Vaccination: An Updated Analysis of the Health Risk, Part II

A 3-part series, by Gary Null, PhD and Martin Feldman, MD

A major controversy is brewing in the United States as people question whether the vaccines we give to children are safe and effective. In this three-part series, we explore the vaccine controversy to help separate the myths from the facts. We have conducted an extensive review of the scientific literature to examine the safety and efficacy of vaccines and the health effects of these often-mandated medical procedures.

Part II


Diphtheria Toxoid
According to the Centers for Disease Control and Prevention (CDC), the incidence of diphtheria was reduced to zero by 2004, from an estimated average of 21,053 cases per year in the 20th century.[1] But as with other infectious diseases, much of the decline in mortality from diphtheria had occurred before the vaccine was used. This mortality rate fell from 40 deaths per 100,000 in 1900 to approximately 16 per 100,000 in 1920, when the diphtheria vaccine was introduced in the US.[2]

Pertussis Vaccine
Despite high levels of childhood vaccination coverage for pertussis (whooping cough), the largest outbreak of this disease in four decades has occurred in recent years. There were 25,827 reported cases of pertussis in 2004 (the actual incidence could be higher due to underreporting), compared with a low of 1,010 in 1976.[3]

According to the CDC, the reported rate of pertussis per 100,000 population increased from 1.8 in 1994 to 8.9 in 2004. The 2004 rate was the third consecutive annual increase in the incidence of pertussis. The CDC notes that two-thirds of reported cases of pertussis now occur among adolescents and adults due to the waning of vaccine-induced immunity. This waning occurs five to ten years after receipt of the vaccine. [4]

Similar trends in pertussis were noted nearly 20 years ago in a 1988 report. After the US mandated whooping cough vaccination in 1978, the incidence of the disease in the next eight years trebled. The highest incidence was in infants less than one year old. However, the highest relative increase was in adolescents and adults.[5]

In 2006, the CDC’s Advisory Committee on Immunization Practices (ACIP) addressed the rise of whooping cough among adolescents by recommending that they receive another dose of pertussis vaccine. The Tdap vaccine (which also contains tetanus and diphtheria toxoids) is now recommended for all children age 11 to 18 and replaces the tetanus-diphtheria booster previously given to adolescents. The Tdap booster adds to the five doses of diphtheria, pertussis, and tetanus that children already receive before their seventh birthday.[6]

Several research papers suggest that immunization programs have not yet brought pertussis under control. A 2006 article reports that pertussis “has reemerged worldwide as a cause of substantial morbidity and mortality in infants, children, and adolescents, despite high vaccination rates.”[7] Another report, published in 2005, states that an increased incidence of pertussis “has been observed worldwide since the introduction of widespread vaccination.” These researchers say that there has been “a general shift in the age distribution of pertussis toward older groups” and that “despite high coverage rates for primary immunization in infants and children, pertussis continues to be a global concern, with increased incidence widely noted.”[8]

On the other hand, the merit of the pertussis vaccine is indicated by a 2006 paper. This research evaluated state-level rates of nonmedical exemptions (those based on religious or personal beliefs) to mandatory vaccination from 1991 to 2004 and the incidence of pertussis among people 18 and younger from 1986 to 2004. The study found that an increased incidence of pertussis was associated with state policies granting personal-belief exemptions and the easier granting of exemptions.[9]

Replacement of the whole cell pertussis vaccine. The US made a major vaccine substitution in the 1990s when it replaced the diphtheria, tetanus, and whole cell pertussis vaccine (DTP) with a diphtheria, tetanus, and acellular pertussis vaccine (DTaP).[10] The whole cell vaccine has been associated with serious adverse reactions (such as seizures and encephalopathy).[11]

Studies have since found a decline in the number of adverse reactions to pertussis-containing vaccines. An analysis of reports made to the Vaccine Adverse Event Reporting System (VAERS) from 1991 to 2001 found that the overall reporting rate decreased substantially after use of the acellular petussis vaccine compared with the whole cell version (12.5 vs. 26.2 reports per 100,000 net doses distributed).[12]

An analysis of VAERS data from 1995 (when the whole cell vaccine was in use) to 1998 (when the acellular vaccine was predominant) found that the number of reports concerning pertussis fell from 2071 in 1995 to 491 in the first half of 1998. Events categorized as “nonfatal serious” fell from 334 in 1995 to 93 (first-half ’98). However, the decrease in reports involving deaths was modest, from 85 deaths in 1995 to 77 in 1997 and 41 in the first half of 1998.[13]

Recent comparisons of the whole cell and acellular pertussis vaccines confirm that the older version caused more adverse reactions. One study of VAERS evaluated the number of emergency room visits, life-threatening reactions, hospitalizations, disabilities, deaths, seizures, infantile spasms, encephalitis/encephalopathy, autism, sudden infant death syndrome (SIDS), and speech disorders that began within three days of receipt of pertussis-containing vaccines. The study found statistical increases for all of these events, except cerebellar ataxia, following whole cell vaccination compared with acellular vaccination.[14] In Japan, an analysis of two decades of use of the acellular vaccine showed that while neurological illnesses were rare with both types of pertussis vaccine, the incidences of encephalopathy/encephalitis and status epileptics/frequent convulsions, febrile seizures/provocation of convulsions, and sudden deaths were significantly lower with the acellular than the whole cell vaccine.[15] A study in Canada reported a 79% decrease in febrile seizures and a 60% to 67% decrease in hypotonic-hyporesponsive episodes following the introduction of the acellular vaccine there.[16]

Other research has associated the whole cell vaccine with neurological complications, including convulsions, hypotonic-hyporesponsive episodes, paralysis, and encephalopathy.[17,18,19,20,21,22] Sadly, the DTP vaccine also has been associated with SIDS, the unexpected death of an infant for which autopsy cannot reveal a determining cause. In 1982 William Torch reported that his investigation of 70 SIDS cases (which was triggered by a report of 12 such deaths occurring within three-and-one-half hours to 19 hours of DPT vaccination) found that two-thirds of the victims had been vaccinated from a half-day to three weeks prior to death.[23]

Torch reaffirmed a link between DTP and SIDS in 1986, when he presented 11 new cases of SIDS and one of near-miss syndrome occurring within 24 hours of DTP injection[24] Analysis of these and more than 150 cases of DTP post-vaccinal deaths reported in the literature – about half of which were sudden or anaphylactic – led Torch to conclude: “Although many feel that the DPT-SIDS relationship is temporal, this author and others maintain a casual relationship exists in a yet-to-be-determined SIDS fraction.”[25]

Other researchers also have uncovered a relationship between DTP and SIDS.[26,27] However, the CDC reported in 1996[28] that several studies conducted in the 1980s did not find an association between DTP vaccination and SIDS.[29,30]

Pertussis vaccination and asthma. A 1994 study found that children immunized against whooping cough were five times more likely to suffer from asthma than those who did not receive the vaccine.[31] Another study of almost 2,000 children born between 1974 and 1984 showed that vaccination against whooping cough was associated with a 76% increased risk of developing asthma and other allergic diseases later in life.[32] On the other hand, a study published by the CDC of more than 160,000 children did not find an association between the DTP vaccine and the risk of asthma.[33] A 2006 report from the Netherlands also found that receipt of the DTP/polio vaccine in infancy was not related to reported atopic disorders at primary school age.[34]

Tetanus Toxoid

The literature includes articles on neurological reactions to the tetanus vaccination[35-40] and other adverse reactions.[41-43]


Three types of polio vaccines have been used throughout the world: 1) the OPV, or oral polio vaccine (Sabin vaccine), consisting of live attenuated poliovirus; 2) the IPV, or inactivated polio vaccine (Salk vaccine), consisting of killed poliovirus and given by injection; and 3) the eIPV, an enhanced potency inactivated polio vaccine, consisting of killed poliovirus with high viral antigen content.

