Why Do Only Some People Experience Severe Antidepressant Withdrawal?


Why do some people experience severe withdrawal symptoms when stopping antidepressants, while others have few symptoms and some have none? Who are these “severe” people? Can we identify them before they start an antidepressant?

With so much debate and discussion about “how many” (including the previous two essays in this series), it’s surprising that so little has been written about “why some and not others?” Yes, being on an antidepressant for a long time increases the risk of severe withdrawal when stopping. That’s clearly one factor. Yet many people who’ve been on antidepressants for years can stop them with little difficulty. It appears clear that after long-term exposure to antidepressants, some sort of adaptation takes place in the central nervous system that takes a long while to reverse, for many people. Yet not everyone. What accounts for the difference?

Blue background, transparent pill bottle spills blue and white pills toward cameraUnfortunately, we don’t even understand how antidepressants really work. Yes, they affect serotonin and/or norepinephrine signaling. But how does that change mood? Yes, there are many known alterations that follow the change in serotonin and/or norepinephrine signaling. One common pathway for multiple antidepressant modalities, from pills to exercise to transcranial magnetic stimulation, is an increase in “neurotrophic factors”: cell fertilizers, if you will, that make neurons more likely to grow, to make connections with other neurons. In the face of chronic stress, neurotrophic factors can help prevent neuronal decline. But how does that change mood?

My point is: we just don’t know enough about the mechanisms of mood to know what the mechanisms of antidepressant withdrawal really are, in order to identify people at high risk for severe withdrawal before they start an antidepressant. Lacking an understanding of mechanism, is there any other way to identify the people who will have severe withdrawal symptoms when they try to stop an antidepressant?

Below, one possibility. But first, my apologies: this idea has been offensive to some people. I hope the following details may help make it less so. The idea comes from 20+ years of experience working with people with complex mood disorders.

The Basis for a Hypothesis

Most patients referred to me were already on an antidepressant, often their third or fourth or more. They usually had also tried many other approaches, but almost always those other treatments were done with an antidepressant. So, in search of something they hadn’t already done, a common alternative would be to try some of those previous treatments without an antidepressant—on the presumption that antidepressants might have interfered with response. Accordingly, the first step would begin with tapering their current antidepressant (while in most cases continuing whatever else they were on or doing). This strategy was so often helpful I used to hope that the next referred patient would be on an antidepressant, giving me at least one strategy to offer.

Here is the key observation: it seemed as though nearly all of these patients had withdrawal symptoms during their antidepressant taper. Despite taking small steps down, even with a month or more between reductions, they would still have a noticeable “wobble” right after the decrease. Their experience led me to the remarkable website, SurvivingAntidepressants.org, where similar experiences are described over and over again.

Now a second key observation: primary care colleagues, with whom I have worked closely, did not seem to be having the same experience. They asked for help with numerous issues, but not antidepressant withdrawal problems. They didn’t ask for help with tapering. So our research team looked at the numbers, finding that 90% of patients in our health care system who stopped their antidepressant did so without a prescription for the lowest available dose. Many of these patients may have had significant withdrawal symptoms, but not enough to go back to their prescriber and describe the problem and obtain a smaller pill to facilitate smaller steps down. In other words, a large majority of primary care patients seemed not to need the careful tapering that nearly all my patients did.

One difference could be trauma. In psychiatry, many of our patients have experienced it. Not quite so much so in primary care. But I’d see significant withdrawal problems even in patients without awful trauma histories (yes, I could have missed it).

So, here’s another possibility. This is a working guess, which could be mostly or completely wrong, but it is testable. I hope you’ll follow along as I explain my hunch. If I lose you, here’s the bottom line: it seems possible that some or much of the vulnerability to antidepressant withdrawal is related to “bipolarity”. Not bipolar disorder, but rather a mostly genetic element underlying bipolar disorders.

Bipolarity Is Not “Bipolar Disorder”

Bipolarity can be present in people who do not have bipolar disorder; i.e. their symptoms are not sufficient for that diagnosis. Really? Yes: most mood specialists around the world now accept that people with depression can have any number or intensity of manic symptoms, on a spectrum from “unipolar” (no manic symptoms, present or past) to “bipolar” (meeting official diagnostic criteria for bipolar disorder) with many patients in between these two poles. For example, in the most recent international guidelines, the mood spectrum is explicitly described (skeptics, see Figure 3 therein).

Instead, think of bipolarity as a kind of energy. Those who have a lot of bipolarity are likely to put a lot of energy into their activities: more drive, more passion, more certainty, more optimism, more likely to take the initiative.  High bipolarity can be a stable trait with no depression problems or mood shifting or obvious cycling, so-called “hyperthymic temperament”. Any degree of bipolarity is possible, from none to hyperthymia to overt bipolar II or bipolar I.

