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Going to start Bac today?

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empyr3al

@cheeto

I hope it works for you.  Seems to be hit and miss for some.  Also seems to be simpler to obtain in large quantities than Baclofen.  Really over 1800mg, but can be pushed to 3600mg at which point if its not doing much for you, its not the drug for you.  It kind of hits a plateau apparently where more doesn't make a difference.  If it fails, push harder on the Baclofen?  We know how hard that is to obtain in quantity here in Canada.  I know this site has a strong taste for Baclofen and it shows real promise!  Its just a pain in the arse to obtain.

Now I do suggest before you absolutely decide that you look at "google" the SE's as if you get even a single hint of increased skin problems like ulcers around the mouth or suicidal tendency.  I have a family member that monitors any behaviours I am not seeing myself.  Any bad SE's you immediately talk to your doctor.

BTW the standard script is 3 x 300mg it seems for back spasm, pain, etc.  I'm not sure why you got 300mg once a day.  Should have no problem getting 3x300.  In my case the bottle says take 1 or 2 capsules 3 times daily as needed, so it can vary as much as I need it too.  The pharmacy fills what the max allowable is, so 180 caps a month.  So its $36 at walmart for APO-Gabapentin 180 capsules + fill if you don't have a plan.  If you were curious.

Good luck!  I'd like to hear if you do use it and what happens, so check in. :)

Edited by empyr3al

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Otter

It's a shame about the side effects.  We're in some ways not a lot further ahead in using baclofen than we were years ago.  The medical profession still has not got to grips with it.   I'm of the view that the prevailing attitude, still, prevents a lot of people from getting the treatment they need.   If someone is coming off an addiction and the drug they are being treated with has side effects which make it impossible to work, then they shouldn't be working.  But, the prevailing attitude is that this is a will power issue, not a medical one, so one is expected to simply "not have" the problem in the first place and not to ask for time off work.  Would an employer be upset because a cancer sufferer on chemo was wiped out by the treatment, or would they be treated with compassion?  It's a mistake to think that one can take a drug which stops drinking at the appropriate dosage with no side effects.  Why would anyone assume it was going to work without side effects?  Baclofen is an anxiolitic. It makes you relax. When you relax, you fall asleep.  Taking it through the day is going to make you relaxed through the day.  If you drank through the day, you would also fall asleep.

As yet, there's no answer to this other than to persevere as best you can or try something else. There isn't the backup or understanding in the medical profession, hospitals, among employers or the public to allow this to work as well as it should.  It may also be that you don't suffer from the crippling anxiety which baclofen treats and that you have a condition which doesn't respond to baclofen.  You may never find out.

I've found, over the years, that there's been no change in the public awareness of alcoholism treatment with baclofen or any meds.  Even now that my wife doesn't drink and isn't relapsing, she is labelled as an alcoholic in a very derogatory fashion, even by people who are drinking heavily, daily.  Such a shame.

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StuckinLA
19 hours ago, cheeto said:

I have been feeling really weird on Bac and super sleepy as I know those are SE's that should go away in time. Thinking about the high doses I will need to take and the reluctance of my Doc to even give me this script I have decided to go with Empry3al's suggestion of Gabapentin which I have taken on and off for years for Sciatica then Menopause hot flashes. Of course now that I read what works for hot flashes it's not 300 mg a day but more like 300 mg, 3 times a day which maybe would work for alcohol cravings too. I am sure my Doc would give me a higher mg prescription with refills too. So yesterday I went down to 20 mg Bac and have some Gabapentin so I took 200 mg X 2. Today I will do the same and work up to 600 mg of Gabapentin and maybe go down to 10 mg of Bac and hopefully in a couple days just go off the Bac?

Eh, that would be entirely up to you. A lot of people around here have taken both bac and gabapentin and found the combo worked well for them. I know there's been a study of gabapentin alone for alcohol cravings, in the 1800+mg/day range, but don't have the results of that study offhand. I know of no one who has found gabapentin on its own to be successful in reducing cravings. In my own case, as I mentioned, I have taken gabapentin off and on a lot in the past for sleep and for what I believe is nerve pain, with no noticeable effect.

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StuckinLA

Oh one more thing, the baclofen side effects don't "get worse" with higher doses. I know how you're thinking right now because I had that same fear: OH MY GOD IF THIS IS WHAT 30MG FEELS LIKE WHAT HAPPENS WHEN I TAKE 200!?

But it doesn't work like linearly like that. I'm not saying higher doses are a walk in the park, but as long as you take things slow and steady it isn't as bad as you think it will be.

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empyr3al

You will need register or log in to read this content  ... Says it warrants more study and its 2014.  Bunch of interesting info.

