Federal Letter
Letter to My Federal Reps
I am a Wisconsin constituent and founder of Kimberly’s Educational Resources. I am an educator and neurodivergence advocate who collaborates with researchers on neurodevelopment and systems biochemistry.
Key Takeaways
Research integrity failures in autism science are influencing federal policy. Independent researchers identifying these issues are being excluded and their methods appropriated by academic institutions.
Princeton University’s 2025 Nature Genetics study on autism subtypes closely mirrors my 2022-24 publicly documented Jigsaw Puzzle Research Methodology. Their preprint referenced hypothesis testing using bioinformatics tools that were later removed before publication. Princeton’s Dean of Faculty is now reviewing this for misconduct.
The Henry Ford Health (HAP) vaccine study misrepresents correlation as causation. It relies on employer-based insurance data that ends when coverage lapses, only considers Michigan vaccination records, and creates false “unvaccinated” categories and misleading conclusions.
The UAMS folinic acid trial was published despite an FDA Full Clinical Hold for investigator non-compliance. Authors held patents on the assay used, creating conflicts of interest. Reported effect sizes were minimal but overstated in media coverage and later cited by policymakers.
Nonverbal autism remains physiologically untested. No standardized medical exam has ever assessed cranial, facial, or vocal nerve function in nonspeaking individuals. This is a diagnostic gap comparable to neglecting hearing tests in deafness. Functional nerve testing must be federally prioritized.
My biochemical model, The Autism and the Comorbidities Theory, maps autism to a BH4-centered redox-sensitive mechanism disrupting excitatory/inhibitory neural balance. Comorbidities arise from parallel stress-response shunts across five “BioToggles”: immune, metabolic, cellular repair, nervous, and genetic regulation.
Vaccine injuries are not autism they’re a comorbidity. They are rare comorbidities affecting genetically susceptible individuals, specifically those with mutations such as metallothoneins. Precision screening protocols are needed to identify risk and ensure appropriate in-office treatment.
Requested actions:
1. Strengthen federal research integrity oversight and prohibit publication while FDA holds remain unresolved.
2. Fund functional nerve testing and treatment protocols for nonspeaking individuals.
3. Advance precision-based genetic screening to identify true risk factors.
4. Enforce protection and attribution rights for independent researchers whose methods are adopted without citation.
Letter:
I am writing to raise urgent concerns about research integrity failures in autism science that are actively shaping public health policy, and about how independent researchers who identify these problems are being systematically excluded and appropriated by academic institutions.
PART I: Academic Appropriation of Independent Research
In November 2022, following significant public interest in my previously nonverbal autistic daughter’s progress using neuroscience-based interventions, I publicly introduced what I termed the “Jigsaw Puzzle Research Methodology” for autism research. This approach, documented via TikTok, ResearchGate, and my published books, is grounded in the Exclusivity Principle: given that over 95% of autistic individuals have comorbidities, autism and its comorbidities must share underlying physiological mechanisms rather than occurring coincidentally.
The methodology involves:
1. Breaking autism and comorbidity traits into their constituent gene-coded proteins
2. Identifying biochemical convergence points where proteins regulate multiple pathways simultaneously
3. Clustering individuals into phenotypes based on these shared mechanisms
4. Linking phenotypic clusters to causal biology rather than behavioral observation alone
I documented this framework publicly throughout 2023, with timestamped records available at:
Kimberlyedu.org
Social media - TikTok (94.6K) Instagram (140K)
ResearchGate.net/profile/Kimberly-Kitzerow (136,738+ reads)
In July 2025, Princeton University researchers published a study in Nature Genetics identifying autism subtypes. Lead author Natalie Sauerwald described their approach using nearly identical language: “It was like trying to solve a jigsaw puzzle without realizing we were actually looking at multiple different puzzles mixed together.”
Their methodology mirrors mine: separate individuals into subtypes based on trait clustering, then link clusters to distinct genetic and biological pathways.
Most significantly: Princeton’s preprint version (medRxiv, August 2024) included references to testing specific hypotheses using bioinformatics tools including ShinyGO. This acknowledgment was removed from the published Nature Genetics version.I utilized a functional biochemical network, while they used post hoc logic and statistical analysis. A peer reviewer even acknowledged the post hoc logic.
Princeton’s Dean of Faculty is currently investigating this matter for potential academic misconduct.
This is not merely about attribution. It demonstrates a systemic problem: when independent researchers identify methodological innovations that later appear in institutional research without citation, it undermines scientific integrity and discourages precisely the kind of parent-driven, community-connected research that can advance understanding of complex conditions like autism.
