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Shelton, 2006 Correspondence from Dr. Richard Shelton about prolonged withdrawal syndrome

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Altostrata

Subject: RE: Antidepressant discontinuation syndrome

Date: Sat, 22 Jul 2006 14:31:17 -0500

From: "Shelton, Richard" <richard.shelton@[e-mail]

To: [altostrata]

 

Sorry for the delay - I have been away at a scientific meeting.

 

I actually think the discontinuation syndrome is pretty bad in some situations and truly horrible in others. Hence, why participated in a scientific focus group that wrote a series of papers teaching docs about the problem (appeared in the Journal of Clinical Psychiatry).

 

First, let's acknowledge one thing: there is a great deal of variability in response, with a lot of people experiencing bad symptoms and others little at all, but almost all resolve; that is, except for a very small group, where the symptoms become persistent. At the core, the variability is related to genetic (actually, more correctly, genomic) differences between people (one of our areas of research).

 

The receptors do down-regulate. In fact, the reaction of the majority of people is consistent with down-regulation. That is, there is an adaptation that occurs in the receptor (actually phosphorylation) that makes it less responsive to serotonin. This, by the way, is probably the serotonin 2A type receptors. When the adaptation occurs, it takes about 10-14 days to re-equilibrate (to de-phosphorylate). The receptor returns to normal, along with related proteins (like the serotonin transporter protein). That is how they work.

 

The variation between people is probably due to genomic variations in the genes coding for proteins involved in this process. However, regardless of the situation, in the average circumstance, the re-adaptation eventually occurs. This is why it can be protracted in some situations. However, even in that situation, there is a limit in time.

 

So, why do some people have these very long effects? There may be several potential causes. For example, it is possible that something has happened to destroy some neurons - either the ones containing serotonin or the others that they connect to.

 

In fact, there is a research literature that says exactly that. However, all the studies have been in cells in culture and have one essential problem that invalidate them (sorry for being so direct). The concentrations used to achieve the toxic effects are a two orders of magnitude above what can ever be found in human tissue - that is, the concentration is 100 times as much as can ever be achieved in humans. Typical concentrations don't do that. This, then, falls into the category that too much of anything is toxic (first postulated by Paracelsus in the 16th century, I think). So, too much water, salt, sun, etc., etc.

 

In fact, a strong effect of antidepressants (including paroxetine) is the opposite - that is, preservation of neurons by stimulating the production of brain derived neurotrophic hormone, and another hormone, bcl-2. Both stimulate the growth of new tissue and preserve the health of the living cells.

 

So, what then? Let's go back to our premise: The discontinuation effect is truly horrific in some people. The direct mechanisms involved in the genesis of the problem can't really be involved in it's persistance. So, what's up with that?

 

In fact, there are long-standing adaptations that can take place in the nervous system. However, as with most things in the body, the problem is a variation of a normal process (otherwise, it wouldn't be there in the first place).

 

There appear to be lots of variation in this reaction in people who develop persistent symptoms, but one salient feature that seems almost invariably present: They become intensely afraid during the experience. People may describe this in different ways, but the way the brain is reacting is an exaggeration of what the brain does during threat. The physical symptoms are consistent with that.

 

So the "threat" systems are "turned on" and don't "turn off" easily. This can happen in a few ways, but has to occur pretty fast.

 

In fact, it is a normal response. Think of a mouse living in a field somewhere. If there is an acute threat that occurs (e.g., chased by a cat) and the mouse escapes, the mouse's brain has to remember that and react. There are a couple of ways to do that. One is to synthesize proteins to "remember." That, actually, is slow (but happens). The second is to actually do something to the genes controlling the system itself: to induce chemical modifications to the genes or the supporting structure to activate some genes and inactivate others. The net effect is for the system to stay "on" so to speak. However, in this situation, it is purely adaptive.

 

Going by the principle, then, that people vary in their response, some people seem particularly prone to have this to occur. That is why when people are exposed to a life threatening situation, some go on to develop post-traumatic stress disorder, and others don't. Now, one important thing is that most people develop trauma related symptoms immediately after an event (e.g., insomnia, dreams of the event, anxiety, etc., etc.). In the normal situation, these symptoms resolve within a month. But some people develop long-standing responses, in which the system is turned "on" and they can't turn it "off." I think that is what is at play here.