You will need register or log in to read this content  Synergy between NAL and Gabapentin combination study.

Just a couple links, I didn't book mark everything that I've read.  Like StuckinLA said it might work well in combo.  My case is that its currently used in combination so maybe I'm getting different results personally than using it stand alone.  Mirtazapine is a strong marker for me also in what I take.  Tons of links on that med.

 

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empyr3al

Interesting, the Mayo Clinic is starting a new study on it.

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Otter
On 9/17/2017 at 10:28 PM, empyr3al said:

Interesting, the Mayo Clinic is starting a new study on it.

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This study is interesting, for me, for one reason.  It illustrates very well how even the Mayo Clinic takes the same approach to this illness which has always been taken.

Look at the inclusion criteria:

Inclusion Criteria:

Prediction of Alcohol Withdrawal Severity Scale (PAWSS) score >4.

Adults age 18 or older.

Sufficient understanding of English.

Hospitalized on Hospital Internal Medicine or Generose.

 

We, and the medical profession, continue to define this illness in terms of the amount of alcohol consumed and consequences, ie., Hospitalization. The other criteria are age and language.

If you think about the research being done with baclofen, for instance, the brain scans which Dr. Childress did, and which led to Ameisen taking baclofen for his anxiety, you can see a neurological disorder, a hyperactivity of the limbic region in the brain.  What is the nature of the illness which the Mayo Clinic is intending to treat?  By settling on Gabapentin as a treatment, they must think there is an anxiety problem, but their inclusion criteria say nothing about this.  Do all people who over-use alcohol and end up in hospital do so because of a neurological problem related to the brain's anxiety coping mechanism (if that's the right way to state it)?  If they don't, then those taking alcohol who don't have any such problem presumably won't respond positively.  

The new DSM-V criteria for "alcohol use disorder" also suffer from the same approach, in my opinion.  Even the term they use shows this approach.  Alcoholism was typically referred to as "alcohol misuse" or "substance abuse".   If someone suffers from severe pain and takes lots of pain-killers such as codeine, would it be right to describe their illness as an "opiate use disorder" or would it be more useful to look at the cause of the pain?  We've moved away from calling it alcohol abuse to a "disorder" of alcohol "use".  What on earth does that mean from a medical perspective? How does is help in finding a treatment to define the illness as either an abuse of alcohol or a disorder of its use?

We've had this debate here and previously, elsewhere, for years now.  What's the precise name for what baclofen treats?  What does baclofen do to which part of the brain and why is this part of the brain not working properly?   I don't even get the impression from the French studies that they have addressed this issue.  The Prescribing Guidelines describe the experience of prescribing doctors who reported that patients would come to them and ask for baclofen, with little discussion about their condition, symptoms or much of anything.   There's no mention in the Guidelines of any neurological or medical "diagnosis" or taking of a case history other than that the patient complained of being addicted to alcohol.  

What this leads to is a division between 12-Steppers...get psycho-social support...baclofen users...lots of advice about dosage...and those who try other meds...advice about dosage.  Most of us are not doctors so we can't diagnose and don't know what questions to ask.   We may see reports of anxiety and then suggest baclofen, and it may or may not work.  The medical profession, even those doctors using baclofen, are no better.  

Am I missing something?

 

 

 

 

 

Edited by Otter
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StuckinLA
11 hours ago, Otter said:

The new DSM-V criteria for "alcohol use disorder" also suffer from the same approach, in my opinion.  Even the term they use shows this approach.  Alcoholism was typically referred to as "alcohol misuse" or "substance abuse".   If someone suffers from severe pain and takes lots of pain-killers such as codeine, would it be right to describe their illness as an "opiate use disorder" or would it be more useful to look at the cause of the pain?  We've moved away from calling it alcohol abuse to a "disorder" of alcohol "use".  What on earth does that mean from a medical perspective? How does is help in finding a treatment to define the illness as either an abuse of alcohol or a disorder of its use?

Interesting point. Seems the attempt to destigmatize "alcoholism" and "addiction" with the language of abuse and disorder may still be missing the point.

In terms of the anxiety, whether it is underlying or not, anyone going through that level of withdrawal is going to have anxiety issues.

