Posts Tagged ‘amyloid and tuberculosis’

Vaccines as an Autism Trigger: A TB Link?

January 27, 2015


Lawrence Broxmeyer, MD

From NEXUS Magazine February–March 2015 (vol. 22,no. 2)

Vaccines as an Autism Trigger: A TB Link?
by Lawrence Broxmeyer, MD
© December 2014 – January 2015


[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, paediatrician 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 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

“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– 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@ For more information, visit

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)
California Department of Developmental Services, Sacramento, 1999
1. Developmental Services System. Changes in the Population of Persons with Autism and Pervasive Developmental Disorders in California’s Developmental Services System: 1987 through 1998,

Division of Communicable Disease Control, Richmond, California, 1999
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Santa Clara County, California, March 2006
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Centers for Disease Control and Prevention, Atlanta, Georgia, September 2008
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Subcommittee on Human Rights and Wellness, Washington, DC, September 2004
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21. Kempf, op. cit., p. 450

Uncommon Valour
22. Statement of William W. Thompson, PhD, regarding the 2004 article examining the possibility of a relationship between MMR vaccine and autism,
23. DeStefano, F.I., Bhasin, T.K., Thompson, W.W., Yeargin-Allsopp, M., Boyle, C. Age at first measles-mumps-rubella vaccination in children with autism and school-matched control subjects: a population-based study in metropolitan Atlanta. Pediatrics 2004 Feb; 113(2):259-66
24. Audio of Sharyl Attkisson telephone interview with CDC’s Dr. Frank DeStefano about his questioned MMR-autism study, August 26, 2014,
25. Child Trends DataBank. Figure 2. Percentage of Children Ages 3-17 with Autism Spectrum Disorders (ASD), by Race/Hispanic Origin, 2007 and 2011/12,
26. Duke, W.D. Multiple Infections – A study of the relation of one infection to another. JAMA 1918 Nov 23; 71(21):1703-1706
27. CDC Factsheet. Tuberculosis In Blacks,

Exhibit 1: Known Contents of the MMR Vaccine
28. Sugarman, S.D. Cases in vaccine court—legal battles over vaccines and autism. N. Engl. J. Med. 2007; 357(13):1275-77
29. U.S. Department of Health and Human Services Food and Drug Administration (FDA). Guidance for Industry. Characterization and Qualification of Cell Substrates and Other Biological Materials Used in the Production of Viral Vaccines for Infectious Disease Indications. Center for Biologics Evaluation and Research. Rockville, MD, February 2010 (50 pp.),
30. Jochems, C. et al. The Use of Fetal Bovine Serum: Ethical or Scientific Problem?. Altern. Lab Anim. 2002 Mar-Apr; 30(2):219-227
31. Norris, Charles C. Gynecological and Obstetrical Tuberculosis, New York & London: D. Appleton & Co., 1923, p. 58: Johne, H.A. Deutsche Zeitschr. f. Thiermed. (Leipzig) 23:207; also Forts. d. Med. 1885; 3:108
32. Dow, C.T. Mycobacterium paratuberculosis and autism: is this a trigger?. Med. Hypotheses 2011 Dec; 77(6):977-81. Epub 2011 Sep 7
33. Whittington, R.J., Windsor, P.A. In utero infection of cattle with Mycobacterium avium subsp. paratuberculosis: a critical review and meta-analysis. Vet J. 2009 Jan; 179(1):60-9. Epub 2007 Oct 24

