Oh Tim, I've just had a most ghastly weekend because I felt so unworthy (Cerejo, 2015).
Surprising as it may seem, this quote was directed by Paul Nurse to Tim Hunt shortly
after they both learned that they received the Nobel Prize, illustrating, more or
less, the so-called Imposter Phenomenon (or Imposter Syndrome). Originally described
in 1978 and increasingly discussed over the last years (with over half of all publications
in the area published in the last 6 years), the imposter syndrome is a psychological
state, in which people express self-doubt on their accomplishments and skills, despite
factual evidence or other people indicating otherwise (Bravata et al., 2020). As a
corollary, syndromal imposters suffer from constant fear of being exposed as a fraud
(bluff ), because they often believe that they have fooled their peers into overrating
their abilities and professional competence (Chrousos and Mentis, 2020). As part of
a vicious cycle, syndromal imposters feel more prone to failure, may become less productive,
and are characterized by insecurity and procrastination (Neureiter and Traut-Mattausch,
2016a,b; Mullangi and Jagsi, 2019). Intriguingly, recent studies suggested that imposter
syndrome sufferers should be distinguished into two broad categories: true imposters
and strategic syndromal imposters, based on the degree of self-doubt (Leonhardt et
al., 2017).
An established body of research has been conducted on the prevalence and consequences
of the imposter syndrome (Parkman, 2016; Bravata et al., 2020). Notably, it affects
up to two out of three people in certain settings (Gravois, 2007); however, in settings
such as academia, its prevalence might be grossly underestimated in the predominant
culture of silence in higher education (Evans et al., 2018). Highly demanding families
and professional environments, psychological traits, such as perfectionism or insecurity,
and social inequalities, are all putative contributors to the imposter syndrome (Want
and Kleitman, 2006; Dickerson, 2019; Mullangi and Jagsi, 2019; Chrousos and Mentis,
2020). Despite its high prevalence and human toll, the potential neurobiological underpinnings
of the syndrome and its evolutionary origin have been scarcely explored.
Here, we emphasize the need to search for the potential psycho-neuro-biological basis
and evolutionary roots of this phenomenon, and to highlight the critical research
questions that should be addressed and answered in order to change clinical thought
and practice. This knowledge will hopefully stimulate novel conceptual approaches
to the phenomenon, which may unravel, in the long term, rational methods for its prevention,
diagnosis and behavioral -cognitive therapy treatment, especially in the younger generation,
especially females, which appear the most afflicted.
In evolutionary terms, it is worth exploring whether the syndromal imposter phenomenon
could be perceived as a contemporary remnant of a selected trait that could have offered
a survival and reproductive advantage to our ancestors, most likely as a result of
universal selection within a social hierarchy structure. Specifically, it would be
crucial to determine to what extent this phenomenon is a manifestation of anticipatory
anxiety, a vestige of a primitive arousal status in the anticipation of potential
threats (i.e., part of the active fight-or-flight response), or of withdrawal from
a potential threat, a valuable response of reducing exposure in the face of danger
(i.e, a manifestation of the defensive flight or passive freezing response), or, perhaps,
a combination of the two (Chrousos, 2009). In the same vein, could a psychological
(not evolutionary) self-induced feeling of failure serve as an internal impetus to
reach higher levels of perfectionism, as part of the obsessive-compulsive comorbid
traits that are present, more or less, in individuals afflicted by the syndrome? Collectively,
could the fear of failure combined with imposter syndrome be associated with the primary
emotion of shame, which may have an evolutionary function in keeping the tribe together
(Jaffe et al., 2014)? Or, at least, in theory, could imposter syndrome sufferers fear
success, in which case links to subclinical anhedonia or alexithymia (i.e., difficulty
to express feeling of pleasure from success) can be proposed?
