“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?

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.

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?)

For the past few years, I’ve felt a primal urge to disengage from the world around me. This inner restlessness is strongest when I’m in public and forced to witness the current state of our culture and values—garbage littering the streets, people Face-timing without headphones, rampant obesity, fourteen year old girls with false eyelashes and lip injections. It’s all inner pain manifested in the physical world, fueled by a system preying on people’s vulnerabilities to make money.

Bit of a bitch for cultivating happiness, eh?

As much as I see evidence of generational cultural improvement—for example, the expansion of gay and women’s rights over the past 50 years (save for the recent Supreme Court idiocy)—the cynic in me doubts we’ll see meaningful change in our lifetime when it comes to the environment, mental health, and ethical technological application. CO2 emissions, Big Pharma, and AI aren’t going anywhere anytime soon. The speed, money, and power generated from these industries is simply too persuasive under the current system. Perhaps a shift will occur one day, but for now, it seems to me that the real game is figuring out how to thrive as an individual in a toxic environment.

Enter Johann Hari and his new-ish book, Stolen Focus: Why You Can’t Pay Attention and How To Think Deeply Again. It’s one of the may books I’ve been reading when I retreat back into my sanctuary to think about how in the hell I’m going to maintain my sanity in a world so far removed from our animal nature.

It’s also a book that sat on my shelf for a long time because I said to myself, “I just wrote and published a book. My focus is just fine.”

Except, in the months since MAY CAUSE SIDE EFFECTS came out, I’ve been a scattered mess. No queue without a scroll through Instagram. No stoplight without an email check. No evening without an iPad.

Finally, after a conversation with a client who told me how he’s been leaving his phone at home and walking to his local library just to have a long stretch of uninterrupted time, I realized it was time for me to address my hijacked attention span.

Stolen Focus is one of the most powerful books I’ve read about living in the modern world. I encourage all of you to buy a hardcopy and read it in full (and I stress the hardcopy part, as opposed to an ebook or audio. People understand and remember less of what they read on screens.) But given that time is currency and that people just don’t read much any more (over 50% of Americans didn’t read a single book in 2022), I’m featuring ten of what I believe to be the most important quotes from Johann’s work. I hope these ideas will get you thinking about the world you live in and encourage you to take control and make active changes in your life and the life of your children.

“Democracy requires the ability of a population to pay attentional long enough to identify real problems, distinguish them from fantasies, come up with solutions, and hold their leaders accountable if they fail to deliver them…people who can’t focus will be more drawn to simplistic authoritarian solutions—and less likely to see clearly when they fail.”

“In 1986, if you added up all the information being blasted at the average human being—TV, radio, reading—it amounted to 40 newspapers’ worth of information every day. By 2007, they found it had risen to the equivalent of 174 newspapers per day. The increase in volume of information is what creates the sensation of the world speeding up.”

Physicist Sune Lehmann, a professor in the Department of Applied Mathematics and Computer Science said of the increase in perceived speed, “ ‘What we are sacrificing is depth in all sorts of dimensions. If you have to keep up with everything and send emails all the time, there’s no time to reach depth. Depth connected to your work in relationships also takes time…all these things that require depth are suffering. It’s pulling us more and more up onto the surface.”

Adam Gazzaley, a professor of neurology, phsiology, and psychiatry at the Univeristy of California explained it this way: “Think of your brain as like a nightclub where, standing at the front of that club, there’s a bouncer. The bouncer’s job is to filter out most of the stimuli that are hitting you at any given moment—the traffic noise, the couple having an argument across the street, the cellphone ringing in the pocket of the person next to you—so that you can think coherently about one thing at a time. The bouncer is essential. This ability to filter out irrelevant information is crucial if you are going to be able to attend to your goals…In addition to switching tasks like never before, our brains are also being forced to filter more frantically than at any point in our past…The bouncer is overwhelmed, and the nightclub becomes full of rowdy assholes disrupting the normal dancing.”

“Sune [Lehmann] had seen a photograph of Mark Zuckerberg, the founder of Facebook, standing in front of a room of people who were all reaching virtual reality headsets. He was the only person standing in actual reality, looking at them, smiling, pacing proudly around. When he saw it, Sune said, ‘I was like—holy shit, this is a metaphor for the future.’ If we don’t change course, he fears we are headed toward a world where ‘there’s going to be an upper class of people that are very aware’ of the risks to their attention and find ways to live within their limits, and then there will be the rest of society with ‘fewer resources to resist the manipulation, and they’re going to be living more and more inside their computers, being manipulated more and more.’ ”

“If you go too fast, you overload your abilities and they degrade. But when you practice moving at a speed that is compatible with human nature—and you build that into your daily life—you begin to train your attention and focus. Slowness nurtures attention, and speed shatters it.”

