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The strongest explanation is a heterogeneous developmental account in which specific cognitive and sensory differences interact with co-occurring conditions and the social environment. No single deficit adequately explains all psychological difficulties experienced by autistic people. For particular emotional difficulties, alexithymia is a well-motivated candidate mechanism; for interpersonal difficulties, mismatched communication and exclusion are important competing or interacting causes. A useful explanation must say which outcome it explains and distinguish evidence from a broad label.

The outcome itself needs clarification. Differences in social communication, distress during unpredictable or sensory-demanding situations, difficulty identifying emotions and anxiety are not one psychological variable. An autistic person may show one without another, and outwardly similar avoidance can reflect different causes. Diagnostic criteria describe a pattern; they do not identify a single neural lesion, establish an absence of empathy or determine an individual’s quality of life. A theory should predict a specified process and explain variation within the autistic population as well as average differences from a comparison group.

A global theory-of-mind deficit is therefore insufficient. Mental-state reasoning can be difficult in some situations, and language, executive demands or spontaneous use can influence performance. Yet explicit task success and fluent conversation need not covary perfectly, while sensory overload and repetitive behaviour are not automatically consequences of failing a false-belief test. Calling every social misunderstanding mindblindness risks redescribing the outcome. The more precise question is which information the person represents, how it is accessed and whether the interaction supplies cues that both participants interpret similarly.

The broken-mirror hypothesis offers a neural mechanism but faces related specificity problems. One child study found preserved goal-imitation and action-representation measures despite differences in theory-of-mind performance. This challenges a universal failure of action matching as the cause of all autistic social difficulties. It does not prove every mirror-related response is typical; it shows why evidence about one imitation task or one activation contrast cannot stand for an entire diagnostic explanation. The developmental origin, current function and social consequences of a matching response require separate tests.^[ref]

Other single-process theories can contribute without becoming universal explanations. Differences in executive control may affect switching, planning or managing competing demands. Weak-central-coherence accounts emphasize local and contextual processing; social-motivation accounts emphasize orienting, reward and developmental experience. Predictive-processing accounts can formulate differences in expectations or the weight given to sensory evidence. Each needs independent measures and competing predictions. Observed withdrawal alone does not distinguish low social interest from anxiety, sensory strain or previous rejection, and a flexible account that explains any behaviour after the event is weak evidence for a mechanism.

For identifying emotions in oneself or others, alexithymia provides a more discriminating hypothesis. Across two psychophysical experiments, alexithymia related to difficulty interpreting emotional expressions, while controls separated expression interpretation from physical discrimination and identity judgments. An interoceptive study likewise associated its measured difficulty more clearly with alexithymia than autism. These results favour measuring a co-occurring dimension rather than treating emotional difficulty as a necessary feature of autism. They do not establish that every autistic person is alexithymic, or that alexithymia explains every communication or sensory difference.^[ref][ref]

This account has testable limits. Alexithymia questionnaires require insight into one’s own emotional abilities, and heartbeat counting can be influenced by beliefs and timing strategies. Anxiety, language and overlapping questionnaire content may create or obscure associations. Consequently, converging behavioural, physiological and longitudinal measures are needed before inferring a causal chain from interoception through emotion identification to social difficulty. A selective association is useful evidence against diagnostic essentialism, but it is not a complete causal theory of autism.

A relational explanation addresses another level. The double-empathy proposal treats mutual understanding across differing experiences as a two-way problem. It was initially a theoretical argument, not proof that all difficulties are socially imposed. Experimental story-transfer work subsequently found that mixed-neurotype chains lost information more readily than same-neurotype chains in the tested setting. This is evidence that communication success depends on partner composition. It supports investigating shared expectations and conventions, while leaving open effects of familiarity, recruitment and the particular task.^[ref][ref]

The wider environment can also contribute. In thin-slice studies, non-autistic observers formed less favourable first impressions of autistic speakers and expressed less willingness to interact; evaluating speech transcripts did not produce the same pattern as audiovisual presentation. Thus some barriers can arise from other people’s reactions to communication style rather than the substantive content conveyed. These controlled judgments do not establish the cause of every real-world relationship difficulty or later mental-health outcome. They nevertheless show why a theory confined to an autistic individual’s presumed deficit omits an experimentally demonstrated part of the interaction.^[ref]

The most plausible explanatory programme combines these levels without treating them as interchangeable. A sensory or cognitive difference may change an interaction; repeated misunderstanding can alter expectations and anxiety; co-occurring emotion-identification difficulties may complicate recognizing or communicating distress. Those pathways are hypotheses to test prospectively, including autistic people with varied language and support needs. Results from verbally fluent research volunteers cannot represent the whole population, and support needs must not be dismissed merely because interpersonal context matters.

The decisive criterion is explanatory specificity. For a facial-emotion task, an alexithymia-related interpretation account can outperform a global autism-deficit explanation. For a difficult conversation, partner mismatch and exclusion may add explanatory power beyond an individual task score. For other outcomes, sensory, developmental or co-occurring clinical factors may dominate. This evidence favours multiple interacting mechanisms and individually measured needs over either a universal inability to understand minds or a claim that the social environment explains everything. It motivates scientifically testable, outcome-specific explanations rather than conclusions about an individual based solely on diagnosis.