For Neurodivergents
Welcome, Neurodivergents!
This page is for neurodivergent individuals who want a clearer understanding of the frameworks Kimberly Kitzerow built to explain the impact of different categories and durations of stress on development and function over time.
What You Need to Know
These frameworks operate as one integrated system. Together, they explain how stress activation alters development and function over time, how those shifts are categorized, how biological timing is disrupted, how neurodevelopment can be guided in response, and how long term outcomes emerge.
Neurodivergent Biochemistry
Neurodivergent Biochemistry is the broader systems framework. It explains how stress-response activation alters development and function over time across the body.
This includes how regulatory systems shift, how timing is disrupted, and how those state changes affect physiology and neurodevelopment.
Autism and the Comorbidities Theoretical Model
The theoretical model is more specific. It explains how one particular downstream outcome can emerge from those broader biological shifts: autism traits and comorbid traits occurring together from a shared upstream root cause.
In other words, Neurodivergent Biochemistry is the broader explanatory system. The Autism and the Comorbidities Theoretical Model consists of the predictions of that system.
Understanding Autism and Comorbid Traits Through Kitzerow’s Model
This section provides an important overview of Kitzerow’s Autism and the Comorbidities Theoretical Model.
To define the underlying system that produces both autism traits and comorbid traits, rather than treating them as separate categories.
The model was created for her nonverbal autistic daughter after identifying the exclusivity principle: autism and comorbid traits occur together at a rate that requires a shared root cause.
The mechanisms that make up the model have been independently supported across research. ( mechanism validation ) The full system has not yet been tested as a complete model.
Autism and comorbid traits are outputs of the same underlying system state. Current research continues to align with the structure of that system rather than contradict it.
One Upstream Cause, Two Downstream Trait Categories
In Kitzerow’s model, autism traits and comorbid traits do not come from separate origins. They branch from the same upstream stress-response shift, but affect different downstream functions.
1. Neural Development Is Affected
When typical development is deprioritized, neural development is affected.
2. Skills and Behaviors Are Encoded in Neural Pathways
Skills and behaviors depend on neural pathways being built, connected, strengthened, and timed in the right way.
3. Skill and Behavior Development Is Changed
When those pathways develop differently, skill development and behavior development are affected too, which leads to autism-specific traits.
4. NeuroToggle Is the Support Framework
Because this category is neurodevelopmental, support focuses on instruction and neuroplasticity. NeuroToggle is the framework used to build, strengthen, expand, and time neural connections and pathways.
1. Body Function Is Affected
When typical function is deprioritized and the stress-response system is prioritized, regulatory system domain activation alters how body systems function.
2. Altered Function Builds Wear and Tear
When body systems stay in altered states over time, stress builds and wear and tear accumulates across those systems.
3. Comorbid Traits Result
Those system-level changes show up as comorbid traits in areas such as immune function, metabolism, repair, pain, sleep, and nervous system regulation.
4. Neurodivergent Biochemistry Explains the Pattern
Because this category involves regulatory system domains, support focuses on symptom mitigation, accommodation, and medical care. Neurodivergent Biochemistry explains how those system-level shifts produce comorbid patterns.
There is no cure for genetic mutations. Because of that, support focuses on symptom mitigation and accommodation across the two downstream categories: neurodevelopmental support for autism traits and medical management for comorbid traits.
Important info: 95% of Autistics Have At Least 1 Comorbidity
If you’re autistic, your experience may involve more than autism traits.
Many people notice patterns that go beyond communication, sensory differences, or behavior. Physical, neurological, and systemic differences often show up alongside them.
These patterns are not random. When the same combinations appear across individuals, it suggests a shared underlying mechanism.
Common comorbidities include sleep disruption, GI issues, metabolic differences, immune changes, neuroinflammation, anxiety, seizures, OCD, ADHD, motor differences, connective tissue differences, autonomic dysfunction, and chronic pain ( Al-Beltagi, 2021; Chung & Kim, 2024; Khachadourian et al., 2023; Bougeard et al., 2021; Burns et al., 2023; Hours et al., 2022; González-Herrero et al., 2022; Owens et al., 2021 ).
