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One theory of antidepressant withdrawal syndrome


Altostrata

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On 5/24/2011 at 10:59 PM, Altostrata said:

THIS IS THE FIRST POST OF THIS TOPIC. LINK TO FULL POST

 

Admin note: For discussion of lamotrigine (Lamictal), see Lamictal (lamotrigine) to calm post-discontinuation withdrawal symptoms

 


 

 

This following is an article that has propagated all over the Web, by someone named Altostrata. It has been updated for this post:

As I've been suffering from Paxil withdrawal syndrome since October 2004, I've studied the medical literature on antidepressant withdrawal syndrome. What I've learned about the alerting system and glutamatergic system in antidepressant withdrawal syndrome may be informative.

Antidepressants cause downregulation of serotonin receptors. In a mechanism of brain self-defense, the receptors actually disappear, becoming more sparse so as to take in less serotonin. It is thought among withdrawal researchers that people who experience the worst withdrawal are slower than others to repopulate serotonin receptors.

Others believe those who suffer the worst are those whose brains are highly neuroplastic and adapted more thoroughly to the influence of the medication.

Relative slowness to upregulate receptors doesn't mean there's anything intrinsically wrong with our brains, it just means there's variability (of course) among nervous systems.

Even among people suffering the most severe antidepressant withdrawal syndrome, repopulation of serotonin receptors probably occurs long before symptoms disappear. However, while the serotonin system is repairing itself, an imbalance occurs in the autonomic nervous system. The locus coeruleus "fight or flight" center becomes disinhibited and the glutamatergic system becomes more active than normal. This is called disinhibition of the alerting system, and it generates symptoms that are awful: panic, anxiety, sleeplessness, and dreadful imagery among them.

 

... link to rest of this post

Stas you might want to read this. This is what I had seen.

Edited by scallywag
delete multiple quoted posts, edit quote by adding link to post loaction

 

2001 Remeron , Celexa, prozac a week on lithium. 

2014 went off effexor and trazadone in 3 weeks. 

2014 zoloft (hyper reaction) put on effexor 75 mg. Was stable until 2017 

2017  Trazadone 50 mg (June) Effexor to 113 mg (2 weeks) Effexor 150 mg for a month . Took 75 mg until November. . Lithium 10 days, Lamactil 10 day  aug-nov15 ativan

October : Prozac bridge to get off 75 mg of effexor Used 10 mg of prozac. Stopped prozac 3 wk 

Dec 6, 7 Upped trazadone from 50 to 100 mg Did it for 3 days Stopped it

Dec 7 , Dec 8 Took prozac again 0.1 , 0.1, 0.6 stopped it

Dec 11 and Dec 12 upped it to 100 again

Dec 15 , 16,17 went back to 50 mg of trazadone

December 18 Began 3 beads of effexor  Dec 25 began 5 beads of effexor take 10 mg of omneprazole daily

 

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  • 2 months later...

I like this explanation of withdrawal syndrome as it relates to sleep homeostasis dysregulation and other kinds of extremely "wired but tired" states not physiologically possible naturally and makes perfect sense. However I think it's only a part of the story. It doesn't explain all the odd visual/sensory/perceptual disturbances that happen and get worse long after the drugs are out of the system, especially if tapered too quickly or cold turkey, which are most definately neurotransmitter related.

2016-2017 (Took mirtazapine on an "as needed" basis when I haven't slept a night as the next day I'd get a guaranteed 11 hours+ sleep, but very seldom. Maybe 5-6 times in total and 2 days at the same max. & never had problems with that ) 

 

21/08/17 - 26/08/17  (Started Mirtazapine because of sleep problems Day 1 - 3,5mg Day 2 - 7,5mg, Day 3 - 15mg Day 4 7,5mg - Day 5 - 7,5mg - Day 6 - 7,5mg then stopped without tapering because of personality changes)


September (Sporadic intake of 3,75mg-7mg  because insomnia, maybe 5-6 times but September 23th- September 25th (Day 1 - 7,5mg, Day 2 - 7,5mg Day 3 7,5mg)


October (Sporadic intake for 3,75mg -7mg because of insomnia. maybe 4-5 times)


October 13th Last dose of mirtazapine 3,75mg (no taper)

 

Sorry, I didn't keep track of when exactly I took some dosages in September or October.

