MESO-Rx

Anabolic Steroids

Une première cure pour septembre 2018

Mephis à dit:
Non j'ai commencé à 40 et je suis monté progressivement.
Niveau diète oui je suis toujours dans une vibes saine et ce depuis mon jeune âge ahaha. 4kg oui mais sûrement parce que c'était la première. Renseigne toi bien sur le desmo et évite le chocolat lol.
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Qu'est ce qui se passe pour le chocolat ?
Pour infos, je ne sais pas si tu l'as vu après être passé sur ma diète, mais il y a un petit carré de chocolat par jour : https://fr.thinksteroids.com/community/threads/diete-saveed.17089/#post-417203
 
Opte pour de vrai hépato protecteurs si déjà on croit aux hépato protecteurs
Chardon marie
Tudca
NAC
Sont ceux qui ont des études liées quand à la protection hépatique ou en tout cas amélioration des enzymes hépatiques sous traitement méd ou pour traitement ou prévention de certains atteintes hépatiques comme la choléstase qui sont une des premières merdes que l'on peut avoir avec les oraux aas alpha alkylé 17 selon les report cases que j'avais mis et que je tiens sur un doc mais qu'on s'en bat les steak royalement @Samuro

Sinon il y a tjrs la méthode à partir sans protection mais là je te dis bonne chance car je n'oserai pas le tester
 
@dvnfit666 : Merci pour ton retour !
La vrai question serait : Le quel opter ? Desmodium vs Chardon Marie.

Les infos que nous avons sur différents sites :
Le desmodium sera plutôt utilisé chez des personnes dont le foie est soumis à des stress très importants (chimiothérapie, hépatite, alcoolisme...). Le chardon marie, qui pousse en France, sera une bonne plante de soutien du foie dans les autres cas.
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https://www.passeportsante.net/fr/C...ert/Question/desmodium-et-chardon-marie-22809


La deuxième, le chardon-Marie, est plus adaptée à des situations de crise, de la crise de foie aux hépatites virales aiguës, voire la cirrhose. C'est aussi une solution pour éliminer les effets secondaires de la chimiothérapie. Non seulement le chardon-Marie protège les cellules du foie, mais il stimule aussi leur renouvellement. S’il s’agit de récupérer d'un excès alimentaire, quelques gélules ou des tisanes suffisent. En cas de troubles graves, il faut évidemment bien plus que des tisanes.
Les gélules de chardon-Marie peuvent convenir, mais les dosages doivent être assez élevés pour donner des résultats dans les troubles sérieux.

Il en va de même pour le remède hépatique suprême, le desmodium, plante dans ce domaine supérieure à toute autre.
Cliquez pour agrandir...
https://www.alternativesante.fr/foie/le-foie-notre-centre-anti-poison


Le Desmo semble donc répondre à notre besoin.
Qu'en pensez-vous ?
 
Tudca
Nac
Chardon marie est le trio pour moi et j'avais posté des liens plus sérieux que passeport santé ou alternative santé poto c'était des études pubmed
Desmodium j'ai pas trouvé de bonnes études sur pubmed ayant un lien direct avec un effet hépato protecteur comme ceux que j'ai trouvé avec tudca nac et Milk thistle
 
Milk Thistle
https://www.ncbi.nlm.nih.gov/pubmed/20564545
https://www.ncbi.nlm.nih.gov/books/NBK118
https://livertox.nih.gov/MilkThistle.htm
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3959115/