In the United States, the IPV (enhanced potency version) has been recommended for routine childhood vaccination against polio since 2000. Before that, the live attenuated OPV was the polio vaccine of choice for more than three decades. This vaccine, however, actually caused polio – vaccine-associated paralytic poliomyelitis (VAPP) – in a small percentage of recipients.[44] The risk of VAPP “became more difficult to justify” as polio was controlled worldwide and importations of wild poliovirus to the US became less likely, according to an article in the Journal of the American Medical Association.[45]

As a result, in 1996 the government recommended a sequential schedule using both IPV and OPV for the childhood polio vaccination series. The ACIP then recommended the all-IPV schedule in 2000.

According to the CDC, the overall risk for VAPP is approximately one case in 2.4 million OPV doses distributed, while the first-dose risk is one case in 750,000 doses distributed. The OPV has caused the only indigenous cases of polio reported in the US since 1979. Between 1980 and 1998, 144 cases of VAPP were reported.[46] Another VAPP case occurred in 1999, and in 2005, a case of imported VAPP was reported in the US after an unvaccinated American woman traveled to Central America and was exposed to an infant vaccinated with OPV.[47] In late 2005, four cases of vaccine-derived poliovirus (VDPV) involving a poliovirus strain used in the OPV were identified in unvaccinated children in an Amish community in Minnesota. The source of these infections is not known, since the OPV has not been used in the US since 2000.[48]

During the time that the trivalent OPV was used in the US (from 1963 to 1999), an inactivated polio vaccine was available. The original IPV, developed by Jonas Salk, was used to immunize American children from 1955 to 1962. According to the JAMA article, the OPV became preferred to the IPV because it provided better intestinal immunity, was able to indirectly vaccinate susceptible contacts through transmission of vaccine polioviruses, was easier to administer, and cost less.[49]

Although IPV does not cause VAPP, the severity profiles of reports to VAERS on IPV and OPV in infants up to six months of age were “remarkably similar.” Among the most frequent symptoms reported for IPV were fever, SIDS, convulsions, agitation, apnea, and stupor. Reports of fatalities in 1998 per 100,000 doses distributed were somewhat higher for IPV than for OPV. Of 142 fatalities reported for both IPV and OPV in 1997-1998, 89 indicated SIDS.[50]

Polio vaccine and Guillain-Barre syndrome. GBS is a disease that involves the nervous system and is characterized by muscle weakness, numbness, loss of reflexes, and paralysis.

In Finland, in 1985, there was an increase in the incidence of GBS a few weeks after the implementation of a nationwide campaign using OPV.[51,52] And in Brazil, an analysis of 38 cases of paralysis diagnosed as GBS led in all cases to the isolation of the vaccine strains of the poliovirus. All patients had been vaccinated with the OPV months or years before the onset of symptoms.[53] In contrast, two other studies failed to find a correlation between GBS and the OPV.[54,55]

Vaccine viruses also have been isolated from patients with paralysis diagnosed as transverse myelitis (TM), and in patients with facial paralysis (FP).[56] Most individuals with TM and FP had received the OPV months or years prior to the onset of disease, indicating that the virus may remain latent and revert to virulence later in time.

Polio vaccine and SV40-related cancers. Research conducted in the past few decades has revealed that several types of cancer may be associated with the receipt of polio vaccines more than 40 years ago that were contaminated with a monkey virus.

In 1960, it was discovered that the Salk IPV was contaminated with SV40 (simian virus 40), which was derived from the monkey cells used to grow the vaccine viruses. The SV40 survived inactivation with formaldehyde, the method used to kill the poliovirus for use in the vaccine. More than 98 million Americans were vaccinated during the time period (from 1955 to 1963)[57] that injectable and oral doses of the polio vaccine were contaminated with SV40. These people today have SV40 sequences integrated into their genetic code.

Animal studies have demonstrated the ability of SV40 to integrate its DNA into that of the host cell and induce malignancy. Unfortunately, studies show that the virus retains these same properties in humans and is associated with increased rates of certain cancers.[58] Integration and replication of SV40 has been documented in 13% to 43% of non-Hodgkin’s lymphomas,[59,60] 47% to 83% of mesotheliomas (malignant tumors of the lining of the lungs),[61,62] 11% to 90% of different types of brain tumors,[63-66] 50% of osteosarcomas,[67] more than 33% of other types of bone tumors,[68,69] and 28% of bronchopulmonary carcinomas.[70]
A continuing concern is that SV40 may be transmitted from person to person. The virus has been detected in people born in the 1980s and 1990s, decades after the tainted polio vaccine was no longer in use.[71] SV40 is now present in children, as noted by Kurt Link, MD, in his 2005 book The Vaccine Controversy, and the CDC takes this as evidence that SV40 is a naturally acquired infection unrelated to exposure to the contaminated polio vaccine. But as Dr. Link states, it is more likely that people infected by the vaccine have transmitted SV40 to others or to their offspring (such as through semen). The implication, he says, is that “any SV40 problems may not, as had been hoped, fade away with time. There is even now, ironically, work being done to provide a vaccine against SV40.”[72]

It should be noted that other research indicates there is no association between SV40 and an increased risk of rare cancers such as ependymomas, osteosarcomas, and mesotheliomas. One study compared rates of cancer after 30 years in birth cohorts who were likely to have received SV40-contaminated vaccine as infants and children with rates in people who not unexposed. Age-specific cancer rates were not significantly elevated for those exposed to the tainted vaccine.[73] Another study found no increased number of cancer deaths among 1,073 people who received SV40-contaminated vaccine,[74] and a 35-year follow-up found no deaths from the types of tumors that have been linked to SV40.[75]


Another example of changes to the US vaccination protocol was the addition in 2006 of a second dose of varicella (chickenpox) vaccine to the childhood immunization schedule. This dose is recommended for universal vaccination of all children at ages four to six and for any child, adolescent or adult who previously has received only one dose. The first dose of the varicella vaccine was recommended for children in 1995.[76]

The ACIP recommended the second dose at four to six years of age “to further improve protection against the disease.”[77] The fact is, outbreaks of varicella have occurred despite increasing coverage with the first dose of the vaccine. In a survey of 59 jurisdictions (states, large cities, and US territories) by the CDC, 45 jurisdictions were notified of at least once varicella outbreak in 2004, and 13 were notified of six or more. Data obtained on 190 outbreaks in 2004 showed that two-thirds occurred in elementary schools.[78]

Varicella outbreaks may occur even in highly vaccinated communities, and vaccinated children are still at risk of contracting the disease.[79-81] According to the CDC, 11% to 17% of vaccinated children have developed chickenpox – so-called “breakthrough varicella” – in recent outbreaks of the disease among vaccinated schoolchildren.[82] In three studies, rates of infection in vaccinated individuals ranged from 18% to 34% anywhere from five to ten years following immunization.[83-85]

In other recent studies of chickenpox outbreaks, vaccine effectiveness against varicella of any severity ranged from 44% to 87%. Effectiveness was as high as 97% for moderate or severe illness.[86-91] Research also shows that people with breakthrough varicella tend to have milder illness than do unvaccinated people who contract the disease,[92] although the vaccinated individuals can be just as infectious.[93]

VAERS received 6,574 reports of adverse events for the varicalla vaccine from March 17, 1995 to July 25, 1998. Approximately four percent of reports concerned serious events (such as anaphylaxis, thrombocytopenia, pneumonia, and convulsions) and deaths.[94] The dangers of adult chickenpox. In most cases chickenpox is a benign, self-limiting disease in children, and the natural immunity derived from contracting the disease is permanent. Vaccine-induced immunity, on the other hand, lasts only an estimated six to ten years. The temporary nature of vaccine-induced immunity can create a more dangerous situation by postponing the child’s vulnerability until adulthood, when death from the disease is 30 times more likely.

