On the concept of psychological risk factor
Stefano Canali
Università degli Studi di Cassino
Topoi. An International Review of Philosophy, 2004, 23, pp. 177-186.
The idea that certain mental phenomena (e.g. emotions, depression, anxiety) can
represent risk factors for certain somatic diseases runs through common thinking on the
subject and through a large part of biomedical science. This idea still lies at the focus of the
research tradition in psychosomatic medicine and in certain interdisciplinary approaches that
followed it, such as psychoneuroimmunology. Nevertheless, the inclusion in the scientific
literature of specifically mental phenomena in the list of risk factors pertaining to a specific
pathological condition would seem, to say the least, problematic when not completely absent,
unlike what happens for certain behavioural factors, such as smoking, sedentary life, and
alcohol abuse. It is also significant that insurance companies and health and welfare services
do not pay for interventions and treatment for states of anxiety, disorders of mood and of the
personality, alexithymia and stress reduction, as means of prevention or treatment of somatic
diseases, as instead they do for the treatment of tobacco addiction.
However, as I shall endeavour to argue here, there are numerous and well grounded
reasons why this different consideration of psychic conditions compared with behaviours is
valid and must be maintained in the evaluation of pathogenetic risk factors.
Behavioural risk factors and psychic risk factors
Several different methods are now available which establish on a firm basis that some
behavioural aspects play a significant role in the etiology and progression of a disease. To
return to the case of smoking, for example, the following types of study have provided
evidence that this kind of behaviour contributes to the development of lung cancer: A) the
epidemiological studies carried out to demonstrate whether smoke represents a risk factor for
cancer of the respiratory system, comparisons between smokers and non smokers, the
demonstration of the existence of a dose-effect relation; control of confusing factors. B)
laboratory studies related to the possible development of lung cancer. C) Short term and
follow-up studies on the effects of the reduction of smoking on the etiology of cancer and its
progression. D) Analysis of the components of cigarettes and of the smoke inhaled and the
isolation of the active ingredients having pathological effects on tissues, experiments on
animals carried out using these components. E) in vitro studies aimed at determining the
molecular path from the active ingredients to pathophysiological changes of lung cancer
development.
None of the mental processes postulated as causes or risk factors for psychosomatic
disorders has ever been examined using such methods. This is due in the first instance to the
very identity of the psychological and psychiatric constructs. Emotion, stress, anxiety and
depression have a complex and multidimensional nature, both as concepts and as actual
nosological entities, and are therefore constitutionally non quantifiable and hard to investigate
using epidemiological studies.
This set of problem elements nevertheless represents a basis for another series of
difficulties of a methodological nature in the psychosomatic approach. One of the main
characteristics of the controlled studies is the capacity to indicate the mechanisms and
transitions that link diseases to the risk factor.
The typical model of psychosomatic conceptualization involves a structuring and a causal
direction by psychological factors of the somatic factors through one or more physiological
mediators. Therefore, in order to acceptably document the hypotheses of psychosomatic
etiology, it would be necessary accurately to identify the psychological factor involved or to
characterize it univocally and then to evaluate its physiological effects and the way the latter
promote the pathogenetic process.
The uncertain identity of psychological constructs
We have seen how the univocal identification or accurate characterization of a
psychological element or process actually proves impossible. Then, despite the efforts made
to detail the various components of mental disorders undertaken by diagnostic handbooks
and international classifications, today embodied in DSM-IV-TR and ICD-10, psychosomatic
tradition tends to use the terms referring to pathological emotions in a rough and ready
fashion. For example, studies based on a psychosomatic approach point to anxiety as a risk
factor in cardiovascular disorders (CVD), and depression in cancer and again for CVDs.
In the case of anxiety, these studies seem completely to neglect the fact that they are
using a multiform and controversial psychological and psychiatric concept. As a clinical
category, the term anxiety disorder comprises several different subtypes characterized by
widely differing symptoms ranging from various phobic manifestations to generalized anxiety,
posttraumatic stress disorders and obsessive-compulsive disorders. According to some
researchers, however, the breakdown into subtypes is still highly ambiguous and
controversial (e.g. Barlow, 1988). The widespread, multidimensional and approximate
appearance of the psychological constructs that, like anxiety or depression, are adopted as
risk factors, makes it impossible to isolate them and to manipulate them experimentally, as is
generally done when active ingredients are being identified.
