Respiratory Vaccines Cannot Work
Respiratory Vaccines Cannot Work
They have never worked, and here’s why.
[This post is too long for e-mail, so please click on the title to see the entire article.]
Vaccines for respiratory diseases have a consistent record of inefficacy regarding the alleged purpose of generating specifically neutralizing antibodies and imparting resilience to the diseases for which each of those vaccines is named. The influenza vaccine, flu shot, has averaged 14% efficacy for seniors, [1] the group most at risk for poor influenza outcomes, in the US, and generally shows no statistically significant differences in antibody profiles between vaccinated and unvaccinated subjects. [2]
This low efficacy is not surprising, given the impossibility of the task. Quickly mutating viruses, such as are involved in respiratory infections, make poor vaccine candidates due to the stark contrast between the quick agility of viral mutation and the clunky slowness of manufacturing and distributing and administering hundreds of millions of vaccine doses. Viral mutation speed running circles around industrial vaccine production was especially visible to the world in the COVID era, as the Wuhan strain spike protein, on which the COVID vaccines were based, quickly disappeared, as Delta, Omicron and subsequent variants pre-dominated, each in turn. Negative efficacy of the COVID vaccines has been scandalous around the world. [3] [4] [5] [6] [7] Risk of COVID infection and death with COVID were found to rise with each successive dose of vaccine for most age groups. [8] [9] The widely disseminated COVID vaccines were obsolete before the vast majority of vaccinees had been injected.
However, there is another reason, a basic microanatomical reason for the inevitable failure of all vaccines for respiratory infectious diseases.
First, let’s review the microanatomy of the alveolus (Plural: alveoli), which is where gas exchange occurs, the route of oxygen into the body, carbon dioxide out from the blood to the lungs to exhalation. The shape of clusters of alveoli looks like bunches of grapes, and this maximizes surface area for oxygen – carbon dioxide exchange.
Now zooming in, there is a 3-layer barrier between the blood and the air in the lungs, called the blood gas barrier (BGB), or the alveolar-capillary barrier. It has enormous surface area, seventy square meters in an individual human, yet is no thicker than 500 nanometers. [10] This structure maximizes both volume and ease of gas exchange between air and blood. A ubiquitous layer of intermeshed capillaries surrounds each alveolar sac, enabling nearly adjacent respiratory air and liquid blood to stay microscopically close, yet always separated.
West illustrates the layers of the blood-gas barrier, also known as the alveolar-capillary barrier. [11]
As shown, the blood gas barrier is only 0.5 micrometers = 500 nanometers thick.
The BGB keeps our lungs from filling with either liquid blood or cells from the blood. Forty different cells comprise this barrier, but the ultimate gatekeepers at that location are both the tight alveolar epithelium and the zonulae occludentes, or tight junctions, which are in turn regulated by “pore and leak” type protein activities. [12] The BGB mainly serves as the filter by which the small molecules oxygen and carbon-dioxide are exchanged between airspace and blood.
Large proteins such as antibodies, however, cannot pass the blood-gas barrier in a healthy person under physiologic conditions. Nor would it be desirable to have plasma proteins leak into the alveolar epithelium or mucosa, to fill the lungs with fluid. Also, capillary oncotic pressure depends on the presence of plasma proteins in the blood. This is also necessary, along with the BGB, to keep blood from escaping the blood vessels and getting into the lungs.
The obstacle of finely meshed filtration at the blood gas barrier has long been thought to be the obstacle to large proteins passing from the blood to the lungs. [13] [14] Taylor and Gaar calculated the pore radius of the alveolar epithelium to be 0.6 to 1.0 nanometers. An IgG antibody is 7.25 nanometer radius, and cannot fit through such tight areas in a healthy individual. Thus the antibody generated by the vaccine does not get to where it was intended to arrive. Joseph Lee compares the size difference between a small water molecule, which cannot easily pass the tight barrier, to the large antibody that is advertised to be able to travel to where it is needed to stop or prevent a respiratory infection. The 18 dalton size of the water molecule to the 145,000 dalton size of an antibody is like the size of a can of soda to the size of an SUV, which is 8,000 times larger. [15] Therefore, not only have antibodies never been observed to pass from the blood to the respiratory epithelium, but it is not feasible in healthy individuals.
