Addressing Dr. Christina Parks’s Claims
There is presently a viral video circulating featuring the testimony of Dr. Christina Parks regarding COVID-19 vaccines and mandating them. In this video, she makes a number of blatantly false claims or prevaricates and they are worth going through in detail. Parks recycles a few of her points so this is mostly chronological but if she returned to a particular subject I discuss it in the same section rather than mentioning it a second time.
Gene therapy
Parks begins her testimony by alleging that the mRNA vaccines are an example of gene therapy. As it happens, I have a recent post addressing this precise question. In short, there is no reasonable basis under which COVID-19 vaccines (or, in general, any vaccine against any infectious disease) could be considered a form of gene therapy. Some regulatory definitions even explicitly state that vaccines against infectious diseases are not gene therapy. The FDA does not regulate them as though they are gene therapy, nor does any other regulatory body that I am aware of. Expression of the spike protein induced by these mRNA vaccines is transient and done only twice (as the vaccines are given only twice- ergo they don’t function as any kind of replacement gene therapy), it fulfills no known therapeutic role (it is preventive to protect against COVID-19, especially severe COVID-19), and it is given to people who are healthy. It does not qualify as gene therapy (though it would be completely irrelevant even if it did as this says nothing about its safety or effectiveness).
The Media
Parks continues by arguing that the science behind the COVID-19 vaccines has been “simplified to take away freedom of choice.” This claim is not scientific and is blatant political pandering to appeal to people’s libertarian instincts, conspiratorial thoughts about the media, and general distrust of governmental institutions. I would remind Dr. Parks that the media at large that communicates with the lay public is not a professional scientific society issuing publications to its members. Things have to be simplified for them to be comprehensible. For the record though, I don’t think the science here is particularly complicated- though the level at which it is examined is a factor.
COVID-19 Vaccines and Transmission
Parks then comes to the central thesis of her testimony: that COVID-19 vaccines do not prevent transmission. This claim is false and readily verifiable as such. Firstly, as a baseline, if infection cannot occur (sterilizing immunity) then there is no potential for onward transmission. mRNA vaccines in particular have demonstrated the ability to prevent infections. This study found that 14 days after the second dose of an mRNA vaccine, the risk of a positive PCR was 90% lower than for an unvaccinated individual. Johnson and Johnson/Janssen’s pre-licensure Phase 3 trial measured an efficacy of 65% against asymptomatic infection. A study of Mayo Clinic patients found that 10 days after 1 dose of mRNA vaccination, the risk of a positive PCR was reduced by about 80%. In a nationwide study in Israel, the Pfizer vaccine was able to reduce asymptomatic infection by 90% 7 days after dose 2. The SIREN study of UK healthcare workers confirmed that the Pfizer vaccine is able to reduce the risk of asymptomatic infection by 85% 7+ days after the second dose. There are additional data to assess transmission risks. This study showed that for every 20% of the population that is vaccinated, the risk of an unvaccinated person having a positive PCR is halved. This study found that the the likelihood of household transmission was approximately 40 to 50% lower in households of index patients who had been vaccinated 21 days or more before testing positive than in households of unvaccinated index patients, with most of the vaccinated participants having received just 1 dose of vaccine in a 2-dose series. This summary by Richterman, Meyerowitz, and Cevik goes through a great deal of the data on the indirect effects of COVID-19 vaccines to stop the spread. In fact, Dr. Cevik herself recently contributed a thorough Twitter thread on how the picture may have changed with the Delta variant- but by and large it hasn’t. This alone would be sufficient to dismiss Dr. Clark’s entire testimony but she makes a number of additional false claims which also should be addressed.