 

People might ask, "why then do I still have some of the same symptoms?" The answer is related to the longer-term synthesis of new proteins. What happens is that the brain activates the pathways associated with that symptom (e.g., electrical sensations in the body), and it stays on. It is like a kind of memory, so to speak. But one that reactivates the sensations.

 

That is the basic story. The question, then, is what's next? There are a few ways to potentially deal with the problem. First, you could use something to directly suppress the symptoms - really not great, but often effective. Drugs related to Valium (e.g., Xanax) activate neurons related to a chemical in the brain called gamma amino butyric acid (GABA). That is an inhibitory transmitter, which can suppress the symptoms. However, it only works when it is present, and the body adapts to it with time, producing physical dependency - not ideal.

 

Another way is to use another serotonin uptake inhibitor antidepressant (probably one with a long half life). Most people don't want to do that since they believe that the first one was toxic (which, as I've described, is untrue). Serotonin is a regulatory chemical in the body, and in the stress-emotional system its primary role is inhibitory. So, it suppresses the activity of the neurons that are "turned on," suppressing the symptoms. In most (but not all) people that will work. It is an acceptible alternative.

 

Given that the mechanism involves "memory," then information processing is important. So, certain forms of cognitive behavioral therapy seem to be effective in reducing the symptoms, at least to a manageable degree. I like that option. It has to start with several ideas - your brain has not actually been "damaged;" the symptoms are not life-threatening; etc. However, a good cognitive therapy may be able to help.

 

A lot of therapists say they do cognitive therapy; however, most who do so are not really compent at the treatment. I'd advise going to the Center for Cognitive Therapy website at the University of Pennsylvania (http://www.uphs.upenn.edu/psycct/). There is a referral list at the bottom of the page (it goes to this site: http://www.uphs.upenn.edu/psycct/referral/states.htm, where you can look up your state to try to find a therapist). If you have the choice, someone that specializes in anxiety disorders is the place to start.

 

Best of luck,

 

Richard C. Shelton, M.D.

James G. Blakemore Research Professor

Department of Psychiatry

Vanderbilt University School of Medicine

Edited by Altostrata
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Altostrata

Date: Sat, 22 Jul 2006 17:32:00 -0700 (PDT)

From: [altostrata] Subject: RE: Antidepressant discontinuation syndrome

To: "Shelton, Richard" <richard.shelton@[e-mail]>

 

Dr. Shelton:

 

Thanks very much for sharing your theory. I can't tell you how much I appreciate your work in educating doctors about discontinuation syndrome and your attention to the prolonged variety. Many practitioners still do not even believe discontinuation syndrome exists.

 

I can confirm that exaggerated anxiety and fear have been a prominent emotional feature in my case, although not as much as for others. Although I have steadily recovered from physical and cognitive symptoms over the last 21 months, I have occasions, perhaps once every few weeks, where perhaps for a minute or so I feel a bolt of pure fear. I can manage those.

 

My main discontinuation-induced difficulties now are 1) concentration and memory problems 2) insomnia 3) emotional numbness 4) occasional intense depression 5) anorgasmia.

 

When you speak of patients whose serotonin 2A type receptors re-adapt slowly, where would you say I am on the continuum? When have you seen "protracted" conditions resolve (at around two years?) or is my profile that of a patient whose problems will be "persistent"?

 

I am consulting with Dr. Owen Wolkowitz at UCSF. I have discussed with him my sense of an anxiety loop corresponding to your description. He may recommend a pharmagenetics evaluation. May I show your letter to him? He is very interested in other doctor's theories.

 

Thank you for your suggestion of cognitive therapy. I am working on cognitive techniques with a therapist now.

 

Sincerely, [altostrata]

 

PS You may be interested to know that I am hypersensitive to GABA-ergics, along with other discontinuation-induced hypersensitivities. A little could go a long way with me. I do not trust antidepressants; from my experience, very few doctors are knowledgeable enough to prescribe them and deal with their side effects.

