The Future of Withdrawal Studies Is Already Written
This is a follow-up to:
Adele Framer, a citizen scientist and patient advocate, has studied psychotropic withdrawal syndromes for 20 years. She founded the peer support site SurvivingAntidepressants.org in 2011 and, in 2023, the nonprofit Psychotropic Deprescribing Council for research and medical education. She is an occasional advisor to the medical tapering service Outro Health.
Dr. Aftab mentioned me in his June 13 article, Some Predictions About the Future of “Withdrawal Studies” and graciously invited me to comment. I respect his call for clarity. I’ll try to briefly offer my perspective.
About my bona fides: I am a citizen scientist and the inventor of “withdrawalology,” a term I coined to describe the specialized study of psychotropic drug withdrawal syndromes and their amelioration by tapering. I have no academic credentials in the medical or scientific fields. My interest was focused by my personal experience of developing protracted antidepressant withdrawal syndrome from going off paroxetine in 2004, which has been recounted elsewhere.
As a withdrawalologist, I stand on the shoulders of grassroots activity dating back to the ‘90s. In 2005, I joined one of a dozen forum-type websites full of thousands of people reporting withdrawal syndrome from the new antidepressants and benzodiazepines, long before social media became populated.
Since then, I have researched drug withdrawal syndromes, corresponded with many researchers, and became recognized as an expert in the field. This is not so special, because throughout medicine, iatrogenic effects are poorly studied in general and drug withdrawal syndromes are even more bereft.
In 2006, psychiatrist Richard Shelton, a co-author of Schatzberg et al., 2006. Antidepressant discontinuation syndrome: consensus panel recommendations for clinical management and additional research (a journal supplement sponsored by Wyeth), wrote me this:
“I actually think the discontinuation syndrome is pretty bad in some situations and truly horrible in others …. almost all resolve; that is, except for a very small group, where the symptoms become persistent.”
Another co-author of Schatzberg et al., 2006, psychiatrist Peter M. Haddad, who had published extensively about antidepressant withdrawal syndrome, mentioned the importance of case reports in another correspondence. Subsequently, under the pseudonym Altostrata, in 2011 I started SurvivingAntidepressants.org, an online forum site designed to collect longitudinal pseudonymous first-person accounts while providing peer support for tapering and psychiatric drug withdrawal syndromes, including protracted conditions. The site accumulated 23,740 registered members before it became read-only in January 2026.
Predating the activity on Facebook, Twitter, Reddit, Inner Compass, etc, discussions within SurvivingAntidepressants.org shaped the current discourse about psychiatric drug withdrawal in the scientific literature as well as throughout the burgeoning social media “withdrawal community.”
I invited many researchers to look at the approximately 6,000 first-person longitudinal case narratives collected on the site. Among my correspondents were Giovanni Fava and his colleagues Carlotta Belaise, Fiammetta Cosci, and Guy Chouinard; Michael Hengartner, Paul Andrews, Jim Phelps, and Brian Harvey. Mark Horowitz was a member of SurvivingAntidepressants.org, where he conceptualized his theory of hyperbolic tapering. All went on to contribute to the more recent stratum of literature about psychiatric drug withdrawal syndromes, including Chouinard, G., & Chouinard, V.A. (2015). New Classification of Selective Serotonin Reuptake Inhibitor Withdrawal.
In late 2023, I founded the nonprofit Psychotropic Deprescribing Council, an interdisciplinary organization to collaboratively research and create unbiased medical education about rational psychotropic deprescribing, tapering, and support for what we view as a significant life event. Our membership includes hundreds of pharmacists, mental health professionals, and physicians, some of them psychiatrists, all interested in sharing their experiences and learning more.
A bird’s-eye view
In the US, the population being treated with psychiatric drugs amounts to a general population, not a population selected for severe mental illness. Recent US Census data shows that at any one time, close to 25% of all US adults are taking drugs for a mental health condition alone; while serious mental illness is estimated to affect 6% of the adult population. Approximately two-thirds of those taking psychiatric drugs are taking antidepressants (17% of all US adults). This is a rolling total; at least half of new antidepressant users will shortly quit their drugs, while others will start.
