7 Reasons Why Antibodies Can’t Possibly Provide Immunity

There is a massive vaccine industry that rakes in billions in profits, based on the belief that if you have antibodies, you are ‘protected’. Here’s 7 reasons why that belief needs a re-think…

ONE.

There are numerous cases in the scientific literature, of people succumbing to illness, even though they had high antibody counts [1-3]. In fact, some of those had antibody titres 100x higher than what is considered sufficient to provide ‘immunity’. On the other hand, there are people with little to no antibody counts (and supposedly susceptible) passing through disease outbreaks completely untouched [4].

Actually, the discovery that antibodies are not responsible for immunity was made more than 80 years ago, by immunologist Dr. Merrill Chase, and his discovery was largely ignored by mainstream medicine, despite a long and illustrious career, and publishing more than 150 research papers [5].

TWO.

According to vaccine logic, the more antibodies you have, the better, but in a NORMALLY functioning immune system, antibody production is tightly restricted (for good reason – more on that later). It’s now common knowledge that Vitamin D is necessary for a healthy immune system…but did you know Vitamin D LIMITS antibody production [6]? It begs the question why, if antibodies really are as vital as we have been led to believe…

 THREE.

The presence of prior antibodies has been found to ENHANCE some diseases. It’s called ‘antibody-dependant enhancement’ and, so far, it has been demonstrated to enhance dengue fever, zika virus, HIV, Ebola, and others [7-12].

FOUR

Antibodies are created in the body as a last resort. It only occurs AFTER the cells have become infected. Remember the selling point of vaccines – about having a ‘primed’ immune system, so that antibodies could respond faster? Well, technically that’s true, but they neglected to mention that, even in a ‘primed’ immune system, antibodies are STILL not called into action, until after infection occurs [13]. Therefore, it’s a biological impossibility for antibodies to prevent infection, even in a ‘primed’ immune system.

FIVE.

By now, you may be wondering why the human body is designed to limit, restrict or delay antibody production. There’s a good reason for this – because antibodies are highly inflammatory and uncomfortable. Those unpleasant symptoms that you experience when ‘sick’ are not symptoms of disease, they are the result of antibodies. Antibodies place a large burden on the body’s excretory systems and, if not excreted in a timely manner, they conglomerate and form ‘antibody complexes’, which are rather large and tend to get stuck in the soft tissues and joints, causing inflammation and tissue damage [14]. If you get ‘arthritis’ after a vaccine or illness, now you know why! Antibodies!

SIX.

True immunity requires a robust innate immune system (also known as Th1 immunity). This is the very first line of defence. As already mentioned, vaccines target antibody production, which is part of the humoral immune system (also known as Th2 immunity) – and the last function called into play by the immune system.

We can look upon these two arms of the immune system (innate and humoral) as being antagonistic – when one is dominant, the other is suppressed. So, a dominant antibody response (caused/exacerbated by repeat vaccinations), means that the innate immune system (first line of defence) is suppressed, leaving you more vulnerable to infection [15].

It should be noted here, that the disease known as ‘AIDS’ is characterised by this very same thing – high antibody counts, and poor function of the innate immune system [16]

Also of note – studies have shown that cancer and autism patients have this particular immune imbalance – high antibody counts and suppressed innate immunity [17-20].

SEVEN.

Antibodies are extracellular, meaning that they are active outside the cells, but cannot actually enter cells…although scientists are trying to genetically engineer antibodies that will do just that [21].

Now, this is quite a conundrum, because antibodies are not called into action until after a pathogen has entered the cells, and antibodies can only bind to antigens on the surface of the cell (NOT inside the cell).

Now you have to rely on T-cells to orchestrate the killing of infected cells, in order to stop the spread of infection – this is the realm of the innate immune system (the one that is suppressed by repeated vaccinations, remember?). Such is the natural sequence of events when a th1-type response is generated, such as seen in natural infection [22].

The natural Th-1 type response is to eliminate infection via externalising it – this is the classic disease symptoms we know so well, such as rash, fever, cough, mucus, swelling etc [23]. Th2 dominance inhibits this natural response, which inevitably must lead to either:

  • altered disease manifestation, so for example, the vaccinated person who has whooping cough, may have a cough, but without the tell-tale ‘whoop’ sound [24].
  • chronic underlying infection, inflammation or auto-immune disease [25-26].

Let’s just re-emphasize that last point, because it’s really important, and once understood, you’ll never again look at vaccines the same way again…

First: Vaccines are designed to stimulate antibody production (Th2 immune system).

Second: Antibodies cannot stop infection, nor can they enter cells that are infected.

Third: Due to immune imbalance caused by vaccination, infected cells harbour infection chronically, causing inflammation and auto-immune conditions.

Fourth: person shows only mild or no signs of acute illness, but becomes progressively burdened down by chronic health issues.

So, what actually happens is that the vaccine has not prevented infection, it has simply prevented the body from expelling the infection.

It goes without saying, that such a state of affairs does wonders for the vaccine ‘efficacy’ statistics, since the vaccinated are less likely to show overt signs of acute disease, and therefore, less likely to be diagnosed, or even tested – meanwhile, chronic ‘non-communicable’ diseases continue to spiral out of control…

Now you know why.

