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I'd never taken librium, but I wonder if it is a safer alternative to valium in this prescribing climate, at least in the United States. Valium is still very vilified here because of its reputation from the 70's. When I asked my then-doctor for valium to taper off of ativan, he looked at me weirdly and said "Are you sure this is what you want?". But he had no problem giving me lorazepam from which I'd suffered severe interdose anxiety and horrible tolerance. I looked at the ProPublica database, and Lorazepam is still the most commonly prescribed benzo in the area I live. But then I am also seeing a lot of old beta-blockers and Gabapentin spiking in popularity. Hmmmm.... Coincidence?

 

There was a mental health warmline nearby that was free to call. It closed last year. I remember that a lot of people answering calls were on some or the other combination of Gabapentin, Propanolol, Risperdone, hydroxizine, etc. etc.

Hmmm....  I wonder why......

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I'd never taken librium, but I wonder if it is a safer alternative to valium in this prescribing climate, at least in the United States. Valium is still very vilified here because of its reputation from the 70's. When I asked my then-doctor for valium to taper off of ativan, he looked at me weirdly and said "Are you sure this is what you want?". But he had no problem giving me lorazepam from which I'd suffered severe interdose anxiety and horrible tolerance. I looked at the ProPublica database, and Lorazepam is still the most commonly prescribed benzo in the area I live. But then I am also seeing a lot of old beta-blockers and Gabapentin spiking in popularity. Hmmmm.... Coincidence?

 

There was a mental health warmline nearby that was free to call. It closed last year. I remember that a lot of people answering calls were on some or the other combination of Gabapentin, Propanolol, Risperdone, hydroxizine, etc. etc.

Hmmm....  I wonder why......

 

Hi LPfree,

 

Hope you are doing well.  In my humble opinion valium is a far safer benzdiazaphine than lorazepam, if there is such thing as a “safe Benzodiazaphine”

 

I think all Benzodiazaphines belong in the dirty waste basket, but i can tell you that from a neurophysiological perspective librium is the least noxious of the Benzodiazaphines. 

 

It shouldn’t suprise us that in the age of supersized everything from 64 ounce soda drinks, to 80” televisions, that they turbocharged librium to valium and valium to the high potency Benzodiazaphines and z drugs, which are simply brutal to our precious nervous system. 

 

Everyone wants a quick fix these days, and they want it in a big explosive way.  Even our iPhones are supersizing and will be the size of my iPad in another few years.  It’s the “evolution” of mankind, and insofar as pharmaceuticals are concerned,  this is a very bad thing.

 

Time is of the essence when dealing with high potency Benzodiazaphines and z drugs.....

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Just wanted to comment on a statement by Liberty earlier for others who read this thread...

 

Librium is absolutely NOT "weak" or a placebo. It's dosage equivalence is simply a higher number of mg compared to other benzos. The Amt of mg has nothing to do with a benzo being "weak" or "strong". All benzos are "strong". Some are shorter acting and some are longer acting.  But none are placebo. All create dependency. All are very difficult to w/d off of and cause w/d sxs. Longer acting ones simply decrease interdose w/d. But please be clear that they are not weak or placebo. I think it's dangerous and misleading to suggest this.

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libr,

 

I appreciate your point. Not to be argumentative, dm123 described Librium's effects as 'placebo'.

 

If I were to be on Librium for years (am anything but fine) I'd expect problems re: dependency.

No idea how to source Librium for a couple of years (Netherlands!) and the truth is that it probably won't work. If only I could liberate the equivalent of a few 100 ,000 USD by selling a house like someone else, for medical treatment or a better and more natural environment. If it's going to last a decade or more. Physical problems, not just the benzo.

 

I'm not sure where I got that story, but in the old days (1980s) when new problems cropped up both doc and patient would agree that something was wrong and the patient would usually accept the judgement of the doc .. these days, people know better. That old doc of mine was stuck in the 1980s and forgot to tell, in oh so many ways. Sorry about the whining. Everybody is different.

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libr,

 

I appreciate your point. Not to be argumentative, dm123 described Librium's effects as 'placebo'.

 

If I were to be on Librium for years (am anything but fine) I'd expect problems re: dependency.

No idea how to source Librium for a couple of years (Netherlands!) and the truth is that it probably won't work. If only I could liberate the equivalent of a few 100 ,000 USD by selling a house like someone else, for medical treatment or a better and more natural environment. If it's going to last a decade or more. Physical problems, not just the benzo.

 

I'm not sure where I got that story, but in the old days (1980s) when new problems cropped up both doc and patient would agree that something was wrong and the patient would usually accept the judgement of the doc .. these days, people know better. That old doc of mine was stuck in the 1980s and forgot to tell, in oh so many ways. Sorry about the whining. Everybody is different.

