The “Psilocybin-Telomere Hypothesis”
An empirically falsifiable prediction concerning the beneficial
neuropsychopharmacological effects of psilocybin on genetic aging
Christopher B. Germann (Ph.D., M.Sc., B.Sc. / Marie Curie Alumnus)
First published: 31.07.2019
We introduce a novel hypothesis which states that psilocybin has beneficial effects on genetic
aging. Ex hypothesi, we predict a priori that psychotherapeutic psilocybin interventions have
quantifiable positive effects on leucocyte telomere length (telomeres are a robust predictor of
mortality and various aging-related diseases). The “psilocybin-telomere hypothesis” is
formalised as a logically valid deductive (syllogistic) argument. Impetus for our theorising
derives from a plurality of converging empirical evidence which indicates that psilocybin has
persistent beneficial effects on various aspects of mental health (e.g., depression, anxiety,
PTSD, addiction, etc.). Additional support is based on a large corpus of studies which
establish reliable correlations between mental health and telomere attrition (improved mental
health is generally correlated with longer telomeres). Another component of our argument is
based on recent studies which demonstrate that “meditative states of consciousness” exert
beneficial effects on genetic aging (i.e., telomere length). Similarly, psilocybin can facilitate
states of consciousness which are neurophysiologically and phenomenologically significantly
congruent with meditative states. Furthermore, prior research has demonstrated that a single
dose of psilocybin can occasion profound and life changing transformative experiences
(≈70% of healthy volunteers rate their experience with psilocybin amongst the five
personally most meaningful lifetime events, viz., the experience is ranked next to giving birth
to a child or losing a loved one). We argue that these profound psychological effects are
quantifiable at the molecular genetic/epigenetic level. Given the widespread availability and
cost effectiveness of telomere length assays, we suggest that telomere analysis should be
regularly included in future psilocybin studies to provide an adjunctive quantitative biological
marker, i.e., in addition to introspective self-reports, psychometrics, and multi-modal
neuroimaging data (viz., scientific consilience/methodological triangulation). In order to
substantiate the “psilocybin-telomere hypothesis” potential neuropsychopharmacological
mechanisms of action are discussed. Scientific research along these lines is thus highly
interdisciplinary and it has deep implications from a philosophy of science perspective as it
connects the epistemic level (qualitative experiential phenomenology) with the ontic level
(quantitative molecular genetics) of analysis. Moreover, innovative multidisciplinary
investigations of the “telomere-psilocybin hypothesis” could contribute to the improvement
This work was funded by the European Union Marie Curie Initial Training Network
Marie Curie Actions: FP7-PEOPLE-2013-ITN-604764
of therapeutic psychological interventions and the identification of novel pharmaceutical
targets to slow down genetic aging and improve quality of life during the aging process. Our
hypothesising follows the Popperian logic of scientific discovery, i.e., bold (and refutable)
conjectures form the very foundation of scientific progress.
