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DeepVersity — a living essay. This text is revised as research advances and the underlying ideas develop.

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A chronic symptom does not arise in a vacuum. It appears in an organism with a biological history of its own: previous illnesses, periods of strain, adaptations, intervals of recovery and learned responses. At the same time, the symptom belongs to the present, in which the nervous system, immune system, metabolism, endocrine function, behaviour and environment continually influence one another.

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Looking at a single symptom or measurement can tell us something extremely important. But it does not always explain why a symptom persists, why other changes accompany it, or why two people in seemingly similar circumstances respond so differently.

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Understanding long-term health may therefore require a different question: not only which part of the system is functioning abnormally, but how the system as a whole came to function in this particular way.

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A symptom tells us something, but not always the whole story.

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Modern medicine can investigate inflammation, endocrine function, blood glucose regulation, gastrointestinal disease, neurological injury and cellular energy production with ever greater precision. More accurate diagnostics and targeted treatments are essential. In many situations, a symptom can be traced to an identifiable disease mechanism that can be addressed directly.

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Yet identifying a symptom is not necessarily the same as understanding its entire course of development. Persistent pain may be accompanied by disrupted sleep; ongoing fatigue may alter physical activity and social life; a prolonged period of illness may affect both physical capacity and the bodily sensations a person begins to anticipate.

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These relationships do not mean that every co-occurring symptom shares a single cause. They mean that the consequences of one problem may, over time, become part of the conditions that shape another. When this happens, investigating an individual change remains necessary, but may no longer be sufficient.

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The body's history lives on in its present physiology

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It is easy to imagine the body beginning each day from the same starting point. Biological systems, however, are not without history. Repeated demands, illnesses, environmental conditions and opportunities for recovery can leave traces in how readily systems are activated and how quickly they return to their previous patterns of activity.

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In stress physiology, this tension has been explored through the concepts of allostasis and allostatic load. Allostasis refers to maintaining stability through adjustment to changing demands; allostatic load describes the potential biological costs associated with prolonged adaptation.¹

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This is more than the claim that stress is harmful. The same response may be protective in one situation and costly in another. Activation, vigilance and the rapid mobilisation of energy can be indispensable. Difficulties may arise when these responses remain necessary for too long, recur repeatedly or become poorly matched to other biological demands.

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Biological history also takes many forms. It does not refer only to memories or psychological experiences. It may include immunological memory, tissue changes, changes in functional capacity and long-term metabolic adaptations. The present state of a living system cannot always be understood without this temporal dimension.

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The nervous system integrates information, but it does not act alone

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The nervous system helps the organism detect change, regulate internal functions and prepare for future demands. It brings together signals from within the body, environmental conditions, previous experience, possibilities for action and the social world.

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But the nervous system is not the sole command centre of biological regulation. The immune and endocrine systems, metabolism and local tissue mechanisms have their own forms of regulation, and they in turn influence nervous system function. This is what makes the interactions so interesting: regulation does not travel along a single pathway in a single direction.

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The interaction between the nervous and immune systems has, for example, been investigated through research on the inflammatory reflex. This work illustrates how neural signalling can participate in the regulation of inflammatory responses.² At the same time, signals from the immune system influence the brain, behaviour and experience. The existence of such a mechanism does not mean that all inflammatory diseases originate in nervous system dysregulation.

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This broader perspective develops the idea of body and mind as one interconnected system. It is not a matter of a psychological event first arising outside biology and then acting upon the body. Experience, action and physiology unfold at different levels of the same living system.

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The body does not merely react, it also anticipates.

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Much of physiology does not wait for a disturbance to occur before preparing a response. The organism anticipates meals, movement, daily rhythms, social situations and potential threats. The significance of anticipatory regulation has been explored, among other places, in theoretical models of allostasis.³

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Anticipation is not limited to conscious expectations. A person need not be thinking about anything threatening for their behaviour and physiology to have adapted to a situation that was previously demanding. Implicitly learned associations and signals from within the body also contribute to these processes.

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Interoception — the sensing and processing of signals from inside the body — is an important part of this picture. Models of predictive interoception propose that incoming bodily information and expectations shaped by previous experience jointly contribute to the interpretation of bodily states.⁴ This is an influential research framework, not a complete explanation for the origins of every chronic symptom.

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If recurring pain, uncertainty associated with illness or physiological instability alters what the organism comes to expect, that change may extend to attention, behaviour and certain regulatory responses. This does not make symptoms imaginary. It means that present physiology and anticipation shaped by past experience may participate in the same process.

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What initiates a disease and what keeps symptoms going are different questions

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This distinction is particularly important when trying to understand chronic conditions. An illness may begin with an infection, an autoimmune process, tissue damage, a genetic predisposition or another identifiable biological mechanism. Over time, however, additional factors may become part of the symptom pattern: sleep becomes disrupted, demands accumulate, activity changes, pain-related processing shifts, or illness restricts the possibilities of everyday life.

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What originally triggered a problem may therefore not, by itself, explain what later maintains or amplifies its symptoms. Conversely, a change observed in regulation may be a consequence of the illness rather than its cause.

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Distinguishing these roles helps prevent a dangerous oversimplification: labelling every chronic condition a problem of the nervous system, stress or prediction. That would merely replace one form of reductionism with another. A systems perspective must not exchange one single-cause explanation for a different one.

