Response to Criticism of Our Serotonin Paper

37
14961

We recently published a paper finding that the serotonin hypothesis of depression (the idea that depression is caused by low serotonin or reduced serotonin activity) is not supported by scientific studies that have been conducted over the last few decades. The serotonin hypothesis was communicated to the public as the “chemical imbalance” theory of depression. In surveys, 85 to 90% of people in western countries report believing that depression is caused by a chemical imbalance.

We suggest that the idea that depression is caused by low serotonin or a chemical imbalance should no longer be communicated to patients as it is not supported by research.

An illustration of a doctor falling headfirst into a door in a giant brain, his feet kicking outside

This also brings into question what antidepressants are doing: if they are not correcting an underlying chemical problem, as people are often told (“like insulin for diabetes”), then other ways of understanding what they are doing, such as providing hope (the placebo effect) or numbing emotions (a common report by patients) may be more accurate descriptions.

Psychiatrists in Britain, some of them with career-long relationships with the pharmaceutical industry, responded to our paper’s findings and its implications here, which were then reported in several media pieces covering our paper. We would like to respond to these criticisms.

We would like to say first that no one should stop their antidepressant medication abruptly—this can be dangerous and is known to cause withdrawal effects, which can be severe and long-lasting in some people, especially those using the medications long-term. If anyone is considering this choice, we advise you to discuss it with your doctor and, if you go ahead, to undertake a gradual and supported reduction as advised by recent Royal College of Psychiatry guidance.

Contradictory responses—the serotonin imbalance theory was both never supported and also is still supported

There are a few remarkable aspects of the criticisms to note before we address specific critiques. The first is that the criticisms of our paper were contradictory, with some prominent psychiatrists saying that there was nothing new in our review (“really unsurprising,” “not news”) as it was already understood that depression was not caused by low serotonin. However, other psychiatrists said it was “premature” to dismiss the serotonin hypothesis and that further studies are required (despite this hypothesis having been studied for more than 50 years now). The existence of contradictory viewpoints reveals the cognitive dissonance in the field.

Disconnect between the public and psychiatrists

The second notable fact is how disparate the response was from psychiatrists and the public, with most psychiatrists shrugging off the finding as a straw man by saying “I don’t think I’ve ever met any serious scientists or psychiatrists who think that all cases of depression are caused by a simple chemical imbalance of serotonin” and that they are “broadly in agreement with the authors’ conclusion about our current efforts.”

In contrast there has been an avalanche of interest from the public—with more than a million reads on The Conversation, and widespread media coverage, so that our paper is now amongst the top 600 papers ever shared (out of 21 million papers that have been tracked). This interest likely stems from how widespread the message is that depression is caused by a chemical imbalance and that antidepressants work by fixing this imbalance. Many people, including journalists, have been shocked to find out this is not true, with one presenter commenting “it blows your mind.”

It may well be the case that psychiatrists have a more “sophisticated” understanding of the role of serotonin than the lay public, but psychiatrists have failed to correct this misunderstanding. Several academics have said that “we never told anybody this explanation.” However, the public clearly is being given this explanation: in England last week, a doctor on BBC radio told the public that in depression “there is a chemical imbalance and antidepressant given at the right time will help with that chemical imbalance.” The same message was given to the public on a leading UK morning television programme earlier in the year by another doctor. It is not surprising that the vast majority of the general public (as shown in surveys) believe this message to be an established scientific fact.

We know from our analysis of textbooks and journal articles that the idea of low serotonin (the “chemical imbalance”) was widespread in medical literature and remains so in many current textbooks. It was only recently that the Royal College of Psychiatrists in Britain removed its reference to chemical imbalances, describing the theory as an “oversimplification,” but without explaining that there is no proof for low serotonin levels, or indeed for any other neurochemical theory of the causes of depression. The American Psychiatric Association continues to tell the public that “differences in certain chemicals in the brain may contribute to symptoms of depression.”

Psychiatrists fail to appreciate the enormous impact for patients of being told that depression is caused by a chemical problem in the brain and that antidepressants can fix this problem. Skating over this issue to turn to alternative hypotheses about the cause of depression or the mechanism of action of antidepressants neglects to address the fact that patients have been misled. It is alarming to hear that there is a problem in your brain and it is misleading to suggest that we know there are drugs which can fix it.

This narrative strongly encourages people to take antidepressants because it seems wholly rational to take a drug which reverses an underlying chemical problem; indeed, it seems irresponsible not to do so. What is being dismissed as trivial semantics by experts has had consequences for the life choices and self-perception of hundreds of millions of patients worldwide. Imagine being told that you had a major problem in your heart that required medication to fix—only to find out that that problem was not truly there.

For the public, the chemical imbalance has been no straw man or semantic approximation, but something that has guided the direction of their lives, choices, and health. We know that believing that your depression is caused by a chemical imbalance tends to make people more pessimistic about recovery (seeing their symptoms as more chronic and intractable), leads them to believe they have less ability to regulate their moods, and also leads them to believe that medication is a more credible solution than therapy. We should actively counter this myth and remove it from medical information conveyed to patients because it is not supported by evidence.

The mechanism of action of antidepressants does not matter, as we know that they work

The other argument raised by critics was that even if antidepressants are not rectifying an underlying chemical problem, they can still be effective by modifying neurotransmitters—and we use many medications whose mechanism we don’t understand. Some critics have said “Many of us know that taking paracetamol can be helpful for headaches and I don’t think anyone believes that headaches are caused by not enough paracetamol in the brain. The same logic applies to depression and medicines used to treat depression.”

First of all, the analogy is misleading because we know that paracetamol works by targeting the mechanisms that produce pain, and it does not produce an alteration in normal emotions and mental experience. With antidepressants, we do not have evidence that they target the underlying biological basis of depressive symptoms, and they do produce mental and emotional changes which can account for their effects.

