Your immune system is stimulated every day and all day long. The system is there to fight infections, contaminations and etc. I have a flu shot each year, required by work. I have had a pneumonia vaccination all to help prevent worse flu and pnumonia illness from occuring. As a nurse I’ve not seen any bad vaccination outcomes think goodness, but I have seen two children not vaccinated die from measles (yes it can, and does happen). But in the U.S. you as a person or you as a parent can decide if you or your child gets immunizations.
This is not true for all States if you want your child to attend public school. Some states are making various vaccines mandatory with no exceptions allowed.
I feel this is a discussion between me, my doctor and my child (when my child is old enough to participate in the conversation).
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So, NVIC is a prominent anti-vacc outlet, and they include this lovely line in the article:
The most frequent kind of diabetes is diabetes mellitus, a chronic degenerative disease caused when the pancreas either fails to produce a protein hormone called insulin or the body’s cells are resistant to the action of insulin.
Given the source of these claims, the cherrypicking from the scientific literature (they cite only sources supporting their position and don’t mention statistical significance of correlations), and the fairly wretched summary of what diabetes is, I feel safe in dismissing this as more anti-vacc propaganda.
As a side-note, I’m a professional researcher with a PhD in the biological sciences, and I read, write, and analyze peer reviewed scientific literature daily. I also have run large-scale biological experiments including dose-response, retrospective, cohort, and both controlled and observational studies. While my laboratory and field focus was on plants and microbes, the underlying science and methods are the same. This whole article screams “bad science” to me.
I would agree completely except for the obvious connection between live viruses and the immune system. As an engineer who deals with hideously complex systems, I know too well (and have the scar tissue to remind me) that any time you poke something in a complex system, you run the significant risk of having something unexpected pop up somewhere else. And biological systems are indescribably more complex than the ones I deal with.
It’s important not to confuse the message with the messenger. There may be absolutely nothing to this (quite possible, even likely) or there may be a germ of reality in it. Very much like the concerns Gary Taubes raises in his latest book, we simply will not know until somebody, somewhere does the rigorous. peer-reviewed research to find out. And nobody has, as far as I can ascertain.
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Every state has immunization exceptions allowed. You would have to go to your individual state to seen exceptions allowed. Almost all states allow medical providers to sign a immunization exception certificate for medical reasons and a child cannot be barred from attending school with that certificate on file.
True. Medical exemptions exist in all the 50 states. However some states have curtailed or removed religious and/or philosophical exemptions.
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So, there is a very simple explanation of a lot of the “ongoing epidemic…not seen in past populations.” It is, however, not an explanation that many people like to hear, because it is entirely unsatisfying. I’ll share it anyways, however, and people can draw their own conclusions. A bit of background to start:
The “Modern” understanding of disease really dates to “germ theory” in the 19th C. (less than 150 years ago), while historical documentation of human obsession with disease itself has a few thousand years of recorded history (some point to Egyptian steles as having the first evidence of viral disease, in the form of poliomyelitis). The modern understanding of genetics, on the other hand, really only dates from the very late 19th C. (with Mendel) and the “evolutionary synthesis” of the early 20th C. The ideas we now think of as the field of medical genetics, that inherited genes can affect human susceptibility or resistance to disease, really only date from the Post-World War II era. The very first theory that human immune system could attack its own tissues dates to 1904. The first population-wide study of autoimmune disease prevalence and societal cost was published in 1997.
So, what does that all mean and suggest to me as a scientific researcher? That the “increase in autoimmune” disorder prevalence is affected by the very recent development of research on autoimmune disorders. Simply enough, fifty years ago, many diseases that are now known to be autoimmune in nature weren’t known at that time to be autoimmune, and were thus classified in other ways. The first criteria for classifying a disease as autoimmune (and see the Wiki article on autoimmune disease for more info) were only described in a paper from 1957.
It doesn’t make any more sense to say that there is an increase in autoimmune disorders in the last few decades (as we’ve finally learned to identify and describe them) than it would to say that there is an increase in viral diseases after 1892. There weren’t any diseases described as viral before that time (because there was, literally, no theory of or evidence for the existence of the virus), and that does not mean that viral diseases didn’t exist before we started to understand them. Smallpox repeatedly devastated Europe of the Middle Ages, and the Middle East before that, and India going back about 10,000 or more years. The disease (complex) was attributed to divine wrath, ill humors, bad air, poison, witchcraft, and the unknown, but never to viruses before the early 20th C. It still existed, and still made people sick.
In a similar fashion, Type 1 diabetes existed (and was even diagnosed) before it was described as an autoimmune disorder. I’m sure that Type 2 existed as well, as well as the MODY and MIDD varieties of DM. These disorders existed before they were recognized as being diseases or disorders at all. The marked increase in diagnoses of diabetes after the 1890s does not necessarily mean that there were many more cases of diabetes mellitus than their had been before the disorder was described, published, and disseminated to the modern medical community. The basics of the disease were described by the Egyptians and Indians around 1500 BCE and the name diabetes came from Greece in 250 BCE. How many children (and adults) died from complications of DM even after it was described and named but before it was understood (even as poorly as it is today)? They weren’t recorded as victims of an autoimmune disorder.
