Conclusion

            This current research yields data that contribute to the growing body of knowledge concerning the role of alexithymia in the etiology of psychosomatic and other disorders of affect regulation. The data support the heuristic value of the alexithymia construct in conceptualizing and explaining some of the deficits involved in disorders characterized by affect dysregulation. The results of this current research are consistent with findings of earlier studies while at odds with the results of others.

            Zeitlin and McNally (1993) found greater association between alexithymia and PD than with OCD. Parker, Taylor, Bagby and Acklin (1993) found higher rates of alexithymia in those with PD compared to those with simple phobia. And Joukamaa and Lepola (1994) found more alexithymia in those with PD than in a healthy control group. The results of this current research are consistent with these studies in finding greater correlation between alexithymia and PD than with other disorders.

            On the other hand, Cox, Swinson, Shulman and Bourdeau (1995) found a non-significant difference in alexithymia between a PD sample and a social phobia sample. Fukunishi, Kikuchi, Wogan and Takubo (1997) found a non-significant difference between PD and social phobia samples. And Bankier, Aigner and Bach (2001) found lower alexithymia scores for a PD sample compared to somatoform, obsessive-compulsive and depression samples.

            While research results may be inconsistent, or even contradictory, the current research results are consistent with the author’s experience in treating those with PD compared to other mental health disorders. The degree of affective unawareness in psychosomatic disorders such as PD is commensurate with the degree of somatization and tendency for catastrophic explanations of somatic experiences. The F1 subfactor on the TAS-20 isolates this trait and identifies the difficulty in distinguishing between emotions and related physiological sensations. It would be expected that there would be significant elevation on F1 by those with PD compared to controls, and this current research confirms this. Some of the inconsistent findings by earlier studies are related to a lack of subfactorial analysis.

            The most prominent implications of this current research derive from two sources. First is the significant involvement of the TAS-20 F1 deficits in PD for both genders. And second is the considerable gender difference in the prevalence of alexithymia. Given the extent of difference between genders in the manifestation of alexithymic traits, it is all the more noteworthy that the only area of congruence between the genders is in the elevation of F1 scores in PD. The implication is that the F1 deficits – difficulty identifying emotions and differentiating them from their related physiological sequelae – are the alexithymic component most involved in PD. The somatization process inherent in this component underscores Nemiah’s (1984) conceptualization of PD as a psychosomatic disorder. The Krystal model (1988) as well as the Lane and Schwartz model (1987) suggest the origin of the somatization in PD to be the arrest at or regression to an earlier, non-verbal and somatized level of affect development. The implications for treatment then would appear obvious – that affects need to become more well identified and verbalized to become more cognitive and less somatic.

Directions for Future Research

            The results of this current research provide additional empirical support for the significance of certain alexithymic traits in the etiology of PD. These current research hypotheses seem to be appropriate directions for future research given the large body of literature supportive of the theory outlined in the literature review. It would be of value for future research to address some of the limitations of this current research that are noted earlier. It would be beneficial for future research to be conducted with larger sample groups, possibly controlling for age and gender using a narrower age range or single gender studies.

            Given the multi-faceted nature of the alexithymia construct, future studies might include additional self-report measures or observer-rating instruments designed to isolate each of the alexithymic traits to provide more information as to which traits are most prominent to PD. Observer-ratings could also address the inherent problem of the accuracy of self-reported data. Valuable future research might involve the use of pre and post testing of specific alexithymic traits to obtain information as to the interconnectedness of traits and whether they respond in tandem or independently to treatment interventions. Additionally, pre and post testing might demonstrate mutability of alexithymic traits, and thereby influence the state or trait controversy regarding the nature of alexithymia.

Closing Statement

            Each is liable to panic, which is exactly, the terror of ignorance surrendered to the imagination. Knowledge is the encourager, knowledge that takes fear out of the heart, knowledge and use, which is knowledge in practice. They can conquer who believe they can. It is he who has done the deed once who does not shrink from attempting again.

- Ralph Waldo Emerson (1803-1882)

            This current research offers validation of the above quotations premise, that ignorance provides opportunity for the imagination to induce fear while knowledge can quell it. The cognitive and affective deficits of alexithymia constitute ignorance – or rather the lack of self-knowledge – that allows the imagination to generate panic attacks. This research provides support for the hypothesis that the aspect of alexithymia most responsible for chronic panic attacks is the limited capacity for identifying emotions and the tendency to confuse them with physical sensations. The cognitive therapy modality strives to increase self knowledge – thereby reduce alexithymic traits – and has demonstrated the greatest success of any modality in reducing the frequency and intensity of the panic attacks of PD. Cognitive therapy aims to facilitate progression in the epigenetic model of affect development, upward from early levels of alexithymic traits to higher levels of desomatized, verbalized affects. Ultimately, the goal of treatment is the facilitation of the successful completion of normal developmental epigenesis – from alexithymia to lexithymia.