“Withdrawal teaches you, as the clinician, that you don’t control the process. Successful tapering is inherently patient-led, and there’s a kind of humility in accepting that.”
This is a nice interview, but for someone who claims to study medication withdrawal, the ideas seem to track remarkably well with what lay people say rather than what researchers write.
Among the more dangerous things I have encountered in psychiatry, I would rank the myth of hyperbolic tapering just below akathisia. People get into terrible trouble with it. I personally know cases where women have spent close to half a decade in hyperbolic tapering loops. In fact, this kind of drawn-out process is more the rule than the exception.
The idea that drug effects can be meaningfully mapped to receptor binding profiles is demonstrably untrue. Most psychiatric drugs have multiple windows of effect. This has been known for a long time. Some drugs, such as SSRIs, do show sharp hyperbolic occupancy curves, but many others do not. Some are sigmoid. Many drugs also have state-dependent binding characteristics or compete with other chemicals.
It is also odd to talk about homeostasis in relation to psychiatric drugs, since it essentially repurposes the chemical imbalance narrative. It is contradictory to claim that the chemicals involved have nothing to do with the illness, except when they supposedly generate similar syndromes during withdrawal. Brain systems operate more on an allostatic principle. Receptors can upregulate and downregulate quite rapidly, assuming receptors are even the central issue. Saying there is too much serotonin (ironically the exact opposite of drug company marketing) is like saying there are too many letters in the postal system on a given day.
This is what I see happening in withdrawal groups. People have been on the medication a long time, they try to come off, and they experience significant withdrawals. Sometimes the withdrawals are truly horrific, but in other cases they are distressing mainly because the person expected to feel nothing. Regardless, they panic and, like a child stuck up a tree, they cling tightly to the branch. They begin lowering themselves slowly, resulting in a shaky descent with a lot of scraping and clawing. When they reach the lower branches, they become so overwhelmed by the myth of hyperbolic tapering that no amount of encouragement can coax them the rest of the way down. Instead, they spend another year or two, often on top of the year or two already spent, measuring out doses in ever smaller fractions. The entire process becomes a neurotic mess of emotion and terror. Eventually they come off and give full credit to the hyperbolic taper. Of course, there is no reason to believe the excruciatingly slow pace made any difference. There is simply no counterfactual.
The whole thing is like that Simpsons episode where Homer gets his arms stuck in two vending machines. Just before the paramedic amputates his arm, they notice that Homer is still holding onto the cans. Of course Homer feels foolish but he really did have his both of his arms stuck, it is just that when you are in a situation like that, and panicking, it is very hard to figure out what is actually going on. I believe that consumers can have excellent empirical insights and should be listened to a hell of a lot more, people know their own bodies. But in this kind of panic striken state, I'm not sure how easy it is to tell what is doing what.
But perhaps you think I am being unfair. In truth, tapering can be very difficult, and for some people slowing things down substantially can help. For others it simply increases their exposure to a drug that may be making them unstable or affecting other physiological systems. There is no evidence that 5 or 10 percent reductions are better than 15 or 20 percent reductions. Current ideas about hyperbolic tapering have no logical endpoint. People just go slower and slower until they are on fractions of a milligram, grinding pills into dust. In some cases, all-cause mortality seems more likely to catch up with them before they finish the taper. It is all very silly but also very sad and I truly feel awful for the people who go through it.
In my experience helping people in withdrawal groups, going a bit slower, perhaps half the original speed, is often as effective as a 10 percent reduction schedule, or at least the difference is not noticeable. That, combined with the judicious use of antidotes, usually gets people better much faster without them getting psychologically stuck. I am also not convinced from what I have seen that tapering speed has anything to do with protracted problems after withdrawal. I have actually seen more cases with ongoing issues among those who followed extremely slow tapers. It could be that the people who cannot go any faster are the ones most harmed by the drug, but it seems at least equally plausible that the harm was already done and dragging out the taper only increased exposure to the problematic medication.