Research in neuroscience, for instance, is showing how the various subtypes of anxiety
are linked to different biological correlates (Kandel, 1983; LeDoux, 1998; Grillon, 2002). The
latter would conceivably have a pathogenetic basis in apparatuses having different
mechanisms and with consequently different morbid outcomes.
The same may be said for depression. It is actually impossible to determine the biology of
“depression” as this condition consists of a complex set of different subjective elements –
anxiety, detachment, loss, despair, etc., of behavioural and relational processes associated
with an extensive array of physiological and pharmacological alterations (Schatzberg et al,
2002, Musselman et al., 1998).
In the case of both anxiety and depression, moreover, there is a high incidence of
reciprocal co-morbidity or the onset of other psychiatric manifestations (Nesse, 1999), which
further complicates the characterization of factors having an etiological role and their possible
interaction.
What has been said above points to the absence of any fundamental assumptions to
characterized anxiety or depression as risk factors for CVDs or more in general for somatic
diseases.
Furthermore, like all other affective states, anxiety is a complex process related to several
domains, from subjective experience to the various physiological equivalents, as far as
behavioural manifestations which in their turn refer in a circular fashion to environmental and
social variables are concerned. The correlation with somatic disorders should therefore be
investigated for each of these domains, also taking account of the fact that, during the
possible pathogenetic process thus triggered, these different aspects of anxiety interact,
reciprocally modifying each other, modifying the biological substrate and being transformed
by the latter.
Imprecision, the overlapping of these psychiatric concepts, the circular relationship
between domains and different processes thus precludes the possibility of making an
adequate assessment of the extent, specificity, biological coherence and even the temporal
relationship of the postulated causal association, qualities that instead represent important
criteria for ascertaining causality in medicine.
The case of stress
Also when confronted with a more neutral concept such as stress, research into
psychosomatic mediators and mechanisms betrays its imprecise nature. Although apparently
better characterized than depression at the biological level, if for no other reason than the
wide use made of animal models, which have been late to appear for depressive states,
stress places a series of exceptional obstacles in the way of studies aimed at isolating
psychological risk factors and the characterization of pathogenetic mechanisms and
processes leading from the psychological to disease in the clinical sense. Above all, stress is
another multidimensional concept used to refer to different psychological and physiological
processes and in this sense ultimately becomes a secondary risk factor. It is potentially linked
to all the affective dynamics and each affective reaction above a given threshold may be
stressful. Furthermore, stress represents a complex variety of psychological processes
ranging from the cognitive dimension to behavioural reaction and passing through a multitude
of intermingled subjective dimensions of affectivity. For instance, emotional response and
stress response are known to be strongly modulated by experience and by the cognitive
dimension. In this sense, the same event or stressor can produce different effects in different
persons, as well as at different stages in the life of the same individual. It is consequently
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impossible to generalize with reference to the exposure to stress as a possible etiological
factor as stress itself actually reproduces a two-fold and mutually related plurality of effects
referring to individuals and to different periods in the life of the same individual: those
dependent on predisposition and on the current biological terrain, and those mediated by
experience and the cognitive dimension. This implies in turn that it is impossible to identify a
consistent biological gradient of responses to exposure to stress or to negative emotions: on
the other hand, this is a fundamental element in the formulation of suitable hypotheses
regarding the causal relationship between risk factors and disease.
At the same time the fact that the emotional reaction and response to stress both depend
on circular relationship with the cognitive level and learning does not allow us to determine
satisfactorily whether a dose response relation exists between emotions and disease, and
what form this takes, as in this case the dose is also a function of the response.
This complexity is related to a large number of mutually interacting physiological
equivalents.
This complexity makes it extremely difficult to isolate the various pathways through which
stress affects the biological terrain and thus to provide an adequate description of any
etiopathogenetic role played by psychological events.
