Wednesday, January 31, 2007
Like many others, I have recieved replies that border on the absurd, the latest from Mr Tim Berridge of the MHRA Licensing Division just does not add up. I won't post the original email they sent me on here because apparently they have now banged a copyright notice on all FOI requests answered by them. I can, however show you my response to them. I see no reason to copyright any of my questions because they ARE IN THE PUBLIC INTEREST.
So here goes...
Dear Mr Berridge,
Firstly I would like to thank you for your response, although why it took 20 working days to basically answer two questions still remains a mystery. I was also concerned to see that you had copied in three other people, Richard Goldfinch I know of but the other two, namely, Muriel Passmore and Ingrid Calvert, I cannot recollect ever seeing their names before in my correspondence with the MHRA. Could you tell me firstly, why these two were copied in on your email to me and secondly what division of the MHRA do they work in (if they work within the MHRA that is)
Now onto my Freedom of Information request and the answers provided by you.
1. Did GSK provide the MHRA background documents giving details about the imbalance of serotonin in the brain?
Yes, a lot of this information has arisen from our knowledge of other antidepressants and from animal studies and animal models. To the best of my knowledge, this has never been directly proven in humans.
I am glad to see we now have it on record that GSK did indeed provide the MHRA documents giving details about the imbalance of serotonin in the brain, I am somewhat confused though because to my knowledge, based purely on my own research, there is NO or never has been any scientific study into the imbalance of serotonin in the brain. The last line of your answer to question )1) you state 'To the best of my knowledge, this has never been directly proven in humans'. Now call me flippant or naive but what on earth are the MHRA doing granting a licence to GSK for a drug that they (GSK) claim, and I quote here from the Seroxat patient information leaflet "...People who are depressed or anxious have lower levels of serotonin than others." To make a broad statement like that surely must mean that there have been some 'human' experiments carried out by GSK regarding the imbalance of serotonin. Is this claim by GSK on the Seroxat patient information leaflet something the MHRA have overlooked or do the MHRA actually agree with GSK that people who are depressed or anxious have lower levels of serotonin than others?
Moving on to question (2) of my Freedom of Information request:
2. Did GSK provide the MHRA documents with figures for the effect the drug had in changing the imbalanced state?
No. To my knowledge, it would not be possible to conduct such a trial in humans.
Once again I bring to your attention the Seroxat patient information leaflet that states "...People who are depressed or anxious have lower levels of serotonin than others."
Could you or any other expert tell me how GlaxoSmithKline arrived at this assumption bearing in mind that, in your own words Mr Berridge, you told me '...it would not be possible to conduct such a trial in humans'
Thirdly, I approach question (3) and its answer by you with a sense of bewilderment.
3. Please forward me documents that GSK supplied the MHRA during the application procedure for Seroxat that relate to the 'correcting effect' regarding people with lower levels of serotonin
Your reply was basically no answer, using instead the exemption rule contained in the FOIA, section 21 - Information accessible to the applicant by other means.
Whilst I have to accept this I was however totally flabbergasted that you suggest that I go to the website of GSK to read of the trials conducted by GSK on Paroxetine/Seroxat.
Flabbergasted because the MHRA are currently investigating GSK regarding the clinical trials of Paroxetine/Seroxat. I, as a member of the public, have grave concerns over anything that comes out of GSK, particularly their 'published' Seroxat clinical trial data.
Why then would someone from the MHRA direct me to a website of a company who are currently under investigation by the MHRA? It just defies belief and all logic.
Finally, a colleague of mine noticed that answers to FOI requests from the MHRA are now carrying a copyright notice at the foot of the response. Are you suggesting to me that whatever information I receive from you via the FOI should remain for my eyes only?
Like you, I have taken the liberty of copying in people in this email, some you or your peers will be aware of, others you will not. I trust I am not breaking any copyright rules here
Mr Robert Fiddaman
Monday, January 29, 2007
Emails from the edge
The Secrets of Seroxat
1,2,3 and now.......
4. Secret emails
How much longer are you going to 'investigate' Glaxo SmithKline?
How much longer are you going to protect MHRA regulators, Prof. Alisdair Breckenridge and Dr Ian Hudson? BOTH former employees of Glaxo SmithKline - BOTH now regulators on your board.
Thursday, January 25, 2007
Shelley Jofre gives an update on her investigation into the antidepressant Seroxat. Shelley has currently made three films about the drug.
Seroxat and the other SSRI antidepressants (including Prozac, Lustral and Ciprimil) may provoke violence in a small number of people who take them, according to a paper published today on the Public Library of Science Medicine website.
The study - which focused primarily on Seroxat - looked at clinical trial data and reports of adverse effects and found possible links between SSRI antidepressants and violent behaviour.
Back in October 2002, Panorama broadcast Secrets of Seroxat.
This film included the disturbing claim that Seroxat had thrown one man into a state of mental turmoil which led him to kill himself and three members of his family.
We also uncovered evidence that the antidepressant was addictive, that it could make some adults self-harm and become suicidal and that clinical trials had shown that these effects were also possible in children who took the drug.
Seroxat's manufacturer, GlaxoSmithKline (GSK) vigorously denied each of these claims at the time and still continued to defend its best-selling drug in two subsequent programmes that we made on the subject.
Gradually though, over the last four years we have been proved right on each of the claims we made in the original programme.
GSK drops the claim you cannot become addicted to Seroxat" from Seroxat packs.
The medicines' regulator bans Seroxat and other SSRIs (except Prozac) for use in under-18s after clinical trials results link them with increase in self harm.
Government Expert Working Group recommends careful monitoring for suicide in 18-30 year olds on SSRIs.
Norwegian study links Seroxat to increased risk of suicide attempts in adults.
GSK's own review of clinical trial data reveals increase in suicide attempts in 18-30 year olds taking Seroxat.
Study suggests possible links between SSRIs and violent behaviour.
Friday, January 19, 2007
The symptoms within their letter to GSK pretty much sum up how I felt. I too suffered from Acid Reflux (still do) I wonder now if Seroxat caused this? Anyway, read on:
The truth about Paxil
by Stephen E. written to GlaxoSmithKline plcPosted Wed June 26, 2002
Drugs have become a booming business today, and your products are very important -- critical even -- to many millions of people. I'm on one of them, and that's why I feel compelled to send you this complaint about effectiveness at your company. Specifically, my complaint is about Paxil. I am really furious about this.
