Winstrol Cycle - Winsrol Stanozolol Cycle with Testosterone
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Boldenone (equipoise) in my humble opinion needs to be run 16 weeks unless you were to frontload it as to get to whatever hormone level your shooting for as soon as possible. I personally didnt know shit about frontloading properly with injectables in my younger years, so have no real world experience doing it properly, but i have frontloaded equipoise for this reason the last time i ran EQ, and I got super sick, I believe from frontloading it , and had to stop everything.
In any case, to be specific to your question, yes i think 16 weeks minimum if your going to use it the traditional way, which is weekly injections, and it takes a while to build up as you know. However i would love to hear some EQ Frontload success stories and ask how fast they were able to get to peak levels and how long they stayed on the EQ, as i think maybe 10 to 12 weeks is possible provided your able to get the boldenone hormone levels peaked and level sooner than you would with traditional methods as i touched on above.
As for long cycle runs with Stanozolol (winstrol, 17aa- injectable or oral) and how to protect and support a healthy liver I will list some solid choices below this post:
Liver Support Agents S-adenosylmethionine and N-acetylcysteine (NAC) Especially Important During Oral / Injectable Steroid Cycles
(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
SAM-e Promotes Liver Health
The liver is unique because it is the only internal human organ capable of regenerating itself. As little as 25% of a liver can regenerate into a whole liver again, and SAM-e plays a leading role in that regeneration. The third highest amount of SAM-e in the body is found in the liver. Only the adrenal and pineal glands contain more.
SAM-e is thought to be beneficial for those with liver disease by acting as a precursor of antioxidant glutathione; repairing the mitochondrial glutathione transport system; inhibiting the toxic effects of proinflammatory cytokines; and increasing DNA methylation.(7)
There are nearly a thousand published studies documenting SAM-e's ability to support prevention and improvement in liver disease.
• In a study of hepatic glutathione levels in patients with liver disease, participants were divided into four groups. Nine patients with alcoholic liver disease were given SAM-e; seven patients with non-alcoholic liver disease were given SAM-e; 8 patients with alcoholic liver disease were given a placebo; and 15 normal subjects served as a control group. Prior to beginning treatment, all patients had very low hepatic glutathione levels compared to controls. Following treatment, patients receiving the SAM-e had a significant increase in their hepatic glutathione levels compared with both the placebo-treated group and controls.(8)
• When SAM-e was given to 62 patients with alcoholic cirrhosis in a clinical trial, they were significantly less likely to die or require a liver transplant within the next two years, compared with 61 patients who had received a placebo.(9)
SAM-e Is Promising for Fibromyalgia Patients
Although SAM-e has not been studied yet as much for support of fibromyalgia patients as for those with some other illnesses, the results thus far are encouraging. In one double-blind study of 44 patients with primary fibromyalgia, improvements were seen in the areas of clinical disease activity, pain, fatigue, morning stiffness and mood.(10)
SAM-e's Role in Alzheimer's Disease
Since extremely low levels of SAM-e were found in the cerebrodpinal fluid and brain regions of Alzheimer's patients in a 1996 study, researchers are examining the potential benefits of supplemental SAM-e in Alzheimer's.(11) A recent study stated, “...our findings suggest that dietary supplementation with SAM... holds promise as a therapeutic approach to prevent or delay AD. A preliminary study indicates that SAM can provide some cognitive improvement in AD patients.”(12)
Facts About SAM-e You Need to Know
Dosage: Recommended therapeutic doses usually range between 400 – 1600 mg a day, although some individuals may require higher doses. Studies suggest that 400 mg per day may be adequate for osteoarthritis patients, while up to 1600 mg a day is often needed for mood support. The usual dose for those with liver disorders has been 1600 mg a day. (As with any addition to your health support regimen, supplementation with SAM-e should be considered only with the approval of your professional healthcare team.)