The primacy of the mind
It should be noted how the idea that the mental contents and dynamics can represent risk
factors is based on the assumption that the mental element, for instance in depression or
anxiety, takes priority over the somatic symptom and is thus the cause of the disease. This
assumption seems to depend solely on the priority given in our culture to the mental, as
opposed to the physical, dimension of the person. Also with reference to neurobiological
evidence it now seems reasonable to investigate the relations between emotions and disease
by examining somatic symptoms as one of the two dimensions making up affective disorders.
It would not thus be totally unreasonable to reverse the causal order and investigate these
morbid conditions as the manifestation of a process of ‘psychologization’ of somatic
phenomena.
On the identity of emotions
Two other problematic aspects of the idea that the psychological content of the emotion
can be taken as representing risk factors must be mentioned. The first of these is dependent
on the substantial continuity and overlapping of the spectrum of the shared affective life, the
customary emotional response to common stimuli and on which, in the approach we are now
analyzing, the onset and progression of certain forms of chronic pathology are believed to
depend. The somatic symptoms would therefore be difficult to relate to specific emotion and
all forms of causal argument would thus be precluded.
Emotional experience also displays aspects of strong relativity and indeterminacy in all
the various theories that have attempted to explain it and that may be related to three main
conceptualizations: peripheral theory, central theory and cognitive theory.
The peripheral theory of emotions
Introduced by William James in 1884 in his famous article in Mind, the peripheral theory
of emotions claims that emotional experience consists in physical sensations, of feedback
from vegetative and behavioural responses. We do not run away because we are afraid, but
we are afraid because we are running away, we tremble, and our pulse and breathing rate
shoot up. But, as Walter Bradford Cannon (1927) had already pointed out, the most intense
emotions generally are accompanied by very similar vegetative modification patterns.
Furthermore, Cannon pointed out that although we are generally conscious of the type of
emotion experienced, visceral activities are not perceived very accurately as these somatic
regions are not highly innervated. These objects reflect the type of difficulty encountered
when it is endeavoured to relate the various emotional states to specific physical symptoms.
The central theory of emotions
The central theory, first proposed in the mental content psychology of Wilhelm Wundt and
Edward Bradford Titchener and then systematized and related to nervous processes by
Cannon (1927), identifies the specificity of emotions as characteristic subject experiences.
The peculiar psychological content of the emotions is thus believed to be the effect of
corresponding brain processes that can nevertheless give them meaning and distinction. In
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this conception the emotional response is subsequent to the activity giving rise to the
emotional experience. The subjective experience, with its variability, its irreducibility, it purely
qualitative nature, becomes the causal agent of the emotional response. Also this conception
of emotional experience is hard to frame within quantitative studies and in causal explanation
models specific to research on risk factors.
The cognitive theory of emotions
In order to explain the differences between emotional experiences also cognitive
representations have been used. In this sense the experience of fear, for example, consists
above all of awareness of having to face a dangerous event or thing. The cognitive theory of
emotions was proposed for the first time in a radical version by Stanley Schachter and
Jerome Singer in 1962. They claimed that emotional experience was above all a process of
attributing significance or of the verbal labeling of processes of physiological activation. In this
case, the emotions become relative to experience, learning and individual culture.
Self-report of emotions and epidemiological investigations
Many of the epidemiological studies on emotions and disease are based on self-reports
of specific affective states and involve the use of a vast array of measurement scales. Despite
some interesting convergence of results, there are obvious methodological gaps and the
absence of studies and procedures to compare the evidence.
Data collection through self-reports is problematic, to say the least. It has long since been
recognized that the perception of emotions is strongly influenced by experience, by cognitive
elements, by the personality, by the capacity to distinguish among the constantly overlapping
emotional states (e.g. Lazarus, 1977; Lazarus et al., 1970). Furthermore, the perception of
possible negative and pathogenic emotions may be falsified by psychological defence and
adaptations mechanisms capable of deceiving the subject as to his/her mental health
(Shedler et al., 1993).