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empyr3al

I'm not sure why its renamed.  Substance use disorder is way to vague too.  Uppers, Downers, Psychedelics, Disassociatives... Like come on.  So to get this straight, its being studied for AWS.  How does this encompass recovery?  Because as far as I know AWS is the term for the first 72 hours and that's the misnomer being pushed as an agenda to stop diazepam use.  AWS.  It should be at least categorized into Immediate Withdrawal Syptoms and Alcohol Recovery Medications.  Then developed further and other characteristics and exhibited behaviors and what we call PAWS might not just be "Oh, it'll pass, its because you drank so much", maybe there is something else wrong you #$#2.  I would think Gabapentin is for long term use not just bing bang boom you are fixed.  Now deal with the rest of the crap.  Maybe the name AUD is to soften the blow those those that want to admit to over using alcohol or are dependent and to take away the shame?  Sometimes I wonder about this whole disease agenda that is going on.  Why are we not looking further into the brain as to why people are self medicating with alcohol.  Its not all because of social influence or damaged past, its often to dampen some other chemical or brain function and physical issues.  Otter I totally agree we are not looking at why these drugs work for some and not for others.  What parts of the brain are damaged that are being compensated for with the medications if they do so in fact work.  Still a shallow study, but at least a study is being done?!  Mind you, this study because its inherently going to be flawed (again) may actually damage a potential medicine for those it can actually help.  If it fails, look at why it failed.  I swear some companies are funding these studies so they can push their patented drugs and not lose their hold on the market, so they are designed to fail... look at cigarettes.

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StuckinLA

Oh, didn't catch that the gaba study was for AWS. That's worthless. Anyway, @cheeto sorry to have hijacked your thread, how are you doing?

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cheeto

Hi StuckinLA and everyone, I am now taking 1200 mg of Gabapentin and 40 mg of Bac a day. I need to read up on Gaba & Bac to see what dosage others took and what the success rate was?

Just found these...

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Conclusions and Relevance  Gabapentin (particularly the 1800-mg dosage) was effective in treating alcohol dependence and relapse-related symptoms of insomnia, dysphoria, and craving, with a favorable safety profile. Increased implementation of pharmacological treatment of alcohol dependence in primary care may be a major benefit of gabapentin as a treatment option for alcohol dependence.

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Will let you all know how it's going but still at 1 1/2 bottles of wine a night!

Thanks for posting...

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empyr3al

Hrm @cheeto, I gave myself no easy options to drink so maybe that's a difference?  (not true, I could right now get in my truck and go get some, but why?).  Normally even typing that would trigger me to contemplate doing just that.  Are you trying to not buy it or is easily accessible and just a habit or is it dependency driving it?  Puts me in a dilemma about GabaP because I think its more so not a reduction drug but used to take the edge off of trying to abstain possibly?  I have had a lot of practice with sobriety so I know the ropes and gabapentin made this time different than previous.  Substantially easier but not without perfection.  Much simpler not to think about it.  I found it harder in prior attempts at sobriety to break patterns of behavior and thoughts than with GabaP.  So I broke my patterns again.  For example I gave up playing certain types of video games (SimCity, Civilization, strategy games, etc) many years ago because I found myself always moving my hand to reach for my "drink" when it was not there (while abstaining from AL).  Even sitting in a different spot to watch TV, or going up the stairs with the other foot breaks up your patterns (believe me its strange, try putting a watch on the other wrist or a bracelet).  I park my truck in a different spot, I walk my dog a different route, the lawn has a different mowing pattern.  Every pattern changed intentionally right in the moment instead of practice.  Only twice in the past 3 weeks has the gremlin come saying I could stop at the lcbo, and a swift moment of cold chill has run over me but I catch it quickly and disregard the thought as nonsensical and move on.  It used to happen without GabaP constantly during a day and would have to know I had it in stock at home or the time to pick it up on the way home.  Now it seems to only happen at the same one instance I can't avoid which is probably a memory mold in terms of where I am driving over a certain big bridge that I've done it before.  I don't dwell on why I thought it for too long other than to recognize where I am, then think about something else.  I haven't drank on GabaP.  I seem to have stopped taking diazepam incidentally using GabaP without real conscious effort which is curious even though they don't touch on the same neurological features.

Now with Baclofen most people I assumed are not drinking with it and are post AWS which takes a concentrated effort on abstaining and obtaining the switch is where you stop thinking or craving?  Maybe I'm way off but I thought Naltrexone was the only drug specifically devised using TSM for some to slow drinking quantity.  Study on Baclofen for intake moderation.  You will need register or log in to read this content

Hoping it works for you still.  Its was always worth a shot and cannot say unless you consciously stop drinking it will be of benefit.  Keep it in your "toolbox" of options as no pill really covers everything fully.