Even transport of small molecules, such as sodium and water, is tightly regulated from blood to the lungs in a healthy person. [16] A sodium molecule is 0.19 nanometers, and a water molecule is 0.27 nanometers in diameter, and fenestration ranges across similar sizes. IgG molecules, on the other hand, the antibodies that are stimulated by vaccines, are typically 14.5 x 8.5 x 4.0 nanometers. [17] The tight junctions are the “functional and structural boundary” which controls the transport of ions, water and other small molecules. [18] These are the connecting pieces between the barrier cells, and function as the gatekeepers of what reaches the lungs. In healthy people, these junctions are so tight that even the smallest proteins, let alone large IgG antibodies, do not have a feasible path from the blood to the surface of the airways. IgG antibodies stimulated by vaccines are about 145,000 to 150,000 daltons, yet even 40,000 dalton molecules are blocked by the BGB. [19] The larger the protein, the less the appearance in the lavage fluid from broncho alveolar washes. [20]
The tight junctions are also mechanically strong, having tensile strength comparable to reinforced concrete, yet adequately supple to distend on inhalation. Scanning electron micrographs show that any breaches of the BGB occurred not at the tight junctions, but rather within the cells themselves, so that any disruptions were within rather than between cells. [21] All of this changes in a person with acute or chronic respiratory disease, in which the respiratory epithelium becomes injured, following a diverse array of possible mechanisms, and in which fluids and proteins can enter the airspace. [22]
There is neither a pressure gradient, either oncotic or diffusion under natural circumstances, that would draw, push, release or otherwise place large proteins such as antibodies across a small barrier to enter the airspace of a healthy person, unless in intense exercise. There would have to be an induced pressure inside the capillaries of 50 mmHg in order for even small 6 nanometer wide hemoglobin proteins to enter the airways, [23] which can occur in elite athletes during intense exercise, and at 100 mmHg in thoroughbred racehorses during peak performance. This exercise must be quite intense for this to happen. Elite human athletes performing at the top level of their oxygen consumption for a few minutes have disrupted the BGB so much as to cause bleeding into their alveoli. Experiments with thoroughbred horses on treadmills at peak performance has shown the same disruption of BGB cells and bleeding into the alveoli at 100 mmHg of pulmonary capillary pressure. [24] Such high pressure is typical of the aorta in humans, but capillary pressure is typically from 10.5 to 22.5 mmHg. [25] Therefore, in ordinary human activity, such bleeding into the lungs does not occur in healthy individuals.
Besides intense exercise, other known stressors that cause failure of the blood gas barrier are all known to be pathological: high-altitude pulmonary edema, high capillary pressure causing edema and hemorrhage, use of ventilators, as in an ICU, to overinflate lungs, and having an abnormal extracellular matrix, such as in Goodpasture’s syndrome, in which bleeding occurs from the pulmonary capillaries into the alveoli. [26]
Even when there are breaks in the BGB, they generally do not disrupt the basement membranes, and they generally close within a few minutes. The vaccine advocates’ promise of appearance of vaccine-induced IgG antibodies from the blood through the BGB to somehow arrive to the alveolar epithelium – to be in the right place at the right time to fight disease or to prevent infection – has not been observed to happen in the entire history of vaccination, despite the relentless hype. Lung epithelia apparently never got the memo from vaccine advocates that such large molecules as vaccine-induced antibodies were supposed to squeeze through such tight spaces to arrive to the area where they might be most useful, the surface of the lung alveoli.
Essentially, injecting a liquid that reaches the bloodstream, in order to stimulate the B-cells of the immune system to produce huge antibodies, results in no observed transport of these huge molecules through to the respiratory epithelia and mucous membranes – the battlefield where respiratory infections are fought – in a healthy person. And the immunity-by-injection strategy has zero chance of succeeding in such a quest. Creating antibodies in the blood to attempt to fight respiratory infections is simply the wrong strategy in the wrong place. Unless the vaccine induces lung disease, as described above, in which case the tight junctions between the blood and the alveoli could be pried apart, or alveolar epithelial cells could be burst apart, to such a degree that such leakage occurs. But in that case, the vaccine induces new disease, and thus the vaccine would be understood a priori to have failed in its alleged and heavily advertised purpose.
Let’s be careful what we wish for. Large proteins do not belong in the airspace of the lungs, and would be difficult to clear. The promise/threat of vaccine-induced antibodies arriving to those surfaces would not necessarily be helpful, even if it were possible. The challenge to clear proteins from airspaces contributes to poor prognosis in patients. Acute respiratory distress syndrome (ARDS) is associated with large quantities of proteins in the airspace. Those who die of this disease have been found to have three times the amount of protein in their airspaces than ARDS survivors. [27]
Likewise, the barrier is protective in the reverse direction. If air leaked into the blood in the form of a sufficiently large bubble, the air embolism arrival to the heart would be fatal. So let’s not wish for such easy blood-lung transport of large proteins.