Secondly, we would suggest that how a drug works, or what exactly it does, is crucially important in evaluating whether it is useful or not. With a drug that modifies brain chemistry in ways we do not fully understand, it would be wise to take a cautious approach and be wary of using it for long periods of time on a continuous daily basis. This is a very different proposition from taking a drug that reverses an underlying deficiency.

With antidepressants, we are looking for heuristics, or rules of thumb, to make sense of what these medications are doing in the context of short-term randomised trials that show marginal differences from placebo (with the vast majority of studies lasting less than 12 weeks). The idea that medications work by rectifying an underlying imbalance is very reassuring. Indeed, who would decline such a “lock and key” treatment? And this seemed to have been the marketing strategy of drug companies in propagating this line. For instance, we are not overly worried about long-term use of insulin in diabetes because supplementing a naturally occurring chemical back to normal levels seems unlikely to be a harmful approach.

However, if the approach to treatment is now reframed as altering brain chemistry in a system that has no underlying detectable problem (or involves a complex and nuanced alteration of serotonin as yet poorly understood) then we are faced with a very different proposition. The human brain has evolved over millions of years and involves thousands of inter-dependent chemical systems to regulate processes in the body and brain. It is a valid question to ask: what is the effect on the brain of modifying the action of a neurotransmitter in this complex, inter-dependent system, especially in the long term?

We may be guided in answering this question by the effects of other substances that affect mental processes such as thoughts and feelings, including recreational drugs like alcohol. These tend to cause tolerance from repeated use, and withdrawal effects when they are stopped; this combination is usually termed physical dependence (a state distinct from addiction). Most such drugs also have detrimental effects on things like concentration and memory when they are used frequently or continuously. We know that these theoretical concerns are borne out in practice with the use of antidepressants: there are withdrawal effects—which can be severe and long-lasting in some people—and negative impacts on memory, concentration and sleep, not to mention sexual and other physical adverse effects.

We should use antidepressants because we know they work, even if we don’t understand their mechanism of action

Many critics have put forward the argument that it does not matter that antidepressants are not rectifying a chemical imbalance because we know that they are effective from clinical trials (and the mechanism of action is a secondary concern).

First, it’s important to remember that the majority of the effect of an antidepressant is due to a combination of the natural course of our moods and placebo effects. When you look at all the randomised controlled trials that have been performed together (as in this meta-analysis paper) they show that antidepressants are a little bit better than a placebo (an inactive sugar pill), but not much. Meta-analyses routinely find that placebos produce a 10-point improvement, while antidepressants produce a 12-point improvement, on a 52-point depression scale after 6 weeks of treatment. Many have argued that this 2-point difference between antidepressants and placebo does not amount to a worthwhile difference.

In fact, it is not certain that there is even as much difference as this, because there are methodological problems with these studies that may explain this small difference between drugs and placebo. These include the possibility that people on antidepressants have an enhanced placebo effect because some will be able to guess that they got the real drug due to side effects and other subtle cues. Indeed, in one trial, in which patients were all given an antidepressant, but half told that it was  a placebo and half told the truth, those who were been told that they had received an antidepressant showed twice the change in anxiety and depression scores compared to those who believed they had received the placebo. Expectations can have a powerful effect on outcome.

Recent criticisms of antidepressant trials are detailed in this paper and this one. Other important points are that these trials are almost all conducted by drug companies, and the vast majority of them last only a few weeks, whereas of course many people end up taking antidepressants for months and frequently years. In general, the effects of drugs tend to diminish over time, especially for drugs associated with withdrawal effects, such as antidepressants.

Even if there are small differences between antidepressant and placebo that are not explained by artefacts of the trial methods, there are other mechanisms that can explain their effects, and we cannot therefore assume that they work by fixing an underlying chemical problem (as outlined further below).

Antidepressants might work via a mechanism other than serotonin

Several critics have said that although antidepressants don’t work by correcting a serotonin deficiency there are many other possible biological mechanisms of depression that they may be targeting. The possible mechanisms included: acting through neurogenesis, “due to complex changes in neuronal functioning,” increasing neurotransmitter levels, or changing cognitive biases by acting on the brain. One psychiatrist pointed out that there are 59 biological hypotheses for why depression may occur and antidepressants might be working on any of these proposed abnormalities. One or more of these hypotheses may pan out, but at the moment they remain hypotheses—that is, they are speculative, unproven ideas about things that might be relevant, and most of them come from work in animals or cells in a dish.

This line of argument illustrates how most critics just assume that there must be something wrong with the brain: “it is very clear that people suffering from depressive illness do have some abnormality of brain function, even if we do not know what it is.” They also assume that antidepressants must be acting on the biological processes that underpin depression and this reveals how they are wedded to what has been called a “disease-centred” model of drug action. This is the idea that drugs for mental health problems can only work by reversing underlying brain abnormalities that are responsible for producing the symptoms of mental health problems.

However, one of us has been arguing for many years now that there is an alternative explanation for how psychiatric drugs work—the “drug-centred” model. This suggests that psychiatric drugs affect mental symptoms and behaviour through altering normal brain functioning and, through this, altering normal mental experiences and activity. When alcohol, for example, reduces social anxiety because of the typical mental and behavioural changes it produces, we recognise that these effects occur in anyone, regardless of whether they suffer from a diagnosed social anxiety disorder or not.

Any drug that changes normal brain activity is likely to have some impact on mood, and indeed, drugs with many different sorts of chemical actions have been shown to have comparable effects to drugs that are classified as antidepressants, including opiates, benzodiazepines, stimulants, and antipsychotics.