Edited by Altostrata
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Altostrata

Date: Sun, 30 Jul 2006 22:54:51 -0700 (PDT)

From: [altostrata]

Subject: Your article in J Clinical Psychiatry

To: richard.shelton@[e-mail]

 

Dr. Shelton --

 

I have just read your article in Journal of Clinical Psychiatry 2006 vol 67 Supplement 4. Your earlier paper, Steps Following Attainment of Remission: Discontinuation of Antidepressant Therapy; Prim Care Companion J Clin Psychiatry. 2001 Aug;3(4):168-174. was one of the few helpful resources I could find last year when it was clear (to me at least) that I was suffering from prolonged discontinuation syndrome.

 

As I read it, in your current paper you define discontinuation syndrome as invariably time-limited to a matter of a few weeks, and any symptoms after that time indicate relapse, recurrence, or another illness altogether.

 

Dr. Shelton, I know you and Dr. Peter Haddad are well aware that prolonged and persistent antidepressant syndrome does occur. I am profoundly grateful you shared your views with me. However, your definition of discontinuation syndrome as short and transient is airtight. Does the working group intend to address the prolonged and persistent conditions separately?

 

I had the "electrical sensations" aka "zaps," among other acute symptoms, for seven months post-Paxil. Your guidelines would lead a clinician to attribute this to anything but discontinuation syndrome.

 

Although I have steadily improved over 21 months, Paxil discontinuation has left me with hypersensitivity to many medications. Following your guidelines, a clinician might diagnose me with depression and prescribe a full dose of an antidepressant that might kill me. Accurate diagnosis and treatment of my condition is crucial to me.

 

After reading the J Clin Psych articles, I realized I will not be able to get appropriate treatment from any psychiatrist in the United States. Please, I beg of you, continue your education of clinicians including information about the prolonged and persistent forms of antidepressant discontinuation syndrome.

 

Sincerely, [altostrata]

Edited by Altostrata
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Altostrata

Subject: RE: Antidepressant discontinuation syndrome

Date: Mon, 7 Aug 2006 at 4:34 PM

From: "Shelton, Richard" <richard.shelton@[e-mail]

To: [altostrata]

 

There is a difference between what is definitional and what is exceptional. I want to be careful in addressing this question.

 

There is a scientific difference between something that is directly caused by an event (such as the discontinuation effects of paroxetine), and something else that may be set off by the action. The differences are subtle, but very important, as they determine what the appropriate next steps should be.

 

Much of what I have heard from people with regard to long-term discontinuation sound consistent with variants of panic attacks. I believe that discontinuation of paroxetine can precipitate panic (pretty well described in the past). This is not surprising, give the fact that paroxetine suppresses panic. This effect is consistent with the pathophysiology of panic.

 

Paroxetine suppresses the activity of parts of the brain thought to be involved in the induction of panic. They are highly activated when paroxetine is discontinued. Note that I think that paroxetine can induce panic in people who have not had them in the past. As often is the case, the symptoms present in the original panic attack are replicated as the illness progresses.

 

Therefore, the pattern of symptoms is established by the originating event, in this case paroxetine discontinuation. This is true, by the way, even for people who have previously had panic attacks. That is, the form changes in a way consistent with the newly experienced symptoms. This is not peculiar to paroxetine discontinuation - it can happen with other drugs as well. Hence, the separation between the originating event (discontinuation) and the ongoing problem (panic). This is important, since there are treatments for panic. We have been successful in dealing with discontinuation using them. For example, variants of cognitive behavior therapy are well-established for panic and are helpful in discontinuation situations. This, then, does not necessarily require a medication, although I do not object to using one if needed (only one with a longer half-life than paroxetine).

 

R

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squirrel

very interesting article.

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Maybe

When he talks about persistent, does he mean prolonged wd or forever?

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Barbarannamated

Has Dr. Shelton informed the FDA of his findings that paroxetine can induce panic disorder in patients treated for depression? He is saying it is not discontinuation syndrome but a new diagnosis, correct?

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alexjuice

It is kind of Dr. Shelton to take the time to anawer these emails. I don't know many who do so. He deserves credit for that.

