1
The Parasite-Mediated Domestication Hypothesis
The Parasite-Mediated Domestication Hypothesis
Janko SKOK
University of Maribor, Faculty of Agriculture and Life Sciences, Department of Animal Science, Hoče, Slovenia
ABSTRACT
Based on the premise that parasites indirectly influence literally all of the main processes that otherwise underlie the 
domestication syndrome, it is hypothesised here that endoparasites (helminths and protozoa) have played an important 
mediating role in the process of (proto)domestication. The hypothesis predicts that the frequency of domestication syndrome 
traits such as tameness, depigmentation, mottling, piebaldism, floppy ears, short and curled tail, reduced size of the adrenal 
gland, etc. in the (wild) population increases i) with decreasing genetic resistance to parasites and/or ii) with increasing parasite 
load. According to the parasite-mediated domestication hypothesis, the features of the domestication syndrome could be 
genetically linked to genes related to resistance/tolerance to parasites, the role of miRNA in the process of epigenetic inheritance 
or the transgenerational inheritance of stress pathology.
Keywords: domestication syndrome, endoparasites, genetic resistance, neural crest cells, endocrine system, miRNA
Agricultura Scientia 20: No 1: 1-7(2023)
https://doi.org/10.18690/agricsci.20.1.1
*Correspondence to: 
E-mail: janko.skok@um.si
BACKGROUND
There are two competing hypotheses about the path of 
initial domestication of animals, with the wolf (Canis lupus) 
being the first animal to undergo this process. The first and 
predominant hypothesis is the commensal scavenger or self-
domestication hypothesis, and the second is the pet keeping 
or cross-species adoption hypothesis (Serpell, 2021; Mech 
and Janssens, 2022). The first states that domestication was 
initiated by individuals of the wild population approaching 
human settlements where the remains of human prey were 
found, while the second states that Palaeolithic humans took 
wolf pups from dens at an early age and raised them.
Either way, to be selected for further breeding by humans, 
the animal had to have an attenuated stress response, as 
individuals with low levels of prosociality were shunned or 
killed (Losey, 2022). In other words, the wild individuals that 
entered the (self-)domestication process had to express at 
least some degree of tameness by nature, which is thus a key 
trait of the domestication syndrome. 
The domestication syndrome is defined as a set of phe-
notypic traits common to different species of domesticat-
ed animals, regardless of the path of domestication and 
the further methodical selection to which they have been 
subjected. The phenomenon was first described by Darwin 
(1868) but not explained until more than a century later by 
Belyaev (1979), whose silver fox domestication experiment 
showed that selection for tameability destabilises the reg-
ulatory systems controlling morphological and behavioural 
development, resulting in changes otherwise characteristic 
of the domestication syndrome, i.e. tameness, floppy ears, 
upturned tail, depigmentation, etc.
Belyaev (1979) proposed that the traits of the domesti-
cation syndrome are genetically linked to genes associated 
with tameness. He proposed that selection for tame behav-
iour, i.e. an impaired stress response, leads to significant 
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The Parasite-Mediated Domestication Hypothesis
changes in the entire ‘hypothalamic-pituitary-adrenal’ 
system (HPA axis) and thus to glucocorticoid secretion - the 
domestication syndrome is thus based on the close relation-
ship between the nervous and endocrine systems and their 
effects on ontogenetic development. Later, Crockford (2002) 
proposed that genetically controlled changes in the rhythm 
of thyroid hormone secretion are crucial for the initiation 
and/or implementation of heterochronic changes and thus 
play an important role in the domestication syndrome. 
Indeed, such changes in the endocrine system alter em-
bryonic and postnatal growth, maturation, stress response, 
brain development, hair/skin production and pigmentation, 
adrenal gland function/size, and gonadal development and 
function, which is crucial in the context of the domestica-
tion [syndrome] (Dobney and Larson, 2006; Lord et al., 2020).
Finally, Wilkins et al. (2014) deepened the understanding 
of the mechanism underlying the domestication syndrome 
by proposing that the main phenotypic components of the 
syndrome are neural crest cell (NCC) derivatives. According-
ly, the multiple phenotypic changes that characterise the 
domestication syndrome reflect a developmental reduction 
in NCC input for the affected phenotypic traits. They further 
suggested that the deficits of NCCs during embryonic devel-
opment could be due to the lower number of NCCs initially 
formed, the lower migratory capacity of NCCs and conse-
quently the lower number of NCCs at the final sites or the 
lower proliferation of these cells at these sites.