A plethora of studies indicate that telomere length is a reliable indicator of biological aging. A
healthy lifestyle is generally associated with longer telomeres while an unhealthy lifestyle is
associated with shorter telomeres (Boccardi, Paolisso, & Mecocci, 2016; Jue Lin, Epel, &
Blackburn, 2012). There are numerous factors which influence telomere attrition, for instance,
quality of diet (Leung et al., 2014; Paul, 2011), alcohol consumption (Pavanello et al., 2011),
tobacco smoking (Mirabello et al., 2009), sleep patterns (K. A. Lee et al., 2014), a variety of
social/interpersonal variables (Beatty Moody et al., 2019; Belinda L. Needham et al., 2014;
Notterman & Mitchell, 2015), fitness and physical exercise (Denham et al., 2013; Puterman et
al., 2010), exposure to environmental toxins such as traffic pollution (Hoxha et al., 2009) and
various chemical compounds found in plastics (Pavanello et al., 2010), etc. pp. (for a
comprehensive review see Shammas, 2011). Furthermore, converging evidence indicates that
telomeres are affected by psychological conditions such as stress, depression, and negative
thought patterns (e.g., rumination) (E. Epel, Daubenmier, Moskowitz, Folkman, & Blackburn,
2009; Gotlib et al., 2015; Price, Kao, Burgers, Carpenter, & Tyrka, 2013; Puterman et al., 2013;
Verhoeven, Révész, Wolkowitz, & Penninx, 2014). The pertinent literature delineates the
following general pattern: Positive psychological states are associated with longer telomeres
whereas depression, chronic stress, and anxiety are inversely related with telomere length
(Hoge et al., 2013). Our hypothesis is based on the major premise that psychological conditions
affect telomeres. In addition, our hypothesis rests on the minor premise that psilocybin exhibits
significant positive therapeutic effects on various aspects of psychological health. Rapidly
accumulation converging empirical evidence supports this claim (Bogenschutz et al., 2015;
Bogenschutz & Johnson, 2016; Bolstridge, 2013; Carhart-Harris et al., 2016; Griffiths et al.,
2016; Kraehenmann et al., 2015a; Lieberman & Shalev, 2016; Nichols, Johnson, & Nichols,
2017; Rucker, Jelen, Flynn, Frowde, & Young, 2016).
Specifically, numerous studies have
demonstrated that psilocybin reduces depression (Griffiths et al., 2016; Ross et al., 2016) and
for the sake of focus and parsimony the present discussion will be primarily concerned with
this factor. However, similar arguments could be articulated with respect to anxiety, PTSD,
chronic stress, addiction, et cetera. Given the well-established comorbidity between
depression, anxiety disorders/PTSD, and addiction (Volkow, 2004) it is cogent to assume that
the underlying cognitive and biochemical mechanisms are in many cases significantly
Contrary to wide spread public doxa (Bourdieu, 1977), epidemiological data indicate that psychedelics are not
linked to psychopathology or suicidal behaviour (Johansen & Krebs, 2015; Krebs & Johansen, 2013; cf. Müller,
Püschel, & Iwersen-Bergmann, 2013). The mass-media utilized propagandistic/PR methods à la Bernays
(Bernays, 1928; L’Etang, 1999) in order justify the governmental “War on Drugs” (initiated by the Nixon
administration) which was clearly politically motivated, for instance, in order to target Vietnam war opponents
and racial minorities and to serve the “prison-industrial complex(Douglas & Pond, 2012; Moore & Elkavich,
Hypothesis as a deductive syllogistic argument
Our hypothesis is based on the empirically founded assumption that neuropsychological factors
affect aging at the genetic level. We postulate that beneficial psychological conditions are
associated with telomeric health (longer telomeres via activation of the enzyme telomerase
reverse transcriptase which adds nucleotide sequences to the ends of DNA). Consequently, we
predict a priori that beneficial psychological and neurobiological changes induced by
psilocybin are ex post facto quantifiable by telomere analysis. The primary hypothesis can be
stated as a deductive argument in the form of a logically valid Aristotelian categorical
Syllogism #1
Major premise:
Minor premise:
Depression is associated with shorter telomeres (telomere attrition).
Psilocybin reduces depression.
∴ Ergo, psilocybin positively affects telomere length.
According to syllogistic logic each of the three distinct terms represents a category, i.e.:
[Depression] — [Telomeres] — [Psilocybin].
In Syllogism #1 the category [Telomeres] is the major term and [Psilocybin] constitutes the
minor term. Crucially, the premises have a single term in common (the middle term)
appears as the subject or predicate of the categorical proposition, in casu, [Depression].
According to the principles of propositional logic, the conclusion follows deductively
iff the
major and minor premise are veridical. In the following sections we will thus provide
empirical evidence which substantiates the major and minor premise, i.e., 1) that depression
is associated with shorter telomeres and 2) that psilocybin reduces depression. Note that our
hypothesis could also be remodelled in the framework of Bayesian epistemology. In this case
the subsequently presented information can be utilised to calibrate or parametrise “informed
priors” which severe as a conditional probabilistic basis for Bayesian prediction, viz.,
“degrees of belief” or credence.
