🧠 Overview
Alexithymia (literally, “no words for emotions”) is a personality-level state that reflects a disrupted or underdeveloped linkage among language–emotion–body to some degree.Individuals with this profile often cannot clearly identify or describe their own feelings, even when they know they feel “uneasy” or “not themselves.”
This condition does not mean a person “has no emotions” — on the contrary, they have a full range of emotions like everyone else. It’s just that the brain systems that translate emotions into words operate slowly or out of sync with internal bodily awareness (interoception).
This creates a gap between “what is felt” and “what can be spoken.”
Alexithymia is not classified as a “disorder” in the DSM-5-TR or ICD-11; rather, it is a trait or dimension of personality that directly affects emotional expression, communication, and overall mental health.
The concept arose in the 1970s within psychosomatic medicine, which sought to explain why some patients manifest physical symptoms under stress without being able to talk about their emotions.
The term “emotion-blindness” is used metaphorically — not because the person lacks a heart, but because “their brain can’t see the language of its own heart.”
Three core deficits stand out:
1️⃣ Difficulty identifying feelings (DIF)
2️⃣ Difficulty describing or conveying feelings (DDF)
3️⃣ Externally Oriented Thinking (EOT) — prioritizing logic and facts over inner feelings
Brains of people with alexithymia often show atypical connectivity among the insula, anterior cingulate cortex (ACC), and amygdala — regions involved in sensing bodily signals and processing emotion.
As a result, they may feel “numb” or “cut off” from their own emotions in some situations, especially under stress or inner conflict.
This condition appears in roughly 10–15% of the general population and is notably higher among individuals with Autism Spectrum Disorder (ASD), depression, anxiety disorders, chronic pain, and eating disorders.
“Emotion-blindness” is also linked with favoring analytical over emotional reasoning, which may make a person seem “cold” or “unfeeling,” when in reality their internal emotion-processing simply runs slower.
In relationships, alexithymia makes emotional communication misaligned — a partner may feel “unloved” or “uncared for,” when in fact the person simply can’t articulate what they feel.
Physically, emotions may emerge as bodily symptoms instead — chest tightness, headaches, or stomach clenching under stress — while the person doesn’t recognize these as “anxiety” or “fear.”
In summary, alexithymia is “a state in which the brain can feel, but doesn’t know how to speak about it.”
It is the gap between emotions that truly arise and language–awareness–expression that fail to align.
And although it isn’t a disorder, it’s a key mechanism underlying tense relationships, chronic emotional distress, and medically unexplained physical symptoms for many people.
💭 Core Symptoms
Alexithymia literally means “no words for emotions.”
Its core symptoms directly concern the recognition and use of emotional language, which is a multi-step process in the brain — from perceiving bodily signals (interoception) → interpreting them as emotions → translating them into words → communicating them outward.
In most people, these systems operate in synchrony. But in those with Alexithymic Type, these systems fall “out of rhythm.”
The result: they can feel, but cannot translate the feeling into words — or even cannot tell what exactly they are feeling.
Thus, the main symptom cluster of Alexithymia consists of four major dimensions as follows:
1️⃣ DIF — Difficulty Identifying Feelings
“I don’t know what I feel — I just feel bad.”
This refers to difficulty in identifying or labeling emotions occurring at a given moment.
The insula (which senses bodily signals) and anterior cingulate cortex – ACC (which interprets sensations into emotional meaning) fail to coordinate efficiently.
Therefore, the person only knows that “something is happening in the body” — such as a racing heartbeat, chest tightness, or shortness of breath —
but cannot determine whether it is fear, anxiety, or something else.
This often leads to misinterpretation, for example:
- Interpreting stress as “illness” rather than “emotional tension.”
- Feeling uneasy without knowing why.
- Uncertain whether one feels sad or angry.
- Using vague general terms like “I feel not okay” instead of precise ones like “I feel disappointed.”
In neurobiological terms, this is called somatization of affect — when emotion is converted into bodily symptoms because the circuits linking emotion and language do not function fully.
