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Sweet and Sensitive: Sensory Processing Sensitivity and Type 1 Diabetes
YJPDN-01683; No of Pages 4 Journal of Pediatric Nursing xxx (2017) xxx–xxx
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Journal of Pediatric Nursing
Sweet and Sensitive: Sensory Processing Sensitivity and Type 1 Diabetes Alon Goldberg, Dr., PhD a,⁎, Zaheera Ebraheem, Dr., MD b, Cynthia Freiberg, BSC c, Rachel Ferarro, BA b, Sharon Chai, MA d, Orna Dally Gottfried, Dr., MD e a
Tel-Hai College, Department of Education, Upper Galilee 12210, Israel The Center for Juvenile Diabetes and Pediatric Endocrinology and Pediatric Outpatient Clinics, Ziv Hospital, Zefat, Israel School of Medicine, Bar Ilan University, affiliated to Ziv Hospital, Zefat, Israel d Department of Field Practice, Tel-Hai College, Upper Galilee 12210, Israel e Diabetes Service Manager, The Center for Juvenile Diabetes and Pediatric Endocrinology and Pediatric Outpatient Clinics, Ziv Hospital, affiliated to The School of Medicine, Bar Ilan University, Zefat, Israel b c
a r t i c l e
i n f o
Article history: Received 9 May 2017 Revised 28 October 2017 Accepted 28 October 2017 Available online xxxx Keywords: Sensory processing sensitivity Autoimmune disease Type 1 diabetes
a b s t r a c t Objective: Sensory processing sensitivity (SPS) is a recently proposed construct that refers to a genetically influenced tendency to more strongly and deeply process a variety of information. The aim of the study was to examine whether SPS is associated with an autoimmune disease such as type 1 diabetes (T1D). Research design and methods: Participants were 128 adolescents (62 with T1D and 66 comparisons [without autoimmune disease]) and their parents who completed the Highly Sensitive Person Scale (HSPS) questionnaire, assessing SPS level. Results: Higher levels of SPS were found in the T1D group than in the comparison group. Furthermore, the frequency of SPS trait was significantly higher in the T1D group than in the comparison group. Conclusions: T1D is associated with higher levels of SPS. Hence, there is a need to develop interventions, treatments, and care focused on the needs of T1D patients with SPS temperament, aimed at better treatment adherence. Furthermore, longitudinal research is needed to evaluate whether SPS is a risk factor in the development of T1D. © 2017 Published by Elsevier Inc.
The fundamental way that individuals perceive and respond to their environment is through the processing of sensory information (Aron & Aron, 1997; Aron, Aron, & Jagiellowicz, 2012; Dunn, 2001; Jerome & Liss, 2005). People have different thresholds for perceiving, responding to, and becoming overwhelmed by sensations, which are reflected in individual lifestyles, moods, and temperaments (Dunn, 2001). Sensory processing sensitivity (SPS), a recently proposed construct, refers to a tendency to more strongly and deeply process a variety of information including the arts, caffeine, other peoples' moods, hunger, and pain. Roughly 20% of the population is hypothesized to be highly sensitive. They tend to process and respond to lower thresholds of information and to better detect subtle differences in the environment. These processing differences are genetically based, present at birth, and located in the central nervous system (Aron et al., 2012; Aron & Aron, 1997), and polymorphisms both in the serotonin and in the dopamine systems have been implicated (Chen et al., 2011; Homberg, Schubert, Asan, & Aron, 2016). People high in SPS also tend to be more in tune with their own thoughts and emotions, to be more aware of the emotions of others, and to be prone to “pause to check” in new ⁎ Corresponding author. E-mail address: [email protected] (A. Goldberg).
situations due to their predisposition to wariness (Aron et al., 2010; Aron et al., 2012; Aron & Aron, 1997). SPS was comprehensively studied in a series of seven studies designed to create and validate the Highly Sensitive Person Scale (HSPS), a self-report measure of sensory processing style (Aron & Aron, 1997). Sensory processing is related, but not identical, to the constructs of behavioral inhibition (Carver & White, 1994; Gray, 1991), introversion (Eysenck, 1991), shyness (Kagan, 1997), and neuroticism (Aron & Aron, 1997). Aron and Aron (1997) argued that SPS has been confused with neuroticism and fearfulness because both highly sensitive and neurotic or fearful individuals may not proceed in the face of novel situations. Overall, highly sensitive people are more likely to experience anxiety disorders such as social phobia (Kinnealey & Fuiek, 1999; Liss, Mailloux, & Erchull, 2008; Neal, Edelmann, & Glachan, 2002), avoidant personality disorder (Meyer & Carver, 2000), and depression (Johnson, Turner, & Iwata, 2003). Thus, highly sensitive people are not necessarily prone to more negative emotional states, but they may be more sensitive to negative parental environments and are more prone to negative affectivity when exposed to negative environments (Aron, Aron, & Davies, 2005; Liss, Timmel, Baxley, & Killingsworth, 2005). Furthermore, SPS is positively correlated with levels of stress and symptoms of ill-health (Benham, 2006).
https://doi.org/10.1016/j.pedn.2017.10.015 0882-5963/© 2017 Published by Elsevier Inc.