TUDCA
https://www.ncbi.nlm.nih.gov/pubmed/23592128
Differences In The Metabolism And Disposition Of Ursodeoxycholic Acid And Of Its Taurine-conjugated Species In Patients With Primary Biliary Cirrhosis
Tauroursodeoxycholic Acid For The Treatment Of HCV-related Chronic Hepatitis: A Multicenter Placebo-controlled Study
Ursodeoxycholic And Tauro-ursodeoxycholic Acids For The Treatment Of Primary Biliary Cirrhosis: A Pilot Crossover Study
Tauroursodeoxycholic Acid For Treatment Of Primary Biliary Cirrhosis. A Dose-response Study
Does Tauroursodeoxycholic Acid (TUDCA) Treatment Increase Hepatocyte Proliferation In Patients With Chronic Liver Disease
The ultimate LIVER thread and info on orals and ORAL TOXICITY!!
This post might deserve a sticky, seeing as though there is no definitive post around here concerning liver health and oral C17 alpha alkylated anabolics. No post stating what specifically happens inside the liver when C7AA steroids are consumed, what they do inside, what happens over prolonged periods, and what is the best thing to do and take in order to solve the problem. The answers to all of these questions have recently piqued my interest because in one of my biochemistry courses, we just so happen to be covering certain aspects of liver function and the biochemical processes that occur inside it. We specifically touched upon the use of ursodeoxycholic acid (UDCA) for regulating proper liver function (specifically, BILE FLOW) in the midst of liver damage from things like alcohol, hepatitis C, etc. I also ran into a small issue post-cycle that I thought may have been a liver issue (lucky it doesn't seem like it was), and that caused me to look further into this. Some or much of this information may already be known, but I feel the need to spread word about it and post this here to educate people who might be asking the same questions.

I'm a really busy guy, and I don't have very much time to take everything I have read and conjure it up into my own words here. So, to save time, I am simply going to copy and paste my findings from other sources into this post, and provide references to them.

I am, for the most part, going to just copy and paste a whole post I already made in a previous thread I posted in where a forum member was asking about liver protection, oral anabolics, etc. where I explained everything to him. Here it is, folks:

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TUDCA (Tauroursodeoxycholic acid) is quite literally the primary and ONLY liver protectant people should be using if they are taking C17 Alpha Alkylated oral anabolic steroids. I think that Liv 52 is okay to use as well. But, if you could only pick ONE product and throw the rest away, I would say TAKE THE TUDCA!!!! Research has shown that it is the ONLY thing that is effective at treating anabolic steroid SPECIFIC induced cholestasis of the liver. Off the top of my head, one company that makes a product with TUDCA in it is Thermolife in their Liver Longer supplement, but they have seemed to be out of stock for a long while now. I know it is possible to pick up generic TUDCA if you look hard enough online. Just google it!

If you can find TUDCA elsewhere, get it as soon as you can.

As a matter of fact, using a liver support supplement such as TUDCA may even INCREASE the oral absorption and bioavailability of the steroid because it prevents cholestasis of the liver. You have to understand what happens in the liver when you use C17 alkylated orals. Cholestasis is defined as an impairment of bile flow in the liver. I don't know if you remember your highschool biology class, but bile is an extremely important component of the liver and of our body, because bile serves dual purposes:

1. In a way, it acts as a waste removal sewage fluid for the liver. All of the byproducts (not all necessarily bad, but stuff that your liver needs to remove on a regular basis or else it will harm the liver from an unhealthy buildup) that your liver creates from all the work it does in metabolizing a bazillion billion different things every day, gets collected as bile. In turn, bile salts really 'clean' the liver out.

2. Bile and the bile salts within it are very important to our digestion, especially of fats. It's stored in the gall bladder and then pumped into your duodenum (upper section of your small intestine) when you eat food to aid in digestion, as it assists in the breakdown of fats and such.

Now, in a nutshell, what happens when your liver gets 'damaged' from oral steroids is: (and i'm not going to get into the specific chemistry of it for ease of explanation to the layman) the liver is overloaded from processing the C17 alkylation on the anabolic steroid you are ingesting. What happens as a result is that it causes a slow down of bile flow in the liver, because the liver is getting so overloaded with the processes it is trying to undergo. The impairment of bile flow in the liver is known as cholestasis, and is a direct result of C17 alkylated steroid use . When bile flow is slowed down too much (or has outright STOPPED), the bile salts, which are very toxic to the liver cells, will start to damage those liver cells. The key idea here is BILE FLOW, and you'll see this repeated a lot in this post! The liver needs to keep churning bile through itself in all of its cells in order to clean out the metabolites resulting from all of the biochemical processes it's doing every second!

