Kitzerow’s Primary Source List

Kitzerow’s Primary Source List documents the concepts, terms, and educational frameworks for which Kimberly Kitzerow is the primary source, developed through organizing protein inductions into a functional biochemical network to clarify physiological regulation and development across baseline and allostatic states.

While individual biological components existed in isolation as biochemical relationships and protein data, Kitzerow is the first to organize them into this specific integrated systems level framework. She coined the terminology and educational frameworks to express these relationships.

The concepts listed here are Kitzerow’s primary sources and require citation when referenced or adapted. Her primary sources are categorized into three sections: concept, terminology, and educational frameworks.

Citations

Frequently Asked Questions

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.

  • 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.

  • 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.

  • 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.

  • 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.

  • 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.

  • 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 to Cite This Work

    The concepts, terminology, and educational frameworks listed on this page are original contributions for which Kimberly Kitzerow is the primary source. When these ideas are used, referenced, or adapted, they must be cited.

    APA Style (7th edition)

    General reference

    Kitzerow, K. (Year). Kitzerow’s Primary Source List. Kimberly’s Educational Resources. URL

    Example in text

    (Kitzerow, Year)

    If referencing a specific concept or framework, name it in the text:

    (Kitzerow, Year, BioToggle™ educational framework)

    MLA Style (9th edition)

    Works Cited entry

    Kitzerow, Kimberly. Kitzerow’s Primary Source List. Kimberly’s Educational Resources, Year, URL.

    Example in text

    (Kitzerow)

    If referencing a specific concept or framework, include it in the sentence:

    (Kitzerow, “BioDial™ Educational Framework”)

    Important Note on Use

    If a concept is used, it must be cited. If citation is not permitted in a given context, the concepts listed on this page should not be used. Use without attribution constitutes plagiarism.

Concept 1: Regulatory System Domains - BioToggle

Categorical physiological regulatory system domains responsible for maintaining internal balance

  • Kimberly Kitzerow is the primary source for the formal conceptualization of the body as organized into a defined set of categorical physiological regulatory system domains, each responsible for maintaining internal balance within a specific functional area of physiology.

    Within this conceptualization, regulatory system domains:

    • Maintain stability within their domain under baseline conditions

    • Continuously monitor internal physiological state

    • Detect deviations from expected ranges

    • Coordinate corrective processes to restore balance when deviation occurs

    • Operate interdependently, with all five domains reallocating resources and participating in feedback loops during allostatic responses to restore balance

    These domains operate continuously across development and throughout the lifespan. When deviation or increased demand is detected, physiological regulation may shift toward prioritized, demand-responsive control until balance is restored.

    This concept is organizational and categorical. It defines how physiological regulation is partitioned into domains, independent of specific molecular mechanisms, signaling pathways, or instructional analogies.

  • Regulatory system domains:


    A term introduced by Kimberly Kitzerow to describe categorical divisions of physiological regulation in which each domain contains a complete regulatory system within its functional scope, while operating as part of an interdependent network of regulatory systems.

    Within this terminology, each regulatory system domain includes the essential components of a regulatory system within its domain of responsibility, including mechanisms for sensing internal state, maintaining a functional operating range, detecting deviation, coordinating control, and activating effectors to restore balance.

    At the same time, no regulatory system domain functions in isolation. Domains are interdependent, share resources, exchange signals, and participate in feedback loops with one another. During allostatic responses, multiple domains may be engaged simultaneously, with coordinated reallocation of resources and cross-domain regulation required to restore overall physiological balance.

    The term refers to functional domains of regulation, not isolated pathways or single mechanisms. Each domain is complete within its scope, yet inherently dependent on the coordinated activity of the other domains.

  • The categorical physiological regulatory system domains identified within this framework are:

    1. Immune system regulatory domain
      Responsible for detecting and responding to biological threats, coordinating inflammatory processes, and maintaining host defense and immune balance.

