April 02, 2019

Why Does the CDC Recommend Hepatitis B Vaccination for Infants?

The CDC’s recommendation for universal hepatitis B vaccination of infants puts most children at unnecessary risk of harm from the vaccine.

 

By Jeremy R. Hammond, Contributing Writer, Children’s Health Defense 

 

Parents are told by public health officials and the media that they should vaccinate their children strictly according to the schedule recommended by the US Centers for Disease Control and Prevention (CDC). The CDC’s routine childhood vaccine schedule is based on solid science, we are told, and it is imperative that all parents comply to reduce the societal disease burden. Anyone who dares to criticize or dissent from public vaccine policy is characterized as dangerously ignorant and irrational. A recent New York Times editorial, for example, characterized anyone who does so as “the enemy” and described all vaccines on the CDC’s schedule as “crucial shots”.

So is the HepB vaccine really necessary for all infants? Why does the CDC treat this vaccine as a one-size-fits-all solution when the vast majority of infants are not at significant risk of infection?

But is it really “crucial” for all children to be so vaccinated? To highlight the rationality and importance of this question, consider the example of the CDC’s recommendation that all newborn babies receive a hepatitis B (HepB) vaccine, typically on their very first day of life. Many parents naturally wonder why it is considered so necessary to vaccinate their baby against a virus that is primarily transmitted sexually or through sharing of needles among injection drug users. The hepatitis B virus (HBV) can also be transmitted to infants at birth if the mother is a carrier, but screening to identify infected pregnant women is done routinely, and an alternative effective treatment has long been available for infants born to carriers. So is the HepB vaccine really necessary for all infants? Why does the CDC treat this vaccine as a one-size-fits-all solution when the vast majority of infants are not at significant risk of infection?

To answer this question, we need look no further than the CDC’s own stated rationale for this policy, which was adopted in 1991. Close examination of the CDC’s reasoning and the evolution of this policy illustrates that, far from being based on science, the decision by the CDC’s vaccine advisory committee to adopt this policy was faith-based and concerned primarily not with the health of infants, but with the agency’s overriding goal of achieving high vaccination rates. Comparing the policy with the science reveals that parents are right to be concerned because the policy unnecessarily puts children who are not at risk of infection at risk of harm from the vaccine.

The Risk to Infants of Hepatitis B Infection

To place the CDC’s stated rationale for this policy into proper context, it’s important to understand a little bit about the nature of the virus and the risk it poses generally to the population and particularly to infants.

According to the CDC’s “Pink Book”, while most acute hepatitis B infections among adults are effectively dealt with by the host’s immune system, chronic infection is a known cause of liver disease, contributing significantly to the disease burden of cirrhosis and hepatocellular carcinomas. Most children and about half of adults with acute infection do not show any symptoms. Those with chronic infection may also be asymptomatic but are known as “carriers” since they still carry and can spread the virus.

Subpopulations at highest risk therefore include sexually active individuals, injection drug users, health care workers, and children who are born to infected mothers…

Transmission of the virus occurs through infected blood or other bodily fluids. Subpopulations at highest risk therefore include sexually active individuals, injection drug users, health care workers, and children who are born to infected mothers or otherwise come into prolonged close contact with infected household members. Mother-to-infant transmission usually occurs during birth. If an environmental surface is contaminated, the virus can remain stable and infectious for seven or more days, so indirect transmission, while unlikely, is also possible. Replication of the virus occurs only in liver tissue.

Most adults completely recover from acute infection and come away with lasting immunity. However, 1 percent to 2 percent of acute cases result in fulminant disease. Among these cases, 63 percent to 93 percent will result in death. About 200 to 300 deaths occur each year in the US due to severe HBV disease.

