IL-6: The Smoking Gun of Vaccine Damage

For years, many in the vaccine awareness community have pondered whether the rise and rise of widespread vaccination could be related to the rise and rise of chronic conditions afflicting our society (in the West, at least). We have even pondered seemingly unrelated issues, like mental illness, depression, suicide and violence, wondering if vaccines might somehow be involved.

Despite our wondering, we haven’t had definitive proof. Just a vague suspicion that we cannot prove. We’ve been accused, by some, of trying to implicate vaccines in *every* malady known to mankind.

It has been my suspicion that severe reactions following vaccination usually require other co-factors to be present – whether that’s existing toxicity or health conditions, genetic mutations causing a reduced ability to detoxify, low Vitamin C status, recent antibiotic use (leading to gut dysbiosis, etc), systemic yeast infection, chronic stress, to name a few.

However, recently I just happened to be up at 3am in the morning – couldn’t sleep – and decided to do plug some random search terms into Pubmed.

I stumbled across a study that, honestly, shocked me so much, all hope of sleep was gone for the night.

In this small (double-blind, placebo-controlled) study, researchers set out to study the effect of inflammation on emotional awareness. In particular, the ability to ‘read’ another person’s mental state (an important social-cognitive skill that allows us to have meaningful social interactions with other humans).

In order to induce inflammation, they vaccinated participants in the treatment group with Typhim Vi (a typhoid vaccine), while participants in the control group received a saline injection. Levels of Interleukin-6 (an important marker of inflammation) increased by more than 400% in the vaccination group. Those in the vaccination group subsequently performed worse in testing that assessed their ability to ‘read’ the mental state of others [1].

Note that this is not the first study to show that vaccination can significantly increase IL-6 levels. Two decades ago, another study, conducted on premature infants, clearly demonstrated that vaccination with the whole-cell DTP vaccine elevated IL-6 levels. [2].

Now, this may not seem like a big deal, until you begin to understand what science has already discovered about Interleukin-6, since it’s discovery in 1986…

What this study clearly demonstrates is that inflammatory reactions, with potentially long-term consequences, take place after vaccination, even without any OUTWARD or IMMEDIATE signs of harm.

Interleukin-6 is a pro-inflammatory cytokine, normal and necessary to facilitate inflammatory processes during the acute phase of infection. It is when interleukin-6 is elevated excessively, especially for long periods of time, that problems – big problems – start to manifest.

There is an overwhelming, and growing, wealth of evidence that links inflammatory levels caused by excessive Interleukin-6, with neurological disorders, chronic diseases and autoimmune conditions.

AUTISM

Recent studies show that interleukin-6 is significantly up-regulated in autistic patients, compared with healthy controls [3].

Studies on mice also reveal that if IL-6 levels are increased in a pregnant female, brain development is altered in the unborn fetus, and offspring grow up to suffer from behavioural changes and social deficits commonly seen in autism [4-5].

BIPOLAR DISORDER

New research (published October, 2019) shows that symptomatic offspring of parents diagnosed with bipolar disorder, have significantly higher levels of IL-6, compared with offspring who display no symptoms of the disorder [6].

In other research, bipolar patients who were experiencing manic episodes also showed increased IL-6 levels, while bipolar patients who were in remission showed similar levels to healthy controls [7].

CANCER

Over-expression of Interleukin-6 has been reported in almost all types of tumours. According to research published in 2016:

“The strong association between inflammation and cancer is reflected by the high IL-6 levels in the tumour microenvironment, where it promotes tumorigenesis by regulating all hallmarks of cancer and multiple signalling pathways, including apoptosis, survival, proliferation, angiogenesis, invasiveness and metastasis, and most importantly, the metabolism” [8].

Therapies that block or inhibit IL-6 are being explored as a treatment, not only for cancer, but other chronic inflammatory diseases, such as autoimmune conditions [9].

SIDS

Research from 1995 showed that babies who died of Sudden Infant Death Syndrome (SIDS) had higher levels of IL-6 in cerebrospinal fluid. Researchers surmised that the presence of these inflammatory cytokines in the central nervous system may cause respiratory depression, especially in vulnerable infants [10].

