14 replies to this topic

[lemon_]

Hi all,

 

May you give advice on what supplements to take for Alcoholism please?.

no fluff.

 

 

thank you.

[aconita]

I assume you mean supplements which may help in ending or reducing the habit. 

 

Since alcohol seems to effect mainly endorphins and GABA it may make sense to emulate that.

 

Guessing that opiates wouldn't be a smart choice in order to raise endorphins, unless you aim to become an opiates addict, of course, I may suggest training as an healthy and very efficient way to achieve that.

 

GABA may be enhanced by glutamine and theanine as the easier compounds to get (and probably safer too).

 

Glutamine has to be taken in relatively high amounts (10-20g/day),

 

 

 

 

 

[jroseland]

Piracetam has 6 human studies showing it as helpful for recovering alcoholics.

 

In an interesting episode of history, Dr. Hoffer introduced the founder of Alcoholics Anonymous, Bill Wilson, to LSD therapy for alcoholics. Dr. Hoffer also introduced Vitamin B3 to Wilson as an option for treating Alcoholism:

“Bill was very curious about it and began to take niacin, 3 g daily. Within a few weeks fatigue and depression which had plagued him for years were gone. He gave it to 30 of his close friends in AA and persuaded them to try it. Within 6 months he was convinced that it would be very helpful to alcoholics. Of the thirty, 10 were free of anxiety, tension and depression in one month. Another 10 were well in two months.”

They went on to conduct studies on much larger groups, the data produced was optimistic:

“A five-year longitudinal field trial of nicotinic acid was conducted on 507 known alcoholics to determine what effects and benefits might result. Our experience strongly suggests that:

1. Nicotinic acid can benefit 50 to 60 percent of alcoholics in the organic stage.

2. Nicotinic acid can benefit about 30 percent of the total alcoholic population.”

Niacin is an inexpensive, and potentially transformative option worth the consideration of those struggling with alcoholism.

 

A handful of studies and clinical reviews have established Tianeptine, as an option for treating alcoholic withdrawal, from a review analyzing multiple trials:

"Tianeptine is effective in the treatment of depression in elderly and post-alcohol-withdrawal patient subgroups. Tianeptine was more effective in reducing psychic anxiety than placebo in patients with major depression or depressed bipolar disorder with or without melancholia."

Although, this doesn't make it good cure for a hangover, combining it with alcohol is a very bad idea.

[Logic]

http://www.longecity...sm-supplements/

 

http://www.longecity...heavy-drinking/

 

Edited by Logic, 18 February 2016 - 12:34 PM.

[GoingPrimal]

Look into butyrate - I've been using it with great success. My n=1 is that it completely annihilates the urge to drink - you still can if you so incline, but that incessant voice in the back of your head telling you to gets muted.

 

I've also noticed that it usually prevents me from wanting to continue drinking. I used to go out and after two drinks, would usually compulsively imbibe 3-4 more. After using butyrate, I can sip on two drink for 4 hours and be content.

 

It also appears to be effective for reducing cravings for amphetamines, cocaine and nicotine, but not opiates.

 

 

The histone deacetylase inhibitor sodium butyrate decreases excessive ethanol intake in dependent animals.

 

Here it is on Amazon. Don't send any money, use it to stock up on butyrate. 1 pill three times a day has worked well, currently experimenting with higher doses.

[Fred C. Dobbs]

Cravings

 

The prescription drug Naltrexone eliminates alcohol cravings for some users like flippiing a switch. It is an opioid receptor antagonist. It is not habit-forming. It does not induce nausea if you drink alcohol. It has minimal side effects. It is cheap and easily available in the U.S. with a prescription.

https://en.wikipedia...wiki/Naltrexone

http://www.webmd.com...naltrexone oral

http://www.drugs.com...dependence.html

http://www.ncbi.nlm....term=naltrexone

http://www.theatlant.../#disqus_thread

https://www.google.c...Sinclair Method

http://www.amazon.co...customerReviews
http://www.amazon.co...customerReviews

 

Naltrexone does not work for everyone. Here are some alternative prescription options:
https://en.wikipedia...iki/Acamprosate
https://en.wikipedia.org/wiki/Baclofen
https://en.wikipedia.../wiki/Nalmefene

 

If none of that works for cravings, a hard to get option is Ibogaine. It is not legal in the U.S. because it is a hallucinogen, but it is legal in Mexico, Canada, Bahamas, and Costa Rica, which are relatively easy access. You need to be in somewhat good physical health to use it because it is a rough "trip." Some users report elimination of cravings after one "trip" on Ibogaine. It is not addictive. Some of the clinics that offer this therapy appear to be sketchy, and some are legit clinics.

