Supplements to protect from negative alcoh...
Alien65
21 Jan 2008
wiserd
03 Nov 2008
The mixed cations help with absorption of high doses. Too much acid isn't healthy.
I've found it works better taken a while before bed, as my absorption slows then.
waldemar
12 Dec 2008
acid neutral ascorbate (vitamin C) helps remove almost any drug or chemical by upregulating glutathione. (even beneficial ones.) My favorite is c-salts.
The mixed cations help with absorption of high doses. Too much acid isn't healthy.
I've found it works better taken a while before bed, as my absorption slows then.
So, this implies that people taking vitamin c should increase some of the other supplements because of the reduced dosage, doesn't it? What about pure ascorbic acid, same effect?
yoyo
13 Dec 2008
3VeRL0ng
24 Mar 2009
hamishm00
26 Mar 2009
As far as brain damage go, who knows. You may be pleased to know that any damage is likely to be short-term anyway.
Barksdale
26 Mar 2009
I reckon Taurine, NAC, Milk Thistle and b6 is a pretty good pre-drink stack.
As far as brain damage go, who knows. You may be pleased to know that any damage is likely to be short-term anyway.
I'm gonna check that out, but isn't taurine dangerous?
VespeneGas
26 Mar 2009
I reckon Taurine, NAC, Milk Thistle and b6 is a pretty good pre-drink stack.
As far as brain damage go, who knows. You may be pleased to know that any damage is likely to be short-term anyway.
I'm gonna check that out, but isn't taurine dangerous?
No.
According to this the oral rat LD50 is 5000 mg per kg. If rat and human metabolisms were the same (they aren't) then it would take 340 GRAMS of taurine orally to kill a 150 pound person. I'm not sure how to do the dose conversion, but you get the picture.
Also, they've done studies on taurine for hypertension and diabetes where they used up to 6 grams per day with no nasty side effects.
Barksdale
27 Mar 2009
http://astronutritio...ess/liver-detox
I guess if I take enough Milk Thistle + C-Vitamin + Nac + Taurine that I will have a less irritating hangover:)
saddlesblazing
30 Mar 2009
maxwatt
30 Mar 2009
renwosing
01 Apr 2009
Ortho-Core should do the trick.
Renwosing
Rejuvena
29 Sep 2012
Too late for prevention and I knwo the old sayin, but is there some hope of repair and if so, could someone provide a list with possible dosages? 27 yr old female:(
Kevnzworld
29 Sep 2012
Sam E, 400 mg activated methionine
Silymarin , 500 mg, twice a day ( milk thistle )
PPC, polyunsaturated phosphatidyl choline
NAC , a precursor to glutathione , which protects the liver.
Lastly, drink water when you drink alcohol, and stay hydrated.
Edited by Kevnzworld, 29 September 2012 - 05:22 AM.
Dorian Grey
29 Sep 2012
Hepatol Res. 2006 Mar;34(3):199-206. Epub 2006 Jan 24.
A dual effect of N-acetylcysteine on acute ethanol-induced liver damage in mice.
Wang AL, Wang JP, Wang H, Chen YH, Zhao L, Wang LS, Wei W, Xu DX.
Department of Toxicology, Anhui Medical University, Hefei 230032, PR China; Toxicology Laboratory, Center for Disease Control of Anhui Province, Hefei 230032, PR China.
Abstract
Reactive oxygen species (ROS) have been associated with acute ethanol-induced liver damage. N-acetylcysteine (NAC) is a glutathione (GSH) precursor and direct antioxidant. In this study, we investigated the effects of NAC on acute ethanol-induced liver damage. Female ICR mice were administered by gavage with a single dose of ethanol (6g/kg). NAC was administered in two different modes. In mode A, mice were injected with different doses of NAC at 30min before ethanol. In mode B, mice were injected with different doses of NAC at 4h after ethanol. Acute ethanol-induced liver damage was estimated by measuring serum alanine aminotransferase (ALT) activity and histopathological changes. Result showed that a single dose of ethanol (6g/kg) caused a significant increase in serum ALT activity, followed by microvesicular steatosis and necrosis in mouse liver. Pretreatment with NAC significantly protected against acute ethanol-induced liver damage in a dose-independent manner. Correspondingly, pretreatment with NAC significantly attenuated acute ethanol-induced lipid peroxidation and GSH depletion and inhibited hepatic TNF-alpha mRNA expression. By contrast, post-treatment with NAC aggravated ethanol-induced hepatic lipid peroxidation and worsened acute ethanol-induced liver damage in a dose-dependent manner. Taken together, NAC has a dual effect on acute ethanol-induced liver damage. Pretreatment with NAC prevent from acute ethanol-induced liver damage via counteracting ethanol-induced oxidative stress. When administered after ethanol, NAC might behave as a pro-oxidant and aggravate acute ethanol-induced liver damage.