By virtue of changing brain chemistry, antidepressants also produce changes to normal mental activity and experiences. The nature of these changes depends on the type of antidepressant—some antidepressants are strongly sedative, for example, but others are less so. Sedative drugs might improve sleep and reduce anxiety, which may be reflected in a lowering of depression symptom scores (because depression scales include several items on sleep and anxiety), but they may also make people feel groggy during the day.

Antidepressants are widely recognised to numb emotions (in a dose-related manner), including not just sadness and anxiety but welcome emotions like happiness and joy. Numbing emotions is also likely to reduce depression scores, and it may be experienced as useful by someone with a mental health problem, but it may not be.

All these effects may account for the small difference found between antidepressants and placebos in randomised trials (if these are not due to methodological artefacts). Hence the difference between placebo and antidepressants does not demonstrate anything about the basis of depression, unless you make the surely indefensible assumption that all the effects described above are not relevant.

Taking a drug that numbs emotions may feel like a relief for someone who is deeply unhappy, fearful or confused. But in the long-term taking a drug that alters normal brain chemistry may have harmful effects. In fact, we know that antidepressants cause physical dependence. The brain alters to try to counteract the effects of the drug, and then when people miss a dose or stop taking the drug they experience withdrawal effects, which are a consequence of the brain changes no longer being opposed by the drug. These can be severe and prolonged, especially if people have used the drugs for a long time.

Long-term use of drugs that numb emotions may also have harmful psychological consequences because it may prevent people from finding other, potentially more lasting ways of managing their emotions. It may also prevent people from identifying and addressing the problems that made them depressed in the first place.

But SSRIs work so there must be a serotonin problem of some sort

Just because SSRI antidepressants show marginal benefits over placebo in randomised trials (as above), does not logically mean that depression is related to serotonin. For example, the fact that alcohol improves social anxiety does not mean that social anxiety is caused by an alcohol deficiency. And we do not think that headaches are caused by a paracetamol deficiency, as even many of the critics pointed out. This line of reasoning is so common there is even a term for this fallacy—the ex juvantibus fallacy (making inferences about the causes of an illness from response to a treatment).

The relationship of serotonin to depression is more nuanced

Many of the expert critics have suggested that although they recognise that a simple serotonin deficiency does not explain people’s depression, “changes in the serotonin system may be contributing to their symptoms,” in a more nuanced, complicated, and still poorly understood way. In one sense this is probably true—that serotonin in some complex way is in involved in depression—and we agree with one critic who said, “it would be surprising if a such a widely distributed brain neuromodulatory system was completely uninvolved in the complex experiences that make up clinical depression.”

Indeed, it is also probably true that noradrenaline, dopamine, inflammation, cortisol, glutamate, and substance P in various interlinking neural networks are all involved in some nuanced, complicated, and poorly understood way in depression—because of course the brain works with electricity and chemistry and so these will be involved in different mood states. It would be equally true to say that serotonin (and all these other substances) is involved in some complex, nuanced way in hunger, fear, joy, thinking, walking, talking, and sleep. It is essentially an untestable and unfalsifiable claim to say that a given chemical is involved in a complex, nuanced way in depression.

However, it is a very different sort of claim to say that a specific neurotransmitter is altered in depression and provides a target for treatment. The non-specific argument that serotonin is involved in some complex, nuanced manner is not a sound basis for manipulating serotonin as a treatment for depression. This is similar to making a general claim that biology is involved in depression (as it surely is) to justify the use of any biological treatment. Biology is involved in diabetes but this does not justify any biological treatment (e.g. blood pressure medication). Instead, a specific biological problem (insufficient insulin production) is used to justify a specific remedy (exogenous insulin).

Alternative understandings of depression

None of the experts who criticised our research or rushed to defend the use of antidepressants acknowledged that there are other ways of understanding depression, and other approaches to helping people who suffer from it.

There is abundant research that shows that stressful life events strongly predict depression. One study found that combining this with personality structure (“neuroticism,” which could be understood as essentially sensitivity to stress) shows an incredibly strong relationship to risk of depression—a strength of relationship entirely absent from research into brain changes.

This is not to dismiss the idea that biology is involved in our moods in some shape or form—genetics plays a significant role in shaping our personality, for example, along with upbringing and perhaps particularly childhood experiences. However, the role of biology in some general way is not the same as proposing a specific biological problem that can be reversed with a supposedly targeted biological treatment.

Some people suggest that even if environmental factors precipitate depression, depressed feelings are still produced by brain chemicals, and therefore modifying these chemicals can help alleviate these feelings. An analogy might demonstrate the limitation of this approach. We know that learning Japanese will produce changes in the electrical signals and chemistry of the brain. However, we would think it odd if a student of Japanese decided that they would like to work out what those chemical and electrical changes were rather than attending more Japanese classes. In the same way, if we know that situations that produce insecurity and stress lead to depression, trying to delineate the specific chemical correlates of depression might be less productive than addressing the challenging situations that are the root cause of it.

Overall, the search for the brain basis of depression in chemistry may be committing a category error, mistaking trouble in the mind for trouble in the brain, like opening up the hood of a computer when a piece of software crashes.

Summary

Overall, although academic psychiatrists may hold a more sophisticated view of the role of serotonin in depression than that it is simply lowered (although some continue to advocate for this explanation), this explanation for depression has been widely communicated to the public as the “chemical imbalance” theory of depression and this has affected their treatment choices and how they view themselves. This likely explains the considerable interest generated by our paper.

Despite opinions to the contrary, being told that a drug acts on the underlying chemical cause of depression is quite distinct from being told that it changes the brain in ways we don’t understand, and may act via placebo effects or numbing. This information is likely to have a profound effect on how people evaluate antidepressants and the decisions they make about them. The effectiveness of antidepressants in clinical trials is still highly contested, and other proposed theories of how antidepressants might target hypothetical biological processes underpinning depression have not been proven or demonstrated in humans.

