The Medical Tales That Shape Our Distress

Two modern myths—“chemical imbalance” and “gender identity”—have justified harmful treatments built on poor evidence.

Aug 26, 2025

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About the Author

Carrie Clark is a writer and researcher focusing on prescribed harm, sex and gender, liberalism and evidence based epistemology. She is the founder of Healix, a platform for people who have been harmed by prescribed psychiatric medications. Healix provides advocacy services to people experiencing adverse and withdrawal effects, and campaigns to prevent prescribed psychiatric drug harm.

Many of us are now wearily familiar with the term “lived experience.” In debates about gender, race, and identity, appeals to lived experience often substitute personal anecdote for systematic evidence. Such accounts are nearly impossible to test or refute, making them a convenient rhetorical tool for those who suspect their argument may not withstand objective scrutiny.

A clear example is the transgender individual who claims that so-called “gender-affirming” care has been lifesaving. While this may be true for that person, systematic evidence increasingly shows poor outcomes for the average person who medically transitions. Nevertheless, lived-experience narratives are often deployed to shut down evidence-based debate on contentious issues.

That is not my aim here. Rather, this essay explores the parallels I see between the questionable research practices, myths, and half-truths used to promote “gender-affirming” care, and those used to assert the safety and efficacy of antidepressants. But it is also, unavoidably, about my own lived experience. Were it not for the admittedly anecdotal, unverifiable events I am about to recount, I might never have been motivated to investigate the shaky evidence supporting antidepressant use, and thus would never have noticed the parallels with the case for “gender-affirming” care in the first place.

I was diagnosed with Acute Antidepressant Discontinuation Syndrome (AADS) in 2023, after attempting to stop taking the antidepressant I had been prescribed 20 years earlier, at age 15. It was an incredibly frightening experience. My case was reported in The Times, which noted that antidepressant withdrawal is far more common than many realize, yet still poorly understood and rarely acknowledged. Current deprescribing guidelines recommend tapering over a few weeks or months, but evidence increasingly suggests that long-term users often need to reduce their dose far more gradually to avoid severe withdrawal. Withdrawal is frequently misdiagnosed as relapse or as the onset of an entirely new condition, with doctors often insisting that antidepressants cannot cause severe or prolonged withdrawal. While some people appear to stop without difficulty, there is currently no way to predict who will or will not struggle. Despite this uncertainty, a 2019 survey found that only 2 percent of antidepressant users recalled being warned about dependence or withdrawal at the time of prescription.

This was certainly true in my case. I was assured that antidepressants were safe, effective, and easy to stop. Yet when I tapered off in 2023, I was overwhelmed by a bizarre array of symptoms unlike anything I had ever experienced: vertigo, visual distortions, pins and needles, tinnitus, burning skin, extreme sensitivity to light and temperature, and—most distressingly—an agonising inner restlessness that made it unbearable to stay still. I was completely unable to sleep, sit, or rest while I had this symptom, which I now know is called akathisia, which can occur when discontinuing most psychiatric medications and is strongly associated with suicidality. During the nine months I endured akathisia, suicide came to seem like an entirely rational choice. The symptoms of AADS were harrowing, and it was deeply unsettling to realize that I had become dependent on a drug I had always been told was safe, effective, and easy to discontinue.

So you can imagine my surprise when I came across a new systematic review of antidepressant withdrawal, published just last month. The authors—psychiatrist Dr. Sameer Jauhar and colleagues—claim that their review of randomized control trials proves that AADS is virtually non-existent, and that withdrawal symptoms are reliably mild, short-lived, and resolved within a few weeks at most. They even advise clinicians against disclosing the risks of physical dependence and withdrawal when prescribing antidepressants, lest patients become unduly alarmed and decline the medication. What was I to make of this seemingly evidence-based finding that stood in such stark opposition to my own lived experience? After examining Jauhar’s research in detail, my immediate—and rather unexpected—reaction was a renewed empathy for the experiences of detransitioners.

Just as with research claiming that detransition is vanishingly rare, Jauhar’s findings were technically correct but utterly irrelevant to the real-world experience of patients. Clinical guidelines recommend taking antidepressants for a minimum of six months. In the UK, 8.7 million people are currently on these drugs, and half have been taking them for more than two years. Of those, 3.8 million—myself included—have been on them for over five years. Existing research has shown that withdrawal risk increases dramatically with duration of use, with the most severe and protracted cases occurring in patients who have taken the drugs for two years or more. Yet Jauhar’s review examined only short-term studies lasting just 8–12 weeks. Only two longer-term studies were included, neither lasting more than 26 weeks; one was ultimately excluded from the final analysis, and the other examined agomelatine, an antidepressant known not to cause dependence or withdrawal.

Detransitioners know this pattern all too well. Transition regret is understood to take between 7 and 11 years to manifest, yet the claim that detransition is rare—and therefore that “gender-affirming” care is safe—is based almost entirely on short-term studies virtually guaranteed to miss the true rate of regret. And the parallels between the experiences of detransitioners and those of people like me—patients harmed by psychiatric drugs who have joined what is sometimes called the “prescribed harm community”—do not end there. Inaccurate medical guidelines that perpetuate harmful practices? Check. Medical gaslighting of harmed patients? Check. Uncertain benefits with no reliable way to predict who will be harmed? Check. Organized efforts to discredit whistleblowers and silence patient testimony? Check. A systemic failure to secure properly informed consent before prescribing life-altering treatments? Check.