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Those symptoms are related to neurotransmitters only in the sense that neurotransmitters and other hormones are the way signals are transmitted throughout the body. They are autonomic symptoms.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

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On 6/21/2011 at 10:39 AM, Altostrata said:

I have verified the information in post #1 with a knowledgeable doctor.

 

I have also been corresponding with Dr. Giovanni Fava. Dr. Fava has not only been a longtime critic of antidepressants, he an expert in Cushing's syndrome, a disorder involving excessive cortisol production due to tumors. (The cortisol production in Cushing's is far, far higher than in withdrawal syndrome. Symptoms of Cushing's include fatigue; muscle weakness; depression, anxiety and irritability; loss of emotional control; cognitive difficulties.)

 

Dr. Fava's theory that antidepressants worsen the course of depression, instilling a greater likelihood of relapse in those who take them, has been getting more attention lately. His statistics of relapse (and those of Dr. Irving Kirsch, see Do Antidepressants Make You Sad?) are based on existing research.

 

I have long contended that many of those post-antidepressant cases of relapse recorded in psychiatric research are actually withdrawal syndrome, from which you may recover. Therefore, while Dr. Fava's theory seems likely in light of existing research, if withdrawal syndrome were factored in, it would show that antidepressants are not effective and increase the risk of withdrawal syndrome rather than relapse.

 

This last week, Dr. Fava and I had this exchange regarding Do Antidepressants Make You Sad?:

 

 

Just quoting this one as..........my brother was in town recently and while visiting a friend of his.........I was referred to a book written by a local pediatrician.     And I WILL search for it.  She, our friend, said it was about how AD's don't work.  And God Bless him........and I so hope he is still practicing, working with the children.  The pediatrician is her brother.  He may well be retired now.

 

About that march???!!!  I mean it's March now.  We best get organized......:o:)

 

Peace, harmony, healing and all that......

mmt

Edited by manymoretodays
oh, I always elaborate somewhere

Late 2023- gone to emeritus status, inactive, don't @ me, I can check who I've posted on, and I'm not really here like I used to be......thanks.

Started with psycho meds/psychiatric care circa 1988.  In retrospect, and on contemplation, situational overwhelm.

Rounding up to 30 years of medications(30 medication trials, poly-pharmacy maximum was 3 at one time).

5/28/2015-off Adderal salts 2.5mg. (I had been on that since hospital 10/2014)

12/2015---just holding, holding, holding, with trileptal/oxcarb at 75 mg. 1/2 tab at hs.  My last psycho med ever!  Tapered @ 10% every 4 weeks, sometimes 2 weeks to

2016 Dec 16 medication free!!

Longer signature post here, with current supplements.

Herb and alcohol free since 5/15/2016.  And.....I quit smoking 11/2021. Lapsed.  Redo of quit smoking 9/28/2022.  Can you say Hallelujah?(took me long enough)💜

None of my posts are intended as medical advice.  Please discuss any decisions about your medical care with a knowledgeable medical provider.  My success story:  Blue skies ahead, clear sailing

 

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  • 1 month later...

Thank you for sharing your knowledge and insight. It helps me to think more carefully about withdrawal and the introduction of  'New' medications. It's like, maybe I'd better be done with the withdrawal process before deciding to add something new into the mix. At least then I'll know if symptoms are from withdrawal or from a new medication.

6+ years of Cymbalta at 90mg. I have taken this since back surgery following car accident. Pain meds caused seizures and failed to address pain. Am now being tapered off. Now at 0 mg, but taking 30mg e/o day for up to 2 wks. Also on Divalproex, Lamotrigine, vitamin D, B12 and Calcium (not so faithfully).

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  • 4 weeks later...
  • Mentor
On 3/12/2018 at 2:29 PM, manymoretodays said:

About that march???!!!  I mean it's March now.  We best get organized......:o:)

@manymoretodays: I'm in! Maybe we could do something like the Womxn's March where there were marches in different cities. I got Seattle 🙂

  • Prozac | late 2004-mid-2005 | CT WD in a couple months, mostly emotional
  • Sertraline 50-100mg | 11/2011-3/2014, 10/2014-3/2017
  • Sertraline fast taper March 2017, 4 weeks, OFF sertraline April 1, 2017
  • Quit alcohol May 20, 2017
  • Lifestyle changes: AA, kundalini yoga

 

"If you've seen a monster, even if it's horrible, that's evidence of divinity." – Damien Echols

 

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Dr. Fava's theory that antidepressants worsen the course of depression, instilling a greater likelihood of relapse in those who take them, has been getting more attention lately. His statistics of relapse (and those of Dr. Irving Kirsch, see Do Antidepressants Make You Sad?) are based on existing research.