https://en.wikipedia.org/wiki/Ibogaine

Example providers for reference (this is in no way an endorsement):

http://ibeginagain.org/
http://bahamianoasis.org/ibo/
http://ibogainebahamas.com/

 

Brain Damage

 

High alcohol consumption and/or malnutrition depletes thiamine in a huge way, causing a dementia that is called by several names, such as "Alcohol-related dementia (ARD)" and "Wernicke–Korsakoff syndrome." This type of dementia mimics Alzheimer's, but it will stop progressing or reverse when thiamine is restored.

 

Ordinary Thiamine is not well-absorbed orally. It is therefore given intravenously (200mg, three times per day) in the form of a "banana bag." A synthetic thiamine called "Benfotiamine" is well-absorbed orally, but it does not significantly increase thiamine in the brain. A synthetic thiamine called "Sulbutiamine" is well-absorbed orally and crosses the blood brain barrier. Sulbutiamine is also used as a smart drug by people without thiamine deficiency. Typical dosage is 400-1000 mg per day. Sulbutiamine is cheap and easy to get, so it is worth a try.

https://en.wikipedia...ki/Sulbutiamine

https://en.wikipedia...elated_dementia

https://en.wikipedia...sakoff_syndrome

 

 

 

 

 

[normalizing]

this is related; http://www.medicalne...cles/305996.php

[kpavel]

Look into butyrate - I've been using it with great success. My n=1 is that it completely annihilates the urge to drink - you still can if you so incline, but that incessant voice in the back of your head telling you to gets muted.

 

I've also noticed that it usually prevents me from wanting to continue drinking. I used to go out and after two drinks, would usually compulsively imbibe 3-4 more. After using butyrate, I can sip on two drink for 4 hours and be content.

 

It also appears to be effective for reducing cravings for amphetamines, cocaine and nicotine, but not opiates.

 

 

The histone deacetylase inhibitor sodium butyrate decreases excessive ethanol intake in dependent animals.

 

Here it is on Amazon. Don't send any money, use it to stock up on butyrate. 1 pill three times a day has worked well, currently experimenting with higher doses.

 

COOL, that is why things like curcumin are mentioned helpful.)

 

 

Protective effect of quercetin on alcohol abstinence-induced anxiety and convulsions.

Chronic administration of ethanol (2 g/kg, p.o.) on days 1-6 and its withdrawal produced an anxiogenic reaction in mice as assessed in the mirrored-chamber test. Daily administration of quercetin (25 or 50 mg/kg, p.o.) prior to ethanol for 6 days prevented withdrawal-induced anxiety in mice. However, acute administration of a single dose of quercetin (50 mg/kg) to animals withdrawn from ethanol, i.e., on day 7, did not prevent withdrawal-induced anxiety. Ethanol withdrawal also induced a significant increase in the locomotor activity of mice indicating an anxiogenic response. Daily administration of quercetin (25 or 50 mg/kg, p.o.) prior to ethanol for 6 days prevented withdrawal-induced increased locomotor activity. Ethanol withdrawal also sensitized the convulsogenic reaction to pentylenetetrazole (PTZ). A non-convulsive dose (40-60 mg/kg) of PTZ produced full-blown convulsions and increased mortality in ethanol-withdrawn mice. Both acute and chronic administration of quercetin (25 or 50 mg/kg, p.o.) produced a significant protection against ethanol withdrawal-induced reduction in PTZ threshold in mice. The result suggests the protective effect of this safe drug, quercetin, in the management of ethanol withdrawal reactions.

 

[bootdoc]

Cravings

 

The prescription drug Naltrexone eliminates alcohol cravings for some users like flippiing a switch. It is an opioid receptor antagonist. It is not habit-forming. It does not induce nausea if you drink alcohol. It has minimal side effects. It is cheap and easily available in the U.S. with a prescription.

https://en.wikipedia...wiki/Naltrexone

http://www.webmd.com...naltrexone oral

http://www.drugs.com...dependence.html

http://www.ncbi.nlm....term=naltrexone

http://www.theatlant.../#disqus_thread

https://www.google.c...Sinclair Method

http://www.amazon.co...customerReviews
http://www.amazon.co...customerReviews

 

Naltrexone does not work for everyone. Here are some alternative prescription options:
https://en.wikipedia...iki/Acamprosate
https://en.wikipedia.org/wiki/Baclofen
https://en.wikipedia.../wiki/Nalmefene