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When pain and sleep begin to influence one another

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The relationship between pain and sleep offers a concrete example of why the temporal structure of symptoms matters.

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Pain can make it difficult to fall asleep, interrupt sleep and increase vigilance at night. Conversely, disturbed sleep can affect pain sensitivity and predict later pain. A review bringing together prospective and experimental research found that poorer sleep predicted subsequent or more severe pain in a number of study designs.⁵

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A feedback relationship can then develop: pain disrupts sleep, while poor sleep may in turn make pain harder to manage or intensify the experience of pain. The strength of this relationship and its biological mechanisms nevertheless vary between individuals and conditions.

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The point is not that sleep is the hidden root cause of pain. Rather, a consequence of a prolonged illness can itself become one factor contributing to its continuation. Understanding the relationships between symptoms may therefore reveal further possibilities even when the original disease mechanism has already been identified and is being treated.

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Health is not immobility, but the capacity to move between states

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Good physiological function does not mean that every measurement remains unchanged. Heart rate, hormone activity, alertness, energy use and many other processes fluctuate continually. What matters is whether the system can respond appropriately to a situation and subsequently move into another functional state.

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One promising field, network physiology, examines how temporal relationships between different physiological functions are organised. In a study by Bashan and colleagues, the structure of physiological networks varied across different sleep and wake states.⁶ This does not establish that chronic illness is simply a form of network rigidity. It does, however, provide a tangible example of how the relationships between systems can themselves be measured and shown to change.

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From this perspective, health can also be understood in terms of adaptive capacity: the ability to activate, recover, allocate resources and change behaviour as circumstances change.

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Flexibility, is not a single number. Even heart rate variability (HRV), which can describe certain aspects of cardiac autonomic regulation, cannot by itself capture the adaptive capacity of an entire organism. Neither a high nor a low value is a universally meaningful indicator of health without context.

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Bodily signals are information, not unequivocal verdicts

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Living with illness over a long period may change how a person notices, interprets and anticipates signals from their body. It is useful to examine this without assuming that bodily sensations are unreal or self-generated.

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A 2024 systematic review and meta-analysis examining pain and interoception reported differences in certain dimensions of interoception between people with chronic pain and control groups. The certainty of the evidence was, however, very low, and the studies could not establish whether the observed differences were causes, consequences or both.⁷

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This uncertainty does not make the field unimportant. On the contrary, it shows why signals arising from the body, their neural processing, conscious experience and symptom-related behaviour need to be distinguished — and why the ways they influence one another deserve careful investigation.

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What can we actually measure?

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When we talk about regulation, there is a danger that the concept becomes too expansive: everything appears to be related to it, while nothing is precisely defined. A systems perspective must therefore set limits on its own explanations.

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Researchers have attempted to quantify allostatic load using indices combining biomarkers from several physiological domains. A large analysis pooling multiple cohorts illustrated both the promise of this approach and the difficulty of standardising the measures involved.⁸ Similarly, physiological flexibility, prediction and recovery capacity need precise definitions within each study.

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Biological plausibility is not the same as observing two variables changing together. And neither is equivalent to demonstrating that changing one variable actually causes a change in another. A rigorous systems interpretation does not bypass these distinctions.

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What does this perspective change?

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Systems thinking does not mean abandoning clinical diagnosis or targeted medical treatment. Nor does it mean that calming the nervous system can generally cure chronic diseases. Some conditions require highly specific, ongoing care, and the value of regulatory practices cannot be generalised across them.

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Instead, this perspective can broaden the questions we ask. Once an underlying illness has been appropriately investigated and treated, it may also be useful to consider what shapes sleep quality, symptom intensity, the distribution of demands, the possibilities for activity and recovery. In some circumstances, carefully selected changes targeting these factors may support the overall situation. Their effects and safety must, however, be assessed in context.

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I find it compelling to think that long-term health is not always only about removing a particular disturbance. It can also be about expanding the range of what becomes possible: the system is no longer bound quite so tightly to one recurring response, everyday life opens up in new ways, and future demands may perhaps be met with greater flexibility. This is a way of understanding health, not a promise of any particular treatment outcome.

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Finally: what should we ask beyond the symptom?

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Instead of asking only what is going wrong in the body, we can also ask:

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• How has this cluster of symptoms changed over time?

• What initiated the condition, and what might be maintaining it now?

• Which changes are primary, and which are consequences?

• In what situations do responses remain flexible, and when do they recur in similar patterns?

• What do present measurements tell us, and what do they leave out?

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These questions do not replace medical investigations, diagnoses or treatment. They deepen the understanding within which those activities take place.

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Viewing chronic health through a systems perspective does not diminish the importance of biological mechanisms. It makes their relationships, history and temporal organisation more visible. A single disturbance may initiate a sequence of events, yet the situation that develops may no longer be explained by that disturbance alone. Sometimes the whole becomes easier to understand when we examine not only the parts of the system, but how they function together. Recovery does not always mean the disappearance of symptoms. Sometimes it means the return of possibilities.

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By Natassa Aaltonen, MSc · Founder of DeepVersity

Published 01 March 2026 · Updated [21 October 2026]

About the author

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Explore the research behind this essay

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Which findings and scientific models inform this essay? The companion page presents references ¹–⁸, examines the methods and limitations of key publications, and explores the questions their findings leave open.

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Explore the research →

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This is an essay integrating scientific research perspectives, not an individual medical assessment or treatment recommendation.