Our overall approach to searching for the chemical equation of depression may not be the most fruitful manner in which to understand depression, given there is such strong evidence that stressful life events are closely linked to the onset of depression.

***

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.

37 COMMENTS

  1. Joanna and Mark

    So glad you shook up the establishment with your recent research and written articles. AND they (psychiatry and Big Pharma) will seemingly NEVER cease to come up with excuses and bogus arguments to justify their past 30 years of rotten science and harmful “treatments” when it comes to depression (and SSRI drugs).

    What stands out most of all in all of these debates is just how desperate those in power are to NOT have people seriously examine what is wrong with their profit based societies (and related culture) in which they have so much power and privilege. For them, it ALWAYS has to be faulty genes and biology to explain troubled human psychological states of mind and related behaviors.

    And when we talk about environmental stressors or other trauma type events in people’s lives, yes, some of these events will exist (through chance happenings) in every society or system.

    However, some systems, have inherent forms of class divisions and other forms of exploitation and trauma built in to their systemic DNA. This creates an environment with overly intense stressors that more often pushes the human genetic genome to its extreme limits of ability to cope in normal ways.

    Of course, most likely all neural chemicals (and their processes) in the brain are somehow connected to depressive or psychotic type thought patterns, HOWEVER, that says nothing about true causation and/or about how to safely resolve (in a positive way) those kinds of extreme human psychological states.

    Human beings have the genetic capability to be very violent, AND also to exhibit very compassionate and loving behaviors. Certain DIFFERENT environments will trigger both of these examples of human thought patterns and behaviors.

    Our vitally important historic task, is to create the environment that will ultimately bring out the very best of what the human species has to offer the planet and the Universe.

    Richard

  2. I really don’t see the point of such papers or discussions. Suppose the data went the other way, would that mean that we should submit to the mental health system?

    Certainly not! What we should be talking about is how to oppose and eradicate the mental health system, not to scientifically prove it wrong.

    Joshua

  3. I think nobody should be given antidepressant pills. But I am only one person with an opinion that many may not want to hear. I do not like people choosing to smoke or drink either, if these are imbibed addictively, but I would never influence them in their choice. I have been unmedicated for years through choice and recently I felt desperate enough to go back on pills for short term respite. They have helped to calm me. But I shall not stay on them longer than needed. Six months maybe. People go on morphine patches for six months and know “it” is not easy to withdraw. Ideally, being pill free is best for the body and brain.

    While here kicking a net ball against a rattling fence, can someone clever explain to me how numbing emotions is an effect of medicine? Oh I know that medicine does have that risk, for sure. But as far as I can understand it science does not yet know exactly what “emotions” are made of.

    Where are they even located?

    Are emotions fuzzy Valentine feelings that emerge from the four chambers of the heart? Are emotions effusive infusions drip fed into people from outside, from eventful stimuli, easy to intake like sooking up strands of spaghetti? Are emotions god-given? Or are emotions electrical fizzles that spark when synapses are tickled? Are emotions therefore chemicals? Neurochemicals?

    I am just spotting our collective avoidance of studying emotions on a metaphysical or quantum or mechanism level. We do not seem to want our emotions to be reduced to levers or buttons or drivers within the oafish blob of the ugly brain. And yet on closer inspection the brain is running the whole show night and day for almost a century.

    So we have this saying that medication, used to treat chemical imbalance, is numbing emotions, but is it possible that emotions are chemical too and at some stage can feel imbalanced? I am thinking of women with post natal depression. Their emotions are numb towards their babies. Some may say it is “trauma” that causes those women to become emotionally numb but the blood samples do point out massive surges or slumps in hormones after birth.

    Dear Joanna and Dear Mark, I am not being nasty in tweezering stray sentences. I am on “the side” of reducing medical intervention these days because it has become an over prescribing nightmare, but I have a disappointment in a concept given to me to read as “truth” when it can only joyfully be intuition. If traditional psychiatry had done the same teasing of its own confident offerings, from the deity of pharma, then we would not be where we are. We lose our double checking lack of confidence at our peril. For it is doubt that really “listens” to each individual, not “certainty”.

    A pill is a symbol of human certitude much like a nuclear missile is a symbol of human certitude.

    Since we do not know what consciousness is yet I believe we cannot confidently say what emotions are. We can only guess. I am fine with my guessing about my emotions. I do not need science to go looking at what makes a feeling of sadness or euphoria. Life is too short to analyse life away to a last award winning paper.

    But I would say for myself that my own feelings in my schizophrenia are interwoven with sublime ineffable chemicals of emotions. I do not like the word chemical. It is so harsh and reductive sounding but the periodic table of elements shows how diamonds and stars can be the chemicals of the skeleton and blood iron and breath. We ought to revere our Earthly chemicals without that being turned into gross treatment of those.

    Chemical is now a devil of a word to be set opposite the grace word “natural”, and so we dislike its artficial clinical evocation. But the human kiss has umpteen biological natural chemicals in it.

    I like Dr Susan Greenfield’s book on the brain. It is called “A Day In the Life of The Brain”. It is an homage to that vital organ, but half way through she goes into depth on her own research into trying to locate emotions and where they are coming from. She was surprised that a feeling like sadness can come from ANYWHERE in the brain. The notion of a blobby bit for anger or a blobby bit for sadness is from science’s old assumptions, instead Dr Greenfield became interested in brain scans that revealled subtle “waves” that ripple all over the brain upon heightened emotion. I am not explaining it well so maybe see the book for yourself, if interested in it.

    The HOOVER DAM is going to explode and when it does so I will prove that the consciousness of an ordinary person like me can see the future. It is all about Waves.

    Learning to swim does wonders for the emotions, whatever they are. That’s all that matters.

