Your symptoms are changing. That does not mean instability.
It is 9:30 a.m. when Sonia L., thirty-four, arrives with a medical record compiled over two years of investigations. Neurology, cardiology, endocrinology, rheumatology, gynaecology, internal medicine: each consultation has addressed a specific question, each examination has helped rule out certain hypotheses, yet none has truly explained why her condition seems to be continually changing.
Pain appears in her back and then disappears. A few days later, profound fatigue sets in from the moment she wakes, despite an apparently adequate amount of sleep. At other times, she experiences tingling in her hands, sudden accelerations in heart rate, or an unusual difficulty maintaining her attention.
The medical reports remain broadly reassuring. No single condition has been identified that could account for the entire clinical picture. Monitoring continues.
Sonia does not dispute these conclusions. She is not asking for a diagnosis to be manufactured simply to give a name to what she is experiencing.
She simply expresses a contradiction.
“My condition changes even though my life does not.”
This sentence already contains part of the problem. What makes the case difficult to interpret is not only the persistence of the symptoms. It is their mobility.
When a symptom changes in location, intensity or nature, the term “instability” easily comes to mind.
The idea seems intuitive: if the manifestations change, the system producing them must itself be unstable.
This interpretation is not unreasonable. Certain conditions can indeed produce significant fluctuations, and some regulatory mechanisms can become less effective.
But the conclusion becomes too rapid when variability itself is equated with dysfunction.
A healthy living organism is not an immobile system.
Heart rate varies with breathing, posture and activity. Blood pressure changes throughout the day. Body temperature, alertness, energy availability, pain perception and numerous hormonal or autonomic parameters vary according to sleep, nutrition, physical activity and internal or environmental demands.
Physiology depends precisely on this capacity for modulation.
The concept of allostasis describes this property from a particular perspective: the organism maintains its viability not by keeping every variable at a fixed value, but by continuously adjusting different systems to the predictable or unpredictable demands of the environment.
The clinical question therefore cannot simply be: “Do the symptoms vary?”
It must become:
How do they vary? In what sequence? Under what constraints? With what amplitude? And above all: does the system subsequently return to a level of functioning compatible with its needs?
In Sonia’s case, previous investigations primarily examined the symptoms at the time they were present.
Back pain led to a musculoskeletal assessment. The palpitations justified a cardiological work-up. The tingling led to a neurological evaluation.
At each stage, the reasoning was coherent.
But these investigations were not necessarily designed to answer another question: what relationship exists between the episodes?
When the record is reconstructed according to a strict chronology, several associations emerge. The pain occurs more frequently after prolonged working days. Palpitations are reported more often when meals are delayed. Morning fatigue becomes more pronounced when sleep is fragmented, even when total sleep duration appears adequate. Less demanding days are sometimes accompanied by a reduction in symptoms without eliminating them completely.
None of these associations demonstrates causality.
But they alter the initial hypothesis.
What appeared random may not be entirely random.
Research on physiological complexity has specifically challenged the idea that optimal biological functioning necessarily corresponds to maximal regularity.
Healthy physiological systems often produce complex fluctuations, structured across multiple timescales. Conversely, ageing and certain diseases may be accompanied by a reduction in this complexity, with a diminished repertoire of responses available when the system is challenged.
This literature obviously does not allow us to conclude that every irregularity is healthy, or that every form of regularity is pathological.
It requires a more demanding distinction: the amount of variation is not equivalent to the quality of adaptation.
One system may produce numerous but disorganised fluctuations. Another may display substantial variability while maintaining a response that is proportionate, context-dependent and reversible.
The question is no longer:
“Why do the symptoms change so much?”
It becomes:
“What does the way they change reveal?”
This new question requires us to observe symptoms not merely as events, but as responses embedded within a temporal sequence.
In Sonia’s case, the manifestations do not accumulate linearly. They follow one another, sometimes replace one another, and intensify in certain contexts before diminishing when the demands placed on the system decrease.
The clinical picture appears incoherent as long as it is read as a juxtaposition of independent symptoms.
It becomes more intelligible when the dynamics connecting them are examined.
One distinction remains essential, however: identifying a temporal organisation does not mean that a cause has been identified.
An association between delayed meals and palpitations does not prove a metabolic mechanism. Worsening after fragmented sleep does not demonstrate that sleep explains the entire clinical picture. Improvement on less demanding days does not justify reducing the symptoms to stress.
Chronology does not automatically produce a diagnosis. It allows more precise hypotheses to be constructed.
Adaptive variability requires more than the mere presence of fluctuations.
It implies that a response can be mobilised when a demand appears, modulated according to its intensity, and then reduced once that demand disappears.
In Sonia’s case, the problem may therefore not be that her organism varies.
It may lie in the increasing cost of certain responses: longer recovery, more symptoms after relatively modest demands, and greater difficulty returning to the previous state.
This interpretation remains a clinical hypothesis. It constitutes neither an independent diagnosis nor a direct measurement of Sonia’s “adaptive capacity.”
It nevertheless allows us to distinguish two phenomena that would be conflated if we simply used the word instability:
variation because a system is capable of adapting,
and variation because each adaptation is becoming progressively more costly.
The next step is to organise observation rather than immediately multiply interpretations.