This doesn't mean I don't believe that we can't improve taper schedules or that going much slower might indeed turn out to be a good idea. My issue is with the way "hyperbolic" tapering has reached heights of popularity that would make the marketing departments of drug companies blush.
I share many of your concerns. In my experience with my patients, most people tolerate a gradual but non-hyperbolic taper just fine. My impression is that hyperbolic tapering seems to be useful for a subset that are really struggling with tapering. I am really curious to see what happens with hyperbolic tapering under randomized, blinded conditions (and my own guess is that on average there will be no advantage)
Pretty much my observations from within the withdrawal groups. I think hyperbolic tapering could be as much psychological as biological. What irritates me is that the hyperbolic crowd all chant the same tune on pharmacodynamics while curiously lacking fundamental information about pharmacodynamics. The hypnotic effects of Seroquel at lower doses come to mind, not to mention metabolics and half-lives.
As much as I feel like a turncoat saying it, the mix in the withdrawal groups is the same mix you see in clinical settings. A good fraction are neurotic, a smaller number may have neurodevelopmental disorders, some may have lability due to past trauma, and a much smaller number are likely bipolar, although curiously few are truly psychotic. Then there are cases of lupus and immune sensitivity. Within that, there are very real experiences that have nothing to do with these factors. Most alarming are the cases of lupus that seem suspiciously well timed to the drug.
My overall impression is that the old psychopharmacologists were mostly right. Benzodiazepines rarely cause dependence in sensible doses, antidepressants are reasonably safe for the first year or so, and anticonvulsants are probably towards the top of the heap in terms of difficult withdrawals. Most striking is that the withdrawal group for lithium is virtually non-existent. This seems difficult explained purely by prescribing rates. While bad experiences on lithium are common, they appear to be much more straightforward and less bizarre, and overall people do not become “entangled” in lithium. Largely, the lithium cases just seem to have taken too much.
I think a large part of the problem stems from the paint-by-numbers approach to medicine that is common in some places. Most of the worst stories I have encountered so far in the groups come from France. French psychiatry seems to be leading the world in mindless practice, as if they are daring local authorities to replace them with convenience store clerks. The US is a distant second. A large part of the issue could be solved if psychiatrists simply took responsibility for piloting the “aircraft” instead of behaving like vending machines. It is largely a problem of deskilling in psychopharmacology as far as I can tell, much like the deskilling that has occurred in psychopathology. The whole thing gives psychiatry the feeling of a “Woozle hunt” or constant reruns of Back to the Future. If we are not careful, we will forget the use of lithium for at least the third time in recorded history.
Amongst all this, David Healy has expressed to me his interest in carefully gathered idiographic case descriptions of withdrawal syndromes. He is particularly interested in case studies that include introspective descriptions from the patient. He wants to know what they are experiencing internally so that similar effects can be differentiated. For example, he’s looking for descriptions like the urge to “leap out of” one’s skin, which seems quite pathognomonic of akathisia. If you read his book The Suspended Revolution, it contains a lot of information about the kinds of descriptions he thinks are useful. He's also interested in trying to find matching pairs of cases or small case series in which the phenotype is strikingly homogeneous between individuals. I'm actually serious, if you have any sensible case vignettes, send them to him.
I'm not an expert but I think figuring out what you are taking them for is probably the most important thing. And by that I mean, really nailing the jello to the wall. Course is usually the most important criterion, as in "course of illness".
"Antidepressant" as a term is a bit of shorthand. There are several types and in my non-expert opinion, there are probably more than a few different things we casually call "depression". The problem is figuring out what you are experiencing.
To be a little less cryptic, for a start and just as an example, the most common antidepressants, SSRIs, probably don't do a lick for the most serious type of depression: melancholia.
In terms of safety, I think it is reasonable to believe people who report that they find it hard to come of them, and it seems to me that most of those people have been on them a few years, whereas the ones who have only been on them a few months seem to report less problems. That's probably about the best data we have to go on. It is anecdotal but it also seems like a fairly straightforward thing that is being reported so I can't see much reason to treat the claim with suspicion.
