by Lawrence Broxmeyer, MD
From NEXUS Magazine, February–March 2015 (vol. 22, no. 2)
http://www.nexusmagazine.com
Vaccines as an Autism Trigger: A TB Link?
by Lawrence Broxmeyer, MD
© December 2014 – January 2015
Email: nyinstituteofmedresearch@yahoo.com
Website: http://lawrencebroxmeyermd.com/
[Sidebar Introduction]
While it can’t be said categorically that vaccines trigger autism, it can’t be denied that many vaccines still contain toxic mercury compounds as well as animal and human components which may be contaminated with tuberculosis mycobacteria, with deleterious effects.
At present, the cause of autism and its related spectrum disorders is unknown. Many hypotheses regarding what causes autism have been and will continue to be put forth, but only one will prevail: its true cause. A conversation as to whether vaccines trigger autism cannot be made in a vacuum but, rather, must be weighed against certain epidemiologic, scientific and historic considerations because its complexity is too great.
California Department of Developmental Services, Sacramento, 1999
California, in 1999, had been on high alert for some time. Level-one autism, without any of its “spectrum”, went from almost 5,000 cases in late summer 1993 to an estimated 20,377 cases by December 2002. As California’s Department of Developmental Services stood by incredulously, it witnessed a tripling of California’s autism rate and all but 15 per cent of cases were in children.
California wasn’t alone, but its autism rates had become the fastest-growing group in that state’s developmental disability system and a number of Bay Area school districts were forced to fill entire classes with youths with different forms of autism.
But even in the midst of California’s mini-epidemic, its Santa Clara County seemed particularly singled out. The California Department of Social Services’ aid, brokered by the San Andreas Regional Center, staggered to its breaking point, and its forecast for autism in Santa Clara wasn’t good.
What was behind this epidemic? A major clue, overlooked from a critical standpoint, was contained in the timeline of the department’s own 1999 autism report1 which concluded that the disease had increased dramatically between 1987 and 1998. What had happened in California in and around 1987 that could have sown the surplus of autism that California now reaped?
Division of Communicable Disease Control, Sacramento, California, 1999
While autism exploded in California, there was also, beginning in 1987, a major spike in the number of tuberculosis cases reported by the Tuberculosis Control Branch of California’s Division of Communicable Disease Control. There, division head Dr Sarah Royce proclaimed a tuberculosis (TB) epidemic in California. The epidemic peaked in 1992, had the same male preponderance as autism, and took off at precisely the same moment in time.
California’s TB epidemic was claimed to have peaked well before 1999, but this didn’t stop it from continuing to contribute the greatest number of cases to the nation’s total tuberculosis morbidity.2 But, as with autism, the problem was worldwide, and even the World Health Organization, traditionally slow to react, had declared a global tuberculosis emergency six years earlier.3
Among children, brain-seeking central nervous system tuberculosis is common in a disease that kills more children each year than any other, with the potential to cause in survivors a withdrawal from social interaction, among other things, in its devastating wake.4
It had to be more than a coincidence, therefore, that since the 1980s California experienced a dramatic increase in the number of children diagnosed with autism as well.
Santa Clara County, California, March 2006
If California was experiencing autistic tremors, then surely its Santa Clara County was at the epicentre. By 2006, Santa Clara had some of the highest rates for autism in the entire USA. Although this was for unknown reasons, again the question became: why Santa Clara? The answer pointed in a similar direction.
By 2002, it had become apparent that tuberculosis was on the rise in Santa Clara. By 2006, that county had the highest number of new TB cases in California. A news report of 2014 mentioned that Santa Clara now has “more tuberculosis cases than most US states”.5 At the same time, the immigrant share of the population in Santa Clara County, mostly from countries where TB is endemic, is at its highest point since 1870.6
Santa Clara’s Health Department sounded the alarm. Santa Clara now knew that it had two problems on its hands. Its medically trained psychiatrists, doctors, personnel and statisticians just never stopped to think that the two problems might be related.