First I want to start off by saying what a horrible company you are and that I am currently talking to a lawyer about joining the many current lawsuits against you people. I started taking paxil when I was 16, soon after losing all inhibitions for life and followed by several suicice attempts and panic attacks, as well as many side effects that I had no idea could be related to paxil. Now after 2 years and one try to try and quit going through horrible withdrawl effects that YOU KNEW ABOUT and didn't tell me or my doctor I now know that these side effects are caused by YOUR product, these side effects iv had for over a year now but never thought it had anything to do with paxil because YOU PEOPLE didn't warn me of: (I also am developing a muscle spasm disorder only after 7 days of wheening off of your product in a 10 mg drop.) And by the way, don't bother asking for a release to see my medical information, because you won't get it. You deserve to pay me and thousands of other people for the pain that you have caused.
My Depression and anxiety sympoms worsed. I never had depression before I started on the meds, and my anxiety actually got worse in some cases. -Panic attacks, I never had a panic attack before on paxil, and experienced them more times then I wanted to after starting on your mind altering poison.-Hot surges running through my body with proufous sweating. -Horrible nightmares or aggressive dreams, dreams of having battles with people from past. Alot of the time I have trouble remembering if something happened in a dream or in real life.. -Obsessive thoughts.-I got these before on the medicine so it is hard to say that paxil is to blame. Though in alot of aspects it has gotten worse, or stayed the same, and isn't paxil supposed to make it go away?
-Just can't seem to feel any more. Just don't care anymore. Feelings of "who cares" and "fuck it"-Perhaps the most common side effect that YOU don't warn us about, the most common one I've ever seen in my research. This happened almost immidiatly after starting the drug, only caring about a video game, not caring if I showered or brushed teeth, not caring if I had a job or went to school, I found myself knowing I would grow up to be a homless loser when I grew up and I didn't care.I didn't care that we were broke and we might now lose the house because of me and my mom has to now work 2 jobs as a single parent to two.
Feeling like a zombie. No emotions. Unable to feel "normal" sadness or cry at all. Excessive or "fake" happiness.-This is also another common side effect YOU don't want people to know. The fact that these drugs are just a "band-aid" of sorts, it made me unable to feel sadness and happiness. This wasn't constant, because at alot of points during the years I would be able to feel sadness, and it was horrible, much worse then sadness I had before I was on the drug. The only thing I couldn't experience was happiness, I had the fake happiness alot, like something good happening in the game I would be extactic, but if something bad happened in the game I would think of suicide, I would begin to cry over anything ect ect.
Severe dizzyness, fear of passing out or losing control.- Alot of the time I would have to hold on to the walls when going to the bathroom or down the stairs to stop myself from falling downstairs. -
Sleeping with lights on because of the fear-this happened alot earlier, I would keep the TV on with no sound just for the light, I never knew why.
-Feeling disconnected,foggy, feeling of unreality or drugged out-This is a big one, which hurts my concentration, which is another side effect i list later.
-Heart palpitations-i get this quite often
-Tightness in the head-i get this alot, also the back of my head gets numb.
-No personal identity/opinions of your own.-This is constant, I never have any opinions of my own and constantly feel like I don't have my own personality.
-Feelings of being unnable to function like a normal human being.-these thoughts have plagued me for years.
-Hate to go out or be around people. Also may hate people, not even comfortable with familiy-this was the problem that got me onto the paxil, though its hard to say if it got worse, I know it hasn't gotten better.
-Feeling like it will never end.-again these feelings have haunted me since I started on these drugs.
-Urge to jump from a moving car.-maybe a few times, it is hard to remember
-Extreme head pain-maybe once or twice a week I will get horrible headaches, I've tried taking asprin etc but nothing works.-I'm not sure I will ever be my old self again or be normal again.-I'm Convinced of having some rare and fatal disease constantly. I have been in and out of hospitals for over a year, thinking I have a heart problem, gunna have a heart attack, thinking I have a tumor, as soon as something went wrong, weather a sour throat to a pain in my toe I thought I was going to die of some rare and fatal disease.
-Fatigue and problem in hands(predominantly left) tingling, mild to severe tremors, more pain and slight stiffness may spread up arm into sholder.-i get this alot, mostly just tinglings and tremors, sometimes pain would move up to my sholder and I would panic thinking I would have a heart attack. This happens 4-8 times daily.
-Heavy bleeding from the nose.-there was a time were I had nose bleeds,(where i was convinced of having some rare disease) it went away in a few weeks.
-Nausia, gastrointestinal problems, feeling bloated and full.
Acid reflux disease, severe flatulance.-I have acid reflux disease, and even though I've tried every drug to treat it, it hasn't gotten any better, I still feel nausiated for a few hours after I eat, as well as severe flatulance, if i were to count, i would guess that I burp at least 2,000 times a day and fart at least 1,000.(keep in mind these are 24-48 hour days) My doctor is stumbled on how I could have gotten Acid Reflux Disease
-Memory loss with apathy, trouble concentrating. Trouble focusing, hard to read words.I have very bad memory, often I'll stop in the middle of the sentance searching for a word to say. I don't concentrate, days that I have gone to school when I'm off of paxil I wouldn't be able to concentrate or focus. Before on these drugs I passed all my classes as well as wrote a novel(I like to write, I used to write alot before I was on the drugs, whereas I just didn't want to write it, and now its at the point where I can't even remember most of the ideas I had for stories.). Also I can watch a movie, and then the next week wonder if I saw it, and tell my mom that I want to go see this movie and she complains that I just saw it.
-Manic/depressive episodes-this happened alot, specially if something bad happened in the game, like I died or lost an important item ect.
-Chills-This happens to me at least 4 times a day, even in the heat my entire body will just shake in one fast jerking motion from the top to the bottom, it only lasts maybe a second or two.
-Head jerking and muscle spasms. REM(rapid eye movement) that leads to insomnia, Tremors, sudden jerky movements of muscles. -I've had these for alittle over a year now. Mostly my legs and arms will jerk suddenly without me wanting them to, it happens more at night. Rapid eye movement keeps me up at night, and I'm up basically till I'm so tired that I just pass out because of REM in conjunction with nausia and constantly having to sit up and burp because of the acid reflux disease -Feelings of hopelessness and feelings that you are out of control.-I have feelings of hopelessness alot, like the only way to get out of it is suicide etc.
-Suicidal-perhaps the most dangerous side effect hidden from our eyes, I have read dozens of stories of suicide because of paxil. I especially found the 8 million dollar reward to the family of the man who shot his wife daughter grandaughter and himself quite interesting. At the drop of a hat I could become suicidal, even if the littlest thing went wrong I thought of it, even though I'm horrified of dieing, and constantly thinking i have some fatal disease. -Inner restlessness, feeling that something is not right but I am not sure what, but it is there haunting me in the back of my brain.and its there all the time, and it drives me crazy, it is hard to explain but best described as Morphius said in the movie the matrix "You don't know what it is but its there, like a blister on your brain, haunting you."