My working guess: people with little or no bipolarity are less likely to have difficulty stopping their antidepressant, whereas people with a lot (but not necessarily meeting diagnostic criteria for “bipolar disorder”) are more likely to have severe withdrawal symptoms.

This hypothesis offends some people because the label “bipolar” carries more stigma than “depression”. I understand that.  But my wish here is to go beyond the labels. Bipolarity—as opposed to bipolar disorder—is not an illness, it is a genetic trait. People can have none of it, or a little, or a lot.

Evidence in Support of the Hypothesis

In the next three subsections of this chapter, I’ll present three lines of evidence that support a connection between bipolarity and antidepressant withdrawal. First, high-energy symptoms during a depression (so-called “mixed state”) strongly resemble many of the symptoms of severe antidepressant withdrawal. Second, antidepressant dose reduction can induce hypomania and mania even in people who did not previously have recognized bipolar disorders. (Think about that for a minute.) And third, antidepressant discontinuation in patients with bipolar disorder is frequently extremely challenging, requiring small decrements and very long taper periods—much like the kind of tapering described on SurvivingAntidepressants.org.

1. Symptom similarity

Have a look at the figure below. Circle A presents physical symptoms of antidepressant withdrawal. Circle C presents symptoms and markers of bipolar disorder.  Circle B presents the relatively more psychological symptoms of antidepressant withdrawal, drawn from two studies which quantify the frequency of withdrawal symptoms.  (These lists are not exhaustive).

Overlapping symptoms of antidepressant withdrawal and mixed state depressions

Circle B also represents symptoms of “mixed states”. Depressive mixed states are simply depression plus bipolarity: typical depressions mixed with symptoms associated with bipolar disorders. Debate continues about which high-energy symptoms qualify a depression for a mixed state diagnosis, but recently, several research teams have found four symptoms particularly prominent: anxiety, anger, agitation, and attention problems (dubbed “the Four A’s” by one specialist). As shown in the figure, all of these symptoms overlap with symptoms of antidepressant withdrawal. Is this just a coincidence?

Bipolarity admixed with depression (mixed state) is an extremely common variation of depression. For example, a recent study identified 29% of a sample of patients with major depression as having a mixed state, using empirically derived criteria. People with mixed depression do not necessarily have “bipolar disorder”, but they’re not “unipolar” either: most are in the broad middle between the two ends of the mood spectrum.

The point is: mixed states indicate bipolarity, and the symptoms of mixed states are remarkably like those of antidepressant withdrawal.

2. Induction of hypomania, mania, and mixed states

Ironically, while antidepressants can induce hypomania, mania, and mixed states when they are initiated, antidepressants can also induce these symptoms when rapidly discontinued. One way to understand this irony is to regard bipolarity as capable of creating unstable mood states. Pushing a person in either direction—toward mania, when antidepressants are started; or toward depression, when they are suddenly discontinued—can further destabilize some people’s depression into rapidly cycling mixtures of mood symptoms.

Antidepressant discontinuation-induced hypomania/mania has been observed even in people who have not previously been diagnosed with bipolar disorder. This suggests that the phenomenon is not simply a worsening of an underlying condition. It’s not limited to people who have bipolar disorder.

As a colleague who has reviewed this idea of mine pointed out, withdrawal from other psychiatric medications can induce hypomania, not just antidepressants. But this is far less frequent than has been described with antidepressant withdrawal (as follows, for the skeptics): hypomania during benzodiazepine withdrawal was described in a patient with severe intellectual disabilities; and during opiate withdrawal in a case series, where the authors noted that “features of hyperthymic temperament and family history of bipolarity were traced in most of the individuals”. Otherwise, in a review of psychotropic withdrawal syndromes, induction of hypomania/mania is not listed for alcohol, benzodiazepines, nicotine, opiates or stimulants.

When tapering my patients’ antidepressants, one goal was to avoid inducing the negative high-energy symptoms of mixed states. Or was I helping them avoid having antidepressant withdrawal? In patients with a diagnosis of bipolar disorder, I don’t think withdrawal and mixed states can be distinguished (except by additional physical symptoms such as nausea and brain zaps). If so, then are we seeing a connection between antidepressant withdrawal and bipolarity? Might this explain why primary care patients, with less complex depressions, appear to have much lower rates of antidepressant withdrawal than my bipolar-rich patient population?

Next, a third line of evidence supporting such a connection.

3. Similar taper rates

People with severe antidepressant withdrawal symptoms discover that to successfully discontinue the medication, they must lower the dose by extremely small steps, very slowly. For example, the website SurvivingAntidepressants.org recommends reducing one’s antidepressant dose monthly by 10% of the previous month’s dose. If the pre-taper dose is 100 mg/day of sertraline, the first step down would be to 90 mg/day, a month later to 81 mg/day, then 73, 66 and so on. Users may go faster, especially initially, but are warned to slow down if they are experiencing any increase in symptoms after a decrement.

