Mar 18, 2013
USA / Europe
Peat has touched upon his views of the immune system in several articles, mostly related to autoimmune disease. In his view, the role of the immune system is not so much to "attack" foreign pathogens that threaten the organism, but is more akin to sanitation workers who clean up trash and other debris that can become food for pathogens and stimulate their growth. It is the energetic status of the organism that determines resistance to infections, and if the immune system gets activated it is to remove bits and pieces of damaged tissue that has necrotized due to insufficient energetic resources. This theory is commonly known as Morphostasis theory of immunity and there the website below describes it in more detail.

Of course, mainstream medicine flatly denies such a role for the immune system and continues to insist that we are constantly under attack by "evil" organisms and we need all sorts of vaccines to protect us, or immunosuppressive therapies when our own immune system turns against us. However, that pernicious view of human biology and the immune system may be beginning to change with studies like the one below. It discovered that during a heart attack, our immune system gets "activated" as if the body is under attack by virus and it is the overactivity of the immune system that leads to scarring of the heart muscle. Suppressing the immune system was therapeutic and prevented the scarring as a result of a heart attack. I think a much better approach would have been to prevent as much as possible cell death during a heart attack and thus avoid the activation of the "garbage disposal" system, instead of suppressing it. Progesterone, niacinamide and inosine are among the chemicals known to prevent cell death during ischemia and unsurprisingly have shown tremendous benefit in animal studies with both stroke and heart attacks. In addition, considering Peat's writing on the role of estrogen in triggering such "autoimmune" attacks, other anti-estrogenic substances like aspirin, vitamin E, vitamin E, emodin, etc should also be quite helpful. Those have also demonstrated highly therapeutic effects in both preventing the occurrence of and limiting the damage from ischemic events like heart attacks and strokes.
Going beyond heart attacks, I think this illustrates that many of the so-called chronic viral conditions (CFS, EBV, JCV, etc) are in fact nothing more but a heightened immune response to disintegrating tissue due to energetic dysfunction. Restoring the energetic levels may be highly therapeutic for those conditions as well. Inosine is chemical with known "anti-viral" properties and has been patented as a prescription drug under the name of Inosine Pranobex. I put the "anti-viral" in quotes because in light of this study and the knowledge of morphostasis, inosine's effects may have nothing to do with stopping an actual virus. Instead, inosine may simply be correcting an energetic deficiency, as it is an effective precursor to ATP. A lack of proper ATP synthesis is well known to quickly leads to cell death and thus "immune" activation. Restoring ATP levels has been shown to be therapeutic in a variety of cases ranging tom from liver disease, to neurodegenerative disease, to infectious disease, to cancer. I posted quite a few studies on inosine's role as ATP precursor in the Cardenosine thread if there is interest in learning more about it.


