A Few Remarks to Brian and Peter

*** Re: https://www.facebook.com/peter.r.leunen/posts/10152773864408275

INTRODUCTORY REMARKS

I have two overall purposes: one practical and the other theoretical. These two purposes arise from separate motivations.

Here’s the practical side. Heretofore, I had made one contribution to this thread, namely, to link to a book by Catherine Diodati. Brian subsequently dismissed this recommendation. So, practically, I want to try to bolster confidence in the continuing relevance of Diodati’s book. I will therefore argue to this conclusion: For all that has been said, Diodati’s book is still a worthwhile read.

In outline, my argument will look like this: In terms of immunization, Diodati’s book covers “history, ethics, law, and health” (as her subtitle reveals). However, at least three-fourths of her book – “history, ethics, and law” – is more or less completely unaffected by advances in the technical study of the innate immune system. Specifically, new discoveries of the function and importance of things such as “toll-like receptors,” while certainly interesting and even vital from the point of view of practitioners in areas like clinical medicine, the physiology of human immunity, and so on, have little impact on the sorts of ethical and legal issues that constitute at least half of Diodati’s book. Since she merely sketches the history of immunization in order to set the stage for her philosophical-legal discussions, and since the philosophical-legal discussions are unaffected by minutiae like “toll-like receptors,” her “history” portion need not make any reference to such niceties either. But then, 75% of her book is still relevant, despite being written before the discovery of (the importance of) “toll-like receptors,” and suchlike. Moreover, the remaining portion of the book – somewhat unhelpfully labeled “health” – is either negligibly impacted (at worst) or completed unaffected (at best). Therefore, the overwhelming proportion of Diodati’s book – if not the entire book – remains relevant, despite the swipe at its publication date. I flesh this argument out in greater detail in PART ONE.

Theoretically, my purpose may seem a bit stranger. Here it is in a nutshell: I suspect that there are various language barriers that obstruct clear and charitable dialog in this area (i.e., discussions of vaccines, autism, and so on). Pursuant to this suspicion, I will try to make salient some of (what I believe to be) these troublesome features. I will discuss my motivation for this aspect further along.

Theoretically, my point will be this: Considering statements of the form “‘vaccines’ [do cause/ do not cause] ‘autism’,” I will argue that the words “vaccine” *and* “autism” are both ambiguous, and that this ambiguity makes *any* claim of the aforementioned form highly suspect, if not entirely non-evaluable – regardless of whether one endorses a “do cause” or “do not cause” reading. (I also note – but do not pursue – the fact that “causation” is, metaphysically speaking, a vexed area also.) Putting meat on this skeletal argument is my burden in PART TWO.

Finally, just for the hell of it, I will remark upon various of Brian’s comments. This section should be considered, if not entirely non-serious, at least less-serious than the previous two portions – PARTS ONE and TWO. I will provide my commentary in PART THREE.

It may be tempting for a person – particularly, although perhaps not exclusively, Brian – to be eager to “skip down” to PART THREE and start firing off a response. Though certainly understandable from a psychological perspective, this would be a mistake for at least two reasons. Firstly, as I said, my comments in PART THREE are intended to carry different – and lesser – weight than those in PARTS ONE and TWO. Additionally, the comments in PART THREE at least partially depend conceptually upon the scaffolding that I erect in PARTS ONE and TWO.

My advice would be this: Either ignore the entire presentation; or, take it in the order that I wrote it – and in the spirit that I have just now indicated it should be taken.

Let me be clear from the outset. At least as far as concerns my important PARTS ONE and TWO, I will not be challenging any of the assertions made hereon (that is, on Peter’s thread) regarding the various findings, somewhat pedantically excerpted, of such-and-such clinical trials (and whatnot). I will simply stipulate that all of the experimental claims that have been made (chiefly by Brian) are correct.

Finally, Peter already knows that I tend to be prolix. To Brian: You are apparently both intelligent and enthusiastic. I trust that nothing I have written could be construed as an attack upon you, personally. (Regarding the phrase “somewhat pedantically excerpted,” shortly you will discover that I am capable of being at least *as pedantic* as you; so, in calling your comments “pedantic,” I mean no disrespect.) If you are a serious student of immunology, or an allied field, I commend you and encourage you to continue. I have only a few philosophical points to sound off about. However, these points have taken some space to unpack. I appeal to the polymath Blaise Pascal who once (in his Provincial Letters) wrote: “I have made this letter longer than usual, because I lack the time to make it short.”

But, without further ado…

PART ONE: THE PRACTICAL, DEFENDING THE RELEVANCE OF DIODATI’S BOOK

Let me begin this way. The full title of Diodati’s book is as follows:

Immunization: History, Ethics, Law and Health.

From this title it may be inferred (and from my close reading of it I can verify) that the book divides roughly into four subsections. (This is not to say, particularly, that what I am here calling “subsections” map neatly onto chapter divisions. They do not. It is to say, rather, that Diodati has four distinct aims and that she deals with each of the four themes in a sustained enough way to count them as, in some sense, more or less equal [proper] “parts” of her overall work.)

The criticism of the book, ostensibly arising from a Brian’s narrow focus upon its publication date, was this: “This [that is, the book] was written before they understood Innate Immunity and the effect of Toll Like Receptors (especially TLR1/2).”

I will stipulate that the responder’s claim is factually correct. So, for discussion purposes, it is agreed: Diodati’s books was written before “they” (whoever they are) wrote the present biological chapter on “toll-like receptors” (TLRs).

My question – and I assure the reader that I am not being a smart-aleck – is: So what?

To bring my confusion more clearly into focus, consider Diodati’s four sections one at a time. We will then ask, of each subsection in turn, what difference details about TLRs are bound to make for section.

Section one covers the *history* of immunization. Clearly, if references to TLRs are now believed by experts in the relevant fields to be indispensable to full scientific explanations of the function of the human immune system, then (insofar as this belief persists), going forward, one will have to incorporate such references in any account of human immune function that purports to comprehensive. However, it is not clear what this, being granted, has to do with the “history of immunization.” Presumably, the history of immunization has not been rewritten on account of this newest chapter being added. But then it follows that Diodati’s discussion of the history of immunization is (almost completely) unaffected by anything to do with TLRs.

Hence, one-quarter of Diodati’s book is – at least presumptively – unaffected by new information concerning TLRs.

Section two covers the *ethics* of immunization. In this portion of the book (which actually cuts across many of the other issues that she raises), Diodati weighs ethics-related issues such as the relationship of present immunization practices to commonly listed medical values. The three chief values are these: respect for patient autonomy, the requirement of beneficence, and the commitment to non-malfeasance.

Here’s a quick sketch of one set of considerations relevant to patient autonomy. “Autonomy,” in its broadest outline, has to do with guaranteeing that the patient enjoys her right of self-determination. It is fairly uncontroversial to say that, in order for a person to exercise self-determination (or at least, in order to do so well), it is needful that said person have access to information that bears on the medical decision that she has to make. However, immunizations are often conducted in such a manner as to leave the patient largely (if not wholly) ignorant of relevant information.

Take just two examples.

Number one, in mass influenza vaccination campaigns, it is not uncommon for nurses to administer the immunization – which is, after all, invasive – in an almost “assembly-line” environment where “[t]he normal opportunity for doctor-patient consultation becomes impeded [at best] and the consent process is reduced to the acquisition of a signature” (p. 165).

Number two, Diodati points out (although I forget where, and I am too lazy to look it up) that vaccine doses come with information packets of the sort that one routinely ignores when opening (oh, say) a bottle of Tylenol. The typical vaccine recipient never so much as lays a finger upon these packets, which are often discarded by the administering personnel. It therefore follows that the average patient receives more information with her purchase of over-the-counter symptom alleviators than she does with the injection, into her body, of a chemical stew by someone who is possibly not even her usual practitioner.

Are these conditions defensible after all? Maybe: I don’t know! But either way, apparently, they themselves – and discussions thereof – have little to do with TLRs.

However, if this last bit is true, we now (for all that has been said so far by way of objection) have preserved one-half of the book.

Section three covers the *law* concerning immunization. Diodati tackles numerous issues in this section, none apparently turning on technical minutiae regarding TLRs.