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Otter
17 hours ago, empyr3al said:

Hrm @cheeto, I gave myself no easy options to drink so maybe that's a difference?  (not true, I could right now get in my truck and go get some, but why?).  Normally even typing that would trigger me to contemplate doing just that.  Are you trying to not buy it or is easily accessible and just a habit or is it dependency driving it?  Puts me in a dilemma about GabaP because I think its more so not a reduction drug but used to take the edge off of trying to abstain possibly?  I have had a lot of practice with sobriety so I know the ropes and gabapentin made this time different than previous.  Substantially easier but not without perfection.  Much simpler not to think about it.  I found it harder in prior attempts at sobriety to break patterns of behavior and thoughts than with GabaP.  So I broke my patterns again.  For example I gave up playing certain types of video games (SimCity, Civilization, strategy games, etc) many years ago because I found myself always moving my hand to reach for my "drink" when it was not there (while abstaining from AL).  Even sitting in a different spot to watch TV, or going up the stairs with the other foot breaks up your patterns (believe me its strange, try putting a watch on the other wrist or a bracelet).  I park my truck in a different spot, I walk my dog a different route, the lawn has a different mowing pattern.  Every pattern changed intentionally right in the moment instead of practice.  Only twice in the past 3 weeks has the gremlin come saying I could stop at the lcbo, and a swift moment of cold chill has run over me but I catch it quickly and disregard the thought as nonsensical and move on.  It used to happen without GabaP constantly during a day and would have to know I had it in stock at home or the time to pick it up on the way home.  Now it seems to only happen at the same one instance I can't avoid which is probably a memory mold in terms of where I am driving over a certain big bridge that I've done it before.  I don't dwell on why I thought it for too long other than to recognize where I am, then think about something else.  I haven't drank on GabaP.  I seem to have stopped taking diazepam incidentally using GabaP without real conscious effort which is curious even though they don't touch on the same neurological features.

Now with Baclofen most people I assumed are not drinking with it and are post AWS which takes a concentrated effort on abstaining and obtaining the switch is where you stop thinking or craving?  Maybe I'm way off but I thought Naltrexone was the only drug specifically devised using TSM for some to slow drinking quantity.  Study on Baclofen for intake moderation.  You will need register or log in to read this content

Hoping it works for you still.  Its was always worth a shot and cannot say unless you consciously stop drinking it will be of benefit.  Keep it in your "toolbox" of options as no pill really covers everything fully.

Here's an article which I found explaining baclofen from a scientific/neurological perspective.  You will need register or log in to read this content     The gist of the article is as follows:

"Relapse is a widely recognized and difficult to treat feature of the addictions. Substantial evidence implicates cue-triggered activation of the mesolimbic dopamine system as an important contributing factor. Even drug cues presented outside of conscious awareness (i.e., subliminally) produce robust activation within this circuitry, indicating the sensitivity and vulnerability of the brain to potentially problematic reward signals. Because pharmacological agents that prevent these early cue-induced responses could play an important role in relapse prevention, we examined whether baclofen—a GABAB receptor agonist that reduces mesolimbic dopamine release and conditioned drug responses in laboratory animals—could inhibit mesolimbic activation elicited by subliminal cocaine cues in cocaine-dependent individuals."

I don't think you've got baclofen right.  You say baclofen people are not drinking and are post AWS.   

There's no AWS with baclofen.   AWS is a result of stopping drinking suddenly as in a detox.  For instance, with the regime of "Seven Weeks to Sobriety" you have to stop drinking and it's recommended in the book that you take an anxiolitic on the first day of the program, but that if you drink very heavily, you should detox in hospital.  All traditional rehabs I am aware of require abstinence before engaging in treatment because they are 12-Step based.  

You take baclofen while drinking but over time the effect is to reduce alcoholic craving.  It's not "required" that you continue drinking while taking baclofen.  You just ease up the dosage of baclofen slowly to avoid side effects and it stops the craving when you reach the right dosage.   There's no AWS because you are weaning yourself off alcohol slowly over a long period.

Imagine a neuroreceptor is like a glass and you can either fill it with alcohol or baclofen. The more baclofen you put in the less the glass "needs" to be filled with alcohol, so when the neuroreceptor is "full up" with baclofen, you don't want to drink alcohol.   You have to keep taking baclofen to keep the glass full and if you get more stress, you take more.  If you stop taking it, you want more alcohol.

Nal is different.  It works on a different neuroreceptor, one responsible for giving you the euphoria of alcohol, rather than taking away anxiety caused by a lack of a brain chemical.  You take Nal before drinking to lessen the need for alcohol, to deaden the "fun" receptor, so in theory when you drink and don't get a buzz, over time your brain says "meh, I don't need this".   This process is supposed to extinguish the desire to drink but it requires continued drinking.

