to make sense in this context, but for me, is extraordinary. I am pulling away from the confines of painting lessons and tutorials in favor of following my intuition in a way that feels less like amateur experimenting and more like remembering how to do something I already know how to do. Even my physical body is responding. I am lighter, literally and figuratively. I am moving it in new ways that, like painting, feel like remembering.

Socially, I am both a better listener and more of a recluse. I haven’t been giving up my time to other people as easily, but when I do, I find I’m more objective. I can listen to what they have to say and, because I don’t have context filtered through some agenda, come to a conclusion or ask questions without as much judgement or assumption.

This is not entirely without its downsides. In July, I got stranded in Long Island for five days and missed a friend’s wedding thanks to a wave of airline disruptions due to storms on the East Coast. Had I been paying an ounce of attention, I might not have made a last minute change to my itinerary that caused me to attempt to fly on the day storms were predicted to be the worst. On the other hand, while I missed the wedding, I spent those five days in Long Island helping a friend who really needed that help. And I got to spend the time devouring a book I randomly pulled off the shelf, Born to Run, which in two back to back readings has transformed me from someone who thought I hated running to someone who is now going on hour long trail runs at whim, for fun.

Just yesterday, the writer Suleika Jaouad shared a prayer she threw up to the heavens in 2015: “May I be awake enough to notice when love appears, and bold enough to pursue it without knowing where it will lead.”

These words bring tears to my eyes as I type, not just in hope of romantic love, but in the courage that it takes to step forward while knowing less. Cutting ties with current events and mass media means I am forced to watch what comes up within myself. A few times, I have spiraled into a loop of worry over whether or not I’m making the right choices. Have I overcorrected? Am I going to miss something I need to know? Am I confusing my intuition with fantasy? Is not knowing what I don’t know leading me down the wrong path?

Bold enough to pursue without knowing where it will lead.

I can’t argue with the wonder that has come out of knowing less. And so, for now, I will continue to keep my distance and watch what comes in its place.

During my sophomore year at Middlebury College, I took notoriously tricky course called Introduction to Modern Logic. An early requirement for philosophy majors (one of the many declarative detours I flirted with before landing on the equally useless History degree), it focused on good reasoning and the technical breakdown of arguments.

A basic example:

If Bellaroo is napping on her dog bed, then Bellaroo is not taking a walk.

Bellaroo is napping on her dog bed.

Therefore, Bellaroo is not taking a walk.

The statement is true in all circumstances, regardless of time, interpretation, or the laws of physics. If Bellaroo is napping on her bed, she is irrefutably not taking a walk.

The point of this course is to help students identify patterns of good reasoning and patterns of bad reasoning, so they have a better idea of what to follow and what to avoid. The tricky part occurs when a statement seems true at first glance, but breaks down when logic is applied. These are called logical fallacies, and they are everywhere.

A few examples:

The Appeal to Ignorance, where we assert a claim because no one can prove otherwise.

People have been praying to God for years. No one can prove He doesn’t exist. Therefore, He exists.

The Bandwagon, where we assume something to be true or good just because many others believe it to be true or good.

Everyone at the gym is wearing Lululemon. I need to buy their yoga pants.

The Red Herring, were we use irrelevant information to distract from an argument.

There are starving children in Africa. Eat your broccoli.

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Psychiatry, more than any other branch of medicine, is saturated with logical fallacies. Hell, we can apply all three of the above examples to cultural rationale within the world of psychiatry and mental health:

The most pervasive logical fallacy in psychiatry and mental health diagnoses, though, is circular reasoning, which is an argument that uses the same statement as both the premise and the conclusion.

The reason why circular reasoning is so pervasive in psychiatry compared to other specialties is because psychiatry doesn’t have any form of objective boundaries. The rest of medicine, generally, agrees on parameters that define a pathological disease. Diabetes in the United States is only diagnosed as diabetes when two fasting A1C blood sugar tests read 6.5% or higher. Doctors—and even different countries—debate 6.5% as the cutoff, but all agree that at a certain point, high blood sugar levels indicate disease.

But psychiatric criteria cannot explain behaviors or experiences through any means beyond subjective opinion. Furthermore, as we’ve been exploring throughout the last few issues, these subjective opinions are rooted in norms and meaning. They can’t be measured independently, and they are not necessarily true across time and culture.

And yet, the flywheel of circular reasoning continues to spin, flinging the world of mental and emotional health further away from the solution. As British child psychiatrist Sammy Tammi said in his open letter on the diagnostic model of psychiatry to the Society of Humanistic Psychology, “The result of this basic [logic] error is that medical scientific knowledge in the area of mental health is at a standstill. No chemical imbalances, consistent neurological differences, genetic abnormalities or markers found. None. Billions of dollars of wasted money on wasted biological research that leads nowhere…higher levels of reported stress and anxiety, higher numbers of people disabled due to a mental health condition and rates of significant improvement from those attending mainstream services hovering at around a quarter to a third of those they see. These are not the outcomes you would expect to see from an effective model of clinical care.”

“When humans do not assume they have rather complete control of their experience, they do not so deeply fear those who have appeared to have lost it.”

—Juli McGruder, anthropologist

As of late, I’ve been learning about the different expressions of perceived mental illness around the world. I use “perceived” in this context because the more I learn, the more I understand that symptoms of mental/emotional distress are tied to cultural expectations. (See the TikTok tics from issue 105.) Said another way, the lifecycle of mental illness is influenced by the macro and micro-level beliefs that surround it. What’s considered crazy in one culture is accepted in another.

On a macro level, the prevalence and intensity of schizophrenia vary from place to place. Men living in urban areas of Sweden, for example, are at a 68% higher risk of being admitted for psychosis than those who live in the countryside. This is also true for urban settings in the United States and Europe, and it remains constant even when migration, drug use, and poverty are taken out of the equation.

Furthermore, a 25 year study conducted by the World Health Organization that began in the 1960s found that people diagnosed with schizophrenia in developing countries have better outcomes, longer periods of remission, and higher levels of social functioning than those in industrialized nations. Known as the International Pilot Study of Schizophrenia, the data showed that over time, 40% of schizophrenics in countries like the United States, Denmark, and Taiwan were considered “severely impaired” compared to 24% of people in countries like India, Nigeria, and Columbia.

Of course, these findings ignited a hot debate because the results are counterintuitive. You’d think all the money, research, and resources would lead to better outcomes. But alas, the data showed the opposite to be true.

(Side note, half a century later, our use of psychotropic medicine continues to reflect what we knew in the 1960s and 1970s. Are poor nations tragically underserved by psychiatry? Or have they avoided the crosshairs?)

This debate is the heart of cross-cultural psychiatry research. While it’s interesting in its own right and the conclusions are, to me, dead obvious, I find the micro influences to be even more interesting. It’s not just about the culture we live in. But the roof we live under.

Expressed emotion (EE) is a term used to describe the way that family members and caregivers interact with a person. High EE is characterized by critical, hostile, and emotionally overinvolved behaviors. Low EE is characterized by warm, supportive, and accepting behaviors. While expressed emotion is not the cause of distress, it can influence the course and outcome in an individual.

We all know that when our actions are met with criticism or hostility, we don’t fare as well. But emotional over-involvement requires more explanation.

Emotional over-involvment is characterized as a range of dramatic behaviors ranging from self-sacrifice, extreme devotion, overprotectiveness, or intrusiveness over a person’s life. Control, essentially.