 

Alex

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Barbarannamated

Alex,

You're a better person than me. :-/ It feels placating to me. He knows there is a serious problem, but only offers advice on how to deal w with the sequelae. No effort to publish (that I am aware of) or perhaps he's being blocked. He's being VERY cautious w what he puts in print. Notice no type of 'apology', even general, for the impact of these meds on Alto's life or the other thousands+. Is he still prescribing them? Ill bet my bottom dollar he is. (What's a bottom dollar, anyway?) I know that Stahl is a drug *****, however, his main Essentials of Psychopharm book (not the handbook) really steers against SSRIs as 1st line for depression. If anyone is near a med school bookstore or has this book, please tell me if you see the same thing. Im NOT defending Stahl! Just thinking about approaching from a backdoor, so to speak.. 'divide and conquer. They obviously aren't going to cut all ties w pharma, but they MAY go up against one drug to start with, alienate only 1 company or group of drugs. Too bad Prozac is off patent. We could leverage use of Prozac for discontinuing/tapering. But oh how I despise Lilly!

I do look forward to speaking with Shelton. Don't worry, I'll be good. ;-)

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alexjuice

Alex,

You're a better person than me. :-/

 

Haha. If you insist! No seriously, barb, I have emailed as sorts of people in the field, even sympathetic figures. Many do not respond. Many do respond but it's either only to say they don't answer email or it's not the principal but a staff member or grad student speaking the doc's company line. If Shelton is really taking time to respond to email for free, I give him credit. My old shrink used to charge $75 if you needed to call him on the telephone in an emergency, that's the profession we're dealing with.

 

I do agree there is hypocrisy here. It does seem that the doctor is playing the politician game. When talking about causes of brain zaps it made me think, "it depends what your definition of the word 'is'...is." Still I give him credit for engaging with random people who are not his patients even if his integrity is not 100% snow white in all areas of his professional interactions. Also, i hate to say this, it's my opinion, after living with a couple dozen doctors for 150 days, that doctors don't see patients as human or as equally human as themselves of their family members. Maybe this because of compassion fatigue or simply a defense. But doctors see sick and miserable and dying people all day long everyday. In my experience this affects empathy and ability to relate as co-humans. So I don't think he means to be dismissive or demeaning. He's just a doctor talking to a pateint and can't help himself that it comes across that way

 

I do want to support and reinforce your emotions. I feel the same way that they don't seem to care on an emotional level. I think it's wrong and disgusting.

 

Too bad Prozac is off patent. We could leverage use of Prozac for discontinuing/tapering. But oh how I despise Lilly!

I do look forward to speaking with Shelton. Don't worry, I'll be good. ;-)

 

I don't follow you here Barb. Why is it too bad Prozac's gone generic? Is it that docs should come out against the short-lived ADs in favor of prozac cross? Since most don't even seem to recognize withdrawal, or treat with due respect, I'm not sure how eager docs would be for this. I'm a little foggy so perhaps your point has eluded me?

 

In any event, docs like Shelton who is both a doctor (MD) and a doctor (professor) should have a bit more latitude to be honest. He's got tenure, I assume. And you mention you have a meeting scheduled.

 

When you speak with Dr. Shelton, what do you plan to ask him, besides what you've already mentioned?

 

Alex

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Altostrata

I believe Dr. Shelton has a guilty conscience.

 

To my knowledge, this information about prolonged withdrawal syndrome has never been communicated to the FDA. As Peter Haddad (on occasion a co-author with Shelton) also alludes to it in several papers, I believe there are unpublished studies in which it surfaces.

 

Perhaps you can ask about unpublished studies or other evidence, Bar.

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Barbarannamated

Subject: RE: Antidepressant discontinuation syndrome

Date: Mon, 7 Aug 2006 at 4:34 PM

From: "Shelton, Richard" <richard.shelton@[e-mail]

To: [altostrata]

 

There is a difference between what is definitional and what is

exceptional. I want to be careful in addressing this question. There is

a scientific difference between something that is directly caused by an

event (such as the discontinuation effects of paroxetine), and something

else that may be set off by the action. The differences are subtle, but

very important, as they determine what the appropriate next steps should

be.

 

Much of what I have heard from people with regard to long-term

discontinuation sound consistent with variants of panic attacks. I

believe that discontinuation of paroxetine can precipitate panic (pretty

well described in the past). This is not surprising, give the fact that

paroxetine suppresses panic.

