Can anyone make sense of this to explain to a layperson?

[[cs...]]

Thanks dm123, it was horrific to say the least. That being said, it appears I tick off the boxes for items 1, 3, 4, and 5 under Areas of Scope. Needless to say, I will be reading your posts with great interest and enthusiasm even if I don't fully understand everything.

Yes, you are definitely a more complex case in terms of scope, but my hope is that we can all identify the buckets of scope that we fall into, and then this will help us identify which parts of the science and clinical studies are relevant to us.  In doing that, we might be able to apply some of the crude adjunctive therapies to help us through our taper.  It seems that most of us in 4 do eventually progress to 5.  I was well on the way.  Your metabolism of Valium is very unique, and I'm glad you've been able to get as far as you have with your fast metabolism. 

[[cs...]]

Hi DM123,

thanks so much for this information, and I'm glad that the references to psychotherapeutic terms of trauma fit in with your thread.

 

The info on kindling is fascinating.....as with everything about this process it's really not understood is it? (pr perhaps it's my unscientific mind)

 

I have never had a seizure, and even though used short acting and pernicious Xanax really didn't even have any interdose w/d until about 17 years of use.  Then it lasted about 9 months before I committed to the taper.  What I'm reading from your posts leads me to think that the kindling phenomena may not be a significant factor in my w/d.  (although length of usage is) and possibly the ridiculously large cuts I made in the beginning -- where glutamate was running the show and I felt so very very unwell will factor into my w/d.  If for nothing else than the learned behaviour state specific learning that occurred.

(I may need to get a new couch!  The old one is where I was living my life...  )

 

Again I want to thank you for putting all of this here on BB.  Every time I read your posts -- although over my head -- I think I learn a wee bit more about the processes happening in my CNS and HPA axis. The science starts to make some sense and the physiology that is impacted becomes a bit more clear.  That helps me with the idea that I really need to get out of the way and let my body heal -- somehow a hard lesson to put into practice!

 

I hope that your presentation of your papers go very well!

All the best to everyone here (and on BB)

SS

 

Yes, you are right.  At first glance kindling seems to be simple upregulation of the Glutamate system, but that term is used very freely.  Even if it is one of the major players involved in kindling (and i do believe it is),  we don't know how much of an impact the other factors are having to make the neuron hyperexcitable, and furthermore we don't know exactly how it gets upregulated.  I'm guessing the research will point to an intracellular process, and also these other factors combining to cause the hyperexcitable neuron. 

 

LTP, which Pers wrote about ultimately caused sensitization and upregulation of AMPARs via intracellular processes. 

 

The hyperexcitable neuron is something I hope we explore in detail.  Keeping our focus on that end goal helps us interpret the clinical studies in the proper  context.....

 

You have very strong physiology.  During the 17 years of xanax did you dose all at once during the day/night or did you spread out the dose.  Dosing a short acting benzo like I did is a sure path to kindling.  If you single dosed 17 years of xanax you have amazing physiology.  Adding in the small amount of V I think was very smart of you.  Was that your idea or the doctor's.?

 

Yes the science is telling us all to get it out of our bodies as fast as possible.

[[cs...]]

dm123, are you able to find any research on benzos and platelets? I've read of people being low in platelets, but mine were as wonky as my blood pressure. Usually, while I was taking Ativan, my platelets were in the 900,000 range. They remained that high throughout the duration of Ativan and into Klonopin. My hematologist had no answers. He kept giving me test after test. He gave me iron infusions, which didn't change a thing. I didn't want a bone marrow biopsy. Then after my TIA in 2015, the platelets bounced up to 1.8 million. I had to get off almost all the pills I was put on in the hospital for them to go down to 700,000. The last time I was tested they were down to 550,000. All my doctor could say was that I had "highly reactive blood."

 

Thank you for all your research so much!! And if you can answer this, I would be grateful!!

 

Hi Terry can you explain more about what pills you were on?  You mentioned it was at 1.8M, then you got off almost all  the pills you were on.  It then dropped to 700K.

 

I noticed many cases of high platelets are idiopathic.(i.e., primary form)

 

Did the hospital do a platelet pheresis?

[[...]]

Thank you dm123 for all your research .......

I can't absorb all of it , but ! A laymans question ..... Where is the hope in all of this ? I tend to feel more hopeless in reading all the research .....

 

I was on high dose hydrocortisone fro 9 months and had to cold turkey when it 'turned ' on me , which I now think was a bad idea , though they were making me so sick I felt I had no choice .

 

Now I am coming up against the same type of reaction to Valium ... Which is very frightening . As I know ct is not an option .

 

Now that I knwo that steroids are PAMS , it makes sense why , after my ct and then starting klonopin , I began to feel a lot better ! I then corssed to Valium when I had a difficult time trying to taper klonopin . The crossover was brutal and I don't think I ever stabilized on Valium . I am also I now find a fast metabolizer of at least the parent drug Diazepam .

 

What does all this mean fro me ? My taper seems impossible with extreme WDs at the slightest reduction . I'm stuck and feel quite trapped now with the benzo.

 

I hope your research leads to some answers for those of us struggling so much .

 

Interestingly ,valium has become extremely sedating fro me this last month , way more than it ever has been before ,to the point where I can only take 1/2 mg in the am and 1/2 at lunch , and the rest at night . The sedative effects are supposed to become quickly tolerant.  I have found the opposite , the anxiolytic effects are pretty much zero , and the sedation over the top !

Complicated is an understatement isnt it!

MiYu

 

 

[[Te...]]

I was given Lipitor (my cholesterol was at 188), clonodine, Plavix (he did no genetic testing to see if I was a fit person for this), Hydralazine, Famotidine, Amlodipine, aspirin, Atenolol. Since I am allergic to NSAIDS, the aspirin had to go first. I am still on 2.5 mg. Amlodipine, but that's the only pill out of all of them that I'm still taking. The Lipitor made my liver enzymes really high, so of course I was tested for Hepatitis a few times.

 

I don't know if the hospital did a platelet apherisis.

 

I know this is a lot to ask you!! I just think that my body couldn't take all the drugs. I only weighed 117 at the time (5'5" tall) and think it was all too much. I was right in the throes of benzo withdrawal, too. At the time, with all the pills, I felt like I had Alzheimer's.

 

Since the last time my platelets were checked, they were at 550,000, and I just think my body had finally settled down somewhat after the benzo mess and everything else.

 

Thank you, dm123!!!

[[li...]]

dm123,

 

'GPCRs, for example. We have not gotten to these, but muscarinic receptors are a type of GPCR.  We know that in studies, stimulation of muscarinic  receptors cause a DECREASE in inhibitory signaling of GABAa receptors.'

I sort of briefly touched on that in my latest PM.

 

Many years ago I took a powerful antimuscarinic drug for two days, it had a half life of between two and three days and an active metabolite.

Weeks or months later I definitely felt a backlash, with cognitive effects during the afternoon, requiring me to take an extra 0.25 mg clonazepam late afternoon.

 

'hyperexcitability' one's hyperexcitability isn't the same as someone else's. I may have that, in the sense of being very sensitive to exercise and not in a good way, strong hormonal reactions. Whether sensitivity to sunlight/weather is part of that I don't know, the same goes for general drug sensitivity.

[[Su...]]

Hi DM123,

thanks so much for this information, and I'm glad that the references to psychotherapeutic terms of trauma fit in with your thread.