Moreover, higher levels of perfectionism or fear of failure or success could make
underestimating one's own abilities an evolutionarily stable strategy. For instance,
and in a converse manner, could the imposter phenomenon be, as some experts have suggested,
a self-deceiving technique aiming to lower anxiety during external judgment of someone's
performance, despite internal self-confidence (Young, 2019)? In this context, there
might be overlaps of imposter syndrome and cognitive distortions (i.e., dysfunctional
though patterns) in various forms of anxiety or depression, especially in relation
to the self, often discussed in the context of evolutionary psychiatry (Nettle, 2004).
In the same vein, could this syndrome represent a cognitively intense, yet self-harming
manifestation of the premeditatio mallorum (i.e., negative visualization, or the pre-meditation
of evils), a concept otherwise defined by Stoic philosophers as a way to reach existential
sobriety (Robertson, 2019)?
Importantly, both anxiety and depression are associated with changes in the activity
of the stress system, which may lead to chronic brain neuromediator imbalances associated
with dysphoric distress (Chrousos, 2009). Pursuing this issue from a neurobiological
standpoint, research should focus on whether stress associated with the imposter syndrome
is linked to elevated release of stress mediators in the Central Nervous System (CNS)
and the peripheral tissues of the organism. Stress normally is associated with activation
of the brainstem locus caeruleus/norepinephrine system, which subserves arousal and
regulates the functions of the autonomic nervous system, and the hypothalamic-pituitary-adrenal
(HPA) axis, which plays modulatory roles (Chrousos, 2009). Mediators involved include
norepinephrine and corticotropin-releasing hormone in the CNS, and the catecholamines
norepinephrine and epinephrine, as well as, the steroid hormone cortisol, in the systemic
circulation. Chronic activation of the stress system may be associated with dysphoria,
anxiety, and depressive symptoms, as well as, somatization phenomena (Iob et al.,
2020); therefore, stress system dysfunction could be linked to some of the most severe
mental and somatic manifestations of syndromal imposters.
That said, considering the HPA axis as the biological basis of, or at least a major
contributor to, the imposter syndrome should be treated with caution, given that this
system is also generally related to stress, anxiety, depression, and somatization,
and many other related psychopathologies. Thus, the specificity of the HPA axis in
the pathophysiology of the imposter syndrome should not be taken for granted, not
least because the predictive power of HPA axis dysfunction for the imposter syndrome
might be quite low. Moreover, imposter syndrome and anxiety disorder could activate
the same stress response network, thus, raising the question whether they are separate
entities or, instead, overlapping ones. Our educated guess is that a major overlap
with often comorbid anxiety and depression might be present in the imposter syndrome.
Persons with low self-confidence or those who live in the certainty that others mistakenly
overestimate them on a permanent basis, and, thus, constantly fear exposure, should
suffer from the burden of the imposter syndrome to a higher degree. Under this prism,
the chronically elevated psychological stress level [e.g., as assessed through the
Trier Social Stress Test (Kirschbaum et al., 1993)] could be the consequence of the
imposter syndrome or, at least, a part of a vicious cycle of cause-causality, with
regard to this syndrome; however, examining possible causal relations (or providing
suggestions on how to address such causal schemes) would extend beyond the scope of
this Opinion article. Collectively, it seems imperative, at least in the decades-to-follow,
to elucidate the neurobiological basis of the imposter syndrome, to diagnostically
and therapeutically approach and its co-morbid disorders in a patient-centered manner
toward relieving the discomfort, no matter the underlying pathologic interconnections
and causal schemes.
It is noteworthy, nonetheless, that other biological systems, such as the Hypothalamic-Pituitary-Gonadal
axis and the associated sex hormones, could be involved in the pathogenesis of the
imposter syndrome as well, let alone explaining, at least partially and beyond social
and psychological reasons, the increased prevalence of the syndrome in women and girls.
Indeed, high testosterone levels have been associated with hierarchy, social dominance,
and competition, while estrogen has been connected to agreeableness and cooperation;
these effects, which are closely linked to the self and social behavior, may in turn
play a role in the genesis of the imposter syndrome (Ehrenkranz et al., 1974; Mccarthy,
1995).
