Kitzerow’s Primary Source List
Kitzerow’s Primary Source List
This page identifies the concepts, terminology, and educational frameworks for which Kimberly Kitzerow is the primary source.
- Concepts
- Terminology
- Educational frameworks
This work organizes isolated biological relationships into a defined systems-level framework.
The Jigsaw Puzzle Methodology
A structured approach to identifying patterns across biological data.
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Primary source here refers to the origin of the framework, not the discovery of each isolated mechanism
What already existed
Individual proteins, pathways, biomarkers, and biochemical relationships already existed in the scientific record as isolated findings.
What was added
This work organizes those findings into a specific systems-level structure, defines how the parts relate, and introduces terminology and frameworks to describe those relationships.
Why that matters
The intellectual contribution is not the existence of isolated biological components. It is the functional organization of those components into a coherent explanatory model.
Why this page is public
This page documents those concepts, terms, and frameworks so they can be identified, evaluated, and cited correctly when referenced or adapted.
Understanding How This Primary Source List Is Being Used
This section clarifies how the page defines primary source, how the concepts were created, and how attribution applies when these concepts, terms, or frameworks are used.
There is a significant difference between:
1. Raw data and isolated findings
“We observed X protein does Y under Z conditions”
2. Organized Knowledge
Understanding how multiple findings relate to each other in a functional system
3. Conceptual Frameworks
Creating models to explain why and how these relationships matter
The intellectual work is in:
- Recognizing which isolated findings are relevant to each other
- Understanding how they interact as a system
- Organizing them into a coherent framework
- Providing terminology that allows others to think and communicate about these relationships
- Making predictions based on the integrated model
Integration and organization is time consuming intellectual work. This took thousands of hours. For this reason, these primary sources must be cited with use.
Use of these concepts, terminology, or frameworks without proper attribution constitutes plagiarism, and in some cases copyright/trademark infringement.
What does “primary source” mean in this context?
In this context, a primary source refers to the original originator of a concept, organizational framework, or terminology. A primary source is the individual who first formulated the idea, defined its structure, and articulated its use, rather than someone who later applied, extended, or referenced it.
Use of these concepts or terms should therefore cite Kimberly Kitzerow as the originating source.
How were these concepts created?
These constructs were developed through the systematic organization of protein inductions and regulatory patterns observed across physiological systems while building a functional biochemical network.
By grouping protein behavior according to regulatory role, timing, and prioritization under demand, these concepts emerged as organizing principles that explain how physiological regulation, development, and adaptation operate across baseline and allostatic states.
The entries below identify each concept, the terminology introduced to describe it, and the educational frameworks used to explain it.
Are the underlying mechanisms new?
The individual components, such as genes, proteins, biochemical pathways, and kinetic principles in classic and quantum individually are not new and are well described in existing literature.
The contribution lies in how these components are organized and interpreted. By grouping protein inductions according to regulatory role, timing, and prioritization under demand, functional relationships become clearer than when components are considered individually.
This approach is comparable to how the periodic table organizes known elements. The elements themselves were not newly discovered, but their arrangement highlighted relationships and patterns that were not obvious when viewed in isolation. Similarly, this work focuses on organization and structure rather than introducing new biological units.
What is the purpose of listing these concepts publicly?
The purpose of this list is to provide clarity for attribution and citation. By documenting the concepts and terms for which Kimberly Kitzerow is the primary source, this page helps educators, researchers, and institutions correctly reference the origin of these ideas, distinguish them from related but preexisting models, and recognize their uncited use.
Why are these concepts not published in a peer-reviewed journal?
Kimberly Kitzerow has chosen to make this work open access and will not submit it to a journal.
This decision reflects a commitment to transparency, accessibility, and public accountability. Journal publication restricts access, limits who may evaluate the work, and places control of dissemination in the hands of private publishers. By remaining open access, these concepts are available for review, critique, and use by educators, researchers, clinicians, and institutions without paywalls or gatekeeping.
The absence of journal publication does not negate authorship, originality, or the requirement for citation. Open-access conceptual work remains subject to the same standards of attribution as any other scholarly contribution.
