After I discussed a new paper yesterday purporting to implicate inflammation as a cause of autism, particularly how unimpressive and of unclear significance its findings were and how it was being used and abused by antivaxers to claim that it supported their idea that vaccines cause autism, some of my readers started mentioning another, related paper published this month about inflammation in autism. It was published online first as an accepted but not yet formatted manuscript on October 8 in Annals of Neurology and comes from a group at Harvard led by a pathologist named Matthew Anderson, the Director of Neuropathology at Beth Israel Deaconess Medical Center, whose lab studies the molecular, cellular and neural network mechanisms responsible for disorders of membrane excitability and synaptic transmission in the central nervous system. It’s the same sort of paper as the last one in that it examines the postmortem brains of people with autism and autism spectrum disorder (ASD) and compared them to controls without ASDs and found…inflammation!
The authors note in the introduction:
Autism spectrum disorder (ASD) manifests in early childhood and is diagnosed based on behavioral deficits including impaired social and increased repetitive behaviors and restricted interests. The study of ASD postmortem brain tissue provides insights into the pathologic processes that underlie this disorder currently defined exclusively by behavioral deficits. Using ASD human postmortem brain tissues, investigators have discovered an increase of cytokines, chemokines, growth factors, and activated astroglia and microglia in the cerebral cortex, white matter, and cerebellum in ASD indicating ongoing activity of the innate immune system1-5. Genome-wide transcriptional profiling has revealed an increase in the expression of a diverse array of genes encoding mediators of this activated innate immune response along with an overall decrease in the expression of many neuron-related genes6-8. Here we applied computer vision algorithms to quantify astrocyte-derived round membranous blebs, multifocal perivascular lymphocytic cuffs, and increased perivascular space and collagen; novel neuropathologic features that we found in a large proportion of ASD brains. The results provide the signatures of a cellular immune response, reflected by T-lymphocyte infiltrates and cytotoxic cell injuries (typical of T-lymphocytes) to CSF-brain barrier astrocytes, in ASD compared to control postmortem brains.
As the press release says:
Not previously linked to autism, perivascular lymphocyte cuffing is a well-known indicator of chronic inflammation in the brain. Lymphocyte cuffs in the brain are telltale signs of viral infections or autoimmune disorders. But the pattern Anderson observed did not match any previously documented infection or autoimmune disorder of the brain. In the brains Anderson examined, the cuffs were subtle but distinct. “I’ve seen enough brains to know you shouldn’t see that,” he said.
I can’t help but note that when I see a finding described as so subtle that I often question its physiologic relevance, but we’ll go with Anderson for the moment.
So Anderson’s group was looking for different indications of inflammation in the brain than Theoharides’ group was in the study discussed yesterday. They approached the problem in a similar way, by looking at postmortem brains. The difference, though, is that Anderson also included adult brains. Overall, they examined brains from the Autism Tissue Program and Autism BrainNet brain banking programs, as well as from the neuropathology archives of the Bett Israel Deaconess Medical Center, for a total of 25 cases of ASD and 30 controls. Their exclusion criteria included evidence of neurodegenerative disease, central nervous system (CNS) infection, or other neuropsychiatric disorder where ASD was absent. For control cases, a further exclusion criterion was a known family member with ASD.
Perusing Table 1, which lists the cases and controls by features including age, sex, brain weight, and cause of death, I was struck by the lack of effort on the authors’ part to summarize the information to compare the ASD cases to controls to determine if the two groups were comparable. I realize that beggars can’t be choosers when it comes to brain specimens, particularly brain specimens of patients with ASD who died and whose bodies or brains were donated to science, but it’s hard to tell how comparable the groups are. I did a few quickie calculations, and they were reasonably comparable, with the controls being older, but not statistically significantly so, but it would have been nice to have this information summarized. Another good thing about the study is that the technicians and pathologists evaluating the tissue sections were blinded to diagnosis.
Anderson and company took the ASD brain sections and compared them to the controls after subjecting them to histology and immunohistology, and looked for lymphocytes as an indication of inflammation. They then used automated lymphocyte detection and an automated segmentation procedure. The specific stain was hematoxylin and eosin (H&E) plus Luxol Fast Blue (H&E+LFB). Blocks containing cerebral cortex were subjected to automated lymphocyte quantification, and blocks with the highest lymphocyte counts were selected for staining with primary antibodies to CD3, CD20, CD4, and CD8 using standard immunohistochemistry (IHC). These are markers for various immune cells, and I list them so that the pathologists reading this can comment freely. For some reason, the authors also stained each case with the largest perivascular space (space around blood vessels) for staining with glial markers. Basically, the authors were looking for “perivascular cuffs” of lymphcytes, a sign of chronic inflammation in the brain.