 

If none of that works for cravings, a hard to get option is Ibogaine. It is not legal in the U.S. because it is a hallucinogen, but it is legal in Mexico, Canada, Bahamas, and Costa Rica, which are relatively easy access. You need to be in somewhat good physical health to use it because it is a rough "trip." Some users report elimination of cravings after one "trip" on Ibogaine. It is not addictive. Some of the clinics that offer this therapy appear to be sketchy, and some are legit clinics.

https://en.wikipedia.org/wiki/Ibogaine

Example providers for reference (this is in no way an endorsement):

http://ibeginagain.org/
http://bahamianoasis.org/ibo/
http://ibogainebahamas.com/

 

Brain Damage

 

High alcohol consumption and/or malnutrition depletes thiamine in a huge way, causing a dementia that is called by several names, such as "Alcohol-related dementia (ARD)" and "Wernicke–Korsakoff syndrome." This type of dementia mimics Alzheimer's, but it will stop progressing or reverse when thiamine is restored.

 

Ordinary Thiamine is not well-absorbed orally. It is therefore given intravenously (200mg, three times per day) in the form of a "banana bag." A synthetic thiamine called "Benfotiamine" is well-absorbed orally, but it does not significantly increase thiamine in the brain. A synthetic thiamine called "Sulbutiamine" is well-absorbed orally and crosses the blood brain barrier. Sulbutiamine is also used as a smart drug by people without thiamine deficiency. Typical dosage is 400-1000 mg per day. Sulbutiamine is cheap and easy to get, so it is worth a try.

https://en.wikipedia...ki/Sulbutiamine

https://en.wikipedia...elated_dementia

https://en.wikipedia...sakoff_syndrome

 

Naltrexone is dosed at 50 mg/day

Acamporsate is dosed at 666mg 3x a day.

 

Acamporsate blocks cravings.

 

Naltrexone decreases the euphoria from alcohol as well.

 

You can combine both - Natrexone at 50 mg/day, and acamporsate at 333mg 3 x a day- naltrexone will increase acomporsate levels.

 

Good luck.

 

Drinking on naltrexone- Sinclair method.
 

[zorba990]

Look into butyrate - I've been using it with great success. My n=1 is that it completely annihilates the urge to drink - you still can if you so incline, but that incessant voice in the back of your head telling you to gets muted.

I've also noticed that it usually prevents me from wanting to continue drinking. I used to go out and after two drinks, would usually compulsively imbibe 3-4 more. After using butyrate, I can sip on two drink for 4 hours and be content.

It also appears to be effective for reducing cravings for amphetamines, cocaine and nicotine, but not opiates.

The histone deacetylase inhibitor sodium butyrate decreases excessive ethanol intake in dependent animals.

Here it is on Amazon. Don't send any money, use it to stock up on butyrate. 1 pill three times a day has worked well, currently experimenting with higher doses.

Very interesting! Does this imply gut disbiosis as a causative factor?
I've only seen info on protective mechanisms
http://www.ncbi.nlm....00/#!po=14.0625

[GoingPrimal]

 

Look into butyrate - I've been using it with great success. My n=1 is that it completely annihilates the urge to drink - you still can if you so incline, but that incessant voice in the back of your head telling you to gets muted.

I've also noticed that it usually prevents me from wanting to continue drinking. I used to go out and after two drinks, would usually compulsively imbibe 3-4 more. After using butyrate, I can sip on two drink for 4 hours and be content.

It also appears to be effective for reducing cravings for amphetamines, cocaine and nicotine, but not opiates.

The histone deacetylase inhibitor sodium butyrate decreases excessive ethanol intake in dependent animals.

Here it is on Amazon. Don't send any money, use it to stock up on butyrate. 1 pill three times a day has worked well, currently experimenting with higher doses.

Very interesting! Does this imply gut disbiosis as a causative factor?
I've only seen info on protective mechanisms
http://www.ncbi.nlm....00/#!po=14.0625

 

 

I'm not qualified to say, but it seems that sodium butyrate works for addiction at least partially through interacting with FosB.