-Worsening or delayed cure of acne.I started getting acne after i started on these damn drugs, since then I've tried everything to get rid of it, and currently on two prescriptions from a dermatoligist.
-Severe hot flashes while asleep, wake up covered in sweat every night
-Severe mood changes. Anger and violent one second, then happy, then very very sad. Very rude and short tempered all the time. At first I hadn't noticed it but my mom often complains about how rude i am, and I am very short tempered about things, fighting with my mother or brother I'll flip out and start screaming and cursing for little arguments.
-Heavy Sweating all the time. -Urge to drink excessively, sever dry mouth.This is constant, I can not leave my house without a water bottle, and if i do my mouth gets very very dry and I start to panic thinking I'm goign to vomit, never happened before I were on these drugs. -Feet stay cold, can never seem to get them warm at all, cept right after I get out of a hot shower. -Need for increased dose for same symtom, tolerance. I started with 10, then 20, then 30, then 40, then doctor wanted me to go to 60. I originally was till I found all the research proving your drug to cause all these problems.
-Sleepy all of the time, but cannot fall asleep, Insomnia caused by REM. When i do fall asleep I sleep ALOT 13+ hours a night. Like I said before about my insomnia, but when I do sleep I sleep for 13+ hours, even if I was awake for a normal 10-12 hours, when I first started and before I got the REM I was awake for 12 hours, then slept the other 12 which led to halting of going to school.-Visual and Audio Hallucinations.If i look at my wall for awhile I can see paterns, or people moiving around, once at a friends house I was looking at his curtains in the dark and saw spiderman swinging from buildings. Audio wise I hear ringing all the time, as well as humming or buzzing, sometimes doorbells and phones ringing.
-Breathing problems. Feelings like I am going to stop breathing, tightness of chest, feeling that something is wrong with my breathing.This happens all the time, and is happening as I'm typing right now, usually its tightening in my chest or feeling like my throat is closing.
-Muscle and joint pains. -Itchy, rashes on legs, knees, under arms and back. This isn't constant but many times during the day I find myself unable to stop scratching these parts of the body. -Pain in the lower left hand side of the stomach which mild to very often, usually its just nauisa tho. -Self mutilation,cutting myself.
-Changing myy mind every minute, decide to do one thing, then decide to do another, decide that a spoon is clean, then decide its dirty and get a new one-Lethargic, very weak, ,no energy to do anything, lost all inhibitions to do anything.
-Mild to Severe constipation on and off, coupled with diareah the times that I've tried to get off of your death pill.
I'd like to direct you to www.drugawareness.org where they have publiciced medical journals about the effects of paxil that YOU do not warn us about, especially including withdrawl and side effects. Now I don't believe in god or anything but I believe you people are sick. You should be taking these pills and see how you like it. I know people will do anything for money but this is just too much, your hurting hundreds of thousands of people for life, and like i said before, don't even think about asking me for medical release because you will not get it. You are a lieing manipulating evil company and I and many other people won't rest until the world knows about these horrible things that you don't want the world to know
Frankly, I guess I'm not surprised by this latest problem because I've been very dissatisfied in the past. I definitely won't be a repeat customer of yours, and I definitely won't recommend you to people I know.
Here's what I think GlaxoSmithKline plc should do: take paxil OFF the market andpay the people you hurt money for thier pain and what it has done to thier lives!.
I hope to get a response from you soon. This is a very important matter, not just for me but for all consumers of your products.
Thursday, January 11, 2007
Poor old Mr Sneeze. Not only is he forever battling his year-round sniffles in Coldland, he's now under investigation by a Government Watchdog who want to scrutinise his association with multinational pharmaceutical firm GlaxoSmithKline.
The rumpus centres on a recent promotional Mr Men book written and illustrated by Adam Hargreaves and titled 'Mr Sneeze And His Allergies'. According to The BBC it was funded by GSK and shows us how, with some help from Little Miss Sunshine, Mr Sneeze is urged to take action against a suspected dose of hayfever. But alas, their good work is undone by the arrival of Mr Silly and his pet chicken, called Rover (!).
After the story there are four pages of allergy information from Allergy UK and - this is the problem area - two pages promoting the use of GSK products.
50,000 copies of the book have been printed so far this year and distributed to Tesco Clubcard holders, allergy road shows, allergy clinics and doctors surgeries. The book was approved by The Proprietary Association of Great Britain, which is responsible for checking marketing material from pharmaceutical companies. And what's more, they're standing by their decision to back the project, citing its confident public health message.
But the Medicines and Healthcare Products Regulatory Agency aren't so convinced, because The Medicines Act of 1994 prohibits the promotion of medicines to children. Of course, GSK rebuke such allegations...
This one might want to run, and run. But really, we hope it doesn't!
Wednesday, January 10, 2007
The following article is from the Washington Post.
Take particular care and attention when reading the final paragraph
Drug May Help Hypochondriacs
And now, a real pill for your unreal illness.
Scientists report that the antidepressant Paxil helped hypochondriacs be less fearful about getting sick. In the first controlled study that compared a group of hypochondriacs given the drug with a group that got psychological talk therapy and another group that received sugar pills, the medication significantly reduced people's fears about imaginary illnesses.
Before the trial, one 40-year-old, who said he had fears starting at age 10 that he was going to die in his sleep, rated his certainty that he was suffering from a serious illness as an 8 on a scale of 1 to 10. After six weeks on Paxil, his fear level dropped to a 4 -- an improvement that led him to continue the medication after the trial.
According to the standard manual of mental disorders, hypochondriasis is a potentially serious condition that can prompt people to go doctor shopping, abuse sick time at work and become complete invalids.
The study found that hypochondriacs who got cognitive behavior therapy, which encourages people to challenge the validity of their disabling beliefs, also improved -- as much as those given the drug. Researchers suggested that a combination of this talk therapy and medication might be especially effective.
The study was published this month in the American Journal of Psychiatry by researchers at Leiden University in the Netherlands and other Dutch centers. It was funded by an "educational grant" from Glaxo SmithKline, which makes Paxil.
Now here's my slant on this:
If Paxil/Seroxat is to be prescribed to hypochondriacs then Glaxo SmithKline and the Medicines Healthcare and products Regulatory Agency can pass their withdrawl symptoms off as nothing more than hyphchondriasis. Their addiction will no doubt also be passed off as a psychological problem.