Anderson then did this:
All available H&E+LFB stained slides were reviewed with a standard bright field microscope and photographs were taken using a 60x objective (600x total magnification; TIFF-format; resolution 2448×1920 pixels) using a 5- megapixel CCD camera (Model DP27, Olympus). On every H&E+LFB-stained section from every ASD and control case, while blinded to the diagnosis, we photographed three blood vessels with the most abundant perivascular lymphocytes in each of the following brain compartments: grey matter, white matter, or leptomeninges. Fields containing single vessels (luminal diameter range 15-500μm) involved by the highest density of lymphocytes were selected from ASD and control cases using a 40x objective. This resulted in a collection of images with identical field of view sizes.
So, basically, sections with the most lymphocytes overall were selected and then of those sections the investigators looked at the blood vessels with the most lymphocytes overall were examined. This double selection makes me wonder a bit right there if there was any sort of bias introduced into the study, although I can see the rationale that focal areas of lymphocyte infiltration might be significant. In any event, the authors found multiple foci of lymphocytic cuffs with increased numbers of lymphocytes in 65% of ASD cases compared to control brains. They emphasize that they found this in males and females, across all ages, in white and grey matter and leptomeninges, and in most brain regions. Looking at their data and figures, I see that they found around two- to five-fold increased numbers of lymphocytes per vessel in all brain regions other than the medulla.
An interesting way to look at the data is to plot it this way, in a cascading plot with box-and whiskers plots showing the median, upper and lower quartile, and upper/lower quartiles ± 1.5 x (interquartile range), with the black cutoff line representing the lymphocyte count of 23/vessel that gives the highest sensitivity for ASD versus control groups:
What you can see is that, yes, by and large the ASD cases have higher lymphocyte counts per vessel, but that there’s a lot of overlap. Most of the rest of the figures show the same thing, overall differences of a similar magnitude with about a third of ASD cases not showing increased lymphocytes per vessel and considerable overlap between the two groups. A second finding of the paper is that the perivascular cuffs examined were made up of killer T-cells, immune cells that normally attack and destroy infected, cancerous, or dying cells, although they can attack normal cells in autoimmune diseases. Also found were increased cellular debris in the perivascular spaces, suggesting that the T-lymphocytes were attacking cells in that space and were associated with membranous blebs (also known as apoptotic bodies), structures associated with programmed cell death. Noting that astrocyte-derived membranous blebs haven’t been observed in other CNS disorders, Anderson speculated that they might have been generated by a targeted attack of astrocyte processes by cytotoxic (killer) T-lymphocytes at CNS blood-brain boundaries.
Anderson further speculates:
We suggest the invading CD8+ lymphocytes in ASD may have T cell receptors that selectively target epitope(s) presented by MHC-expressing astrocytes localized at the glia limitans where CD8+ T-cell cytotoxic effectors such as granzyme B may be locally released to generate these GFAP+ astrocyte membranous blebs in ASD. An MRI study has revealed dilated Virchow-Robin spaces in the centrum semiovale white matter in 7 of 16 subjects with ASD13; a possible correlate to the dilated perivascular spaces we identified in white matter. Astrocyte debris released into the Virchow- Robin CSF spaces and leptomeningeal fibrosis (collagen deposition) could contribute to other brain pathologic processes such the obstruct of CSF absorption consistent with the evidence of increased extra-axial cerebrospinal fluid in high-risk infants that develop ASD14. The astrocyte-targeted damage could have direct or indirect (cytokine-mediated) immune effects on the ability of astrocytes to provide metabolic support to axons causing action potential transmission failures15 as one explanation for the long-range functional connectivity deficits documented in ASD16.
And concludes:
Our study provides signature features of this T-lymphocyte immune subtype of ASD in postmortem cases and identifies astrocyte debris as a potential source of CSF or serum biomarkers for clinical diagnosis and monitoring of the pathology in living patients. Finally, with biomarkers that define the T-lymphocyte immune subtype of ASD, the efficacy of T-lymphocyte-targeted immunotherapies on biomarker levels and behavioral symptoms could be tested.