I do not make this comparison to diminish the experiences of detransitioners, nor am I claiming that psychiatric medications have caused me as much direct harm as puberty blockers, cross-sex hormones, or sex-reassignment surgeries have caused them. Nonetheless, it is essential to recognize the commonalities between these two forms of medical harm, particularly given the growing push by some critics of gender medicine to steer gender-distressed individuals toward conventional psychiatric treatments that are, in many respects, no safer, more effective, or more evidence-based than “gender-affirming” care.

Both treatment pathways involve misleading patients about the nature of their condition, overstating the benefits of invasive medical interventions, and downplaying—or outright denying—the risks. The remainder of this essay will make these parallels explicit, drawing on both lived experience and evidence-based analysis to argue that both “gender-affirming” care and the overprescription of antidepressants ought to be recognized as medical scandals.

Misleading People About the Causes of Their Distress

For people with a psychiatric diagnosis, discovering that our mental health problems are not caused by an innate “chemical imbalance” in the brain can be as disorienting as a detransitioner realizing that “gender identity” theory is not actually supported by evidence. In both cases, it undermines the very framework we were taught to use to understand our most distressing feelings.

When I was prescribed antidepressants at 15, I was told I had a lifelong, incurable medical condition caused by a chemical imbalance in my brain—something I would need to manage with psychiatric medication for the rest of my life, much as a diabetic must take insulin. The view that mental health conditions are precisely analogous to physical health problems has been ever-present in my interactions with mental health professionals over the past two decades. Any doubts I expressed about taking psychiatric medication were always rejected by reference to this analogy. After all, someone with diabetes wouldn’t refuse to take insulin, would they?

What I did not expect was to one day learn how little evidence exists to support the chemical-imbalance theory of mental illness. I had always assumed that, while the explanation might be simplified for patients, there must be at least some solid basis for it. Yet despite decades of research, the serotonin theory of depression and the dopamine theory of schizophrenia have never been proven. A 2023 umbrella review led by Professor Joanna Moncrieff of University College London examined studies testing the serotonin theory of depression and concluded:

[T]he research consisted of small studies that either showed no link between serotonin and depression or yielded inconsistent results. Moreover, few of them accounted for the likely impact of antidepressants.

Controlling for the effects of antidepressants is important, because these drugs predictably alter brain chemistry in ways unrelated to any underlying condition. When such changes are misinterpreted as evidence of a pre-existing imbalance, the drug’s side effects can be mistaken for proof of the very theory used to justify the prescription.

Indeed, much early research on serotonin and dopamine theories fell into exactly this trap. Neither theory began with the discovery of an actual chemical imbalance in patients with depression or schizophrenia. Instead, researchers inferred the existence of such an imbalance based on the observed effects of psychiatric drugs and their presumed efficacy (more on that later). Because antipsychotics alter dopamine sensitivity and were believed to reduce schizophrenia symptoms, the dopamine theory posited that schizophrenia must be caused by abnormalities in the dopamine-system. Likewise, because antidepressants were thought to treat depression by altering serotonin sensitivity, the serotonin theory posited that depression must be caused by abnormalities in the serotonin system.

Both theories, then, began by reasoning backwards, and making a series of unwarranted assumptions in the process. The fact that psychiatric medications alter sensitivity to certain brain chemicals does not, by itself, prove that symptoms are caused by a pre-existing imbalance of those chemicals. Nor does the fact that antipsychotics and antidepressants produce characteristic mood changes. Effects such as sedation, stimulation, and emotional blunting may indeed be useful in alleviating distress, but these drugs exert such effects whether or not the patient has a diagnosable mental health condition.

As Moncrieff explains, much of the early research collapses under closer scrutiny:

Findings of increased D2-receptor density in the brains of people diagnosed with schizophrenia were first reported from post-mortem studies in the 1970s. At first these findings were regarded as evidence of a pre-existing dopamine abnormality in the brains of people with schizophrenia…However, the patients whose brains were examined had been taking antipsychotic drugs for long periods before they died. No one asked the obvious question of whether the observed effects were due to drug treatment, even though it had already been established that antipsychotic drugs increase brain concentrations of D2-receptors in animal studies. Subsequent post-mortem studies found that the abnormalities of dopamine receptors were entirely attributable to the effects of drugs…Therefore research has not shown any consistent abnormalities in dopamine receptors in schizophrenia per se. It has demonstrated that neuroleptic drugs…cause a compensatory increase in the number and density of these receptors in the brain.

Perhaps the most compelling refutation of the “chemical imbalance” theory is that laboratory tests of serotonin and dopamine levels have never been used to diagnose depression or schizophrenia, nor to determine the “correct” dosage of medication needed to restore balance. The reason is simple: these theories have no predictive value. Objective measurements of serotonin or dopamine cannot determine whether someone has depression or schizophrenia, nor can they predict who will benefit from antidepressants or antipsychotics.