Ethan Watters uses an example in his book, Crazy Like Us, that describes a mother who was so emotionally over involved with her son’s schizophrenia that she “dropped all other interests from her life. Her sole activity, she reported, was to take care of him and protect him, ‘like a pearl of a diamond.’ This same mother said that she often became so distraught over her son’s plight that she considered committing suicide by throwing herself down the family staircase.”

In addition to raising stress levels in the sufferer—which in this case, could trigger schizophrenic episodes—this maligned strategy is a constant reminder to the person suffering that those around him perceive him to be ill, which in turn, reinforces the idea that something is wrong.

Watters gives a contrasting example of a family in Zanzibar with a schizophrenic daughter, Kimwana, who overdosed her medication and nearly died. Juli McGruder, an anthropologist who witnessed the scene said, “There was no noisy woe-is-me talk or dramatic wringing of hands. [The family] seemed to take it in stride like everything else…When I asked what I could do, [the mother] told me I could take a carton of milk to Kimwana in the hospital.”

The ability for the family unit to keep calm and carry on benefitted Kimwana. The family’s perspective, in part because of Zanzibarian beliefs include spiritual possession, allowed everyone to embrace the idea that difficulties—and even voices in the head—are a natural part of life. Therefore, disruptive behavior as a result of these difficulties was more understandable and forgivable. Kimwana wasn’t viewed as other, or as someone to be feared. She was viewed as a strong expression of what we all have inside of us. This kept her within the social group.

Anglo-Americans have the highest level of expressed emotion compared to different groups around the world. Given that we no longer let our kids have sleepovers, have unsupervised play, or breathe without parental supervision, this shouldn’t be surprising. According to researcher Jill Hooley, Anglo-Americans have a strong “locus of control,” which means they believe a person can be master of their own fate and control their own issues through force of will. The critical, hostile, and emotionally over involved actions stemming from this locus of control aren’t necessarily cruel in intent, but are instead an expression of assumed (and flawed) human nature.

Cultures with more fatalistic or spiritual values place less focus and/or blame on those with mental and emotional distress. Conversely, in cultures that value personal accountability and individualism, highly emotionally involved relatives are actually more hopeful about the disease because they are convinced recovery is a matter of will—both on their part and the part of the sufferer.

But as they say in football (soccer), “It’s the hope that kills you.”

Watters says, “One typical father described his reaction to the schizophrenic break of his son: ‘I went to the library and began reading books about mental illness…I thought: “No, I’m going to fix this.” That is your first instinct as a parent. You’re going to fix it. I thought, “I can get him help. I can get him cured.”…That intense focus, even when it springs from a hopeful engagement of the problem, might be the very thing that exacerbates the illness.”

Furthermore, our obsession with the biomedical model of mental illness only exacerbates emotional over involvement. Take the following Euro-American norms:

By applying these norms to an individual, we separate them from the group by labeling them as Other, all while promoting the idea that recovery is never really possible. How could it be, if mental illness is nothing more than a stroke of bad luck and questionable genetics?

In 1997, Sheila Mehta of Auburn University got curious about whether or not the “brain disease” narrative of mental illness actually reduced stigma, as promised.

In her experiment, she paired up people for what test subjects thought was a simple learning experiment. Unbeknownst to the test subjects in the study, their partners were actors and were instructed to inform the test subjects during the get-to-know-you phase that they suffered from mental illness.

The actor told the test subject that the distress occurred because of the “things that happened to me when I was a kid or that they had “a disease just like any other, which affected my biochemistry.”

In the experiment, the test subject was assigned to teach the actor a pattern of button presses. When the actor got the pattern wrong, the test subject was told to give the actor a “barely discernible” to “somewhat painful” electric shock.

Test subjects who believed their partner had a “disease like any other” increased the severity of shocks at a faster rate than those paired with the actor whose issues were caused by childhood events.

Mehta said, “The results of the study suggest that we may actually treat people more harshly when their problem is described in disease terms. Viewing those with mental disorders as diseased sets them apart and may lead to our perceiving them as physically distinct. Biochemical aberrations make them almost a different species.“

And what is our instinct when we encounter Other? Critical, hostile, and emotionally over-involved behaviors.

So it goes.

As of late, I’ve become fascinated with the idea that mental illness is contagious.

The fascination started with a New York Times article about a wave of thousands of female and gender-nonbinary teens who developed Tourette’s-like tics during the pandemic—because of TikTok.

Arriving in the zeitgeist when people were forced to stay home, TikTok exploded during the pandemic. Videos of people claiming to have Tourettes multiplied on the platform, and because TikTok’s algorithm is built on showing users a wide variety of content—regardless of the user’s preferred interests—Tourette’s videos began popping up on people’s feeds. As of this writing, #Tourettes on TikTok has 8.7 billion views.

Like mental illness, there aren’t any scans or biological markers to diagnose or identify Tourettes. However, Tourettes is categorized as a movement and neurological disorder marked by uncontrolled physical or verbal tics, not a mental illness. It typically presents in males and first appears in childhood, with waxing and waning symptoms.

For the girls with “TikTok Tics,” however, the Tourettes-like symptoms arrived suddenly, with a wave of new cases popping up all over the world. Notably, though, when life began to regain some normalcy and the stress of the pandemic waned, the wave of TikTok Tics receded as well. Thus, it is hypothesized that the unique stress of the pandemic + the unique vulnerability of teenage girls created a tinderbox of stress that manifested in psychologically contagious tics.

This isn’t the first time we’ve observed psychological contagion. This phenomenon repeats itself across both time and cultures. In the Middle Ages, it was believed that humans could be possessed by the spirits of demonic animals, leading a group of nuns at a French convent to meow like cats.

In the 1800s, “hysteria” was a known psychological diagnosis that afflicted women. It included a diverse range of symptoms, including paralysis, stomach pain, amnesia, and day blindness. Hysteria was almost worshiped and certainly fetishized by popular magazines, newspapers, and even public hygiene literature. Much like today, male doctors and scholars of the time filled lecture halls and pontificated on the “quintessential illness of womanhood,” as Ethan Watters said in his book, Crazy Like Us. But by the time the 20th century rolled around, hysteria had largely evaporated from the collective consciousness. Women stopped reporting paralysis and leg weakness, and the symptoms of psychosomatic illness moved on to other expressions.

Even the human reaction to war is tied to the cultural temperature. Medical records of war veterans show that the psychological and even physical effects of war are a reflection of time and place. For British soldiers in the Boer War, the psychological trauma manifested as muscle weakness and joint pain, while American soldiers during the Civil War complained of a weak heartbeat and an aching in the left side of the chest. During World War I, both British and American soldiers experienced “shell shock,” with symptoms that included tremors, ticks, and sensory disturbances. Today, addiction affects veterans of modern war.

As Watters explains, “Although the potential psychic damage of war is indisputable, the process by which that damage becomes an outward symptom is a reflection of the cultural beliefs in a particular time and place.”

Said another way, whether as a PTSD response to war or TikTok, people will unconsciously produce symptoms that reflect the culture’s prevailing cultural diagnosis of the time. The TikTok Tics were not so much a measurable illness, but a subconscious yearning for recognition of internal distress.

The implications of viewing mental illness through this lens, in my opinion, destabilize the entire foundation of psychiatry and psychology. I know, for example, that as a young ballet dancer, the eating disorders I experienced as a teenager were created through community. Anorexia is rampant in ballet not just because thinness is an aesthetic ideal, but because everyone else is doing it. Toss in the death of my father and the emergence of the internet in the early 2000s, and the fixation on thinness festered as a direct result in order to satisfy a need to belong to something while expressing suffering. There wasn’t ever anything wrong with my brain. If anything, it was a sign that my psyche was doing exactly what it should be expected to do in times of great stress. I was simply exhibiting symptoms consistent with the time—no different than if I had started meowing with nuns in the Middle Ages.