Acellular Pertussis Vaccines
She draws a comparison of COVID-19 vaccines to acellular pertussis vaccines, stating that the acellular pertussis vaccines do not reduce transmission. This is not quite true. Certainly, the effect of the acellular pertussis vaccine on reducing spread is less than what we would like and its key role is indeed in the prevention of disease (which is why maternal immunization during pregnancy is so critical). However, it cannot be ignored that herd protection effects have been observed with the acellular pertussis vaccine that indicate a reduction in transmission. Parks is correct to point out that the DTaP vaccine is not without flaws and she is correct to point out that it does not do as good a job at preventing transmission as we would like, but the acellular vaccines remain our best tools for controlling spread and preventing disease due to pertussis. James Cherry, one of the leading infectious disease experts on the matter of pertussis, has in fact argued that boosters of acellular pertussis vaccines should be offered every 3 years to reduce spread. The current acellular vaccines do not induce Th1/Th17 immunity that seems to be essential for clearing B. pertussis once infection has occurred, which has lead to the pursuit of additional candidates like BPZE1, a live attenuated strain of Bordetella pertussis that does induce this profile of immunity. Parks also argues that the reason for the shift to acellular vaccines from the previous-generation whole-cell version was concerns of safety but this is not, strictly speaking, true. Whole-cell pertussis vaccines never demonstrated legitimate safety concerns per se but were highly reactogenic (especially before methods to remove endotoxin from them were produced)- they provoked intense side effects such as high-grade fevers, but safety concerns were largely the result of anti-vaccine propaganda, as Dr. Cherry writes in his seminal review linked earlier. Parks furthermore argues that acellular vaccines are less effective than whole-cell pertussis vaccines in the prevention of pertussis which is also an incomplete remark at best. Acellular pertussis vaccines performed non-inferiorly to (sometimes even better than) whole-cell vaccines in clinical trials. Their principal issue is waning (which Dr. Cherry proposes addressing through regular boosting), and in replacing them with next-generation vaccines spanning more antigens there may be challenges in increasing the breadth of the immune response in those who have been primed by the acellular vaccines due to linked-epitope suppression (wherein memory cells specific to antigens from the acellular vaccines will outcompete those for novel antigens; this comment by Dr. Cherry has been distorted previously by anti-vaccine advocates to claim that it means that those who received acellular vaccines are at greater risk than the unvaccinated. This is untrue). Some have argued that the emergence of pertactin-deficient strains has caused a drop in the effectiveness of acellular vaccines because pertactin is a key antigen in the vaccines, but evidence for this is lacking. In sum, a completing a series of pertussis vaccines are estimated to be 80-90% effective against pertussis disease. Their effects on transmission are less than what we would hope, though not zero, and work is underway to create better pertussis vaccines. In the interim, staying up to date on pertussis vaccines, and especially vaccination during pregnancy, remain critical tools to protect against pertussis.
Influenza Vaccines and Transmission
Parks similarly argues that influenza vaccines do not prevent transmission. This requires a bit of framing and context before getting into the details, so bear with me for a moment. Influenza has many strains, unlike many other pathogens (SARS-CoV-2 does not have multiple strains per se- the variants are not distinct enough from one another that they have been classified as separate strains), mutates extremely rapidly (it is a negative-sense RNA virus that has a genome comprising 7 or 8 segments depending on the subtype and no proofreading activity in its RNA-dependent RNA polymerase unlike coronaviruses), and has many host species and animal reservoirs. Thus each year, surveillance centers coordinated by the WHO have to guide which strains of influenza are selected in the annual flu vaccine, which typically includes 4 strains (2 influenza A and 2 influenza B). Unfortunately, some years, matching is imperfect and vaccine effectiveness is poor. Most years, the flu vaccine has a computed vaccine effectiveness of 40-60% against influenza-like illness (ILI; essentially symptomatic influenza, but coded as such for epidemiological purposes due to undertesting of influenza cases). While that number is certainly much lower than that for many of our vaccines, the flu vaccines still save lives and prevent hospitalizations each year. CDC estimates that vaccination against flu prevents thousands of deaths, tens of thousands of hospitalizations, and millions of symptomatic infections every year. Regarding the specific evidence for influenza vaccines and their ability to reduce transmission of the virus, data are somewhat sparse with most studies overwhelmingly focusing on the ability of the vaccine to prevent ILI, but there certainly is positive data. In particular strong effects are observed when vaccinating children as they tend to be critical vectors for the influenza virus. For instance, Japan initially did not vaccinate their schoolchildren and had a mortality rate due to influenza 3-4 times of the US; upon initiating a pediatric vaccination program the values became similar to US levels. This effect has also been seen in smaller studies (this one too). Influenza vaccine uptake may also be particularly important among staff in certain congregant settings such as nursing homes where risk is particularly high for residents to protect them, which has also been shown here, as well as here, and here. Certainly, influenza vaccines are imperfect, but they still prevent considerable suffering through their lifesaving and morbidity-saving effects. Work is underway to attain better influenza vaccines, but for now, we should not allow perfect to be the enemy of good. Furthermore, it is worth noting that the fact that influenza vaccines do not confer sterilizing immunity is not entirely bad, as it it allows the immune system to evolve cross-reactive responses which may be protective against future encounters with flu.