References:

[1] Crone NE, Reder AT. Severe tetanus in immunized patients with high anti-tetanus titers, Neurology, 1992, 42(4): 761-764.

[2] Maselle SY, Matre R, Mbise R, Hofstad T. Neonatal tetanus despite protective serum antitoxin concentration, FEMS Microbiol Immunol, 1991, 3(3): 171-175.

[3] Pitisuttithum P, Gilbert P, Gurwith M, et al. Randomized, double-blind, placebo-controlled efficacy trial of a bivalent recombinant glycoprotein 120 HIV-1 vaccine among injection drug users in Bangkok, Thailand. J Infect Dis, 2006, 194(12):1661-1761.

[4] Brodie M, Park W. Active Immunization Against Poliomyelitis, Am J Pub Health, 1936, 26:119–125.

[5] O’Connor A, Merrill W Chase, 98, Scientist Who Advanced Immunology, New York Times, Jan 22, 2004. https://www.nytimes.com/2004/01/22/nyregion/merrill-w-chase-98-scientist-who-advanced-immunology.html. Accessed October, 2018.

[6] Røsjø, E., Lossius, A., Abdelmagid, N., Lindstrøm, J. C., Kampman, M. T., Jørgensen, L., … Holmøy, T. (2017). Effect of high-dose vitamin D3 supplementation on antibody responses against Epstein–Barr virus in relapsing-remitting multiple sclerosis. Multiple Sclerosis Journal, 23(3), 395–402.

[7] Halstead SB, O’Rourke EJ. Antibody-enhanced dengue virus infection in primate leukocytes, Nature, 1977, 265(5596):739-741.

[8] ] Dejnirattisai W, Jumnainsong A, Onsirisakul N, et al. Cross-reacting antibodies enhance dengue virus infection in humans, Science, 2010, 328(5979):745-748.

[9] Dejnirattisai W, Supasa P, Wongwiwat W, et al. Dengue virus sero-cross-reactivity drives antibody-dependent  enhancement of infection with zika virus, Nat Immunol, 2016, 17(9):1102-1108.

[10] Homsy J, Meyer M, Tateno M, et al. The fc and not CD4 receptor mediates antibody enhancement of HIV infection in human cells, Science, 1989, 244(4910):1357+.

[11] Furuyama W, Marzi A, Carmody AB, et al. Fcy-receptor Ila-mediated Src signaling pathway is essential for the antibody-dependent enhancement of ebola virus infection, PLoS Pathogen, 2016, 12(12):e1006139.

[12] Biryukov S, Angov E, Landmesser ME, et al. Complement and antibody-mediated enhancement of red blood cell invasion and growth of malaria parasites, EBioMedicine, 2016, 9:207-216.

[13] Janeway CA Jr, Travers P, Walport M, et al. Immunobiology: The Immune System in Health and Disease. 5th edition. New York: Garland Science; 2001

[14] Cochrane CG, Dixon FJ. Cell and tissue damage through antigen-antibody complexes. Calif Med. 1969;111(2):99-112.

[15] Brad Spellberg, John E. Edwards; Type 1/Type 2 Immunity in Infectious Diseases, Clinical Infectious Diseases, Volume 32, Issue 1, 1 January 2001, Pages 76–102.

[16] Kaur R, Dhakad MS, Goyal R, Bhalla P, Dewan R (2016) Study of TH1/TH2 Cytokine Profiles in HIV/AIDS Patients in a Tertiary Care Hospital in India. J Med Microb Diagn 5:214

[17] Sato M, Goto S, Kaneko R, et al. Impaired production of Th1 cytokines and increased frequency of Th2 subsets in pBMC from advanced cancer patients. Anticancer Res, 1998, 18:3951-3955.

[18] Huang M, Wang J, Lee p, et al. Human non-small cell lung cancer cells express a type 2 cytokine pattern. Cancer Res, 1995, 55:3847-3853.

[19] Filella X, Alcover J, Zarco MA, et al. Analysis of type T1 and T2 cytokines in patients with prostate cancer, prostate, 2000, 44:271-274.

[20] Gupta, S., Aggarwal, S., Rashanravan, B., Lee, T., TH1 and TH2-like cytokines in CD4+ and CD8+ T cells in autism, J of Neuroimmunol, 1998; 85:106-109.

[21] Coghlan A. Super-antibodies break the cell barrier, New Scientist, https://www.newscientist.com/article/dn4881-super-antibodies-break-the-cell-barrier/. Accessed December 2018.

[22] Kim EJ, Cho D, Kim TS. Efficient induction of T helper type 1-mediated immune responses in antigen-primed mice by anti-CD3 single-chain Fv/interleukin-18 fusion DNA, Immunology, 2004, 111(1): 27–34.

[23] Abbas AK, Murphy KM, Sher A. Functional diversity of helper T lymphocytes, Nature, 1996, 383(6603):787-93.

[24] Nelson KE, Williams C. Infectious Disease Epidemiology: Theory and practice 2007), Jones and Bartlett Learning, pp 131.

[25] Hayflick, L. Slow Viruses, Executive Health Report, Feb. 1981, pp 4.

[26] Talai, N., “Autoimmunity,” in Fudenberg, Basic Clinical Immunology, 3rd Ed., Lange, 1980, p. 222.

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