The Shocking Truth About Spike Proteins, Sugar And Inflammation

Updated on December 4, 2025, with new English,, Latin American Spanish and Mandarin audio versions to help readers worldwide access this content.

🎧 ▶️ Press the play button below to listen in English.

🇪🇸 Spanish (Latinoamérica)

Hoy descubrirás cómo las proteínas de pico y el exceso de azúcar pueden encender la inflamación silenciosa en tu cuerpo.

Presiona el botón de reproducir para escuchar.

🇨🇳 中文(简体)

今天你将了解刺突蛋白和过量糖分如何在体内引发看不见的慢性发炎。

请按下方的播放按钮收听。

This article delves into the emerging evidence and scientific insights surrounding the persistence of SARS-CoV-2 spike proteins in the body after COVID-19 and vaccination.

It explores how these spike proteins, acting as foreign agents, contribute to chronic inflammation and trigger health issues across multiple organs, including the heart, brain, and blood vessels.

Additionally, it examines the role of mRNA vaccines in inducing IgG4 antibody production, which can impair immune response, lead to autoimmune diseases, and promote new or exacerbate conditions like cancer.

The article further highlights the detrimental interplay between persistent or recurrent hyperglycemia—whether diabetic or not—and the chronic inflammatory state caused by spike proteins, explaining its potential role in accelerating disease progression and contributing to the observed excess deaths since 2021.

This comprehensive discussion, drawing on extensive research and references, aims to provide a clearer understanding of these interconnected health challenges.


Part 1: Evidence for the Persistence of SARS-CoV-2 Spike Proteins Post-Infection and Vaccination

Introduction

The SARS-CoV-2 spike protein, a hallmark of natural infection and mRNA-based COVID-19 vaccines persists in the human body long after the acute phase of infection or vaccination.

This persistence has raised significant concerns about its potential role in chronic inflammation, autoimmune diseases, and other long-term health consequences.


Evidence for Spike Protein Persistence

1. Post-Infection Persistence:

  1. A study by Bansal et al. (2022) detected circulating spike protein fragments in individuals months after infection, even when viral RNA was no longer detectable.
  2. Researchers found viral antigens, including spike protein, in the gut mucosa of individuals up to seven months after infection.

2. Post-Vaccination Persistence:

3. Mechanism of Persistence:

The SARS-CoV-2 spike protein causes inflammation
SARS-CoV-2 spike protein. Source: Wikipedia

Part 2: Chronic Inflammation Induced by Persistent Spike Proteins

Mechanism of Chronic Inflammation

The spike protein interacts with angiotensin-converting enzyme 2 (ACE2) receptors, expressed in various tissues, including the heart, lungs, kidneys, and blood vessels. This interaction leads to cellular damage and a prolonged inflammatory response.

1. Endothelial Damage and Vascular Inflammation:

2. Cardiac Effects:

3. Neurological Inflammation:

4. Multi-Organ Impact:


Part 3: mRNA Vaccines, IgG4, and Autoimmune Diseases

mRNA Vaccines and IgG4 Production

1. Switch to IgG4 Antibodies:

2. Autoimmune Diseases:


SARS-CoV-2 particles emerging from cultured cells.
Source: Wikipedia

Part 4: Spike Proteins and Cancer

Recurrent and New-Onset Cancers

1. Impaired Immune Surveillance:

2. Proliferative Effects of Spike Protein:


Part 5: Persistent Hyperglycemia and Its Role in Aggravating Spike Protein-Induced Inflammation

Hyperglycemia, whether resulting from diabetes or other metabolic dysregulations, is a well-established contributor to chronic inflammation.

When combined with the persistent presence of SARS-CoV-2 spike proteins in the body, the inflammatory cascade is amplified, exacerbating existing disease conditions or hastening the onset of new ones.

This synergistic effect may partially explain the excess mortality observed globally since 2021.


How Hyperglycemia Fuels Inflammation

1. Pro-Inflammatory State:

  • Chronic hyperglycemia induces the production of advanced glycation end products (AGEs) and their interaction with receptor proteins (RAGEs), which trigger oxidative stress and the release of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α).
    • Reference: Yan, S. F. et al. (2009). “The RAGE Pathway: Implications for Diabetic Complications and Inflammation.” Nature Reviews Endocrinology.