PART II: The HAP Study – Flawed Research Shaping Policy
The Henry Ford Health and Health Alliance Plan (HAP) study is being used to suggest vaccines are linked to chronic illness, but its design is fundamentally flawed:
Data Structure Problems:
- Used employer-based insurance data (HAP) that only tracks families while covered under that specific plan
- When parents change or lose jobs, family coverage ends and data collection stops
- Children who later developed conditions or received vaccines elsewhere became invisible to researchers
- Created false “unvaccinated” vs. “vaccinated” comparisons based on data gaps, not actual vaccination status
Registry Limitations:
- Drew vaccination data from Michigan Care Improvement Registry (MCIR)
- Registry only includes vaccines given in Michigan
- Children vaccinated out-of-state or at non-reporting clinics would be miscategorized as unvaccinated
Surveillance Bias:
- Compared children with regular medical care (more documentation) to those rarely seeing doctors (less documentation)
- Children who see doctors more frequently naturally have more recorded diagnoses
- Those with less medical contact appear healthier simply because less is recorded
Confounding Variables Ignored:
- Family income levels
- Environmental exposures
- Geographic access to healthcare
- Socioeconomic factors strongly associated with health outcomes
The result: Differences attributed to vaccines are actually driven by data gaps, uneven observation periods, and systemic confounders. This is correlation misrepresented as causation, and it is influencing public health conversations. This is dangerous, not due to disruption, but due to the sheer incompetence.
PART III: UAMS Folinic Acid Trial – Publishing Despite FDA Hold
ClinicalTrials.gov (NCT01602016) lists this trial as terminated for investigator non-compliance and placed on Full Clinical Hold by the FDA. Despite this status, results were published.
I personally contacted the University of Arkansas for Medical Sciences (UAMS) to clarify the regulatory status and received email confirmation that issues leading to the FDA hold were not resolved prior to publication.
- Two coauthors are listed as inventors on the folate autoantibody receptor test patent utilized in the study (ID: 7846672)
- Raises serious conflict-of-interest questions about patent-holders evaluating their own assay
- Study reported improvements of 5.7–7.3 points out of possible 150–155 on standardized measures
- Despite minimal effect size, lead author Dr. Frye appeared in CBS news coverage suggesting folinic acid as treatment for nonverbal autism
- Current administration has referenced this study in discussing autism treatments
This represents a failure of research integrity oversight at multiple levels: trial termination, conflict-of-interest management, post-publication accountability, and public communication of effect sizes. The fact that this influenced our national announcement on autism treatment options is extremely concerning.
PART IV: Why This Matters – My Daughter’s Story and the Testing Gap
My daughter was diagnosed with Nonverbal Autism and qualified for Wisconsin’s Children’s Long Term Support Plan (CLTS). This is a program that requires qualification for institutionalization. On her 4th birthday, she was unable to blow out a candle on her birthday cake.
In that moment, I realized: nonverbality is not part of autism itself, it is a physiological comorbidity.
Not being able to blow out a candle revealed a physical impairment affecting motor neuron control, likely impacting her ability to produce speech. This was later supported research documenting facial muscle anomalies in nonverbal autism.
I then learned something shocking: There has never been a standardized functional test to measure nerve and muscle function required for speech production in individuals who cannot speak. The cranial, facial, and vocal nerves controlling fine-tuned coordination of sound into words have never tested. Quite literally. Not once, in either research or clinical settings.
Nonverbal individuals deserve established diagnostic, prognostic, and treatment protocols. Just as those who cannot see or hear do. Currently, parents receive only behavioral support resources to manage emotional responses to what is an unrecognized physical limitation. We are treating trapped cognizance as if it were a behavioral choice.
I have launched a petition to prioritize functional nerve testing for speech production: you can find it here.
After discovering this gap, I developed NeuroToggle®, a neuroplasticity-based instructional framework targeting motor neurons in cranial, facial, and vocal nerves and associated brain pathways. NeuroToggle focuses on restoring functional neural signaling between brain and muscles responsible for speech production by optimizing conditions for neural circuit reorganization. It helped my daughter go from nonverbal and aggressive, to speaking and emotionally regulated. Each behavior and skill is a neural circuit that can be optimized.
I have documented this work in two published books:
- 1st Edition: Why neuroplasticity-based strategies are relevant for neurodivergent learners
- 2nd Edition: How to build, strengthen, time, and expand neural connections through targeted instruction
PART V: My Biochemical Framework – Beyond Behavior to Biology
Autism has long been described through behavior rather than biology. To bridge that gap, I created The Autism and the Comorbidities Theory a biochemical model mapping causal genetic/epigenetic mechanisms that produce autistic traits and comorbidities.
The Exclusivity Principle emerged from observing that over 95% of individuals diagnosed with autism experience one or more comorbid conditions. If this co-occurrence rate is not coincidental, autism and comorbidities must be physiologically linked through shared mechanisms.