How to Take SAM-e: SAM-e works best when taken on an empty stomach. Because it is absorbed mainly in the intestine, enteric-coated tablets that allow it to pass through the stomach intact are preferable. Leave tablets in their foil or foil blister packs until you are ready to take them in order to maintain their stability.
Adverse Effects: There seem to be few adverse effects with SAM-e, even at high doses. Occasionally mild gastrointestinal distress has been reported. Since SAM-e can sometimes lead to insomnia, it is usually best to take it early in the morning. Because it plays a role in mood support, SAM-e may trigger manic episodes in people with bipolar disorder.
Contraindications: While there are no confirmed drug interactions with SAM-e, individuals using prescribed medications such as antidepressants, including serotonin re-uptake Inhibitors and MAO inhibitors, should consult a physician before using. Individuals with Parkinson's disease, bipolar disorder or manic depression should not take SAM-e.
In Summary
More than three decades of solid research support the use of SAM-e to help promote natural improvement in symptoms of osteoarthritis, depression and liver disease. Ongoing research is also revealing its promising potential for those with a number of other conditions.
______
References:
1. Williams AL, et al. “S-adenosylmethionine (SAMe) as treatment for depression: a systematic review.” Clin Invest Med. 2005 Jun;28(3):132-9.
2. Rosenbaum JF, et al. “The antidepressant potential of oral S-adenosyl-l-methionine.” Acta Psychiatr Scand. 1990 May;81(5):432-6.
3. Bell KM, et al. “S-adenosylmethionine blood levels in major depression: changes with drug treatment.” Acta Neurol Scand Suppl. 1994;154:15-8.
4. Soeken KL, et al. “Safety and efficacy of S-adenosylmethionine (SAMe) for osteoarthritis.” J Fam Pract. 2002 May;51(5):425-30.
5. Wadie IN, et al. “S-Adenosyl methionine (SAMe) versus celecoxib for the treatment of osteoarthritis symptoms: A double-blind cross-over trial.” BMC Musculoskelet Disord. 2004;5:6.
6. Konig H, et al. [Magnetic resonance tomography of finger polyarthritis: morphology and cartilage signals after ademetionine therapy] Aktuelle Radiol. 1995 Jan;5(1):36-40.
7. Purohit V, Russo D. “Role of S-adenosyl-L-methionine in the treatment of alcoholic liver disease: Introduction and summary of the symposium.” Alcohol. 2002 Jul;27(3):151-4.
8. Vendemiale G, et al. “Effects of oral S-adenosyl-L-methionine on hepatic glutathione in patients with liver disease.” Scand J Gastroenterol. 1989 May;24(4):407-15.
9. Mato JM, et al. “S-adenosylmethionine in alcoholic liver cirrhosis: a randomized, placebo-controlled, double-blind, multicenter clinical trial.” J Hepatol. 1999 Jun;30(6):1081-9.
10. Jacobsen S, et al. “Oral S-adenosylmethionine in primary fibromyalgia. Double-blind clinical evaluation.” Scand J Rheumatol. 1991;20(4):294-302.
11. Morrison LD, et al. “Brain S-adenosylmethionine levels are severely decreased in Alzheimer's disease.” J Neurochem. 1996 Sep;67(3):1328-31.
12. Tchantchou F, et al. “S-adenosyl methionine: A connection between nutritional and genetic risk factors for neurodegeneration in Alzheimer's disease.” J Nutr Health Aging. 2006 Nov-Dec;10(6):541-4.
__
* Karen Lee Richards is Lead Expert specializing in Fibromyalgia and ME/CFS, for HealthCentral's ChronicPainConnection (www.chronicpainconnection.com). Karen is co-founder of the National Fibromyalgia Association (NFA) and was Executive Editor of Fibromyalgia AWARE magazine for four years.
Note: This information has not been reviewed by the FDA. It is general and is not meant to diagnose, prevent, treat or cure any condition, illness, or disease. It is very important that you make no change in your healthcare plan or health support regimen without researching and discussing it in collaboration with your professional healthcare team
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:
LiverSupport.com
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
Research Summary
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.