Auxiliary hypothesis
We hypothesise that a negative psilocybin experience does not produce the predicted effects.
Thus, our hypothesis is directional (one-tailed) in the case of a positive phenomenological
experience, but bidirectional without any additional specification as we expect that negative
psilocybin experiences can cause, stress, anxiety, and in the worst-case scenario psychological
traumata. Ex hypothesi, negative psychological conditions shorten telomers (Malan,
Hemmings, Kidd, Martin, & Seedat, 2011). However, from a longitudinal perspective even a
prima facie negative psilocybin experience can have beneficial therapeutic/cathartic effects
The absence of the middle term in both premises leads to a syllogistic fallacy, i.e., the fallacy of the
undistributed middle (viz., non distributio medii).
From a philological vantage point the term “deduction” is etymologically derived from the Latin deducere “to
lead, to derive”. Thus, the premises lead (automatically) to the conclusion, i.e., the conclusion is logically
derived. This formalisation constitutes the basis of the deductive-nomological model (PopperHempel model)
of scientific explanation.
which take time to unfold. In a more generic form, the “psilocybin-telomere hypothesis” could
be reformulated as in Syllogism #2. However, for the sake of specificity
(operationalism/experimental testability) we will focus the subsequent discussion on the more
specific formalisation which focuses on depression.
Syllogism #2
Major premise:
Minor premise:
Beneficial neuropsychological changes positively effect telomere length.
Psilocybin has quantifiable beneficial neuropsychological effects.
∴ Ergo, psilocybin positively effects telomere length.
It should be emphasised that we selected depression as a representative exemplar to
demonstrate a much broader line of thought. Psilocybin has multifarious beneficial effect on
psychological health and the predicted effects on genetic health are thus multifactorial. In this
context the term psychology
is semantically used in original etymological sense viz., the
study of the soul, spirit, and breath. That is, the effect of psilocybin go far beyond the treatment
of psychopathology and the improvement of general well-being. Psilocybin (and its
serotonergic structural relatives) has the potential to induce ineffable life-transforming
spiritual/mystical transpersonal experiences (Griffiths, Richards, McCann, & Jesse, 2006;
Griffiths, Hurwitz, Davis, Johnson, & Jesse, 2019) which transgress the primarily implicit
demarcation criteria which delineate mainstream “rational” academic psychological discourse.
Evidence in the support of the major premise: Depression shortens telomers
Numerous studies indicate that depression has quantifiable effects on telomeres (B. L.
Needham et al., 2015; Wikgren et al., 2012; Wolkowitz et al., 2012) and animal models support
this finding (Wei, Backlund, Wegener, Mathé, & Lavebratt, 2015). The pertinent literature
indicates a general pattern: Positive mental psychological states have beneficial effects on
telomere length while the opposite holds true for negative states such as stress, depression, and
anxiety (Malan et al., 2011; Okereke et al., 2012). Accumulating evidence thus indicates that
depression accelerates genetics aging (telomere attrition) and it has been hypothesised that the
link between depression and genetic aging is, inter alia, mediated by the hypothalamic
pituitaryadrenal axis (HPA axis) (Vreeburg et al., 2009). The HPA axis is crucial for the
elicitation of stress responses in respect to a given stressor, e.g., release of the stress hormones
cortisol, epinephrine/adrenalin, and norepinephrine. Inflammation is another important
interrelated factor in the context of stress, depression, and genetic aging (Kiecolt-Glaser, Derry,
& Fagundes, 2015). The exact psychoneuroendocrinological mechanisms are a matter of an
ongoing scientific debate (for an evolutionary account see Miller & Raison, 2015).