Let me draw attention to just two of her many illuminating discussions in this portion of the book.

Number one, she analyzes the justifications provided (in the relevant literature) for the implementation of compulsory vaccination schemes.

Number two, she talks about the (potential and actual) consequences of failing to establish comprehensive vaccine injury programs.

She mentions other issues and much else that is worthy of consideration, but these two examples (I think) are quite sufficient for me to state the following. Short of a clear argument to the contrary, I think it exceedingly unlikely that her discussion of the ethical implications of (hypothetical) compulsory vaccination schemes and the absence of comprehensive vaccine injury programs, will depend much on technical details of innate immune system functionality (e.g., things like TLRs) – however interesting those details may be in other contexts.

At the end of my sketch of Diodati’s treatment of the ethics of immunization, I posed a few questions. Similar questions may be posed, here. For instance: Can compulsory schemes be defended? Perhaps: I don’t know! Also, we may ask: Is the absence of a (genuine) vaccine injury program a sever liability? Who knows?!?

Notice that our answers to the difficult ethical and legal questions are prone to be nuanced. But what I think is straightforward is this: none of these questions anything obviously to do with TLRs.

If, all appearances to the contrary, there *is* something that TLRs have to do with history, ethics, and law, I should think that we are owed at last the sketch of an argument demonstrating as much. However, since no argument has yet been produced, I conclude the following, provisionally.

We have preserved three-quarters of Diodati’s book!

To put it another way, at this point, I have shown that no less than 75% of the book that I recommended is still relevant – even stipulating that the book says nothing whatever about TLRs (because I am granting that you’re correct when you say that the book predated the development of the present understanding of TLRs).

I think, though, that I can press this line of inquiry a little farther.

Section four covers “health.” Here, at last, one might suspect that not mentioning TLRs would be at least somewhat detrimental to Diodati’s presentation. However, the worst case scenario would be that one-quarter of the book is no longer as valuable as it once was. On this picture, 75% of Diodati’s book would continue to be relevant, despite having no discussion of TLRs. That’s pretty good, it seems to me. And, remember, that’s the *worst case* scenario.

Better scenarios can easily be envisaged. Let me imagine two of them.

Number one, I can image that, while relevant at the highly detail-oriented, experimental-clinical level (geared toward the laboratory specialist), TLRs are irrelevant (or at least not *as* important) at the “overall picture,” low-detail-oriented level of introductory presentation (geared towards someone other than a clinician). Diodati’s discussion climaxes in her analyses of ethics and law. The history and science (“health”) overviews are merely ground laying adventures.

If this is so, then – given that she is writing something other than a clinical study – the absence of TLRs is either not detrimental to her presentation at all or, if it is, the detriment is minimal. Personally, for all I have so far seen, I am tempted to guesstimate that the percentage of relevance of the “health” section is somewhere around 80%. To put it slightly differently, even assuming some damage to a general-introduction-style presentation (in virtue of having no discussion of TLRs), I think that’s fair to suppose that 80% of the presentation is still relevant. After all, there are more things to talk about than TLRs. There are immunoglobulins, macrophages (in their other, non-TLR-related roles), helper t-cells, killer t-cells, b-cells, antibodies, and so on. (In fact, given the breadth of what could profitably be discussed, and the observation that Diodati discusses much of it, I think that docking her 20% is arguably too severe.)

However, 80% of 25% (that is, 80% of the quarter of her book that deal only with “health”) still leaves 20%. Therefore, on this picture, 95% of Diodati’s book (the 75% already shown to be relevant, plus the 20% salvaged in her health section) still has continuing relevance *despite having no mention of TLRs*.

Number two, as you have no doubt surmised, I am not a biologist. I am not a medical student, either. I am not engaged in clinical studies of any sort. I had to Google TLRs just to get an idea of what the responder was all worked up about ;-) But one of the things that I did read – in the opening paragraph of the handy Wikipedia article on the topic, was this:

“They [TLRs] are …usually expressed in sentinel cells such as macrophages and dendritic cells…”.

Given this, it seems fair to say something like something like the following. Macrophages are important components of the innate immune system. Given the present state of the study of the immune system, TLRs must be invoked in any comprehensive discussion of *why* , exactly, macrophages are so important. For TLRs help to explain *how it is* that macrophages participate in the innate immune system. However, in an introduction to the immune system, designed for the non-clinician, it is not clear that one is obliged to describe precisely *how* the macrophages perform their functions. For some purposes and audiences, the mere fact that macrophages *are* important might be good enough to note.

Indeed, Diodati does note the importance of macrophages in the innate immune system. But given her purposes and intended audience, it’s not at all clear to me that her neglect (for whatever reason) is any problem at all. [See APPENDIX 1.]

If this picture is sound, then Diodati gets another one-quarter of her book to pass muster.

In summary: In light of the TLR deficit, the worst case scenario seems to be that 75% of her book is still relevant. Better cases go up from 75%, all the way up to 100%, depending upon other details. These details need not detain us, I think, since 75% relevance suits me fine. After all, of her coverage of “History, Ethics, Law, and Health,” the first three categories are – as far as I can see – entirely unaffected by the state of macrophage science and the discovery (or lack thereof) of the cellular-level roles of TLRs. (Bear in mind that I recommended to the book to Peter, who, I take it, has a special interest in *law*.)

[APPENDIX 1] There are questions – that I cannot answer – regarding whether Diodati would be, variously, permitted or advised to leave off discussing TLRs were she revising her book today.

On the one hand, I am not convinced that she mightn’t be better off leaving out any mention of TLRs. From the point of view of a general introduction, simply serving to prepare the way for a discussion of ethics and law, they may be far too detail-oriented. It is not at all clear to me that such technical matters will be profitable additions into overviews of human immune function for non-specialists.

However, there is another possibility congenial to my thesis (that is, that her book is still entirely relevant and worthy of careful study).

I think that at least one of Diodati’s arguments might actually be strengthened by the TLR science. One argument that Diodati gives is directed against one type of immunization procedure. Consider a certain respiratory pathogen, call it P1. Given that P1 is a respiratory pathogen (ex hypothesi), the natural path of (pathological) exposure would be through the lungs. In a natural situation, an infected person would be one who, to put it crudely, in some way inhaled, aspirated, or otherwise got into their respiratory system, a bit of pathogenic material.

Diodati: “When a disease is encountered naturally, the body reacts quickly by initiating an immune response at the point of entry as well as throughout the body where the various elements of the immune system become primed. Essentially, as the pathogens attempt to overtake the cells they are continually weakened and eliminated as they pass through a series of interdependent protective levels. In most cases, excluding tetanus and rabies among the ‘vaccine preventable diseases,’ the respiratory and gastrointestinal systems (secretory IgA systems) encounter the pathogens first” (p. 50).

Let’s now suppose that there is a vaccine against P1. Suppose further that it is live-matter and injectable. (I note that even on the supposition that the vaccine is “deactivated,” there may be residual live-matter. I want to leave this aside. For those interested – and as I have been advising all along – see Diodati!)

Diodati: “Vaccines, on the other hand, *bypass* many of the body’s initial immune defences. This may be likened to a Trojan Horse, wherein the invaders are allowed to bypass the usual primary defensive mechanisms to initiate an internal ‘surprise attack,’ causing the defensive players to scramble into action. Unlike natural infection, which immediately functions to weaken the pathogen and simultaneously send out chemical ‘messages’ to activate other immune system elements, there is no opportunity to ‘prime’ the immune system as a whole. In this way, vaccines do not elicit an immune response that can be considered comparable to natural immunity. In fact, the immune system is so hard pressed to respond to the internal ‘attack’ that it compensates by utilizing far more immune cells than it normally would during a natural infection” (p. 50).

Diodati’s point, here, might be glossed this way: the human body has a subtle, graduated response-system for reacting to pathogenic invasion. Like police officers implementing steps on some sort of “threat response continuum,” the innate immune has various mechanisms for escalating its response to pathogens. This response system is coordinated and complicated.