Detransitioners were often misled by their doctors in a strikingly similar way. They were told their distress was caused by an innate mismatch between their sexed bodies and their inner “gender identities,” and—much like me—they were assured this was a lifelong condition that would worsen, perhaps even leading to suicide, without medical intervention. Instead of “chemical imbalance” theory, the field of so-called “gender-affirming” care produced the equally discredited “brain sex” theory.

The brain sex theory posits that transgender individuals have brains that exhibit a “cross-sex shift”—more closely resembling the neuroanatomy typical of the sex they identify with rather than their biological sex. These findings are presented as proof of an inborn, biological gender identity and are frequently invoked to justify medical transition. But as investigative journalist Christina Buttons has shown, these studies consistently fail to control for sexual orientation—and when they do, the purported cross-sex shift vanishes:

A clear pattern emerges when comparing these and similar studies: the magnitude of the cross-sex shift reported in trans-identified individuals’ brains correlates with the proportion of homosexuals in the sample. For example, in Simon et al.’s study, all transgender participants were homosexual, potentially amplifying participants’ sex-atypical neuroanatomical features. In contrast, Luders et al.’s cohort had a much lower proportion of homosexual participants, coinciding with null findings overall regarding brain feminization. Savic and Arver’s rigorous control for sexual orientation further demonstrates that some neuroanatomical differences previously attributed to gender dysphoria likely reflect—or are confounded by—sexual orientation-related brain variations.

Nonetheless, people experiencing gender-related distress are routinely encouraged to view themselves as having an innate, lifelong medical condition of biological origin. As Buttons has documented, this false narrative is promoted not only by clinicians, but also by media outlets, activists, popular television programs, and transgender individuals themselves.

So what does cause conditions like depression and gender-related distress? After completing a PhD aimed at identifying a biochemical basis for depression, University College London psychiatric researcher Mark Horowitz reached the following conclusion:

Depression is related to the number of stressful life events you experience in any given period of time…The relationship between the number of stressful life events in your life and your risk of being depressed are the steepest relationships I’ve ever seen in psychiatry. If you have none of those events in your life you have a very small chance of being depressed. If you have lots of them you have a very high chance of being depressed.

Similarly, research shows that individuals with gender-related distress are disproportionately likely to have experienced adverse life events. For example, young people treated at the NHS Gender Identity Development Service were more likely to be in foster care, to have experienced childhood neglect or sexual abuse, or to have a parent with a mental health or substance abuse problem.

Of course, adverse experiences do not guarantee that someone will develop depression or gender-related distress. Human resilience is extraordinary, and the vast majority of people recover spontaneously after experiencing traumatic events. But far from being evidence of an innate biological defect within the individual, both conditions appear to be part of the natural human spectrum of responses to adversity. They are ways of manifesting and communicating distress that, while deeply real, are shaped by life circumstances rather than immutable brain chemistry or “gender identity.”

For both detransitioners and members of the prescribed-harm community, accepting the narrative that we suffered from an innate medical condition fundamentally altered the course of our lives. It shaped our beliefs about recovery and led us to embrace risky medical treatments we might otherwise have avoided. As Moncrieff writes—on a point that applies as much to gender-related distress as to depression:

How we think about depression is not just an academic or philosophical exercise. It profoundly effects how we understand and cope with our own emotions, and how we respond to other people’s emotions.

The consequences of this mindset are easy to see. Consider the intense fear often expressed by people with gender-related distress whenever any restriction on “gender-affirming” care is proposed. Many have been persuaded to believe they have an innate, biological disease that will drive them to suicide without medical treatment. Under that belief system, it is not irrational to feel terrified when access to such treatment is withdrawn or threatened.

The same dynamic is documented in Moncrieff’s work on depression. People who believe that depression is caused by a chemical imbalance tend to be more pessimistic about recovery, show poorer long-term outcomes, and are reluctant to taper off antidepressants, even when those drugs are no longer clinically indicated. And again, this reaction is entirely rational if you have been convinced that you suffer from an incurable biological condition that can only be managed through ongoing medical intervention.

Misrepresenting the Risks and Benefits of Treatment

The term iatrogenic refers to harm caused by medical treatment itself. Iatrogenic injury is a shared experience for both detransitioners and members of the prescribed-harm community. We followed our doctors’ advice, accepting medical interventions we were told were safe, effective, and evidence-based. Not only did these treatments fail to resolve our distress, but they also caused lasting damage to our physical and mental health.

Like many detransitioners, I only began scrutinizing the evidence on the risks and benefits of antidepressants after I had been harmed by them. In hindsight, that may seem foolish, but I trusted my doctor’s judgment. When I eventually realized how little evidence supports the claim that antidepressants are safe and effective, I felt deeply betrayed by the medical profession. Detransitioners often express the same sense of betrayal. A survey by researcher Lisa Littman found that 76 percent did not inform their prescribing clinician that they had been harmed by medical transition. After all, why return to the very professional whose guidance destroyed your health and wellbeing? I, for one, have no desire to see another psychiatrist ever again.