In my clinical practice, a similar small-decrement/slow-taper process evolved as I focused increasingly on patients with bipolar disorders and sub-threshold bipolarity. In 2011, I suggested a four-month average taper based on cataplexy rates after antidepressant discontinuation.

Over time I received more and more referrals of people who had already tried four or more antidepressants. The probability that switching to a different antidepressant will alleviate your depression is very low once you’ve tried that many. But I slowly learned that some people can get better, at least a little better, by gradually stopping their antidepressant (while usually continuing everything else they’d ended up on by that time). A resident whom I supervised was so impressed with this approach, we published together a report of 12 cases in which we saw improvement in severe anxiety and suicidal ideation just by tapering patients’ antidepressants.

SurvivingAntidepressants.org suggests small steps down for people with antidepressant withdrawal. My target was a presumed underlying bipolarity. The taper programs are very similar. Of course, the necessity for very slow taper rates in both conditions does not by itself establish any direct relationship between these two groups. But this similarity in taper programs, together with the other two lines of evidence above suggests a possible connection.

At least this hypothesis leads to testable questions. If my hypothesis is correct, markers of bipolarity should be more common in people with severe antidepressant withdrawal symptoms than in people who can stop antidepressants with little or no difficulty. These markers include family history of bipolar disorder, early age of onset of depressions (around late teens or very early 20s), highly recurrent episodes of depression, postpartum depression, and strongly adverse reactions to antidepressants when or not long after they are started (although I reported one patient’s experience of having mixed state symptoms develop after seven years on sertraline that helped her “join the human race”).

For detecting bipolarity, a single simple two-page questionnaire combines three validated screening tools. Called MoodCheck, it consists of the Bipolar Spectrum Diagnostic Scale, a family history screener, and the Bipolarity Index. On this questionnaire, there is no “cut-off”, no threshold for a bipolar diagnosis. Rather, the point is to allow people to estimate their position on the spectrum of bipolarity, from none to a little to a lot.

If my hypothesis proves to be correct, more people with intermediate and high scores would have severe antidepressant withdrawal symptoms than people with low or zero scores. If so, a questionnaire like this could be used to identify patients who will need slow careful tapering; or better yet, patients who are at high risk for severe antidepressant withdrawal and who therefore should be even more cautious about starting one.


Again, my apologies to anyone who reads this essay and finds themselves angry or hurt. Bipolarity is not “bipolar disorder”, which though it is being actively destigmatized (e.g. BrainStorm the Film) is still more frightening to many than “depression”. If bipolarity really does correlate with severe antidepressant withdrawal, then identifying it could prevent a lot of suffering. If not, the question remains: why some people and not others—because the risk of antidepressant withdrawal does not seem to be similar for all users.


Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.


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  1. The author’s point should rather be: “we just don’t know enough about the mechanisms of mood” to prescribe any drug or suggest any form of “brain stimulation” for anyone. And even though “anti-depressants” have become part of our everyday language we should acknowledge that it is a marketing term and not a medical term like anti-hypertensives as we now know it actually causes depression with long term use.

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  2. Just a quick question: hyperthymic temperament – I was not clear how this was “bipolarity”?, in the sense that the word bipolarity suggests two poles. Hyperthymic as you described may be a stable state. I was curious about your use of language. Why call this bipolarity – why not just mark out the 4 A’s or mixed state?
    But really enjoyed the article and felt t matched what I see, and my own lived experience of this class of drug.
    A very interesting idea..

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  3. A thought..is it possible that those withdrawing from antidepressants under only PCP care might be more likely to self medicare with things like alcohol, etc, during the pr9cess, since people without a huge psychatric dx tend to be less careful about “acceptable” over the counter drugs, therefore blurring withdrawal results?

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  4. There is so much presumption of science in this article that has no basis in actual scientific evidence to date. Additionally how does any of this explain people who took these medications for non-mental health related issues and don’t have a history of this in their family? People who took these for nerve pain, for menopausal symptoms, and the whole host of other off-label conditions that these drugs are prescribed for? Have you taken into consideration why people don’t talk to their doctors about symptoms? What about the fact that certain populations trust doctors more than others? And the list of questions that are variables to this “hypothesis” goes on. You cannot assume that the fact that primary care doctors weren’t dealing as much with this issue as you that their patients were not experiencing it-this has no basis in science. Again there are many perspectives and considerations not taken here that are essential to this issue-culturally, scientifically, politically, economically, medically etc. Also a lot has been written and talked about, about the fact that some people respond in certain ways and others don’t when it comes to withdrawal. This is a huge topic of conversation and scientific inquiry amongst those that are actively involved in research in this field and in fields that relate to these conditions. It feels undermining to not address the myriad of factors actually at play here in the complex reality of why this issue exists and why it is so complex to determine who might have severe withdrawal verses those who don’t. There is much actual scientific conjecture being relayed right now on this from other scientists and fields of study. Where are those voices and perspectives in this article? Have those been considered? Your hypothesis does not take into account previous health history from a virology perspective either and the role post-viral changes in immunology play, for one example of the multiplicity of factors involved here. To state that it comes from “bipolarity” is a deeply unscientific statement that discounts lots of other research into why people develop disease in general. This hypothesis misses the mark in so many ways for me and seems to really neglect pertinent areas of research (like peripheral neuropathy for instance) that are highly relevant to antidepressant withdrawal conditions.

