LIVER PROTECTORS- the list, don't run a cycle without them
- 06-17-2008, 02:28 PM
LIVER PROTECTORS- the list, don't run a cycle without them
I decided to list all the liver protectors I know , since a lot of guys here use a lot of methylated oral steroids I think they should never run a cycle without this baby's, health comes in a first place and its better safe than sorry so lets go:
1) SAMe- Only a few look at SAMe as a liver protector but this is one of the most important ones, the facts;
SAMe: The Liver Super- Nutrient
The evidence is definitely in. SAMe (S-adenosylmethionine) is serious medicine against liver disease. Almost a thousand published studies document the ability of this bioactive form of methionine to prevent and treat liver disorders, including cancer.
SAMe, the amazing "super-nutrient," can single-handedly normalize liver function. How? SAMe is the central player in liver biochemistry. It does two crucial things: It methylates, and it transforms itself into the liver's most vital substance, glutathione.
The liver contains the third highest amount of SAMe in the body, after the adrenal and pineal glands. SAMe is so important for liver function that it can be considered an essential nutrient for that organ. In addition to its many other functions, SAMe plays a leading role in liver regeneration. The liver has special SAMe enzymes just for regenerating tissue.
The liver has a tough job. It has to break down every chemical the body encounters, including drugs. It has to filter blood, chase after bacteria, make bile, and create various other substances such as lipoproteins. In short, there is a reason the liver is the only organ that readily regenerates: It has to.
SAMe is the product of a biochemical reaction between ATP and methionine. Half of all methionine in the body is used in the liver to make SAMe. SAMe has been compared to ATP in its importance for the body. It is used in many different cellular processes, from replication to biochemical reactions that create melatonin and phosphatidylcholine. SAMe is particularly important for the liver because glutathione is synthesized from it. Glutathione is crucial for liver function. A good portion of liver SAMe is turned into glutathione. Glutathione is the liver's natural antioxidant.
SAMe has been isolated from yeast and purified. It is currently sold in Europe as an antidepressant. Many clinical studies have been conducted with this supplemental form of SAMe. It has been used in trials against depression, osteoarthritis and other conditions. Of all the published studies, the ones on the liver are perhaps the most comprehensive.
The Liver Super-Nutrient
SAMe is the liver super-nutrient. Nothing comes close to providing the spectrum of health benefits that SAMe provides for the liver. Based on published clinical trials, elevating SAMe levels can have a powerful effect on many conditions. As a preventive agent, SAMe is so powerful that it can reverse the effects of chemicals and alcohol as they occur. Studies show that low SAMe levels create the conditions for liver cancer, and that SAMe can prevent these conditions from occurring. Anyone concerned about the effects of drugs, chemicals, alcohol and aging on their livers should look into the benefits of SAMe.
dosage required : 400mgs /day
2) NAC- everybody knows this one,N-acetylcysteine (NAC), which is used as a mucolytic agent in COPD and other diseases, was also found to be a powerful antioxidant, as a precursor of reduced glutathione, and a potential therapeutic agent in the treatment of diseases characterized by free radical and oxidant damage and a must have for sure,look at this study;
Patients who have had a recent heart attack, ulcerative colitis, or adult respiratory distress syndrome may be deficient in glutathione (GSH), an important protector of liver cells, red blood cells, and lymphocytes.
Lower glutathione levels in plasma and lung fluid have also been seen in patients with human immunodeficiency virus (HIV) infection. It is thought that low glutathione levels speed up the development of emphysema in HIV-positive patients, especially if they have a history of smoking. Patients who are co-infected with HIV and hepatitis C (HCV) have even further diminished levels of glutathione.
A new study by De Rosa and colleagues, published in the European Journal of Clinical Investigation, investigated the use of N-acetylcysteine (NAC), a mucolytic agent used to reduce the viscosity of mucus and to build up glutathione levels in HIV-positive patients. In an 8-week test, 31 patients received NAC and 30 received a placebo. Both groups began the study with low glutathione levels.
Results showed that the patients who received NAC had near-normal glutathione levels, whereas levels in the placebo group remained the same. No side effects were reported, although occasional dose reduction was necessary to diminish gastrointestinal effects.