Parks also made a comment about how getting multiple consecutive vaccines for influenza increases your risk of severe influenza. Truthfully, I am unsure what she is referencing. The best I can tell, she is misinterpreting how original antigenic sin works in influenza. Original antigenic sin is the concept that the first encounter we have from influenza generates immunological memory that gets recalled with subsequent encounters. However, influenza differs greatly between strains and the immune system may end up focusing on a conserved site between the different strains but one that does not offer good protection. As the discussion by Yewdell and Santos linked previously mentions however, epidemiological evidence for a significant role of original antigenic sin in influenza is at best mixed. When I asked Dr. Jenna Guthmiller about this concept, as I wasn’t sure what was being referred to (and she is a literal expert on the immunology of influenza), she explained to me that there isn’t really a harm per se but after successive boosting you eventually hit a ceiling with your antibodies where you can’t really productively generate new responses effectively, and that you are definitely better off getting your flu vaccine annually than not. I think that if I didn’t know, and Dr. Guthmiller didn’t know, this probably doesn’t have sound basis.
Pre-Licensure Trial Endpoints
Parks argues that the vaccines were assessed on their ability to prevent symptoms alone. This is false. For instance, here is the FDA briefing document for the Pfizer/BioNTech COVID-19 vaccine which gives the following as its endpoints:
Primary Efficacy Endpoints Study C4591001 has two primary endpoints:
First primary endpoint: COVID-19 incidence per 1000 person-years of follow-up in participants without serological or virological evidence of past SARS-CoV-2 infection before and during vaccination regimen – cases confirmed ≥7 days after Dose 2
Second primary endpoint: COVID-19 incidence per 1000 person-years of follow-up in participants with and without evidence of past SARS-CoV-2 infection before and during vaccination regimen – cases confirmed ≥7 days after Dose 2
Secondary Efficacy Endpoints Study C4591001 has secondary endpoints based on different approaches to COVID-19 case evaluation criteria as follows:
COVID-19 confirmed at least 14 days after Dose 2: COVID-19 incidence per 1000 person-years of follow up in participants either (1) without or (2) with and without serological or virological evidence of past SARS-CoV-2 infection before and during vaccination regimen – cases confirmed ≥14 days after Dose 2
Severe COVID-19: incidence per 1000 person-years of follow-up in participants either (1) without or (2) with and without evidence of past SARS-CoV-2 infection before and during vaccination regimen – cases confirmed either (1) ≥7 days after Dose 2 or (2) ≥14 days after Dose 2 CDC-defined COVID-19: incidence per 1000 person-years of follow-up in participants either (1) without or (2) with and without evidence of past SARS-CoV-2 infection before and during vaccination regimen – cases confirmed either (1) ≥7 days after Dose 2 or (2) ≥14 days after Dose 2.
For the primary efficacy endpoint, the case definition for a confirmed COVID-19 case was the presence of at least one of the following symptoms and a positive SARS-CoV-2 NAAT within 4 days of the symptomatic period:
• Fever;
• New or increased cough;
• New or increased shortness of breath;
• Chills;
• New or increased muscle pain;
• New loss of taste or smell;
• Sore throat;
• Diarrhea;
• Vomiting.
For a secondary efficacy endpoint, a second definition, which may be updated as more is learned about COVID-19, included the following additional symptoms defined by CDC (listed at https://www.cdc.gov/coronavirus/2019-ncov/symptoms-testing/symptoms.html):
• Fatigue;
• Headache;
• Nasal congestion or runny nose;
• Nausea.
For another secondary endpoint, the case definition for a severe COVID-19 case was a confirmed COVID-19 case with at least one of the following:
• Clinical signs at rest indicative of severe systemic illness (RR ≥30 breaths per minute, HR ≥125 beats per minute, SpO2 ≤93% on room air at sea level, or PaO2/FiO2 <300 mm Hg);
• Respiratory failure (defined as needing high-flow oxygen, noninvasive ventilation, mechanical ventilation, or ECMO);
• Evidence of shock (SBP <90 mm Hg, DBP <60 mm Hg, or requiring vasopressors)
• Significant acute renal, hepatic, or neurologic dysfunction;
• Admission to an ICU;
• Death.
