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 .
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. .
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.
Recent studies show that interleukin-6 is significantly up-regulated in autistic patients, compared with healthy controls .
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].
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 .
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 .
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” .
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 .
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 .
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 .
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) . Furthermore, those who performed violent suicide attempts displayed the highest IL-6 levels .
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”. 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 .
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’ .
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 .
Elevated levels of IL-6 have also been reported in women suffering from post-partum depression .
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 .
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 .
According to Professor Gherardi in France, aluminium deposits may persist for up to 12 years at injection site, in some individuals . 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 .
PS: If you’d like to support my work, please consider purchasing my book, or telling others about it! I would really appreciate that.
 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.
 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.
 Eftekharian MM, Ghafouri-Fard S, Noroozi R, et al. Cytokine profile in autistic patients, Cytokine, 2018, 108:120-126.
 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.
 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.
 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).
 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.
 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.
 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.
 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.
 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.
 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.
 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.
 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.
 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.
 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.
 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.
 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.
 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.
 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.
 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.
 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.
 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.
 Khan Z, Combadiere C, Authier FJ, et al. Slow CCL2-dependent translocation of biopersistent particles from muscle to brain, BMC Med, 2013, 11:99.