For an affliction to be pathological, it seems to me that it should ring true across both time and culture. A cancerous mass viewed under a modern microscope looks the same in Taiwan as it does in the United States. But if mental illness and psychological distress cannot be separated from the culture in which it is experienced, how is a blanket biomedical response ever going to be the answer?

Hi friends,

I’m writing to you today from Brooklyn, where I’ve been for a month. I’m here taking a six-week public speaking workshop in the hopes of creating a straight-ish shot to a career that can be supported by speaking on antidepressant withdrawal and depression recovery. Like most endeavors, there’s a way to have a small impact and there’s a way to go big. I want to go big, so I’m taking the time to dedicate focus and level up.

(Now would be a good time to mention that I am available for booking for 2024. I’d love to speak at your business, conference, or university event. Please reach out to me at brooke@brookesiem.com.)

Spending an extended period of time in another environment illuminates cracks in the world I’ve built for myself. I first discovered this in the depths of antidepressant withdrawal, when I boarded a one way ticked to Malaysia six months after getting off of Effexor. I’d committed to a year of international travel before I took my last antidepressant, thinking that I had plenty of time to get off the cocktail of prescriptions I’d been on as a teenager. I figured I’d feel like I had the flu for a week or two, start taking a new antidepressant that would surely work wonders, and flit off around the world in an Eat, Pray, Love fantasy.

Instead, I had a withdrawal experience so horrific, I would eventually sell a book about it. LOLz.

As difficult as it was to travel while in antidepressant withdrawal, it accelerated my healing. I was changing countries every five weeks, which meant I had enough time to settle into a new place, but not enough time to create a home. This forced me into a minimalist lifestyle. If it didn’t fit in one suitcase and a backpack, it couldn’t come with me.

This exercise in pairing down spotlighted what was actually important and what was a story I was telling myself. Prior to leaving the United States, for example, I made room in my suitcase for a travel steamer to keep my clothes crisp. After three weeks in Malaysia, both the steamer and most of the clothes I brought with me were given to goodwill. The steamer was useless in the oppressive humidity, as were clothes that required steaming. It wasn’t just about lightening up the suitcase. It was about changing the focus from how I thought I needed to present myself to what I actually needed to feel good. In Malaysia, I wasn’t surrounded by folks who looked like me or thought like me, so I didn’t have a chance to be influence by their choices. It was about what I needed and how I wanted to feel. But it took being in a completely different physical location for me to start understanding that.

Emotionally, I went through the same process. For years, I’d created a story for myself that blamed my problems on outside influences. I was depressed because of my business partner, my finances, or a lack of romance. But in choosing to leave my life, I stripped myself of all those external factors. I couldn’t blame my misery on my business partner when I was no longer part of the business.

Unlike the practicalities of luggage, unpacking my emotional baggage took longer than three weeks. I needed to move around a few times to notice what triggers came with me and what didn’t. It was only after I noticed that I had the same problem in Malaysia as I did in Cambodia that I was able to come to the conclusion that maybe the problem was me.

This was terrible news. And great news! It meant I had the power to do something about it but I also had to do something about it, which is always unpleasant and involves a lot of ugly crying. But as I practiced the muscle of identifying the issues inside me, I got better at clearing them up without all the drama.

Over and over again, with each new country, I evaluated the contents of my suitcase in relation to where I was in the world. By the end of the experience, I was traveling only with a carry on, the contents of which could sustain me on chilly Argentinian nights or warm Mexican days. And I’d stripped myself off all the emotional bullshit too.

Over the years, I’ve continued this practice (save for that pesky pandemic which complicated matters.) Here and there I seem to spend a couple of months in another place and see what it has to teach me. It slows down time, puts what matters into focus, and shows me what to clear out. A few months in Vancouver, Canada ultimately led to an important relationship and semi-permanent relocation to the Great White North. A summer in Seattle produced MAY CAUSE SIDE EFFECTS. This time in Brooklyn is showing me how much I’ve healed since I left New York City seven years ago, while also highlighting the need for me to leave the comfortable but anemic existence I fell into during covid. Honing, honing, honing.

I realize that I’m in a unique position to do this. I don’t have kids and my work is relatively flexible. But the lesson can be learned without getting on a plane. All it takes is an honest assessment of what’s not working in your life and forcing yourself to experiment with different choices around that issue. Few things in life are irreversible. Commit for two months and see what happens. Maybe you cut out coffee, stop watching the news, or finally see a therapist or counselor. Whatever it is, it’s got to be long enough to settle into, but short enough to know you can handle the inevitable unease that comes with it. Two months, I think, is the sweet spot.

What comes of this practice is the ability to question what you believe about the world. This intellectual flexibility makes for interesting and resilient people who are thoughtful, adaptable, and unlikely to be manipulated. It also has the beautiful side effect of slowing down time, because when you’re consciously paying attention to the reverberations of new choices, you can’t act on autopilot. With a world moving at an ever increasing speed, any chance to slow it down is a welcome gift.

In the 100th issue of Happiness Is A Skill, I revealed that I underwent genetic testing through GeneSight in order to get an insight into how my body metabolizes psychiatric drugs. My results are in, and we’re going to take a look at them together in order to better understand this technology, while also examining some of the limitations and concerns around this type of testing.

I recommend reading through issue 100 before diving in here.

Please note that I have no affiliation with GeneSight, and this is in no way an advertisement or medical advice.

The GeneSight report focuses on three different aspects of psychiatric drug metabolism: psychotropic, which indicates how a person is likely to metabolize a wide variety of psychiatric drugs; genotype and phenotype, which is the organism’s genetic information and its observable traits; and a gene-drug interaction chart.

In theory, this information aims to optimize medication choices by reducing trial-and-error prescribing. Given that I’m not in the business of taking psychiatric drugs ever again, I’m more interested in the insight this gives me into my own body, and what it might mean for psychiatric drug withdrawal. Big emphasis on might. I won’t be running any double blind, placebo controlled trials on the hypothesis any time soon, but seeing this information and understanding what it means does make me think twice about blindly taking prescription drugs. Personally, I think that’s the power of a test like this. It shows the layperson that pharmaceutical intervention is extremely complicated, while also increasing the patient’s medical literacy. Given that on average, doctors only spend 17 minutes with each patient—and 4.5 hours per day on electronic medical records—it behooves the patient to have some basic medical literacy before walking into an appointment.

Genesight gives psychotropic results for five drug categories: antidepressants, anxiolytics and hypnotics (anti-anxiety and sedatives), antipsychotics, mood stabilizers, stimulants & non stimulants.

The results are coded in green (use as directed), yellow (moderate gene-drug interaction), and red (significant gene-drug interaction.)

Intuitively, you can gather that green medications are not associated with any known genetic issues that would be expected to change patient medication outcomes; yellow medications may require dose adjustments in order to have the desired effect and may be less likely to work/may cause side effects; and red mediations are likely to require significant dose adjustments in order to have the desired effect, or they not work at all, and may cause side effects.

The number to the right indicates the rationale for the reason why a drug is in the yellow or red column. This is where things get interesting when viewed through the lens of my personal history.

Before my child psychiatrist landed on a combination of Wellbutrin XL and Effexor XR, he gave me at least two other drug that created obvious, immediate side effects. I don’t remember which drugs they were and the medical records have long been destroyed, but given the antidepressant market in 2001/2002, it was likely to be Prozac, Celexa, or Zoloft—all of which exist in my yellow column.