For me it's not so much a matter of having a "tool box".  Yes, there are lots of methods out there.  I have been slogging away on this project for years because the baclofen science sets out what the illness in the brain is that needs to be treated...in some people.  Whether it's all people, or just some, I don't know but everyone has the same brain chemicals.  We don't really get an idea of why baclofen may work for some but not for others because there's virtually no discussion of anything which could be used as a diagnosis. No one goes for a brain scan or has blood tests which would show GABA shortages in the brain.   It's still a matter of doctors asking if you drink, how much, and then handing over a prescription on an almost trial and error basis.  That's also how they work with anti-depressants, trying SSRI's then newer drugs like Mirtazapine.  They just start with what's approved by the authorities after they thumb through the index of available medicines. 

 

I hope that makes sense.

 

 

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Otter
On 9/20/2017 at 8:36 AM, StuckinLA said:

Interesting point. Seems the attempt to destigmatize "alcoholism" and "addiction" with the language of abuse and disorder may still be missing the point.

In terms of the anxiety, whether it is underlying or not, anyone going through that level of withdrawal is going to have anxiety issues.

The article I posted above describes the underlying condition of drug addiction (presumably alcoholis is the same for the purposes of a discussion of baclofen) as drug-induced or drug cue-induced mid-brain (mesalimbic) neural activation and dopamine release.   This seems to be a better scientific/medical description of what baclofen treats by "attenuating" dopamine release by acting on the GABAB receptor. The feeling in the brain/mind of the addict, without the attenuating effects of baclofen is a "dysphoria" or "anxiety".  These last two terms are confusing because they are primarily used in psychiatry and are not neurological terms referring to recognised medical/neurological illnesses.  The problem is that Ameisen, et al, picked up on these terms and applied them to alcoholism or what he saw as the underlying condition of "alcoholism".  Alcoholism or drug addiction and all the behaviour and thoughts that goes with it is, in the article's terminology, a "downstream effect" of the illness.  

The illness is therefore better described as "alcohol-induced and alcohol cue-induced midbrain (limbic or mesalimbic) neural activation and dopamine release" which is attenuated by the dopamine reducing effects of baclofen.    The diagnostic tools doctors should use for this would be what?  A brain scan?  Certainly a comprehensive medical case history conducted by a doctor with some idea of neurology and the illness should be overseen by a neurologist who has training in this disorder and the use of baclofen and knows how to treat the side effects of baclofen.   At present, we are just getting to the point where there is a fairly sparse sprinkling of general practice doctors who are willing to give a prescription for baclofen based on a self-diagnosis by the patient of "alcoholism" based on the negative consequences of drinking and the volume of alcohol consumed.  

I don't think that this treatment is being pursued by professionals in the field in a way which is thoroughgoing enough to allow it to succeed as well as it could.  The whole history and philosophy of alcohol treatment hamstrings anyone trying to use baclofen or prescribe it for a patient.  We are still hacking our way through the dense undergrowth of a forest of confused terminology and philosophies of treatment.  We need to define what is being treated, then diagnose it, then get the dosage right, deal with side effects and then, figure out ways of helping recovering sufferers deal with all the crap in their lives.  This last part in itself is a huge battle because society treats all this treatment as a hoax and baclofen users, ie., alcoholics as...well...alcoholics, and therefore beyond cure or redemption and not deserving of any help or support.  

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empyr3al

@Otter, like my GP.  Its easy to dismiss effects in sobriety as being caused by alcohol use and not why alcohol use was initiated in the first place.  Or even if something happened during the course of normal drinking that caused a major spike in consumption.  The concept that once you have your first drink at 16 you opened a door doesn't nearly work in that situation as possibly you had a fall, a stroke, a car accident and alcohol or substance use spikes and becomes the fill in gap measure.  So much assumption made by AA and the gen pop.  Many may have been normal drinkers before something happened.

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Otter
1 hour ago, empyr3al said:

@Otter, like my GP.  Its easy to dismiss effects in sobriety as being caused by alcohol use and not why alcohol use was initiated in the first place.  Or even if something happened during the course of normal drinking that caused a major spike in consumption.  The concept that once you have your first drink at 16 you opened a door doesn't nearly work in that situation as possibly you had a fall, a stroke, a car accident and alcohol or substance use spikes and becomes the fill in gap measure.  So much assumption made by AA and the gen pop.  Many may have been normal drinkers before something happened.

Also, dopamine imbalance is a cause of other problems.  