Industry Turns a Blind Eye
34. USDA Factsheet: Bovine Tuberculosis. Animal and Plant Health Inspection Service, Maryland, August 2002
35. Youmans, G.P. Tuberculosis. Philadelphia: W.B. Saunders Co., 1979
36. Mutalib, A.A., Riddell, C. Epizootiology and Pathology of Avian Tuberculosis in Chickens in Saskachewan. Can. Vet. J. 1988 Oct; 29(10):840-842
37. Stabel, J.R., Steadham, E.M., Boilin, C.A. Heat Inactivation of Mycobacterium paratuberculosis in Raw Milk: Are Current Pasteurization Conditions Effective?. Applied and Environmental Microbiology 1997; 63:4975-77
38. Greger, M. Paratuberculosis and Crohn’s Disease: Got Milk? USDA Farce? section. January 2001,
39. Higuchi, K., Harada, N., Yamada, H., Kobayashi, K., Takeda, M. The invasion of Mycobacterium tuberculosis into non-phagocytic cells. Kekkaku 2000 Nov; 75(11):649-59
40. Hayflick, L., Moorhead, P.S. The serial cultivation of human diploid cell strains. Exp. Cell Res. 1962; 25:585-621
41. Hull, T.G. Diseases Transmitted from Animals to Man. Springfield, Illinois: Charles G. Thomas Publisher, 1947, 3rd ed.
42. Trylich, C. Some Thoughts on Tuberculosis of Domestic Animals Particularly as Relating to Meat Inspection. Canadian Journal of Comparative Medicine 1957 Apr; 21(4):121-133
43. Romanenko, V.F., Diachenko, A.M., Kravchenko, N.A., Mikitin, O.O. Experimental findings on the role of chicken eggs in the epidemiology of tuberculosis. Probl. Tuberk. 2001; 6:40-1
44. Package Insert. M-M-R® II (Measles, Mumps, and Rubella Virus Vaccine Live). Merck & Co., Inc., Whitehouse Station, NJ 08889. Revised June 2014,
45. Rock, R.B., Olin, M., Baker, C.A., Moliter, T.W., Peterson, P.K. Central Nervous System Tuberculosis: Pathogenesis and Clinical Aspects. Clinical Microbiology Reviews 2008 Apr; 21(2):243-261

The Science of Denial
46. Abrams, L. This is the infectious disease you should be worried about. October 24, 2014,
47. Reuters. Los Angeles health officials concerned about TB outbreak on skid row. February 22, 2013,
48. Walia, R., Hoskyns, W. Tuberculous meningitis in children: problem to be addressed effectively with thorough contact tracing. Eur. J. Pediatr. 2000 Jul; 159(7):535-38
49. WHO. TB Is Single Biggest Killer Of Young Women. Press Release, Geneva, Switzerland. WHO/40, 26 May 1998
50. Waecker, N.J. Jr, Connor, J.D. Central nervous system tuberculosis in children: a review of 30 cases. Pediatr. Infect. Dis. J. 1990; 9:539-543
51. Garg, P.K. Tuberculosis of the central nervous system. Postgraduate Med. J. 1999; 75:133-40
52. Rzhetsky, A., Wajngurt, D., Park, N., Zheng, T. Probing Genetic Overlap among Complex Human Phenotypes. Proceedings of the National Academy of Sciences 2007 Jul 10; 104(28):11694-99
53. Norris, Charles C., Gynecological and Obstetrical Tuberculosis, New York & London: D. Appleton & Co., 1923, pp. 46, 56, 54
54. Kobrinsky, S. Pregnancy and Tuberculosis. Canad. M.A.J. 1948 Nov; 59:462-64
55. Warthin, A.S., Cowie, D.M. A Contribution in the Causuitry of Placental and Congenital Tuberculosis. J. Infectious Diseases 1904; 1:140-169
56. Weber, F.P. Congenital tuberculosis. Br. J. Children’s Dis. 1916; 13:321,359
57. Dorozhkova, I.R., Deshkekina, M.F., Ereneeva, A.S., Zemskova, Z.S., Ilyiash, N.I, Zhukova, E.K. Congenital Tuberculosis. Probl. Tuberk. 1972; 50(10):80-83
58. Insanov, A.B., Gadzhiev, F.S. Comparative Analysis of the Results of Spinal Fluid Microbiological Study in Children and Adults Who Suffered from Tuberculous Meningitis. Probl. Tuberk. 1996; 5:25-28
59. Adhikari, M., Pillay, T., Pillay, D.G. Tuberculosis in the Newborn: An Emerging Problem. Pediatr. Infect. Dis. 1997; 16:1108–12
60. Welch, W.H. Papers and Addresses, Vol. 2: Bacteriology. Baltimore: Johns Hopkins University Press, 1920
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62. Gourion, D., Pélissolo, A., Orain-Pélissolo, S., Lepine, J.P. Neonatal Tuberculous Meningitis in a Patient with Asperger’s Syndrome. Journal of Autism and Developmental Disorders 2003 Oct; 33(5):559-60
63. Broxmeyer, L. Autism: An Ancient Foe Becomes a Modern Scourge – The Return of a Stealth Pathogen. North Charleston, SC: CreateSpace, 2012 (159 pp.)
64. Tsukamura M., Mizuno, S. Occurrence of Mycobacterium tuberculosis and strains of the Mycobacterium avium–M. intracellulare complex together in the sputum of patients with pulmonary tuberculosis. Tubercle 1981; 62:43-46
65. Carlson, B.C., Jansson, A.M., Larsson, A. The Endogenous Adjuvant Squalene Can Induce a Chronic T-Cell-Mediated Arthritis in Rats. American Journal of Pathology 2000 Jun; 156(6):2057-65
66. Pandey, A.K., Sassetti, CM. Mycobacterial Persistence Requires the Utilization of Host Cholesterol. PNAS 2008 Mar 18; 105(11):4376-80