I don't have much time on me, so for further explanation I am going to quote a couple articles I found that explain in more detail what TUDCA does and how it literally is the ONLY liver support compound that is useful, to a much larger degree than anything else, at combating cholestasis:


A few words on the hepatotoxicity of 17a-methylated androgens/anabolics
1. 17a-methylated androgens/anabolics are hepatotoxic.
The liver toxicity of steroids is an under-researched field, but there seems to be a strong correlation between how easily the body can metabolize a steroid & its toxicity. Metribolone -- a truly excessively toxic compound -- is often referred to in the literature as a 'non-metabolizable androgen'. (1, 2, 3, etc.) Mibolerone , another deadly-toxic anabolic steroid, is also effectively 'non-metabolizable': The main metabolite of mibolerone in humans is... unchanged mibolerone. And by a very wide margin.

Methylstenbolone, which is resistant to 17b-HSD and 3b-HSD, is obviously difficult for the body to clear. It should therefore be no safer, no less toxic, than Superdrol or M1T -- compounds which share very similar traits.


2. Liver injury due to oral anabolic use typically manifests itself as cholestasis.
Hepatotoxicity induced by oral anabolic compounds tends to be characterized by enlargement of periportal hepatocytes, impairment of bile flow & dramatically increased serum levels of AST, ALT and GGT. In other words, cholestasis... but let's examine this a little bit further.

The word "cholestasis" gets thrown around a lot, but it can mean two very different things: The physical obstruction of hepatic bile flow -or- the impairment of bile secretion. In the former case, there is a mechanical block in the bile duct system; in the latter, bile is held in hepatocytes or cholangiocytes as it cannot be secreted. In both cases, what happens thereafter is that the retained hydrophobic bile salts -- which are strongly cytotoxic -- lead to cellular injury, then apoptosis, then necrosis, often followed by an inflammatory reaction and tissue fibrosis. This tissue damage, if advanced enough, can physically destroy bile ducts, worsening the condition.

The obstruction of bile flow is typically not something you'd experience after exposure to any toxin; it is the almost exclusive domain of inherited or autoimmune diseases which leave fibrotic lesions or scar-tissue in the liver, such as cystic fibrosis, primary biliary cirrhosis, and so on. Exposure to oral anabolic compounds can, however, result in the second form of cholestasis -- bile retention in hepatocytes -- thus the enlarged hepatocytes observed after their use.


3. There are three fundamental ways of preventing/treating cholestasis:
1. Metabolic induction of hydrophobic bile acid detoxification
2. Stimulation of impaired bile secretion
3. Protection of hepatocytes from the toxic effects of hydrophobic bile acids and/or inhibition of hepatocyte apoptosis.

Cholestatic liver damage is caused by bile acid accumulation... But not all bile acids are toxic. Generally speaking, the fewer hydroxyl groups they bear, the more hydrophobic and cytotoxic they are. Hence lithocholic acid is markedly cytotoxic, deoxycholic acid is very slightly cytotoxic, and cholic acid is essentially non-cytotoxic. Treatment #1 would involve hastening the metabolic conversion of the more toxic bile acids to hydrophilic, less toxic compounds --- or increasing the synthesis of hydrophilic bile acids from cholesterol, which would decrease the cytotoxicity of the entire bile pool as a whole. This can seemingly be achieved with the oral administration of ursodeoxycholic acid (UDCA), which has been reported to activate the PXR/SXR nuclear receptor in hepatocytes, which then activates bile acid–metabolizing enzymes. It is reasonable to assume that Tauroursodeoxycholic acid (TUDCA), the taurine conjugate of UDCA, should have the same effect.

As for #2... Bile secretion at the level of the hepatocyte is carried out by a group of transporter proteins: The bile salt export pump (BSEP), the phospholipid export pump (MDR3), the canalicular bilirubin conjugate export pump (MRP2), and a chloride-bicarbonate anion exchanger (AE2) for bicarbonate excretion. BSEP is the driving factor behind bile-acid dependent secretion, and MRP2/AE2 are the major forces behind bile-acid-independent bile secretion. Hydrophilic bile acids such as UDCA & TUDCA (and even, partially, cholic acid) have been shown to increase expression of BSEP mRNA; they activate BSEP coactivators by binding to the Farnesoid X Receptor (the "bile acid receptor"); they phosphorylate the BSEP protein via a Ca+/PKCa-mediated mechanism; lastly, they stimulate Cl -/HCO3 - exchange via this same PKCa induction, thus increasing AE2 levels.
Taken together, the above effects drastically enhance secretion of potentially toxic bile acids.