 

Liberty,

 

The context of “placebo” is that for me, i feel nothing. It prevents withdrawal symptoms.  So biologically it is doing a whole bunch of stuff, but the feeling is completely “placebo”. Always has been even at the higher doses, and even now on the fumes and chips.  I prefer it this way as a non-recreational user that finds the drug class reprehensible.  It did get me out of tolerance as well.

 

I once looked at some librium threads on bluelight a long time back.  They make fun of the drug for obvious reasons.  It does very little in terms of what many of the other Benzodiazaphines do, and this is in part due to its slow onset of action and as you know, its GABAaR affinity subunit binding profile.

 

Others might have a completely different reaction to the drug than i do depending on their genetic neurophysiology. I’ve learned that we are all similar in many ways, but also very different in how we react to various drugs.

 

Behind the scenes at a neurophysiological level Librium is doing a whole lot of stuff,  preventing the fast unwind in plasticity that would inevitably and forcefully occur without it.  So in this way it prevents a lot of pain and anguish.

 

One other point, the cuts and tapering can be brutal. Make no mistake about it. It’s when you cut, that you realize just how much it’s actually doing,  and how much it is holding things together.  Kind of like a dam holding back a bunch of water. You only realize how much water is being held back when the dam breaks....Things are calm as long as the dam is intact........

 

Hope this helps

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Dm123- with all due respect, I would say that if L got you out of tolerance, that is not a placebo effect. ;)

 

I don't "feel" it either but I didn't feel any effect from K either. I felt a LOT of effect from 120 mg Magnesium glycinate. I even felt tremendous effect from homeopathic mag phos although that effect was very short lived like 15 minutes.

 

I don't consider 5mg L to be "low dose". Dose size is so relative. Regular Vs high vs low are based on the effects on a 70 kg middle aged white male. I am middle aged but none of hose other things. I am a smaller woman and what is "low" dose for a large man is "high" dose for a thin woman. What is "normal" dose is in the context of men. Women require lower doses than men to get the same effect. Weight and genetics matter too. We don't know much abt the genetics it we do know gender and weight. The effect of benzos is absolutely dependent on a person's weight and gender.

 

That is scary abt the neonatal brain. But neonatal and adult brains are very different. An adult brain had neuro plasticity but is not the same as a developing brain. Which hopefully means our brains aren't permanently damaged like a developing brai would be.

 

I appreciate this group and wish you all a safe journey out of this mess.

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Dm123- with all due respect, I would say that if L got you out of tolerance, that is not a placebo effect. ;)

 

I don't "feel" it either but I didn't feel any effect from K either. I felt a LOT of effect from 120 mg Magnesium glycinate. I even felt tremendous effect from homeopathic mag phos although that effect was very short lived like 15 minutes.

 

I don't consider 5mg L to be "low dose". Dose size is so relative. Regular Vs high vs low are based on the effects on a 70 kg middle aged white male. I am middle aged but none of hose other things. I am a smaller woman and what is "low" dose for a large man is "high" dose for a thin woman. What is "normal" dose is in the context of men. Women require lower doses than men to get the same effect. Weight and genetics matter too. We don't know much abt the genetics it we do know gender and weight. The effect of benzos is absolutely dependent on a person's weight and gender.

 

That is scary abt the neonatal brain. But neonatal and adult brains are very different. An adult brain had neuro plasticity but is not the same as a developing brain. Which hopefully means our brains aren't permanently damaged like a developing brai would be.

 

I appreciate this group and wish you all a safe journey out of this mess.

 

Hi Libr,

 

I think I should have simply used a different term.  Placebo has all kinds of connotations.

I think we are all individual, but for me personally, i never felt the onset of librium after taking it, even at the initial dosages which were much much higher.  That was the point i was trying to get across. Biologically, I have always known that its doing a lot in the background keeping things stable. So not a true placebo by any means.  I would think that during crossover and tapering this is exactly the drug response that we want to achieve. Something that is removing symptoms or making symptoms more tolerable, but not giving us any type of buzz or high.  Much like aspirin relieves a headache, but doesn’t produce euphoria or a buzz or a high. (I am not comparing librium to aspirin, but i think you get the point)

 

There are websites on the internet that are looking to use Benzodiazaphines for recreational use. Why they are using benzos of all drugs to experiment with is beyond me.  This is most dangerous thing that they could do, because no one knows beforehand if they are going to quickly reach tolerance or be kindled by these types of drugs, especially when they dose erratically and at very very high doses. In that sense, librium is completely “placebo”’, and that’s how they refer to the drug. I don’t find it funny myself.