Vaccines bypass some (or even much) of this system’s early-warning triggers and first-responder activities. Hence, vaccines may cause an immune response that is escalated well-beyond what that response would be in the case of natural exposure to the relevant pathogen. Perhaps we could call this sort of thing “putting the immune system into shock.” Such a “shock” situation, Diodati worries, could be a contributing causal factor to many conditions, from auto-immune disorders and autism to Alheimer’s Disease.

This is one of her arguments. Let’s leave aside the question of whether she’s correct or not. Interested readers are, once again, directed to consult her presentation directly.

What I want to suggest is that, given the structure of her argument, it seems plausible to suppose that the added layer of complexity attributable to the new scientific understanding of TLRs strengthens her case.

For one might think that this business about TLRs could be glossed (albeit roughly) this way: TLRs add a layer of subtlety onto an already subtle system.

THEREFORE (one might think), Diodati’s argument is made stronger for this reason: The discovery of the importance of TLRs just shows that the body’s graduated system has even more complex and vital steps than thought previously. Insofar as certain vaccine procedures bypass any of this system, those vaccines could cause unpredictable effects (at best) or immune system haywire (which might show up as a “worst case” in autoimmune disorders).

Suppose that I am entirely incorrect. These flourishes aside, my main point stands, I think:

Diodati’s book is still worth reading!

PART TWO: THE THEORETICAL, RAISING WORRIES ABOUT THE PRECISION OF WORDS SUCH AS “VACCINE” AND “AUTISM”

I will be interested, in this section, to simply make a few scattered remarks about (potentially or actually) troubling terminology. My underlying point will simply be this: the relevant issues are complex and far from clear, and this complexity and obscurity is only made worse by imprecise and even ideology-laden words.

Let me disclose my *motivation*. I was struck by Peter’s comments:

“So, contaminants in a vaccine may cause autism” and, further on, “However, immunization does not cause autism.”

I came about it this way. (Bear with me!) We can conceive of three distinct “definition strategies” (for lack of a better phrase) regarding the word “vaccine,” and they correspond to three, distinguishable psychological sets.

Number one: We might be antecedently skeptical of immunization – rationally (i.e., for some reasons) or irrationally (i.e., for no reasons at all) – and “poison the terminological well” in the manner in which we believe that the vaccines themselves are poisoned. If we’re like this, we might define “vaccine” as “poisoned needle” (or something relevantly similar).

Number two: We might be enthusiastic supporters of immunization – again, either rationally or irrationally. In this case, we might define “vaccine” as “salubrious needle” (or whatever – you get the idea, I hope).

Before I map a third possible strategy, let’s assess these two. Clearly, they both have this in common: Whether they are grounded in reason or not (i.e., whether they are rational or irrational), they assign merit or demerit to immunization methods a priori. To put it differently, these first two definitions do not trouble to assess individual immunization strategies. They merely assume, apart from inspecting anything, that “vaccines” are such that they are either good (period) or bad (period).

Why did Peter’s comment make me think of this?

Let me try to sharpen the issue with two more examples.

In epistemology, that is, the branch of philosophy that makes a study of questions such as “how can human beings *know* anything?”, received opinions demand that a distinction be drawn between “knowing” and less successful cognitive states such as “truly believing” (and certainly “falsely believing”).

To truly *know* some proposition, p – and one must say the word “know” with suitable gravity in order to grasp my purport – roughly speaking, one has to have all of the following in place.

(1) There is a psychological condition; namely, one has to *believe* that p is true.

(2) There is a distinctly epistemological condition; that is, one has to have suitable *reasons* for believing that p is true. (This is called having “justification” or “warrant” for one’s belief.)

(3) There is a metaphysical condition. In fact, p has to *be* true.

On the standard account of knowing (and I am ignoring complications such as Gettier cases, and much else besides), if any of the three conditions fails, then one fails to *know* p.

One way of glossing the definition of “knowing” might be this: “Knowing” is “successfully believing something true.” (This is all very impressionistic, mind you.)

As such, “knowing” – by definition – can never go wrong. On the standard view of knowledge, one cannot “know” something that is false. For instance, according to the received view of geography, I cannot “know” that the earth is flat – because it isn’t flat, it’s spheroidal. To be sure, I could (mistakenly, in the prevailing view) *believe* that the earth is flat. And there’s no question that, historically speaking, many people have (mistakenly) believed this. But – insofar as the earth is, in fact, spheroidal – no one, at any time, has ever “known” that the earth was flat.

Here’s the point: We (i.e., human beings) can sometimes use words in this way. We can choose to use the word “know” such that it picks out only successful cases of true-proposition-grasping. Philosophers *could* have used a different word. We could now stipulate a different word. These things are neither here nor there. The point is that we can have certain words play these sorts of “purist” functions.

So, Peter, I could use the word “lawyer” in the way that someone such as Plato might have preferred. To be exact, we could define “lawyer” as “someone who really knows the law, always acts justly,” etc. In other words, we *could* use the word “lawyer” in such a way as to rule out of court – by definition – the possibility that there could ever be an “unscrupulous lawyer.”

If “lawyer” has the notion of “infallible legal expertise” baked into it, then a person who is mistaken on some point of law doesn’t count as a lawyer. Similarly, if our concept of “lawyer” entails “being unfailingly just,” then a shyster will never count as a “lawyer” – even if he is posing as one.

Don’t get me wrong, here. I am *not* saying that this word use is advisable. I am simply making my *motivation* known. To put it succinctly, your comment prompted me to consider what “vaccine discourse” might look like if conducted in this sort of “purist”-exclusionary way.

So, when you wrote: “So, contaminants in a vaccine may cause autism,” it may be that our a priori vaccine-booster, mentioned earlier, thinks (my comments are [bracketed]):

“On the one hand, ‘vaccines’ are salubrious things [by definition!]. Salubrious things do not cause ailments, conditions, disorders, illnesses, or maladies [etc. – by definition!]. Autism is an ailment, condition, disorder, illness, or malady [or something like these, etc. – by definition!]. Therefore, vaccines do not cause autism. [And all of this has simply been ‘established’ *by definition*!] On the other hand, ‘contaminants’ [in the relevant medical sense] are morbific things [by definition!]. Morbific things cause ailments, conditions, disorders, illnesses, or maladies [etc. – by definition!]. Autism is an ailment, condition, disorder, illness, or malady [or something like these, etc. – by definition!]. Therefore, contaminants cause [or at least are a candidate cause for] autism.”

(There is a parody of this sort of argument on the website “vaxtruth.org.” It runs thus: “Autism is a behavioral diagnosis. In order to receive the diagnosis of ‘Autism’ a child must exhibit a certain number of behaviors over a certain time frame. If he or she does not do so, the diagnosis of ‘autism’ is not warranted. There is no blood test for ‘autism.’ ‘Autism’ can’t be confirmed or ‘ruled-out’ by laboratory analysis. It’s strictly a behavioral diagnosis. Therefore, anything that causes physiological damage cannot directly ‘cause’ autism. Ergo… vaccines cannot ‘cause’ ‘autism.’” Of course, as the post proceeds to explain, there are numerous other serious physiological conditions that “vaccines” plausibly *do* cause, some of which are typically presented by those with diagnoses of “autism.” See <http://vaxtruth.org/2011/08/vaccines-do-not-cause-autism/>)

Again: this whole train of argument proceeds swimmingly without any bothersome folderol like a clinical investigation or an experiment. Of course, a parallel can be constructed to mirror the a priori vaccine-skeptic’s thinking as well. It’s shorter.

“‘Vaccines’ are morbific things [by definition!]. Morbific things cause ailments, conditions, disorders, illnesses, or maladies [etc. – by definition!]. Autism is an ailment, condition, disorder, illness, or malady [or something like these, etc. – by definition!]. Therefore, vaccines cause [or at least are a candidate cause for] autism.”

These ways of “arguing” may strike the reader as foolish. Value judgments aside, however, the key point is that they are uninformative. As strings of a priori declarations, nothing is learned in the conclusions that isn’t already contained in the premises. And the truth of the premises is dependent upon the accuracy of our definitional assumptions. There are no experimental checks.

Having analyzed these two a priori possibilities, a third avenue becomes clear.

Number three: We might put aside our antecedent suspicions and enthusiasms and just look to see whether vaccines causes autism or not. This is the a posteriori route.