Effexor, too, is on my yellow list. While I know I didn’t have immediate side effects from my 37.5mg dose, Effexor withdrawal was pure hell. While there aren’t any clinical studies looking at the relationship between the CYP450 system and psychiatric drug withdrawal, it doesn’t seem like a radical leap to assume that someone’s ability to metabolize a drug also affects the body’s ability to get the drug out of the system. Anecdotally, this hypothesis is further bolstered by my relative ease when it came to getting off the Wellbutrin, a drug in my green column. I know this isn’t the whole story, but it seems unlikely that it’s not somehow related.

Another reason why I find this test valuable is because of the information buried in the anxiolytics and hypnotics results. Many of these drug are commonly prescribed as part of surgical procedures in hospitals. If I ever needed major surgery, I’d want my anesthesiologist to have these results. Whether or not they’d take them into consideration is another matter, but I’ve given a copy to my emergency contact, just in case.

The genotype and phenotype type results show specific variants for each gene. These results explain why drugs end up in the green/yellow/red column.

It is broken down into two categories: Pharmacodynamic and pharmacokinetic.

Pharmacodynamic genes provide insights into how medications interact with the body. Variations in these genes can impact the likelihood of response or the risk of side effects with certain medications.

While it is important to note that many genes—including ones not tested by GeneSight—are involved in the process of metabolizing psychiatric drugs, GeneSight has identified a handful of issues known to come with specific gene variants. SLC6A4, for example, encodes for the serotonin transporter, which is the main site of action for SSRIs. People have either a long allele (variation) or short allele of SLC6A4. According to GeneSight, “Studies have shown that the short [SLC6A4] allele results in less serotonin transporters than the long allele. Individuals who have the short allele may be less likely to respond to certain SSRIs based on this genotype.” Thus, my short SLC6A4 allele contributes to the reason why SSRIs like Celexa, Paxil, and Zoloft are on my yellow list.

The same goes for pharmacokinetic genes, which provide information about how the body processes medications.

What stands out here is my CYP2D6 and CYP1A2. CYP2D6 is involved in a wide range of drug metabolism, psychiatric and otherwise. My intermediate metabolizer status indicates that I metabolize these drugs more slowly than normal. This is important because it means that while I may not have immediate adverse reactions, I am more likely to encounter them long term as the drug slowly builds up in my system.

On the other end of the spectrum, I am an ultra rapid metabolizer for CYP1A2. CYP1A2 is involved in the metabolism of a not only some antipsychotics, but also melatonin and caffeine. This explains two things I’ve known to be true about myself: I can drink caffeinated coffee or tea late in the day without it affecting my sleep, and melatonin has little to no effect on me. This makes sense—thanks to my quick CYP1A2, both caffeine and melatonin rush right through my system.

Additionally, vegetables like cabbages, cauliflower and broccoli are known to increase levels of CYP1A2, whereas spices like turmeric and cumin inhibit CYP1A2. So much so that a Sydney based researcher concluded that the “different diets and lifestyles of South Asians compared to Europeans could lead to the two groups requiring very different doses of medicines commonly used to treat illnesses such as depression and psychosis.”

Said another way: diet affects drug metabolism.

Of course, most of us aren’t thinking about how that chai tea affects the efficacy of our Rx cocktail. For the majority of people, it’s this particular quirk probably irrelevant. But for others—say, someone living in a Sri Lankan household who is struggling with a particular prescription drug—the knowledge might be more akin to low hanging fruit.

Furthermore, it speaks to the nuance of drug prescription that is all but ignored. Now, I know that any drug or supplement I take should be crossed checked to see if it’s metabolized by CYP1A2 or CYP2D6. If so, maybe I need to stay away from Indian food while I take it or consider a change in dose.

The last chunk of the GeneSight test is a handy chart outlining gene-drug interaction. The chart is supplementary, and only tells you which genes are involved in metabolizing each drug.

The real limitation here is that the second multiple drug are involved, all of this goes out the window.

You now know that a drug-gene interaction occurs when a person’s genetic makeup affects how their body metabolizes or responds to a medication. A drug-drug-gene interaction occurs when the effects of two or more medications are altered by a person’s genetic makeup.

For example, someone who is an intermediate metabolizer for CYP3A4—one of the enzymes involved in Zoloft (sertraline) metabolizatoin—may have no issue with the Zoloft alone, even as an intermediate metabolizer. But serotonin toxicity, also know n as serotonin syndrome, becomes a real risk if they start taking the antibiotic erythromycin. Erythromycin uses the CYP3A4 pathway and therefore inhibits the metabolism of Zoloft, leading increased and potentially toxic Zoloft levels in the body.

While the Zoloft or the erythromycin individually may not create an issue, combine them together with an intermediate or slow metabolizer, and you’ve got a problem.

GeneSight isn’t of any help when it comes to drug-drug-gene interaction, a giant limitation given how many people are on multiple drugs. But again, it gives us more information than we had before, which I think is a net positive.

In general, I went down the GeneSight rabbit hole for no reason other than pure curiosity. I have no plans to take psychiatric drugs in the future, nor do I know how my trajectory might have been different had I had this information back when I was medicated in 2001.

There is plenty of debate about the use of genetic testing in the world of mental health, most of it focusing on questions about privacy, accuracy, over interpretation of the results, lack of FDA approval, and cost.

From my perspective, there’s not enough compelling evidence to convince me that people shouldn’t take it into consideration. We do all sorts of things that aren’t approved by the FDA—drinking wine and taking multivitamins, for example—so that argument is moot. Privacy concerns are ubiquitous these days, but I personally don’t care what they do with my results. Some think that the results could inhibit people from getting insurance to pay for psychiatric care down the line, but again, I haven’t seen direct evidence of this.

Like anything, it’s up to the individual to decide what’s best for them.

It’s the 100th issue of Happiness Is A Skill, and I’m marking the occasion by going down a rabbit hole of genetic testing through GeneSight. This isn’t your usual, turns out I’m 1% Korean type of genetic testing (true story). It’s relatively new science that analyzes the body’s ability to process psychiatric drugs through the cytochrome P450 system (CYP), a group of enzymes responsible for metabolizing many medications and other substances in the body.

Though I personally have zero plans to ever swallow a psychiatric drug again, the more time I spend in the world of antidepressant withdrawal, the more interested I am in the why of it all. Why is it that some people have no issue stopping psychotropic drugs cold-turkey, while other people, like the man I wrote about in Issue 99, have permanent brain damage from psychiatric drug use and withdrawal?

My hunch is that it has something to do with genetics and the CYP system. Though there are no known studies on the CYP system and withdrawal specifically, there is some emerging research on CYP system and medication side effects. My assumption is that if the CYP system affects how a daily dose of drugs is metabolized, it’s likely involved in clearing the drug out of the system even when a daily dose is no longer being taken.

Hopefully we’re not too far from formal research on the subject, but in the meantime, I’m going to share what I’ve learned about this genetic testing and my results.

The CYP450 pathway is a group of enzymes found in the liver that are responsible for the metabolism of a wide variety of drugs, including antidepressants and antipsychotics. Specifically, the CYP450 enzymes are involved in the breakdown of these drugs in the liver, which can affect their efficacy and potential side effects.

Most antidepressants are metabolized by the CYP450 enzymes through variant alleles (versions) of the CYP450 pathways. For example, allele CYP2C19 is primarily responsible for metabolizing citalopram/Celexa and escitalopram/Lexapro while allele CYP2D6 is primarily responsible for fluoxetine/Prozac, paroxetine/Paxil, and venlafaxine/Effexor.

