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The relevance of maintaining and worsening processes in psychopathology

Published online by Cambridge University Press:  08 June 2015

Francesco Mancini
Affiliation:
Scuola di Psicoterapia Cognitiva (SPC), 00185 Rome, Italy. mancini@apc.it
Amelia Gangemi
Affiliation:
Department of Cognitive Science, University of Messina, 98122 Messina, Italy. gangemia@unime.it

Abstract

The states called “psychopathology” are very diverse, but Lane et al.'s single-process explanation does little to account for this diversity. Moreover, some other crucial phenomena of psychopathology do not fit this theory: the role of negative evaluations of conscious emotions, and the role of emotions without physiological correlates. And it does not consider the processes maintaining disorders.

Type
Open Peer Commentary
Copyright
Copyright © Cambridge University Press 2015 

The target article proposes a unifying theory of psychopathology based on two hypotheses, one concerning the genesis of psychological disorders and the other concerning the psychotherapeutic process leading to change. We focus on the first hypothesis: Psychopathology depends on poor processing of emotions related to traumatic experiences. Four crucial phenomena do not fit this single-process explanation. First, the states called “psychopathology” are very diverse, but Lane et al.'s theory does little to account for this diversity. Indeed, how can a common cause yield a diversity of psychological illnesses? For example, if all psychopathologies are ascribable to the same sequence – trauma→no mentalization of the concomitant emotion→psychopathology – how can different psychological disorders occur? And why does one patient become borderline whereas another patient becomes agoraphobic?

Second, how does patients' awareness of traumatic emotions contribute to psychopathological suffering? Many patients can be aware of traumatic emotions and even evaluate them negatively. This evaluation, not a lack of awareness, exacerbates their suffering. Anxious patients, for example, evaluate their fear as a proof of their weakness. Patients are depressed, for example, not only because they judge their retirement as a sign of uselessness, but also because they consider their lack of interest and energy as a further evidence of uselessness. Such ruminations about depressive symptoms are a key risk factor in clinical depression (Nolen-Hoeksema Reference Nolen-Hoeksema1991; Reference Nolen-Hoeksema2000). Patients are often disturbed about their disturbances (Ellis Reference Ellis1980) and unintentionally give themselves two problems for the price of one (Clark & Beck Reference Clark and Beck2010; Dryden Reference Dryden2000).

Third, how does psychopathology arise from explicit components of emotions? In some cases, an awareness of an emotion and the safety-seeking behaviors that are elicited, such as avoidance of the feared object, can occur without any physiological correlates of the emotion itself (Mauss et al. Reference Mauss, Wilhelm and Gross2003). This lack of correspondence between subjective reports of anxiety and physiological arousal in anxious patients is supported in a number of studies, showing a dissociation between state anxiety and physiological arousal (heart rate, blood pressure, noradrenaline, cortisol response), with the former being stronger compared with the latter (Alpers et al. Reference Alpers, Abelson, Wilhelm and Roth2003; Van Duinen et al. Reference Van Duinen, Schruers and Griez2010).

