covid notes - brain and immune function

COVID Notes: Random Thoughts On Brain and Immune Function

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This is the third in series of short posts adapted from twitter threads contemplating various aspects of COVID-19 pandemic. The first two posts can be found here and here, and of course, on twitter.

COVID, the Brain, and Immune Function

The neuroinvasive potential of SARS‐CoV2 may play a role in the respiratory failure of COVID‐19 patients.

“The most characteristic symptom of patients with COVID‐19 is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously…”

…where the brainstem was heavily infected…”

Key sentences points: could not breathe spontaneously and brainstem involvement. Reading further we get thalamic involvement – as was reported in COVID-19–associated Acute Hemorrhagic Necrotizing Encephalopathy: CT and MRI Features.

As soon as I see this pattern, brainstem degradation>thalamic involvement, I immediately think dysautonomia>beriberi>thiamine deficiency>mito-hypoxia>disrupted immune function>inflammation overkill>leaky BBB >leaky junctions.

Then a few, more philosophical questions, niggle in the background. I have long had this theory that these pathogens have always already been with us and are just ‘activated’ when the circumstances align. I have no real basis for this and certainly much evidence against it.

But the idea remains – what if everything was already there? That the threats that we face are not entirely external but internal as well. This doesn’t mean that there are not external pathogens to which we fall prey, there absolutely are, but what if we constitutionally mirror those pathogens – they exist in us already but remain quiescent, mostly, until some confluence of events activates them.

If that were the case, then potential for any pathogen to ‘reach’ any part of the body, the brain included, would not be so much about the uniqueness of the pathogen, although that would play role certainly, but more about the uniqueness of the ‘host’.

This would then bring us back to Matzinger’s danger theory, where the immune system has advanced beyond the overly simplistic self vs non-self model – because everything is self, the pathogens were always already a part of us, and it is our response to them that engenders danger.

That brings us back to host response being the key variable to address with any illness. And with that, two questions. 1) what does the individual need to survive/be healthy and 2) are they getting it?

Reframed for this pandemic. 1) What molecular resources does the patient require to mount an effective immune response, with the appropriate amount of inflammation and at the appropriate time?  2) Are they getting them? Likely they are not, because they are ill, sometimes seriously.

Reframed one more time. 1) What are the molecular resources one needs to beat this illness altogether – to be an asymptomatic carrier? 2) Are they getting them?

In this regard, everything comes back to host resources availability. That places the determinants of health versus illness squarely onto host health or more specifically, host mitochondrial health because question always comes back to mitochondrial fitness, to the energy/ATP needed to either stave off illness altogether or fight it and survive if this fails.

Then where the pathogen attacks becomes an equation that includes equal parts pathogen to host variability e.g. host genetics/epigenetics/diet/lifestyle/environment etc., which is moderated by energy availability.

And from that perspective, as meandering and incompletely argued as it was, maybe it still provides a clue to how we fight this – bolster host defenses. Maybe that’s too simple in the age of technology. Maybe not.

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Chandler Marrs, PhD

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.

2 Comments

  1. MedCram wonders about possible oxidative stress and ATP production failure as central to covid19 damage (https://www.youtube.com/watch?v=Aj2vB_VITXQ, https://www.youtube.com/watch?v=gzx8LH4Fjic).

    Is there anything you folks can think of that might help along this path?

    Looks to me like vitamin D supplementation might help via reducing ROS (since I believe vitamin D increases ACE2 which is occupied/inactivated by SarsCov2 and which (ACE2) decreases superoxides) but that’s just a dot-connecting guess.

    • Thiamine. We have lots of articles on this.
      Of course, other nutrients are needed, but thiamine is key to mitochondrial health, easily depleted with illness and often missed in treatments.

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