  4. I don’t know that I want to say too much about this.

    I totally support the basic argument of the original paper. But the bad reactions are partly due to the fact that while the paper knocked out a basic stable datum of “mental illness,” it failed to replace it with a new (hopefully more workable) stable datum. Simply destroying a stable datum leads only to confusion. You must be willing to supply a new stable datum if you want to reduce the confusion and clamor around changes in science.

    If the best we can come up with is that we should start addressing the events that trigger depression (and other non-optimum mental reactions) then let us state that.

    The fact remains that the depth of the reaction often is not consistent with the depth of the triggering event. Most people can bounce back from “depressing” events, even including the death of a spouse, parent, or sibling. There must be some other variable at work.

    I think better answers already exist and have simply been suppressed by a criminal mental health system. But you don’t have to agree with me to agree that the academic world does not have a complete picture of these processes, nor of course really effective treatments. Those people need to change something in their thinking, or they will never arrive at more workable answers.

    • Hi Larry, you write;

      “The fact remains that the depth of the reaction often is not consistent with the depth of the triggering event. Most people can bounce back from “depressing” events, even including the death of a spouse, parent, or sibling. There must be some other variable at work.”

      Why MUST there be some other variable at work? Why might it not be a compounding of events, which then cause the observable (over) reaction? We don’t see the build up to an earthquake, but some people surely see the effects of that accumulation. And if I were thinking along the lines of psychiatry, I might even attribute the earthquake to me dropping a cup of tea or some such unrelated event.

      Quite fascinated by this “ex juvatibus fallacy” presented in the article.

      I wonder what Dr Moncrieff thinks about the claim that the use of electricity can ‘shock’ the brains chemicals back to their normal functioning. Not unlike the ‘treatment’ our economies might require given the way things are going (see Naomi Klein The Shock Doctrine).

      https://www.youtube.com/watch?v=B3B5qt6gsxY&t=10s

      “Milton Friedman understood the utility of a crisis. Only a crisis, actual or perceived, produces real change. When that crisis occurs, the actions taken depend on the ideas that are laying around.”

      • Well, I guess my explanation of my understanding of how the mind works was not that convincing.

        The fact that different people react in different ways to life events is obvious but the reasons why really aren’t, are they?

        I know there is more to it than meets the eye, because people recover when those hidden factors are brought to the surface. But it is not a convincing argument intellectually.

        I would probably do better by refraining from describing the theory that I have studied and stick to my main message, which is that Psychiatry is purposely ignoring information that would lead it out of the woods, indicating that it would prefer to remain ignorant of its own subject.

        • My best guess is that there are some things we were never meant to know. Though I must say I find the ex juvantibus fallacy an interesting way of explaining the ‘three card Monte’ being done by psychiatrists.

          “I would probably do better by refraining from describing the theory that I have studied and stick to my main message, which is that Psychiatry is purposely ignoring information that would lead it out of the woods, indicating that it would prefer to remain ignorant of its own subject.”

          Personally, i’d be interested in the theory you have studied, but I understand why you might feel that way. (just between you and me, they don’t much like Muslims either)

          And your comment about preferring to remain ignorant of it’s own subject reminded me of the ‘copper’ who found it best he didn’t know about the attempt to ‘outcome’ me as a direct result of the misconduct of his fellow officers. How often do we hear of psychiatrists saying “it might be best I don’t know about that”. Which is possibly the reason this particular article has been so popular. It might just be best they DO know about this, or at least not be able to deny they were told.

          I heard today on the radio that they have an ‘anti psychotic’ drug which can be injected twice a year for ‘schizophrenia’, saving all the problems of taking pills everyday (check the ‘chemical handcuffs’ twice a year, saving doctor a heap of time). Not heard much of the details, just a general skipping over the facts to prepare the public for the ‘scientific breakthrough’ from psychiatry.

          It might be a good time to enter the discussion and ask if the shortened life expectancy, lack of recovery etc with those pills is the same with this new injectable. ‘new and improved’?

      • Boans,

        I like the earthquake metaphor. If an earthquake happens in the middle of the ocean, it might go completely undetected. Or it might go undetected until it results in a tsunami. Or it might be detected as a large earthquake in the ocean and the scientists will then post tsunami warnings based on the size they determine the earthquake to be. Maybe a tsunami will happen, maybe it won’t. Maybe it will affect one geographical area more than another even though perhaps the prediction was the opposite.

  5. Tremendous Chapter and Verse Rebuttable! Amazing how steadfast these “academic psychiatrist” remain in maintaining their large scale grift. But totally understandable since their daily life is dependent on writing prescriptions that insure no cure. In other words, the last thing they want is for a patient to be cured. They are the very disease/contagion they purport to cure

  6. Medicine has made numerous advances since adopting a particular ontological approach since 1800 – see Foucault’s ‘Birth of the Clinic’. Except in psychiatry. Here an ethics first approach is more important. Dethroning ontology is all important. Numerous philosophers have said this (e.g. Wittgenstein, Levinas, even Husserl). For those who don’t understand these terms – I’m saying the relationship comes first in psychiatry – and what a thing (such as the likes of what we call “depression”, “schizophrenia”, “obsessive-compulsive”, etc) is is unimportant. There is ample evidence that when we get the relationship right the ontological problem disappears (or dissipates, or “dissolves like sugar in water” – Wittgenstein).

    For Daiphanous Weeping, you must have a good reason for writing such long replies, but I couldn’t help noticing that you claimed science doesn’t know what emotions are. Yes they do. The enactive cognition approach, which sees “mind” as located in the body, describes emotions as subtle neurological-muscular movements often exhibited as we anticipate events.

    • Hey, Nick,

      I really appreciated the first part of your comment – I agree that psychiatry has relied on ‘naming’ and ‘categorizing’ to the detriment of understanding and using actual relationships between two human beings as the primary ‘healing’ agent. But of course, it should be understood that relationships are not really within the aegis of medical practice in the first place, so perhaps the first error is for medical folks to try and ‘heal’ emotional/spiritual/relationship concerns.