"Several important diseases of the nervous system are associated with dysfunctions of the dopamine system, and some of the key medications used to treat them work by altering the effects of dopamine. Parkinson's disease, a degenerative condition causing tremor and motor impairment, is caused by a loss of dopamine-secreting neurons in an area of the midbrain called the substantia nigra. Its metabolic precursor L-DOPA can be manufactured, and in its pure form marketed as Levodopa is the most widely used treatment for the condition. There is evidence that schizophreniainvolves altered levels of dopamine activity, and most antipsychotic drugs used to treat this are dopamine antagonists which reduce dopamine activity.[2] Similar dopamine antagonist drugs are also some of the most effective anti-nausea agents. Restless legs syndrome and attention deficit hyperactivity disorder (ADHD) are associated with decreased dopamine activity.[3]" Wikipedia

What we are seeing are a lot of new treatments for conditions like Parkinson's Disease using baclofen, for instance, You will need register or log in to read this content

Arbaclofen was developed to treat autism.  When doctors treat alcoholism, they tend to think that they need to get the patient first to stop drinking (just like that) and then treat the underlying mental illness.  But, the underlying illness and "alcoholism" are likely to be one and the same thing.  Alcohol comsumption is just a way of self-medicating.   Because we  a haven't seen the association of both alcoholism and things like autism and ADHD with dopamine, we talk about alcoholics who say they are only self-medicating with alcohol as being irresponsible when, in fact, they are right.  Alcohol does medicate this dysphoria.  It's an anxiolytic, but it isn't specific to the illness in its effect. It affects the whole body and causes behaviours which people don't like, which are anti-social and unpleasant.  Baclofen is specific to the GABAB receptors so it is a better, more effective "treatment" than alcohol.

My beef with people who downplay baclofen is that they overlook the science behind it but you can't blame them because even the scientists and doctors involved in baclofen research and treatment haven't even got to grips with isolating and identifying the illness and just call it alcoholism, which allows detractors to ignore the science.  If we could get proper diagnosis of a clearly defined, identifiable disorder of the neurological system it would make it easier to explain and treat, without all the misinformation and antagonism between supporters of this research and others who are committed to AA or some other method.  We could look at each form of treatment and measure it in terms of whether it works for this neurological condition and we could say whether or not the patient actually has the illness or drink for social reasons.  I used to drink every day and I had anxiety, but not to the extent that I couldn't chocoose to have a coke rather than a glass of wine.  I don't drink at all now and I don't have overwhelming anxiety so I don't have the illness.  My alcohol consumption when I was in a stressful job did cause me to have worse anxiety, particularly Sunday night job anxiety so I'd always drink on a Sunday night to calm my pre-Monday, back to work anxiety.  But, that's not "alcohollism".  I didn't have an organic disorder. although continued alcohol consumption and stress may, I suppose, have pushed me towards having a bit of a problem and I found it hard to quit.    

 

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StuckinLA
On 9/22/2017 at 10:42 AM, cheeto said:

Conclusions and Relevance  Gabapentin (particularly the 1800-mg dosage) was effective

Yeah the study is with 1800 - I saw a psych who was going to put me on 2400-2800 or something like that, and I've taken up to 3600mg a day on my own. But like I've said here and elsewhere, gabapentin really seems to have no effect on me whatsoever. So I don't want to present my experience with it as typical, just possible.

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Mom2JTx3

@cheeto  Otter is correct in saying that you don't have to quit drinking before or while taking Baclofen.  However Gabapentin may work differently.  There are Baclofen users who had terrible side effects until their dose was over 100mg, then it got better.  @Ne1 comes to mind.  I eventually found my drinking decreasing after a period of time, but then going back up again until I reached indifference.  Even at that point I still had to decide to put down the bottle because of habit and just being emotionally dependent on the stuff.  

 

 

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empyr3al

@Otter I was going to mention this documentary earlier when you mentioned cue's.  If you aren't in Canada, you'd need to use a VPN to watch it some other method.  There are CT scans and MRI's taken of cue's and a discussion about Naltrexone.  Even if you cannot watch the video the summary is there and some images.

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Nicnak

When I first titrated up in bac over 2 years ago I got all sorts of SE's early on.Since my 2nd time of titrating I find the side effects come much later on and I have failed to reach indifference at way over my 2 previous switches,don't know if this is related by interesting 

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Otter
On 9/24/2017 at 6:46 AM, empyr3al said:

@Otter I was going to mention this documentary earlier when you mentioned cue's.  If you aren't in Canada, you'd need to use a VPN to watch it some other method.  There are CT scans and MRI's taken of cue's and a discussion about Naltrexone.  Even if you cannot watch the video the summary is there and some images.

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I read the article.  I grew up watching David Suzuki.   

Here's the thing.  Naltrexone was approved for opioid addiction twenty, thirty years back on the basis of studies which showed it had some effect as an antagonist.  Back then any drug which showed some effect could get approval because something is better than nothing.  Then, someone has the idea that it might work for alcoholism.  Even in drug addiction, Nal was only supposed to be effective in reducing drug taking for three months.  That was supposed to give the addict a helping hand in getting off the drug, but abstinence was to be attained through will power. After three months Nal became ineffective because the effects of antagonists are lost after the brain adjusts to them.  

