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Rachel Hotez was born in the early 1990s. Peter Hotez was on the faculty at Yale, developing a vaccine for hookworm. Ann Hotez had two older children already. Rachel, the third of what would become four, is described in the book as an easy baby, “content to sit in her car seat, in the dining room or another quiet place and read.”¹ Her first year was, in her mother’s words, unremarkable. She sat unsupported later than her siblings, at nine months rather than six, but her parents attributed the delay to individual variation. “Children do not all learn and grow in the same ways, or at the same speed,” Ann later wrote.¹

By eighteen months, Rachel was not walking. She was not talking. Her pediatrician, Simone Simon, raised the concern. Ann Hotez writes that she and Peter had not seen it: “How could it be that Peter, a pediatrician himself, and I, an experienced mother, hadn’t noticed? I think we had seen differences, but we attributed them to what we knew, or thought we knew, about child development.”¹

The referral was to the Birth-to-Three intervention team at the Darcey School. Rachel was starting to talk by twenty months. By twenty-nine months she was functioning at the eighteen-month level in most areas. At Yale in the spring of 1995, she was diagnosed by Dr. Wendy S. Levine with pervasive developmental disorder, not otherwise specified. She was three years old.

Between eighteen and twenty-four months, Rachel had lost the trajectory she was on. Her father’s book identifies this window precisely, as a matter of clinical description, and returns to it as the central subject of his Chapter 9.

The timeline that contradicts itself

Chapter 9 of Hotez’s book is titled “What Does Cause Autism? The Scientific Evidence.” It is the book’s central scientific move. Hotez cites a series of brain imaging studies, most prominently a 2017 paper from Joseph Piven’s group at the University of North Carolina–Chapel Hill.² Piven’s team scanned the brains of infants whose siblings already had autism, and who were therefore considered at higher risk, at multiple points during infancy. They found measurable changes in the brains of children later diagnosed as early as six to twelve months of age. Specifically, the outer layer of the brain, the cortex, expanded faster than normal between six and twelve months, and the brain as a whole grew larger than expected between twelve and twenty-four months. The larger brain size coincides with the age at which most parents first recognize the condition.

Hotez presents this as decisive. If measurable brain changes are present at six months of age, he argues, then the vaccines given at twelve and eighteen months cannot have caused those changes. He writes: “The changes in the brains of kids with ASD are set into motion well before (about a year) many parents recognize any signs of alterations in communication or social behavior.”¹

The argument depends on what a reader does not know, or does not pause to consider.

The current injection schedule for an American newborn begins within hours of birth, with the compound marketed as vitamin K. That injection is not formally part of the vaccine schedule but is administered nearly universally. The formal vaccine schedule begins on the same day, with hepatitis B. It resumes at two months, with DTaP, Hib, pneumococcal conjugate, inactivated polio, rotavirus, and a second hepatitis B dose. At four months, most of the same combination is repeated. At six months, most of it is repeated again, along with the first influenza dose. By six months of age, a child has received approximately twenty vaccine doses, several of which contain aluminum adjuvant. The cumulative aluminum burden by six months of age has been estimated at approximately 4.4 milligrams,³ a figure Hotez himself cites in Chapter 8 while comparing it favorably to dietary aluminum in infant formula.¹

The comparison is where the omission is starkest. When aluminum is eaten in food, less than one percent is absorbed into the body. When aluminum is injected as part of a vaccine, it is designed to stay. The compound is added to vaccines because it holds at the injection site and provokes the inflammatory response that makes the vaccine work. French research groups have documented that aluminum-loaded white blood cells remain at injection sites for years,⁴ and that these particles are then carried through the lymphatic system to distant tissues, including the brain.⁵ Aluminum has been recovered from brain tissue of autism decedents at concentrations substantially higher than in age-matched controls.⁶ Christopher Shaw and Lucija Tomljenovic have documented dose-response relationships between pediatric aluminum burden and autism prevalence across multiple countries.⁷ None of this literature appears in Hotez’s book. Aluminum adjuvant is addressed in a single dismissive paragraph in Chapter 8, primarily by reference to the Children’s Hospital of Philadelphia comparison to formula.¹

The Piven timeline does not exonerate the vaccine schedule. It identifies the window in which vaccine-induced injury would produce measurable effects. Whatever is producing the cortical expansion Piven documented at six to twelve months of age is happening after the birth-through-six-month injection schedule, not before it. Hotez names the window. He does not name the exposures inside it.