Please cite this article as: Goldberg, A., et al., Sweet and Sensitive: Sensory Processing Sensitivity and Type 1 Diabetes, Journal of Pediatric Nursing (2017), https://doi.org/10.1016/j.pedn.2017.10.015
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A. Goldberg et al. / Journal of Pediatric Nursing xxx (2017) xxx–xxx
Given that many SPS individuals experience sensory bombardment (Aron & Aron, 1997), they are more susceptible to environmental influences; for example, they are more affected than others by negative developmental experiences and environmental exposures (Hartman & Belsky, 2015) and may experience higher levels of stress (Aron et al., 2005; Liss et al., 2005), which can also lead to diseases and further life experiences that strongly affect the sensitivity genotype by increasing its phenotype expression (Pluess, 2015) and activating the sympathetic nervous system (Shoenfeld et al., 2008). The present study examined whether SPS is associated with an autoimmune disease such as diabetes mellitus type 1 (also known as juvenile diabetes or type 1 diabetes [T1D]). Since Hawkins, Davies, and Holmes (1957) first proposed the link between stress and illness, stressful life events have been found to be positively associated with chronic diseases (Renzaho et al., 2014; Shoenfeld et al., 2008; Stojanovich & Marisavljevich, 2008). The loss of body self-tolerance, as in the case of autoimmune diseases, is considered to be caused by genetic, hormonal, immunological, and environmental factors (Shoenfeld & Isenberg, 1989). N80% of patients reported emotional stress before disease onset (Stojanovich, 2010), and the disease can cause further stress that may in turn lead to other autoimmune diseases (Shepshelovich & Shoenfeld, 2006). The role of stress as a pathogenic factor in autoimmune diseases has been discussed in the literature (Carter, Herrman, Stokes, & Cox, 1987; Herrmann, Schölmerich, & Straub, 2000; Persson, Berglund, & Sahlberg, 1999; Wolfe, 1999), and it is presumed that neuroendocrine hormones triggered during stress may lead to dysregulation/altered or amplified cytokine production. This response can trigger the hypothalamic-pituitary-adrenal axis and sympathetic nervous system (Shoenfeld et al., 2008). The current study focuses on T1D, as a case of autoimmune disease. T1D is one of the most common chronic diseases among children; 15,000 children are diagnosed each year in the United States alone (Juvenile Diabetes Research Foundation, 2016). The disease is caused by autoimmune destruction of insulin-producing beta cells of the pancreas, leading to deficient insulin production, which renders the body unable to control the amount of sugar in the blood. The total dependence on an outside source of insulin has short- and long-term implications (e.g., cardiovascular diseases and problems with the limbs, blindness, kidney failure, coma, and even death) (Compas, Jaser, Dunn, & Rodriguez, 2012). Adolescents with T1D are more likely to be at risk of peer-group ridicule and violence than their healthy counterparts and to exhibit high internalizing and externalizing symptoms and high involvement in risky behaviors (Luyckx, Seiffge-Krenke, & Hampson, 2010; Silverstein et al., 2005; Storch et al., 2004). Furthermore, adolescents with T1D are at risk for diabetes complications, which can be exacerbated by their need for individualization and independence (Silverstein et al., 2005). Hence, the complex treatment and new lifetime regime affect the routines of the adolescent and his/her family, posing emotional challenges for and exerting stress on the whole family system (Cunningham, Vesco, Dolan, & Hood, 2011; Landolt, Vollrath, Laimbacher, Gnehm, & Sennhauser, 2005). Taken together, the study objectives were to compare SPS levels between a group of adolescents with T1D and a comparison group (without autoimmune diseases) to investigate whether adolescents with T1D have higher SPS levels than those in the comparison group, and to compare the frequency of the SPS trait within each group. Thus, we hypothesized as follows: Hypothesis: The T1D group will show significantly higher levels of SPS than the comparison group, and the frequency of SPS traits will be higher in the T1D group. Research Design and Methods Participants Participants (N = 128) included 62 adolescents with T1D and 66 adolescents without an autoimmune disease for comparison, matched to
T1D participants. All come from middle-class homes, and all speak Hebrew as a native language. The T1D group (n = 62) includes 35 males (56.5%) and 27 females (43.5%); their average age was 16.06 years (SD = 3.47). Participants in the T1D group were diagnosed at a mean age of 10.97 years (SD = 5.57), and with an average Hb1Ac level of 7.17 (SD = 1.54). Participants diagnosed with diseases in addition to T1D were excluded from the study. The comparison group (n = 66), participants without an autoimmune disease, includes 38 males (56.7%) and 29 females (43.3%); their average age was 15.09 years (SD = 4.09). Participants' demographics are shown in Table 1. Instruments a) Demographic questionnaire. A six-item questionnaire gathered information about gender, age, parents' marital status, socioeconomic status, and the T1D disease (i.e., onset of T1D, Hb1Ac level). b) The Highly Sensitive Person Scale (HSPS)—child report and parent report (Aron & Aron, 1997). This 27-item questionnaire evaluates the SPS trait. Both versions, child and parent, have showed solid reliability and discriminant and convergent validity (Acevedo et al., 2014; Aron et al., 2005; Aron & Aron, 1997; Liss et al., 2005). Respondents are asked to respond to items using a Likert scale ranging from 1 (not at all) to 7 (extremely). Example items include “Do other people's moods affect you?” and “Are you easily overwhelmed by strong sensory input?” In the current study, Cronbach's alphas for the T1D group were α = 0.86 (self-report), α = 0.89 (parent report), and for comparisons α = 0.85 (self-report) and α = 0.86 (parent report). Self-report and parent report were highly correlated (r = 0.73, p b 0.0001). Procedure The Helsinki Committee for Experiments on Humans, at a major medical center, approved the study protocol. At the recruitment stage, families were invited to participate in the study by diabetes clinic staff. In the second stage, a comparison group with matched demographic characteristics was recruited, using social media and advertisements. After signing informed consent forms, participants (adolescents with T1D/healthy adolescents, and parents) were asked to complete questionnaires. Participants were told that their anonymity would be preserved throughout the study, that the data collected would be used for research purposes only, and that their names would remain confidential. They were also assured of their right to discontinue their participation in the study at any time and were offered the option to receive the final general research findings. Results Preliminary Analyses To determine whether any demographic and personal characteristics might interfere with the analysis and thus should be controlled for in the analyses, we conducted some preliminary analyses. A t-test Table 1 Participants' Demographic Data. Characteristic Gender Males, n (%) Females, n (%) Age, M (SD) Diabetes onset age, M (SD) Hb1Ac level, M (SD)
T1D group (n = 62)
Comparison (n = 66)
35 (56.5%) 27 (43.5%) 16.06 (3.47) 10.97 (5.57) 7.17 (1.54)
38 (56.7%) 29 (43.3%) 15.09 (4.09) – –
T1D = Type I diabetes.