[medievil]

I willinclude both medications and supplements as i  never excludeany working interventions

 

ote

Combined Pharmacotherapies and Behavioral Interventions for Alcohol DependenceThe COMBINE Study: A Randomized Controlled Trial FREE

Raymond F. Anton, MD; Stephanie S. O’Malley, PhD; Domenic A. Ciraulo, MD; Ron A. Cisler, PhD; David Couper, PhD; Dennis M. Donovan, PhD; David R. Gastfriend, MD; James D. Hosking, PhD; Bankole A. Johnson, MD, PhD; Joseph S. LoCastro, PhD; Richard Longabaugh, EdD; Barbara J. Mason, PhD; Margaret E. Mattson, PhD; William R. Miller, PhD; Helen M. Pettinati, PhD; Carrie L. Randall, PhD; Robert Swift, MD; Roger D. Weiss, MD; Lauren D. Williams, MD; Allen Zweben, DSW; for the COMBINE Study Research Group

[+] Author Affiliations

JAMA. 2006;295(17):2003-2017. doi:10.1001/jama.295.17.2003.Text Size: A A A

 

 

Article

 

Figures

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Anchor

ABSTRACT

ABSTRACT | METHODS | RESULTS | COMMENT | ARTICLE INFORMATION |REFERENCES

 

Context Alcohol dependence treatment may include medications, behavioral therapies, or both. It is unknown how combining these treatments may impact their effectiveness, especially in the context of primary care and other nonspecialty settings.

 

Objectives To evaluate the efficacy of medication, behavioral therapies, and their combinations for treatment of alcohol dependence and to evaluate placebo effect on overall outcome.

 

Design, Setting, and Participants Randomized controlled trial conducted January 2001-January 2004 among 1383 recently alcohol-abstinent volunteers (median age, 44 years) from 11 US academic sites with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, diagnoses of primary alcohol dependence.

 

Interventions Eight groups of patients received medical management with 16 weeks of naltrexone (100 mg/d) or acamprosate (3 g/d), both, and/or both placebos, with or without a combined behavioral intervention (CBI). A ninth group received CBI only (no pills). Patients were also evaluated for up to 1 year after treatment.

 

Main Outcome Measures Percent days abstinent from alcohol and time to first heavy drinking day.

 

Results All groups showed substantial reduction in drinking. During treatment, patients receiving naltrexone plus medical management (n = 302), CBI plus medical management and placebos (n = 305), or both naltrexone and CBI plus medical management (n = 309) had higher percent days abstinent (80.6, 79.2, and 77.1, respectively) than the 75.1 in those receiving placebos and medical management only (n = 305), a significant naltrexone × behavioral intervention interaction (P = .009). Naltrexone also reduced risk of a heavy drinking day (hazard ratio, 0.72; 97.5% CI, 0.53-0.98; P = .02) over time, most evident in those receiving medical management but not CBI. Acamprosate showed no significant effect on drinking vs placebo, either by itself or with any combination of naltrexone, CBI, or both. During treatment, those receiving CBI without pills or medical management (n = 157) had lower percent days abstinent (66.6) than those receiving placebo plus medical management alone (n = 153) or placebo plus medical management and CBI (n = 156) (73.8 and 79.8, respectively; P<.001). One year after treatment, these between-group effects were similar but no longer significant.

 

Conclusions Patients receiving medical management with naltrexone, CBI, or both fared better on drinking outcomes, whereas acamprosate showed no evidence of efficacy, with or without CBI. No combination produced better efficacy than naltrexone or CBI alone in the presence of medical management. Placebo pills and meeting with a health care professional had a positive effect above that of CBI during treatment. Naltrexone with medical management could be delivered in health care settings, thus serving alcohol-dependent patients who might otherwise not receive treatment.

 

 

 

Que

Pharmacotherapy for Adults With Alcohol Use Disorders in Outpatient SettingsA Systematic Review and Meta-analysis FREE

Daniel E. Jonas, MD, MPH1,2; Halle R. Amick, MSPH2; Cynthia Feltner, MD, MPH1,2; Georgiy Bobashev, PhD3; Kathleen Thomas, PhD2; Roberta Wines, MPH2; Mimi M. Kim, PhD4,5; Ellen Shanahan, MA2; C. Elizabeth Gass, MPH1; Cassandra J. Rowe, BA6; James C. Garbutt, MD7,8

[+] Author Affiliations

JAMA. 2014;311(18):1889-1900. doi:10.1001/jama.2014.3628.Text Size: A A A

 

 

Article

 

Figures

Tables

 

Supplemental Content

References

 

 

CME

 

 

Anchor

ABSTRACT

ABSTRACT | METHODS | RESULTS | DISCUSSION | CONCLUSIONS | ARTICLE INFORMATION | REFERENCES

 

Importance  Alcohol use disorders cause substantial morbidity and early mortality yet remain greatly undertreated. Medications are considerably underused.

