Genetic influences on alexithymia and their relationship with depressive symptoms

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Abstract

Objective

The factors involved in the etiology of alexithymia are still unclear. While a few studies suggested substantial genetic influences on alexithymia, it remains to be determined if these influences are independent of genetic influences on other mental health variables correlated with alexithymia, such as depression. This study is aimed at confirming previous findings of a genetic contribution to alexithymia, examining whether there are genetic or environmental influences common to alexithymia facets, and investigating whether genetic influences on alexithymia are independent of genetic influences on depression.

Methods

The 20-item Toronto Alexithymia Scale and a validated measure of depression were administered to a sample of 729 twins (45% males) aged 23–24 years drawn from the population-based Italian Twin Register. Genetic structural equation modeling was performed with the Mx program.

Results

Genetic factors accounted for 42% of individual differences in alexithymia. Unshared environmental factors explained the remaining proportion of variance. There was a substantial (0.65) genetic correlation between alexithymia and depression. The inclusion of depression as a covariate in the genetic models reduced the heritability estimate for alexithymia to 33%.

Conclusions

Despite some limitations, this study corroborates the notion that genetic factors contribute substantially to individual differences in alexithymia, with unshared environmental factors also playing an important role. Also, it suggests a genetic link between alexithymia and depression.

Introduction

The term ‘alexithymia’ (from the Greek a = lack, lexis = words and thymos = emotion, mood) was introduced in the early seventies to describe some cognitive and affective characteristics that were often observed among patients with so-called psychosomatic disorders [1], [2]. The alexithymia construct, which has gradually taken on a key role within psychosomatic medicine, encompasses limited ability to identify and verbally express emotions, to distinguish emotions from bodily sensations, impoverished fantasy life, and reduced symbolic thinking with a concrete, stimulus-bound, action-oriented thinking style similar to the ‘pensée opératoire’ [3].

While considerable research has been devoted to the association between alexithymia and physical and mental health problems and its possible causal implications, only relatively few studies have attempted to identify which factors are involved in the etiology of alexithymia. Most of these studies pointed to a role of childhood family factors [4], [5], [6], [7], [8], [9], [10], [11]. Although such factors seem to be entirely environmental in nature, in recent years behavioral genetic studies revealed that the exposure to many features of the family environment is at least partly under genetic influence [12], [13].

There are several mechanisms that may account for the contribution of genetic factors to individual differences in alexithymic characteristics. The genes potentially involved in variation in alexithymia may influence the transcription of neuronal receptors or neurotransmitters, or may affect neurodevelopment. Genetic factors significantly contribute to variation in brain structures [14], [15], and a recent study reported an association between alexithymia and the catechol O-methyltransferase Val108/158Met gene polymorphism [16]. Some family studies found a significant association of mothers' [17], [18], [19] and fathers' [19] alexithymia scores with alexithymia scores in the offspring. While these studies suggest an intergenerational transmission of alexithymia, they cannot establish whether the observed familial aggregation originates from genetic or environmental influences shared by family members.

The twin study design is the most suitable to disentangle the role of nature and nurture. Given that monozygotic (MZ) twin pairs share all genes, while dizygotic (DZ) pairs share on average 50% of them, a higher phenotypic resemblance observed among MZ pairs for a trait suggests a substantial role of genetic factors in its expression. To date, only three twin studies of alexithymia have been performed. Two pioneer studies suggested genetic influences on alexithymia [20] or at least its externally oriented thinking facet [21]. However, these studies suffered from limitations in sample size [20], [21] and measurement [20]. Recently, a very large population-based study of 8785 twin pairs strongly supported a genetic contribution to individual differences in all facets of alexithymia [22].

While these studies suggest genetic effects on alexithymia, there are several related issues that deserve further investigation. First, no study used multivariate models to examine whether there are genetic or environmental influences common to alexithymia facets. Second, it remains to be determined if genetic influences on alexithymia are independent of genetic influences on other mental health variables, such as depression, which are correlated with alexithymia [23], [24], [25] and are known to be genetically influenced [26], [27].