Let's just look at this segment from the above article shall we?
"... After six weeks on Paxil, his fear level dropped to a 4-- an improvement that led him to continue the medication after the trial."
Well done GSK - Another group of people to target your drug at.
How can a GP diagnose a hypochondriac who walks into his/her surgery complaining of withdrawal symptoms... or worse still that the hypochondriac wants to kill themselves? I find this latest trial sickening and nothing more than a money making project for GSK.
Glaxo SmithKline - YOU ARE A DISGRACE TO THE HUMAN RACE
lot longer than 3 months. I have it for more than 2 years; I was
unable to work for 6 months because of it. It's only been in the last
6 months that I've been able to function at all normally, and I still
Here's a little essay I wrote about the monoamine theory of
depression on paxilprogress.org, an online support group for people
with paroxetine withdrawal syndrome:
It is true that manipulating the serotonin receptors (and other
neurohormone receptors) appears to relieve the symptoms of depression
and some other psychiatric disorders. However, that is not proof that
a deficiency of serotonin or any other neurohormone is the cause of
What it demonstrates is that if you alter the neurohormone balance
and, doing that, the interaction of hormones throughout the body, it
can have positive mood effects. In a minority of people, altering the
hormonal balance has adverse effects, sometimes fatal, as they become
suicidal or homicidal.
The mechanism controlling mood can be anywhere in the body's hormonal
system. Sometimes it's the thyroid. Sometimes it seems to be
metabolic, based on a lack of omega-3 fatty acids, essential
minerals, vitamin B12, or other nutrient. Sometimes it is in the HPA
axis, such as noradrenergic hypersensitivity.
The statistics are further contaminated because quite often
antidepressants are prescribed on the basis of misdiagnosis. A third
of all untreated cases of "depression" resolve spontaneously because
the condition was situational or, who knows, a transient hormonal
imbalance. This means that antidepressants often are credited with
successful treatment when the patient would have recovered anyway
In general, medicine operates on the assumption that the widespread
hormonal disruption caused by antidepressants, on balance, is
beneficial. Danger signs such as weight gain, hypoglycemia, and
adverse effects on sexual response (this last affecting approximately
50 percent of patients) are ignored.
Those of us who are suffering severe discontinuation syndrome are the
canaries in the coal mine. Our problems reveal that the hormonal
disruption may not be benign. Whether occurring during treatment with
antidepressants or in withdrawal, it is certainly vastly underreported
The calculations that net out a benefit for antidepressant use may be
highly distorted, by accident and by design -- there is vast profit
in the defense that, overall, side effects are minor.
And patients should be made aware of the risks so they can make
Tuesday, January 09, 2007
"...People who are depressed or anxious have lower levels of serotonin than others."
There is plenty of information on this blog that suggests otherwise.
Here is an email I recieved today.
----- Original Message -----
From: Dan Adams
Sent: Tuesday, January 09, 2007 8:04 PM
Subject: RE: Serotonin
Dear Mr. Fiddaman,
Currently, as far as I understand, there is no way to determine proper serotonin levels in the brain. One major problem is that cerebral serotonin levels are difficult to measure (brain barrier issues). Another problem is determining whether the serotonin is interacting the way it should. This is why treating depression and serotonin deficiency is largely a guessing game. Doctors prescribe selective serotonin reuptake inhibitors in an effort to keep serotonin in the system longer, but they have to do it in increasing doses until the patient either responds well or has an overdose reaction. Typically, doctors try a number of combinations until something works (I’m sure you already understand this.)
However, some progress is being made, particularly with serotonin tracers, molecular compounds which bind with serotonin and can be traced in the brain. These compounds are radioactive and can be measured in an fMRI or PET scan. We have some friends at the University of Liege, in Belgium, who are pioneers in this area and are very close to developing a traceable serotonin marker in humans. Perhaps within a few years, we’ll have better answers as to how serotonin works in the brain, and how to measure the proper amount/balance.
In the meantime, I’m sure you recognise the importance of light therapy and receiving light in general. Light does what SSRIs cannot; light produces serotonin in the brain, while SSRI’s work to keep serotonin from being absorbed too quickly. This is why several studies have shown that a combination of light and medicine are synergistic, that is they work better than either alone. These studies have been done on seasonal and non seasonal major depression.
A good site to review is: http://www.moodrelief.com/ Also, I would be a bit concerned that the over use of light therapy and or the overuse of the combination of both light and medication can lead to an ‘over reaction’. If one feels jittery, nausea, anxiety or mania, one should discontinue the use of light for a few days and then very gradually increase the amount again.
People who are depressed or anxious have lower levels of serotonin than others.
Take a bow.
‘The Emperors New Drugs’ journal article pretty much substansiates what this scholar wrote over three years ago! http://www.seroxat.pwp.blueyonder.co.uk/namiscc.org_Research_2002_DrugEfficacy.pdf
It has been suggested that depression results from the depletion of certain brain neurotransmitters such as Norepinephrine for example, Richelson (1991). However biochemical theories of depression fail to account for environmental causes of depression which undoubtedly cause the illness in the majority of cases, the past experiences of the individual leading to lowered amounts of neurotransmitter and it can therefore be argued resulting in depression as a consequence perhaps as an evolutionary adaptation, Nesse (2000). Farvolden, Kennedy, & Lam (2003) suggest that effective treatments include the existing range of therapeutic drugs: SSRI (Selective Serotonin Reuptake Inhibitors), SNRI (Selective Norepinephrine Reuptake Inhibitors), MAOI’s (Monoamine Oxidase Inhibitors) and Tricyclic antidepressants. However there is significant evidence to suggest that such drugs rather than resulting in remission merely treat the symptoms rather than the cause, Farvolden et al (2003).
Indeed it has even be suggested that the aforementioned antidepressants are little better than placebos, any pill whether containing an inert substance such as talc or the active drug Paroxetine (Seroxat) one of the SSRI class of medications having pretty much the same therapeutic effect perhaps as a result of a release of neurotransmitters instituted by the brain in response to placebo, Kirsch, Moore, Scoboria, and Nicholls (2002).
To determine which biochemical theory of depression is most strongly supported by the available evidence the remainder of this essay will look at the current evidence, evaluating and interpreting the suggested causes of depression leading to a valid conclusion.
