Rethinking Statistics and Causality: Why Mechanisms Cannot Be Inferred from Data Distributions

1National Taiwan University
Project teaser

TL/DR:   Persistent failures of statistical and causal inference to match real-world behavior across disciplines reveal a deeper limitation: mechanisms cannot be recovered from data distributions. These mismatches motivate a revisit of both paradigms, showing that statistical inference collapses into geometric alignment, while causal inference extends the same error by conflating probability with causality.

Psychology Mismatch

Psychology: Low Effects, Fragile Replication
Across psychology, average effects hover around ~0.3 and fail to replicate at scale. The field remains fragmented because statistical significance consistently fails to translate into stable, real-world behavior.

Economics Mismatch

Economics: Wrong Origins, Unrealistic Agents
Economics inherits a false origin story—exchange emerges from reciprocity, not barter—and relies on agent models (selfish, rational) that fail in real human behavior. Yet the discipline continues producing theories that appear mathematically rigorous, but are built on the wrong mechanisms.

Biomedicine Mismatch

Biomedicine & Neuroscience: Significance Without Mechanism
Biomedicine triggered the first replication crisis, and cognitive neuroscience shows correlations so low that many results fail to replicate across studies. Statistical patterns rarely translate into reliable biological mechanisms.

Why Statistics & Causal Inference Need Rethinking

Across psychology, neuroscience, and applied economics, many findings fail to replicate or disappear outside the lab. Even without fraud, statistically “significant” effects often fail to match real-world behavior. These breakdowns are not discipline-specific—they reflect a deeper mismatch between how real systems generate phenomena and how statistical inference interprets the data left behind.

In practice, statistics and causal inference operate entirely within data space. But data are already a compressed projection of a much higher-dimensional world; most semantic structure is lost before analysis even begins. Once mechanisms are removed in this projection, no amount of geometry or factorization applied to the remaining traces can reconstruct how the system actually works.

Many failures stem from two assumptions: that alignment in data space reflects structure in the underlying system, and that probabilistic factorizations reveal the process that generated the outcomes. Yet these tools operate in a domain where the mechanism is no longer present, which is why they break even when used correctly.

The Two Roots of the Error

Two foundational mistakes that pushed statistics and causal inference off course.

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No Generative Mechanism

Many fields never had a generative mechanism. With no account of how observations arise, inference collapsed into geometry and statistics—treating data-space patterns as if they revealed real structure, even though they cannot.

No mechanism → no grounding

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Minimal Data, Big Conclusions

Many fields relied on minimal data. With only small, sparse, convenience samples, inference collapsed into geometric patterns—treating limited observations as if they captured the structure of the world, even though they do not.

Sparse data ≠ world structure

The Three Foundational Failures of Statistical Inference

Sampling, correlation, and conditioning fail for the same structural reason: they operate on low-dimensional shadows, not on the generative system itself.

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Sampling Assumes the Wrong World

Statistics assumes observations come from a fixed distribution. But real-world data are low-dimensional projections of a high-dimensional generative process. A “distribution” is only the shadow, never the source.

Projection ≠ generative process

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Correlation Mistakes Geometry for Mechanism

Correlation is the cosine between centered vectors—pure geometry. Across different spaces, this angle has no meaning at all. Even within the same space, it measures only surface similarity, never the mechanism that produced the data.

Geometry ≠ structure

Conditioning Has No Set-Level Meaning

Conditioning is probability division. But division has no corresponding set operation, so a conditional has no event-level meaning of “given”. Also, probability is not closed under division. Therefore, Bayes’ theorem inherits this illegality — its “update” cannot represent information, belief, or any generative mechanism.

No set → no semantics → no update

Abstract

Statistical and causal inference have become universal currencies of explanation across the sciences, particularly in domains where underlying mechanisms remain opaque. Their apparent rigor—spanning psychology, economics and biomedicine—rests on the assumption that patterns within data can reveal the processes that generate them. Yet persistent mismatches between empirical predictions and real-world behaviour expose a deeper limitation: mechanisms cannot be inferred from data distributions alone.

To address this limitation, we revisit the foundations of both paradigms, showing how statistical inference reduces explanation to geometric alignment, while causal inference, evolved from Bayes’ theorem and graphical models, extends this misstep by conflating probabilistic structure with causal truth. Both expose the same epistemic gap: data encode a lower-dimensional projection of structure, not the mechanism that generates it.

We argue that understanding the world follows two routes: one is data-driven, expanding models toward richer function classes to achieve high-precision prediction, as exemplified by modern deep learning; the other is mechanism-driven, proposing and testing structural hypotheses as in the physical sciences. A robust framework requires both: data-driven models for high-precision prediction, and mechanistic models for reconstructing how the world produces the data we observe.

Why It Matters?

These failures do not stay inside statistics. They propagate across every discipline that relies on data-space reasoning. Psychology, neuroscience, political science, and applied economics routinely draw conclusions from patterns that could never reveal how the system actually works. Entire literatures grow around correlations, regressions, and conditional probabilities whose quantities have no mechanism-level meaning.

Causal inference amplifies the problem. Its algebra multiplies probabilities into joint events that do not exist in real systems. Because observed variables are low-dimensional projections of a richer generative world, the true joint distribution is undefined—yet causal formulas fabricate it through factorization. The machinery operates on objects that have no semantic or generative counterpart in reality.

Machine learning and statistical learning theory inherit the same statistical ontology, but their actual behavior no longer matches their notation. Quantities like likelihoods, expected risk, factorizations, and losses survive as syntactic artifacts, even though the true system has no mechanism that corresponds to them. Models work through optimization heuristics and implementation patches, not through the semantics their formulas suggest. What runs in practice is not what the notation claims.

That is why the foundation must be rebuilt. As long as inference is performed in data space, every downstream field will continue scaling the same structural error — operating on quantities that do not correspond to the systems they aim to explain.

Cite This Work

@misc{diau_2025_17633314,
  author       = {Diau, Egil},
  title        = {Rethinking Statistics and Causality: Why
                   Mechanisms Cannot Be Inferred from Data
                   Distributions
                  },
  month        = nov,
  year         = 2025,
  publisher    = {Zenodo},
  doi          = {10.5281/zenodo.17633314},
  url          = {https://doi.org/10.5281/zenodo.17633314},
}