“Alexithymia is a dimensional personality trait that varies in intensity from person to person. Alexithymia is measured on a continuum and is defined by; (1) a difficulty identifying feelings (certain ones or all of them) and distinguishing between feelings and bodily sensations of emotional arousal (2) difficulty describing feelings to others (3) constricted imaginal process, as evidence by scarcity of fantasies.” (Thanks Wikipedia!)
In Greek, Alexithymia means “not having words for feelings” and it causes people to register their emotions as a physical problem/ailment rather than a sign or distinct inner feeling that signals us to the fact that something needs our attention. For example, instead of registering a feeling of anger (more specifically a degree of mental anguish never experienced before) they cannot process it at the cognitive level because it’s beyond what their psyche can handle, so it gets experienced as a headache, indigestion or muscle pain and stiffness, or worse, according to Dr. Bessel Van Der Kolk, in his bestselling book, “The Body Keeps The Score- Brain, Mind, and Body in the Healing of Trauma.”
Traumatized children and people are often alexithymic because they’ve learned to shut down their emotions because they were too overwhelming (during abuse, trauma, etc.) and as a result, they have lost touch between their mind and body and can no longer identify what they’re feeling. This condition causes people to use “action” instead of “language” to express what they’re feeling. For example, a child that was bullied at school may not appear to be too upset about it but may spend that evening and the following days with an unexplained headache or stomach and gastrointestinal distress.
Alexithymia also causes changes in the immune system which lead to autoimmune illnesses and diseases. Below is an academic article (review) that helps explain the process, which includes increases in Tumor Necrosis Factor (TNF).
*************************************************************************************************
*From Website; https://link.springer.com/content/pdf/10.1007/BF03379564.pdf
“ALEXITHYMIA AND IMMUNE DYSREGULATION: A CRITICAL REVIEW”
By, Tomas Uher* Department of Neurology, Faculty Hospital Bulovka, Prague, Czech Republic Received January 5, 2010; accepted February 14, 2010
ABSTRACT; Numerous recent studies have documented that alexithymia is significantly related to dysregulation of immune functions. These findings implicate that stressors related to alexithymia could underlie the process of immune dysregulation that likely presents a significant risk factor in pathogenesis of several psychosomatic illnesses.
In close relationship with above mentioned data it was hypothesized that responses of autonomic nervous system (ANS) to emotion-evoked stimuli in alexithymic subjects are exaggerated or excessively persistent (Nemiah, 1975; Papciak et al., 1985; Martin & Pihl, 1985). In agreement with this assumption sympathetic overactivation in alexithymic persons has been found (Martin et al., 1986; Martin & Pihl, 1986; Rabavilas, 1987; Infrasca, 1997; Fukunishi et al., 1999; Gundel et al., 2002). This sympathetic over-activation frequently disturbs the autonomic, neuroendocrine and immune systems, and may result to tissue pathology. Recent findings also indicate that a main factor in this process present HPA axis (hypothalamus pituitary adrenal) and SAM system (sympathetic adrenal medullary), which significantly influence functioning of the immune system by regulation of proinflammatory and antiinflammatory cytokines.
ALEXITHYMIA AND IMMUNE CHANGES; According to recent findings glucocorticoides and catecholamines present key stress hormones produced by HPA and SAM system, that prompt the production of anti-inflammantory cytokines such as IL-4, IL-10 and TGF-β, whereas they inhibit production of proinflammantory cytokines, such as IL-12, TNF-α (Tumour Necrosis Factor Alpha) and INF-γ (Interferon Gamma) (Elenkov & Chrousos, 2002). According to recent evidence, cytokine production may be also directly stimulated by stressful experiences and negative emotions (Kiecolt-Glaser et al., 2002) and conversely cytokines may be responsible for influence of the HPA and SAM system (Zarkovic et al., 2008; Marques et al., 2009; Locatelli et al., 2010). Recent findings suggest that interleukine dysregulation presents important factor responsible for chronic impairment of pro/antiinflammatory cytokine balance in alexithymia with psychological and somatic adverse effects (Corcos et al., 2004). Guilbaud et al. (2003) suggests that immune dysregulation observed in alexithymia, in many aspects seems to follow the same pattern as in subjects afflicted with chronic stress with a predominance of depressed cell-mediated immunity and a skewed Th1/Th2 ratio towards Th2 response. Contemporary studies also demonstrated that acute stress increases cardiac sympathetic activation and plasma catecholamine levels, while chronic stress is associated with a higher blood pressure and plasma levels of ACTH (Adrenocorticotropic Hormone) and diminished cellular immune response with decreased levels of interleukin-1β (Caioppo et al., 1998). According several studies acute stress seems to induce cell-mediated immunity (Th-1 immune response) while chronic stress induces humoral (Th-2) immune responses (Elenkov et al., 1996; Marshall et al., 1998; Glaser et al., 2001; Agarwal & Marshall, 2001). From this perspective and according to PubMed search, there are only a few studies examining immune response in alexithymia. For example, a study performed in 17 healthy young women demonstrated that alexithymia (measured by Toronto Alexithymia Scale – TAS) was significantly positively correlated with serum levels of IL-4 (Corcos et al., 2004). In this context increased level of IL-4 was hypothesized as an important factor responsible for chronic impairment of pro/anti-inflammatory cytokine balance in alexithymia with psychological and somatic adverse effects (Corcos et al., 2004). Another investigation by Pedrosa Gil et al. (2007) compared 24 subjects with somatoform disorder (SFD) and clinically significant alexithymia (TAS) with 9 healthy controls. They found significant relationship of alexithymia with decreased Th1-mediated immune function and increased activation of Th2 immune function. These finding were confirmed by the augmented serum levels of IL-6 and IL-10, elevated immunoglobulin E, and decreased levels of IL-2 Ralpha. Similarly, in the study by Guilbaud et al. (2008) performed in fifty-one healthy 18-27 year old women significant correlations of alexithymic scores (TAS) with decreased interleukin 1beta, IL-2 and IL-4 production were found. Guilbaud et al., (2008) also found reduced ratios of Th1/Th2 (IL-2/IL10) and CD4/CD8, as well as reduced CD4 percentages indicating that alexithymic women have altered immune function, with a predominance of depressed cellmediated immunity and a skewed Th1/Th2 ratio towards Th2 response. Also other authors have demonstrated altered cellmediated immunity in alexithymia. For example, study of Dewaraja et al. (1997) performed in 97 male subjects has reported hypo-activation of Th1 immune functions with significantly lower numbers of the most cytotoxic natural killer (NK) subset and killer effector T cell count in alexithymic subjects (TAS). In further study by Todarello et al. (1994) performed in 62 women (36 healthy and 26 affected by cervical intraepithelial neoplasia CIN I, II, III), who were not aware of their condition, lower rates of almost all lymphocytic subsets in alexithymic women compared to non-alexithymic ones were found. These results were successfully replicated by Todarello et al. (1997) performed in bigger sample of 43 women affected by cervical dysplasia and 67 healthy women. These studies by Todarello et al. (1994, 1997) are in agreement with results reported by other authors who hypothesized that a certain personality trait characterized by emotional inhibition is related to greater cancer vulnerability, and that type of personality might be an important factor responsible for the outbreak of cancer. Such relationship might be mediated by certain lymphocytic functions and alexithymic status. It was proposed that immune system has an important role as a possible mediator between personality and cancer and that lowered cytotoxic lymphocytes trigger a mechanism, that may be responsible for the association between alexithymia and psychosomatic illnesses (Dewaraja et al., 1997). Also further studies demonstrated immune changes associated with alexithymia. For example, strong positive correlation was found between pro-inflammantory cytokine IL-18 levels and alexithymia score (TAS) in ischemic stroke patients, particularly in patients with right–hemisphere lesions (Bossù et al., 2009). In the study by Temoshok et al. (2008) performed in 200 HIVinfected subjects, alexithymic scores (TAS) were positive correlated with significantly lower stimulated production of HIV-inhibiting MIP-1 alpha. They also observed association of strong maladaptive Type C coping with significantly higher IL-6 that presents a second key immune parameter in HIV pathogenesis. Close relationship between immune response and alexithymia was also found in the study by Lin et al. (2005) performed in 60 healthy male students where positive correlation of elevated alexithymic scores (TAS) with significantly lower levels of saliva IgA (Imunoglobulin A) one month before stress situation was observed. Recent study by Vadacca et al., (2008) found increased prevalence of alexithymia (TAS) in patients with rheumatoid arthritis (RA) (54%) and also in patients with systemic lupus erythematosus (SLE) (42%). Both groups of patients had increased values of IL-6 and TNF-alpha. Similar study (Bruni et al., 2006) reported association between alexithymia (TAS) and increased TNF levels in RA patients.
CONCLUSION; Recent results indicate significant relationships among stress, alexithymia and immune dysregulation, although there are certain limitations that mainly include relatively small sample sizes in several studies and heterogeneous patient populations. In the majority of these studies alexithymia related reduction in Th1-mediated immune functions (Todarello et al., 1994, 1997; Dewaraja et al., 1997; Pedrosa et al., 2007; Guilbaud et al., 2008) and an increase in the activation of the Th2 immune functions have been observed (Pedrosa et al., 2007; Guilbaud et al. 2008). But also other support hypothesis of cytokine dysregulation in alexithymia (Corcos et al., 2004; Bruni et al., 2006; Vadacca et al., 2008; Temoshok et al., 2008; Bossù et al., 2009). In addition an influence of the neuroendocrine dysregulation on immune functions is relatively well documented (Elenkov & Chrousous, 2002). Open question is, to what extent alexithymia may be modified by psychotherapeutic interventions (Grabe et al., 2008). Reduction of alexithymic features by psychotherapeutic interventions was tested in the several studies with optimistic results (Beresnevaite, 2000; Kennedy & Franklin 2002; Simha-Alpern, 2007; Gay et al., 2008 & Grabe et al., 2008). In this context assumed biological effect of psychotherapy on the structure and functions of the brain (Kandel, 1988, Gabbard, 2000) could present an important topic for future research of alexithymia and its therapy.
For references, please click on the link above, to this critical review. Thank you for reading
DONATIONS; If you find this website educational or interesting, please consider making a donation to help with website and bookmaking costs, as I am currently writing my very first book about my experiences with each of these subject matters. THANK YOU!!!🌺🌺🌺
