The MHRA & Serotonin

I’ve been just been copied in with an email to Tim Berridge at the MHRA:

Dear Mr Berridge

I’m writing because I have kindly been copied in with your recent email to Mr Fiddaman regarding Serotonin and its alleged link to the cure of depression.

I’m confused by all this, so to help me understand matters could you confirm that the MHRA’s current position is that depression is in fact a medical condition caused by a chemical imbalance and that by increasing levels of serotonin in the brain chemistry this condition can be cured.

I only ask as it seems the Royal College of Psychiatrists and the Institute of Psychiatry have accepted that depression isn’t caused by a chemical imbalance.

Also, could I ask you to consider the following statements which are directly linked to this discussion:

“Although it is often stated with great confidence that depressed people have a serotonin or norepinephrine deficiency, the evidence actually contradicts these claims”. Professor Emeritus of Neuroscience Elliot Valenstein, in Blaming the Brain (1998), which reviews the evidence for the serotonin hypothesis.

“Given the ubiquity of a neurotransmitter such as serotonin and the multiplicity of its functions, it is almost as meaningless to implicate it in depression as it is to implicate blood”. Science writer John Horgan, in his critical examination of modern neuroscience, TheUndiscovered Mind (1999).

“A serotonin deficiency for depression has not been found”. Psychiatrist Joseph Glenmullen, clinical instructor of psychiatry at Harvard MedicalSchool, in Prozac Backlash (2000).

“So far, there is no clear and convincing evidence that monoamine defi ciency accounts for depression; that is, there is no “real” monoamine deficit”. Psychiatrist Stephen M. Stahl, in a textbook used to teach medical students about psychiatric medications, Essential Psychopharmacology (2000).

“Some have argued that depression may be due to a deficiency of NE [norepinephrine] or 5-HT [serotonin] because the enhancement of noradrenergic or serotonergic neurotransmission improves the symptoms of depression. However, this is akin to saying that because a rash on one’s arm improves with the use of a steroid cream, the rash must be due to a steroid deficiency”. Psychiatrists Pedro Delgado and Francisco Moreno, in “Role of Norepinephrine in Depression,” published in the Journal of Clinical Psychiatry in 2000.

“…I wrote that Prozac was no more, and perhaps less, effective in treating major depression than prior medications…. I argued that the theories of brain functioning that led to the development of Prozac must be wrong or incomplete”. Brown University psychiatrist Peter Kramer, author of Listening to Prozac, which is often credited with popularizing SSRIs, in a clarifying letter to the New York Times in 2002.

“I spent the first several years of my career doing full-time research on brain serotonin metabolism, but I never saw any convincing evidence that any psychiatric disorder, including depression, results from a deficiency of brain serotonin. In fact, we cannot measure brain serotonin levels in living human beings so there is no way to test this theory. Some neuroscientists would question whether the theory is even viable, since the brain does not function in this way, as a hydraulic system”. Stanford psychiatrist David Burns, winner of the A.E. Bennett Award given by the Society for Biological Psychiatry for his research on serotonin metabolism, when asked about the scientific status of the serotonin theory in 2003.

“Indeed, no abnormality of serotonin in depression has ever been demonstrated”. Psychiatrist David Healy, former secretary of the British Association for Psychopharmacology and historian of the SSRIs, in Let Them Eat Prozac (2004).

“We have hunted for big simple neurochemical explanations for psychiatric disorders and have not found them”. Psychiatrist Kenneth Kendler the coeditor-in-chief of Psychological Medicine, in a 2005 review article.

Although SSRIs are considered “antidepressants,” they are approved treatments for eight separate psychiatric diagnoses, ranging from social anxiety disorder to obsessive-compulsive disorder to premenstrual dysphoric disorder. Some consumer advertisements (such the Paxil Web site) promote the serotonin hypothesis, not just for depression, but also for some of these other diagnostic categories.

Thus, for the serotonin hypothesis to be correct as currently presented, serotonin regulation would need to be the cause (and remedy) of each of these disorders.

I await you reply with baited breath

Me too.

10 Responses to “The MHRA & Serotonin”

  1. Matthew Holford Says:

    Ouch. Nice one. Don’t be holding your breath, though: Mr Berridge will be taking the full 20 working days, over a reply, I suspect!

