In developmental psychopathology, differentiating between the coexistence and the clinical entity of two problem areas is of utmost importance. So far, logistic regression analysis has already provided helpful answers, as shown in studies on comorbidity of tic disorders. While the concept of bridging symptoms may be investigated adequately by both logistic regression and the network approach, the former (latent variable) seems to be of advantage with regard to the problems of multiple comorbidities and development.

If Knobe is right that ordinary judgments are normatively suffused, how do scientists free themselves from these influences? I suggest that because science is distributed and externalized, its claims can be manipulated in ways that allow normative influences to be hived off. This allows scientists to deploy concepts which are not normatively suffused. I suggest that there are good reasons to identify these normatively neutral concepts with the folk concepts.

We agree with Cramer et al. that pure cases of behavioral disorders with no symptom overlaps are rare. However, we argue that disorders do exist and the network idea is limited and limiting. Networks of symptoms are observed mainly at behavioral levels. The core deficit is commonly at the cognitive or brain levels, and there the story is completely different.

Knobe considers two explanations for the influence of moral considerations on “non-moral” cognitive systems: the “person as moralist” position, and the “person as [biased] scientist” position. We suggest that this dichotomy conflates questions at computational and algorithmic levels, and suggest that distinguishing the issues at these levels reveals a third, viable option, which we call the “rational scientist” position.

We propose Knobe's explanation of his cases encounters a dilemma: Either his explanation works and, counterintuitively, morality is not at the heart of these effects; or morality is at the heart of the effects and Knobe's explanation does not succeed. This dilemma is then used to temper the use of the Knobe paradigm for discovering moral norms.

As psychiatric illnesses have correlates in the brain, it is surprising that Cramer et al. make almost no reference to the brain's network character when proposing a network approach to comorbidity of psychiatric diseases. We illustrate how data from combined neuropsychological and functional and structural brain-imaging investigations could inform theoretical models about the role played by overlapping symptoms in the etiology of psychiatric comorbidity and the pathways from one disorder to another.

I agree with Knobe's claim in his “Person as Scientist, Person as Moralist” article that moral considerations are integral to the workings of people's competence in making causal judgments. However, I disagree with the particular explanation he gives of the way in which moral considerations influence causal judgments. I critically scrutinize his explanation and outline a better one.

We suggest that the network approach to comorbidity (Cramer et al.) is best examined by using longitudinal, multi-measurement, intra-individual data. Employment of time-series analysis to the examination of the generalized anxiety disorder and major depressive disorder comorbidity enables a detailed appreciation of fluctuations and causal trajectories in terms of both symptoms and cognitive vulnerability.

We are neither scientists nor moralists. Our mental capacities (such as attributing intentionality) are neither akin to the scientist's exact reasoning, nor are they “suffused through and through with moral considerations” (Knobe's target article, sect. 2.2, last para.). They are more similar to all those simple capacities that humans and animals are equally capable of, but with enhanced sensitivity to counterfactual situations: of what could have been.

Cramer et al's proposal to view mental disorders as the outcome of network dynamics among symptoms obviates the need to invoke latent traits to explain co-occurrence of symptoms and syndromes. This commentary considers the consequences of such a network view for genetic association studies.

Cramer et al.'s article is an example of the fruitful application of complex dynamic systems theory. We extend their approach with examples from our own work on development and developmental psychopathology and address three issues: (1) the level of aggregation of the network, (2) the required research methodology, and (3) the clinical and educational application of dynamic network thinking.

Knobe reports that subjects' judgments of whether an agent did something intentionally vary depending on whether the outcome in question was seen by them as good or as bad. He concludes that subjects' moral views affect their judgments about intentional action. This conclusion appears to follow only if different meanings of “intention” are overlooked.

Knobe cites both relevant alternatives and defaults on a continuum to explain how moral judgments influence intuitions about certain apparently non-moral notions. I ask (1) how these two accounts are related, (2) whether they exclude or supplement supposedly competing theories, and (3) how to get positive evidence that people consider relevant alternatives when applying such notions.

We welcome network theory as a tool for modelling the multi-directional interactions that characterise disease. However, we feel that Cramer et al. have neglected one important aspect: how diseases change over developmental time. We discuss principles such as fan in, fan out, bottlenecks, and common pathways, and argue that modelling these developmental aspects can be vital, particularly in deriving properly targeted treatments.

Knobe relies on unhelpful analogies in stating his main thesis about the mind. It isn't clear what saying the mind works, or doesn't work, “like a modern university” or “a scientific investigation” means. We suggest he should say that some think that human cognition respects a ban on fallacies of relevance, where considerations actually irrelevant to truth are taken as evidence. His research shows that no such ban is respected.

Cramer et al.'s network approach reconceptualizes mental comorbidity on the basis of symptom space originating from psychometric signatures. We argue that the advantages of this approach need to be regarded in the context of the multi-level functional organization of the neural substrate, ranging from neurogenetic to psychometric. Neuroelectric oscillations are proposed as a level-integrating principle.

Cramer et al.'s critique of latent variables implicitly advocates a type of scientific anti-realism which can be extended to many dispositional constructs in scientific psychology. However, generalizing Cramer et al.'s network model in this way raises concerns about its applicability to psychopathology. The model could be improved by articulating why a given cluster of symptoms should be considered disordered.

Knobe contends that in making judgments about a wide range of matters, moral considerations and scientific considerations are “jumbled together” and thus that “we are moralizing creatures through and through.” We argue that his own account of the mechanism underlying these judgments does not support this radical conclusion.

Depressive mood can be involved in the moral judgments made by people with depression. Here, we focus on the negative judgments depressed patients have of themselves and the world. Possibly, the alterations in moral judgment in subjects with depression can be understood by taking into account the neural basis of depression.

The majority of commentators agree on one thing: Our network approach might be the prime candidate for offering a new perspective on the origins of mental disorders. In our response, we elaborate on refinements (e.g., cognitive and genetic levels) and extensions (e.g., to Axis II disorders) of the network model, as well as discuss ways to test its validity.