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The day has come and your little bundle is here. The wonder of it is overwhelming: this human grew out of two cells, inside you, and despite those last couple of days feeling like a year each, all of this happened in 9 months, without your doing much but standing by. If you are in a hospital, your baby is likely to be snatched away from you upon entry into the world, and subjected to all manner of empirical interventions aimed at damage control for all of his weaknesses and lurking dysfunctions – antibiotics in his eyes, vitamin K in his blood, a good scrubbing with some 1, 4-dioxane and formaldehyde-containing baby wash, and, since 1991, the Hepatitis B vaccine.
What is that? Why does my baby need it?
According to the CDC, everyone needs it. As far as we understand it, this is a communicable infection that can, in debated percentages, progress to cirrhosis, liver cancer, and death. Populations at risk are those having unprotected sex, using IV drugs (not most babies!), those transfused, or in blood contact with an infected party. Of adults infected, 90-95% clear the virus on their own, without intervention, according to my medical school textbook, Harrisons Principals of Internal Medicine. The concern for infant contraction of the virus is that the immature neonatal immune system "allows" for the virus to hang out chronically in up to 90% of cases. Then, in the 2nd or 3rd decade of life, most of these infected infants enter the "HBeAg+ phase" where they may be at escalating risk for cirrhosis, progressive liver damage, and cancer. Viral replication, the genotype of the virus (there are 8 known), liver cell damage as measured by enzymes, and characteristics of the host immune response render the movement through different phases of chronic infection quite variable. So, in those mothers with active infection as determined by testing for viral DNA and antigen/antibody, managing the transmission to the baby is a compelling concern. I will address how we may be failing to address this compelling concern in an effective way.
But what about the rest of the babies born to non-infected mothers? Your newborn, fresh-out-of-the womb, baby needs this injection of genetically engineered recombinant viral DNA inserted into a yeast cell because they are reportedly easy to "capture" at that point, and to assure compliance (unlike higher risk adults); however, prevention of vertical transmission from mother to child is thought of as the primary indication (despite ease of assessing whether or not the mother is actually infected) as this is a primary source of disease burden.
Is this working?
Much is unknown and difficult to quantify about the effects of the vaccine including that antibody production, if it occurs, may be very short-lived and certainly may not be carrying children into their teen years when they may be at higher behavioral risk for contraction. Assessments of prevalence pre and post vaccine introduction seem to have suggested that vaccination was responsible for a decrease in chronic hepatitis B infection in children age 6-19, but these papers use blood levels of HBcore antigen and surface antigen rather than polymerase chain reaction testing for viral DNA. What if all of this data were invalidated by outdated testing that fails to truly identify chronic infection?
An illuminating paper, just published in the Journal of Viral Hepatitis may shed light on the true outcomes of this approach and its basis in a flawed conceptualization of the virus and its interaction with our immune system. This trial assessed for the infectious status of 259 pregnant women with Hepatitis B by looking at the presence of viral DNA, viral antigens called HBeAg and HBsAg which indicate that the body is actively infected, and antibodies to both antigens.
All of the babies in the study were vaccinated at 0,6,10, and 14 weeks, so, as has been the case in every study of vaccine efficacy and safety, there was no naturalistic placebo group. One group of these babies received hepatitis immunoglobulin (HBIG) which is derived from actively infected adults, and the other group did not, and they assessed their levels of infection over a two year period. They looked deeper than in previous studies because they looked at the presence of the viral DNA in these babies over time, not just the antibody production or "immune response."
Here's what they found:
"The results of this large prospective longitudinal study show that 42% of babies born of HBsAg-positive mothers develop occult HBV infection, which is not prevented by administration of recombinant HBV vaccine to the new- born."
What does this mean?
The implication of this is that immune response to the vaccine, which is heralded as "proof of efficacy", in fact had no statistical bearing on infectious outcomes. Only exposure to active maternal infection at birth correlated with future outcomes. Giving the babies HBIG (not the vaccine) may have suppressed overt infection in some cases, but it just sent it underground, to something called covert infection, so that fully 49% of babies remained infected after these interventions.
Contrary to claims (often industry-funded: refs 5 and 9; ref 11) of cited studies which assert 85-95% efficacy of the vaccine alone and in combination with HBIG in preventing acute and chronic infection in babies born to infected mothers, this study found that, not only were babies going on to develop chronic infection, but the type of infection they developed did not prompt the expected antibody response and would likely smolder there chronically without routine detection including when these individuals may go on to donate blood, donate organs, and have sex.
No historical studies claiming vaccine efficacy have ever actually tested for the persistent presence of viral DNA. In fact, most have assessed only for the presence of antibodies.
This covert infection is theorized to develop as a result of "immune pressure" from these treatments, which result in viral mutations eluding the host, and result in failure to produce detectable antibodies. These mutations accumulate in vaccinated children and can be transmitted from mother to child.
