by Dr. Kelly Brogan
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?
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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.