By looking at the genetic variations in these alleles, we can see how the body metabolizes psychiatric drugs via the CYP450 pathway. Everyone falls into one of the following categories: extensive (normal) metabolizer, intermediate metabolizer, poor metabolizer, rapid or ultra-rapid metabolizer.

An extensive metabolizer is a person with normal enzyme activity levels, meaning they can metabolize drugs normally, and therefore require standard doses of medications.

In contrast, an intermediate metabolizer has reduced activity levels of the CYP enzyme, which means they metabolize drugs slower than expected. As a result, intermediate metabolizers may experience higher overall drug levels or longer exposure to drugs, which can lead to increased risk of side effects or toxicity.

Poor metabolizers have significantly reduced or absent activity of a specific CYP enzyme, which leads to impaired drug metabolism. As a result, poor metabolizers may need to avoid certain drugs altogether due to the risk of adverse effects.

Conversely, ultra rapid metabolizers are individuals with increased activity levels of CYP enzymes, which means they metabolize drugs faster than expected, potentially leading to lower overall drug levels and reduced or absent effectiveness of medications.

The work of Selma Eikelenboom-Schieveld, a Dutch forensic scientist based out of New Mexico, focuses on the association between genetic variants of the CYP450 enzymes and violence-related adverse drug reactions in patients receiving psychoactive medication.

In her 2016 research paper “Psychoactive Medication, Violence, and Variant Alleles for Cytochrome P450 Genes,” Eikelenboom-Schieveld compared 55 violent individuals—whose behavior ranged from an altered emotional state (30 subjects), to assault, attempted or completed suicide and homicide (25 subjects)—against 58 persons with no history of violence as the controls.

In the nonviolent group, 38 subjects did not use prescription medication. In the violent group, all the subjects were on prescription medication. Of the 75 subjects on medication, 52 (almost 70%) were on three or more medications.

Her research showed that there is an “association between prescription drugs, most notably antidepressants and other psychoactive medication; having variant alleles for CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 and CYP3A4; and the occurrence of an altered emotional state or acts of violence. Based on these results, genotyping patients for these six CYP450s would provide information as to who might be susceptible to adverse drug reactions, e.g., the development of an altered emotional state or assault/suicide/homicide.”

To say it another way: if someone is a normal metabolizer or has limited CYP gene variations and is only on one medication, chances are acts of violence are also limited. But in someone with many variants and many medications, the enzymatic pathway effectively gets clogged up, causing a buildup of drugs in the system that can lead to an altered emotional state or violence. These undesirable actions are often mistaken for mental illness, so more drugs added, increasing the likelihood of violence.

Welcome to Science Corner by Happiness Is A Skill, where I take a few minutes to teach you about the relevant neuroscience of antidepressants and antidepressant withdrawal. No more half assed assumptions without evidentiary support, like the whole chemical imbalance theory of mental illness. The idea that “too little” serotonin causes depression? Or that “too little” dopamine causes ADHD? Obsolete, oversimplified, hogwash conveniently packaged by marketing departments of pharmaceutical companies in order to convince you to “talk to your doctor about Zoloft, because when you know more about what’s wrong, you can help make it right.”

That’s the actual tagline for Zoloft by the way, from 2001. Brilliant, isn’t it? Here’s a very simple explanation for your distress. It has nothing to do with your life or your choices or the bad things that happened to you, but instead has to do with some chemicals in your brain you can’t control. So take this pill and the sun will shine and flowers will bloom and scary thoughts will go away and we’ll all be content. Right? Right? 

If one could die of bullshit overload, I would long be gone.

Instead, let’s talk serotonin transporter (SERT) occupancy, something researchers have actually measured and analyzed in labs.

Let’s start with some background information. The serotonin transporter is a protein in the brain that helps regulate levels of serotonin. When someone takes an antidepressant, the drug binds to the SERT protein and blocks it from transporting serotonin out of the brain, disturbing the brain’s longstanding homeostasis by increasing the amount of serotonin available. When early test subjects reported an elevated mood after taking antidepressants in clinical trials, the assumption was that the increase in serotonin was responsible for this relief, therefore thus forming the basis of the serotonin theory of depression. If more serotonin = happier people, then less serotonin = sad people. And that’s how Prozac was born!

Too bad it was all a pipe dream.

Over time, the brain adapts to the presence of the drug and learns to produce less serotonin on its own. The body is always trying to get back to homeostasis, remember. The pharmaceutical industry spends billions of dollars trying to convince you that they can override hundreds of thousands of years of evolutionary physiology, but the bottom line is the body has to remain in equilibrium to stay alive. If you’re hot, you sweat to cool down. If you’re cold, you shiver to warm up. If either of those systems don’t work like they should, you die.

So let’s say you’ve been on 20mg Prozac (fluoxetine) for ten years and you decide it’s time to come off. Your doctor drops you to 10mg for a few weeks and you tolerate it. Maybe you’re a little emotional and antsy but you can handle it. Your doctor has heard about all this withdrawal stuff so he thinks he’s got it all figured out and tells you not to drop from 10mg to 0, but to instead cut the capsule in half and take 5mg for a week or two. You don’t feel great and wonder if it’s the depression coming back. But you figure you’ll drop to zero and give it a few weeks to know for sure. After all, 5mg is miniscule. Smaller than the smallest dose on the market! They give 5mg of Prozac to six year olds!

You drop to zero and all hell breaks loose—akathisia, huge emotional swings, paranoia, brain fog, gut issues. Back to the doctor you go, because clearly you’re sick and how stupid you were to think that you could operate without the Prozac. So you go back on 20mg. Hell, make it 40mg this time. Clearly, you need it. Your doctor suggests an antipsychotic as well because the paranoia suggests an emergence of Bipolar Disorder. Life, now, is all about managing symptoms.

Where did everyone go wrong? A fundamental misunderstanding of SERT occupancy.

Let’s look at the following graphs, courtesy of researcher Mark Horowitz:

The black curve is the measure of SERT occupancy as determined through brain-imaging techniques called PET scans that allow researchers to see the biological workings of the body. As you can see, at 25mg of fluoxetine, 80% of the serotonin transporters are occupied.

Figure (a) is a representative of the conventional line of thinking for linear tapering of antidepressants. Rather, the idea of lowering dosages by equal, measured steps—5mg, in the case of this graph. The problem is that if you lower the dose of Prozac from 20mg to 5mg—a 75% reduction—SERT occupancy only reduces by 20%. This means that not only are there fewer operating receptors, there is also less serotonin in the brain because the body long ago lowered its production. It is likely that withdrawal occurs at least in part because of this chemical imbalance created through linear tapering. And yes, it is ironic that this time, a true chemical imbalance is responsible.

Due to the hyperbolic nature of SERT occupancy, this dissonance is even more extreme at lower dosages, as seen in Figure (b). At 2.5mg of Prozac—20% of the lowest dose available on the market—SERT occupancy is 40%, just half of what it is at a robust dose of 25mg. This explains why it can be more difficult for people taper as they get closer and closer to zero.

Though SERT occupancy occurs with all antidepressants, the levels of SERT occupancy vary from drug to drug, as shown by this systematic analysis of 10 different psychiatric drugs, done by Anders Sorenson, et al.

The reason why you need to know about this is because it’s likely your prescriber is completely unaware. More understanding of SERT occupancy, as well as more robust research (especially when multiple drugs are involved), would lead to better de-prescribing practices that will likely lessen or eliminate severe withdrawal effects.

