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With the recent release of a provocative children's book entitled Melanie's Marvelous Measles, a debate has ensued regarding the effectiveness and wisdom surrounding measles vaccinations. When I first heard about the book, I went to Amazon to order a copy for myself. The amount of negative reviews was staggering. People were claiming that the information was "dangerous", "harmful" and "ill-informed". Some were even calling for the book to be banned. It took me a few minutes to read it from cover to cover. Rather than critique the book, which has already been done quite eloquently by others, I would like to talk about the widespread fear surrounding measles and the misinformation regarding the vaccine.
References to measles can be found as far back as the 7th century. Measles is an RNA virus that was first isolated in 1954. A typical infection produces a characteristic skin rash starting at the head and progressing down the trunk and extremities. The rash is typically preceded by a high fever. Around this time, blue-white spots (Koplik spots) can be found on the mucous membranes. These are considered pathognomonic for measles. Other symptoms may include cough, runny nose, conjunctivitis, diarrhea, anorexia and lymphadenopathy.
According to the CDC, prior to the introduction of the vaccine, measles was a nearly universal infection occurring most commonly in 5-9 year olds with 90% of U.S. children immune by age 15. Most kids recovered fully within a few weeks with life-long immunity. Reported complications from data collected between 1985-1992 included pneumonia (6%), encephalitis (.1%), seizures (.6-.7%), and death (.2%). These occurred most frequently in children under 5 and adults over 20. These complications may, in fact, have been exacerbated by allopathic interventions to treat common symptoms such as fever reduction using antipyretics.[15,16]
Many people are aware that the first licensed live-virus vaccine was introduced in 1963 (Edmonston B strain) but few know that there was also a killed measles vaccine (KMV) licensed that same year. That vaccine was pulled in 1967, however, after it was discovered that individuals who received the KMV and were subsequently exposed to the wild virus were afflicted with a more severe atypical form of measles. Today's vaccine, known as MMR, contains attenuated, live-measles virus (Edmonston-Enders strain) mixed together with mumps and rubella virus. There is an alternate version of the vaccine, known as MMRV, that combines MMR with the varicella virus. The measles virus is cultured on chick embryo fibroblast tissue and the vaccine contains human albumin, neomycin, sorbitol and gelatin. The 2013 CDC recommendations include 2 doses of MMR, the first at 12-15 months and the second at 4-6 years.
CDC data appears to indicate that the live-virus vaccine has been very effective at decreasing classic measles incidence in our population, however, it can take little credit for the decreased mortality in the developed world considering the death rate had decreased over 98% prior to the vaccine. Never the less, vaccine advocates hail this as a victory. The problem is that few of them question whether it was wise to prevent children from acquiring this infection naturally. Many well-respected doctors and researchers believe that measles is a right of passage that allows a child's immune systems to develop and strengthen. It has been documented that kids in 3rd world countries who get a wild measles infection are less susceptible to malaria and parasitic infections. Medical literature from the 1940's documents children being cured of a kidney disorder known as nephrotic syndrome following measles.
The number of classic measles cases in the US appears to have declined but any protection afforded by the vaccine is limited and often short-lived. Natural infection with wild measles creates long-lasting viral-specific and viral-neutralizing antibodies that are not acquired following vaccine-introduced infection. There are numerous documented cases of measles occurring in highly vaccinated communities [6-8, 17] which can be attributed primarily to short-term efficacy (secondary vaccine failure). This has important implications considering the fact that measles has an increased rate of complications in adults when compared to school age children. In 1973, persons 20 years of age or older accounted for approximately 3% of cases, however, by 2001 that number had increased to 48%.
Not only are measles complications more frequent and severe in adults, but infection during pregnancy increases the risk of spontaneous abortion, premature labor and low-birth weight infants. Additionally, vaccination appears to have increased infants susceptibility to measles.
"Infants whose mothers were born after 1963 had a measles attack rate of 33% compared with 12% for infants of older mothers."
[M]easles susceptibility of infants younger than 1 year of age may have increased. During the 1989-91 measles resurgence, incidence rates for infants were more than twice as high as those in any other age group.
Women of childbearing age, who in the pre-vaccine era acquired measles naturally in childhood, no longer have the robust, life-long viral-specific and viral-neutralizing immune factors to pass to their infants from their serum through the placenta. This is likely the case for breast-milk as well. Secretory IgA (sIgA) antibodies are produced in the mammary gland and can provide passive immunity to breast-fed infants. Natural & vaccine-acquired measles infections have been shown to produce mucosal antibodies. Although I have found no study that looks at the difference between sIgA production in the breast-milk of vaccinated moms versus those who experienced a natural measles infection, it's reasonable to suspect, given what occurs in the serum and the increased susceptibility of infants in the post-vaccine era, that naturally infected moms provide more robust antibody protection through their breast-milk.
Measles in infancy is a risk factor for a fatal degenerative central nervous system condition known as Subacute Sclerosing Panencephalitis (SSPE). Could we be setting the stage for disaster if and when measles reignites here in the U.S. due to either imported cases from abroad or a novel mutated strain caused by the vaccine itself? I can predict, with absolute certainty, the response from our government health officials...more vaccines!
