barano90 / przygotowania PP NAC jesień 2013

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prz1993 Zawodnik IFBB

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Jest liderem w tym dziale Szacuny 21595 Napisanych postów 30819 Wiek 30 lat Na forum 13 lat Przeczytanych tematów 870875

Jakiś czas temu pamiętam polecałeś jakiś olej na problemy z trawieniem. Mógłbyś podać nazwę? Bo zacząłem metę i zaczęła się lipa lekka... A Ty chyba jesteś najbardziej ogarniętą osobą w tematach wątrobowo-trawiennych

Lecą probiotyki, NAC, esseliv, ale od kilku dni sraka i wzdęcia...

http://www.sfd.pl/Przemek_Górynowicz_&_IHS__MASA!-t1021799.html
http://www.sfd.pl/Droga_do_debiutów_2014__Przemek_Górynowicz_&_IHS_-t967941.html
http://www.sfd.pl/prz1993_/_Natural_Pałer_%_-t955065.html

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Anonim

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Szacuny 11148 Napisanych postów 51569 Wiek 31 lat Na forum 24 lat Przeczytanych tematów 57816

warto spróbować tego TUDCA,

NAC, TAD czy heparegen te leki działają głownie na poniesienie glutationu i tu sie spisują działac działają lepiej sie czujemy szybciej wywala syf z organizmu ale nadal nie usuwają przyczyny, Esseliv to jedynie może wspomóc pracę wątroby i wspomóc przy odbudowie.

Zagłębcie się w temat jak głownie działają saa na wątrobę a wszystko się wyjaśni.

skutki uboczne zastoju żółci dodatkowo można zaobserwować na dietach VLCD czy nisko tłuszczowych gdzie po wyjśćiu z redukcji idziemy na całęgo z żarciem. Jak sie nie myle to karpiu dobrze zna temat bo wylądował w szpitalu głownie chyba przez to

posty Ś.P bokita na animalu powinni oprawić w ramkę i chronić, szkoda że nie ma takich ludzi więcej co bez celowo po prostu pomagają innym i to z taką wiedzą jak on nie ma już chyba nikogo w pl, wiedzą praktyczną, teoretyczna no i podpiętą pod saa

TUDCA zamówiony zamiennik 100kaps/250mg 89zl na receptę ale już wszystko ogarnięte w przyszłym tyg będe miał recepte a w zamian w aptece dostałem Raphacholin C ma pomóc zapewniała farmaceutka

2 tyg na TUDCA, NAC, TAD, kwas ALA, esseliv jak nie zejdą próby ide do rodzinnego po skierowanie na USG jamy brzusznej + na reszte badań

Zmieniony przez - barano90 w dniu 2014-05-31 14:10:15

Zmieniony przez - barano90 w dniu 2014-05-31 14:16:51

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rkarpinski Natural SFD Team

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Szacuny 1596 Napisanych postów 56736 Wiek 40 lat Na forum 15 lat Przeczytanych tematów 264393

Daj nazwę tego tudca aptecznego. Pytałem u mnie i nic im to nie mówi.

Doświadczenia wszystkich kulturystów są podobne
Ludzie się na nich gapią, wytykają palcami
Są jak wybryki natury ale nie mają cyrkowego namiotu aby się w nim skryć.

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Anonim

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Szacuny 11148 Napisanych postów 51569 Wiek 31 lat Na forum 24 lat Przeczytanych tematów 57816

bo ci farmaceuci wiedzą tyle, że więcej w google sie dowiesz niż od nich

Proursan, Ursocam, Ursofalk, Ursopol najtaniej wychodzi proursan około 80-90zl reszta koło 120zl

TUDCA=UDCA działanie to samo

Zmieniony przez - barano90 w dniu 2014-05-31 14:35:07

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Anonim

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Szacuny 11148 Napisanych postów 51569 Wiek 31 lat Na forum 24 lat Przeczytanych tematów 57816

Ciekawa lekturka sporo wyjaśni

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:

Metabolic induction of hydrophobic bile acid detoxification
Stimulation of impaired bile secretion
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.

źródło : http://www.ironmagazineforums.com/

Zmieniony przez - barano90 w dniu 2014-05-31 14:46:00

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Anonim

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Szacuny 11148 Napisanych postów 51569 Wiek 31 lat Na forum 24 lat Przeczytanych tematów 57816

mm1986
Ja sie akurat kompletnie nie znam na tych suplementach wspomagajacych watrobe itp, bo jak narazie to moja watroba nawet przyjmujac 10miesiecy orale, w niemalych dawkach sluzy jak najbardziej - narazie ale Barano, tu u mnie w stanach kazdy szamie obowiazkowo suplement o nazwie Tudca, co prawda nie nalezy do najtanszych ale kazdy to chwali ze naprawde pomaga, ale jaki jest sklad, tego Ci nie powiem, musisz sprawdzic

widać odrazu, że w stanach wiedzą co robią a nie esseliv + ziólka na wiadro orali

może się przczynisz do dokształcenia polskiego piwniczanego bodybuildingu i przetłumaczysz trochę chłopaką