When Mercury in Vaccines Aggravates Existing Conditions to Create Autism
Subcommittee on
Human Rights and Wellness, Washington, DC, September
2004
2004
https://lawrencebroxmeyermd.wordpress.com/2017/08/11/vaccines-as-an-autism-trigger-a-tb-link-2/
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
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
colonises 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 centre 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
(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
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
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.31Macroscopically 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– foetal 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 foetus 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 foetal 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.
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.
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