Long COVID May Be a Systemic Microvascular Disease: How SPED (Spike Protein Endothelial Disease) May Explain “Post-COVID Anxiety”

A very interesting paper from 2021 demonstrates how SARS-CoV-2 (read Spike Protein) may induce stress-related disorders.

• The SARS-CoV-2 virus triggers endothelial senescence by usurping host serine proteases, the renin angiotensin system, and mitochondria.

• Senescent endothelial cells disrupt the BBB tight junctions, allowing stress molecules, including ANGc II, ET-1 and PAI-1, access to the amygdala, hippocampus, and mPFC, increasing the susceptibility for PTSD and other stress related disorders.

• Virus-damaged mitochondria predispose to PTSD by shifting cellular metabolism from OXPHOS to glycolysis in a Warburg effect.

• Virus-usurped furin and plasmin alter the pro-BDNF/BDNF ratio, predisposing to PTSD.

In the above set of bullet points – let’s be real. The first one should most certainly begin with “The SARS-CoV-2 Spike Protein triggers endothelial senescence...”

One of the more unusual aspects of Long COVID is the development of what has been called Post-COVID Anxiety.

Anxiety is considered one of the longer-term symptoms of Post-COVID syndrome (PCS), aka Long-COVID — a recently identified diagnosis.

Research shows that between 23% and 26% of people have mental health challenges (including anxiety) after recovering from the disease, particularly females.

Some studies place that figure higher, hovering closer to the 50% mark.

Post-COVID anxiety has overlapping symptoms with other mental health conditions, including:

• generalized anxiety disorder (GAD)

• obsessive-compulsive disorder (OCD)

• post-traumatic stress disorder (PTSD)

• major depressive disorder (MDD)

• Illness anxiety

• panic disorder

Post-COVID Anxiety: An Emerging Condition
https://psychcentral.com/anxiety/anxiety-after-covid

This intrigued me, as I believe it may actually be a manifestation of what I have called SPED (Spike Protein Endothelial Disease). Let’s go back to 2015. A study was published that showed a definitive relationship between higher anxiety levels and the incidence of stroke.

Results

A total of 419 incident stroke cases were identified from hospital/nursing home discharge reports and death certificates. Reporting more anxiety symptoms at baseline was associated with increased risk of incident stroke after adjusting for standard biological and behavioral cardiovascular risk factors (hazard ratio, 1.14; 95% confidence interval, 1.03–1.25). Findings persisted when additionally controlling for depression. Exploratory analyses considering the role of potential confounding versus pathway variables suggested that behavioral factors may be a key pathway linking anxiety to stroke risk.

Conclusions

Higher anxiety symptom levels were associated prospectively with increased risk for incident stroke independent of other risk factors, including depression. Anxiety is a modifiable experience that is highly prevalent among the general population. Its assessment and treatment may contribute to developing more effective preventive and intervention strategies for improving overall cardiovascular health.

Prospective Study of Anxiety and Incident Stroke
https://pmc.ncbi.nlm.nih.gov/articles/PMC4354776/

So, we have a correlation between anxiety and stroke – microvascular disease. Now, let us look at a 2021 paper which demonstrates that PTSD is itself an endothelial disease. The mechanisms involve BBB disruption and endothelial cell senescence – well known as part of the Spike Protein’s repertoire.

COVID-19 has been associated with a high PTSD prevalence, suggesting that aside from the psychological burden of the disease itself, the virus may directly interfere with the stress-processing brain areas. The virus-host interactome reveals several pathogen-induced states, such as cellular senescence and associated glycolysis, that facilitate viral replication, while at the same time disrupt the BBB. The virus likely increases PTSD susceptibility as, even in the absence of viral infection, this disorder has been associated with EC senescence and glycolytic states. This two-strike model not only may explain the high comorbidity of COVID-19 and PTSD, but also opens vistas for novel interventions, including ARBs, ACEi, ASIC1a blockers, senolytics, furin inhibitors, BRD4 inhibitors and anti-glycolytic interventions.

PTSD as an Endothelial Disease: Insights From COVID-19
https://www.frontiersin.org/journals/cellular-neuroscience/articles/10.3389/fncel.2021.770387/full

What do these findings tell us? Essentially, they begin to build a hi-resolution image showing Long COVID being a microvascular disease. And a systemic one at that. This leads to several questions. Among the most important being; is it reversible? Another that I am continually researching is centered on the whole subclinical nature of microvascular disease. Is this happening, more or less, to anyone who has been exposed to SARS-CoV-2 and/or its Spike Protein? After all, smoking causes subclinical damage long before clinical signs develop. The same is true for many other chronic – and fatal – conditions. I will continue the search for truth and understanding. Please have a blessed week.