Balancing the risks and benefits of any medical intervention is always a tricky business, but the rationale for treatment collapses when the condition in question already has a high rate of spontaneous recovery. This is a critical fact typically withheld from both gender-distressed individuals and those with depression—and the introduction of medical interventions may, in fact, have made outcomes worse.

Before the advent of medical transition procedures, roughly 85 percent of gender-distressed young people saw their symptoms resolve naturally after puberty. Under a non-medical “watchful waiting” approach, the prognosis for spontaneous recovery was strong. But with the rise of “gender-affirming” care, the trajectory has shifted dramatically: nearly 100 percent of gender-distressed young people placed on puberty blockers now proceed to sterilizing cross-sex hormones. Today, natural recovery is far less likely, and irreversible treatment far more so.

Depression, too, was historically recognized as a condition with high rates of natural remission. In Anatomy of an Epidemic, medical journalist Robert Whitaker cites multiple statements from National Institute of Mental Health (NIMH) officials in the 1960s and 1970s—before the widespread use of antidepressants—acknowledging this fact:

In the treatment of depression one always has as an ally the fact that most depressions terminate in spontaneous remission. This means that in many cases regardless of what one does the patient eventually will begin to get better. Nathan Kline, NIMH official, 1964
[Most depressive episodes] will run their course and terminate with virtually complete recovery without specific intervention. Dean Schuyler, head of the NIMH depression section, 1974
Depression is, on the whole, one of the psychiatric conditions with the best prognosis for recovery with or without treatment. Jonathan Cole, head of the NIMH psychopharmacology service centre, 1964

As with gender-distressed youth—whose symptoms may only resolve after several years of puberty—recovery from depression can be slow and arduous. Yet in 1974, Dean Schuyler reported a spontaneous recovery rate for depression of about 50 percent within four months. More recent data are equally encouraging. Moncrieff cites two studies finding recovery rates of 85 percent and 86 percent for untreated depression after one and two years, respectively. Large population-based surveys report a median time to recovery of just three months.

Like gender-related distress, then, depression has long been a condition with high natural recovery rates. So why is this good news so rarely communicated to patients weighing the risks and benefits of undergoing medical transition or taking antidepressants? One might assume it’s because both treatments have been shown to be so remarkably effective that they dramatically improve on these already high natural recovery rates. Unfortunately, that is not the case.

The evidence that “gender-affirming” care—puberty blockers, cross-sex hormones, and sex-reassignment surgeries—is not an effective treatment for gender-related distress is now so well-established that it hardly needs repeating. This is an area of medicine where randomized control trials (RCTs) are effectively impossible, as blinding is unfeasible when the intervention produces obvious physical changes. As a result, there is no RCT evidence showing that “gender-affirming” care is more effective at relieving distress than a placebo. In fact, uncontrolled studies suggest that sex-reassignment surgery is associated with higher risks of depression, anxiety, suicidality, and substance abuse—hardly the outcomes one would expect from a truly effective medical treatment.

By contrast, antidepressants do at least have systematic reviews of RCTs showing they are slightly more effective than placebo in reducing depressive symptoms. But the effect size is minuscule. As Moncrieff notes, meta-analyses using the 52-point Hamilton Depression Rating Scale (HDRS) find an average difference of two points or less between placebo and antidepressant groups. Clinical guidelines suggest that a change of seven or eight points is needed to indicate even “mild improvement,” while a change of three points or less equates to “no change.” As Moncrieff writes, “a difference of 2 points does not even register as a difference on the Clinical Global Impressions Scale.”

Given these negligible treatment effects, how have antidepressants and “gender-affirming” care come to be so widely promoted as safe and effective? Critics of gender medicine will recognise the pattern: the case for both has been built on a foundation of dubious research practices designed to exaggerate benefits and obscure harms. In gender medicine, the original Dutch Protocol and the NHS Early Intervention Study downplayed negative results, ignored the implications of high dropout rates, inverted validated survey findings, and inflated positive outcomes. As Moncrieff shows, similarly dubious methods have been used to overstate the benefits of antidepressants.

One telling example comes from the Sequenced Treatment Alternatives to Relieve Depression (STAR-D) study, in which participants were randomised to receive different therapies while taking antidepressants. The researchers abandoned the validated Hamilton Depression Rating Scale (HDRS) as their primary outcome measure, replacing it with an unvalidated tool of their own creation—thereby inflating apparent benefits. Psychologist Ed Pigott’s reanalysis of STAR-D data found that only 46 percent of the 4,041 participants improved at any point, and a mere 2.7 percent (108 people) were still in the study and had recovered at the 12-month mark. Pigott also discovered that STAR-D counted as “recovered” some participants who had no depressive symptoms at the start of the study, and excluded early dropouts—likely those who experienced severe side effects—from the final analysis.