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    • Very negligent and scary for the people he’s treating. He’s going to be going to all of them with this presumption on personality traits and in some cases doing more damage.

      I appreciate he wants to help and is looking for a clue, but to presume it’s innate personality traits is really tonedeaf

      My withdrawal CREATED these clusters of personality characteristics due to how the withdrawal and subsequent adverse reaction made me feel- I wasn’t like this before – and this “neurotic” picture that he paints as a basis of the “type” of person this affects is offensive to say the least – most of us WEREN’T like this before, and it’s why we are so so desperate when it happens.

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      • Great point, Jennifer. Most of us weren’t neurotic or having bipolarity (not sure what that means) prior to being put on psych drugs. Do clinicians not recognize that when people start to experience a host of disabling symptoms and never being heard or believed by health care workers could cause someone to think, feel or behave differently?

        It seems that prescribers of psychiatric drugs have an enormous blind spot that leads them to find a problem with the patient again and again rather than consider how destructive their drugs are.

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  5. A better area to look to for hypotheses concerning antidepressant withdrawal and other withdrawal conditions like PSSD, that’s actually based in science, would be the intersection of polyneuropathy, polyvagal theory, and neuroscience (particularly the relationship between the limbic system, immune system, brain stem, and the vagus nerve). This condition also heavily overlaps with many other “neuro-immune” conditions like Long-COVID, POTS, ME/CFS, Fibromyalgia, MS, Lyme, and other autoimmune diseases. It would be pertinent of researchers to collaborate across these fields to determine the underlying mechanisms of action in these strikingly similar conditions to see what is causing them and why some people might develop them verses others. Researchers are already in fact doing this but getting psychiatric drug withdrawal conditions included is challenging precisely because of their relationship to psychiatry and the incredible campaign psychiatry in the US in particular has embarked on to stop these conditions from coming to light. Underlying trauma to the autonomic nervous system or to the limbic system from adverse childhood experiences for example could have a role to play, allostatic load could have a role to play, etc. But basing a hypothesis on, what is fundamentally an understanding of the brain and body that does not include neuroscience or neuropathy at its core, would be to completely ignore how the body functions and the incredible reliance on our sensory systems for life. A hypothesis related to an understanding of health based on psychiatry or psychology is not going to get us to figuring out why some people develop severe withdrawal and others don’t.

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  6. Okay, I need to re-read this article when I don’t have COVID, brain fog is a bit of an issue just at this particular moment…

    But dear God, thank you for trying to use diagnostic terms in the way they were intended– just as a common language to describe certain constellations of symptoms– rather than some kind of medicalized post-digital “If you see this, it must have been caused with that, and must be treated with this!”

    There are a lot of things that drove me batsh*t about the DSM V, but one that’s not talked about enough was dumping ‘cyclothymia’ and ‘mood disorder due to a medical condition.’ These diagnoses imply a spectrum of bipolarity– they encourage clinicians to think that way, that bipolarity isn’t… well, binary. Not something you either have or you don’t.

    Working with young adults, I wish there were actually MORE diagnoses in this continuum. The one I’d love to invent would be: “Developmentally Normative Cyclothymia.”

    Okay, I’m going to stop now… well, in a moment. I guess I’m wondering why bipolarity has to always be genetic? I mean, I’m asking because I really don’t know. There’s a lot of literature on the connection between trauma and bipolar– enough to convince me that there was something there, but I could never figure out exactly what. I have a chronic medical condition with well-documented symptoms that come and go with no rhyme or reason, so hell yeah, I got a mood disorder! When I feel good, I go as hard as I can to make up for lost time, and when I feel like crap, I have to slow down which bums me out. You could say that pisses me off– or puts me in a ‘mixed state.’ And those patterns got burned in during adolescence, so during rare periods of longer remission, it’s hard to break out of them.

    I’m really not thinking clearly. But you were, and outside the box, so thanks for that! (And for taking Surviving Antidepressants seriously.)

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    • I hope you get better soon.

      I do have doubts about the genetic link too. I am guessing is in the “family history” part of JP, but that’s my guess.