The vast majority of psychiatric patients were initially prescribed antidepressants by primary care doctors, very often without formal diagnosis. The majority of clinical guidelines recommend that maintenance of antidepressants may continue 6 months after symptomatic remission, though this arbitrary rule of thumb is rooted in clinical trials confounded by unrecognized withdrawal symptoms, such as those reviewed in Geddes et al., 2003. Antidepressants are not routinely recommended for mild to moderate depression. According to Luo, et al., 2020, only about 14% of US adults who are taking antidepressants meet the Kessler-6 Index for a severe condition; more than 86% have mild to moderate scores. A meta-analysis showed that in mild to moderate cases, their gradual discontinuation should not lead to the relapse of severe mental illness – though it could lead to withdrawal symptoms.
Psychotropics are psychotropics; regular use of any of them brings about neurobiological adaptation, physiological dependence, and when drug steady-state drops too precipitously, their withdrawal syndromes have remarkably similar features.
As with other psychotropics, psychiatric drug withdrawal symptoms appear among neonates and animals, who have no capacity for expectancy bias or nocebo effect. They occur when people accidentally forget their drugs. They occur when people deliberately stop their drugs with full but misplaced confidence that they’ll be among those who get away with it.
Other post-drug syndromes – emotional anesthesia, sexual dysfunction, hypersensitivity, and neurological kindling – have been documented for many decades in the literature regarding discontinuation after chronic alcohol, opioid, benzodiazepine, and amphetamine use. They can be sequelae of any chronic psychotropic exposure.
Some may be related to homeostatic disruption in the discontinuation process, and therefore true withdrawal symptoms; in other cases, they may be tragically ineluctable consequences of long chronic drug exposure, which so often involves a history of fruitless dosage escalation, bumpy drug switches, forgotten doses, unsuccessful discontinuation attempts, and other neurobiological missteps.
No one knows, because aside from the recent interest in withdrawalology, in-depth investigations of these iatrogenic conditions are rare.
Psychotropic drug withdrawal syndromes offer ample opportunity for misidentification of equally enigmatic ME/CFS, POTS, post-viral syndromes, fibromyalgia, or FND. Throughout the withdrawal literature, including that by psychiatrists regarding antidepressants, common withdrawal symptoms and protracted withdrawal symptoms are described as autonomic. ME/CFS, POTS, post-viral syndromes, fibromyalgia, and FND also have autonomic features.
Differential diagnosis is essential in distinguishing withdrawal syndromes from FND or dysautonomias, which also fluctuate and can be drug-induced. Among the millions taking psychiatric drugs, certainly there are small numbers with any of these conditions, even some with brain tumors. Crucially, the chronology of dosage reduction indicates withdrawal symptoms. If they appear, you’d want to quickly reinstate a low dose of the suspect drug. In protracted withdrawal syndrome, you’d want to be very careful about drug interventions, which, due to withdrawal-induced hypersensitivity, might cause paradoxical reactions or neurological kindling.
How often does withdrawal syndrome occur after discontinuation of chronic psychotropics? In addiction medicine, it is presumed to occur so often that drug substitution is routinely utilized to avert it, while gradual tapering is recommended for benzodiazepines.
There is no reason to presume that antidepressants and other psychiatric drugs are exempted from the general consequences of psychotropic discontinuation. As with other psychotropics, when dosage is decreased, withdrawal syndrome is the horse, not the zebra.
We have no words
Always concerned with ontology and semantics, Dr. Aftab is correct that the vocabulary used in public discourse about prescribed drug withdrawal is confusing. Medical terminology itself is confusing, particularly in psychiatry and addiction medicine, the two medical specialties inescapably fixated on but eternally flummoxed by human nature.
Linguistically siloed, psychiatry itself is prone to paraphrases, poetic license, misnomers, misappropriations, and misinterpretations of pharmacological terms, such as “dependence”, evidenced by the vast numbers of synonyms listed in systematic searches for review articles.
Withdrawalology has made do with what it can find in the existing terminology. “Withdrawal” has long been used colloquially and medically as a noun for both the process and the consequence. However, across psychotropics, withdrawal clearly proceeds from a chronology after a psychotropic drug dose has been reduced or discontinued, whether the drug has been prescribed or not.
If the literature says “depression” is a possible withdrawal symptom, how does it differ from “relapse”? What does “rebound” mean? What is “protracted withdrawal syndrome”? Defined as following acute withdrawal, which is supposed to only last for a matter of weeks, it is scarcely detailed anywhere, though Lerner & Klein, 2019 listed 11 synonyms for it collected by SAMHSA.