Diabetes Mellitus, Tuberculosis And the Science of Denial

August 15, 2012

by Lawrence Broxmeyer, M.D.

©2011 US Library of Congress, All Rights Reserved



Summary The thought that tuberculosis and its family of mycobacteria could cause diabetes seems farfetched, but is not.

If this weren’t true, then why would Dr. Denise Faustman of the Massachusetts General Hospital have announced human trials with dilute cow tuberculosis (BCG) to attempt cure of type 1 juvenile diabetes, a disease historically thought by some to be caused by human tuberculosis. The first trial at Mass General, involving a handful of humans has already suggested that tuberculous BCG therapy can cure Type 1 diabetes.

It’s postulated that the BCG kills the cells that are attacking the pancreas in such patients and the trials chief investigator, Faustman has gone ahead to gear up for a larger phase 2 clinical trial using the same technique.

BCG or Bacille Calmette–Guérin, BCG. The only known vaccination against tuberculosis. Not formally approved in the US because of its limited benefits and possible complications. Essentially it is prepared from a strain of the attenuated (weakened) live bovine (cow) tuberculosis bacillus, Mycobacterium bovis, that has lost its virulence in humans by being specially sub-cultured (230 passages) in an artificial medium for 13 years.

The precise terminology used to describe the study said  “……..a commonly used vaccine that provides protection against tuberculosis, called Bacillus Calmette-Guerin (BCG) was used effectively to deplete the abnormal immune cells that attack and destroy the insulin producing cells of the pancreas.”

But instead of couching things in the vaguery of “abnormal immune cells”, what if there was simply some infection going on in these pancreatic cells that cannot be picked up by today’s commonly utilized technology. Certainly to many, with the possible exception of died-in-wool immunologists, this makes more sense.

In that case, the explanation for the efficacy of BCG as a treatment for  Diabetes would go like this. BCG is a mycobacteria, and in nature most strains of the mycobacteria including human and cow tuberculosis (BCG) have long been known to compete, change and destroy one another. And they do this through attack with their viral mycobacteriophage armament, which live inside all virulent strains of tuberculosis. Usually such viral mycobacteriophage is species specific, and so we would expect a mycobacterial phage to attack another mycobacteria. Were diabetes of mycobacterial origin, the explanation would follow that the ‘phages’ within the BCG itself are attacking the very tubercular strains that are infecting the insulin producing Islet cells of the pancreas.

A TM4 Mycobacteriophage virus landing on and then injecting its DNA through a mycobacterial cell wall. When a virus called a bacteriophage or mycobacteriophage infects a bacteria or mycobacteria such as tuberculosis, the mycobacteria itself becomes the mycobacteriophage’s workshop, which hijacks the machinery of the mycobacteria, turning it from its usual purposes to the sole task of replicating the virus’s genetic material and protein coat. So effectively can this happen, with so many copies of the bacteriophage or mycobacteriopage being produced – that the germ hosting it can eventually, in effect, commit suicide, bursting under the pressure of phage offspring. If this happens then the multiplying bacteriophages are set free –to infect other germs, continuing the cycle.