Discussion
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.
http://www.blackwell-synergy.com/doi...ournalCode=tri
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:
Abstract
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
(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
SAM-e Promotes Liver Health
The liver is unique because it is the only internal human organ capable of regenerating itself. As little as 25% of a liver can regenerate into a whole liver again, and SAM-e plays a leading role in that regeneration. The third highest amount of SAM-e in the body is found in the liver. Only the adrenal and pineal glands contain more.
SAM-e is thought to be beneficial for those with liver disease by acting as a precursor of antioxidant glutathione; repairing the mitochondrial glutathione transport system; inhibiting the toxic effects of proinflammatory cytokines; and increasing DNA methylation.(7)
There are nearly a thousand published studies documenting SAM-e's ability to support prevention and improvement in liver disease.
• In a study of hepatic glutathione levels in patients with liver disease, participants were divided into four groups. Nine patients with alcoholic liver disease were given SAM-e; seven patients with non-alcoholic liver disease were given SAM-e; 8 patients with alcoholic liver disease were given a placebo; and 15 normal subjects served as a control group. Prior to beginning treatment, all patients had very low hepatic glutathione levels compared to controls. Following treatment, patients receiving the SAM-e had a significant increase in their hepatic glutathione levels compared with both the placebo-treated group and controls.(8)
• When SAM-e was given to 62 patients with alcoholic cirrhosis in a clinical trial, they were significantly less likely to die or require a liver transplant within the next two years, compared with 61 patients who had received a placebo.(9)
SAM-e Is Promising for Fibromyalgia Patients
Although SAM-e has not been studied yet as much for support of fibromyalgia patients as for those with some other illnesses, the results thus far are encouraging. In one double-blind study of 44 patients with primary fibromyalgia, improvements were seen in the areas of clinical disease activity, pain, fatigue, morning stiffness and mood.(10)
SAM-e's Role in Alzheimer's Disease
Since extremely low levels of SAM-e were found in the cerebrodpinal fluid and brain regions of Alzheimer's patients in a 1996 study, researchers are examining the potential benefits of supplemental SAM-e in Alzheimer's.(11) A recent study stated, “...our findings suggest that dietary supplementation with SAM... holds promise as a therapeutic approach to prevent or delay AD. A preliminary study indicates that SAM can provide some cognitive improvement in AD patients.”(12)
Facts About SAM-e You Need to Know
Dosage: Recommended therapeutic doses usually range between 400 – 1600 mg a day, although some individuals may require higher doses. Studies suggest that 400 mg per day may be adequate for osteoarthritis patients, while up to 1600 mg a day is often needed for mood support. The usual dose for those with liver disorders has been 1600 mg a day. (As with any addition to your health support regimen, supplementation with SAM-e should be considered only with the approval of your professional healthcare team.)
How to Take SAM-e: SAM-e works best when taken on an empty stomach. Because it is absorbed mainly in the intestine, enteric-coated tablets that allow it to pass through the stomach intact are preferable. Leave tablets in their foil or foil blister packs until you are ready to take them in order to maintain their stability.
Adverse Effects: There seem to be few adverse effects with SAM-e, even at high doses. Occasionally mild gastrointestinal distress has been reported. Since SAM-e can sometimes lead to insomnia, it is usually best to take it early in the morning. Because it plays a role in mood support, SAM-e may trigger manic episodes in people with bipolar disorder.
Contraindications: While there are no confirmed drug interactions with SAM-e, individuals using prescribed medications such as antidepressants, including serotonin re-uptake Inhibitors and MAO inhibitors, should consult a physician before using. Individuals with Parkinson's disease, bipolar disorder or manic depression should not take SAM-e.
In Summary
More than three decades of solid research support the use of SAM-e to help promote natural improvement in symptoms of osteoarthritis, depression and liver disease. Ongoing research is also revealing its promising potential for those with a number of other conditions.