Before routine childhood vaccination, more than 80 percent of acute infections occurred in adults, about 8 percent in adolescents, and about 4 percent in children infected through perinatal transmission. Although at lower risk of becoming infected, such children are at higher risk of their infection becoming chronic, disproportionately accounting for about 24 percent of chronic infections. While chronic infection occurs in only about 5 percent of adult cases, the risk of an acute infection becoming chronic increases as the age of the host decreases. An estimated 30 percent to 50 percent of infections occurring in children aged one to five years become chronic, and for infants infected from their mothers, the rate is as high as 90 percent.

An estimated 25 percent of individuals with chronic infection will die prematurely from liver disease. About 3,000 to 4,000 people die from HBV-related cirrhosis each year, and another 1,000 to 1,500 die from HBV-related liver cancer.

It is primarily these fatal outcomes in adults—the few hundred deaths from fulminant disease and the few thousand deaths from liver disease—that public health officials have aimed to prevent through mass vaccination.

The hepatitis B virus has a number of different antigen components. (This gets a bit technical, but it’s important context, so bear with me.) The CDC defines an “antigen” as any foreign substance in the body, including but not limited to viruses or bacteria, which is capable of causing disease, and the presence of which triggers an immune response, including but not limited to the production of antibodies. As the CDC’s Pink Book explains, “Several well-defined antigen-antibody systems are associated with HBV infection.” These are the HBV core antigen (HBcAg), another protein contained in the viral core called the HBV e antigen (HBeAg), and a surface antigen (HBsAg).

The presence of HBsAg in the blood indicates infection, but only the complete virus is infectious, not individual antigen components. The presence in the blood of antibodies to this antigen, called “anti-HBs”, is considered indicative of immunity. Infection may also stimulate production of antibodies to HBcAg, or “anti-HBc”, the presence of which indicates past infection. The presence of anti-HBc of the immunoglobulin M class (IgM-anti-HBc) indicates recent infection. Chronic infection is determined by a positive result for HBsAg along with a negative result for IgM-anti-HBc.

The HepB vaccine contains just one viral antigen, HBsAg. Unlike natural infection, the vaccine does not stimulate production of anti-HBc.

For nearly three decades now, the CDC has treated vaccination during early childhood as a one-size-fits-all solution despite the variability in individual immune responses, individual risk from the virus, and individual risk from the vaccine.

Despite the advancements of modern science, much remains unknown about the human immune system and the full impact of viral infection or vaccination. And reading through the CDC’s Pink Book chapter on hepatitis B raises as many questions as it answers. Why do some individuals develop protective anti-HBs to fight off infection while others don’t and hence become carriers? What is the clinical significance of the development of anti-HBc in addition to anti-HBs versus the development only of the latter? In what other ways does natural immunity differ from vaccine-conferred immunity? Why would an individual’s immune system—and particularly children’s immune systems—fail to generate protective antibodies in response to the live virus, yet still be capable of doing so in response to the vaccine? Why do some individuals also fail to develop protective antibodies in response to the vaccine?

One would think that such questions would be relevant for understanding how to develop more effective methods of disease prevention, but answers to them cannot be found in the Pink Book. Indeed, answers to them are not readily found by perusing the broader scientific literature. The most obvious reason for this curiosity is the influence of the pharmaceutical industry and government policies on the direction of scientific research.

For nearly three decades now, the CDC has treated vaccination during early childhood as a one-size-fits-all solution despite the variability in individual immune responses, individual risk from the virus, and individual risk from the vaccine.

The evolution of the CDC’s HepB vaccine recommendation

Before the introduction of the vaccine, numerous effective prevention measures had already been implemented to some degree in the US, including blood screening and administration of hepatitis B immune globulin (HBIG) to infants born to HBsAg-positive women. HBIG contains protective antibodies obtained from the blood plasma of selected donors, conferring passive immunity to the infant. It’s estimated to be about 75 percent effective in preventing chronic infection when given soon after exposure. Additionally, newborn infants may have maternal antibodies passively acquired through the placenta.