So injecting BCG into diabetic patients has nothing to do with “bolstering their immunity”, a favored explanation among trial investigators. It has to do rather with hand-to-hand viral phage (mycobacteriophage) combat between the mycobacteriophages in the dilute cow tuberculosis (BCG) being injected and a prime suspect for the cause of the disease itself, human tuberculosis. (See:

Bacteriophages (viruses which target bacteria) are injecting their DNA (upper left) into a bacteria. In return, once inside the bacteria they can go through a rapid lytic cycle in which they multiply and burst the bacteria’s cell wall (bottom left) or their DNA can join with the bacterias (in green) to form a prophage, which can later enter at any time into a lytic cycle which will also implode and kill the bacteria.

If this is the case though, then why is it not being detected? As Nobel nominee Mattman never tired of emphasizing – for survival, the preferred form of the virulent mycobacteria, including tuberculosis, is its cell-wall-deficient (CWD) forms, some of which are viral themselves in size. Cell-wall-deficient mycobacteria and bacteria are also known as “L-forms”.

Mattman taught and used a new method to diagnose tuberculosis in 72 hours. The conventional method took three to four weeks. Her book, Cell Wall Deficient Forms: Stealth Pathogens, Third Edition describes these techniques to spot extremely difficult to identify cell-wall-deficient (CWD) tuberculosis using methods widely used abroad, but not nearly enough in US labs. Cell-wall-deficient or “L-forms” come into being because of a breach in their cell wall, which gives them the plasticity to assume many different forms.

Furthermore, if the favored form of tuberculosis, either inside or outside the pancreas, is its CWD form,  it turns out that a June, 2012 study by Nadya Markova and team also have identified such filterable CWD and L-forms in the BCG vaccine from cow tuberculosis itself. This appeared in the journal of Human Vaccines and Immunotherapeutics:

Certainly mycobacteriophages are prevalent in the CWD forms of any mycobacteria including those of BCG. As a matter of fact, although many agents, antibiotics included, have been claimed to be behind CWD forms, according to Nelson and Pickett, who appeared in the Journal of Infectious Diseases back in 1951, it is ‘phages’ which are themselves behind CWD formation, with other factors, such as antibiotics merely being contributory causes.


The peculiar relationship and frequent association of diabetes mellitus and tuberculosis has been observed for more than 2000 years, yet the reason for this is, to this day, not known. Before the discovery of insulin, a diagnosis of diabetes was a death sentence within 5 years, and the usual cause of that death was tuberculosis. And to this day, physicians in many parts of the world subscribe to the dictum that if diabetes mellitus is not controlled, look for tuberculosis; and, if tuberculosis is not controlled, look for diabetes mellitus.

Despite this, in the 5th century, tuberculosis was already being portrayed as a ‘‘complication’’ of diabetes, a view little changed to this day, parroting Root’s original 1934 description of ‘‘a one-sided relationship’’: tuberculosis still seen as a common complication of diabetes, while diabetes is thought to be no more common among TB patients than in the population at large. . To be sure, Roots paper has methodology flaws, relying at one point in his study to differentiate through a Mantoux TB skin test, those who had contracted TB (skin test positive) as opposed to those who he felt had not (skin test negative). In reality a negative TB skin test means nothing, as immunosuppressive forces inside the TB patient could be so great that the body cannot muster a positive skin test.

To Nichol’s, Roots ideas were ‘‘not logically tenable’’ and in Nichol’s study of 178 otherwise healthy, non-diabetic military men with tuberculosis at Fitzsimmons Army Hospital, one-third had abnormal glucose screening tests. But despite Nichol’s findings and those of Reaud in New York as well as others, this was not being recognized elsewhere, and Nichols wanted to know why. His conclusion: that the incidence of diabetes among tuberculosis patients was considerably underestimated and that in tuberculosis patients, diabetes develops quite commonly. Diabetes was easy to detect. Tuberculosis and the mycobacteria were not. (

The evidence for a tubercular cause of diabetes is mounting. Schwartz and Haas both linked Type-2 diabetes to tuberculosis. And the pancreatic islet amyloid deposits that they found as a by-product of systemic tubercular infection have recently been dissolved by rifampicin, a first line drug against tuberculosis. Engelbach spoke of ‘‘transitory’’ diabetes in TB and Karachunskii noted that patients with tuberculosis commonly wound up with insulin deficiency and persistently high blood sugars. Furthermore tubercular proteins have been shown recently not only to cause ‘‘autoimmune’’ Type-1 diabetes in NOD (non-obese diabetic) mice, but act as a vaccine to stop the inevitable diabetes that would otherwise materialize. The documentation of patient cases where TB has preceded and come before the development of diabetes is extensive yet underplayed. Both Lin and Tsai’s studies speak of tuberculosis complicated by diabetes. Diabetes has been around since the first century AD, in a perpetual state of coping and managing. It is time, it is long past time, to cure diabetes. But current models as to its cause are not equipping us to do so.

Tuberculosis of the Pancreas. Considered “rare”, it’s incidence is growing, and its true incidence unknown. Extremely difficult to diagnose and sometimes can only be spotted by doing a PCR (Polymerase Chain Reaction) of biopsied or autopsied pancreatic tissue.


In 1991, two years before The World Health Organization belatedly issued its first ever global emergency – regarding tuberculosis, a disease estimated to result in a human death every 10 seconds [1], a WHO ad hoc committee announced that an apparent epidemic of diabetes had occurred – or was occurring – in adult people throughout the world. The developing countries, as well as the minorities of disadvantaged communities in industrialized nations, particularly in the United States, seemed to be taking the brunt of the epidemic [2]. CDC maps for US Diabetes and TB at the time showed, for both diseases, a predominantly Southern US distribution, with major inroads along much of the Eastern seaboard.

The intimate relationship between Tuberculosis and Diabetes presented on a poster from the International Union Against Tuberculosis and Lung Disease. The open and nagging question remains, as the artwork suggests: which causes which?

American Diabetes: the Pimas

American Indians have some of the highest diabetes rates in the world, nearly four times greater than other Americans. In one screening study, using three geographic areas, 40–70% of American Indian adults aged 45–74 were found to have diabetes [3]. But it is within this subgroup, that the highest levels of diabetes in the world are found, in the Pima Indians of Arizona [4].

Bar graph of ethnic distribution of US diabetes showing the highest rate among the Pima Indians.

This drew investigators worldwide to grapple with questions such as why those Pimas who chose to stay in the mountains of Mexico, away from the reservations, had incredibly lower rates of diabetes.

Although Mexican Pimas have the ‘‘genes’’ for Type-2 diabetes, fewer than 1 in 15 get the disease. This argued against a genetic basis for the disease. Diabetes, however, was not the only problem facing the American Indians and the Pimas. For if Indian diabetes soared, their rate of TB was more than five times greater than that for other Americans, most American Indian children becoming tuberculin positive by the age of 10 to 15 [5].

By 1900, tuberculosis had become the most serious health problem among North American Indians [6], as well as their leading cause of infectious death [7]. And some of the most dreadful manifestations of tuberculosis susceptibility on record can be found when this group was compelled to change their ancestral ways and live on reservations [8]. The first well documented outbreak of US Indian TB was among 2,800 Sioux, made US prisoners of war around 1880. Not in evidence during incarceration, and soon thereafter, TB deaths, in their most acute form occurred in the barracks, reaching, by 1913 Sioux mortalities at a level 10 times greater than any in Europe during the worst of its 19th century TB epidemics. And similar events were unfolding on other Indian Reservations. Runaway epidemics among North American Indians such as the Arizona Navajo and the Qu’Appelle Valley Canadian Indians left in their wake TB mortality rates of up to 9,000 per 100,000, the highest anywhere at any time. (Ibid)

General Douglas MacArthur, Commander-in-Chief of the Allied Forces in the Southwest Pacific on an inspection trip met with representatives of 5 different American Indian tribes, one of which (on far left) was Sgt. Virgil Brown, a Pima Indian.

Despite the warm, arid Arizona climate, TB still remains the greatest cause of Navajo death, a byproduct of their confinement to reservations and adopting the white man’s diet and way of life. Although tuberculosis reached the Americas with the coming of the North American Indian migrants, it only persisted at a low level of endemicity until an epidemic began 1500 years ago, thought to have originated in the Andean region of South America. Unfortunately, this epidemic did not have an opportunity to reach its apex or subside, leaving highly susceptible American Indians in the direct path of European colonizers. [9]

The single worst disease present in European cities was tuberculosis and by 1800 it was understood that no other disease was as common, nor as deadly. Young noted that it caused one in four premature deaths in England, while major Parisian hospitals simultaneously recorded 40% of their deaths as resulting from tuberculosis. This set the backdrop for a US eastern seaboard death rate of approximately 400 per 100,000 by 1830, a reservoir with which to infect the ultra-susceptible American Indians with virulent European strains.