 

I have long contended that many of those post-antidepressant cases of relapse recorded in psychiatric research are actually withdrawal syndrome, from which you may recover. Therefore, while Dr. Fava's theory seems likely in light of existing research, if withdrawal syndrome were factored in, it would show that antidepressants are not effective and increase the risk of withdrawal syndrome rather than relapse. 

 

 

This. I wonder how much of the "worsening" is just that people are being inappropriately put onto meds, and then inappropriately withdrawing from them. I hope that's the case, anyway.

2005 St John's Wort / 2006-2012 Lexapro 20mg, 2 failed attempts to stop, tapered over 4.5 months in early 2012

January 2013 started Sertraline, over time worked up to 100mg

July 2014 Sertraline dropped from 100mg to 75mg, held for six months, slower tapering until 2019 22 Dec 3.2mg

2020 Sertraline 19 Jan 3.1mg, 26 Jan 3.0mg; 1 Mar 2.9, 7 Mar 2.8, May (some drops here) 24 May 2.5, May 29 2.4, June 21 2.3, June 28 2.2mg,  July 4 2.1mg, July 24 (or maybe a bit before) 2mg, early Nov switched to home made suspension; 29 Nov 1.8mg; approx 25 Dec 1.6mg)

2021 Some time in about Jan/Feb realised probably on more like 1.8mg and poss mixing error in making suspension; doses after 10 Feb accurate; 10 Feb 1.6mg; 7 Mar 1.4, continued monthly

10% drops until 1mg, then dropped 0.1mg monthly.

May 2022,0.1mg, now dropping 0.01mg per week

29 August 2022 - first day of zero!

My thread here at SA: https://www.survivingantidepressants.org/topic/1775-bubbles/page/21/

Current: Armour Thyroid

 

 

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  • 1 year later...

The title information has been very valuable to me.

 

i have found my symptoms of what I consider the brain have mostly gone and is now replaced by symptoms that are fight-flight in nature.

 

the symptoms that I feel are related to upregulation of receptors have seem to cleared, I even believe that my brain has completely restored itself, as I was on SSRI for only 6 months overall.

 

the issue I have now seem CNS related and it’s usually the agitation and anxious jittery type feeling, unable to focus or stay still, it’s like being in a nervous state without external factors causing it, it comes and goes but it is mild.

 

this also influences my thoughts, an anxious body will create anxious thoughts. Sometimes I feel like someone with GAD, although before SSRI I was a very cool customer.

 

ive tested the idea with taking a myriad of supplements, ie. nootropics and also vitamins..they have initial calming effects followed by the contradictory effects for hrs following, and this I believe is the triggering of the autonomous fight flight mechanism. I even reduce my doses eg. 5HTP to 20% of the recommended dose and got quite severe reaction which could last a day, and the reaction feels very CNS and not like WD symptoms,

 

another is low resislience, when I am having a nice conversation with friends I will suddenly feel agitated, spaced out and numb, and the need to lie down after 15 mins of stimulation.the same occurs with stress, the tolerance level is quite low, compared to my normal self before SSRI, I could have hr long heated debates or party all night, even backpack across Europe for months. The shocks were easily shouldered. I am surprised that coming off lexapro left me in such a weakened state, I can barely enjoy a conversation for more than 15 min before feeling overwhelmed.

 

i can only give this time and hope I recover, as said, the paradigm shift occurred and the symptoms I felt with initial discontinued have turned into what feels more link CNS.. pardon me if I don’t know the medical language for this, but the feeling and experience is certainly different. I can test this just by taking some tryptophan or SAMe, even fish oil or vitaminB and in a few hrs I will being to feel very uncomfortable. Even things like coffee and nicotine can cause me to feel this internal buzzing which quickly turns into a throbbing headache..now in the past I could easily slam down 5 coffees a day or stack up piles of vitamins with little effect. Its a big difference today, so I am sure there is something that needs healing until things go back to normal

Lexapro

10mg 11/2018 -  4 weeks

20mg 12/2018 - 4 weeks

20mg - 0mg - 01/2019 - 02/2019  - taper 6 weeks - WD symptoms

10mg - 03/2019 - 6 week reinstate

03-04/2019 taper 10,7.5,5,2.5,0mg as instructed by dr.

