liver result after epistane cycle
- 01-04-2008, 11:04 PM
- 01-04-2008, 11:05 PM
01-04-2008, 11:18 PM
01-04-2008, 11:53 PM
01-04-2008, 11:59 PM
I know for me, on anything I can make better gains that most people. In terms of things like anabolics im sure that it will have a more pronounced effect in terms of mass gains as well as sides. Ive been known to get hit hard with sides sometimes. Its just how my body reacts. Making a vague general assumption that a compound doesnt affect your liver based on YOUR own personal results does not mean that others will get the same.
01-05-2008, 12:00 AM
01-05-2008, 12:05 AM
my results were great and went from benching around 250 x5 to 280 x5 and gained alot of muscle about 8-10lbs while losing fat and actually I just tapered down after 5 weeks for pct and it worked great I ran 40mg for 5 weeks then went to 2 pills for abou a week than 1 for a week it worked great the doctor said my liver values were absoutly perfect it suprised me to it was a very simple cycle using only one comound other than protein powder and creatine which I consider essential anyways
01-05-2008, 12:10 AM
the test numbers are at my moms house but I'll get them and post them I'm 30 by the way just I had to go to the hospital for something else(tore knee cartliage)and asked for the test while I was there I was shoked when the came back perfect I expected them to be a little off. Because to be honest I ran this cycle half hazard. The taper pct worked great to I figured it would with this compound because of its ai properties.
01-05-2008, 12:10 AM
01-05-2008, 05:49 AM
01-05-2008, 09:17 AM
01-05-2008, 06:34 PM
i also had pefect liver values and ideal cholesterol and test levels about 600 ng/dl..after a 6 week cycle of epi...dosing it 20,30,30,40,40,40..........tha t was about 5 days after my last pill....and i used torm for pct
01-05-2008, 06:52 PM
Perfect is rather ambiguous when you consider the ranges:
SGOT (AST) (normal range: 0 - 40 IU/L)
SGPT (ALT) (normal range: 0 - 40 IU/L)
Knowing your pre and post values would be more indicative. This also applies to lipids as well.
Because your values are in range does not tell you how much thay have changed as a result of the consumption of this product.
Someone could have 38/38 ast/alt and 180 total cholesterol and this does not tell you anything about how this supplement has effected your health.
Consider that if you had a 18/18 ast/alt before hand and your lipids are now 10hdl/160ldl post cycle...this is not perfect.
That is a silly statement. They certainly are whether you feel they are or not.I dont feel supports supplements are scentificaly proven.
01-06-2008, 11:40 AM
hears my numbers
the perfect range is sgot10-45
I do not have the choleserol results but that would be kind of hard to determine with out knowing before numbers as bodybuilding diets tend to give you high choleserol
01-06-2008, 11:54 AM
I must admit you're all coming across pretty f'n cynical . Can someone please let me know what he would have had to post for all to say something "nice, good job"?
01-06-2008, 11:58 AM
01-06-2008, 11:59 AM
01-06-2008, 08:22 PM
01-07-2008, 12:09 AM
01-07-2008, 11:01 AM
let me defend myself after being flamed eating a lot of red,meat,eggs,milk and many other high protien foods can raise cholesterol in my opinion that a big reason for bodybuilders having heart trouble. And show me one definitive scentific report saying milk thistle helps liver support in the steroid using community you cant because as far as I know there are none. And as far as this being my first post I can tell you I read on tis site and many others a lot I have just never posted on here I just figured everyone would like to see the actual liver results after a epistane cycle and I did post the actual numbers.
01-07-2008, 11:12 AM
This is simply an excerpt from Dinoiii's pct articles--------------------------------------------------------------------------------
So, we see this term thrown about, but not too often do we hear, what in the world is this, but somehow, I am sure not many of you know (but your secret’s safe with me). I will allow you now to act smart in front of your friends free of charge with your silymarin knowledge. In short, silymarin is a fancy, shmancy name for a mixture of flavonoid components (i.e. – silybin, silidianin, and silichristine) from milk thistle. The concentration of silymarin is highest in the fruit, but it is also found in the seeds and leaves. Milk thistle extracts standardized for silymarin usually find their way into your favorite supplements at about a 70-80 percent concentration.