The National Vaccine Information Center (NVIC), Vienna, Va., advises parents to seriously consider not using the chickenpox vaccine in healthy children. According to Barbara Loe Fisher, cofounder and president, “The case/fatality ratio in healthy children is one death per 100,000 children. In adults, it rises to 31 deaths per 100,000. So it basically is an experiment. That is really what happens with most of these vaccines that they bring out. They really don’t know what the long-term effect is going to be.” Dr. Link, however, cautions that if most children are immunized according to the current US policy of universal vaccination, “it may be unwise to try to avoid vaccination because of the hazard of later acquiring varicella as an adult.”[95]

The temporary immunity provided by the vaccine is a particular concern for pregnant women. Normally, 90% of adult women are immune to varicella and transfer this immunity to their babies during pregnancy. But the immunity induced by vaccination, which lasts only five to ten years, may be gone by the time a woman enters her reproductive stage, leaving pregnant women at risk of contracting the infection and transmitting it to the fetus. Fetal varicella syndrome is characterized by multiple congenital malformations and is often fatal for the fetus.[96] In addition, children born to women whose vaccine-induced immunity has faded are unprotected during the first year of life, when their immune system is still developing, and may suffer fatal complications if exposed to the infection.

Another potential problem in the coming years is an increase in the rate of shingles due to widespread use of the varicella vaccine. As Dr. Link explains, the varicella zoster virus causes both chickenpox and herpes zoster (shingles). The virus could lie dormant for many years and later become active and cause shingles due to a reduction in immunity. One report states that mass vaccination with varicella “is expected to cause a major epidemic of herpes zoster.”[9]7 And while some research has not found in increase in the rate of shingles, reports Dr. Link, it will be years before we know whether the vaccine virus is too weak to be activated or the immunity produced by the vaccine is too weak to control the virus.[98]

It is of interest that the FDA approved the first vaccine for herpes zoster in 2006. Zostavax is a live vaccine licensed for use in people age 60 and older. In a study of approximately 38,000 people, the vaccine reduced the incidence of herpes zoster by about 50% overall. Effectiveness ranged from 64% for people age 60-69 to 18% for those 80 and older.[99]


The hepatitis B vaccine became commercially available in the US in 1982 and was recommended for certain high-risk groups of people. However, when vaccination programs aimed at these groups did not stem an increase in hepatitis B infections, the ACIP recommended universal immunization of infants against this disease in 1991.[100]

An analysis of reports made to VAERS over 11 years – from 1991 to 2001 – found that hepatitis B was the most frequently mentioned vaccine in 1991-1995 reports and the second-most commonly mentioned (after varicella) in 1996-2001 reports.[101]

An earlier study found that 12,520 adverse reactions to hepatitis B were reported to VAERS from 1991 to 1994, with 14% of these reactions involving newborns and infants.[102] Approximately one-third of reactions involved an emergency room visit or hospitalization, according to the Association of American Physicians and Surgeons (AAPS). There were 440 deaths, about 180 of which were attributed to SIDS.[103]

Dr. Jane M. Orient, executive director of AAPS, has stated that according to a federal government study, “Children younger than 14 are three times more likely to die or suffer adverse reactions after receiving hepatitis B vaccines than to catch the disease.”[104]

In adults, hepatitis B vaccination was associated with serious autoimmune disorders in one analysis of VAERS data and a review of the literature, published in 2004. These disorders included arthritis, pancytopenia/ thrombocytopenia, multiple sclerosis, rheumatoid arthritis, myelitis, Guillain-Barre syndrome, and optic neuritis. In adult use of the hepatitis B vaccine, there were 465 positive re-challenge adverse events.[105]

Other articles associate the hepatitis B vaccine with complications of the nervous system[106-110] and joints[111-116] and other adverse effects.[117] The Institute of Medicine stated in 2002 that “the epidemiological evidence favors rejection of a causal relationship between the hepatitis B vaccine in adults and multiple sclerosis.” (The evidence was inadequate to accept or reject a causal association with other demyelinating conditions.)[118] A case-control study published by the CDC in 2003 also found that the hepatitis B vaccine is not associated with an increased risk of multiple sclerosis or optic neuritis.[119] However, a case-control study published in 2004 concluded that its findings “are consistent with the hypothesis that immunization with the recombinant hepatitis B vaccine is associated with an increased risk of MS, and challenge the idea that the relation between hepatitis B vaccination and risk of MS is well understood.”[120]

The purpose of vaccinations is to reduce the risks of complications associated with the diseases they are designed to prevent. Complications from a vaccine should not outweigh those derived from the disease. And yet, according to Dr. Philip Incao, who has studied vaccinations and the immune system for three decades, in the case of hepatitis B, “…the conclusion is obvious that the risks of hepatitis B vaccination far outweigh its benefits.”[121]

Are vaccine-induced antibodies only temporary? Vaccine supporters claim that the development of an antibody response to a vaccine virus equals protection against the disease. So we now vaccinate children against hepatitis B to prevent them from contracting the disease later in life. But for this to occur, the level of antibodies that are supposed to be protective must remain high for very long periods of time.

A study published in 2004 reports that antibodies to hepatitis B surface antigen (anti-HBs) had disappeared by five years of age in most of the low-risk children studied who were vaccinated from birth against hepatitis B.[122] A study in the Gambia found that fewer than half of vaccinees had detectable anti-HBs 15 years after vaccination and that vaccine efficacy against infection among 20- to 24-year-olds was 70.9%. A positive finding was that hepatitis B vaccination in early life can provide long-lasting protection against carriage of the hepatitis B virus – a major risk factor for liver cirrhosis and hepatocellular carcinoma – despite decreasing levels of anti-HBs.[123]

One study of adult hepatitis B vaccination evaluated the persistence of anti-hepatitis-B antibodies in 635 homosexual men immunized against the virus. After five years, antibodies no longer existed in 15% and had declined sharply – below levels deemed to be protective – in another 27%. Hepatitis B developed in 55 men, and two became carriers of the virus.[124] Another study found that after three years, 36% of individuals who initially responded to the hepatitis B immunization lost anti-hepatitis-B antibodies.[125]

Why then are we needlessly vaccinating millions of children if by the time they’ll be adults and might be exposed to the virus, they won’t have the antibodies that are supposed to protect them? And, in any case, are these antibodies offering protection against the disease?


In recent years, two of three diseases targeted by the MMR vaccine – measles and rubella – have been virtually eliminated in the United States. The last major resurgence of measles occurred in 1989-1991, when more than 55,000 cases and approximately 120 deaths were reported. The ACIP recommended in 1989 that a second dose of measles-containing vaccine be added to the childhood vaccination schedule, and the incidence of measles began to fall in 1992. A record low of 37 cases were reported in 2004.[126,127] In 2000, a panel of experts convened by the CDC determined that measles was no longer endemic in the US.[128] Similarly, the incidence of rubella fell to nine cases in 2004, and it was determined that rubella is no longer endemic in the US.[129]

Despite this success, concerns remain about adverse effects of MMR vaccination. The Institute of Medicine has found evidence that this vaccine can cause anaphylaxis, thrombocytopenia, and acute arthritis.[130,131] Other research has associated the vaccine with adverse effects on the nervous system[132-137] gastrointestinal tract,138 and joints.[139-141]

Meryl Dorey, editor of the Australian publication Vaccination? The Choice is Yours and president of the Australian Vaccination Network, points out that the MMR vaccine is associated with Guillain-Barre paralysis, multiple sclerosis, and aseptic meningitis, a swelling of the lining of the brain that can be fatal. The CDC has noted that while cases of Guillain-Barre syndrome following MMR vaccination have been reported, the IOM has found the evidence “insufficient to accept or reject a causal relationship.”[142]

Measles Vaccine

Vaccine failures. A study published in 1994 evaluated all US and Canadian articles reporting measles outbreaks in schools and found that, on average, 77 % of these infections occurred in vaccinated people. The authors concluded, “The apparent paradox is that as measles immunization rates rise to high levels in a population, measles becomes a disease of immunized persons.”[143] The New England Journal of Medicine has reported that 60% of all measles cases among American schoolchildren between 1985 and 1986 occurred in those who were vaccinated.[144] Other studies confirm a high percentage of measles among vaccinated subjects.[145,146]

Vulnerabilities related to the measles vaccine. Natural immunity to measles – derived from contracting the disease – is permanent and is transferred from mothers to babies in utero through the placenta. Babies born to mothers who have had the disease are protected from the infection during their first year of life by the presence of a high concentration of natural antibodies circulating in their blood. Measles vaccination, on the other hand, induces lower antibody titers than does natural infection. Neutralizing measles antibodies passed by vaccinated women to their newborns disappear rapidly, leaving the babies susceptible to the infection in their first year of life, when they are more at risk of complications.