Another important factor associated with depression is oxidative stress (Lopresti, Maker, Hood,
& Drummond, 2014). Again, it has been demonstrated that oxidative stress contributes to
Accordingly, the etymology of the term “psychedelics” is derived from the Ancient Greek ψυχή (psukh,
“mind, soul, spirit”) + δλος (dêlos, “to manifest, to reveal”), i.e., “psychedelic substances” could be adequately
translated as “mind manifesting” or “soul revealing” substances. Previously, psychedelics were also labelled as
“psychotomimetics (Osmond, 1957) because they were thought to produce (mimic) symptoms similar to those
of a psychosis.
genetic aging, i.e., it accelerates telomere attrition (Von Zglinicki, 2002) (cf. Boonekamp,
Bauch, Mulder, & Verhulst, 2017). In fact, inflammatory and oxidative stress biomarkers can
be regarded as “peripheral biomarkers” in major depression (for a review see Lopresti et al.,
2014). In addition, effects on various brain growth factors have been associated with stress and
depression. Specifically BDNF (brain-derived neurotrophic factor) has been thoroughly
investigated in this context (Martinowich, Manji, & Lu, 2007) and it appears to be decreased
in clinically depressed populations (Castrén, Võikar, & Rantamäki, 2007; Erickson, Miller, &
Roecklein, 2012; Groves, 2007). Lower BDNF-levels may be responsible for neuroanatomical
changes that accompany depression. Interestingly in the context at hand, it has been suggested
that telomerase mediates the cell survival-promoting actions of BDNF (Fu, Lu, & Mattson,
2002). Consequently, it would be of great interest to examine the effects of psilocybin on
BDNF concentrations (Idell et al., 2017) as this might provide basic insights into an
intermediary mechanism which mediates between psilocybin and its postulated effects on
genetic aging. In sensu lato, various forms of stress (including chronic rumination) set in
motion a cascade of detrimental effects which negatively affect telomeres (Kiecolt-Glaser &
Glaser, 2010; J Lin, Epel, & Blackburn, 2009; Monaghan, 2014). Stress magnifies the body’s
inflammatory responses which in turn inhibit telomerase activity (see also Zhang et al., 2016).
Again, the exact mechanisms are currently a topic of active research (see Elissa S. Epel, 2009).
It has been hypothesised that exposure to stress activates a broad array of biological mediators
which results in the shortening of telomeres (Kotrschal, Ilmonen, & Penn, 2007). As discussed,
stress arousal increases stress hormones, inflammation, and oxidative stress, which in turn leads
to a shortening of telomeres (Blackburn & Epel, 2012; E. S. Epel et al., 2004; Monaghan,
2014). However, there are various protective factors which can modulate these detrimental
events. Certain neurosteroid hormones counteract the negative effects of excessively high
levels of cortisol. For example, the endogenous steroid hormone dehydroepiandrosterone
(DHEA) has been shown to possess antiglucocorticoid properties which offer protection
against the deleterious effects of cortisol (Young, Gallagher, & Porter, 2002), thereby reducing
neurocognitive deficits in depression. Likewise, BDNF induced hippocampal neurogenesis has
positive protective effects on chronic stress levels (Levone, Cryan, & O’Leary, 2015; Mahar,
Bambico, Mechawar, & Nobrega, 2014; Schoenfeld & Gould, 2012; Warner-Schmidt &
Duman, 2006) and reduces social avoidance (Hill, Sahay, & Hen, 2015; Lagace et al., 2010).