It thus appears odd, to say the least, to indicate as a cause or risk factor of a somatic
disease a fact determined by interpolating constitutionally subjective values. Moreover, if the
emotions depend on other psychological elements rather than on affective states it is more
likely that the primary risk factors will be cognitive type constructs, an individual’s culture,
his/her personality. In this case, it would thus actually be impossible to identify the active
ingredient, the causal agent, the specific correlate, as the cognitive type constructs, individual
culture, the personality, are all elements that are difficult to break down as they are specified
by value systems and meanings.
Expression of emotions and biological coherence of symptoms
Another singular aspect of psychosomatic conceptualization and the identification of
emotions as risk factors in certain diseases is the fact that the various explanatory
hypotheses have indicated as potential etiopathogenetic factors all the different and
conflicting dimensions of emotional experience. Risk factors for identical psychosomatic
phenomena, for instance, affecting the cardiovascular system, have been observed to some
extent in alexithymia, that is, in the incapacity to verbalize affective processes, in the
unconscious repression of emotions (e.g. Davison and Petrie, 1997, Marshall, 1972), in the
conscious inhibition of emotions in the face of emotional arousal (e.g. Weinberger et al.,
1979), in the excessive outpouring of emotions (e.g. Gross and Levenson, 1993, Pennebaker
and Beall, 1986). This radical uncertainty conflicts with all criteria of coherence and biological
logic which should instead be observed in postulating a causal link between emotion and
disease.
State or traits? From emotions to personality
Another significant question in the analysis of emotions as risk factors in somatic
diseases is the problematic nature of the distinction between emotional states and traits. The
distinction between the two is considered a function of their duration: the former are thought
to refer to transient emotional phenomena, while the latter are constituent elements of the
personality, permanent characteristics. Although appreciable at the extremes of the temporal
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continuum, in normal everyday conditions the distinction between states and traits is seen to
be arbitrary (e.g. Allen and Potkay, 1981).
This has important logical consequences with regard to the hypotheses concerning the
links between emotions and somatic diseases. Investigation of the relations between
emotions and disease could sometimes measure traits and on other occasions more or less
transient emotional states. The impossibility of distinguishing the object of the observation
would therefore lead to the impossibility of ensuring the comparability of studies.
Personality and disease
The idea that personality type is causally linked to specific somatic disorders is an old
one, and was to some extent already formulated in the Hippocratic doctrine of the relations
between humours, or vulnerability and character traits. It was Helen Flanders Dunbar who
gave this belief systematic form prior to World War II through an extensive use of
psychological tests, statistics and the comparison of character traits with clinical signs
(Dunbar, 1935 and 1943). According to Dunbar a kind of character cliché existed for each
disease. The patient with coronary problems, for example, was a person who worked and
struggled tenaciously, possessed strong self-control and tended to be successful and to fully
attain his/her goals. The peptic ulcer patient, on the other hand, was a hyperactive and overenterprising type. Dunbar’s ideas were given wide circulation in the subsequent literature. The
public at large was quite familiar with Friedman and Rosenman’s (1959) theories on the
associations between CVD and personality type, which had been in the limelight of the
medical debate ever since the 1980s. Claus Bahnson (1969, 1980, 1981), on the other hand,
attempted to find a correlation between personality type and cancer.
However, let us examine the meaning and the implications of the idea of personality types
as risk factors in the relative somatic diseases. The idea that a certain type of personality is
prone to a particular disease generally leads to the conviction that a causal link may be
hypothesized between an inclination towards certain emotions and somatic symptoms. In the
final analysis this idea may lead to two distinct meanings: 1) It may mean that a person tends
to experiment certain emotions and to be predisposed towards certain events and
experiences. In this case, it is therefore evident that the causal agent that is supposed
somehow to link the psychological side to the symptom is not the personality type but perhaps
the emotion. 2) It may mean that both proneness to certain emotions and emotional
responses and the symptoms depend on a certain type of individual constitution that reacts to
certain experiences in specific ways that are psychologically and somatically coordinated.
Also in this case, therefore, there is no true causal relation between personality and symptom,
while the link between psychological dimension and somatic disease ought to be related to
the general framework of proneness, the individual constitution.