HYPOTHESIS ON THE POSSIBLE ROLE 
OF ENDOPARASITES IN THE PROCESS OF 
DOMESTICATION
Since the domestication of animals, there appears to 
have been a large increase in the number of parasites 
common to humans and domesticated animals (McNeill, 
1976; Morand et al., 2014). This relationship seems to be an 
expected consequence of the advent of domestication, a 
suitable condition for intraspecific transmission of parasites. 
However, another aspect should be highlighted here, namely 
the causality of this relationship, whereby the evolutionary 
adaptation of parasites to maximise their dispersal may 
have played an important role in making this relationship 
possible in the first place. Therefore, they might have played 
an important role in (proto-)domestication, particularly in 
self-domesticated mammals, i.e. at a very early stage of the 
domestication process initiated by the animals themselves. 
Behavioural changes are usually mediated by many, 
often interacting, endocrine and neuromodulatory mecha-
nisms (Kaushik et al., 2012; Del Giudice, 2019). Although not 
all behavioural changes are adaptive, parasites can influence 
these mechanisms and alter host behaviour in ways that 
increase their likelihood of transmission and give them a 
specific adaptive advantage (Poulin, 2010; Poulin, 2013; Del 
Giudice, 2019; Hughes and Libersad, 2019). In particular, par-
asites can influence fear responses and anxiety, i.e. reduce 
them in order to increase inter- and intraspecific contacts. 
In the early stages of domestication, such tame behaviours 
aimed at reducing animals' fear of humans were necessary 
for life in an anthropogenic environment (Herbeck et al., 
2022). 
The fear response is controlled by the HPA axis, in par-
ticular by the secretion of glucocorticoids (GC), which is 
also deviated by parasite infestations. Although GC levels 
increase on average in affected individuals, their secretion 
varies greatly depending on the phase of parasite infestation 
(O'Dwyer et al., 2020). The temporal activation of the HPA 
axis is also highly dependent on the severity and duration of 
the stressor(s) and the extent to which the organism can an-
ticipate or cope with the challenge. However, stress respons-
es are usually inhibited by negative feedback mechanisms, 
with GC reducing drive/instinct (processed in the brainstem) 
and promoting trans-synaptic inhibition by limbic struc-
tures, e.g. the hypothalamus (Herman et al., 2016). However, 
if either stimulus is intense enough, the facilitation will 
still override the feedback inhibition (Gann et al., 1977). In 
contrast, under certain conditions (e.g. chronic drive), GC 
can also induce positive feedback in some brain structures 
and increase the reactivity of the HPA axis (Herman et al., 
2016).
Elevated GC indeed have different effects, which also 
depend on the particular time window in which the eleva-
tions occur. For example, prenatal stress of various kinds, in-
cluding parasite-induced stress, can cause postnatal changes 
in HPA activity, including a reduction in adrenal weight and 
thus an inappropriate stress response (Welberg and Seckl, 
2001; O'Dwyer et al., 2020). 
Parasites also affect the function of the thyroid gland, 
a gland that secretes thyroid hormones in a distinctly pul-
satile manner and is crucially involved in the regulation 
of developmental processes. Indeed, a certain level of its 
hormones is required to initiate migration, differentiation 
and maturation of early embryonic cells, growth, central 
nervous system development, hair growth, adrenal gland 
function, pigment (eumelanin) production, etc. Given the 
importance of the thyroid gland in the timing of develop-
mental processes, it has been suggested that disruption of 
thyroid function leads to the heterochronic changes that 
are otherwise characteristic of domesticated animals (see 
Crockford, 2004). And parasites may also play a role in this 
aspect of domestication, as endoparasites, especially hel-
minths, have been shown to cause various thyroid disorders, 
including thyroid nodules, hypo- and hyperthyroidism 
(Raizada, 2021). 
Further, parasite infestation confined to the maternal 
intestine has been shown to positively influence postnatal 
brain development in the context of long-term potentiation 
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The Parasite-Mediated Domestication Hypothesis
related to learning and cognition (Haque et al., 2019). Ac-
cordingly, there is evidence that domestication, artificial 
selection and breeding lead to an improvement in spatial 
memory in human-made experimental settings, which has 
been explained as an adaptation to the anthropogenic en-
vironment that enables more efficient task solving (Lewejo-
hann et al., 2010). However, this could also be partly due to 
the higher threshold for acute stressors in domestic animals, 
i.e. less anxiety and fear, as mentioned earlier, because acute 
stress can impair cognition, learning and (spatial) memory 
(Wolf 2003; Sandi et al., 2005). 
