The Heart Disease No One Is Diagnosing

Dr. Job Mogire, MD, FACP, FACC Board-Certified Cardiologist | Carle Foundation Hospital, Champaign, IL

In 1996, Juha Kauhanen and colleagues published a study in the Finnish Kuopio Ischemic Heart Disease Risk Factor cohort that has received far less attention than it deserves.

They measured alexithymia, the difficulty identifying and describing one’s own emotional states, in 2,297 middle-aged Finnish men using the Toronto Alexithymia Scale. They followed them for an average of six years. Men in the highest quartile of alexithymia had more than double the all-cause mortality risk of men in the lowest quartile, after controlling for age, smoking, blood pressure, and other established cardiovascular risk factors. 4 / Promising (Kauhanen et al. 1996, PMID: 9032717)

More than double.

That finding has not entered standard cardiovascular clinical practice. No physician routinely screens for alexithymia. It is not in the cardiovascular risk calculators. It is not in the standard annual physical.

What Alexithymia Is

Alexithymia was named by Peter Sifneos in 1973 from the Greek: a (without), lexis (word), thymos (emotion). Without words for emotion. It is measured most commonly by the Toronto Alexithymia Scale (TAS-20), a 20-item validated self-report instrument that assesses three subscales:

1. Difficulty Identifying Feelings (DIF): Not knowing what one is feeling at any given moment.
2. Difficulty Describing Feelings (DDF): Having no language for internal states even when they are dimly sensed.
3. Externally Oriented Thinking (EOT): A cognitive preference for the concrete and external rather than the internal and emotional.

The prevalence of clinically significant alexithymia (TAS-20 score above 61) is estimated at approximately 10 percent in the general population and substantially higher in specific populations. 4 / Promising Men score higher than women on average. Professional populations in high-demand, low-reflective environments show higher rates than average.

It is not a psychiatric disorder. It is not autism spectrum disorder, with which it is sometimes confused. It is a dimension of emotional awareness that exists on a continuum in the general population and that carries, at higher levels, a documented mortality cost.

The Mechanism: How Alexithymia Produces Cardiovascular Risk

Pathway 1: HPA Axis Without Regulatory Feedback

Under normal conditions, emotional processing provides regulatory feedback to the stress response. The person who recognizes, names, and processes a stressful experience resolves the emotional activation more completely than the person who cannot name what they are experiencing.

In the alexithymic individual, the stressor produces the same physiological activation: HPA axis engagement, cortisol release, sympathetic arousal. But the regulatory feedback loop, the processing of the emotional meaning of the stressor, is impaired or absent. The activation continues beyond the duration it would otherwise.

This is the mechanism by which alexithymia maintains chronic HPA activation and its downstream cardiovascular consequences: blood pressure elevation, visceral fat accumulation, insulin resistance, systemic inflammation, and endothelial dysfunction.

Pathway 2: The Help-Seeking Deficit

The man who cannot identify what he is feeling is unlikely to seek help for it. He does not have a language for the cardiac tightness that comes and goes. He does not have a word for the chronic fatigue that is qualitatively different from tiredness. He experiences the symptom but lacks the internal vocabulary to flag it as something requiring attention.

This produces the delayed help-seeking pattern that characterizes cardiovascular events in high-alexithymia men. The symptom is present. The internal signal processing that would translate it into a clinical concern is impaired.

Pathway 3: Social Disconnection

Alexithymia impairs the interpersonal signaling that maintains social connection. The person who cannot identify or describe their emotional states has difficulty being known by others. Relationships stay at a functional level. The deeper social connection that serves as a buffer against the physiological consequences of chronic stress is unavailable.

This connects the alexithymia mechanism directly to the social isolation mechanism: the same internal inability to name emotion that prevents HPA resolution also prevents the development of the social bonds that would buffer the autonomic and inflammatory consequences of that HPA activation.

The Population It Hits Hardest

The profile of high alexithymia in the general population matches, in striking ways, the profile of the man Stop Dying Early is built to reach.

Professional men in high-demand occupations with extensive training in managing complexity through external systems rather than internal reflection. Men who have been reinforced throughout their career for decisiveness, composure, and analytical rather than emotional processing. Men who are exceptional at understanding everything external to themselves and have applied correspondingly little attention to the internal domain.

This is not a character failure. It is a trained cognitive pattern that carries a cardiovascular cost. The man who has spent twenty years being rewarded for not feeling his feelings, or at least not showing them, has developed an autonomic nervous system that is chronically activated by load it cannot process through the normal regulatory pathway.

The Evidence Base: What We Know and Its Limits

The Kauhanen finding remains the most cited mortality data. Subsequent research has explored the association with less consistent methodology and smaller samples. What the evidence supports at a clinical level:

What is well-established: Alexithymia is associated with autonomic dysregulation, impaired cortisol reactivity and recovery, elevated inflammatory markers, and social isolation, each of which is independently associated with cardiovascular risk. 4 / Promising

What is established but less replicated: The direct association with cardiovascular mortality in the Kauhanen cohort. This is a single large prospective study, which represents strong but not yet replicated evidence of the mortality association specifically. 3 / Early

What is not yet established: Whether treating alexithymia, through psychotherapy or other interventions, reduces cardiovascular events. There are no clinical trials addressing this question. The mechanism is plausible. The intervention evidence does not yet exist. 2 / Theoretical

This is an honest grading. The mortality association is real and deserves clinical attention. The treatment pathway is not yet proven at the level that would make it a clinical recommendation.

Alexithymia and Cardiac Rehabilitation Outcomes

Following an acute myocardial infarction, the standard of care includes a structured cardiac rehabilitation program: supervised exercise, risk factor modification, dietary guidance, and psychological support. Completion rates are already suboptimal in the general population. In patients with high alexithymia, the problem is worse.