SARS-CoV-2, as with all respiratory viruses, arrives to the upper airways first, and then to the lungs in natural infection. This is where antibodies might be useful, at the mucous membranes of the respiratory tract, where plasma cells produce secretory IgA antibodies, and at the alveolar epithelium. However, antibodies cannot arrive there from the bloodstream, due to the barrier examined herein. Nor can those antibodies exert their influence from across the tight blood gas barrier. Those vaccine-induced antibodies are in the wrong place to have a useful effect, and they always have been. Therefore, injected vaccines against respiratory pathogens are useless.
[1] K Russell, J Chung, et al. Influenza vaccine effectiveness in older adults compared with younger adults over five seasons. Feb 28 2018. Vaccine. 36 (10): 1272-1278. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5812289/
[2] K Nicholson, D Baker, et al. Immunogenicity of inactivated influenza vaccine in residential homes for elderly people. May 1992. Age Ageing. 21 (3): 182-188. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7110073/
[3] K Beattie. Worldwide Bayesian causal impact analysis of vaccine administration on deaths and cases associated with COVID-19: A big data analysis of 145 countries. Preprint. Nov 15 2021. https://drive.google.com/file/d/1DLlRa9rUqvW9pG1vNEsWMEydWwsmSMbe/view
[4] C Hansen, A Schelde, et al. Vaccine effectiveness against SARS-CoV-2 infection with the Omicron or Delta variants following a two-dose or booster BNT162b2 or mRNA-1273 vaccination series: A Danish cohort study. https://www.medrxiv.org/content/10.1101/2021.12.20.21267966v3.full.pdf
[5] Status of the SARS-CoV-2 variant Omicron in Denmark. COVID-19 Omicron variant report. Dec 31 2021. Statens Serum Institut. https://files.ssi.dk/covid19/omikron/statusrapport/rapport-omikronvarianten-31122021-ct18
[6] Public Health Scotland. Public Health Scotland COVID-19 & Winter Statistical Report. Jan 17 2022. https://publichealthscotland.scot/media/11802/22-01-19-covid19-winter_publication_report_revised.pdf
[7] Office for National Statistics. Coronavirus (COVID-19) infection survey, UK: Characteristics related to having an Omicron compatible result in those who test positive for COVID-19. Dec 21 2021. https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/conditionsanddiseases/adhocs/14107coronaviruscovid19infectionsurveyukcharacteristicsrelatedtohavinganomicroncompatibleresultinthosewhotestpositiveforcovid19
[8] UK Health Security Agency. COVID-19 vaccine surveillance report. Week 9. Mar 3 2022. https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/1058464/Vaccine-surveillance-report-week-9.pdf
[9] UK Office for National Statistics. Death by vaccination status, England. https://www.ons.gov.uk/peoplepopulationandcommunity/birthsdeathsandmarriages/deaths/datasets/deathsbyvaccinationstatusengland
[10] Y Fung. Blood flow in the lung, in Biomechanics: Circulation. 1997. Springer. 333-445. https://books.google.com/books/about/Biomechanics.html
[11] J West. Comparative physiology of the pulmonary blood-gas barrier: the unique avian solution. Dec 2009. Am J Physiol Regul Integr Comp Physiol. 297 (6). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803621/
[12] L Shen, C Weber, et al. Tight junction pore and leak pathways: a dynamic duo. 2011 Annu Rev Phsiol. 73: 283-309. https://pubmed.ncbi.nlm.nih.gov/20936941/
[13] A Taylor, K Gaar, Jr. Estimation of equivalent pore radii of pulmonary capillary and alveolar membranes. Apr 1970. Am J Physiol. 218 (4) https://journals.physiology.org/doi/abs/10.1152/ajplegacy.1970.218.4.1133
[14] K Leiby, M Brickman, et al. Bioengineering the blood gas barrier. Mar 12 2020. Compr Physiol. 10 (2): 415-452. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7366783/
[15] J Lee. Fatal design mistake of “efficacy and safety of the mRNA-1273 SARS-CoV-2 vaccine trial. Oct 21 2021. https://img1.wsimg.com/blobby/go/1a1e8981-e255-4a9c-835e-30861d098294/downloads/Letter%20to%20FDA%20Vaccine%20Clinical%20Study%20Paper%20Aut.pdf?ver=1665016632949
[16] D Eaton, M Helms, et al. The contribution of epithelial sodium channels to alveolar function in health and disease. 2009 Annu Rev Physiol. 71: 403-423. https://pubmed.ncbi.nlm.nih.gov/18831683/
[17] Y Tan, M Liu, et al. A nanoengineering approach for investigation and regulation of protein immobilization. Nov 25 2008. ACS Nano. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4512660/
[18] N Godbole, A Chowdhury, et al. Tight junctions, the epithelial barrier, and toll-like receptor 4 during lung injury. Dec 2022. Inflammation 45 (6): 2142-2162. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9649847/