2. Endothelial Dysfunction:

  • Elevated glucose levels impair endothelial cell function, leading to increased vascular permeability and a heightened inflammatory response.
  • When spike proteins bind to endothelial ACE2 receptors, the combination accelerates vascular damage, raising the risk of heart attacks, strokes, and microvascular complications.
    • Reference: Saltiel, A. R., & Olefsky, J. M. (2017). “Inflammatory Mechanisms Linking Obesity and Metabolic Disease.” The Journal of Clinical Investigation.

3. Immune Dysfunction:

  • Hyperglycemia suppresses key immune responses, including the activity of neutrophils and macrophages.
  • This allows persistent spike proteins to evade clearance, prolonging their tissue inflammatory effects.
    • Reference: Marik, P. E. (2012). “The Role of Glucose and Glycemic Control in Critical Illness.” Chest.

Spike Protein and Hyperglycemia: A Vicious Cycle

1. Spike Protein-Induced Insulin Resistance:

  • Studies suggest that SARS-CoV-2 infection and spike protein presence can impair pancreatic beta-cell function and exacerbate insulin resistance, even in non-diabetic individuals.
  • This creates a feedback loop in which hyperglycemia worsens inflammation, further damaging metabolic regulation.
    • Reference: Sathish, T., & Kapoor, N. (2021). “SARS-CoV-2 and Hyperglycemia: A Double-Edged Sword.” Diabetes Research and Clinical Practice.

2. Increased Susceptibility to Complications:

  • Hyperglycemia amplifies the inflammatory and thrombotic risks associated with persistent spike protein activity, contributing to the development or worsening of cardiovascular diseases, kidney dysfunction, and neuroinflammation.

The Link to Excess Deaths

Since 2021, a notable increase in excess deaths has been reported globally. Several factors point to the interaction between persistent spike proteins, chronic hyperglycemia, and inflammation as contributing mechanisms:

1. Accelerated Disease Progression:

  • Persistent inflammation triggered by spike proteins, combined with hyperglycemia, may lead to faster progression of atherosclerosis, heart failure, and other chronic conditions.

2. Increased Cancer Incidence:

  • Hyperglycemia enhances the proliferation of cancer cells by providing a favorable metabolic environment. The impaired immune surveillance caused by spike protein persistence and hyperglycemia further facilitates tumor growth.

3. Weakened Resilience to Infections:

  • Individuals with chronic hyperglycemia exhibit impaired immunity, leaving them vulnerable to secondary infections, sepsis, and other complications, which may explain part of the excess mortality.

Articles about excess deaths

  1. The Complete Measure of Excess Deaths
  2. Cardiac Arrhythmias Explain Excess Deaths
  3. The Rise in Deaths Among Canadian Doctors
  4. Lincoln National Insurance paid out 163% more for deaths of working people ages 18-64 in 2021
  5. Pfizer COVID shot Lot Numbers with the most deaths
  6. Excess deaths continue in 2022
  7. Excess deaths in Scotland 2021
  8. More COVID jabbed dead from COVID-19 than the unvaxxed in Scotland
  9. Above-average deaths of 5 to 74 years old for the year 2021
  10. US data: High numbers of autopsies done in 2021 among 15-64-year-olds.
  11. CDC data shows higher deaths from 25-54 years old in 2021 compared to 2018-2020
  12. 145 countries with higher COVID-19 cases and deaths after the COVID shots
  13. Indiana life insurance CEO says deaths are up 40% among people ages 18-64
  14. Vaccine-induced deaths in the US and Europe are way higher than the CDC reports!
  15. German Analysis: The Higher the Vaccination Rate, the Higher the Excess Mortality

Take Away Message

Given that almost everyone has been exposed to SARS-CoV-2 through infection, vaccination, or both, it is impossible to determine who may still harbor persistent viral remnants, such as spike proteins, in their bodies.

These remnants can trigger or exacerbate chronic inflammation, autoimmune conditions, or other medical complications.

With the insights from this article, one critical step is to maintain optimal blood sugar levels.

Persistent hyperglycemia can amplify the inflammatory state caused by SARS-CoV-2 remnants, accelerating the onset and worsening of associated diseases.

By controlling blood sugar through healthy lifestyle choices, regular monitoring, and timely medical intervention, we can reduce the risk of these complications and promote overall health.