Over several weeks, the episodes are placed back into context: sleep quality and continuity, meal timing, physical activity, prolonged working days, recovery periods and the circumstances in which symptoms appear.
The objective is not to transform every daily fluctuation into a biomarker.
It is to identify reproducible relationships.
Gradually, certain sequences become more intelligible. Prolonged working days are more frequently followed by increased pain. Delayed meals more often precede certain episodes of palpitations. Fragmented nights are associated with less satisfactory recovery the following day.
The variability has not disappeared.
It has become more structured within the analysis.
Another element in the record illustrates the difference between controlling a symptom and understanding a trajectory.
Faced with particularly troublesome episodes of tachycardia, a cardiologist proposes a low-dose treatment intended to reduce the palpitations.
The decision addresses a specific clinical indication and naturally remains within the remit of the prescribing physician.
The episodes decrease.
Yet Sonia simultaneously reports greater fatigue and recovery that remains unsatisfactory.
“My heart is calmer… but I don’t feel better.”
This observation does not allow these manifestations to be attributed to the treatment. An individual clinical course is never sufficient to establish a causal relationship.
It nevertheless highlights a fundamental clinical distinction: improvement in a targeted symptom and improvement in overall functioning are not necessarily synonymous.
Reassessment with the prescribing physician then allows benefits, tolerability and the overall clinical course to be considered together.
Sonia’s case does not require her previous assessments to be declared incorrect.
Each addressed a legitimate question.
The difficulty emerges when each manifestation generates a new sequence of investigations without reconstructing its relationship with the manifestations that preceded it.
The pain then belongs to one record. The palpitations to another. Sleep to a third. Fatigue to a fourth.
Sonia, however, is not living four separate medical records.
She is living one biological trajectory.
The question is no longer:
“How can Sonia be stabilised?”
but:
“What is progressively reducing her capacity to absorb certain demands,
modulate her response, and then recover?”
This reformulation does not provide an immediate answer.
It does, however, change what deserves to be observed.
Sleep is no longer considered solely in terms of duration, but also in terms of continuity and its relationship with the following day. Physical activity is no longer assessed solely according to quantity, but according to its place within periods of exertion and recovery. Meals are not interpreted as the cause of the palpitations, but their timing may become a piece of information to compare with the other available data.
Adjustments that fall within the medical field remain matters to be discussed with the treating physician or the relevant specialist.
The objective is not to impose artificial regularity on a living organism.
It is to understand why certain variations become symptomatic, more costly, or take longer to resolve.
Changing symptoms prove neither successful adaptation nor system failure.
Variability must be interpreted.
Its structure, amplitude, timing, relationship with demands, and the capacity for recovery provide more information than the simple observation that “the symptoms change.”
Research on physiological complexity has shown why apparent regularity is an insufficient criterion for characterising the functioning of a living system. Models of allostasis, meanwhile, remind us that adaptation itself involves coordinated changes that enable the organism to respond to environmental demands.
These theoretical frameworks do not allow Sonia to be diagnosed.
They allow a more rigorous question to be asked.
The most important information may not be that her symptoms vary.
It may lie in the way they vary, in what precedes those changes,
and in the organism’s capacity subsequently to return to a level of functioning compatible with its needs.
Sonia’s condition may not be changing without an underlying logic.
That logic may simply become invisible when each manifestation is examined separately and at a different point in time.
Reconstructing that logic does not mean inventing a common cause for every symptom.
It means distinguishing what has been demonstrated, what is associated, what remains hypothetical and what now warrants further investigation.
A living organism is not defined by the absence of variation.
It is also defined by its capacity to vary without losing coherence.
When symptoms change but successive investigations fail to explain their trajectory, the problem is not necessarily a lack of information.
It may lie in the way that information has been separated throughout the medical journey.
Clinical Biological Decoding® reconstructs the chronology, compares the available data, examines the interactions between symptoms, biology, treatments, constraints and clinical evolution, and then reviews 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 interpret.
This analysis does not replace medical diagnosis, prescription, or follow-up by the treating physician.
Lipsitz LA, Goldberger AL. Loss of “complexity” and aging. Potential applications of fractals and chaos theory to senescence. JAMA. 1992;267(13):1806–1809.
Goldberger AL, Peng CK, Lipsitz LA. What is physiologic complexity and how does it change with aging and disease? Neurobiology of Aging. 2002;23(1):23–26.
McEwen BS, Wingfield JC. The concept of allostasis in biology and biomedicine. Hormones and Behavior. 2003;43(1):2–15.
Manor B, Lipsitz LA. Physiologic complexity and aging: implications for physical function and rehabilitation. Progress in Neuro-Psychopharmacology & Biological Psychiatry. 2013.
Dr Farida Sebbag works on the strategic analysis of complex medical situations in which symptoms persist, fluctuate or remain difficult to explain despite investigations that may remain reassuring. Her work focuses on the chronological reconstruction of data, the identification of interactions between them, and their examination in light of the international scientific literature.
HypnoCorpe® is a private practice based in Geneva and working internationally. Its analyses do not replace medical diagnosis, prescription, or follow-up by the treating physician.
Clinical Analysis · Complex Medical Situations