Maybe, but what does this all mean? Well, of course antivaxers think they know what it means, and what they think it means is highly predictable. They thinks that this is slam-dunk evidence that vaccines done it when it comes to autism:
The association between vaccination and autism was first reported by medical historian Harris L. Coulter and Barbara Loe Fisher, co-founder of the National Vaccine Information Center, in their 1985 book DPT: A Shot in the Dark (Harcourt Brace Jovanovich). Among the case history descriptions of DPT vaccine injury and death were cases of healthy children who suffered brain inflammation and brain damage after DPT vaccinations and were diagnosed with autism.
Of course, because if inflammation is involved in any condition or disease, then to antivaxers vaccines must be able to cause that condition or disease. There’s just one problem. Large scale well-designed epidemiological studies have repeatedly failed to find an association between vaccination and autism. Actually, there are two problems in that, as I mentioned yesterday, even though there is evidence of chronic inflammation in the brains of many autistic people in postmortem samples (for which this study just provides more evidence), it’s still very much up in the air whether this inflammation described in studies like this is causative for ASDs or epiphenomenon (i.e., a secondary effect or byproduct that arises from but does not causally influence a process). This study changes this no more than the study I discussed yesterday.
Of course, with the epidemiological evidence being what it is, namely negative for an association between vaccination and autism, even assuming that Anderson’s speculation that autism might be an autoimmune disease is correct and the inflammation being observed is not an epiphenomeon, then we know one thing with a high degree of certainty: Vaccines don’t cause it. (Seriously, there isn’t even a hint of a whiff of a signal in the literature looking for correlation between vaccines and autism.) That would mean that, even if autism has an autoimmune component to its pathophysiology, it’s not due to vaccines. That doesn’t stop antivaxers from twisting studies like this to fit their agenda, though, and I expect that they will continue to do so. That is, of course, one of the easiest predictions to make, because twisting science to suit their agenda is what they do.
32 replies on “Brain inflammation, autism, and antivaxers”
Hilariously, Greg commented on yesterday’s post that he is waiting for someone else to comment. It is more and more evident that Greg lacks the capacity to grok the content of these studies and relies upon others’ comments to attack; such is the life of a scientifically-illiterate. So I’ll help him out. I can’t comment on the histopath but it is becoming increasingly clear how/why ASDs are highly complex genetic disorders that are influenced by perhaps scores of genes. Height is influenced by scores of genes so it seems likely that ASDs are even more complex. Investigators have yet to solve the “chicken and egg” problem i.e. is the ASD influenced by inflammatory activity or is the inflammatory activity a response to the ASD. Studies like this and tissue donations will help to elucidate this. It’s always a shame that anti-vaxxers weaponise such studies using a single finding in isolation and unable/unwilling to look at the entirety of the study.
Is there also a possibility that the same genes that lead to ASD lead to something related to the immune system?
Damn, you are good. On a forum filled with scientific minds; it was a lawyer who asked the most relevant question, lol.
The answer; is yes. Genetic variants on genes IL1-10 (Interleukin) are correlated with Autism. Genetic variants on genes IL1-10 are also correlated with immune-mediation.
Note that I was not supporting your desire to believe vaccines cause autism, in spite of the evidence. If the same genetic factors that lead to autism lead to immune issues, there is a genetic cause. Immune issues did not cause autism. A common genetic issue caused each separately.
There’s a third possibility that there’s a root cause that induces both inflammation and autism, without one leading to the other. I admit, Occam’s Razor tells us that’s unlikely, something causing two unrelated issues in the brain, but this is an early enough study that I’m not entirely comfortable saying we should assume a 1:1 relationship of the correlation.
How cute, they drew a line through a scatterplot of medians. It’s almost as if they told their biostats intern who is working on a bachelor’s in computer programming to make something pretty for them.
Orac is correct, those box plots have a ton of overlap between cases and controls — and within cases and within controls. Anyone taking this seriously as showing some sort of difference between the two groups needs to take a refresher. What is shows is that there is a lot of variation between and within the groups. And how do you fix that, you ask?
Google it. 😉
“medical historian Harris L. Coulter”
Um, yeah… sure. Coulter’s PhD was in Russian studies, including language. His day job was as an interpreter: https://www.legacy.com/obituaries/washingtonpost/obituary.aspx?n=harris-l-coulter&pid=135222393
His “medical” training was in homeopathy. His medical histories are based on fairy tale science, here is one: https://homeopathic.com/product/homeopathic-medicine/
ScienceMom: “Investigators have yet to solve the “chicken and egg” problem i.e. is the ASD influenced by inflammatory activity or is the inflammatory activity a response to the ASD.”