PMID: 16439183
---------------------------
SAM-e, B-Complex, Lecithin (eggs), and V-8 (potassium), Taurine, and Vitamin-C are yer best morning after "repair" tonics.
Edited by synesthesia, 29 September 2012 - 03:55 PM.
Dorian Grey
29 Sep 2012
Effect of genistein and quercetin on proliferation, collagen synthesis, and type I procollagen mRNA levels of rat hepatic stellate cells. PMID: 11749858
http://www.ncbi.nlm....pubmed/11749858
CONCLUSION: GE and QU inhibited hepatic stellate cell proliferation and collagen synthesis that might have a protective role against liver fibrosis.
-----------------------------
Study on antifibrotic effects of curcumin in rat hepatic stellate cells. PMID: 19152370 http://www.ncbi.nlm....pubmed/19152370
Our results suggest that curcumin exerted antifibrotic effects, possibly through two different mechanisms depending on its concentrations. At lower concentrations (1.25 approximately 10 microM), curcumin exerted antifibrogenic effects, whereas at higher concentrations (20 approximately 40 microM), curcumin exerted induction of apoptosis in HSCs.
--------------------------------------------
The antifibrogenic effect of epigallocatechin gallate results from the induction of de novo synthesis of glutathione in passaged rat hepatic stellate cells. PMID: 16682975
http://www.ncbi.nlm....pubmed/16682975
"our results, for the first time, demonstrate that the antioxidant property of EGCG derived from de novo synthesis of intracellular GSH plays a critical role in its antifibrogenic effect. These results provide novel insights into the mechanisms of EGCG as an antifibrogenic candidate in the prevention and treatment of liver fibrosis."
Cheers!
Dorian Grey
29 Sep 2012
Iron-dependent activation of NF-kappaB in Kupffer cells: a priming mechanism for alcoholic liver disease.
Xiong S, She H, Sung CK, Tsukamoto H.
Source
Department of Pathology, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA.
Abstract
"Alcoholic liver disease is associated with hepatic iron accumulation, and iron supplementation exacerbates alcoholic liver disease, suggesting the pathogenic role of iron in alcoholic liver disease.
We have tested a hypothesis that iron plays a signaling role in activation of redox-sensitive nuclear factor-kappa B (NF-kappaB and that increased iron content results in heightened expression of proinflammatory cytokines in Kupffer cells because of this signaling.
In cultured Kupffer cells isolated from normal rats, treatment with a lipophilic iron chelator, 1,2-dimethyl-3-hydroxypyrid-4-one (L1), markedly reduced lipopolysaccharide (LPS)-induced NF-kappaB activation and expression of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6.
Kupffer cells, isolated from rats with experimentally induced alcoholic liver disease, had significant increases in nonheme iron content, NF-kappaB binding, and mRNA expression for TNF-alpha and macrophage inflammatory protein-1. Ex vivo L1 treatment normalized all these parameters.
Addition of ferrous iron to cultured normal rat Kupffer cells increased I-kappa B kinase (IKK) activity at 15 min and NF-kappaB binding at 30 min. L1 pretreatment completely abrogated both effects. Moreover, the iron treatment increased TNF-alpha release and TNF-alpha promoter activity in a NF-kappaB-dependent manner.
Ferrous iron also transiently decreased cytoplasmic I-kappa B-alpha (IkappaB-alpha), with concomitant increases in nuclear p65 protein and DNA binding of p65/p50.
Taken together, these results support the existence of iron-dependent signaling for activation of IKK/NF-kappaB in Kupffer cells, and this iron signaling serves as a target for a potential priming effect for the pathogenesis of experimental alcoholic liver disease".
PMID: 12957294
-----------------------------------
Get Thee to a Blood Bank!
Edited by synesthesia, 29 September 2012 - 05:15 PM.
Dorian Grey
29 Sep 2012
Increased lipid peroxidation and impaired antioxidant enzyme function is associated with pathological liver injury in experimental alcoholic liver disease in rats fed diets high in corn oil and fish oil.