Furthermore, parasites cause changes in the host profile 
of miRNA, small non-coding RNAs that can control gene ex-
pression (Paul et al., 2020), not only through parasite infes-
tation itself, but also through the secretion of vesicles con-
taining miRNAs into host cells (Buck et al., 2014). miRNAs are 
significantly involved in many prenatal and postnatal de-
velopmental and physiological processes (Floris et al., 2016). 
In the context of the domestication syndrome, it is particu-
larly important to note that miRNAs are also substantially 
involved in the formation of the neural crest during em-
bryonic development; either in the induction, specification, 
delamination, migration or differentiation of NCCs (Weiner, 
2018). In addition, there are some miRNA families involved 
in parasitic diseases caused by endoparasites as well as in 
NCCs differentiation (Table 1). Since small non-coding RNAs, 
including miRNAs, are known to enter the foetus via the 
placenta to regulate foetal development (Li et al., 2015), it 
is reasonable to assume that parasites indirectly influence 
embryonic development along the ‘miRNA-transplacental 
transport-NCCs’ axis and may also mediate the phenotypic 
changes that characterise the domestication syndrome. 
In addition to the NCCs, miRNAs are involved in the 
activity of the endocrine system and regulate hormone pro-
duction, activity and responsiveness of target cells. They can 
directly act on target genes encoding hormones or enzymes 
involved in hormone production or metabolism, thus af-
fecting hormone concentrations (Peng and Wang, 2018; 
Peng and Li, 2022). For example, miRNA-21, miRNA-let-7, 
miRNA-16 and miRNA-24 are among the miRNAs involved in 
various parasitic diseases (see Table 1 for references), as well 
as possible neuroendocrine cell function (Park, 2017). 
Finally, parasites have been shown to cause disruptive 
selection (favouring otherwise extreme phenotypes) in 
animals and thus can rapidly increase genetic variance 
within a host population (Duffy et al., 2008; Blanchet et al., 
2009). High phenotypic variability (i.e. a high frequency of 
extreme phenotypes) is otherwise observed in populations 
of domestic animals in which breeds of the same species 
differ from each other to the same extent as species of the 
same genus in the natural state (Darwin, 1868). Barker (2001) 
reported that much of the genetic variance of a domesti-
cated species is due to differences between breeds, while 
Groeneveld (2010) stated that the uniqueness of a breed is 
not evident from molecular data, which on the contrary 
show that most of the genetic diversity exists within a breed 
and not between breeds. 
The genetic background for the possible role of parasites 
in the process of domestication remains to be explored, but 
few starting points are suggested here. First, since resist-
ance and tolerance to parasites are genetically determined 
and heritability is relatively high (Steer and Wakelin, 1998; 
Mazé-Guilmo, 2014), the characteristics of the domestication 
syndrome could be genetically linked to genes related to re-
sistance/tolerance to parasites, with the (proto-)domestica-
tion selection favouring less genetically resistant individuals. 
Second, given the influence of parasites on the host profile 
of miRNA, the role of miRNA in the process of epigenetic 
inheritance (Sharma, 2014; van Otterdijk and Michels, 2016) 
should also be considered. Finally, manipulating the foetal 
Table 1: Some miRNAs involved in various parasitic diseases as well as in neural crest (NC) development
miRNAs Influence during NC development References
miRNA-140 bone development, chondrogenesis
Buck et al., 2014 
Weiner, 2018 
Paul et al., 2020 
Antonaci and Wheeler, 2022 
He and Pan, 2022
miRNA-27 chondrogenesis
miRNA-124 chromaffin cells
miRNA-let-7a craniofacial development
miRNA-17~92 NC induction/specification, craniofacial development, chondrogenesis
miRNA-24 NC induction/specification
miRNA-21 Schwann cells
miRNA-let-7 epithelial to mesenchymal transition/migration, chondrogenesis
miRNA-1 craniofacial and hart development, pigment cells
miRNA-20a NC induction/specification
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The Parasite-Mediated Domestication Hypothesis
environment by exposing the mother to adverse conditions 
during pregnancy - in our case parasites - can alter the 
response to stress not only in the offspring but over several 
generations (Matthews and Phillips, 2012). Therefore, in the 
context of changes in the HPA system (stress response) asso-
ciated with domestication, transgenerational programming 
of HPA function and behaviour, i.e. inheritance of para-
site-induced stress pathology, should not be neglected. 
