Several years ago, I was standing in the Capitol Building in D.C. in a long-sleeved maroon dress that stretched tightly over my 37-week pregnant belly. I was sweating my ass off and berating myself for wearing a long-sleeves in July when the baby inside of me was practically crowning. I couldn’t focus on how hot I was for too long, though. I needed to get my head back in the game.
The woman from the lobbying firm that was organizing our group tapped the paper I held in my hand and asked me if I knew where I was going. I assured her I did, or at least I would figure it out, and I scanned the list of senators and representatives whom I’d be seeing over the next few hours. Each had a few notes scribbled next to their names, potential intel that we could use in our conversations about the eating disorder bill we were there to support. One mentioned that the representative had a mentally ill sibling that he’d talked about in the media. Another was a military veteran himself and had talked publicly about the importance of mental health for service members.
The lobbyist looked at my sweaty face and sympathetically handed me a bottle of water. “Just remember,” she said firmly. “Focus on the biology stuff. Tell them about genetics research. That’s what they need to hear. They need to know mental health is not a choice.” She drew out the last sentence slowly, emphasizing each word.
I nodded and glanced down at my notes. I’d written out some of the most compelling findings about eating disorders, the ones that were making all the waves in our little corner of the clinical world, but that were hardly mainstream knowledge. I’d written, for example, that up to 83% of the variance in who develops bulimia could potentially be accounted for by genetics. There were notes too about large-scale studies – studies of almost 75,000 people – that were helping to show eight particular genomic regions that seemed to be associated with anorexia.
We were there to help this bill pass, one that would help to secure more funding for research and identification resources for eating disorders, and we suspected that the way to do this was to help these politicians see that these conditions were not just serious, but biologically rooted.
It was the strategy that had led in recent years to greater recognition and funding for some of eating disorders’ cousins, things like major depression and schizophrenia. The previous few decades’ intense focus on mental illness as based in the brain had seemed to revolutionize our field. Sure, we’d always called these conditions “mental,” but now we weren’t thinking about that in some abstract way, but in a very literal and tangible way, one that could be seen in colorful images up on screens.
This neurological work by scientists had helped us move far beyond things like the “refrigerator mother” theory, painfully inaccurate ideas that had emerged in the 1940s and held on for far too long and suggested conditions like autism and schizophrenia were caused by a lack of maternal warmth. These theories had desperately needed revision, and the new research strategies and technologies that were emerging, things like genetic twin studies and brain imaging, gave us a path to debunk some of the most harmful ideas.
By the early 2000s and 2010s, this paradigm shift had taken strong root. Academics, clinicians, and the public were excitedly pointing to the biological bases for the conditions that had once been mistakenly attributed to everything from the devil to laziness to moral failings. People around the world were beginning to talk more openly about their mental health conditions, now emboldened by their apparent ties in their own brain wiring, something they couldn’t have been responsible for. We could finally make jokes about our silly brains not making enough serotonin and no longer hide our pill bottles deep in the recesses of our bathroom cabinets. The world seemed to be having a true mental health revolution, one that promised no more stigma for the millions of people suffering with mental health conditions.
Back in D.C., armed with this arsenal of biological evidence, I was excited to talk to lawmakers about how far we’d come in our understanding of eating disorders and of mental health more widely. How could we continue to dismiss something for which we now had stacks of biological journal articles and such pretty brain imaging? And the people I talked to that day – mostly staffers – nodded enthusiastically and seemed genuinely interested in all this fancy data.
But when the time came for the bill to move forward, it was dropped. It wasn’t that it was controversial. No one was arguing against it. For them, it didn’t matter so much if the illnesses were caused by Barbie or genetics. They just had other things more pressing, I heard, than worrying about a bunch of girls with eating disorders.
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The promise that the biological paradigm brought to the field of mental health has been slowly eroding in recent years, leaving sufferers and professionals alike demoralized. In a cruel irony, the actual result of mental illnesses having a biogenetic explanation has actually increased sigma in some significant ways. Research published in the last ten years shows that when genetic and neurological explanations are given for mental illness, individuals do tend to blame themselves less, hardly an insignificant benefit. However, tragically, these explanations are shown to make others want greater distance from the person, perceive them as potentially scary, and have less optimism for their recovery.
It seems that when we perceive someone with mental illness as suffering from something beyond their control, something more essential to their biological makeup, we find ourselves even more averse to them.
But perhaps the greatest and cruelest irony of the biological paradigm is this: it’s not only failing to make the world better and kinder for people suffering, but it may not be nearly as much of a reality as we’ve thought.
