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

Abstract

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

E-Mail: christopher-germann@cognovo.net

URL: https://www.cognovo.net/christopher-germann

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.

Introduction

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

congruent.

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,

2008).

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.

Syllogism #1

Major premise:

Minor premise:

Conclusion:

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)

that

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 (Popper–Hempel 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:

Conclusion:

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–

pituitary–adrenal 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 (psukhḗ,

“mind, soul, spirit”) + δῆλος (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”

(Crick,

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

1A/2A

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”.

Conclusion

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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