0mg - 04-06/2019 - WD symptoms again.

accute symptom cleared follow by protracted symptoms still ongoing

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Hello, regarding this statement, "Antidepressants cause downregulation of serotonin receptors. In a mechanism of brain self-defense, the receptors actually disappear, becoming more sparse so as to take in less serotonin. It is thought among withdrawal researchers that people who experience the worst withdrawal are slower than others to repopulate serotonin receptors"  can someone explain the process to reverse this? What makes the receptors come back/go back to normal? Does it happen automatically with the absence of the SSRI?

Paxil 40 mgs started January 1999, many withdrawal attempts since then, with two cold turkey.
Paxil 10 mgs since 2011. I had been unable to go lower for seven years.
Paxil 9 mgs began September 17, 2018. Continued for 12 weeks.
12-10-18 began 8.5 mgs. 01-21-19 began 8 mgs. 03-04-19 began 7.5 mgs. 04-15-19 began 7 mgs. 06-24-19 began 6.8 mgs.

07-29-19 began 6.6 mgs. 08-19-19 began 6.4 mgs. 09-30-19 began 6.2 mgs.
I've been through hell the past several months, tapering down from 7 mgs. I can't live like this, so I will increase, and remain there for the foreseeable future.  10-21-19 began 7 mgs.

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10 hours ago, tmzddz said:

can someone explain the process to reverse this? What makes the receptors come back/go back to normal? Does it happen automatically with the absence of the SSRI?

It happens on its own, but also on its own time. It's been almost a year and I still have debilitating symptoms.

- March 2017: 50mg Sertraline starts

- August 2017: up to 100mg

- February 2018: down to 50mg

- November 2018: one-week taper down to 0mg

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Herod, thanks for responding. I'm sorry you still have debilitating symptoms. I am in a bad way myself, so I understand and am sending you (((HUGS))).

Paxil 40 mgs started January 1999, many withdrawal attempts since then, with two cold turkey.
Paxil 10 mgs since 2011. I had been unable to go lower for seven years.
Paxil 9 mgs began September 17, 2018. Continued for 12 weeks.
12-10-18 began 8.5 mgs. 01-21-19 began 8 mgs. 03-04-19 began 7.5 mgs. 04-15-19 began 7 mgs. 06-24-19 began 6.8 mgs.

07-29-19 began 6.6 mgs. 08-19-19 began 6.4 mgs. 09-30-19 began 6.2 mgs.
I've been through hell the past several months, tapering down from 7 mgs. I can't live like this, so I will increase, and remain there for the foreseeable future.  10-21-19 began 7 mgs.

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  • 9 months later...
On 5/24/2011 at 7:59 PM, Altostrata said:

Admin note: For discussion of lamotrigine (Lamictal), see Lamictal (lamotrigine) to calm post-discontinuation withdrawal symptoms

 


 

 

This following is an article that has propagated all over the Web, by someone named Altostrata. It has been updated for this post:

As I've been suffering from Paxil withdrawal syndrome since October 2004, I've studied the medical literature on antidepressant withdrawal syndrome. What I've learned about the alerting system and glutamatergic system in antidepressant withdrawal syndrome may be informative.

Antidepressants cause downregulation of serotonin receptors. In a mechanism of brain self-defense, the receptors actually disappear, becoming more sparse so as to take in less serotonin. It is thought among withdrawal researchers that people who experience the worst withdrawal are slower than others to repopulate serotonin receptors.

Others believe those who suffer the worst are those whose brains are highly neuroplastic and adapted more thoroughly to the influence of the medication.

Relative slowness to upregulate receptors doesn't mean there's anything intrinsically wrong with our brains, it just means there's variability (of course) among nervous systems.

Even among people suffering the most severe antidepressant withdrawal syndrome, repopulation of serotonin receptors probably occurs long before symptoms disappear. However, while the serotonin system is repairing itself, an imbalance occurs in the autonomic nervous system. The locus coeruleus "fight or flight" center becomes disinhibited and the glutamatergic system becomes more active than normal. This is called disinhibition of the alerting system, and it generates symptoms that are awful: panic, anxiety, sleeplessness, and dreadful imagery among them.

