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Re: hope that you don't end up dying from liver or kidney damage
 
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Published: 6 years ago
 
This is a reply to # 2,286,175

Re: hope that you don't end up dying from liver or kidney damage


I would like to say that my responses are not meant to be inflammatory but thought provoking. This is not an issue which side is right for the sake of argument but rather a journey of learning so people can find their cure.

I have read more accounts of people getting well from pharmas than natural remedies. parasites create a living hell in the body via immune reactions (ROS/RNS) reactive oxygen/nitrogen species, immune shifting, endocrine disturbances, pain etc, than any pharma could ever hope to. Furthermore the ROS/RNS damage tissues (liver, kidney, cell membranes, etc).

This is an article on liver damage caused by oxidative stress. Note the author points out that endotoxins created by pathogens create damage, not just drugs. The author goes on to say that the ROS from the immune cycles damage mitochondrial functioning (damages cells and cell membranes rendering them weakened).

AbstractSend to:
J Gastroenterol Hepatol. 2011 Jan;26 Suppl 1:173-9. doi: 10.1111/j.1440-1746.2010.06592.x.
Reactive oxygen and mechanisms of inflammatory liver injury: Present concepts.
Jaeschke H1.
Author information
Abstract
Liver cell death induced by stresses such as ischemia-reperfusion, cholestasis and drug toxicity can trigger a sterile inflammatory response with activation of innate immune cells through release of damage-associated molecular patterns (DAMPs). A similar inflammatory response can be induced by pathogen-associated molecular patterns (PAMPs) such as endotoxin. Both DAMPs and PAMPs activate through toll-like receptors the resident macrophages (Kupffer cells) and recruit activated neutrophils and monocytes into the liver. Central to this inflammatory response is promotion of reactive oxygen species (ROS) formation by these phagocytes. ROS are the principal toxic mediators by which inflammatory cells kill their targets, e.g. bacteria during host defense but also hepatocytes and other liver cells. The mechanism of ROS-induced cell killing during inflammation involves the promotion of mitochondrial dysfunction through an intracellular oxidant stress in hepatocytes leading mainly to oncotic necrosis and less apoptosis. The additional release of cell contents amplifies the inflammatory injury. However, an inflammatory oxidant stress insufficient to directly cause cell damage can induce transcription of stress defence genes including antioxidant genes. This preconditioning effect of ROS enhances the resistance against future inflammatory oxidant stress and promotes the initiation of tissue repair processes. Despite the substantial progress in our understanding of mechanisms of inflammatory liver injury during the last decade, more research is necessary to better understand the role of ROS in acute liver inflammation and to develop clinically applicable therapeutic strategies that selectively target the detrimental effects of oxidant stress without compromising the vital function of ROS in host defense.
© 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd.
 

 
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