http://www.ncbi.nlm..../pubmed/9581686
Abstract
Increased hepatic oxidative stress with ethanol administration is hypothesized to be caused either by enhanced pro-oxidant production or decreased levels of antioxidants or both. We used the intragastric feeding rat model to assess the relationship between hepatic antioxidant enzymes and pathological liver injury in animals fed different dietary fats. Male Wistar rats (5 per group) were fed ethanol with either medium-chain triglycerides (MCTE), palm oil (PE), corn oil (CE), or fish oil (FE). Control animals were fed isocaloric amounts of dextrose instead of ethanol with the same diets. The following were evaluated in each group: liver pathology, lipid peroxidation, manganese superoxide dismutase (MnSOD) levels, copper-zinc SOD (CuZnSOD) levels, glutathione peroxidase (GPX) levels, and catalase (CAT) levels. All enzymes were evaluated using activity assays and immunoblots. Rats fed FE showed the most severe pathology (fatty liver, necrosis, and inflammation), those fed CE showed moderate changes, those fed PE showed fatty liver only, and those fed MCTE were normal. Parameters indicative of lipid peroxidation (conjugated dienes and thiobarbituric acid-reactive substances) were also greater in rat livers from animals fed the diets high in polyunsaturated fatty acids (CE and FE). CuZnSOD, GPX, and CAT activities showed an inverse correlation (r=-.92, P < .01) with severity of pathological injury, with the lowest levels for both enzymes found in FE-fed rats. Decreased enzyme activity in CE- and FE-fed rats was accompanied by similar decreases in immunoreactive protein. Ethanol administration did not cause significant decreases in enzyme activity in groups that showed no necroinflammatory changes (MCTE and PE). MnSOD activity showed no significant change in any ethanol-fed group. Our results show that decreases in CuZnSOD, GPX, and CAT occur in rats showing pathological liver injury and also having the highest levels of lipid peroxidation. These results suggest that feeding dietary substrates that enhance lipid peroxidation can exacerbate both ethanol-induced oxidative damage as well as necroinflammatory changes. The decrease in activity of antioxidant enzymes observed in animals fed diets high in polyunsaturated fatty acids and ethanol could possibly increase the susceptibility to oxidative damage and further contribute to ethanol-induced liver injury.
PMID: 9581686 [PubMed - indexed for MEDLINE]
Edited by synesthesia, 29 September 2012 - 04:48 PM.
Rejuvena
29 Sep 2012
Rejuvena
29 Sep 2012
niner
30 Sep 2012
And how does all that translate to skin? Liver regenerates, we know alcoholic brains regenerate after drinking cessation, weren't there any studies conducted on the way skin behaves and how to help it rejuvenate, ie - reverse the sag, dryness, ugly tone... Supps for that? Sometimes the effects of excessive partying to not appear overnight - once they appear can they be reversed at all? and I dont mean plastic surgery...:(
Skin is damaged in several different ways, the most important being UV light, with glycation, oxidation, and inflammation playing their part. Too much partying could contribute to oxidation, inflammation, and maybe glycation, as well as make you less able to deal with UV. So, what to do? You need a skin care regimen. We have a skin forum here, and there are a lot of good threads in there. There are some other forums on the net that are dedicated to skin care and beauty, and there is a lot of expertise there. Briefly, you'll want a good quality photostable UVA-blocking sunscreen, and you should use it 365 days a year. Most of a skin program is topicals- retinoids, alpha hydroxy acids, a vitamin C/E preparation, and niacinamide are some things to consider. There are a few oral supplements of note, such as silicon. (BioSil and JarrowSil are two that are commonly used). Gelatin and hyaluronic acid could be on the list. Another thing to think about is your diet. Diet has a big role in skin health and appearance. Avoid sugar, industrial seed oils, and refined carbohydrates. Eat lots of vegetables. Avoid things cooked at high temperatures, as they contain Advanced Glycation Endproducts that are highly inflammatory. Get some good olive oil and use it liberally.
Skin can definitely get better, but it takes time. It doesn't happen overnight.
ViolettVol
08 Oct 2012
Thanks for your answer,And how does all that translate to skin? Liver regenerates, we know alcoholic brains regenerate after drinking cessation, weren't there any studies conducted on the way skin behaves and how to help it rejuvenate, ie - reverse the sag, dryness, ugly tone... Supps for that? Sometimes the effects of excessive partying to not appear overnight - once they appear can they be reversed at all? and I dont mean plastic surgery...:(
Skin is damaged in several different ways, the most important being UV light, with glycation, oxidation, and inflammation playing their part. Too much partying could contribute to oxidation, inflammation, and maybe glycation, as well as make you less able to deal with UV. So, what to do? You need a skin care regimen. We have a skin forum here, and there are a lot of good threads in there. There are some other forums on the net that are dedicated to skin care and beauty, and there is a lot of expertise there. Briefly, you'll want a good quality photostable UVA-blocking sunscreen, and you should use it 365 days a year. Most of a skin program is topicals- retinoids, alpha hydroxy acids, a vitamin C/E preparation, and niacinamide are some things to consider. There are a few oral supplements of note, such as silicon. (BioSil and JarrowSil are two that are commonly used). Gelatin and hyaluronic acid could be on the list. Another thing to think about is your diet. Diet has a big role in skin health and appearance. Avoid sugar, industrial seed oils, and refined carbohydrates. Eat lots of vegetables. Avoid things cooked at high temperatures, as they contain Advanced Glycation Endproducts that are highly inflammatory. Get some good olive oil and use it liberally.
Skin can definitely get better, but it takes time. It doesn't happen overnight.
I was wondering about the HA supplements especially - I do already take biosil, just have to work on doing it regularly instead of just when I remember.:/
Back to hylauronic acid - any good supp brands to recommend that are known for best absorption?