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This is a fairly recent study on Naltrexone which suggests that Nal doesn't work for abstinence and makes users feel more intoxicated, which explains, they say, why it is effective in reducing drinking, at least initially.  It seems to suggest that Nal makes you feel more drunk and from this they draw the conclusion that it works on the reward circuitry of the brain.  Nal, they say, increases craving for alcohol...

I'm not sure if I've read this right so don't quote me.

Bac is different, works on a different part of the brain, as an agonist, not an antagonist.  Ameisen and the French baclofen researchers are very critical of Nal and TSM.  They just think it's a con, from what I gathered from them.  None of them was at all interested in it.

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Nicnak
On 24/09/2017 at 1:11 AM, Mom2JTx3 said:

@cheeto  Otter is correct in saying that you don't have to quit drinking before or while taking Baclofen.  However Gabapentin may work differently.  There are Baclofen users who had terrible side effects until their dose was over 100mg, then it got better.  @Ne1 comes to mind.  I eventually found my drinking decreasing after a period of time, but then going back up again until I reached indifference.  Even at that point I still had to decide to put down the bottle because of habit and just being emotionally dependent on the stuff.  

 

 

I was different,I was drinking up to 3 bottles of wine a day till bang,I titrated up the next day to 160 and didn't drink for 4 months.But as you know I then got the urge to drink,slowly at first till about 4 months then I was back to drinking in the old way 

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empyr3al

@Otter curious study. At what level were these individuals drinking I wonder. A bottle of two of wine or 40oz of vodka? So Nal might make controlled drinking but the individual has increased intoxication? So in fact it is saying that the 40oz of vodka will potentially reduce to a bottle of wine? I say this because I wonder what the tipping point of levels of intoxication Naltrexone might be most effective at in curbing excessive drinking. The fact the cue's are higher in the NTX than PLC group does lead me to wonder something I have been pondering for a while. That NTX not only mutes alcohol but all highs including eating, so introduction of a flood of AL in this study may mean that the individual is still wanting and seeking an escape from discomfort and at such a point any trigger or cue can induce a craving and therefore abstinence is a struggle. In my case experiment Mirtazapine and Gabapentin to take the struggle (anxiety) off the cue based issues shown to be inherent of NTX in this study.

I lapsed hard on NAL after 6 months and lost a ton of weight which had to be curbed differently. So NTX is an interesting topic but I am still cautious of swinging all for one method such as Baclofen and eliminating potentials of others for modification or a synergy of medications.  Neither here nor there, but NAL alone seems in my case not be the end all.  Baclofen with NAL may have been effective for me had I been given that opportunity to experiment.

" Of note, our data do not establish an absolute deficit in the ability of alcohol to activate the VS in our clinical population. Because ethical considerations limit the level of brain alcohol exposure that can be assessed in treatment seeking subjects, the deficit was detected at blood alcohol levels lower than those that typically result from heavy drinking. It is therefore possible that a VS response to alcohol would occur in this population at higher levels of intoxication."  This in the results is interesting that the cue's were instigated at very low levels and thats an interesting sign.

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Nicnak
19 minutes ago, empyr3al said:

@Otter

I lapsed hard on NAL after 6 months and lost a ton of weight which had to be curbed differently. So NTX is an interesting topic but I am still cautious of swinging all for one method such as Baclofen and eliminating potentials of others for modification or a synergy of medications.  Neither here nor there, but NAL alone seems in my case not be the end all.  Baclofen with NAL may have been effective for me had I been given that opportunity to experiment.

" Of note, our data do not establish an absolute deficit in the ability of alcohol to activate the VS in our clinical population. Because ethical considerations limit the level of brain alcohol exposure that can be assessed in treatment seeking subjects, the deficit was detected at blood alcohol levels lower than those that typically result from heavy drinking. It is therefore possible that a VS response to alcohol would occur in this population at higher levels of intoxication."  This in the results is interesting that the cue's were instigated at very low levels and thats an interesting sign.

I was the other way,I put on loads of weight whilst drinking and lost 3.5 stone last year over 4 months of not drinking.Since drinking again I've put on 1.5 stone

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Otter
20 hours ago, empyr3al said:

@Otter curious study. At what level were these individuals drinking I wonder. A bottle of two of wine or 40oz of vodka? So Nal might make controlled drinking but the individual has increased intoxication? So in fact it is saying that the 40oz of vodka will potentially reduce to a bottle of wine? I say this because I wonder what the tipping point of levels of intoxication Naltrexone might be most effective at in curbing excessive drinking. The fact the cue's are higher in the NTX than PLC group does lead me to wonder something I have been pondering for a while. That NTX not only mutes alcohol but all highs including eating, so introduction of a flood of AL in this study may mean that the individual is still wanting and seeking an escape from discomfort and at such a point any trigger or cue can induce a craving and therefore abstinence is a struggle. In my case experiment Mirtazapine and Gabapentin to take the struggle (anxiety) off the cue based issues shown to be inherent of NTX in this study.

