Borsboom and colleagues provide an informative account of the challenges inherent in the widespread adoption of traditional biology-oriented explanations of mental conditions. Nonetheless, while the network approach may offer a more integrative depiction of psychopathology, we contend that it is, in part, similarly based on an impoverished view of the term “biological,” as is generally the case in the fields of medicine and psychology (Brüne Reference Brüne2016). Specifically, the prevailing undertaking of biological interpretations of mental conditions has largely focused on so-called proximate descriptions (e.g., biological mechanisms), while disregarding their “ultimate” or evolutionary dimensions (i.e., their phylogeny and adaptive value; Nesse Reference Nesse2013). When viewed through the lens of Tinbergen's framework encompassing both the proximate and the ultimate levels of explanations of specific design features or traits, a couple of key issues arise that render the network approach no more useful than the standard biological model in medicine and psychology (Brüne Reference Brüne2014; Nesse Reference Nesse2013).
The first claim is that the network approach offers a unique way of looking at psychopathology, whereby the synergism involving associated symptoms in a system of connections is purported to be key in the development of such conditions. Although it does make sense that symptoms of many psychological conditions are likely to affect one another in a progressive and reciprocal manner, the network approach fails to clarify as to why this is the case. Is it because some symptoms are naturally influential on others? If so, why is this the case? Borsboom et al. contend that the logical interpretation of intentional narratives behind certain symptoms could explain why. However, it begs the question as to why such relationships are rational or comprehensible.
The second claim is that, in the context of a network approach, psychopathological features are believed to be engendered either as a result of individual developmental trajectories or as an outcome of environmental circumstances (i.e., akin to the proximate level). It is similarly ambiguous as to why these proposed antecedents would effectively bring about psychopathological symptoms. As an example, why exactly might exposure to thin models on media induce self-esteem issues and extreme eating habits in females? If it is because of social comparison, then why do humans compare so much? It is quite apparent that such explanations seem to pose more questions than answers.
We suggest that an evolutionary framework could plug these gaps by providing a comprehensive, ultimate account to complement such an otherwise detailed theoretical perspective relating to the proximate viewpoint. Specifically, two main evolutionary concepts, one relating to evolutionary mismatch (Durisko et al. Reference Durisko, Mulsant, McKenzie and Andrews2016), and the other to life history theory (LHT) (Stearns Reference Stearns2000; cf. Del Giudice Reference Del Giudice2014), respectively, are proposed to be highly valuable in shedding light on the actual origins of psychopathology.
For instance, the notion of evolutionary mismatch has been touted as a major underlying cause of a variety of mental conditions (Durisko et al. Reference Durisko, Mulsant, McKenzie and Andrews2016). It refers to the manifestation of problems among people because relevant genes and cognitive/biological mechanisms (broadly useful in the ancient context) could not evolve fast enough to match the dramatic metamorphoses in existential conditions that have materialized in the contemporary world (Grunspan et al. Reference Grunspan, Nesse, Barnes and Brownell2018; O Reference O, Shackelford and Weekes-Shackelford2018a). To illustrate, consider the proposition that depression is an outcome of residing in an evolutionarily novel setting whereby one's personal, occupational, and social experiences are drastically different from that of prehistoric individuals (Hidaka Reference Hidaka2012). Such a contextual framework would have provided important elucidations for the existence of depressive symptoms (e.g., having a sense of hopelessness and anhedonia or entrapment in a seemingly hopeless situation), which the network approach might merely attribute to the occurrence of a precipitating event (e.g., failing an exam). Although it is conceivable that an exam failure could indeed play a role in the emergence of depression, such a proximate explanation precludes a sufficient understanding of why one is susceptible to feeling hopeless (and subsequently develop depression) following such an event. Apart from banking mainly on rationality and the general acknowledgement of extrinsic influences as is the case with the network model, Hidaka's (Reference Hidaka2012) theorization (e.g., the existence of evolutionarily novel inadequacy of social support in the current context) could uniquely explain why contemporary humans may be more vulnerable to develop the condition. Similar formulations relating to evolutionary mismatch could likewise describe the pathogenesis of a wide assortment of many other disorders, ranging from animal phobias (O Reference O, Shackelford and Weekes-Shackelford2018b) to schizophrenia (Abed & Abbas Reference Abed and Abbas2011).