Fancy Shmancy, maybe. However, silymarin is at least ten times more potent in antioxidant activity than vitamin E and also increases the liver’s own antioxidant, glutathione (which we have spoken about at great lengths thus far in this series) by OVER 35%!
EVIDENCE-BASED EFFICACY: Positive effects have been seen with 70-80% concentration in treating several types of liver disease, including hepatitis and cirrhosis. The therapeutic effect of milk thistle extracts in these disorders has been confirmed by biopsy as well as by clinical and laboratory data.
Although milk thistle extract has shown benefits in treating acute and chronic viral hepatitis, the results with milk thistle extract are most impressive when looking at studies evaluating its effectiveness in alcohol- or toxic-chemical-induced hepatitis, which is why it applies readily to the post-cycle time frame. For example, in one double-blind study in workers exposed to toxic toluene and/or xylene vapors for five to twenty years, milk thistle extract (Thisilyn) was shown to significantly lower levels of AST and ALT, while significantly improving other blood measurements, such as platelet count, white blood cell count, and percentage of lymphocytes compared to other white blood cells (but it’s use can also create an inaccurate picture for clinician’s, so we must be wary in our question asking during history taking).
Even in cirrhosis of the liver, milk thistle extract has shown some benefits. Although not all studies have shown significant effects, in one controlled study the four-year survival rate was 58% in the milk thistle group compared to 39% in the control group.
There have been no studies to date examining the potential of milk thistle to treat gallstones through it’s ability to increase bile solubility (gallstones form when bile components fall out of solution). When there are drastic body re-composition events, namely fat loss – this is ABSOLUTELY AN IMPERATIVE POINT as gallstones have a tendency to readily form.
FORMS & DOSAGES: Milk Thistle is available as bulk and dried seeds, as tea bags, as a tincture, as a fluid extract, and as a solid extract in tablet and capsule forms. Extracts standardized for silymarin content are preferred as it is the component proposed to be responsible for the extract’s mechanism of action (recall bioflavinoid complex discussed earlier). There is some preliminary data to suggest combinations of Silybin, the key component in silymarin within milk thistle, and phosphatidylcholine would help aid absorption. It is too early to tell and the data available was thus far only published by those with vested interest, so I cannot say definitively. The regular version standardized should be good enough anyway – so why get fancy?
The goal of therapy here will be based on silymarin content. If using the dried seeds, a much lower dose is necessary to see positive effects of the compound.
POTENTIAL SIDE EFFECTS / INTERACTIONS: The earliest side noted is a looser stool (due to increase of bile output). Aside from that, it tends to be a rather safe supplement with a great track record.
If you are taking the following drugs: thyroid hormone, acetaminophen, butyrophenones, phenothiazines, phenytoin, and even alcohol, I advise AGAINST the use of milk thistle as it has a tendency to drive down efficacy of these agents.
(1) If loosened stool side effect occurs, it is a good idea to take some sort of fiber source (i.e.- guar gum, pectin, psyllium, and/or oat bran) with your milk thistle dose if it is desired to continue to use the product. This will help aid bile binding preventing irritation.
-----------------------------------------IN-HOUSE STUDY -------------------------------------
Houser, D. The Efficacy of Various OTC Hepatoprotectants in the Post-Cycle time frame following use of C17 alkylated PH/PS – a double-blind, placebo controlled look. (2004) [Unpublished to date-see below]
Study Group: 34 clients in Post-Cycle Therapy after the use of upper-limit dosing of various C17 alkylated PH/PS products. The breakdown of the in-house participants was as follows:
Group A: 15 Solitary M1T (Dosing Parameters: 20 to as high as 60 mg per day x 6-10 week cycles).
Group B: 7 M1T + MD (Dosing Parameters: 12 to as high as 30 mg per day of each x 4-12 week cycles).
Group C: 12 MD + MOHN (Dosing Parameters: 12 to as high as 20 mg per day of each x 4-18 week cycles).