Important for the present hypothesis is the empirical finding that psilocybin induces
neurogenesis in the dentate gyrus of the hippocampus and that it facilitates fear extinction in
animal models (Catlow, Song, Paredes, Kirstein, & Sanchez-Ramos, 2013). Studies have
demonstrated that stress and depression are associated with a reduction of hippocampal volume
due to atrophy and loss of neurons (Warner-Schmidt & Duman, 2006). Several studies indicate
that hippocampal neurogenesis may be required for some of the cognitive-behavioural effects
of antidepressants (Sahay & Hen, 2007). Current evidence indicates that plasma BDNF levels
are decreased in unmedicated depressed patients and that antidepressant treatment (e.g., SSRIs)
can increase BDNF to normal concentrations (B. H. Lee & Kim, 2010). In addition to these
mediators there are several moderators which influence the effects of depression and stress on
telomeres. Many studies have investigated the moderating role of genetic predispositions that
are responsible for a heightened vulnerability to various life stressors. Given that personality
traits have a strong heritability component (as indicated by twin studies (Bouchard, Lykken,
McGue, Segal, & Tellegen, 1990)) it is not surprising that some individuals are much more
resilient when exposed to stress, compared to others who are hypersensitive and display
negative reactions even to minor life-stressors. Metanalytic research indicates that a specific
polymorphism of the serotonin transporter promoter (5-HTTLPR) moderates the correlation
between stress and depression (Karg, Burmeister, Shedden, & Sen, 2011). In addition to genetic
differences, epigenetic changes are thought to play a moderating role (e.g., via DNA
methylation which alters gene expression by inhibiting the binding of transcription factors; see
Moore, Le, & Fan, 2013). That is, in contrast to genetic changes, epigenetic changes alter the
expression of genes (but, by definition, not the genetic code itself). Epigenetic changes can be
reversible and non-reversible depending on specific conditions (also see Choudhuri, 2011). We
suggest that that the psychologically profound “transformative” experiences which can be
induced by psilocybin are accompanied by significant epigenetic changes. That is, we predict
that the qualitative phenomenological aspects of psilocybin are reflected at the epigenetic level.
A landmark study conducted at Johns Hopkins University by MacLean, Johnson & Griffiths
(2011) experimentally demonstrated that a single high-dose of psilocybin can induce long-
lasting personality changes in the personality trait “Openness to Experience” (as measured by
the widely used NEO Personality Inventory). This finding is very intriguing because there is
broad scientific consensus that personality traits are relatively stable over time (i.e., a genetic
basis is assumed; Bouchard et al., 1990) and that they can only be altered by major life events
(e.g., McCrae & Costa, 1997). Ergo, it is logically cogent to predict that the personality changes
induced by psilocybin are accompanied by epigenetic changes. This line of thought connects
neatly with the previously presented results. A genetic pilot study (Stoltenberg et al., 2002)
found that OTE is related to SERT polymorphism (5-HTTLPR which is associated with
SLC6A4, the serotonin transporter gene discussed previously in the context of depression and
PTSD, inter alia). Based on this empirical background it is thus logically sound to assume that
psilocybin has epigenetic effects on genes related to serotonin. Specifically, 5-HTTLPR is a
plausible candidate gene given its association with depression, anxiety-related personality
traits, and addiction (for a metanalyisis of the moderating role of 5-HTTLPR in stress and
depression see Karg et al., 2011). Given that psilocybin has been used therapeutically to treat
all of these disorders (Tylš, Páleníček, & Horáček, 2014) a common genetic mechanism is thus
predictable on an a priori basis. To recapitulate: We provided evidence which substantiates the
major premise of our syllogistic argument (the predicate of the conclusion): Telomere length
is a reliable indicator of genetic aging and it has been repeatedly demonstrated that telomeres
are affected by psychological conditions such as chronic stress, anxiety, and depression, inter
alia. In the next section we will provide a synopsis of the evidence which indicates that
psilocybin exerts beneficial effects on various aspects of mental health, and we will specifically
focus on its postulated effects on depression.