 

I think the 5 mg response is also relative to one’s starting dose as well (ie, total daily dose at crossover).

 

You had started with 20 mg and you are at 25% of your original dose. 

 

I started much higher and am at a much lower dose in percentage terms.  So we might respond differently at that same dose because our recovery paths are all very unique.

 

I do agree that body weight, absorption, genetics, metabolism, body fat, etc do also play a big role.  These interplay with the pharmacokinetics of the drug in a very complex fashion.  Ultimately, we are are all very individual in how we respond to these types of drugs.  This is one reason, among many, why crossover amounts don’t always strictly adhere to table conversion. Another reason is how tolerant or kindled a person is at the time of crossover.

 

The neonatal brain article is scary, but these studies are so specific in nature that they rarely apply to our own real life circumstances in any meaningful way. 

 

Best wishes and hope you are doing fine

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"...but these studies are so specific in nature that they rarely apply to our own real life circumstances in any meaningful way."

 

I disagree, these studies on non-human species serve as the basis for most drug approvals by legislative bodies. With the exception of off the record research eg. MKUltra, Tuskegee, etc., these are the primary basis by which medications are or are not made available to the public. 

 

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"...but these studies are so specific in nature that they rarely apply to our own real life circumstances in any meaningful way."

 

I disagree, these studies on non-human species serve as the basis for most drug approvals by legislative bodies. With the exception of off the record research eg. MKUltra, Tuskegee, etc., these are the primary basis by which medications are or are not made available to the public.

 

Hi FI Addendum,

I disagree.

We first need to differentiate between clinical studies like this one and drug specific clinical trials.

Relative to psychoactive pharmaceuticals, which we are discussing, both are very lacking.

 

 

Clinical studies:

 

Can we extract something useful from this particular clinical study?  Perhaps.  Can it be applied to the effects of the drug on neonatals and babies?  Yes.

Can it be applied to our current circumstances on this forum.  Not without further study on **adult** human beings. And we know that this cannot be ethically done.  This particular study cannot be applied to us, and that was the point that i was making above. 

 

This particular study concerns neonatal and postnatal.. I’ve written about neurogenesis extensively on this thread.  Pre and early in brain development GABAaRs are actually excitatory and they play a crucial part in AMPAR development (“uncloaking of AMPARs)  See this study for example. One of literally hundreds.  Also read the conclusion of this citation.

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2859806/

 

 

Quotes

 

One of the unique features of GABAergic functional plasticity is that in early development, activation of GABAA receptors results in depolarizing (mainly excitatory) responses and Ca2+ influx. Although there is strong evidence from several areas of the CNS that GABA plays a significant role in neurite growth not only during development but also during adult neurogenesis, surprisingly little effort has been made into putting all these observations into a common framework in an attempt to understand the general rules that regulate these basic and evolutionary well-conserved processes.

 

In addition to early developmental aspects, we also consider the GABAergic role in dendritic growth during adult neurogenesis, extending our discussion to the roles played by GABA during dendritic proliferation in early developing networks versus adult, well established networks

 

......

 

 

In the mature brain, GABAA receptor activation leads to Cl− influx, resulting in hyperpolarization (inhibition) of the cell. In immature neurons (both during early development and adulthood), however, GABAA receptor activation is depolarizing and mainly excitatory (LoTurco et al., 1995; Ben-Ari et al., 2007; Ge et al., 2007; Wang and Kriegstein, 2009).

 

........

 

Depolarizing GABAergic activity is present at the earliest stages of network activity, long before the onset of sensory experience, when the developing CNS is spontaneously active, neurons extend dendrites and axons, and they establish synaptic connections.

 

......

 

The GABAergic transition from excitation to inhibition is activity-dependent. An initial in vitro study reported that GABAergic activity regulates its own switch from excitation to inhibition (Ganguly et al., 2001).

 

End quotes

 

 

 

So GABAaRs are strictly depolarizing in early brain development.

 

The question then becomes, how do we apply a neonatal and post natal study to fully developed adults when the function of the GABAaR in excitatory receptor development and plastiicty is completely and thorougly different?  We cannot.  This study is completely non applicable to adult human beings.  For those of us on this forum, We cannot draw any conclusions about plasticity related glutamate receptor effects of clonazepam.

 

In addition, Human neurophysiology is quite different from animal physiology in many many different ways.  We aren’t even able to fully characterize all the many different elements and dynamics and facets  of human adult Neuroplasticity.    And Neuroplasticity is what really comes into play when you want to figure out the long lasting effects of drugs like Benzodiazaphines, and discontinuing from them.  This is why i said that these studies rarely apply to our real life circumstances in real life.