The reason I say what I say about benzos is that, despite the problems reported by the benzo withdrawal community being very real, benzos came up in an era of drug restriction and were the subject of a war on drugs launched by the FDA. They got dragged over hot coals and nothing came out. If benzos caused problems as frequently as people think these days, they would never have survived the intense scrutiny. The only way I can think of to square the circle on benzos is to suggest that either benzo withdrawals are a relatively rare reaction or, alternatively, work on a principle similar to alcohol, i.e. a glass of red wine a day will probably never cause a serious addiction.
For a bit of an insider scoop on antidepressants and other drugs, you can go and read interviews with the discovers of the drugs on the INHN website. Here is an interview with Roland Kuhn, who discovered the use of one of the very first antidepressants, and he had strong views about exactly "which depression" they should be used in which he called "vital depression": https://inhn.org/about/interviews/leonanrdo-tondo-interview-of-roland-kuhn
A lot to address here. What do researchers write that contradicts what Anders says here?
It’s pretty ironic that you call hyperbolic tapering dangerous. I really hope you’re kidding. Hyperbole about hyperbolas? Dangerous because of the “neurotic” worrying? Dangerous because it extends the duration of time someone is on a medication you would likely deem relatively safe in the case of SRIs?
Drug effects are more than receptor binding, yes. Binding is a degree or two removed from biological effect, but there isn’t yet a more biologically accurate model available, unless you have one to provide. SRIs have hyperbolic occupancy curves, as do antipsychotics, the main drugs Anders discusses. Most psych drugs have hyperbolic curves. Which drugs are you thinking of with sigmoid curves?
How quickly receptors up or down regulate after chronic drug treatment is an open question and differs significantly by receptor system. Making a blanket statement like that is overly reductive. Saying serotonin levels influence withdrawal isn’t necessarily contradictory; 5HT levels are known to increase with SRI treatment, and are correlated with both treatment effects and side effects. The point is that raised levels are not a sufficient explanation and there is much more to the story mechanistically.
I don’t quite understand what basis you have to assume that hyperbolic tapering is a myth. The principles, eg tapering by a % rate each month, were initially largely derived from patients themselves, who had to look to each other for guidance (in the face of no institutional guidance) , not fabricated just from dose occupancy curves. The PET radioligand studies more so provided a biological underpinning to validate what patients had discovered themselves. So it’s been grounded clinically from the beginning. The reason to believe that the method makes a difference is because it gained traction specifically because it helped a subset of patients. It may be over applied, or excessively cautious in some patients, but that’s exactly why more research is needed. And to assume that it’s a myth at that point is to simply assume that patients are just being “neurotic” and it’s “all in their heads”— a very bad stance for a psychiatrist to take.
Hyperbolic tapering is entirely consistent with 20% reductions. The “evidence” that some patients need smaller reductions is simply that they’ve found that to be the case. I’m not saying psychological factors don’t play a role in some cases, but I think you’re leaning too far into assuming they are the primary factor. I think the best stance in these situations is to give credence to your patients. What is it that makes you dubious of some patients actually needing very slow tapers? Because you think it’s improbably biologically? Because there isn’t “evidence” of the need? Please think about how evidence in medicine is created, ie money is needed for research and financial incentives to study this are limited to non existent.
And most patients go to this method after failing traditional tapers, often multiple times. The picture you paint is just not representative of the majority.
And I can promise you that pharma companies have done a great job marketing.They literally branded SRI withdrawal as “discontinuation” syndrome and are the reason people are generally dubious of protracted syndromes!
I'm not a doctor. My wife developed the form of akathisia described by Teicher and Cole in the early 1990s. This event very nearly ended both our lives. I take this problem seriously which is why I don't want to see people go swerving from one dangerous myth to another.
The primary basis is comes from interviewing people who are part of a hyperbolic tapering group, who along with their terrifying tales of drug side effects and withdrawals tell me they feel pressured to follow a hyperbolic taper and they're too scared to speak up because the group will ridicule them and ostracise them if they criticise hyperbolic tapering, and to thank me for saying something that made them feel safe to try another way.