 

The info on kindling is fascinating.....as with everything about this process it's really not understood is it? (pr perhaps it's my unscientific mind)

 

I have never had a seizure, and even though used short acting and pernicious Xanax really didn't even have any interdose w/d until about 17 years of use.  Then it lasted about 9 months before I committed to the taper.  What I'm reading from your posts leads me to think that the kindling phenomena may not be a significant factor in my w/d.  (although length of usage is) and possibly the ridiculously large cuts I made in the beginning -- where glutamate was running the show and I felt so very very unwell will factor into my w/d.  If for nothing else than the learned behaviour state specific learning that occurred.

(I may need to get a new couch!  The old one is where I was living my life...  )

 

Again I want to thank you for putting all of this here on BB.  Every time I read your posts -- although over my head -- I think I learn a wee bit more about the processes happening in my CNS and HPA axis. The science starts to make some sense and the physiology that is impacted becomes a bit more clear.  That helps me with the idea that I really need to get out of the way and let my body heal -- somehow a hard lesson to put into practice!

 

I hope that your presentation of your papers go very well!

All the best to everyone here (and on BB)

SS

 

Yes, you are right.  At first glance kindling seems to be simple upregulation of the Glutamate system, but that term is used very freely.  Even if it is one of the major players involved in kindling (and i do believe it is),  we don't know how much of an impact the other factors are having to make the neuron hyperexcitable, and furthermore we don't know exactly how it gets upregulated.  I'm guessing the research will point to an intracellular process, and also these other factors combining to cause the hyperexcitable neuron. 

 

LTP, which Pers wrote about ultimately caused sensitization and upregulation of AMPARs via intracellular processes. 

 

The hyperexcitable neuron is something I hope we explore in detail.  Keeping our focus on that end goal helps us interpret the clinical studies in the proper  context.....

 

You have very strong physiology.  During the 17 years of xanax did you dose all at once during the day/night or did you spread out the dose.  Dosing a short acting benzo like I did is a sure path to kindling.  If you single dosed 17 years of xanax you have amazing physiology.  Adding in the small amount of V I think was very smart of you.  Was that your idea or the doctor's.?

 

Yes the science is telling us all to get it out of our bodies as fast as possible.

 

Yes I dosed once a day -- at bedtime -- for the 17 years that I was on the medication.... weird huh?  For most of that time, around 10 years I tool .25 only.  It was when I went off the .25 for a week -- during a meditation retreat --  in a feeble attempt to get off Xanax  that I started to need to take more and more of the med....

 

I think that was one of the reasons I was under the mistaken idea that I might have and easier time getting off (that and DENIAL!!!)  When I started to get the interdose w/d towards the end of the reign of xanax I started to take about .03-.06mg  around 4:00am, but that was really for less than a year I believe.  I feel extremely lucky and unlucky with my physiology.  It allowed me to be on this drug for far too long -- and I think it's allowing me to come off with a relative ease -- some days though -- yowza!

 

  It was my docs idea to add the valium which I'm very grateful for.  And I've been able to come down very quickly on the Xanax -- perhaps too quickly, although my pace has slowed way down atm...

 

I'm very very aware after reading your posts that I do not want to allow the glutamate to get too active in my system as I think it causes damage.....if I'm reading you right.  And slowing down the pace has allowed my CNS and the HPA axis to catch up in the healing process. 

I've said on this forum before the most helpful modality has been osteopathy -- very helpful and not much recognized in  N. America, where I live....

 

I want to get this out of my body as quickly as possible but without leading to the acuity that I read so much about from people who appear to have gone off too quickly.  How did you come off?  quickly or with a slow steady taper or a combo of both.  ( If that's in your sig I'll read it there)

 

Again that you!

[[Be...]]

I had platelets on the low side when I got tested while in tolerance w/d.  I was also diagnosed with Thrombophilia.  My SED rate was low, too, at 2.  Blood coag problems.  Antibody response.  I was diagnosed with Lupus and I think that it's drug-induced. 

[[cs...]]

Thank you dm123 for all your research .......

I can't absorb all of it , but ! A laymans question ..... Where is the hope in all of this ? I tend to feel more hopeless in reading all the research .....

 

I was on high dose hydrocortisone fro 9 months and had to cold turkey when it 'turned ' on me , which I now think was a bad idea , though they were making me so sick I felt I had no choice .

 

Now I am coming up against the same type of reaction to Valium ... Which is very frightening . As I know ct is not an option .

 

Now that I knwo that steroids are PAMS , it makes sense why , after my ct and then starting klonopin , I began to feel a lot better ! I then corssed to Valium when I had a difficult time trying to taper klonopin . The crossover was brutal and I don't think I ever stabilized on Valium . I am also I now find a fast metabolizer of at least the parent drug Diazepam .

 

What does all this mean fro me ? My taper seems impossible with extreme WDs at the slightest reduction . I'm stuck and feel quite trapped now with the benzo.

 

I hope your research leads to some answers for those of us struggling so much .

 

Interestingly ,valium has become extremely sedating fro me this last month , way more than it ever has been before ,to the point where I can only take 1/2 mg in the am and 1/2 at lunch , and the rest at night . The sedative effects are supposed to become quickly tolerant.  I have found the opposite , the anxiolytic effects are pretty much zero , and the sedation over the top !

Complicated is an understatement isnt it!

MiYu

Hi MiYu,

 

I hope the research helps as well.  We are in the same boat.  The waves are horrible.

 

Although I do feel hydrocortisone is a PAM, it's officially not a neurosteroid and is not in the official listings. https://en.m.wikipedia.org/wiki/Category:GABAA_receptor_positive_allosteric_modulators

My Benzo doc did say it does influence the Cl- influx, and I know Pers indicated it was a modulator as well, so these two resources are reliable.

 

I know where you are at.  I was on HC for 2.5 years.  It is really is tough on the body.  I tapered it very slowly over a 6 month period.  I was just finishing off the taper when I crossed over to Librium.  So I definitely know the feeling.  When you crossed over did the doc titrate you up on the Valium until your wd symptoms faded or did he not do this?

It sounds like you were never stabilized to start.

 

What are these wd symptoms that you are feeling?  It does not sound like hyperexcitability, because you mentioned you feel overly sedated.  That might not be such a bad thing. I've tapered the morning and after noon doses, and am just on nightly.  You should ask your doc if you can just take all 8 mgs at night. (See also Ashton manual taper schedules)However, phsiologically, the .5 mgs should not make a difference due to the long half life. 

  Don't make any changes without consulting your doctor.   

 

Also how long ago did you drop the HC?  It takes a while for the pituitary and hypothalamus to pick up the drop and normalize the ACTH.  Especially that you cold turkeyed it.

 

You should be going by symptoms, and if you feel ill, don't make the cut, and tell your doc.  I know you are on gabapentin.  I unfortunately could not tolerate it, (too stoned and spaced out)and can't use it as an adjunctive med.

 

can you ask your doc if that's what is making you so sedated.?  Perhaps your excitatory system does not need as much of the gabapentin to blunt the neuron potential at this point. 

 

You would need to ask your doc about the current dose

 

So you are sedated at the same time anxious?.  Horrible feeling. I've felt that.  Are you able to sleep well?

 

Yes my next ADDENDUM will go deep into the different physiological aspects of tolerance for benzos and how that correlates to the subunit configuration of the receptor.  Yes, the sedation and hypnotic is supposed to wear off week (tolerance builds fast) and anxiolytic effect wears off slow, so you are just the opposite.  I found my tolerance to Librium sedation to wear off fast. 

