My ResearchGate Papers
Why Kitzerow Chose ResearchGate
Kimberly Kitzerow chose to publish her work on ResearchGate to ensure it remains open access and freely available to the autistic community. This platform allows her to retain full intellectual property rights while providing transparent analytics that show how many people have read her work, from which institutions, and from which countries. To date, her publications have been read over 137,000 times worldwide.
Traditional peer review is exclusively a journal publishing process, it is not open to those who choose open access. It involves 2-3 unpaid reviewers who evaluate a paper before a journal decides to publish it. This process represents a publication step rather than scientific consensus, and authors often relinquish their intellectual property rights in the process. By using ResearchGate, she maintain ownership of my work and provide transparency to the autistic community while contributing to open scientific dialogue and accessibility.
There have been successful replications, and derivatives, however they did not cite her. Kitzerow is legally published across websites, videos, books, and ResearchGate articles with public time stamps. Her work is legally published and copyrighted, with trademarks where applicable.
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Autism & the Comorbidities Along the BH4 Pathway
Date: Jan 2024
Abstract: Autism spectrum disorder (ASD) is a neurodevelopmental disorder affecting approximately 1 in 45 individuals in the United States, characterized by impaired social communication and repetitive behaviors (Delhey et al., 2018). Evidence increasingly suggests that both genetic and environmental factors play a part in its pathogenesis. A notable contributor is the tetrahydrobiopterin (BH4) pathway, influenced by genetic and environmental factors. It regulates many biological processes potentially leading to the onset of autism and its associated comorbidities.
To Cite:
APA – Kitzerow, K. (2024). Autism & the Comorbidities Along the BH4 Pathway. ResearchGate. https://doi.org/10.13140/RG.2.2.23124.37761/1
MLA – Kitzerow, Kimberly. “Autism & the Comorbidities Along the BH4 Pathway.” ResearchGate, 2024, https://doi.org/10.13140/RG.2.2.23124.37761/1
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Genomic and Proteomic Regulation in Cellular Homeostasis: From Molecular Mechanisms to Clinical Implications
Date: August 2024
Abstract: This review explores the intricate relationship between the genome, proteome, and cellular regulatory networks in maintaining homeostasis and responding to stress. It emphasizes how the genome provides the blueprint for cellular function, highlighting the role of coding and non-coding DNA in protein synthesis and regulation. The proteome is crucial in regulating homeostasis within the metabolome, a process continuously monitored through signal transduction. When cellular stress occurs, it triggers alterations in protein isoforms, which in turn regulate the metabolome to restore homeostasis. Disruptions in these systems can lead to various pathological conditions.
To Cite:
APA - Kitzerow, K. (2024). Genomic and Proteomic Regulation in Cellular Homeostasis: From Molecular Mechanisms to Clinical Implications. Research Gate. https://doi.org/DOI: 10.13140/RG.2.2.31853.19682/3
MLA - Kitzerow, Kimberly. “Genomic and Proteomic Regulation in Cellular Homeostasis: From Molecular Mechanisms to Clinical Implications.” Research Gate, 2024, https://doi.org/DOI: 10.13140/RG.2.2.31853.19682/3.
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The BH4 Pathway as an Allostatic Mechanism in the Pathology of Autism and Systemic Comorbidities
Date: August 2024
Abstract: Autism Spectrum Disorder (ASD) is a biomedical neurodevelopmental disorder in which cellular stress triggers biochemical shifts that alter developmental pathways during critical periods and continue to impact the individual into adulthood. These disruptions extend beyond early brain development, resulting in long-term systemic consequences, as chronic allostatic overload imposes a sustained physiological burden throughout the autistic individual’s life. ASD is frequently accompanied by systemic comorbidities—including cardiovascular, metabolic, autoimmune, neuromuscular, and connective tissue disorders—yet the underlying biochemical mechanisms unifying these conditions remain poorly understood. This paper proposes that the BH4 shunt functions as a central allostatic mechanism, redirecting tetrahydrobiopterin (BH4) activity under cellular stress to prioritize redox balance over neurotransmitter synthesis.
To Cite:
APA - Kitzerow, K. (2024a). The BH4 Pathway as an Allostatic Mechanism in the Pathology of Autism and Systemic Comorbidities. Research Gate. https://doi.org/DOI: 10.13140/RG.2.2.18927.96167
MLA - Kitzerow, Kimberly. “The BH4 Pathway as an Allostatic Mechanism in the Pathology of Autism and Systemic Comorbidities.” Research Gate, Aug. 2024, https://doi.org/DOI: 10.13140/RG.2.2.18927.96167.
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The Shift in Kinetic Laws Under Systemic Load
Date: April 2025
Abstract: This paper proposes that dynamic systems do not operate under a single fixed set of kinetic laws. Under baseline conditions, classical kinetics apply: rate-governed interactions proceed according to concentration gradients, thermodynamic favorability, and continuity-based modulation. However, when a system is exposed to systemic load-defined here as the accumulation of inputs, demands, or conditions that exceed the system's regulatory bandwidth and necessitate a shift from baseline operation to adaptive response. The system transitions into a high-intensity adaptive state in which kinetic behavior shifts categorically. Linear progression is replaced by threshold-governed reconfiguration and emergent behaviors optimized for survival. This paper hypothesizes that under systemic overload, systems shift from classical kinetic behavior to an alternate regulatory mode driven by conditional logic, toggled thresholds, and quantum-aligned mechanisms such as tunneling, probabilistic activation, and state switching. These processes do not indicate disorder but structured urgency. There is order to the disorder.