Rachel’s regression was observed at eighteen months. She had received the standard childhood schedule available at the time. What Piven’s MRI cannot see, because his study was not conducted until decades later, is what Rachel’s brain looked like at six months, or at twelve months. What is preserved in the record is Ann Hotez’s testimony that she had bonded less to Rachel than to her older children, that Rachel was “quiet” and “content,” that Rachel’s motor milestones were behind but her attention span seemed strong. What is also preserved is Peter Hotez’s own observation that Rachel cried longer and more intensely at the needle than her siblings did.

What happens in the window

Piven’s timeline identifies when brain changes become measurable. It does not identify what causes them. Hotez’s book, having named the timeline, moves on. The question of what happens in the birth-through-six-month window remains open. Answering it requires setting the book aside.

Aluminum hydroxide and aluminum phosphate are added to vaccines because they persist. The industry term for a compound added to a vaccine to intensify the body’s response is adjuvant. Aluminum functions as an adjuvant because it resists clearance. The body’s repair processes engage the compound and cannot dispatch it. The resulting sustained inflammation is what the industry calls efficacy.

The design depends on a biological assumption medicine does not defend openly. It assumes that the body will confine its response to the injection site. It will not.

Beginning in 1998, Romain Gherardi and colleagues at the French National Institute of Health and Medical Research described a condition in adults who had received aluminum-adjuvanted vaccines. Muscle biopsies at the injection sites showed distinctive lesions: aggregates of white blood cells called macrophages, filled with aluminum hydroxide. The lesions were present years after the injection. Aluminum, in other words, did not clear. It remained at the site, engulfed by cells that could not digest it.⁴

Fifteen years later, Zakir Khan and Gherardi’s group published a follow-up study. Using fluorescent aluminum hydroxide particles injected into the muscle of mice, they demonstrated that the particles were carried away from the site by macrophages, drained through the lymphatic system, and arrived in distant tissues, including the brain, over weeks and months. The transport depended on a specific signaling molecule, CCL2, that summons macrophages to sites of inflammation. Blocking CCL2 stopped the process. Restoring CCL2 restored it.⁵

Aluminum is injected. It provokes the inflammation it was designed to provoke. White blood cells arrive to engulf it. They cannot digest it. They carry it, embedded within themselves, through the lymphatic system to wherever the body is calling for their services. In an infant whose blood-brain barrier is still developing, they carry it into the brain.

Christopher Exley’s group at Keele University has recovered aluminum from brain tissue samples of people who died with autism, at concentrations substantially higher than in age-matched controls without autism.⁶ Christopher Shaw and Lucija Tomljenovic at the University of British Columbia have documented dose-response relationships across countries: as the pediatric aluminum injection burden has risen, so has autism prevalence.⁷ The correlations do not prove causation. They form the kind of convergent signal the studies Hotez cites in Chapter 8 would have been designed to test, if the field had been oriented toward asking the question.

In 1913, Charles Richet was awarded the Nobel Prize in Physiology or Medicine for his description of anaphylaxis. What Richet actually demonstrated, in a series of experiments on dogs beginning in 1901, was that injecting a foreign protein into an animal produced a heightened response to any subsequent exposure to the same protein. The first injection sensitized. The second could kill. Richet named the process anaphylaxis, from the Greek for “without protection.”¹⁹ His finding, that the injection route sensitizes the body against future encounters with the same substance, is Nobel-documented history.

Every childhood vaccine contains foreign proteins injected in the presence of aluminum designed to hold. The Richet mechanism is not disputed. It is simply not applied to childhood vaccination in the mainstream literature, because to apply it would be to concede what the industry is designed to deny.

The reader does not need to accept every step of this reasoning to hold the essay’s central point. Aluminum accumulates. It travels. It has been recovered from the brains of people who died with autism. The mechanism that would produce sensitization from injected foreign proteins won a Nobel Prize. None of this appears in the book Hotez wrote to close the question.