As Professor Michael Biggs has shown, the Dutch research team used similar sleight-of-hand to inflate the benefits of “gender-affirming” care. They excluded from their final results patients who had suffered serious adverse effects, including one who died as a direct consequence of treatment. This patient, placed on puberty blockers, lacked sufficient penile tissue for conventional vaginoplasty and instead underwent a high-risk bowel-based procedure, dying of sepsis shortly after. He was one of 15 patients—out of an original sample of just 70—whose outcomes the Dutch team failed to report. Such omissions are not rare; both the gender medicine and antidepressant literatures are littered with examples of poor research practice and selective reporting.

The trivial treatment effects matter because neither intervention is risk-free. Puberty blockers, cross-sex hormones, and sex-reassignment surgeries carry well-documented risks, as has been amply demonstrated by numerous systematic reviews. Puberty blockers do not improve mental health or reduce gender dysphoria but are linked to cognitive impairment and reduced bone density. Cross-sex hormones cause infertility, irreversible reproductive damage, and increased risks of cardiovascular disease, certain cancers, and stroke. Sex-reassignment surgeries can result in sexual dysfunction, incontinence, and a host of other surgical complications, and are associated with a significantly increased risk of suicidality. These risks are especially difficult to justify given the high natural recovery rates for gender-related distress.

Antidepressants, likewise, have an extensive side-effect profile. In a minority of users—particularly those under 25—they can trigger paradoxical and dangerous effects: worsening depression, new-onset psychosis, sudden and intense suicidal ideation, or impulsive and violent behavior. A 2006 meta-analysis found that children on antidepressants were twice as likely as their placebo-treated peers to develop suicidal thoughts and behaviors. Andrew Mosholder, the FDA drug safety specialist who first identified this doubling of suicidality, was blocked by his agency from publishing his findings. Both pharmaceutical companies and the FDA have faced accusations of downplaying antidepressant risks to protect the psychiatric drug market. While these extreme adverse events affect a minority, they remain under-researched and are seldom disclosed to patients before prescribing.

More common side effects of antidepressants include—but are not limited to—emotional blunting, sedation or insomnia, weight gain, nausea, agitation, cognitive decline, dry mouth, metabolic disorders, genital numbness, and sexual dysfunction. For some, these effects are mild and short-lived; for others, they can be chronic and debilitating, persisting long after the drug is discontinued. It is increasingly recognized that Post-SSRI Sexual Dysfunction (PSSD) can last for years and may occur even after brief use. Some people with PSSD also experience anhedonia—an inability to feel pleasant emotions—further compounding the impact on quality of life. Although PSSD remains under-researched, a 2024 survey estimated that as many as 13.2 percent of antidepressant users may develop the condition.

Intriguingly, there may even be a link between the numbing effects of antidepressants and the development of gender-related distress. Taylor Murphy, prescribed antidepressants as a teenager, identified as transgender for 13 years before detransitioning. She believes the drugs inhibited her sexual development and induced a dissociation from her body, feelings she misinterpreted as signs of being transgender. Her gender-related distress resolved entirely after discontinuing the medication.

Given their minimal treatment effects and significant side-effect profile, do antidepressants at least deliver substantially better outcomes than no treatment at all? It doesn’t look like it. Uncontrolled studies comparing medicated and unmedicated individuals find better outcomes for those who do not take antidepressants—even after controlling for initial severity of depression. Depressive episodes tend to last longer in those taking antidepressants, and medicated individuals are less likely to return to work following sickness absence.

The truth is, we know remarkably little about the long-term outcomes of antidepressant use—and the same is true for “gender-affirming” care. In both cases, the medical profession has largely failed to follow up with patients over meaningful timeframes. A 2018 University of Oxford meta-analysis found that only 2 percent of antidepressant trials lasted longer than three months, with three-quarters running just eight weeks or less. Yet, as mentioned earlier, the NHS still advises patients to take antidepressants for at least six months, and 3.8 million people in the UK have been on them for more than five years—despite the absence of long-term safety or efficacy data.

Duration of use matters enormously, because the longer someone takes an antidepressant, the harder it becomes to stop. A recent survey by Horowitz et al. found that:

In fully adjusted models those using antidepressants for over 24-months prior to stopping were more likely to experience a withdrawal syndrome…report severe withdrawal effects…report longer lasting symptoms…and be less likely to be able to stop than those using for less than six-months.

Like me, 40 percent of those surveyed experienced withdrawal symptoms so severe that they were forced to reinstate the drug. Fortunately, Horowitz has developed a method known as “hyperbolic tapering,” which allows long-term users to discontinue medication safely over an extended period. Yet clinical practice has been slow to adapt; most doctors still recommend a rapid taper, even for long-term patients for whom it will very likely cause severe withdrawal.

The scale of the problem is staggering. If 40 percent of long-term users cannot stop antidepressants safely under current guidelines, that could mean as many as 1.5 million people in the UK are physically dependent on these drugs. If supply chain disruptions ever caused shortages, the consequences would be catastrophic.

At the risk of leaning too heavily on my lived experience, I feel compelled to share a personal reason why I am especially shocked that patients are not warned about the risks of antidepressant dependence and withdrawal before starting these drugs. In line with the clinically insignificant effects described by Moncrieff, I never experienced any substantial benefit from antidepressants. They made me somewhat numb, somewhat detached from my feelings—but withdrawal was agony. It struck like a thunderbolt, shattering the stability of my otherwise happy and stable life.