      As to your second statement, your explanation of emotions seems extremely shallow and limited, and not particularly scientific. ‘Seeing’ ‘mind’ as located in the body sounds a lot more like philosophy, as does ‘describing’ emotions in terms of ‘subtle neurological-muscular movements.’ I don’t think it’s fair to claim an irrefutable or even generally agreed-upon scientific understanding of emotions. Sure, there are lots of theories, but all that I’ve seen doesn’t come close to a fully tested falsifiable understanding of what emotions really ARE.

      • Hi Steve

        I try to keep my comments very brief. So my bad if I’ve made it appear very shallow. This was a description of radical enactivism – which is all the rage in cognitive science since 2000. It goes way beyond the Cartesian dualism – mind is no longer in the head – but firmly centred in the body. In a way it is the body. People are usually so entrenched in a form of Cartesian dualism that it takes quite a bit to get your head around (ha ha – given that mind is not in the head) this new paradigm. I would suggest some Hutto – although he is a little obtuse at first. I hope to have an article out shortly explaining it for the armchair philosophers.

        • I am not saying you are wrong. I’m just saying we’re not talking science any longer. When you have to talk about moving away from Cartesian dualism and ‘centering’ the mind in the body, not to mention declaring that something is ‘all the rage,’ we are definitely not talking about straight science anymore. We are talking about philosophy. Nothing wrong with talking philosophy, in fact, one of psychiatry’s most fundamental weaknesses is its lack of any coherent philosophical agreements and structure, but a possible viewpoint on what the mind or a thought or an emotion might be is a very far cry from a scientific understanding of it. I defy you or anyone else to design a scientific experiment to prove where the mind is located. I guarantee you can’t do it. So whether the mind is in the brain, in the body as a whole, or impinging on the body/brain from some exterior viewpoint, is simply not a question science can answer at the moment, and may never be able to answer.

          But I am still interested in hearing the ideas involved. I love philosophy, actually.

          • I am intrigued by your assertion that an experiment could not be designed to determine the location of the mind.

            Perhaps this is due to the reluctance of Science to use the being itself as an observer capable of reporting facts and observations. Odd, since humans are often involved in the chain of data produced by experiments, and also design the experiments and interpret their results.

            On the one hand, it could be imagined that one day “mental energy” could be described and detected using electronic devices, the way we do for radio, infrared, and other non-visible wavelengths today.

            On the other hand, we already have people themselves, who obviously interact with at least their own minds and could possibly learn how to locate that mind relative to other related spaces such as the body. Attempts already made along this line have come up with visualizations such as “an array of golden balls surrounding the body.”

            I personally don’t see the point of pursuing this particular question. We know from past life recall research that the mind, whatever its exact location and shape, is portable, can be taken with the spiritual being to its next body, where it can be used to inform the being of various past events and skills that may seem relevant in the current life.

            It is the reluctance of Science to accept these findings, not the absence of data, that is the problem. This is not simply “philosophical.” The data derived from past life research has been used to create therapeutic processes that help people. So this data is in the realm of applied science, just like basic quantum physics can be applied to the manufacture of light emitting diodes and other working electronic equipment.

          • Steve – we are somewhat apart on this. Radical enactivism originated in philosophy – (Moyal-Sharrock 2016 – “Wittgenstein today”, the quote “father of enactivism”) – but now it is answering empirical questions. Philosophy comes first in any endeavour that later develops an empiricism. You agree, hopefully, that there is a discipline called ‘Cognitive Science’ that employs thousands of academics in universities around the world, hold conferences, write papers etc etc. Now when a revolution occurs in a science it generally also shakes up some philosophical foundations. For example, it was thought for a long time that just as a bell struck in a vacuum makes no sound, so light must also need a medium to travel through. So the luminous aether was postulated to exist. Then Einstein showed that light waves are different from sound waves in that they don’t need a medium to travel thru. So the luminous aether was dropped from science – a philosophical assumption we found we could do without.
            Cognitive science is currently gripped by papers wrestling with this new paradigm. If you google “4E Cognition” you will find your way to many papers that explain this paradigm far better than I.

          • There have been plenty of groups of ‘scientists’ who have been dead sure and published lots of papers and so on. Sorry, but if this makes any kind of sense, it ought to be readily explainable to the lay person. Einstein’s theory of relativity is as complex mathematically as any theory known to man, but it can be explained in terms of bending space and the effects of travel as the speed of light is approached, etc.

            I have yet to hear anything from you that suggests any kind of grasp on the practical implications of this philosophy. Surely, you can come up with a simple example showing how this approach works out in the real world. But I am skeptical that such a thing can really be done, as we simply haven’t the vaguest idea what a ‘mind’ is or how it ‘arises’ or where it resides. Nothing, not a clue.

            I will give this a quick look, but it sounds like a very complex and difficult theory to explain, and in the end, good science tends to provide simpler solutions, not more complex ones. In any case, we really need to see a falsifiable premise that is vigorously tested before admitting something to be scientifically valid. I see no such premise here. The idea that the mind is distributed throughout the body is not one I can see being testable. Though I’ve been wrong before, I’ll have to see the actual hard testing before I get too excited about a particular philosophical viewpoint.

          • OK, I did a quick search for concrete evidence of 4e cognition and found exactly nothing. I found a LOT of philosophizing on the ASSUMPTION that cognition is a full-body process, but there is nothing I’ve seen so far that even slightly approaches a falsifiable premise, let alone an actual experiment. To suggest that this very arcane theory is a scientific explanation of emotion doesn’t appear to be close to a valid claim, from what I’ve read so far. Perhaps you can direct us to an article that exemplifies an actual scientific experiment demonstrating the validity of 4e cognition and its applicability to emotions.