Rachel’s regression window opened at eighteen months, months after the aluminum-containing doses at two, four, and six months would have completed the biopersistence and transport described above. What her brain looked like at six months of age is not preserved in the record. Neither is her cerebrospinal fluid aluminum concentration at any age. Neither is any measurement that would let a family ask, decades later, whether their daughter’s condition was set in motion by exposures her father’s book does not consider possible.

The years of intervention

By age five, Rachel had a formal IQ evaluation. Her verbal IQ was 84, near the low end of normal. Her performance IQ was 60. Later testing put her performance IQ in the 40s.¹ She was placed on Prozac, then Zoloft, then Luvox, then Risperdal. Each medication, in Hotez’s account, produced worse effects than the last. She was eventually taken off all psychiatric medication.

Rachel had two psychiatric admissions at Yale-New Haven’s Winchester 1 inpatient unit. An EEG revealed right-sided temporal lobe spike discharges. She was placed on tegretol for a period, with what Hotez describes as “possibly some improvement.”¹ The tegretol was eventually discontinued because Rachel would not comply with the blood draws needed for level monitoring. The Hotez family lived through years that Peter describes with candor: “dreary or frightening,” “wearing us down,” “she seldom gave much back emotionally, compared with the other children.”¹

The family relocated to Houston in 2011, where Peter had accepted a position at Baylor College of Medicine. Rachel finished her secondary education at Lamar High School with a certificate. She could not sustain the transition program at Houston Community College. Two brief residential placements failed. She lived, and continues to live, at home with her parents.

By 2016, Hotez had begun writing what he calls “science tikkun” pieces for PLOS. In early 2017 he published an op-ed in the New York Times titled “How the Anti-Vaxxers Are Winning.”⁸ The book followed in 2018.

The name that does not appear

Hotez names his opponents. Andrew Wakefield, characterized as an “elaborate fraud” quoting Brian Deer’s BMJ series. Robert F. Kennedy Jr., named in connection with campaigning around thimerosal and working with the parent group Safe Minds. The film Vaxxed, called “phony.” Hotez identifies a “toxic combination of hysteria and pseudoscience,” “phony propaganda,” “fake news, half-truths, and conspiracy theories.”¹

He does not name William Thompson.

William Thompson is a senior scientist at the U.S. Centers for Disease Control and Prevention. In August 2014, through his attorneys at Morgan Verkamp LLC, Thompson issued a public statement about a 2004 study he had co-authored in the journal Pediatrics.⁹ The study, DeStefano et al., examined children in the Atlanta area, comparing when they received the MMR vaccine to whether they later developed autism. It concluded there was no link.¹⁰ Thompson’s 2014 statement was direct:

I regret that my coauthors and I omitted statistically significant information in our 2004 article published in the journal Pediatrics. The omitted data suggested that African American males who received the MMR vaccine before age 36 months were at increased risk for autism. Decisions were made regarding which findings to report after the data were collected, and I believe that the final study protocol was not followed.⁹

Thompson provided documents to Congressman Bill Posey. On July 29, 2015, Posey read Thompson’s statement into the Congressional Record on the floor of the U.S. House of Representatives.¹¹ Thompson has never recanted the statement. He remains employed at the CDC. His full statement, released through his attorneys at Morgan Verkamp LLC, is archived among the Vermont Legislature’s official witness testimony documents from its 2015 hearings on vaccine policy.⁹

Vaxxed, the film Hotez dismisses in his book as “phony,” is a documentary built around Thompson’s disclosure. It contains recordings of Thompson’s conversations with the biologist Brian Hooker. Hotez’s characterization of the film appears in a book that never names its subject.

The DeStefano 2004 study Thompson repudiated is one of the studies Hotez cites in Chapter 8. It appears in the list of investigations that, in his summary, demonstrate no link between MMR and autism.¹ The reader is not told that a senior author of one of those investigations has publicly stated that statistically significant findings were omitted.

The pattern extends beyond Thompson. Hotez’s Chapter 10, titled “Struck by Lightning,” offers his central injury statistic: approximately one severe adverse event per one million vaccine doses. He derives the figure by dividing roughly 300 annual compensated claims from the National Vaccine Injury Compensation Program by roughly 300 million annual doses.¹ The comparison to being struck by lightning is presented as authoritative.