 

I think you need to talk to your doc about the gabapentin. Are you taking any other adjunctive meds?

 

Glad you and I are off the HC.

 

How did you find out you are a fast metabolizer of Valium?

 

 

 

 

[[cs...]]

Thank you dm123 for all your research .......

I can't absorb all of it , but ! A laymans question ..... Where is the hope in all of this ? I tend to feel more hopeless in reading all the research .....

 

I was on high dose hydrocortisone fro 9 months and had to cold turkey when it 'turned ' on me , which I now think was a bad idea , though they were making me so sick I felt I had no choice .

 

Now I am coming up against the same type of reaction to Valium ... Which is very frightening . As I know ct is not an option .

 

Now that I knwo that steroids are PAMS , it makes sense why , after my ct and then starting klonopin , I began to feel a lot better ! I then corssed to Valium when I had a difficult time trying to taper klonopin . The crossover was brutal and I don't think I ever stabilized on Valium . I am also I now find a fast metabolizer of at least the parent drug Diazepam .

 

What does all this mean fro me ? My taper seems impossible with extreme WDs at the slightest reduction . I'm stuck and feel quite trapped now with the benzo.

 

I hope your research leads to some answers for those of us struggling so much .

 

Interestingly ,valium has become extremely sedating fro me this last month , way more than it ever has been before ,to the point where I can only take 1/2 mg in the am and 1/2 at lunch , and the rest at night . The sedative effects are supposed to become quickly tolerant.  I have found the opposite , the anxiolytic effects are pretty much zero , and the sedation over the top !

Complicated is an understatement isnt it!

MiYu

 

Don't let the research bring you down.  The body heals.  It's all temporary.  We just have to get the benzodiazaphine out to fully heal, and leave those receptors alone. 

[[cs...]]

dm123,

 

'GPCRs, for example. We have not gotten to these, but muscarinic receptors are a type of GPCR.  We know that in studies, stimulation of muscarinic  receptors cause a DECREASE in inhibitory signaling of GABAa receptors.'

I sort of briefly touched on that in my latest PM.

 

Many years ago I took a powerful antimuscarinic drug for two days, it had a half life of between two and three days and an active metabolite.

Weeks or months later I definitely felt a backlash, with cognitive effects during the afternoon, requiring me to take an extra 0.25 mg clonazepam late afternoon.

 

'hyperexcitability' one's hyperexcitability isn't the same as someone else's. I may have that, in the sense of being very sensitive to exercise and not in a good way, strong hormonal reactions. Whether sensitivity to sunlight/weather is part of that I don't know, the same goes for general drug sensitivity.

 

Hi liberty, I agree, one's hyperexcitability can be different from another person's hyperexcitability.....  physiologically the same, but for each person manifests itself differently.  Hyperexcitability is a term used quite a bit in the epilepsy literature.  It's an oversensitization of the CNS.  It can manifest itself as anxiety, nerve pain and even panic attacks and agoraphobia.  At its worst, SE, and seizing with very little input stimuli.  Lucklily most of us never reach that point, with a proper taper.

[[cs...]]

Hi DM123,

thanks so much for this information, and I'm glad that the references to psychotherapeutic terms of trauma fit in with your thread.

 

The info on kindling is fascinating.....as with everything about this process it's really not understood is it? (pr perhaps it's my unscientific mind)

 

I have never had a seizure, and even though used short acting and pernicious Xanax really didn't even have any interdose w/d until about 17 years of use.  Then it lasted about 9 months before I committed to the taper.  What I'm reading from your posts leads me to think that the kindling phenomena may not be a significant factor in my w/d.  (although length of usage is) and possibly the ridiculously large cuts I made in the beginning -- where glutamate was running the show and I felt so very very unwell will factor into my w/d.  If for nothing else than the learned behaviour state specific learning that occurred.

(I may need to get a new couch!  The old one is where I was living my life...  )

 

Again I want to thank you for putting all of this here on BB.  Every time I read your posts -- although over my head -- I think I learn a wee bit more about the processes happening in my CNS and HPA axis. The science starts to make some sense and the physiology that is impacted becomes a bit more clear.  That helps me with the idea that I really need to get out of the way and let my body heal -- somehow a hard lesson to put into practice!

 

I hope that your presentation of your papers go very well!

All the best to everyone here (and on BB)

SS

 

Yes, you are right.  At first glance kindling seems to be simple upregulation of the Glutamate system, but that term is used very freely.  Even if it is one of the major players involved in kindling (and i do believe it is),  we don't know how much of an impact the other factors are having to make the neuron hyperexcitable, and furthermore we don't know exactly how it gets upregulated.  I'm guessing the research will point to an intracellular process, and also these other factors combining to cause the hyperexcitable neuron. 

 

LTP, which Pers wrote about ultimately caused sensitization and upregulation of AMPARs via intracellular processes. 

 

The hyperexcitable neuron is something I hope we explore in detail.  Keeping our focus on that end goal helps us interpret the clinical studies in the proper  context.....

 

You have very strong physiology.  During the 17 years of xanax did you dose all at once during the day/night or did you spread out the dose.  Dosing a short acting benzo like I did is a sure path to kindling.  If you single dosed 17 years of xanax you have amazing physiology.  Adding in the small amount of V I think was very smart of you.  Was that your idea or the doctor's.?

 

Yes the science is telling us all to get it out of our bodies as fast as possible.

 

Yes I dosed once a day -- at bedtime -- for the 17 years that I was on the medication.... weird huh?  For most of that time, around 10 years I tool .25 only.  It was when I went off the .25 for a week -- during a meditation retreat --  in a feeble attempt to get off Xanax  that I started to need to take more and more of the med....

 

I think that was one of the reasons I was under the mistaken idea that I might have and easier time getting off (that and DENIAL!!!)  When I started to get the interdose w/d towards the end of the reign of xanax I started to take about .03-.06mg  around 4:00am, but that was really for less than a year I believe.  I feel extremely lucky and unlucky with my physiology.  It allowed me to be on this drug for far too long -- and I think it's allowing me to come off with a relative ease -- some days though -- yowza!

 

  It was my docs idea to add the valium which I'm very grateful for.  And I've been able to come down very quickly on the Xanax -- perhaps too quickly, although my pace has slowed way down atm...

 

I'm very very aware after reading your posts that I do not want to allow the glutamate to get too active in my system as I think it causes damage.....if I'm reading you right.  And slowing down the pace has allowed my CNS and the HPA axis to catch up in the healing process. 

I've said on this forum before the most helpful modality has been osteopathy -- very helpful and not much recognized in  N. America, where I live....

 

I want to get this out of my body as quickly as possible but without leading to the acuity that I read so much about from people who appear to have gone off too quickly.  How did you come off?  quickly or with a slow steady taper or a combo of both.  ( If that's in your sig I'll read it there)

 

Again that you!

Hi SS, I don't have a sig, but I have a detailed post on what I've gone through.  I don't post progress because I don't want to jinx it 

 

As I indicated to Mi Yu I'm done with morning and afternoon doses and working on the nightly.  I'm slow tapering. She and I are at similar places, but most likely I started out from a bit higher

[[cs...]]

I was given Lipitor (my cholesterol was at 188), clonodine, Plavix (he did no genetic testing to see if I was a fit person for this), Hydralazine, Famotidine, Amlodipine, aspirin, Atenolol. Since I am allergic to NSAIDS, the aspirin had to go first. I am still on 2.5 mg. Amlodipine, but that's the only pill out of all of them that I'm still taking. The Lipitor made my liver enzymes really high, so of course I was tested for Hepatitis a few times.

