Research ArticlesWorking papers, published research & mechanistic foundations

Using IMIG, IVIG, and MSC therapy as parallel pathways to neuropeptide cascade recovery. Proposes the three-state SST-14 interneuron model, a six-component adjunctive metabolic support framework, and a biomarker-stratified trial architecture with state-assignment decision algorithm and neuropeptide cascade restoration as the primary endpoint. Includes convergent evidence from Naviaux's cell danger response framework and Morrow's GPT2 mitochondrial research as independent proof-of-concept for the State 2 model. 61 references. Companion to The Anatomy of Autism. Authorship under discussion — under expert review prior to journal submission.

A systems biology dissection of immune-derived autism presenting a two-layer model: the convergent cascade tracing founding conditions through gut pH dysregulation, immune activation, IDO1, and NF-κB to SST-14 interneuron silencing; and a constitutional susceptibility architecture identifying seven tipping points that determine who the cascade propagates in. Includes the three-state clinical framework, the CREB/CBP/CRE transcriptional suppression mechanism, the estrogen-cAMP sex ratio explanation, and ten testable predictions. Working document — under expert review prior to journal submission.

A mechanistic framework for SST-14 transcriptional restoration through a sequenced five-month supplement cascade — sulforaphane, NMN/NR, luteolin, fisetin, and forskolin — addressing both NF-κB-mediated CREB suppression and adenosine-driven adenylyl cyclase starvation through convergent but distinct molecular angles. Presented as a companion to IMIG and as a standalone protocol for patients outside trial access. Includes full constitutional susceptibility context, patient selection criteria, and the biological latch mechanism explaining why the protocol requires months rather than weeks. Working paper — May 2026 · Version 3.

How Roundup disrupts gut microbiome function, depletes tryptophan availability, and feeds directly into the IDO1 cascade — a mechanistic connection with direct implications for the Biology of Autism framework.

IL-6, IL-17A, and fetal microglial priming. How prenatal immune events establish the inflammatory baseline that persists throughout neurodevelopment and shapes the ASD phenotype.

The CCK/opioid peptide → somatostatin no-off-switch mechanism, the upstream cholinergic suppression arm, and downstream consequences across seven gut peptides. Companion to Chapter 11 of the core framework.

How acetaminophen use around vaccination depletes sulfate availability, disrupts glycosaminoglycan synthesis, and may impair the detoxification capacity needed to clear adjuvant load in susceptible children.

Microbiome differences, lifestyle, vaccine exposure differential, and what lower observed ASD rates in Amish communities do and don't mean for the biological cascade model.

The metabolic mechanism linking estrogen signaling to IDO1 activity, adenylyl cyclase, and the male-to-female ASD population ratio — why the sex difference in ASD prevalence may be hormonally mediated.

What each receptor system does, how E/I imbalance develops, and how the kynurenine pathway and calcium dysregulation drive excitatory overload in the autism cascade.

One condition fails to open plasticity or keep it open. The other has plasticity closing prematurely later in life. The shared biology of synaptic remodeling failure and what connects them mechanistically.

When pepsin cannot break proline bonds at low pH, casomorphin and gliadorphin peptides remain intact. Which amino acids stay trapped, what opioid-like signaling results, and what this means for tryptophan availability, CCK, and the ASD cascade.

Persistent anti-streptococcal serology without active infection points to molecular mimicry — the immune system attacking self-tissue that resembles strep antigens. How this connects to basal ganglia autoantibodies, PANS, and immune-triggered regression in ASD.