Therefore, the following question has arisen: can we explain and possibly treat the
imposter syndrome by targeting the stress system and certain stress mediators? Further
research should be conducted, notably by assessing the levels of these mediators in
imposter syndrome sufferers. Neuro-imaging studies, which, to our knowledge, have
not been conducted in affected subjects as yet, would complement the above research
efforts.
From a psychobiological perspective, the perceived effort-reward imbalance stress
model suggests that a disparity between effort, which relates to duties and obligations,
and reward, which includes social and/or financial rewards, can lead to chronic activation
of the stress system with all that this entails (Siegrist, 1996; Ota et al., 2014).
We are tempted to theorize that imposter syndrome sufferers might subjectively perceive
effort-reward imbalance, which could inhibit them from feeling rewarded for their
successes or failing to be optimistic for any kind of upcoming rewards in the future.
In the same context, the role of disturbed levels of stress mediators in contributing
to the link between the imposter syndrome and effort-reward imbalance cannot be excluded,
as examined elsewhere (Ota et al., 2014). It is quite plausible that stress mediators,
which are either elevated or decreased as a result of chronic stress (Chrousos, 2009),
suppress, or fail to activate, the reward system of the brain. For the time being,
we contend that in the quest of achieving happiness through success, modern society
stimulates activities that ultimately boost the brain reward system, which, however,
is known to exhibit tolerance. Thus, on the one hand, intermittently secreted mediators,
such as serotonin, oxytocin, and dopamine, the so-called happiness, affiliation/altruism/compassion,
and reward hormones, respectively, participate in achieving constitutional happiness
and optimism, while, on the other hand, continuous or very frequent activation of
the stress system could lead to desensitization of the reward system and constitutional
unhappiness and pessimism about the future.
Similarly, a chronic decrease in the production of stress mediators, which characterizes
some chronic stress states, could cause an inadequate activation of the reward system
also accompanied by concurrent dysphoria and pessimism about the future (Chrousos,
2009). In this context, exploring the serotonin, oxytocin, and dopamine systems among
imposterism sufferers could be a worthy research pursuit. Likewise, it would be intriguing
to know how these neuro-hormones and other bioactive molecules are functionally interconnected
(Quintana et al., 2019), and how they are related to the feelings of self-doubt in
the syndromal imposters.
Could the imposter syndrome be explained and tackled, if its evolutionary and psycho-neuro-biological
underpinnings are deciphered? This scientific journey may be long-lasting and may
entail associating complex psychobiological, neurochemical, and neuroimaging experiments,
with scores in imposter syndrome scales [for a review on these scales, see Mak et
al. (2019)]. For the time being, the syndromal imposter phenomenon should be named
and acknowledged by those who suffer from it, and it should be tackled by a sufferer's
realistically appreciation of his/ her own strengths and weaknesses, not by being
influenced from misperceived internal or external judgments.
Receiving proper mentoring, seeking the help of experts, and embarking on appropriate
psychotherapies may be worthy avenues to pursue in this prevalent syndrome (Chrousos
and Mentis, 2020). The latter approaches are of particular importance for the younger
generation of high-achievers, because, of note, the age of the majority of PhD and
MD-PhD students overlaps with the peak of mental health issue prevalences. These approaches
can also be applied to the treatment of broader clinical conditions (such as anxiety
disorders), as well as issues of social stigma, thus, offering a holistic approach
to the discomfort of imposter syndrome–anxiety sufferers. Last, but not least, in
our highly competitive era, one should openly acknowledge that toning down our expectations
concerning our own goals to justify potential failures may create vicious cycles of
self-discomfort, at least in the so-called true syndromal imposters (Leary et al.,
2000). The ancient approach of ethos, pathos, and pragma, i.e., the ethically-, emotionally-,
and realistically-oriented approach to life, continues to be pertinent, including
suffering from impostor syndrome, and it should always be a worthy salutary goal to
pursue.
Author Contributions
GC, A-FM, and ED conceived and designed the study, prepared the first draft, and reviewed
the final version of the manuscript. All authors have read and approved the final
version of the manuscript.
Conflict of Interest
The authors declare that the research was conducted in the absence of any commercial
or financial relationships that could be construed as a potential conflict of interest.