That’s a lot of words but the short version is that the trial did not evaluate the ability to prevent symptoms- it evaluated the ability to prevent clinically and virologically confirmed SARS-CoV-2 infection. This point is perhaps less disingenuous to some than to others because some might not be aware of the distinction between signs and symptoms. Symptoms are the subjective perceptions that we may feel when we are ill- things like pain, fatigue, nausea, etc. Signs are objective and can be detected by the other person or through diagnostic testing, like a positive PCR for SARS-CoV-2 infection. Suggesting that the vaccines prevent symptoms only is dishonest. They demonstrated spectacular efficacies of ~95% against symptomatic COVID-19, which includes the disease processes it contributes to. The Johnson & Johnson/Janssen (JJJ) vaccine had slightly different primary endpoints:
The structure of various IgA antibodies. Secretory IgA is shown in panel f, defined by the presence of a secretory component, J chain, and dimeric structure. Secretory IgA must be produced locally at the site of the mucosa, and cannot enter mucosal sites from the bloodstream.
Figure 11.1 from Society for Mucosal Immunology. Principles of mucosal immunology. (CRC Press, 2020).
The co-primary endpoints were efficacy of a single dose of vaccine to prevent centrally confirmed, moderate to severe/critical COVID-19 occurring (1) at least 14 days after vaccination and (2) at least 28 days after vaccination in study participants without evidence of prior SARS-CoV-2 infection at baseline. Evaluation of the co-primary endpoints was triggered by prespecified criteria:
1. The first 50% of participants have at least 2 months of follow-up after vaccination
2. At least 42 moderate to severe/critical cases of COVID-19 with onset at least 28 days after vaccination
3. At least 6 cases of COVID-19 among participants ≥60 years of age (onset ≥28 days after vaccination)
4. At least 5 severe/critical cases of COVID-19 in the placebo group (onset ≥28 days after vaccination) with a favorable vaccine-to-placebo split for both co-primary endpoints.
However note here that the vaccine was not evaluated on the basis of its ability to prevent symptoms as Parks states in her testimony.
Mucosal Immunity by the mRNA vaccines
Parks argues seemingly from the basis of acellular pertussis vaccines that vaccines against COVID-19 that mRNA vaccines cannot be protective against transmission (we have already established this as false) because they do not induce mucosal immunity. As it happens, recent preprints demonstrate that this is untrue. This one is more comprehensive than the related one so I will focus on it. One way to profile mucosal immunity, at least its humoral components, in the upper airway is through examining saliva for the presence of neutralizing antibodies. In this study, Nahass and colleagues examined vaccinees for the presence of such antibodies and convalescent individuals to make comparisons. At the mucosal surfaces, most antibody is indeed IgA; more precisely, it is secretory IgA. The Tal lab has previously found evidence of secretory IgA following mRNA vaccination, suggesting a mucosal response. There is a relevant caveat here though in that antibodies to commensal microbiota may also crossreact with the spike receptor-binding domain, and thus whether these are elicited from the vaccines is not confirmed (though the fact that the levels of salivary antibodies does vary with the specific vaccine used is encouraging as far as mucosal immunity resulting from intramuscular vaccinations). However, salivary IgG and IgA antibodies against the spike protein in vaccinees did prove capable of neutralizing a VSV pseudovirus expressing the SARS-CoV-2 spike protein. It’s worth noting that even parenteral (e.g. intramuscular) routes of administration have been shown in the past to elicit varying degrees of mucosal immunity. For instance, one model of protection against SARS-CoV-2 via these vaccines posits that high levels of antibodies (mainly IgG) are actively imported into the lungs and then rise to the upper airway via mucociliary clearance. As a note for anyone who is interested- it is known that mRNA vaccines can induce circulating monomeric IgA production against the spike protein. However, this is not the same as mucosal IgA. IgA in circulation does not end up in the mucosa. Hence why I have limited the refutation of this portion of the claims to evidence explicitly demonstrating the presence of anti-spike secretory IgA in pertinent mucosal compartments rather than showing published and peer-reviewed data showing IgA induction by mRNA vaccines. It is very difficult to study mucosal immunity relative to the systemic compartment, which is why information on this is more scarce and preprints are only really starting to trickle in now. I will also note that Parks was largely correct in classifying SARS-CoV-2 as a mucosal, respiratory pathogen. Viremia (virus in the blood) is rare, generally only occurring in very severe disease. Still, there are open questions about its ability to invade other organs (e.g. the brain, pancreas, kidney) and the role that retained viral reservoirs may play in persistent COVID-19 symptoms.
Viral Loads and Delta Variant
Vaccinated individuals who have breakthrough cases (predominantly due to the delta variant in this study) are less likely to have culture-positive virus.