Perhaps the most meaningful post-mortem examination of pancreatic tissue from diabetic and non-diabetic Pima Indians ever done showed that 77% of the diabetic group had amyloidosis of the islets of the pancreas compared with only 7% in non-diabetic subjects [10].

Phillip Schwartz and amyloidosis

Type 2 diabetes constitutes approximately 90% of all diabetes. And type 2 diabetes is intimately linked to the production of amyloid. A review of four autopsy studies (two in the US, one in Germany, and one in Japan) revealed an average of 70% of type-two patients have diabetic islet amyloid by light microscopy But to experts at University College in London, amyloid deposits are universally present in the pancreas in maturity onset diabetes and indeed may be related to islet failure itself.

The association of amyloidosis and tuberculosis is and has been well known for some time. And that tuberculosis can produce the same type of amyloid found in the pancreas of diabetics can no longer be denied in lieu of recent studies.

As a pathologist and lead researcher, Dr. Phillip Schwarz knew all about amyloid and amyloidosis. Once a Professor of General Pathology at the University of Frankfurt-am-Main in Germany, when he came to the US and when no explanation of diabetes or its amyloid  cause came close to what Schwartz, in a 50 year autopsy-driven study uncovered, he published [12]. In a report of 331 autopsied cases of amyloid, ages ranging from 16 to 87, Schwartz showed tuberculous lesions somewhere in the body in practically all of them. He speculated that most of these were from childhood infection. A remarkable 224 out of 331 diabetics had, in Schwartz’s study amyloidosis of the pancreas secondary to tuberculosis. Moreover, most of those diagnosed as diabetic prior to death showed intense islet cell amyloidosis and Schwartz hypothesized that once amyloidosis of the pancreatic islet cells from tuberculosis hit a critical mass, the result was diabetes mellitus [12].

The Warren State Hospital were Philip Schwartz MD served as pathologist and Chief Researcher until the mid-1970′s.

Thus, according to Schwartz, most cases of pancreatic amyloidosis, as well as the inflammatory infiltrate of the islet cells characteristic of Juvenile diabetes, ought to be considered an immunopathy induced by tuberculosis. Like Nichols, Schwartz noted that diabetes was easy enough to pick up with routine laboratory tests, TB was not, its main weapon being its insidious nature, often taking decades to discover, if then.

Schwartz knew that there were two conceivable ways in which the pancreas could be attacked by tuberculosis: First and foremost was by its toxins and inflammatory proteins, dumped into the blood. [13] The germ need not be present and indeed often could not be found in the pancreatic tissue of diabetics, which Schwartz knew would lead to “autoimmune” speculation.

The other, much less frequent means by which tuberculosis attacked was through the direct invasion of the pancreas by tubercle bacilli, either through the blood or by direct penetration of the pancreas by nearby infected lymph nodes [13]. But even in the few cases where microbes of tuberculosis were present in the pancreas, it could take up to 14 weeks to grow out in the laboratory [14], a practice not routinely followed.

Knowles, by 1990, reported on the anti-TB effects from pancreatic extracts themselves and actual injections of T.B. into the pancreas only proved destructive if an enormous amount of inoculum was used.

In any scenario, Chaudhry et al. [15] concluded, a clinical diagnosis of pancreatic tuberculosis was not possible. Biopsy, autopsy or serology were the only means.

To further prove the connection between tuberculosis and amyloidosis, Schwartz injected M. tuberculosis into the peritoneum of 22 guinea pigs, all of whom promptly died within 28–96 days. All but four exhibited amyloidosis. Yet only one of the control animals, not injected with tuberculosis, came down with amyloidosis. [12] Schwartz’s guinea pig experiment was supported by Hass’s studies. , In a large series of rabbits, Hass found that three out of every four animals developed amyloidosis within 15 days of being infected with bovine (or cow) tuberculosis. Furthermore, the injection of tuberculin, a protein derivative of tuberculosis into these animals only hastened the development of such amyloidosis [16].