In the fictional example I gave above, our now “bipolar” patient needed a much slower taper that followed the hyperbolic curve and was adjusted only once she stabilized from the previous dose reduction. Had she tolerated a 10% reduction—from 10mg to 9mg to 8.1mg to 7.29mg and so on to 0—her brain likely would have had much more time to fire up dormant receptors and naturally ramp up serotonin production, leading to a more gentle, symptom-free re-introduction into a world without SSRIs.

Instead, when she was pulled off too quickly, her system went haywire because neurotransmitters are responsible for regulating the entire body. Instead of recognizing this as withdrawal, both she and her doctor assumed it was mental illness and plunked her back in the system with a shiny new diagnosis. This happens all the time. All. The. Time.

I hope you’ve enjoyed this Science Corner issue of Happiness Is A Skill. Please keep in mind that we are very much in the infancy of antidepressant withdrawal research, and that no single piece of information is the whole answer. But as they say on NBC, the more you know! Ding ding dong!

In the midst of the pandemic, a 35 year old man I’ll call Sav, began shooting hoops in his hometown in Italy. First, he shot from the three point line. Then, he turned around and shot backward, sinking the basketball into the net. A few weeks later, he did it blindfolded. Then backward, blindfolded, and while jumping on a trampoline. 

The trick shot obsession grew to kicking ping pong balls into narrow-mouthed water jugs and launching soccer balls into basketball hoops with a golf club. In less than a year, he amassed millions of followers and cashed fat checks from merch and ad sales. 

Then, in the summer of 2022, Sav went dark. 

As it turns out, the followers, the money, the trick shots—all of it was a result of psychiatric drug withdrawal-induced akathisia, a constant state of tortuous restlessness and burning agitation that Sav described as “dishumane.” Unable to sleep or stop moving, Sav channeled his distress into intricate human tricks.

The circus nature of it all kept him occupied in between months long hospitalizations over 30 sessions of controversial electroconvulsive therapy (ECT). He spoke to every known doctor, expert, and advocate on the subject of withdrawal—including me—in hopes that someone could stop the pain. Nothing helped. Most suggestions just made things worse.

Today, Sav is in the process of ending his life through an assisted suicide organization in Switzerland. 

There is an aphorism in medicine, coined by former Dean of Medicine at Harvard Dr. Charles Sidney Burwell that says, “Half of what we are going to teach you is wrong, and half of it is right. Our problem is that we don’t know which half is which.”

I think about this quote constantly, both in the context of my own health and when people like Sav reach out to me for help. I can’t give medical advice since I’m not a doctor, but I can talk about my experience and share resources. Even when I’m passing along research done by other people, it’s a paralyzing to know how much we don’t know, how much I don’t know. What works for one person causes havoc in another. That’s all well and good if the body is strong enough to recover from all the self experimentation. But in a case like Sav’s, any little change seems to set off a cascade of irreversible negative effects.

So much of medicine, and especially a new field like psychiatric drug withdrawal, is focused on the how, not the why. The why is too expensive, requiring oodles of money and serious research. Sav’s case is the perfect example. He followed the leading theory of tapering off psychiatric drugs—hyperbolic tapering—a strategy that encourages small dose reductions, each one smaller than the one before, over a long period of time. Research shows that generally, this method lessens or eliminates withdrawal symptoms by allowing the brain and body to adjust without getting overwhelmed by the sudden lack of drug presence.

But there is a subset of people like Sav who don’t seem to tolerate this method. Instead, it’s like their body hits a limit with how much of the drug they can process, and these long tapers basically become prolonged poisoning. Sav told his doctors over and over again that he thought the taper was hurting him. He was dismissed and told to stay the course. Not knowing what else to do, he followed their advice. And he’s now going to Switzerland because of it.

I’ve heard similar stories from enough people to know that Sav’s story is not a one off. For these folks, there’s something going on physiologically that’s outside of the norm. My hunch is that it has something to do with the genetic component of their body’s CYP system, a complex bodily function involved in the metabolism of drugs, chemicals, hormones, and neurotransmitters. But until someone designs a study for people in withdrawal that analyzes genetic variants in the CYP system, it’s all just a guess. And I’m sure it’s not that simple. I’d also like to see fMRIs, qEEG, hormone panels, and VO2 max tests for people in withdrawal. Until that actually happens (if it ever happens), people like Sav are going to suffer thanks to well intended but myopic views.

Personally, I don’t know know how to deal with this. I’m heartbroken over Sav. I feel like the community failed him. It’s an impossible position for everyone. What percentage of people are sacrificial lambs on the path to truth and understanding? How do you instill hope in the hopeless? How do you help when sometimes the help is poison?

If there is any silver lining to this story, it is this: Sav told me he does not want to go quietly. He wants the world to know his story. We have a little bit of time. The checks and balances in Switzerland are many, for good reason, and he does not yet have a date.

Of course, I hope that between now and then some miracle shows up and he finds some relief. If not, I have to assume that he is a player in a bigger game. That somehow, his suffering won’t be in vain because it will lead to more awareness and education. He is, after all, a bit of a showman. Every trick shot sunk not just to distract himself, but to prove that nothing is impossible.

I will share his real name when he is ready to fully go public. In the meantime, he has given me permission to share his story. Thank you for reading.

In the year before and months after MAY CAUSE SIDE EFFECTS released, I didn’t read a single book. I’d just finished writing one, and reading other people’s work did nothing but invite comparison and insecurity. But something shifted when we flipped the page to 2023, and I’m back to devouring books at all hours of the day.

Among the stack I’ve recently finished is Dr. Ellen Vora’s The Anatomy of Anxiety: Understanding and Overcoming the Body’s Fear Response.

Ellen is a Yale and Columbia University educated, board-certified psychiatrist who speaks openly about antidepressant withdrawal and the overprescription epidemic. Though Ellen and I haven’t ever met, we’re in occasional contact since she’s one of the few working psychiatrists with the balls to speak out about the pill for every ill “strategy” that seems to be doing more harm than good. Also an acupuncturist and yoga teacher, she practices from a functional-medicine foundation, meaning she believes most (if not all) mental health issues are caused not by disease or a chemical imbalance but by everything from unresolved trauma to lifestyle choices to blood sugar crashes.

The perk of this approach is that unresolved trauma, lifestyle choices, and blood sugar crashes are all things we have the power to fix. What a concept!

The conventional theory of anxiety is that it exists in the head and causes downstream, emotional and physical effects. In The Anatomy of Anxiety, Ellen argues that anxiety begins in the body, and that it’s the physiological stress response that causes mental anguish. Said another way, our brain chemistry changes as a result of an imbalance in the body, not the other way around. This is good news, she says, because this anxiety is both preventable and responsive to basic adjustments to habits, diet, and lifestyle.

Just as I did with Johann Hari’s Stolen Focus, I’ve compiled what I think are the 10 most important and interesting ideas from Ellen’s book. One caveat: The Anatomy of Anxiety is an outstanding starting point for those beginning to explore the mind-body connection and the basic science of anxiety. For those of you who spend a lot of time in this space, you’ll likely recognize much of the content. I worry that my familiarity with the topic means I’ve skimmed over obvious lightbulb moments. Thus, if you’re someone who struggles with anxiety and you don’t spend your free time nerding out over the science like I do, I highly recommend you take my word for it and get a copy for yourself. Understanding how your body works and why it reacts the way it does is a key first step in managing and healing anxiety.

Onward to the good stuff! (Bold emphasis mine.)