Fourth, the theory in the target article fails to account for the persistence of psychological disorders. It does not consider research suggesting the existence of two classes of processes that maintain and worsen psychological disorders: those linked to cognitive processes (e.g., Harvey et al. Reference Harvey, Watkins, Mansell and Shafran2004) and those linked to interpersonal ones (e.g., Alden & Taylor Reference Alden and Taylor2004). Regarding cognitive processes, together with Johnson-Laird we have argued that psychological illnesses arise from pathological emotions, and different emotions lead to characteristic pathologies. Cognitive processes, such as reasoning, strive to reduce the impairments giving rise to the hyper emotions, but they often serve to maintain or exacerbate the illness (Johnson-Laird et al. Reference Johnson-Laird, Mancini and Gangemi2006). A hypochondriac patient, for example, focuses on a danger, such as a bodily feeling, which leads to an unconscious transition to a great anxiety that he or she is seriously ill. The anxiety drives cognitive processes in a prudential way: The patient is more likely than others to attend to information related to the illness (see Owens et al. Reference Owens, Asmundson, Hadjistavropoulos and Owens2004), to identify harmless physical sensations as signs of serious illness (see Haenen et al. Reference Haenen, Schmidt, Schoenmakers and van den Hout1997), and to be biased toward confirming its occurrence (see de Jong et al. Reference de Jong, Haenen, Schmidt and Mayer1998; Gilbert Reference Gilbert1998). The processes aimed at preventing harm have the opposite effect. They strengthen patients' beliefs that they are ill and help to maintain or increase the hypochondria. Likewise, patients suffering from anxiety, OCD, or depression use their emotions as a source of evaluations. If they feel anxious about something, they overestimate the danger (Arntz et al. Reference Arntz, Rauner and van den Hout1995). This mechanism is common to those with a tendency to obsessive compulsions (Davey et al. Reference Davey, Startup, Zara, MacDonald and Field2003; Gangemi et al. Reference Gangemi, Mancini and van den Hout2007), and those suffering from depression (Kaney et al. Reference Kaney, Bowen-Jones, Dewey and Bentall1997). This process too implies vicious circles that strengthen negative emotions, appraisal, and beliefs that cause these psychological disorders.

For the interpersonal processes, several studies have demonstrated that anxious people behave in ways that lead to negative reactions from other people, thus establishing dysfunctional interpersonal cycles between themselves and others (Clark Reference Clark, Crozier and Alden2001). These interpersonal cycles could be responsible for the maintenance of the disorders. For example, people with social anxiety and with social phobia display distinctive and less-functional social behavior (i.e., anger, criticism, dependency) than people without those conditions (Alden & Taylor Reference Alden and Taylor2004). They also fail to reciprocate others' self-disclosures, a strategy that led others to perceive targets as dissimilar and uninterested in them, factors that weigh heavily in relationship formation (Alden & Bieling Reference Alden and Bieling1998; Papsdorf & Alden Reference Papsdorf and Alden1998). Depression is also associated with negative social responses (Alden et al. Reference Alden, Bieling, Meleshko, Craig and Dobson1995). Segrin (Reference Segrin2001) found for example, a relationship between social skills deficits and interpersonal connections as maintaining factors of depression.

In sum, the sequence of events following traumas, including inadequate emotional reactions, may lead to certain psychological illnesses. But, other factors matter too. They include the nature of the emotions themselves, which tend to characterize different illnesses; the subjective experience of emotions, which, even in the absence of physiological reactions, can contribute to illnesses; the differences in how individuals react to emotions; the interplay between their emotions and cognitions; and interpersonal processes in maintaining illnesses.

ACKNOWLEDGMENT

We would like to thank Philip N. Johnson-Laird for valuable comments and suggestions on an earlier draft of this manuscript.