Nevertheless, the number of cases occurring in the US annually continued to increase until it peaked in 1985 at about 26,000 reported cases. The increase in prevalence was occurring particularly among young adults. The decline seen during the second half of the 1980s through the early 1990s is attributed to a reduction in transmission among gay men and drug users as a result of efforts to prevent transmission of the human immunodeficiency virus (HIV), which causes acquired immunodeficiency syndrome (AIDS). From 1990 to 2004, incidence of acute hepatitis B infection declined by 75 percent, with most of the decline occurring among children and adolescents, coinciding with greater vaccination coverage.

Persons considered at “substantial risk” included various categories of health care workers, gay men, illicit injectable drug users, recipients of certain blood products, household and sexual contacts of HBV carriers, Alaskan Eskimos, immigrants or refugees from countries where HBV is highly endemic, and prison inmates.

The hepatitis B vaccine was first licensed for use in the United States in 1981. The following year, the CDC’s Advisory Committee on Immunization Practices (ACIP) issued a recommendation for vaccination of high-risk individuals. The estimated lifetime risk of HBV infection at the time was approximately 5 percent for the US population as a whole, but rose to almost 100 percent for the highest-risk groups. Persons considered at “substantial risk” included various categories of health care workers, gay men, illicit injectable drug users, recipients of certain blood products, household and sexual contacts of HBV carriers, Alaskan Eskimos, immigrants or refugees from countries where HBV is highly endemic, and prison inmates.

For infants born to HBsAg-positive mothers, the CDC recommended administration of HBIG. For infants whose mothers were chronic carriers (positive HBsAg but negative IgM-anti-HBc), the CDC additionally recommended a 3-dose vaccination regimen starting no sooner than 3 months of age. The CDC added that “Studies to determine the immunogenicity and efficacy of vaccine at birth, with or without HBIG, are currently under way.” (Emphasis added.)

The CDC admitted that, with respect to the developing fetus, safety data were not available, but assumed that the risk should be negligible on the grounds that the viral antigen contained in the vaccine was non-infectious. However, since the viral antigen was not the only component of the vaccine, the CDC’s conclusion did not logically follow.

The CDC did not say whether studies were being done to determine the safety of vaccinating infants at birth. This curious oversight was made despite the CDC’s acknowledgment that the vaccine included aluminum—a known neurotoxin—as an “adjuvant”. An adjuvant, as defined by the CDC, is “an ingredient used in some vaccines that helps create a stronger immune response in people receiving the vaccine.” Inasmuch as aluminum is a foreign substance in the body capable of causing disease and which triggers an immune response, aluminum also meets the CDC’s definition of an “antigen”.

Additionally, the hepatitis B vaccine being used at the time included another known neurotoxin: mercury.

Furthermore, the CDC included high-risk pregnant women within the scope of its recommendation by stating that pregnancy “should not be considered a contraindication to the use of this vaccine”.

The CDC admitted that, with respect to the developing fetus, safety data were “not available”, but assumed that the risk “should be negligible” on the grounds that the viral antigen contained in the vaccine was non-infectious. However, since the viral antigen was not the only component of the vaccine, the CDC’s conclusion did not logically follow.

This glaring non sequitur fallacy by the CDC is illustrative of a complete lack of concern among public health officials about the neurotoxicity of mercury and aluminum, both of which are known to pass through both the placental and blood-brain barriers.

In fact, the CDC issued its recommendations that high-risk pregnant women and infants of carrier mothers be vaccinated despite a complete absence of studies demonstrating that either practice was safe. The clinical trials used to obtain licensure for the vaccine had included only gay men.

Additionally, the CDC acknowledged that the duration of protection conferred by the vaccine had “not yet been determined.”

In 1984, the CDC revised its recommendation to include vaccination of infants at birth. Under the new policy, women belonging to high risk groups were to be tested routinely during prenatal visits, and if positive for HBsAg, HBIG was to be administered to the infant as soon as possible after delivery and preferably within twelve hours of birth. Now, instead of waiting until at least a week to initiate the vaccine regimen, the CDC advised giving the first dose within seven days of birth, further implying that this should preferably be done on the very first day of life by stating that the effectiveness of HBIG administered concurrently with vaccination increased the effectiveness of preventing chronic infection from 75 percent up to 90 percent. (According to the Pink Book, vaccination alone is 70 percent to 95 percent effective, while vaccination concurrent with HBIG within twenty-four hours of birth is 85 to 95 percent effective.)