      Funny, thinking out of the box suggests to me I might be bipolar less prone, despite being “strong” willed, persistent, determined, sometimes relentless. Never been manic, never beed depressed…

      And I have come down from SSRIs without mania/hypomania, despite developing anxiety, or god forbids, even akathisia. So, I can see the parallel, so I guess I just got one A, instead of 4. Good for me! 🙂

      Sad because it might not have been anxiety but akathisia…and not even bipolarity since I just got one A.

      And one psychiatrist told me no chance I had bipolar, and I am guessing because of that. Odd fellow, but quite emphatic.

      Saddly, apparently covertly, with the ill-will of relatives I might have been covertly diagnosed as bipolar, even druged as such. Poor me, but here I am still…apparently since childhood, but they didn’t told me that. Oh, the irony.

      But I did hear comments that I got “cured” of whatever I was covertly diagnosed in childhood by someone who should have been told that. But a couple of psy unprofessionals never, as adult, told me that either. Oh, the irony, gasslighting and an attact on my right to know and guard my health. 😛

      I do hope you feel better soon, as ironies go, I might have had “the fog”, despite negative blood work suggesting didn’t had covid. Hey, labs, they make mistakes, and it was top covid season. I am less foggy now. 🙂

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  7. thanks for this thoughtful analysis. However I wonder if you can speculate on what is going on at a neurochemical level to explain the fact that some people have a lot more trouble getting off depression pills than others? People with bipolarity are likely more reactive to events in their environments. How could this happen again at neurochemical level?

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  8. Given the fact that the “mental health” industry didn’t know brain zaps – which are not a symptom of either “depression” or “bipolar” – were a common symptom of antidepressant discontinuation until 2005.


    Despite the fact the “mental health professionals” have been force and coerce drugging millions with their newer antidepressants – psychiatry’s “new wonder drugs” – since the 1980s/1990s.

    And the “mental health professionals” did supposedly know – until the 2013 DSM5’s creation – that misdiagnosing the adverse and withdrawal symptoms of the antidepressants as “bipolar” was morally and ethically wrong … even according to their DSM “bible,” until 2013. (Read the “Note.”)


    But this was changed in the “bipolar” definition of the 2013 DSM5 – likely to spite Robert Whitaker for his award winning 2010 “Anatomy of an Epidemic” – where he pointed out that a million children had already had the common adverse effects of the antidepressants and ADHD drugs misdiagnosed as “bipolar.”


    I know we have a huge lack of ethics problem amongst the force and coerce treating “mental health professionals.” But this is also a sign we have huge lack of ethics problems with how the entirety of the medical / pharmaceutical industrial complex functions.

    And since big Pharma chose to respond to this lack of ethics and credibility problem of their force treating “cash cow” psychiatrists, by trying to replace their scientifically “invalid” psychiatric “cash cows,” with the “cash cow” of Covid, and the forced drugging of everyone.


    Honestly, everyone must now question the ethics of the entirety of the medical / pharmaceutical industrial complex. And make no mistake, I’m not a big fan of Dr. Robert Malone, who is quoted at the end of that video, since he has possibly inappropriately sued “the Conscience of Psychiatry” … who is, to my knowledge, the very honest psychiatric and medical truth teller, Dr. Peter Breggin.

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  9. Do I have bipolar or simply bipolarity? Whichever – my life got back on track once I learned how to the condition and started guarding my stability. Mostly by strict adherence to lifestyle measures. I don’t have time for stigma. I’ve got a life I want to live. So I say I have bipolar because then health care providers who don’t understand bipolarity will take care not to prescribe other meds that might set off an episode.

    BTW thank you, Dr. Phelps, for those amber glasses. Major piece of resolving my sleep issues, which is a major piece of maintaining my stability, which is priceless.

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  10. The terms “trauma” and “bipolarity” may seem devoid of meaning when not linked to specific experiences and observable symptoms in one person (they cannot be used for abstract faceless humans as if they mean an arm or a leg). What exactly constitutes trauma? This ambiguity is a factor that diminishes people’s respect for psychiatry, as it appears to use words as if they were tangible entities. If we are using language, then we need to use it effectively not just one has power to say whatever they want.

    This situation brings to mind the Positive Disintegration Theory proposed by Kazimierz Dąbrowski. He eloquently delves into the excitability factor in humans, emphasizing its role in managing and regulating mood and fostering psychological growth and transcendence. the more I read MIA, the more I feel the whole psychiatry is set to diminish human excitability! making everybody standardized!

    But if I attempt to approach this topic objectively, one might perceive depression as a form of regression (deep child like state) and mania as a transcendent state (adult form), often without conscious awareness of either condition at any given moment. And I really think this polarity is very normal human thing at minimum.