5 participants – 600mg NAC
5 participants – 400mg enteric-coated SAMe
3 participants – 600mg NAC + 400mg enteric-coated SAMe
2 participants – placebo-control
“Cliff-Notes” Summary: 4 of 5 participants in SAMe-only group and all 3 participants in NAC + SAMe group had an average 5-day faster return to baseline of AST/ALT elevations than NAC and placebo-control. The addition of NAC in the dual-coverage group seemed to offer no additional benefit without statistically significant results between the two. NAC + placebo-control groups saw no statistically-significant changes in AST/ALT levels. Results seem to suggest SAMe is superior, at least in the post-cycle realm, to NAC in returning transient LFT elevations to baseline INDEPENDENT of cycle length. The essential caveat was the unanswered question in regard is why one of the SAMe-only participants mimicked results of NAC and placebo. Author’s Note: A current follow-up series of serum studies in specific regards to this individual are underway as we speak in hopes of offering answers.
3 participants – 600mg NAC
3 participants – 400mg enteric-coated SAMe
1 participant – 600mg NAC + 400mg enteric-coated SAMe
(Author’s Note: not enough participants in this arm for placebo-control)
“Cliff-Notes” Summary: Similar results to Group A were seen in this arm. The SAMe-only and SAMe + NAC participants saw an average 3-day faster return to baseline of AST/ALT elevations. The faster return to baseline of transient LFT elevations was again INDEPENDENT of cycle length. It is truly unfortunate that there was no ability to gain a placebo-control group here, but M1T + MD in a concurrent run was not one of the most popular cycles when these PH/PS products were still being marketed legally. With the support of the first and third arms of the study, some definite inferences can be made. It would appear that the SAMe inclusion is what offered aid in the post-cycle realm for expedited returns to baseline LFT.
4 participants – 600mg NAC
4 participants – 400mg enteric-coated SAMe
2 participants – 600mg NAC + 400mg enteric-coated SAMe
2 participants – placebo-control
“Cliff-Notes” Summary: Once again, the SAMe-only and SAMe + NAC participants saw an average 8-day faster return to baseline (inferences about the strength of PH and subsequent elevation in transaminase can likely explain the difference 5 vs. 3 vs. 8 respectively for the three arms) SPECIFICALLY in cycles under 8 weeks. Cycles that extended beyond this time frame tended to exhibit results that were not statistically significant when compared with either the NAC-alone or placebo-control groups. Of note, 2 participants in this arm did NOT see LFT elevation (1 in NAC only and 1 in NAC + SAMe groups). This is likely to be attributed to one of two things: specificity to elevation to particular PH/PS run or irregularly low-level baseline LFTs (of which has not been explored to date due to lack of participant follow-up).
* Author’s note: All information gathered here was done prior to the October 2004 ban. Due to legal issues, follow-ups for replicability are thwarted by the Steroid Control Act of that year. The aforementioned 3-arm study will appear in an upcoming book with complete lab values verified by Quest Diagnostics reports.
Summary of Hepatoprotectant Use in PCT: Despite certain supplement companies’ claims, the attempts to replicate NAC results in oral (PO) form have been less than stellar and shows these particular supporters simply either not doing their homework or just attempting to “kitchen sink” their products with a bell and whistle. You can get away with very cheap brands quality-tested, but it is imperative to be careful in choosing which brand to go with. Fortunately enough, many brands of SAMe have been tested independently and it would appear this to be the OFFICIAL dinoiii agent of choice at this time, especially post-C17 alkylated oral use.
Quality Dose: 400mg enteric-coated SAMe (keeping in mind concentration of stabilizers we learned about above) two times per day (bid) + Milk Thistle (dose accordingly).
Dana Houser, MD, MHSA, CISSN
R&D Consultant; Diector of Pharmacovigilance Program MAN Sports, Inc.
01-07-2008, 11:14 AM
I also didn't think anyone mentioned milk thistle other than you. There are a slew of support supplements that help to alleviate the side effects of 17aa substances. They have a slew of scientific support to back them up as well.
01-07-2008, 11:17 AM
1: Med Pregl. 2003;56 Suppl 1:79-83.Links
[Hepatoprotective effects of silymarin in androgenic-anabolic steroid-induced liver damage]
[Article in Serbian]
Radovanović D, Jovanović D, Mihailović D, Ranković G, Stojiljković N, Dimitrov V.