 

I don't know if the hospital did a platelet apherisis.

 

I know this is a lot to ask you!! I just think that my body couldn't take all the drugs. I only weighed 117 at the time (5'5" tall) and think it was all too much. I was right in the throes of benzo withdrawal, too. At the time, with all the pills, I felt like I had Alzheimer's.

 

Since the last time my platelets were checked, they were at 550,000, and I just think my body had finally settled down somewhat after the benzo mess and everything else.

 

Thank you, dm123!!!

 

Hi Terry, you were on all of those at once?

 

From what I see benzodiazaphines cause low platelet count, not high. This is very interestingly...

 

https://www.karger.com/Article/Pdf/206797

 

https://www.ncbi.nlm.nih.gov/pubmed/2990062

Quote

These findings suggest that: (a) flurazepam, as compared to diazepam, is 106% - 357% more effective in inhibiting platelet aggregation and serotonin secretion induced by arachidonic acid, collagen and phospholipase C; (b) flurazepam inhibits platelet activation by inhibiting the release of arachidonic acid, its conversion into prostaglandins and by blocking the action of prostaglandins on platelets; © diazepam does not inhibit thrombin-induced release of arachidonic acid, conversion of exogenously added arachidonic acid into MDA, or the action of prostaglandins; (d) both flurazepam and diazepam inhibit PLC-mediated activation of platelets; and (e) neither diazepam nor flurazepam achieve their antiplatelet actions by affecting platelet cyclic nucleotide levels.

End quote

 

 

Was your platelets low during benzo and other med use?.  The spike you had might have been after you got off of it, as the body seeks to achieve homeostatic balance.  As mentioned in an earlier ADDENDUM, it often overcorrects initially, then settles down as other systems normalize.  Benzos seem to be good a creating chaos in a lot of different systems in the body.  I think it is utterly amazing that the body heals itself if we just let it do so.  Your platelets are just a bit north of normal, so you appear to be on the right track in this area.

 

Since you were on so many different drugs they could have acted synergistically as well to further lower  platelets and cause a severe rebound when getting off them.  I find it very strange that a lot of these drugs are approved in isolation or with minimal cross reactivity , yet doctors combine them into all kinds of concoctions.  Almost like a nutty professor approach .  I was just thinking about this the other day.

 

I also noticed some of the drugs were contraindicated with others in your list.  Did the pharmacist warn you of these?

 

 

Lipitor also lowers platelets

https://www.ncbi.nlm.nih.gov/pubmed/15255464

 

Clonidine lowers platelets as well.  2% is significant

http://www.ehealthme.com/ds/clonidine/low-platelet-count/

 

32,994 people reported to have side effects when taking Clonidine.

Among them, 574 people (1.74%) have Low platelet count

 

It's listed as a rare side effect in the clonidine pamphlet

 

 

Plavix does the same

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014541/

Platelets did recover

 

 

Interesting article on low platelets

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1993236/

 

Hydralazine

You can read this and the area of lupus.  It can also lower platelets

http://www.netdoctor.co.uk/medicines/heart-and-blood/a6223/apresoline-tablets-hydralazine/

 

 

Flamotidine

http://www.globalrph.com/thrombo.htm

Many other references

 

Same with amlodipine

https://www.ncbi.nlm.nih.gov/pubmed/8519039

 

Aspirin is known as a platelet inhibitor.

 

Atenolol same thing 2%

http://www.ehealthme.com/ds/atenolol/platelet-count-decreased/

 

 

 

I don't think the platelets were reduced primarily by the benzodiazaphine, but we will never really know.  It looks like your platelet count was suppressed while on the drugs, and you had a large overcorrection once you got off all of those meds.

 

Amazingly it looks like you are normalizing.    It's starlting to see you were rx'ed all of these drugs. 

You have an amazing recovery story.

 

Amazing bodies that we have.

[[li...]]

Side note: I've tried to find that 'medical wiki' but for some reason it's nigh impossible unless I know the URL. It's a medical wiki, isn't it ?

 

As in https://en.m.wikipedia.org/wiki                                /Category:GABAA_receptor_positive_allosteric_modulators#/search

 

I couldn't find it with google. Unless it's related to a language or country ...

[[...]]

Thank you dm123 for all your research .......

I can't absorb all of it , but ! A laymans question ..... Where is the hope in all of this ? I tend to feel more hopeless in reading all the research .....

 

I was on high dose hydrocortisone fro 9 months and had to cold turkey when it 'turned ' on me , which I now think was a bad idea , though they were making me so sick I felt I had no choice .

 

Now I am coming up against the same type of reaction to Valium ... Which is very frightening . As I know ct is not an option .

 

Now that I knwo that steroids are PAMS , it makes sense why , after my ct and then starting klonopin , I began to feel a lot better ! I then corssed to Valium when I had a difficult time trying to taper klonopin . The crossover was brutal and I don't think I ever stabilized on Valium . I am also I now find a fast metabolizer of at least the parent drug Diazepam .

 

What does all this mean fro me ? My taper seems impossible with extreme WDs at the slightest reduction . I'm stuck and feel quite trapped now with the benzo.

 

I hope your research leads to some answers for those of us struggling so much .

 

Interestingly ,valium has become extremely sedating fro me this last month , way more than it ever has been before ,to the point where I can only take 1/2 mg in the am and 1/2 at lunch , and the rest at night . The sedative effects are supposed to become quickly tolerant.  I have found the opposite , the anxiolytic effects are pretty much zero , and the sedation over the top !

Complicated is an understatement isnt it!

MiYu

Hi MiYu,

 

I hope the research helps as well.  We are in the same boat.  The waves are horrible.

 

Although I do feel hydrocortisone is a PAM, it's officially not a neurosteroid and is not in the official listings. https://en.m.wikipedia.org/wiki/Category:GABAA_receptor_positive_allosteric_modulators

My Benzo doc did say it does influence the Cl- influx, and I know Pers indicated it was a modulator as well, so these two resources are reliable.

 

I know where you are at.  I was on HC for 2.5 years.  It is really is tough on the body.  I tapered it very slowly over a 6 month period.  I was just finishing off the taper when I crossed over to Librium.  So I definitely know the feeling.  When you crossed over did the doc titrate you up on the Valium until your wd symptoms faded or did he not do this?

It sounds like you were never stabilized to start.

 

What are these wd symptoms that you are feeling?  It does not sound like hyperexcitability, because you mentioned you feel overly sedated.  That might not be such a bad thing. I've tapered the morning and after noon doses, and am just on nightly.  You should ask your doc if you can just take all 8 mgs at night. (See also Ashton manual taper schedules)However, phsiologically, the .5 mgs should not make a difference due to the long half life. 

  Don't make any changes without consulting your doctor.   

 

Also how long ago did you drop the HC?  It takes a while for the pituitary and hypothalamus to pick up the drop and normalize the ACTH.  Especially that you cold turkeyed it.

 

You should be going by symptoms, and if you feel ill, don't make the cut, and tell your doc.  I know you are on gabapentin.  I unfortunately could not tolerate it, (too stoned and spaced out)and can't use it as an adjunctive med.

 

can you ask your doc if that's what is making you so sedated.?  Perhaps your excitatory system does not need as much of the gabapentin to blunt the neuron potential at this point. 

 

You would need to ask your doc about the current dose

 

So you are sedated at the same time anxious?.  Horrible feeling. I've felt that.  Are you able to sleep well?

