Borsboom et al. contrast the symptom network model with biological explanations of psychopathology and conclude that mental disorders cannot be explained in terms of biology. In fact, their conclusion is based on a biased and flawed description of the biological study of human mind and behavior. They reduce biological explanations of mental symptoms and disorders to abnormal neurobiological mechanisms and defective brain circuits. Even though such a reductionist model is still frequently encountered in the research and clinical literature, it is not illustrative of how biological explanations can improve our understanding of the origin of mental disorders. After the Darwinian revolution, biology is not only the study of the operation and interaction of structural elements, from molecules up to organs and whole individuals (functional biology). Modern biology is also the study of adaption and phylogenetic history (evolutionary biology) (Mayr Reference Mayr1982). When applied to psychiatry, the evolutionary approach shows that the biology of mental disorders is not just “neurobiology and genetic constitution” but also the study of evolved reactions to adverse environmental circumstances, including adaptive symptoms and calibrated life history strategies (Troisi Reference Troisi2017).
Keller and Nesse (Reference Keller and Nesse2006) introduced and tested a new framework for understanding the adaptive significance of depressive symptoms. Their hypothesis (the “situation-symptom congruence” hypothesis) predicts that, if different depressive symptoms serve different evolved functions, then different events that precipitate a depressive episode should give rise to different symptom patterns that increase the ability to cope with the adaptive challenges specific to each situation. The hypothesis was tested by asking 445 participants to identify depressive symptoms that followed a recent adverse situation. Guilt, rumination, fatigue, and pessimism were prominent following failed efforts; crying, sadness, and desire for social support were prominent following social losses. These significant differences were replicated in an experiment in which 113 students were randomly assigned to visualize a major failure or the death of a loved one. The results of the study confirmed the prediction that symptoms eliciting comfort (e.g., crying) should be especially prominent when social bonds are threatened, lacking, or lost, whereas symptoms dissuading the individual from pursuing current and potential goals (e.g., pessimism and fatigue) should arise when the environment is unpropitious and future efforts are unlikely to succeed. Strong support for the evolutionary hypothesis came subsequently from a study of 4,856 individuals who experienced different patterns of depressive symptoms associated with nine categories of adverse life events (Keller et al. Reference Keller, Neale and Kendler2007). These findings offer a biological explanation of the origin of depressive symptoms without implying defective brain circuits and argue against “reductive models that suggest that neural and molecular levels are the only ones at which we will find true explanations for the phenomenon of clinical depression” (Keller et al. Reference Keller, Neale and Kendler2007, p. 1528).
Environment (and especially social environment) is a crucial variable in evolutionary explanations of mental disorders, which are at the same time biological and non-reductionist. The concept of developmental plasticity is based on the understanding that the phenotype and genotype do not have a fixed relationship and that the phenotypic attributes of individuals are affected by developmental processes. The relationship between environmental influences and the consequential phenotypic change may have directional components of adaptive value (Belsky Reference Belsky2016).
Life history theory is a mid-level evolutionary framework that explains individual differences in various correlated behaviors and outcomes such as mating strategies, risky behaviors, reproductive development, and health. These phenotypic variables are conceptualized as indicators of individual differences along a fast-slow life history continuum. Individuals adopting a fast strategy (that theoretically is most adaptive under harsh and unpredictable environmental conditions) employ short-term mating tactics, engage in risky behaviors, are less future oriented, and devote less time to their offspring (Chua et al. Reference Chua, Lukaszewski, Grant and Sng2017). Consistent with the notion that evolution is incapable of forward thinking, life history theory offers a biological explanation of how early social experiences provide the cues that calibrate individuals’ systems for adapting to their future social environments. Adverse early experiences (e.g., childhood maltreatment) tend to regulate development toward a so-called fast life history characterized by behaviors that would maximize fitness when life is short and the future cannot be controlled or predicted, including heightened risk-taking, early reproduction, and decreased prosocial traits. The life history theory has been especially productive in helping to understand unstable attachments, social antagonism, sexual promiscuity, and early reproduction in some individuals not simply as behavioral disorders, but as a natural outcome of context-sensitive developmental mechanisms that are adaptive for genes, even if not for individual and social well-being (Del Giudice et al. Reference Del Giudice, Ellis and Shirtcliff2011). Several personality disorders, as currently described by psychiatric classifications, seem to reflect “fast life history strategies” caused by a combination of genetic characteristics and early unpredictable or adverse experiences (Brüne Reference Brüne2016). An important implication of life history theory is that the biological prevention of psychiatric disorders should target social risk factors like poverty, maltreatment, and affective deprivation.
Mental health professionals continue to employ a mind-brain dichotomy when reasoning about clinical cases. In clinical discourse, references to “mind” and “brain” have become a form of code for different ways to think about the etiology of psychiatric disorders and their treatment. The etiology and pathogenesis of “biological” disorders would depend mainly on genetic predisposition and neural dysfunction, whereas environmental factors and interpersonal problems would be the main causal factors of “psychological” disorders. The divide between mind and brain fades away if one reasons in terms of adaptive function and employs the concept of behavioral systems. A behavioral system (e.g., the attachment system) can be defined as an integrated group of functionally related components consisting of specific psychological processes, physiological mechanisms, anatomical structures, and genetic influences. No component has an intrinsic priority over the others, and malfunctioning can originate anywhere in the system. When this happens, malfunctioning propagates to all of the components. From such a perspective, it does not make any sense to say that a psychiatric disorder is a “brain disorder” or a “mind disorder.”