Based on the premise that parasites indirectly influence 
literally all the main processes that otherwise underlie the 
domestication syndrome, it is hypothesised that parasites 
(specifically endoparasites: helminths and protozoa) played 
an important mediating role in the process of domestica-
tion. However, it is important to stress at this point that a 
heavy, persistent parasite load would be detrimental to the 
health of the animals and could result in the parasite load 
being too high for the animals to survive even under ideal 
living conditions. It is therefore difficult to imagine how this 
situation could be maintained over hundreds or thousands 
of generations. Moreover, wild animals can be infected with 
various parasites that only make them sick, but not domes-
ticated or even more accessible to humans.
The hypothesis presented here assumes that a 'parasite 
effect' is primarily involved in the emergence of the do-
mesticated state (proto-domestication) and not necessarily 
in its continuous maintenance. According to the para-
site-mediated domestication hypothesis, it is predicted that 
the frequency of domestication syndrome traits, such as 
tameness, depigmentation and mottling, floppy ears, short 
and curled tail, reduced adrenal gland size etc. in the (wild) 
population increases i) with decreasing genetic resistance 
to parasites, i.e. the frequency of parasite resistance alleles 
in the population and/or ii) with increasing parasite load. 
Therefore, it would also be expected that domestic animals 
are genetically less resistant to the parasites. In this regard, 
there have already been some comparative studies exam-
ining the parasite load in wild and domestic animals, with 
slightly contradictory results. In pigs, for example, Ineson 
(1954) showed differences in parasite load depending on the 
parasite species, with domestic pigs having a slightly higher 
parasite load than wild pigs. In contrast, Alwin et al. (2015) 
found that parasite loads were higher in wild boars than in 
semi-free-range domestic pigs and on-farm domestic pigs, 
with the latter having the lowest parasite load. The studies 
on wild and domestic canines cannot provide a clear answer 
either (see Eguía-Aguilara et al., 2005; Mitrápková et al., 2015; 
Čabanová et al., 2016; Čabanová et al., 2017). However, in such 
studies comparing wild and domestic counterparts, the 
living conditions and the general possibility of the animals 
to be exposed to the parasites are most likely determining 
factors for the parasites incidence, so that the parasite load 
cannot simply be considered as an indicator of the degree of 
genetic resistance to parasites.
To test the hypothesis proposed here, genetic resistance 
should be tested primarily in wild individuals showing signs 
of the domestication syndrome or secondarily in domestic 
animals or domestic-wild hybrids and compared with 
their fully wild counterparts. However, this requires that 
the genetic markers for resistance to parasites are known. 
The parasite load should be investigated either in the wild 
population consisting of individuals showing signs of the do-
mestication syndrome (tameness, specific morphology and 
colouration, etc.) or in the population of domestic animals, 
domestic-wild hybrids and wild animals of the same species 
sharing the same environment.
It can then be predicted that the wild individuals 
showing signs of the domestication syndrome, as well as the 
domestic animals and domestic-wild hybrids, are geneti-
cally less resistant to parasites and/or more infested with 
parasites than the fully wild individuals.
Last but not least, special caution must be taken with do-
mesticated animals that may have been artificially selected 
for parasite resistance, because in this case the results are 
inevitably misleading and the conclusions biased.
Acknowledgements
Many thanks to Prof. Oleg V. Trapezov and Prof. Adam Wilkins 
for their willingness to discuss the issue and for their valuable 
comments and constructive criticisms. Thanks are also due 
to the anonymous reviewers for their valuable reviews and 
comments.
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7
The Parasite-Mediated Domestication Hypothesis
Hipoteza o udomačitvi preko parazitov
IZVLEČEK
Izhajajoč iz predpostavke, da paraziti posredno vplivajo pravzaprav na vse glavne procese, ki sodelujejo pri pojavu sindroma 
udomačevanja, domnevamo, da so imeli endoparaziti (helminti in protozoji) pomembno posredniško vlogo v procesu (proto)
domestikacije. Hipoteza predvideva, da se pogostnost lastnosti sindroma udomačitve, kot so krotkost, depigmentacija, lisavost, 
pegavost, povešena ušesa, kratek in zavit rep, zmanjšana velikost nadledvične žleze itd., v (divji) populaciji povečuje i) z manjšo 
genetsko odpornostjo proti parazitom in/ali ii) z naraščajočo obremenitvijo s paraziti. V skladu s hipotezo o udomačitvi preko 
parazitov, bi lahko bile značilnosti sindroma udomačitve genetsko povezane z geni, povezanimi z odpornostjo/toleranco na 
parazite, vlogo miRNA v procesu epigenetskega dedovanja ali transgeneracijskega dedovanja stresne patologije.
Ključne besede: sindrom udomačitve, endoparaziti, genetska odpornost, celice nevralnega grebena, endokrini sistem, miRNA