While most of my symptoms eased after I reinstated the drug, some appear permanent. I now live with withdrawal-induced tinnitus: a ceaseless ringing in my ears that feels like a tiny violin bow scraping my brain stem. I have been diagnosed and treated for post-traumatic stress disorder brought on entirely by the existential horrors of withdrawal. There were moments when I truly believed I was going to die.

Discovering that your doctor failed to warn you of a life-altering risk is devastating. It destroys trust in the medical profession. I never consented to the risk of withdrawal—because I was never told it was possible. This has given me a renewed empathy for detransitioners, many of whom were also denied crucial information about the serious adverse effects of “gender-affirming” care.

Take the case of detransitioner Prisha Mosley. After undergoing a “gender-affirming” double mastectomy, she became pregnant. Her doctors had not warned her that mastectomy does not remove all the milk ducts in the female chest and that, during pregnancy, breast milk would painfully build up in the chest wall. She was in such excruciating pain that she could barely hold her newborn son. She has spoken at length about the trauma of this experience and the loss of faith in medical professionals that followed. She, too, had not consented—because she had not been informed.

If “gender-affirming” care or antidepressants produced dramatic, lasting improvements in functioning, one could at least argue about whether such risks might be worth it. But the evidence does not support any strong long-term benefit for either. People deserve full, honest disclosure of the risks involved, and the high probability that—given the natural recovery rates—neither treatment will meaningfully improve their lives.

Medical Gaslighting and Attacks on Whistleblowers

The most striking parallel I see between the experiences of detransitioners and members of the prescribed-harm community is what happens when we try to speak publicly about the medical harm we’ve experienced: we are often disbelieved, dismissed, or accused of endangering vulnerable people. Disturbingly, psychiatrists and providers of “gender-affirming” care often lead the way in pouring scorn on harmed patients. Medical whistleblowers who raise doubts about either treatment are routinely attacked, their character impugned and professional integrity questioned. Meanwhile, individuals who feel they have benefited from these interventions can respond with hostility, perceiving that stories of harm threaten the validity of their own choices.

Many readers will be familiar with the hostility detransitioners encounter when sharing their stories. Detransitioner Ritchie Herron, who regretted his sex-reassignment surgery the moment he awoke from it, described in an article last year how his doctors flatly denied his feelings:

I told them that I thought I had regret and they told me that I didn’t. Instead they said I had OCD and that what I was feeling was all part of my OCD…All I really wanted was an acknowledgement that I’d made this huge mistake, but no one would let me say that.

Others have been told they are merely entering a new phase of their “gender journey.” Gender GP, a UK clinic offering “gender-affirming” care, states on its website that detransition is “part of a much larger, diverse set of gender experiences.” Johanna Olson-Kennedy, a physician and leading proponent of such treatments, has even downplayed regret over double mastectomies by noting that detransitioned women can just get breast implants later: “Here’s the other thing about chest surgery. If you want breasts at a later point in your life, you can go and get them!” These kinds of minimizations compound the suffering of those already grappling with irreversible harm.

Members of the prescribed-harm community face similar dismissal. Clinical indifference to the suffering caused by psychiatric drug withdrawal is rooted in a long-standing failure to distinguish between withdrawal symptoms and relapse of the underlying condition. In fact, the predictable withdrawal syndrome triggered by discontinuing antidepressants has often been reframed in the medical literature as evidence of the drugs’ supposed “relapse prevention” properties. Even when withdrawal symptoms bear no resemblance to a patient’s original condition, doctors frequently interpret them as proof that the medication is essential to keep the patient from “relapsing.”

Horowitz compares this to telling someone they should keep smoking because they become irritable and anxious when they quit. Irritability and anxiety in that case are clearly signs of nicotine withdrawal—not proof that smoking is treating an innate nicotine deficiency.

Psychiatrist and former FDA specialist in psychiatric drug safety, Josef Witt-Doerring, has shown how the design of antidepressant discontinuation trials enables the widespread medical gaslighting of patients in withdrawal. These trials are structured in a way that virtually guarantees withdrawal will be mistaken for “relapse”—just as studies reporting low rates of detransition are designed in ways that cannot capture true regret rates.

In a typical antidepressant discontinuation trial, participants are split randomly into two groups. The continuation group remains on their medication, while the discontinuation group is either abruptly switched to a placebo or rapidly tapered off the drug before receiving an inert tablet. The outcomes of both groups are then compared. As Horowitz et al. summarized in a 2022 paper:

In these discontinuation studies people have their antidepressants stopped abruptly, or rapidly, making withdrawal symptoms very likely, and little effort is made to measure withdrawal symptoms or distinguish them from relapse. We conclude that there is currently no robust evidence for the relapse prevention properties of antidepressants.