Borsboom et al. contrast the symptom network model with biological explanations of psychopathology and conclude that mental disorders cannot be explained in terms of biology. In fact, their conclusion is based on a biased and flawed description of the biological study of human mind and behavior. They reduce biological explanations of mental symptoms and disorders to abnormal neurobiological mechanisms and defective brain circuits. Even though such a reductionist model is still frequently encountered in the research and clinical literature, it is not illustrative of how biological explanations can improve our understanding of the origin of mental disorders. After the Darwinian revolution, biology is not only the study of the operation and interaction of structural elements, from molecules up to organs and whole individuals (functional biology). Modern biology is also the study of adaption and phylogenetic history (evolutionary biology) (Mayr Reference Mayr1982). When applied to psychiatry, the evolutionary approach shows that the biology of mental disorders is not just “neurobiology and genetic constitution” but also the study of evolved reactions to adverse environmental circumstances, including adaptive symptoms and calibrated life history strategies (Troisi Reference Troisi2017).
Keller and Nesse (Reference Keller and Nesse2006) introduced and tested a new framework for understanding the adaptive significance of depressive symptoms. Their hypothesis (the “situation-symptom congruence” hypothesis) predicts that, if different depressive symptoms serve different evolved functions, then different events that precipitate a depressive episode should give rise to different symptom patterns that increase the ability to cope with the adaptive challenges specific to each situation. The hypothesis was tested by asking 445 participants to identify depressive symptoms that followed a recent adverse situation. Guilt, rumination, fatigue, and pessimism were prominent following failed efforts; crying, sadness, and desire for social support were prominent following social losses. These significant differences were replicated in an experiment in which 113 students were randomly assigned to visualize a major failure or the death of a loved one. The results of the study confirmed the prediction that symptoms eliciting comfort (e.g., crying) should be especially prominent when social bonds are threatened, lacking, or lost, whereas symptoms dissuading the individual from pursuing current and potential goals (e.g., pessimism and fatigue) should arise when the environment is unpropitious and future efforts are unlikely to succeed. Strong support for the evolutionary hypothesis came subsequently from a study of 4,856 individuals who experienced different patterns of depressive symptoms associated with nine categories of adverse life events (Keller et al. Reference Keller, Neale and Kendler2007). These findings offer a biological explanation of the origin of depressive symptoms without implying defective brain circuits and argue against “reductive models that suggest that neural and molecular levels are the only ones at which we will find true explanations for the phenomenon of clinical depression” (Keller et al. Reference Keller, Neale and Kendler2007, p. 1528).
Environment (and especially social environment) is a crucial variable in evolutionary explanations of mental disorders, which are at the same time biological and non-reductionist. The concept of developmental plasticity is based on the understanding that the phenotype and genotype do not have a fixed relationship and that the phenotypic attributes of individuals are affected by developmental processes. The relationship between environmental influences and the consequential phenotypic change may have directional components of adaptive value (Belsky Reference Belsky2016).
Life history theory is a mid-level evolutionary framework that explains individual differences in various correlated behaviors and outcomes such as mating strategies, risky behaviors, reproductive development, and health. These phenotypic variables are conceptualized as indicators of individual differences along a fast-slow life history continuum. Individuals adopting a fast strategy (that theoretically is most adaptive under harsh and unpredictable environmental conditions) employ short-term mating tactics, engage in risky behaviors, are less future oriented, and devote less time to their offspring (Chua et al. Reference Chua, Lukaszewski, Grant and Sng2017). Consistent with the notion that evolution is incapable of forward thinking, life history theory offers a biological explanation of how early social experiences provide the cues that calibrate individuals’ systems for adapting to their future social environments. Adverse early experiences (e.g., childhood maltreatment) tend to regulate development toward a so-called fast life history characterized by behaviors that would maximize fitness when life is short and the future cannot be controlled or predicted, including heightened risk-taking, early reproduction, and decreased prosocial traits. The life history theory has been especially productive in helping to understand unstable attachments, social antagonism, sexual promiscuity, and early reproduction in some individuals not simply as behavioral disorders, but as a natural outcome of context-sensitive developmental mechanisms that are adaptive for genes, even if not for individual and social well-being (Del Giudice et al. Reference Del Giudice, Ellis and Shirtcliff2011). Several personality disorders, as currently described by psychiatric classifications, seem to reflect “fast life history strategies” caused by a combination of genetic characteristics and early unpredictable or adverse experiences (Brüne Reference Brüne2016). An important implication of life history theory is that the biological prevention of psychiatric disorders should target social risk factors like poverty, maltreatment, and affective deprivation.
Mental health professionals continue to employ a mind-brain dichotomy when reasoning about clinical cases. In clinical discourse, references to “mind” and “brain” have become a form of code for different ways to think about the etiology of psychiatric disorders and their treatment. The etiology and pathogenesis of “biological” disorders would depend mainly on genetic predisposition and neural dysfunction, whereas environmental factors and interpersonal problems would be the main causal factors of “psychological” disorders. The divide between mind and brain fades away if one reasons in terms of adaptive function and employs the concept of behavioral systems. A behavioral system (e.g., the attachment system) can be defined as an integrated group of functionally related components consisting of specific psychological processes, physiological mechanisms, anatomical structures, and genetic influences. No component has an intrinsic priority over the others, and malfunctioning can originate anywhere in the system. When this happens, malfunctioning propagates to all of the components. From such a perspective, it does not make any sense to say that a psychiatric disorder is a “brain disorder” or a “mind disorder.”