Centers for Disease Control and Prevention, Atlanta, Georgia, September 2008
Time passed. More information came in. In September 2008, the Centers for Disease Control and Prevention (CDC) published a study7 by lead author, pediatrician and researcher Dr Laura J. Christie of the California Department of Public Health entitled “Diagnostic Challenges of Central Nervous System Tuberculosis”. Christie and colleagues identified 20 cases of unexplained encephalitis referred to the California Encephalitis Project that were indeed tubercular. The team importantly began with this significant statement: “Tuberculosis (TB) of the central nervous system (CNS)” as thought of by physicians “is classically described as meningitis. However, altered mental status, including encephalitis, is within the spectrum of [its] clinical manifestations.”
In most of the 20 cases, the California Encephalitis Project cultured out tuberculous encephalitis, the same tuberculosis considered the least likely cause for encephalitis. Yet there it was. But, as Christie pointed out, as little as 25 per cent of patients with a diagnosis of CNS TB actually cultured out TB, which was a criterion for this particular study. That means that only a quarter of possible cases were confirmed.
Subcommittee on Human Rights and Wellness, Washington, DC, September
2004
[Photo caption]
Congressman Dan Burton, Chairman of the Hearing before the Subcommittee on Human Rights and Wellness, 8 September 2004
The following excerpts are from the transcript of the “Hearing before the Subcommittee on Human Rights and Wellness of the Committee on Government Reform, House of Representatives, One Hundred Eighth Congress, Second Session, September 8, 2004”.8
[The Subcommittee’s Chairman, Congressman Dan Burton (R-Indiana), is thanking Dr Melinda Wharton, Acting Deputy Director of the National Immunization Program, Centers for Disease Control and Prevention, for her opening testimony.]
Mr Burton: Thank you for your testimony. Everybody knows the value of vaccinations. And every time you testify, you tell us how valuable they’ve been. And we already know that.
We’re not here to say that vaccinations aren’t important. They’re very important. They’ve given us the highest quality of life of any civilization in the history of mankind. That isn’t what we’re talking about. We’re talking about why they’re putting mercury in vaccinations and why it’s never been tested since 1929 when Lilly developed it.
[Congressman Burton turns his attention to Dr William Egan, the Acting Director of the Office of Vaccines Research and Review, Center for Biologics Evaluation and Research, Food and Drug Administration (FDA).]
Mr Burton: Has thimerosal ever really been tested? Has thimerosal ever been tested by our health agencies?
Mr Egan: Only in those early tests that you know of that were done by Lilly.
Mr Burton: When was that? That was done in 1929. Let’s follow-up on that. In 1929, they tested this on 27 people that were dying of meningitis. All of those people died of meningitis, so they said there was no correlation between their death and the mercury in the vaccines. That is the only test that’s ever been done on thimerosal that I know of. Can you think of any other?
Mr Egan: No, in people, no. Except for accidental exposures over time.
Mr Burton: So we have mercury that’s being put into people’s bodies in the form of this preservative, and has been since the 1930s, and it’s never been tested by our health agencies. And yet you folks come here and you testify that there’s no conclusive evidence, and the IOM [Institute of Medicine] says, they favor, get this, they don’t say they’re sure, they say they favor rejection of a causal relationship between mercury and autism and other neurological disorders. Nobody ever gives a categorical statement, that no, mercury does not cause this, no, it doesn’t. And that’s because you can’t do it…
Mr Egan: We are diligently working, as we have testified today and previously, toward eliminating thimerosal mercury from vaccines as quickly as can be done. But there are many issues that are involved in doing this. If we were to say tomorrow that all vaccines, for example, all flu vaccines could only be administered in single dose syringes or single dose vials [thus eliminating the need for thimerosal], the capacity to fill those does not exist…
Mr Burton: OK. Now, my grandson got nine shots in one day, seven of which contained mercury. So if he got the very small amount, he’d be getting maybe nine micrograms, right?
Mr Egan: No, much less than that. Because the maximum that we calculate that a child could receive now during the first six months of life is somewhat less than three. A number of these vaccines [have] defined trace as less than one, some of them have considerably less than one.
Mr Burton: But that amount of mercury would not do any neurological damage to anybody?
Mr Egan: Not according to any guideline.
Mr Burton: No, no, no, no. I want you to say yes or no.
Mr Egan: I do not believe so.
Mr Burton: You do not believe so. I didn’t say believe. Can you say to me right now that amount of mercury being injected into a baby will not hurt it?