However, and this is where the bulk of my interest lies, I think that there are potential, grave impediments to following this route. The impediments are not necessarily inherent in the a posteriori approach. (Although, surely, there are perennial philosophical puzzles like Hume’s problem of induction, and so on.) Rather, the impediments arise given certain relevant linguistic features.

I will limit myself to two problematic words: “vaccine” and “autism.” Let me try to explain why both of these terms is problematic. (Incidentally, in the discipline of metaphysics, the word “cause” is notoriously problematic as well. This would mean that, arguably, in the statement “vaccines do/do not cause autism,” it happens that every constituent word is problematic. That ought to be a little alarming.)

The first word that strikes me as requiring a bit of “precisification” is the word “vaccine.” To put it slightly differently, the word “vaccine” is not, I fear, suitably precise for serious scientific purposes.

Why would I say this? Consider: A tempting first-pass (non-a-priori) definition for the word might be something like “active immunization vehicle or agent.” To put it a different way, a “vaccine” is a sort of colloquial term for some sort of chemico-pharmacological “brew” (for lack of a better term) that is designed to elicit in its recipient an active immunological response towards one or more “pathogens” (that is, disease-causing agents such as bacteria, fungi, viruses, etc.).

What we – for convenience – label “vaccines” are therefore really *combinations* of several, discrete substances. “Vaccine” is a word that picks out a whole lot of different such combinations.

For instance, vaccines may contain quite a few different substances, such as: toxoids (i.e., bacteria-secreted toxins), detoxification agents (e.g., formaldehyde), live micro-organisms (whether bacterial or viral), inactivated micro-organisms (whether bacterial or viral), preservatives (e.g., thimerosal), adjuvants (e.g., aluminum gels or aluminum salts), and so on.

Even though what I have said so far is rough; it is not – I hope! – controversial. The simple point, here, is that “vaccine” is term that picks out a class of complex “objects” (in the broad sense of the word “object”).

In this way, the word “vaccine” is similar to words such as “protein.” “Protein” is a word that picks out a class of objects. “Protein” is, if you like, shorthand for particular assortments of amino acids. There are many different amino acids, and many different ways in which amino acids can be arranged. In considering two “proteins,” one may in fact be considering two strikingly different constellations of amino acids. It is of little use (not to mention comprehensibility) to speak of “proteins” being “useful” or “useless.” And this is not just because such words arguably assign value judgments. It’s (at least partly) because “proteins” are so variable in their constituent parts that it is unlikely any sweeping value claims can be made about “proteins.” The devil is in the amino acid details and in the function of various amino acid combinations.

Intuitively, some claim like that “proteins are useful” really amounts to the claim that “certain amino acids will be useful, in certain combinations.” But this does not rule out that *different* amino acids, or the same amino acids in *different* combinations, will be “useless” (whether non-salubrious or even morbific).

Similarly, in considering two “vaccines,” one may be considering two quite divergent collections of substances. By way of *illustration* (not *documentation*), one may consult the simple list on Wikipedia. (http://en.wikipedia.org/wiki/List_of_vaccine ingredients ) Even if the list is not entirely correct in terms of its details (I don’t know whether it is or isn’t), still, the list illustrates the point: different “vaccines” have quite different ingredients from one another.

What is the significance of this point? I think that the significance of the point is that, given the wide divergence of ingredients from one “vaccine” to the next, generalizations about “vaccines” should probably sound to us a bit suspicious. To put it differently, when we realize that one vaccine may be composed of ingredients that vary markedly from another, we begin to realize that statements such as “vaccines [do or do not] cause [some condition]” are over-generalizations that ignore the details of actual vaccine composition. However, as with “proteins” where it makes quite a lot of difference to protein “usefulness” what the constituent amino acid components *are*, so with “vaccines”: it seems reasonable to think that it will makes quite a lot of difference to judgments about “vaccine safety” and “vaccine utility” (and so on) what, exactly, the “vaccine” components *are*. Intuitively, some “vaccines” may have “use” and be “safe,” while other may be, variously, “useless” or “unsafe” or both. And the reason is clear: “vaccines” differ widely from each other compositionally.

Consider again the Wikipedia write up. The first entry is titled “adenovirus vaccine.” This is listed as being composed of the following ingredients: “Acetone, alcohol, anhydrous lactose, castor oil, cellulose acetate phthalate, dextrose, D-fructose, D-mannose, FD&C Yellow #6 aluminum lake dye, fetal bovine serum, human serum albumin, magnesium stearate, micro crystalline cellulose, plasdone C, polacrilin potassium, potassium phosphate, sodium bicarbonate, [and] sucrose. ”

Forget the question about whether this is precisely correct. For the sake of the point, let’s simply grant that this description is accurate.

Now compare the adenovirus components with the ingredients of the vaccine, listed further down the list, labeled “polio vaccine (IPV-IPOL)”: “Calf serum protein, formaldehyde, neomycin, 2-phenoxyethanol, polymyxin B, [and] streptomycin.”

There is some vagueness, admittedly. For example, reading the rough list, I wonder: Do “fetal bovine serum” and “Calf serum protein” pick out the same substance or different substances? But let’s put this aside as well.

The key observation, I think, is that two “vaccines” can be constituted in such a way as to have virtually no ingredients in common.

What, then, is the sense of a statement like: “‘vaccines [do or do not] cause x”?

Such statements as “‘vaccines [do or do not] cause x” must really be translated into longer statements such as “Acetone, alcohol, anhydrous lactose, castor oil, cellulose acetate phthalate, dextrose, D-fructose, D-mannose, FD&C Yellow #6 aluminum lake dye, fetal bovine serum, human serum albumin, magnesium stearate, micro crystalline cellulose, plasdone C, polacrilin potassium, potassium phosphate, sodium bicarbonate, [and] sucrose.” [do or do not] cause x; AND “Calf serum protein, formaldehyde, neomycin, 2-phenoxyethanol, polymyxin B, [and] streptomycin” [do or do not] cause x; AND… so on for every conceivable combination of ingredients.

Is this even remotely plausible?

Clearly, two “vaccines” might be made up of (nearly completely or completely) different pharmacological combinations. Given that “vaccines” differ considerably from each other in terms of ingredients, any generalizations about “cause” will be far too coarse-grained to be taken seriously.

Intuitively, it is possible that one ingredient be (<-subjunctive) found to be autism-“causing” (or cancer-causing, or what have you). I am not saying that this has or has not happened, merely that it is possible. In such a case, it would then be true to say of that ingredient that *it* “causes” autism. But would it be correct to say, on the basis of this hypothetical, single wayward ingredient, that “a vaccine” has been shown to cause autism?

I think that we have choices about how we wish to speak. When we speak loosely, we often make broad claims out the sort: x caused y.

For example, suppose that a defect in a particular device often results in a fire. Suppose, further, that the device is really a complex arrangement of various components – say, electrical components, mechanical components, optical components, whatever. Finally, suppose that the defect is somewhere inside of the electrical components.

Would it be correct to say the “device” (period) causes fires? Or would it be correct that the “electrical components of the device” cause fires?

I think that it probably depends on the context of use. Let’s pick out two such contexts, for illustration purposes.

If we’re in quality control, then we probably want to use the more specific determination. After all, if we want to advise the company about to improve the device, it matters quite a lot which component, specifically, is in need of redesign.

If we’re consumers wanting to know what products to stay away from, we can probably get by with speaking more broadly. After all, given the device in question is a composite of different components, and that one cannot buy the device without buying all of the components, if really doesn’t make much difference to our buying decisions whether the defect is electrical, mechanical, or otherwise. All we care about is that there is a defect somewhere (and that defect, wherever it is, is enough to dissuade us from purchasing the device).

This may apply to "vaccines" as well. If one ingredient, say some aluminum salt, is shown to cause autism (or whatever), if we’re being specific, and detail-conscious, we probably want to know which specific ingredient is the culprit and should therefore probably say “aluminum salt causes autism.” Loose speaking won’t serve us well.

On the other hand, if we’re consumers trying to decide which vaccines to avoid or to accept, it probably will be enough for us to speak more broadly. We might say, “avoid the hepatitis A vaccine because it causes autism.” Of course, it is well to realize, in this hypothetical case, that what we really mean is “avoid the hepatitis A vaccine because it contains aluminum salt and aluminum salt causes autism.”