 

Yes my next ADDENDUM will go deep into the different physiological aspects of tolerance for benzos and how that correlates to the subunit configuration of the receptor.  Yes, the sedation and hypnotic is supposed to wear off week (tolerance builds fast) and anxiolytic effect wears off slow, so you are just the opposite.  I found my tolerance to Librium sedation to wear off fast. 

 

I think you need to talk to your doc about the gabapentin. Are you taking any other adjunctive meds?

 

Glad you and I are off the HC.

 

How did you find out you are a fast metabolizer of Valium?

 

So ....thanks  for answering Dm .... My story is a bit complex but I'll try and keep it as simple as possible .

I was on HC fro adrenals....which I think was actually just hormonal in the end ...the HC didn't help me at all , I never improved on it , in fact I got worse , so doctors kept raising my dose as they thought I want absorbing it or something.

I ended up on 60-80 mgs , a lot ! I tried to taper it a few times and couldn't . I tried prednisone too , that was a bit better and not so "sudden" in onset , but I still ended up having a bad reaction to it , so I went back to HC , and finally was able to taper down to 20 mgs . Fairly rapidly . At that point I ended up on ER one day , just crazy reaction , perhaps it was WDs , I don't know . Anyway , I pretty much dropped to zero in a month. I was super sick . I actually thought I was going to die . I could barely move , totally opposite response to what steroids should do .

During that time I couldn't sleep , so I was prescribed ambien and Xanax as needed . I started having panic attacks after the steroids , and my stress tolerance was zero as you can imagine .

I took 5 mgs ambien to sleep most nights during the nine months , and the Xanax initially only .125 a couple of times a week .

The gabapentin , I've been on for some years befor all this , for restless legs , always only between 100-3oo mgs . But the steroids made my RLS so bad I had to go up to 900 !

 

So then , a life trauma , right after the steroid cT , and I couldn't cope without the benzo or the ambien . So now 5 mgs ambien , and either .125-.25 Xanax , or 1/2 mg of Ativan which I also had been prescribed as needed.

 

I had no idea during all this about the addictive nature of benzos .

 

On to dec 2016 ( this all started in November 2014) , I was so sick my friend took me to a naturopath ,who prescribed me klonopin! I dropped the ambien , still on 900 sometimes more gabapentin .

I took .25 mgs klonopin and .125 mgs Xanax for two months at that point . Then decided I wanted off the klonopin and Xanax.

Dropped the Xanax and discovered benzo WD hell!

Bad ......

Upped the K To .375 in Feb 2016 to cover the Xanax .

 

March began cross to Valium .... Really hard , I had terrible WDs from K for three months , like I had CTd it , even with crossing to 10 mgs Valium .

 

So I guess I was never really stable , and my body had been through so much with the steroids and the ups and downs of meds .

 

I'm on 360 mgs gabapentin now , I tapered that this last year . Seemed a lot easier than the Valium in terms of WDs .,

As for the Valium , I can't get below where I'm at . Each cut i try to  make makes me very sick .

 

Bottom line now -

360 mgs gabapentin

7.93 Valium ( that's 8 mgs minus the 1/8 th I microtapered in June , still having horrible WDs from that cut)

 

Just holding and hoping things even out . I haven't cut back the gabapentin since March this year .

 

Well that wasn't exactly short! Writing it makes me realize what my body has been through these last 2-1/2 years . I really was only on benzos daily fro six months before I started trying to taper . But I had the steroid ct 8 months before that.

 

Not sure if any of this means anything except a good old mess!

 

MiYu 

 

 

[[...]]

And as far as the WDs I feel..... So tired all the time , no stress tolerance at all , difficulty walking , weakness, stomach issues , burning skin and fingers , head stuff , memory issues , sometimes shakes , stress jerks , unable to talk much as I find it stressful . Back pain . Liver area burning pain . Cortisol surges . Anxiety .

 

The weird thing is the Valium makes me less tired at night , which maybe suggests it's suppressing cortisol in the daytime? Like today I took 1/2 mg at lunch and was knocked out for three hours . And tonight I've taken 4 mgs and it hasn't had that effect at all !

It didn't do this in the beginning either , make me sedated during the day . Not at all . This is fairly recent ....

 

Complicated bodies we have !

[[Te...]]

I was given Lipitor (my cholesterol was at 188), clonodine, Plavix (he did no genetic testing to see if I was a fit person for this), Hydralazine, Famotidine, Amlodipine, aspirin, Atenolol. Since I am allergic to NSAIDS, the aspirin had to go first. I am still on 2.5 mg. Amlodipine, but that's the only pill out of all of them that I'm still taking. The Lipitor made my liver enzymes really high, so of course I was tested for Hepatitis a few times.

 

I don't know if the hospital did a platelet apherisis.

 

I know this is a lot to ask you!! I just think that my body couldn't take all the drugs. I only weighed 117 at the time (5'5" tall) and think it was all too much. I was right in the throes of benzo withdrawal, too. At the time, with all the pills, I felt like I had Alzheimer's.

 

Since the last time my platelets were checked, they were at 550,000, and I just think my body had finally settled down somewhat after the benzo mess and everything else.

 

Thank you, dm123!!!

 

Hi Terry, you were on all of those at once?

 

From what I see benzodiazaphines cause low platelet count, not high. This is very interestingly...

 

https://www.karger.com/Article/Pdf/206797

 

https://www.ncbi.nlm.nih.gov/pubmed/2990062

Quote

These findings suggest that: (a) flurazepam, as compared to diazepam, is 106% - 357% more effective in inhibiting platelet aggregation and serotonin secretion induced by arachidonic acid, collagen and phospholipase C; (b) flurazepam inhibits platelet activation by inhibiting the release of arachidonic acid, its conversion into prostaglandins and by blocking the action of prostaglandins on platelets; © diazepam does not inhibit thrombin-induced release of arachidonic acid, conversion of exogenously added arachidonic acid into MDA, or the action of prostaglandins; (d) both flurazepam and diazepam inhibit PLC-mediated activation of platelets; and (e) neither diazepam nor flurazepam achieve their antiplatelet actions by affecting platelet cyclic nucleotide levels.

End quote

 

 

Was your platelets low during benzo and other med use?.  The spike you had might have been after you got off of it, as the body seeks to achieve homeostatic balance.  As mentioned in an earlier ADDENDUM, it often overcorrects initially, then settles down as other systems normalize.  Benzos seem to be good a creating chaos in a lot of different systems in the body.  I think it is utterly amazing that the body heals itself if we just let it do so.  Your platelets are just a bit north of normal, so you appear to be on the right track in this area.

 

Since you were on so many different drugs they could have acted synergistically as well to further lower  platelets and cause a severe rebound when getting off them.  I find it very strange that a lot of these drugs are approved in isolation or with minimal cross reactivity , yet doctors combine them into all kinds of concoctions.  Almost like a nutty professor approach .  I was just thinking about this the other day.

 

I also noticed some of the drugs were contraindicated with others in your list.  Did the pharmacist warn you of these?

 

 

Lipitor also lowers platelets

https://www.ncbi.nlm.nih.gov/pubmed/15255464

 

Clonidine lowers platelets as well.  2% is significant

http://www.ehealthme.com/ds/clonidine/low-platelet-count/

 

32,994 people reported to have side effects when taking Clonidine.