Mark Lumley and colleagues at Wayne State University have published extensively on alexithymia and health outcomes across medical contexts. Their work, along with studies of cardiac rehabilitation cohorts, points to a consistent pattern: patients with high alexithymia scores have lower rates of program completion, worse engagement with the psychological components of rehabilitation, and higher rates of recurrent cardiac events at follow-up. 3 / Early

The mechanism is not simply non-compliance in the ordinary sense. The psychological components of cardiac rehabilitation, including education about stress and its physiological effects, group support, and anxiety management, depend on the patient having access to their own emotional states. He needs to be able to identify that he is frightened of another cardiac event, or that he is carrying unprocessed distress about his diagnosis, for those components to do anything useful.

The high-alexithymia patient does not experience what he would describe as fear or anxiety about his cardiac event. He experiences “nothing.” There is no aversive motivating signal tied to the diagnosis. There is no internal alarm telling him that what just happened is serious and that he needs to change. The behavioral change circuit is architecturally incomplete: the input that would drive the output is missing.

This is not stubbornness. It is not denial in the psychodynamic sense. It is a processing pattern that, at the moment when motivated health behavior is most needed, leaves the patient without the internal signal that would produce it.

The Somatization Pattern

In the absence of emotional labeling, physical symptoms carry the load that emotions would otherwise carry. The alexithymic individual does not experience “anxiety” or “stress” as identifiable internal states. He experiences back pain, headaches, or gastrointestinal symptoms. The body is generating output that corresponds to emotional activation, but the cortical labeling step, the one that would assign that output to a psychological category, does not occur.

This somatization pattern has been extensively documented in the alexithymia literature. Multiple studies using the TAS-20 show significant positive correlations between high alexithymia scores and medically unexplained symptoms, particularly in the cardiovascular and gastrointestinal domains. 4 / Promising

The clinical relevance in cardiology is specific: the man who experiences chronic chest tightness and attributes it, accurately from his perspective, to musculoskeletal causes or acid reflux rather than to emotional or cardiac causes is in a diagnostically ambiguous position. High alexithymia makes that position more dangerous in two directions simultaneously. First, genuinely cardiac symptoms may be attributed to the pre-existing somatic pattern and not escalated clinically. Second, the somatic symptoms generated by unprocessed emotional load are real physiological events, not invented complaints, and they carry their own cardiovascular consequences through the HPA and autonomic pathways described above.

The physician who asks “any chest pain?” and receives “sometimes, but I think it’s just muscle tension” is not getting an uninformative answer. He is getting an answer that is shaped by a processing architecture that deserves its own clinical attention.

The Sleep-Alexithymia Interface

Sleep is not simply rest. REM sleep in particular is the period during which the brain consolidates emotional memories and regulates affect: the brain processes emotionally salient events from the prior day, reducing their autonomic charge. This is why acute distress often feels different, and somewhat reduced, after a night of sleep.

The alexithymic individual has impaired access to the emotional processing that this system requires as input. The REM processing system depends on emotionally tagged memories being available for consolidation. When that tagging is incomplete, the sleep architecture that depends on it is disrupted. Multiple studies show that high alexithymia is associated with poor sleep quality, more fragmented sleep architecture, and reduced slow-wave sleep proportion. 3 / Early

The cardiovascular consequences of disrupted sleep are well-characterized at this point: elevated nocturnal cortisol, elevated nocturnal blood pressure, reduced heart rate variability, impaired glucose metabolism, and accelerated atherosclerotic processes. These are not subtle effects. They are substantial and cumulative.

What connects this to the clinical encounter is the presentation. The man with high alexithymia and disrupted sleep architecture may report sleeping through the night without difficulty. He does not experience what he would call insomnia. He wakes unrefreshed but attributes this to schedule or age or the amount of work he is carrying. The sleep study, if one were done, would show fragmented architecture and reduced slow-wave proportion. But the patient has no subjective framework that would lead him to request one.

He is accumulating nocturnal cardiovascular burden without any awareness of it as a sleep problem. The signal is present. The receiver is offline.

What Belongs in the Clinical Record

Alexithymia is unlikely to enter standard cardiovascular risk calculators in the near term. It is not a biomarker that can be quantified from a blood draw.

What can happen in a clinical encounter is a question. One question: “When you are under significant stress or pressure, do you find it easy or difficult to identify what you are actually feeling?” Or: “Who in your life knows the real version of how you are doing?”

These questions surface the processing pattern that is clinically relevant. They can be answered in 30 seconds. They add information that the standard cardiovascular risk assessment does not contain.

The Platform That Addresses This

Stop Dying Early exists in part because alexithymia and its cardiovascular consequences are operating in the background of clinical encounters that never surface them. The Signal Check assessment maps five domains of the pattern: the performance identity, body signal awareness, sleep quality, load management, and genuine connection. The Connection and Performance domains specifically probe the behavioral signatures of high alexithymia.

This is not therapy. It is a clinical instrument that maps cardiovascular risk factors that standard cardiology encounters do not measure.

Three Actions

1. Take the TAS-20, the Toronto Alexithymia Scale. It is publicly available and takes five minutes. A score above 61 is clinically significant. A score between 52 and 60 is borderline. Either warrants reflection and potentially a conversation with a skilled clinician.

2. Notice the question “what are you feeling right now?” If the answer is consistently effortful or blank, not suppression but genuine absence of access, that is clinically relevant information.

3. Take the Signal Check. It maps the behavioral pattern that includes but is not limited to alexithymia, and places it in the cardiovascular context where it belongs.

This paper is educational and does not constitute medical advice. Discuss your individual clinical situation with your physician.