This difference in infants’ immunity levels is reflected in a 1995 study. Researchers found that 71% of nine-month-olds and 95% of 12-month-olds had no detectable neutralizing measles antibodies in their blood. All infants with detectable measles antibodies at nine or 12 months had mothers born before 1963, before the vaccine era.[147]

Research confirms that antibody response to the vaccine virus is only temporary. One study shows that four years after MMR vaccination, measles antibodies fell below the putative protective levels in 28% of children and were no longer present in another three percent of vaccinees.[148] Experimenting with high-potency vaccines produced even poorer results.[149]

Jamie Murphy, author of What Every Parent Should Know About Childhood Immunization, argues that rather than preventing measles, the vaccine may simply suppress it, only to have it manifest as other forms of disease with age.[150] He asserts that quite a few diseases are associated with the measles vaccine, including “encephalopathies (brain damage), aseptic meningitis, cranial nerve palsy, learning disabilities, hyperkinesis, and severe mental retardation….”[151] Several studies have documented that measles vaccination produces immune suppression that contributes to an increased susceptibility to other infections.[152,153] One study links measles vaccination to Crohn’s disease.[154]

Problems with vaccine testing. In a response to information provided by the World Health Organization, author and lecturer Trevor Gunn has identified shortcomings in the testing of vaccines and the rationale for mass immunization, particularly with regards to measles.[155] One problem is that vaccine studies use seroconversion, or antibody presence in the bloodstream, to indicate effectiveness. When UK health authorities say that the measles vaccine is 90% effective, they do not mean that it reduces the incidence, severity, or death rate of the disease by 90%, but rather that 90% of recipients produce a certain level of antibodies to the viral agents. However, the level of serum antibodies does not correlate with the body’s ability to fight illness. People with low antibody levels may demonstrate immunity, while people with higher antibody levels may have no immunity.

Given this disconnect, says Gunn, we must “place a greater reliance on obtaining efficacy results of immunisation from population studies.” These studies measure the level of disease protection in populations after they’ve been inoculated, using cohort groups matched for age, population, and disease exposure similarities, and so forth. Although WHO quoted references to a number of population studies in its communication with Gunn, the author says that all of the studies were conducted in developing countries. Thus, the results cannot be “directly extrapolate to developed countries,” where people may fear that the risks of vaccination outweigh the risk of contracting a disease such as measles.

In addition, notes Gunn, population studies referenced by WHO show the difficulties of vaccine testing. One study, for example, suggests that measles vaccination reduces childhood mortality by 30%. However, the control group was not non-vaccinated, but rather included children who did not seroconvert and thus were assumed to have no immune response to the vaccine. In this case, we would not know whether deaths in the control group were due directly to the vaccine, to its lack of effectiveness, or to lack of natural immunity provided by the measles itself. In another group in this study, 15 of 123 did not have antibody conversion after vaccination, so their results were excluded as well. Three of this group actually died. We do not know the cause of these deaths, or whether the remaining 12 in the group were prevented from getting the disease.[156] In another study, the cohort group was cherry-picked for people who did not have a history of measles. This group may have been less likely to die from measles in general or may be heartier in general than the people who were selected against in the study.[157]

Mumps Vaccine

Although mumps infection is a largely benign disease when contracted during childhood, it becomes more dangerous in older children and adults, who are more susceptible to severe neurological, testicular, and ovarian complications from the infection. It is alarming to see that vaccination is clearly shifting the occurrence of this disease from young children toward those who are older.[158]

A large outbreak of mumps occurred in the United States in 2006, with 5,783 cases being reported to the CDC in less than ten months (from January 1 to October 7). The median age for the mumps patients was 22 years, and the highest age-specific rate was among people 18 to 24 years of age, many of them college students.[159]

Questions about efficacy. The resurgence of mumps raises concerns about vaccine failure. Although the CDC does not know the vaccination history of all the 2006 cases, it has reported that 63% of 1,798 patients in Iowa (which had the highest number of cases) had received one or two doses of the MMR vaccine.[160]

Other mumps outbreaks have occurred in highly vaccinated populations in the US and Europe.[161-163] The populations in several of these studies had virtually complete vaccination coverage. In a high school population with more than 95% coverage, 53 of 54 students who got the disease were vaccinated.[164] In a Tennessee school with 98% coverage, 67 of 68 students who got mumps were vaccinated. Thus, mumps cases in this instance were attributed mostly to vaccine failure.[165]

Perhaps the boldest statement on the efficacy of the mumps vaccine comes from the authors of an epidemiological study conducted in Switzerland. They found a fivefold increase in the number of mumps cases from 1990 to 1993, especially in vaccinated children. Among the authors’ conclusions was: “The Rubini [mumps] strain vaccines, which are the most commonly used in Switzerland, seem to have played an important role in the clear increase in mumps cases since 1990.”[166]

Urabe strain and meningitis. Another strain of mumps virus used in vaccines has been associated with the development of aseptic meningitis.[167] The Urabe strain is not used in vaccines in the US, but it has been used in Canada and the United Kingdom in the past. This strain of mumps virus was identified as the cause of aseptic meningitis in 1989 in patients who developed meningitis 21 days after injection. The virus isolated from these patients was identical to that used in the vaccine.

The Urabe strain of the mumps virus was removed from Canadian vaccines in 1989[168] because of a meningitis outbreak. The strain was removed in the UK in 1992. According to Trevor Gunn, when laboratory and hospital reports were cross-linked to vaccination records there, “the [perceived low risk of meningitis from this particular vaccine] rose to between one in 4,000 and one in 21,000.”[169] Despite these vaccine withdrawals, a mass immunization campaign targeting children one to 11 years old was carried out in 1997 in Salvador, Brazil, with a Urabe-containing MMR vaccine. An outbreak of aseptic meningitis followed, with 58 cases diagnosed.[170]

Rubella Vaccine

A study published in 1981 found that 15 years after receiving rubella vaccination, one in 11 children lost protection and became susceptible to re-infection.[171] This is worrisome because rubella infection is especially dangerous when contracted during pregnancy, since the fetus may develop malformations if exposed to the virus. Again, the lack of permanent immunity offered by vaccinations is creating serious problems down the line.

th-2Viera Scheibner, a retired research scientist, notes that in a 1991 report on the adverse effects of pertussis and rubella vaccines from the Institute of Medicine, “the evidence indicated a causal relationship between RA 27/3 rubella vaccine and acute arthritis in 13% to 15% of adult women. Also some individuals were shown to go on to develop chronic arthritis.”[172]


Organizations and Websites

Association of American Physicians and Surgeons
1601 N. Tucson Blvd., Suite 9
Tucson, AZ 85716-3450
Tel: 800-635-1196
Opposes vaccine mandates that violate the medical ethic of informed consent.

Gary Null’s Website
Provides information on optimizing health through nutrition, lifestyle factors and alternative medicine.

Immunization Action Coalition
1573 Selby Avenue, Suite 234
St. Paul, MN 55104
Tel: 651-647-9009
Provides educational materials on vaccination for health professionals and the public to help increase immunization rates and prevent disease.

The Institute for Vaccine Safety
Johns Hopkins Bloomberg School of Public Health
615 N. Wolfe Street
Room W5041
Baltimore, MD 21205
Provides independent assessment of vaccines and vaccine safety; works to prevent disease using the safest possible vaccines.