Among them, 574 people (1.74%) have Low platelet count

 

It's listed as a rare side effect in the clonidine pamphlet

 

 

Plavix does the same

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014541/

Platelets did recover

 

 

Interesting article on low platelets

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1993236/

 

Hydralazine

You can read this and the area of lupus.  It can also lower platelets

http://www.netdoctor.co.uk/medicines/heart-and-blood/a6223/apresoline-tablets-hydralazine/

 

 

Flamotidine

http://www.globalrph.com/thrombo.htm

Many other references

 

Same with amlodipine

https://www.ncbi.nlm.nih.gov/pubmed/8519039

 

Aspirin is known as a platelet inhibitor.

 

Atenolol same thing 2%

http://www.ehealthme.com/ds/atenolol/platelet-count-decreased/

 

 

 

I don't think the platelets were reduced primarily by the benzodiazaphine, but we will never really know.  It looks like your platelet count was suppressed while on the drugs, and you had a large overcorrection once you got off all of those meds.

 

Amazingly it looks like you are normalizing.    It's starlting to see you were rx'ed all of these drugs. 

You have an amazing recovery story.

 

Amazing bodies that we have.

 

Thank you so  much, dm123, for all of the research you did on those pills!!! Yes, I was given all of them, and I wonder if the doctor was just trying to cover his hind in doing that. I learned a very good lesson from that hospital stay - to try and do everything in my power to remain vigilent about my health so that I don't have to go to the hospital. There, you are under their direction and guidance, and have to take the pills you are given. You don't have a say, per se.

 

In looking back on my plog, I was taking all the pills above when my platelets jumped to 1.8 million, so even though they lower platelet count in others, that didn't work for me for some reason. Synergistically they could have caused an opposite effect, that of rising the platelets. And aspirin didn't do a thing to lower them ever. I was taking that for quite awhile. It was only AFTER I got off them that my platelets went down.  It seems my body is telling me that it can only do its work well without the added pills. Something always goes haywire when I'm on pills, no matter what they are.

 

Well, thanks for listening and for being so kind and knowledgeable!!! And thanks so much for the time you take out of your day to look all this information up. It's really helpful to me just to have a caring person on the other side!!!

[[Su...]]

Hi DM123,

thanks so much for this information, and I'm glad that the references to psychotherapeutic terms of trauma fit in with your thread.

 

The info on kindling is fascinating.....as with everything about this process it's really not understood is it? (pr perhaps it's my unscientific mind)

 

I have never had a seizure, and even though used short acting and pernicious Xanax really didn't even have any interdose w/d until about 17 years of use.  Then it lasted about 9 months before I committed to the taper.  What I'm reading from your posts leads me to think that the kindling phenomena may not be a significant factor in my w/d.  (although length of usage is) and possibly the ridiculously large cuts I made in the beginning -- where glutamate was running the show and I felt so very very unwell will factor into my w/d.  If for nothing else than the learned behaviour state specific learning that occurred.

(I may need to get a new couch!  The old one is where I was living my life...  )

 

Again I want to thank you for putting all of this here on BB.  Every time I read your posts -- although over my head -- I think I learn a wee bit more about the processes happening in my CNS and HPA axis. The science starts to make some sense and the physiology that is impacted becomes a bit more clear.  That helps me with the idea that I really need to get out of the way and let my body heal -- somehow a hard lesson to put into practice!

 

I hope that your presentation of your papers go very well!

All the best to everyone here (and on BB)

SS

 

Yes, you are right.  At first glance kindling seems to be simple upregulation of the Glutamate system, but that term is used very freely.  Even if it is one of the major players involved in kindling (and i do believe it is),  we don't know how much of an impact the other factors are having to make the neuron hyperexcitable, and furthermore we don't know exactly how it gets upregulated.  I'm guessing the research will point to an intracellular process, and also these other factors combining to cause the hyperexcitable neuron. 

 

LTP, which Pers wrote about ultimately caused sensitization and upregulation of AMPARs via intracellular processes. 

 

The hyperexcitable neuron is something I hope we explore in detail.  Keeping our focus on that end goal helps us interpret the clinical studies in the proper  context.....

 

You have very strong physiology.  During the 17 years of xanax did you dose all at once during the day/night or did you spread out the dose.  Dosing a short acting benzo like I did is a sure path to kindling.  If you single dosed 17 years of xanax you have amazing physiology.  Adding in the small amount of V I think was very smart of you.  Was that your idea or the doctor's.?

 

Yes the science is telling us all to get it out of our bodies as fast as possible.

 

Yes I dosed once a day -- at bedtime -- for the 17 years that I was on the medication.... weird huh?  For most of that time, around 10 years I tool .25 only.  It was when I went off the .25 for a week -- during a meditation retreat --  in a feeble attempt to get off Xanax  that I started to need to take more and more of the med....

 

I think that was one of the reasons I was under the mistaken idea that I might have and easier time getting off (that and DENIAL!!!)  When I started to get the interdose w/d towards the end of the reign of xanax I started to take about .03-.06mg  around 4:00am, but that was really for less than a year I believe.  I feel extremely lucky and unlucky with my physiology.  It allowed me to be on this drug for far too long -- and I think it's allowing me to come off with a relative ease -- some days though -- yowza!

 

  It was my docs idea to add the valium which I'm very grateful for.  And I've been able to come down very quickly on the Xanax -- perhaps too quickly, although my pace has slowed way down atm...

 

I'm very very aware after reading your posts that I do not want to allow the glutamate to get too active in my system as I think it causes damage.....if I'm reading you right.  And slowing down the pace has allowed my CNS and the HPA axis to catch up in the healing process. 

I've said on this forum before the most helpful modality has been osteopathy -- very helpful and not much recognized in  N. America, where I live....

 

I want to get this out of my body as quickly as possible but without leading to the acuity that I read so much about from people who appear to have gone off too quickly.  How did you come off?  quickly or with a slow steady taper or a combo of both.  ( If that's in your sig I'll read it there)

 

Again that you!

Hi SS, I don't have a sig, but I have a detailed post on what I've gone through.  I don't post progress because I don't want to jinx it 

 

As I indicated to Mi Yu I'm done with morning and afternoon doses and working on the nightly.  I'm slow tapering. She and I are at similar places, but most likely I started out from a bit higher

Thanks Terry I'll look it up.  :smitten:

[[Te...]]

SS, thank you, although I'm not sure what you're looking up! 

[[Su...]]

progress log?  Or maybe I misunderstood    That would be pretty normal these days.

SS

[[Te...]]

Oh, don't go there, SS. It's too depressing. I like to note things because it's good to go back and see where I did wrong, as I invariably do. I'm also healing v-e-r-y slowly.

[[li...]]

About hyperexcitability. For those who are not familiar with teh concept, this seems like a very nice introduction : https://www.ncbi.nlm.nih.gov/books/NBK2510/

Many things referenced to in this thread are mentioned. Even a hint about sodium channels, perhaps related to glutamate ?

[[Sw...]]

Following.  I have read parts of this thread.  Am interested in the material covered, have trouble "digesting" the "meaty" parts of the discussion.  Thanks for all your work dm123, and the questions posed by everyone else as well.

 

Sweet pea

[[...]]

a

Thanks for this thread .... I've no idea if this is at all of interest or relevant ,

but I'd like to add a little something that I've thought about relative to the brain and healing. I feel there's possibly a trauma factor in cold turkeys and rapid withdrawals that maybe causes brain lesions and ongoing symptoms.