2️⃣ DDF — Difficulty Describing Feelings
“I know I’m sad... but I can’t explain why.”
Even when they recognize that they are feeling something, the words for those emotions are missing.
This results from underfunctioning in Broca’s area, the left inferior frontal gyrus, and the insula–ACC network, which connects language to emotion.
Common behavioral patterns include:
- When asked, “How do you feel?” they respond, “I don’t know,” or “I’m fine.”
- They talk about events, not emotions, e.g.:
“I got scolded by my friend,” instead of “I felt embarrassed and hurt.”
- They favor logical phrasing over emotional phrasing, e.g.:
“Because he was wrong,” instead of “I was angry that he didn’t value my effort.”
This makes others perceive them as “emotionally closed” or “insincere,” while in truth, they simply don’t know how to put it into words.
3️⃣ EOT — Externally Oriented Thinking
“Focusing on facts rather than feelings.”
This is a thinking style directed outward — focusing on external events, information, and logic rather than internal experience.
The prefrontal cortex, especially the dorsolateral PFC, takes the lead, while the limbic system, which generates emotion, is downregulated.
For example,
when a friend says, “I feel terrible about failing the exam,”
a person with high EOT may respond:
“Just study more next time; you’ll pass.”
instead of
“I understand — that must really hurt your confidence.”
As a result, they appear “highly logical but emotionally detached.”
On the positive side, such people often excel in analysis, problem-solving, and rational decision-making.
EOT is also associated with reduced fantasizing and low interest in art or literature, because these activities rely heavily on emotional interpretation.
4️⃣ Interoceptive Deficits
“The brain doesn’t understand what the body is saying.”
This refers to deficits in perceiving bodily signals such as heartbeat, breathing, muscle tension, or body temperature.
Individuals with interoceptive deficits cannot match these signals to the emotions they represent.
For instance, a fast heartbeat may not be recognized as excitement or fear.
The anterior insula, which serves as the hub of interoceptive awareness, operates below normal levels.
This leads to a state of emotional numbness or emptiness.
Many report physical symptoms like headaches, stomachaches, or chest tightness from chronic stress without realizing the emotional cause.
🔁 Behavioral Manifestations
When the “feel–interpret–express” system lacks coordination, downstream behavioral patterns emerge, such as:
- Difficulty communicating emotions
- Slow emotional responses
- Using logic in place of emotion
- Frequent misreading of others’ emotions
- Appearing “unfeeling” while internally carrying high stress
Clinically, this reflects a functional disconnection between the emotional system (limbic) and the executive–linguistic system (PFC).
🌍 Real-World Impact
- Personal relationships: Partners may feel “unloved” or “misunderstood” because the person stays quiet and unemotional.
- Workplace: Often seen as “cold” or “unempathetic,” yet capable in analytical or planning roles.
- Physical health: Suppressed stress manifests as bodily symptoms like headaches, fatigue, or chronic indigestion.
- Mental health: Feelings of emotional emptiness and loss of meaning in life.
- Therapy: Progress in psychotherapy tends to be slower, since hidden emotions are not easily accessed or verbalized.
🧩 Diagnostic Criteria
💡 Note: Alexithymia is not a disorder,
and therefore has no official diagnostic criteria in the DSM-5-TR or ICD-11.
However, there are standardized assessment tools used globally to measure severity and subtype patterns of alexithymia.
1️⃣ Toronto Alexithymia Scale (TAS-20)
The most widely used and validated instrument.
Developed by Bagby et al. (1994).