 

This effect is consistent with the pathophysiology of panic. Paroxetine

suppresses the activity of parts of the brain thought to be involved in

the induction of panic. They are highly activated when paroxetine is

discontinued.

 

Note that I think that paroxetine can induce panic in people who have

not had them in the past. As often is the case, the symptoms present in

the original panic attack are replicated as the illness progresses.

Therefore, the pattern of symptoms is established by the originating

event, in this case paroxetine discontinuation.

 

This is true, by the way, even for people who have previously had panic

attacks. That is, the form changes in a way consistent with the newly

experienced symptoms. This is not peculiar to paroxetine discontinuation

- it can happen with other drugs as well.

 

Hence, the separation between the originating event (discontinuation)

and the ongoing problem (panic).

R

 

Looking more closely at this. Anyone, PLEASE feel free to set me straight!

1) what area of brain is he referring to w panic? Is this documented somewhere?

2) he is clearly attempting to dissociate the panic disorder from paroxetine use or discontinuation. Way to CYA, doc.

3) 'symptoms replicate as illness progresses' Sounds a bit like kindling, ie. worsening of panic rather than improving w more time away from drug.

4) 'Note that I think paroxetine can induce panic in people who have not had them in the past.'

* I assume he MEANT to say 'discontinuation of paroxetine can induce....' but, bottom line, it IS the med THAT WAS NEVER ASSESSED FOR LONG TERM USE or Safety that is the cause. The panic disorder was not present prior to paroxetine EXPOSURE. He wants to separate the tardive neuroendocrine dysregulation, manifesting as panic, from the treatment. New diagnosis, new treatment rendered by psychiatry/ology. Interesting how he advises CBT. Short term psychotherapy to reverse iatrogenic changes in the panic center of the brain? Would it not follow that mania induced by ADs should also be treatable w CBT and not mood stabilizers and APs? I would like to discuss the mechanism of tardive dyskinesia w him, then extrapolate. May also be interesting to chat w a/neurologist specializing in movement disorders.

IF we were talking about a med used in general med and not mental health, this would be a known Public Health crisis-- an antibiotic creating a mutated resistant superbug, for example.

 

Sorry if this is all review for all of you who have been analyzing and fighting for so long.

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Barbarannamated

Just one more thing.... the 'unmasking' of bipolar I now see is a convenient way to shift blame to patient and 'underlying psychpathology' rather than place responsibility on drug.

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Barbarannamated

I will definitely chat w you before I see him, Alto.

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alexjuice

Would it not follow that mania induced by ADs should also be treatable w CBT and not mood stabilizers and APs? I would like to discuss the mechanism of tardive dyskinesia w him, then extrapolate.

 

I'd be interested in his response if this comes up. I've heard several explanations for seemingly permanent effects from antipsychotics. Mostly doctors dismiss the notion of 'permanent' change, so far as I've seen. Yes, I'd definitely like to know what mechanism he attributes tardive dyskinesia to.

 

I look forward to your report. As to your other questions, I'm not able to help with the technicals, unfortuntately.

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Barbarannamated

Alex, my thinking is that any pharma company is looking to expand usage of currently marketed drugs still patent protected. It has become very hard to get new drugs through the FDA approval process and especially CNS compounds. Docs see most SS/NRIs as me-too drugs w a few exceptions: Prozac is more activating, Paxil better w anxious depression, Cymbalta is a slam dunk w any pain pts. Similar w AAPs. Seroquel for sleep, Ability for activation/energy, Zyprexa... no f***g clue how that is still on the market. I worked w researchers on sertindole which never made it to market due to cardiac issues, I believe. Ive never heard a doc discuss half life w ADs or APs. They are aware of slight diffs (much more so w AAPs) and just keep trying until something seems to work, but they have no idea why.

So, my thought was that Prozac could carve out a niche, be the hero and help all the people trying to DC the other nasty ADs w shorter T1/2 and anticholinergic probs. They'd get so many scripts not only for DCing but also b/c they'd be perceived as safer for newly diagnosed (not a good part of my plan). In the process, the problems w discontinuation would get some attention.

