Psychextrical Interpretation as the Missing Bridge in Science: Why Observation With Psychological-Method Produces Confusion

BY: OMOLAJA MAKINEE

18 January 2026

Introduction: Observation Is Not Understanding

Science often mistakes observation for explanation. Data is gathered, correlations are plotted, and conclusions are announced—yet disagreement persists, reversals occur, and certainty collapses. This is not because science lacks data, but because it lacks interpretive discipline.

Observation answers what is happening. Interpretation answers why it is happening. Between the two lies method.

Modern behavioural science remains tethered to psychological-methods, a framework that prioritises observed behaviour and epigenetic influence while treating biological inheritance as background noise. Neuroscience and psychiatry inherited the lens of psychology wholesale—and as a result, they frequently talk past one another. One field asserts; another debunks. Both observe accurately. Both interpret incompletely.

Nowhere is this methodological failure more visible than in the recent public controversy surrounding claims that paracetamol use during pregnancy causes autism.

1. The Paracetamol–Autism Claim: When Observation Outruns Interpretation

The claim—popularised publicly by Donald Trump—did not arise in a vacuum. It drew from observational cohort studies that analysed historical pregnancy data.

What These Studies Did Correctly

The primary studies examined:

• Maternal paracetamol use during pregnancy.
• Later autism diagnoses in children.

They relied on:

• Maternal self-reporting (retrospective surveys).
• Biomarker analysis (e.g. cord blood).

Their findings showed correlation between prenatal paracetamol exposure and autism diagnoses. In Psychextrics, this observation was not false.

Where Psychological-Methods Failed

Psychological-methods treat correlation as behavioural causation candidates. Yet these studies could not isolate:

• Whether autism arose from paracetamol itself.
• Or from the reason paracetamol was taken (fever, infection, inflammation).

High maternal fever and infection are themselves independent risk factors for neurodevelopmental differences. Psychological-methods lack the tools to disentangle biological susceptibility from environmental trigger.

Thus, the claim leapt prematurely from association to cause.

2. The Scientific Rebuttal: Stronger Method, Same Limitation

To counter the claim, major health bodies invoked sibling-comparison models—considered the “gold standard” within psychological-methods.

What Sibling Models Achieved

Researchers compared:

• Siblings born to the same mother.
• One exposed to paracetamol in utero.
• One unexposed.

Because siblings share genetics and home environment, this method successfully eliminated:

• Broad genetic variation.
• Socio-economic confounders.

The result was decisive:

The autism association disappeared.

From this, the scientific community concluded:

Paracetamol does not cause autism.

Within psychological-methods, this conclusion was valid. Yet it was still incomplete under Psychextrics.

3. Why Psychextrics Says Both Sides Were Right—and Wrong

Psychextrics introduces a fundamentally different interpretive framework. It begins with a structural premise:

Behavioural conditions are fixed in susceptibility within the diencephalon at conception.

The diencephalon—thalamus, hypothalamus, epithalamus, subthalamus—is the brain’s meaning-generating and decision-making engine. It integrates:

• Genetic Index Markers (GIM).
• Hormonal Index Markers (HIM).
• Epigenetic Index Markers (EIM).
• Hormonal Fluidity Index (HFI).

From this integration, the thalamic nuclei produce neurotype-specific behavioural susceptibilities—not behaviours themselves, but conditions of possibility.

The cortex does not debate these outcomes. It displays them.

4. Susceptibility, Not Causation

From birth to roughly age three, GIM and HIM aggressively seek expression. They are not blank slates, but latent architectures awaiting compatible triggers.

EIM and HFI—diet, environment, stressors, chemicals, infections—do not create behavioural conditions. They present stimuli to GIM/HIM. The response depends entirely on what is already biologically present.

If a behavioural susceptibility does not exist within GIM/HIM:

• No environment can activate it.
• No exposure can manufacture it.

This explains why:

• One child develops autism.
• Another remains immune.
• Under the same exposure.

5. Re-interpreting the Paracetamol Question

Under psychextrical-methods:

• Paracetamol can activate autism if the susceptibility already exists in GIM/HIM.
• Paracetamol is irrelevant if the susceptibility is absent.
• The same mother may produce different outcomes across pregnancies.

Thus:

• Observational studies were right to see associations.
• Sibling studies were right to see no universal causation.

Both failed because psychological-methods assume uniform susceptibility. Psychextrics rejects this assumption.

6. Pregnancy Is Not a Repeated Experiment

Each pregnancy represents a unique biological snapshot:

• Maternal age.
• Hormonal state.
• Immune profile.
• Epigenetic exposure.
• Paternal sperm quality.

This is why:

• Cravings differ across pregnancies.
• Some foods suddenly become intolerable.
• Others become urgently desired.

Cravings are not “whims.” They are epigenetic signals interacting with GIM/HIM windows.

A woman may crave apples in one pregnancy and reject them entirely in another—not because her DNA changed, but because the changes in the maternal susceptibility window interacted differently with the unique biological fingerprint of each embryo, shaped by aging spermatozoa, fertilisation dynamics, and pregnancy-specific epigenetic conditions.

7. Age, Timing, and Biological Windows

A mother in her 20s may carry a vulnerability marker that activates under certain exposures. In her 30s, that same marker may be dormant—or vice versa.

Likewise:

• Older paternal age increases the likelihood of sperm mutations.
• Split spermatozoas raise developmental variability.
• These factors interact with maternal biology, not independently.

Autism—and all behavioural spectra—emerge from timed interactions, not single causes.

8. Why Psychological-Methods Keep Failing

Psychological-methods prioritise:

• Epigenetic influence.
• Environmental causation.
• Behavioural observation.

They struggle with:

• Individualised biology.
• Latent susceptibility.
• Timing-dependent activation.

As a result, they produce endless “ifs” and “buts”:

• This causes autism… except when it doesn’t
• This gene matters… except when it doesn’t

The problem is not data. The problem is interpretation.

9. Psychextrical-Methods: Individualised Interpretation

Psychextrics reverses the order:

1. What exists biologically (GIM/HIM).
2. When susceptibility windows are open.
3. What epigenetic inputs are presented (EIM/HFI).

Behaviour is not imposed. It is revealed. This is why:

• One exposure harms one child.
• Leaves another untouched.
• And strengthens a third.

Conclusion: Science Needs Better Interpretation, Not More Data

The paracetamol debate is not a failure of science—it is a failure of methodological interpretation. Observation without interpretive architecture produces contradiction. Interpretation without biological grounding produces ideology.

Psychextrics does not ask whether something causes autism. It asks:

In whom, when, and under what biological conditions can it activate what already exists?

Until science crosses this bridge—from observation to interpretation—it will continue to argue with itself, loudly and endlessly, while mistaking correlation for understanding.

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Introducing Psychextrics