To Cite:
APA - Kitzerow, K. (2025). The Shift in Kinetic Laws Under Systemic Load. ResearchGate. https://doi.org/10.13140/RG.2.2.22013.06886/1
MLA - Kitzerow, Kimberly. “The Shift in Kinetic Laws Under Systemic Load.” ResearchGate, 2025, https://doi.org/10.13140/RG.2.2.22013.06886/1
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Beyond Saturation: Enzymatic Kinetic Thresholds, Systemic Load, and the Impact of Oversupplementation
Date: April 2025
Abstract: his paper explores the kinetic consequences of substrate oversaturation inenzymatic systems, particularly under conditions of chronic stress and allostatic load.While supplementation is often employed to restore metabolic balance, excessivesubstrate availability can exceed enzymatic capacity, surpassing the catalytic ceilingdefined by k-cat value. In these cases, the intended therapeutic eCect may reverse,pushing the system toward instability. This paper proposes that oversaturation should berecognized as a state distinct from classical saturation, with unique implications fornetwork behavior and systemic regulation. When combined with allostatic overload, supplementation that exceeds enzymatic limits poses a risk to regulatory capacity. This model reframes supplementation through a systems-level kinetic lens, offering a new framework for understanding biochemical thresholds in vulnerable populations
To Cite:
APA - Kitzerow, K. (2025). Beyond Saturation: Enzymatic Kinetic Thresholds, Systemic Load, and the Impact of Oversupplementation. ResearchGate. https://doi.org/10.13140/RG.2.2.33337.68968
MLA - Kitzerow, Kimberly. “Beyond Saturation: Enzymatic Kinetic Thresholds, Systemic Load, and the Impact of Oversupplementation.” ResearchGate, 2025, https://doi.org/10.13140/RG.2.2.33337.68968
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BioToggle Categorical Delineation: A Functional Framework for Timing-Sensitive Intervention in Neurodivergent Biochemistry
Date: April 2025
Abstract: This delineation table organizes the five BioToggle™ in the Neurodivergent Biochemistry™ Framework—Immune, Metabolic, Cellular Repair, Nervous System, and Gene Regulation—into three mechanistic categories: Situational, Chronic, and Genetic. Each reflects a redox-sensitive adaptive system that contributes to phenotype variability in which proteins shift, which systems are disrupted, and when in the developmental or aging process this occurs. Understanding this framework may provide a conceptual foundation for precision-aligned, time-sensitive support strategies—shifting away from checklist-based diagnostic labels toward a mechanistic, systems biology interpretation of neurodivergence. Disclaimer: As an educator, I analyze, synthesize, and translate peer-reviewed scientific literature into original, proprietary frameworks designed to enhance interdisciplinary understanding. These materials are conceptual in nature and are not intended to diagnose, treat, or serve as clinical protocols. Their purpose is to advance scientific literacy and spark informed exploration by qualified professionals within their respective fields. All rights, including intellectual property and derivative use, are reserved by Kimberly’s Educational Resources. Any clinical application, diagnostic development, or derivative research must be conducted by licensed professionals through appropriate research channels and with proper attribution.
To Cite:
APA - Kitzerow, K. (2025). BioToggle Categorical Delineation: A Functional Framework for Timing-Sensitive Intervention in Neurodivergent Biochemistry. ResearchGate. https://doi.org/10.13140/RG.2.2.18927.96167
MLA - Kitzerow, Kimberly. “BioToggle Categorical Delineation: A Functional Framework for Timing-Sensitive Intervention in Neurodivergent Biochemistry.” ResearchGate, 2025, https://doi.org/10.13140/RG.2.2.18927.96167
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Neurodivergent Biochemistry and the Autism and the Comorbidities Theory
Date: July 2025
Abstract: Neurodivergent Biochemistry is a universal molecular systems biology explanatory framework that delineates how prolonged allostatic activation disrupts typical development and function over time. It centers on the regulatory system’s influence over five epigenetically responsive BioToggles: immune, metabolic, cellular repair, nervous system, and genomic regulation. These BioToggles collectively monitor and modulate the human kinetic flow-state that maintains physiological stability, adaptability, and survival. Each BioToggle responds to internal and external stressors and can exist in one of three states: Situationally flipped in response to acute stress. Chronically stuck when stress remains unresolved. Genetically locked due to inherited or spontaneous gene mutations that lead to the activation of the BioToggles. This can either occur due to a gene mutation within the regulatory proteins, or gene mutations that create the conditions that breach the set point of a BioToggle regulatory system. This framework delineates why neurotypical individuals may exhibit neurodivergent traits when exposed to persistent stress, and why those traits may become enduring if regulatory systems fail to return to baseline. It also is the foundation for the Autism and the Comorbidities Theory, in which gene mutations initiate a biochemical stress response that is prioritized over typical development and function. This creates an atypical developmental trajectory in which stress-adapted signaling dominates. Over time, the persistence of this response leads to cumulative allostatic overload. This accelerates age-related physiological decline and contributes to the broad spectrum of comorbidities observed in autism. Neurodivergent Biochemistry reframes autism as a systemic, redox-regulated shift in biological priority from growth and integration toward stress adaptation and survival.
To Cite:
APA - Kitzerow, K. (2025a). Neurodivergent Biochemistry and the Autism and the Comorbidities Theory. Research Gate. https://doi.org/DOI: 10.13140/RG.2.2.30248.89606
MLA - Kitzerow, Kimberly. “Neurodivergent Biochemistry and the Autism and the Comorbidities Theory.” Research Gate, July 2025, https://doi.org/DOI: 10.13140/RG.2.2.30248.89606.