______
References:
1. Williams AL, et al. “S-adenosylmethionine (SAMe) as treatment for depression: a systematic review.” Clin Invest Med. 2005 Jun;28(3):132-9.
2. Rosenbaum JF, et al. “The antidepressant potential of oral S-adenosyl-l-methionine.” Acta Psychiatr Scand. 1990 May;81(5):432-6.
3. Bell KM, et al. “S-adenosylmethionine blood levels in major depression: changes with drug treatment.” Acta Neurol Scand Suppl. 1994;154:15-8.
4. Soeken KL, et al. “Safety and efficacy of S-adenosylmethionine (SAMe) for osteoarthritis.” J Fam Pract. 2002 May;51(5):425-30.
5. Wadie IN, et al. “S-Adenosyl methionine (SAMe) versus celecoxib for the treatment of osteoarthritis symptoms: A double-blind cross-over trial.” BMC Musculoskelet Disord. 2004;5:6.
6. Konig H, et al. [Magnetic resonance tomography of finger polyarthritis: morphology and cartilage signals after ademetionine therapy] Aktuelle Radiol. 1995 Jan;5(1):36-40.
7. Purohit V, Russo D. “Role of S-adenosyl-L-methionine in the treatment of alcoholic liver disease: Introduction and summary of the symposium.” Alcohol. 2002 Jul;27(3):151-4.
8. Vendemiale G, et al. “Effects of oral S-adenosyl-L-methionine on hepatic glutathione in patients with liver disease.” Scand J Gastroenterol. 1989 May;24(4):407-15.
9. Mato JM, et al. “S-adenosylmethionine in alcoholic liver cirrhosis: a randomized, placebo-controlled, double-blind, multicenter clinical trial.” J Hepatol. 1999 Jun;30(6):1081-9.
10. Jacobsen S, et al. “Oral S-adenosylmethionine in primary fibromyalgia. Double-blind clinical evaluation.” Scand J Rheumatol. 1991;20(4):294-302.
11. Morrison LD, et al. “Brain S-adenosylmethionine levels are severely decreased in Alzheimer's disease.” J Neurochem. 1996 Sep;67(3):1328-31.
12. Tchantchou F, et al. “S-adenosyl methionine: A connection between nutritional and genetic risk factors for neurodegeneration in Alzheimer's disease.” J Nutr Health Aging. 2006 Nov-Dec;10(6):541-4.
__
* Karen Lee Richards is Lead Expert specializing in Fibromyalgia and ME/CFS, for HealthCentral's ChronicPainConnection (www.chronicpainconnection.com). Karen is co-founder of the National Fibromyalgia Association (NFA) and was Executive Editor of Fibromyalgia AWARE magazine for four years.
Note: This information has not been reviewed by the FDA. It is general and is not meant to diagnose, prevent, treat or cure any condition, illness, or disease. It is very important that you make no change in your healthcare plan or health support regimen without researching and discussing it in collaboration with your professional healthcare team
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:
LiverSupport.com
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
Research Summary
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.
Discussion
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.
http://www.blackwell-synergy.com/doi...ournalCode=tri
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:
Abstract
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
Optimizing Cutting Cycles: Advanced Strategies with Winstrol and Testosterone
Optimizing Cutting Cycles: Advanced Strategies with Winstrol and Testosterone
Enhancing Your Winstrol Cycle: The Role of Testosterone
Incorporating Testosterone into your Winstrol cycle can significantly enhance muscle retention and strength. Testosterone, often considered the foundation of most steroid cycles, complements Winstrol's cutting effects by preserving muscle mass and improving overall body composition.
Strategic Dosing for Maximum Efficiency
To optimize the benefits of Winstrol and Testosterone, strategic dosing is essential. For beginners, lower dosages are advisable to gauge the body's reaction, while experienced users might opt for higher doses within safe limits. Regular blood tests are recommended to monitor the body’s response and adjust dosages accordingly.
