When being stressed is no longer enough to explain what is happening
It is shortly after five o’clock when Julien D., thirty-nine, arrives at the practice. His suit is still immaculate, his laptop under his arm, his phone in his hand. He apologises before he even sits down.
“Sorry I’m late. I was still on a video call.”
Julien manages international projects and coordinates teams across several time zones. He exercises regularly, does not smoke and reports no major medical history that would immediately explain what is happening to him.
For a long time, his reasoning was straightforward. If he slept too little, his work required it. If he remained constantly available, his responsibilities demanded it. If he was tired, a few quieter days should be enough for him to recover.
But for several months, that last assumption has no longer held true.
His lapses in memory are becoming more frequent. Certain words escape him in the middle of a conversation. At times, he remains in front of his screen for several seconds before recovering the thread of what he was doing. On several occasions, he has unintentionally fallen asleep on the train or in front of his computer.
And yet he continues to work.
That is precisely what makes the case difficult to interpret.
“I’m not ill. I’m simply exhausted.”
The investigations correctly answer the questions they were designed to address
The initial investigations are reassuring. The available endocrine, metabolic and cardiovascular data do not, when considered separately, reveal an abnormality capable of explaining the entire clinical picture.
This information matters.
Depending on the investigations actually performed and the context in which they were conducted, it allows certain hypotheses to be excluded or considered less likely.
It does not, however, establish that Julien’s overall functioning has necessarily returned to its previous state.
Because while the investigations remain reassuring, Julien continues to report intermittent palpitations, night sweats, sensations of numbness and, above all, an impression that has become almost constant:
“I feel as though I’m ready to react even when nothing is happening.”
The question is therefore no longer simply: “Is Julien stressed?”
It becomes: what happens when the pressure stops, but the sense of vigilance persists?
Logical, but incomplete
Initially attributing Julien’s fatigue to his lifestyle is not irrational. His professional demands are substantial, his working days are long and the time available for recovery appears insufficient.
The reasoning becomes incomplete when this explanation is maintained even as new information emerges.
The problem is no longer simply that he works too much.
It is that he no longer recovers as he once did when the work stops.
That distinction changes the hierarchy of the questions that need to be asked.
Activation and recovery are not two versions of the same state
The stress response is not, in itself, pathological. It belongs to the normal mechanisms of adaptation.
When a situation requires a rapid response, several systems participate in the organism’s adjustment: the autonomic nervous system, neuroendocrine axes, cardiovascular function, energy metabolism and attentional processes.
But adaptation is not simply the ability to become activated.
It also requires the ability to modulate that activation once the situation that triggered it has disappeared.
This is where an essential distinction emerges in Julien’s case: the presence of a demand and the persistence of activation are not necessarily the same thing.
The capacity to adapt therefore cannot be measured solely by the amount of pressure an individual can withstand.
It also depends on the ability to recover when that pressure decreases.
Sleep provides information that daytime investigations cannot show
Given the episodes of drowsiness and insufficient recovery, sleep becomes a central dimension of the case.
Depending on the clinical context, a specialised sleep assessment may therefore be relevant in order to investigate sleep-disordered breathing, fragmentation, abnormalities in sleep continuity or other causes capable of impairing its restorative function.
In Julien’s case, the important element is not simply the number of hours spent in bed. It is the discrepancy between a sleep duration that may appear relatively preserved and the persistent feeling that recovery is no longer taking place.
This distinction is consistent with research on hyperarousal, particularly in insomnia: in some patients, markers of cognitive, autonomic or cortical activation may persist even while the individual is attempting to sleep.
This does not, by itself, allow us to diagnose Julien with a “physiological hyperarousal syndrome”.
It does, however, provide a working hypothesis: recovery needs to be investigated as a function in its own right, rather than inferred simply from the fact that Julien sleeps for several hours.
The turning point
The initial question was:
“How much stress is Julien under?”
It becomes:
“Does his body retain the same capacity it once had to move from activation into recovery?”
Allostasis: maintaining stability through continuous adjustment
The concept of allostasis allows the reasoning to go further, provided once again that it is not turned into a diagnosis.
The body does not maintain its parameters by remaining static. It maintains them through continuous adjustments across multiple systems.
The work of Bruce McEwen and other researchers developed the concept of allostatic load to investigate the cumulative cost associated with repeated or prolonged adaptation.
This is a multisystem concept.
It cannot be inferred from a normal or elevated cortisol value, a heart rate, a blood pressure measurement or an isolated symptom.
The data presented in Julien’s case therefore do not allow us to conclude that he has a “high allostatic load”.
The model is being used here to ask a question, not manufacture a conclusion: are several systems showing, during the same period, changes compatible with recovery becoming less effective?
What becomes visible when the case is reconstructed over time
Considered separately, Julien’s symptoms are relatively non-specific.
A palpitation does not summarise the autonomic nervous system. A poor night’s sleep does not demonstrate neuroendocrine dysregulation. An occasional lapse in memory does not constitute neurological disease. A cortisol measurement cannot, on its own, describe the overall stress response.
But a chronology allows different questions to be asked.
When did his recovery begin to change? Did the attentional difficulties appear before or after the fragmentation of his sleep? Do the palpitations follow particular periods of overload? Do the symptoms diminish during periods that are genuinely free from professional demands? Do certain medications, stimulants, dietary changes, infections or personal events coincide with a change in the trajectory?
This work does not transform non-specific symptoms into a diagnosis.
It helps determine which relationships genuinely need to be investigated.
Then an event requires the medical reasoning to be reopened
During a business trip, Julien describes an unusual episode: for a few moments, he experiences what feels like a disruption in his ability to organise the information he is receiving.
An event of this kind should not automatically be absorbed into a theory of stress.