It consists of 20 self-report items, rated from 1–5 (total score 20–100), and measures three dimensions:
| Dimension | Description |
|---|---|
| DIF | Difficulty Identifying Feelings — trouble distinguishing one’s own emotions |
| DDF | Difficulty Describing Feelings — trouble describing emotions to others |
| EOT | Externally Oriented Thinking — focus on logic and external facts over internal feelings |
Interpretation Cutoffs:
- ≥ 61 → alexithymic range
- 52–60 → borderline / possible
- ≤ 51 → non-alexithymic
Strengths:
- Available in multiple languages (including Thai)
- High reliability (Cronbach’s α ≈ 0.80–0.86)
- Applicable for both research and clinical practice
Limitations:
- Relies on self-report
- Individuals with severe emotional unawareness may underrate their difficulties
2️⃣ Bermond–Vorst Alexithymia Questionnaire (BVAQ)
A more detailed companion measure than TAS-20.
It includes 40 items, divided into two main dimensions:
- Cognitive dimension: emotional reasoning and cognitive processing
- Affective dimension: emotional experiencing and feeling capacity
The BVAQ distinguishes between “those who cannot think emotions” and “those who cannot feel emotions.”
For example:
Some may understand emotions but not feel them (affective deficit).
Others may feel emotions but lack words to express them (cognitive deficit).
3️⃣ Other Research Instruments
- Observer Alexithymia Scale (OAS): rated by peers or clinicians
- Structured Interview for Alexithymia (SIA): for clinical research settings
- LEAS (Levels of Emotional Awareness Scale): measures granularity in emotional perception
4️⃣ Clinical Use of Scores
- Cutoff ≥ 61 indicates presence of alexithymic traits
- High EOT vs low DIF/DDF → “logic-dominant” emotional style
- High DIF/DDF → greater risk of depression and psychosomatic issues
- Often paired with mental health tools like BDI-II (depression) and STAI (anxiety)
5️⃣ Follow-Up Assessments
- Recommended every 6–12 months to track psychotherapy progress
- Decreasing TAS-20 scores, especially in DIF/DDF, indicate improved emotional awareness and integration
🔬 Clinical Summary
Although “Alexithymia” is not a formal disorder in diagnostic manuals,
these instruments allow accurate understanding of the brain–body–language link that underlies emotional awareness.
They form the foundation for designing targeted interventions such as:
training interoceptive awareness, emotion labeling, and emotional mirroring exercises.
Subtypes or Specifiers
Common subtype groupings in the literature:Primary (Trait) Alexithymia – a relatively stable personality characteristic linked to early emotional system development/biobiology → tends to be more persistent and slower to respond to therapy. PMC+1
Secondary (State/Situational) Alexithymia – arises after psychological/physical factors, e.g., chronic psychological trauma, medical/neurological conditions (injury, stroke), or chronic stress → can fluctuate and remit as precipitating factors improve. There is an “organic subtype” when directly associated with brain pathology. old.jpsychopathol.it
Specifiers by TAS-20 dimensions: profiles dominated by DIF/DDF/EOT (e.g., “DIF-dominant”) to plan targeted support. sciencedirect.com
Contextual/comorbid: co-occurring with ASD, depression, anxiety, chronic pain, and eating disorders, which may alter the clinical picture compared to non-comorbid cases. PMC+1
🧠 Brain & Neurobiology
Over more than 30 years, neuroscience has shown that alexithymia is not just a behavioral personality style but a condition with distinctive signatures in brain structure and connectivity — especially within the interoceptive–emotional–regulatory network, a set of regions that coordinate with great subtlety.1️⃣ Insula — The Interoceptive Hub
The insula links “bodily signals” to “emotional awareness.”It acts as a “central receiver” for internal data — heartbeat, breathing, temperature, muscle tension — relaying this to emotion and language systems.
Multiple studies find that people with high alexithymia show reduced insula activity, especially in the anterior insula, which supports the sense of “I’m feeling X.”
fMRI work shows that when presented with emotional images or sounds, their insula responses may be minimal.
They may know something is happening in their body (e.g., pounding heart) but the brain does not interpret it as fear or excitement.
Conversely, the posterior insula, more tied to sensory–bodily processing, may be overactive in some cases.
This could explain why emotions are often misread as physical symptoms — “tight chest” instead of “sadness” — the body signals are detected, but not translated into emotion words.