Before looking at the biochemical theories of depression it is important to look briefly at things that are known to cause depression in the first instance such as childhood anxiety disorders, Muris, Meesters, & Van Melick (2002). Muris et al (2002) carried out a study with children aged 9-12 years to compare the effectiveness of cognitive behavioural therapy with a psychological placebo such as emotional disclosure. Participants in the study were either assigned to cognitive behavioural therapy (a), emotional disclosure (placebo) (b), or (c) no treatment (control). The results of the study indicated that cognitive behavioural therapy (CBT) was superior to emotional disclosure, and the no treatment conditions. The researchers concluded from the results that only the CBT condition resulted in significant reductions in anxiety, trait anxiety and depression. It can easily be argued from the results of the Muris et al (2002) study that the cognitive behavioural therapy method of treatment caused a remission of psychiatric symptoms of the young participants in the study. However what is unclear is exactly what the method achieved, i.e. was it an increase in neurotransmitters or something else entirely?
Healy (2002) highlights that there exist two separate biochemical theories of endogenous depression: the amine, and catecholamine theories. Schildkraut (1965) proposed in the catecholamine hypothesis that depression resulted from a decrease in available Norepinephrine at central adrenergic receptor sites, Norepinephrine inhibitors such as Reserpine resulting in depression, and MAOI’s increasing levels of Norepinephrine, relieving depressive symptoms. Whereas in the Indoleamine hypothesis there exists evidence to suggest that there is an imbalance or disturbance in three main areas;
Amine metabolism, electrolyte distribution and, or hormonal function result in depression and other affective disorders, Toru, & Itokawa (2001).
There is a problem with the catecholamine hypothesis however. If depression resulted simply as a result of lowered catecholamine levels within the brain one would expect that alpha-methyl-paratyrosine would cause depression in humans as it inhibits the enzyme tyrosine hydroxylase limiting catecholamine synthesis, and the introduction of the chemical does not have that effect, Berman, Sanacora, Anand, Roach, Fasula, Finkelstein, Wachen, Oren, Heninger, and Charney (2002). Berman et al (2002) carried out a study to assess the integrated role of the monoamine system in depressed patients. It was decided that un-medicated depressed subjects would be asked to partake in a 2 week double blind, random ordered crossover study. Subjects were placed in active indoleamine (via tryptophan depletion the precursor of Serotonin) plus catecholamine (via alpha-methyl-paratyrosine administration) depletion and separately Indoleamine plus sham (via diphenhydramine administration) catecholamine depletion.
The results of the Berman et al (2002) study suggests that simultaneous disruptions of the indoleamine and catecholamine systems do not make depression worse in previously un-medicated subjects. This finding lends support to the theory that monoamines regulate mood by some as yet unknown indirect mechanism such as the suggestion that neurotransmitters interact with one another, and that imbalances of these neurotransmitter systems result in depression. The currently held hypothesis is that monoamine depletion results in depression, Leonard (2000). Leonard suggests that the monoamine hypothesis predicts that there is some form of impairment of the monoaminergic system with lower than normal levels of Norepinephrine, Serotonin or both. Depletion studies have indicated a correlation between such deficiencies and depression, researchers measuring the active neurotransmitters and their metabolites in cerebrospinal fluid and urine, Sobczak, Honig, Van Duinen, Riedel, (2002). This would suggest that no one neurotransmitter is implicated in isolation and that instead of proposing that there is an abnormality in a singular neurotransmitter system perhaps more than one of the neurotransmitters interacting together results in depression. There have been several attempts to propose such a biogenic hypothesis, Prange, Wilson, Lynn, Alltop, & Stikeleather (1974). Researchers have found that drugs that act by increasing the amount of neurotransmitter in the synaptic cleft take a number of weeks to take effect, and can in some cases result in increasingly severe depression and anxiety in the mean time before the drug becomes effective, Bourin, David, Jolliet, & Gardier (2002).
During Paroxetine withdrawal, patients are known to experience very severe symptoms including electric shock like sensations, mood instability, hypomania, suicide, paresthesia’s etc., Haddad, Devarajan, & Dursun (2001), again suggestive that a reduction in Paroxetine (Seroxat) results in not only a lowering of Serotonin but perhaps also in Dopamine causing coordination problems similar to those found in Parkinson’s disease. Haddad et al (2001) highlight that 2 patients presented with stroke like symptoms which were later attributed to withdrawal from Paroxetine. The manufacturer GlaxoSmithKline have recently been found guilty of homicide where a grandfather murdered his wife, daughter and baby granddaughter before committing suicide after only two days on Paxil (Seroxat) resulting in law suits in several countries including the United States and United Kingdom, patients claiming that the drug is addictive and causes a range of very unpleasant side effects and withdrawal symptoms including those already mentioned, Boseley (2001).
Since SSRI and SNRI medications do not elicit immediate improvements in depression despite evidence that such drugs stop Serotonin or Norepinephrine from being reabsorbed in the synaptic cleft almost immediately, resulting in more of the neurotransmitter becoming available. This would suggest that indeed neurotransmitters do interact with one another, the increase in Serotonin leading to increases or decreases in other neurotransmitters, and thus reductions in symptoms of depression. The antidepressant medication Venlafaxine has a clinical effect upon both Serotonin and Norepinephrine and has been shown to elicit a much quicker response rate in terms of action again supporting the notion that several neurotransmitters are implicated and perhaps interacting together, Artigas, Nutt, & Shelton (2002). There is some evidence to suggest that SSRI medications such as Prozac and Paroxetine for example result in emotional blunting, Opbroek, Delgado, Laukes, McGahuey, Katsanis, Moreno, & Manber, (2002). It can be argued therefore that this could lead to the individual prescribed such drugs losing interest and pleasure in pursuits that they previously found enjoyable for example sex. SSRI’s often result in loss of libido, Hsu, & Shen (1995).
It can be hypothesised that Paroxetine and other SSRI medications increase Serotonin but also interfere with the Dopamine system since it has been demonstrated that the neurotransmitter Dopamine is involved in sexual function, Giuliano, & Allard (2001), and pleasure, Davis, & Woodside (2002). Therefore based on this argument it is easy to see how a grandfather might murder his entire family before turning the gun upon him-self after a very short period of time taking an SSRI ‘supposed’ to treat depression, his emotions blunted by Paroxetine to such an extent that he no longer found any pleasure in life.
This hypothesis is consistent with there being an interaction between the neurotransmitters Serotonin, Norepinephrine, Dopamine and depressive illnesses.