What if I want to use these concepts but my institution only permits citation of peer-reviewed journal articles?
If a concept is being used, it must be cited. If citation is not permitted, then the concept should not be used.
The concepts listed on this page are original organizational and conceptual contributions for which Kimberly Kitzerow is the primary source. Using these ideas without attribution, regardless of the reason, is not acceptable. Institutional policies that restrict citation to journal publications do not override basic standards of intellectual attribution.
If a concept is considered sufficiently rigorous or useful to inform work, then it is sufficiently rigorous to cite. Use without citation constitutes plagiarism. Instances of uncredited use will be documented and reported.
How This Primary Source List Is Organized
The entries on this page are organized into three sections so concepts, terminology, and educational frameworks can be distinguished clearly.
Concepts
These are the underlying ideas and organizing principles that describe how the system functions.
This section identifies original conceptual structures used to explain regulation, development, and system behavior.
Terminology
These are the original terms used to name, define, and communicate the structures and relationships identified in the framework.
This section clarifies which words and phrases originated within this work.
Educational Frameworks
These are the instructional and explanatory frameworks built from the conceptual structure and used to apply it in practice.
This section distinguishes the formal frameworks from the concepts and terms that support them.
Regulatory System Domains · BioToggle
BioToggles are regulatory system domains that epigenetically influence gene expression based on categorical protein induction patterns.
Concept Explanation
BioToggles are regulatory system domains that organize how gene expression is influenced through epigenetic regulation based on categorical patterns of protein induction.
In this framework, biological regulation is not treated as a collection of isolated pathways acting independently. It is organized into broader regulatory domains that shape how protein induction patterns influence gene expression across categories of physiological function.
These domains provide the categorical structure for understanding how the body shifts priorities under changing conditions. They define domain-based influence over gene expression rather than temporal sequence, task completion, or downstream phenotype by itself.
BioToggles therefore function as the regulatory side of the broader system. They identify which type of regulatory domain is influencing gene expression through epigenetic changes in protein induction patterns.
Functional Role
BioToggles define how regulatory system domains influence gene expression by shifting categorical patterns of protein induction within those domains.
This influence occurs through epigenetic regulation. As protein induction patterns change within a given regulatory domain, gene expression is influenced in ways that alter physiological prioritization across that domain.
BioToggles do not define timing. They define regulatory category.
Within the broader framework, they help explain which kind of regulatory pressure is shaping biochemical activity at a given point in the system.
Conceptual Scope
This concept is organizational and operates at the level of regulatory system domains.
It provides a structure for understanding how gene expression is influenced across categories of biological regulation rather than at the level of isolated proteins or single pathways viewed independently.
Within the broader system, BioToggles define domain-based influence over gene expression, while BioDials define temporally regulated gene expression patterns.
This makes BioToggles foundational to the system architecture, because they classify the regulatory domains through which physiological prioritization is organized.
The 5 Regulatory Domains
Immune System
The regulatory domain associated with immune surveillance, inflammatory signaling, host defense, and broader immune-state prioritization.
Metabolism
The regulatory domain associated with energy handling, substrate use, nutrient allocation, and broader metabolic prioritization.
Cellular Repair
The regulatory domain associated with tissue maintenance, repair processes, structural restoration, and broader recovery priorities.
Nervous System
The regulatory domain associated with signaling, state regulation, responsiveness, coordination, and broader nervous system prioritization.
Genetic Regulation
The regulatory domain associated with gene-regulatory control, epigenetic influence, and broader regulation of expression patterns across physiological conditions.
Temporal System Domains · BioDial
BioDials are temporally regulated gene expression patterns, epigenetically regulated by ultradian, circadian, circannual, developmental, and age-related temporal system domains.
Concept Explanation
BioDials are temporal system domains that organize gene expression through epigenetic regulation across ultradian, circadian, circannual, developmental, and age-related cycles.
In this framework, gene expression is not only influenced by regulatory category. It is also patterned across time. BioDials provide the temporal structure through which gene expression is coordinated, repeated, sequenced, and carried across functional and developmental conditions.