Evidence in support of the minor premise: Psilocybin reduces depression
Psilocybin has been reliably associated with numerous mental health benefits and a number of
studies demonstrated that psilocybin significantly reduces symptoms in depressed populations
(Carhart-Harris et al., 2018; Cowen, 2016; Ross et al., 2016b). For instance, it has been reported
that psilocybin improves emotional face recognition in treatment-resistant depression and this
improvement was statistically significantly correlated with a reduction in ahedonia (Stroud et
al., 2018). From a neuroimaging point of view a reduction of depressive symptoms was
associated with increased resting-state functional connectivity (RSFC) within the default-mode
network (DMN; 5 weeks post-treatment). Furthermore, post treatment response was associated
with increased ventromedial prefrontal cortex RSFC and bilateral inferior lateral parietal cortex
RSFC, in addition to decreased RSFC in the the parahippocampal-prefrontal cortex (Carhart-
Harris et al., 2017). Moreover, brain-wide analyses revealed post-treatment decreases in
cerebral blood flow (CBF) in the temporal cortex and the amygdala. Importantly, reductions in
in amygdala CBF were statistically significantly correlated with a reduction in depressive
symptoms. The study (op. cit.) demonstrated that the acute effects of psilocybin differ from the
longitudinal effects. In the following paragraphs we will primarily focus on the role of the
DMN and the amygdala in depression. According to the DSM-V, one of the categorical
diagnostic criteria of depression is rumination. It is pertinent for the “psilocybin-telomere
hypothesis” at hand that rumination has been associated with telomere shortening. Rumination,
in turn, has been associated with hyperactivity of the default-mode-network
(DMN) (Berman
et al., 2011; Cooney, Joormann, Eugène, Dennis, & Gotlib, 2010). Experimental studies have
demonstrated that psilocybin significantly downregulates DMN activity (Carhart-Harris et al.,
2017). Interestingly, a recent experimental study indicated that psilocybin-assisted mindfulness
training modulates DMN connectivity with lasting effects (Smigielski, Scheidegger, Kometer,
& Vollenweider, 2019). Therefore, we argue that the downregulation of DMN activity is an
important neuroanatomical component of the “telomere psilocybin hypothesis”. Rumination is
a persistent symptom of depressive disorders and therefore a reduction in rumination is like to
positively affect telomere length. We suggest that the reduction of rumination is an aspect
which is common between psilocybin interventions and mindfulness training and mediation.
That is, different methods predict a similar outcome criterion, viz., a reduction in unwanted
repetitive thought patterns. Rumination is a cause for chronic stress and chronic, in turn, is
associated with various inflammatory processes and downregulation of the immune system, all
of which have been associated with shorter telomeres (Andrews, Fujii, Goronzy, & Weyand,
2010; E. S. Epel et al., 2004; Weng, 2012). Further, psilocybin can occasion profound
transformative experiences. For example, in longitudinal study ≈70% of healthy volunteers
rated their experience with psilocybin amongst the five most meaningful and significant
experiences of their lives, ranked next to giving birth to a child, losing a loved one (Griffiths,
Richards, Johnson, McCann, & Jesse, 2008; similar results where recently replicated Griffiths
et al., 2019). We argue that these phenomenological/experiential effects have a quantifiable
genetic counterpart. That is, these profound experiences should be accompanied by equally
profound genetic changes (i.e., in proportion to the profundity phenomenological experience).
This ideas is motivated by recent genetic studies which reintroduce Lamarckian elements into
quantitative biology and thereby challenge the “central dogma of molecular biology”
1970) which was for a long time axiomatic to genetic research. For instance, it has been shown
that acquired olfactory conditioning can be epigenetically inherited by subsequent
generations(at least up to F2) (Dias & Ressler, 2014). The odorant receptor (Olfr151) was used
to condition F0 mice and subsequent generations (which were utterly naïve to the olfactory
Specifically, various connectivity differences have been demonstrated which differentiate healthy individuals
from individuals diagnosed with major depressive disorder, i.e., more neural functional connectivity between
the posterior-cingulate cortex and the subgenual-cingulate cortex during rest periods, but not during task
engagement (but see Berman et al., 2011).