While emphasizing that studies had shown vaccination to be effective, the CDC mentioned no studies demonstrating that it was safe to vaccinate newborn babies or to expose developing fetuses to mercury and aluminum by vaccinating pregnant women.

In an updated recommendation the following year, the CDC explicitly recommended vaccinating infants born to infected mothers concurrently with HBIG within twelve hours of birth. Once again, safety studies were not forthcoming.

In 1986, a new version of the hepatitis B vaccine was licensed for use in all ages. The older version was manufactured by isolating and purifying HBsAg from the blood plasma of infected individuals. The new vaccine, Merck’s Recombivax HB, instead contained viral proteins that were genetically engineered, manufactured by cloning the virus’s genetic coding for HBsAg into “recombinant” yeast.

Under federal law, vaccine manufacturers are required to include package inserts with their products providing adequate warnings about the risks of using them. These are publicly available on the FDA’s website. The current package insert for Recombivax HB, with respect to its effectiveness, states that “The duration of the protective effect of RECOMBIVAX HB in healthy vaccinees is unknown at present and the need for booster doses is not yet defined.” The vaccine may also be ineffective if administered to an individual who is already infected.

It’s not known whether the vaccine’s contents are excreted in human milk, and there are no studies of the effects on breastfed infants or milk production. There are no studies to determine whether the vaccine can cause genetic mutations or cancer, or whether it can impair fertility.

With respect to its safety, Merck states that “There are no adequate and well-controlled studies designed to evaluate RECOMBIVAX HB in pregnant women.” Additionally, “Developmental toxicity studies have not been conducted with the vaccine in animals.” It’s not known whether the vaccine’s contents are excreted in human milk, and there are no studies of the effects on breastfed infants or milk production. There are no studies to determine whether the vaccine can cause genetic mutations or cancer, or whether it can impair fertility.

Merck does refer to post-licensure clinical studies relevant to pregnant women, but these were not actually designed to test the safety of the vaccine for this group. Instead, twenty-three pregnant women were vaccinated “inadvertently” early in their first trimester, four of whom ended up having a miscarriage. Merck states that this 17 percent miscarriage rate is “consistent with estimated background rates”, but given the fact these studies weren’t designed to determine whether fetal harm might occur, included a very small number of pregnant women, and didn’t include a placebo control group, this information is totally worthless in terms of risk assessment.

The only information about safety with respect to vaccinating infants refers to three clinical trials including a total of only “147 healthy infants and children (up to 10 years of age)”. Since the infants were grouped with older children and their number unspecified, this information is uninterpretable with respect to the safety of vaccinating infants still in the earliest stages of childhood development. The number of children included was also too low for these studies to have the statistical power necessary to detect any harms apart from those that occur very frequently. There was no placebo control group even to determine the statistical significance of reported adverse events, such as fever or rhinitis. Furthermore, these children were monitored for adverse events for only five days, so any adverse events occurring after that period of time were entirely missed.

This is particularly concerning given that symptoms of neurological damage from toxins like mercury and aluminum might not be noticeable for many weeks, months, or even years following exposure—not to mention the fact that it is not only single exposures that need to be taken into consideration, but the cumulative impact of all environmental toxic exposures.

Despite the total inadequacy of the clinical trials for determining the safety of vaccinating pregnant women and infants, a microbiologist from the Food and Drug Administration (FDA), Richard Daemer, assured the public of the new vaccine’s safety by stating that it “just can’t do any damage, period”.

The sole premise upon which that fallacious conclusion was based was, once again, that the vaccine did not contain a live virus capable of infection. It was a statement that once again demonstrated the complete lack of consideration among public health officials that mercury and aluminum, both of which were also included in Recombivax HB, could potentially cause neurodevelopmental harm to vulnerable fetuses and young infants.

