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Vaccination Policy Lags Behind Vaccination Science
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Vaccination policy lags behind vaccine science
by Teresa Binstock December 9, 2007
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Although vaccinologists have long enjoyed the prominence of their field's orthodoxy, skepticism is arising in respected venues. The British Medical Journal allows the question, "Are US flu death figures more PR than science?" and the journal vaccine presents an article titled, "Why is evidence-based medicine so harsh on vaccines?" Debate about the safety of vaccinations continues.

Many parents believe their child's neurologic, behavioral, or certain other physiological problems were caused or exacerbated by vaccinations. The CDC, which receives gargantuan funding to promote vaccinations (1-2), assures the public of their safety. Despite these assurances, a reporting system for vaccine-related adverse effects exists (3-4). A growing body of medical research suggests that subgroups of individuals can be adversely affected by environmental exposures that, for most people, seem not to generate untoward effects (eg, 5).

Consider some new words: pharmacogenomics, pharmacogenetics, and nutrigenomics. Each calls attention to the interplay between environmental factors and the human genome. Pharmacogenetics refers to how drugs interact with various gene alleles. An example is that some people detoxify an anti-cancer drug before it can do its work. Conversely, some individuals detoxify a given drug so poorly that a therapeutic dose normal for most people is far too high. Nutrigenomics refers to relationships among proper levels of intra-body nutrients, a person's gene alleles, and his or her need for nutritional boosting of one metabolic pathway or another (6). The word toxicogenomics refers to the interplay between gene alleles and environmental chemicals (5). Each of these fancy words has an inherent principle. People are not identical. There is much inter-individual variation in the human genome, and these differences often cause people respond to differently to otherwise similar chemical exposures. A major ramification is that medical treatments based upon a "one size fits all" policy often create problems for some individuals. This may be what is occurring as childhood vaccinations become more numerous.

In fact, the new insights about pharmacogenomics and nutrigenomics ought be applied to the nation's vaccination policy. Might subtle genetic variations account for why some children experience adverse reactions to vaccinations? If so, are one-size-fits-all mandates for vaccinations likely to injure some children? Ought a sick child not be vaccinated? Certainly, some contraindications against vaccinations are known and declared, but findings in pharmacogenomics and nutrigenomics suggest that officially declared vaccination contraindications circa 2007 may be insufficient for protecting infants and toddlers whose gene alleles and nutritional status indicate enhanced likelihood of risk. These concerns are not theoretical.

Vaccine guidelines are virtually compulsory in most states. Most parents are informed that they consent. School attendance is one of the primary levers by which vaccinations are enforced. Recently, Maryland prompted a flurry of news articles describing school-related vaccination-enforcement (eg, 7). Similarly, New Jersey is likely to add four vaccinations as conditions for preschool and kindergarten registration (eg, 8). These events proceed even as many physicians, researchers, and parents question the wisdom of infants, toddlers, and young children receiving so many vaccinations so early in life.

Gregory A. Poland, M.D., is a Mayo researcher. He and his colleagues have published numerous findings about gene alleles and their effects upon an individual's ability to produce titers to vaccinal antigens. Needless to say, their research and similar studies by others help us understand the genomic basis for inter-individual responses to vaccinations (eg, 9-19). Some individuals are low responders, they hardly generate a titer to a vaccinal antigen. Other individuals are high responders, they generate antibody responses far higher than normal. These differences provide possible clues regarding why vaccinations are not safe for every child, why many parents describe post-vaccinal adverse effects, and do so while the CDC and AMA continue to trumpet vaccine safety, even as some states seek increased enforcement of compulsory vaccinations in accord with a one-size-fits-all policy.

For more than ten years, many parents of autistic children have purchased titer-based immune screens for vaccinal antigens and for herpes viruses. Many such parents report that their autistic child who had been vaccinated has one or several missing titers for a vaccinal antigen. Since some vaccines contain live-viruses (described as attenuated), if some individuals have one or more alleles that impair immune responses to a specific vaccine's antigen, might that vaccine's live-virus be effectively less attenuated for that subgroup of individuals? Since some viruses are known to have the potential of affecting the central nervous system of humans (20-26), would vaccinal injections with attenuated versions of those viruses be more likely to generate adverse effects in individuals with missing or weak titers against those viruses? As suggested by findings in pharmacogenetics and in the work of Dr. Poland and colleagues, the answer may well be Yes! Some individuals are likely to be affected by injections of live-viruses, even those claimed to be attenuated. Furthermore, the work of Merrill Chase and others has made clear that a missing titer may represent additional immune weaknesses.