[19] E Schneeberger. Ultrastructural basis for alveolar-capillary permeability to protein. 1976. Ciba Found Symp. 38 (3). 3-28. https://pubmed.ncbi.nlm.nih.gov/181220/
[20] K Kim, A Malik. Protein transport across the lung epithelial barrier. Feb 1 2003. Am J Physiol- Lung Cellular and Molecular Physilogy. 284 (2). https://journals.physiology.org/doi/full/10.1152/ajplung.00235.2002#B112
[21] J West. Thoughts on the pulmonary blood-gas barrier. 2003 Lecture Lung Cellular and Molecular Physiology.. Am J Physiology. https://journals.physiology.org/doi/full/10.1152/ajplung.00117.2003#REF10
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[23] G Pietra, J Szidon, et al. Hemoglobin as a tracer in hemodynamic pulmonary edema. Dec 26 1969. Science. 166 (3913): 1643-1646. https://pubmed.ncbi.nlm.nih.gov/5360588/
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[25] A Shore. Capillaroscopy and the measurement of capillary pressure. Dec 2000. Br J Clin Pharmacol. 50 (6): 501-513. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2015012/
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This is a great article! Thank you. Makes so much sense. Something always told me to steer clear of the flu vaccines. More recently there's been evidence that the more flu vaccines you get, the more likely it is you'll get the flu. Anecdotally, the only people I know who get a flu shot regularly also get sick every winter, sometimes more than once. Over the last 3 years, I've become more skeptical of ALL vaccines. Seems like the principle "you can't get something for nothing" applies to vaccines as well. Maybe a vaccine will cause your immune system to become more likely to fight off a specific pathogen, but at what cost? What damage are you doing to your immune system and your overall health by taking that vaccine? Answer: A lot more than we've been led to believe.
Superb! As a Cardiothoracic surgeon, with experience treating "Shock lung" - "cytokine storm" - whatever the name of the day is popular.. This explains it nicely - Superbly well written and graphics show detail. I feel I should repost on my substack and add some of my experience into the flow of information. basically this --Exactly.. but the spike protein, circulating through capillaries in the alveolar sac wall, is so very very close that when it triggers an inflammatory white cell to explode into an aggressive killer cell (see below).. then the damage extends into the alveolar cell wall, destroys its function if not destroying the sac itself, and that sac is now out of commission for O2 exchange.. Do this with enough (thousands) of air sacs and you see “Shock lung..” Or “Cytokine storm lung. “ Dump in Remdesivir (poison) and put patient on HPV - with the pneumatic barotrauma following and you have 80% mortality of those ICU patients. Hospital collects and extra 29,000 or more in Medicare dollars if a positive COVID test can be somewhere on the chart.. Frees up the ICU bed for another victim, another cytokine storm, and another Medicare check for the administrators bottom line.
Example… WBCs are charged with the mission to clean up problem proteins/cells/viruses/etc etc. There fore.. when a patient has RBCs leaking out into the extravascular and extra cellular space the trash piles up. Let’s say I have chronic venous hypertension from genetically inferior collagen tissue in my lower extremity venous valves.. I develop varicose vein.. then ambulatory upright posture makes the hydrostatic pressure even higher as the “check valves” down the leg are incompetent.. and the veins dilate up making the incompetence worse, the pressures higher. Eventually (women) complain about the unsightliness of the serpiginous varicose veins.. with time there is chronic diapedesis of RBCs out of the venous capillaries at the ankle and the trash builds up. Eventually the WBCs go do their work to eat up the fragments of RBCs and that iron is returned to the circulation where new RBCs are made (spleen, bone marrow etc)..
However, in the clean up, WBCs leave behind proteases that attack other proteins in the area of the ankle and eventually a red area replaces the “rust colored” medial malleolar area.. untreated, the inflammation continues and eventually a “venous ulcer” is evident and it can spread. We spend BILLIONS of health care dollars on these venous ulcers. Usually not deadly and not risk for limb loss.. just a pain in the butt to care for and they look like hell. Imagine that mess in your lungs… thank you spike protein.