I don't know how widespread this issue is but it is clear that some groups latch on to the idea and it has spread far beyond SSRIs and benzos. Tapering is a terrifying process, hyperbolic taper gives people hope. Some people benefit from it tremendously, others become very stuck and spend years in a vicious cycle.
What people fail to recognise is that the notion is strikingly similar to the marketing language used by pharmaceutical companies who have constructed a narratives around "chemical imbalances".
I say it's a myth because it largely attempts to reverse engineer research that has been promoted and influenced by pharmaceutical companies.
The windows of effects of antipsychotic drugs were not established by the manufacturer's research but from psychiatrists talking to patients and observing them first hand. This sort of research is no longer done and is probably the reason no one noticed the new problems.
Nervous illness, otherwise known as neuroticism is a serious thing and I apologise for speaking flippantly about it. Many people with nervous illnesses are prescribed benzos and SSRIs, many of these people already suffer from severe medical anxiety and rumination. Hyperbolic tapering can become a source of great distress for them and they can easily become trapped in cycle of anxiety and despair. Due to how long the typical tapers can go on for, it is not unusual to see people go through this for several years.
I having nothing against hyperbolic tapering per se. If someone has been on a drug for a long time, it seems sensible to slow things down. But there isn't much evidence it works.
There are other problems, drug bioavailability is not consistent and the binding curves start to breakdown at lower doses. Add in the half life of the drug and in many cases at lower doses the variance is greater than the taper amount.
If we want solve this problem we need to believe people and help them figure out what is going on. But offering them new biologically plausible narratives isn't helping them. Hyperbolic tapering didn't come from victims, it came from well meaning doctors. The fact that some victims think it helped isn't very helpful. Better to listen to the ideas that came out of their experiences that are theirs and not put in their heads by others. Easier said than done.
Anyway, let's not fight. This is a problem to be solved. I'm as frustrated as you are.
This is a nice interview, but for someone who claims to study medication withdrawal, the ideas seem to track remarkably well with what lay people say rather than what researchers write.
Among the more dangerous things I have encountered in psychiatry, I would rank the myth of hyperbolic tapering just below akathisia. People get into terrible trouble with it. I personally know cases where women have spent close to half a decade in hyperbolic tapering loops. In fact, this kind of drawn-out process is more the rule than the exception.
The idea that drug effects can be meaningfully mapped to receptor binding profiles is demonstrably untrue. Most psychiatric drugs have multiple windows of effect. This has been known for a long time. Some drugs, such as SSRIs, do show sharp hyperbolic occupancy curves, but many others do not. Some are sigmoid. Many drugs also have state-dependent binding characteristics or compete with other chemicals.
It is also odd to talk about homeostasis in relation to psychiatric drugs, since it essentially repurposes the chemical imbalance narrative. It is contradictory to claim that the chemicals involved have nothing to do with the illness, except when they supposedly generate similar syndromes during withdrawal. Brain systems operate more on an allostatic principle. Receptors can upregulate and downregulate quite rapidly, assuming receptors are even the central issue. Saying there is too much serotonin (ironically the exact opposite of drug company marketing) is like saying there are too many letters in the postal system on a given day.
This is what I see happening in withdrawal groups. People have been on the medication a long time, they try to come off, and they experience significant withdrawals. Sometimes the withdrawals are truly horrific, but in other cases they are distressing mainly because the person expected to feel nothing. Regardless, they panic and, like a child stuck up a tree, they cling tightly to the branch. They begin lowering themselves slowly, resulting in a shaky descent with a lot of scraping and clawing. When they reach the lower branches, they become so overwhelmed by the myth of hyperbolic tapering that no amount of encouragement can coax them the rest of the way down. Instead, they spend another year or two, often on top of the year or two already spent, measuring out doses in ever smaller fractions. The entire process becomes a neurotic mess of emotion and terror. Eventually they come off and give full credit to the hyperbolic taper. Of course, there is no reason to believe the excruciatingly slow pace made any difference. There is simply no counterfactual.