Timing Your Cycle for Peak Results
Timing is crucial in a Winstrol and Testosterone cycle. Starting with Testosterone and introducing Winstrol mid-cycle can help maintain muscle hardness and definition. Alternatively, beginning with Winstrol can offer a 'kickstart' for rapid gains, followed by the sustaining effects of Testosterone.
Winstrol Only vs. Stacked Cycles
While a Winstrol-only cycle is common for cutting, stacking with Testosterone can offer enhanced benefits. This combination provides a balance between muscle definition and strength, making it a preferred choice for many bodybuilders.
Managing Side Effects for a Safe Cycle
Understanding and managing potential side effects is crucial. Winstrol's hepatotoxicity and Testosterone's estrogenic effects, such as water retention and gynecomastia, require attention. Using liver protectants and aromatase inhibitors can mitigate these risks.
Advanced Cycle Options: Incorporating Other Steroids
For more experienced users, adding a third steroid like Trenbolone or Equipoise can further enhance the cycle's effectiveness. These combinations can offer more pronounced muscle definition and strength gains.
The Importance of Post-Cycle Therapy (PCT)
Post-Cycle Therapy is essential in restoring the body’s natural hormone production. A well-planned PCT, typically involving Clomid or Nolvadex, is crucial following a Winstrol and Testosterone cycle.
Conclusion
A Winstrol and Testosterone cycle, when planned and executed correctly, can be a powerful tool in achieving cutting goals. By understanding the nuances of dosing, timing, and side effect management, bodybuilders can maximize their results while maintaining safety.
Optimizing Cutting Cycles: Advanced Strategies with Winstrol and Testosterone
Enhancing Your Winstrol Cycle: The Role of Testosterone
Incorporating Testosterone into your Winstrol cycle can significantly enhance muscle retention and strength. Testosterone, often considered the foundation of most steroid cycles, complements Winstrol's cutting effects by preserving muscle mass and improving overall body composition.
Strategic Dosing for Maximum Efficiency
To optimize the benefits of Winstrol and Testosterone, strategic dosing is essential. For beginners, lower dosages are advisable to gauge the body's reaction, while experienced users might opt for higher doses within safe limits. Regular blood tests are recommended to monitor the body’s response and adjust dosages accordingly.
Timing Your Cycle for Peak Results
Timing is crucial in a Winstrol and Testosterone cycle. Starting with Testosterone and introducing Winstrol mid-cycle can help maintain muscle hardness and definition. Alternatively, beginning with Winstrol can offer a 'kickstart' for rapid gains, followed by the sustaining effects of Testosterone.
Winstrol Only vs. Stacked Cycles
While a Winstrol-only cycle is common for cutting, stacking with Testosterone can offer enhanced benefits. This combination provides a balance between muscle definition and strength, making it a preferred choice for many bodybuilders.
Managing Side Effects for a Safe Cycle
Understanding and managing potential side effects is crucial. Winstrol's hepatotoxicity and Testosterone's estrogenic effects, such as water retention and gynecomastia, require attention. Using liver protectants and aromatase inhibitors can mitigate these risks.
Advanced Cycle Options: Incorporating Other Steroids
For more experienced users, adding a third steroid like Trenbolone or Equipoise can further enhance the cycle's effectiveness. These combinations can offer more pronounced muscle definition and strength gains.
The Importance of Post-Cycle Therapy (PCT)
Post-Cycle Therapy is essential in restoring the body’s natural hormone production. A well-planned PCT, typically involving Clomid or Nolvadex, is crucial following a Winstrol and Testosterone cycle.
Conclusion
A Winstrol and Testosterone cycle, when planned and executed correctly, can be a powerful tool in achieving cutting goals. By understanding the nuances of dosing, timing, and side effect management, bodybuilders can maximize their results while maintaining safety.
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