This paper is not just about cancer but is relevant to understanding the role of angiotensin receptors in inflammation. It suggests the use of AT1 receptor antagonists in treating inflammatory and autoimmune disorders.
http://www.journal-inflammation.com/content/1/1/3
I understand very little of it, but what's interesting is that the type of drugs it suggests include olmesartan (Benicar) which is used in the Marshall protocol. Has anyone experimented with Benicar without doing the whole Vit D avoidance thing?
From a review of the current disease literature, it has been demonstrated that the role of AT1 and AT2 in inflammation is not limited to cancer-associated inflammation, but is generally consistent and system wide. Potential therapy by manipulation of these receptors, although at an early stage, has been demonstrated for some of these diseases and it is proposed that this approach will provide an effective basis for the treatment of autoimmune, inflammatory and neurodegenerative disorders using existing drugs. AT1 receptor blockade should, in addition, provide a treatment to alleviate the damage caused by bacterial and viral infections, where their destructive action is through chronic inflammation. Given the importance of the immune suppressant effect of inflammation in cancer, it is anticipated that AT1 blockade should also serve to elicit a more effective immune response to other invaders that seek to corrupt the wound recovery process.
Manipulation of the AT1 and AT2 receptors has profound and exciting implications in the control of disease.
Jenny
http://www.journal-inflammation.com/content/1/1/3
I understand very little of it, but what's interesting is that the type of drugs it suggests include olmesartan (Benicar) which is used in the Marshall protocol. Has anyone experimented with Benicar without doing the whole Vit D avoidance thing?
From a review of the current disease literature, it has been demonstrated that the role of AT1 and AT2 in inflammation is not limited to cancer-associated inflammation, but is generally consistent and system wide. Potential therapy by manipulation of these receptors, although at an early stage, has been demonstrated for some of these diseases and it is proposed that this approach will provide an effective basis for the treatment of autoimmune, inflammatory and neurodegenerative disorders using existing drugs. AT1 receptor blockade should, in addition, provide a treatment to alleviate the damage caused by bacterial and viral infections, where their destructive action is through chronic inflammation. Given the importance of the immune suppressant effect of inflammation in cancer, it is anticipated that AT1 blockade should also serve to elicit a more effective immune response to other invaders that seek to corrupt the wound recovery process.
Manipulation of the AT1 and AT2 receptors has profound and exciting implications in the control of disease.
Jenny