Shamier, M. C. et al. Virological characteristics of SARS-CoV-2 vaccine breakthrough infections in health care workers. medRxiv 2021.08.20.21262158 (2021) doi:10.1101/2021.08.20.21262158.
Parks repeated the persistently misunderstood claim that viral loads are equal between vaccinated and unvaccinated individuals. This has not been demonstrated, and in fact there is considerable evidence to the contrary. Parks is conflating qPCR Ct values with viral load, which is inappropriate. Ct values are a metric with PCR that reflect how much DNA there is in the sample you run the reaction on (which is itself a proxy for how much viral RNA there is in people’s noses). The issue is that viral RNA does not equate to replication competent virus. In particular, coronaviruses make large quantities of subgenomic RNA, and depending on what the primers used for the PCR are set to (often it is the N gene, which comprises the bulk of subgenomic RNA), the reaction may detect RNA not associated with intact virus that lowers the Ct value, suggesting a higher viral load. Different variants produce different quantities of subgenomic RNA, and thus Ct value alone cannot be used to make comparisons of viral load. Formally, this requires a viral titration, but this is subject to certain challenges. Specifically, working with SARS-CoV-2 requires a Biosafety Level 3 facility, which is not widely available- hence the need for pseudovirus assays as these can be performed at lower biosafety levels. Regardless, this is easy enough to rebut with two studies. Firstly, vaccinated cases who experience breakthrough infections with the delta variant demonstrate a lower likelihood of having positive virus cultures. Notably, this is still not a viral titration, which would be valuable information regarding the relative infectiousness of those cases which do have positive virus and which do not. Additionally, it is noted that patients who experience breakthrough infections with the delta variant have much more rapid clearance of the virus (meaning less opportunity to transmit); though this is noted through longitudinal PCR testing and not directly viral load, there is no clear process to me by which one could selectively diminish the RNAs without affecting viral load and further these cases are matched with naive controls who also had the same variant (delta). While it is possible for post-vaccine infections to transmit, it is a priori less likely for those infections to occur and even when they do they will not be infectious for as long and they may not even have enough virus in their nose to produce new productive infections. However, given the substantial spread of the delta variant, the heterogeneity in vaccine uptake throughout the US (i.e. large pockets of unvaccinated), and the still nontrivial number of positive viral cultures among vaccinated individuals, nonpharmaceutical interventions are needed to control COVID-19 in addition to vaccination.
Barnstable County Outbreak
Parks claims the Barnstable County Outbreak is proof the vaccines are ineffective in curbing transmission. I discussed the Barnstable County outbreak before:
Stock then brings up the Barnstable County outbreak and he gets applauded for some stupid reason, again ignoring context and misrepresenting data. We have no idea what the denominator for the outbreak described here was (i.e. how many people were exposed to the virus). There is no way to make a conclusion about vaccine effectiveness from that study, despite him trying to imply it shows the vaccine doesn’t work. Here’s a thought experiment for you to understand why this isn’t useful. Suppose I take 100 fully vaccinated people and put them in a room where I introduce aerosolized measles virus. We might expect a few of them to get sick because vaccines aren’t 100% effective (2 doses of MMR-II are 97-99% effective against measles). 100% of the cases will be in people who were fully vaccinated. Does that mean the vaccines don’t work? Secular trends in the incidence of measles would suggest otherwise. See this excellent animation by Dr. Kristen Panthagani in this post from Dr. Jeremy Faust’s Inside Medicine Bulletin showing how breakthrough cases and disease prevalence change with vaccination rates. Provincetown has a 95% vaccination rate. If 74% of the cases were in vaccinated people, that gives vaccines (and this is across all 3 available in the US) 84% effectiveness (assuming everyone in Provincetown had equal likelihood of exposure) against symptomatic COVID-19 under conditions that would really stress test them. In short, this case series does not impugn the effectiveness of vaccines for COVID-19 and anyone claiming that it does either doesn’t understand how vaccine effectiveness works or has an agenda.
ADE/VAERD
There is no evidence that vaccinated individuals experience more severe COVID-19 either due to the delta variant or any other variant as a result of being vaccinated. It is still overwhelmingly unvaccinated individuals that experience the burden of severe disease in the US. I have discussed ADE specifically here. San Diego County for example has released a recent report on the burden of SARS-CoV-2 infections and how it splits among vaccinated vs. unvaccinated here. The unvaccinated are 4 times more likely to have a case of COVID-19, and 86 times more likely to be hospitalized due to COVID-19 than fully vaccinated people.