I tend to look at things from a point of 'who stands to benefit/have a vested interest in getting the information out there?' IF there was a product indicated for AD discontinuation, it would be genius and also hated by every AD manufacturer and generic companies. Even if someone performed AND PUBLISHED studies using Prozac to DC, it would shed some light. Has that been done in a controlled setting? I think Wikipedia mentions Prozac on the SSDI Discontinuation page.

It's a very tangled web to try to penetrate. Creating some infighting MAY be a step.

Once a product is off patent, they won't invest in it for research or marketing. That's why so many companies tweak the molecule or change delivery system. Extends patent life.

That said, there ARE branded generics which I don't fully understand. The new trazodone, Aplenzin (bupropion HBr or budeprion? ). They've morphed Wellbutrin so many ways--Zyban, etc.

Hope this makes sense! It's a stretch.

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Altostrata

Bar, why don't you ask him what he means by this?

 

I believe he may be part of the wing that thinks withdrawal symptoms are a form of PTSD: The patient experiences the horrific physical symptoms and thereafter has a psychosomatic reaction based in the mechanisms of PTSD. The drug isn't the problem, the patient's reaction to the trauma is the problem.

 

This is ridiculous when you consider what the symptoms can be. But then, PTSD can cause a wide range of symptoms as well -- and its definition is becoming broader and broader.

 

Personally, I find "There is a difference between what is definitional and what is exceptional" to be offensively patronizing.

 

One hallmark of rationalization in the service of cognitive dissonance is a lack of logical coherence and a reliance on blither. Do you think that's what's going on here?

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Barbarannamated

Oh, absolutely! He is a master of doublespeak to cover his ass, not commit, confuse the issue and avoid responsibility.

I didn't know what he meant by the definitional vs exceptional comment, but it didn't feel good. He is all over the place.

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Barbarannamated

And I still go back to ... the panic/PTSD did not exist prior to exposure to med. Doesn't prove causation, but sure looks like an association or correlation.

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Altostrata

What he's saying is that severe or prolonged withdrawal syndrome is so exceptional as to be negligible. This without any statistics of frequency -- unless he's hidden those somewhere.

 

So that's another question to ask him: How often does prolonged withdrawal occur and what is is evidence?

 

I would not waste any time discussing withdrawal as PTSD with him. That's an artifact of doctors not listening to patients, or reinterpreting what they say to suit their own prejudices. Just dismiss it as nonsensical.

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compsports

""I believe he may be part of the wing that thinks withdrawal symptoms are a form of PTSD: The patient experiences the horrific physical symptoms and thereafter has a psychosomatic reaction based in the mechanisms of PTSD. The drug isn't the problem, the patient's reaction to the trauma is the problem. ""

 

The problem is psychiatry in general never views their drugs as the problem. It doesn't matter what the situation is.

 

CS

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alexjuice

Has anyone (Alto, Gia, others) had any recent correspondence with academicians?

 

The Shelton emails in the thread are very thought provoking and it's over a year later so perhaps there are some new ideas in circulation?

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Barbarannamated

Alex,

 

I never got to talk to him, but agree his research is very interesting.

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Altostrata

Later on, Dr. Shelton got on the pharma gravy train:

 

http://focus.psychiatryonline.org/article.aspx?articleID=1391085 September 01, 2012 Author and Article Information:

 

Richard C. Shelton, M.D., Charles Byron Ireland Chair of Psychiatric Research, Vice Chair for Research, Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham.

 

Dr. Shelton reports the following disclosures: Consultant: Lilly, Cyberonics, Janssen, Medtronic, Pamlab, Pfizer, Ridge Diagnostics, Takeda; Grant/Research Support: Bristol-Myers Squibb, Lilly, Elan Corp, Euthymics Bioscience, Forest, Janssen, Novartis, Otsuka, Pamlab, Pfizer, Repligen Corp, Ridge Diagnostics, St. Jude Medical Inc., Takeda.