As has been mentioned previously Kirsch, Moore, Scoboria, and Nicholls (2002) analysed the efficacy data submitted to the Food and Drugs Administration (FDA) for approval of the 6 most widely prescribed antidepressants: Fluoxetine (Prozac), Paroxetine (Paxil), Sertraline (Zoloft), Venlafaxine (Effexor), Nefazodone (Serzone), and Citalopram (Celexa) between the years 1987 and 1999 respectively. The results of the study indicated that 80% of participant responses to the medications were as a result of a placebo effect. Based on this finding it can be argued that antidepressant medications are little more than expensive placebos that cause severe side effects and withdrawal symptoms. Indeed Kirsch et al (2002) discuss in detail that researchers and participants alike knew without a doubt when the active drug was being given because placebos do not produce such side effects since they are inert substances used as a control to highlight that it was the drug having the clinical effect rather than a non-drug.
Healy (2002) suggests that psychotropic drugs were placebo controlled from the 1960s to 1984, but that the majority of trials following this period were merely a comparison between old and new medications, and therefore it is impossible to determine whether or not such ‘new’ dugs are actually better, or indeed if they even have any clinical efficacy. This has allowed pharmaceutical companies to state that their products are superior ‘magic bullets’ that are effective over a range of psychiatric illnesses where Serotonin has been implicated such as social anxiety disorder and obsessive compulsive disorder, based on dubious clinical trials that indicate only modest effectiveness, Healy (2002).
Healy purports that, “The clinical trial results are not compatible with the idea of a Serotonin lesion or a magic bullet effect in any of these disorders.”
It can be suggested that pharmaceutical companies such as the aforementioned GlaxoSmithKline have purposefully kept clinical trial data confidential because the data from such studies doesn’t back up their claim that the drugs are as effective in the treatment of depression or any of the other disorders for which they have gained a license to treat. The Government licensing body, the Medicines Control Agency and their expert advisors the Committee on Safety of Medicines have shares and other financial interests in both the drugs and companies they license drugs on behalf of. Therefore it can be argued that Seroxat (Paroxetine) and other SSRI’s gained a license not because they were effective, but rather because members sitting on the licensing committee had a conflict of interest, and still do, Committee on Safety of Medicines (1999). This view is supported by a recent Guardian newspaper article where an expert review was invalidated by the Committee on Safety of Medicines members having undisclosed interests in the SSRI’s they were supposed to be conducting a safety review of, Boseley (2003).
Based on the available evidence it is clear that the neurotransmitters Serotonin, Norepinephrine and Dopamine are all implicated in depression supporting the Indoleamine theory of depression. It is far from clear however whether or not the current range of new antidepressants, i.e. the SSRI and SNRI class of medications have any conclusive evidence to support the view that they benefit patients to the levels purported by pharmaceutical companies.
Any effect during clinical trials could it can be argued be a result of a placebo effect, participants perhaps believing that because they are experiencing side effects that this will lead to remission or partial remission of their depressed condition the levels of neurotransmitters in turn increasing or normalising due to the placebo effect. The fact that SSRI and SNRI medications take a number of weeks to elicit any antidepressant effect despite evidence to suggest that they act almost immediately also supports the view that decreased levels of a specific neurotransmitter is not the cause of depression but rather merely one of the causes. The study conducted by Berman et al (2002) where catecholamines were ruled out as the cause of depression supports the hypothesis that Amines, and perhaps hormonal imbalances result in depression and disorders where Serotonin and Norepinephrine have been implicated, Healy (2002).
Further research is necessary to determine whether or not the current ‘wonder drugs’ such as Seroxat and Prozac are as effective at treating depression as their manufacturers claim, and perhaps more importantly to dispel patient anxiety as to whether or not the SSRI class, Paroxetine (Seroxat) in particular are drugs of dependence, and can cause serious adverse reactions including suicide. Another important suggestion might be for the Government to tighten the rules governing who can and cannot sit on drug licensing bodies, as it is clear that many of the current members of the Committee on Safety of Medicines have intolerable conflicts of interest and it can be argued licensed unsafe drugs for the treatment of depression during the late 1980s and early 1990s resulting in it can be argued innumerable deaths as a result of suicide and withdrawal symptoms caused by adverse reactions to the medications.
Artigas, F., Nutt, D. J., Shelton, R. (2002). Mechanism of action of antidepressants. Psychopharmacological Bulletin, 36, 2: 123-132. Abstract from Endnote, Pubmed.
Berman, R. M., Sanacora, G., Anand, A., Roach, L. M., Fasula, M. K., Finkelstein, C. O., Wachen, R. M., Oren, D. A., Heninger, G. R., & Charney, D. S. (2002). Monoamine depletion in un-medicated depressed subjects. Journal of Biological Psychiatry, 51, 6: 469-473.
Boseley, S. (2001). Four People Dead is Four too Many. Guardian Unlimited. Online Resource:
Boseley, S. (2003). Drug review halted over company links. Guardian Unlimited. Online Resource:
Bourin, M., David, D. J., Jolliet, P., & Gardier, A. (2002). Mechanism of action of antidepressants and therapeutic perspectives. Therapie, 57, 4: 385 - 396. Abstract from Endnote, Pubmed.
Committee on Safety of Medicines, (1999). Market Towers, London. Online Resource:
Davis, C., & Woodside, D. B. (2002). Sensitivity to the rewarding effects of food and exercise in the eating disorders. Journal of Comparative Psychiatry, 43, 3: 189-194. Abstract from Endnote, Pubmed
Farvolden, P., Kennedy, S. H., & Lam, R. W. (2003). Recent developments in the psychobiology and pharmacotherapy of depression: optimising existing treatments and novel approaches for the future. Expert Opinion Investigating Drugs, 12, 1: 65 – 86. Abstract from Endnote, Pubmed.
Giuliano, F., Allard, J. (2001). Dopamine and sexual function. International Journal of Impotence Research, 13, 3: 18-28. Abstract from Endnote, Pubmed.
Haddad, P. M., Devarajan, S., & Dursun, S. M. (2001). Antidepressant discontinuation (withdrawal) symptoms presenting as 'stroke'. Journal of Psychopharmacology, 15, 2: 139-142. Abstract from Endnote, Pubmed.
Healy, D. (2002). The Creation of Psychopharmacology. Harvard University Press, pp, 114, 143, 209, 290, 299, 307.
Hsu, J. H., & Shen, W. W. (1995). Male sexual side effects associated with antidepressants: a descriptive clinical study of 32 patients. International Journal of Psychiatry Medicine, 25, 2: 191 – 201.
Kirsch, I., Moore, T. J., Scoboria, A. & Nicholls, S. S. (2002). The Emperor's New Drugs: An Analysis of Antidepressant Medication Data Submitted to the U.S. Food and Drug Administration. Prevention & Treatment, Volume 5, Article 23. Online Resource:
Leonard, B. E. (2000). Evidence for a biochemical lesion in depression. Journal of Clinical Psychiatry, 61, 6: 12-7. Abstract from Endnote, Pubmed.