That same year, the US Congress passed the National Childhood Vaccine Injury Act, which granted broad legal immunity against vaccine injury lawsuits to the pharmaceutical industry and established the Vaccine Injury Compensation Program, funded by an excise tax on each vaccine dose, to effectively shift the financial burden for vaccine injuries away from the manufacturers and onto the taxpaying consumers. The Supreme Court in 2011 upheld legal immunity for vaccine manufacturers on the grounds that adverse reactions are “unavoidable” and design defects are “not a basis for liability”.

In 1988, the CDC once again revised its policy by recommending screening for all pregnant women, not just those in high risk groups, in an effort to reduce the number of perinatally infected infants who become chronic carriers. The number of such infants born each year was estimated to be about 3,500, which represented about one-fifth of the estimated number of births to HBsAg-positive women annually (16,500). A study done ten years later estimated that 97 percent of pregnant women in the US receive prenatal screening.

Once again, there was no placebo control group, and the researchers solicited only certain pre-selected adverse events by providing a symptom checklist. Once again, subjects were monitored for a very short term, which was only four days.

In 1989, a second recombinant HepB vaccine was licensed for use in all ages: GlaxoSmithKline’s Engerix‑B. Its package insert includes similar warnings as are included with Merck’s product. In thirty-six clinical trials, Engerix‑B was administered to 5,071 healthy adults, children, and newborn infants. Once again, including the unspecified number of infants with older children and adults renders this information uninterpretable with respect to the risks of vaccinating infants. Once again, there was no placebo control group, and the researchers solicited only certain pre-selected adverse events by providing a symptom checklist. Once again, subjects were monitored for a very short term, which was only four days.

The CDC’s rational for universal HepB vaccination of infants

Given the low risk to most newborns of Hepatitis B Virus (HPV) infection, the routine screening during pregnancy to identify at-risk newborns and the availability of HBIG treatment for exposed infants (that is 75 percent effective at preventing chronic infection), coupled with the lack of studies to determine the safety of vaccinating pregnant women and infants, what was the scientific medical rationale underlying the CDC’s decision in 1991 to recommend that all newborn babies be vaccinated?

The simple answer is that there wasn’t one. The ACIP’s recommendation was not based on science, but on the CDC’s desire to achieve its goal of eliminating transmission of HBV by achieving high vaccination rates. Indeed, the CDC was actually quite explicit about this at the time.

The stated reason why the CDC wanted to vaccinate all infants was not because all infants were at risk of infection, but simply because its strategy to vaccinate high-risk populations was failing.

The CDC’s “rationale for a comprehensive strategy to eliminate transmission of hepatitis B virus in the United States” was published in its journal Morbidity and Mortality Weekly Report (MMWR) on November 22, 1991. The new strategy included “making hepatitis B vaccine part of routine vaccination schedules for all infants.” The stated reason why the CDC wanted to vaccinate all infants was not because all infants were at risk of infection, but simply because its strategy to vaccinate high-risk populations was failing.

In the CDC’s own words, “In the United States, most infections occur among adults and adolescents. The recommended strategy for preventing these infections has been the selective vaccination of persons with identified risk factors. However, the strategy has not lowered the incidence of hepatitis B, primarily because vaccinating persons engaged in high-risk behaviors, life-styles, or occupations before they become infected generally has not been feasible.” (Emphasis added.)

As the CDC reiterated, “Efforts to vaccinate persons in the major risk groups have had limited success.” Furthermore, “Educational efforts alone are not likely to fully eliminate the high-risk behaviors responsible for HBV transmission.”

Infants, of course, do not engage in those high-risk behaviors. The CDC’s reasoning was simply that, since adults tended for various reasons to not get the vaccine, it would eliminate the choice by vaccinating everyone at birth, regardless of individual risk.