Mr Egan: It’s impossible to make those categorical statements with 100 percent—
Mr Burton: That’s right. So it is possible that the amount of mercury that’s being injected, even in trace amounts, could damage a child neurologically, right?
Mr Egan: I don’t think it has that capacity, no. We can argue.
Mr Burton: I know, but you don’t think it is, but you can’t say categorically, can you?
Mr Egan: Do I have evidence for every single child, for every possible dose, the answer is no…
As it turns out, the doses of thimerosal referenced in micrograms cited by Egan were small change compared to what is in certain current multidose flu shots.9 The CDC’s 2014–2015 guidelines for eligible child influenza vaccinations advise: “To protect their health, all children 6 months and older should be vaccinated against the flu each year.”10 With some multidose influenza preparations containing as high as 25 micrograms per dose of thimerosal or higher, this can add up to a lot of thimerosal. And on top of this, concurrently, the CDC still insists: “Pregnant? Get a Flu Shot!”11
Congressman Burton had established, as of 2004, that the only study ever done to conclude that thimerosal was not neurotoxic or could not precipitate the first signs and symptoms of autism was done by its manufacturer, Ely Lilly, in 1929—a study in which 22 meningitis patients (not 27, as Congressman Burton mentioned) in an Indianapolis epidemic were treated with thimerosal, all of whom died.
Lilly showcased and funded the study for one reason and one reason only: its scientist Smithburn, the study’s lead author, out of the sheer desperation of having nothing with which to cure his patients, had injected 22 of those patients dying of meningitis with large doses of thimerosal (up to 10 milligrams per kilogram intravenously) with supposedly no significantly grave consequences.12 That is, no grave consequences other than the fact that seven out of 22 of Smithburn’s patients died within one day after receiving the thimerosal. Only one patient made it to day 62 before succumbing—hardly enough of a window to investigate for chronic mercury damage from the thimerosal. Nevertheless, Lilly would next try to turn a lemon into an orange, sponsoring other scientists13 to say that the thimerosal had nothing to do with the deaths of Smithburn’s meningitis patients.
Unknown to either Burton or Egan, there was one other study testing a mercury compound on humans—a sizeable series which also appeared in the same publication, The Journal of the American Medical Association (JAMA), which had published the Lilly study. Hartz14, looking for a cure for his chronic TB patients, concluded that his trial with a mercury compound was “positively injurious and detrimental to one afflicted with tuberculosis”. Of the 14 patients to whom Hartz administered six or more injections (consisting of 1/5 gram or 13-milligram doses every second day), 12 died within from two weeks to six months after their last injection. Hartz was only using a small fraction of what Smithburn had used, yet his results for those on the receiving end of multiple injections of the mercury compound were disastrous. Hartz wrote:15
“This enormous percentage of deaths, namely, 85.7 per cent, among those [TB] patients who received six or more injections [of mercury], can be attributed only to the use of mercury, simply from the fact that the expectation of life in many of the cases chosen was very favorable indeed. In fact, on account of the age of the patients and the chronic arrested type of the disease, they were the kind of patients who live long and have a favorable prognosis.”
Also unknown to the scientists and the congressman present at the hearing was that although the 1929 Lilly investigators purportedly had an epidemic of meningococcal meningitis on their hands, as the epidemic wore on they were considering it as having originated as a mixed infection with an underlying tubercular infection—making the Hartz and Lilly publications have more in common than might at first meet the eye. It was an era when Mycobacterium tuberculosis and Neisseria meningitidis (the meningococcus) were the two most common causative organisms responsible for meningitis.16 And to this day, TB meningitis is in the differential rule-out for meningococcal meningitis.17
In back-to-back studies of the Indianapolis outbreak of 1929, Smithburn, present in the initial investigation, left the second-phase probe to Kempf, Gilman and Zerfas.18 Both publications showed how anti-meningococcal serums were of little or no use for the Indianapolis outbreak—an unexpected finding for a meningococcal meningitis epidemic.