Because of time limitations, I will have to leave it here with respect to “vaccines.”

Let us turn now to the second word that I earlier identified as “problematic,” namely, the word “autism.”

In an article dated January 21, 2014 titled “Lack of Clear Diagnostic Boundaries Remain, Despite New Classification for Autism” and posted by the Murdoch Children’s Research Institute (MCRI), we read: “Despite changes implemented last year to modernise and clarify diagnostic boundaries for autism spectrum disorder (ASD), there is still a 'grey zone' which could lead to both over and under diagnosis, according to a new overview of autism [which was conducted by Murdoch Childrens Research Institute and the University of Melbourne].” (<https://www.mcri.edu.au/news/2014/january/lack-of-clear-diagnostic-boundaries-remain,-despite-new-classification-for-autism/>.)

Bearing in mind the working definition, cited above, for the words “know,” “knowledge,” and cognates thereof, the article (supra.) continues by stating that: “Whilst there are no *known* causes for autism, researchers say *it's time to give up on a single explanation for autism*.” (Loc. cit. Emphasis added.)

Let’s review the initial proposition:

“‘Vaccines’ [do cause/do not cause] ‘autism’.”

We firstly observed that “vaccine” is a generic term that picks out a class of complex objects. Enough differences exist amongst different “vaccines” to justify skepticism regarding claims made about “vaccine” “causal powers.” Sweeping claims about “vaccines” obscure the fact that “vaccines” differ from one another in remarkable ways. (See the discussion, above.)

However, now it also appears that the word “autism” is also problematic. For “autism” does not pick out a single condition with clear-cut “diagnostic boundaries.”

It therefore appears that there are various subsorts of “autism.”

It appears that Brian made a comment in this vicinity when he wrote: “Immunization with fungal contaminated vaccines (TLR2 agonists) will cause autism (one of the 2 types, non genetic).”

However, in light of the MCRI analysis of the “diagnostic boundaries” for “autism,” even Brian’s statement fails adequately to capture the linguistic disarray.

Brian’s comment seems to imply – although, admittedly, it does not state as much explicitly – that “autism” is such that is has two clearly differentiated “subtypes” (hence his comment “one of *the 2 types*”, emphasis added.)

This does not appear to be the judgment of the MCRI. According to the MCRI, even the newly rejiggered diagnostic classification leaves a “gray area.” This “gray area” leads, in part, to MCRI’s advice that people forego speaking of “a single explanation for autism.” How many distinguishable “conditions” lie within the “gray area”? Who knows?

Thus, talk of “vaccines” causing “autism” is not simply slippery due to the ambiguity built into the class noun “vaccines,” but also due to the diagnostic fuzziness built into the term “autism.”

“Autism,” I take it, is something like an “umbrella term.” It marks out a cluster of conditions that, to borrow from Ludwig Wittgenstein, might be thought to “bear a family resemblance to one another,” but which do not answer to a definite “check list” of features. “Autism” is a generic term for several discrete, although possibly related, subtype maladies.

I could proceed with a discussion of the problems associated with the word “cause,” and make a “trifecta” of problematic sentence components. But I will forebear. The discussion of “cause,” while interesting in metaphysics, will probably be construed as even more “out there” than the points that I have been making.

PART THREE: THE COMMENTARY, ON BRIAN’S REPLIES AND LINKS

Let me venture just a bit farther from the language-oriented points and critique – just a bit – some of the comments that Brian made (at least as far as I follow him). Most of what is in this section won’t rise much past the level of verbal jousting. I take it that my most substantial points have already been made in PARTS ONE and TWO, above. I am really only doing this section in order to demonstrate that I have not tried to disregard Brian’s contributions to the thread.

Let me begin by continuing – in a speculative trajectory – the train of thought with which I ended PART TWO.

There I had just noted that the MCRI had explicitly rejected a “single cause” theory for “autism” – not least because “autism” is an umbrella term for a cluster of (seemingly) related conditions, albeit ones with indefinite diagnostic boundaries, rather a term for a precise condition with definite diagnostic boundaries.

It isn’t even that are faced with one imprecise condition but that we can define two precise subtype conditions. The diagnostic boundaries themselves are fuzzy. Going further, then, we may with some plausibility say that nothing in the brief overview of the MCRI’s findings suggests that the “single explanation” model simply ought to be amended to (something like) a double-explanation model. To put it differently, if “autism” has fuzzy diagnostic boundaries, it is far from established, even if Brian is correct that autism is presently believed to subdivide *roughly* into “two subtypes,” that it divides *definitely* into exactly “two subtypes” still less that each “subtype” will have *one* definite “cause.”

In fact, this “two cause”/“two subtype” arrangement is implausible, at least for the following reason. It seems plausible to suppose that cases presently falling into the “gray area” will resist clear etiological analyses and that, following an effort to clarify diagnostic boundaries, some cases that are presently regarded as cases of “autism” will cease to be so considered.

Furthermore, due to the lack of clear diagnostic boundaries, it seems *possible* that at least *one* case will be found having both of these features: (1) the case bears the diagnosis “autism,” and (2) the likely causal culprit is some non-”contaminant”-component of some “vaccine” or other.

I take it that this is, antecedently, extremely plausible.

All we need to motivate this view is the existence of some typical “vaccine” component with a “suspicious past” (from the medical point of view). Didodati lists numerous non-“contaminant”-components that warrant concern. Take just one concrete example: formaldehyde. As the poster surely knows, formaldehyde is sometimes used in “vaccine” mixtures because is both a germicide and a fungicide. However, there is (according to Diodati’s research – and see her book for the citations!) credible evidence to suggest that formaldehyde is (possibly among other things) carcinogenic.

Remember, all that I need to *motivate* (not demonstrate) my view is a “suspicious” pharmacological agent. I have at least one. It seems at least possible, that formaldehyde – a.k.a. embalming fluid – besides being carcinogenic, might also be linkable to (at least some subtypes of) “autism.” For all that has been said so far this is surely *possible*. And, given formaldehyde’s “suspicious past” – that is, its cancer-correlation – it is also a credible “threat,” prima facie.

Notice my caveat: “For all that has been said so far…”! I mean to say that, from all that has so-far been posted, Brian has not even remotely foreclosed on this possibility, evidentially speaking. For all that he has posted (remarks, links, etc.), evidentially speaking, *even if* fungal contamination is the “cause” of one specific, subtype of “autism” – and here I break in to remind the reader that there is arguably no such thing as a “specific” subtype of “autism,” since the diagnostic boundaries of the entire condition are fuzzy – it does not follow that *other* subtypes of “autism” will not be shown to have “causes” stemming from one or more “vaccine” ingredients – say, formaldehyde.

Again, I don’t wish to be misunderstood. I am not arguing that formaldehyde *is* the ingredient that makes the best candidate for the “cause of [certain subtypes of] autism.” I am not even arguing that there *is* any such wayward component, necessarily. I am simply arguing that it is BOTH *possible* that there is and that suspecting that there is one is a *defensible* suspicion. The mention of formaldehyde is merely supposed to illustrate these two points.

Let me now shift to assessing some of Brian’s comments, directly.

Because I just mentioned the fungicide, formaldehyde, let me consider first (a portion of) his remark stamped “April 23 at 6:13pm”:

“…The reason why, or one of the reasons why Autism has exploded has been the LACK of Thimerisol in vaccines. The Rockefeller Institute knew that Eperythazoons (Mycoplasmas) in vaccines caused adverse events via fungal contamination.”

Ignoring the flourish about what “the Rockefeller Institute” “knew” – which, for all I know may well be the case, but certainly hasn’t been evidenced, here – the fact is that, up until now, I have simply stipulated that Brian is correct that “…Eperythazoons (Mycoplasmas) in vaccines caused adverse events via fungal contamination.”

This seems entirely plausible. I have seen nothing to doubt it.

“That’s why they put mercury in the vaccines (Thi-MER-isol).”