This paper explains the mechanism in withdrawal causing alerting disinhibition: Harvey, et al: Neurobiology of antidepressant withdrawal: implications for the longitudinal outcome of depression; Biological Psychiatry. 2003 Nov 15;54(10):1105-17.

Once disinhibition of the alerting system takes hold, it becomes self-perpetuating. The whole question of neurotransmitter imbalance -- a chimera of psychiatry anyway -- becomes moot. No manipulation of serotonin, norepinephrine, or dopamine is going to help. In fact, it usually makes the condition worse.

Noradrenergics -- buproprion or Wellbutrin; mirtazapine or Remeron; SNRIs such as Cymbalta, Serzone, Effexor; and St. John's Wort, rhodiola -- stimulate "fight or flight" activation, as will most SSRIs. Drugs and substances that are stimulating should be avoided.

Even drugs that are calming may cause a paradoxical reaction as the alerting system fights to stay in control.

My guess is: The first phase of withdrawal, the acute phase, is the initial shock of withdrawal, with the most defined symptoms, such as brain zaps and nausea and possibly waves of unusually intense "depression" and "anxiety" -- actually, emotions generated by the neurological upset. Later, glutamatergic hyper-reactivity and autonomic instability take over. Often the autonomic instability causes wide hypersensitivity to drugs, supplements, and even foods.

Out of control, unrelated to environmental or psychological triggers, the alerting system sends intense, spontaneous signals to the adrenals, which produce the stress hormones cortisol and adrenaline.

This is not strictly brain damage. Brain damage means some physical part has been permanently removed and can never be recovered. Rather, this is iatrogenic neuropsychiatric damage.

According to established principles of neuroplasticity, the nervous system can repair itself and regain functioning that is close to normal. In cases where there is no apparent iatrogenic cause for autonomic dysfunction, it often spontaneously resolves. Low stress, good nutrition, and as much sleep and gentle exercise as possible are key.

[ironically for those suffering from lamotrogine (Lamictal) withdrawal -- too-fast Lamictal withdrawal causing glutamatergic rebound -- lamotrigine is a drug that tempers the activity of the glutamatergic system, incidentally reinforcing an intact GABA system. Microdoses of lamotrigine can assist recovery from antidepressant withdrawal syndrome. I am being treated with about 5mg per day and it is helping me recover.

Cautionary note: Lamotrigine may not be a universal treatment for withdrawal syndrome. If you want to try it, make sure you consult a doctor who is very familiar with using it and start with very small doses -- .5mg to begin, slowly titrate up to 5mg or more; stay at the lowest effective dose. Nausea and headaches are signs of too high a dose. (2mg tablets are available by request from GlaxoSmithKline; 5mg tablets are available by prescription; lamotrigine can be made into a liquid by a compounding pharmacy.) In too large a dose, lamotrigine, like everything else, can make your symptoms worse.]

In the medical literature on antidepressant withdrawal, symptoms of alerting system disinhibition -- anxiety, panic, sleeplessness, irritability, agitation among them -- are sometimes misidentified as "unmasking" or emergence of bipolar disorder. This leads the clinician to medicate with a cocktail of drugs upon which the patient does poorly, the neuropsychiatric damage from antidepressant withdrawal being compounded by additional medication and attendant reactions.

In Anatomy of an Epidemic, Robert Whitaker describes this process as the way many children, suffering adverse effects from antidepressants, are led into a lifetime of medications for misdiagnosed bipolar disorder.

It's always the victim who's blamed, not the drug. It's about time we took a closer look at what withdrawal does to the nervous system, and question whether the chronic downregulation of serotonergic receptors caused by long-term antidepressant prescription is a benign condition.

 

 


For discussion of lamotrigine (Lamictal), see Lamictal (lamotrigine) to calm post-discontinuation withdrawal symptoms

 

Two questions:

 

if downregulation leads to an excited rebound effect that can last for years. Is there any evidence of how to regrow receptors?

 

second thing, you said the brain can repair itself close to normal? Does close to normal mean not entirely normal?

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You can't do anything about downregulation except to let your body go through natural processes to re-calibrate receptors. Not much is known about this process. For some people, it seems to be very gradual and take a long time.