Ellen likes to differentiate from “true anxiety” and “false anxiety” in order to help her patients understand what is anxiety they can control (false), and what is anxiety that’s baked into human existence (true)

“False anxiety is the body communicating that there is a physiological imbalance, usually through a stress response, whereas true anxiety is the body communicating an essential message about our lives. In false anxiety, the stress response transmits signals up to our brain telling us, something is not right. And our brain, in turn, offers a narrative for why we feel uneasy…this type of anxiety is not here to tell you something meaningful about your deeper self; rather, it’s offering a more fundamental message about your body. When we recognize that we are experiencing anxiety precipitated by a physiological stress response, we can address the problem at the level of the body, by altering our diet or getting more sunshine or sleep. In other words, false anxiety is common, it causes immense suffering, and it’s mostly avoidable.”

True anxiety arises from having strayed from a vital sense of purpose and meaning. This anxiety is what it means to be human—to know the inherent vulnerability of walking this earth, that we can lose the people we love and that we too, will one day die…it is essentially a guide for how to make our lives as full as they can be.

Between 2019 and 2021, the Kaiser Family Foundation estimated that rates of anxiety and depression skyrocketed by 270 percent.

Genes simply don’t adapt that quickly, which punctures quite the hole in the theory of anxiety as a genetic disorder. (Never mind the fact that an “anxiety gene” has never been identified.”

Ellen says: “These rates would not have risen so precipitously if these disorders had a predominantly genetic basis—which was our presiding understanding over the last several decades. Our genes cannot adapt so quickly as to account for our recent catapult into anxiety. It stands to reason that we are increasingly anxious because of the new pressures and exposures of modern life—such as chronic stress, inflammation, and social isolation. So, odd as it may sound, this recent acceleration is actually good news because it means there are straightforward changes we can make.”

Though we have the same stress response as we did thousands of years ago—when stress meant running from a saber-tooth tiger or finding consistent food supply—modern life gives us a very different set of circumstances to cope with. Rarely are we in life or death situations and instead experience regular, low-grade stressors like a bloated email inbox or road rage.

Still, “with our modern diets and habits—which frequently trigger stress responses in our bodies—many of us live in a near constant state of feeling under siege. Your blood sugar is crashing after eating something sweet? The body interprets this as a mild threat to survival. You stay dup too late doom scrolling on your phone? The body feels surrounded by danger. Sleep deprivation, chronic inflammation from eating foods you don’t tolerate, and the comment section on Twitter—these are all, from your body’s perspective, indications that your environment is not safe. So, the body releases stress hormones into your bloodstream, and this invisible chemical cascade manifests as the feelings and sensations of false anxiety.”

Because false anxiety is often caused by outside stressors, it’s also manageable if you know what to look for. The book goes into the science behind each of these bullet points, but as a starting point, here are Ellen’s recommendations for “pausing in the midst of turmoil” in order to understand the particular false anxiety that’s occurring as well as how to address it:

“I’m anxious, and I’m not sure why. Am I…

• Hungry? (eat something)
• Sugar-crashing or having a chemical comedown? (Did I just eat something sweet, processed, or laden with food coloring or preservatives? Have a snack and focus on making different choices next time.
• Overcaffeinated? (Perhaps this jittery anxiety is really caffeine sensitivity; tomorrow, drink less caffeine.)
• Undercaffeinated? (I drank less caffeine today than usual; dose up and aim for consistent daily caffeine consumption going forward)
• Tired? (Take a nap; prioritize an earlier bedtime tonight.)
• Dehydrated? (Drink some water.)
• Feeling sluggish? (Take a quick walk outside; dance.)
• Dysregulated? (Did I just engage in an internet rabbit hole or social media binge? Dance or go outside to rest the nervous system.)
• Drunk or hungover? (File this away to help inform future choices around alcohol.)
• Due for a dose of psychiatric medication? (Right before the next dose, I’m at the pharmacological nadir—or the point where the level of medication in my bloodstream is at its lowest, and this can affect mood. Time to take meds.)

(A note from Brooke in bold: I’d argue that the last bullet point could also include, “Time to take meds or if coming off meds, recognize this as a sign of psychiatric drug withdrawal and be kind to yourself.” )

True anxiety serves a purpose in society, as demonstrated by this fascinating 1980s study of primates:

“Studies of primates show that some members of the tribe are more anxious than others—these are the ones that tend to hang back, gathering the peripheries of the main group. In the 1980s, the late zoologist Dian Fossey decided to remove these more sensitive members of one group of chimpanzees to see how it would affect the rest of the community. Six months later, all the chimps were dead. ‘It was suggested that the anxious chimps were pivotal for survival,’ Sarah Wilson writes compellingly of this experiment in her book First, We Make the Beast Beautiful. ‘Outsiders, they were the ones who were sleeping in the trees on the edge, on the border, on the boundary of the community. Hyper-sensitive and vigilant, the smallest noise freaked them out and disturbed them, so they were awake much of the night anyway. We label such symptoms anxiety, but back when we were in trees, they were the early warning system for the troop. They were the first to scream, “Look out! Look out!”’”

(Side note, I’ve never used that many quotation marks before. My 10th grade English teacher Mrs. Utter would be proud.)

Though this study was on monkeys, the same can be said about more sensitive and anxious folks in the world. They alert everyone else to potential problems and dangers. (I.E., climate activists.)

The most positive (and counterintuitive) change I ever made to my sleep hygiene was when I started eating a hefty portion of starchy carbs at dinner.

Prior to this directive—which came from a high performance nutritionist and professor of muscle science at Cal Fullerton—I’d often skimp on starchy carbs at dinner in order to rationalize dessert, or go low-carb all together in a misguided attempt to cut calories and stay lean. My shitty sleep, I assumed, was unrelated.

As it turned out, this strategy was causing blood sugar spikes and crashes (with dessert) or causing overall low blood sugar (low-carb) that disturbed my sleep. When I added about a cup of cooked white rice or potatoes to the meal, my sleep issues evaporated. What happened?

Ellen explains: “If you typically get ‘hangry’—angry and irritable when you’re hungry—at 3pm, the overnight equivalent is waking up at 3am with racing thoughts, unable to fall back asleep. This typically happens when your blood sugar crashes overnight and your body counters with a stress response…a stress response can make your sleep more superficial, shunting you out of the deeper stages of sleep and making it more likely you’ll be jolted awake.”

The solution is to stabilize blood sugar throughout the night. I do this with a big, starchy carb heavy (but low sugar) meal. Ellen likes to eat a spoonful of almond butter before bed, and eats another spoonful if she wakes up jittery and anxious.

“Our bodies are increasingly bombarded with unrecognizable chemicals and food—ranging from pesticides to phthalates to Pop-Tarts (essentially, foreign agents our bodies didn’t evolve to deal with)—that provoke the immune system in much the same way a genuine infection would. A daily ingestion of Doritos, for instance, leaves the immune system belligerent and confused. It keeps fighting, thinking it stands a chance at killing off the ‘infection’ of Doritos, but our immune system isn’t build to defeat chips—not to mention that we get ‘reinfected’ with every snack. Over time, a consistently inflammatory diet can result in a dysregulated, hyper-vigilant immune system, an inflamed body, and sustained feelings of depression or anxiety.”

“The body is hardwired for survival,” Ellen says, “not for feeling calm.”

She’s says this in the chapter about psychiatric drug withdrawal, specifically in relation to benzodiazepines. But what I find most interesting about the statement is that we’re all walking around under the assumption that calm should be the norm and anxiety a pathogen to eradicate.