As I was reading through this, and the previous study, I kept wondering why they did not screen the samples for the several known genetic sequences that have been found in the last ten years.
Orac: ” That would mean that, even if autism has an autoimmune component to its pathophysiology, it’s not due to vaccines”
Needless to say, there is great possibility that this occurs at a stage of development prior to any vaccination.
In addition:
One of Orac’s critics proposed testing cytokine profiles as though that might provide the much desired ‘smoking gun’ against vaccines: in reality, testing would have to be an oft-repeated process because infants/ children receive many insults to their immune systems that are NOT vaccines – like every day. How could you tell WHICH CHANGE is due to vaccines, not a scraped knee or cold ? So , Ok, thrice daily test for 2 years: that’ll work.
Thank you! I was feeling a bit an idiot with obsessive-compulsive disorder thinking “couldn’t they have included at least some average or median value for age? Or at least ordered the cases along it, or the cause of death?”
Anderson et al’s study looks interesting and has some commendable features (like the pathologists reviewing tissue sections being blinded to diagnoses i.e. of ASD).
The chain of postulates leading to the suggestion that at least some ASDs have an autoimmune etiology does seem to contain weak links.
While I’m not a neuropathologist, one thing I wonder about is that while Anderson et al observed perivascular cuffs of T-lymphocytes, I don’t see a description of lymphocytes cuffing/attacking identifiable astrocytes or lymphocytes aggregating with the “membranous blebs”. Shouldn’t they have seen this if the ASD patients’ immune systems were targeting astrocytes?
I gather that the researchers used glial fibrillary acidic protein (GFAP) to identify astrocytes as the source of the degenerate membranous blebs. A potential problem here is that GFAP is a pretty messy stain. I’m used to seeing a lot of bleed-over into material that isn’t clearly brain tissue (including necrotic debris from tumors metastatic to the brain). Thus, one could question the origin of these GFAP-positive blebs.
The conclusion that such blebs result from lymphocyte “attack” may also be questionable, even though their number supposedly correlated with the degree of perivascular lymphocyte cuffing. Blebbing has been observed in many different tissue for a variety of reasons, including anoxia (lack of oxygen), viral infection, toxins etc.
“Cellular blebbing is a unique form of dynamic protrusion emanating from the plasma membrane which can be either apoptotic or nonapoptotic in nature. Blebs have been observed in a wide variety of cell types and in response to multiple mechanical and chemical stimuli. They have been linked to various physiological and pathological processes including tumor motility and invasion, as well as to various immunological disorders.”
http://ncbi.nlm.nih.gov/pmc/articles/PMC5588526/
Is there greater cell turnover in the brains of ASD patients for reasons other than immune system activation?
I’d be interested to see what other pathologists think about these and additional points.
Lastly, since no RI post should be entirely without snark, I have to say that Orac’s color map of brain regions is incomplete, since it doesn’t show the enormous black area radiating out from the basal ganglia in antivaxers, which correlates strongly with a reptilian impulse to blame vaccines for everything.
The work up here was very basic, CD3 (a pan T cell marker), CD20 (a B cell marker), and the markers for T cell subsets, CD4 and CD8. I’m not sure what information you get out of those four markers beyond being able to say that the infiltrate is non-neoplastic. I fail to see how one gets from there to autoimmune easily. Certainly, based upon the markers, I don’t see how one could determine cause and effect.
I am not a neuropathologist, but it seems to me to be a stretch to pin anything on the presence of cytoplasmic blebs.
I agree that the evidence may have been over interpreted. This is an interesting finding, but that is all. It would be very useful to figure out what the inflammatory infiltrate is reacting to. I doubt that this paper tells us anything useful about ASD, but it may suggest a line of research to pursue.
Personally, I sort of doubt that anything useful will come out of this, but you never know.
One last comment, as has already been said, we know from other studies that this has nothing to do with vaccines.
My brain hurts, you goddamn specialist!
Holy fucking Screeching Weasel:
K drug dealers, I did promise to respond to this post and perhaps some of you were waiting. My initial thought was to gloat that indeed Orac proved me correct that he wouldn’t be able to muster enough manure to fling at Anderson . So dry are his criticisms, that, surprisingly, we even have this..
I heard a –damn!– there Orac..