Steering well clear of the acute phase, Chouinard and Chouinard (2015) somewhat arbitrarily put the start of protracted antidepressant withdrawal at 6 weeks of symptomology, with duration of “several months or more.” (Hengartner et al., 2020, of which I was a co-author, estimated median duration to be about 2 years.)
Surely observant clinicians have seen continuous withdrawal symptoms lasting more than 6 weeks – that would be protracted withdrawal syndrome. But how do patient reports of “delayed withdrawal” on social media make sense? In my experience, asking people more questions about their recent history usually revealed that “delayed withdrawal” was preceded by initial mild withdrawal symptoms, perhaps ignored, that had progressed to marked withdrawal syndrome. Due to withdrawal-induced hypersensitivity, one innocent glass of alcohol or a course of antibiotics or a strenuous workout session could trigger or revive more obvious withdrawal symptoms.
(There is also the possibility of individual neurology holding out against withdrawal-induced dysregulation for a time, but finally falling like a trail of dominoes into a more conventional pattern of protracted withdrawal syndrome.)
When human nature meets psychotropic drugs, we’re utterly in the dark, linguistically. No language has the words to describe the symptoms that patients feel when they experience an alien drug-induced neurobiological effect. They struggle to communicate and clinicians struggle to understand them.
Nebulous terms at best, “depression,” “anxiety,” and “anhedonia” only dimly convey withdrawal sensations. I made up the term “emotional anesthesia” to indicate a post-drug symptom that is distinct from the usual use of “depression,” drug-induced “blunting,” and “anhedonia.”
Dr. Aftab may have over-interpreted language that the withdrawal community uses on social media. The participants are doing the best they can, but they are mostly unaware of the existing literature about withdrawal. Like many researchers, they are describing the leg of the elephant closest to them, sometimes in detail that does not stand up to generalization.
Patients’ words are all that clinicians have to go on, and clinicians are confused. The haze around identification of withdrawal syndrome appears to be the appearance of emotional symptoms in the symptom lists. This carries over into research: even if physical withdrawal symptoms were present, Lewis, et al., 2021 put subjects with any appearance of emotional symptoms on the “relapsed” side of the ledger. This is a conceptual error leading to questionable conclusions.
It is a curious blind spot that psychiatry analyzes emotional symptoms out of context. In the midst of drug discontinuation, people may well react to odd symptoms with fear or distress – aside from actual withdrawal-induced emotional symptoms. If the chronology is pointed in the right direction and the patient reports odd physical symptoms, you’re seeing withdrawal whether emotional symptoms are present or not. If only emotional symptoms are present, differential diagnosis should presume the chronology is the key.
“Discontinuation” for antidepressant withdrawal syndrome is an unnecessary euphemism. Very widely used for centuries throughout medicine and society to describe what happens after people stop psychotropics, “withdrawal” will be in use forever. However, as various clinical interests converge on improving the process, the future of withdrawal studies will inevitably shift to “tapering,” a term that has gotten scant attention in medical education.
Start low and go slow
Even in 1904, Watson knew that he had to gradually wean Sherlock Holmes off cocaine over years. Systematically gradual tapering practices have never been applied to the newer psychiatric drugs. Perhaps it’s time to try something different?
Insisting on extensive data before psychiatry acts to recommend clinical deprescribing practices is an insurmountable barrier to addressing avoidable treatment risk affecting millions. With little inclination in the medical profession to study iatrogenic conditions, it is unlikely that large randomized controlled trials will define the process of psychiatric drug discontinuation. (The more recent ANTLER RCT, one of the few investigations that might have true withdrawal symptom data, summarized all their other patient-level data in Lewis, et al., 2021, but not the withdrawal data, which has been sequestered.)
Meanwhile, minimizing drug burden is simply good medicine, as the American Society of Clinical Psychopharmacology agrees.
If we truly want to improve outcomes, we shall have to make do with general medical and pharmacological principles, case reports, clinician experience, and common sense – like so much clinical practice does.
Mark Horowitz, co-author of The Maudsley Deprescribing Guidelines, has attempted to give clinicians some pointers. As he has specified repeatedly, his protocol for hyperbolic tapering is only a place to start. The receptor occupancy curves that he has so painstakingly mapped out allow all parties involved to visualize the process.