Please cite this article as: Goldberg, A., et al., Sweet and Sensitive: Sensory Processing Sensitivity and Type 1 Diabetes, Journal of Pediatric Nursing (2017), https://doi.org/10.1016/j.pedn.2017.10.015
A. Goldberg et al. / Journal of Pediatric Nursing xxx (2017) xxx–xxx Table 2 Means, standard deviations, and T-values of sensory processing sensitivity levels (N = 128). Sensory processing sensitivity level
Self-report Parent report
Comparison (n = 66)
T1D group (n = 62)
M
SD
M
SD
T(126)
4.38 4.33
0.90 1.08
4.00 3.60
0.85 1.33
2.42⁎⁎ 3.58⁎⁎⁎
T1D = Type I diabetes. ⁎⁎ p b 0.01. ⁎⁎⁎ p b 0.001.
analysis revealed no significant differences in age between the T1D and the comparison groups, and a chi-square test showed no correlation between gender and group. A Pearson correlation test showed no significant correlations between SPS level (self- and parents' report) and HB1Ac, age, or diabetes onset age. We also found no differences in SPS level between males and females. To examine the research hypothesis regarding differences in SPS levels between the T1D and comparison groups, we conducted t-tests of the independent variables, with SPS level (child and parent report separately) as the dependent variable. Results showed significant differences in SPS level between the T1D and comparison groups, with higher SPS levels in the T1D group (self-report, M = 4.38, SD = 0.90; parentreport, M = 4.33, SD = 1.08) than in the comparison group (self-report, M = 4.00, SD = 0.85; parent-report, M = 3.60, SD = 1.33), as shown in Table 2. For further analysis, we computed SPS levels with a cut point of the highest 20% scores as H-SPS (high SPS) and the lowest as non-SPS. To examine whether the SPS individuals are more frequent in the T1D group, we conducted a 2 × 2 chi-square analysis with the two dichotomous variables: group (T1D/Comparison) and SPS (H-SPS/non-SPS). Both self-report and parent report revealed significant correlations [χ(1) = 10.20, p b 0.001] and [χ(1) = 7.33, p b 0.01] (respectively), with higher frequencies of SPS individuals in the T1D group (40.3%; 43.5%) than in the comparison group (15.2%; 23.2%), as shown in Table 3. Discussion The current research examined whether SPS is associated with T1D. The main hypothesis was that participants in the T1D group would show higher levels of SPS than those in the comparison group, and that the frequency of the SPS individuals would be higher in the T1D group. As hypothesized, we found higher levels of SPS in the T1D group than in the comparison group. Moreover, we observed a significantly higher frequency of SPS individuals in the T1D group than in the comparison group. Autoimmune diseases are considered to be caused by genetic, hormonal, immunological, and environmental factors (Shoenfeld et al., 2008; Shoenfeld & Isenberg, 1989; Stojanovich, 2010; Stojanovich & Marisavljevich, 2008). Research suggests that individuals with the SPS temperament are more likely to experience higher stress levels and illness symptoms (Benham, 2006). The current study suggests that they may also develop an autoimmune disease, such as T1D, as autoimmune diseases are associated with a highly activated sympathetic nervous Table 3 Frequencies (%) of sensory processing sensitivity individuals (N = 128). Sensory processing sensitivity individuals
T1D group (n = 62)
Comparison (n = 68)
χ(1)
Self-report Parent-report
40.3% 43.5%
15.2% 23.2%
1.20⁎⁎⁎ 7.33⁎⁎
T1D = Type I diabetes. ⁎⁎ p b 0.01. ⁎⁎⁎ p b 0.001.
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system (Shoenfeld et al., 2008). Moreover, everyday T1D experiences and environmental influences may increase the expression of temperamental genes, which might be reflected in higher SPS levels (Pluess, 2015). SPS individuals detect, process, and respond to lower thresholds of information and better detect subtle differences in the environment (Aron & Aron, 1997); they also experience more emotional sensitivity and “pause to check” behavior due to their predisposition to wariness (Aron & Aron, 1997; Carver & White, 1994). Although they have been found to be more anxious and depressed (Kinnealey & Fuiek, 1999; Meyer & Carver, 2000; Neal et al., 2002), highly sensitive people are not necessarily prone to more negative emotional states, but they may be more sensitive to negative environments and more prone to negative affect and illness when exposed to such environments (Aron et al., 2005; Benham, 2006). The role of stress as a pathogenic factor in autoimmune diseases was highly discussed in the literature (Carter et al., 1987; Herrmann et al., 2000; Shepshelovich & Shoenfeld, 2006; Wolfe, 1999), and it is presumed that neuroendocrine hormones triggered during stress may lead to dysregulation/altered or amplified cytokine production and activate an autoimmune disease. Furthermore, this response can trigger the hypothalamic-pituitary-adrenal axis and sympathetic nervous system (Shoenfeld et al., 2008), which may further enhance the expression of sensitivity genes (Hartman & Belsky, 2015). Adolescents with T1D are more likely to experience stress because of their need for individualization and independence (Silverstein et al., 2005), on one hand, and their potential dependence on and conflicts with their parents as a result of the complex treatment, on the other hand, posing emotional challenges for and exerting stress on the whole family system (Cunningham et al., 2011; Landolt et al., 2005). This process may highly expressed in the case of highly sensitive adolescents with T1D. Implications Although additional research is needed, the current findings would suggest that SPS may be associated with T1D. These findings are important to understanding the association between temperament and T1D and the mechanism of stress in disease pathogenesis, in treatment adherence, and within the diabetes care clinic. SPS is a genetically based trait, present at birth (Aron & Aron, 1997); it can be regulated by a supportive environment that reduces and manages stress. SPS individuals may be more sensitive to negative environments (Aron et al., 2005), but they are also more sensitive to positive environments (Pluess & Belsky, 2013), so they may greatly enjoy the contribution of interventions to regulate stress and lower