What this means is that, current practice, as applied to the group of people most appropriate for the intervention (those infants of infected mothers we were hoping to protect), is not effective at preventing infection and may contribute to mutations in the virus that allow for covert infection.
So, if it works even 1% more than a coin toss in preventing infection, than why not just do it?
Because it is a toxic exposure that has unknown and unpredictable effects. It has never been appropriately studied in humans (true placebo control), and what we are observing from population-based reports is that 443,093 adverse events (headache, irritability, extreme fatigue, brain inflammation, convulsions, rheumatoid arthritis, optic neuritis, multiple sclerosis, lupus, Guillain-Barre Syndrome (GBS) and neuropathy ) have been registered including >1500 deaths, often labeled as Sudden Infant Death Syndrome. NVIC discusses:
An historic report in 1994 published by the Institute of Medicine, National Academy of Sciences, reviewed the medical literature for evidence that vaccines, including hepatitis B vaccine, can cause a variety of immune and neurological health problems. An independent committee of physician experts concluded that there were no case controlled observational studies or controlled clinical trials conducted on hepatitis B vaccine either before or after licensure to scientifically evaluate persistent reports that hepatitis B vaccine can cause sudden infant death syndrome; Guillain-Barre syndrome (GBS) and other central demyelinating diseases including transverse myelitis, optic neuritis, and multiple sclerosis; and immune system dysfunction including chronic arthritis.
The Institute of Medicine feels that causal relationships cannot be established between vaccination and adverse events because of inadequate data. This data seems imperative to begin formally accumulating.
Why is it so toxic?
It is made of:
Recombinant adsorbed hepatitis B vaccine is prepared from transformed Chinese hamster ovary cells, and is a liquid product that contains hepatitis B surface antigen that is rendered insoluble by adding aluminum salt.
Hepatitis B vaccine has a broad spectrum of activity, and 144 genes with different functions, including metabolism and inflammation, were differentially expressed after vaccination.
As someone interested in the role of inflammation in chronic diseases including mental illness, cardiac disease, cancer, and autoimmunity, this quoted mouse study concerned me in that it demonstrated cumulative inflammatory stimulation and damage with vaccine exposure lasting after the first day of injection.
Who cares about aluminum?
Aluminum activates microglia in the brain and is strongly linked to Alzheimers, Parkinson's disease and autoimmune disorders. This is a known neurotoxin and potent immune stimulant – added because the newborn immune system is actually built not to respond. This has been referred to as the anti-inflammatory phenotype and speaks to the powerful interplay between an infant, their mother's milk, and the priming of their immune system in the first 2 years of life. Several exploratory analysis have argued for a causative role for aluminum in autism incidence including one by Lucija Tomeljenovic and Shaw and by MIT researcher, Stephanie Seneff who states:
"Mentions of autism in VAERS increased steadily at the end of the last century, during a period when mercury was being phased out, while aluminum adjuvant burden was being increased. Using standard log-likelihood ratio techniques, we identify several signs and symptoms that are significantly more prevalent in vaccine reports after 2000, including cellulitis, seizure, depression, fatigue, pain and death, which are also significantly associated with aluminum-containing vaccines. We propose that children with the autism diagnosis are especially vulnerable to toxic metals such as aluminum and mercury due to insufficient serum sulfate and glutathione."
Another study found that children who received the Engerix B Hepatitis B vaccine were 74% more likely to develop "central nervous system inflammatory demyelination" than children who did not receive the vaccine, and 177% more likely to develop multiple sclerosis.
Stimulating immune response in the presence of a toxic additive or "adjuvant" like a metal, likely also contributes to autoimmune phenomenon according to current immune theories that I discuss here and is corroborated conceptually by similarity between HBV amino acid structure and human proteins.
The only primate study done with an unvaccinated control group, concerningly demonstrated delayed acquisition of neurodevelopmental reflexes in the thimerosol (ethylmercury-forming preservative) Hep B vaccinated group (particularly in those with low birth weight and gestational age) relative to the unexposed group. Studies such as this, along with those like this that determined a 9x greater risk for receipt of special educational services in boys receiving the pre-2001 Hep B vaccine series, and one that suggested a 3-fold greater risk of autism diagnosis likely led to the removal of thimerosol from the product in 2001. The thimerosol-containing vaccine was on the market for 19 years before this change (and it is still an ingredient of the flu vaccine and tetanus), which may raise concerns for some about the delay in remediating dangers associated with these products. These dangers are learned of post-hoc, in the field, after many children have paid the price of inadequate placebo-controlled, long-term study.
What to do?
As a clinician, I go to great lengths to support healthy immunity in my pregnant patients. I do this through diet, minimization of environmental exposures, promoting exercise and mitigation of stress response through meditation. There is much to be learned about our immune system and particularly about its interaction with environmental factors, and other systems in the body, including neuroendocrine. Until we know more, we must tread lightly, lest we "first do harm" – something we doctors promised not to do.