#3 can be complicated, but I will explain briefly: Certain toxic bile salts activate the Fas Death Receptor on hepatocytes. This leads to a cascade of dozens of protein interactions & ultimately to cell death. TUDCA, UDCA, and certain other compounds can diminish Fas–induced apoptosis, but, as far as I am aware, the exact mechanism is not known at this time. Fas activation here is not ligand-dependent, so the 'obvious' mechanism is out the window. The mechanism could, however, involve activation of the EGFR, which activates MAPK & the MAPK-mediated 'survival pathway' in hepatocytes; it might also involve inhibition, somewhere along the line, of the proapoptotic proteins Bax and Bid.


4. Recommendations
I strongly recommend TUDCA or UDCA to anybody considering a cycle containing oral androgens, for what should by now be obvious reasons. They are extremely potent at preventing or reversing 17aa-androgen-mediated liver damage. There's really no excuse not to take them, in my opinion, and I would advise you not to run a cycle if you can't afford them. Oral androgens can send you straight to the ER if the right precautions are not taken, & your health is much more important than a few more pounds of here-today-gone-tomorrow muscle.

Silymarin and silybin, the milk thistle extracts, are very strong antioxidants and free-radical scavengers in hepatic tissue. They impede hepatic lipid peroxidation, increase glutathione concentrations, and even have anti-inflammatory and tissue-regenerative properties... Other plant-extracted compounds, such as celastrol, have similar effects... But while these extracts are excellent to take for general liver health, they are weak protection and not an appropriate treatment for cholestasis, as they do not appear to impact bile acid secretion/metabolism at pharmacologically-relevant doses. Silymarin did increase bile secretion and improve bile acid metabolism in rats -- but that effect was primarily noticed at a dose of 100mg/kg, administered via i.p. injection (100% bioavailability), and therefore doesn't have much bearing on humans who take much smaller amounts orally (~10% bioavailability).
...But Primordial Performance's "Liver Juice" is silymarin/silybin attached to an excellent delivery complex, and should be quite effective if taken 3x/day. It is the best milk thistle supplement out there, in my opinion.

NAC is also a fine antioxidant and glutathione-booster, but it suffers from poor bioavailability & is usually very underdosed in commercially-available supplements... So I wouldn't bother with it.

Sanofi-Aventi (or is it just 'Sanofi' these days?) manufactures the popular phospholipid-complex product "Essentiale" and "Essentiale Forte". The phosphatidylcholine therein has been shown to help protect hepatic cell membranes against the damaging effects of chenodeoxycholic acid, can inhibit lipid peroxidation, and can induce cytochrome P450, which stimulates the metabolic clearance of bile acids... So there's a reason that it's the most popular OTC liver support in Europe and Asia... But "Essentiale" can be hard to find in the USA -- and, on its own, I don't believe that it is totally adequate protection for users of oral androgens.

And Liv-52? Mostly a waste of money. A blend of mild antioxidants is all there is to it.

The bottom line here is this: Oral anabolics/androgens are hepatotoxic. Period. If you are going to use them, I implore you to take sensible precautions. Antaeus shall release a novel and powerful liver-support product in the very near future. In the meantime, there's Thermolife's "Liver Longer" and Primordial's "Liver Juice". Both are cheap enough that there's no excuse not to take them.Another article:


How do 17-aa oral steroids cause liver damage?

Despite a lot of discussion on the forums about the "toxicity" of different oral steroids, most users are unaware of the mechanism or implications around these "toxic effects" (which is probably the reason why most users have yet to find an effective cure for the toxic effects).

Let me shed some light on this ambiguous topic.