The whole thing is like that Simpsons episode where Homer gets his arms stuck in two vending machines. Just before the paramedic amputates his arm, they notice that Homer is still holding onto the cans. Of course Homer feels foolish but he really did have his both of his arms stuck, it is just that when you are in a situation like that, and panicking, it is very hard to figure out what is actually going on. I believe that consumers can have excellent empirical insights and should be listened to a hell of a lot more, people know their own bodies. But in this kind of panic striken state, I'm not sure how easy it is to tell what is doing what.
But perhaps you think I am being unfair. In truth, tapering can be very difficult, and for some people slowing things down substantially can help. For others it simply increases their exposure to a drug that may be making them unstable or affecting other physiological systems. There is no evidence that 5 or 10 percent reductions are better than 15 or 20 percent reductions. Current ideas about hyperbolic tapering have no logical endpoint. People just go slower and slower until they are on fractions of a milligram, grinding pills into dust. In some cases, all-cause mortality seems more likely to catch up with them before they finish the taper. It is all very silly but also very sad and I truly feel awful for the people who go through it.
In my experience helping people in withdrawal groups, going a bit slower, perhaps half the original speed, is often as effective as a 10 percent reduction schedule, or at least the difference is not noticeable. That, combined with the judicious use of antidotes, usually gets people better much faster without them getting psychologically stuck. I am also not convinced from what I have seen that tapering speed has anything to do with protracted problems after withdrawal. I have actually seen more cases with ongoing issues among those who followed extremely slow tapers. It could be that the people who cannot go any faster are the ones most harmed by the drug, but it seems at least equally plausible that the harm was already done and dragging out the taper only increased exposure to the problematic medication.
This doesn't mean I don't believe that we can't improve taper schedules or that going much slower might indeed turn out to be a good idea. My issue is with the way "hyperbolic" tapering has reached heights of popularity that would make the marketing departments of drug companies blush.
I share many of your concerns. In my experience with my patients, most people tolerate a gradual but non-hyperbolic taper just fine. My impression is that hyperbolic tapering seems to be useful for a subset that are really struggling with tapering. I am really curious to see what happens with hyperbolic tapering under randomized, blinded conditions (and my own guess is that on average there will be no advantage)
Pretty much my observations from within the withdrawal groups. I think hyperbolic tapering could be as much psychological as biological. What irritates me is that the hyperbolic crowd all chant the same tune on pharmacodynamics while curiously lacking fundamental information about pharmacodynamics. The hypnotic effects of Seroquel at lower doses come to mind, not to mention metabolics and half-lives.
As much as I feel like a turncoat saying it, the mix in the withdrawal groups is the same mix you see in clinical settings. A good fraction are neurotic, a smaller number may have neurodevelopmental disorders, some may have lability due to past trauma, and a much smaller number are likely bipolar, although curiously few are truly psychotic. Then there are cases of lupus and immune sensitivity. Within that, there are very real experiences that have nothing to do with these factors. Most alarming are the cases of lupus that seem suspiciously well timed to the drug.
My overall impression is that the old psychopharmacologists were mostly right. Benzodiazepines rarely cause dependence in sensible doses, antidepressants are reasonably safe for the first year or so, and anticonvulsants are probably towards the top of the heap in terms of difficult withdrawals. Most striking is that the withdrawal group for lithium is virtually non-existent. This seems difficult explained purely by prescribing rates. While bad experiences on lithium are common, they appear to be much more straightforward and less bizarre, and overall people do not become “entangled” in lithium. Largely, the lithium cases just seem to have taken too much.