Just as it is a well-guarded secret that glucose intolerance occurs in the setting of TB without diabetes, and is reversible following adequate anti-tuberculosis treatment [17]; so too is it glossed over that initial, pronounced, enhanced insulin secretion with TB leads to signs of relative insulin deficiency and persistent high blood sugars. [18] It is just this higher secretion of insulin, leading in turn to lower functional insulin reserves, that sets the stage for the more frequent development of severe diabetes mellitus in patients with pulmonary tuberculosis. (Ibid)

Moreover, such hyperglycemia, in addition to stimulating insulin over- secretion, causes the over-secretion of pancreatic islet amylin, setting in motion the sort of destructive pancreatic islet cell amyloidosis that Schwartz regularly documented [12].

The ultimate importance of amyloidosis of the pancreas towards the pathogenesis of age-related diabetes shows similarities between cats and man. Thus the typical diabetic cat is obese and middle-aged, and has low but detectable circulating insulin levels. However, the most striking similarity between the species is the occurrence of islet amyloidosis (IA) in nearly all diabetic cats and in over 90% of humans with Type-2 diabetes mellitus [19]. Even before Koch discovered the causative organism of human tuberculosis in 1882, it was recognized in dogs and cats [20]. Up to 13% of cats [21] harbored the disease, often unsuspected. In addition, it soon became obvious that cats were also susceptible to Avium or fowl tuberculosis [22–24].

The historical roll-call referenced by Schwartz of scientists linking amyloid in man to TB is extensive and in the past amyloid’s usual precipitating cause was acknowledged to be primarily tuberculosis [25]. However, in recent years scientific thought has shifted towards non-infectious inflammatory diseases as the most commonly associated cause of amyloidosis. In the case of rheumatoid arthritis and Crohn’s disease, this is specious thinking, as these along with other ‘non-infectious’ conditions implied in amyloidosis have themselves been linked indirectly to infectious causes.

But Schwartz, after a 50-year-based investigative study at autopsy found important omissions in those who stipulated  so-called ‘‘primary’’ or non-infectious amyloidosis, [12] in their lack in ruling out the possible presence of active or inactive tuberculosis. Many of these investigators, said Schwartz, simply never looked for or preformed the tests that would have ruled it out.

By 1994, de Beer and Nel [26], studying the relationship between a major rise of serum amyloid, and having tuberculosis, saw a rapid descent in amyloid levels in patients treated with anti-tubercular drugs. Tomiyama and Asano [27] dissolved beta-amyloid plaque with rifampin, a first line drug for TB, and one of the few agents, to this day, that is able to dissolve amyloid plaque. In 2004,Fink similarly  dissolved amyloid, in vitro, with rifampin.

The science of denial

A century ago diabetics were virtually doomed to die of tuberculosis, if not fatal diabetic ketoacidosis [28]. Root, in reviewing the history of the association of diabetes and tuberculosis, noted that ‘‘in the latter half of the 19th century the diabetic patient appeared doomed to die of pulmonary tuberculosis if he succeeded in escaping coma’’. In 1883, Bouchardat stated ‘‘at autopsy every case of diabetes has tubercles in the lungs’’ [29].

Apollinaire Bouchardat (1806-1886). Bouchardat was one of the outstanding diabetologists of the 19th Century, often credited as the founder of diabetology.

Root presented an interesting analysis of 1121 autopsied diabetics in 1934, from which he concluded that active tuberculosis occurred two to three times more frequently than expected [30]. But because in studies like Root’s diabetes seemed to usually precede tuberculosis, it was concluded that the 5th century notion [31] that diabetes comes first was valid. To Nichols [32], this came from a ‘‘peculiar consensus’’, which ‘‘did not seem proper’’. Even Munkner [33] objected to Root’s conclusions, writing that one would expect a somewhat increased number of diabetics within a group of tuberculosis patients as well. Yet it was Root’s [36] 1934 ‘‘one-sided association’’ between TB and diabetes, that others would blindly follow to this day. Yet, Nichols insisted , it was not a question of whether diabetes developed commonly in TB patients. He knew it did.

Certainly in his paper, Root’s ‘‘remarkable cases’’ often point more towards Nichol’s views of TB coming before diabetes, than they did towards his own hypothesis. [30] Were Root and others ignoring the obvious?