Immune cells mistake heart attacks for viral infections

"...The team, which also includes researchers from the Center for Systems Biology at Massachusetts General Hospital (MGH), Brigham and Women’s Hospital, Harvard Medical School, and the University of Massachusetts, presents the findings in the journal Nature Medicine. Ischemic heart disease is the most common cause of death in the world and it begins with a heart attack. During this process, heart cells die, prompting immune cells to enter the dead tissue, clear debris and orchestrate stabilization of the heart wall. But what is it about dying cells in the heart that stimulates the immune system? To answer this, researchers looked deep inside thousands of individual cardiac immune cells and mapped their individual transcriptomes using a method called single cell RNA-Seq. This led to the discovery that after a heart attack, DNA from dying cells masquerades as a virus and activates an ancient antiviral program called the type I interferon response in specialized immune cells. The researchers named these “interferon inducible cells (IFNICs).” When investigators blocked the interferon response, either genetically or with a neutralizing antibody given after the heart attack, there was less inflammation, less heart dysfunction, and improved survival. Specifically, blocking antiviral responses in mice improved survival from 60 percent to over 95 percent. These findings reveal a new potential therapeutic opportunity to prevent heart attacks from progressing to heart failure in patients. “We are interested to learn whether interferons contribute to adverse cardiovascular outcomes after heart attacks in humans,” said King, who did most of the work on the study while he was a cardiology fellow at Brigham and Women’s Hospital and at the Center for Systems Biology at MGH in Boston. The immune system has evolved innate antiviral programs to defend against a diverse range of invading pathogens. Immune cells do this by detecting molecular fingerprints of pathogens, activating a protein called IRF3, and secreting interferons, which orchestrate a defense program mediated by hundreds of interferon-stimulated genes. Investigators found that surprisingly, the antiviral interferon response is also turned on after a heart attack despite the absence of any infection. Their results point to dying cell DNA as the cause of this confusion because the immune system interprets it as the molecular signature of a virus. Surprisingly, the immune cells participating in the interferon response were a previously unrecognized subset of cardiac macrophages. These cells could not be identified by conventional flow sorting because unique markers on the cell surface were not known. By using single cell RNA Seq, an emerging technique that combines microfluidic nanoliter droplet reactors with single cell barcoding and next generation sequencing, the researchers were able to examine expression of every gene in over 4,000 cardiac immune cells and found the specialized IFNIC population of responsible cells."

Broken man

Sep 11, 2016
This is exactly my story. Its 1 month that I started with inosine. For me, its the best supplement now . I have alot of energy, lost some weight, good mental clarity, better muscle recovery. My lupus is away too but dont know if its because of inosine.


Feb 20, 2013
Mainstream medicine is so contradictory. On the one hand they say you need an immune system to protect you from germs, but at the same time they give you immunosuppressive drugs to treat auto-immune conditions. This makes you more sensitive to getting infections and also increases tissue breakdown and cell death (cortisol causes tissue breakdown). This increased cell death then activates your immune system to clean it up, resulting in even stronger auto-immune flares when the drug is removed. Using immunosuppressive drugs to treat auto-immune problems just makes the situation worse.


Apr 5, 2016
Would you be able to apply this theory to type 1 diabetes. As in the immune system attacks the pancreas due to chronic metabolic stress in an ill fated attempt to maintain its structure?


Thread starter
Mar 18, 2013
USA / Europe
Would you be able to apply this theory to type 1 diabetes. As in the immune system attacks the pancreas due to chronic metabolic stress in an ill fated attempt to maintain its structure?

I don't think the immune system attacks the pancreas. The pancreas is failing due to very high levels of FFA (PUFA), estrogen, and cortisol and the immune system clears up the dead tissue. High doses niacinamide has been shown in some studies to reverse type I diabetes in children, which is consistent with the high FFA destroying the pancreas. Peat also spoke about this mechanism behind the type I "diabetes". Most adult onset of diabetes I are a result of severe stress of some sort. Special forces soldiers have a very high incidence for that very reason - chronic VERY high stress levels.


Sep 10, 2014
Not Uganda
- Beyond Host Defense: Emerging Functions of the Immune System in Regulating Complex Tissue Physiology
Abstract said:
The essential roles played by the immune system in the discrimination between self- versus non/altered-self and its integral role in promoting host defense against invading microbes and tumors have been extensively studied for many years. In these contexts, significant advances have been made in defining the molecular and cellular networks that orchestrate cell-cell communication to mediate host defense and pathogen expulsion. Notably, recent studies indicate that in addition to these classical immune functions, cells of the innate and adaptive immune system also sense complex tissue- and environment-derived signals, including those from the nervous system and the diet. In turn these responses regulate physiologic processes in multiple tissues throughout the body, including nervous system function, metabolic state, thermogenesis, and tissue repair. In this review we propose an integrated view of how the mammalian immune system senses and interacts with other complex organ systems to maintain tissue and whole-body homeostasis.


Sep 24, 2016
Everything is intertwined, and physiology is very "efficient" meaning that every part of it fullfills as many roles as needed, as little as possible.
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