(Dr. Shelton moved from Vanderbilt to University of Alabama at Birmingham in 2012 http://www.uab.edu/medicine/psychiatry/faculty/30-faculty/faculty-bios/409-richard-c-shelton-md-test )

 

Also see http://www.uab.edu/medicine/psychiatry/research/mood-disorders-research

Current research programs include:

  • AHRQ CHOICE Comparative Effectiveness Study, which is comparing the effects of two common treatments for bipolar disorder, quetiapine and lithium (Shelton)
  • Impact of chronic stress and environmental enrichment on the organization of brain circuits underlying stress-elicited behavioral responses (Kerman)
  • Impact of circadian misalignment induced by off-shift sleep strategies in hospital shift work nurses (Gamble)
  • Impact of dysregulation of GSK3 (therapeutic target for lithium and several of psychotropic drugs) on circadian rhythms (Gamble)
  • Impact of neonatal handling vs. maternal separation on the development of depressive- and anxiety- like behaviors and the organization of emotional-motor brain circuitry. A basic science study investigating neurobiology of somatic symptoms of mood disorders (Kerman)
  • Ketamine Treatment of Acute Suicidal Ideation in the ER, a project that is testing the possible benefits of ketamine, a rapid treatment of depression, for suicidal depressed patients in the emergency department setting (McCullumsmith and Shelton)
  • L-methylfolate for Treatment Resistant Major Depression, which is testing the possible benefits of a natural treatment, a metabolite of folic acid, for depression that is not fully responsive to antidepressant therapy (Shelton)
  • Neural correlates of fear conditioning in major depression, a translational study of brain structure and function following early life trauma and stress sensitization within unipolar depression (Grant)
  • NIMH RAPID Trials, a program of research that focuses on the development of rapidly effective treatments for depression (Shelton)
  • Obesity, Inflammation, and Depression, which is studying inflammation as a possible link between obesity and depression (Shelton)
  • Paliperidone and Lithium in the Treatment of Suicidality, an assessment of the effectiveness of two treatments for suicidal thoughts, coupled with a study of the regulation of specific genes in suicidal patients (Shelton and May)
  • Ramelteon for Bipolar Depression, a study of a completely new approach for the management of the depressed phase of bipolar disorder, the use of a medicine that helps to normalize circadian rhythms (Shelton and May)
  • Resting-state connectivity and trauma, an investigation of resting state-connectivity within unipolar depression based on differential trauma history (Grant)
  • Suicide Assessment Validation Study, a project which is comparing three ways of assessing suicide risk (May and Shelton)
  • Testing the efficacy, and safety of OPC-34712, a new medicine, as add-on treatment for people with major depression (Fargason)
  • Testing the efficacy, safety , and tolerability of desvenlafaxine succinate sustained release in the treatment of children and adolescent outpatients with major depressive disorder (Cullinan)
  • Ziprasidone Augmentation in Treatment-Resistant Depression, a study testing a new approach for the treatment of depression that does not fully respond to antidepressant therapy (Shelton)

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alexjuice

Later on, Dr. Shelton got on the pharma gravy train:

 

http://focus.psychiatryonline.org/article.aspx?articleID=1391085 September 01, 2012 Author and Article Information:

 

Richard C. Shelton, M.D., Charles Byron Ireland Chair of Psychiatric Research, Vice Chair for Research, Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham.

 

Dr. Shelton reports the following disclosures: Consultant: Lilly, Cyberonics, Janssen, Medtronic, Pamlab, Pfizer, Ridge Diagnostics, Takeda; Grant/Research Support: Bristol-Myers Squibb, Lilly, Elan Corp, Euthymics Bioscience, Forest, Janssen, Novartis, Otsuka, Pamlab, Pfizer, Repligen Corp, Ridge Diagnostics, St. Jude Medical Inc., Takeda.

(Dr. Shelton moved from Vanderbilt to University of Alabama at Birmingham in 2012 http://www.uab.edu/medicine/psychiatry/faculty/30-faculty/faculty-bios/409-richard-c-shelton-md-test )

 

Well, I'm sorry to hear this news.

 

Dr. Shelton's having to reside in Birmingham, Alabama is a minor consolation.

 

Alex

 

PS - I've never been to Birmingham but it's one of only three American cities for which I've never heard a positive report.

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Narcissus

 

 

Well, I'm sorry to hear this news.

 

Dr. Shelton's having to reside in Birmingham, Alabama is a minor consolation.

 

This made me laugh out loud.  No small feat as I feel like **** right now.  

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