17-aa steroids are toxic to the liver because they inhibit the excretory functions of the liver. (1-7)

More specifically, the more "liver toxic" a 17-aa steroid is, the more it inhibits the production and flow of bile from the liver.

Bile salts are known as the liver's "cleansing agents" because they act as "soaps" that carry away the toxins and flush them into the intestines for excretion. If the bile flow is restricted in the liver, then the liver cannot rid itself of toxins. When the liver loses its ability to excrete toxins, it creates a buildup of toxins throughout the entire body. (1-13)

This condition is known as cholestasis [Kola-sta-sis]. By definition, cholestasis is a condition where the flow of bile cannot flow from the liver. (1) This is the most common liver condition developed from 17-aa steroids. (1-7)

If a liver becomes cholestatic for too long, the condition can begin damaging liver cells by causing necrosis (premature death of liver cells) from excessive toxin build up in the liver. This can eventually lead to cirrhosis of the liver (development of fibrous scar tissue) when the liver attempts to regenerate the damaged liver cells. This leads to loss of liver function from the replacement of healthy liver cells with fibrous connective tissue. (2)

Although cholestasis is reversible and generally not a lethal condition, it can lead to the more serious problems mentioned above if left untreated -- not to mention costly medical bills.

To avoid serious health complications it's important to protect the liver before it becomes cholestatic or seriously damaged from prolonged cholestasis (which I will explain later).



What are signs that my liver is damaged?

When the liver has been damaged by oral steroids there are certain signs that may become obvious to the user.

Here are some of the most common signs indicating you may have a serious liver issue. Warning signs usually appear in the following order, with the later signs being the most serious -

• Reduced appetite
• Nausea and fever
• Excessive Itchiness
• Yellow eyes or skin (jaundice)
• Very dark urine (dark amber colored)
• Bloody stools


Waiting for all these signs to appear means you have waited too long. You want to take action BEFORE these signs appear. This is why I advise getting full lab values on liver function before, during and after any 17-aa oral steroid cycle. If performing lab tests for liver function, the following values are considered normal.


Normal Values -

Total bilirubin range: 0.3-1.7 mg/dl

Alanine aminotransferase (ALT) range: 10-40 IU/L

Aspartate aminotransferase (AST) range: 10-40 IU/L

Alkaline phosphatase (ALP) range: 34-125 IU/L

Gamma-glutamyl-transpeptidase (GGT) range: 7-32 IU/L

Levels above these normal values doesn't necessarily mean you have liver damage. It is common for healthy weight training athletes or bodybuilders to be slightly outside of the "normal" ALT, AST and ALP values. Therefore these "Danger Values" have been established as more appropriate levels to indicate a serious liver toxicity issue. (1-7)


Danger Values -

Total bilirubin: 10 mg/dl or higher

Alanine aminotransferase (ALT): 50 IU/L or higher

Aspartate aminotransferase (AST): 50 IU/L or higher

Alkaline phosphatase (ALP): 150 IU/L or higher

Gamma-glutamyl-transpeptidase (GGT) range: 50 IU/L or higher
NOTE: Historical research from 17-aa oral steroid induced liver toxicity suggests that lab values higher than the "Danger Values" indicate that you may be suffering from cholestasis (1-7) If your lab values are higher than the "Danger Values" listed above you should discontinue any current oral steroid use and seek medical treatment.

If the above lab tests are not an option, it is possible to get an affordable at home test for bilirubin levels, which can help diagnose a liver damage from a 17-aa oral steroid. There are tests available, such as the TestMedica Liver Home Scan, which can be purchased online for less than $5 per test. Although these home based tests lack accuracy or true diagnosis ability, it can offer a valuable insight about the condition of the liver and is recommended for any steroid user not able to get lab tests done in a clinical setting.



How can I protect my liver?

To prevent cholestasis, the primary condition caused by oral steroid use, it is important to ensure there is ample hydrophilic bile acid available in the liver for the proper clearance of toxins. There are two reliable options for this.

