The Labels Multiply Because the Ledger Sorts Outcomes
It is early in this literature review, so I am not drawing any conclusion. Think of this as a field note.
The more papers I read around autism, ADHD, anxiety, sensory processing, eating disorders, peptides, amino acids, DPPIV, mitochondria, gut signaling, and oxidative stress, the more convinced I am that our diagnostic labels name observed behaviors. I would like to have clean biological kinds.
I do not consider labels to be fake. I consider them descriptive.
It means labels may sit too far downstream for my tastes and research interests.
A child becomes a label only after the child’s nervous system has been expressed in a social atmosphere. A child is an organism. The child has to digest food, break down peptides, clear metabolic residues, hold mitochondrial reserve, regulate excitation and inhibition, manage immune signals, sleep, repair, filter sensation, and survive social threat.
But none of that gets done through language.
Those are physiological processes for the most part.
Behavior is what leaks out when that stack runs under load.
One organism gets called autistic. Another gets called ADHD. Another gets called anxious. Another gets called oppositional. Another gets called gifted but difficult. Another gets called bipolar. Another gets called eating disordered. Another gets called fine until collapse.
The ledger sorts outcomes.
Biology sorts bottlenecks.
That is the thing I keep seeing.
Inside autism itself, the literature does not show one smooth object. It shows clusters. Sensory features cluster. Amino-acid patterns cluster. Gut and peptide findings appear in subgroups. Oxidative stress and mitochondrial dysfunction recur as background machinery. Autophagy and cellular cleanup enter the story. DPPIV/CD26 appears as one of the body’s peptide editors: part enzyme, part immune-signaling protein, part metabolic regulator, part stress-chemistry junction.
That is not an autism explanation by itself.
But it is a definite heads-up signal.
It is a warning. The literature I’m looking at suggests neurodivergence may involve metabolic dysregulation at a fundamental level. By metabolic, I do not mean junk food diet or obesity. I mean the living machinery of the organism: fuel, substrates, enzymes, peptides, transport, clearance, inflammation, repair, and signaling.
The snapshot is seasoned researchers across multiple disciplines of the biological basis of behavior admitting their frustration with massive confounding factors.
The label “autism” is silent on which metabolic account the organism is running. “Anxiety” does not tell us whether the organism is dealing with peptide load, immune activation, autonomic instability, relational threat, sensory overload, or depleted repair capacity. “ADHD” does not point to whether attention is failing from dopamine salience, sleep issues, mitochondrial drag, glucose instability, screen ecology, or chronic nervous-system arousal.
The same visible behavior can have different biological routes.
Each route may capture a different individual presentation within the group of people having observed and labeled neurodivergent presentations.
The same biological bottleneck can present through different behaviors.
That is why the literature looks confounded. Some of the confounding may be sloppy method. But some of it may be the architecture of the thing itself.
Human beings are not spreadsheets with symptoms attached. They are living regulatory economies.
When ordinary life chemistry stops passing through and starts accumulating, life changes character. Amino acids become excitatory pressure. Food peptides become immune or opioid-like signals. Damaged organelles become cleanup burden. Oxidative stress taxes repair. Poor sleep blocks restoration. Social threat raises the cost of masking. Attention-capture environments keep the system from settling.
Then the institution arrives late and writes a label on the visible behavior.
A label may help. It may open services. It may give a person language. It may reduce shame and organize accommodation.
But labeling can also hide the organism.
The better question is not, “Which label is this person?”
My preferred track is to investigate the neurobiology.
Which regulatory stack produced this presentation?
What is the organism trying to metabolize?
What is failing to clear?
What is being over-signaled?
What is being under-repaired?
What is being mistaken for character, attitude, personality, or identity?
My instincts are telling me the next useful account of neurodivergence will not come from replacing one grand label with another. “It is all autism” will fail. “It is all trauma” will fail. “It is all mitochondria” will fail. “It is all gut” will fail. “It is all dopamine” will fail.
The object is stacked.
Metabolism, peptides, immune signaling, mitochondrial reserve, sensory filtering, GABA/glutamate balance, autonomic regulation, sleep, trauma, and attention ecology do not operate in separate rooms.
They braid.
They jam.
They compensate.
They overload.
The labels multiply because the ledger sorts outcomes.
The organism keeps the actual accounts scripted in physiology.
References:
Dell’Osso, L., Carpita, B., Nardi, B., et al. “Autistic traits distribution in different psychiatric conditions: A cluster analysis on the basis of the Adult Autism Subthreshold Spectrum questionnaire.” Psychiatry Research 326, 115270.
Lyons-Warren, A. M., Wangler, M. F., & Wan, Y.-W. “Cluster Analysis of Short Sensory Profile Data Reveals Sensory-Based Subgroups in Autism Spectrum Disorder.” International Journal of Molecular Sciences 23, 13030.
Ferraro, S., Saielli, L., Biganzoli, D., Tosi, M., et al. “Amino Acid Patterns in Children with Autistic Spectrum Disorder: A Preliminary Biochemical Evaluation.” Nutrients 17, 274.
Sebastián-Martín, A., Sánchez, B. G., Mora-Rodríguez, J. M., Bort, A., & Díaz-Laviada, I. “Role of Dipeptidyl Peptidase-4 (DPP4) on COVID-19 Physiopathology.” Biomedicines 10, 2026.
Golub, Y., Stonawski, V., Plank, A. C., et al. “Anxiety Is Associated With DPPIV Alterations in Children With Selective Mutism and Social Anxiety Disorder: A Pilot Study.” Frontiers in Psychiatry 12, 644553.
Jarmołowska, B., Bukało, M., Fiedorowicz, E., Cieślińska, A., et al. “Role of Milk-Derived Opioid Peptides and Proline Dipeptidyl Peptidase-4 in Autism Spectrum Disorders.” Nutrients 11, 87.
Miao, C., Shen, Y., Lang, Y., et al. “Biomimetic nanoparticles with enhanced rapamycin delivery for autism spectrum disorder treatment via autophagy activation and oxidative stress modulation.” Theranostics 14(11), 4375–4392.