Anyway, getting in these argument there is a tendency to lose sight of the significance of the discussions. This leads me to say, if truth be told, Anderson’s findings are some of the most significant and pivotal ones in autism research. Consider the long research history suggesting brain abnormality in autism. For instance, we’ve had aberrant fMRI autism findings, but perhaps those could’ve been excused as the autistic brain behaving ‘differently’ or quirky. Exley also found excessive concentrations of aluminium in autistic brains, but even if that was a reason for serious concern, it still wasn’t confirmation of damage. The same can be said of Theoharis Theoharides and their recent finding of significant amounts of inflammatory citokines in autistic brains. With Anderson’s findings, however, we now have concrete evidence of inflammation leading to actual brain damage in autism.
The issue then is why are we not sounding the alarm about these findings? What’s with the pedestrian reception? Never mind if it’s not vaccines causing the inflammation as many here contends (not me of course!), but where is the call to arms to get to the bottom of the cause or causes, and figure out if we can prevent them? If Anderson is correct about close to 70% ‘cuffing’ or brain damage, that would translate to over 50,500 annual cases in the US alone! In what other arena, outside of autism, would we be so complacent with over 50,500 kids yearly developing brain damage?!
Of course you guys don’t need to answer these questions; they’re rhetorical. We all know the answers.
That wasn’t the point of discussing the study; I know that’s what you’re mired in with what passes as vaccine critique for you but you (yet again) just look like you’re trying to mask your ignorance with aggression.
No “we” don’t. No one established pathology (as far as I can tell) let alone aetiology so you can’t make that claim.
It’s merely caution over preliminary results. If you want to go all hair-on-fire, have at it but no one outside your echo chamber will join in.
My initial thought was to gloat that indeed Orac proved me correct that he wouldn’t be able to muster enough manure to fling at Anderson .
That wasn’t the point of discussing the study; I know that’s what you’re mired in with what passes as vaccine critique for you but you (yet again) just look like you’re trying to mask your ignorance with aggression.
Indeed – what was the point of Orac discussing these studies? Was he simply out to inform by offering ‘balanced’ critique, or was he more interested in grinding his axe and raising enough suspicions about the findings, and thereby undermining their possible indictment of vaccines? If it was the latter, then calling him out was the most appropriate response. You suggesting it was the former may be more a matter of you ‘masking’.
How about simply to show that such a preliminary study cannot be used by anti-vaxxers to support their claim that vaccines cause autism and studies such as these “prove” it. As usual, you’ve done nothing to support your claims and just keep attacking those who you disagree with.
“Consider the long research history suggesting brain abnormality in autism”
What? You thought there might NOT be brain abnormality in ASD? Really? I mean, ASD is a disorder of the brain, isn’t it? Don’t you agree? In that case, there must be some abnormality in the brain in people with ASD. Don’t you agree? If so, then what is your point?
“We all know the answers.”
No, we do not. You are missing the point. The point is that we do know that the answer is NOT vaccines. That has already been eliminated as a cause. And the lesson is: don’t waste any more resources on that dead end. If we want to find the answer(s), then spend time, money, and manpower on possible causes that have not already been eliminated.
Note to non-scientist readers:
When a scientist, upon reading an article, says “that sounds interesting”, that means “if you draft a new project for further research into this topic, and include the findings of this article, and I was tasked by the NIH or some other agency to review it for grant approval, I will be favorably inclined to tell the powers-that-be that yes, this project should go ahead”.
Assuming of course the new project is scientifically sound.
It also means “that’s not conclusive”, but in fairness most science never is. The most-often written sentence in conclusion of scientific articles is “more research in needed on this topic”.
But that definitely beats up “that’s garbage”.
Now, when a scientist says “Uh! That’s funny” or “eureka!”, things are about to be very exciting.
This post and the one before mentioned the number of samples being involved in the study as a critical factor. The more people involved, the more likely the results will mean something and not just be some random fluke. Imagine yourself going out of your home and picking someone at random in the street and deciding this person is a typical human being. Depending on your luck, you can end up with a blind woman, a drunk homeless guy, or a dog. Pick a thousand people, you are more likely to have a good sampling of the human population. It’s exactly like when polling people.
To give you a sense of scale, back when I was doing some cancer biomarker research, my sample sizes were typically around 40 patients, it took ages to analyze all samples, and that was not enough.
I know some people look like their dogs, but if you are picking a person randomly off the street and end up with a dog, you are doing it all wrong.
It is a good illustration of how anti-vaxxer research works though.