It would be cheaper and easier, the CDC argued, just to vaccinate everyone at birth than to continue targeting high-risk populations. “In the long term,” the CDC judged, “universal infant vaccination would eliminate the need for vaccinating adolescents and high-risk adults.”

Continuing, the CDC noted that the older, plasma-derived vaccine was no longer produced in the US, having been replaced by the recombinant vaccine technology. Like the older vaccine, both brands of the newer HepB vaccine contained aluminum and mercury.

The CDC acknowledged that no long-term studies had been done to determine the effectiveness of the new vaccine. Instead, its effectiveness was judged on the basis of studies done for the older, plasma-derived vaccine. With the older vaccine, protective antibody levels were initially provoked in most subjects, but waned over time so that after nine years as many as 60 percent of subjects no longer had detectable antibodies. However, the vaccine seemed to induce immunologic memory so that subjects remained immune despite waning antibody titers. For children vaccinated at birth, the protective effect of the vaccine persisted for “at least 5 years”.

Hence, the CDC’s recommendation was not based on scientific studies demonstrating that the recombinant HepB vaccine administered in early childhood would confer immunity throughout adulthood. Instead, the CDC’s policy was faith-based, resting on the mere assumption that it would do so.

… it’s very easy to say that there is no apparent evidence of harm when studies to determine the risk have not been done.

The CDC’s new policy was even more faith-based when it came to the question of the new vaccine’s safety. It produced no studies demonstrating that exposing fetuses and infants to these neurotoxins was safe. Instead, citing its own unpublished data, the CDC judged on the basis of “limited experience” that there was “no apparent risk” to developing fetuses of vaccinating pregnant women. Of course, it’s very easy to say that there is no apparent evidence of harm when studies to determine the risk have not been done.

The CDC also once again employed the non sequitur fallacy that, since the viral antigen particles in the vaccine were noninfectious, the vaccine “should cause no risk to the fetus”—thus once again demonstrating the institutionalized failure to consider the potential for neurodevelopmental harms from mercury and aluminum.

Beyond that, the best the CDC could do to reassure the public about the vaccine’s safety was to add that “Hepatitis B vaccines have been shown to be safe when administered to both adults and children. Over 4 million adults have been vaccinated in the United States, and at least that many children have received hepatitis B vaccine worldwide.”

Of course, this, too, was a non sequitur fallacy, as the conclusion that the vaccine is safe does not follow from the premise that it had been injected into four million children globally. (Consider how many cigarette smokers there must have been in the world already before the government and tobacco industry finally acknowledged that smoking can cause lung cancer.)

In the CDC’s faith-based judgment, the benefit of possibly preventing an estimated 2,000 to 5,000 annual deaths from HBV-related liver disease outweighed any potential harms, including the risks of unnecessarily exposing millions of fetuses and newborn babies to the neurotoxic effects of mercury and aluminum.

In 1999, the decision was made to eliminate the mercury-based preservative thimerosal from most vaccines routinely recommended for children. This was done because it had become known that the CDC’s schedule was exposing children to cumulative levels of mercury that exceeded the safety guidelines of the US Environmental Protection Agency (EPA). However, thimerosal is still used in multi-dose vials of influenza vaccines, and both hepatitis B vaccines licensed for use in infants still contain aluminum.

Evidence of Neurological Harm from the HepB Vaccine

Despite widespread concerns about the possibility of neurodevelopmental harm from the HepB vaccine, which is administered to more than 70 percent of newborns worldwide, still twenty-five years after the CDC implemented its universal infant vaccination regimen, as a team of Chinese researchers noted in a study published in the journal Psychoneuroendocrinology, “Whether this neonatal vaccination affects brain development is unknown.”