Importantly, elevated levels of IL-6 were not necessarily accompanied by outward symptoms of infection or inflammation (fever, etc), even though IL-6 is known to cross the brain barrier and affect the body’s temperature ‘set-point’ in the hypothalamus [11].

SUICIDE AND VIOLENCE

Research shows that IL-6 levels are increased in people who attempt suicide, when compared with those who suffer from depression (but are not suicidal) [12]. Furthermore, those who performed violent suicide attempts displayed the highest IL-6 levels [13].

Research published in 2014 showed that IL-6 levels were significantly higher in patients with intermittent explosive disorder, compared to normal controls. In addition, both C-Reactive Protein (another inflammatory marker) and IL-6 were “directly correlated with a composite measure of aggression and, more specifically, with measures reflecting history of actual aggressive behavior in all participants”[14]. Plasma levels of IL-6 significantly correlated with impulsivity and monotony avoidance (a factor in thrill-seeking or dangerous behaviours).

DEPRESSION AND ANXIETY

IL-6 levels are increased in patients suffering from anxiety disorders, compared with control subjects [15].

One study of older women found that those who reported the most depression, anger, fatigue or mood disturbance, had significantly increased levels of IL-6. Although it is known that IL-6 increases psychological disorders, the feelings of anxiety or stress also increase IL-6, so the process can become a ‘vicious cycle’ [16].

At least two meta-analyses have shown that IL-6 is the most consistently elevated cytokine in the blood of patients with major depressive disorder, and that peripheral levels of IL-6 positively correlate to symptom severity [17-18].

It has also been shown that children with higher circulating IL-6 levels at age 9, had a 10% higher risk of developing depression by age 18 [19].

Elevated levels of IL-6 have also been reported in women suffering from post-partum depression [20].

Monoclonal antibodies against IL-6 receptors are currently being used as treatment for rheumatoid arthritis, and are being tested as potential treatment for mood disorders.

TYPE 2 DIABETES

Research shows that elevated levels of both IL-6 and C-Reactive Protein can predict the development of type 2 diabetes [21].

Clearly, there are consequences to up-regulating IL-6 in the body. The question is, if vaccination can increase IL-6 levels by more than 400%, how long do the levels stay elevated for? I feel this is the critical issue at stake here, given that chronic up-regulation seems to be a major factor in many of the disorders mentioned above. Unfortunately, the studies mentioned don’t address this issue, however, we do know that aluminium adjuvants selectively up-regulate IL-6, possibly via oxidative stress processes [22].

According to Professor Gherardi in France, aluminium deposits may persist for up to 12 years at injection site, in some individuals [23]. In mice studies, the aluminium slowly moves from injection site to distant organs, such as brain and spleen, where it can still be detected 1 year following vaccination [24].

PS: If you’d like to support my work, please consider purchasing my book, or telling others about it! I would really appreciate that.

References:

[1] Balter LJT, Hulsken S, Aldred S, et al. Low-grade inflammation decreases emotion recognition – Evidence from the vaccination model of inflammation, Brain Behav Immun, 2018, 73: 216-221.

[2] Pourcyrous M, Korones SB, Crouse D, Bada HS. Interleukin-6, C-Reactive Protein, and abnormal cardiorespiratory responses to immunization in premature infants, Pediatrics, 1998, 101(3):E3.

[3] Eftekharian MM, Ghafouri-Fard S, Noroozi R, et al. Cytokine profile in autistic patients, Cytokine, 2018, 108:120-126.

[4] Smith SE, Li J, Garbett K, et al. Maternal immune activation alters fetal brain development through interleukin-6, J Neurosci, 2007, 27(40):10695-702.

[5] Wu WL, Hsiao EY, Yan Z, et al. The placental interleukin-6 signaling controls fetal brain development and behaviour, Brain Behav Immun, 2017, 62:11-23.

[6] Lin K, Shao R, Wang R. Inflammation, brain structure and cognition interrelations among individuals with differential risks for bipolar disorder, Brain Behav Immun, 2019, S0889-1591(19).