2️⃣ Anterior Cingulate Cortex (ACC) — Emotional Regulator
The ACC supports decision-making and evaluating emotional conflicts.In typical brains, the ACC and insula collaborate to answer “what am I feeling, and how should I respond?”
In alexithymia, this collaboration is often downregulated — the ACC–insula communication loses synchrony.
That lag produces delays in recognizing and interpreting feelings.
The brain senses something is happening, but it can’t categorize or respond with words, leading to outward flatness or numbness while internal arousal is strong.
Several fMRI studies also associate reduced ACC activation with greater use of emotional suppression.
When naming a feeling fails, the brain may choose to switch it off.
3️⃣ Amygdala & Frontolimbic Connectivity
The amygdala detects threat and generates basic emotions (fear, anger).In alexithymia, communication between the amygdala and prefrontal cortex (especially vmPFC and dlPFC) is atypical.
Normally, the amygdala alerts the PFC to help understand and label the emotion.
In alexithymia, this channel is often cut or slowed, preventing timely categorization — “this is fear,” “this is anger.”
People feel a strong bodily impulse but don’t understand what it is; they may automatically withdraw, go silent, or shut down.
Some studies also find reduced amygdala responsiveness, helping explain why certain individuals seem unmoved by typically emotional stimuli (sad films, love songs, reassurance).
4️⃣ Inferior Parietal Lobule & Insula Connectivity (New 2025 evidence)
A 2025 medRxiv preprint reports altered connectivity between the insula and inferior parietal lobule during emotion suppression and working memory tasks among high-alexithymia groups.The parietal cortex manages attentional shifting and the body schema in space.
This impaired linkage may hinder capturing internal signals and focusing on one’s own emotions in the moment, supporting a newer view that alexithymia involves a deficit in self-directed emotional attention.
5️⃣ Neurochemistry
Though still under study, evidence suggests roles for serotonin, oxytocin, and dopamine in emotional linkage.- Low serotonin → greater avoidance of sad/anxious affect.
- Low oxytocin → difficulty sensing others’ feelings (affective empathy) and reduced warmth in relationships.
- Dopamine dysregulation → blunted reward experience, e.g., “I know I should be happy, but I don’t feel it.”
🔬 Neural Systems Summary
Alexithymia reflects a mismatch across three brain layers:
- Feeling (limbic) → amygdala
- Interoceptive awareness (insula, ACC) → interpret the feeling
- Language (PFC–Broca) → express it
When these three don’t synchronize, “felt emotion” can’t become “understood emotion.”
Lacking understanding, the brain doesn’t know how to release it, and thus chooses to mute the heart.
🌱 Causes & Risk Factors
The causes of the Alexithymic Type are multifactorial — biology, early development, emotional experiences, and sociocultural context.It’s not a single “disease,” but a pattern of constructing emotional selfhood gradually shaped by brain and environment.
1️⃣ Biological & Genetic Factors
Twin studies show a genetic component; roughly 30–40% of population variance may be heritable.Variants in serotonin transporter (5-HTTLPR) and oxytocin receptor (OXTR) have been proposed to influence sensitivity of emotional and interoceptive systems.
Additionally, congenitally smaller/weaker interoceptive networks (e.g., a thinner left insula) can raise risk for primary alexithymia, a form embedded in personality from early life and often persistent.
2️⃣ Early Developmental Experiences
Ages 0–6 are critical for learning the language of emotions from caregivers.If adults don’t talk about feelings — “Don’t cry,” “Don’t be scared,” “It’s nothing, forget it” — the child receives insufficient emotional mirroring.
Thus, the neural systems that should learn to name/regulate emotions (insula–ACC–PFC) aren’t adequately trained.
By contrast, children in families that frequently name feelings (e.g., “You seem tired — how was your day?”) tend to develop broader emotional vocabulary and stronger insula responses.
For many adults, alexithymia is a legacy of emotional neglect rather than an innate absence of emotion.
3️⃣ Psychological Trauma
Emotional trauma — especially complex trauma or chronic invalidation — plays a major role.Repeated experiences of harm, rejection, or dismissal teach the brain that “to feel = danger.”
