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Blog #3: Stress: The kind we have in us and the kind outside of us (Lay Version)

Updated: Jun 29, 2023

When I did the research for my book, The Paradox of the Immune System, I began to realize that “stress” disrupts the normal state of our body in ways we have never considered. Whether it’s mental, physical or caused by environmental factors like foreign, “antigen” or “non-self” substances (Einstein once said, “The environment is everything that isn’t me”). It has been scientifically proven that stress produces a loss of the normal balance in the functions, cells and fluids that control our health and well-being (this balance is called "homeostasis"). That being the case, we can conclude that external and internal forms of stress create a “dysregulation” (a loss of homeostasis) or an abnormal state in our body, including our immune system. This imbalance leads to injury and death of cells and tissues within our body, all of which are constantly accumulating as abnormal debri. The immune system interprets this debri as an “autoantigen,” that is, a substance produced by the body itself, i.e., “auto,” but foreign to it, “antigen.” It treats this “non-self” autoantigen substance as it would any antigen. As such, the immune system is now reacting to both this autoantigenic stimulus along with the originating (stress) factors. This combination produces a cycle sometimes referred to as the ”clinical autoimmune cycle” or the “danger hypothesis” intoning a dangerous situation.

Taking this process to its logical conclusion, if we recall from the previous blog on the cause of chronic inflammation being an unrelenting immune response, we can conclude that this stress “cycle” is a potential cause of chronic inflammation. And when considering the driving force of a stress-related immune response being autoantigens, along with its originating external or internal cause(s), we can begin to see the basis for chronic inflammation and stress as the basis for all disease categories. Such categories include autoimmune diseases, cancers and the range of almost all other diseases.


Based on this immunology logic about stress as the basis for chronic inflammation and all diseases, why aren’t all humans in a constant state of clinical or subclinical “disease”? Could it be that we actually are in varying stages of stress-related dysregulation, but controlled by forces in the body (genetic, immunologic, neurologic and more) yet undetermined? Certainly, more research must be conducted to identify such forces that amplify or mitigate human disease in the presence of stress antigenicity.

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