But does personalityactually exist?
Intuitively we believe that our actions are coherent, that is, that they depend on some
profound element in our individual nature: our personality. On closer examination, however,
the idea of personality is seen to be fraught with controversial aspects. It has been
incorporated in a large number of conflicting theories: to cite but a few – from behaviouralism
to the theory of individuality, from psychoanalysis to the biosocial theory, and even in radical
approaches in which the personality is a mere psychological concept. A cognitive construct,
an intellectual product, as Boethius wrote as early as the 6th century: “Persona est substantia
individua rationalis naturae”
This multiplicity of conceptions developed parallel with the emergence of an astonishing
array of instruments for measuring the personality. Unlike for other psychological concepts,
however, research has failed to identify any satisfactory definition of a simple operational
nature, which is only further evidence of the elusive nature of the reference of this category.
It is problematic, to say the least, to consider personality as a risk factor for
psychosomatic symptoms, as the cause or correlate of a somatic disease.
Psychological research itself has begun to question the concept of personality. In the late
1960s, Walter Mischel suggested that personality possibly accounted for less than 10% of the
variations in the behaviour of individuals and among individuals (Mischel, 1969). Mischel also
considered that the perception of continuity and coherence of behaviour was a cognitive
construction and that therefore personality practically did not exist.
Measuring of personality traits and representation of the temporal dimension
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Let us however assume that personality exists and that psychometric instruments are
capable of measuring the traits properly. Epidemiological studies on the relations among the
various personality types and somatic diseases are based on psychometric measures. In this
case we would have a snapshot of the person fixed on a single time frame. The exclusion of
the temporal dimension leads however to two serious epistemological inconsistencies. In the
first instance the time dimension appears to be fundamentally specific to the doctrines aimed
at investigating personality, as it represents the only quantity within which it would be possible
to understand and explain the fact that it apparently remains constant even in changing
circumstances. In the second place, this synchronic description of the personality is found to
be inconsistent with the theoretical framework surrounding it when it is used as a risk factor in
epidemiological type investigations and to seek explanations of a psychosomatic type.
Indeed, as a causal element in this case, personality is considered an active element
precisely because it is spread over the whole period of the individual’s existence. The single
snapshot portraying the personality thus becomes relatively unimportant in understanding or
identifying any physiological mediation mechanisms, in order to explain how personality traits
act at the etiological level and contribute to determining the pathogenetic progression of
morbid conditions of a chronic nature, such as the disorders for which today we seek a
correlation with factors of the psychosocial type probably linked to very lengthy time scales.
Emotions and disease: from problems of time frame to the indefinite complexity of the
web of causation
Reference to the temporal dimension introduces a gap between the limited time frame
surrounding emotional phenomena and the larger one in which chronic diseases develop and
in which emotions are viewed as risk factors. Also in the case of negative emotions
associated with long-term psychiatric conditions, such as untreated depression which may
last from 6 months to more than one year, we are dealing with periods of time that are
certainly shorter than those needed to bring about and maintain the lengthy process of a
disease such as CVD, cancer or diabetes, which are instead often associated with depressive
syndromes.
It is therefore impossible in the narrow sense to attribute an etiological role to certain
psychological conditions. It is therefore necessary to speak of relations, of the action of
psychological elements inside a multi-stage process made up of successive exposures to
pathogenic elements. And this is ultimately what the psychosomatic approach has actually
started to do, reformulating its basic epistemological elements and shifting from a search for
the causes to the identification of the relations (Mizrachi, 2001).
Nevertheless, also in this new approach investigations of the relations between emotions
and disease continue to perpetuate a mentalistic model and tend to assign a predominant role
to the psychological dimension of the emotions. However, considering mental phenomena
and emotional experience, as a risk factor leads to an inadequate thematization of the role of
behaviours associated with emotional disorders, mood and in general all the psychiatric
conditions involved in the causation of a somatic type of pathological condition. And it stands
in the way of reflecting on another causal circularity, that between psychological experiences,
behaviour and nervous processes. In this way, the persistence of a mentalistic approach on
the one hand hinders the development of research strategies focused on the objectivizable
plane of behavioural risk factors and, on the other, limits the perspectives and variables with
which to investigate as required the individual portions and the different planes of the close
network of relations between emotions and somatic symptoms.