To reduce suffering, the brain automatically closes access to emotion — a self-protection strategy.
This yields secondary alexithymia, where the brain grows accustomed to not feeling to avoid pain.
Common in survivors of family violence, emotional abuse, or PTSD.
4️⃣ Organic Causes (Brain & Medical Conditions)
In some, alexithymia arises after brain injury, such as:- Frontal head trauma
- Stroke affecting the insula or ACC
- Early neurodegenerative processes
This group is termed organic alexithymia.
Because it stems directly from neuropathology, people lose emotional awareness they previously had.
For example, some with Parkinson’s disease or multiple sclerosis report they no longer feel joy or sadness as before.
5️⃣ Comorbid Psychiatric & Medical Conditions
Alexithymia commonly co-occurs with:- ASD: overlapping interoceptive–social circuitry differences
- Depression & Anxiety: chronic stress and low mood dampen internal awareness
- Eating disorders: especially anorexia nervosa — many cannot distinguish hunger from anxiety
- Chronic pain disorders: distorted body awareness blurs physical and emotional pain
These comorbidities can worsen alexithymia and slow psychotherapy response.
6️⃣ Sociocultural Factors
Cultures that valorize toughness and reason over feeling often show higher alexithymia.In many Asian contexts, men are expected not to cry or show emotion, training the brain to suppress affect as habit.
Some cultures that welcome emotion talk (e.g., parts of Scandinavia/Western Europe) tend to show lower rates.
Thus, cultures that forbid feeling quietly shape alexithymia as a social risk factor.
7️⃣ Chronic Stress & Cognitive Overload
Chronic stress locks the brain into fight-or-flight.The limbic system becomes overactive while the PFC downshifts nuanced emotion processing.
Stuck in survival mode, the brain ignores emotional signals to conserve energy.
Over time, this hardens into persistent emotional numbness.
🔬 Causal Summary
Alexithymia doesn’t come from one place.It’s the sum of genetic vulnerabilities in interoceptive circuitry,
caregiving that lacked emotional mirroring,
trauma teaching the brain to shut feeling off,
and cultures that prize reason over emotion.
Simply put, it’s “a brain that learned to close the heart to survive in a world unsafe for feeling.”
Treatment & Management
The goal is to build a “language of emotion” and train interoception–emotion labeling–communication, rather than “treating a disorder.”1) Psychotherapies with Supporting Evidence
- CBT (emotion-adapted): focus on labeling emotion–thought–behavior, use emotion diaries, and graded exposure to internal cues. A 2024 review reports CBT is most used and often reduces alexithymia scores (within-group effect sizes from moderate to large, though methods vary). MDPI
- Emotion-Focused / Mentalization-Based approaches: emphasize identifying, exploring, naming, and processing feelings, plus understanding one’s and others’ mental states (mentalization). Evidence is growing, especially with comorbidities. PubMed
- Mindfulness-based (MBSR/MBCT): observe body–emotion signals non-judgmentally to strengthen interoception and regulation; moderate evidence. ResearchGate
- Group therapy / Psychoeducation: teach emotion vocabulary, emotion-cycle models, and social reflection exercises to support relationship communication. Frontiers
2) Skills to Include in the Plan
- Interoceptive training: body scans, pulse/breath counting, body–emotion silhouette mapping, and daily sensation–emotion comparisons. viejo.medwave.cl
- Emotion labeling drills: feelings wheels/word tables; daily “Event–Feeling–Thought–Action” exercises.
- Structured journaling: (1) event, (2) body signals, (3) emotion name, (4) supporting/contradicting evidence, (5) communication options.
- Social homework: reflect feelings with a partner (“I notice my stomach is tight — I might be anxious”) to build automatic language–emotion behavior.
3) Clinical Tips
- Adapt therapy formats: use visuals and schematics (visual scaffolding), mix closed/open questions, short logs, and word banks.