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Even with the best of intentions, we as humans really like our binaries and want to put things in them. This is certainly true when it comes to understanding the etiology of mental conditions, even among those of us who would readily espouse what researchers and clinicians call the biopsychosocial model. The idea of this model is that we are acknowledging that mental conditions have roots in our personal biologies, our psychologies, and our social worlds. Almost every clinician I know would say they use this model in their thinking. And yet I don’t know if there’s anyone I know who doesn’t lean more toward one of those three dimensions a little more heavily.
That’s to say that we all come to looking at mental health with our own biases, and perhaps it’s natural to want to take the latest research or social media trend and feel sure that we now finally have a solid understanding of where this all comes from.The reality, one that most of us know but struggle to actually hold, is that there is far more that we don’t know in this field than what we do know. And what we “know” is continuously shifting, becoming embedded in new context, being examined through new lenses.
So as this particular discussion continues, one that will challenge some of what we have held as reality, I urge us to recognize how unhelpful a binary (or even a triad) is here. Said more plainly: I’m going to tell you why a biogenetic model isn’t what we thought it was, but that’s not to say it’s all wrong. Said even more plainly: Don’t hate me.
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If you’re even remotely interested in these topics, and I’m supposing you are if you’re still reading, and if you have a social media feed, you are all too aware that trauma is having a moment. It’s a moment that I feel confident even the trauma studies folks, experts like Judith Herman and Bessel van der Kolk, could have never imagined seeing in their lifetimes.
Back in my own graduate learning and early days of practice, trauma was a chapter in a book, a topic generally covered on the syllabus, but often at the end of a course in the “special considerations” section. Oh yes, and there’s this trauma thing to think about.. Some of the things you are trying might not actually work because there are a handful of people who have PTSD. Don’t forget about them.
Those people, it was still assumed, were most the military veterans and, after some advocacy to finally recognize them, women who had experienced sexual assault. While it was foot-noted that trauma could involve repeated exposure to a stressor, we were at that point still trained to look for what at some point became known as the Big T-trauma, those seminal events that rocked someone’s world – car accidents, intimate partner violence, watching someone die.
The statistics would suggest that a not-insignificant number of people had experienced a seminal event like this, but it certainly wasn’t everyone. And those people could be served by the trauma specialists, the doctors and therapists trained in special protocols that hoped to reduce the impact of the trauma in twelve to sixteen sessions, usually by asking people to repeatedly recount what happened until the memories seemed to lose their edge.
Then came TikTok. Well, actually, then came a number of other things, including interest in more body-based interventions for mental health and books like The Body Keeps the Score, but arguably nothing would have gained any attention outside of the narrow bubble of clinicians without the virality of social media. And viral these ideas did become.
Within a couple of years, my own feed each day was filled with dozens of creators explaining that the way I couldn’t get started on the report I needed to write or the way I reacted to my son’s tantrum were actually trauma responses. I wasn’t sure if my own algorithm was particularly steeped given my job, but I soon realized that I was hardly the only one hearing daily about attachment styles and the vagus nerve. As the word trauma was seeping into our more general lexicon online, I quickly noticed the shift in IRL too. My friends and patients were referring to early traumas with a newfound recognition and even casualness.
There have been plenty of critiques of this phenomenon, both from well-intentioned mental health experts fearful of trauma losing its gravity and from agitated social conservatives seemingly fearful that everyone is claiming to have been victims. I won’t say that there isn’t worthy commentary out there, but my take, on the whole, is that any paradigm shift requires at least an initial phase of what feels extreme.
Should we be calling not getting into one’s top choice college trauma? We could debate it, but we might miss something important. And that is the fact that all the trauma talk was rewiring our brains in its own way, this time toward an openness to considering how our experiences, particularly our early experiences, have shaped our mental health.
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Gabor Mate is also having a moment. He’s an unlikely social media star given his advanced age of 80 years old, but his work has gained a voracious steam in recent years. In his soothing Hungarian accent, he explains on podcasts, reels, and countless YouTube videos why we’ve gotten mental health all wrong. His most recent book, The Myth of Normal, is a deep dive into these topics, highlighting how western culture not only ignores the impact of stress and trauma, but then perpetuates it.
Mate shares openly in the media about his own story of early abandonment, and it’s a powerful one. His grandparents were killed in Auschwitz and his mother, in an attempt to protect his safety, left him in the care of a stranger for five weeks when he was a year old. He describes being unable to look at her for several days upon their reunion, so wounded he was by this period of separation and perceived abandonment. Mate believes that the challenges in trust and the rage he can easily experience can be directly traced back to this early trauma.