“When people think they’re doing several things at once, they’re actually “juggling” as Professor Earl Miller at the Massachusetts Institute of Technology explains. He continues, “ ‘They’re switching back and forth. They don’t notice the switching because the brain sort of papers it over, to give a seamless experience of consciousness…but if you spend a lot of this brain processing time switching and error correcting, you are simply giving your brain less opportunity to follow your associate links down to new places and really [have] truly original and creative thoughts.’ “

In short: “If you spend your time switching along, then the evidence suggests you’ll be slower, you’ll make more mistakes, you’ll be less creative, and you’ll remember less of what you do.”

“The cognitive neuroscientist Dr. David Strayer at the University of Utah conducted detailed research where he got people to use driving simulators and tracked how safe their driving was when they were distracted by technology—something as simple as their phone receiving a text. It turned out their level of impairment was “very similar” to if they were drunk. The distraction all around us isn’t just annoying, it’s deadly: around one in five car accidents are now due to a distracted driver.”

“We evolved to get a rush of energy when the sun began to set. This was very helpful to our ancestors…[who] got a fresh rush of energy just as the light waned so they could safely get back to their tribe and finish the things they needed to do that day. But now we control the light. We decide when the sunset happens. So if we keep bright lights switched on right until the moment we decided to go to sleep, or we watch TV on our phones in bed, when we switch them off we accidentally trigger a physical process—our bodies think this budding waning of light is the arrival of sunset, so they release a rush of fresh energy to help you get back to your cave.”

Johann spends a good chunk of the book exploring the ADHD topic, but in my opinion, it boils down to the following:

“To pay attention in normal ways, you need to feel safe. When children can’t pay attention, it’s often a signal that they are under terrible stress. If you’re medicating a child in that situation, you’re colluding with them remaining in a violent or unacceptable situation.”

Aza Raskin, former creative lead at Firefox, designed the now-ubiquitous “infinite scroll” that keeps content continuous on Instagram, Facebook, Twitter, etc. What started off as a way to make browsing more convenient has now been usurped by Big Tech to keep eyeballs on screens, because “the longer you make people look at their phones, the more advertising they see—and therefore the more money Google gets.”

Aza says, “one of the ironies is there are these incredibly popular workshops at Facebook and Google about mindfulness–about creating the mental space to make decisions nonreactively—and they are also the biggest perpetrators of non-mindfulness in the world.”

Chamath Palihapitiya, Facebook’s former Vice President of growth, explained in a speech that the effects [of Facebook] “are so negative that his kids ‘aren’t allowed to use that shit.’”

James Williams, former Google strategist, once “addressed an audience of hundreds of leading tech designers and asked them a simple question: ‘How many of you want to live in the world you are designing?’ There was a silence in the room. People looked around them. Nobody put up their hand.”

It’s been a frigid and snowy year winter in the Washoe Valley, and much of our infrastructure is being tested. Trees are down all over town, the weight of heavy snow too much for delicate branches. Reno’s signature neon lights are dim and patchy, presumably due to wiring shorts. My house lost power and cell service for three days over the New Year’s weekend, leaving the dog and me to head across town and huddle next to my mother’s fireplace.

I am struck by the obvious metaphor: it is in times of extreme events where cracks— disregarded for so long—become too big to ignore. It was only in the aftermath of the power outage that support from Oregon and Idaho was brought in, despite long-standing signs of a grid too fragile to handle a heavy winter.

The timing of these storms plus the entry into a new year has pushed me into a state of reflection and repair. The extreme personal events of 2022—the release of MAY CAUSE SIDE EFFECTS, the death of a friend, discovering a genetic mutation, and the slow, torturous separation from a long-term partner—didn’t just reveal cracks, it shorted the entire system and is now forcing me to rebuild.

At the center of this restructure is the question: What am I optimizing for?

Said another way: What kind of life do I want? How do my choices support or work against that goal?

For each answer that comes to mind, I look for the core value underneath. For example, a big goal is to never send out a resume or apply for a job ever again. This means my past work feeds the flywheel that creates future work. Practically, it means I need to keep producing so the flywheel has a steady stream of energy.

But the bigger question is why it’s so important for me to never again go through a formal job search, and that comes down to how I want to live my life. I value my independence and ability to be in charge of my own schedule above all else. If I’m going through a traditional application process, it means I’d be working for someone else, therefore giving up a core value to meet external expectations. It’s just not going to work for me.

Following this train of thought, I’ve come up with the following North Star: I am optimizing to create a life where I work as much as I want and earn as much as I need.

Simplifying the goal to a single sentence will, in theory, help me make choices that support this goal. A shiny opportunity with a lot of money may come along, but if I already have as much money as I need and the new job requires me to work more than I want, why would I go down a path that works against my core values?