Likewise, LHT is believed to be comparatively useful in deciphering the etiology of psychiatric conditions (Del Giudice Reference Del Giudice2014), because the concept is not only valuable in comparing species but also in explaining within-species variations (Stearns Reference Stearns2000). It is a concept derived from behavioral ecology, which focused on the adaptive tradeoffs (e.g., a faster LH strategy involving spreading meagre resources across many offspring who will experience earlier sexual maturity and a higher mortality rate, versus a slower LH strategy encompassing heavy investment in a few offspring with sexual maturity/death occurring at a later age) in relation to the nature of external circumstances (e.g., residing in a highly dangerous vs. predictably safer environment) as a means to realize favourable procreative outcomes (Stearns Reference Stearns2000).
According to this approach, psychopathological problems are manifestations of either a slow (e.g., autism) or a fast LH strategy (e.g., attention deficit hyperactivity disorder [ADHD]) (Del Giudice Reference Del Giudice2014). While a network model would argue that a child develops ADHD because of parental neglect, for instance, LHT can explain why the condition may emerge in the context of gene-environment correlation, which is fully compatible with the mismatch approach. For example, some psychological traits nowadays associated with ADHD were once adaptive in harsh and uncertain environments in relation to survival and reproduction over much of human evolutionary history. These traits are less profitable in the evolutionarily novel world and may become “symptoms,” depending on the quality of parental input (Bakermans-Kranenburg & Van Ijzendoorn Reference Bakermans-Kranenburg and Van Ijzendoorn2006).
Taken together, we contend that a combination of the LHT and the evolutionary mismatch approach, to name just two major evolutionary concepts, would provide a fundamental framework to complement the network model in understanding psychopathology.
Borsboom and colleagues provide an informative account of the challenges inherent in the widespread adoption of traditional biology-oriented explanations of mental conditions. Nonetheless, while the network approach may offer a more integrative depiction of psychopathology, we contend that it is, in part, similarly based on an impoverished view of the term “biological,” as is generally the case in the fields of medicine and psychology (Brüne Reference Brüne2016). Specifically, the prevailing undertaking of biological interpretations of mental conditions has largely focused on so-called proximate descriptions (e.g., biological mechanisms), while disregarding their “ultimate” or evolutionary dimensions (i.e., their phylogeny and adaptive value; Nesse Reference Nesse2013). When viewed through the lens of Tinbergen's framework encompassing both the proximate and the ultimate levels of explanations of specific design features or traits, a couple of key issues arise that render the network approach no more useful than the standard biological model in medicine and psychology (Brüne Reference Brüne2014; Nesse Reference Nesse2013).
The first claim is that the network approach offers a unique way of looking at psychopathology, whereby the synergism involving associated symptoms in a system of connections is purported to be key in the development of such conditions. Although it does make sense that symptoms of many psychological conditions are likely to affect one another in a progressive and reciprocal manner, the network approach fails to clarify as to why this is the case. Is it because some symptoms are naturally influential on others? If so, why is this the case? Borsboom et al. contend that the logical interpretation of intentional narratives behind certain symptoms could explain why. However, it begs the question as to why such relationships are rational or comprehensible.
The second claim is that, in the context of a network approach, psychopathological features are believed to be engendered either as a result of individual developmental trajectories or as an outcome of environmental circumstances (i.e., akin to the proximate level). It is similarly ambiguous as to why these proposed antecedents would effectively bring about psychopathological symptoms. As an example, why exactly might exposure to thin models on media induce self-esteem issues and extreme eating habits in females? If it is because of social comparison, then why do humans compare so much? It is quite apparent that such explanations seem to pose more questions than answers.