    However, the question arises: why medicalize mental illness instead of incorporating it into educational frameworks at early age? One can be as happy in depth as much as they can be depressed in depth – as unique as their fingerprints. If we teach them early on rather than ritalining them into zombie, I think most people can manage their cycles as adults in much more creative and healthier given the opportunity. All these meds are just blocking people from increasing their consciousness to regulate and self soothe and keeping them into compliance of the state sanctioned behaviour.

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  11. I think your survey on which dosage patients stop their antidepressants may have a caveat.
    In my experience, not even a psychiatrist will prescribe the lowest dose, because you can often just cut the second-lowest dose in half. I don’t think my insurance would cover the lowest dose for this reason.

    When I was on sertraline the lowest dose I was given a prescription for was 50mg, not 25mg. I was instructed to cut the pills in half. When I returned describing insufferable symptoms, I was instructed to take halfs on alternating days or to numb the pain with benzos (which I refused). I did not return to this doctor and instead got a second expert opinion, which was equally unhelpful: “I have not heard of these problems before, my patients tend to have good experiences with this drug. Are you sure you aren’t having a panic attack right now?” This doctor then suggested voluntary inpatient treatment where I could be put on additional drugs, to help with the other drugs, which I also refused.

    The bottom line both of these experts conveyed to me is that my adverse reaction was a sign that I need to be on higher doses of the drug or on more drugs. I quit the drug cold turkey, with a short but extremely unpleasant period of withdrawal. The symptoms subsided completely and didn’t return. I think I got lucky, because I only took the drug for a short time.

    So yes, I am opposed to your explanatory effort using the term bipolarity, for dialectic reasons. I think this terminology supports the current trend of increasing dosage and adding more drugs, because the adverse effect are a sign of an uncovered underlying issue (i.e. bipolarity). To me, it is not a middle-ground solution as you called it in a previous article.

    You seem to have extensively read symptom reports on the surviving antidepressants forum. Cascading polydrugging with increasingly worse outcomes is not a rare experience there, it is in fact common. Many people end up with atypical antipsychotics or mood stabilizers for their underlying bipolar condition, which was just an adverse reaction to an antidepressant.
    The thing we all need is rather simple: A prescriber who takes our symptom descriptions at face value and helps us get rid of the offending drug(s). You seem to honor this approach in your practice, which I think is great. I have never met anyone like you in my time in the mental healthcare system, though. The worst part of the experience for me was the complete lack of care I received.

    For the record, I would say the descriptions of manic symptoms on your questionnaire don’t describe me at all and this has always been the case throughout my life. However, the adverse drug reactions for antidepressants on the second page were all present for me to an alarming degree. I’m not sure how this could have helped before trying sertraline, even if my prescribers had bothered inquiring.

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  12. As the meme curse decrees: “Every single person who confuses correlation and causation ends up dying”.

    The presumption that antidepressant withdrawal symptoms indicate unmasked bipolar disorder or other pre-existing psychiatric condition is very old and very wrong.

    There are so many confounds in Phelps et al., 2023, it’s hard to know where to begin. Lack of prescription refill could have many explanations other than lack of withdrawal. People may not have refilled because they’d already been cutting up their tablets for a while to taper off.

    People may have had withdrawal symptoms after stopping their antidepressants, but when they went back to their doctors, neither they nor their doctors recognized the symptoms as withdrawal. We know this ignorance is still near-universal (Framer, 2021). Or the patients and doctors may not have known to reinstate the drugs to stop withdrawal symptoms — we spend a lot of time on SurvivingAntidepressants explaining this, it’s still not common knowledge.

    Or it could be that patients just didn’t talk to those doctors about their withdrawal symptoms, having concluded their prescribers were dunderheads about the drugs anyway. Maybe they went to other doctors and got other drugs.

    The catalog of antidepressant withdrawal symptoms is vast. Choosing a subset of withdrawal symptoms, one may draw Venn diagrams showing overlap of antidepressant withdrawal with many medical conditions, such as ME/CFS, fibromyalgia, covid-19, long covid, traumatic brain injury, brain tumor, pheochromocytoma, Parkinson’s, multiple sclerosis, vitamin deficiencies.

    In fact, antidepressant withdrawal has a lot in common with withdrawal syndromes across psychotropics (Lerner and Klein, 2019; Nielsen et al., 2012). Are you prepared to generalize your theory of unmasked “bipolarity” to, let’s say, heroin withdrawal?

    You say: “SurvivingAntidepressants.org suggests small steps down for people with antidepressant withdrawal. My target was a presumed underlying bipolarity. The taper programs are very similar….But this similarity in taper programs, together with the other two lines of evidence above suggests a possible connection.”

    No, it does not. What is shows is that tapering causes fewer withdrawal difficulties than not tapering, and that it can be successful even if the premise for it is wrong.