 

 

Drug Specific clinical trials:

 

 

Drug specific clinical trials are very highly politicized and incentivized in the United States. They do provide great visibility into drug toxicity and pharmacokinetics.  They provide absolutely no visibility into long lasting processes like the psychoactive drug related effects on Neuroplasticity.

Profitability inevitably interferes with clinical trail integrity.  Statistics are tweeked, control elements are modified, all in an effort to get the drug released with minimal amount of R&D and clinical study overhead.  That is real life.  They are good for short term therapeutic characterization of the drug. Not long term profile characterization of the drug.  A study like the one above could be used perhaps for pregnancy code characterization of clonazepam but I doubt it will be actually used for that.

 

The tragic part about all of this, is that even when clinical trials and pharmaceutical companies do disclose dosing instructions on drugs like Benzodiazaphines, they are thorougly and completely ignored by the medical practitioners. This is no fault of the clinical trial, but it says a lot about what all these trials and clinical studies do when it really matters.

 

And i am by no means anti-drug.  There are some wonderful pharmaceuticals out there, but Benzodiazaphines are not one of them, because it’s never been fully characterized in clinical trials.

 

I am a neuroscience guy. I like all these studies.  But one has to be very very careful drawing conclusions from them, for those of us here on the forum.....

 

Hope this helps

 

 

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Dm123- with all due respect, I would say that if L got you out of tolerance, that is not a placebo effect. ;)

 

I don't "feel" it either but I didn't feel any effect from K either. I felt a LOT of effect from 120 mg Magnesium glycinate. I even felt tremendous effect from homeopathic mag phos although that effect was very short lived like 15 minutes.

 

I don't consider 5mg L to be "low dose". Dose size is so relative. Regular Vs high vs low are based on the effects on a 70 kg middle aged white male. I am middle aged but none of hose other things. I am a smaller woman and what is "low" dose for a large man is "high" dose for a thin woman. What is "normal" dose is in the context of men. Women require lower doses than men to get the same effect. Weight and genetics matter too. We don't know much abt the genetics it we do know gender and weight. The effect of benzos is absolutely dependent on a person's weight and gender.

 

That is scary abt the neonatal brain. But neonatal and adult brains are very different. An adult brain had neuro plasticity but is not the same as a developing brain. Which hopefully means our brains aren't permanently damaged like a developing brai would be.

 

I appreciate this group and wish you all a safe journey out of this mess.

 

Hi Libr,

 

I think I should have simply used a different term.  Placebo has all kinds of connotations.

I think we are all individual, but for me personally, i never felt the onset of librium after taking it, even at the initial dosages which were much much higher.  That was the point i was trying to get across. Biologically, I have always known that its doing a lot in the background keeping things stable. So not a true placebo by any means.  I would think that during crossover and tapering this is exactly the drug response that we want to achieve. Something that is removing symptoms or making symptoms more tolerable, but not giving us any type of buzz or high.  Much like aspirin relieves a headache, but doesn’t produce euphoria or a buzz or a high. (I am not comparing librium to aspirin, but i think you get the point)

 

There are websites on the internet that are looking to use Benzodiazaphines for recreational use. Why they are using benzos of all drugs to experiment with is beyond me.  This is most dangerous thing that they could do, because no one knows beforehand if they are going to quickly reach tolerance or be kindled by these types of drugs, especially when they dose erratically and at very very high doses. In that sense, librium is completely “placebo”’, and that’s how they refer to the drug. I don’t find it funny myself.

 

I think the 5 mg response is also relative to one’s starting dose as well (ie, total daily dose at crossover).

 

You had started with 20 mg and you are at 25% of your original dose. 

 

I started much higher and am at a much lower dose in percentage terms.  So we might respond differently at that same dose because our recovery paths are all very unique.

 

I do agree that body weight, absorption, genetics, metabolism, body fat, etc do also play a big role.  These interplay with the pharmacokinetics of the drug in a very complex fashion.  Ultimately, we are are all very individual in how we respond to these types of drugs.  This is one reason, among many, why crossover amounts don’t always strictly adhere to table conversion. Another reason is how tolerant or kindled a person is at the time of crossover.

 

The neonatal brain article is scary, but these studies are so specific in nature that they rarely apply to our own real life circumstances in any meaningful way. 

 

Best wishes and hope you are doing fine

 

Agree w/ everything you wrote, dm123.  L has a slow, gradual onset; hence, no "high".  That's the point. That's why I agree it's a good taper drug. That's why it is the taper drug of choice at least in the US for alcohol.  L is not abused.  No street value.  But it is certainly doing it's work/damage on our CNS! 