I think a large part of the problem stems from the paint-by-numbers approach to medicine that is common in some places. Most of the worst stories I have encountered so far in the groups come from France. French psychiatry seems to be leading the world in mindless practice, as if they are daring local authorities to replace them with convenience store clerks. The US is a distant second. A large part of the issue could be solved if psychiatrists simply took responsibility for piloting the “aircraft” instead of behaving like vending machines. It is largely a problem of deskilling in psychopharmacology as far as I can tell, much like the deskilling that has occurred in psychopathology. The whole thing gives psychiatry the feeling of a “Woozle hunt” or constant reruns of Back to the Future. If we are not careful, we will forget the use of lithium for at least the third time in recorded history.
Amongst all this, David Healy has expressed to me his interest in carefully gathered idiographic case descriptions of withdrawal syndromes. He is particularly interested in case studies that include introspective descriptions from the patient. He wants to know what they are experiencing internally so that similar effects can be differentiated. For example, he’s looking for descriptions like the urge to “leap out of” one’s skin, which seems quite pathognomonic of akathisia. If you read his book The Suspended Revolution, it contains a lot of information about the kinds of descriptions he thinks are useful. He's also interested in trying to find matching pairs of cases or small case series in which the phenotype is strikingly homogeneous between individuals. I'm actually serious, if you have any sensible case vignettes, send them to him.
“Benzodiazepines rarely cause dependence in sensible doses, antidepressants are reasonably safe for the first year or so,”
Would you say that after a couple years antidepressants become less safe? Less effective?
I'm not an expert but I think figuring out what you are taking them for is probably the most important thing. And by that I mean, really nailing the jello to the wall. Course is usually the most important criterion, as in "course of illness".
"Antidepressant" as a term is a bit of shorthand. There are several types and in my non-expert opinion, there are probably more than a few different things we casually call "depression". The problem is figuring out what you are experiencing.
To be a little less cryptic, for a start and just as an example, the most common antidepressants, SSRIs, probably don't do a lick for the most serious type of depression: melancholia.
In terms of safety, I think it is reasonable to believe people who report that they find it hard to come of them, and it seems to me that most of those people have been on them a few years, whereas the ones who have only been on them a few months seem to report less problems. That's probably about the best data we have to go on. It is anecdotal but it also seems like a fairly straightforward thing that is being reported so I can't see much reason to treat the claim with suspicion.
The reason I say what I say about benzos is that, despite the problems reported by the benzo withdrawal community being very real, benzos came up in an era of drug restriction and were the subject of a war on drugs launched by the FDA. They got dragged over hot coals and nothing came out. If benzos caused problems as frequently as people think these days, they would never have survived the intense scrutiny. The only way I can think of to square the circle on benzos is to suggest that either benzo withdrawals are a relatively rare reaction or, alternatively, work on a principle similar to alcohol, i.e. a glass of red wine a day will probably never cause a serious addiction.
For a bit of an insider scoop on antidepressants and other drugs, you can go and read interviews with the discovers of the drugs on the INHN website. Here is an interview with Roland Kuhn, who discovered the use of one of the very first antidepressants, and he had strong views about exactly "which depression" they should be used in which he called "vital depression": https://inhn.org/about/interviews/leonanrdo-tondo-interview-of-roland-kuhn
A lot to address here. What do researchers write that contradicts what Anders says here?
It’s pretty ironic that you call hyperbolic tapering dangerous. I really hope you’re kidding. Hyperbole about hyperbolas? Dangerous because of the “neurotic” worrying? Dangerous because it extends the duration of time someone is on a medication you would likely deem relatively safe in the case of SRIs?
Drug effects are more than receptor binding, yes. Binding is a degree or two removed from biological effect, but there isn’t yet a more biologically accurate model available, unless you have one to provide. SRIs have hyperbolic occupancy curves, as do antipsychotics, the main drugs Anders discusses. Most psych drugs have hyperbolic curves. Which drugs are you thinking of with sigmoid curves?
How quickly receptors up or down regulate after chronic drug treatment is an open question and differs significantly by receptor system. Making a blanket statement like that is overly reductive. Saying serotonin levels influence withdrawal isn’t necessarily contradictory; 5HT levels are known to increase with SRI treatment, and are correlated with both treatment effects and side effects. The point is that raised levels are not a sufficient explanation and there is much more to the story mechanistically.