The Maudsley Deprescribing Guidelines’ more conservative recommendation is an initial reduction of 25% with smaller reductions from there. (An estimated 5-6 half-lives only reaches the threshold of the mean drug plasma steady-state plateau. Six half-lives plus a stabilization period at least as long between dosage reductions allows re-adaptation to a new lower steady-state, a homeostasis based on lower drug input, or, if you will, receptor occupancy. For psychiatric drugs dosed daily, I suggest this will be a minimum interval between reductions of about 2 weeks. However, re-adaptation is individual; making a reduction while the drug plasma level is still in flux or the patient reports withdrawal symptoms disrupts the re-establishment of homeostasis, elevating risk.)
If you’re a hyperbolic taper doubter, you can design your own nonlinear tapering schedule, as long as you maintain a tolerable drug plasma steady-state, stay in close communication with your patient, and correct course as needed to avoid withdrawal symptoms.
Any taper is better than no taper. Don’t do this:
Tell your patient to simply stop taking their drug.
Tell patients to “cut in half, then half again, then off” over a few weeks. These very instructions have driven hundreds of thousands to the withdrawal communities and social media.
Tell patients to skip doses to taper. How could this even be considered when clinicians know it’s important to maintain drug steady-state?
All of the above are demonstrated failures that create outraged consumers. If 50% reductions are a bad idea, what’s left? Try more gradual reductions. Trial and error is a central tenet in psychiatric drug treatment. Embrace uncertainty. Modify as you get feedback from the patient. Don’t make your patients mad at you.
Expectancy bias goes both ways
All that psychiatry knows about SSRI withdrawal syndromes – the catalog of symptoms, the misinterpretation of acute withdrawal, the high expectation of relapse – comes from early trials that utilized abrupt cessation, placebo substitution, or inadequate tapering, yet almost never included protocols to identify withdrawal symptoms. (Not only were subjects in these trials generally antidepressant-naive, they had no expectation that the drugs might cause withdrawal syndrome.)
No conclusions about rate or relapse or withdrawal can be drawn from these compromised and confounded studies. There is no scientific basis for presuming that relapse is the usual outcome of discontinuation of prescribed psychotropics and withdrawal syndrome is uncommon.
The negativity that is visible in the withdrawal community on social media is a mirror image of clinicians’ expectancy bias. All that the withdrawal community knows about withdrawal comes from clinicians utilizing inadequate tapering practices, which from the patient point of view have produced disasters for many years. And that is why they radiate fearfulness and distrust.
The DSM already expects clinicians to differentially characterize subtle permutations of depression. If clinicians update their priors and stop conflating withdrawal symptoms and relapse, I predict tapers that are gradual and in collaboration with the patient will bring about very little real relapse and protracted withdrawal syndrome will become very rare.
Foster self-efficacy
It is an axiom in the mental health field that a strong therapeutic alliance produces better outcomes. The 2026 International Conference on Deprescribing (where psychiatry was hardly represented) featured a poster titled “Personality traits predicting benzodiazepine discontinuation failure in older adults.” The study found that no personality traits were germane but “discontinuation self-efficacy” was the strongest predictor of successful cessation, “consistent with evidence identifying perceived capability as a key determinant of deprescribing behaviour.”
For a successful discontinuation process, a positive attitude on the part of the clinician should facilitate patient self-efficacy – recognized as a central goal of mental health interventions.
Wherever people go, there they are. They’ll react to discomfort or pain in characteristic ways that are not necessarily pathological. Among the millions taking psychiatric drugs, some may be querulous, some may dramatize because they think they’re being ignored, some may expect bad things to happen, some may be inclined to the nocebo effect. Or, most likely, they may be reliable narrators. This is where a clinician who knows their patient and asks questions can calibrate — who needs reassurance, who needs the taper slowed, who needs both. If a withdrawal-induced symptom is suspected, stop or slow down the taper until vague symptoms resolve. Respecting the patient’s report and acting to reassure them if needed can only strengthen the therapeutic relationship.
Patient confidence in the process of deprescribing depends on the clinician’s skill and attitude. If the clinician radiates uncertainty about the deprescribing process and expects patient fragility and relapse, that will elevate patient apprehensiveness and corrode their confidence, producing worse outcomes.
Give consumers what they’re asking for: They want to go off their unnecessary drugs without having the risk of withdrawal syndrome hanging over them. Try gradual tapering with a positive attitude in cooperation with your patient! If it’s slow enough, what can you lose?
If you go slowly enough, you’ll be able to tell if your patient is in trouble. As you guide your patients off their drugs, if you have good communication with your patient, you should be able to forestall both withdrawal symptoms and relapse. This is your responsibility. If you see a lot of relapse, you’re doing it wrong.
It’s a consumer movement
Twenty years ago, as now, fear of and anger about withdrawal syndrome from inappropriate discontinuation techniques were fueling the patient complaints now being broadcast on social media. Theories about this movement being driven by ideology or outside agitators are an irrational defense.
The vast majority of people in these online communities would not know who Thomas Szasz is if he reared up from his cold, cold grave and bit them on the leg; they don’t read journal articles; and they have no ideology except the very human impulse of looking for someone to blame. People can avow any identity on social media, but there’s no reward in a “withdrawal identity” – there’s too much misery.
Except for those in forced treatment, every one of those consumers was once a hopeful patient. Now they’re customers who think they’ve been lied to. Their ranks are constantly replenished by what now amounts to treatment error. If clinicians stopped creating outraged consumers, there would be much less noise from social media.
If appropriate tapering methods were adopted, the picture of psychiatric drug withdrawal syndrome as a clinical and personal disaster would become history. There will be no resistance to this from the online “withdrawal community.” It’s an amorphous consumer movement, not a crazed monolithic beast.
No patient is going to stand in the way of clinical practice improvement.
Comments are open.
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I personally think that all the hubbub about antidepressant withdrawal is pretty pointless. First of all, I am not "confused". When patients complain of withdrawal symptoms (meaning they complain of various problems after decreasing or stopping an antidepressant), I appreciate as much variability as I do with patients' starting antidepressants.
Second of all, since the dosing and side effect information in the inserts is completely inadequate to encompass all the reactions my patients have when they start antidepressants, why would I expect less variability when they decrease or stop antidepressants?
Third of all, every single discussion I have seen (both about starting an antidepressant and stopping an antidepressant), presupposes that a doctor makes clinical decisions for a passive patient based on his total mastery of total knowledge. That is not anything like the reality. Each of my patients has different values related to stability, uncertainty, risk, and taking medication itself. All I can or should do is tell them what I know, which isn't much because patients are so unique, and promise close follow-up and the use of my clinical intincts.
Fourth, we speak about patients as if they form some collective unity that can be treated as one individual about whom guidelines shift depending on the prevailing wind of online chatter and literature. They can't. I have found that I solved every every clinical problem with intense follow-up and close collaboration with the patient, unless I failed to form an alliance (and that can happen, for example I didn't give the patient the Xanax they wanted or the patient didn't feel heard beacuse of my own anxiety and high volume practice). Since we know most antidepressants are prescribed by non-psychiatrists, this is where the challenges lie, most patients are on their own.
Fifth, after that most antidepressants are prescribed by non-psychiatrists, the worst problem is that most information traded between both non-clinicians and clinicians for the past quarter century has been heavily contaminated by pharma marketing efforts. Refusing pens and lunches has done nothing to eliminate or even reduce this issue. Prescribers' knowledge about the meds they prescribe, or even reasonable decision making, is useless because they are based on a marketing hype that has nothing to do with reality or even real knowledge or evidence.
None of this is anti-psychiatry. This is anti-fake psychiatry.
I was diagnosed with major depressive disorder over 40 years ago, suffered from depression starting in my early teens. I started taking Prozac after the birth of my third child when I was suffering from severe postpartum depression. I remember the experience when it finally started working, it was like a gray cloud was lifted from my brain. I tried tapering off with the help of a medical doctor about 20 years ago, but relapsed into a major depressive incident. So now I’ve been on Prozac for probably 40+ years. I still have ups and downs. My psychiatrist and I have talked about tapering off, but he does not think that in my situation it’s a good idea, and I agree. It still works for me. The only thing I get worried about is the long-term effects on my brain, as I am 75 years old. But I think every patient is different and it’s really important to listen to what their experience is. My biggest fear in life has been my depression. At one time prior to Prozac I knew that that’s how my life would end, with a depressive incident. I appreciate all the studies that are being done and I love reading articles like this. Thank you.