 

As for studies - how applicable they are to real life and how accurate they are given the financial incentives and pressures to get positive results...well, that's a very difficult topic for another thread. The idea of studies is necessary - the scientific method. The reality isn't always pretty unfortunately...and which studies are good and which are garbage...well, therein lies the dilemma.

But a neonatal brain is definitely very different than an adult brain and I agree that studies on neonatal brains cannot be used to make conclusions for adult brains.

 

One question I have is does our CNS really go back to normal 100%???  I mean, will it be as if we never took a benzo???  If so, then why do people say subsequent tapers are more difficult?  Are we forever changed and will we be "sensitive" to things forever? 

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I once looked at some librium threads on bluelight a long time back.  They make fun of the drug for obvious reasons.  It does very little in terms of what many of the other Benzodiazaphines do, and this is in part due to its slow onset of action and as you know, its GABAaR affinity subunit binding profile.

 

Honestly, I would not have minded a librium prescription instead of the ativan to begin with. The way how my anxious tendencies ran, I would have been better off with it. I don't endorse benzos, but I do think that librium as needed in people with a lot of generalized anxiety with panicky spikes makes more sense than ativan or klonopin, if benzo should be prescribed in the first place. But just like my mother, I also had a propensity for shorter acting bzds due to these spikes. It's just that, for her, the short acting bzds were much more appropriate as she had this ability to bring herself down very quickly from panic. Basically, her panic amplitude would be higher than mine, but her recovery rate from panic would be much quicker than mine. So, I am sure that due to my genetic makeup, drugs such as Xanax, Ativan and Klonopin were totally inapropriate for my system. The one that actually helped me for real many years ago was Oxazepam (Serax). I know it's a short-acting one, but the slower onset of action and its much lower potency than of the Xanax, Ativan and Klonopin made it a much safer choice for me instead of Loazepam. Looking back I wish I'd been prescribed Serax in place of Ativan. But I'd read recently that Actavis discontinued making generic oxazepam, and it was the only mfg. that made it in the United States. It's a shame because it's one of the safest benzos, as far as benzos are concerned. The rebounds would have not beat me up into the ground the way Lorazepam did.

 

 

I do find bluelight very informative and useful resource, although I tend to avoid those threads of people bragging about how much benzo they can take and the miraculous recoveries of getting off 10 yeas benzos in 3 months. If it is true, I'm jealous, and if it's not, I am annoyed.

 

But yes, I'd never partaken in recreational use of anything (except for sugary coffee drinks and desserts - all the stuff I can't touch now). I always felt my brain was on a different wavelength by nature, so no reason to bend the reality even more. But I did have a history of taking antihistamines for anxiety/sleep, as well as natural supplements, teas, coffee (coffee worked as a sedative for me for the longest time), etc. etc.

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All I know that my body threw a horrific revolt when reducing L from 1mg to 0.5mg. Apparently, that 0.5mg was doing a lot and the brain is now permanently angry now with me.

 

But I wonder if there's something about L and decision making circuitry because it has absolutely affected it in that area to the level I didn't think imaginable

 

I look at myself before taking L and right now, and yes, I've gotten older and all that, BUT....I can't even believe just how much of a profound impact it had had on my brain and my body. Yes, I had panic attacks before taking it, but I wasn't living in a panic attack. Big difference.

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Dm123- with all due respect, I would say that if L got you out of tolerance, that is not a placebo effect. ;)

 

I don't "feel" it either but I didn't feel any effect from K either. I felt a LOT of effect from 120 mg Magnesium glycinate. I even felt tremendous effect from homeopathic mag phos although that effect was very short lived like 15 minutes.

 

I don't consider 5mg L to be "low dose". Dose size is so relative. Regular Vs high vs low are based on the effects on a 70 kg middle aged white male. I am middle aged but none of hose other things. I am a smaller woman and what is "low" dose for a large man is "high" dose for a thin woman. What is "normal" dose is in the context of men. Women require lower doses than men to get the same effect. Weight and genetics matter too. We don't know much abt the genetics it we do know gender and weight. The effect of benzos is absolutely dependent on a person's weight and gender.

 

That is scary abt the neonatal brain. But neonatal and adult brains are very different. An adult brain had neuro plasticity but is not the same as a developing brain. Which hopefully means our brains aren't permanently damaged like a developing brai would be.

 

I appreciate this group and wish you all a safe journey out of this mess.

 

Hi Libr,

 

I think I should have simply used a different term.  Placebo has all kinds of connotations.