The actual genesis of meningococcal disease was and still is not fully understood. Meningococcus colonizes large numbers in the general population harmlessly, with only a very small percentage of individuals having serious illness from it—notably in the limbs and the brain. Front and center in the follow-up study done by Smithburn’s colleagues was a mysterious “micrococcus” found in both phases of the Indianapolis outbreak. Just prior to Lilly’s publications, a similar micrococcus was uncovered by Sweany19, also published in JAMA, and subsequently by Mellon and Fisher20 in The Journal of Infectious Diseases. But both Sweany and Mellon’s micrococcus proved to be a (pleomorphic) form of cell-wall-deficient (CWD) tuberculosis (see figure 1 for an example of CWD TB). According to Kempf et al.:21
“The fact that the meningococcus could not be recovered from the blood, spinal fluid or nasopharynx does not necessarily mean that it was not there. However, it [the mysterious micrococcus] was readily recovered from the few meningococcic [meningococcal] cases that we have observed during the last few months and during the first and second years of this epidemic. One might expect to find an organism of this nature in traumatic meningitis or as a complication in tuberculosis…”
As he left the congressional hearing, very much on Congressman Dan Burton’s mind, after having grilled the FDA’s Dr William Egan, was that despite promises time and again to remove mercury from vaccines it never seemed to happen.
Figure 1: One of the stealth, viral-like forms of “cell-wall-deficient” atypical tuberculosis colonies that grew from the brain of a child who expired from the disease. Such forms of tuberculosis are extremely difficult to detect and require special stains and culture media not used routinely in today’s laboratories.
(Source: Korsak, T., Acta Tuberc. Pneumol. Belg. 1975; 66[6]:445-469)
Uncommon Valour
“My name is William Thompson. I am a Senior Scientist with the Centers for Disease Control and Prevention, where I have worked since 1998. I regret that my coauthors and I omitted statistically significant information in our 2004 article published in the journal Pediatrics. The omitted data suggested that African American males who received the MMR vaccine before age 36 months were at increased risk for autism. Decisions were made regarding which findings to report after the data were collected, and I believe that the final study protocol was not followed…”22
On 27 August 2014, CDC scientist Dr William Thompson spoke out, admitting that he had co-authored a study23 which purposely cooked the data to avoid showing that African-American infants and toddlers given the MMR (measles, mumps, rubella) vaccine before 36 months of age were at a 340 per cent increased risk for coming down with autism. At the time of the study, and for a decade after, Thompson was silenced—but troubled. This was no average witness; this was a man who knew the intricacies of the study and the original data obtained like the back of his hand.
Obviously, the CDC’s doctored 2004 study was an attempt to clear the MMR vaccine of troublesome implications—an attempt to give the vaccine a clean bill of health. But if the study’s purpose was to examine honestly the possibility of a causal relationship between the MMR vaccine and autism, it failed miserably.
After Thompson came out, the CDC’s Director of Immunization Safety and Thompson’s co-author, Dr Frank DeStefano, defended the study as originally published. But Thompson was already on record. Thompson believed that the removal of some of the study’s subjects because of the lack of a Georgia birth certificate not only went against the original study protocol, but, by reducing the study size by 41 per cent, obscured the strong statistical association between the timing of the MMR vaccination and the appearance of autism in African-American male toddlers. DeStefano was lead investigator in the 2004 paper. Subsequently, DeStefano had a telephone interview with investigative reporter Sharyl Attkisson.24 Here are a few verbatim excerpts from their exchange:
Attkisson: Were you aware of any of his [whistleblower William Thompson’s] concerns of, you know, have you been aware before today of any of his concerns about this?
DeStefano: Uh, uh, yeah, I mean I’ve continued to see, uh, uh, see him for over the past ten years and we’ve interacted fairly frequently, and, uh, uh, no I wasn’t aware of this.
Attkisson: So whoever he raised his concerns to, he didn’t, he didn’t raise it to you or anybody you knew of?
DeStefano: No, I mean the last time I saw him was probably about two months ago, and he didn’t mention anything about this…
[Ms Attkisson turns up the heat, relating to lead author DeStefano, that she thought that leaving out anything in the results of the study, especially through a birth certificate criterion which went against the study’s protocol, didn’t seem appropriate. It was also hiding the true conclusion of the study, which otherwise found a 340 per cent increase in autism in black children given the MMR before 36 months.]