National Immunization Program
(Including the Advisory Committee on Immunization Practices)
NIP Public Inquiries
Mailstop E-05
1600 Clifton Road, NE
Atlanta, GA 30333
Tel: 800-232-4636
(Dec. 2007: Page redirects to
A website of the Centers for Disease Control and Prevention, with information on vaccines, vaccine safety, diseases, other immunization topics, and resources.

National Network for Immunization Information
301 University Blvd.
CH 2.218
Galveston, TX 77555-0351
Tel.: 409-772-0199
Provides up-to-date, scientifically valid information about immunization to help the public, health professionals, and policymakers make informed decisions.

National Vaccine Information Center
204 Mill Street, Suite B1
Vienna, VA 22180
Tel.: 703-938-DPT3
Oldest and largest parent-led organization advocating reformation of the mass vaccination system. MedAlert, a service of the NVIC, has organized information from the Vaccine Adverse Event Reporting System for online searching (go to

Thinktwice Global Vaccine Institute
P.O. Box 9638
Santa Fe, NM 87504
Provides information on childhood vaccines and others to facilitate informed decisions; supports the right to accept or reject vaccines.

Vaccination Liberation
P.O. Box 457
Spirit Lake, Idaho 83869-0457
Opposes compulsory vaccination laws; provides information on vaccinations not often made available to the public.

Vaccine Adverse Event Reporting System (VAERS)
P.O. Box 1100
Rockville, MD 20849-1100
Tel: 800-822-7967
Cooperative program of the FDA and CDC that collects reports on adverse events occurring after vaccinations.

Vaccine Information and Awareness Website
Works to ensure freedom of choice for parents regarding vaccination.
For information on exemptions, go to

Vaccination News
P.O. Box 111818
Anchorage, AK 99511-1818
Provides a wide range of news and views on vaccinations and vaccination policy.

Provides information on vaccines, adverse events, vaccine critics, diseases targeted by vaccines, medical politics, and more.

Vaccination Exemption Information

Vaccination Liberation:

Vaccine Information and Awareness website:

National Vaccine Information Center:

Joseph Mercola, D.O.:

Books, Videos, and DVDs

The Consumer’s Guide to Childhood Vaccines
by Barbara Loe Fisher
National Vaccine Information Center, 1997

Evidence of Harm: Mercury in Vaccines and the Autism Epidemic
by David Kirby
New York: St. Martin’s Press; 2005

Immunization: The Reality Behind the Myth
by Walene James
2nd Edition
Boston: Bergin & Garvey; 1995

Reverse the Aging Process Naturally
by Gary Null and Martin Feldman, M.D.
New York: Villard Books: 1993

A Shot in the Dark
by Harris L. Coulter and Barbara Loe Fisher
New York: Avery Publishing Group; 1991

State of Immunity: The Politics of Vaccination in Twentieth-Century America
by James Colgrove
University of California Press: 2006

Vaccination and Immunization: Dangers, Delusions & Alternatives
by Leon Chaitow
Wappingers Falls, New York: Beekman Books; 1994

The Vaccine Controversy: The History, Use, and Safety of Vaccinations
by Kurt Link, M.D.
New York: Praeger Publishers; 2005

The Vaccine Guide: Risks and Benefits for Children and Adults
by Randall Neustaedter
Berkeley, California: North Atlantic Books; 1996, 2002

The Virus and the Vaccine: Contaminated Vaccine, Deadly Cancers, and Government Neglect
by Debbie Bookchin and Jim Schumacher
New York: St Martin’s Press; 2004

What Every Parent Should Know About Childhood Immunization
by Jamie Murphy
Earth Healing Products;1993

“Vaccines: The Risks, the Benefits, the Choices” (DVD)
by Sherri J.Tenpenny, DO

“Vaccines: What the CDC Documents and Science Reveal” (DVD)
by Sherri J.Tenpenny, DO

“Building the Immune System Naturally” (VHS)
by Gary Null

“Supercharge Your Immune System” (VHS)
by Gary Null

“Total Health” series, Steps 1 – 7 (DVD or VHS) by Gary Null

About the Authors

Gary Null, PhD
2307 Broadway
New York, New York 10024 USA
646-505-4660/ Fax 212-472-5139

Gary Null, PhD has authored more than 50 books on health and nutrition and numerous articles published in research journals. He holds a PhD in human nutrition and public health science from the Union Graduate School. Null maintains a website at that presents information on how to optimize health through nutrition, lifestyle factors, and alternative medicine.

Martin Feldman, MD practices complementary medicine. He is an Assistant Clinical Professor of Neurology at the Mount Sinai School of Medicine in New York City.

Notes – Part Two

1. Centers for Disease Control and Prevention. Comparison of 20th century estimated U.S. annual morbidity and 2004 morbidity from vaccine-preventable diseases. Available at Immunization Action Coalition, United States diphtheria mortality rate from 1900-1967. Available at: Pertussis Outbreak Digest 2004. (Dec. 2007: Link not working.)4. Jajosky RA, Hall PA, Adams DA, et al. Summary of notifiable diseases – United States, 2004. MMWR 2006; 53(53):1-79.

5. Hutchins SS, et al. Current epidemiology of pertussis in the United States. Tokai J Exp Clin Med 1988; 13 Suppl:103-109.

6. Broder KR, Cortese MM, Iskander JK, et al. Preventing tetanus, diphtheria, and pertussis among adolescents: use of tetanus toxoid, reduced diphtheria toxoid and acellular pertussis vaccines recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep 2006; 55(RR-3):1-34.

7. Munoz FM. Pertussis in infants, children, and adolescents: diagnosis, treatment, and prevention. Semin Pediatr Infect Dis 2006; 17(1):14-19.

8. Tan T, Trinade E, Skowronski D. Epidemiology of pertussis. Pediatr Infect Dis J 2005; 24(5Suppl):S10-18.

9. Omer SB, Pan WK, Halsey NA, Stokley S, et al. Nonmedical exemptions to school immunization requirements: secular trends and association of state policies with pertussis incidence. JAMA 2006; 296(14):1757-1763.

10. Centers for Disease Control and Prevention. Surveillance for safety after immunization: Vaccine Adverse Event Reporting System (VAERS) – United States, 1991-2001. MMWR Surveill Summ 2003; 52(No. SS-1):1-24.

11. Geier DA, Geier MR. An evaluation of serious neurological disorders following immunization: a comparison of whole-cell pertussis and acellular pertussis vaccines. Brain Dev 2004; 26(5):296-300.

12. Centers for Disease Control and Prevention, op. cit.

13. Braun MM, Mootrey GT, Salive ME, et al. Infant immunization with acellular pertussis vaccines in the United States: assessment of the first two years’ data from the Vaccine Adverse Event Reporting System (VAERS). Pediatrics 2000; 106(4):E51.

14. Geier DA, Geier MR. An evaluation of serious neurological disorders following immunization: a comparison of whole-cell pertussis and acellular pertussis vaccines. Brain Dev 2004; 26(5):296-300.
15. Kuno-Sakai H, Kimuar M. Safety and efficacy of acellular pertussis vaccine in Japan, evaluated by 23 years of its use for routine immunization. Pediatr Int 2004; 46(6):650-655.

16. Le Saux N, Barrowman NJ, Moore DL, et al. Decrease in hospital admissions for febrile seizures and reports of hypotonic-hyporesponsive episodes presenting to hospital emergency departments since switching to acellular vaccine in Canada: a report from IMPACT. Pediatrics 2003; 112(5):e348.

17. Miller DL, et al. Pertussis immunisation and serious acute neurological illness in children. Br Med J 1981 May 16; 282(6276):1595-1599.

18. Gale JL, et al. Risk of serious acute neurological illness after immunization with diphtheria-tetanus-pertussis vaccine. A population-based case-control study. JAMA 1994 Jan 5; 271(1):37-41.