            Sorry, my question mark doesn’t work. I urgently need a new keyboard.

  7. Hi Steve – this is becoming a bit drawn out for me. Although Wittgenstein thought Freud’s psychoanalysis a “foul practice” that’s done “no end of harm”, he was in agreement that it’s a person’s will that gets in the way of understanding – not intellectual argument. Many sciences don’t have experiments – astronomy, anthropology, etc – they are straight descriptive sciences, and every now and then someone comes up with a “fertile new point of view” (Wittgenstein). You and l.e. Cox consider “mind” as a noun; in the new paradigm “mind” is used more as a verb.
    You’ve no doubt heard of “fast” and “slow” thinking – animal intuitions and human social language based thinking. Most of our thinking turns out to be the fast animal kind. Especially relevant is social thinking – we are excellent “mind readers” – we mostly understand each other instantly – there is no interpretation involved in this – think of an obvious example – a friend in pain – Now the Cartesian paradigm gave rise to various ‘Theories of Mind’ – everyone was an imaginary psychologist or anthropologist and understood others by putting their expressions through your theory of mind and your ‘biocomputer’ chugged out “Oh they are hurting”. Now Dreyfus and Dreyfus had a chess grandmaster playing fast chess and at the same time adding numbers delivered at 1 a second. The grandmaster computing ability was taken up with adding – but they still won the majority of games against skilled players – so this shows that you rely on the fast animal intuitions – think of driving, you daydream or have an intense conversation with your passenger. Haidt calls the animal part “the elephant” and the slow social reasoning “the rider”. You can, for example, show the rider an argument for this new paradigm but if the elephant doesn’t want to go there – you’re pissing in the wind.
    Seikkula says he prefers to call open dialogue “a way of life” in preference to calling it a psychotherapy (The Australian & NZ Journal of Family Therapy, 32, 3: 179-193). This fits with this new paradigm – and is where I came in – saying that the relationship (ie ethics) comes first ontology a distant second. [Notice our discussions have focused on questions of ontology rather than ethics].
    I must leave it there – but I will post on other topics on MiA in the future. Thanks for the conversation.

    • Still sounds like straight up philosophy to me. I have never doubted the value of instincts, but while they are an excellent guide to personal action, they don’t provide a structure to build a mutual understanding upon. To claim a scientific explanation for emotions, we need some kind of verifiable agreement, whether by measurement or by predictive ability or elegance of explanatory power – like the sun-centered view of the planets – which is clearly simpler and more useful in predicting future events. It seems you have an interesting hypothesis and some possible theories on how it might apply, but I don’t see a useful explanation of the origins and location of emotions that helps understand and predict emotional events and outcomes in the future.

      Best to you in your future.

    • I sent my animal ideas to Hait way back over a decade ago. I fertilize, as does the wind and rain. Nobody thanks the wind and rain. Everyone thinks they grew the crop out of logical arguements themselves. They then make more and more barren certainty out of the gifts of wind and rain. I am Scottish. We listen to the beloved wind and the sacred rain.

      Alas, something is wrong with the MAGNETOSPHERE. The Earth’s cosy quilt of magnetizm is compromized in some way. I keep hearing this word. So along with my prophecy of the HOOVER DAM going to be carpet bombed I feel we will hear more about changes in the magnetosphere. It is not a bad change as such and the future will have good in it. We must be patient while we as individual people in humanity deal individually with humanity’s lure to entice everyone en masse into collective destructive nonsense. By this I mean each of us is learning how powerful we each are at breathing in love and exhaling out peace.

  8. And on and on it goes. Now the people who rebutted the rebutters of the original paper will rebut the rebutters. I have read the original paper and the rebuttal and find value in both of them. Does the answer have to be one or the other? As has been pointed out, the most common theory of mental health today is the biopsychosocial model. In my experience, the medicalization of mental health problems has more to do with insurance companies greed than anything else. When I started in the mental health field, many people came into psychiatric hospitals voluntarily and often stayed for a month or more, while a team of psychiatrists, psychologists, social workers, and other therapists worked to find the right combination of medicine, therapy, and social supports to help people. Even those who were committed and resistant often came to value the treatment they received and asked to stay longer. We could send people out on passes so they could see how they’re functioning had improved or not, and they were grateful for the care they got. But the insurance industry put a stop to that. The insurers said, keeping people in the hospital that long was not “cost effective” for them. Get them in and get them out fast, and if you don’t give them medication, you won’t get paid! Therapy? We’re not paying for that! Just give them the drugs! Passes? If they’re well enough to go out on a pass, they’re well enough to go home! Capitation, a concept that reduced payments to mental health providers, forced hospitals and providers to cut staff and services. Hospitals and providers struggled to provide adequate care, being told they had to do “more with less,” but nobody ever said how this was to be accomplished. Public funding entities began to use the same approach, and funding dried up. As I have said elsewhere, there are good psychiatrists and very bad psychiatrists, and finding the good ones isn’t easy. Medication helps some people and not others, but when the reviewer at the insurance company says “we’re not paying”, it becomes a matter of survival and that makes for bad decision-making and leads to abuse. If we want to improve the mental health system, we need to take on the insurance companies and take the profit motive out of it. The mental health system is not perfect by any stretch of the imagination (is any system?). Do we have to have to throw the baby out with the bath water? Do we have to be at each other’s throats? Nobody goes into the mental health field to become rich–including psychiatrists, who are the worst compensated physicians. Everyone started out with good intentions, but the need to survive and corporate greed turned many people in the wrong direction.