These domains organize temporally regulated gene expression patterns rather than domain-based regulatory influence. They define the temporal side of the broader system.
BioDials therefore function as the timing architecture of the framework, describing how gene expression patterns are epigenetically regulated across recurring and lifespan-based cycles.
Functional Role
BioDials regulate when gene expression patterns occur by structuring epigenetic activity across defined temporal cycles.
This temporal regulation influences how biological processes are carried out across short-term, daily, seasonal, developmental, and age-related timescales.
BioDials do not define which regulatory system domain is influencing gene expression. They define the temporal patterning through which gene expression is organized over time.
Within the broader framework, they help explain how function and development are shaped not only by what is being regulated, but by when that regulation is patterned and expressed.
Conceptual Scope
This concept is organizational and operates at the level of temporal system domains.
It provides a structure for understanding how gene expression is coordinated across time rather than at the level of isolated cycles or individual biological events.
Within the broader framework, BioDials define temporally regulated gene expression patterns, while BioToggles define regulatory system domains that epigenetically influence gene expression based on categorical protein induction patterns.
This makes BioDials foundational to the timing architecture of the system, because they classify the temporal domains through which biological regulation is patterned over time.
The 5 Temporal Domains
Ultradian
The temporal domain associated with gene expression patterns regulated across cycles shorter than 24 hours.
Circadian
The temporal domain associated with gene expression patterns regulated across approximately 24-hour biological cycles.
Circannual
The temporal domain associated with gene expression patterns regulated across longer seasonal or annual biological cycles.
Developmental
The temporal domain associated with gene expression patterns regulated across stages of growth, maturation, and developmental progression.
Age-Related
The temporal domain associated with gene expression patterns regulated across aging and lifespan-based physiological change.
Biochemical Regulation · Neurodivergent Biochemistry
Neurodivergent Biochemistry is the broader systems framework that explains how different categories and durations of stress alter gene expression, protein function, development, and physiological function over time through changes in regulatory system domain prioritization and temporal system domain coordination.
Concept Explanation
Neurodivergent Biochemistry is the broader systems framework that explains how biochemical regulation shifts under stress across the body.
Within this framework, biological regulation is shaped by the interaction between BioToggles, which define regulatory system domain influence over gene expression, and BioDials, which define temporally regulated gene expression patterns across ultradian, circadian, circannual, developmental, and age-related cycles.
Different categories of stress do not produce identical biological effects, and duration matters. The type of stress influencing the system and how long that influence persists affect how regulatory system domains are prioritized, how temporally regulated gene expression patterns are altered, and how protein induction and protein function shift over time.
As stress becomes prolonged, repeated, or developmentally embedded, the impact on development and physiological function also changes. Neurodivergent Biochemistry therefore describes how different categories and durations of stress produce coordinated shifts in gene expression, protein induction, protein function, development, and physiological function over time.
Functional Role
The functional role of Neurodivergent Biochemistry is to explain how different categories and durations of stress produce coordinated biological change across systems rather than isolated pathway disruption.
It does this by describing how regulatory system domains shift influence over gene expression, how temporal system domains alter gene expression patterning across time, and how these changes affect protein induction and protein function throughout the body.
Duration is a core variable in this framework. Short-term stress, prolonged stress, repeated stress, and developmentally embedded stress do not shape the system in the same way. As duration changes, the impact on development, physiological function, and system-level adaptation also changes.
Within the broader framework, Neurodivergent Biochemistry integrates BioToggles and BioDials to explain how regulatory category and temporal patterning interact across different durations of stress to shape biological state.
The 5 Allostatic States
Within this framework, allostatic regulation is organized into five distinct states based on origin, duration, and resolution pattern. Each state reflects a different relationship between regulatory system domain prioritization and temporal system domain coordination.
1. Situational Allostatic State
A transient regulatory state in which regulatory system domains are prioritized in response to an acute deviation or demand. Protein induction and biochemical pathway activity shift temporarily and resolve once the situational demand passes, allowing return to baseline temporal system domain coordination.
2. Chronic Allostatic State Due to Environmental Allostatic Overload
A prolonged regulatory state resulting from sustained or repeated environmental, physiological, or psychosocial demand. Regulatory system domains remain persistently prioritized due to ongoing activation, despite intact baseline regulatory and resolution capacity.
3. Chronic Allostatic State Due to Genetic Constraint in Allostatic Resolution Proteins
A persistent regulatory state arising from genetic variation affecting proteins responsible for resolving, terminating, or downregulating allostatic responses, such as those involved in feedback inhibition, repair, clearance, or restoration of baseline function.
In this state, stress detection and activation are intact, but inefficient resolution prevents timely return to baseline, resulting in prolonged regulatory system domain prioritization in the absence of ongoing stress.
4. Developmentally Induced Allostatic State
A persistent regulatory state arising from genetic variation affecting proteins required for normal developmental processes. Mutations in genes governing developmental progression prevent completion of developmental programs, resulting in continued regulatory system domain prioritization as the system remains in a compensatory allostatic state.
5. Genetically Induced Allostatic State Due to Impaired Baseline Regulatory Maintenance
A persistent regulatory state caused by genetic variation affecting proteins required for maintaining baseline function, even in the absence of external stress. Because homeostatic maintenance cannot be sustained efficiently, regulatory system domains remain engaged beyond baseline demand, producing a chronic shift in biochemical regulation.
Conceptual Scope
Neurodivergent Biochemistry operates at the systems level. It does not isolate single pathways or single proteins as independent explanations.
It provides the broader structure for understanding how regulatory system domains, temporal system domains, gene expression, protein induction, protein function, and allostatic states interact to shape physiological function and development.
Its scope includes the impact of both category and duration. Different categories of stress influence different regulatory domains, and different durations of stress alter how deeply those effects shape development and physiological function over time.
Within the broader model, it serves as the biochemical foundation. BioToggles define regulatory system domain influence, BioDials define temporally regulated gene expression patterns, and Neurodivergent Biochemistry explains how those systems interact across different categories and durations of stress.
The BH4 Shunt
The central allostatic mechanism through which physiological resources are reallocated within regulatory system domains until balance is restored.
Concept Explanation
The BH4 Shunt is the central allostatic mechanism through which physiological resources are reallocated within regulatory system domains until balance is restored.
In this framework, tetrahydrobiopterin (BH4) functions as a central regulatory molecule during allostatic states. When the BH4 Shunt is engaged, BH4-dependent pathways are reprioritized in response to physiological deviation or increased demand.
This reprioritization shifts biochemical pathway activity, alters protein induction patterns, and changes how physiological resources are allocated across regulatory system domains.
The BH4 Shunt therefore functions as the central mechanism linking allostatic demand to coordinated downstream biochemical regulation.
Terminology
BH4 Shunt is the term used to describe the central allostatic redistribution of BH4-dependent pathway activity within regulatory system domains under conditions of demand.
In this terminology, the BH4 Shunt refers to the reprioritization of BH4-dependent physiological processes in response to deviation from baseline regulation. This reprioritization alters which downstream biochemical pathways are emphasized until balance is restored.
The BH4 Shunt is not used here to describe a single isolated reaction. It describes a systems-level reallocation mechanism that organizes downstream regulatory change across physiology.
BH4-Dependent Regulatory Shunts
Within this framework, activation of the BH4 Shunt produces downstream BH4-dependent regulatory shunts that organize coordinated adaptive responses across physiology.
AAAH Shunt
Organizes BH4-dependent shifts affecting aromatic amino acid hydroxylase pathways and downstream neurotransmitter-related regulation.
NOS Shunt
Organizes BH4-dependent shifts affecting nitric oxide synthase regulation and downstream redox-sensitive signaling and stress-response patterns.
AGMO Shunt
Organizes BH4-dependent shifts affecting alkylglycerol monooxygenase-related regulation and downstream lipid, repair, and broader adaptive system responses.
Educational Framework
Within Neurodivergent Biochemistry, the BH4 Shunt functions as an educational framework for explaining how allostatic demand is translated into coordinated biochemical reprioritization.
It provides a structured way to describe how stress-responsive regulation is redistributed across physiological systems rather than interpreted as unrelated pathway disruption.
In this role, the BH4 Shunt clarifies how one central regulatory mechanism can generate multiple downstream shunts and shape broader phenotypic patterns across physiology and development.
Physiological Load Kinetics
Describes how biological systems shift from predominantly classical kinetic control to increased reliance on quantum-facilitated mechanisms as capacity constraints alter the thresholds required to sustain function across physiological load states.
Concept Explanation
Physiological Load Kinetics describes how biochemical systems operate under different kinetic states as physiological load changes relative to regulatory and energetic capacity.
In this conceptualization, biochemical behavior is governed by capacity to sustain function under load, not solely by reaction rates. Under low physiological load, sufficient capacity supports classical, rate-governed kinetic behavior and coordinated temporal regulation. As physiological load increases, available capacity becomes constrained and the thresholds required to sustain baseline kinetic behavior shift.
When classical rate-governed processes can no longer meet these altered thresholds, biochemical activity transitions into a high-load kinetic state. In this state, pathway engagement is determined by which reactions remain viable under constrained capacity rather than by baseline efficiency.
This produces a functional shift in kinetic dominance, in which quantum-facilitated enzymatic mechanisms that are already present become more consequential because they can operate under reduced energetic and regulatory reserve.
Physiological load kinetics therefore describe capacity-dependent shifts in kinetic dominance driven by functional necessity, explaining how biological systems preserve organized, adaptive operation across increasing levels of physiological load without invoking changes to underlying physical laws.
As physiological load increases, rising demand shifts kinetic thresholds beyond what classical kinetics alone can sustain, resulting in an ordered transition toward quantum-facilitated enzymatic mechanisms to meet functional needs. There is order to the disorder.
Terminology
A term used by Kimberly Kitzerow to describe the capacity-dependent regulation of kinetic behavior as physiological systems respond to increasing or sustained physiological load.
Within this usage, physiological load kinetics refer to how changes in regulatory and energetic capacity alter the thresholds that govern which biochemical reactions can be sustained, resulting in shifts in the relative dominance of classical and quantum kinetic mechanisms across the continuum from homeostasis to allostatic overload.
Under low physiological load, biochemical activity is governed predominantly by classical, rate-based kinetic laws.
As physiological load increases and available capacity becomes constrained, reactions increasingly rely on quantum-facilitated enzymatic mechanisms that remain viable under altered threshold conditions.
These shifts do not represent disorder or a breakdown of physical law. Rather, they reflect a structured, functional reweighting of kinetic mechanisms in which classical and quantum kinetics operate within an ordered hierarchy determined by capacity and demand. In this terminology, physiological load kinetics describe how biological systems preserve organized, adaptive function under constraint by operating within, not outside of, established chemical and physical principles.
What Are the 5 Physiological Load States?
Within this framework, physiological regulation is described across five physiological load states, defined by the relationship between physiological demand, regulatory capacity, and the dominant kinetic rules governing biochemical activity.
1. Homeostasis
Physiological demand remains within available capacity. Biochemical activity is governed predominantly by classical, rate-based kinetic rules, supporting stable physiological function, development, and maintenance.
2. Systemic Load
Physiological demand increases but remains manageable. Regulatory systems engage while classical kinetic rules remain dominant, with adaptive modulation of pathway activity.
3. Systemic Overload
Physiological demand exceeds available capacity such that the system can no longer meet requirements under classical kinetic rules alone. Kinetic thresholds are crossed, necessitating a change in operating behavior.
4. Allostasis
Alternate regulatory operating rules take over to sustain function under conditions exceeding baseline capacity. Biochemical activity reflects a functional shift toward quantum-facilitated enzymatic mechanisms that can operate under constrained capacity.
5. Allostatic Overload
Prolonged reliance on high-load operation results in cumulative wear and tear. Sustained dependence on constrained, non-baseline kinetic behavior leads to progressive loss of maintenance, repair, and recovery capacity.
Conceptual Scope
This concept is organizational and state-based. It defines how biochemical systems shift in dominant kinetic behavior as physiological demand changes relative to available capacity.
It is used to describe ordered transitions in biochemical operating behavior across increasing physiological load rather than to describe disorder, collapse, or violation of physical principles.
Within the broader framework, Physiological Load Kinetics provides a way to classify how function is preserved under constrained conditions and how load shapes the biochemical rules under which the system continues to operate.
Kitzerow’s Autism and the Comorbidities Theory
Proposes that autism and its associated comorbidities arise from genetically induced allostatic states that consistently activate regulatory system domains, and the BH4 Shunt, reprioritizing resources within temporal system domains, which alter physiological function and development over the lifespan.
Concept Explanation
Kitzerow’s Autism and the Comorbidities Theory proposes that autism and its associated comorbidities arise from genetically induced allostatic states characterized by persistent activation of regulatory system domains and the BH4 Shunt, resulting in resource reprioritization within temporal system domains and altered physiological function and development across the lifespan.
Within this theory, autism and comorbid traits are not treated as separate, unrelated categories. They are understood as coordinated downstream outcomes of the same persistent upstream regulatory state.
The theory therefore provides a unified explanatory model in which altered biochemical regulation, developmental timing, and persistent allostatic prioritization generate both autism traits and system-wide comorbid expression.
Autism as a Genetically Induced Allostatic State
In this theory, autism is understood as a genetically induced, developmentally stable allostatic condition in which regulatory system domains are persistently prioritized over temporal regulatory system domains for the duration of the lifespan.
When this prioritization occurs during critical developmental periods, it produces enduring neurodevelopmental traits.
Persistent displacement of temporal regulatory domain function drives altered biochemical pathway activity, resulting in consistently altered physiological function and development.
Comorbidities as Predictable Physiological Consequences
Comorbidities are not viewed as secondary, coincidental, or independent conditions. Instead, they are understood as predictable physiological consequences of the same genetically induced allostatic state, expressed across multiple systems over time.
Variation in comorbid presentation reflects which regulatory system domains are most affected, the degree of sustained prioritization, and how temporal coordination is displaced, altering biochemical pathway activity in each phenotype.
Within this framework, biochemical regulation and protein induction mediate how genetically induced allostasis shapes both neural development and systemic physiology, explaining why autism reliably co-occurs with immune, metabolic, neurological, gastrointestinal, and connective tissue differences.
Conceptual Scope
This concept is organizational and explanatory, not diagnostic or prescriptive.
It provides a unified framework for understanding autism and its comorbidities as coordinated outcomes of persistent allostatic regulation.
Within the broader structure of the primary source list, this theory is downstream from Neurodivergent Biochemistry. Neurodivergent Biochemistry defines the broader regulatory system and variables, while this theory applies that structure to a specific predicted phenotype pattern.
How the Primary Source Concepts Fit Together
These concepts do not function as isolated ideas. Together, they form one integrated systems-level structure.
Regulatory System Domains · BioToggle
Defines the major physiological regulatory domains that determine which systems are being prioritized.
Temporal System Domains · BioDial
Defines the temporal domains that determine when biological tasks are completed, whether functional or developmental.
Biochemical Regulation · Neurodivergent Biochemistry
Explains how regulatory domain prioritization and temporal coordination interact across allostatic states to shape development and function.
The BH4 Shunt
Defines the central allostatic mechanism through which physiological resources are reallocated within regulatory system domains until balance is restored.
Physiological Load Kinetics
Explains how biological systems shift in kinetic dominance as physiological load changes relative to available capacity.
Kitzerow’s Autism and the Comorbidities Theory
Applies the broader systems structure to a specific predicted phenotype pattern, explaining autism and associated comorbidities as coordinated downstream outcomes of the same persistent upstream regulatory state.
In sequence, the structure works like this:
BioToggle defines what is being regulated.
BioDial defines when biological tasks are completed, whether functional or developmental.
Neurodivergent Biochemistry explains how those systems interact across allostatic states.
The BH4 Shunt describes the central mechanism of biochemical resource reallocation.
Physiological Load Kinetics explains how operating behavior shifts as load exceeds available capacity.
Kitzerow’s Autism and the Comorbidities Theory explains the outcomes produced by that system.