19. Menkes JH, et al. Workshop on neurologic complications of pertussis and pertussis vaccination. Neuropediatrics 1990; 21(4):171-176.

20. Murphy JV, et al. Recurrent seizures after diphtheria, tetanus, and pertussis vaccine immunization. Onset less than 24 hours after vaccination. Am J Dis Child 1984; 138(10):908-911.

21. Stetler HC, et al. History of convulsions and use of pertussis vaccine. J Pediatr 1985; 107(2):17517-9.

22. Hirtz DG, et al. Seizures following childhood immunizations. J Pediatr 1983; 102(1):14-18.

23. Torch, WS. Diphtheria-pertussis-tetanus (DPT) immunization: a potential cause of the sudden infant death syndrome (SIDS). Neurology 1982; 32(4):A169 (abstract).

24. Torch WC. Diphtheria-pertussis-tetanus (DPT) immunization may be an unrecognized cause of sudden infant death (SIDS) and near-miss syndrome (NMS): 12 case reports. Neurology 1986 b (suppl 1); 36:149 (abstract).

25. Torch WC. Characteristics of diphtheria-pertussis-tetanus (DPT) postvaccinal deaths and DPT-caused sudden infant deaths syndrome (SIDS): a review. Neurology 1986 a (suppl 1); 36:148 (abstract).

26. Baraff LJ, et al. Possible temporal association between diphtheria-tetanus toxoid-pertussis vaccination and sudden infant death syndrome. Pediatr Infect Dis 1983; 2(1):7-11.

27. Walker AM, et al. Diphtheria-tetanus-pertussis immunization and sudden infant death syndrome. Am J Public Health 1987; 77(8):945-951.

28. Update: vaccine side effects, adverse reactions, contraindications, and precautions recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1996; 45(RR-12):1-35.

29. Hoffman HS, Hunter JC, Damus K, et al. Diphtheria-tetanus-pertussis immunization and sudden infant death: results of the National Institute of Child Health and Human Development Cooperative Epidemiological Study of Sudden Infant Death Syndrome Risk Factors. Pediatrics 1987; 79:598-611 [cited by CDC].

30. Bouvier-Colle MH, Flahaut A, Messiah A, et al. Sudden infant death and immunization: an extensive epidemiological approach to the problem in France. Int J Epidemiol 1986; 18:121-126 [cited by CDC].

31. Odent MR, et al. Pertussis vaccination and asthma: is there a link? JAMA 1994; 272(8):592-593.

32. Farooqi IS, Hopkin JM. Early childhood infection and atopic disorder. Thorax 1998; 53(11):927-392.

33. DeStefano F. Gu D, Kramarz P, et al. Childhood vaccinations and risk of asthma. Pediatr Infect Dis J 2002; 21(6):498-504.

34. Bernsen RM, de Jongste JC, Koes BW, et al. Diphtheria tetanus pertussis poliomyelitis vaccination and reported atopic disorders in 8-12-year-old children. Vaccine 2006; 24(12):2035-2042.

35. Bakshi R, et al. Guillain-Barre syndrome after combined tetanus-diphtheria toxoid vaccination. J Neurol Sci 1997; 147(2):201-202.

36. Bolukbasi O, et al. Acute disseminated encephalomyelitis associated with tetanus vaccination. Eur Neurol 1999; 41(4):231-232.

37. Read SJ, et al. Acute transverse myelitis after tetanus toxoid vaccination. Lancet 1992; 339(8801):1111-1112.

38. Topaloglu H, et al. Optic neuritis and myelitis after booster tetanus toxoid vaccination. Lancet 1992; 339(8786):178-179.

39. Schlenska GK. Unusual neurological complications following tetanus toxoid administration. J Neurol 1977; 215(4):299-302.

40. Baust W, et al. Peripheral neuropathy after administration of tetanus toxoid. J Neurol 1979; 222(2):131-133.

41. Fardon DF. Unusual reactions to tetanus toxoid. JAMA 1967;199(2):125-126.

42. Rose I. Adverse reactions to tetanus toxoid. Lancet 1973; 1(7799):380.

43. Sutter RW. Adverse reactions to tetanus toxoid. JAMA 1994; 271(20):1629.

44. Centers for Disease Control and Prevention. Poliomyelitis prevention in the United States: updated recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2000 May 19; 49(RR-5):1-22.

45. Alexander LN, Seward JF, Santibanez TA, Pallansch MA, Kew OM, et al. Vaccine policy changes and epidemiology of poliomyelitis in the United States. JAMA 2004; 292(14):1696-1701.

46. Ibid.

47. Centers for Disease Control and Prevention. Imported vaccine-associated paralytic poliomyelitis – United States, 2005. MMWR 2006; 55(4):97-99.

48. Centers for Disease Control and Prevention. Poliovirus infections in four unvaccinated children – Minnesota, August-October 2005. MMWR 2005; 54(41):1053-1055.

49. Alexander, op. cit.

50. Wattigney WA, Mootrey GT, Braun MM, et al. Surveillance for poliovirus vaccine adverse events, 1991 to 1998: impact of a sequential vaccination schedule of inactivated poliovirus vaccine followed by oral poliovirus vaccine. Pediatrics 2001; 107(5):e83.

51. Kinnunen E, et al. Nationwide oral poliovirus vaccination campaign and the incidence of Guillain-Barre Syndrome. Am J Epidemiol 1998; 147(1):69-73.

52. Uhari M, et al. Cluster of childhood Guillain-Barre cases after an oral poliovaccine campaign. Lancet 1989 Aug 19; 2(8660):440-1.

53. Friedrich F, et al. Temporal association between the isolation of Sabin-related poliovirus vaccine strains and the Guillain-Barre syndrome. Rev Inst Med Trop Sao Paulo 1996; 38(1):55-8.

54. Rantala H, Cherry JD, Shields WD, et al. Epidemiology of Guillain-Barry syndrome in children: relationship of oral polio vaccine administration to occurrence. J Pediatr 1994; 124(2):220-223.

55. Ismail EA, Shabani IS, Badawi M, et al. An epidemiologic, clinical, and therapeutic study of childhood Guillain-Barre syndrome in Kuwait: is it related to the oral polio vaccine? J Child Neurol 1998; 13(10):488-492.

56. Friedrich F. Rare adverse events associated with oral poliovirus vaccine in Brazil. Braz J Med Biol Res 1997; 30(6):695-703.

57. Centers for Disease Control and Prevention. Simian virus 49 (SV40), polio vaccine, and cancer. Last modified April 22, 2004.

58. Vilchez RA, Kozinetz CA, Arrington AS, et al. Simian virus 40 in human cancers. Am J Med 2003; 114(8):675-684.

59. Vilchez RA, Madden CR, Kozinetz CA, et al. Association between simian virus 40 and non0Hodgkin’s lymphoma. Lancet 2002; 359(9309):817-823.

60. Shivapurkar N, Harada K, Reddy J, et al. Presence of simian virus 40 DNA sequences in human lymphomas. Lancet 2002; 359(9309):851-852.

61. Testa JR, et al. A multi-institutional study confirms the presence and expression of simian virus 40 in human malignant mesotheliomas. Cancer Res 1998; 58(20):4505-4509.

62. Carbone M, Pass HI, Rizzo P, Marinetti M, Di Muzio M, et al. Simian virus 40-like DNA sequences in human pleural mesothelioma. Oncogene 1994; 9(6):1781-1790.

63. Martini F, et al. Simian virus 40 footprints in normal human tissues, brain and bone tumours of different histotypes. Dev Biol Stand 1998; 94:55-66.

64. Martini F, et al. SV40 early region and large T antigen in human brain tumors, peripheral blood cells, and sperm fluids from healthy individuals. Cancer Res 1996; 56(20):4820-4825.

65. Huang H, et al. Identification in human brain tumors of DNA sequences specific for SV40 large T antigen. Brain Pathol 1999; 9(1):33-42.