 

As the process takes a long time, some years may pass. Your body and brain naturally want to get back to normal functioning. "Normal" may change as years go on. You can never step in the same river twice.

 

For example, if you went on antidepressants when you were 19 and went off when you were 34, your brain and nervous system will not revert to what you remember "normal" to be as a 19-year-old. That's life.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

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2 hours ago, Altostrata said:

You can't do anything about downregulation except to let your body go through natural processes to re-calibrate receptors. Not much is known about this process. For some people, it seems to be very gradual and take a long time.

 

As the process takes a long time, some years may pass. Your body and brain naturally want to get back to normal functioning. "Normal" may change as years go on. You can never step in the same river twice.

 

For example, if you went on antidepressants when you were 19 and went off when you were 34, your brain and nervous system will not revert to what you remember "normal" to be as a 19-year-old. That's life.

ok so we don't know how up regulation works. got it. 

 

but by "normal" you dont mean it can cause permanent changes or damage to the brain, but that the natural aging process will continue 

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The aging process, whatever you've done while you're recovering, your general health -- they all affect your "normal" at any one time.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

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  • 1 month later...
On 5/25/2011 at 7:59 AM, Altostrata said:

The locus coeruleus "fight or flight" center becomes disinhibited and the glutamatergic system becomes more active than normal. This is called disinhibition of the alerting system, and it generates symptoms that are awful: panic, anxiety, sleeplessness, and dreadful imagery among them.

This paper explains the mechanism in withdrawal causing alerting disinhibition: Harvey, et al: Neurobiology of antidepressant withdrawal: implications for the longitudinal outcome of depression; Biological Psychiatry. 2003 Nov 15;54(10):1105-17.

Noradrenergics -- buproprion or Wellbutrin; mirtazapine or Remeron; SNRIs such as Cymbalta, Serzone, Effexor; and St. John's Wort, rhodiola -- stimulate "fight or flight" activation, as will most SSRIs. Drugs and substances that are stimulating should be avoided.

 

Alto, could you please clarify the bolded statements. These appear to be contradictory, the way I understand them.

 

So you're saying the WD effect leads to activation of fight and flight. I read this as stimulating the LC and Amygdala.

 

In the second statement: SSRIs are also stimulants. (presumably for the same fight and flight centers.)

 

I always thought SSRIs depressed the flight/fight activity, thus decreasing anxiety and other emotions.

 

Am I getting this wrong?

2012- Citalopram 40- Axal 0.5mg  2017- Stopped Axal CT. No WD.

2017 - Effexor XR 75 mg.

For Epilepsy:1983 - Tegral 400 mg/day  2009 - Lumark 1000 mg/day- Biotim eyedrops for glaucoma.

27 April 2019 - Effexor XR taper started. 40 beads removed - 16% - 63mg20 May - 10% - 20 beads. 57mg / 3 June - 10% - 20 beads - 51mg / 18 July - 6% -10 beads - 48mg / 20 July - 7% -10 beads- 44.5mg/ 1 Sept - 75 mg alternate days = 37.5 mg/ 14 Sept - 75 mg every 3rd day = 25mg/  22 Sept - Effexor XR stopped.

27 Oct - Tegral = 300mg. Citalopram = 30 mg. Lumark = 500mg Busron = 10 mg. Somna = 2.5 mg

1-Jan 2020 Tegral 200mg BD- Citalopram 20mg OD- Lumark 500BD

25 Apr 2020 Tegral 200 mg BD- Citalopram alternate days 20 mg and 10 mg OD - Lumark 500BD

May June 2020 Dropped to 10 mg citalopram due to drug shortages.

Early July 2020: CT'ed citalopram - nonavailability of medicine. Tegral + Lumark remains same as before.

 

 

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  • 8 months later...
On 5/24/2011 at 7:59 PM, Altostrata said:



This is not strictly brain damage. Brain damage means some physical part has been permanently removed and can never be recovered. Rather, this is iatrogenic neuropsychiatric damage.

According to established principles of neuroplasticity, the nervous system can repair itself and regain functioning that is close to normal. In cases where there is no apparent iatrogenic cause for autonomic dysfunction, it often spontaneously resolves. Low stress, good nutrition, and as much sleep and gentle exercise as possible are key.
 

 

does "close to normal" mean no one ever achieves a complete reversal back to what they were before starting meds? just curious as to what you meant by that. 