their risk of developing the disease. In the case of highly sensitive T1D patients, they may benefit more than T1D patients who are not highly sensitive from patient-centered nursing and a trust-based alliance between the clinic staff (physicians, nurses, or social workers) and them and their families. Strength, Limitations, and Future Studies It is important to mention that the present study examined a small sample of participants, using a cross-sectional design, and any conclusions regarding causality are limited. Hence, with regard to this limitation, the high SPS levels within T1D individuals points to the need to develop interventions, treatments, and care that are focused on their needs and on their higher sensitivity to family and clinic environments, and that aim at better adherence to treatment. Such environments would be better tuned to regulating SPS individuals' negative affect and enhancing their positive experiences. Finally, although the data were collected using several sources of reports (self and parent), the use of more objective measures to examine SPS and T1D stress, such as fMRI (Functional Magnetic Resonance Imaging; for further information, see Acevedo et al., 2014) and skin conductivity, are recommended. Furthermore, longitudinal research is needed
Please cite this article as: Goldberg, A., et al., Sweet and Sensitive: Sensory Processing Sensitivity and Type 1 Diabetes, Journal of Pediatric Nursing (2017), https://doi.org/10.1016/j.pedn.2017.10.015
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to evaluate whether SPS is a risk factor for the development of T1D; expanding the research to other autoimmune diseases is also suggested. Acknowledgments The authors thank the study participants and the clinic staff at the Ziv Medical Center juvenile diabetes clinic, and the volunteer participants, without whom the study would not have been possible. We express gratitude to Prof. Arthur Aron, Prof. Michael Pluess and Prof. Miri Scharf for their comments on an early version of the article. There are no potential conflicts of interest relevant to this article. Author contributions AG acquired, analyzed, and interpreted the data; drafted the manuscript; reviewed the manuscript for important intellectual content; and approved the final version of the manuscript submitted. AG is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. ZE, CF, and RF recruited the participants at the Juvenile Diabetes clinic, collected and coded the data to the computer. SC initiate the collaboration between Tel-Hai college and Ziv Hospital’ juvenile diabetes clinic and approved the final version of the manuscript submitted. ODG was in charge of carrying out and implementing the research program, responsible for its acceptable and appropriate ethical standards, and oversaw the provision for full clinical services, which was enhanced by the patient's participation and cooperation with the research project. References Acevedo, B. P., Aron, E. N., Aron, A., Sangster, M. -D., Collins, N., & Brown, L. L. (2014). The highly sensitive brain: An fmri study of sensory processing sensitivity and response to others' emotions. Brain and Behavior, 4(4), 580–594. https://doi.org/10.1002/ brb3.242. Aron, A., Ketay, S., Hedden, T., Aron, E. N., Rose Markus, H., & Gabrieli, J. D. E. (2010). Temperament trait of sensory processing sensitivity moderates cultural differences in neural response. Social Cognitive and Affective Neuroscience, 5(2–3), 219–226. https://doi.org/10.1093/scan/nsq028. Aron, E. N., & Aron, A. (1997). Sensory-processing sensitivity and its relation to introversion and emotionality. Journal of Personality and Social Psychology, 73(2), 345–368. https://doi.org/10.1037/0022-3514.73.2.345. Aron, E. N., Aron, A., & Jagiellowicz, J. (2012). Sensory processing sensitivity: A review in the light of the evolution of biological responsivity. Personality and Social Psychology Review, 16(3), 262–282. https://doi.org/10.1177/1088868311434213. Aron, E. N., Aron, A. F., & Davies, K. M. (2005). Adult shyness: The interaction of temperamental sensitivity and an adverse childhood environment. Personality and Social Psychology Bulletin, 31(2), 181–197. https://doi.org/10.1177/0146167204271419. Benham, G. (2006). The highly sensitive person: Stress and physical symptom reports. Personality and Individual Differences, 40(7), 1433–1440. https://doi.org/10.1016/j. paid.2005.11.021. Carter, W. R., Herrman, J., Stokes, K., & Cox, D. J. (1987). Promotion of diabetes onset by stress in the bb rat. Diabetologia, 30(8), 674–675. https://doi.org/10.1007/ BF00277327. Carver, C. S., & White, T. L. (1994). Behavioral inhibition, behavioral activation, and affective responses to impending reward and punishment: The bis/bas scales. Journal of Personality and Social Psychology, 67(2), 319–333. https://doi.org/10.1037/00223514.67.2.319. Chen, C., Chen, C., Moyzis, R., Stern, H., He, Q., Li, H., ... Dong, Q. (2011). Contributions of dopamine-related genes and environmental factors to highly sensitive personality: A multi-step neuronal system-level approach. PLoS One, 6(7), e21636. https://doi. org/10.1371/journal.pone.0021636. Compas, B. E., Jaser, S. S., Dunn, M. J., & Rodriguez, E. M. (2012). Coping with chronic illness in childhood and adolescence. Annual Review of Clinical Psychology, 8, 455–480. https://doi.org/10.1146/annurev-clinpsy-032511-143108. Cunningham, N. R., Vesco, A. T., Dolan, L. M., & Hood, K. K. (2011). From caregiver psychological distress to adolescent glycemic control: The mediating role of perceived burden around diabetes management. Journal of Pediatric Psychology, 36(2), 196–205. https://doi.org/10.1093/jpepsy/jsq071. Dunn, W. (2001). The sensations of everyday life: Empirical, theoretical, and pragmatic considerations. American Journal of Occupational Therapy, 55(6), 608–620. https:// doi.org/10.5014/ajot.55.6.608. Eysenck, H. J. (1991). Biological dimensions of personality. In L. A. Pervin (Ed.), Handbook of personality (pp. 244–276). New York, NY: Guilford. Gray, J. A. (1991). The neuropsychology of temperament. In J. A. Strelau, & A. Angleitner (Eds.), Explorations in temperament: International perspectives on theory and measurement (pp. 105–128). New York, NY: Plenum.