I don’t quite understand what basis you have to assume that hyperbolic tapering is a myth. The principles, eg tapering by a % rate each month, were initially largely derived from patients themselves, who had to look to each other for guidance (in the face of no institutional guidance) , not fabricated just from dose occupancy curves. The PET radioligand studies more so provided a biological underpinning to validate what patients had discovered themselves. So it’s been grounded clinically from the beginning. The reason to believe that the method makes a difference is because it gained traction specifically because it helped a subset of patients. It may be over applied, or excessively cautious in some patients, but that’s exactly why more research is needed. And to assume that it’s a myth at that point is to simply assume that patients are just being “neurotic” and it’s “all in their heads”— a very bad stance for a psychiatrist to take.
Hyperbolic tapering is entirely consistent with 20% reductions. The “evidence” that some patients need smaller reductions is simply that they’ve found that to be the case. I’m not saying psychological factors don’t play a role in some cases, but I think you’re leaning too far into assuming they are the primary factor. I think the best stance in these situations is to give credence to your patients. What is it that makes you dubious of some patients actually needing very slow tapers? Because you think it’s improbably biologically? Because there isn’t “evidence” of the need? Please think about how evidence in medicine is created, ie money is needed for research and financial incentives to study this are limited to non existent.
And most patients go to this method after failing traditional tapers, often multiple times. The picture you paint is just not representative of the majority.
And I can promise you that pharma companies have done a great job marketing.They literally branded SRI withdrawal as “discontinuation” syndrome and are the reason people are generally dubious of protracted syndromes!
I'm not a doctor. My wife developed the form of akathisia described by Teicher and Cole in the early 1990s. This event very nearly ended both our lives. I take this problem seriously which is why I don't want to see people go swerving from one dangerous myth to another.
The primary basis is comes from interviewing people who are part of a hyperbolic tapering group, who along with their terrifying tales of drug side effects and withdrawals tell me they feel pressured to follow a hyperbolic taper and they're too scared to speak up because the group will ridicule them and ostracise them if they criticise hyperbolic tapering, and to thank me for saying something that made them feel safe to try another way.
I don't know how widespread this issue is but it is clear that some groups latch on to the idea and it has spread far beyond SSRIs and benzos. Tapering is a terrifying process, hyperbolic taper gives people hope. Some people benefit from it tremendously, others become very stuck and spend years in a vicious cycle.
What people fail to recognise is that the notion is strikingly similar to the marketing language used by pharmaceutical companies who have constructed a narratives around "chemical imbalances".
I say it's a myth because it largely attempts to reverse engineer research that has been promoted and influenced by pharmaceutical companies.
The windows of effects of antipsychotic drugs were not established by the manufacturer's research but from psychiatrists talking to patients and observing them first hand. This sort of research is no longer done and is probably the reason no one noticed the new problems.
Nervous illness, otherwise known as neuroticism is a serious thing and I apologise for speaking flippantly about it. Many people with nervous illnesses are prescribed benzos and SSRIs, many of these people already suffer from severe medical anxiety and rumination. Hyperbolic tapering can become a source of great distress for them and they can easily become trapped in cycle of anxiety and despair. Due to how long the typical tapers can go on for, it is not unusual to see people go through this for several years.
I having nothing against hyperbolic tapering per se. If someone has been on a drug for a long time, it seems sensible to slow things down. But there isn't much evidence it works.
There are other problems, drug bioavailability is not consistent and the binding curves start to breakdown at lower doses. Add in the half life of the drug and in many cases at lower doses the variance is greater than the taper amount.
If we want solve this problem we need to believe people and help them figure out what is going on. But offering them new biologically plausible narratives isn't helping them. Hyperbolic tapering didn't come from victims, it came from well meaning doctors. The fact that some victims think it helped isn't very helpful. Better to listen to the ideas that came out of their experiences that are theirs and not put in their heads by others. Easier said than done.
Anyway, let's not fight. This is a problem to be solved. I'm as frustrated as you are.