His conceptualization of his own struggles aligns with much of what we know about attachment, memory, and enduring nature of relational wounding. One of the more meaningful aspects of his story, for me personally, is that parents can cause harm even when doing what is absolutely necessary, protective, or loving. It’s a reminder that we don’t get spared from trauma even with well-meaning caregivers.
Mate’s work as a physician led him to treating plenty of people just like him, ones who had early experiences of fear, loss, or invalidation, and who were later suffering with debilitating physical and mental health issues. He was particularly drawn to working with people with addiction, and this was where he truly formulated his ideas about trauma as the root of mental illness.
His perspectives are among the most hardline of trauma theorists, asserting essentially that there is no real biological basis for the vast majority of mental illness, at least not in the way that we typically talk about biology. He holds that this is true even for conditions that seem to have a strong base of evidence for neurological divergence from the norm, like ADHD. This is where some understandably struggle to get on board with Mate.
The nuance in his argument about a genetic role in mental health is that he asserts that a substantial portion of the population are born with genes that don’t predispose them specifically to certain conditions, like depression, but rather with genes that make them particularly sensitive to the outside environment. Mate says that people higher on the sensitivity spectrum are going to be more influenced than others by their surroundings, including their early caregiving and the tricky experiences they endure. This isn’t to say we aren’t all affected by our environment, as we absolutely are. But this is where, Mate believes, paths diverge. This is why two siblings, for instance, might be subject to many of the same experiences (though, to be sure, never all) and have very different long-term mental health outcomes.
Relatedly, two students in the same class may also end up with very different outcomes, not just as a function of their sensitivity, but also their birthdates. In an interesting study from the University of British Columbia, researchers examined the medication records of almost one million British Columbian children over eleven years. What they found was that children born in December were 39 percent more likely to be diagnosed with ADHD than their schoolmates born in January of the same year. The explanation for this is that (due to the local age/grade regulations), the December kids were almost a year younger than their January peers and in the same grade. That eleven-month gap in brain development, particularly executive functioning and emotion regulation, were interpreted by adults as symptoms of a disorder.
To be absolutely clear, I’m not personally suggesting that ADHD isn’t a real condition or that it doesn’t have genetic ties. What this research and others like it suggest to me is that it’s critical to understand the lens through which we are identifying and assessing symptoms. When we don’t, we risk interpreting feelings and behaviors as a function of a pathology when they may be better explained by developmental or cultural factors. This is, at least in part, how the healthcare system has ended up over-pathologizing poor people and people of color.
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And at the same time, the truth – shocking to some given how definitively we’ve come to discuss the biogenetic origins of mental health – is that we’ve not yet found a single gene that codes for a specific mental health condition. Not one, despite a lot of effort to find one by a lot of really smart people.
What we do have more of, rather, are gene sequences that we find associated with different symptom expressions. Let me explain with an example. There are two genes that are involved in how our cells get coded for the flow of calcium into our neurons. When someone has variation from the norm in these genes, it affects the brain circuitry that’s involved in processing our emotions, how well we can pay attention, and how well we think and remember. More people end up being diagnosed with conditions like bipolar disorder and major depression have variation in these genes than people who are not diagnosed with these conditions. To be fair, this is a far cry from saying those genes – or any specific others – cause bipolar or depression.
What we have here are more associations than causations. This is not to say that a gene doesn’t exist, but we haven’t identified it yet. What we have are some really interesting and important findings about the relationships between our genes and our mental processes. What we don’t have are definitive genetic causes.
One of the disorders where we see this tension play out and we tend to go quickly beyond the biogenetic evidence we have is obsessive compulsive disorder. Recently in the The Guardian, a mental health advocate, Rose Cartwright, who had literally written the book-turned-movie on her own OCD, wrote a mind-blowing think piece on how she has more recently learned how scant the actual evidence is for a model of OCD as an innate illness. She was shocked to talk with neuroscientists and other professionals who explained that psychiatric illnesses were not nearly as well understood or defined as the world seemed to think. Even Professor Allen Frances, one of the lead authors of the literal manual for diagnosis, the DSM, had been critical of diagnosis and said, “These concepts are virtually impossible to define precisely with bright lines at the boundaries.”
In the piece, Cartwright beautifully narrates her own journey of rethinking mental illness, including the reckoning and pain involved. She writes, “This felt like an attack on my identity, like I was being told my suffering wasn’t serious. If my thoughts weren’t illness, did that mean they were “me”? Did I want the shit in my head? Did I choose this? I would later come to understand that to question the medical model is not to question whether mental health problems exist: they are real and devastating. I would learn that, yes, there are brain changes that correlate with poor mental health, changes that entrench and compound distress. But that neuroscience is far from being able to understand these correlations, much less categorise them into discrete conditions, or explain why brains start to become disordered in the first place. Mental health far more complex and mysterious than any doctor had ever admitted.”