Muris, P., Meesters, C., & Van Melick, M. (2002). Treatment of childhood anxiety disorders: a preliminary comparison between cognitive-behavioral group therapy and a psychological placebo intervention. Journal of Behavioural Therapy Experimental Psychiatry, 33, 3-4: 143-158. Abstract from Endnote, Pubmed.
Nesse, R. M. (2000). Is depression an adaptation? Archive of Gen Psychiatry, 57, 1: 14 – 20. Abstract from Endnote, Pubmed.
Opbroek, A., Delgado, P. L., Laukes, C., McGahuey, C., Katsanis, J., Moreno, F. A., Manber, R. (2002). Emotional blunting associated with SSRI-induced sexual dysfunction. Do SSRI’s inhibit emotional responses? International Journal of Psychopharmacology, 5, 2: 147-151. Abstract from Endnote, Pubmed.
Prange, A.J, Wilson, I.C, Lynn, C.W, Alltop, L.B, Stikeleather, R.A. (1974). L-tryptophan in mania: contribution to a permissive hypothesis of affective disorders. Archives of General Psychiatry, 30: 56–62. Abstract from Endnote, Pubmed.
Richelson, E. (1991). Biological basis of depression and therapeutic relevance. Journal of Clinical Psychiatry, 52: 4 – 10. Abstract from Endnote, Pubmed
Schildkraut, J. J. (1965). The catecholamine hypothesis of affective disorders: a review of supporting evidence. American Journal of Psychiatry, 122, 5: 509-522. Abstract from Endnote, Pubmed.
Sobczak, S., Honig, A., Van Duinen, M. A. Riedel, W. J. (2002). Serotonergic dysregulation in bipolar disorders: a literature review of serotonergic challenge studies. Journal of Bipolar Disorder, 4, 6: 347-356. Abstract from Endnote, Pubmed.
Toru, M, & Itokawa, M. (2001). A history of famous hypotheses and the future development of studies on affective disorders. Nippon Rinsho, 59, 8: 1437-1443. Abstract from Endnote, Pubmed.
Saturday, January 06, 2007
Two must see blogs
Moral excellence comes about as a result of habit. We become just by doing just acts, temperate by doing temperate acts, brave by doing brave acts.
Friday, January 05, 2007
BY CARL ELLIOTT
When the FDA’s Psychopharmacologic Drugs Advisory Committee holds its public hearing on December 13 to consider yet again the possible links between suicidality and the SSRI/SNRI antidepressants, one distinguished member of the advisory committee will be Dr. Bruce Pollock. Pollock used to be on the faculty at the University of Pittsburgh, but last year he was appointed to the Sandra A. Rotman Chair in Neuropsychiatry and Head of the Division of Geriatric Psychiatry at the University of Toronto. Pollock is also one of three committee members with extensive financial ties to antidepressant manufacturers. Pollock will not be allowed to vote, but his expertise was deemed so important by the FDA that his conflicts of interests were waived so that he could be included on the committee.
Pollock’s name may be familiar to scandal watchers. Two years ago, Congress was holding hearings on the question of whether GlaxoSmithKline had suppressed studies unfavorable to Paxil, and the New York attorney general had charged GlaxoSmithKline with consumer fraud. (GlaxoSmithKline settled the lawsuit without admitting wrongdoing, but paid a $2.5 million fine.) In December 2004, ABC News aired an investigative report on GlaxoSmithKline titled “Drug Maker Withheld Paxil Study Data: ABC News Uncovers Documents Unknown to Regulators and Many Study Doctors.” One of those documents concerned Pollock’s work for GlaxoSmithKline.
In the late 1990s, worries had emerged that patients might become dependent on the SSRIs. To combat the perception that people who stopped using Paxil might experience withdrawal symptoms – or “discontinuation” symptoms, as they were often called – GlaxoSmithKline (then still known as SmithKline Beecham) hired a public relations agency called Ruder Finn. Ruder Finn drafted letters that they planned to submit to scientific journals and that downplayed the idea that Paxil was associated with discontinuation symptoms. According to internal memos, Pollock was one of four psychiatrists whom they planned to invite to “author” the letters.
A letter from Pollock eventually appeared in the Journal of Clinical Psychiatry. Although the wording of Pollock’s letter was somewhat different from the draft written by Ruder Finn, it made all the same points. It even made them in the same order. But there was no disclosure, no mention of industry funding, no mention of “editorial assistance,” and no mention of Ruder Finn. Pollock concluded his letter by saying, “Rather than directing our efforts towards the relatively infrequent, minor and transient discontinuation symptoms associated with SSRI therapy, clinicians may be well advised to focus their energies on the greater issues of efficacy, safety, and patient outcome.” The bottom line: concerns about discontinuation symptoms were overblown
Pollock was on the GlaxoSmithKline advisory board at the time, but he told ABC News that he had written the letter to the Journal of Clinical Psychiatry himself and had no knowledge of the draft letter prepared by the PR firm with his name on it. He did admit, however, that "could imagine a scenario where a representative from the makers of Paxil said, 'Could you make this point?'" According to ABC News, Pollock’s letter later appeared in an internal business plan guide prepared for GlaxoSmithKline sales reps. It cited Pollock's letter as "an effective tool for addressing discontinuation."
Writing about the Paxil fraud case last year in the Hastings Center Report, Leemon McHenry described today’s pharmaceutical company marketing strategy as “defending the molecule.” Rather than drawing conclusions from the evidence, wrote McHenry, the strategy is to select the data that promote the drugs, ignore the unfavorable data, pay a prominent academic to sign onto ghostwritten articles about the positive data, and publish the ghostwritten article in the best journals. Then you complete the circle by citing the ghostwritten articles in your marketing literature.
Actually, McHenry left out one crucial part of the circle. If you are the person who signs the ghosted article, you just may get a seat on an FDA advisory committee and a named chair at the University of Toronto.