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Please cite this article as: Goldberg, A., et al., Sweet and Sensitive: Sensory Processing Sensitivity and Type 1 Diabetes, Journal of Pediatric Nursing (2017), https://doi.org/10.1016/j.pedn.2017.10.015
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Journal of Pediatric Nursing
Sweet and Sensitive: Sensory Processing Sensitivity and Type 1 Diabetes Alon Goldberg, Dr., PhD a,⁎, Zaheera Ebraheem, Dr., MD b, Cynthia Freiberg, BSC c, Rachel Ferarro, BA b, Sharon Chai, MA d, Orna Dally Gottfried, Dr., MD e a
Tel-Hai College, Department of Education, Upper Galilee 12210, Israel The Center for Juvenile Diabetes and Pediatric Endocrinology and Pediatric Outpatient Clinics, Ziv Hospital, Zefat, Israel School of Medicine, Bar Ilan University, affiliated to Ziv Hospital, Zefat, Israel d Department of Field Practice, Tel-Hai College, Upper Galilee 12210, Israel e Diabetes Service Manager, The Center for Juvenile Diabetes and Pediatric Endocrinology and Pediatric Outpatient Clinics, Ziv Hospital, affiliated to The School of Medicine, Bar Ilan University, Zefat, Israel b c
a r t i c l e
i n f o
Article history: Received 9 May 2017 Revised 28 October 2017 Accepted 28 October 2017 Available online xxxx Keywords: Sensory processing sensitivity Autoimmune disease Type 1 diabetes
a b s t r a c t Objective: Sensory processing sensitivity (SPS) is a recently proposed construct that refers to a genetically influenced tendency to more strongly and deeply process a variety of information. The aim of the study was to examine whether SPS is associated with an autoimmune disease such as type 1 diabetes (T1D). Research design and methods: Participants were 128 adolescents (62 with T1D and 66 comparisons [without autoimmune disease]) and their parents who completed the Highly Sensitive Person Scale (HSPS) questionnaire, assessing SPS level. Results: Higher levels of SPS were found in the T1D group than in the comparison group. Furthermore, the frequency of SPS trait was significantly higher in the T1D group than in the comparison group. Conclusions: T1D is associated with higher levels of SPS. Hence, there is a need to develop interventions, treatments, and care focused on the needs of T1D patients with SPS temperament, aimed at better treatment adherence. Furthermore, longitudinal research is needed to evaluate whether SPS is a risk factor in the development of T1D. © 2017 Published by Elsevier Inc.
The fundamental way that individuals perceive and respond to their environment is through the processing of sensory information (Aron & Aron, 1997; Aron, Aron, & Jagiellowicz, 2012; Dunn, 2001; Jerome & Liss, 2005). People have different thresholds for perceiving, responding to, and becoming overwhelmed by sensations, which are reflected in individual lifestyles, moods, and temperaments (Dunn, 2001). Sensory processing sensitivity (SPS), a recently proposed construct, refers to a tendency to more strongly and deeply process a variety of information including the arts, caffeine, other peoples' moods, hunger, and pain. Roughly 20% of the population is hypothesized to be highly sensitive. They tend to process and respond to lower thresholds of information and to better detect subtle differences in the environment. These processing differences are genetically based, present at birth, and located in the central nervous system (Aron et al., 2012; Aron & Aron, 1997), and polymorphisms both in the serotonin and in the dopamine systems have been implicated (Chen et al., 2011; Homberg, Schubert, Asan, & Aron, 2016). People high in SPS also tend to be more in tune with their own thoughts and emotions, to be more aware of the emotions of others, and to be prone to “pause to check” in new ⁎ Corresponding author. E-mail address: [email protected] (A. Goldberg).
situations due to their predisposition to wariness (Aron et al., 2010; Aron et al., 2012; Aron & Aron, 1997). SPS was comprehensively studied in a series of seven studies designed to create and validate the Highly Sensitive Person Scale (HSPS), a self-report measure of sensory processing style (Aron & Aron, 1997). Sensory processing is related, but not identical, to the constructs of behavioral inhibition (Carver & White, 1994; Gray, 1991), introversion (Eysenck, 1991), shyness (Kagan, 1997), and neuroticism (Aron & Aron, 1997). Aron and Aron (1997) argued that SPS has been confused with neuroticism and fearfulness because both highly sensitive and neurotic or fearful individuals may not proceed in the face of novel situations. Overall, highly sensitive people are more likely to experience anxiety disorders such as social phobia (Kinnealey & Fuiek, 1999; Liss, Mailloux, & Erchull, 2008; Neal, Edelmann, & Glachan, 2002), avoidant personality disorder (Meyer & Carver, 2000), and depression (Johnson, Turner, & Iwata, 2003). Thus, highly sensitive people are not necessarily prone to more negative emotional states, but they may be more sensitive to negative parental environments and are more prone to negative affectivity when exposed to negative environments (Aron, Aron, & Davies, 2005; Liss, Timmel, Baxley, & Killingsworth, 2005). Furthermore, SPS is positively correlated with levels of stress and symptoms of ill-health (Benham, 2006).
https://doi.org/10.1016/j.pedn.2017.10.015 0882-5963/© 2017 Published by Elsevier Inc.