Attkisson: …I still think it would be pretty important to know…
[DeStefano’s reply below apparently was his way of deflecting Attkisson’s probing comment by saying that autism probably developed in the womb before 36 months anyway and that somehow this meant that an MMR vaccination given before 36 months was already too late for the vaccine to cause or precipitate the first signs of autism.]
DeStefano: No, I mean, I think, you know, the other, the other important consideration here is looking at what, what time period we’re talking about. We’re, you know, autism, as you probably are aware, is a condition that really probably has its start while the child is still in the womb. And, you know, it doesn’t, some of the behaviors and such don’t come apparent, become apparent until maybe the child is one, two, three years old. But, uh, uh, what we know about autism that, uh, the, uh, characteristics or behavioral signs do become ava–, you know, apparent by 24 months of age, so. So we had different cut-offs, before 18 months of age, there was no difference in, in any group in terms of, uh, vaccination levels, between the cases and controls. At 24 months of age, when, uh, au—you know—behaviors of autism or some features of autism become apparent, there was no difference between the, uh, cases and controls in any group, it was at 36 months where there was a slight differen—and the difference was, we’re talking about a difference between 93% versus 91%, not a, a big difference. But, so that’s at 36 months. And at 36 months, an exposure around that time period is just not biologically plausible to have a uh, uh, a causal association with autism. I mean autism would’ve already started by then…
Attkisson: Let me just, let me just interrupt, before I lose that thought. So you already made up your mind regardless of what the stats show that if it, certain things show that it didn’t make sense, you wouldn’t, you would try to find out a way to…
DeStefano: No, that’s not what we said. I’m just saying, you know, you interpret, you interpret findings, also, you know, there’s the statistics, then you have to also interpret, bring in things like biological plausibility, how do you interpret these results? So I think we had pretty strong evidence that these results at 36 months were primarily a reflection of requirements to attend early intervention special education programs for the, for the children with autism…
Attkisson: Is there any possibility that it is biologically plausible and you just haven’t, you know, that that’s, the consensus is that it’s not, among you guys, but that it is and you’re overlooking that?
DeStefano: I’m, I’m not aware of any data that would say, you know, that would s-, you know, that would say that, uh, you would have, um, onset of autism after 36 months.
Granted DeStefano’s remark that “autism, as you probably are aware, is a condition that really probably has its start while the child is still in the womb”, which many believe, what did this have to do with a vaccine like MMR exacerbating or bringing on the first signs or symptoms of an autism, perhaps from chronic infection first acquired in the womb—even if the vaccination was given just before 36 months of age? Moreover, now that the real results of the 2004 autism–vaccine study were revealed, why did they show a 340 per cent increase in young black children given the MMR before age 36 months? Autism is certainly not more prevalent in African-American children than in whites. In fact, the rates of autism in black children are considerably less.25
Sir William Osler, co-founder of Johns Hopkins Hospital and frequently described as the Father of Modern Medicine, mentioned that “a quiescent malady” such as congenital syphilis and tuberculosis “may be lighted into activity by vaccination”.26 So, perhaps the differential with the MMR might lie in the racial differential in one of the diseases which Osler mentioned. The CDC’s own statistics, for example, show that the percentage of tuberculosis in blacks is way out of proportion to their percentage in the US population, with TB rates being seven times higher in blacks than in whites.27
The MMR, then, could very well be acting adversely in the fashion described by Osler through statistical evidence alone—but there was much, much more.
Exhibit 1: Known Contents of the MMR Vaccine
Of all the issues of concern regarding a vaccination–autism link, one of the most prominent is, according to Sugarman28, the continued use of thimerosal in certain influenza shots, especially the widely used and economical multidose influenza vials through which many patients can be vaccinated using the same vial of influenza vaccine. Most of the legal battles over vaccines and autism, Sugarman mentions, have alleged that the first signs and symptoms of autism were precipitated by this mercury-containing preservative, which used to be an ingredient in many childhood vaccines and still is found in some of the multidose flu shots used by paediatricians.
Others have argued that the culprit is the measles, mumps and rubella vaccine (MMR) or perhaps MMR in combination with thimerosal. Yet in many other autistic cases, a direct causal link is not there for either. Nevertheless, the thought lingers that these agents as well as other vaccines could, in certain cases, still trigger the first signs and symptoms of autism. In the meantime, the lay term pointing to “toxins” in the vaccines is inadequate.
