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Relieving human suffering is a challenging goal in every aspect. It requires powerful conceptual tools that will parse human complexity into a manageable number of issues. It requires clinical creativity that will lead to the successful targeting of key domains and dimensions of human functioning. It depends on methodological tools that permit the development of generalizable knowledge from detailed experience with myriad individuals. Two disciplines, psychiatry and behavioral sciences, share the same goal to relieve human suffering. However, they operate off of different paradigms and utilize different tools to accomplish this goal. In the early days of the behavior therapy movement, the late Gordon Paul (1969), then just a few years past his PhD, asked one of the most widely cited questions about the proper goal of a science of evidence-based interventions: “What treatment, by whom, is most effective for this individual with that specific problem, under which set of circumstances, and how does it come about?” (p. 44). This incited a new scientific approach to therapeutic intervention: specified and tested interventions for specific problem areas that fit the needs of individuals based on known processes of change. This promising beginning did not quite extend far enough into the field, however, because the early days of behavior therapy relied on learning principles and theories that were largely drawn from the animal laboratory, in the absence of similarly well-developed theories of human cognition and emotion. Indeed, excessive confidence in learning principles may explain why 2 years earlier Paul (1967) had not included the phrase “and how does it come about” in the original formulation of this question, focusing entirely on contextually specific evidence-based procedures. The early behavior therapists generally assumed that the learning laboratories could be trusted to map out needed principles of change for intervention science (Franks & Wilson, 1967). Our argument is that the field has now developed sufficiently to return to an expanded form of Paul’s original vision. We believe that the time is ripe for modern psychotherapy and intervention science to focus on a new foundational question: “What core biopsychosocial processes should be targeted with this client given this goal in this situation, and how can they most efficiently and effectively be changed?” Answering this question is the goal of any form of process-based therapy (PBT), which can be defined as the contextually specific use of evidence-based processes linked to evidence-based procedures to help solve the problems and promote the prosperity of particular people. In contrast to treatments focused on syndromes, PBT targets theoretically derived and empirically supported processes that are responsible for positive treatment change. It is our view that such a process-based approach is the key for the future of evidence-based care. For the following discussion, it is important to clarify a few key terms. Most importantly, we need to distinguish the underling therapeutic processes from the therapeutic procedures that are utilized in treatment. Therapeutic procedures are the techniques or methods that a therapist utilizes to achieve the treatment goals of the client: the defined and measurable outcomes upon which the therapist and client have agreed. Such goals are not static goal posts, but they may change as treatment progresses. Usually, therapy is directed toward multiple goals, which can often be arranged in a hierarchy depending on priority, immediacy, difficulty, or related dimensions. Therapeutic processes are the underlying change mechanisms that lead to the attainment of a desirable treatment goal. We define a therapeutic process as a set of theory-based, dynamic, progressive, and multilevel changes that occur in predictable empirically established sequences oriented toward the desirable outcomes. These processes are theory-based and associated with falsifiable and testable predictions, they are dynamic because processes may involve feedback loops and nonlinear changes, they are progressive in the long term in order to be able to reach the treatment goal, and they form a multilevel system because some processes supersede others. Finally, these processes are oriented toward both immediate and long-term goals. It should be noted that the term therapeutic process is sometimes used in the literature to refer broadly to the patient-therapist relationship that includes so-called common factors, such as the therapeutic alliance and other factors of the therapeutic relationship. The term therapeutic process, as we use it, can include this more traditional use of the term as long as such processes are based on a clearly defined and testable theory and meet the empirical standards we are suggesting. It is not, however, synonymous with that traditional use. Our argument is not new. In fact, it brings us back to the very beginning of behavior therapy and its foundational element—functional analysis. Functional analysis utilizes idiographic assessments of a target behavior and the history and context in which it occurs to identify the functional relationship between variables that cause or contribute to the occurrence of this behavior (for a review, see Haynes & O’Brien, 1990). The historical and philosophical roots of functional analysis are based on Skinner’s (1953) approach to the analysis of action in its historical and situational context. In clinical contexts, it has expanded beyond contingency analysis to include “the identification of important, controllable, causal functional relationships applicable to a specified set of target behaviors for an individual client” (Haynes & O’Brien, 1990, p. 654). This approach has been a guiding principle since the early days of behavior therapy and has been embraced by many notable scholars, including Albert Bandura, David Barlow, Walter Mischel, Arthur Staats, and Gerald Davison, to name only a few. The early emphasis on functional analysis changed, however, when modern psychiatry adopted structuralism for its nosology. The Latent Disease Model of Psychiatry Mental health care professionals have been engaged in a long and heated debate over how to best define, classify, and treat mental disorders (Varga, 2012). The official definition of a mental disorder in the contemporary psychiatric nosology is “a syndrome characterized by clinically significant disturbance in an individual’s cognition, emotion regulation, or behavior that reflects a dysfunction in the psychological, biological, or developmental processes underling mental functioning” (American Psychiatric Association [APA], 2013, p. 20). To explain such a “dysfunction,” the Diagnostic and Statistical Manual of Mental Disorders (DSM) has adopted a medical illness model. This model makes the assumption that symptoms reflect underlying and latent disease entities. Earlier versions of the DSM were based on psychoanalytic theory and assumed that mental disorders are a result of deep-seated conflicts; modern versions point to dysfunctions in biological, genetic, psychological, and developmental processes as the primary cause. The view of the National Institute of Mental Health (NIMH), the major funding agency for clinical science in the United States, has been that “mental illnesses are brain disorders” and that “in contrast to neurological disorder with identifiable lesions, mental disorders can be addressed as disorders of brain circuits” (Insel et al., 2010, p. 749). Thus, the NIMH is attempting to utilize findings from modern brain sciences to define and diagnose mental disorders, rather than relying on clinical impressions, which may result in arbitrarily defined and consensus-derived diagnostic groups that show a high degree of heterogeneity and comorbidity (Insel et al., 2010). The motive behind this exploration is that eventually the acquired information may be used to develop better treatments or to tailor existing treatments to the individual. Similarly, the DSM–5 noted that “the diagnosis of mental disorders should have clinical utility: it should help clinicians to determine prognosis, treatment plans, and potential treatment outcomes for their patients” (APA, 2013, p. 20). Specifically, the hope is that the DSM–5 validates diagnostic criteria: “Approaches to validating diagnostic criteria for discrete categorical mental disorders have included the following types of evidence: antecedent validators (similar genetic markers, family traits, temperament, and environmental exposures), concurrent validators (similar neural substrates, biomarkers, emotional and cognitive processing, and symptom similarity), and predictive validators (similar clinical course and treatment response)” (p. 20). However, although the DSM–5 recognizes the importance of such validators, it concludes that the empirical support for these validators is insufficient. Therefore, “until incontrovertible etiological or pathophysiological mechanisms are identified to fully validate specific disorders or disorder spectra, the most important standard for the DSM-5 disorder criteria will be their clinical utility” (APA, 2013, p. 20). Unfortunately, there is scant evidence that the latent disease model has met that criterion for success.