My own doctors were certain there was no way my symptoms could be caused by stopping antidepressants. They accepted the conventional wisdom that withdrawal is mild, self-limiting, and resolved within a few weeks. Yet my symptoms were so severe—and so completely unlike anything I had experienced before—that clinicians concluded I must be suffering from the onset of an entirely new condition. Over nine months, I was misdiagnosed three times: first with new-onset panic attacks, then migraine, and finally Functional Neurological Disorder. I underwent blood tests, MRI scans, blood pressure monitoring, and neurological evaluations—all while my actual problem remained unrecognized.

I did not reinstate my antidepressant because my doctor recommended it; I did so out of sheer desperation, hoping it might bring relief from my unrelenting symptoms. Only when I gradually improved over the next six weeks did my GP realize what had truly been happening. I was officially diagnosed with Acute Antidepressant Discontinuation Syndrome (AADS), and—to her credit—she has since used my case to educate herself on safe deprescribing practices.

Others in the prescribed-harm community have not been so fortunate. Withdrawal symptoms are often misdiagnosed as chronic fatigue syndrome, narcolepsy, health anxiety, or dismissed entirely as “psychosomatic” or “medically unexplained.” Worst of all, withdrawal can be mistaken for the onset of a new psychiatric disorder, leading to prescriptions for additional dependency-forming medications, each capable of producing its own withdrawal syndrome upon cessation. Patients caught in this polypharmacy doom loop can end up dependent on multiple unnecessary psychiatric drugs, while the true cause of their symptoms—withdrawal—remains unidentified and untreated.

This dynamic mirrors the way gender-distressed young people are often funneled toward increasingly invasive medical transition procedures, while the underlying causes of their distress remain unexamined. When puberty blockers fail to alleviate gender-related distress, this is typically framed as evidence that cross-sex hormones are needed; when those fail, the “solution” is assumed to be sex-reassignment surgery. A 2022 survey found that 70 percent of detransitioners stopped transitioning after realizing their distress stemmed from deeper issues—such as trauma, homophobia, or bullying—that clinicians had overlooked in their rush to recommend medical interventions. Many report reaching the end of the medical transition pathway, having made irreversible changes to their bodies, only to discover—too late—that their problems were never treatable with hormones or surgery.

For both detransitioners and members of the prescribed-harm community, this form of medical gaslighting can be devastating. Given the lack of long-term outcome data, our lived experiences are easily dismissed as mere anecdotes or statistical outliers. Worse still, even whistleblowers with impeccable credentials are often vilified for raising concerns about “gender-affirming” care or the lack of informed consent in antidepressant prescribing.

American gender clinics have become especially adept at demonizing and discrediting medical professionals who question the safety of “gender-affirming” care. Jamie Reed worked at the Washington University Transgender Centre (WUTC) in Missouri for four years before becoming a whistleblower. She observed that medical transition often failed to improve the well-being of the vulnerable young people she treated, and that WUTC was not adequately informing patients or families about the risks. In 2022, her employer told her to “Get on board, or get out,” dismissing her ethical concerns as “defensiveness and hostility.”

Similarly, surgical resident Eithan Haim exposed Texas Children’s Hospital in 2023 for continuing to provide “gender-affirming” treatments to minors despite having publicly pledged to stop in 2022, after the Texas attorney general deemed the procedures unsafe. Federal prosecutors attempted to charge Haim with illegally disclosing medical data, only dropping these baseless charges in 2025.

Psychiatrists who raise concerns about overprescription of psychiatric drugs face similarly groundless attacks from defensive colleagues. Mark Horowitz is a notable case because his critique draws on both “lived experience” and evidence-based expertise. Once convinced that a “chemical imbalance” underlies mental illness—so much so that he dedicated his PhD to finding the biochemical cause of depression—Horowitz began taking antidepressants as an anxious trainee psychiatrist. But when he went into severe withdrawal after discontinuing the drug, he realized the official guidelines he had been trained to follow were in fact making some patients seriously ill. He has since devoted his career to developing evidence-based deprescribing protocols and helping patients safely stop their psychiatric medications.

Horowitz—an accomplished science communicator who is not campaigning to ban psychiatric medications—is nonetheless treated by some colleagues as if he were intent on harming patients. Jauhar, the author of the flawed withdrawal review cited in the introduction, has been one of his most persistent (if inept) critics. In response to Horowitz’s evidence-based critiques of that review, Jauhar and his supporters have accused him of fostering “polarization,” and of being “abusive” and “bullying.” Horowitz has replied:

I and colleagues have been repeatedly called anti-drug ideologues. I do not think pointing out that short-term trials does [sic] not extrapolate to long-term use constitutes a particularly ideological position.

Jauhar also spearheaded public attacks on the umbrella review by Moncrieff and Horowitz that found no evidence for the serotonin theory of depression. Ironically—given the questionable research methods in his own withdrawal review—Jauhar accused them of data manipulation and poor research practice, claiming they were misleading the public. Moncrieff’s book Chemically Imbalanced: The Making and Unmaking of the Serotonin Myth contains a detailed refutation of these criticisms, as do a persuasive blog post by Horowitz and a jointly authored article in Nature. Nonetheless, Jauhar has continued to recycle what Moncrieff calls “inconsequential and contradictory” arguments, even three years after the umbrella review’s publication.