Anti-HIV protease inhibitors are known to be toxic to the liver, especially in patients with both HIV and hepatitis, and the NAC results are therefore significant. In a study of 24 patients, interferon and NAC treatment reduced liver abnormalities better than interferon alone.
dosage required: 2000 mg ed
3) liv 52
dosage required: 9 tabs/day
4)milk thistle, sylmarin
dosage required: 1800 mg ed
everybody knows this 2 but if you have doubts check this link you got millions of studies to prove their efficacy:
one note on the milk thistle , some say it inder gains, where`s why:
Milk Thistle: Good for Livers, Potentially Bad for Gains
Title: Silymarin inhibits function of the androgen receptor by reducing nuclearlocalization of the receptor in the human prostate cancer cell line LNCaP.Authors: Zhu W, Zhang JS, Young CY.Source: Carcinogenesis 2001 Sep;22(9):1399-403
Agents with novel mechanisms of blocking androgen receptor (AR) function may be useful for prostate cancer prevention and therapy. Previous studies showed that silibinin (SB), the major active component of Milk Thistle, could inhibit cell proliferation of a human prostate cancer cell line by stopping the cell cycle without causing cell death. This study further demonstrates the potential molecular mechanism by which Milk Thistle acts on androgen-responsive prostate cancer cells by inhibiting function of the AR. We observed that Silymarin (SM) and SB inhibited androgen-stimulated cell proliferation as well as androgen-stimulated secretion of both prostate-specific antigen (PSA) and human glandular kallikrein (hK2).Additionally, for the first time, we show that SM and SB diminished transactivation activity of the AR. However, SM did not affect AR levels and steroid-binding ability of total AR in western blotting and ligand-binding assays. Intriguingly, we found that nuclear AR levels are significantly reduced by SM and SB in the presence of androgens. This study provides a new insight into how Milk Thistle negatively modulates androgen action in prostate cancer cells.
Milk Thistle is a popular bodybuilding supplement and is currently the most well researched plant for the treatment of liver disease (with over 450 published peer review papers). Silymarin, a flavonoid extract from Milk Thistle, has been used clinically for alcoholic liver disease treatment in Europe and Asia for almost 2,000 years. Currently it?s used by bodybuilders as a protective measure for the liver when using high doses of orals.Silymarin is not water soluble and is typically administered as an encapsulated standardized extract. The absorption with oral administration is rather low, with only two to three percent being effectively taken up. The peak plasma levels after an oral dose are achieved in four to six hours. The reason this study is significant is because of the described mechanism that Milk Thistle is working in the prostate. It is showing effectiveness in treating prostate cancer because it prevents the androgen receptor from making it to the nucleus of the cell. This may be good if you are fighting cancer of the prostate, but it is bad if you are trying to get a muscle cell to grow larger.In order for testosterone to work, it must pass from the blood to the inside of a muscle cell, bind to the androgen receptor inside the cell, then travel inside the nucleus where it binds to your DNA.These researchers were able to show that Milk Thistle did not reduce the number of androgen receptors, nor did it prevent androgens (i.e., testosterone) from binding to the receptors. All it seemed to do was prevent the androgen receptor from traveling to the nucleus, and in our case, this prevents the desired effect. The androgen receptor, once bound to the androgen, must make it to the nucleus in order to increase protein synthesis.Bottom line: Use Milk Thistle if you are sure you are having liver toxicity problems. Then, only use it for a few weeks at a time. There are other herbs with tremendous hepatoprotective effects, so you might give them a try instead.
As seen controversial to say the least, do your choice...