This may be correct in some cases. My main comments, here, are two. Firstly, I refer the interested back to my discussion of the problem with the word “vaccine.” Of course, not all “vaccines” utilize thimerosal as a fungicide. I mentioned another common fungicide already, namely, formaldehyde. Brian may not dispute this. So the point doesn’t seem especially worth lingering on.

“The ‘Jenny McCarthy’s’ of the world believe the mercury CAUSED the contamination.”

Frankly, I doubt that this sentence is true. I am not quite sure what is supposed to be the denotation of the definite description “The ‘Jenny McCarthy’s’ of the world…”. (Why is it possessive?) However, it seems altogether possible to ignore this bit and rewrite the sentence:

“[Some people] believe [that] …mercury [additives in a vaccine] CAUSED the contamination.”

However, this restructured sentence doesn’t seem to me to be entirely acceptable either. My trouble arises from the phrase “CAUSED the contamination.” I am not sure what this is supposed to mean. Let me try out two possible ways (as I see it) of clarifying the sentence.

(1) “Some people believe that adding mercury to a vaccine causes the vaccine to become ‘contaminated’ *with fungus*.”

(2) “Some people believe that mercury additives in vaccines themselves cause ‘adverse events’ – e.g., ‘autism’ and possibly Alzheimer’s, etc.”

The sentence that I have marked (1) seems close to what you actually wrote. The problem is that it just strikes me as false. It is, to be sure, an empirical matter! We could take a poll and ask people to report their beliefs about mercury vis-à-vis fungal contamination in vaccines. Having our poll results, surely, we would seemingly have the makings of an answer.

I’m just shooting from the hip, here, but I would put money (although, not much – I’m both poor and cheap) on people either believing that mercury *inhibits* fungus (in the case of, say, medical students who happened to be among our respondents) or people *having no beliefs at all* about how mercury relates to fungus (in the case, for instance, of most people who are not medical students).

However, to say that I doubt that “average Joes” have any articulable opinions regarding how mercury-in-vaccines relates specifically to *fungus* is not to say that “average Joes” have no opinions at all about mercury-in-vaccines. I think that a fair number of people surely do have opinions about *mercury*.

I would suspect, though, that (non-medical student) responders with opinions about mercury would report overwhelmingly something more like what I have labeled sentence (2) than what I have labeled sentence (1).

However, if I am on target with my suspicions, then you’re essentially attacking a straw-man, here. You say:

“It didn’t.”

You seem to mean that you take it that mercury did not *cause* “fungal contamination.” However, I doubt that this is really a genuine concern to most people who profess to “worry” about mercury-in-vaccines. I think that most (non-medical student) mercury-worriers are concerned that mercury itself directly causes (what you termed) “adverse events” (two of which I listed as “autism” and Alzheimer’s), rather than that mercury causes “fungal contamination.”

If so, then your response here, even if true (which I have all along been assuming) is entirely irrelevant.

“So now there is a LESS effective adjuvant in the vaccines.”

Here, I do actually have to raise a factual concern about your claim. In my (admittedly limited) reading, it does not appear to me that thimerosal is listed as an “adjuvant.” The CDC defines “adjuvant” as “a substance that is added to the vaccine to increase the body’s immune response to the vaccine.” (<http://www.cdc.gov/vaccinesafety/concerns/adjuvants.html>.)

It appears to me that the typical “adjuvants” are aluminum salts.

Thimerosal is listed as a “preservative” and sometimes as a “fungicide.” (See Diodati.)

However, I can easily correct the sentence:

“So now [upon the removal of thimerosal] there is a LESS effective fungicide in the vaccines.”

This is perhaps true. However, I do not find it particularly compelling. After all, I want to know whether “vaccines” are the sorts of things that I want in my – and my children’s – bodies. Thimerosal may be a first-class fungicide. It doesn’t follow, though, in virtue of its fungicidal properties that it’s safe to inject into a living human being. Clearly, thimerosal’s being a swell fungicide will not, by itself, guarantee against the eventuality that thimerosal can precipitate “adverse events.” Intuitively, Spectracide Immunox, Ortho Dormant Disease Control, and Terraclor may also be top-notch fungicides. However, it seems inadvisable to inject any of these into a human being.

I want to know more about the safety of thimerosal. For example, although I am no expert, Diodati voices one concrete concern. “[T]here appears to be a cumulative effect to thimerosal: persons who have received successive treatments (e.g., immunoglobulin serum preserved with thimerosal) show elevated mercury levels in their urine. Even tiny very tiny amounts of mercury are known to be cytotoxic (destructive to cells) and can be particularly destructive to brain, kidney and liver cells. Ingested mercury has been associated with chromosome damage, depletion of zinc in the brain tissues, systemic poisoning, and genetic defects. Recently the FDA banned the use of thimerosal is over-the-counter drugs since its safety and efficacy have not been established. The effects of mercury are currently being examined, particularly regarding its use in dental amalgams (affecting autoimmune disease), and undoubtedly more information will soon be available” (p. 70. Note: I am excluding all of the details of her numerous journal citations. I recommend the book to anyone who wants to learn more).

Here’s her summary statement: “In light of the evidence thus far available, it is clear that the bioaccumulation of thimerosal poses a serious health risk. [Additionally, and based upon evidence, the references to which I am neglecting to reproduce:] Like formaldehyde, thimerosal appears to be unreliable in protecting vaccines from contamination and, like phenol, thimerosal has a toxic effect upon white blood cells” (ibid.).

But you continue:

“That is ONE reason [presumably, for increased diagnoses of ‘autism’].”

I am not denying that bona fide fungal contamination may cause (some forms of) “autism.” However, I personally am not at all confident that additives such as formaldehyde, phenol, and thimerosal do not cause “adverse events” themselves. Possibly, one or more of these additives will be shown to have a causal relationship with (some forms of) “autism” (perhaps forms other than those precipitated by fungus – perhaps the same forms …maybe this is a case of causal over-determination, or maybe they are co-factors).

However, I also wish to point out – what you already probably realize: People are not just worried about “autism.” I mean, suppose that (some forms of) “autism” are, as you say, due to fungal antagonism of various crucial components of the innate immune system. And suppose further that thimerosal does, indeed, reduce the number of adverse fungal incidents. Still, it may be that thimerosal accumulates in brain tissue and that, despite being helpful in terms of preventing (some forms of) “autism,” it also ends up causing Alzheimer’s.

To put the point somewhat facetiously: Some people – like me – just think that an element which previously caused hatters to go mad ought not be intentionally injected into babies.

If the thimerosal goes, maybe the result *will be* that many “vaccines” become clearly “unsafe” due to the risk of fungal contamination. And maybe the consequence is that said “vaccines” become impermissible to administer. I am inclined to say: So be it.

“…[Some babies are] Born immune suppressed and given multiple innoculations too close together in time. …”

This combination surely applies to some infants. However, Diodati offers (yet again) another, complementary hypothesis. It may be that the inoculation frenzy *by itself* is enough to overwhelm the not-yet-fully-developed immune system of the newborn and perhaps lead to “immune suppression” – and perhaps even (some forms of) “autism.” (Some of this depends on how we define “immune suppression.” I mean, given that baby’s immune system is not yet fully developed (according to Diodati), this immaturity might be enough by itself to count the baby as “immune-suppressed.”)

Together with the “bypass” problem, which I sketched above, it seems to me not at all implausible (and certainly nothing said so far rules it out), that vaccines administered to newborns might very well cause more problems than they solve.

One area that I haven’t space (or patience) to get into – but which is to my mind crucial to the overall topic – is the possibility (explored by Diodati at length) that vaccine benefits are largely (if not entirely) overestimated.

I will just fire off a few quick examples – and hope the reader follows up with Diodati. She argues (but, given my already long reply, I will not rehearse her points) that the “defeat of Polio” had at least as much to do (and, she suggests, quite possibly even more to do) with improved sanitation systems and a reclassification of some forms of “Polio” as Meningitis, as it did with “vaccines.” She argues that “childhood” diseases such as chickenpox, measles, and mumps are (statistically) mostly mild when encountered naturally, during childhood (and the natural immunity thus conferred lasts a lifetime and – I believe, although I am going from memory, here – can be transferred passively through breast milk), but are often quite severe when encountered in older individuals (e.g., in cases of “shingles”), particularly after their artificial immunity has “worn off” (which makes evident the fact that artificial immunity does not confer lifetime protection, but must be augmented at intervals by “boosters,” at the added expense of additional exposure to potentially hazardous additives; and which artificial “immunity” cannot be transferred passively… I think, but if I am wrong, it’s my error …I am tired and am not looking this last bit up).