1. The first option is the drug known as Ursodiol - a.k.a. ursodeoxycholic acid. This naturally occurring bile acid is used for its ability to detoxify the liver by clearing out less hydrophilic bile acids and other toxins that cause a toxic build up, such as 17-aa oral steroids. (4,5)

Ursodiol is typically prescribed to patients admitted to the hospital for steroid induced liver toxicity, but unfortunately, it is an expensive prescription drug, and not easily obtainable.

Typical dose - 1000-1200mg/day before, during and after cycleOne more small thing I found someone post on another forum:


Everytime now that I take an oral AAS, I get massive heartburn within 3 days. I even tried an injectable oral and still got acid reflux within a week. So, I did some research and found some interesting information. This is just a random post I found on Google.


http://www.********.com/forums/archi...p/t-36636.html
Everyone seems to miss what is happening here. If an oral kills your appetite, it is because it is too toxic for the liver. I forget exactly what happens, but to summarize, when the liver is overloaded it causes a slowing of digestion, and a backflow of bile, which is why you also see people complaining of acid reflux on harsh 17aa's. The only way to really cure your appetite is to drop the anadrol . Perhaps next time around run with liv. 52 and alpha lipoic acid?



From what I read, bile helps with digestion. Now, when I take an oral AAS, the pain I get is similar to acid reflu/heartburn, but not exactly. It feels more like the food I eat just sits in my stomach and rots, never digesting. Lets say I eat some tacos on Tuesday, by Thursday morning I am still burping that taste up.That always made me wonder if orals cause heartburn or something similar.




Now read this
http://www.emoryhealthcare.org/liver...blems.html#PBC

In primary biliary cirrhosis, inflammation destroys the bile ducts and prevents bile from escaping the liver. The accumulated bile damages healthy liver tissue, eventually leading to cirrhosis (scarring). As scar tissue replaces healthy liver tissue, the liver loses its ability to function. All this happens very slowly. People with PBC can lead healthy, symptom-free lives for 10 years or more after diagnosis.

Though primary biliary cirrhosis is often asymptomatic, especially early on, the most common symptom is extreme itching, especially in the arms, legs and back. Other symptoms include fluid buildup in the abdomen or legs, jaundice (yellowing of the eyes and skin), or fatty deposits and darkening of the skin under the eyes.

The standard treatment for PBC is a daily dose of a medication called ursodiol. Ursodiol improves liver function and increases life expectancy in people with PBC. Other medications may be indicated for controlling symptoms
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Chardon marie je prends comme second poto le premier au tout haut de la liste c'est tudca pour moi dosé à min. 250mg par pills
 
Pour le TUDCA, je note plusieurs points suivants suite à la lecture de tes liens et contenus :
Code: 
They are extremely potent at preventing or reversing 17aa-androgen-mediated liver damage. There's really no excuse not to take them, in my opinion, and I would advise you not to run a cycle if you can't afford them

Code: 
TUDCA reduced both ALT and Knodell's score in the 5 patients in whom a significant increase of PCNA-LI (p < 0.05) was observed after treatment


Update de la cure au 23 juin

Dès S-5 : Début de la nouvelle diète
S-3 : PDS complète
S-2 : Chardon-Marie Okygen 300mg (1 comprimé)
S-1 : Chardon-Marie Okygen 300mg (1 comprimé)
S1 : Tbol 30mg / Samarin 140mg / TUDCA Premium Powders 250mg
S2 : Tbol 30mg / Samarin 140mg / TUDCA Premium Powders 250mg // PDS simple fin S2
S3 : Tbol 40mg / Samarin 140mg / TUDCA Premium Powders 250mg
S4 : Tbol 50mg / Samarin 140mg / TUDCA Premium Powders 250mg // PDS simple fin S4
S5 : Tbol 50mg / Samarin 140mg / TUDCA Premium Powders 250mg
S6 : Tbol 50mg / Samarin 140mg / TUDCA Premium Powders 250mg // PDS simple fin S6
S+1 : Clomid 50mg / nolvadex 20mg / TUDCA Premium Powders 250mg
S+2 : Clomid 50mg / nolvadex 20mg / TUDCA Premium Powders 250mg
S+3 : Clomid 50mg / nolvadex 20mg / TUDCA Premium Powders 250mg
S+4 : OFF
S+5 : PDS complète
Cliquez pour agrandir...