What about the possibility of vaccine-induced disorders not typically associated with a measles infection? Wild measles exposure occurs through contact with the human respiratory tract. The measles vaccine introduces a lab altered, live-virus through an unnatural route of exposure. This weakened, man-made virus can bury deep into the tissues and create a slow infection in practically any area of the body including the gastro-intestinal (GI) tract and central nervous system (CNS). The consequences of these vaccine-induced infections may not show up for months, years or decades later.
A vaccine induced form of SSPE known as Measles Inclusion-Body Encephalitis (MIBE) has been documented in children months to years following measles vaccination. Could the rapid rise in chronic inflammatory bowel and neurological disorders be caused by these slow infections? How many doctors would ever think to investigate the possibility that these illnesses may be with a distant vaccination? To further complicate the issue, in a phenomenon known as recombination, the measles virus can combine with other live viruses in the vaccine to create a novel virus with unknown effects.
There is one additional thing that I would like people to consider ... could the whole premise behind artificially stimulating antibody production in order to provide protection from measles be flawed?
[R]esearchers have noted that children with simple agammaglobulinemia in whom measurable measles antibodies do not develop after measles virus infection recover from the disease normally...In contrast to antibody data, patients with defects in the cell-mediated immune system clearly do poorly...and quickly succumb to progressive infection despite administration of large doses of measles antibody-containing immunoglobulin.
The fear surrounding measles stems from ignorance. In a well-nourished child with a properly functioning immune system, viral infections are typically subclinical or exceedingly mild. Certain infections, such as measles, even appear to provide long-term health and immune system benefits. Malnourishment, in particular vitamin A deficiency, is a primary cause of poor outcomes. One of the most effective ways to ensure that a viral illness runs a mild or benign course is to provide children with adequate stores of vitamin A prior to exposure.
As well, high doses of vitamin A given during an acute measles infection has been shown to prevent mortality. Vitamin A works by signaling cell-mediated immune cells known as macrophages to produce an anti-viral messenger known as interferon. Young infants are unable to produce high-levels of interferon  and, therefore, rely on passive immunity from mom for protection. It should be noted that measles vaccination has been shown to deplete levels of serum vitamin A.
Many fruits and vegetables provide beta-carotene which is converted by the liver into active vitamin A (retinoids), however, the efficiency of uptake and conversion can vary based on a variety of factors. Particularly during illness, I prefer pre-formed vitamin A from high quality, whole-food sources like cod liver oil and high-vitamin butter oil. I should mention that Melanie's Marvelous Measles will be one of the first books that I read to my daughter.
-  CDC. 2012. Chapter 12. The Pinkbook: Course Textbook – 12th Edition.
-  Yalcin, S. M.D.; Yurdakok, K. M.D. "Sex specific differences in serum vitamin A values after measles immunization." The Pediatric Inf Dis J. 1999, p.747
-  Rooth IB. 1992. "Suppression of plasmodium falciparum infections during measles or influenza." Am J Trop Med Hyg 47(5):675-81.
-  Richard W. Blumberg, M.D.; Harold A. Cassady, M.D. 1947. "Effect of Measles On The Nephrotic Syndrome." Am J Dis Child 73(2):151-166.
-  Obukhanych, T. 2012. Vaccine Illusion.
-  Nkowane, B.M., S.W. Bart, W.A. Orenstein, and M. Baltier. 1987. "Measles outbreak in a vaccinated school population: epidemiology, chains of transmission and the role of vaccine failures." Am J Public Health 77:434-438.
-  Boulianne, N, et al. "Major measles epidemic in the region of Quebec despite a 99% vaccine coverage." Can J Public Health 1991, 82:189-190.
-  De Serres, G, et al. "The largest measles epidemic in North America in a decade--Quebec, Canada, 2011: Contribution of susceptibility, serendipity and super-spreading events on elimination." J Infect Dis 2012
-  Feigin, R. Textbook of Pediatric Infectious Diseases, Volume 1. 2004, p.2289
-  Papania, M, et al. "Increased susceptibility to measles in infants in the United States." Pediatrics 1999, Nov;104(5):e59
-  Bitnun A, et al. "Measles inclusion-body encephalitis caused by the vaccine strain of measles virus." Clinical Inf Dis 1999, Oct;29(4):855-61.
-  Huiming, Y., et al. "Vitamin A for treating measles in children." Cochrane Database Syst Rev 2005, CD001479
-  Trottier, C, et al. "Retinoids inhibit measles virus through a type 1 IFN-dependent bystander effect." FASEB J 2009, 23:3203-3212.
-  Wilson, C.B., et al. "Decreased production of interferon-gamma by human neonatal cells. Intrinsic and regulatory deficiencies." J Clin Invest 1986, 77:860-867.
-  Ahmady, A.S., and A.R. Samadi. "The adverse effects of antipyretics in measles." Indian Pediatr 1981, 18:49-52.
-  Sugimura, T, et al. "Risks of antipyretics in young children with fever due to infectious disease." Acta Paediatr J 36:375-378
-  Poland, G.A., R.M. Jacobson. "Failure to reach goal of measles elimination. Apparent paradox of measles infections in immunized persons." Archives of Int Med 1994, 154(16):1815-20.
-  Historical statistics of the United States – Colonial Time to 1970 Part 1
-  Simon, J.K., et al. "Mucosal IgA Responses In Healthy Adult Volunteers following Intranasal Spray Delivery of a Live Attenuated Measles Vaccine." Clin Vaccine Immunol. Mar 2011; 18(3): 355–361.