Using bioinformatics tools and established autism biomarkers, I:
1. Delineated each physiological protein contributing to both autism traits and comorbid traits
2. Clustered traits by shared proteins regulating multiple bodily systems
3. Identified distinct biochemical cluster regions responsible for groups of traits (“cluster symptom disorders”)
4. Mapped a specific cluster corresponding to DSM-5 diagnostic criteria for autism
5. Mapped surrounding clusters aligning with comorbid traits and medical conditions
Within this framework:
- Autism results from a specific epigenetic redox-sensitive protein shunt (the BH4 Shunt) that upregulates transamination pathways within the cortico-striatal-thalamic loop (CSTL)
- This disrupts excitatory/inhibitory (E/I) balance in neural circuits governing movement, habit formation, and reward processing
- Produces core behavioral and physiological features consistent with DSM-5 criteria
- Comorbidities emerge from additional biochemically simultaneous epigenetic redox-sensitive shunts activated under allostatic (stress-response) conditions
My framework introduces five categorical regulatory systems I call BioToggles:
1. Immune system
1. Metabolism
1. Cellular repair
1. Nervous system
1. Genetic regulation
Each regulatory system operates as a reflex loop: sensor, setpoint, error detector, controller, and effector. Feedback loops between BioToggles maintain physiological balance.
BioToggles can be:
- Situationally flipped under setpoint deviations
- Chronically stuck if setpoint is not restored
- Genetically locked due to mutations creating regulatory system set point deviations or direct dysregulation.
When activated, the stress response and regulatory system epigenetic redox sensitive effectors are prioritized over typical development in predictable ways. This epigenetically regulates which proteins are on and off.
Important clarification on genetics:
Genetic does not mean hereditary. A gene mutation is simply a change in instructions used to make a protein. Because each protein carries out a specific physiological function, faulty instructions produce predictable effects. Genes are 99.9% conserved across humans. Meaning which proteins manage viral clearance, glucose metabolism, or folate processing (MTHFR, DHFR), etc. are identical in everyone, with variation within minimal variation.
This is why precision medicine matters: Because proteins are genetically coded, both beneficial and adverse reactions can be genetically predictable when mapped functionally.
Within this framework, vaccine injuries are not autism. They represent a comorbidity that can occur in genetically vulnerable individuals, such as those with metallothionein variants affecting metal detoxification. These represent a small subset within the broader stress-response model.
The focus should be on:
- Identifying rare genetic risk factors
- Improving screening protocols
- Ensuring emergency in-office treatment (comparable to EpiPens) is available when rare adverse reactions occur
It is harmful to inflate risk through poorly designed studies like the HAP study that mislead the public and distract from precision-based solutions. It is responsible to acknowledge risk, albeit rare, exists. Therefore, a protocol to identify those who are at risk should be established. Along with a treatment plan for these rare adverse events.
Detailed documentation is available at:
- Kimberlyedu.org
- ResearchGate.net/profile/Kimberly-Kitzerow
REQUEST FOR SUPPORT
I respectfully ask for your support in:
1. Stronger Federal Oversight of Autism Research Integrity
- Mandate repercussions for lack of resolution of FDA clinical holds before publication of trial results
- Establish post-publication accountability for research used to inform public health policy
2. Medical Research into Functional Nerve Testing for Nonverbal Individuals
- Fund development of standardized diagnostic protocols for cranial, facial, and vocal nerve function in nonverbal individuals
- Establish therapeutic standards comparable to those for blindness or deafness
- Move beyond purely behavioral definitions to physiological assessment for nonverbality and acknowledge it as its own comorbidity and condition to allocate resources to.
3. Precision-Based Approaches Distinguishing Genetic Vulnerability from Generalized Causation
- Promote research identifying specific genetic risk factors for adverse reactions
- Support development of screening protocols and emergency interventions
- Counter misleading studies that inflate risk without accounting for genetic variability
4. Protection and Attribution Rights for Independent Researchers
- Establish consequences for academic institutions that appropriate methodological frameworks from independent researchers
- Create pathways for independent researchers to receive formal recognition and collaboration opportunities
- Ensure publicly timestamped research receives proper attribution in institutional publications
Autism must be understood through physiology and genetics, not fear or flawed data.
When independent researchers identify critical gaps, like the absence of nerve testing for nonverbal individuals, or develop novel methodologies for understanding complex conditions, that work must be protected and credited, not appropriated.
When studies with fundamental design flaws shape public health conversations, federal oversight must intervene.
When clinical trials terminated for non-compliance are published anyway, accountability must follow.
Thank you for your time and for your continued service to the people of Wisconsin.
All the best,
Kimberly Kitzerow
Founder, Kimberly’s Educational Resources (NeuroToggle® & Neurodivergent Biochemistry™)
Neuroplasticity Educator & Neurodivergence Advocate
Connect with me: