It is unclear what causes alexithymia, though several theories have been proposed. Early studies showed evidence that there may be an interhemispheric transfer deficit among people with alexithymia; that is, the emotional information from the
right hemisphere of the brain is not being properly transferred to the language regions in the left hemisphere, as can be caused by a decreased
corpus callosum. This is often present in psychiatric patients who have suffered severe childhood abuse. A
neuropsychological study in 1997 indicated that alexithymia may be due to a disturbance to the right hemisphere of the
brain, which is largely responsible for processing emotions. In addition, another neuropsychological model suggests that alexithymia may be related to a dysfunction of the
anterior cingulate cortex. These studies have some shortcomings, however, and the empirical evidence about the neural mechanisms behind alexithymia remains inconclusive. French psychoanalyst
Joyce McDougall objected to the strong focus by clinicians on neurophysiological explanations at the expense of psychological ones for the genesis and operation of alexithymia, and introduced the alternative term "
disaffectation" to stand for psychogenic alexithymia. For McDougall, the disaffected individual had at some point "experienced overwhelming emotion that threatened to attack their sense of integrity and identity", to which they applied psychological defenses to pulverize and eject all emotional representations from consciousness. McDougall has also noted that all infants are born unable to identify, organize, and speak about their emotional experiences (the word
infans is from the Latin "not speaking"), and are "by reason of their immaturity inevitably alexithymic". Based on this fact McDougall proposed in 1985 that the alexithymic part of an adult personality could be "an extremely arrested and infantile psychic structure". A similar line of interpretation has been taken up using the methods of
phenomenology. The first language of an infant consists of nonverbal
facial expressions. The parent's emotional state is important for determining how any child might develop. Neglect or indifference to varying changes in a child's facial expressions without proper feedback can promote an invalidation of the facial expressions manifested by the child. The parent's ability to reflect self-awareness to the child is another important factor. If the adult is incapable of recognizing and distinguishing emotional expressions in the child, it can influence the child's capacity to understand emotional expressions. The attention-appraisal model of alexithymia by Preece and colleagues describes the mechanisms behind alexithymia within a cognitive-behavioral framework.
Molecular genetic research into alexithymia remains minimal, but promising candidates have been identified from studies examining connections between certain genes and alexithymia among those with psychiatric conditions as well as the general population. A study recruiting a test population of Japanese males found higher scores on the Toronto Alexithymia Scale among those with the
5-HTTLPR homozygous long (L)
allele. The 5-HTTLPR region on the
serotonin transporter gene influences the transcription of the serotonin transporter that removes serotonin from the
synaptic cleft, and is well studied for its association with numerous psychiatric disorders. Another study examining the
5-HT1A receptor, a receptor that binds
serotonin, found higher levels of alexithymia among those with the G allele of the
Rs6295 polymorphism within the HTR1A gene. Also, a study examining alexithymia in subjects with
obsessive–compulsive disorder found higher alexithymia levels associated with the Val/Val allele of the
Rs4680 polymorphism in the gene that encodes
Catechol-O-methyltransferase (COMT), an enzyme that degrades
catecholamine neurotransmitters such as
dopamine. These links are tentative, and further research will be needed to clarify how these genes relate to the neurological anomalies found in the brains of people with alexithymia. Although there is evidence for the role of environmental and neurological factors, the role and influence of genetic factors for developing alexithymia is still unclear. A single large scale Danish study suggested that genetic factors contributed noticeably to the development of alexithymia. However, some scholars find
twin studies and the entire field of
behavior genetics to be controversial. Those scholars raise concerns about the "equal environments assumption".
Traumatic brain injury is also implicated in the development of alexithymia, and those with traumatic brain injury are six times more likely to exhibit alexithymia. Alexithymia is also associated with newborn circumcision trauma.
Substance abuse, or substance use disorders There is evidence to propose a significant correlation between substance abuse and alexithymia and a meta-analysis found a large effect size between the two measures. A bi-directional relationship was suggested, where substance abuse increases alexithymic traits and alexithymia correlated with increased substance abuse. In a study that explored cocaine-dependent individuals, it was found that the mechanism between alexithymia and substance abuse may be mediated by differences in reward processing in alexithymic individuals although more research is needed. ==Relationships==