 

There's a German man called dr . Hamer ( passed away recently) who spent a lot of his life researching cancer and trauma , and how shock effects the brain , he was able to image parts of the brain and make connections to other parts of the body where specifically,  cancers would manifest.

In his work ( he was an oncologist) , he found that he had over 90% cure  success rate with cancer patients simply by dealing with the traumas / shocks.

He had his license taken away in Germany for this research ! And lived abroad to continue his research .

Anyway , relative to benzos , it's not the whole picture , but I wonder how , if the brain is shocked, perhaps it causes lesions that then cause symptoms ongoing ....in the case of abrupt discontinuation this would  not neccesarily be a conscious shock, ( also can very much be) but  then not are shocks in those that develop cancers always... They are repressed in the subconscious.

I also wonder if this plays some roll in kindling ? Repeated feelings / symptoms of WD that the brain then patterns subconsciously,and physically in both the brain and thus the body ..... I'm not a scientist so I don't if any of this makes sense .

 

If you want to check out his work you can google Dr. Hamer ,German  new medicine .

He was against antianxiety meds , antidepressants , also steroids , as he felt they also suppressed the emotional roots of disease . Remarkable man ....he did go on to explore all kinds of other body illnesses related to trauma and shock . He found always that if the original shock was brought to consciousness , and a different meaning found in present time , the body would start to "reverse" the imbalance / illness.

 

MiYu

( both he and his wife developed cancer after their son died in a tragic accident , this initiated his research . He survived his cancer, his wife did not. He had access to many patients as he was an oncologist . So began his work )

 

Hi, thanks for this very interesting post.  I'm going to look into his work.  Speaking of trauma, the field of long term potentiation is huge, and very interesting.  This might interest you in the context of repeated traumas and fear processing,,,,,

 

 

 

LTP in fear processing

Quote

 

 

While the long-term potentiation of synapses in cell culture seems to provide an elegant substrate for learning and memory, the contribution of LTP to behavioral learning — that is, learning at the level of the whole organism — cannot simply be extrapolated from in vitro studies. For this reason, considerable effort has been dedicated to establishing whether LTP is a requirement for learning and memory in living animals. Because of this, LTP also plays a crucial role in fear processing.

 

End quote

 

 

 

Quote

 

In 2006, Jonathan Whitlock and colleagues reported on a series of experiments that provided perhaps the strongest evidence of LTP's role in behavioral memory, arguing that to conclude that LTP underlies behavioral learning, the two processes must both mimic and occlude one another.[50] Employing an inhibitory avoidance learning paradigm, researchers trained rats in a two-chambered apparatus with light and dark chambers, the latter being fitted with a device that delivered a foot shock to the rat upon entry. An analysis of CA1 hippocampal synapses revealed that inhibitory avoidance training induced in vivo AMPA receptor phosphorylation of the same type as that seen in LTP in vitro; that is, inhibitory avoidance training mimicked LTP. In addition, synapses potentiated during training could not be further potentiated by experimental manipulations that would have otherwise induced LTP; that is, inhibitory avoidance training occluded LTP. In a response to the article, Timothy Bliss and colleagues remarked that these and related experiments "substantially advance the case for LTP as a neural mechanism for memory."[51]

End quote

 

 

LTP in contextual cues to instigate anxiety(fear)

 

From Pers’ paper on LTP

 

In this study, rats were administered diazepam (DZ) for 18 days then abruptly taken off the drug.  The rats exhibited symptoms of withdrawal anxiety for 4 days after the drug was withdrawn.  On the 15th day the rats were re-exposed to the same environment (a plus maze, or PM) where they had originally experienced the withdrawal symptoms.  The contextual cues in the environment of the PM triggered a recurrence of the withdrawal symptoms. If the contextual cues were changed in the environment of the PM, the rats did not experience a recurrence of the withdrawal symptoms on re-exposure. 

 

“In the present investigation we demonstrated that changes in the environmental cues associated with DZ withdrawal prevented the expression of the anxiety-like behavior observed during PM test re-exposure.” (19)

 

 

The researchers attributed the recurrence of symptoms in conjunction with contextual cues to a lowered threshold to generate LTP.  Next they repeated the experiment, but this time they administered the PKMζ inhibitor ZIP two hours prior to re-exposure and observed the following:

 

“In the present study we found that inhibition of PKMζ prior to re-exposure to the withdrawal environment with preserved contextual cues not only prevented the anxiety expression but also reversed the facilitated LTP in all DZ-dependent animals, suggesting that plasticity in the hippocampus has a crucial role in maintenance of these memories that were vulnerable to the amnesic effects of ZIP.” (19)

 

It was interesting that this study showed environmental cues could trigger withdrawal symptoms in conjunction with LTPs, which may demonstrate an overlap in functional characteristics between memory LTPs and BZ withdrawal LTPs.  This poses a question as to whether LTPs which occur during withdrawal could share other commonalities with memories.  Other LTPs, such as LTPs involved in chronic pain conditions, have been shown to share characteristics with memory LTPs:

 

 

“…these findings point to a spinally encoded mechanism for the persistence of nociceptive sensitization with molecular underpinnings that closely resemble those involved in L-LTP and the maintenance of long-term memory traces.” (24)

 

 

Functional similarities between withdrawal LTPs and memory LTPs might include such things as distraction and time, which are two concepts discussed frequently with regards to benzo withdrawal.  Distraction appears help reduce withdrawal symptoms, and ironically is also a factor in both avoidance and fading of memories.  Time has been suggested to be the only known cure for withdrawal, similarly it is also the cure for painful memories as ‘time heals all wounds.’  Just as withdrawal symptoms can seemingly pop up again out of the blue, so can memories.  As demonstrated in the previous study, this may be due to contextual cues in the environment, either consciously or subconsciously, triggering the ‘biological memory’ stored in the Central Nervous system (CNS).  Contextual cues may be varied and might result from single or multiple environmental perceptions involving visual, tactile, olfactory, or gustatory senses.  Formation of LTPs may be the reason why withdrawal symptoms can persist for such a long time.

 

 

End quote

Thanks DM ..... This confirms my feelings that trauma triggers can indeed bring on WD symptoms....

And I believe this is why for some who experience protracted WD after CTs are actually being subconsciously triggered by things they ar not aware of .

 

In German new medicine they call them 'tracks '. Becoming conscious of the tracks or triggers are essential to healing the brain .

Dr Hamer was actually able to observe circular patterns in areas of the brain , that , on trauma resolve would just disappear . These circles would correspond to certain areas of the body , and also specifically to how the individual responded emotionally to the trauma , and also the meaning they made out of it . Changing the meaning was also key to healing .

 

What is LTP , sorry , I've missed that somewhere !

 

Time and distraction , yes , for sure .

I think fro some of us healing is much harder once we have an associated trauma 'sensation '. I speak fro myself .

 

I am working with someone who cured herself of epilepsy by identifying all tracks that stimulated her seizures. I hope she can help me .

I believe I now have a trauma 'track ' from my CT of steroids , as I have many similar symptoms during this attempt to withdraw from Valium .

It's also interesting to me how some people can try several times to withdraw and sometimes on their final try have very few symptoms .....

 

 

All very interesting , thank you for your research DM ,

MiYu 

[[Su...]]

a

Thanks for this thread .... I've no idea if this is at all of interest or relevant ,

but I'd like to add a little something that I've thought about relative to the brain and healing. I feel there's possibly a trauma factor in cold turkeys and rapid withdrawals that maybe causes brain lesions and ongoing symptoms.

 

There's a German man called dr . Hamer ( passed away recently) who spent a lot of his life researching cancer and trauma , and how shock effects the brain , he was able to image parts of the brain and make connections to other parts of the body where specifically,  cancers would manifest.

In his work ( he was an oncologist) , he found that he had over 90% cure  success rate with cancer patients simply by dealing with the traumas / shocks.

He had his license taken away in Germany for this research ! And lived abroad to continue his research .

Anyway , relative to benzos , it's not the whole picture , but I wonder how , if the brain is shocked, perhaps it causes lesions that then cause symptoms ongoing ....in the case of abrupt discontinuation this would  not neccesarily be a conscious shock, ( also can very much be) but  then not are shocks in those that develop cancers always... They are repressed in the subconscious.

I also wonder if this plays some roll in kindling ? Repeated feelings / symptoms of WD that the brain then patterns subconsciously,and physically in both the brain and thus the body ..... I'm not a scientist so I don't if any of this makes sense .

 

If you want to check out his work you can google Dr. Hamer ,German  new medicine .

He was against antianxiety meds , antidepressants , also steroids , as he felt they also suppressed the emotional roots of disease . Remarkable man ....he did go on to explore all kinds of other body illnesses related to trauma and shock . He found always that if the original shock was brought to consciousness , and a different meaning found in present time , the body would start to "reverse" the imbalance / illness.

 

MiYu

( both he and his wife developed cancer after their son died in a tragic accident , this initiated his research . He survived his cancer, his wife did not. He had access to many patients as he was an oncologist . So began his work )

 

Hi, thanks for this very interesting post.  I'm going to look into his work.  Speaking of trauma, the field of long term potentiation is huge, and very interesting.  This might interest you in the context of repeated traumas and fear processing,,,,,

 

 

 

LTP in fear processing

Quote

 

 

While the long-term potentiation of synapses in cell culture seems to provide an elegant substrate for learning and memory, the contribution of LTP to behavioral learning — that is, learning at the level of the whole organism — cannot simply be extrapolated from in vitro studies. For this reason, considerable effort has been dedicated to establishing whether LTP is a requirement for learning and memory in living animals. Because of this, LTP also plays a crucial role in fear processing.

 

End quote

 

 

 

Quote

 

In 2006, Jonathan Whitlock and colleagues reported on a series of experiments that provided perhaps the strongest evidence of LTP's role in behavioral memory, arguing that to conclude that LTP underlies behavioral learning, the two processes must both mimic and occlude one another.[50] Employing an inhibitory avoidance learning paradigm, researchers trained rats in a two-chambered apparatus with light and dark chambers, the latter being fitted with a device that delivered a foot shock to the rat upon entry. An analysis of CA1 hippocampal synapses revealed that inhibitory avoidance training induced in vivo AMPA receptor phosphorylation of the same type as that seen in LTP in vitro; that is, inhibitory avoidance training mimicked LTP. In addition, synapses potentiated during training could not be further potentiated by experimental manipulations that would have otherwise induced LTP; that is, inhibitory avoidance training occluded LTP. In a response to the article, Timothy Bliss and colleagues remarked that these and related experiments "substantially advance the case for LTP as a neural mechanism for memory."[51]

End quote

 

 

LTP in contextual cues to instigate anxiety(fear)

 

From Pers’ paper on LTP

 

In this study, rats were administered diazepam (DZ) for 18 days then abruptly taken off the drug.  The rats exhibited symptoms of withdrawal anxiety for 4 days after the drug was withdrawn.  On the 15th day the rats were re-exposed to the same environment (a plus maze, or PM) where they had originally experienced the withdrawal symptoms.  The contextual cues in the environment of the PM triggered a recurrence of the withdrawal symptoms. If the contextual cues were changed in the environment of the PM, the rats did not experience a recurrence of the withdrawal symptoms on re-exposure. 

 

“In the present investigation we demonstrated that changes in the environmental cues associated with DZ withdrawal prevented the expression of the anxiety-like behavior observed during PM test re-exposure.” (19)

 

 

The researchers attributed the recurrence of symptoms in conjunction with contextual cues to a lowered threshold to generate LTP.  Next they repeated the experiment, but this time they administered the PKMζ inhibitor ZIP two hours prior to re-exposure and observed the following:

 

“In the present study we found that inhibition of PKMζ prior to re-exposure to the withdrawal environment with preserved contextual cues not only prevented the anxiety expression but also reversed the facilitated LTP in all DZ-dependent animals, suggesting that plasticity in the hippocampus has a crucial role in maintenance of these memories that were vulnerable to the amnesic effects of ZIP.” (19)

 

It was interesting that this study showed environmental cues could trigger withdrawal symptoms in conjunction with LTPs, which may demonstrate an overlap in functional characteristics between memory LTPs and BZ withdrawal LTPs.  This poses a question as to whether LTPs which occur during withdrawal could share other commonalities with memories.  Other LTPs, such as LTPs involved in chronic pain conditions, have been shown to share characteristics with memory LTPs:

 

 

“…these findings point to a spinally encoded mechanism for the persistence of nociceptive sensitization with molecular underpinnings that closely resemble those involved in L-LTP and the maintenance of long-term memory traces.” (24)

 

 

Functional similarities between withdrawal LTPs and memory LTPs might include such things as distraction and time, which are two concepts discussed frequently with regards to benzo withdrawal.  Distraction appears help reduce withdrawal symptoms, and ironically is also a factor in both avoidance and fading of memories.  Time has been suggested to be the only known cure for withdrawal, similarly it is also the cure for painful memories as ‘time heals all wounds.’  Just as withdrawal symptoms can seemingly pop up again out of the blue, so can memories.  As demonstrated in the previous study, this may be due to contextual cues in the environment, either consciously or subconsciously, triggering the ‘biological memory’ stored in the Central Nervous system (CNS).  Contextual cues may be varied and might result from single or multiple environmental perceptions involving visual, tactile, olfactory, or gustatory senses.  Formation of LTPs may be the reason why withdrawal symptoms can persist for such a long time.

 

 

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Thanks DM ..... This confirms my feelings that trauma triggers can indeed bring on WD symptoms....

And I believe this is why for some who experience protracted WD after CTs are actually being subconsciously triggered by things they ar not aware of .

 

In German new medicine they call them 'tracks '. Becoming conscious of the tracks or triggers are essential to healing the brain .

Dr Hamer was actually able to observe circular patterns in areas of the brain , that , on trauma resolve would just disappear . These circles would correspond to certain areas of the body , and also specifically to how the individual responded emotionally to the trauma , and also the meaning they made out of it . Changing the meaning was also key to healing .

 

What is LTP , sorry , I've missed that somewhere !

 

Time and distraction , yes , for sure .

I think fro some of us healing is much harder once we have an associated trauma 'sensation '. I speak fro myself .

 

I am working with someone who cured herself of epilepsy by identifying all tracks that stimulated her seizures. I hope she can help me .

I believe I now have a trauma 'track ' from my CT of steroids , as I have many similar symptoms during this attempt to withdraw from Valium .

It's also interesting to me how some people can try several times to withdraw and sometimes on their final try have very few symptoms .....

 

 

All very interesting , thank you for your research DM ,

MiYu 

 

That makes so much sense MiYu!  I'm at a place where I can see how my thoughts will start a physical sensation that leads to more anxiety snd the spiral goes down, down, down.... So why not get that spiral to go Up, up up?  Not easy but doable with the right techniques and modalities.....

Hope you are having a good day.

SS

:smitten: