Q-) Are the unusual experiences seen in synaesthesia caused by an inborn

genetic trait – or are they a product of learning and experience?

Synaesthesia derived from the Greek word meaning synth - together / combined
and Aesthesis - perceptions or sensations is a fascinating neurological
phenomenon in which stimulation of one sensory or cognitive pathway leads to
automatic, involuntary experiences in a second sensory pathway. This condition
results in the extraordinary sensory associations, where sounds may evoke
colours, or numbers may carry distinct tastes. Researchers characterise
synaesthesias in terms of the inducer - a true stimulus that initiates synaesthetic
association - and the synchronous stimulus, which generates a nonveridical
experience. Synesthetic experiences are highly subjective, diverse, and often
difficult to comprehend for those who do not share this intriguing trait.
Synaesthesia can vary greatly from person to person, both in terms of types of
sensory associations and their intensity. It is believed to be a result of increased
connectivity between different brain regions, particularly those involved in
sensory processing. It is suggested by some research that some individuals are
generally born with it but it can also be adapted at a later stage of life. Certain
studies also indicate that drugs like LSD, psilocybin, and mescaline and alcohol
may cause transient synesthesia. (Sinke et al, 2012).

Numerous studies have been conducted to determine if synaesthesia is primarily

manifested by genetics or if the external factors are the cause. While the exact
genetic pathways underlying synesthesia remain mostly unknown, research
suggests that hereditary factors account for most cases of the illness. However,
experiences and environmental circumstances can also influence the
manifestation of synesthesia. This essay will explore the role of genetics and
factors beyond genetics, contributing to synesthesia and how this condition is
induced.

While a definitive genetic basis for synesthesia has yet to be established, the
phenomenon often shows familial patterns with approximately 40% of
synesthetes reporting a first-degree relative with the condition. (Brang &
Ramachandran, 2011). Considering vast heterogeneity of the condition, one
might readily assume that each type of synesthesia is attributed to a distinct
gene or group of genes. A number of psychophysical studies were carried out to
evaluate the perceptual experiences of synesthetes and contrast them with those
of non-synesthetes. A cross-modal matching task was one of the main
experiments in which participants were given coloured patches and instructed to
choose the colour that corresponded to a given letter or number. The purpose of
this activity was to find out if synesthetes regularly connected particular
graphemes to particular colours. Additionally, the brain activity linked to
synesthetic experiences was examined using neuroimaging techniques including
functional magnetic resonance imaging (fMRI). The conclusions of the study
shed important light on the processing of the brain of synesthetes. They
proposed that synesthetes experience sensory experiences through enhanced
neural connection between brain regions in charge of processing several
modalities, including vision and colour perception. It strongly implies that
synaesthesia is a genuine perception possibly caused by the cross wiring in
specific area.

Researchers have worked with autistic patients to gain a thorough understanding

of the hereditary component of synaesthesia. Not surprisingly, there exists
evidence of genetic connections that run in the family and intersect with autism
and synaesthesia. It is clear that there is a connection between synaesthesia and
autism, as per a paper by Bouvet et al., 2019. Rather, the mechanisms founding
synaesthesia may constitute a special kind of autistic vulnerability. In an effort
to thoroughly evaluate the genetic component implicated in synaesthetes
exhibiting autistic symptoms, a recent study by Taylor et al. (2023) revealed that
genetics may influence individual variability in synaesthesia and that
non-shared environment is a crucial factor in the aetiology of synaesthesia.
Moreover, it was thought that the majority of the association between
synaesthesia and autistic traits was due to shared genetics and a small degree of
non-shared contextual element.

A study by Barnett et al, 2008, gives a conclusive statement that synaesthesia

runs in families, and a by chance occurrence is not possible. They were able to
ascertain the exact type of synaesthesia experienced by each participant based
on their answers to comprehensive questionnaires. Through the study they
found that 42% of synaesthetes have a family member with synaesthesia. Even
in the improbable event that synaesthesia were as widespread as 1 in 20 people
(Simner et al., 2006), this number would not likely be explained by chance.
Their data, together with those from multiple other investigations (Baron-Cohen
et al., 1996; Rich et al., 2005; Ward and Simner, 2005), offer strong support for
the hereditary nature of synaesthesia.

Given the sufficient evidence that synesthesia runs in families, it is reasonable

to assume that a mutation results in defective pruning of neural connections
between adjacent brain maps, such as between V4 and fusiform gyrus, which is
primarily responsible for colour perception, might be causing the condition in
some people. (Brang & Ramachandran, 2011)

The high degree of variation expressed in synaesthesia does indicate a

significant genetic component in the development of synaesthesia. However, the
influence of environmental factors and other external influences cannot be
disregarded. Below is a detailed explanation of the external causes impacting
the condition.

Although, a study conducted in 2008 by Bargary & Mitchell provides a

controversial evidence that supports the idea that developmental synesthesia is
majorly caused by structural differences in the brain. This is likely due to
direct connections between nearby brain areas. The results from the
electroencephalogram (EEG) studies' findings imply that synaesthetes may
differ in how they receive sensory information at an early age in both the visual
and auditory domains. A recent Diffusion Tensor Imaging tractography (DTI)
study supports the idea of altered structural connectivity in synesthetes. DTI
tracks water molecule diffusion in the brain, revealing differences in white
matter integrity. Higher fractional anisotropy (FA) was found in temporal,
parietal, and frontal regions of synesthetes compared to controls. These areas
correlate with increased blood-oxygen-level-dependent (BOLD) response to
grapheme stimuli inducing colour percepts. FA in the right inferior temporal
cortex, near V4, correlated with the nature of synesthetic experience. While no
differences were found on the left side indicating lateralisation variability,
tractography didn't show specific tract differences. This suggests structural
differences in the brains of synesthetes, but the microstructural details still
remain unclear. These studies have the potential to significantly enhance
cognitive and neurophysiological models of synesthesia and its connection to
typical sensory processing and multisensory integration.

According to the previous research, genetics has been shown to play a

significant role in synesthesia however it is not the sole determinant of this
condition. Bosley and Eagleman's 2015 twin study, which includes single case
studies, partially aligns with previous findings regarding genetic influence.
However, their large sample size study confirms that synesthesia is not
exclusively determined by genetics. If it were, monozygotic twins would exhibit
a 100% concordance rate, which in this case exhibited only 73.9%. They
suggest that while genetics may contribute to CSS development, extragenic
factors such as epigenetics or environmental influences are likely significant.
The existence of six discordant monozygotic twin pairs in this study further
supports the influence of extragenic factors in synesthesia development.

Moreover, intriguing studies have been conducted to determine whether

training, drugs, alcohol, etc. might cause someone to experience synaesthesia. A
fascinating evidence can be drawn from the paper by Kallio et al, 2017
suggesting that hypnosis can effectively produce a condition similar to
synaesthesia. The fact that the hypnotically induced analogue of synaesthesia
differs from congenital synaesthesia phenomenologically suggests that the
underlying brain process is distinct.

In my view, synesthesia arises from a deviation in the analogical processing of

the brain, which accounts for the variability observed among synesthetes and
explains why only approximately 5% of the adult population experiences it.
Additionally, external factors such as environmental influences, epigenetics
(Bosley & Eagleman, 2015) and structural differences (Bargary & Mitchell,
2008) contribute to the development of synesthesia. However, acquiring the
condition through learning and experiences seems unlikely. In concert with the
findings of Kallio et al.’s 2017 study, while it may be possible to elicit
experiences similar to synesthesia, inducing the actual condition itself appears
to be improbable. While many studies rely on self-reported questionnaires, this
approach may have limitations. However, a more thorough understanding could
be achieved by employing a more suitable research method to analyse the data
throughout the study. But, based on the study outlined above, I think that the
unusual experiences associated with synaesthesia are a result of an inborn
genetic trait rather than an acquired condition over time.
References-

Bargary, G., & Mitchell, K. J. (2008). Synaesthesia and cortical

connectivity. Trends in Neurosciences, 31(7), 335–342.
https://doi.org/10.1016/j.tins.2008.03.007

Barnett, K. J., Finucane, C., Asher, J. E., Bargary, G., Corvin, A. P.,
Newell, F. N., & Mitchell, K. J. (2008). Familial patterns and the origins of
individual differences in synaesthesia. Cognition, 106(2), 871–893.
https://doi.org/10.1016/j.cognition.2007.05.003

Baron-Cohen, S., Burt, L., Smith-Laittan, F., Harrison, J., & Bolton, P.
(1996). Synaesthesia: Prevalence and familiality. Perception, 25(9),
1073–1079. https://doi.org/10.1068/p251073

Bosley, H. G., & Eagleman, D. M. (2015). Synesthesia in twins:

Incomplete concordance in monozygotes suggests extragenic factors.
Behavioural Brain Research, 286, 93–96.
https://doi.org/10.1016/j.bbr.2015.02.024

Bouvet, L., Amsellem, F., Maruani, A., Tonus-Vic Dupont, A., Mathieu,
A., Bourgeron, T., Delorme, R., & Mottron, L. (2019). Synesthesia &
autistic features in a large family: Evidence for spatial imagery as a
common factor. Behavioural Brain Research, 362, 266–272.
https://doi.org/10.1016/j.bbr.2019.01.014
Brang, D., & Ramachandran, V. S. (2011). Survival of the synesthesia
gene: Why do people hear colors and taste words? PLoS Biology, 9(11).
https://doi.org/10.1371/journal.pbio.1001205

Kallio, S., Koivisto, M., & Kaakinen, J. K. (2017). Synaesthesia-type

associations and perceptual changes induced by hypnotic suggestion.
Scientific Reports, 7(1). https://doi.org/10.1038/s41598-017-16174-y

Rich, A. N., Bradshaw, J. L., & Mattingley, J. B. (2005). A systematic,

large-scale study of synaesthesia: Implications for the role of early
experience in lexical-colour associations. Cognition, 98(1), 53–84.
https://doi.org/10.1016/j.cognition.2004.11.003

Simner, J., Mulvenna, C., Sagiv, N., Tsakanikos, E., Witherby, S. A.,
Fraser, C., Scott, K., & Ward, J. (2006). Synaesthesia: The prevalence of
atypical cross-modal experiences. Perception, 35(8), 1024–1033.
https://doi.org/10.1068/p5469

Sinke, C., Halpern, J. H., Zedler, M., Neufeld, J., Emrich, H. M., & Passie,
T. (2012). Genuine and drug-induced synesthesia: A Comparison.
Consciousness and Cognition, 21(3), 1419–1434.
https://doi.org/10.1016/j.concog.2012.03.009

Taylor, M. J., van Leeuwen, T. M., Kuja-Halkola, R., Lundström, S.,

Larsson, H., Lichtenstein, P., Bölte, S., & Neufeld, J. (2023). Genetic and
environmental architecture of synaesthesia and its association with the
autism spectrum—a twin study. Proceedings of the Royal Society B:
Biological Sciences, 290(2009). https://doi.org/10.1098/rspb.2023.1888

Ward, J., & Simner, J. (2005). Is synaesthesia an X-linked dominant trait

with lethality in males? Perception, 34(5), 611–623.
https://doi.org/10.1068/p5250