A previous study by the same team, published in the Journal of Neuroimmunology a year prior (2015), was the first to examine the question of “whether neonatal vaccination could influence brain development in a physiological manner.” Studying the effects of vaccination in rats, among their findings was that it triggered an increase in “pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α”, which research had focused on “as having a detrimental effect on neuronal function and synaptic plasticity.” The increase in pro-inflammatory cytokines was part of “a neurotoxic expression profile” exhibited by HepB-vaccinated rats. Their data confirmed “that altered immune status induced by vaccination modulates hippocampal synaptic plasticity during early life”. The vaccine induced a bias toward an antibody response, or humoral immunity, in relation to cell-mediated immunity. This skewing of the immune system, they concluded, “exerted detrimental effects”.

… early vaccination with [hepatitis B vaccine], which induces strong immune activation, is suspected to influence brain development and behavior.

In their study the following year, the researchers elaborated: “Perinatal immune activation has been demonstrated to influence brain development and behavior. The brain is still developing in the early postnatal time period and thus immune activation can impact the developmental programming of the brain. . . . Therefore, early vaccination with [hepatitis B vaccine], which induces strong immune activation, is suspected to influence brain development and behavior.”

Furthermore, the balance between cell-mediated (Th1) and humoral immunity (Th2) “serves as an important mediator for the effects of immune activation on the central nervous system (CNS).” The HepB vaccine, as previously reported, induced a Th2 bias, which “is regarded as neurodetrimental” and “has been reported to be associated with cognitive deficits”. Their new study demonstrated that early HepB vaccination impaired the behavior, the synaptic plasticity of the hippocampal part of the brain, and the growth of nerve tissue of mice in early adulthood. These detrimental outcomes were all possible effects of “the alterations in the brain neuroimmune milieu following the systemic Th2 bias.”

The researchers concluded that early HepB vaccination “induces impairments in behavior and hippocampal neurogenesis”, with their data “supporting the long suspected potential association of [hepatitis B vaccine] with certain neuropsychiatric disorders such as autism and multiple sclerosis.”

In a third rodent study published in the journal Cytokine in October 2018, the researchers highlighted how HepB vaccination “induced an instant anti-inflammatory cytokine response and a subsequent proinflammatory cytokine response in the hippocampus.” Notably, behavioral impairment appeared in mice vaccinated on the day of their birth at eight weeks of age, coinciding with “the delayed hippocampal neuroinflammation”. A dramatic increase in pro-inflammatory cytokine levels (IL-1β, IL-6, and TNF-α) as compared to controls was observed between thirty-five to forty-two days post-vaccination.

Naturally, such evidence of delayed neurological harm couldn’t possibly have been detected in the uncontrolled clinical trials with only four or five days of follow-up that were used by Merck and GlaxoSmithKline to obtain the FDA’s stamp of approval for getting their products to market.

As Children’s Health Defense contributing writer J.B. Handley has remarked with respect to this series of studies, “It’s reasonable to say that the way Hepatitis B vaccine was tested and the way Hepatitis B causes brain damage (on a delayed schedule) means our health authorities have no idea how much brain damage Hepatitis B vaccine is causing our children. None.”

Conclusion

While public health officials and the corporate news media mock and scorn anyone who dares to question the wisdom of vaccinating children strictly according to the CDC’s recommended childhood schedule, including vaccination of newborn babies on the very first day of their lives, what the science is telling us is that there are very legitimate reasons for concern. At the very least, there ought to be open discussion and debate about the practice of vaccination, yet instead we are witnessing a concerted effort to silence critics and more strictly enforce vaccine mandates required for school entrance.

While we’re told that the hepatitis B vaccine is a “crucial shot” for infants, the reality is that the vast majority of children are not at significant risk of infection. The CDC’s recommendation to vaccinate newborns universally was not based on science, but on the assumptions that the vaccine would effectively reduce HBV-related liver disease mortality and—to paraphrase the words of FDA microbiologist Richard Daemer—would be incapable of causing harm to pregnant women’s developing fetuses or newborn babies.

Instead, what science is telling us is that the CDC’s recommendation to universally vaccinate newborns at birth puts the majority of children in the US at a completely unnecessary risk of neurodevelopmental harm from the hepatitis B vaccine, with incalculable costs to society.

 

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