 

Objective  To conduct a systematic review and meta-analysis of the benefits and harms of medications (US FDA-approved and others) for adults with alcohol use disorders.

 

Data Sources  PubMed, Cochrane Library, PsycINFO, CINAHL, EMBASE, FDA website, and clinical trials registries (January 1, 1970, to March 1, 2014).

 

Study Selection  Two reviewers selected randomized clinical trials (RCTs) with at least 12 weeks’ duration that reported eligible outcomes and head-to-head prospective cohort studies reporting health outcomes or harms.

 

Data Extraction and Synthesis  We conducted meta-analyses using random-effects models and calculated numbers needed to treat for benefit (NNTs) or harm (NNHs).

 

Main Outcomes and Measures  Alcohol consumption, motor vehicle crashes, injuries, quality of life, function, mortality, and harms.

 

Results  We included 122 RCTs and 1 cohort study (total 22 803 participants). Most assessed acamprosate (27 studies, n = 7519), naltrexone (53 studies, n = 9140), or both. The NNT to prevent return to any drinking for acamprosate was 12 (95% CI, 8 to 26; risk difference [RD], −0.09; 95% CI, −0.14 to −0.04) and was 20 (95% CI, 11 to 500; RD, −0.05; 95% CI, −0.10 to −0.002) for oral naltrexone (50 mg/d). The NNT to prevent return to heavy drinking was 12 (95% CI, 8 to 26; RD −0.09; 95% CI, −0.13 to −0.04) for oral naltrexone (50 mg/d). Meta-analyses of trials comparing acamprosate to naltrexone found no statistically significant difference between them for return to any drinking (RD, 0.02; 95% CI, −0.03 to 0.08) or heavy drinking (RD, 0.01; 95% CI, −0.05 to 0.06). For injectable naltrexone, meta-analyses found no association with return to any drinking (RD, −0.04; 95% CI, −0.10 to 0.03) or heavy drinking (RD, −0.01; 95% CI, −0.14 to 0.13) but found an association with reduction in heavy drinking days (weighted mean difference [WMD], −4.6%; 95% CI, −8.5% to −0.56%). Among medications used off-label, moderate evidence supports an association with improvement in some consumption outcomes for nalmefene (heavy drinking days per month: WMD, −2.0; 95% CI, −3.0 to −1.0; drinks per drinking day: WMD, −1.02; 95% CI, −1.77 to −0.28) and topiramate (% heavy drinking days: WMD, −9.0%; 95% CI, −15.3% to −2.7%; drinks per drinking day: WMD, −1.0; 95% CI, −1.6 to −0.48). For naltrexone and nalmefene, NNHs for withdrawal from trials due to adverse events were 48 (95% CI, 30 to 112) and 12 (95% CI, 7 to 50), respectively; risk was not significantly increased for acamprosate or topiramate.

 

Conclusions and Relevance  Both acamprosate and oral naltrexone were associated with reduction in return to drinking. When directly compared with one another, no significant differences were found between acamprosate and naltrexone for controlling alcohol consumption. Factors such as dosing frequency, potential adverse events, and availability of treatments may guide medication choice.

 

 

Alcohol use disorders (AUDs) are common, cause substantial morbidity, and result in 3-fold increased rates of early mortality (eTable 1 in the Supplement).1- 8 Treating AUDs is difficult but may be aided by using medications. Pharmacotherapy for AUDs was initiated in the 1950s and consisted only of disulfiram (Antabuse). In the 1990s, naltrexone (oral and intramuscular formulations) and acamprosate were approved by the US Food and Drug Administration (FDA) (eTable 2 in the Supplement).

 

 

Fewer than one-third of patients with AUDs receive treatment,6 and only a small percentage (<10%) receive medications to assist in reducing alcohol consumption. To evaluate the benefits and harms of medications for the treatment of adults with AUDs, we conducted a systematic review. A larger, more comprehensive technical report for the Agency for Healthcare Research and Quality was prepared (eTable 3 in theSupplement).9 This article summarizes findings from the larger report on the efficacy of various medications used for the treatment of AUDs in reducing alcohol intake or improving health outcomes and on the adverse effects of these medications.

 

 

ote

Alcohol Alcohol. 2013 Nov-Dec;48(6):687-93. doi: 10.1093/alcalc/agt053. Epub 2013 Jun 28.

Combining medical treatment and CBT in treating alcohol-dependent patients: effects on life quality and general well-being.