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  • Moderator Emeritus

Hi Ryguy,

 

I'll go with the new improved version of self, once healing sets in.

 

And then what follows, in context of that statement is nice to focus on, I think:

 

According to established principles of neuroplasticity, the nervous system can repair itself and regain functioning that is close to normal. In cases where there is no apparent iatrogenic cause for autonomic dysfunction, it often spontaneously resolves. Low stress, good nutrition, and as much sleep and gentle exercise as possible are key.

 

So anyway.....my take, is that recovery happens, the damage can reverse.

 

And best,

L, P, H, and G,

mmt

 

Late 2023- gone to emeritus status, inactive, don't @ me, I can check who I've posted on, and I'm not really here like I used to be......thanks.

Started with psycho meds/psychiatric care circa 1988.  In retrospect, and on contemplation, situational overwhelm.

Rounding up to 30 years of medications(30 medication trials, poly-pharmacy maximum was 3 at one time).

5/28/2015-off Adderal salts 2.5mg. (I had been on that since hospital 10/2014)

12/2015---just holding, holding, holding, with trileptal/oxcarb at 75 mg. 1/2 tab at hs.  My last psycho med ever!  Tapered @ 10% every 4 weeks, sometimes 2 weeks to

2016 Dec 16 medication free!!

Longer signature post here, with current supplements.

Herb and alcohol free since 5/15/2016.  And.....I quit smoking 11/2021. Lapsed.  Redo of quit smoking 9/28/2022.  Can you say Hallelujah?(took me long enough)💜

None of my posts are intended as medical advice.  Please discuss any decisions about your medical care with a knowledgeable medical provider.  My success story:  Blue skies ahead, clear sailing

 

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  • 1 month later...

So is NAC a supplement worth trying as it regulates the glutamatergic system?

Nardil 1985-1988
Paxil ?-1998

Effexor150  1998-November 2018 

Bupoprion150 2002-November 2018

Fluoxetine approximately 1/4 mg trial for WD symptoms December 2020. Took for 3 days but  it seemed to compound the dizziness significantly so I had to discontinue the trial. 

 

Current Medications: Levothyroxine, Acyclovir 

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@Patti2057

 

There are many existing topics on SA.  Use a search engine and add site:survivingantidepressants.org to the search term.

 

n-acetylcysteine-nac

 

* NO LONGER ACTIVE on SA *

MISSION ACCOMPLISHED:  (6 year taper)      0mg Pristiq  on 13th November 2021

ADs since ~1992:  25+ years - 1 unknown, Prozac (muscle weakness), Zoloft; citalopram (pooped out) CTed (very sick for 2.5 wks a few months after); Pristiq:  50mg 2012, 100mg beg 2013 (Serotonin Toxicity)  Tapering from Oct 2015 - 13 Nov 2021   LAST DOSE 0.0025mg

Post 0 updates start here    My tapering program     My Intro (goes to tapering graph)

 VIDEO:   Antidepressant Withdrawal Syndrome and its Management

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  • 4 months later...

Hey Altostrata, 

 

I read this thread and it was very interesting.

 

What exactly do you mean with this statement:

According to established principles of neuroplasticity, the nervous system can repair itself and regain functioning that is close to normal. In cases where there is no apparent iatrogenic cause for autonomic dysfunction, it often spontaneously resolves. Low stress, good nutrition, and as much sleep and gentle exercise as possible are key.

 

 

 

What do you mean with ,,no apparent iatrogenic cause for autonomic dysfunction,,? 

 

I wondered.

 

Greetings Tomster!

 

 

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However, while the serotonin system is repairing itself, disruption occurs in the autonomic nervous system. The locus coeruleus "fight or flight" center becomes disinhibited and the parasympathetic system becomes more active than normal.

 

@Altostrata   I just read your post, and it makes so much sense as to what I am experiencing. 

 

I hope you have some time to respond to a few questions - 

 

1.  Does the FF disinhibition manifest itself as "irrational resistance/fear" of any change?  For example, I find it takes a couple of days for me to get used to changing my wardrobe to warmer clothing (full sleeves, warmer fabrics, socks to bed), and I don't get much sleep the first night. It helps to try and defuse/distract the brain by wearing the clothes earlier in the day when I am moving around, rather than change before bed.  There appears to be a valid reason for that resistance - an aggravation of symptoms - the hypersensitivity to fabric, the change in blood circulation, and overheating/cooling, that happens when I am lying down to sleep.   But in many cases, I find that the same type of resistance to do any work sitting /lying down, while I am perfectly fine moving around.