Not only does glucose intolerance occur in the setting of TB without diabetes, it is reversible following adequate anti-tuberculosis treatment [21]. And lung resection of tuberculosis in patients with severe diabetes mellitus reduces the severity of their diabetes [34]. Engelbach [35] spoke of ‘‘transitory’’ diabetes in some of his TB patients prior to treatment.

By 1990, a landmark article appeared in the February issue of the Proceedings of The National Academy of Science. Elias and Markovits carefully laid out their case. Insulin-dependent juvenile diabetes, all along thought to be from ‘‘autoimmune’’ destruction of the insulin-producing pancreatic islet beta cells, had been shown to be caused, in mice, by a protein by-product related to Mycobacterium tuberculosis [36]. In the study, Elias and Markovits actually saw the onset of pancreatic beta-cell destruction occur when lymphocytes (white blood cells), developed to destroy and rid the body of these tubercular proteins – also called heat shock protein 65 (HSP-65). This did not occur when HSP-70, common to all bacteria, was used. Some weeks after HSP-65 inoculation, antibodies formed not only to the HSP-64 but anti-insulin antibodies. And as all of these antibodies began to decline, overt insulin-dependent diabetes developed.

The researchers also concluded that the HSP-65 manufactured by Mycobacterium tuberculosis could not only be used to induce diabetes but to serve as a vaccine against it. (Ibid) This was direct laboratory evidence that tuberculosis, through its tubercular proteins, could either cause or prevent diabetes, and it was not alone.[37] Other studies of support appeared [38], [39] [40]. But the possible causative responsibility of the tuberculosis and the mycobacteria in diabetes was still being all but ignored.


An old Insulin preparation by Connaught Labs.

In 1995, the number of adults with diabetes mellitus was estimated to be 135 million worldwide. this number is expected to increase to 300 million by 2025. Diabetes has been around since the first century AD in a perpetual state of coping and managing, but with no cure in sight.

Schwartz and Haas’s studies, linking diabetes, tuberculosis and the mycobacteria, laid the foundation for such a cure and a series of studies done only within the last decade or two further solidify that link. Nichols [32] stated outright that on the basis of his evaluation that diabetes, where it looked for, should be quite common in tuberculosis patients. The problem is, it never has been.

Thus while mankind continues its struggle to come to grips with the cause and thereby win the war against diabetes, tuberculosis and the mycobacteria continue their silent destructive path towards causing it, unobstructed by the advance of today’s “science”.

Recently, specific tuberculosis and mycobacterial proteins have been shown to directly cause insulitis, hyperglycemia and diabetes in mice thru the production of anti-insulin antibodies [36]. No microbes are present in just the sort of situation that many would interpret as the ‘‘autoimmune’’ destruction of pancreatic islets in Type-1 diabetes. The problem is, there’s nothing ‘‘autoimmune’’ about the process other than the fact that you cannot recover the actual bacteria doing the damage against targeted pancreatic tissue.

That there is nothing regarding the current theory of diabetes that is set in stone has recently come to our attention. Presently under scrutiny are the long-relished, age-based categories, only first differentiated in 1957 [11], insisting that the vast majority of children and teenagers had Type-1 diabetes (‘‘insulin dependent’’ or ‘‘IDDM‘‘) – a lifelong problem which occurs when cells in the pancreas fail to produce insulin, the controller of blood sugar. In contrast, experts saw Type-2 diabetes (non-insulin dependent or NIDDM) as a disease primarily of the middle-aged and elderly who no longer responded properly to insulin and have some pancreatic failure.

But, the lines between these 1957 age categories are crumbling, swiftly. If, in the US, you are now diagnosed with diabetes in your late teens or early 20’s, you are more likely to have Type-2 diabetes than Type-1. Moreover, although this increasing prevalence of Type-2 diabetes in US children is mostly in minority groups, it is fast gaining a foothold in non-minority children as well [41,42]. And the same holds true in the UK where the child or adolescent need not be in a minority group to have Type-2.

Although it is conceivable that a complete eradication of tuberculosis and related mycobacteria might prevent diabetes mellitus of the aging, and perhaps the young, Schwartz preferred to leave this question open to further investigations by other authors. However such studies, although they have appeared in limited numbers and are supportive, have come at what for diabetics has been a painfully slow rate.


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