Whenever one deals with biologicals originating from the cow, the calf, the chicken, the chicken embryo, the swine or from another human in the form of albumen or a foetal cell line—all found in the MMR—one hits upon the potential of such biologicals used in the vaccine bearing or being contaminated by mycobacterial infection. This holds particularly true of a vaccine like MMR, whose components can potentially carry Mycobacterium tuberculosis from human fluids or tissue, Mycobacterium avium from poultry (a subspecies of which is Mycobacterium paratuberculosis) or Mycobacterium bovis from cows or the foetal tissue of cows. And in this case, we are not talking about mere environmental exposure: we are talking about direct injection through vaccination.
To say that the US Department of Health and Human Services’ Food and Drug Administration is aware of this is a stark understatement. One just need download its “Guidance for Industry”29 for viral vaccines—a 50-page paper—each page carefully framed under the heading “Contains Nonbinding Recommendations”. In such a “Guidance for Industry”, the words and warnings for human Mycobacterium tuberculosis as well as mycobacteria from animal sources are scattered throughout.
The MMR vaccine is generally administered to children around the age of one year (12 months), with a second dose before starting school (i.e., at age 4–5).
MMR is front-loaded with such entities as foetal bovine serum (FBS). Foetal bovine serum or foetal calf serum is the blood fraction remaining after the natural coagulation of blood, followed by centrifugation to remove any remaining red blood cells. FBS comes from the blood drawn from a bovine foetus via a closed system of collection at the slaughterhouse.30
This presents a problem.
Johne was the first to report a case of congenital TB in animals, his specimen consisting of the very same bovine foetus.31 Macroscopically though, he noted, the uterus and placenta of the pregnant cow were normal.
Autism has already been linked to be triggered in certain cases by an atypical tuberculosis called paratuberculosis, frequently found in cattle.32 A critical review found that this same form of tuberculosis can infect bovine cow foetuses about nine per cent of the time when the bovine mother has subclinical disease, and an average of 39 per cent of cow foetuses in cases where the expectant cow shows signs of clinical paratubercular disease.33
Industry Turns a Blind Eye
Once the most prevalent infectious disease of cattle in the US, yet today largely ignored and purportedly no longer nearly the problem it once was, bovine TB caused more losses among US farm animals in the early part of the 20th century than all other infectious diseases combined.34
By 1917, the situation had become so grave in hogs and cattle that the Cooperative State–Federal Tuberculosis Eradication Program, administered by the US Department of Agriculture (USDA) and the Animal and Plant Health Inspection Service (APHIS), had to be instituted. For in 1917, it was estimated that 25 per cent of deaths from tuberculosis in adult humans were caused by animal tuberculosis.35
Although it is claimed that in the United States TB “once was” a common disease of farm poultry flocks, cattle, swine and people, this author remains unimpressed with present governmental agency attempts to diagnose both the bacilli and, moreover, their predominant cell-wall-deficient forms.
As another strategy to hide the true incidence of TB, our domestic animals and poultry are often killed young before the onset of tubercular disease becomes obvious.36 Furthermore, most inspection is done visually.
In the meantime, the USDA continues to downplay and ignore the actual incidence of TB not only in cows and their milk (especially with regard to paratuberculosis) but in poultry and eggs. For example, when forced to address the issue of finding paratuberculosis in containers of milk, the USDA initiated a study in 1998, but first used methods like freezing and ultrasound to damage the very mycobacteria being tested for, and then ignored established techniques to isolate mycobacteria related to TB, growing samples on a culture medium which was considered inadequate—and for not nearly a long enough time.37, 38 Not surprisingly, the USDA results in that study were all negative.
MMR vaccine also contains WI-38 human lung fibroblasts. A fibroblast is the most common type of cell found in our connective tissue. Although no study has addressed the possibility of mycobacteria contaminating such fibroblasts, Higuchi et al. in 2002 found that the all too common and dangerous strain of tuberculosis H37Rv can invade and grow in a WI-38 foetal cell line quite efficiently.39
Actually, WI-38 is a human cell culture line composed of fibroblasts which were derived from the lung tissue of a three-month-old white female foetus. It is commercially known as “WI-38 (ATCC® CCL-75™)”. First sequestered by Hayflick and Moorhead40 in the 1960s, WI-38 has been used ever since in the production of many of our vaccines.