    Matt

  2. truthman30 Says:

    I feel I must draw attention to the fact that Seroxat is in fact NOT and never was an anti-depressant. It was originally licensed as a “hypnotic drug for human use” before being aquired by GSK. (see Link below)

    http://www.paxilprogress.org/forums/showthread.php?t=11984&highlight=paroxetine+hypnotic

    Make of that what you will. But, it seems to me that the reason it has been marketed for so many different “psychiactric disorders”, is purely because of its powerful sedative and hypnotic properties. It numbs , and when a drug numbs it can be quite effective in “masking” conditions, not curing them. A pain killer will numb pain but it will not cure the source of it. I have no doubt that the properties of paroxetine do affect the serotonin system, but it certainly is not as selective as the term SSRI seductively suggests. It has an awful adverse effect on all the bodies systems, from dopamine, to cortisol, testosterone and serotonin amongst others. I also believe that the propeties of Paroxetine do in fact CAUSE and MIMIC “psychiactric disorders”. And also i have reason to believe that the chemical paroxetine is mostly intolerable to the human body.
    The fact that Seroxat is now known to cause strange kinds of genetic malformations and deformeties in foetuses and new born babies leads me to believe that it is causing similar damage to Adults … The damage it does to these newborns (if properly researched) might explain the painful seroxat side effects such as the withdrawal headpressure and the common stomach issues from Seroxat amongst other things…

    (see link) : http://www.paxilprogress.org/forums/showthread.php?t=25390

  3. Matthew Holford Says:

    Actually, as an afterthought, has anybody asked the Department of Health what its position is, with respect to the Chemical Imbalance theory? I only ask, because I note that the DoH has a very similar approach to GSK on the suicide risk to the 18-29 age group.

    Matt

  4. Matthew Holford Says:

    A quick note additional to truthman’s: I saw a piece in the Indy, a week or two ago, which discussed research, made public back in August, 2006, which demonstrated that ketamine (ie, “Angel Dust”, the former human and veterinary tranquilizer) had some kind of therapeutic effect, with respect to depression. PCP was used as an anaesthetic, too, before its side effects became known!

    Matt

  5. truthman30 Says:

    The department of health should have called for a Seroxat ban a long time ago…

  6. truthman30 Says:

    Of course any mind numbing drug would have an affect on a depressed person, any drug which biologically and chemically numbs the depressed individual would seem to have a “therapeutic” effect, you could say the same for alcohol and MDMA. But none of them cure or treat the route causes which are due to lifestyle, circumstances and the individuals perception and reaction to trauma. SSRI’s are nothing but “chemical band-aids”. And in some cases , they can be more of a “chemical lobotomy”…

  7. Matthew Holford Says:

    “The department of health should have called for a Seroxat ban a long time ago…”

    So, not only are we interested in demonstrating the inefficacy and dangers of Seroxat, such that further argument is impossible, we’re also concerned with understanding the motive behind this lack of action. If we understand the motive, it should be straight forward enough to undermine it.

    Matt

  8. truthman30 Says:

    Well, I figure that Seroxat will not be banned until the Patent has run its course and expires, which if you check the GSK website says “during or after 2006” { http://www.gsk.com/financial/reports/ar/report/descrip_of_bus/intell_property/intell_prop.html }

    , why stop a money train in its tracks when you can milk it until it hits its destination? (ie. the end of the tracks)..Seroxat Deformed babies, Seroxat withdrawal, Seroxat addiction and Seroxat suicides aside, this drug is still a big cash flow earner for GSK. The money they pay out in damages and liability claims is a drop in the ocean compared to the massive profit machine it has become for them…
    Although I have good reason to believe that the only reason it is still selling is due to the fact that current users are unable to come off it, proving that is another matter…

  9. Matthew Holford Says:

    Well, dependant upon which figure you believe (GSK’s 25%, or the highest figure I’ve seen, which is 80%), there will be plenty of addicts in the Seroxat universe, who aren’t able to move on to anything else, anyway, expired patent, or not.

    Matt

  10. truthman30 Says:

    Another Pharma/Psych trick is to switch the Seroxat Addict on to another SSRI instead of weaning them off it , that way they can blame the new SSRI for creating the side effects of the withdrawals from Seroxat….


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