Well folks, it’s happened. After a year that I will henceforth refer to as, “The Year That Changed Everything,” I have completely, utterly, all the overused adverbs in the world-ly, hit a wall of systemic exhaustion. 

Not that I can stop. 

I’ve got four trips planned in the next eight weeks, all for work or book-related endeavors. Los Angeles —> Las Vegas (lord help me) —> San Francisco —> Virginia Beach. 

I’ve put myself on a work embargo in between trips, which means after I write this, I’m going skiing. (That’s how embargoes work, right? They’re conditional upon finishing work, right? RIGHT?)

Burnout is a manifestation of chronic, unmitigated stress. Or, as the World Health Organization defines it, an “occupational phenomena” characterized by “feelings of energy depletion or exhaustion; increased mental distance from one’s job, or feelings of negativism or cynicism related to one’s job; and reduced professional efficacy.”

One google of “burnout” provides a whole host of solutions, but frankly, I’m too burned out to even look through it and throw some research at you. Instead, I’ll share my unscientific philosophy on the matter: the BBC.

Boundaries

Bordem

Creativity

The thing about publishing memoir is that everyone wants to talk to you about it. If you’re trying to sell as many books as possible, which I am, this means taking every opportunity to chat. MAY CAUSE SIDE EFFECTS is gaining traction and the bigger the opportunity, the more focused I need to be. 

Thus, for the next eight weeks, I’m postponing, cancelling, or avoiding any work that’s not directly MCSE related. No more bullshit meetings. No more “picking my brain.” The same goes for social obligations. If I don’t fully want to be in an experience or around a group of people, it’s just not happening. I don’t have the bandwidth. 

The only cure I’ve ever found for burnout is boredom followed by creativity. Not standing-in-line-at-the-grocery-store-boredom, but true boredom. Like pandemic levels of boredom. The kind of boredom that transitions from agitation to openness, where the brain shuts down and the instinct to pick up a paintbrush, go for a walk, or play an instrument kicks in. 

In my experience, true rest only occurs in this state. And it’s why vegging out in front of the TV for an hour isn’t all that rejuvenating. What the mind and body needs is primal rest, the sort that occurs in nature or in the nurturing presence of close friends or family. 

It’s a cumulative process, too. One that isn’t all that compatible to modern life. But there are little things we can do to facilitate boredom, like leaving your phone at home when you go for a walk or taking a social media break. One of the more amusing strategies I heard involved locking yourself in your bathroom with nothing but a pen and paper, setting an hour-long timer, and not allowing yourself to do anything but scribble or doodle while you’re in there. No reading lotion labels, no organizing the makeup drawer. No bubble baths. Just pure, private, glorious boredom. 

The great tragedy of the digital world is that fewer people—kids, especially—get bored enough to pick up a pen, eliminating countless writers and artists who might be filled with talent but are instead wasting away playing Fortnite.

I don’t think it’s an accident that our abhorrent collective mental health coincides with the massacre of arts funding in schools. As the beloved author Kurt Vonnegut said, “The arts are not a way to make a living. They are a very human way of making life more bearable. Practicing an art, no matter how well or badly, is a way to make your soul grow, for heaven’s sake.”

Making art for art’s sake is the only thing that rejuvenates my brain during times of burnout. But purposeless creativity does not exist without boredom, which is why the two need to go together. The second moneymaking is involved, it moves into the realm of adding to burnout rather than removing it. 

Of course, I don’t have kids or an elderly parent to care for. Caregiving burnout is its own beast; one that trickier to address. So I’m not even going to try. But if you’re burned out keeping other humans alive, consider yourself hugged. You’re doing a hard thing. 

With that, I’m going skiing. Without my phone. If I have time left in the day while it’s still light out, I’ll paint something. And then in 36 hours I’ll get on a plane. Rinse and repeat.

Last weekend, I did something I rarely do: I went out. Like out out. I put on heels, wore makeup, and made chitchat with strangers at a fundraiser for a local museum. 

I was invited as a date for a friend whose husband went on a last minute business trip, leaving her as the lone stag in a group of eight couples. My butt did a great job of filling the seat, but a table of familiar faces brought not a sense of inclusion, but the sting of loneliness. 

The experience highlighted a nagging feeling I’ve had since MAY CAUSE SIDE EFFECTS was published in September. The book was, in many ways, my best friend. A constant, intimate presence, it persisted through the ebbs and flows of my life, the work often reflecting my reality. It gave me a sense of purpose, never wavered in its dedication, and showed up when I needed it. When it hit bookshelves, it’s like it moved away. It isn’t mine any more. It belongs to other people now, influencing their lives while I scramble to fill the void. 