Finally, in the MMR we have the chick embryo cell culture used to propagate the mumps and rubella (German measles) viruses.
Although authorities seem totally unconcerned today, Hull41, Trylich42 and Romanenko43 all certainly saw the danger of tuberculosis from tubercular hens getting into embryonated chicken eggs.
Chick embryo cell cultures also consist of hydrolysed gelatin as well as human albumen. Hydrolysed gelatin is the hydrolysed connective tissue from an animal—usually from the skin and bones of an animal, generally a pig. The process involves adding enzymes which break down the proteins. It separates the proteins along hydrogen bonds. Then the foetal calf serum from the blood drawn from a bovine foetus through a closed system at a slaughterhouse is also added.
Against all of this you have the antibiotic neomycin added to the MMR in an attempt to contend with any unknown mycobacterial content in the vaccine—which neomycin by itself is totally unequipped to do.
Almost lost in the package insert of Merck’s popular MMR II vaccine is the admission that no studies have been reported to date of the effect of the measles virus vaccine in the MMR on untreated tuberculous children: “However, individuals with active untreated tuberculosis should not be vaccinated.”44 Although infants and children are “individuals”, so difficult is it to isolate TB in them that some paediatric experts recommend a spinal tap in all children under 12 months of age.45 Yet it is specifically at 12 months of age that mandatory MMR vaccination first cuts in.
The Science of Denial
“They believe that TB is an extinct disease. I don’t know why.”46 So said Mario Raviglione, MD, infectious diseases specialist and Director of the World Health Organization’s Global Tuberculosis Programme about a disease which WHO admits infects a third of the world.
While frontal assaults on thimerosal, the MMR vaccine and the overburdened vaccine schedule have justifiably sprung up, a satisfactory and comprehensive explanation as to why and how vaccines might trigger autism has not.
In a 2013 interview, Mel Spigelman, MD, President and CEO of the TB Alliance, a nonprofit TB drug research group based in New York, said of tuberculosis: “It’s still in the US, we just don’t recognize it.”47 Perhaps this is because we just don’t want to recognise it—in ourselves, in our livestock, in the products from our livestock, and in the biologicals used in our vaccine manufacture. But it won’t let us not recognise it.
Meanwhile, we have with tuberculosis one of the few diseases that could possibly account for the soaring rate of autism—a disease which is not only the most common cause of infectious death in children48 but, according to WHO, in their child-bearing mothers aged 15–44, one million of whom die from it each year49; a disease which is extremely neurotropic (nerve-seeking) and remains, worldwide, the most common type of central nervous system infection, particularly among children50; and a disease in which 20–25 per cent of such children can manifest mental retardation as well as other anomalies often associated with neurodevelopmental disorders and the autistic spectrum.51
By 2007, Rzhetsky, in a proof-of-concept biostatistical analysis of 1.5 million patient records, had found significant genetic overlap in victims of autism and those with TB.52
No one who has done a serious study of the literature, old and new, can doubt for a second that the incidence and transfer of maternal tuberculosis, even when there are no maternal symptoms and the disease is latent, are being grossly underestimated. This has been duly noted in recent publications, but more in depth in the past writings and solid research of Charles C. Norris, Pennsylvania physician, gynaecologist, obstetrician and medical investigator. Norris wrote:53
“Pregnancy is prone to light up a latent or chronic tuberculosis, and thus produce a condition in which a bacillemia [blood-borne infection] is likely to be present. Secondary infection and metastasis [by TB] occur in the placenta in the same manner in which they affect other portions of the body.”
“Baumgarten’s theory…has done much to show that congenital tuberculosis may occur, and that tubercle bacilli may remain latent in the child for quite prolonged periods. It has been shown that the tubercle bacillus may remain latent for some time. Under such circumstances congenital tuberculosis is probably mistaken for, and classified as, a postnatal infection [of childhood].”
“Undoubtedly the strong uterine contractions incident to labor constitute a most important factor in the transmission of tubercle bacilli at the end of pregnancy. Organisms that, prior to the onset of labor, were lodged in the placenta or in the intervillous spaces, may, as the result of these contractions, be forced into the fetal circulation. Schlimpert, Schmorl and Geipel, Warthin and Cowie, Dardeleben, and others are very insistent on this point.”