Let this knowledge empower proactive measures for better long-term health outcomes.

Don’t Get Sick!

Stay current by subscribing. Feel free to share and like.

If you find value in this website, please consider buying a coffee or two or five to show your support.

References

  1. Rijkers GT, Weterings N, Obregon-Henao A, et al. Antigen Presentation of mRNA-Based and Virus-Vectored SARS-CoV-2 VaccinesVaccines (Basel). 2021;9(8):848. Published 2021 Aug 3. doi:10.3390/vaccines9080848
  2. Kowarz E, Krutzke L, Reis J, et al. “Vaccine-Induced Covid-19 Mimicry” Syndrome: Splice reactions within the SARS-CoV-2 Spike open reading frame result in Spike protein variants that may cause thromboembolic events in patients immunized with vector-based vaccines. Research Square; 2021. DOI: 10.21203/rs.3.rs-558954/v1
  3. Ogata AF. et al. Circulating SARS-CoV-2 Vaccine Antigen Detected in the Plasma of mRNA-1273 Vaccine Recipients [published online ahead of print, 2021 May 20]. Clin Infect Dis. 2021;ciab465. doi:10.1093/cid/ciab465
  4. Hervier B, Ribon M, Tarantino N, Mussard J, Breckler M, Vieillard V, Amoura Z, Steinle A, Klein R, Kötter I, Decker P. Increased Concentrations of Circulating Soluble MHC Class I-Related Chain A (sMICA) and sMICB and Modulation of Plasma Membrane MICA Expression: Potential Mechanisms and Correlation With Natural Killer Cell Activity in Systemic Lupus Erythematosus. Front Immunol. 2021 May 3;12:633658. doi: 10.3389/fimmu.2021.633658. PMID: 34012432; PMCID: PMC8126610.
  5. Salih, Helmut & Goehlsdorf, Dennis & Steinle, Alexander. (2006). Salih HR, Goehlsdorf D, Steinle A. Release of MICB molecules by tumor cells: mechanism and soluble MICB in sera of cancer patients. Hum Immunol 67: 188-195. Human immunology. 67. 188-95. 10.1016/j.humimm.2006.02.008.
  6. Edgar JR. Q&A: What are exosomes, exactly?BMC Biol. 2016;14:46. Published 2016 Jun 13. doi:10.1186/s12915-016-0268-z
  7. Raposo G, Nijman HW, Stoorvogel W, Liejendekker R, Harding CV, Melief CJ, Geuze HJ. B lymphocytes secrete antigen-presenting vesicles. J Exp Med. 1996 Mar 1;183(3):1161-72. doi: 10.1084/jem.183.3.1161. PMID: 8642258; PMCID: PMC2192324.
  8. Bansal et al. Cutting Edge: Circulating Exosomes with COVID Spike Protein Are Induced by BNT162b2 (Pfizer–BioNTech) Vaccination prior to Development of Antibodies: A Novel Mechanism for Immune Activation by mRNA Vaccines. J Immunol November 15, 2021, 207 (10) 2405-2410
  9. Nuovo, G.J. et al. (2021) Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein. Ann. Diagn. Pathol. 51, 151682, https://doi.org/10.1016/j.anndiagpath.2020.151682
  10. Gu, T. et al. (2020) Cytokine signature induced by SARS-CoV-2 spike protein in a mouse model. Front. Immunol. 11, 621441,
  11. Aboudounya MM, Heads RJ. COVID-19 and Toll-Like Receptor 4 (TLR4): SARS-CoV-2 May Bind and Activate TLR4 to Increase ACE2 Expression, Facilitating Entry and Causing Hyperinflammation. Mediators Inflamm. 2021 Jan 14;2021:8874339. doi: 10.1155/2021/8874339. PMID: 33505220; PMCID: PMC7811571.
  12. Shirato K, Kizaki T. SARS-CoV-2 spike protein S1 subunit induces pro-inflammatory responses via toll-like receptor 4 signaling in murine and human macrophages. Heliyon. 2021 Feb 2;7(2):e06187. doi: 10.1016/j.heliyon.2021.e06187. PMID: 33644468; PMCID: PMC7887388. https://pubmed.ncbi.nlm.nih.gov/33644468/