Laaksonen E1, Vuoristo-Myllys S, Koski-Jannes A, Alho H.

Author information

 

Abstract

AIMS:

The aim of the study was to examine how the combination of medication and a brief cognitive behavioral intervention for alcohol dependency can affect patients' quality of life (QL), symptoms of depression and smoking habits.

METHODS:

We conducted a randomized, open-label, multicenter naturalistic study for 243 voluntary-treatment-seeking alcohol-dependent adult outpatients in two phases: first, 12 weeks with continuous medication followed by targeted medication for up to 52 weeks, and second, a follow-up period of 67 weeks (altogether 2.5 years). The subjects were randomized 1:1:1 to receive supervised naltrexone, acamprosate or disulfiram, plus a brief manual-based cognitive behavioral intervention (CBT).

RESULTS:

All three study groups showed a significant reduction in drinking from baseline to the end of the study. In the QL test EQ-5D, patients exhibited significant positive changes in sleeping, action, pain and mood dimensions. Severity of depression decreased during the whole study. Smoking decreased more in the disulfiram group than in the naltrexone and acamprosate groups.

CONCLUSION:

A combination of medical treatment (naltrexone, acamprosate or disulfiram) with the CBT-booklet (patient guide) appears to help reduce patients' symptoms of depression and improve their QL. Treatment is also associated with success at quitting smoking, especially among patients using disulfiram.

Quote

Pellagrous encephalopathy presenting as alcohol withdrawal delirium: a case series and literature review.

Oldham MA1, Ivkovic A.

Author information

 

Abstract

BACKGROUND:

Alcohol withdrawal delirium (AWD) is associated with significant morbidity and mortality. Pellagra (niacin deficiency) can be a cause of delirium during alcohol withdrawal that may often be overlooked.

OBJECTIVES:

We present a three-patient case series of pellagrous encephalopathy (delirium due to pellagra) presenting as AWD.

METHODS:

We provide a brief review of pellagra's history, data on pellagra's epidemiology, and discuss pellagra's various manifestations, particularly as related to alcohol withdrawal. We conclude by providing a review of existing guidelines on the management of alcohol withdrawal, highlighting that they do not include pellagrous encephalopathy in the differential diagnosis for AWD.

RESULTS:

Though pellagra has been historically described as the triad of dementia, dermatitis, and diarrhea, it seldom presents with all three findings. The neurocognitive disturbance associated with pellagra is better characterized by delirium rather than dementia, and pellagra may present as an isolated delirium without any other aspects of the triad.

DISCUSSION:

Although endemic pellagra is virtually eradicated in Western countries, it continues to present as pellagrous encephalopathy in patients with risk factors for malnutrition such as chronic alcohol intake, homelessness, or AIDS. It may often be mistaken for AWD. Whenever pellagra is suspected, treatment with oral nicotinamide (100 mg three times daily for 3-4 weeks) prior to laboratory confirmation is recommended as an inexpensive, safe, and potentially life-saving intervention.

Qote

Alcohol Alcohol. 2013 Jan-Feb;48(1):88-92. doi: 10.1093/alcalc/ags120. Epub 2012 Nov 16.

Supplementary thiamine is still important in alcohol dependence.

Rees E1, Gowing LR.

Author information

 

Abstract

AIMS:

To assess the effect of mandatory thiamine enrichment of wheat flour on blood thiamine levels in an alcohol-dependent population.

METHODS:

Alcohol-dependent clients (n = 100) entering an inpatient service for the management of alcohol withdrawal had thiamine blood tests and diet interviews. Approximately half (n = 46) the alcohol-dependent participants reported taking vitamin supplements prior to admission. Standard treatment included thiamine supplementation in the form of an intramuscular injection and 100 mg tablets. If consent was gained, a second thiamine blood test was taken prior to discharge (n = 77). Control participants (n = 20) with no history of treatment for alcohol abuse had thiamine blood tests and diet interviews.

RESULTS:

Control participants consumed significantly larger amounts of thiamine in their diet compared with alcohol-dependent participants (P < 0.0001). Alcohol-dependent participants who reported no use of vitamin supplements had significantly lower (P < 0.05) blood thiamine levels compared with controls, whereas controls and those who reported using vitamin supplements had no significant difference. No significant correlation was found between thiamine blood levels and reported levels of alcohol consumption.

CONCLUSION:

Reduced blood levels of thiamine in people who are alcohol dependent, compared with those with no history of alcohol abuse, are likely to be because of the poor diet. Consumption of vitamin supplements appears to bring thiamine levels closer to those seen in control participants. Supplementation of dietary intake of thiamine in people who are alcohol dependent remains an important measure for the prevention of Wernicke-Korsakoff's syndrome in this population.