@ Chris Preston
That depends on your inclusion criteria for your cohorts 🙂
Anderson did not speak autism as a whole, even he said 60 % of brain showed inflammation. And required some “optimization” of data. He did not check were known autism genes either (PTEN was included, though). It would be interesting to know were really high levels inflammation caused by some of known genes.
Why are the error bars so much larger in the autism sample?
It sounds like the controls came from a different data set, which makes sense, but why is the control data set of much higher quality? That implies a different procedure to me. Or even a selection bias.
@ Christine
I would interpret the large error bars as reflecting the biological heterogeneity of the autism sample.
As autism is a spectrum with a large variety, I believe we already know that there are a lot of heterogeneity present.
Interestingly, a lot more than in the (presumably) neurotypical control samples. Either the autism brains show a lot of differences not only between them and the controls, but also, and more importantly between themselves, or indeed there is some unaccounted element in the sample selection.
Given the relatively low numbers in each group, I’m right into speculation territory, and sinking.
GETTING MEASLES ‘RESETS’ THE BODY’S IMMUNE SYSTEM
Orac blogged about this years ago. This study is just more proof.
I was wondering about that too – is the difference that previous studies looked at infections after measles, but this study used blood tests to look at antibodies etc?
I think the study also provided a mechanism, why this was happening and it made the evidence stronger.
Greg@Athaic
In the Beth Israel Medical Center report about the Anderson study we found this..
Yet, Orac also said this….
Although close, greater than two-thirds does not equal 65%, and you also said there was no ‘cuffing’ in the controls. Anyway, there seems to be some confusion about the findings for lymphocytes count and ‘cuffing’. Is this understanding correct: They found increased lympocytes in 65% of ASD cases compared to control brains, and ‘cuffing’ in more than two-thrids of the ASD but none in the controls?
Try reading the abstract if you can’t read the whole paper, genius.
See? Autism IS Immune-Mediated.
Of course, with the epidemiological evidence being what it is, namely negative for an association between vaccination and autism, even assuming that Anderson’s speculation that autism might be an autoimmune disease is correct and the inflammation being observed is not an epiphenomeon, then we know one thing with a high degree of certainty: Vaccines don’t cause it
Right. The epidemiology does not support that vaccines are causative for autism. Of course, epidemiology cannot prove causation anyway; without supporting etiological proof of causation.
What is your different etiological hypothesis?
Autism is a multifactorial (genetic) immune-mediated disorder.
The anecdotal evidence from parents who claim that the vaccines caused their child’s autism continues to defy the epidemiology.
The etiological evidence is pointing to immune-mediation. Vaccines are immune-mediating.
Genetic variants on genes IL1-10 (Interleukin) are correlated with Autism. Genetic variants on genes IL1-10 are also correlated with immune-mediation.
This satisfies the multifactorial equation of autism, which, combined with the anecdotal evidence’s defiance of the epidemiology; SHOULD cause concern for bias in the EPIDEMIOLOGY.
Not restricting control groups to those with suspect variants on IL 1-10 could be causing the bias in the epidemiology.
But instead of voicing any concerns; it ‘makes sense’ to start dissecting already published etiological studies to find some clue for bias.
IL-10 is not a gene, it’s a protein. Do tidy up your performance art.
@ Narad,
IL-10 is a GENE on chromosome #1.Like this: https://www.ncbi.nlm.nih.gov/snp/rs3024498
(that’s actually my own rs report).
The gene encodes the protein. https://www.genecards.org/cgi-bin/carddisp.pl?gene=IL10
@ doritmi
Note that I was not supporting your desire to believe vaccines cause autism, in spite of the evidence. If the same genetic factors that lead to autism lead to immune issues, there is a genetic cause. Immune issues did not cause autism. A common genetic issue caused each separately
You were not trying to support anything, lol;. You asked a question. I answered.
Not only are genes associated with both autism & immune regulation but the SAME genes are associated with both autism & immune regulation & oddly (not really); those same genes are important in regulating vaccine response & the variants on those genes are known for implying a higher risk for adverse events.
It is YOU; who’s desires to believe vaccines are NOT causing autism that is in spite of the evidence. I have way more skin in this game, than you do, to want to believe that they are not. Knowing that they are is of no benefit to me whatsoever; it only means I suffer extreme guilt for having been complicit in my child’s disability.
I have no recourse based on vaccines having caused his autism. No treatments, no financial assistance; nothing but regrets.
I was just giving you props for asking a question that your ‘sciencey’ counterparts cannot bring themselves to consider. They know why but you would not.