66. Bergsagel DJ, et al. DNA sequences similar to those of simian virus 40 in ependymomas and choroid plexus tumors of childhood. N Engl J Med 1992; 326(15):988-993.

67. Lednicky JA, et al. SV40 DNA in human osteosarcomas shows sequence variation among T-antigen genes. Int J Cancer 1997; 72(5):791-800.

68. Carbone M, et al. SV40-like sequences in human bone tumors. Oncogene 1996; 13(3):527-535.

69. Rizzo P, et al. Evidence for and implications of SV40-like sequences in human mesotheliomas and osteosarcomas. Dev Biol Stand 1998; 94:33-40.

70. Galateau-Salle F, et al. SV40-like DNA sequences in pleural mesothelioma, bronchopulmonary carcinoma, and non-malignant pulmonary diseases. J Pathol 1998; 184(3):252-257.

71. Centers for Disease Control and Prevention. Simian virus 49 (SV40), polio vaccine, and cancer. Last modified April 22, 2004.

72. Link K. The Vaccine Controversy: The History, Use, and Safety of Vaccinations. Westport, Conn.; Praeger Publishers; 2005:29.

73. Strickler HD, Rosenberg PS, Devesa SS, et al. Contamination of poliovirus vaccines with simian virus 40 (1955-1963) and subsequent cancer rates. JAMA 1998; 279(4):292-295.

74. Mortimer EA, Lepow ML, Gold E, et al. Long-term follow-up of persons inadvertently inoculated with SV40 as neonates. Medical Intelligence 1981; 305:1517-1518 [cited by CDC].

75. Carroll-Pankhurst C, Engels EA, Strickler HD, et al. Thirty-five year mortality following receipt of SV40-contaminated polio vaccine during the neonatal period. Br J Cancer 2001; 85(9):1295-1297 [cited by CDC].

76. National Immunization Program. New ACIP recommendations. NIP’s Immunization Works! Newsletter, July 2006.

77. Ibid.

78. Centers for Disease Control and Prevention. Public health response to varicella outbreaks — United States, 2003-2004. MMWR 2006; 55(36):993-995.

79. Centers for Disease Control and Prevention. Outbreak of varicella among vaccinated children – Michigan, 2003. MMWR 2004; 53(18):389-393.

80. Centers for Disease Control and Prevention. Varicella outbreak among vaccinated children – Nebraska, 2005. MMWR 2006; 55(27):749-752.

81. Buchholz U, et al. Varicella outbreaks after vaccine licensure: should they make you chicken? Pediatrics 1999; 104(3 Pt 1):561-563.

82. National Immunization Program, op. cit.

83. Clements DA, et al. Over five-year follow-up of Oka/Merck varicella vaccine recipients in 465 infants and adolescents. Pediatr Infect Dis J 1995; 14(10):874-879.

84. Johnson CE, et al. A long-term prospective study of varicella vaccine in healthy children. Pediatrics 1997; 100(5):761-766.

85. Takayama N, et al. High incidence of breakthrough varicella observed in healthy Japanese children immunized with live attenuated varicella vaccine (Oka strain). Acta Paediatr Jpn 1997; 39(6):663-668.

86. Galil K, Lee B, Strine T, et al. Outbreak of varicella at a day-care center despite vaccination. N Engl J Med 2002; 347(24):1909-1915.

87. Lee BR, Feaver SL, Miller CA, et al. An elementary school outbreak of varicella attributed to vaccine failure. J Infect Dis 2004; 190(3):477-483. Epub 2004 Jun 29.

88. Haddad MB, Hill MB, Pavia AT, et al. Vaccine effectiveness during a varicella outbreak among schoolchildren: Utah, 2002-2003. Pediatrics 2005; 115(6):1488-1493.

89. Lopez AS, Guris D, Zimmerman L, et al. One dose of varicella vaccine does not prevent school outbreaks: is it time for a second dose? Pediatrics 2006; 117(6):e1070-1077.

90. Galil K, Fair E, Mountcastle N, et al. Younger age at vaccination may increase risk of varicella vaccine failure. J Infect Dis 2002; 186:102-105.

91. Tugwell BD, Lee LE, Gilette H, et al. Chickenpox outbreak in a highly vaccinated school population. Pediatrics 2004; 113(3 Pt 1):455-459.

92. Bernstein HH, et al. Clinical survey of natural varicella compared with breakthrough varicella after immunization with live attenuated Oka/Merck varicella vaccine. Pediatrics 1993; 92(6):833-837.

93. Galil K, Lee B, Strine T, et al. Outbreak of varicella at a day-care center despite vaccination. N Engl J Med 2002; 347(24):1909-1915.

94. Wise RP, Salive ME, Braun MM, et al. Postlicensure safety surveillance for faricella vaccine. JAMA 2000; 284(10):1271-1279.

95. Link, op. cit., p.52-53.

96. Connan L, et al. Intra-uterine fetal death following maternal varicella infection. Eur J Obstet Gynecol Reprod Biol 1996; 68(1-2):205-207.

97. Brisson M et al. Exposure to varicella boosts immunity to herpes zoster. Vaccine 2002; 20:2500-2507.

98. Link, op. cit., p. 52-53.

99. U.S. Food and Drug Administration. Product approval information – licensing action. Zostavax questions and answers. Updated May 26, 2996.

100. Freed GL, Bordley WC, Clark SJ, et al. Reactions of pediatricians to a new Centers for Disease Control recommendation for universal immunization of infants with hepatitis B. Pediatrics 1993; 91(4):699-702.

101. Centers for Disease Control and Prevention. Surveillance for safety after immunization: Vaccine Adverse Event Reporting System (VAERS) – United States, 1991 – 2001. MMWR 2003 52(SS-1):1-24.

102. Niu MT, Davis DM, Ellenberg S. Recombinant hepatitis B vaccination of neonates and infants: emerging safety data from the Vaccine Adverse Event Reporting System. Pediatr Infect Dis J 1996; 15(9):771-776.

103. Statement of the Association of American Physicians and Surgeons on Vaccines: Public Safety and Personal Choice before the Committee on Government Reform and Oversight U.S. House of Representatives. From

104. Dunbar B. Hearing before the Subcommittee on Criminal Justice, Drug Policy and Human Resources of the House Government Reform Committee. May 8, 1999, transcript by Federal News Service.

105. Geier MR, Geier DA. A case-series of adverse events, positive re-challenge of symptoms, and events in identical twins following hepatitis B vaccination: analysis of the Vaccine Adverse Event Reporting Systom (VAERS) and literature review. Clin Exp Rheumatol 2004; 22(6):749-755.

106. Tourbah A, Gout O, Liblau R, et al. Encephalitis after hepatitis B vaccination: recurrent disseminated encephalitis or MS? Neurology 1999; 53(2):396-401.

107. Herroelen L, et al. Central-nervous-system demyelination after immunisation with recombinant hepatitis B vaccine. Lancet 1991; 338(8776):1174-1175.

108. Viral Hepatitis Prevention Board. Hepatitis B vaccine and central nervous system demyelinating diseases. Pediatr Infect Dis J 1999; 18(1):23-24. Review.

109. Nadler JP. Multiple sclerosis and hepatitis B vaccination. Clin Infect Dis 1993; 17(5):928-929.

110. Hall A, et al. Multiple sclerosis and hepatitis B vaccine? Vaccine 1999; 17(20-21):2473-2475.

111. Geier DA, Geier MR. A one year followup of chronic arthritis following rubella and hepatitis B vaccination based upon analysis of the Vaccine Adverse Events Reports System (VAERS) database. Clin Exp Rheumatol 2002; 20(6):767-771.

112. Birley HD, et al. Hepatitis B immunisation and reactive arthritis. BMJ 1994; 309(6967):1514.

113. Pope JE, et al. The development of rheumatoid arthritis after recombinant hepatitis B vaccination. J Rheumatol 1998; 25(9):1687-1693.