PMID:

 

23161892

 

[PubMed - indexed for MEDLINE] 

Free full te

Qute

Coll Antropol. 2011 Dec;35(4):1225-30.

The use of a food supplementation with D-phenylalanine, L-glutamine and L-5-hydroxytriptophan in the alleviation of alcohol withdrawal symptoms.

Jukić T1, Rojc B, Boben-Bardutzky D, Hafner M, Ihan A.

Author information

 

Abstract

We described the use of a food supplementation with D-phenylalanine, L-glutamine and L-5-hydroxytriptophan in the alleviation of alcohol withdrawalsymptoms in patients starting a detoxification therapy. Since abstinence from ethanol causes a hypodopaminergic and a hypoopioidergic environment in the reword system circuits, manifesting with withdrawal symptoms, food supplements that contains D-phenylalanine a peptidase inhibitor (of opioide inactivation) and L-amino-acids (for dopamine synthesis) were used to replenish a lack in neurotransmitters and alleviate the symptoms of alcohol withdrawal. 20 patients suffering from alcohol addictions starting a detoxification therapy have been included in a prospective, randomized, double blind study. The patients have been randomly devided in two groups. One group recieved for a period of 40 days a food supplement containing D-phenylalanine, L-glutamine and L-5-hydroxytriptophan (investigation group), and the control (placebo) group. On the first day of hospitalization the patients performed a SCL-90-R test, and blood samples were taken for measuring liver enzymes, total bilirubin, unbound cortisol and lymphocyte populations. The same was done on the 40th day of hospitalization. During the therapy a significant decrease in SCL-90-R psychiatric symptoms scores and a significant increase in CD4 lymphocyte count was observed in the investigation group. The cortisol values were significantly, but equally decreased in both groups, the same was with the liver enzymes and the total bilirubin values. We conclude that abstinence causes a major stress for the patients. The use of food supplement containing D-phenylalanine, L-glutamine and L-5-hydroxytriptophan alleviates thewithdrawal symptoms and causes a rise in CD4 lymphocyte population, but it dose not affect the serum cortisol levels, which are probably more affected by liver inflammation and the liver restitution.

Coll Antropol. 2011 Dec;35(4):1225-30.

The use of a food supplementation with D-phenylalanine, L-glutamine and L-5-hydroxytriptophan in the alleviation of alcohol withdrawal symptoms.

Jukić T1, Rojc B, Boben-Bardutzky D, Hafner M, Ihan A.

Author information

 

Abstract

We described the use of a food supplementation with D-phenylalanine, L-glutamine and L-5-hydroxytriptophan in the alleviation of alcohol withdrawalsymptoms in patients starting a detoxification therapy. Since abstinence from ethanol causes a hypodopaminergic and a hypoopioidergic environment in the reword system circuits, manifesting with withdrawal symptoms, food supplements that contains D-phenylalanine a peptidase inhibitor (of opioide inactivation) and L-amino-acids (for dopamine synthesis) were used to replenish a lack in neurotransmitters and alleviate the symptoms of alcohol withdrawal. 20 patients suffering from alcohol addictions starting a detoxification therapy have been included in a prospective, randomized, double blind study. The patients have been randomly devided in two groups. One group recieved for a period of 40 days a food supplement containing D-phenylalanine, L-glutamine and L-5-hydroxytriptophan (investigation group), and the control (placebo) group. On the first day of hospitalization the patients performed a SCL-90-R test, and blood samples were taken for measuring liver enzymes, total bilirubin, unbound cortisol and lymphocyte populations. The same was done on the 40th day of hospitalization. During the therapy a significant decrease in SCL-90-R psychiatric symptoms scores and a significant increase in CD4 lymphocyte count was observed in the investigation group. The cortisol values were significantly, but equally decreased in both groups, the same was with the liver enzymes and the total bilirubin values. We conclude that abstinence causes a major stress for the patients. The use of food supplement containing D-phenylalanine, L-glutamine and L-5-hydroxytriptophan alleviates thewithdrawal symptoms and causes a rise in CD4 lymphocyte population, but it dose not affect the serum cortisol levels, which are probably more affected by liver inflammation and the liver restitution.

 

Anesth Analg. 2004 Mar;98(3):738-44, table of contents.

Intrathecal and oral clonidine as prophylaxis for postoperative alcohol withdrawal syndrome: a randomized double-blinded study.