  13. Suzuki YJ, et al. SARS-CoV-2 Spike Protein Elicits Cell Signaling in Human Host Cells: Implications for Possible Consequences of COVID-19 VaccinesVaccines (Basel). 2021;9(1):36. Published 2021 Jan 11. doi:10.3390/vaccines9010036
  14. Cao, X. et al. (2021) Spike protein of SARS-CoV-2 activates macrophages and contributes to induction of acute lung inflammation in male mice. FASEB J. 35, e21801
  15. Biering et al. SARS-CoV-2 Spike triggers barrier dysfunction and vascular leak via integrins and TGF-β signaling. bioRxiv 2021.12.10.472112
  16. Avolio E et al.  The SARS-CoV-2 Spike protein disrupts human cardiac pericytes function through CD147 receptor-mediated signaling: a potential non-infective mechanism of COVID-19 microvascular disease. Clin Sci (Lond). 2021 Dec 22;135(24):2667-2689. doi: 10.1042/CS20210735. PMID: 34807265; PMCID: PMC8674568.
  17. Lei, Y. et al. SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2. Circulation Research. 2021;128:1323–1326
  18. Grobbelaar, L.M. et al. (2021) SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: implications for microclot formation in COVID-19. Biosci. Rep. 41 (8)
  19. Patterson B. et al. Persistence of SARS CoV-2 S1 Protein in CD16+ Monocytes in Post-Acute Sequelae of COVID-19 (PASC) Up to 15 Months Post-Infection.bioRxiv 2021.06.25.449905
  20. Yu J, Yuan X, Chen H, Chaturvedi S, Braunstein EM, Brodsky RA. Direct activation of the alternative complement pathway by SARS-CoV-2 spike proteins is blocked by factor D inhibition. Blood. 2020.
  21. Nyström et al. Amyloidogenesis of SARS-CoV-2 Spike Protein. bioRxiv 2021.12.16.472920. 
  22. Idrees D, Kumar V. SARS-CoV-2 spike protein interactions with amyloidogenic proteins: Potential clues to neurodegeneration. Biochem Biophys Res Commun. 2021 May 21;554:94-98. doi: 10.1016/j.bbrc.2021.03.100. Epub 2021 Mar 24. PMID: 33789211; PMCID: PMC7988450
  23. Nunez-Castilla, J et al. Spike mimicry of thrombopoietin may induce thrombocytopenia in COVID-19. bioRxiv 2021.08.10.455737
  24. Ehrenfeld M et al. Covid-19 and autoimmunity. Autoimmun Rev. 2020;19:102597.
  25. Kanduc D, Shoenfeld Y. On the molecular determinants of the SARS-CoV-2 attack. Clin Immunol. 2020;215. 
  26. Vojdani A, Kharrazian D. Potential antigenic cross-reactivity between SARS-CoV-2 and human tissue with a possible link to an increase in autoimmune diseases. Clin Immunol. 2020;217:108480
  27. Chen Y, Xu Z, Wang P, Li XM, Shuai ZW, Ye DQ, Pan HF. New-onset autoimmune phenomena post-COVID-19 vaccination. Immunology. 2021 Dec 27. doi: 10.1111/imm.13443. Epub ahead of print. PMID: 34957554.
  28. Jiang H, Mei YF. SARS-CoV-2 Spike Impairs DNA Damage Repair and Inhibits V(D)J Recombination In VitroViruses. 2021;13(10):2056. Published 2021 Oct 13. doi:10.3390/v13102056
  29. BRCA1 gene. Medline [website]
  30. Mirza-Aghazadeh-Attari M, et al.  53BP1: A key player of DNA damage response with critical functions in cancer. DNA Repair (Amst). 2019 Jan;73:110-119. doi: 10.1016/j.dnarep.2018.11.008. Epub 2018 Nov 20. PMID: 30497961.
  31. Segal, Y., Shoenfeld, Y. Vaccine-induced autoimmunity: the role of molecular mimicry and immune crossreactionCell Mol Immunol 15, 586–594 (2018). https://doi.org/10.1038/cmi.2017.151

© 2018 – 2024 Asclepiades Medicine, LLC. All Rights Reserved
DrJesseSantiano.com does not provide medical advice, diagnosis, or treatment

As an Amazon Associate, I earn from qualifying purchases.


Discover more from Don't Get Sick!

Subscribe to get the latest posts sent to your email.