    2. Metabolic regulatory domain
      Responsible for energy allocation, substrate utilization, storage, and metabolic homeostasis across varying physiological demands.

    3. Nervous system regulatory domain
      Responsible for sensory integration, threat detection, arousal, attention, and coordination of rapid adaptive responses.

    4. Cellular repair regulatory domain
      Responsible for cellular maintenance, damage control, detoxification, recycling, and structural repair processes.

    5. Genetic regulation domain
      Responsible for transcriptional control, epigenetic modulation, and longer-term regulatory adjustments that support adaptation and stability.

  • BioToggle™

    BioToggle™ is the educational framework developed by Kimberly Kitzerow to explain how regulatory system domainsfunction, interact, and reprioritize under conditions of physiological demand.

    Within this framework, regulatory system domains are visualized using on–off toggle representations to illustrate shifts in regulatory priority when deviation is detected. The on–off visualization is used to show when a domain is actively prioritized versus when it is not, while maintaining that each domain remains operational and interdependent with the others at all times.

    BioToggle™ is used to teach how physiological regulation can shift away from baseline temporal system domains and toward demand-responsive control, how multiple domains may be engaged concurrently, and how resolution involves coordinated reduction of prioritized activity and reintegration across domains.

    This framework is explicitly educational. The toggle representation is a visualization tool used to support understanding of regulatory prioritization and state change, not a claim that biological systems function as literal binary switches.

Concept 2: Temporal System Domains - BioDial

Temporal cycles of protein synthesis that regulate physiological function and development over time

  • Kimberly Kitzerow is the primary source for the formal conceptualization of physiological function and development as governed by temporal cycles of protein synthesis that operate across multiple time scales.

    Within this conceptualization, protein production, repair, and turnover are coordinated through recurring temporal patterns that manage growth, maintenance, learning, adaptation, and aging. These cycles ensure that physiological processes occur in appropriate sequence, duration, and proportion over time.

    Temporal regulation operates continuously across the lifespan and includes short-term, long-term, and developmental timing processes. These cycles remain active at all times but may be temporarily altered or deprioritized during periods of increased regulatory demand.

    This concept is temporal and organizational. It defines how time structures physiological regulation, independent of specific molecular clocks or instructional analogies.

  • The categorical temporal system domains identified within this framework are:

    • Ultradian temporal domain, which regulates short-cycle timing of protein synthesis and physiological processes occurring multiple times within a day.

    • Circadian temporal domain, which regulates daily timing of physiological processes across approximately 24-hour cycles.

    • Circannual temporal domain, which regulates longer-term, seasonal timing of physiological regulation across months or seasons.

    • Developmental temporal domain, which regulates timing of protein synthesis and physiological processes across stages of development.

    • Aging temporal domain, which regulates gradual, lifespan-related changes in protein turnover, repair capacity, and regulatory prioritization.

  • Temporal system domains:


    A term introduced by Kimberly Kitzerow to describe categorical divisions of physiological regulation based on time-dependent coordination of protein synthesis and function.

    Within this terminology, each temporal system domain represents a distinct scale of biological timing that governs when proteins are produced, repaired, integrated, and retired in support of physiological function and development. Temporal system domains operate continuously across the lifespan and structure regulatory activity over short, intermediate, and long time horizons.

    The term refers to organizational timing domains, not to individual molecular clocks or isolated rhythmic processes. Temporal system domains interact with regulatory system domains and may be temporarily altered or deprioritized during periods of increased regulatory demand.

  • BioDial™ is the educational framework developed by Kimberly Kitzerow to explain how temporal system domains coordinate physiological function, development, learning, and aging through time-dependent regulation of protein synthesis.

    Within this framework, temporal system domains are visualized using dial-based representations to illustrate how the timing of biological processes can be adjusted, accelerated, delayed, or deprioritized in response to physiological conditions. The dial visualization is used to show relative timing emphasis rather than binary activation, emphasizing gradation and proportional change across temporal scales.

    BioDial™ is used to teach how ultradian, circadian, circannual, developmental, and aging temporal domains interact to structure physiological function, development, learning, and aging, and how temporal coordination may be temporarily altered during periods of increased regulatory demand.

    This framework is explicitly educational. The dial representation is a visualization tool used to support understanding of temporal regulation and timing shifts, not a claim that biological systems operate through literal mechanical dials or discrete control interfaces.

Concept 3: Biochemical Regulation - Neurodivergent Biochemistry

Biochemical regulation of physiological function and development is shaped by regulatory system domain prioritization and temporal system domain coordination across allostatic states

  • Kimberly Kitzerow is the primary source for the formal conceptualization of biochemical regulation as the system-level control of protein synthesis, repair, modification, and functional allocation governing physiological function and development, shaped by the interaction between regulatory system domains and temporal system domains and modulated through allostatic states.

    Within this conceptualization, biochemical regulation reflects how physiological systems prioritize regulatory control and temporal coordination in response to deviation, demand, and developmental context. Shifts in regulatory system domain prioritization and alterations in temporal system domain timing influence how protein synthesis, repair, and turnover are organized across physiological function and development through modulation of protein induction.

    Which regulatory system domain is activated, and how resources are reallocated in response to a specific set point deviation, determines which effectors engage. These coordinated biochemical pathway shifts alter physiological function and development in predictable ways, allowing delineation of phenotypic patterns.

    At the center of this process is the BH4 Shunt, which reallocates resources through BH4 trifurcation within regulatory system domains until balance is restored. Engagement of the BH4 Shunt produces predictable downstream effects across systems, including the following regulatory shunts.

    BH4-Dependent Regulatory Shunts

    1. AAAH Shunt
      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 cortico–striatal–thalamic loop circuitry governing movement, habit formation, reward processing, and executive function, thereby altering neural development and behavior. As well as neural development and function in brain neural circuits (processing), afferent (sensory), and efferent (motor) neural circuits that are impacted by these allostatic neurotransmitter activity alterations.

    2. NOS Shunt
      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 activates downstream epigenetic redox-sensitive protein shunts that function as regulatory system effectors.
      Within this architecture:

      • Regulatory system domains 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 these systems disrupts temporal system domain activity, prioritizing regulatory demands over baseline development and function in biochemically predictable ways.

      • Temporal system domains are five time-regulated protein synthesis systems that maintain the body’s steady kinetic flow of protein production across ultradian, circadian, circannual, developmental, and aging domains. Preservation of this kinetic flow is essential for continued physiological function. Prolonged displacement of temporal system domain–regulated protein synthesis by allostatic activity results in allostatic overload and the emergence of predictable comorbidities.

    3. AGMO Shunt
      The AGMO shunt impacts ether lipid cleavage required for endocannabinoid signaling, cellular repair, 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.

    Individual Variation

    Individual differences arise from two interacting mechanisms: experience-driven neural development, which is primarily shaped postnatally by environmental input, and regulatory system domain activation, in which genetically and epigenetically constrained regulatory systems are activated beyond baseline phenotype. The degree, duration, and timing of regulatory system domain activation disrupt temporal system domain–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 domain it affects, when regulatory system domains are activated relative to temporal system domain–regulated protein synthesis, and how experience shapes neural development and function. Regulatory system domain 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.

  • Biochemical Regulation:


    A term used by Kimberly Kitzerow to describe the biochemical regulation of physiological function and development as shaped by regulatory system domain prioritization and temporal system domain coordination across allostatic states. In this usage, biochemical regulation refers to the system-level regulation of protein induction as it is modified by allostatic conditions, through which biochemical pathway activity governs physiological function, development, learning, adaptation, and aging.

    Within this terminology, biochemical regulation describes how patterns of protein induction change in response to internal physiological state, regulatory demand, developmental context, and allostatic state. Protein induction determines which biochemical pathways are active at a given time and, in turn, which physiological functions are prioritized, which molecular effectors are available, how long they remain active, and how physiological resources are allocated across systems.

    Biochemical regulation operates through the coordinated interaction of regulatory system domains and temporal system domains. Under baseline conditions, temporal system domains structure protein induction to support maintenance, development, and coordinated physiological function. During allostatic states, regulatory system domains reprioritize protein induction in response to deviation or demand, altering biochemical pathway activity to support adaptive or survival-oriented regulation. The degree, duration, and developmental timing of these state-dependent shifts determine whether temporal coordination is transiently altered or persistently displaced.

    In this terminology, biochemical regulation is understood as an organizational and state-dependent process, not a single biochemical pathway or isolated reaction. It encompasses the dynamic control of protein induction and biochemical pathway activity that shapes both short-term physiological function and long-term developmental outcomes.


  • Allostatic States

    Within this framework, allostatic regulation is categorized into five distinct states based on origin, duration, and capacity for resolution, each altering regulatory system domain prioritization relative to 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 stable regulatory state in which genetic variation affects proteins required to maintain physiological balance under baseline conditions. As a result, regulatory system domains are consistently prioritized, producing ongoing allostatic regulation rather than episodic activation.

  • Neurodivergent Biochemistry is the educational framework developed by Kimberly Kitzerow to explain how biochemical regulation of physiological function and development is shaped by regulatory system domain prioritization and temporal system domain coordination across distinct allostatic states.

    Within this framework, biochemical regulation is taught through the combined use of BioToggle™ and BioDial™models:

    • BioToggle™ is used to visualize how regulatory system domains become prioritized or deprioritized in response to deviation, demand, or constraint. The toggle representation illustrates shifts in regulatory emphasis across immune, metabolic, nervous system, cellular repair, and genetic regulation domains during different allostatic states.

    • BioDial™ is used to visualize how temporal system domains coordinate the timing of protein induction across ultradian, circadian, circannual, developmental, and aging scales. The dial representation illustrates how baseline temporal coordination supports maintenance, development, learning, and aging, and how this coordination may be displaced during allostatic regulation.

    To explain differences in the duration and persistence of allostatic regulation, the framework also employs stress toggle visualizations (AlloToggle), described as:

    • Situationally flipped
      Represents a transient allostatic state in which regulatory system domain prioritization occurs briefly in response to situational demand and resolves with return to baseline temporal coordination.

    • Chronically stuck
      Represents a persistent allostatic state in which regulatory system domains remain prioritized due to unresolved stress, impaired resolution, or sustained demand, resulting in prolonged displacement of temporal system domain–regulated protein induction.

    • Genetically locked
      Represents a structurally constrained allostatic state in which genetic factors prevent restoration of baseline regulatory balance, producing ongoing prioritization of regulatory system domains across development and time.

    Together, BioToggle, BioDial, and AlloToggle are used to illustrate how which systems are prioritized, when protein induction is coordinated to alter biochemical pathway activity, and how long allostatic regulation persists interact to shape physiological function, developmental trajectories, and comorbidity patterns.

    This framework is explicitly educational. It is designed to support conceptual understanding of system-level biochemical regulation and its developmental consequences. It does not assert diagnostic criteria, treatment protocols, or clinical authority.

Concept 4: The BH4 Shunt

The central allostatic mechanism through which physiological resources are reallocated within regulatory system domains until balance is restored.

  • Kimberly Kitzerow is the primary source for the formal conceptualization of the BH4 Shunt as a central allostatic mechanism through which physiological resources are reallocated within regulatory system domains until balance is restored.

    In this framework, the BH4 Shunt describes how tetrahydrobiopterin (BH4) functions as a regulatory fulcrum during allostatic states. Engagement of the BH4 Shunt results in BH4 trifurcation, in which BH4-dependent pathways are differentially prioritized across regulatory system domains in response to deviation or demand. This reallocation alters protein induction patterns and biochemical pathway activity in predictable, system-level ways.

    Activation of the BH4 Shunt produces downstream regulatory shunts that mediate adaptive responses across nervous system function, immune system response, cellular repair, metabolism, and genetic/epigenetic regulation. The specific shunts engaged and their duration depend on the nature, intensity, and persistence of the allostatic state.

    BH4-Dependent Regulatory Shunts

    1. AAAH Shunt
      The AAAH shunt diverts aromatic amino acids away from dopamine, serotonin, and melatonin synthesis and toward glutamate production through stress-induced transamination. This shift disrupts excitation–inhibition balance within cortico–striatal–thalamic loop circuitry governing movement, habit formation, reward processing, and executive function. These neurotransmitter alterations also affect neural development and function across central processing circuits, afferent sensory pathways, and efferent motor pathways.

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

      Within this architecture:

      • Regulatory system domains are interdependent regulatory systems that respond to physiological stress through coordinated activation and context-dependent allostatic resource reallocation, prioritizing regulatory demands over baseline function in predictable ways.

      • Temporal system domains are time-regulated protein synthesis systems that maintain the body’s steady kinetic flow of protein production across ultradian, circadian, circannual, developmental, and aging domains. Prolonged displacement of temporal system domain–regulated protein synthesis by allostatic activity results in allostatic overload and predictable comorbidity patterns.

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

    Conceptual Scope

    This concept is organizational and state-based. It defines how BH4-dependent regulatory shunts coordinate system-level biochemical responses during allostatic regulation, independent of diagnostic classification, treatment claims, or instructional metaphors.

  • The Five BH4-Dependent Enzymatic Pathways

    1. Phenylalanine hydroxylase (PAH)
      BH4 is required for the hydroxylation of phenylalanine to tyrosine. This reaction regulates aromatic amino acid availability upstream of catecholamine synthesis and broader amino acid metabolism.

    2. Tyrosine hydroxylase (TH)
      BH4 is required for the rate-limiting conversion of tyrosine to L-DOPA in the synthesis of dopamine and downstream catecholamines. This pathway supports baseline monoaminergic neurotransmission and is sensitive to BH4 availability during stress.

    3. Tryptophan hydroxylase (TPH)
      BH4 is required for the conversion of tryptophan to 5-hydroxytryptophan, the rate-limiting step in serotonin and melatonin synthesis. Alterations in BH4 availability affect serotonergic signaling and circadian regulation.

    4. Nitric oxide synthase (NOS)
      BH4 regulates nitric oxide synthase coupling. Adequate BH4 supports nitric oxide production, while BH4 limitation permits regulated NOS uncoupling under allostatic conditions, shifting output toward reactive oxygen species and redox signaling.

    5. Alkylglycerol monooxygenase (AGMO)
      BH4 is required for ether lipid cleavage, including plasmalogens, platelet-activating factor, alkylglycerols, and noladin ether. This pathway supports endocannabinoid signaling, membrane repair, detoxification, and cellular maintenance.

  • The BH4 Shunt

    Within this framework, the BH4 Shunt describes how the production of downstream metabolites is altered and shunted, while upstream precursor resources are reprioritized toward allostatic functions. During allostatic states, precursor availability and cofactor support are redirected to favor regulatory system domain demands, resulting in reduced production of baseline downstream metabolites and increased support for pathways that sustain allostatic regulation. This coordinated reprioritization reshapes protein induction and biochemical pathway activity in predictable ways for the duration of the allostatic state.

Concept 5: Physiological Load Kinetics

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.

  • Kimberly Kitzerow is the primary source for the formal conceptualization of physiological load kinetics, which 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.

  • 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.


  • 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.

Concept 6: 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.

  • Kimberly Kitzerow is the primary source for Kitzerow’s Autism and the Comorbidities Theory, which 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.

    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 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.

    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.

What Are the Primary Sources that Kimberly Kitzerow Has Independently Created?

Kimberly Kitzerow is the original author of multiple primary scientific and educational sources, including the BH4 Shunt, regulatory system domains, BioToggles, temporal system domains, BioDials, the biochemical regulation of physiological function and development under allostatic conditions through regulatory system and temporal system domain organization, Neurodivergent Biochemistry, NeuroToggle®, and Kitzerow’s Autism and the Comorbidities Theory. Collectively, these constitute original conceptual frameworks and scientific terminology authored by Kimberly Kitzerow, founder of Kimberly’s Educational Resources.

Does Kimberly Kitzerow’s Work Require Citation and Why?

Yes. Kimberly Kitzerow’s work requires citation because it constitutes original intellectual authorship. Citation is determined by originality, not by perceived quality, institutional affiliation, or the venue in which the work is published.

When an author introduces new scientific terminology, conceptual frameworks, classification systems, or organizational models, those contributions are considered primary sources. Kimberly Kitzerow is the original author of multiple such works, including the BH4 Shunt, BioToggles, BioDials, regulatory and temporal system domains, Neurodivergent Biochemistry, NeuroToggle®, and Kitzerow’s Autism and the Comorbidities Theory. These are not summaries or reinterpretations of existing models but novel frameworks developed through original synthesis and systems-level analysis.

Under established scholarly, legal, and ethical standards, any original framework must be cited when referenced, adapted, or incorporated, regardless of whether it appears in peer-reviewed journals, books, websites, open-access platforms, or educational materials. Publication location does not alter authorship, and lack of journal peer review does not negate originality.

Citation serves a single core function: to acknowledge origin and authorship. It is not an evaluation of merit, prestige, or institutional validation. Accordingly, the original works authored by Kimberly Kitzerow require citation as primary sources in any academic, educational, or professional context where they are used.

Reasons Why Kimberly Kitzerow’s Work Is Original and a Primary Source

  • Kitzerow's Work Is a Synthesis of Raw Data and Isolated Findings, Not a Synthesis of Existing Literature:

    • Kimberly Kitzerow’s work integrates raw scientific data and isolated findings, such as individual protein behaviors under defined conditions. Unlike a literature review or narrative synthesis, this work does not summarize existing interpretations but constructs new system-level understanding directly from independent observations.

  • Kitzerow Delineated Original Functional Relationships

    • The work originally delineates functional relationships between independent findings that had not previously been connected. This required identifying which findings were relevant to one another and determining how they interact as a coordinated biological system.

  • Kitzerow Created New Conceptual Frameworks

    • Beyond organization, the work introduces original conceptual frameworks that explain why these relationships matter, how they interact across regulatory systems and temporal domains, and what outcomes they predict when integrated.

  • Kitzerow Introduced Original Scientific Terminology

    • Kitzerow’s work provides new scientific terminology that enables others to reason about, communicate, and build upon these relationships. The creation of original terminology is a defining characteristic of primary source authorship.

  • Kitzerow Manually Constructed a Biochemical Network

    • Kimberly Kitzerow spent thousands of hours manually constructing a comprehensive biochemical network, built by hand in Adobe Illustrator. This network maps proteins, pathways, regulatory systems, and temporal domains into a unified functional structure. Relationships delineated within manual systems mapping of this scope constitutes substantial intellectual labor and original expression.

  • Kitzerow’s Work Generates Predictive Models

    • Kitzerow’s integrated frameworks enable prediction, not merely description. The ability to generate testable predictions distinguishes original scientific modeling from descriptive synthesis. Recent research does fall within the predictive framework of Kitzerow’s model.

  • Kitzerow’s Work Constitutes Intellectual Property and Primary Sources

    • The resulting frameworks, terminology, organizational logic, and visual architectures constitute intellectual property and qualify as primary sources. Citation requirements are determined by originality of authorship, not by publication venue, institutional affiliation, or perceived prestige.

    • Therefore, use of these concepts, terminology, or frameworks without proper attribution constitutes plagiarism and, where protected terminology or branded frameworks are involved, may also constitute copyright or trademark infringement.