References

Alden, L. E. & Bieling, P. J. (1998) The interpersonal consequences of the pursuit of safety. Behaviour Research and Therapy 36:19.Google Scholar
Alden, L. E., Bieling, P. J. & Meleshko, K. G. (1995) An interpersonal comparison of depression and social anxiety. In: Anxiety and depression in adults and children, ed. Craig, K. & Dobson, K. S., pp. 5781. Sage.Google Scholar
Alden, L. E. & Taylor, C. T. (2004) Interpersonal processes in social phobia. Clinical Psychology Review 24:857–82.CrossRefGoogle ScholarPubMed
Alpers, G. W., Abelson, J. L., Wilhelm, F. H. & Roth, W. T. (2003) Salivary cortisol response during exposure treatment in driving phobics. Psychosomatic Medicine 65:679–87.Google Scholar
Arntz, A., Rauner, M. & van den Hout, M. (1995) “If I feel anxious, there must be danger”: Ex-consequential reasoning in inferring danger in anxiety disorder. Behaviour Research and Therapy 33:917–25.Google Scholar
Clark, D. A. & Beck, A. T. (2010) Cognitive therapy of anxiety disorders: Science and practice. Guilford Press.Google Scholar
Clark, D. M. (2001) A cognitive perspective on social phobia. In: International handbook of social anxiety: Concepts, research and interventions relating to the self and shyness, ed. Crozier, R. & Alden, L. E., pp. 405–30. Wiley.Google Scholar
Davey, G. C. L., Startup, H. M., Zara, A., MacDonald, C. B. & Field, A. P. (2003) The perseveration of checking thoughts and mood-as-input hypothesis. Journal of Behavior Therapy and Experimental Psychiatry 34:141–60.CrossRefGoogle ScholarPubMed
de Jong, P. J., Haenen, M., Schmidt, A. & Mayer, B. (1998) Hypochondriasis: The role of fear-confirming reasoning. Behaviour Research and Therapy 36:6574.Google Scholar
Dryden, W. (2000) Invitation to rational emotive behavioural psychology, second edition. Whurr.Google Scholar
Ellis, A. (1980) Rational-emotive therapy and cognitive behavior therapy: Similarities and differences. Cognitive Therapy And Research 4(4):325–40.Google Scholar
Gangemi, A., Mancini, F. & van den Hout, M. (2007) Feeling guilty as a source of information about threat and performance. Behaviour Research and Therapy 45:2387–96.Google Scholar
Gilbert, P. (1998) The evolved basis and adaptive functions of cognitive distortions. British Journal of Medical Psychology 71:447–63.Google Scholar
Haenen, M. A., Schmidt, A. J., Schoenmakers, M. & van den Hout, M. A. (1997) Tactual sensitivity in hypochondriasis. Psychotherapy and Psychosomatics 66:128–32.CrossRefGoogle ScholarPubMed
Harvey, A., Watkins, E., Mansell, W. & Shafran, R. (2004) Cognitive behavioural processes across psychological disorders: A transdiagnostic approach to research and treatment. Oxford University Press.Google Scholar
Johnson-Laird, P. N., Mancini, F. & Gangemi, A. (2006) A hyper emotion theory of psychological illnesses. Psychological Review 113:822–41.Google Scholar
Kaney, S., Bowen-Jones, K., Dewey, M. E. & Bentall, R. P. (1997) Two predictions about paranoid ideation: Deluded, depressed and normal participants' subjective frequency and consensus judgements for positive, neutral and negative events. British Journal of Clinical Psychology 36:349–64.Google Scholar
Mauss, I. B., Wilhelm, F. H. & Gross, J. J. (2003) Autonomic recovery and habituation in social anxiety. Psychophysiology 40:648–53.CrossRefGoogle ScholarPubMed
Nolen-Hoeksema, S. (1991) Responses to depression and their effects on the duration of depressive episodes. Journal of Abnormal Psychology 100(4):569–82.CrossRefGoogle ScholarPubMed
Nolen-Hoeksema, S. (2000) The role of rumination in depressive disorders and mixed anxiety/depressive symptoms. Journal of Abnormal Psychology 109:504–11.Google Scholar
Owens, K. M. B., Asmundson, G. J. G., Hadjistavropoulos, T. & Owens, T. J. (2004) Attentional bias toward illness threat in individuals with elevated health anxiety. Cognitive Therapy and Research 28:5766.CrossRefGoogle Scholar
Papsdorf, M. P. & Alden, L. E. (1998) Mediators of social rejection in socially anxious individuals. Journal of Research in Personality 32:351–69.Google Scholar
Segrin, C. (2001) Interpersonal processes in psychological problems. Guilford.Google Scholar
Van Duinen, M. A., Schruers, K. R. & Griez, E. J. (2010) Desynchrony of fear in phobic exposure. Journal of Psychopharmacology 24:695–9.Google Scholar