Qu'en pensez vous ?
Merci les potos !
 
Qu on soit d accord
Aucun hepato protecteur n a fait sa preuve dans la prophylaxie de traitements hepatotoxiques (aka prévention d une hepatite médicamenteuse)
Le mieux qu on a pu avoir c est une réduction des transas dans des études de merde, avec aucune incidence sur la survie


Tu peux prendre ce que tu veux aux dosages qui te chantent l ami, ça changera pas grand chose

Les différents liens qui t ont été proposé parlent de cirrhose biliaire primitive ou d hepatopathies chroniques, ce qui n a absolument rien à voir

Pour rappel, une part non négligeable d hépatite médicamenteuse est due à des suppléments divers et variés

Mon message, ça te dispensera pas d un suivi, suivi qui doit dépasser les transas sur la PDS, pour rappel un des éléments les plus préoccupants avec les oraux c est la peliose hépatique, et ça t en entendra pas parler sur les forums et ça se voit pas à la PDS

Ça sera ma seule intervention sur le sujet, le "débat" a déjà était fait
 
saveed à dit:
Pour le TUDCA, je note plusieurs points suivants suite à la lecture de tes liens et contenus :
Code: 
They are extremely potent at preventing or reversing 17aa-androgen-mediated liver damage. There's really no excuse not to take them, in my opinion, and I would advise you not to run a cycle if you can't afford them

Code: 
TUDCA reduced both ALT and Knodell's score in the 5 patients in whom a significant increase of PCNA-LI (p < 0.05) was observed after treatment


Update de la cure au 23 juin



Qu'en pensez vous ?
Merci les potos !
Cliquez pour agrandir...
Je pense que ça a l'air bon pour ton procotole de cure si les PDS sont faites consciencieusement et que tu suis ce que les bilans t'indiquent
Enfin perso si je devais faire une cure de tbol je ferai probablement de cette manière
 
havah à dit:
pour rappel un des éléments les plus préoccupants avec les oraux c est la peliose hépatique, et ça t en entendra pas parler sur les forums et ça se voit pas à la PDS
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Effectivement j'avais jamais entendu parler de cette bête là... Merci de l'info poto.
Mais du coup comment on fait pour voir si on est pas atteint de cette merde ?
 
  1. Pharmaceutical hepatitis; in that case, liver transaminases are elevated (>100). These elevations are attributed to the intake of oral steroids, are usually asymptomatic, transient and return to baseline levels within several weeks after cessation. Such elevations have been most closely linked to fluoxymesterone and oxymethalone. Occasionally this is mis-diagnosed with muscle damage/rhabdomyolysis (CPK>500) rather than hepatic dysfunction, since both hepatocytes and muscle cells posses receptors for SGOT and SGPT enzymes. Recently, studies demonstrated that GGT is the most distinctive enzyme for the detection of hepatic dysfunction.
  2. Cholestasis; a condition where jaundice occurs. There is not proper elimination of bile, through bile duct and bile tubules intracellular of liver parenchyma. The onset is usually accompanied with development of nausea, fatigue and itching followed by dark-brownish urine (elevated urobilinogen) and jaundice (elevated bilirubin). Jaundice can be prolonged even if the AAS are discontinued. Typically, serum elevations of cholestatic markers such as ALP, γGT, bilirubin-direct/indirect, are present. Liver biopsy typically shows cholestasis with inflammation, hepatocellular necrosis and hyperplasia of hepatocytes. This clinical phenotype of cholestasis is typical of the use of AAS.
  3. Hepatic peliosis; is a rare syndrome in which liver lobes are covered with nodulation that contain blood cysts. The liver may be enlarged, deep red in color. Serum enzyme levels are usually normal or mildly elevated. Patients may present with right upper discomfort. This is a critical and sometimes fatal condition. However, peliosis associated with AAS usually reverses, at least in part, in case the patient discontinuates AAS abuse for good.
  4. Hepatocellular carcinoma; the most serious complication of AAS use is the development of hepatic tumors, either adenoma (HCA) or hepatocellular carcinoma (HCC). Clinical presentation is generally with right upper quadrant discomfort and a hepatic mass found clinically or on imaging studies (U/S,C/T). Routine liver tests are often normal, unless there is extensive spread or rupture or any accompanying liver disease. While fluoxymesterone is associated with HCA formation, other substances like oxymetholone, respectively, methyltestosterone can lead to HCC. There are different therapeutic strategies for HCC without metastasis. In general liver transplantation is the therapy of choice for selected patients with HCC without the possibility of extrahepatic metastasis. Abuse of AAS over a long period of time has a risk of developing an HCC and users should therefore be well monitored. Periodic hepatic ultrasound seems to be an adequate screening procedure to detect the development of hepatic lesions.
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Le toubib BB de anabolic en parle mais ce n'est pas le cas le plus fréquent, sur tous les sites sérieux que je lis et les cases reports c'est bel et bien la choléstase qui revient...
 