I think we are all individual, but for me personally, i never felt the onset of librium after taking it, even at the initial dosages which were much much higher.  That was the point i was trying to get across. Biologically, I have always known that its doing a lot in the background keeping things stable. So not a true placebo by any means.  I would think that during crossover and tapering this is exactly the drug response that we want to achieve. Something that is removing symptoms or making symptoms more tolerable, but not giving us any type of buzz or high.  Much like aspirin relieves a headache, but doesn’t produce euphoria or a buzz or a high. (I am not comparing librium to aspirin, but i think you get the point)

 

There are websites on the internet that are looking to use Benzodiazaphines for recreational use. Why they are using benzos of all drugs to experiment with is beyond me.  This is most dangerous thing that they could do, because no one knows beforehand if they are going to quickly reach tolerance or be kindled by these types of drugs, especially when they dose erratically and at very very high doses. In that sense, librium is completely “placebo”’, and that’s how they refer to the drug. I don’t find it funny myself.

 

I think the 5 mg response is also relative to one’s starting dose as well (ie, total daily dose at crossover).

 

You had started with 20 mg and you are at 25% of your original dose. 

 

I started much higher and am at a much lower dose in percentage terms.  So we might respond differently at that same dose because our recovery paths are all very unique.

 

I do agree that body weight, absorption, genetics, metabolism, body fat, etc do also play a big role.  These interplay with the pharmacokinetics of the drug in a very complex fashion.  Ultimately, we are are all very individual in how we respond to these types of drugs.  This is one reason, among many, why crossover amounts don’t always strictly adhere to table conversion. Another reason is how tolerant or kindled a person is at the time of crossover.

 

The neonatal brain article is scary, but these studies are so specific in nature that they rarely apply to our own real life circumstances in any meaningful way. 

 

Best wishes and hope you are doing fine

 

Agree w/ everything you wrote, dm123.  L has a slow, gradual onset; hence, no "high".  That's the point. That's why I agree it's a good taper drug. That's why it is the taper drug of choice at least in the US for alcohol.  L is not abused.  No street value.  But it is certainly doing it's work/damage on our CNS! 

 

As for studies - how applicable they are to real life and how accurate they are given the financial incentives and pressures to get positive results...well, that's a very difficult topic for another thread. The idea of studies is necessary - the scientific method. The reality isn't always pretty unfortunately...and which studies are good and which are garbage...well, therein lies the dilemma.

But a neonatal brain is definitely very different than an adult brain and I agree that studies on neonatal brains cannot be used to make conclusions for adult brains.

 

One question I have is does our CNS really go back to normal 100%???  I mean, will it be as if we never took a benzo???  If so, then why do people say subsequent tapers are more difficult?  Are we forever changed and will we be "sensitive" to things forever?

 

Hi Libr

 

Yes, I should have qualified my use of the word “placebo”. It is doing a lot.  I know it by the cuts. It is not pleasant, but it is most likely the most gentle way to get out of this mess.  It is a dam holding back a ton of water.

 

I love these clinical studies. The neonatal paper was a great read.  It’s just that sometimes I see panic from a lot of people when it is not necessary, because the studies are not applicable. I can tell you that adult neurogenesis and neonatal neurogenesis are very very different (see my response above) simply because the GABAaR literally goes from completely depolarizing (making membrane potential more positive, ie more apt to fire off an action potential) to a mix of depolarizing and hyperpolarizing and finallly to mostly hyperpolarizing in the adult brain.  So GABAaRs and especially GABAbRs affect adult neurogenesis and i wrote some very long papers posted in this thread on this very subject.  And neurogenesis is one of the main 4 component systems in the Benzodiazaphine model.  Neurogenic activity and neuroplastic activity are both profoundly affected by benzodiazaphines and this manifests itself in altered physiological function at the neuronal level and at the neural circuit level.  I just don’t think the specifics in that particular paper are applicable to us as adults. In a generic sense, we already know that the excitatory receptors plastically adapt when Benzodiazaphines are used chronically.  I just don’t think the specifics in that paper apply to us directly.

 

Best wishes

 

 

 

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I once looked at some librium threads on bluelight a long time back.  They make fun of the drug for obvious reasons.  It does very little in terms of what many of the other Benzodiazaphines do, and this is in part due to its slow onset of action and as you know, its GABAaR affinity subunit binding profile.

