Liver damage VS liver stress
As a general rule, hepatobiliary adverse effects of ASA use are usually limited to agents alkylated in 17α charcoal and consumed orally.
These androgens are synthesized by replacing hydrogen with a methyl or ethyl group in the C17α position, thus preventing its deactivation during the first step of hepatic metabolism and allowing greater oral bioavailability, since most would have almost no bioavailability without it.
However, although SARMs do not have this chemical structure, it does not make them free of possible side effects on the liver. With the use of conventional ASA, what is usually observed is liver damage caused mainly by cholestasis. This is a condition where bile cannot flow correctly through the liver to the duodenum. In short, this bile accumulates in the liver and subsequently It causes damage to the liver by accumulation, damaging cells and subsequently causing cell death.
Con el uso de SARM lo que comúnmente se observa son elevaciones de transaminasas sin ningún efecto a nivel biliar en las analíticas. Esto, sumado a la gran cantidad de reportes de casos de daño hepático inducido por el uso de SARMs en la literatura científica actual, podríamos extrapolar que el daño que producen es un tipo de daño directo por su interacción con los receptores andrógenicos.
Como arreglarlo
n estos casos (uso de SARMs), lo mejor es utilizar agentes antioxidantes en la dosis más baja/efectiva posible para intentar atenuar ligeramente el daño a nivel hepático sin afectar negativamente a la masa muscular, dado que una cantidad alta de antioxidantes disminuye la ganancia de masa muscular.
-NAC: 600-1200 mg al día.
-R-ALA: 600-1800 por día.
-Vitamina C: 1000 mg al día.
Taking NAC is already more than enough in most cases, all the products mentioned above are easily available everywhere.
If we use other types of oral PEDs we can always take TUDCA, 300-1200 mg of TUDCA daily should be enough to reverse any type of temporary damage.