The findings mentioned in this brief essay indicate an important concern. Is enforcement of a one-size-fits-all vaccination policy certain to induce adverse effects in some children? Again, the answer appears to be Yes. Perhaps the policy of enforcing mandatory vaccinations needs be tempered by genomic testing of children so that individuals with relevant alleles or weakened immunity can be identified before they are placed at risk by vaccination incidents. Such testing would not be inexpensive, but establishing a pre-vaccination testing policy might reduce the number of adverse events and thus inhibit the growing costs of long-term care for severely affected individuals.






  5. Toxicogenomics: a pivotal piece in the puzzle of toxicological research. Gatzidou ET et al. J Appl Toxicol. 2007 Jul-Aug;27(4):302-9.

  6. Nutrigenomics: The Genome - Food Interface



  9. Variation in vaccine response in normal populations. Pharmacogenomics. 2004 Jun;5(4):417-27.

  10. The genetic basis for measles vaccine failure. Acta Paediatr Suppl. 2004 May;93(445):43-6;

  11. Correlations among measles virus-specific antibody, lymphoproliferation and Th1/Th2 cytokine responses following measles-mumps-rubella-II (MMR-II) vaccination. Clin Exp Immunol. 2005 Dec;142(3):498-504.

  12. Human leukocyte antigen polymorphisms: variable humoral immune responses to viral vaccines. Expert Rev vaccines. 2006 Feb;5(1):33-43.

  13. Human leukocyte antigen haplotypes in the genetic control of immune response to measles-mumps-rubella vaccine. J Infect Dis. 2006 Mar 1;193(5):655-63. Epub 2006 Jan 27.

  14. Immune activation at effector and gene expression levels after measles vaccination in healthy individuals: a pilot study. Hum Immunol. 2005 Nov;66(11):1125-36. Epub 2006 Jan 4.

  15. Importance of HLA-DQ and HLA-DP polymorphisms in cytokine responses to naturally processed HLA-DR-derived measles virus peptides. vaccine. 2006 Jun 19;24(25):5381-9. Epub 2006 May 3.

  16. Associations between measles vaccine immunity and single-nucleotide polymorphisms in cytokine and cytokine receptor genes. J Infect Dis. 2007 Jan 1;195(1):21-9. Epub 2006 Nov 20.

  17. Human leukocyte antigen and interleukin 2, 10 and 12p40 cytokine responses to measles: is there evidence of the HLA effect? Cytokine. 2006 Nov;36(3-4):173-9. Epub 2007 Jan 17.

  18. Variations in measles vaccine-specific humoral immunity by polymorphisms in SLAM and CD46 measles virus receptors.J allergy Clin Immunol. 2007 Sep;120(3):666-72. Epub 2007 Jun 8.

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  20. measles virus in the CNS: the role of viral and host factors for the establishment and maintenance of a persistent infection. J Neurovirol. 1999 Dec;5(6):613-22.

  21. Increase in adhesion molecules in cerebrospinal fluid of children with mumps and mumps meningitis. Scand J Immunol. 2006 Oct;64(4):420-4.

  22. An adult case of mumps brainstem meningoencephalitis with a past measles-mumps-rubella (MMR) vaccination. Korean J Intern Med. 2006 Jun;21(2):154-7.

  23. Neurological aspects of rubella virus infection. Intervirology. 1997;40(2-3):167-75.

  24. Congenital rubella syndrome due to infection after maternal antibody conversion with vaccine. Jpn J Infect Dis. 2003 Apr;56(2):68-9.

  25. Congenital rubella syndrome despite repeated vaccination of the mother: a coincidence of vaccine failure with failure to vaccinate. Acta Paediatr. 1994 Jun;83(6):674-7.

  26. Complications of varicella in children: emphasis on skin and central nervous system disorders. J Microbiol Immunol Infect. 2000 Dec;33(4):248-52

  27. Polymerase chain reaction analysis and oligoclonal antibody in the cerebrospinal fluid from 34 patients with varicella-zoster virus infection of the nervous system. J Neurol Neurosurg Psychiatry. 2006 Aug;77(8):938-42.

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