Copies of Ruder Finn's letters can be found here:
PDF RUDER FINN (right click and save as)
PDF DR POLLOCK'S WAIVER BY THE FDA (right click and save as)
PDF DR POLLOCK'S CONFLICT OF INTERESTS (right click and save as)
Your question about the proper chemical balance of Serotonin in the brain is difficult to answer. Serotonin levels, like the levels of other neurotransmitters in the brain, are in a constant state of change, depending upon our thoughts, feelings, and actions. Serotonin is released when needed (if available) and reabsorbed when not actively needed. Serotonin is released and absorbed in the brain on a minute-to-minute basis. It's similar to trying to estimate the "normal" level of muscle tension when muscle tension is a factor of what we are doing at the time such as relaxing, lifting weights, etc
The biggest problem in measuring brain Serotonin is the nature of the brain. It's a closed system and highly resistive to invasive procedures. Any attempt to sample brain fluid or tissue not only creates a high risk of infection but possible brain injury as well. While we can draw blood, spinal fluid, urine, etc for chemical analysis - we can't draw substances from inside the brain tissue. The closest we can come is a Positron-Emission Tomography (PET Scan - non-invasive) which can color-code and display levels of glucose metabolism and other chemicals in the brain. That fluid snapshot is still of the levels at the time - depending on the activity, feeling, and thoughts of the individual.
Over the years, attempts have been made to estimate Serotonin levels based on the byproducts of Serotonin as evidenced in blood or urine. Several "natural" or herbal labs on the internet have reported they can measure Serotonin levels, suggesting brain Serotonin. This is a false claim and they draw samples from urine and the gastrointestinal tract. Serotonin is located in the brain and gastrointestinal tract (that's why antidepressants give you an upset stomach). Levels of Serotonin in the GI tract are unrelated to levels in the brain.
In clinical practice, we must estimate the "level" of Serotonin in the brain by it's impact and influence on recognized and connected systems. Like muscle tension - the ability to use our muscles within a certain range of relaxation and lifting suggests normal levels. The inability to pick up a small object would suggest low muscle tension while spasms of the muscles would suggest abnormally high muscle tension. Changes in sleep, appetite, energy level, body temperature, etc. are recognized to reflect low levels of brain Serotonin - something confirmed by PET scans. Flu-like symptoms and dehydration are associated with too much brain Serotonin. During clinical examinations, we ask about physical and emotional symptoms related to neurotransmitter levels in the brain. Patient responses then dictate what medications might be appropriate to stabilize those levels.
In short, we can't accurately measure something we can't easily access, especially when the levels change on a minute to minute basis. All treatments associated with brain neurotransmitters are based on well-recognized clinical symptoms directly associated with specific neurotransmitters and supported by PET scan research. On-going research is focusing on better ways to estimate brain neurotransmitter levels but obviously, any accurate measure that can be used by a clinician in the community is still probably decades away.
While this response may not provide a number, percentage, or other accurate "normal" level for Serotonin, it may shed some light on the difficult task of working with neurotransmitters without using an invasive procedure.
Joseph M Carver, Ph.D.
Wednesday, January 03, 2007
Tuesday 2nd Jan 2007
Could you please provide me with answers to the following:
On the Seroxat Patient Information Leaflet (PIL) it states;
'Seroxat is one of a group of medicines called SSRIs (selective serotonin reuptake inhibitors). Everyone has a substance called serotonin in their brain. People who are depressed or anxious have lower levels of serotonin than others. It is not fully understood how Seroxat and other SSRIs work but they may help by increasing the level of serotonin in the brain'
I would like to bring to your attention the statement in blue, 'People who are depressed or anxious have lower levels of serotonin than others.'
In a recent communication with your MHRA Vigilance and Risk Management of Medicines (VRMM) Division, I was told,
"...we are not aware of an internationally agreed "proper chemical balance of serotonin in the brain"
Therefore, this begs the question how Glaxo SmithKline can issue such a statement on their PIL for Seroxat?
1. Did GSK provide the MHRA background documents giving details about the imbalance of serotonin in the brain?
Please answer Yes or No
2. Did GSK provide the MHRA documents with figures for the effect the drug had in changing the imbalanced state?
Please answer Yes or No
3. Please forward me documents that GSK supplied the MHRA during the application procedure for Seroxat that relate to the 'correcting effect' regarding people with lower levels of serotonin.
Meantime, I look forward to your reply.
Mr Robert Fiddaman
I will, of course, upload answers from the MHRA to this blog when I recieve them
Tuesday, January 02, 2007
----- Original Message -----
From: MHRA Information Centre
Sent: Tuesday, January 02, 2007 1:58 PM
Subject: FW: Serotonin
Dear Mr Fiddaman
In reply to your question of 4th December, please see the response below from our Vigilance and Risk Management of Medicines (VRMM) Division:
A variety of factors can contribute to an individual's predisposition to depression. Although it is believed that depression may be caused by a biochemical imbalance and it is recognised that serotonin plays a role in the development of depression it is considered that there is more than one final common pathway in the aetiology of depression, and we are not aware of an internationally agreed "proper chemical balance of serotonin in the brain" that would prevent or reduce the likelihood of experiencing depression.
As you are aware the role of the MHRA is to license medicinal products and ensure that medicines and medical devices on the UK market work, and are acceptably safe. As the precise role that serotonin plays in depression is still subject to ongoing research we really are not best placed to provide you with a response on this particular issue. You may wish to contact professional organisations such as the Royal College of Psychiatrists to seek their view on this matter.
I hope this is helpful to you.
Central Enquiry Point Information Centre
Medicines and Healthcare products Regulatory Agency
Tel: 020 7084 2000
Let's examine the following MHRA statement shall we?
"Young adults (18-29 years of age) are at a higher
background risk of suicidal behaviour than older adults and
therefore should be monitored particularly closely."
Firstly, a seach on Wikipedia for the term 'Young Adult' provides us with the following:
From Wikipedia, the free encyclopedia
Young adult refers to:
a person in the early years of adulthood
in human development, the stage between adolescence and adulthood, roughly ages 16 to 30.
Young adult (psychology), persons aged 20 to 40
in the Catholic Church, persons aged 18 to 34
in Unitarian Universalist circles, persons aged 18 to 35
Young adult literature, works targeted to ages 12 to 18.
in the computer game The Sims 2, "young adult" is the life stage associated with The Sims 2: University.
Basically, the MHRA are saying that the risk of suicidal behaviour is higher in 'young' adults up to the age of 29. In effect they think that if you are over the age of 29 then you DO NOT fall into the background risk of suicidal behaviour.
Now I find this quite absurd as each human being... or 'Young Adult' are made up of individual components. It seems the MHRA only think people between the ages of 18-29 should be monitored 'particularly closely' Bad news if you are 30+ then eh?
The MHRA need to change the wording from 'Young Adult' to 'Adult', there should be no age restrictions. Quite why they use this terminology is baffling - particularly as many of the adverse withdrawal reactions reported to them regarding Seroxat come from people over the age of 29.
Try this link on Wikipedia for the word 'Transparency'