**6. Conclusion**

The opening quotation from Rutter, made in 2010, applies also today. In this paper, we respond to Rutter's challenge by reporting empirical evidence of three behavioral phenomena in the determination of recurrence risk. Our interpretation of these phenomena in terms of empowerment and imperilment theory, and selfselectivity into reproductive stoppage is less important than their statistical salience. Perhaps other interpretations exist. However, behavioral theory provides axioms, which predicted these effects. By contrast neurodevelopmental theory does not.

The result that recurrence risk is smaller among informed parents is consistent with them being more resilient. This does not mean that they are better parents. It simply means that parents who knowingly or consciously decided against reproductive stoppage are different to parents who conceived before their index child was diagnosed. Nor do we claim that the neurodevelopmental model is false. Indeed, our results are consistent with this model. However, they are not exclusively so. We find that the three behavioral parental phenomena significantly improve predictions of recurrence risk when they are added to the neurodevelopmental model. However, standard neurodevelopmental covariates such as birth gaps and birth orders continue to be statistically significant; they are not superseded by the three behavioral parental phenomena.

Can these behavioral results be confounded by neurodevelopmental effects? This would be the case if the difference between the dates of diagnosis of elder siblings and the dates of conception or birth of younger siblings happened to be correlated with neurodevelopmental phenomena. This difference is positive for uninformed families and negative for informed families. This difference also equals age at diagnosis minus sibling age gaps. There is no reason to suspect that sibling age gaps are directly or indirectly correlated with neurodevelopmental genotypes. However, age at diagnosis might be negatively correlated, if severer cases of ASD are diagnosed more quickly. If so, recurrence risk should vary inversely with age at diagnosis, and birth gaps should have no effect on recurrence risk. Since our results reject both of these predictions, we do not think that they are an artifact of confounding.

Standard neurodevelopmental covariates, such as birth order, might also bear behavioral interpretations. The neurodevelopmental interpretation is that birth order is naturally larger in families that have had more regular children. These families are presumed to be genetically less susceptible to ASD recurrence. A behavioral interpretation might be that parents who have had more experience in raising children are more resilient, which is why recurrence risk varies inversely with birth order. The same applies to covariates such as the ages of parents, which have behavioral as well as neurodevelopmental interpretations. In observational studies results are inevitably ambiguous. On the other hand, whereas most neurodevelopmental covariates have behavioral interpretations, the three behavioral phenomena studied here do not have neurodevelopmental interpretations.

We make a methodological contribution by exploiting the randomness in the timing of diagnoses as a source of natural experimentation. Randomized trials are obviously not feasible because parents cannot be assigned into treatment groups who are informed and controls who are uninformed. By contrast, natural experimentation induced by the timing of diagnosis most probably reveals the same

The first group has odds ratios that are slightly less than 1, while the second group,

*Autism Spectrum Disorder - Profile, Heterogeneity, Neurobiology and Intervention*

In **Figure 6** we plot the relationship, implied by **Table 8**, between recurrence risk (on the vertical axis) and the difference between the birth dates of younger siblings and the dates at which index children were diagnosed (on the horizontal axis). Parents are 'informed' if this difference is positive because younger siblings were born (or conceived) after their index siblings were diagnosed. If this difference is negative, parents were 'uninformed'. Therefore, the shadow of ASD

increases to the right of 0 on the horizontal axis, and the veil of ignorance increases to the left. The baseline for recurrence risk is 4.5 percent as in the data because logit models replicate sample means. Notice that the origin for the shadow of ASD is 2.91 percent because informed parents have lower odds ratios according to **Table 8**. **Figure 6** shows that recurrence risk varies directly with the gap between dates of birth and dates of diagnosis. **Figure 6** also shows that recurrence risk varies

inversely with the shadow of ASD and the veil of ignorance. At one year, the veil of ignorance reduces recurrence risk from 4.5 percent to 3.87 percent and to 2.03 percent after 5 years. At one year, the shadow of ASD reduces recurrence risk from

which is smaller, has odds ratios that are about 1.3.

*Recurrence risk and shadow of ASD or veil of ignorance.*

**Figure 5.**

**Figure 6.**

**78**

*Distribution of family specific odds ratios.*

information with greater reliability provided recurrence risk is sufficiently independent of the timing of diagnosis.

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In summary, the Bettelheim Affair blighted behavioral research into the etiology of ASD. However, the distinction should be made between discredited psychoanalytical theories and untested psychopathological theories that are behavioral. We close with some further quotations from Rutter [28]. "At first sight, it might seem that autism is the diagnostic category least likely to require a developmental psychopathology perspective." However, in reference to grand discredited theories they add, "There is a continuing need to remain skeptical about the new evangelisms that have come to take their place, but equally the imperative must be to replace doubt with programmatic research that truly tests competing hypotheses." Hopefully, the present paper will be judged in this light.