Brian wrote:

“MRSA [Methicillin-resistant Staphylococcus aureus] is a TLR2 agonist as well. Left untreated, you become immune suppressed.”

According to the Mayo Clinic, “[m]ost MRSA infections occur in people who’ve been in hospitals or other health care settings, such as nursing homes and dialysis centers. When it occurs in these settings, it’s known as health care-associated MRSA (HA-MRSA). HA-MRSA infections typically are associated with invasive procedures or devices, such as surgeries, intravenous tubing or artificial joints.” (<http://www.mayoclinic.org/diseases-conditions/mrsa/basics/definition/con-20024479>.)

Based on this statement, it seems to me antecedently plausible that “most MRSA infections” afflict persons who are already “immune suppressed.” However, the mention of a correlation “with invasive procedure or devices” such as “artificial joints” raises the further possibility that MRSA occurs in persons at least some of whom have had their immune intentionally suppressed in order to thwart the rejection of artificial appliances or transplants. (See infra.)

Quoting the article titled “Inhibition of Methicillin-resistant Staphylococcus aureus-induced cytokines mRNA production in human bone marrow derived mesenchymal stem cells by 1,25-dihydroxyvitamin D3,” Brian wrote:

“Quantitative PCR data revealed that MRSA-infection predominantly induced expression of TLRs 1, 2, 6, NR4A2, and inflammatory cytokines IL-8, IL-6, TNFα in hMSCs [“hMSC” apparently designates things called “human mesenchymal stem cells” – MJB]. MRSA-mediated TLR ligands reduced osteoblast differentiation and increased hMSCs proliferation, indicating the disrupted multipotency function of hMSCs.”

Frankly, I question the motivation for reproducing – without explanation – dense, jargon-laden texts such as this in a forum such as Facebook. I mean, I am “guilty” of posting involved responses. However, part of the reason for my wordiness is that I try to thoroughly explain my points. Perhaps I utterly fail to do so; but I try. It seems to me that virtually no explanatory effort has been put forward, here. The impenetrable lingo seems calculated mainly ad vulgus stupet (“to amaze the crowd”).

That stylistic quibble aside, it appears to me that Brian intends the above quotation to serve as evidence for his claim that “untreated …MRSA” leads to immune suppression. So understanding the quotation is important for the purposes of the discussion.

I will have to try to rephrase the point, or, if you like, to translate from technical jargon into the vulgar tongue. Regarding the statement:

“Quantitative PCR data revealed that MRSA-infection predominantly induced expression of TLRs 1, 2, 6, NR4A2, and inflammatory cytokines IL-8, IL-6, TNFα in hMSCs. MRSA-mediated TLR ligands reduced osteoblast differentiation and increased hMSCs proliferation, indicating the disrupted multipotency function of hMSCs.”

The meaning seems to be (something like) this:

“Assorted laboratory tests have revealed that antibiotic-resistant staph infections sometimes induce TLRs to secrete particular substances. These secretions, the result of this staph-TLR interaction, tend to reduce the ability of various stem cells to differentiate – for example, into specialized bone cells called osteoblasts – and, instead, tend to prompt an increase in stem cell populations. Researchers further believe that these results indicate that, in these staph-TLR interactions, the stem cell’s characteristic ability to differentiate into numerous specialized cell types has been disrupted.”

However, from this alone it is not obvious – to the non-specialist, at least – what these things (even granted that they are true) have to do with immune suppression.

A quick Google search clued me in on some possible ways to bridge this gap.

After establishing that “[m]esenchymal stem cells, or MSCs, …can differentiate into a variety of cell types, including: osteoblasts (bone cells), chondrocytes (cartilage cells), and adipocytes (fat cells),” the Wikipedia article goes on to explain the role of “MSCs” in “immunomodulation.”

“Numerous studies have demonstrated that human MSCs avoid allorecognition, interfere with dendritic cell and T-cell function, and generate a local immunosuppressive microenvironment by secreting cytokines. It has also been shown that the immunomodulatory function of human MSC is enhanced when the cells are exposed to an inflammatory environment characterised by the presence of elevated local interferon-gamma levels. Other studies contradict some of these findings, reflecting both the highly heterogeneous nature of MSC isolates and the considerable differences between isolates generated by the many different methods under development.” (<http://en.wikipedia.org/wiki/Mesenchymal_stem_cell>.)

As far as I can tell, the idea is that (at least some) stem cells, in their undifferentiated manifestations, are capable of handicapping certain components of the innate immune system. The key statement appears to be as follows. Various stem cells are capable of “interfere[ing] with …T-cell function, and generate a local immunosuppressive microenvironment by secreting cytokines.”

Two things strike me about this statement.

First, the word “local” is, I presume, not thrown in for nothing. It seems, therefore, that the evidence collected by means of the aforementioned “Quantitative PCR data” only licenses the conclusions of local immune suppression – not necessarily “global” (i.e., full body).

One has to bear in mind – as Brian surely knows – that “PCR data” is not collected via human trials (for ethical reasons that are, I hope, quite obvious). Rather the “polymerase chain reaction” (PCR) method involves the use of test tubes and technology that runs chemical tests in a controlled environment – abstracted away from many of the vagaries of actual, living human organisms.

Thus, the use of PCR technique leads to another point. Second, as the Wikipedia article continues: “Other studies *contradict* some of these findings [that is, regarding the local immune-suppressive effects of stem cells under the relevant conditions], reflecting both the *highly heterogeneous nature of MSC isolates* and the considerable *differences between isolates* generated by the *many different methods* under development” (loc. cit.).

Translation: Some researchers point to very different conclusions, reached during attempts to replicate the previously cited experimental results. These differences possibly arise due to variations in the PCR mixtures tested, variations in PCR testing methods themselves, or some combination thereof.

The Wikipedia article cites Donald G. Phinney and Darwin J. Prockop’s article, “Concise Review: Mesenchymal Stem/Multipotent Stromal Cells: The State of Transdifferentiation and Modes of Tissue Repair—Current Views” (Stem Cells, vol. 25, no. 11, pp. 2896–2902, Nov., 2007, published online Sep., 2007, <http://onlinelibrary.wiley.com/doi/10.1634/stemcells.2007-0637/full>), which concluded by stating that “MSC populations express a diverse array of regulatory proteins that reflect the complexity of bone and marrow as an organ system. These proteins contribute to the broad therapeutic efficacy of MSCs but may also confound evaluation of their transdifferentiation potential” (loc. cit.).

Fundamentally, I take this to mean that the diversity of the stem cells in terms of their “expression” of various proteins is so complex as to elude tidy explanation given the present state of scientific investigation.

Hence – and here is my main point – even the “local immune suppression” findings are tentative.

Googling a bit more, one discovers that (at least some of) the research pertaining to the immune-suppressive tendencies of stems cells (the conditions spelled out above) was conducted pursuant to the investigation of “allo-reactions” that is (mainly), state of affairs in which “[d]irect and indirect alloantigen recognition …by which T cells …lead to transplant rejection after an organ transplant.” (<http://en.wikipedia.org/wiki/Alloantigen_recognition>.)

Some researchers now believe that “[e]vidence has emerged that MSC interact directly with T cells to suppress alloreactivity.” (Jennifer M Ryan, Frank P Barry, J Mary Murphy, and Bernard P Mahon, “Mesenchymal stem cells avoid allogeneic rejection,” Journal of Inflammation [U.K.],vol. 2, no. 8, 2005, <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1215510/>.)

I take it that immune suppression is at least somewhat desirable in cases of organ transplantation (and cases relevantly similar to that).

These last considerations do not show that T-cell suppression via the stem cell interactions does not have applicability for virology or immunology. It likely does.