So, to really sum it up as simply as possible, one of the reasons there is an increase in the prevalence of autoimmune disorders compared to “past populations” is because their were no disorders described as autoimmune to compare modern numbers to. Even with modern record keeping, autoimmune disease is a fairly new concept, so even the recent increase is almost impossible to characterize as an actual increase, rather than a statistical artifact caused by changing definitions and diagnostic criteria.
tl;dr: There isn’t enough evidence to determine whether autoimmune disorders are actually increasing in frequency: the recent description of the mechanisms; the lack of comprehensive current or historical medical records (and even medical systems); and the ever increasing number of “new” or reclassified autoimmune disorders means it’s impossible to make meaningful comparisons with past frequencies overall.
As a last little thought experiment, related to the 1957 paper describing the autoimmune nature of some cases of chronic thyroiditis, consider this: before 1957, there were zero confirmed cases of autoimmune thyroiditis (Hashimoto’s is the most common form); in 1957 there were, if I recall, seven cases documented in that famous paper; after 1957, there has been an exponential increase in the cases of autoimmune thyroiditis. Does that reflect an increase in the underlying frequency of the disease in a given population, or does that exponential increase result from the dissemination of diagnostic criteria for a disease that existed before '57 but wasn’t able to be appropriately diagnosed because it wasn’t recognized as autoimmune? Thyroiditis is still sometimes caused by infection, sometime by autoimmune disorder. That was true before '57 and after '57. The only difference is that we now have a way to distinguish different types of thyroiditis by causal mechanism.
It’s always risky to confuse simply having more data about something with an actual delta in the thing being observed. The classic example is the FBI’s Uniform Crime Reports. More than once the data have seemed to indicate a sharp increase in certain categories of crime, when the reality was that there was just an increase in reporting. Rape is a textbook example.
That being said, the opposite can happen, too: a genuine increase can be mistaken for an increase in reporting because there’s no way to tell the difference, and thus dismissed—the “boy who cried wolf” effect. What really needs to happen is research with more discriminating instruments to determine the actual truth. With data that is continually improving, the only way to do that is to apply very specific controls and filtering while collecting data over a longer time: no quick answers and no instant gratification. Dissatisfying, but that’s just how it is.
The unpleasant fact is that we simply don’t know what we don’t know.
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This is correct, on all fronts. But, and this is important, with something like autoimmune disorder prevalence, retrospective studies will never be able to work (because we can’t generate data which doesn’t exist from the pre-reporting phase). What we can do is create a carefully stated baseline (this happened for the U.S. with the 1997 study I linked above), and then we can continue to use the same methods used to establish the baseline to record prevalence in the same diseases from that study. If that is done (and it is being done by NIH and CDC), then we will be able to make some generalizations about trends in prevalence in the future.
There has been only twenty years since the first baseline study of autoimmune prevalence was published. This means that meaningful results are going to have to wait a few more decades. That’s why the science on this it is unsatisfying for many people: people want to know now, but the data just doesn’t exist. Even a doubling of prevalence (or halving) in the U.S. population over 20 years wouldn’t actually mean much in the grand scheme of things. In thirty more years, there will be some pretty solid analysis of trends in autoimmune disorders in this country, but they still won’t be complete for humans in general (due to issues of time, reporting, geographic distribution, inequality, etc.).
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Precisely my point, though you stated it more fully. It’s impossible to make such a determination retrospectively. It can only be done by moving forward from a known starting point. And that takes time; sometimes a lot of time.
There simply is no shortcut. None. Too bad, but there it is.
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Postscript: notwithstanding the statistical gyrations necessary to arrive at a trustworthy conclusion, I still think it’s worthwhile to do the primary research on how immune systems react to these specific scenarios. If there truly is a cause-effect mechanism in play, it might be possible to prove it in less time than the decades potentially needed for statistical analysis. And anyway, that kind of research frequently produces serendipitous benefits that aren’t anticipated (or anticipatable) going in.
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Big Thumbs Up !!!
I’m definitely for research on pretty much anything and everything, and I agree entirely that research into the mechanisms of autoimmune disease are likely to produce all kinds of interesting knowledge. That being said, there is active research into these subjects. The literature is extensive and growing, and we’ve already learned a lot from it. Some of the interesting recent work in this field indicates that there may be a correlation between autoimmune disease, inflammatory responses, and Type 2 diabetes.
It’s really going to annoy some of the “diet and exercise” haters if it turns out many cases of Type 2 are autoimmune in nature and we’ve just lacked the antibody tests and a theory in order to confirm it in the past…
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