Accessibility long description for Image 2 on the Originator Erasure page: Kitzerow's Autism and the Comorbidities Framework vs Stanford Study

The image is titled “Kitzerow’s Autism and the Comorbidities Framework.”

On the left side of the image, the following text appears in sequence:

Step 1: Eureka Moment.
Nonverbal autistic daughter can’t blow out a candle on her birthday cake leads to the realization that autism and the comorbidities, including nonverbality, are physiologically linked rather than being independent traits.

Step 2: Hypothesis.
It is biologically implausible for autism traits and comorbid traits to co-occur systematically in each phenotype without a shared biochemical root mechanism. This is now called the Exclusivity Principle.

Step 3: Testing Methodology.
Created a biochemical network of gene-coded proteins and mapped autism-associated biomarkers onto the network to identify convergent points of regulatory dysregulation.

Step 4: Conclusion.
The Autism and the Comorbidities Theory.

Below these steps is a section labeled “Core Mechanism.”
The text states:
Autism arises from gene mutations and epigenetic factors that alter regulatory system behavior and constrain neural development and function. Comorbidities arise when stress-responsive BioToggle activation reallocates proteins via epigenetic redox-sensitive BH4 shunt trifurcation, producing predictable comorbidity clusters based on which regulatory system effectors are engaged. The timing and duration of BioToggle activation shape the comorbidity profile, with sustained activation increasing cumulative physiological impact via allostatic overload.

A section labeled “Systems-Level Impact” follows.
The text states that BioToggles may be situationally triggered by environmental encounters, chronically activated when resolution fails, or genetically locked when mutations impair regulatory reset. Activation generates an allostatic response that is biochemically mediated through BH4-dependent regulation. Under cellular stress conditions GCH1 regulates BH4-dependent trifurcates of three epigenetic, redox-sensitive shunts, producing predictable downstream effects across systems.

Numbered points then appear describing three shunts:

1. The AAAH shunt diverts aromatic amino acids away from dopamine, serotonin, and melatonin synthesis and toward glutamate production via stress-induced transamination. This disrupts excitation-inhibition balance within CSTL circuitry governing movement, habit formation, reward processing, and executive function, thereby altering neural development and behavior.

2. The NOS shunt reflects redox-regulated, BH4-mediated control of nitric oxide synthase. The BH4 shunt modulates NOS coupling state, permitting regulated NOS uncoupling under stress conditions and shifting nitric oxide production toward reactive oxygen species generation. This redox shift selectively activates downstream epigenetic redox-sensitive protein shunts that function as regulatory system effectors.

3. The AGMO shunt impacts ether lipid cleavage required for endocannabinoid system activity, cellular repair activity, and detoxification. AGMO is the only enzyme capable of cleaving ether lipid bonds, including plasmalogens, platelet-activating factor, alkylglycerols, and noladin ether. Disruption of noladin ether cleavage to 2-AG alters endocannabinoid signaling. Prolonged AGMO impairment contributes to lysosomal dysfunction, reduced repair capacity, and cumulative system wear.

Epigenetic Redox-Sensitive Protein Shunt Effectors Regulatory Architecture:

• The BioToggles are five interdependent regulatory systems that respond to physiological stress through conserved, coordinated activation and context-dependent allostatic resource reallocation to support survival. Activation of the stress response disrupts the BioDials, prioritizing regulatory and survival demands over typical development and typical function in biochemically predictable ways.

• The BioDials are four time-regulated protein synthesis mechanisms that maintain the body's steady kinetic flow of protein production across circadian, seasonal, developmental, and lifespan timescales. Preservation of this kinetic flow state is essential for continued physiological function and survival. Prolonged displacement of BioDial-regulated synthesis by stress-responsive BioToggle activity results in allostatic overload with biochemically predictable consequences, the comorbidities.

Individual Variation: Individual differences arise from two mechanisms: experience-driven neural development, which is primarily shaped postnatally by environmental input, and regulatory system activation, in which genetically and epigenetically constrained BioToggles are situationally activated beyond the genetic phenotype. The degree, duration, and timing of this BioToggle activation disrupt BioDial-regulated protein synthesis, reallocating resources toward survival and producing variation in development and function.

Timing Effects: Trait severity and presentation depend on when a gene mutation is functionally relevant, which regulatory system it affects, when BioToggles are activated relative to BioDial-regulated protein synthesis, and how experience shapes neural development and function.

BioToggle activation during sensitive developmental windows more strongly displaces developmental and maintenance processes, while experience-driven neural plasticity during these periods further refines or amplifies functional outcomes.

On the right side of the image is a circular diagram titled “Autism and the Comorbidities Theory by Kimberly Kitzerow.”
At the center of the diagram is a label reading “Autism & Comorbid Traits BH4 Shunt.”
Surrounding this center are five labeled systems: Nervous System Comorbid Traits, Immune System Comorbid Traits, Metabolism Comorbid Traits, Cellular Repair Comorbid Traits, and Genetic Regulation Comorbid Traits.

Outside the diagram are condition labels reading: Dysautonomia Anxiety ADHD, Metabolic Disorders G I Conditions, Autoimmune MCAS, and Altered Circadian Rhythm.

On the left side of the image, a red arrow points to the text from a vertical yellow text box.
The yellow box contains the following text:
“Stanford targeted excitation/inhib ition balance within a specific CSTL region, the reticular thalamus, as an intervention approach for autism-related traits.”

The red arrow visually connects this yellow annotation to the explanatory framework text.