 

Honestly, I would not have minded a librium prescription instead of the ativan to begin with. The way how my anxious tendencies ran, I would have been better off with it. I don't endorse benzos, but I do think that librium as needed in people with a lot of generalized anxiety with panicky spikes makes more sense than ativan or klonopin, if benzo should be prescribed in the first place. But just like my mother, I also had a propensity for shorter acting bzds due to these spikes. It's just that, for her, the short acting bzds were much more appropriate as she had this ability to bring herself down very quickly from panic. Basically, her panic amplitude would be higher than mine, but her recovery rate from panic would be much quicker than mine. So, I am sure that due to my genetic makeup, drugs such as Xanax, Ativan and Klonopin were totally inapropriate for my system. The one that actually helped me for real many years ago was Oxazepam (Serax). I know it's a short-acting one, but the slower onset of action and its much lower potency than of the Xanax, Ativan and Klonopin made it a much safer choice for me instead of Loazepam. Looking back I wish I'd been prescribed Serax in place of Ativan. But I'd read recently that Actavis discontinued making generic oxazepam, and it was the only mfg. that made it in the United States. It's a shame because it's one of the safest benzos, as far as benzos are concerned. The rebounds would have not beat me up into the ground the way Lorazepam did.

 

 

I do find bluelight very informative and useful resource, although I tend to avoid those threads of people bragging about how much benzo they can take and the miraculous recoveries of getting off 10 yeas benzos in 3 months. If it is true, I'm jealous, and if it's not, I am annoyed.

 

But yes, I'd never partaken in recreational use of anything (except for sugary coffee drinks and desserts - all the stuff I can't touch now). I always felt my brain was on a different wavelength by nature, so no reason to bend the reality even more. But I did have a history of taking antihistamines for anxiety/sleep, as well as natural supplements, teas, coffee (coffee worked as a sedative for me for the longest time), etc. etc.

 

Hi LPfree

 

I agree with what you are saying in terms of the safety of Benzodiazaphines.  As i said before, i have a dislike of all Benzodiazaphines at this point, because of what happened, but if there is one that i wished i had been given, it would have been Librium.  It is tolerated very well even at very very high doses and tolerance is less apt to form with this Benzodiazaphine.

 

 

 

Best wishes......

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I take it noone has a picture of how L affects neural circuits/pathways vs. clonazepam ? I would think it to be different, but ...

 

Hi Liberty, i do not.

Some others might have better insight into this.

I understand the effects of the drug class on the various forms of plasticity of circuits, but i do not know about specific differences in circuit plasticity with the various Benzodiazaphines.

 

 

I am guessing that the differential subunit binding characteristics do play a role in differences in plasticity and adaptability at the circuit level, but i do not have the sources to back that up. It’s just an intuitive feeling that i have, based on the effects these two different Benzodiazaphines have on people in this forum.

 

Best wishes,

Dm123

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I don't recall if this was on a w-bad.org site or somewhere else, but there was a paragraph somewhere that L can affect GABA receptors in the peripheral part of the front lobe more, while K can affect GABA receptors in the central part of the front lobe more profoundly. There was a paragraph about L affecting the peripheral receptors in a very profound way.
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One question I have is does our CNS really go back to normal 100%???  I mean, will it be as if we never took a benzo???  If so, then why do people say subsequent tapers are more difficult?  Are we forever changed and will we be "sensitive" to things forever?

 

 

Regarding the last question, i can only offer you my personal experience after studying the material for the last few years.  There’s another thread going on about kindling.  Believe me when I say it, neuro-kindling is a very real phenomenon.  I think lots of us confuse the symptoms of tolerance with kindling. They are quite different.

1.So the subsequent tapers can be more difficult because the model tells us that plastically the brain takes a very long time to “unwind”.  The brain does plastically adapt to compensate for the effects of the Benzodiazaphine on the circuit.

By unwind i mean plastically revert back to how it was prior to the Benzodiazaphine. 

2.Subsequent tapers becoming more challenging can also be due to a long term kindling effect on the CNS that never fully reverts prior to the reinstatement of the Benzodiazaphine.  From my experience true neuro-kindling takes years to revert, but very few of us here are neuro-kindled going into this thing.

 

I do not think that we ever revert back to the exact same way that we were before the Benzodiazaphine if tolerance or kindling stages are reached. However, this simply means that we are different, not necessarily worse off.  I know this is the case for me, and i do realize that each of us is different and i cannot speak for others. One area that i do think we will always be challenged with is stress resiliency, which is the brain’s ability to adapt to stress. Stress can take many many different forms and can be negative or positive. Adaptability of the brain i believe is can be decompensated for some of us for a very long time......

 

 

This is interesting.  Dm, a couple of questions from me, wondering if you can clarify the following:

 

a)  What is your specific definition of "kindling"? 

b)  Can you elaborate on the specific symptoms of kindling and how they're different from those of "tolerance". 

c)  How exactly does one recognize when one has reached "kindling stage"?

d)  You're saying that becoming tolerant to one's benzo is as bad for the brain as "kindling"?  (Not sure I'm fully understanding that part).

 

I ask because your definition appears to be very different from the definition the rest of us are familiar with, which is very simply that each withdrawal will lead to a more severe withdrawal than the previous one.  Because, no, this is *NOT* an absolute fact.  You can believe me when I say it because I personally have cold turkeyed 4 or 5 times or more, without experiencing even one teeny tiny symptom. 

 

So, of course we're all different.  Just also trying to wrap my head around why you'd be in disagreement with the stance of the OP in the "other" thread?

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One question I have is does our CNS really go back to normal 100%???  I mean, will it be as if we never took a benzo???  If so, then why do people say subsequent tapers are more difficult?  Are we forever changed and will we be "sensitive" to things forever?

 

 

Regarding the last question, i can only offer you my personal experience after studying the material for the last few years.  There’s another thread going on about kindling.  Believe me when I say it, neuro-kindling is a very real phenomenon.  I think lots of us confuse the symptoms of tolerance with kindling. They are quite different.

1.So the subsequent tapers can be more difficult because the model tells us that plastically the brain takes a very long time to “unwind”.  The brain does plastically adapt to compensate for the effects of the Benzodiazaphine on the circuit.

By unwind i mean plastically revert back to how it was prior to the Benzodiazaphine. 

2.Subsequent tapers becoming more challenging can also be due to a long term kindling effect on the CNS that never fully reverts prior to the reinstatement of the Benzodiazaphine.  From my experience true neuro-kindling takes years to revert, but very few of us here are neuro-kindled going into this thing.

 

I do not think that we ever revert back to the exact same way that we were before the Benzodiazaphine if tolerance or kindling stages are reached. However, this simply means that we are different, not necessarily worse off.  I know this is the case for me, and i do realize that each of us is different and i cannot speak for others. One area that i do think we will always be challenged with is stress resiliency, which is the brain’s ability to adapt to stress. Stress can take many many different forms and can be negative or positive. Adaptability of the brain i believe is can be decompensated for some of us for a very long time......

 

 

This is interesting.  Dm, a couple of questions from me, wondering if you can clarify the following:

 

a)  What is your specific definition of "kindling"? 

b)  Can you elaborate on the specific symptoms of kindling and how they're different from those of "tolerance". 

c)  How exactly does one recognize when one has reached "kindling stage"?

d)  You're saying that becoming tolerant to one's benzo is as bad for the brain as "kindling"?  (Not sure I'm fully understanding that part).

 

I ask because your definition appears to be very different from the definition the rest of us are familiar with, which is very simply that each withdrawal will lead to a more severe withdrawal than the previous one.  Because, no, this is *NOT* an absolute fact.  You can believe me when I say it because I personally have cold turkeyed 4 or 5 times or more, without experiencing even one teeny tiny symptom. 

 

So, of course we're all different.  Just also trying to wrap my head around why you'd be in disagreement with the stance of the OP in the "other" thread?

 

Hi abcd,

I do not remember who asked a similar question about the physiology behind neuro-kindling, but it was several months ago on this thread.  I wish the thread was indexed precisely, but it is in this thread somewhere.  The general thought is that it involves altered phosphorylation and alterations in the expression of what are called protein kinases.

 

You might be able to find it in this thread. 

 

I edited the response because of some points that might cause some to be very uncomfortable.

Kindling is a very controversial topic.

 

Best wishes

 

 

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LPF,

 

I think you get two things mixed up: L as in Librium, L as lorazepam !!!! I have taken lorazepam, not Librium and in recent posts in was referring to Librium.

 

Dm123 or neuroscienguy,

 

I think that kindling is related to a great extent to the 4 pillars you mentioned.

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You seriously got them to change your name, that has to be a first here, omfg quite hilarious, now I've really seen everything!

 

Will come back to respond to post.  Thanks.

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[18...]

You seriously got them to change your name, that has to be a first here, omfg quite hilarious, now I've really seen everything!

 

Will come back to respond to post.  Thanks.

 

 

:clap: :clap: :clap::laugh: :laugh: :laugh:

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You seriously got them to change your name, that has to be a first here, omfg quite hilarious, now I've really seen everything!

 

Will come back to respond to post.  Thanks.

 

 

:clap: :clap: :clap::laugh: :laugh: :laugh:

 

:laugh: :laugh: :laugh:  I wanna change mine too now, umm thinking, thinking ... How wild would that be if we all changed our names periodically ...  So much fun!  :laugh:

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