It first requires appropriate medical evaluation to exclude, according to its presentation, neurological, cardiovascular, metabolic or other causes that might require specific management.
If the corresponding investigations remain reassuring, that is important information.
It does not, however, demonstrate that the episode was “caused by stress”.
The absence of an identified serious cause and the identification of the responsible mechanism are two different conclusions.
What is established, what is plausible, what remains to be demonstrated
This distinction protects the reasoning from two opposing errors.
The first would be to consider the symptoms no longer important because several investigations are reassuring.
The second would be to invent systemic dysregulation simply because the symptoms persist.
It is established that Julien reports a change in his ability to recover, disturbances in sleep or vigilance, and several symptoms that emerged during a period of substantial demands.
It is physiologically plausible that insufficient or fragmented sleep, prolonged cognitive activation and repeated demands may interact with autonomic and neuroendocrine systems.
What has not been demonstrated, on the basis of this information alone, is that a single mechanism explains the entire clinical picture.
A hypothesis becomes useful when it organises what needs to be investigated.
It becomes dangerous when it is presented as something that has already been proven.
Why normal results do not necessarily close the case
A biological test answers a particular question. An electrocardiogram answers another. Brain imaging investigates certain abnormalities. A sleep assessment describes yet another dimension.
None of these investigations is designed, on its own, to summarise an individual’s overall capacity to recover.
Their normality should therefore neither be minimised nor overinterpreted.
It means that the abnormalities being investigated were not identified under the conditions in which the examination was performed.
When symptoms persist, the next step may sometimes be less about immediately ordering another investigation and more about determining whether the information already available has been reconstructed within the same chronology.
Shifting the question
The question is no longer simply:
“Are you stressed?”
It becomes:
“What happens when the pressure disappears: does your body actually recover its usual capacity to restore itself?”
What this new question changes
First, it prevents management from being reduced to a single instruction: “slow down”.
It requires us to identify more precisely what is actually interfering with recovery.
Sleep duration and continuity, exposure to late-night demands, schedules, stimulants, physical activity, medications, sleep-disordered breathing, anxiety or mood symptoms, metabolic, endocrine, neurological or cardiovascular factors: their hierarchy depends on the actual case and on what has already been investigated.
Certain interventions may be relevant without constituting proof of the presumed mechanism.
Restoring sufficient sleep duration, reducing certain late-night demands or temporarily reorganising workload may have clinical or behavioural justification.
But if Julien improves after these changes, that improvement does not retrospectively demonstrate that “autonomic nervous system dysregulation” was the sole cause of his symptoms.
It provides another piece of information to integrate into the trajectory.
What this case teaches us
Stress is too broad a description to constitute, on its own, a clinical explanation.
Two people may be exposed to substantial demands and follow very different trajectories.
What becomes informative in Julien’s case is therefore not simply the amount of work he performs.
It is the progressive change in what happens after the effort: less restorative sleep, slower recovery, more frequent symptoms and a reduction in the reserve that previously allowed him to absorb those demands.
This trajectory does not automatically provide a diagnosis.
It indicates where the reasoning needs to continue.
Conclusion
Julien is stressed.
But that observation is probably the least informative part of his case.
What needs to be understood is the progressive change in his capacity to recover while several investigations continue, within their respective domains, to produce reassuring results.
This discrepancy allows us neither to dismiss his symptoms nor to invent a hidden disease.
It requires reconstruction.
What has changed?
In what order?
What has already been reasonably excluded?
And what still remains a hypothesis to be investigated?
It is often between these questions that the information an isolated result could never provide becomes visible.
HypnoCorpe®
When investigations remain reassuring but recovery, symptoms or the overall trajectory continue to change, the problem is not necessarily a lack of information.
It may lie in the way that information has been separated across consultations and medical specialties.
Clinical Biological Decoding® reconstructs the chronology, compares the available data, examines the interactions between symptoms, biology, treatments, sleep, constraints and clinical evolution, and then searches the scientific literature for evidence that may help clarify the remaining inconsistencies.
The objective is not to produce an additional diagnosis.
It is to reconstruct a situation that has become difficult to read.
This analysis does not replace medical diagnosis, medical prescription or ongoing care by the treating physician.
References
McEwen BS. Protective and damaging effects of stress mediators. New England Journal of Medicine. 1998;338:171–179.
McEwen BS, Wingfield JC. The concept of allostasis in biology and biomedicine. Hormones and Behavior. 2003;43(1):2–15.
Juster RP, McEwen BS, Lupien SJ. Allostatic load biomarkers of chronic stress and impact on health and cognition. Neuroscience & Biobehavioral Reviews. 2010;35(1):2–16.
Chrousos GP. Stress and disorders of the stress system. Nature Reviews Endocrinology. 2009;5(7):374–381.
Brosschot JF, Gerin W, Thayer JF. The perseverative cognition hypothesis: a review of worry, prolonged stress-related physiological activation, and health. Journal of Psychosomatic Research. 2006;60(2):113–124.
Riemann D, Spiegelhalder K, Feige B, et al. The hyperarousal model of insomnia: a review of the concept and its evidence. Sleep Medicine Reviews. 2010;14(1):19–31.
About the author
Dr Farida Sebbag
Founder of HypnoCorpe®
Dr Farida Sebbag works on the strategic analysis of complex medical situations in which symptoms persist or the clinical trajectory remains difficult to explain despite investigations that may continue to be reassuring. Her work focuses on reconstructing the chronology of the available data, identifying their interactions and confronting them with the international scientific literature.
HypnoCorpe® is a private practice based in Geneva and working internationally. Its analyses do not replace medical diagnosis, medical prescription or ongoing care by the treating physician.
Category
Clinical Analysis · Complex Medical Situations