Please cite this article as: Goldberg, A., et al., Sweet and Sensitive: Sensory Processing Sensitivity and Type 1 Diabetes, Journal of Pediatric Nursing (2017), https://doi.org/10.1016/j.pedn.2017.10.015
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A. Goldberg et al. / Journal of Pediatric Nursing xxx (2017) xxx–xxx
Given that many SPS individuals experience sensory bombardment (Aron & Aron, 1997), they are more susceptible to environmental influences; for example, they are more affected than others by negative developmental experiences and environmental exposures (Hartman & Belsky, 2015) and may experience higher levels of stress (Aron et al., 2005; Liss et al., 2005), which can also lead to diseases and further life experiences that strongly affect the sensitivity genotype by increasing its phenotype expression (Pluess, 2015) and activating the sympathetic nervous system (Shoenfeld et al., 2008). The present study examined whether SPS is associated with an autoimmune disease such as diabetes mellitus type 1 (also known as juvenile diabetes or type 1 diabetes [T1D]). Since Hawkins, Davies, and Holmes (1957) first proposed the link between stress and illness, stressful life events have been found to be positively associated with chronic diseases (Renzaho et al., 2014; Shoenfeld et al., 2008; Stojanovich & Marisavljevich, 2008). The loss of body self-tolerance, as in the case of autoimmune diseases, is considered to be caused by genetic, hormonal, immunological, and environmental factors (Shoenfeld & Isenberg, 1989). N80% of patients reported emotional stress before disease onset (Stojanovich, 2010), and the disease can cause further stress that may in turn lead to other autoimmune diseases (Shepshelovich & Shoenfeld, 2006). The role of stress as a pathogenic factor in autoimmune diseases has been discussed in the literature (Carter, Herrman, Stokes, & Cox, 1987; Herrmann, Schölmerich, & Straub, 2000; Persson, Berglund, & Sahlberg, 1999; Wolfe, 1999), and it is presumed that neuroendocrine hormones triggered during stress may lead to dysregulation/altered or amplified cytokine production. This response can trigger the hypothalamic-pituitary-adrenal axis and sympathetic nervous system (Shoenfeld et al., 2008). The current study focuses on T1D, as a case of autoimmune disease. T1D is one of the most common chronic diseases among children; 15,000 children are diagnosed each year in the United States alone (Juvenile Diabetes Research Foundation, 2016). The disease is caused by autoimmune destruction of insulin-producing beta cells of the pancreas, leading to deficient insulin production, which renders the body unable to control the amount of sugar in the blood. The total dependence on an outside source of insulin has short- and long-term implications (e.g., cardiovascular diseases and problems with the limbs, blindness, kidney failure, coma, and even death) (Compas, Jaser, Dunn, & Rodriguez, 2012). Adolescents with T1D are more likely to be at risk of peer-group ridicule and violence than their healthy counterparts and to exhibit high internalizing and externalizing symptoms and high involvement in risky behaviors (Luyckx, Seiffge-Krenke, & Hampson, 2010; Silverstein et al., 2005; Storch et al., 2004). Furthermore, adolescents with T1D are at risk for diabetes complications, which can be exacerbated by their need for individualization and independence (Silverstein et al., 2005). Hence, the complex treatment and new lifetime regime affect the routines of the adolescent and his/her family, posing emotional challenges for and exerting stress on the whole family system (Cunningham, Vesco, Dolan, & Hood, 2011; Landolt, Vollrath, Laimbacher, Gnehm, & Sennhauser, 2005). Taken together, the study objectives were to compare SPS levels between a group of adolescents with T1D and a comparison group (without autoimmune diseases) to investigate whether adolescents with T1D have higher SPS levels than those in the comparison group, and to compare the frequency of the SPS trait within each group. Thus, we hypothesized as follows: Hypothesis: The T1D group will show significantly higher levels of SPS than the comparison group, and the frequency of SPS traits will be higher in the T1D group. Research Design and Methods Participants Participants (N = 128) included 62 adolescents with T1D and 66 adolescents without an autoimmune disease for comparison, matched to
T1D participants. All come from middle-class homes, and all speak Hebrew as a native language. The T1D group (n = 62) includes 35 males (56.5%) and 27 females (43.5%); their average age was 16.06 years (SD = 3.47). Participants in the T1D group were diagnosed at a mean age of 10.97 years (SD = 5.57), and with an average Hb1Ac level of 7.17 (SD = 1.54). Participants diagnosed with diseases in addition to T1D were excluded from the study. The comparison group (n = 66), participants without an autoimmune disease, includes 38 males (56.7%) and 29 females (43.3%); their average age was 15.09 years (SD = 4.09). Participants' demographics are shown in Table 1. Instruments a) Demographic questionnaire. A six-item questionnaire gathered information about gender, age, parents' marital status, socioeconomic status, and the T1D disease (i.e., onset of T1D, Hb1Ac level). b) The Highly Sensitive Person Scale (HSPS)—child report and parent report (Aron & Aron, 1997). This 27-item questionnaire evaluates the SPS trait. Both versions, child and parent, have showed solid reliability and discriminant and convergent validity (Acevedo et al., 2014; Aron et al., 2005; Aron & Aron, 1997; Liss et al., 2005). Respondents are asked to respond to items using a Likert scale ranging from 1 (not at all) to 7 (extremely). Example items include “Do other people's moods affect you?” and “Are you easily overwhelmed by strong sensory input?” In the current study, Cronbach's alphas for the T1D group were α = 0.86 (self-report), α = 0.89 (parent report), and for comparisons α = 0.85 (self-report) and α = 0.86 (parent report). Self-report and parent report were highly correlated (r = 0.73, p b 0.0001). Procedure The Helsinki Committee for Experiments on Humans, at a major medical center, approved the study protocol. At the recruitment stage, families were invited to participate in the study by diabetes clinic staff. In the second stage, a comparison group with matched demographic characteristics was recruited, using social media and advertisements. After signing informed consent forms, participants (adolescents with T1D/healthy adolescents, and parents) were asked to complete questionnaires. Participants were told that their anonymity would be preserved throughout the study, that the data collected would be used for research purposes only, and that their names would remain confidential. They were also assured of their right to discontinue their participation in the study at any time and were offered the option to receive the final general research findings. Results Preliminary Analyses To determine whether any demographic and personal characteristics might interfere with the analysis and thus should be controlled for in the analyses, we conducted some preliminary analyses. A t-test Table 1 Participants' Demographic Data. Characteristic Gender Males, n (%) Females, n (%) Age, M (SD) Diabetes onset age, M (SD) Hb1Ac level, M (SD)
T1D group (n = 62)
Comparison (n = 66)
35 (56.5%) 27 (43.5%) 16.06 (3.47) 10.97 (5.57) 7.17 (1.54)
38 (56.7%) 29 (43.3%) 15.09 (4.09) – –
T1D = Type I diabetes.