The math depends on the pieces used. Hotez’s numerator is the number of NVICP claims that were compensated. NVICP dismisses more claims than it pays. Claims must be filed within three years of the injury appearing. Causation must be proven to a narrow list of conditions the program formally recognizes. Conditions that appear months or years later are not included. The denominator, 300 million doses, is total administered doses. The Vaccine Adverse Event Reporting System, VAERS, is meant to be the surveillance instrument that catches adverse events at the population level. In 2011, a study conducted by Harvard-Pilgrim Health Care under a grant from the Agency for Healthcare Research and Quality, principal investigator Ross Lazarus, was submitted to the federal government. Its finding on VAERS capture rate was that “fewer than 1% of vaccine adverse events are reported.”¹²

Hotez does not mention the Lazarus report. The underreporting problem does not appear in his book. His lightning comparison depends on the Lazarus figure being wrong by a factor of a hundred, and that dependence is not addressed. A correction of two orders of magnitude would move his rate from one per million to one per ten thousand. At the CDC’s own current estimate of 1 in 36 children diagnosed with autism,¹³ the question of what a serious adverse event actually is, and how it is counted, is the question the book was written to close.

Hotez closes it by not opening it.

The perpetual gene

In 2017, Peter and Ann Hotez arranged with the Baylor Department of Genetics to sequence their own DNA and Rachel’s. Whole exome sequencing produces the sequences of the protein-coding regions of the genome. The stated purpose was to identify any variants that might be linked to autism or intellectual disability.

Hotez describes the result with unusual restraint. Rachel had “some genetic variants, including one affecting a gene that could be linked to ASD or mental disabilities.”¹ He writes that the family plans to submit her results to the Baylor Johns Hopkins Center for Mendelian Genetics and to the NIH-supported Undiagnosed Diseases Network, “in order to determine if Rachel’s genetic variants might also be present in other individuals on the autism spectrum or with other mental health conditions.”¹

The sentence is worth reading twice. The whole exome sequencing did not identify a cause of Rachel’s condition. It identified variants of uncertain significance that Hotez hopes might one day be shown to be relevant.

This is the outcome the book has been building toward. Chapter 9 promises that autism is genetic. Hotez cites work from the Simons Foundation and Princeton estimating that as many as one thousand genes may eventually be identified as contributing to autism.¹⁴ At the time of the book’s publication, sixty-five had been identified. The remaining nine hundred and thirty-five are described as awaiting discovery.

The reader is asked to accept a paradigm that has produced sixty-five candidate genes across three decades of intensive investigation, and to expect that the next three decades will produce the remaining nine hundred and thirty-five. The larger project has similar dynamics. The Human Genome Project promised to identify the genetic basis of common disease, and produced approximately twenty thousand genes rather than the one hundred thousand originally predicted. Its subsequent genome-wide association studies for autism have identified small-effect variants that account for a modest fraction of the heritability those studies were designed to explain. The gene has been coming for thirty years.

Meanwhile the environmental candidates Hotez does name in Chapter 9 are curated. He cites Phillip Landrigan’s 2010 review identifying prenatal exposures associated with autism-like presentations: valproic acid, thalidomide, misoprostol, chlorpyrifos.¹⁵ He cites maternal rubella exposure during pregnancy as a cause of congenital rubella syndrome, which he says “can closely resemble autism.”¹ From this he draws a conclusion that returns the reader to the book’s title with a strange inversion: “The ‘R’ component of the MMR vaccine is actually the rubella vaccine that protects a mother from transmitting rubella virus to her baby, and in so doing functions as an effective vaccine against autism.”¹

The MMR vaccine, according to Hotez, prevents autism. This appears in a book titled Vaccines Did Not Cause Rachel’s Autism.

He raises maternal fever and points to Ian Lipkin’s Columbia group work on maternal viral exposures.¹⁶ He notes a 2017 Kaiser Permanente study that found a 1.2 odds ratio for autism among children whose mothers received influenza vaccine in the first trimester.¹⁷ He dismisses the finding as “not statistically significant after adjusting for multiple comparisons.” An odds ratio of 1.2 in a study of nearly two hundred thousand children is not a finding a scientist would dismiss if he were looking for the cause. It is a finding a scientist would dismiss if he had already located the cause elsewhere.