Use of androgenic steroids is associated with a variable rate of serum enzyme elevations which are usually asymptomatic and self limited. Such elevations have been most closely linked to danazol and oxymethalone, but are usually transient and do not require dose adjustment or discontinuation.

More importantly, therapy with anabolic steroids is linked to a distinctive form of acute cholestasis.

livertox.nih.gov/AndrogenicSteroids.htm

Almost any subject abusing AAS will experience adverse effects. Therefore, adverse effects from these exposures, including liver toxicity, are expected to increase in the years to come. The present manuscript describes a representative case of intrahepatic cholestasis with the intention to discuss AAS-related liver toxicity
Anabolic-androgenic steroids and liver injury (PDF Download Available). Available from: https://www.researchgate.net/publication/5945001_Anabolic-androgenic_steroids_and_liver_injury [accessed Jun 23 2018].


Results
As demonstrated by the cases in this report, synthetic AAS caused a remarkable cholestatic hepatotoxicity.
Despite a relatively uneventful recovery, their clinical courses were associated with considerable morbidity.
Conclusion
Synthetic AAS that are not classified as controlled substances continue to fall outside the Food and Drug
Administration (FDA) jurisdiction. They are still available in over-the-counter supplements and are a cause for
serious hepatotoxicity in the United States. Stricter control of their use outside the medical necessity should be
applied and healthcare providers should recognize the significance of the problem.

Hepatotoxicity Associated with Anabolic Androgenic Steroids Present in Over-The
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dvnfit666 à dit:
Je pense que ça a l'air bon pour ton procotole de cure si les PDS sont faites consciencieusement et que tu suis ce que les bilans t'indiquent
Enfin perso si je devais faire une cure de tbol je ferai probablement de cette manière
Cliquez pour agrandir...

Merci !
Pour la PDS, ça sera très rigoureux, j'ai noté tous les points que je vais contrôler ici : https://fr.thinksteroids.com/commun...-pour-septembre-2018.17098/page-4#post-421246

Si tu as des remarques sur cette liste, n'hésite pas ;)
 
Pourquoi ne pas en parler à ton médecin je comprends vraiment pas poto
Encore une fois si un jour tu as une merde ce n'est pas le forum qui va te soigner ou te promulguer les premiers soins en vrai

Et surtout si ton toubib sait de suite que tu es sous traitement aas il pourra mieux comprendre certaines choses
 
dvnfit666 à dit:
Pourquoi ne pas en parler à ton médecin je comprends vraiment pas poto
Encore une fois si un jour tu as une merde ce n'est pas le forum qui va te soigner ou te promulguer les premiers soins en vrai

Et surtout si ton toubib sait de suite que tu es sous traitement aas il pourra mieux comprendre certaines choses
Cliquez pour agrandir...

C'est surtout parce que c'est le médecin de famille, celui qui me suit depuis tout jeune.
Je sais d'entré que mon médecin n'est pas réceptif à ce genre de chose, même s'il est très sympa.

Solution : Changer de médecin traitant je pense :D !
 
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