5) Tauroursodeoxycholic acid (TUDCA) - this is a relatively recent new liver aid , introduced in the market as a supplement by thermolife(LIVER LONGER) it looks like a very good help in preventing cholestasis, one of the major risk with 17 alkylated steroids:
TUDCA prevents cholestasis and canalicular damage induced by ischemia-reperfusion injury in the rat, modulating PKCα–ezrin pathway
Cholestasis, induced by liver ischemia-reperfusion injury (IRI), is characterized by dilatation of bile canaliculi and loss of microvilli. Tauroursodeoxycholic acid (TUDCA) is an anti-cholestatic agent, modulating protein kinase C (PKC) α pathway. PKC reduces ischemic damage in several organs, its isoform α modulates ezrin, a key protein in the maintenance of cell lamellipoidal extensions. We evaluated the effects of TUDCA on cholestasis, canalicular changes and PKCα–ezrin expression in a rat model of liver IRI. Livers flushed and stored with Belzer solution or Belzer + 10 mm TUDCA (4 °C for 6 h) were reperfused (37 °C with O2) with Krebs–Ringer bicarbonate + 2.5 μmol/min of Taurocholate or TUDCA. Bile was harvested for bile flow assessment. Liver tissue was employed for Electron Microscopy (EM) and for PKCα and ezrin immunoblot and immunofluorescence. The same experiments were conducted with the PKCα inhibitor Go-6976. TUDCA-treated livers showed increased bile flow (0.25 ± 0.17 vs. 0.042 ± 0.02 μl/min/g liver, P < 0.05) and better preservation of microvilli and bile canalicular area at EM. These effects were associated with increased PKCα and ezrin expression (P = 0.03 and P = 0.04 vs. control respectively), as also confirmed by immunofluorescence data. PKCα inhibition abolished these TUDCA effects. TUDCA administration during IRI reduces cholestasis and canalicular damage in the liver modulating PKCα–ezrin pathway.
dosage required: 2 X 250 mg ed with meals
6) Essential forte N - this is a otc(at least in europe) Multivitamins and phospholipids complex that really helps keeping the liver in shape when a steroid cycle its done, if money its not a problem put it on your arsenal:
Introduction. Androgenic-anabolic-steroids (AAS)-induced hepatotoxicity typically occurs with C-17 alkylated oral agents abused by exercising individuals at clinically recommended doses. Injectable compounds appear to have the same risk for hepatotoxicity, but are applied in doses three to six times higher than clinically recommended. AAS users occasionally try to avoid the well-known hepatotoxic effects associated with the abuse of a multitude of AAS agents, by using the pharmaceutical agent compound N a phospholipid/vitamin preparation. Primary Objective. The investigation of the actual hepatoprotective effect of compound N against AAS-induced toxicity. Methodology. This was an observational cohort study of 320 athletes; 160 were AAS users and the other 160 were not abusing any substances. Of the 160 users, 44 were using AAS and compound N (group A), and 116 were using solely AAS (group B). The 160 athletes abstaining from substances abuse acted as controls (group C). All athletes were tested for alterations in serum levels of hepatic enzymes. Enzyme levels before the study's onset and after the end of the 8-week AAS regimes were compared among the three groups, in order to delineate the hepatoprotective effect of compound N. Results. Prior to our research all groups showed normal values in all enzymes except creatine kinase (CK). After the 8-week period, CK levels were slightly lower in group A, but without variation in Groups B and C; γ-Glutamyl Transferase (γGT) levels remained normal. Groups A and C had no elevations in any of the enzymes, except CK, while in group B all enzymes' values were elevated above the normal range. The only factor differentiating AAS users in group A from those in group B was the use of compound N, thus the results being suggestive of the compound's detoxification effect. The severity of AAS abuse was positively associated with the degree of changes (Δ values) in all measured enzymes except γGT and CK. Conclusions. Previous suggestions that serum hepatic enzyme elevations in exercising AAS abusers are connected to muscle fiber damage rather than the abuse itself, are contradicted by our results. Since all AAS abusing athletes were prone to exhibit elevations in enzymes' values, the mean values of group A were to be similar to those observed in group B, exceeding normal values. The group hepatic enzyme values of group B were significantly higher than the group C (control). Notably, group A did not have any statistically significant difference in the hepatic enzyme values compared to group C. The effect of exercise on these enzymes' elevations was ruled out by the comparability of training regimens and AAS toxicity was correlated to the severity of AAS abuse.
Multivitamins and phospholipids complex protects t...[Clin Toxicol (Phila). 2008] - PubMed Result
dosage required: at least 2 caps 3 times day with meals
7) Sesamin- Cheap and as the following study show a liver protector:
Protective effects of sesamin against liver damage caused by alcohol or carbon tetrachloride in rodents.