Though the loss has gifted me oodles time, it also illuminates neglect. All of my relationships have suffered over the past five years, particularly my friendships. As a single person with no kids and a minuscule family unit—it’s just me and my mom, no siblings or notable extended family—I’ve always kept a mental running list of friends who would step up in a crisis, no questions asked. 

I don’t know if there’s anyone on that list anymore. 

Years ago I might have blamed this development on the failure of the parties involved, assuming we just didn’t try hard enough. Now, I understand that biology and social psychology is at play, and that itinerant life I’ve led isn’t conducive to creating and maintaining intimate friendships.

The number and quality of friendships is the single most important indicator of longevity and happiness and as we age, friendships become more important for health than family. 

But in 2021, 12 percent of American adults said they had no close friends, contributing to the loneliness crisis that began well before, but was exacerbated by, the pandemic. 

So how do we make friends as adults? More importantly, how do we create meaningful friendships that increase happiness? I dove into the research of evolutionary psychologist and friendship expert Robin Dunbar to find out.

Robin Dunbar is best known for Dunbar’s Number, which he defines as the number of relationships people are able to cognitively able to manage and maintain at once. He puts this number at 150, which unsurprisingly, is just about the size of the average American wedding guest list. 

These 150 people are made up both friends and family and sorted into a sort of circular hierarchy. The closer the ring of people around you, the fewer the people in the ring. 

In the bullseye with you is an spouse or intimate partner, followed by three to five people who make up the first ring, usually family members and a close friend or two. The next ring expands and holds secondary characters. Grandma, perhaps. Friends you know very well but maybe not the one you call in a crisis. From there, we expand through the rings of fair weather friends, colleagues, extended family, old friends who live in different places, and so on through the target.

Meaningful friendship is woven by shared experience and regular exposure. Therefore, the best way to make new friends is to engage in a consistent, social activity like a weekly meetup group. 

When we’re kids, this is automatic. We go to school or an after school activity, see the same people every day, and become friends. As adults, we lose opportunities for that natural interaction. Some people get it through work, but for someone like me who works alone and at home, I have to create it. It’s no surprise, then, that the people in my “close” and “best” friend circles over the years have come from going to the same CrossFit class, at the same time, five days a week for years. 

It’s also not surprising that over the past six years, when I was either traveling internationally or splitting my time between Canada and the US, my friendships suffered. I’d be in town for three weeks and leave for two months. People had babies in the time I was away. 

In my head, they still remained in the “close” or “best” category because I didn’t stay in one place long enough to forge a friendship strong enough to fill the space. But while I was away, my place in their hierarchy shifted, knocking me to outer circles. 

Where people stand in the hierarchy is constantly shifting. When you see less of someone because you see more of somebody else, it pushes people in and out of different circles. We see this happen all the time when people enter new relationships. In an interview with Dan Harris on the Ten Percent Happier Podcast, Dunbar said that falling in love can actually take the place of two close relationships, because the mental energy and attention devoted to the new person inevitably boots two people out of the ring. This explains why people disappear when they get into a relationship. It’s not because they don’t care or are blinded by love. It’s because we have limited capacity.

When life separates “close” and “best” friends, the instinct is to hold those people in their circles by keeping in touch through social media or phone calls. Though social media has a reputation for, you know, toppling democracy and obliterating societal mental health, it’s actually supports relationship intimacy. But with limited energy to devote to friendships, time spent on Facebook eats into opportunities for in-person connection. 

For relationships in the outer rings, this isn’t a big deal. But at the inner rings, intention is crucial. As Dunbar says, people might be “better off finding a new shoulder to cry on just round the corner, so when the world does fall apart, they can walk around the block, knock on their door and get a hug.”

Said another way by the lyricist Stephen Stills: “If you can’t be with the one you love, love the one you’re with.” 

The hardest part of making friends—especially in a new place—is the beginning. But once you engage in a community and show up consistently, proximity will eventually lead to connection. Once those connections are made, the circles naturally expand as people get introduced to one another, creating a flywheel affect that ultimately leads to the sort of event I found myself at last weekend. 

As I felt sorry for myself at the table, envious that these sixteen (!) adults had so much support for one another, I wondered what it was about me that made me feel so separate. 

The answer is that while I was off in Cambodia or Croatia for a month at a time, they were all moving back to Reno and starting their families. All of them have kids around the same age. They get together for play dates and PTA meetings. When the kids aren’t around, they share the common ground gained from so many years of similar experience, often within walking distance of one another. 

It’s a barrier I’m just not going to be able to crack. But that’s okay. There’s plenty of room for them in my “good friends” category, and now I won’t beat myself up wondering why I can’t bring them closer.