The obvious question is: Should science ever be dogmatic?
conditioning paradigm) revealed CpG hypomethylation in the Olfr151 gene. We argue that if
simple olfactory conditioning can cause quantifiable quasi-Lamarckian epigenetic effects than
a profound and life-changing psilocybin experience (cf. Griffiths et al., 2008) should be equally
quantifiable at the genetic level. We suggest that genes associated with the serotonins system
(e.g., SLC6A4 gene associated with sodium-dependent serotonin transporter) are a likely
genetic locus for planned comparisons (specifically in the context of depression and anxiety).
For instance, it has been reported that individuals with specific serotonin transporter (5-HTT)
promoter polymorphism (associated with reduced 5-HTT expression) exhibit greater amygdala
neuronal activity (fear and anxiety-related behaviours) as assessed by BOLD functional
magnetic resonance imaging (Hariri, 2002; see also Heinz et al., 2005). Interestingly, it has
been experimentally demonstrated that psilocybin decreases amygdala reactivity and that this
limbic downregulation correlates with enhanced positive mood (Kraehenmann et al., 2015b).
These effects of psilocybin on emotional processing are specifically relevant for the hypothesis
at hand because the central nuclei of the amygdala are centrally involved in the genesis of
various fear responses such as the fight flight response, ANS responses such as changes in heart
rate (tachycardia), elevation of blood pressure, and neuroendocrine responses such as cortisol
release. A related study investigated the spatiotemporal brain dynamics of emotional face
processing and reported that psilocybin modulates emotional processing presumably via
agonism of the 5HT
serotonin receptor subtypes (Bernasconi et al., 2014). In conclusio,
the general idea which connects genetic research to psychological research is that cellular
mechanisms (i.c. telomeres/telomerase activity) are intimately coupled with cognitive
processes (anxiety, depression, mood, stress, etc.). To use a “sticky formulation” used by
Professor Elissa Eppel in a lecture at the University of California in 2011 “our cells are
listening to our thoughts”.
In conclusio, we provided converging empirical evidence from a plurality of independent
sources which substantiates the stipulations entailed in the major and minor premises of
Syllogism #1. Based on this evidential background we argue that our thesis (i.e., that
psilocybin has beneficial effects on telomeres) is logically sound and therefore warrants
systematic experimental testing. Specifically, we argue that the convergence of evidence
indicates scientific consilience.
According to this pivotal scientific concept strength of
evidence increases when multiple sources of evidence converge. The generalisability and
robustness of converging evidence for a specific logical conclusion is based on the number of
different research approaches in support of the conclusion. Furthermore, if equivalent
conclusions are reached from multiple perspectives this provides evidence in support of the
reliability and validity of the utilised research methodologies themselves. Resilience reduces
the impact of confounding factors (e.g., method related measurement errors) because these
errors do not influence all research methods equally. Resilience thus “balances-out” method
specific confounds. Perhaps more importantly, the same principle also applies to logical
confounds (e.g., logical fallacies and cognitive biases). In the philosophy of science, this has
The etymological root of the term consilience is derived from the Latin consilient, from com "with, together"
and salire "to leap, to jump," hence it literally means “jumping together” (of knowledge). Scientific resilience is
thus semantically synonymous with the expression “concordance of evidence”.
been termed “consilience of inductions” (Fisch, 1985; Hesse, 1968). Inductive consilience
can be described as the accordance of multiple inductions drawn from different classes of
phenomena. Or, in somewhat more elaborate terms, the “colligation of facts” through
“superinduction of conceptions” (Laudan, 1971). The term has recently been adopted by
neuroscientists as exemplified by a SCIENCE paper by (Glimcher, 2004) where the
converge of evidence from multiple (hierarchically arrangeable) sources (molecular, cellular,
neuroanatomical, cognitive, behavioural, social, etc.) plays a crucial role for the development
of meta-disciplinary (unifying) theoretical frameworks. Following this line of thought,
experiments which investigate the effects of psilocybin across multiple levels of analysis and
explanation would be of great value. The “psilocybin-telomere hypothesis” provides impetus
for this endeavour as it connects the epistemic and the ontic level of analysis.
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