    Love you, Jim, you are a good doctor, you’ve listened to your patients, but I’m still not buying your idea that antidepressant withdrawal reveals pre-existing “bipolarity” or any such pseudo-biopsychiatric source.

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    • ‘”Every single person who confuses correlation and causation ends up dying”’… not necessarily at the same time.

      “The presumption that antidepressant withdrawal symptoms indicate unmasked bipolar disorder or other pre-existing psychiatric condition is very old and very wrong.”, I agree, causation seems way too lacking for simple correlation to stich the quilt…

      “Or it could be that patients just didn’t talk to those doctors about their withdrawal symptoms, having concluded their prescribers were dunderheads about the drugs anyway. Maybe they went to other doctors and got other drugs.” like more sensitivity among psychiatrists than GPs leads to more false positivies?. Or more equivocations?.

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  13. Hi Jim

    similarly to what people have already written in the comments above I also think it is a problem to speculate on the question of the different experiences for people in anti-depressant withdrawal and then link it to another highly speculative theory like your bipolarity hypothesis.

    I don’t think that it will pan out that it is people with a certain personality type that have difficulties with tapering off medication. Still I find your work interesting and valuable. Especially the bipolarity hypothesis. What about focusing on that subject only and dig deep in this place to actually find some robust insights?

    I am a follower of the nine-type-personality theory (Enneagram) that was first developed by the Chilean psychiatrist Oscar Ichazo in the 1950. It has since seen a spreading among religious people. Their books are not very valuable. On the other hand there is also a psychological tradition with thought leaders like David Daniels (MD) and Virginia Price, and Don Riso and Richard Hudson (all psychologists).

    Their books The Essential Enneagram (a qualitative test) and The Wisdom of the Enneagram (a very good description of the nine personality types) I can very much recommend.

    I bet you will be surprised that under type four you will find your “bipolarity theory” already fully formulated. Here is a short introduction to the theory and type four:


    Oscar Ichazo was a psychiatric genius of his own and I consider his insights as groundbreaking for psychology and psychiatry as was the late medieval astronomer’s insight that not the earth but the sun was at the center of our solar system!

    It is said that his insights were gained on a thorough understanding of the psychiatric theory of the so called personality disorders and a very deep experience of the reality of the different personality styles from working with people in psychotherapy.

    I am well aquainted with the theory and I haven’t yet met anyone who did not have type four as their main or at least side personality style and had experienced to be able to access the patterns of mania as a means to protect themselves from a unwanted life reality that they couldn’t find a way to deal with anymore.

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  14. Dr. Phelps, I think that the experience you have with your patients (where most DO have withdrawal issues) is the correct one.

    For most primary care physicians (and even most psychiatrists), everything is viewed through the lens of disease and illness. Patients are reporting these problems with the drugs and with withdrawal but they are NOT seen as drug issues, but as evidence of further mental disorder…

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  15. “Lacking an understanding of mechanism, is there any other way to identify the people who will have severe withdrawal symptoms when they [WE] try to stop an antidepressant?”, not scientifically, to prove the correlation of an intervention with an outcome requires causality.

    Simple observational correlation does not have that issue, but interventional correlation does.

    Proving causality requires a proven mechanism beyond doubt, i.e. a theory in the scientific sense.

    Bipolarity expressed as such sounds to me not like energy or drive, there might be a part of that, but sounds more like commitment, resolve, in the sense of firmness of purpouse. “a promise to yourself to do or to not do something”.

    And that apparent equivocation seems important to me because it is opposite to clamining SSRI on the way up or the way down cause instability. That is, because increasing being more resolved, more determined causes oneself to be more unstable.*

    As such, it would cause the opposite of the hypothesized. And as such, a harm not a part of bipolarity but a weakining of it. Removing a quality for firmness in purpose to replace it with instability.

    And that makes my view, I think firmer: Maybe you see more patients with more difficulty withdrawing not by bipolarity, admitting they overlap symptomatically, but because by the referal they are already selected as more harmed by the treatment than patients that stay with the primary provider.

    And that may or may not be bipolarity, and it would be despite bipolarity, overcoming it, defeating it, if it could be understood as firmness of purpose.

    Which saddly, sounds sadder…

    But, maybe the correlation with bipolarity is a proxy of “toxic” sensitivity, just the why, ironically, might rear its back into making hypotheses out of correlations alone, paired with acute clinical eye, I admit. 🙂

    *Like overheating?. Well, I can see as a metaphor that might look appealing, but it might be at least a strained one. And I get the feeling there are hidden hypotheses in the argument, that make it appealing as “overheating”, despite, as I formulated originally sounds contradictory.

    And I could look for the hiddens, but I feel quirky going mainstreamy on the bipolar or bipolarity. It makes me uncomftable, but I am ok “engaging”, if options are provided. 🙂

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  16. Where is Dr. Philip Hickey when we need him! There is so much wrong with this author’s blog series it is hard to know where to begin.