Why are so many mainstream psychiatrists reluctant to accept evidence that current professional practice is unsound and actively harming patients? Why do some, like Jauhar, even argue that patients should not be fully informed about issues such as dependence and withdrawal? Perhaps—like certain providers of “gender-affirming” care—they fear confronting the possibility that they have harmed patients under their care. Another shared feature of both fields is the tendency to frame ethical, evidence-based critiques as “bigoted,” “transphobic,” “stigmatizing,” or otherwise dangerous to patients.

These accusations often come from people who believe they have benefited from the treatment in question—whether “gender-affirming” care or antidepressants. Moncrieff recalls some of the public response to her umbrella review of serotonin:

Other people were angry with me…Had I not considered how publishing our research would upset millions of people, one emailer asked me, adding a sarcastic ‘congrats’? Another felt our findings could be ‘extremely dangerous’ and one suggested we were causing people distress for no reason…Some people felt the research undermined their choice to take medication, and this filled them with fear and anxiety.

Likewise, many currently trans-identified individuals appear to feel threatened by detransitioners’ stories and attempt to undermine or discredit their accounts of harm. Trans-identified commentator Brianna Wu, for instance, has called for stricter gatekeeping around “gender-affirming” care, yet routinely dismisses the harm reported by detransitioners. Maia Poet detransitioned after identifying as a transgender man and binding her breasts for 12 years. Of Poet, Wu wrote:

Literally never medicalized transition with testosterone, lied about it, misleads the public. Has made a career out of trying to dismantle health care for actual trans people. This is someone who gets attention and money for lying about being trans

Speaking about Cristina Hineman—a detransitioner suing Planned Parenthood for prescribing her testosterone after almost no assessment—Wu stated: “I think she should take responsibility…This woman is an adult and made her choices.”

Bioethicist Carl Elliott’s recent book, The Occasional Human Sacrifice, examines a series of medical scandals, including the Tuskegee syphilis experiments and the Willowbrook hepatitis study. Elliott himself is a whistleblower, having exposed unethical practices in clinical trials of the antipsychotic drug Seroquel in the 2000s. His book outlines the recurring features of such scandals, including the defensiveness and outright hostility faced by whistleblowers and harmed patients.

The medical scandals surrounding both “gender-affirming” care and the lack of informed consent around antidepressants are sustained by the same culture of fear—one that punishes doubt, suppresses regret, and attacks those who speak out. As a result, patients continue to suffer iatrogenic harm long after serious ethical concerns should have been acknowledged and addressed.

Conclusion

That is why I feel a bit like a detransitioner, even though I have never identified as transgender. I have detransitioned from the “chemical imbalance” theory of mental illness, just as detransitioners move on from the belief that their distress is caused by a mismatched “gender identity” or a cross-sex shift in the brain. Both of us were misled into pursuing risky medical treatments that might have temporarily dulled our distress but never addressed its root causes.

It is increasingly important to recognize the parallels between the experiences of detransitioners and those living with prescribed psychiatric harm. The Cass Review rightly emphasized the need for gender-distressed youth to be rigorously assessed for co-occurring conditions such as autism, depression, anxiety, and ADHD. Yet the recommended treatment for these conditions is often psychiatric medication—most commonly antidepressants. Many critics of “gender-affirming” care have reassured themselves that antidepressants are a safe alternative to puberty blockers, cross-sex hormones, and surgeries. But in the UK alone, hundreds of thousands of young people under 19 now take antidepressants, and prescription rates are rising rapidly. While the harms of antidepressants may be less immediately visible than those of medical transition, both interventions can carry devastating long-term consequences. Steering gender-distressed individuals toward yet another questionable, poorly evidenced medical pathway is not a wise substitute for helping them understand—and learn to manage—their distress.

If we regard “gender-affirming” care as a medical scandal, then we must also be willing to see the overprescription of antidepressants in the same light. Even if my argument has not fully persuaded you, I hope it prompts you to keep an open mind when you next hear someone describe psychiatric drug harm—just as you might when listening to a detransitioner speak about regret.

I’ll close with a quote from Moncrieff, which offers a reframing of mental distress that I believe could benefit both those with psychiatric diagnoses and those with gender-related distress:

[O]ur moods and emotions are reflections of our nature as complex, biological organisms that have the ability to make choices. Within the varying constraints of our lives, we are free to shape who we become. This freedom is both a burden, when we realise the responsibility is on us, and an opportunity. For, unlike with a brain disorder, we can change at least some of our circumstances and we can change ourselves. We may be able to do this on our own, we may need help from family, friends or professionals, and sometimes we may need to take collective action to change society…Forging a life in today’s world is not easy. Most of us will experience anxiety, uncertainty and disappointments; for some, these will be difficult to overcome. Emotional crises are the understandable result. The meaning of these is not in our brain chemistry, it is in the world. And that is where the solutions lie too.

Follow Carrie Clark’s work and writing over at Healix, a platform for people who have been harmed by prescribed psychiatric medications. Healix provides advocacy services to people experiencing adverse and withdrawal effects, and campaigns to prevent prescribed psychiatric drug harm.

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