The effects of sesamin, a potent inhibitor of delta 5-desaturase in polyunsaturated fatty acid biosynthesis, on the fatty acid compositions of tissue lipids and liver functions were examined in rodents. When a mixture of sesamin and episesamin (51.1:48.2, w/w) was given to rats at a dietary level of 0.5% for 13 days, the proportions of dihomo-gamma-linolenic acid significantly increased not only in the liver but also in plasma and hemocytes, suggesting an interference with delta 5-desaturation by these lignans. The sesamin preparation at the dietary level of 1% improved changes in various blood parameters of the mouse, such as aspartate aminotransferase and alanine aminotransferase activities, and the concentrations of total cholesterol, triglyceride and total bilirubin, caused by continuous inhalation of ethanol. In addition, sesamin showed a significant protective effect against the accumulation of fat droplets and vacuolar degeneration in the mouse liver, as confirmed on histological examination. Sesamin, at the level of 100 mg/kg body weight, also tended to prevent liver lipid accumulation by carbon tetrachloride in mice. These results indicate that sesamin and a related lignan compound have an ability to improve liver function.
Protective effects of sesamin against liver damage...[Ann Nutr Metab. 1993] - PubMed Result
dosage requeired :2000 mg ed
For me this are the magnificent 7 and if money its not a problem I`m sure your liver will thank you when you do your oral cycles...
- 06-17-2008, 02:41 PM
so according to your post, cycle support (which almost everyone on this board uses) is not good for gains, and we should be using other supps?
06-17-2008, 02:51 PM
I personally take at least 600 mg ed but I try not to overdose it...
06-17-2008, 04:48 PM
Good stuff Nunes!! I know Dinoiii has written alot about SAMe's benefits esp with these methylated orals. Gets overlooked alot by most, can be pricey but well worth it.
06-17-2008, 05:06 PM
Interesting read. Where did you get the dosage info for Liv-52? My bottle says 1-2 caps twice per day (450mg per cap.)
06-17-2008, 05:53 PM
06-17-2008, 06:55 PM
Soy Lecithin is also very good for your liver. Unfortunatly I'm at work and don't have the info to back that claim up.
06-17-2008, 07:17 PM
06-17-2008, 08:12 PM
06-17-2008, 08:29 PM
06-17-2008, 08:31 PM
Where's the alpha lipoic acid?????
The LORD is my rock, my fortress, and my savior; my God is my rock, in whom I find protection. He is my shield, the power that saves me, and my place of safety.-Psalm 18:2
06-17-2008, 08:33 PM
06-17-2008, 09:38 PM
06-17-2008, 09:42 PM
I've been on 400 mgs/day of SAMe for 3 months now. Will continue during my H-50/Methyl-E/3-AD cycle.
I really got on it for my joints. The liver abilities are a side benefit to me.
06-17-2008, 10:07 PM
Good stuff Nunes. Liv.52, Milk Thistle, & SAMe are all you need IMO. I've never been big on NAC. I've also heard dandelion extract is outstanding too, but I've never personally used it. This list could be potentially endless.
06-17-2008, 10:31 PM
I agree 100% with the ALA recommendation. It's truly an amazing anti-oxidant.
Nice job nunes!
Evolutionary Muse - Inspire to Evolve
06-18-2008, 12:17 PM
Thanks guys, as ziquor said the list can be endless but I tried to made a compilation of the most common given them the scientific backup.
When I was a newbie trying to find what was the best supps to a perfect cycle I saw a lot of post saying take this and take that but sometimes without explaining why, I tried to answer those questions trying to help people who is searching for a good liver protection and telling them why .
of course there are other good liver aids but with a few of the listed here I think people should be fine .
06-25-2008, 11:50 AM
06-25-2008, 05:52 PM
06-25-2008, 06:15 PM
OK guys since some of you were not satisfied with ALA omission, I decided to post this link:
Alpha Lipoic Acid and Liver Disease (Dec 2007) Townsend Letter for Doctors & Patients
There's some good information about ALA and the liver
Alpha-Lipoic Acid (ALA) is a powerful antioxidant that is produced naturally in the body and stimulates the production of glutathione (GSH). It is a compound that contains sulfur in the form of two thiol groups (a thiol consists of one sulfur and one hydrogen). Once inside the cells, ALA is converted to a more potent antioxidant, dihydrolipoic acid. Research has indicated that ALA, like Vitamin C is an effective water-soluble antioxidant protecting tissues such as the blood from dangerous free radicals. * It was also indicated that when ALA converts to dihydrolipoic acid, it is an effective fat-soluble antioxidant, like that of Vitamin E, protecting fatty tissues as well as membranes.* This unique quality makes ALA the most potent antioxidant because it offers protection against free radicals both inside and outside the cell. Other antioxidants may only provide extracellular protection. Its ability to increase GSH, recycle both fat and water soluble antioxidants and act as a powerful free radical scavenger, makes ALA a necessity for supporting overall immune and liver health.*
08-18-2008, 05:28 PM
08-19-2008, 01:33 AM
i personally loved TUDCA, its the ingredient in thermolife liver longer.
