Chandler Marrs, PhD
Read Chandler’s important discussion on immune function and the connection to mitochondrial dysfunction.
When you have a hammer, everything becomes a nail, or so they say. I worry about this as I dig deeper into mitochondrial dysfunction. Could all of these disparate symptoms and conditions have their roots in the mitochondria? Could it be that simple? Perhaps. More and more, as I search for explanations for the devastating symptoms that so many of our readers report, the research I find points to mitochondrial dysfunction. Sure, changes in gut microbiota and function are apparent and often related and certainly immune dysregulation is a component of these illnesses, but the underlying connection among these disturbances seems inevitably and inextricably linked to dysfunctional mitochondria as the central hub of illness.
Heal the mitochondria, heal the body, is quickly becoming my new mantra.
Mitochondria as Danger Sensors
Some researchers argue that the mitochondria are the danger sensors for host organisms; having evolved over two billion years to identify and communicate signs of danger to the cells within which they reside. The signaling is simple and yet highly refined, involving a series of switches that control cellular energy, and thus, cellular life or death. When danger is present, energy resources are conserved and the immune system fighters are unleashed. When danger is resolved, normal functioning can resume.
If the danger is not resolved and the immune battles must rage on, the mitochondria begin the complicated process of reallocating resources until the battle is won or the decision is made to institute what can only be described as suicide – cell death. Cell death is a normal occurrence in the cell cycle of life. Cells are born and die for all manner of reasons. But when cell death occurs from mitochondrial injury, it is messy, and evokes even broader immune responses, setting a cascade in motion that is difficult to arrest.
And, if the on the battlefield, the host army is understaffed and under-resourced, no matter how hard the immune fighters battle, the fight will be lost, maybe not immediately, but eventually. All sorts of mechanisms will be employed to reallocate and reinforce needed battlements, but they will be for naught, further depleting already scarce host resources, until the decision is made, within the mitochondria, to begin pulling back, withdrawing, and ultimately casting the final orders of cell death.
It’s not Autoimmunity, but Impaired Immunity
I never much liked the war model of health and disease, but it seems to work well as metaphor for immune functioning, as it is far more illustrative and useful than the self-versus non-self-characterization. Really, what army with two billion years of experience, one that contains all of the memories and skills of battles past, would misidentify itself and begin broad scale fratricide – kill itself and its brethren for no other reason but mistaken identify and do so for years on end? Sure, there can be errors, over compensation and other weaknesses in the immune system, but not continued aggression towards itself in some maladaptive response. That makes no sense and contradicts the very notion and function of an immune system – to keep the host organism alive and well. Indeed, when we consider the trillions of microbes – clear non-self entities – that live inside and upon us, the idea that the immune system evolved simply to kill the non selves seems laughable. And so, I reject the concept of autoimmunity, not because the patients who suffer from continued immune system activation are not ill, they are, but because the concept of autoimmunity belies the very nature of immune function and severely limits possible approaches to recovery.
About the Author
Chandler Marrs MS, MA, PhD spent the last dozen years in women’s health research with a focus on steroid neuroendocrinology and mental health. She has published and presented several articles on her findings. As a graduate student, she founded and directed the UNLV Maternal Health Lab, mentoring dozens of students while directing clinical and Internet-based research. Post graduate, she continued at UNLV as an adjunct faculty member, teaching advanced undergraduate psychopharmacology and health psychology (stress endocrinology). Dr. Marrs received her BA in philosophy from the University of Redlands; MS in Clinical Psychology from California Lutheran University; and, MA and PhD in Experimental Psychology/ Neuroendocrinology from the University of Nevada, Las Vegas. Follow her on Twitter and check out her work at HormonesMatter.com.
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