 

2. That brings me to the second question about parasympathetic overactivity..  I find that most of my symptoms occur when I am tired or need to rest or sleep..   I am wondering if this could be due to "parasympathetic excess", which is a type of autonomic dysfunction?  The symptoms described in the link seem to be very similar to what I am dealing with, and I have to carefully manage going into rest state, to avoid triggering the sympathetic activation (adrenaline rushes falling asleep etc)  - https://touchneurology.com/neurometabolic-disease/journal-articles/autonomic-nervous-system-monitoring-of-patients-with-excess-parasympathetic-responses-to-sympathetic-challenges-clinical-observations/

 

I am really trying to piece together what can be directly attributed to withdrawal and what may be due to a underlying autonomic dysfunction (currently diagnosed as a vagus nerve disorder, which I think may be due to a high vagal tone) that was destabilized by CT withdrawal from mirtazapine.  

 

The same page has a description of vagal excess/syncope (https://franklincardiovascular.com/vasovagal-syncope-and-chronic-vagal-excess/) , and I think I may have this, given my syncope events in teenage years, followed by chronic IBS (I never really had the classic IBS-D/IBS-C, only reflux/burping/bloating), so my IBS may be due to autonomic dysfunction, which really flared up with the withdrawal.  Currently,  most of my symptoms appear to flare up following a drastic temperature, pressure, or humidity change, usually a drop in temperature,  and it takes a day or two for the body to find balance.  It gets harder of course, when we have rapid changes like this week in the bay area.  These two articles seems to give credence to the assumption that IBS suffers may have excess parasympathetic activity due to vagal dysfunction and baroreflex sensitivity, given my sensitivity to pressure, cold, and highly symptomatic splenic flexure - https://www.nature.com/articles/s41598-019-43455-5

-  https://journals.physiology.org/doi/full/10.1152/ajpregu.00607.2004 

-  https://journals.physiology.org/doi/full/10.1152/ajpregu.00607.2004

 

However, I don't have any of my chronic IBS symptoms in withdrawal except burping, which is confounds me. The areas most frequently affected seem to be gut/pelvic region (burps, gas, gut noises, multiple bouts of BMs or urination),  extremities (cold feet, burning legs, paresthesia, fabric sensitivity) and head (sinus pressure, disorientation), and most often when going to bed or waking up early AM. 

 

I have seen many improvements over the last couple of months ( reduced FF on wakeups, better digestion/food tolerance and gut motility, better temperature tolerance as long as there is no drastic change or a combination of heat and cold (hot sun/cold winds),  but sleep time continues to be a challenge due to the other physical symptoms.  

 

 

 

Chronic IBS since 1990

Former smoker (1992- Jun 2017)

Prescribed mirtazapine for sleep in Aug 2017 after IBS flare-up following Nicotine cessation.

Mirtazapine 7.5mg 8/17 to 5/18

Mirtazapine 3.75mg 5/18 to 1/19

Off Mirtazapine since 2/19.

Vit B, Vit D+K2 and Magnesium Glycinate as needed.

On Ayurvedic herbs for GI issues - Guduchi since Jul 2020, Indukantham since Oct 2020

On Ashwagandha 1g since Nov 2020

 

 

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I don't think a withdrawal symptom pattern can be attributed to any one body system. The entire web of interactions is trying to stabilize.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

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14 minutes ago, Altostrata said:

I don't think a withdrawal symptom pattern can be attributed to any one body system. The entire web of interactions is trying to stabilize.

Absolutely..  In my case, it seems to target my weakest spot (my gut) most often.

Chronic IBS since 1990

Former smoker (1992- Jun 2017)

Prescribed mirtazapine for sleep in Aug 2017 after IBS flare-up following Nicotine cessation.

Mirtazapine 7.5mg 8/17 to 5/18

Mirtazapine 3.75mg 5/18 to 1/19

Off Mirtazapine since 2/19.

Vit B, Vit D+K2 and Magnesium Glycinate as needed.

On Ayurvedic herbs for GI issues - Guduchi since Jul 2020, Indukantham since Oct 2020

On Ashwagandha 1g since Nov 2020

 

 

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