In this study, we measured alexithymia and depression in a general population sample of MZ and DZ twins reared together, with the aim of confirming previous findings of a genetic contribution to individual differences in alexithymia, examining whether there are genetic or environmental influences common to alexithymia facets, and investigating whether genetic influences on alexithymia are independent of genetic influences on depression.

Section snippets

Participants

The study sample was derived from the population-based Italian Twin Register (ITR) [28], which currently contains information on approximately 23,000 Italian twins belonging to different age groups and geographical areas and is involved in both general population- and clinical-based studies on various complex phenotypes, some conducted within large European networks [29].

A total of 2930 twins enrolled in the ITR and aged 23–24 years were contacted by mail and invited to participate in a study

Sample descriptives

Table 1 shows means and standard deviations of the total TAS-20 and its subscales, computed for twins as individuals, according to gender and zygosity.

The TAS-20 total score was moderately correlated (r=0.44) with PDS score. Females scored, on average, significantly higher on the DIF dimension and significantly lower on the EOT dimension compared to males. No significant zygosity differences were detected.

Correlations

Table 2 provides the observed correlation structure for the total TAS-20 and its subscales.

Discussion

We found a substantial contribution of genetic factors to individual differences in alexithymia and all its facets as measured by the TAS-20. This finding is consistent with a recent large Danish study, though our heritability estimates are slightly higher than those reported in that study [22]. This discrepancy may be due to age differences between study samples, as all our twins were of young age whereas the Danish twins had a broad age range of 20–71 years. Our finding of substantial genetic

References (60)

  • RM Bagby et al.

    The twenty-item Toronto Alexithymia Scale. I. Item selection and cross-validation of the factor structure

    J Psychosom Res

    (1994)
  • RD Lane et al.

    Is alexithymia the emotional equivalent of blindsight?

    Biol Psychiatry

    (1997)
  • CG Kooiman et al.

    The assessment of alexithymia: a critical review of the literature and a psychometric study of the Toronto Alexithymia Scale-20

    J Psychosom Res

    (2002)
  • HCM Vorst et al.

    Validity and reliability of the Bermond–Vorst Alexithymia Questionnaire

    Pers Individ Dif

    (2001)
  • PE Sifneos

    The prevalence of ‘alexithymic’ characteristics in psychosomatic patients

    Psychother Psychosom

    (1973)
  • JC Nemiah et al.

    Alexithymia: a view of the psychosomatic process

  • P Marty et al.

    Das operative Denken (pensée opératoire)

    Psyche Stuttgart

    (1978)
  • B Mallinckrodt et al.

    Family dysfunction, alexithymia, and client attachment to therapist

    J Couns Psychol

    (1998)
  • S Kench et al.

    Alexithymia and childhood family environment

    J Clin Psychol

    (2000)
  • I Fukunishi et al.

    Mothers' low care in the development of alexithymia: a preliminary study in Japanese college students

    Psychol Rep

    (1997)
  • CG Kooiman et al.

    Childhood adversities as risk factors for alexithymia and other aspects of affect dysregulation in adulthood

    Psychother Psychosom

    (2004)
  • C Evren et al.

    Childhood abuse and neglect as a risk factor for alexithymia in adult male substance dependent inpatients

    J Psychoactive Drugs

    (2009)
  • M Joukamaa et al.

    Alexithymia and childhood abuse among patients attending primary and psychiatric care: results of the RADEP study

    Psychosomatics

    (2008)
  • O Mason et al.

    Alexithymia: its prevalence and correlates in a British undergraduate sample

    Psychol Psychother

    (2005)
  • R Plomin et al.

    Why are children in the same family so different from one another?

    Behav Brain Sci

    (1987)
  • R Plomin et al.

    Behavioral genetics

    (2008)
  • JE Schmitt et al.

    Review of twin and family studies on neuroanatomic phenotypes and typical neurodevelopment

    Twin Res Hum Genet

    (2007)
  • JS Peper et al.

    Genetic influences on human brain structure: a review of brain imaging studies in twins

    Hum Brain Mapp

    (2007)
  • BJ Ham et al.

    Association between the catechol O-methyltransferase Val108/158Met polymorphism and alexithymia

    Neuropsychobiology

    (2005)
  • MA Lumley et al.

    Family factors related to alexithymia characteristics

    Psychosom Med

    (1996)
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