SPED AND THE OBSERVED CACHEXIA IN LONG COVID

Building the SPED hypothesis as the foundation of Long COVID and SADS pathology

As with the progressive clarity and assurance of finding the next piece that fits in a jigsaw puzzle you are solving, I will be posting these found “pieces” as I discover how SPED is causing Long COVID and SADS.

Please see my previous posts for an explanation of SPED (Spike Protein Endothelial Disease).

PRELUDE

Six-month follow-up results

Out of 413 discharged patients, 29 patients died and 29 were lost to follow-up. In total, 250 patients completed remote follow-up and 105 patients completed ambulatory follow-up (Fig. 1).

The median age of the 29 dead patients was 82 years (first quartile 76, third quartile 88). Post-COVID respiratory failure and/or cachexia were the causes of the three COVID-related deaths. Other causes of death included multi-morbidity (15), cancer (3), heart failure (5), and other factors.

“Long COVID” results after hospitalization for SARS-CoV-2 infection
https://www.nature.com/articles/s41598-022-13077-5

INTRODUCTION

Cachexia is a multifactorial syndrome characterized by inducing continuous and involuntary weight loss. This complex comorbidity occurs in association with malignant disease and with various other chronic diseases. Cancer cachexia consists of chronic systemic inflammation and catabolism, decreasing treatment response and survival.

Several factors contribute to inflammation in cancer cachexia, as eicosanoids, augmented fatty acid content in the circulation, and increased circulation of pro-inflammatory cytokines, among which tumor necrosis factor (TNF), interferon (IFN), interleukin-6 (IL6), and interleukin 1 beta (IL1B) play a prominent role.

In fact, nonneoplastic cells within the tumor microenvironment and surroundings, including immune cells fibroblasts and endothelial cells, play an important role in regulating the secretion of cachexia-inducing factors by the tumor.

Tumor Microenvironment Autophagic Processes and Cachexia: The Missing Link?
https://hal.sorbonne-universite.fr/hal-03148595/document

THE SPIKE PROTEIN AS “TUMOR,” INDUCING CACHEXIA

What is most important here, is that the Spike Protein is, with regards to cancer cachexia, functionally a TUMOR. And one that has “metastasized” SYTEMICALLY! The reason being, of course, is that it is in the circulation either freely, or attached to virions, and anchors itself to the endothelium.

How does it function as a “tumor?” It causes the endothelial cells to secrete THE VERY SAME CYTOKINES THAT TUMORS DO.

PASC is not associated with autoantibodies, but with elevated IL-1b, IL-6, and TNF plasma levels, which we confirm in a validation cohort with 333 additional participants and a longer time from infection of 10 months.

The IL-1b, IL-6, and TNF cytokine triad is associated with post-acute sequelae of COVID-19
https://www.cell.com/cell-reports-medicine/pdf/S2666-3791(22)00195-1.pdf

This should be of no surprise, as it was known (in 2007) that the original SARS Spike Protein had the exact same properties.

To understand how cells response in the early stage of virus-host cell interaction, in this study, a purified recombinant S protein was studied for stimulating murine macrophages (RAW264.7) to produce proinflammatory cytokines (IL-6 and TNF-alpha) and chemokine IL-8. We found that direct induction of IL-6 and TNF-alpha release in the supernatant in a dose-, time-dependent manner and highly spike protein-specific, but no induction of IL-8 was detected.

Up-regulation of IL-6 and TNF-alpha induced by SARS-coronavirus spike protein in murine macrophages via NF-kappaB pathway
https://pubmed.ncbi.nlm.nih.gov/17532082/

That the virus (now we know it is the Spike Protein) was inducing cachexia was observed early on in the pandemic.

Anorexia is a component of COVID-19. This is, in part, due to the anosmia and loss of taste that occurs in COVID-19, but is also secondary to the elevated levels of inflammatory cytokines, which are common causes of anorexia.

When Syrian hamsters are injected with coronavirus-2, they develop typical signs of COVID-19 as well as weight loss. This is associated with increases in interferonδ and tumour necrosis alpha. Mice infected with coronavirus-2 had had significant weight loss which was reversed by a ribonucleoside analog.

COVID-19: a major cause of cachexia and sarcopenia?
https://onlinelibrary.wiley.com/doi/10.1002/jcsm.12589

THE INVOLVEMENT OF THE DYSFUNCTIONAL ENDOTHELIUM: CARDIAC CACHEXIA INDUCED VIA CANCER CACHEXIA MECHANISMS

Perhaps the most interesting aspect of Cachexia in relation to COVID and SPED is how patients exhibit all of the symptoms of Cardiac Cachexia, yet it seems to be driven by more of a Spike Protein “tumor” approach than an induced advanced Congestive Heart Failure (CHF) approach.

Of interest:

As mentioned above, inflammatory cytokines are activated in advanced CHF, and this activation is particularly marked in cachectic patients. Levels of inflammatory cytokines and catabolic hormones correlate significantly with the reduction in muscle, fat and bone tissue content that occurs in cardiac cachexia.

In CHF patients with cardiac cachexia, skeletal muscle blood flow is an important predictor of exercise capacity, whereas in patients without wasting it is not. Furthermore, there is a positive correlation between impairment in endothelium-dependent vasodilatation in forearm conduit vessels and serum TNF levels in CHF.

There is increasing evidence that the abnormalities in peripheral blood flow and skeletal muscle function that occur in CHF are responsible for symptom generation in this condition. Furthermore, it may be hypothesized that drugs such as angiotensin-converting enzyme inhibitors may exert their beneficial effects on CHF via their influence on endothelial and peripheral muscle function, rather than their central haemodynamic effects.

From tissue wasting to cachexia: changes in peripheral blood flow and skeletal musculature
https://academic.oup.com/eurheartjsupp/article/4/suppl_D/D12/593240

Perhaps we are dealing with an overlap, as SARS-CoV-2 and the Spike Protein have also been shown to be involved with induction of/exacerbation of Congestive Heart Failure. If so, I believe SPED will certainly be a significant factor in the development of COVID related CHF.

Association between COVID-19 and cardiovascular disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7359796/

THINKING OF SOLUTIONS AND ATTENUATING CONSTANT EXPOSURE TO THE SPIKE PROTEIN

Clearly, the best way to avoid all the complications of COVID-19 and PASC is to avoid the virus and especially the Spike Protein. If you read my recent posts, I discuss several therapeutics which I believe should be trialed to see if they ameliorate the observed pathologies. I believe MAINTAINING ENDOTHELIAL INTEGRITY AND PROTECTING ITS MITOCHONDRIA may offer the best hope at mitigating this crisis.

I am working on detailing how the Mitochondria of the Endothelium are as significant as the Endothelium itself in the pathogenesis of SARS-CoV-2 and its Spike Protein.