Depression as a risk factor in CVD. Critical observations
Let us take for instance the idea that depressive conditions represent a risk factor in CVD.
This now represents a rather widespread conception in the modern approach to
psychosomatic research as it is supported by a large body of epidemiological studies (e.g.
Anda et al., 1993; Barefoot and Schroll, 1996; Carney et al., 2002; Glassman and Shapiro,
1998; Frasure-Smith, Lespérance, 1998; Hippisley-Cox et al., 1998; Ford et al., 1998, Wulsin
et al. 1999), to the point that François Lespérance and Nancy Frasure-Smith, two of the most
distinguished workers in the field, have written: It is time that depression replaced type A
behavior as the number one psychological concern for cardiologists (Lespérance, FrasureSmith, 2000).
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A vast literature has now been produced by research on the possible biological
mechanisms underlying the relationship between depressive symptomatology and CVD. It
suggests a wide range of potential mechanisms and also present numerous contradictory
aspects. One of the explanations considered more plausible suggests that depression can
cause CVD through neurohumoral dysregulation. Alteration of the functionality and of the
parameters of the autonomous nervous system and the endocrine system is actually found
both in depression and in CVD. Neurohumoral dysfunctions lead to the alteration of blood
supply to the heart and to the lowering of the variability of the heart rate, thus contributing to
the progression of a CVD. However, in this case it cannot be demonstrated that depression is
the cause of these neurohumoral alterations or that the latter represent the origin of the
neurohumoral dysfunctions observed in CVDs. Depression and CVDs could therefore be two
different manifestations, with different clinical expression times, of these alterations.
Another widely supported explanation points to a possible causal mechanism in
inflammatory processes. One of the ways in which CVDs can be understood is in fact to
consider them as chronic inflammations caused by damage to the vascular endothelium. In
this hypothesis, depression could facilitate and thus increase the inflammatory response by
altering the secretion and lowering the anti-inflammatory action of cortisol. In depressed
patients a hypersecretion of cortisol is found together with the down-regulation of expression
of gluco-corticoid receptors, a phenomenon which thus reduces the anti-inflammatory action
of corticosteroids. Further evidence in support of this explanation is that in depression an
increased level of cytokines, C-reactive protein and tumoral necrosis factors are observed,
which are all risk markers for cardiovascular morbidity and mortality. The objection raised in
connection with hypotheses regarding the causal relationship between depression,
neurohumoral alterations and CVD is valid also in this type of explanation: depression and
CVDs might just represent two different ways of clinical entities manifesting themselves in
time. This observation is reinforced for example by the large body of research pointing to the
presence of depressive symptoms as the side effects of cortisone and interferon therapy.
Emotions and CVDs: a web of causation model
At the current state of affairs a less problematic explanation would thus have to place the
main focus on behavioural variables as the causal nexus between depressive conditions and
CVDs and possibly pursue the analysis of possible relations among individual biological
aspects of depression and CVD.
Depression brings with it alterations in varying degrees to eating and grooming habits,
exercise, smoking and the use of substances with psychotropic effects and so on. These
behavioural changes represent risk factors for CVD. At the same time, however, these
behaviours contribute, on the one hand, to certain mental experiences and, on the other, to
certain alterations of biological processes. Moreover, the psychological experience of
depressive disorders is related to a series of transformations in the functioning of the nervous
system, which then have an effect on all the control and organic regulation processes
governed by the nervous system and ultimately on behaviour itself.