I lapsed hard on NAL after 6 months and lost a ton of weight which had to be curbed differently. So NTX is an interesting topic but I am still cautious of swinging all for one method such as Baclofen and eliminating potentials of others for modification or a synergy of medications.  Neither here nor there, but NAL alone seems in my case not be the end all.  Baclofen with NAL may have been effective for me had I been given that opportunity to experiment.

" Of note, our data do not establish an absolute deficit in the ability of alcohol to activate the VS in our clinical population. Because ethical considerations limit the level of brain alcohol exposure that can be assessed in treatment seeking subjects, the deficit was detected at blood alcohol levels lower than those that typically result from heavy drinking. It is therefore possible that a VS response to alcohol would occur in this population at higher levels of intoxication."  This in the results is interesting that the cue's were instigated at very low levels and thats an interesting sign.

The paper mentions ethical considerations which means they couldn't make them drink a lot because it would make their alcoholism worse.

The point I'm trying to make is that if a person was diagnosed properly then it wouldn't become a question of swinging for one drug.  It would be a question of taking the right drug for the condition.  Because we say that the condition is "alcoholism" we don't know which treatment is best.  

My thinking, from the baclofen studies, is that baclofen works by calming over-activation in the mid-brain or mesalimbic region resulting from alcohol and alcohol cues.   If a person does not suffer from this, then baclofen won't work.   This isn't the same thing as getting euphoria from drinking.  Naltrexone would seem to me to work for people who drink for the enjoyment or euphoria of drinking, burt not because they have this hyperactivity of the limbic system from drinking cues and alcohol.  

One of the issues with using Naltrexone is that the brain adapts to it by creating more neuroreceptors.  If you get rid of the "fun" of drinking, the brain continues to seek pleasure so it creates new pleasure receptors.  This is why TSM just aims at long term reduction of drinking.  Sure it works, but it's for those who drink for pleasure, not because, like Ameisen, they had unbearable anxiety.  My wife didn't drink for fun, except when she was young.  She drank out of anxiety but some of that anxiety may have been caused, over time, by drinking alcohol.

I don't know if it's a question of how much you drink but, rather, the motivation, anxiety or pleasure.    I only ever drank socially or with a meal but after many years of drinking, I got no pleasure from it.  I didn't get a high, so after a while, I think, most people probably don't get such a buzz from alcohol as they did when the first started so for most people it's not so hard to stop, if that's why they started.  It's like anything you do for a buzz, it wears off with time.  That's why I'm not sure it's the Nal which is causing them to stop drinking, if they do, or the continued drinking under the TSM regime.  The studies I've read say that Nal is for drink reduction, not for abstinence.  Baclofen replaces alcohol in the brains circuitry so in people who drink for anxiety can stop drinking by taking baclofen.

 

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cheeto

Well I am done, I give up!. I am titrating down off of Bac & Gabapentin as I have been feeling super drugged,sick and really tired all the time. I can't remember words when speaking or things that I have done. The other day I couldn't remember my address or phone number so this is playing havoc with my brain. I also find I am getting so drunk with these drugs and have lot's of blackouts.

I can't do my work or anything as I am so exhausted all day then can't sleep all night. I finally went to sleep at 7:30am this morning for a few hours and I feel awful. I may end up losing my job if I can't sleep or remember things. Sounds like Gabapentin won't work on it's own and I can't get any more Bac. I don't know anything else that can help me? As I said I was on TSM for almost 3 years so I took a ton of Naltrexone and really need to give my body a break from all these drugs. I have really been trying to cut down or go AF from alcohol but the side effects from titrating down on the pills make me edgy so a few drinks helps right now.

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Nicnak

Don’t give up totally.Leave if a few months then try bac on it’s own.I did this last year after being indifferent then loosing my switch.It only took me just over a 2 week period

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cheeto

How much were you taking of the Bac? The only problem I have is I can't get anymore from my Dr after I use up the ones he prescribed.

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Nicnak

First time I became indifferent at 180mg and the second time it was 160mg

But in between that and after I got up to higher amounts without a switch.I think if you are not successful after a while you need to come right off it and start again.

I get mine from abroad from goldpharma 

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empyr3al

@cheeto its too bad we can't send each other drugs in this country or I would give you what little baclofen I have.  I'm sorry this experiment didnt work out for you.

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