We suggest that an evolutionary framework could plug these gaps by providing a comprehensive, ultimate account to complement such an otherwise detailed theoretical perspective relating to the proximate viewpoint. Specifically, two main evolutionary concepts, one relating to evolutionary mismatch (Durisko et al. Reference Durisko, Mulsant, McKenzie and Andrews2016), and the other to life history theory (LHT) (Stearns Reference Stearns2000; cf. Del Giudice Reference Del Giudice2014), respectively, are proposed to be highly valuable in shedding light on the actual origins of psychopathology.
For instance, the notion of evolutionary mismatch has been touted as a major underlying cause of a variety of mental conditions (Durisko et al. Reference Durisko, Mulsant, McKenzie and Andrews2016). It refers to the manifestation of problems among people because relevant genes and cognitive/biological mechanisms (broadly useful in the ancient context) could not evolve fast enough to match the dramatic metamorphoses in existential conditions that have materialized in the contemporary world (Grunspan et al. Reference Grunspan, Nesse, Barnes and Brownell2018; O Reference O, Shackelford and Weekes-Shackelford2018a). To illustrate, consider the proposition that depression is an outcome of residing in an evolutionarily novel setting whereby one's personal, occupational, and social experiences are drastically different from that of prehistoric individuals (Hidaka Reference Hidaka2012). Such a contextual framework would have provided important elucidations for the existence of depressive symptoms (e.g., having a sense of hopelessness and anhedonia or entrapment in a seemingly hopeless situation), which the network approach might merely attribute to the occurrence of a precipitating event (e.g., failing an exam). Although it is conceivable that an exam failure could indeed play a role in the emergence of depression, such a proximate explanation precludes a sufficient understanding of why one is susceptible to feeling hopeless (and subsequently develop depression) following such an event. Apart from banking mainly on rationality and the general acknowledgement of extrinsic influences as is the case with the network model, Hidaka's (Reference Hidaka2012) theorization (e.g., the existence of evolutionarily novel inadequacy of social support in the current context) could uniquely explain why contemporary humans may be more vulnerable to develop the condition. Similar formulations relating to evolutionary mismatch could likewise describe the pathogenesis of a wide assortment of many other disorders, ranging from animal phobias (O Reference O, Shackelford and Weekes-Shackelford2018b) to schizophrenia (Abed & Abbas Reference Abed and Abbas2011).
Likewise, LHT is believed to be comparatively useful in deciphering the etiology of psychiatric conditions (Del Giudice Reference Del Giudice2014), because the concept is not only valuable in comparing species but also in explaining within-species variations (Stearns Reference Stearns2000). It is a concept derived from behavioral ecology, which focused on the adaptive tradeoffs (e.g., a faster LH strategy involving spreading meagre resources across many offspring who will experience earlier sexual maturity and a higher mortality rate, versus a slower LH strategy encompassing heavy investment in a few offspring with sexual maturity/death occurring at a later age) in relation to the nature of external circumstances (e.g., residing in a highly dangerous vs. predictably safer environment) as a means to realize favourable procreative outcomes (Stearns Reference Stearns2000).
According to this approach, psychopathological problems are manifestations of either a slow (e.g., autism) or a fast LH strategy (e.g., attention deficit hyperactivity disorder [ADHD]) (Del Giudice Reference Del Giudice2014). While a network model would argue that a child develops ADHD because of parental neglect, for instance, LHT can explain why the condition may emerge in the context of gene-environment correlation, which is fully compatible with the mismatch approach. For example, some psychological traits nowadays associated with ADHD were once adaptive in harsh and uncertain environments in relation to survival and reproduction over much of human evolutionary history. These traits are less profitable in the evolutionarily novel world and may become “symptoms,” depending on the quality of parental input (Bakermans-Kranenburg & Van Ijzendoorn Reference Bakermans-Kranenburg and Van Ijzendoorn2006).
Taken together, we contend that a combination of the LHT and the evolutionary mismatch approach, to name just two major evolutionary concepts, would provide a fundamental framework to complement the network model in understanding psychopathology.