The relation between clinical expression of CVD and the depressive event is however the
expression of an individual history of successive exposures to factors and elements able to
cause alterations in the functioning of the cardiovascular system. However, this historical
process is extremely complex in nature. It represents the effect of the two-fold, peculiar
sequence of instances of exposure to pathogenic elements undergone by the individual, at
both the somatic and the psychological level. The relation between clinical expression of the
CVD and the depressive event is an expression both of the peculiar relationship between
events and activating behaviours and the individual biological terrain – vulnerability -, the
latter being determined at the genetic level and thus linked to a further historical level of the
philogenetic path. On the other hand, in the course of life and thus during possible CVD
progression, this given relation gradually becomes more and more modulated by the cognitive
and behavioural levels, since the response to the events and stimuli having
psychopathogenetic potential is modified through experience and its cognitive elaboration in
both the somatic sphere and that of psychological experience. Furthermore, even before an
acute event or an appreciable clinical sign is produced, the pathogenetic trajectories followed
by the cardiovascular system may trigger or mediate some of the depressive symptoms, thus
modifying emotional reactivity and therefore, in a circular fashion, all that is reproduced on the
cardiovascular system as an activating element.
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The idea of depression as a risk factor in CVD is thus linked to a series of processes laid
out on different causal and temporal planes, which are characterized individually and in their
mutual relations both by linear mechanisms and circular dynamics. Such complexity can only
be penetrated through particular sections or individual perspectives, from a certain point of
view, or for particular purposes, for the purpose of identifying a significant criterion and thus
isolating a portion, a limited plan of the processes under way.
In this sense, the unshakeable complexity of this idea, in its generically accepted version,
is such as to make it impossible to come up with any effective causal explanation or concrete
clinical application. It rather represents a suggestive image, an appeal for research without
being a scheme that can be translated into an investigation.
The idea of depression as a risk factor in CVDs is therefore an exemplification of the
epistemological difficulties that arise when it is attempted to considered the “web of causation”
notion of McMahon, Pugh and Ipsen (1960) as something more than a heuristic tool, a
metaphor for expressing the idea that the causal processes of etiopathogenetic pathways are
complex and interrelated (Krieger, 1994).
An emerging model
To some extent paradoxically, in recent years, investigations carried out at a high level of
analysis and reduction have been clarifying the issues at stake more fully in the
characterization of our understanding of the etiopathogenesis of diseases in the psychosocial
approaches, holistic perspectives implicit in the idea of web of causation and of
multifactoriality. By focusing on gene transcription processes, molecular biology and
functional genomics these investigations have been identifying the fundamental mechanisms
underlying the integration of the various physiological systems involved in emotional and
individual adaptation processes, the causal network by which experience and individual
history moulds the shape and functions of organisms, the circular nature and continuity of the
interactions between mental events and somatic phenomena, the overlapping and
concatenation of metabolic and plastic events by means of which the psychological dimension
produces or contributes to the triggering or development of a morbid process.
On the other hand, the very acquisitions of molecular genetics are revealing the need to
reflect on the cascade of biological phenomena related to emotions and to psychosocial
dynamics that also converge on the regulation of gene expression in order to more fully
understand and cope more effectively with all morbid conditions.
Internal and external stimuli such as stages of development, hormone and chemical
mediator concentrations, stress, learning and social interaction affect the formation and
behaviour of gene transcription factors, which is referred to by the term epigenetic regulation.
In other words, just as a combination of genes shapes behaviour, including social behaviour,
so behaviour and social factors – through their action on the organism and on the central
nervous system – modify gene expression and thus the functions of the nerve cells, then
modulating, again in a circular fashion, the behaviour and projection of the individual in the
psychosocial dimension (Andreasen, 1997; Kandel, 1998; Gabbard, 2000).
The regulation of gene expression in nerve cells literally incorporates the various
environmental and psychosocial factors. In the processes of gene transcription culture can
thus become nature, without any mysterious leaps from the mental to the somatic. Thus, in
effect, the evidence that has accumulated in recent years has actually done away with the
very need to seek out the socalled “psycho/somatic transducer”. Psychosomatic transduction
actually does not exist insofar as all the stimuli, whether environmental, physiological or
psychosocial, have one and the same final target – gene regulation. At the same time, gene
regulation represents the initial element in a cascade of behavioural and biological processes
aimed at adapting the organism or which conversely are moving towards a possible gradual
detachment from homeostasis and thus towards disease.
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