INTRODUCTION: The use and abuse of anabolic-androgenic steroids (anabolic steroids) commonly induces liver damage. MATERIAL AND METHODS: The study included 40 male Wistar rats, divided into 4 groups of 10 rats each. Animals in the first experimental group (M), were subjected to progressive systematic forced swimming test, 5 days a week, during 8 weeks. Animals in this group were treated with anabolic steroids methandienone, 2 mg/kg BW/day, per os, before swimming, 5 d/w for 8 weeks. After swimming, animals were given three times more food than the laboratory animals of the same age and kind. Animals in the second group (M+S), were subjected to progressive forced swimming test, 5 d/w 8 weeks. Animals in this group were treated with methandienone equally as the experimental group M and received the same amount of food. Apart from that, they received silymarin 20 mg/kg BW/day. Animals in the third group (K), represented the control group, which was neither subjected to swimming test, nor treated with methandienone or silymarin. Animals in this group received the same amount of food as animals in groups M and M+S. Animals in the fourth group (C), also represented a control. This group was not exercised nor treated, and animals received a standard amount of food for laboratory animals of this kind and age. Quantitative analysis of obtained hemataxylin-eosin, periodic acid shift and enzymohistochemical preparations was processed using Digital Image Analysis System: Microimage 3.0. RESULTS: It was established that processes in the nuclei of animals in groups M and K were significantly more intensive (p<0.001) in relation to groups M+S and C. The investigation of glycogen showed significantly higher density in the cells of groups M and M+S in comparison to groups K and C. Also, there was a significant difference between groups M+S and M. Density of enzyme activity of glutamate dehydrogenase in hepatocytes of animals in the group M+S was significantly higher in relation to the remaining three groups. A statistically significant difference was not found in enzyme activity of succinate dehydrogenase and lactate dehydrogenase. DISCUSSION: In cell nuclei of animals in the experimental group M, in the absence of silymarin effect, methandienone causes damages which induce regenerative processes and in this way increase high intensity activity. Silymarin significantly increases the glycogen density in hepatocytes. Increased activities of GDH are attributed to cell vitality. CONCLUSION: The present results show hepatoprotective effects of silymarin in androgenic-anabolic steroid induced liver damage.
PMID: 15510919 [PubMed - indexed for MEDLINE]
1: Planta Med. 1998 Mar;64(2):138-42.Links
Silymarin inhibits the development of diet-induced hypercholesterolemia in rats.
Krecman V, Skottová N, Walterová D, Ulrichová J, Simánek V.
Institute of Medical Chemistry, Medical Faculty, Palacký University, Olomouc, Czech Republic.
To study the ability of silymarin, a standardized mixture of antioxidant flavonolignans from the medicinal plant Silybum marianum, and of silybin, the main flavonolignan of silymarin, to inhibit the development of diet-induced hypercholesterolemia the rats were fed high cholesterol diet (HCD). Silymarin or silybin were given as dietary supplements, and their influences on serum cholesterol levels were compared to those of probucol, an antioxidant hypocholesterolemic drug. Anticholesterolemic effect of silymarin was parallel to that of probucol, and dose-dependent at dietary drug concentrations of 0.1-0.5-1.0% (w/w). However, in contradistinction to probucol, silymarin caused an increase in high density lipoprotein (HDL)-cholesterol and a decrease in liver cholesterol content, changes considered to be of benefit. In addition to its anticholesterolemic effect silymarin partially prevented the HCD-induced decrease in liver reduced glutathione, an endogenous antioxidant. Silybin was not so effective as silymarin suggesting that either other constituent(s) of silymarin may be responsible for its anticholesterolemic effect or the bioavailability of silybin alone might be lower than that of silybin as a compound of silymarin.
PMID: 9525106 [PubMed - indexed for MEDLINE]
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01-07-2008, 11:17 AM
01-07-2008, 04:32 PM
the only point of my post was to let everyone know my liver was a ok after a epistane cycle not to argue the benifit of support supplements.
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