i did 7 weeks of 60mg dbol ED, and 100mg anadrol ED. i only used the recommended dosage for liver longer, and two days after my dbol/drol i got bloodwork done. my AST and ALT levels were both under 90. they were in the "slightly elevated" range. thats amazing considering my dosages of a simultaneous dbol/drol stack.
08-19-2008, 01:34 AM
08-19-2008, 03:54 PM
08-19-2008, 03:57 PM
Hmm i've never ran a cycle WITH liver protection.
That being said be sure to clarify that standardized milk thistle is key. A strong standardized milk thistle does not need to be dosed that high.
Also, IMO there isnt enough science to say milk thistle truly hinders gains.
Great post though
08-19-2008, 04:08 PM
what about just plain L gluthione???? seems very important, most things synthesize into it, or gluthione is depleted and needs to be regenerated.....
08-19-2008, 04:45 PM
supplementation of l glutathione
08-19-2008, 06:00 PM
08-20-2008, 01:04 AM
What about HepatoPro (Polyenylphosphatidylcholine)
1: Clin Toxicol (Phila). 2007 Aug 30;:1-10 [Epub ahead of print] Links
Multivitamins and phospholipids complex protects the hepatic cells from androgenic-anabolic-steroids-induced toxicity.
Introduction. Androgenic-anabolic-steroids (AAS)-induced hepatotoxicity typically occurs with C-17 alkylated oral agents abused by exercising individuals at clinically recommended doses. Injectable compounds appear to have the same risk for hepatotoxicity, but are applied in doses three to six times higher than clinically recommended. AAS users occasionally try to avoid the well-known hepatotoxic effects associated with the abuse of a multitude of AAS agents, by using the pharmaceutical agent compound N a phospholipid/vitamin preparation. Primary Objective. The investigation of the actual hepatoprotective effect of compound N against AAS-induced toxicity. Methodology. This was an observational cohort study of 320 athletes; 160 were AAS users and the other 160 were not abusing any substances. Of the 160 users, 44 were using AAS and compound N (group A), and 116 were using solely AAS (group B). The 160 athletes abstaining from substances abuse acted as controls (group C). All athletes were tested for alterations in serum levels of hepatic enzymes. Enzyme levels before the study's onset and after the end of the 8-week AAS regimes were compared among the three groups, in order to delineate the hepatoprotective effect of compound N. Results. Prior to our research all groups showed normal values in all enzymes except creatine kinase (CK). After the 8-week period, CK levels were slightly lower in group A, but without variation in Groups B and C; gamma-Glutamyl Transferase (gammaGT) levels remained normal. Groups A and C had no elevations in any of the enzymes, except CK, while in group B all enzymes' values were elevated above the normal range. The only factor differentiating AAS users in group A from those in group B was the use of compound N, thus the results being suggestive of the compound's detoxification effect. The severity of AAS abuse was positively associated with the degree of changes (Delta values) in all measured enzymes except gammaGT and CK. Conclusions. Previous suggestions that serum hepatic enzyme elevations in exercising AAS abusers are connected to muscle fiber damage rather than the abuse itself, are contradicted by our results. Since all AAS abusing athletes were prone to exhibit elevations in enzymes' values, the mean values of group A were to be similar to those observed in group B, exceeding normal values. The group hepatic enzyme values of group B were significantly higher than the group C (control). Notably, group A did not have any statistically significant difference in the hepatic enzyme values compared to group C. The effect of exercise on these enzymes' elevations was ruled out by the comparability of training regimens and AAS toxicity was correlated to the severity of AAS abuse. http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum
08-20-2008, 07:27 AM
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