What Causes High Sensitivity? A Historical Look

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Part 1 of this series explored how Victorian and contemporary medicine talked about hysteria and sensory processing sensitivity (SPS), respectively, as sensorial-emotional maladies.

If the Victorian hysteric and today’s highly sensitive person (HSP) appear to share similar triggers (catalysts) and experiences of overwhelm (crisis), what makes the hysteric and the HSP sensitive to senses and emotions in the first place? In other words, what is the “cause” in these psychological narratives?

During the Victorian era, doctors claimed that women were more prone to this process because of their greater capillary circulation, nervous sensibility, and propensity to emotion. Their biological constitutions provided the perfect trifecta for hysteria.

One physician, leaning on a long line of predecessors, argued that women had more capillary development and more sensitive nervous systems than men. [1] According to other physicians, whenever a woman saw or even remembered an object, emotions would arise immediately. [2] If the emotions traveled through the sympathetic nerves to other parts of the body—and women were, by nature, more emotional and more nervous—then their emotional experience was more likely to cause physical ailments. As the medical texts of the day had it, women were—simply by nature—more sensitive and more likely to experience distress because of this sensitivity.

While sensory processing sensitivity (SPS) is still, in part, understood as an innate condition of a person’s nervous system (like hysteria was understood to be a part of women’s innate nervous constitution) research has recently come to suggest that SPS is epigenetic in nature; it has also begun to tease out the different genetic and environmental aspects.

So if both genes and environments contribute to people’s differential susceptibility to stimuli, then the question becomes: What genes and what environments, in particular, “cause” this trait in 15 to 20 percent of individuals?

Identifying the Role of Genes in High Sensitivity

Researchers have been actively asking the question of which genes cause sensitivity for the last decade, but haven’t yet come to an agreed-upon consensus.

Belksy and Pluess, for example, studied HSPs' genetic predisposition by studying the interaction between various genes and the environment. They concluded that those carrying multiple plasticity alleles will be more susceptible than those individuals carrying fewer plasticity alleles. [3] Another research team, Acevedo et. al., studied the S-allele (serotonin transporter) and concluded that the serotonin transporter might come into play in the genetics of SPS. [4] Homberg also claims that 5-HTTLPR (serotonin-transporter-linked promoter region) may be involved in SPS, but that more research needs to be done. [5]

Conversely, more recently in 2020, Licht et. al. concluded that SPS was not associated with serotonin. [6] Since 5-HTTLPR (serotonin transporter) was discovered in the mid-1990s—just as Elaine Aron’s work on the HSP was also beginning—much research has been done, but researchers continue to debate the genetic predisposition for sensitivity to the environment.

Exploring the Role of Environmental Factors

If SPS is truly epigenetic in nature, as recent research suggests, the second element (besides the genetic predisposition) is the study of the environment and how it influences the genetic expression. The idea that the nature of childhood experience strongly influences the genetic expression of SPS emerges frequently in the literature.

Here, parenting styles and family dynamics come strongly into play in a way we do not really see in the nineteenth-century hysteria literature. The literature seems to agree that people with SPS will reap the benefits of an emotionally attuned childhood environment but will feel the negative repercussions of an emotionally unsupportive childhood environment. [7] Those with genetic predisposition but with better childhood experiences will remain sensitive but will not fall under the double-risk model of not only sensitivity but also anxiety and depression, etc.

Moreover, the literature suggests that supportive childhood environments that understood and responded appropriately to the child’s sensitivity can actually lead the child to emotional regulation with “increases [in] self-awareness, arousal, self-control, and calm, which are so important when responding to any emotion-laden situation.” [8] In other words, a supportive childhood will not suppress the gene expression of innate genetic sensitivity but it will provide a child, and by implication the adult later in life, with the proper tools for negotiating this sensitivity.

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Sensitivity and Gender

Learned behavior from the environment can also influence a person’s sensitivity—and this is where gender also strongly intersects with HSP, as it does with hysteria. Of import, the current literature on SPS and HSPs claim that there is no gender indicator for HSP. Unlike nineteenth-century women who were thought to be more nervously predisposed to hysteria than men, neither the twenty-first woman nor the twenty-first man is genetically more predisposed to be sensitive. Rather, as Elaine Aron and others consistently mention, their studies indicate that there are as many boys and girls in the 15 to 20 percent HSP population. [9]

However, Western gender expectations can alter the expression of sensitivity. For example, if a boy receives a negative reaction from his environment in response to his crying, it can condition him to underreact emotionally in future situations. Other literature states that Western gender stereotypes can make women score slightly higher on the HSP scale, as men may be fearful of identifying with the stereotype of the sensitive person. [10]

Even if the hysteric and the HSP share similar triggers (catalysts) and experiences of overwhelm (crisis), the literature on high sensitivity today stresses not only the condition of the nervous system but also parenting and the emotional climate of one’s childhood.

As I will discuss in Part 3, these differences greatly alter what the literature proposes as the final step in the medical narrative: the cure.