- Set realistic expectations: especially in primary/trait alexithymia, change can be slow; emphasize practical skills over immediate “deep insights” to prevent discouragement. ResearchGate
Note: there’s no specific medication for alexithymia; meds target comorbidities (depression/anxiety, etc.). Emotional skills rely on practice and psychotherapy. (Recent evidence shows TAS-20 score reduction is achievable across multiple protocols.) MDPI
Notes
- Not a disorder — a dimension: avoid stigma; use neutral language + exercises rather than “you have no emotions.”
- Culture/language: limited emotion words in one’s mother tongue and low family mirroring raise risk — therapy should be culturally and linguistically adaptive.
- Relationships/teams: explain the mechanism to partners/teams (“I need time to name what I feel”) and use a 5-minute end-of-day feelings check-in.
- Research continues: recent neuroscience reaffirms roles of the insula–ACC–frontolimbic network and interoception; treatment outcomes improve when protocols emphasize emotion labeling and inner awareness. MDPI+1
References
Moriguchi Y., Komaki G. Neuroimaging studies of alexithymia: physical, affective, and social perspectives. Frontiers in Human Neuroscience (2013). Overview of insula/ACC/amygdala. PMCSchroeders U., et al. The Structure of the Toronto Alexithymia Scale (TAS-20). Diagnostics (2021). Factor structure and psychometrics. PMC
Messina A., et al. Towards a classification of alexithymia: primary, secondary and organic. Journal of Psychopathology (2014). Primary/secondary/organic framework. Journal of Psychopathology
Wang X., et al. Prevalence and Correlates of Alexithymia and Its Relationship With Depression in Chinese Engineering Students. Frontiers in Psychiatry (2021). General prevalence ~10% and 7–30% in youth. PMC
Mattila A.K., et al. Age is strongly associated with alexithymia in the general population. Journal of Psychosomatic Research (2006). ~9.9% prevalence and age/sex differences. sciencedirect.com
Tsubaki K., et al. Psychological Treatments for Alexithymia: A Systematic Review. Frontiers in Psychology (2024). CBT/EFT/mindfulness effects on TAS-20. PMC
Critchley H.D., Garfinkel S.N. Interoception and emotion. Current Opinion in Psychology (2017). Interoception/insula roles. sciencedirect.com
Scarpazza C., et al. Disentangling interoceptive abilities in alexithymia. Psychol Res Behav Manag (2021). Interoception and insula in high-alexithymia groups. PMC
Bird G., Cook R. The alexithymia hypothesis of autism spectrum disorder. (Concept/review: ASD affective differences explained by co-occurring alexithymia). Neurosci Biobehav Rev/related outputs. PubMed+1
de Vroege L., et al. Psychometric Properties of the Bermond–Vorst Alexithymia Questionnaire (BVAQ). Frontiers in Psychiatry (2018). BVAQ cognitive/affective dimensions. Frontiers
Fernández-Jiménez E., et al. Psychometric properties of a revised Spanish TAS-20. (2013). TAS-20 cutoffs: ≤51 non-alexithymia; 52–60 borderline; ≥61 alexithymia. Redalyc
Goerlich K.S. Neuroimaging Studies of Alexithymia (book chapter, 2018). Frontolimbic/insula-ACC overview. research.rug.nl
Lopes C.P., et al. Prevalence of alexithymia and depression among athletes. Frontiers in Sports and Active Living (2025). Updated prevalence 8–27% (sports context/contemporary sample). Frontiers
Health.com explainer (2023). Public-facing summary: trait not disorder, ~10% prevalence, TAS-20/BVAQ tools, care tips (popular-science/SEO). Health
TAS-20 cutoffs primarily from ref. 11; for a reader-friendly page with matching cutoffs, you can also cite Embrace Autism. Embrace Autism
0 Comments
🧠 All articles on Nerdyssey.net are created for educational and awareness purposes only. They do not provide medical, psychiatric, or therapeutic advice. Always consult qualified professionals regarding diagnosis or treatment.