Thus, throughout the first half of the 20th century, the method of choice for an expectant mother with proven TB—if it was found—was early termination of pregnancy.54
Others, like Norris, also saw the possibility of maternal– fetal transfer of even non-symptomatic TB as not uncommon.55-59 Dr Henry William Welch, often called the Dean of American Medicine and a colleague of Osler at Johns Hopkins, was already on record as saying that the mere inability to pick up TB in the fetus or newborn wasn’t an argument against frequent transmission to them.60 There were just too many factors involved, such as the hostile, low-oxygen environment of fetal blood, which could tame even the most virulent TB bacilli into dormant forms for some time, making diagnosis difficult to impossible. The history of associating what we presently call “autism” with tuberculosis is an old one, going back to John Langdon Down, a subset of whose young patients clearly were the first cases of “autism” on record. Such associations persist.61-63
While a blanket statement that vaccinations cause autism cannot be supported, the assertion that certain vaccines can aggravate and precipitate the first signs of an autism originating from chronic disease cannot be denied. A vaccine or group of vaccinations could trigger autism simply by inadvertently introducing, through their human, animal and poultry components, mycobacterial elements into the mother, foetus or young child. Mixed tubercular infection in man with human and fowl TB isn’t a new discovery: Tsukamura and Mizuno64 found it rather commonly in their 1981 study. Once introduced, one tubercular form can potentiate and make more virulent an existing tubercular infection.
Another way in which vaccine components can trigger autism was laid out by Hartz in his JAMA probe regarding how mercury compounds like thimerosal activate and make much worse an existing tubercular infection.
Finally, in vaccinations there are adjuvant oils or lipids, many of which do not have to be reported, used to increase a vaccine’s potency. Such oils or lipids are cholesterol precursors, becoming cholesterol in the body.65 Such a cholesterol surge is a big boost for any dormant systemic tuberculosis already in the body, whose very ability to maintain infection is linked to its ability to acquire and utilise cholesterol. So crucial is this unique ability of TB to use cholesterol in the body for both carbon and energy sources that if it were not for its ability to consume cholesterol, tuberculosis, unlike other pathogens, would be unable to resist eradication through cytokine attack and the attempts of certain activated white blood cells called macrophages to starve it of essential nutrients.66
In comparative and simpler terms, one might look at an injection of certain vaccine oil or lipid adjuvants, squalene among them, whether inside or outside of a vaccination, as lighting up chronic foci of tuberculosis like a Christmas tree; or, in the words of Sir William Osler, chronic tuberculosis “may be lighted into activity by vaccination”—for a few reasons, key to why vaccines, in certain cases, can trigger what a child’s parents clearly see as the first signs of autism in their toddler.
About the Author:
Pennsylvania internist and medical researcher Lawrence Broxmeyer, MD, was on the staff at NY affiliates of Downstate, Cornell and NYU for 14 years. He was the originator and lead author of a novel way to kill AIDS mycobacteria (J. Infectious Diseases 2002; 186[8]:1155-60). His ideas on phagotherapy are still in use today. He contributed a chapter to the textbook Patho-Biotechnology (Landes Bioscience, 2008). His peer-reviewed articles are on PubMed. He is the author of several books including AIDS: What the Discoverers of HIV Have Never Admitted (new edition, July 2014; see review in 20/01) and Autism: An Ancient Foe Becomes a Modern Scourge (2012). He has had several articles published in NEXUS: “Ebola…or African Strains of Tuberculosis” (22/01); “Influenza and the TB Connection” (19/01-02); and “The Untold Truth About Cancer” (17/01-02).
Dr Broxmeyer can be contacted by email at nyinstituteofmedicalresearch@ yahoo.com. For more information, visit http://lawrencebroxmeyermd.com.
Endnotes accompanying the article “Vaccines as an Autism Trigger: A TB Link?”
by Lawrence Broxmeyer, MD
Article published in NEXUS Magazine, February–March 2015 (vol. 22, no. 2)
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Industry Turns a Blind Eye
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Lawrence Broxmeyer M.D. 