At the end of the day, the problem with mental health diagnosis is an issue of circular reasoning. We observe a bunch of symptoms and then put a label on it – let’s say generalized anxiety. At its core, that label is only that – a word – a series of letters – that we’ve used to describe something that we are seeing. But soon our minds treat that label as an explanation. We turn it from the abstract into the concrete. She seems to worry unnecessarily, we say, so she must have generalized anxiety. How do we know she has generalized anxiety? Because she worries unnecessarily. And round and round we go.
And we want these constructs to have a tangible basis, perhaps because being able to see something on a scan or under a microscope feels oddly reassuring. It makes it feel manageable, in a way. How do we fight the monsters we can’t see? The unfortunate reality is, of course, that concretizing these conditions hasn’t resulted in their elimination. Far from it. We have a global mental health crisis on our hands, one that’s giving no sign of slowing. And if the studies I mentioned before about how the biogenetic explanations of mental illness tend isolate people from others, we can expect that the loneliness and mental health epidemics will only increase as a result.
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It would be reasonable to wonder where all of this leaves us. If we lack the certainty in a biological model that we once longed for and if our diagnostic systems are in some ways just spiraling in on themselves, how do we ever get out of this mental health mess we’re in?
Any big paradigm shift is going to require something that humans never like, but particularly loathe these days: sitting in uncertainty. That’s partly where we are right now, in my view, as we try to coalesce all of what we know – and don’t know – about mental illness.
That said, I think we can hold on to a few important pieces of the puzzle here. One is that diagnosis, while circular to a degree and far from perfect, can still be a useful construct. To me, its utility comes in the sense-making it can offer. Even if there is no gene that explains my depression on its own, having a name and a way of talking about what I’m experiencing is significant. It’s shorthand for the way that I’m suffering, and while the shades of my own blue might be different than yours, it helps you know my experience better. Diagnosis also helps to guide research, and that research is still vitally important.
What’s exciting about this paradigm shift is that it necessitates an individualization that we haven’t had in our field in a long time, and perhaps ever. When I can no longer say, “Oh, you have ADHD. I see it right here on your lab tests. I know exactly why you have this condition and how it presents in your life,” then I have to start saying instead, “Tell me your story. Tell me your life.”
It also helps us to ask other important questions, like: How might environmental factors like social media, remote work, capitalism, the constant threat of sexual violence, weight stigma, disconnection from nature, a financial recession, anti-aging marketing, and so many more creating stress for us? How are we not built to endure this socio-political landscape? How are our lives out of step with our psyches?
When we release our attachment to a biologically predestined model, we also get the chance to explore revolutionary treatment approaches that rely not on the dampening or ignoring of symptoms but on actually resolving them. This looks like some of the modalities that you’re likely hearing more about in recent years, like EMDR, Internal Family Systems, and psychedelic-assisted therapies. While each of these has some unique mechanisms of action, of course, they all presuppose that each of us has an innate healing capacity, that we aren’t biologically broken.
As Dr. John Krystal, the head of psychiatry at Yale and one of the foremost thought-leaders on addiction and mental illness, explains when it comes to psychedelics, these treatment approaches restore the brain’s intrinsic capacity to build and maintain connection and healthy functioning. When he was doing his ground-breaking ketamine research back in the 1990s, he realized quickly that the brains of people with severe depression, for example, were not in fact fundamentally different from those without. It wasn’t about needing to go in and fix the brain; it was about removing the barriers that were blocking it from fixing itself.
Those barriers, as I see them, are both within us – as a result of the stuck points we’ve run into from our own adverse experiences and traumas – and outside of us – as a result of the very stressful and dysfunctional modern world we live in. And so our approach to mental health has to similarly be multi-dimensional.
We need good therapy. We need good novels. We need good sunlight and good sleep and less work and less war and less bigotry and better relationship skills and fewer commitments.
We also do need better policy and better funding, which is why I am saddened by the failure of that bill I was lobbying for all those years ago. Ironically, the bill itself was to fund prevention and early identification of eating disorders in schools by educating parents, teachers, and coaches. We knew that changing the outcomes for people suffering needed to be done as early as possible, that their important adults’ influence mattered. We knew that their environments mattered. I wish we could have seen beyond our own biological talking points.