    This 3 part series on antidepressant drugs should be titled:

    “How to manipulate patients to take more antidepressant drugs, Uphold the DSM while creating new diagnoses, and ALL the while pretending to be a more “enlightened” psychiatrist who is trying to save psychiatry from its rightful place in the dustbin of history.”

    And so far the author has not responded to any criticism directed his way, nor do I expect he will.

    Because this author pretends to be a more “enlightened” psychiatrist, it makes the content of these blogs especially dangerous to be published at MIA without a thorough going critique exposing the pseudoscience and harm contained within.

    For example, in order for this author to minimize the overall damage done by the main effects of antidepressant drugs AND for their horrible withdrawal problems, he invents a new diagnoses called “Bipolarity.” He should have actually named it “Bipolar Light;” which sounds kinda cute and more clever. THEN he DECLARES that it is probably “genetic.” Ahhh , more “genetic theories of original sin,” as if we didn’t have enough.

    After inventing this new diagnosis (and never critiques what is wrong with the original “Bipolar” diagnosis), he uses this pseudoscience to allegedly explain why some people (he minimizes how many) end up experiencing horrible withdrawal effects.

    Yes, once again, the ultimate culprit (you guessed it) is actually is in our bad human genes. No, it just couldn’t be the actual drugs themselves and those institutions (Big Pharma and psychiatry) that have colluded for decades (spending billions on PR campaigns) to get hundreds of millions of people on these toxic drugs.

    Please, someone step forward and brutally critique this blog series. MIA and its readers deserve better!


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  17. I also want to say upon re-reading this article and having recently listened to a talk given by Dr. Raymond Perrin (The Perrin Technique) that serious consideration of his work and his theories on the relationship between the autonomic nervous system, the spine, and the lymphatic system also needs to be taken into account when theorizing on why some people develop severe withdrawal and some do not. The Perrin Technique is now widely used across the UK to treat ME/CFS which has striking similarity to similar “neuro-immunological” conditions of which withdrawal highly resembles. There are so many variables from across a spectrum of medical and scientific specialities that need to be considered and looked at together in a coordinated scientific effort to discover why withdrawal occurs and why with varying severity. The answer most certainly does not lie within psychiatry or psychology alone, by any means.

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  18. Doctor, I’m curious as to what you think about kindling? If you have tried several different antidepressants in the past that means you’ve experienced multiple withdrawal experiences. In alcohol rehab facilities they’ve long recognized that each time alcoholics “fell off the wagon” then went back to rehab, the alcohol withdrawal symptoms experienced was more intense.
    Could this be a factor in why it’s harder for some than others to stop their antidepressants?

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  19. I have to disagree. First, he brought up traumatic experiences but he never really said how those experiences affect a person or even a person going through a medication discontinuation! When someone goes through a traumatic experience, especially as a child, it sets their nervous system to be more or permanently on the sympathetic side (always in flight or flight). He never talked about how he helped anyone and taught them how to calm the nervous system down. When someone is going through a medication discontinuation it is not possible to teach them this until they are off and healed somewhat. I don’t believe in disorders, especially from the DSM, which was written by the pharmaceuticals, to benefit them through profit!

    He never talked about how diet and lifestyle might affect a person being put on or taken off a medication! He never talked about the barriers in the body system. Like the gut barrier, the brain barrier, and even the blood barrier. Every organ has a barrier that our immune system lives in and helps to protect that organ from chemicals, bacteria, etc… When that barrier is broken in any area within the body, it causes inflammation, and the inflammation itself causes broken barriers. So if these medications, chemicals, vaccines, diet, lifestyles, bacteria, mold, etc.. get into areas those areas they were not meant to be in what kind of damage do you think they will cause? Especially if it gets into the nervous system and the brain!

    I have been in many different diet and lifestyle groups and the one diet that seems to help heal these supposed MENTAL disorders is the carnivore diet. Many people claim it has helped dramatically. The ones that it doesn’t seem to help completely are people that have CIRS (chronic inflammatory response syndrome). But the diet helps these people some.

    So if someone has had a traumatic experience that sets their nervous system to flight or fight (this itself will cause inflammation in the body by raising cortisol which then raises blood sugars, causing inflammation all over the body), has a really bad diet that has broken the barriers within the body, and then goes to a doctor that doesn’t really educate themselves, just goes by what they were taught for profit for the system. So the doctor prescribes a medication or maybe even a vaccine (medications and vaccines can break these barriers also), but as they say, they don’t really know what they do! What do you think the symptoms this person will have?

    I will never be a doctor but if I can think outside the damn box and do my own research and come up with this on my own then why can’t doctors? They are so smart!

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