[7] Brietzke E, Stertz L, Fernandes BS, et al. Comparison of cytokine levels in depressed, manic and euthymic patients with bipolar disorder, J Affect Disord, 2009, 116(3):214-217.

[8] Kumari N, Dwarakanath BS, Das A, Bhatt AN. Role of interleukin-6 in cancer progression and therapeutic resistance, Tumour Biol, 2016, 37(9):11553-11572.

[9] Rath T, Billmeier U, Waldner MJ, et al. From physiology to disease and targeted therapy: interleukin-6 in inflammation and inflammation-associated carcinogenesis, Arch Toxicol, 2015, 89(4):541-554.

[10] Vege A, Rognum TO, Scott H, et al. SIDS cases have increased levels of interleuking-6 in cerebrospinal fluid, Acta Paediatr, 1995, 84(2):193-196.

[11] Haynes RL. Biomarkers of Sudden Infant Death Syndrome (SIDS) Risk and SIDS Death. SIDS Sudden Infant and Early Childhood Death: The Past, the Present and the Future, University of Adelaide Press, South Australia, 2018, pp. 731–758.

[12] Janelidze S, Mattei D, Westrin A, et al. Cytokine levels in the blood may distinguish suicide attempters from depressed patients, Brain Behav Immun, 2011, 25(2):335-339.

[13] Lindqvist D, Janelidze S, Hagell P, et al. Interleukin-6 is elevated in the cerebrospinal fluid of suicide attempters and related to symptom severity, Biol Psych, 2009, 66(3):287-292.

[14] Coccaro EF, Lee R, Coussons-Read M. Elevated plasma inflammatory markers in individuals with intermitten explosive disorder and correlation with aggression in humans, JAMA Psychiatry, 2014, 71(2):158-165.

[15] O’Donovan A, Hughes BM, Slavich GM, et al. Clinical anxiety, cortisol and interleukin-6: evidence for specificity in emotion-biology relationships. Brain Behav Immun. 2010;24(7):1074–1077.

[16] Lutgendorf SK, Garand L, Buckwalter KC, et al. Life stress, mood disturbance, and elevated interleukin-6 in healthy, older women, J Gerentology, 1999, 54(9):434-439.

[17] Dowlati Y., Herrmann N., Swardfager W., Liu H., Sham L., Reim E.K., Lanctot K.L. A meta-analysis of cytokines in major depression. Biol. Psychiatry. 2010;67:446–457.

[18] Haapakoski R., Mathieu J., Ebmeier K.P., Alenius H., Kivimaki M. Cumulative meta-analysis of interleukins 6 and 1beta, tumour necrosis factor alpha and C-reactive protein in patients with major depressive disorder. Brain Behav. Immun. 2015;49:206–215.

[19] Khandaker G.M., Pearson R.M., Zammit S., Lewis G., Jones P.B. Association of serum interleukin 6 and C-reactive protein in childhood with depression and psychosis in young adult life: a population-based longitudinal study. JAMA Psychiatry. 2014;71:1121–1128.

[20] Boufidou F, Lambrinoudaki I, Argeitis J, et al. CSF and plasma cytokines at delivery and postpartum mood disturbances. J. Affect Disord, 2009, 115:287–292.

[21] Pradhan AD, Manson JE, Nader R, et al. C-Reactive Protein, Interleukin-6 and risk of developing Type 2 diabetes, JAMA, 2001, 286(3):327-334.

[22] Viezeliene D, Beekhof P, Gremmer E, et al. Selective induction of IL-6 by aluminium-induced oxidative stress can be prevented by selenium, J Trace Elem Med Biol, 2013, 27(3): 226-229.

[23] Gherardi RK, Cadusseau J, Authier FJ. Biopersistence and systemic distribution of intramuscularly-injected particles: what impact on long-term tolerability of alum adjuvants? Bull Acad Nat Med, 2014, 198(1):37-48.

[24] Khan Z, Combadiere C, Authier FJ, et al. Slow CCL2-dependent translocation of biopersistent particles from muscle to brain, BMC Med, 2013, 11:99.

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.