Please cite this article as: Goldberg, A., et al., Sweet and Sensitive: Sensory Processing Sensitivity and Type 1 Diabetes, Journal of Pediatric Nursing (2017), https://doi.org/10.1016/j.pedn.2017.10.015
A. Goldberg et al. / Journal of Pediatric Nursing xxx (2017) xxx–xxx Table 2 Means, standard deviations, and T-values of sensory processing sensitivity levels (N = 128). Sensory processing sensitivity level
Self-report Parent report
Comparison (n = 66)
T1D group (n = 62)
M
SD
M
SD
T(126)
4.38 4.33
0.90 1.08
4.00 3.60
0.85 1.33
2.42⁎⁎ 3.58⁎⁎⁎
T1D = Type I diabetes. ⁎⁎ p b 0.01. ⁎⁎⁎ p b 0.001.
analysis revealed no significant differences in age between the T1D and the comparison groups, and a chi-square test showed no correlation between gender and group. A Pearson correlation test showed no significant correlations between SPS level (self- and parents' report) and HB1Ac, age, or diabetes onset age. We also found no differences in SPS level between males and females. To examine the research hypothesis regarding differences in SPS levels between the T1D and comparison groups, we conducted t-tests of the independent variables, with SPS level (child and parent report separately) as the dependent variable. Results showed significant differences in SPS level between the T1D and comparison groups, with higher SPS levels in the T1D group (self-report, M = 4.38, SD = 0.90; parentreport, M = 4.33, SD = 1.08) than in the comparison group (self-report, M = 4.00, SD = 0.85; parent-report, M = 3.60, SD = 1.33), as shown in Table 2. For further analysis, we computed SPS levels with a cut point of the highest 20% scores as H-SPS (high SPS) and the lowest as non-SPS. To examine whether the SPS individuals are more frequent in the T1D group, we conducted a 2 × 2 chi-square analysis with the two dichotomous variables: group (T1D/Comparison) and SPS (H-SPS/non-SPS). Both self-report and parent report revealed significant correlations [χ(1) = 10.20, p b 0.001] and [χ(1) = 7.33, p b 0.01] (respectively), with higher frequencies of SPS individuals in the T1D group (40.3%; 43.5%) than in the comparison group (15.2%; 23.2%), as shown in Table 3. Discussion The current research examined whether SPS is associated with T1D. The main hypothesis was that participants in the T1D group would show higher levels of SPS than those in the comparison group, and that the frequency of the SPS individuals would be higher in the T1D group. As hypothesized, we found higher levels of SPS in the T1D group than in the comparison group. Moreover, we observed a significantly higher frequency of SPS individuals in the T1D group than in the comparison group. Autoimmune diseases are considered to be caused by genetic, hormonal, immunological, and environmental factors (Shoenfeld et al., 2008; Shoenfeld & Isenberg, 1989; Stojanovich, 2010; Stojanovich & Marisavljevich, 2008). Research suggests that individuals with the SPS temperament are more likely to experience higher stress levels and illness symptoms (Benham, 2006). The current study suggests that they may also develop an autoimmune disease, such as T1D, as autoimmune diseases are associated with a highly activated sympathetic nervous Table 3 Frequencies (%) of sensory processing sensitivity individuals (N = 128). Sensory processing sensitivity individuals
T1D group (n = 62)
Comparison (n = 68)
χ(1)
Self-report Parent-report
40.3% 43.5%
15.2% 23.2%
1.20⁎⁎⁎ 7.33⁎⁎
T1D = Type I diabetes. ⁎⁎ p b 0.01. ⁎⁎⁎ p b 0.001.
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system (Shoenfeld et al., 2008). Moreover, everyday T1D experiences and environmental influences may increase the expression of temperamental genes, which might be reflected in higher SPS levels (Pluess, 2015). SPS individuals detect, process, and respond to lower thresholds of information and better detect subtle differences in the environment (Aron & Aron, 1997); they also experience more emotional sensitivity and “pause to check” behavior due to their predisposition to wariness (Aron & Aron, 1997; Carver & White, 1994). Although they have been found to be more anxious and depressed (Kinnealey & Fuiek, 1999; Meyer & Carver, 2000; Neal et al., 2002), highly sensitive people are not necessarily prone to more negative emotional states, but they may be more sensitive to negative environments and more prone to negative affect and illness when exposed to such environments (Aron et al., 2005; Benham, 2006). The role of stress as a pathogenic factor in autoimmune diseases was highly discussed in the literature (Carter et al., 1987; Herrmann et al., 2000; Shepshelovich & Shoenfeld, 2006; Wolfe, 1999), and it is presumed that neuroendocrine hormones triggered during stress may lead to dysregulation/altered or amplified cytokine production and activate an autoimmune disease. Furthermore, this response can trigger the hypothalamic-pituitary-adrenal axis and sympathetic nervous system (Shoenfeld et al., 2008), which may further enhance the expression of sensitivity genes (Hartman & Belsky, 2015). Adolescents with T1D are more likely to experience stress because of their need for individualization and independence (Silverstein et al., 2005), on one hand, and their potential dependence on and conflicts with their parents as a result of the complex treatment, on the other hand, posing emotional challenges for and exerting stress on the whole family system (Cunningham et al., 2011; Landolt et al., 2005). This process may highly expressed in the case of highly sensitive adolescents with T1D. Implications Although additional research is needed, the current findings would suggest that SPS may be associated with T1D. These findings are important to understanding the association between temperament and T1D and the mechanism of stress in disease pathogenesis, in treatment adherence, and within the diabetes care clinic. SPS is a genetically based trait, present at birth (Aron & Aron, 1997); it can be regulated by a supportive environment that reduces and manages stress. SPS individuals may be more sensitive to negative environments (Aron et al., 2005), but they are also more sensitive to positive environments (Pluess & Belsky, 2013), so they may greatly enjoy the contribution of interventions to regulate stress and lower their risk of developing the disease. In the case of highly sensitive T1D patients, they may benefit more than T1D patients