However, as far as I could detect in my quick-and-dirty investigation:

(1) Evidence for immune suppression via stem cell interactions (of the relevant sort) has come mainly via test-tube (PCR) experimentation in the area of alloreactivity. Whether this is relevant or irrelevant will only be discovered (one might plausibly think) if and when immune-suppression studies are conducted in a broader cross-section of laboratory experimentation.

(2) Even if the alloreactivity investigations *are* more widely applicable, still, some researchers have expressed doubts that the conclusions of the above-summarized preliminary experimentation can be replicated – due to considerations such as the variation of samples run through the test tube (PCR) methods as well as a lack of uniformity in test tube (PCR) methodology itself.

(3) Finally, even if the experimentation is both widely applicable and ultimately replicable, still, the experimental conclusions are – presently – framed in terms of *local* suppression. It remains to be seen what broader effect – if any – this suppression would have (and we are here reminded that these tests were not conducted in the highly variable environment of an actual, living human organism, but in test tubes).

Notice, though: I am emphatically *not* suggesting that these scattered concerns show that Brian is *incorrect*. It may well be that TLR agonists cause system-wide (not merely local) immune-suppression. Although this seems to be a plausible way to interpret the current state of the relevant science, it remains to some degree speculative. Brian’s conclusions do not seem to me to have yet been precisely established. To put it slightly differently, Brian’s statements go beyond the conclusions warranted by the experimental data. Sticking scrupulously to the evidence, the *most* that can be said is that *some* (but not all) laboratory-based test-tube (PCR) experimentation suggests that *local* immune suppression is a real phenomenon. This is a far cry from showing that this happens in all (or even most) cases in an human bodies. It is possible that the laboratory tests reveal nothing whatever about what goes on in a real live human being.

Additionally, it is not at all clear how these results – even ignoring the caveats that I just expressed – have to do with immunology, specifically as it pertains to the administration of vaccines to otherwise (presumably) healthy individuals. Nothing at all has been said in the cited articles regarding such matters.

As a final “word” in this section, let me just say something briefly about a few other of Brian’s comments.

Initially, he typed: “Immunization with fungal contaminated vaccines (TLR2 agonists) will cause autism (one of the 2 types, non genetic).”

By now I hope that I do not need to point out two things; but I will do so anyway.

First, the bulk of my reply – what I really want to concentrate on – is in PARTS ONE and TWO. In those sections, I discussed statements of the general form “vaccines [cause/don’t cause] autism” and I made a case (however badly!) for the idea that the terms “vaccine” and “autism” are too fuzzy to really be usefully invoked in sweeping generalizations about “cause” (which “cause” itself is problematic, but I am ignoring this!). So I won’t repeat any of that here.

Second, I hope that it is clear that I do not dispute (since, for one thing, I am not in a position to do so!) that “fungal contaminations” of *some sorts of* “vaccines” (for, surely, not all vaccines are equally susceptible – not to mention that “fungal” is also vague: what sort of fungus? Etc. But let’s ignore this as well) may cause *some forms of* what now flies under the broad diagnostic banner of “autism” (even though “autism” still lacks “definite diagnostic boundaries,” as previously discussed).

What I want to say, here, is about the articles that Brian posted links to subsequent to posting his statement “Immunization with fungal contaminated vaccines (TLR2 agonists) will cause autism (one of the 2 types, non genetic).” I presume, although Brian does no say so explicitly, that these articles were supposed to stand as evidence for the quoted assertion. Do they?

Number one, he posted a link to a CNN article by Tom Watkins titled “Rotarix rotavirus vaccine contaminated, officials say” (Mar. 22, 2010, <http://www.cnn.com/2010/HEALTH/03/22/rotavirus.vaccine/>.) In this article the words “fungus” and “fungal” do not show up at all. In the case under review, the contaminating agent was, according to the article, “material from a pig virus” (loc. cit.). I do not see, therefore, how this article counts as evidence for assertions about fungal contaminants.

Now, in a subsequent comment, Brian mentions “improper manufacturing”. It’s not clear that he intended the CNN article to be evidence for “improper manufacturing” (rather than fungal contamination). But, I think, if it’s evidence for “improper manufacturing,” then the criticism of the “vaccine” manufacturing process that can be made on account of the article cuts far more deeply than merely being one instance of a pharmaceutical company “not catching” the introduction of an animal pathogen.

Again I defer to Diodati: “[V]accine preparation begins with the propagation of antigens, usually in human or animal host tissues. These host tissues can contain myriad of their own distinct pathogens. Past experience has demonstrated that vaccines can become infected by these extraneous, and undetected, pathogens, leading not only to disease within the individual but, sometimes, introducing animal diseases into a new human reservoir” (op. cit., p. 66).

Specifically, “with animal cell-based vaccines, there are viruses that cannot be identified and children [for example] would be injected with ‘a whole lot of micro-organisms that he or she normally wouldn’t come into contact with if they were living a normal life’” (Diodati, op. cit., p. 74; quoting Neil Pearson, Connaught Labs).

One obvious difficulty is that animal diseases can only be screened out once they are known to exist. “Vaccine” manufacturers do not simply run host tissue samples under microscopes, exhaustively mapping every detectable micro-structure, checking for pathogens. In cases such as possible exposure of human beings to, among other things, Simian Immunodeficiency Virus (SIV) and chicken-originated “reverse transcriptase,” there were no “filters” in place to screen for these diseases in host tissues until the diseases had already “crossed species” and been detected in human “vaccine” recipients. The number of these (as-yet undetected animal pathogens) is, of course, unknown. Also unknown is the subset of these pathogens that might pose health risks for human beings.

This provides the basis for an entirely different reason why people might (reasonably, in my judgment) oppose “vaccine” administration – wholly apart from issues about “autism” or “fungal contamination,” etc.

The other link (that I have not already addressed) was due to the journalist Peter Eisler, writing in the USA Today (of Mar. 6, 2013). Titled “Deaths, infections tied to ‘compounding’ drugs,” the article does make a single reference to “fungus” (or a cognate). It reads:

“More than two dozen deaths since 2001 have been linked to contaminated or mismeasured doses of medications produced by compounding pharmacies, according to USA TODAY's review of state and federal records, academic journals, and industry reports. Scores more patients have been badly injured, sometimes resulting in permanent disability. Among the cases: In March, 33 patients in seven states developed fungal eye infections after surgery in which they were injected with contaminated drugs prepared by a compounding pharmacy in Florida, according to Centers for Disease Control and Prevention (CDC) reports. Three-quarters of the patients suffered vision loss, some severe; 80% required additional surgery” (loc. cit.).

33 patients “developed fungal eye infections”. The USA Today summary does not state that patients were administered doses of fungus-contaminated “vaccines.” Maybe they were! But the article does not explicitly say this. Rather, the report indicates that the fungus was in their eyes, and that these fungal eye infections were believed to have resulted from “contaminated or mismeasured doses of medications produced by compounding pharmacies”. For all that the article explicitly says these “medications” – which were either “contaminated *or mismeasured*” – may not even have been “vaccines.” For that has been written, they could have been antibiotics.

This article does not appear to support the poster’s contentions about fungal contamination. This article *does* seem pertinent to the issue of “improper manufacturing.” However, the does author not seem concerned, particularly, about the manufacturing of *vaccines* (e.g., there is no mention of “vaccine” or “immunization”). The issue is “compounding” and may pertain either to (unspecified) “contaminants” or to cases of “mismeasured” ingredients.

CONCLUDING REMARKS

I hope that nothing herein is taken to have been written by me in any mean-spirited or snarky way.

At bottom, I believe that these are subtle questions and that the answers are not obvious. I have tried to make my main points – about some of the limits and pitfalls of language, etc. – in PARTS ONE and TWO.

PART THREE is, more or less, loosely slung.

I appreciate the opportunity that you afforded me to think a bit more about some of these issues. I am not even sure that our degree of disagreement is particularly great. Your comments (and links) were most enlightening; I commend you for your enthusiasm; and I encourage you in your endeavors.

Due to other, pressing projects I will likely not be able to devote any additional time to this discussion in the foreseeable future. I hope, however, that you may find some useful tree in my forest of text! (I apologize for any typographical errors. Perhaps I will get around to correcting them…eventually.)

Best wishes,

Matthew J. Bell (30 April 2014)