Kimberly Kitzerow’s model explains the biochemical link between autism and comorbid traits:
Genetic and epigenetic factors trigger stress-driven activation across regulatory systems.
BH4-dependent pathways shift and redox balance changes under sustained stress.
Epigenetic redox-sensitive protein shunts alter how biological resources are allocated.
Survival functions are prioritized while typical development and typical function are deprioritized.
These shifts show up as consistent comorbid patterns across regulatory systems domains rather than isolated conditions.
What Are the BioToggles?
Kitzerow categorized the regulatory system domains into 5 categories that she named the BioToggles. Comorbidities fall within those 5 categories.
Immune System Differences Can Show Up Alongside Autism
In this framework, immune-related comorbidities fall under the immune system domain because they affect inflammation, immune signaling, and how the body responds to stress and illness.
What It Regulates
Inflammation, immune response, illness signaling, and how the body reacts to internal and external stressors.
What It Can Look Like
Autoimmune patterns, autoinflammatory responses, frequent illness, strong inflammatory responses, or broader immune dysregulation.
Why It Matters
When this system is persistently activated, it can affect regulation across the body and contribute to broader physiological stress patterns.
Relevant Sources
Meltzer and Walter, 2017
Park et al., 2025
Erbescu et al., 2022
In this model, immune comorbidities are part of the broader biological pattern, not separate add-ons.
Metabolic Differences Can Shape Daily Function
In this framework, GI and metabolic comorbidities fall under the metabolic domain because they affect digestion, nutrient handling, energy production, and physical regulation.
What It Regulates
Digestion, nutrient use, energy production, metabolic balance, and how the body fuels development and function.
What It Can Look Like
GI problems, food sensitivities, unstable energy, feeding issues, metabolic differences, or obesity.
Why It Matters
When metabolism is strained, the effects can show up in both daily function and broader physical regulation.
Relevant Sources
Al-Beltagi, 2021
Khachadourian et al., 2023
Aziz-Zadeh et al., 2025
In this model, GI and metabolic patterns are part of the same systems picture, not separate unrelated problems.
Cellular Repair Differences Affect Structure and Recovery
In this framework, connective tissue and repair-related comorbidities fall under the cellular repair domain because they affect structural integrity, resilience, and how the body maintains itself.
What It Regulates
Connective tissue integrity, structural support, tissue maintenance, and physical repair processes.
What It Can Look Like
Joint instability, slow recovery, chronic pain, tissue fragility, or reduced or altered pain perception.
Why It Matters
Structural and repair differences can shape physical stability, comfort, and how stress is carried through the body.
Relevant Sources
In this model, chronic pain or altered pain perception can be part of the same repair and structural pattern.
Nervous System Differences Affect Regulation and Stability
In this framework, autonomic, psychiatric, and neurological comorbidities fall under the nervous system domain because they affect internal regulation, state stability, and how the body responds to demand.
What It Regulates
Stress response, autonomic function, emotional processing, neurological stability, and internal state regulation.
What It Can Look Like
PoTS, anxiety, OCD, ADHD, seizures, tics, FND, burnout, dysregulation, or unstable nervous system states.
Why It Matters
When nervous system regulation is unstable, the effects can shape cognition, emotion, movement, and daily function all at once.
Relevant Sources
Owens et al., 2021
Khachadourian et al., 2023
Soghomonian, 2024
Owens et al., 2021
In this model, nervous system comorbidities reflect system-level instability, not isolated failures of will or character.
Genetic Regulation Shapes Timing Across the Body
In this framework, sleep and circadian-related comorbidities fall under genetic regulation because they reflect timing, coordination, and regulation across biological systems.
What It Regulates
Sleep timing, circadian rhythm, biological coordination, and broader regulatory timing across development and daily function.
What It Can Look Like
Sleep disorders, irregular energy rhythms, circadian disruption, or timing-related learning and regulation differences.
Why It Matters
Timing systems influence when biological processes happen, so disruption here can ripple across the rest of the body.
Relevant Sources
In this model, circadian and sleep differences are part of broader regulatory timing, not just isolated sleep issues.