Aluminum adjuvant does not appear in Chapter 9. In a chapter titled “What Does Cause Autism,” the compound most commonly injected into infants under six months of age, one with documented biopersistence, translocation, and central nervous system deposition, is not discussed as a candidate.

Nor does the chapter engage the growing literature comparing vaccinated to unvaccinated cohorts. Anthony Mawson’s 2017 pilot study of homeschooled U.S. children reported that the vaccinated group had substantially higher rates of neurodevelopmental disorders, allergies, and chronic conditions than the unvaccinated group.¹⁸ Studies of this design remain the most direct empirical test of the question Hotez’s book is written to close. None appear in his citations. The one study design that could definitively answer the question, he dismisses in a single line elsewhere in the book: a randomized trial of vaccinated versus unvaccinated children would, he writes, be “unethical.”¹

The book’s opening dedication lists the funding sources for Hotez’s Center for Vaccine Development at Texas Children’s Hospital. Among them: the Bill & Melinda Gates Foundation. The Carlos Slim Foundation. Gavi, the Vaccine Alliance. UNICEF. The World Health Organization. The Kleberg Foundation. The Blavatnik Charitable Foundation. The Brockman Medical Research Foundation. The Japanese Global Health Innovative Technology Fund. The Southwest Electronic Energy Medical Research Institute. The National Institutes of Health. The Centers for Disease Control and Prevention. The Walter Reed Army Institute of Research. The United States Public Health Service. Baylor College of Medicine. Texas Children’s Hospital.¹

Hotez addresses this preemptively in Chapter 8. He notes that he holds patents on his vaccines but has “not received a penny” and has “no real prospects for financial gain.”¹ The disclaimer is technically accurate. It is also beside the point. Institutional capture does not require kickbacks. It requires career. A scientist whose salary, laboratory, institutional affiliation, and public standing all depend on the paradigm the book defends is not neutral, whether or not he personally profits from any particular product.

Rachel at twenty-five

At the end of the book, Rachel is twenty-five. She lives with her parents in Montrose, Houston. Her routine is fixed. She wakes at four in the morning to Skype her friend Sabrina in Denver. Her morning walk takes her to Randall’s supermarket for a plain bagel, no butter. Later she walks to Subway for a six-inch tuna sandwich, no cheese, mustard on hearty Italian. Along the way she talks to shopkeepers, asks strangers about their dogs, and occasionally brings home men she meets on the street, whom her father has to ask to leave.

She has, at the time of the book’s writing, just been enrolled in a Goodwill training program. A chance airport encounter between her parents and the wife of the Goodwill Houston board chairman produced the introduction. Rachel sorts donated clothes for stains and rips. She works two hours a day. After taxes, Ann Hotez writes, “it is about $14 a day and $215 so far.”¹

This is what the book’s title is defending. A young woman with a performance IQ in the 40s who cannot count money, cannot sustain a classroom, cannot hold employment for more than two hours per day, and lives with her aging parents in a neighborhood where they worry, in the book’s own words, about her safety at night. Hotez writes with clear love for his daughter. He describes Rachel as loyal to her friends, curious about people, empathetic toward animals, quick to strike up conversation in the neighborhood. She is all of these things. She is also a young woman whose life was, at some point, altered.

Her father spent two hundred pages arguing that the alteration cannot be attributed to what he did for a living. The William Thompson statement of August 2014 is not addressed. The aluminum burden accumulated during the first six months of life is not examined as a candidate cause. The injury statistic in Chapter 10 depends on assuming that VAERS captures nearly all vaccine-related injuries, an assumption the Harvard-Pilgrim report says is wrong by a factor of a hundred. The alternative causation runs through a genetic paradigm that has produced sixty-five candidate genes in thirty years and promises another nine hundred and thirty-five to come. On one page inside a book denying vaccine-autism links, the MMR vaccine is inverted into an anti-autism intervention.

The book was written to close the question. What it does instead is document, in loving and exhaustive detail, the life of the girl whose story the question was always about. Rachel cried at the injections longer and more intensely than her siblings did. Between eighteen and twenty-four months, she lost skills. Her EEG showed spike discharges. Her intellectual disability is profound. She sorts clothes at Goodwill.

The door her father wrote his book to close is still open. He walked past it in every description of his own daughter.

References

1. Hotez PJ. Vaccines Did Not Cause Rachel’s Autism: My Journey as a Vaccine Scientist, Pediatrician, and Autism Dad. Baltimore: Johns Hopkins University Press; 2018.
2. Hazlett HC, Gu H, Munsell BC, Kim SH, Styner M, Wolff JJ, et al. Early brain development in infants at high risk for autism spectrum disorder. Nature. 2017;542(7641):348–351.
3. Offit PA, Jew RK. Addressing parents’ concerns: do vaccines contain harmful preservatives, adjuvants, additives, or residuals? Pediatrics. 2003;112(6 Pt 1):1394–1397.
4. Gherardi RK, Coquet M, Cherin P, Belec L, Moretto P, Dreyfus PA, et al. Macrophagic myofasciitis lesions assess long-term persistence of vaccine-derived aluminium hydroxide in muscle. Brain. 2001;124(Pt 9):1821–1831.
5. Khan Z, Combadière C, Authier FJ, Itier V, Lux F, Exley C, et al. Slow CCL2-dependent translocation of biopersistent particles from muscle to brain. BMC Med. 2013;11:99.
6. Mold M, Umar D, King A, Exley C. Aluminium in brain tissue in autism. J Trace Elem Med Biol. 2018;46:76–82.
7. Tomljenovic L, Shaw CA. Do aluminum vaccine adjuvants contribute to the rising prevalence of autism? J Inorg Biochem. 2011;105(11):1489–1499.
8. Hotez PJ. How the anti-vaxxers are winning. New York Times. February 8, 2017.
9. Thompson WW. Statement of William W. Thompson, Ph.D., regarding the 2004 article examining the possibility of a relationship between MMR vaccine and autism. Released through Morgan Verkamp LLC; August 27, 2014. Archived by the Vermont Legislature, H.98 witness testimony, May 6, 2015. Available at: https://legislature.vermont.gov/Documents/2016/WorkGroups/House%20Health%20Care/Bills/H.98/Witness%20Testimony/H.98~Jennifer%20Stella~William%20Thompson%20Statement~5-6-2015.pdf
10. DeStefano F, Bhasin TK, Thompson WW, Yeargin-Allsopp M, Boyle C. Age at first measles-mumps-rubella vaccination in children with autism and school-matched control subjects: a population-based study in metropolitan Atlanta. Pediatrics. 2004;113(2):259–266.
11. Posey B. Remarks on the William Thompson statement. Congressional Record. July 29, 2015;161(120).
12. Lazarus R, Klompas M, Bernstein S, et al. Electronic Support for Public Health–Vaccine Adverse Event Reporting System (ESP:VAERS). AHRQ Grant Final Report, Grant No. R18 HS 017045; 2011.
13. Maenner MJ, Warren Z, Williams AR, Amoakohene E, Bakian AV, Bilder DA, et al. Prevalence and characteristics of autism spectrum disorder among children aged 8 years — Autism and Developmental Disabilities Monitoring Network, 11 sites, United States, 2020. MMWR Surveill Summ. 2023;72(2):1–14.
14. Krishnan A, Zhang R, Yao V, Theesfeld CL, Wong AK, Tadych A, et al. Genome-wide prediction and functional characterization of the genetic basis of autism spectrum disorder. Nat Neurosci. 2016;19(11):1454–1462.
15. Landrigan PJ. What causes autism? Exploring the environmental contribution. Curr Opin Pediatr. 2010;22(2):219–225.
16. Mahic M, Mjaaland S, Bøvelstad HM, Gunnes N, Susser E, Bresnahan M, et al. Maternal immunoreactivity to herpes simplex virus 2 and risk of autism spectrum disorder in male offspring. mSphere. 2017;2(1):e00016-17.
17. Zerbo O, Qian Y, Yoshida C, Fireman BH, Klein NP, Croen LA. Association between influenza infection and vaccination during pregnancy and risk of autism spectrum disorder. JAMA Pediatr. 2017;171(1):e163609.
18. Mawson AR, Ray BD, Bhuiyan AR, Jacob B. Pilot comparative study on the health of vaccinated and unvaccinated 6- to 12-year-old U.S. children. J Transl Sci. 2017;3(3):1–12.
19. Richet C. Anaphylaxis. Nobel Lecture, December 11, 1913. Nobel Media AB. Available at: nobelprize.org.