114. Bracci M, et al. Polyarthritis associated with hepatitis B vaccination. Br J Rheumatol 1997; 36(2):300-301.

115. Hachulla E, et al. Reactive arthritis after hepatitis B vaccination. J Rheumatol 1990; 17(9):1250-1251.

116. Vautier G, et al. Acute sero-positive rheumatoid arthritis occurring after hepatitis vaccination. Br J Rheumatol 1994; 33(10):991.

117. Grotto I, et al. Major adverse reactions to yeast-derived hepatitis B vaccines-a review. Vaccine 1998; 16(4):3293-34.

118. Institute of Medicine. Immunization safety review: hepatitis B vaccine and demyelinating neurological disorders. May 30, 2002.

119. DeStefano F, Verstraeten T, Jackson La, et al. Vaccinations and risk of central nervous system demyelinating diseases in adults. Arch Neurol 2003; 60(4):504-509.

120. Hernan MA, Jick SS, Olek MJ, Jick H. Recombinant hepatitis B vaccine and the risk of multiple sclerosis: a prospective study. Neurology 2004; 63(5):838-842.

121. Incao, Philip, M.D. Letter to Representative Dale Van Vyven, Ohio House of Representatives. March 1, 1999. Provided to by The Natural Immunity Information Network.

122. Petersen KM, Bulkow LR, McMahon BJ, et al. Duration of hepatitis B immunity in low-risk children receiving hepatitis B vaccinations from birth. Pediatr Infect Dis J 2004; 223(7):650-655.

123. Van der Sande MA, Waight P, Mendy M, et al. Long-term protection against carriage of hepatitis B virus after infant vaccination. J Infect Dis 2006; 193(11):1528-1535.

124. Hadler SC, et al. Long-term immunogenicity and efficacy of hepatitis B vaccine in homosexual men. N Engl J Med 1986; 315(4):209-214.

125. Pasko MT, et al. Persistence of anti-HBs among health care personnel immunized with hepatitis B vaccine. Am J Public Health 1990; 80(5):590-593.

126. Centers for Disease Control and Prevention. Measles, mumps and rubella – vaccine use and strategies for elimination of measles, rubella, and congenital rubella syndrome and control of mumps: recommendations of the Advisory Committee on Immunization Practices. MMWR 1998; 47(RR-8):1-67.

127. Centers for Disease Control and Prevention. Measles – United States, 2004. MMWR 2005; 54(48):1229-1231.

128. Centers for Disease Control and Prevention. Measles – United States, 1999. MMWR 2000; 49(25):557-560.

129. Centers for Disease Control and Prevention. Elimination of rubella and rubella congenital syndrome – United States, 1969 – 2004. MMWR 2005; 54(11):279-282.

130. Stratton KR, Howe CJ, Johnston RB Jr. Adverse events associated with childhood vaccines other than pertussis and rubella. Summary of a report from the Institute of Medicine. JAMA 1994; 271(20):1602-1605.

131. Howson CP, Fineberg HV. Adverse events following pertussis and rubella vaccines. Summary of a report of the Institute of Medicine. JAMA 1992; 267(3):392-396.

132. Landrigan PJ, Witte JJ. Neurologic disorders following live measles virus vaccination. JAMA 1973; 223:1459-1462 [cited by CDC].

133. Davis RL, et al. MMR2 immunization at 4 to 5 years and 10 to 12 years of age: a comparison of adverse clinical events after immunization in the Vaccine Safety Datalink project. The Vaccine Safety Datalink Team. Pediatrics 1997; 100(5):767-771.

134. Miller D, et al. Measles Vaccination and neurological events. Lancet 1997; 349(9053):730-731.

135. Sackey AH, et al. Hemiplegia after measles, mumps, and rubella vaccination. BMJ 1993; 306(6886):1169.

136. Kazarian EL, et al. Optic neuritis complicating measles, mumps, and rubella vaccination. Am J Opthalmol 1978; 86(4):544-547.

137. Kline LB, et al. Optic neuritis and myelitis following rubella vaccination. Arch Neurol 1982; 39(7):443-444.

138. Akobeng AK, et al. Inflammatory bowel disease, autism, and the measles, mumps, and rubella vaccination. J Pediatr Gastroenterol Nutr 1999; 28(3):351-352.

139. Chiba Y, et al. Abnormalities of cellular immune response in arthritis induced by rubella vaccination. J Immunol 1976; 117(5 Pt 1):1684-1687.

140. Tingle AJ, et al. Postpartum rubella immunization: association with development of prolonged arthritis, neurological sequelae, and chronic rubella viremia. J Infect Dis 1985; 152(3):606-612.

141. Roberts RJ, et al. Reasons for non-uptake of measles, mumps, and rubella catch up immunization in a measles epidemic and side effects of the vaccine. BJM 1995; 310(6995):1629-1632.

142. Centers for Disease Control and Prevention. Measles, mumps, and rubella – vaccine use and strategies for elimination of measles, rubella, and congenital rubella syndrome and control of mumps. Op. cit.

143. Poland GA, Jacobsen RM. Failure to reach the goal of measles elimination. Apparent paradox of measles infections in immunized persons. Arch Intern Med 1994; 154(16):1815-1820.

144. Markowitz LE, Preblud SR, Orenstein WA, et al. Transmission in measles outbreaks in the United States, 1985-1986. N Engl J Med 1989; 32:75-81. 145. Edmonson MB, Addiss DG, McPherson Jt, et al.

Mild measles and secondary vaccine failure during a sustained outbreak in a highly vaccinated population. JAMA 1990; 263:2467-71.

146. Gustafson TL, et al., Measles outbreak in a fully immunized secondary-school population. NEJM 1987; 316(13):771-4.

147. Maldonado YA, et al. Early loss of passive measles antibody in infants of mothers with vaccine-induced immunity. Pediatrics 1995; 96(3 Pt 1):447-450.

148. Miller E, et al. Antibodies to measles, mumps and rubella in UK children 4 years after vaccination with different MMR vaccines. Vaccine 1995; 13(9):799-802.

149. Whittle H, et al. Poor serologic responses five to seven years after immunization with high and standard titer measles vaccines. Pediatr Infect Dis J 1999; 18(1):53-57. 150. Murphy J. What Every Parent Should Know About Childhood Immunization. Boston; Earth Healing Products; 1993:114. 151. Gary Null Interview with Jamie Murphy, April 7, 1995.

152. Auwaerter PG, Hussey GD, Goddard EA, et al. Changes within T cell receptor V beta subsets in infants following measles vaccination. Clin Immunol Immunopathol 1996; 79(2):163-170.

153. Ward BJ. Changes in cytokine production after measles virus vaccination: predominant production of IL-4 suggests induction of a Th2 response. Clin Immunol Immunopathol 1993; 67(2):171.

154. Thompson NP, Montgomery SM, Pauder, et al. Is measles vaccination a risk factor for inflammatory bowel disease? Lancet 1995; 345(8957):1071-1074.

155. Gunn T. Response to W.H.O. evidence for vaccine safety and effectiveness.

156. Aaby P, et al. Child mortality related to seroconversion or lack of seroconversion after measles vaccination. Pediat Infec Dis J 1989; 8(4):197-200.

157. Clemens JD, Stanton BF, Chakraborty J. Measles vaccination and childhood mortality in rural Bangladesh. Am J Epidemiol 1988; 128(6 ):1330-1339.

158. Hersh BS, et al. Mumps outbreak in a highly vaccinated population. J Pediatr 1991; 119(2):187-193

159. Centers for Disease Control and Prevention. Brief report: Update: Mumps activity—United States, January 1 – October 7, 2006. MMWR 2006; 55(42):1152-1153.

160. Ibid.

161. Cheek, JE, Baron R, Atlas H, et al. Mumps outbreak in a highly vaccinated school population. Evidence for large-scale vaccination failure. Arch Pediatr Adolesc Med 1995; 149(7):774-778.

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This article was published at Arizona Center for Advanced Medicine.