Dobrydnjov I1, Axelsson K, Berggren L, Samarütel J, Holmström B.

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Abstract

In this study, we evaluated the effect of intrathecal and oral clonidine as supplements to spinal anesthesia with lidocaine in patients at risk of postoperative alcohol withdrawal syndrome (AWS). We hypothesized that clonidine would have a prophylactic effect on postoperative AWS. Forty-five alcohol-dependent patients (daily ethanol intake >60 g) scheduled for transurethral resection of the prostate were double-blindly randomized into three groups. All patients received hyperbaric lidocaine 100 mg intrathecally. The diazepam group (DiazG) was premedicated with diazepam 10 mg orally; the intrathecal clonidine group (Clon(i/t)G) received a placebo (saline) tablet and clonidine 150 microg intrathecally; and the oral clonidine group (Clon(p/o)G) received clonidine 150 microg orally. For patients diagnosed with AWS, the Clinical Institute Withdrawal Assessment for Alcohol, revised scale, was used. Twelve patients in the DiazG had symptoms of AWS, compared with two in the Clon(i/t)G and one in the Clon(p/o)G. The median Clinical Institute Withdrawal Assessment for Alcohol, revised scale, score was 12 in the DiazG versus 1 in the clonidine-treated groups. Two patients in the DiazG had severe delirium. Patients receiving oral clonidine had a slightly decreased mean arterial blood pressure 6-12 h after spinal anesthesia (P < 0.05); patients in the DiazG had a hyperdynamic circulatory reaction 24-72 h after surgery. In conclusion, preoperative clonidine 150 microg, intrathecally or orally, prevented significant postoperative AWS in ethanol-dependent patients.

IMPLICATIONS:

In this randomized, double-blinded study, clonidine 150 microg both intrathecally and orally prevented postoperative alcohol-withdrawal symptoms in alcohol-dependent men. The effect was superior to that with a single dose of diazepam 10 mg orally.

 

J Acupunct Meridian Stud. 2016 Feb;9(1):4-10. doi: 10.1016/j.jams.2015.05.007. Epub 2015 Jun 4.

Hypothalamic Norepinephrine Mediates Acupunctural Effects on Hypothalamic-Pituitary-Adrenal Axis DuringEthanol Withdrawal.

Zhao ZL1, Kim SC2, Zhang J1, Liu HF1, Lee BH2, Jang EY2, Lee CW2, Cho IJ2, An WG3, Yang CH2, Kim YW2, Zhao RJ4, Wu YY5.

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Abstract

A previous study demonstrated that acupuncture at ST36 (Zu-San-Li) attenuates ethanol withdrawal (EW)-induced hyperactivation of the hypothalamic-pituitary-adrenal axis in rats. The current study investigated the involvement of hypothalamic norepinephrine (NE) in that process. Rats were intraperitoneally treated with 3 g/kg/d of ethanol or saline for 28 days. After 24 hours of EW, acupuncture was applied to rats at bilateral ST36 points or at nonacupoints (tail) for 1 minute. A high-performance liquid chromatography analysis showed that EW significantly increased both the NE and the 3-methoxy-4-hydroxy-phenylglycol (MHPG) levels in the hypothalamic paraventricular nucleus (PVN). Western blot analysis also revealed that EW markedly elevated the phosphorylation rates of tyrosine hydroxylase (TH), but spared TH protein expression in the PVN. However, acupuncture at ST36, but not at nonacupoints, greatly inhibited the increase in the hypothalamic NE, MHPG, and phosphorylation rates of TH. Additionally, postacupuncture infusion of NE into the PVN significantly attenuated the inhibitory effects of acupuncture at ST36 on the oversecretion of plasma corticosterone during EW. These results suggest that acupuncture at ST36 inhibits EW-induced hyperactivation of the hypothalamic NEergic system to produce therapeutic effects on the hypothalamic-pituitary-adrenal axis.

Copyright © 2016. Published by Elsevier B.V.

[Ark]

Something different you might not have considered and treatment. http://grantome.com/...R01-AA018151-02

[Ark]

In conjunction with http://www.rxwiki.com/clonazepam and some strong will power.
I have a few other ideas, but I'll wait and see as to what you think of the above.

[Science+Nature]

Gabapentin is available with prescription.  It is commonly prescribed for alcoholism and anxiety that is associated with alcohol withdrawal.  I think the starting dosage is 300mg three times a day, it is metabolized by the kidneys not the liver.  As for supplements vitamin B complex and NAC.