who are not highly sensitive from patient-centered nursing and a trust-based alliance between the clinic staff (physicians, nurses, or social workers) and them and their families. Strength, Limitations, and Future Studies It is important to mention that the present study examined a small sample of participants, using a cross-sectional design, and any conclusions regarding causality are limited. Hence, with regard to this limitation, the high SPS levels within T1D individuals points to the need to develop interventions, treatments, and care that are focused on their needs and on their higher sensitivity to family and clinic environments, and that aim at better adherence to treatment. Such environments would be better tuned to regulating SPS individuals' negative affect and enhancing their positive experiences. Finally, although the data were collected using several sources of reports (self and parent), the use of more objective measures to examine SPS and T1D stress, such as fMRI (Functional Magnetic Resonance Imaging; for further information, see Acevedo et al., 2014) and skin conductivity, are recommended. Furthermore, longitudinal research is needed
Please cite this article as: Goldberg, A., et al., Sweet and Sensitive: Sensory Processing Sensitivity and Type 1 Diabetes, Journal of Pediatric Nursing (2017), https://doi.org/10.1016/j.pedn.2017.10.015
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to evaluate whether SPS is a risk factor for the development of T1D; expanding the research to other autoimmune diseases is also suggested. Acknowledgments The authors thank the study participants and the clinic staff at the Ziv Medical Center juvenile diabetes clinic, and the volunteer participants, without whom the study would not have been possible. We express gratitude to Prof. Arthur Aron, Prof. Michael Pluess and Prof. Miri Scharf for their comments on an early version of the article. There are no potential conflicts of interest relevant to this article. Author contributions AG acquired, analyzed, and interpreted the data; drafted the manuscript; reviewed the manuscript for important intellectual content; and approved the final version of the manuscript submitted. AG is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. ZE, CF, and RF recruited the participants at the Juvenile Diabetes clinic, collected and coded the data to the computer. SC initiate the collaboration between Tel-Hai college and Ziv Hospital’ juvenile diabetes clinic and approved the final version of the manuscript submitted. ODG was in charge of carrying out and implementing the research program, responsible for its acceptable and appropriate ethical standards, and oversaw the provision for full clinical services, which was enhanced by the patient's participation and cooperation with the research project. References Acevedo, B. P., Aron, E. N., Aron, A., Sangster, M. -D., Collins, N., & Brown, L. L. (2014). The highly sensitive brain: An fmri study of sensory processing sensitivity and response to others' emotions. Brain and Behavior, 4(4), 580–594. https://doi.org/10.1002/ brb3.242. Aron, A., Ketay, S., Hedden, T., Aron, E. N., Rose Markus, H., & Gabrieli, J. D. E. (2010). Temperament trait of sensory processing sensitivity moderates cultural differences in neural response. Social Cognitive and Affective Neuroscience, 5(2–3), 219–226. https://doi.org/10.1093/scan/nsq028. Aron, E. N., & Aron, A. (1997). Sensory-processing sensitivity and its relation to introversion and emotionality. Journal of Personality and Social Psychology, 73(2), 345–368. https://doi.org/10.1037/0022-3514.73.2.345. Aron, E. N., Aron, A., & Jagiellowicz, J. (2012). Sensory processing sensitivity: A review in the light of the evolution of biological responsivity. Personality and Social Psychology Review, 16(3), 262–282. https://doi.org/10.1177/1088868311434213. Aron, E. N., Aron, A. F., & Davies, K. M. (2005). Adult shyness: The interaction of temperamental sensitivity and an adverse childhood environment. Personality and Social Psychology Bulletin, 31(2), 181–197. https://doi.org/10.1177/0146167204271419. Benham, G. (2006). The highly sensitive person: Stress and physical symptom reports. Personality and Individual Differences, 40(7), 1433–1440. https://doi.org/10.1016/j. paid.2005.11.021. Carter, W. R., Herrman, J., Stokes, K., & Cox, D. J. (1987). Promotion of diabetes onset by stress in the bb rat. Diabetologia, 30(8), 674–675. https://doi.org/10.1007/ BF00277327. Carver, C. S., & White, T. L. (1994). Behavioral inhibition, behavioral activation, and affective responses to impending reward and punishment: The bis/bas scales. Journal of Personality and Social Psychology, 67(2), 319–333. https://doi.org/10.1037/00223514.67.2.319. Chen, C., Chen, C., Moyzis, R., Stern, H., He, Q., Li, H., ... Dong, Q. (2011). Contributions of dopamine-related genes and environmental factors to highly sensitive personality: A multi-step neuronal system-level approach. PLoS One, 6(7), e21636. https://doi. org/10.1371/journal.pone.0021636. Compas, B. E., Jaser, S. S., Dunn, M. J., & Rodriguez, E. M. (2012). Coping with chronic illness in childhood and adolescence. Annual Review of Clinical Psychology, 8, 455–480. https://doi.org/10.1146/annurev-clinpsy-032511-143108. Cunningham, N. R., Vesco, A. T., Dolan, L. M., & Hood, K. K. (2011). From caregiver psychological distress to adolescent glycemic control: The mediating role of perceived burden around diabetes management. Journal of Pediatric Psychology, 36(2), 196–205. https://doi.org/10.1093/jpepsy/jsq071. Dunn, W. (2001). The sensations of everyday life: Empirical, theoretical, and pragmatic considerations. American Journal of Occupational Therapy, 55(6), 608–620. https:// doi.org/10.5014/ajot.55.6.608. Eysenck, H. J. (1991). Biological dimensions of personality. In L. A. Pervin (Ed.), Handbook of personality (pp. 244–276). New York, NY: Guilford. Gray, J. A. (1991). The neuropsychology of temperament. In J. A. Strelau, & A. Angleitner (Eds.), Explorations in temperament: International perspectives on theory and measurement (pp. 105–128). New York, NY: Plenum.
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Please cite this article as: Goldberg, A., et al., Sweet and Sensitive: Sensory Processing Sensitivity and Type 1 Diabetes, Journal of Pediatric Nursing (2017), https://doi.org/10.1016/j.pedn.2017.10.015