Variants and Immunity
Parks also claims that variants are so distinct from each other they are essentially different viruses. This is untrue. The ICTV has not even delineated different variants as being discrete strains, indicating a true difference in their properties. While antibody responses to the vaccines may vary some with different variants (although even then, the effect isn’t particularly large), T cell responses remain largely invariant (pun not intended). In fact, even boosting vaccine recipients with the same vaccine for dose 3 shows substantial improvements in neutralization of variants of concern (Pfizer, Moderna).
Who is hesitant to take vaccines?
Parks makes a curious claim that PhDs and those with the highest level of education are the most hesitant to take these vaccines. This is a puzzling claim and I could not find evidence for it- rather I found the opposite. The Kaiser Family Foundation found that those with less education were less likely to be willing to be vaccinated, though it does not have a statistical bin for PhD education. Also worth noting that an extreme supramajority of physicians are vaccinated against COVID-19. Regardless, this claim is irrelevant to the merits of whether or not vaccination is safe and effective.
Tuskegee Syphilis Study
While the history of the Tuskegee Syphilis Study is extremely important, it is completely irrelevant to the discussion here. The Tuskegee Syphilis Study represents the archetype of an unethical clinical study and in bioethics courses is frequently taught as such (in fact when I took bioethics I was given a set of principles that defined whether or not a clinical trial was ethically appropriate and asked to systematically demonstrate that the Tuskegee Syphilis Study failed all of them). It in fact resulted in tremendous changes to the bioethics of clinical trial, leading to publications like the Belmont report, which defined 3 key principles for studies being ethical (respect for persons, beneficence, and justice) among numerous other changes. The CDC even has a page explaining in detail why the study was unethical. One pervasive myth that is important for historical accuracy however is that the trial participants were infected with T. pallidum (the bacteria that causes syphilis) for the study- they were not. They were, however, denied treatment for it.
There is no question that this study and many others like it have resulted in a legacy of justified distrust among BIPOC individuals as they have undeniably been wronged at the hands of the medical system. Dr. Kimberly Manning has written eloquently about her decision to enroll in a vaccine trial despite being a Black woman physician intimately familiar with the legacy of abuse here. She notes quite critically that she had the option of leaving the trial any time she chose. Furthermore, as part of Operation Warp Speed, efforts were taken to recruit a representative sample of trial participants, including BIPOC individuals, such that there would be similar proportions of them in the study as in the general population. The trial composition is given in the briefing documents linked above, which approximates that of the US (note that the trials were conducted across multiple sites in multiple countries and thus cannot be perfectly representative of the US’s composition). It cannot be ignored that the risk to BIPOC individuals from COVID-19 is disproportionate owing to syndemic vulnerabilities they experience. I wrote the following before:
COVID-19 has massively exploited structural racism in our society to spread. COVID-19 disproportionately affects people of color, and many explanations have been proposed to explain this, most of which are sociological in nature rather than biological. People of color are more likely to be essential workers and thus more likely to be exposed (an inoculum size effect may contribute to their heightened disease severity). They are also more likely to be un- or under-insured. People of color also bear a disproportionate burden of many of the risk factors for severe COVID-19, including diabetes, heart disease, obesity, renal disease, and liver disease. Curiously, mortality from influenza and pneumonia for the elderly are lower among African American and Latino individuals compared with people of white background.
Thus weaponizing lies about the COVID-19 vaccines to discourage vaccination is especially unconscionable as it could save the life of the vaccinated person, especially if they are high risk.
MMR Vaccine and Autism
No anti-vaccine rant would be complete without a false claim about MMR vaccines causing autism, which as a cherry on top, Parks claims has been covered up. The Logic Of Science has done an absolutely marvelous post on the matter generally, so I refer you there for details. There is perhaps nothing more exhaustively disproved in the history of science than the idea that vaccines cause autism. Specifically, Parks references a study wherein it was initially found that receipt of the MMR vaccine in Black boys was associated with autism spectrum disorder. Brian Hooker subsequently tried to publish a study making this claim (of note, he has no expertise in epidemiology) which was summarily retracted. In reality, this was a case of reverse causation. The black boys in question who could present for vaccination were more likely to receive a diagnosis of autism because a qualified pediatric provider was there to give it. Those who could not access the pediatric care didn’t get vaccinated, and thus didn’t get a diagnosis of autism. Vincent Ianelli discusses the ridiculous idea that the evidence for vaccines causing autism has been covered up in this Vaxopedia article and Left Brain Right Brain has an article dealing specifically with the claims about black boys here.