In reality, a part of our body is always looking out for dangers. It’s why we startle when we hear an unfamiliar thunk. Debilitating anxiety needs to be dealt with, of course, but bouts of it is just the body doing its job of trying to stay alive.

“We’re taught from a young age that when something is difficult, it is necessary to distract ourselves. When a child has a tantrum, we think, How can I make the crying stop? We know that if we hand the kid some sugar or a screen, they’ll probably be satisfied. Problem solved, right? Well, actually, now we’ve taught the kid: I can’t handle your big emotions, you can’t handle your big emotions, and should ever feel big emotions in your future life, quickly find something that will distract you, offer you a hit of dopamine, or numb you out. It’s no wonder even we adults turn to our phones or emotional eating when in fact we just need to feel our feelings and let our tantrums run their course.”

This is where true anxiety comes into play. Safety is an illusion. All our effort put into keeping our kids “safe,” building equity, or eating clean could be undone in a matter of moments. We do these things to bring a sense of order into our lives, but trying to white-knuckle our way to control often creates the exact anxiety we’re trying to prevent.

“We are anxious and exhausted because wee are fighting with reality, beliving things are supposed to go a certain way. Instead of showing us where we need more control, anxiety actually alerts us to where we need to let go; when we need to take a breath and patiently, courageously see where our particular path will take us.”

Last weekend, I was invited to sign copies of MAY CAUSE SIDE EFFECTS at a new bookstore in Santa Monica called Zibby’s Bookshop. A dozen or so other authors, including my writing mentor, were signing at the event as well. Afterwards, we all gathered in the lobby of a fancy hotel to drink wine, eat cheese, and bitch about the disaster that is publishing books. Everyone had a horror story, from “my Gen Z publicist will no longer talk on the phone because she says the phone is too stressful” to “my book came out two days before Covid shut the world down” to “my former agent stole my royalties and fled town in a Winnebago.” (I get to take credit for that last one.)

As nurturing and fulfilling as the evening was, I was exhausted from the intensity of it all. As a few of the ladies were transitioning from the party to the after party, I declined, instead deciding it was time to head back to my AirBnB.

“Brooke’s got strong boundaries,” my mentor said, her eyes scanning me like I was some sort of curious, alien species. “I need to work on that.”

This observation stuck with me because it butted up against a series of recent encounters where my “boundaries” caused confusion, discontent, or outright pain in other people. I put boundaries in quotes because to me, it doesn’t feel like a boundary. It feels like the most obvious thing in the world. By doing what’s best for me—in this case, getting a good night’s sleep—I guarantee that I won’t be exhausted in the morning. I’m nicer and more patient when I’m rested, which leads to more pleasant encounters with others, which means my day and everyone else’s is going to be easier. A win for me, a win for the world.

This is called egotistical utilitarianism, a phrase I first heard coined by Matthew McConaghy in an interview with Tim Ferris.

It’s a counterintuitive concept. An egoist does whatever is best for them. A utilitarian does whatever is best for others. How can such opposition fit together?

Because when we take action based on what benefits us the most, it also benefits those around us.

As McConaghy put it, “The decisions we make for the I, for ourselves, the selfish decisions are actually what’s best for the most amount of people — utilitarian — they are where the ‘I’ meets the ‘we’, where the selfish is the selfless.”

Don’t get confused by the “egotistical” part of this. Our negative connotation of the word, in the sense that people who are egotistical operate as if they’re the only mattering person on Earth, disappears when egotistical utilitarianism is fully understood. In this sense, it is about the reason for the action, not the action itself.

As an example, a fireman spends hours at the gym lifting weights, running on the treadmill, and staring at himself in the mirror. His friends and family are chuffy because he isn’t around that much or comes off too rigid in his adherence to the gym schedule. They want him to spend time with them. To tend to their emotional needs. But what’s really happening is the fireman’s inner drive to be in the best shape possible also allows him to have the physical ability and confidence to carry heavy firehoses, pull people out of burning buildings, and trust in his body’s carbon dioxide capacity. His usefulness as an individual, in this specific area where he excels, benefits the collective every time he goes out on a call. And when he is able to do his job to the best of his ability, he is more fulfilled in his life. The more fulfilled his life, the better and more present he can be with the people around him during the time he makes for them.

In my life, it plays out like this:

My work on antidepressant withdrawal is my priority. Full stop. It takes a tremendous amount of energetic effort to navigate a topic this heavy, leaving little energy in the tank to manage the needs of other people. It’s why I’m not married and don’t have kids. I simply don’t have the bandwidth.

As a result, most of my day to day choices are based on what’s best for me and my energy conservation. That means I’m often non-committal, have zero issues cancelling social plans, and don’t express a natural interest in other people’s lives. This comes off as flaky and uncaring, especially to the people in my inner circle who feel they deserve to be put ahead.

But the reality is I can’t do this work and impact the collective if I’m constantly shifting my focus because someone wants attention or pat on the back. If they’re dying or in a real crisis, then of course I’ll drop everything and show up. And I make a conscious effort to speak their love language and spend time with them when I do have the bandwidth. The folks who understand this balance—and more importantly, practice it themselves and manage their own feelings around it—are the people who have staying power.

To harness our drive and use it for the good of the whole is a powerful strategy for both individual and collective happiness. It’s doesn’t mean there won’t be times where you are called to perform an entirely selfless or selfish act, or where obligations and ethics won’t trump individual wants. But it’s worth exploring what exactly is best for you, and to watch what happens around you when to act upon it.

Today, I’d like to share with you an essay by Dr. Bonnie Burstow, a professor and psychotherapist who spent most of her career at the University of Toronto’s Ontario Institute for Studies in Education.

The essay, published in the academic journal Ethical Human Psychology and Psychiatry in 2017, is the sort of work that burrows into your psyche. The core idea presented—that psychiatric drugging of children (including with ADHD drugs) is a form of child abuse—seems radical at first glance. But the deeper you get into the paper, the more difficult it is to argue with the claim.

I am going to refrain from injecting my own thoughts on the essay and instead leave you to process it on your own. However, the paper is quite dense and the language has an academic bent that can make it difficult to understand if you don’t speak academic-ese. Thus, I have pulled key highlights from the work and added them below. Everything blow is a direct quote from the essay. All emphasis (in bold) is my own.

I have also linked to the full paper through a public Google document. I encourage you to read the full piece and share it with your friends and family.

To learn more about Dr. Bonnie Burstow, who died on January 4, 2020, in this New York Times profile.

“Abuse is any behaviour that is used to gain and/or maintain power and control over another person” (Kelowna Women’s Shelter)

“Child abuse refers to any form of physical, psychological, social, emotional, or sexual maltreat- ment of a child whereby the survival, safety, self-esteem, growth, and development of the child are endangered. There are four main types of child abuse: neglect, emotional, physical, and sexual. (Royal Canadian Mountain Police, 2012)”

The United Nations Convention on the Rights of the Child, Article 6:

1. State parties recognize that every child has the inherent right to life

2. State parties shall ensure to the maximum extent possible the survival and the development of the child (UNCRC, Article 6).

The United Nations Convention on the Rights of the Child, Article 37:

1. No child shall be subjected to torture or other cruel or unusual punishment.

2. No child shall be deprived of his or her liberty unlawfully or arbitrarily (UNCRC, Article 37).

If something constitutes abuse, it is not in the best interests of the person being subjected to it—not with women being battered, not with children being assaulted with harmful drugs.

There are, of course, people who would argue that a definition like this cannot cover the area of child abuse because, irrespective of other considerations, it is always critical to do what is in the best interests of the child. (Don’t claims like this frequently underlie oppression?)