    • I agree with your sentiments in a lot of ways – insurance companies do drive what ‘services’ are available and reimbursable. However, if we really want to ‘just be friends,’ it is going to require an acknowledgement of psychiatry’s role in perpetuating a lot of dishonest nonsense. There is good quality evidence, not even disputed among research psychiatrists, that antipsychotics don’t have long-term benefits and probably decrease chances of survival over time, that the ‘seriously mentally ill’ die 20-25 years younger than their non-diagnosed counterparts, and that the drugs play a role in shortening lives, that antidepressants’ effectiveness is pretty limited and fades with time, that some who take antidepressants become manic and often end up with ‘bipolar’ diagnoses, that there are no long-term outcomes that are improved by long term use of stimulants, and on and on. When these studies and reviews are brought to light, just as with Johanna’s honest hard work, the authors are attacked with accusations of connections with unsavory or dishonest people, their motivations are impugned, their characters are attacked, their observations are minimized, and they are ridiculed and often shunned for speaking the truth.

      Having any kind of respectful relations begins with psychiatry’s leaders agreeing to acknowledge and abide by honest research findings instead of trying to spin everything to make psychiatry look right and anyone questioning their absolute authority to declare what is ‘true’ as insane or ill-intended. And I don’t see that happening any time soon. Psychiatry in the institutional sense has cast their lots in with the pharmaceutical industry, and many people’s reputations and standing in the medical community depend on maintaining the fiction of the DSM and the fictionalized ‘research’ that is used to back it up. I’m not opposed to folks on the front lines who are trying to do the best they can. I am opposed to the massive amounts of false information that is forwarded and enforced on those who do have to do that hard work up front.

    • It would help if the good psychiatrists made sure the very bad psychiatrists lost their licenses. I’ve never seen any psychiatrist take action against another psychiatrist no matter how egregious the behavior or how severe the harm to patients.

    • J Q, Though your data about how insurance companies have handled payments for mental health issues is valuable, a lot more is going on here than the profit motive.

      The whole history of health (medical) insurance is a rather strange one. In earlier times, doctors and hospitals had to work on a charity basis if patients weren’t able to pay. Now it is assumed that most patients will not pay for their care, but that insurance companies will. Many medical providers are involved in the insurance industry, and I can see why, as insurance helps to guarantee the income of doctors.

      Yet we must not forget the overarching “rule” of human interaction, which is that “help” should actually help. In the case of medicine, care should result in remission or cure, from the viewpoint of the patient.

      And in the case of mental health care in particular, it is not even logically obvious that doctors should be in the business of mental health. In the case of healing in general, MDs have been largely successful in crowding out other healing professions (chiropractic, functional medicine, etc.) This is also blatantly true in the field of mental health. Even if my church took insurance, I could not get the mental health care provided by my church (“spiritual counseling”) covered by any insurance company.

      If mental health providers really cared about the results obtained by their patients, they would be fiercely decrying the use of drugs that do no good and very actively searching out effective remedies for the mental problems of their patients. I know that this society and the corporate world does not always reward effectiveness, but people who get into this field should demand it. In this field, the provider could always become the patient at some point in their lives.

  9. The papers are good in respect to getting it out to the public.

    And exactly, what are the chemicals doing?
    It seems that even psychiatry readily will admit, TO the RIGHT people, that it’s not
    “imbalance”.
    So they sim[ply change terminology, as they always do and keep selling “chemicals”.
    So what chemicals are missing? Did they do a test as they do with illness?

    They created chemicals that will mess with the brain,and whole body. period.

    Yet even top neurologists do not have a clue what goes on inside our brains, surprisingly, psychiatry does 🙂

    • The reviews on antidepressants of all types are very similar. The fact that something that works on dopamine instead of serotonin is still considered an “antidepressant” shows that they doctors haven’t the slightest idea what is causing “depression” nor whether “depression” has anything to do with “disordered brain chemistry” at all. Any drug you use is an experiment on your own brain, which you’re entitled to do, of course, but it’s not based on any good literature support for Wellbutrin over any other kind of drug. I am of the opinion that it’s similar to trying alcohol or marijuana to deal with your issues. Some people find it helpful to have a few drinks, while others lose control of their lives. But alcohol is not “treating” anything, it’s just a way to temporary feel better. Same with Wellbutrin or SSRIs or any other psych drug. Until and unless someone really finds a subgroup of “depressed” people who actually have some specific, testable issue with brain chemistry, drug “treatment” is similar to taking aspirin for leg pain. It might make the pain go away temporarily, but it’s not going to fix what’s causing the problem.

      • Thank so much, Steve! What I’m understanding is that there’s no evidence linking dopamine levels to depression, either… Just like there’s no link with serotonin.

        I’ve been on Wellbutrin for 8 years, mostly for anxiety. I’m 55. When I was younger (and not on antidepressants), the more athletic I was, the happier, more confident and less anxious I was. There’s definitely a link there! It’s been proven time and again. Exercise really DOES help treat a lot of issues, both physical and psychological.

        I’ve experienced the numbing that comes with this medication. I’m ready to stop it. So as I increase my daily exercise, I’m going to taper off the pills. I’m at 150mg 2x a day. My understanding is 300mg a day is a medium dose. So I’ll go with 150mg ONCE a day for 2 weeks, then every other day for 2 weeks. Wish me luck!

        • Numbing seems to be the most common experience for ANY “antidepressant.” I think it’s the main “therapeutic effect.” If you’re too worried about everything, not giving a crap might feel like “relief.” Of course, if you were not murdering someone because you were worried about the consequences, not giving a crap might turn you into a murderer. It’s a very dangerous game.

          Exercise is probably the #1 best health treatment for almost anything, but particularly good for depression/anxiety!

          Remember there WILL be withdrawal effects, so be prepared for them and don’t give up just because it happens. You can do this!!!

        • That is a massively fast withdrawal… perhaps – a suggestion, not telling you what to do – you could read around on the site and have a look at a likely more successful protocol. Or you might be one of the lucky ones who had a few rough days and no other problems… I wish you well _/\_

LEAVE A REPLY