Self silencing mediates the effects of adverse childhood

experiences and Fibromyalgia symptoms

Thesis submitted to the University of Plymouth for the MSc in

Psychology by Eugenie Walker

2020
Statement of Ethical Compliance

The work reported in this thesis received ethical approval from the Faculty of Health

and Human Science and complies within the guidelines set by the British

Psychological Society.

1
Acknowledgment

A very big thank you to my supervisor, Alison Bacon who’s unstinting patience and

encouragement kept me going. Her enthusiasm and support throughout the last two

years has been invaluable and I feel very lucky to have had her as my supervisor.

I would also like to thank Jacko, whose encouragement throughout the MSc meant

so much. I’m grateful to him for getting me to start the first paragraph of this

dissertation and sad that he will not be able to see the finished product.

This is for you.

Thank you to the rest of my family – Elliot, Mia, Chloe, Marv, Tom, Ruth, Suzy and

Elly for all your support and guidance over the past few years. You’ve been amazing.

2
Contents

Table of Figures…………………………………………………………………….4

List of Tables………………………………………………………………………..5

1. Abstract………………………………………………………...……………………6

2. Introduction…………………………………………………………………………7

2.1 Adaptive Network theory…………………………………………………...…10

2.2 Adverse Childhood Experiences…………………………………….……... 11

2.3 Silencing the Self…………………………………………………………...…12

3. Methods…………………………………….…………………………………...…17

3.1 Participants…………………………………………..................................…17

3.2 Materials and procedures…………………………………………...………..17

4. Results…………………………………………………………………………...…21

4.1 Data analysis………………………………...……………………………...…21

4.2 Correlational analysis…………………………………………...…………….22

4.3 Regression analysis…………………………………………...………………25

4.4 Mediation analysis…………………………………………...………………..26

5. Discussion…………………………………………...…………………………….28

5.1 Limitations………………………………………………………………………32

6. Reference List…………………………………………...………………………..34

7. Appendices……………………………………………………………...……...…46

Appendix A - Brief…………………………………………..............................…46

Appendix B - Debrief…………………………………………...………………….48

3
Table of Figures

Figure 1

Mediation effects of externalised self-perception and divided self on the direct effect

of ACEs on FMS symptoms……………………………………………………………27

4
List of Tables

Table 1
Symptom Clusters and Diagnostic Category (Melidis et al., 2017) …………………18

Table 2
Means and standard deviations measured by diagnosis…………………………..…21

Table 3
Correlations among symptoms, ACEs and silencing the self for non-diagnosis
sample………………………………………………………………………………………22

Table 4
Correlations among symptoms, ACEs and silencing the self for diagnosis sample..23

Table 5
Correlations among ACEs, silencing the self and symptom clusters for diagnosis
sample ……………………………………………………………………..…………….…24

Table 6
Results of hierarchical multiple regression analysis on FMS symptoms, ACEs and
silencing the self. ……………………………………………………………………….…25

Table 7
Indirect effects on the association between ACEs and FMS symptoms observed…27

5
Abstract

Fibromyalgia Syndrome (FMS) is a functional disorder causing widespread

pain with an aetiological relationship to Adverse Childhood Experiences (ACEs). The

present study examined this relationship and also whether FMS symptomatology is

mediated by the construct of self-silencing. Participants completed the Adverse

Childhood Experiences questionnaire, the General Symptoms Questionnaire of FMS

and the Silencing the Self Scale (N = 153). The results showed positive associations

between ACEs and FMS. The symptoms of FMS were enhanced when mediated by

the self-silencing factors of Externalised Self Perception and the Divided Self. The

data supports previous literature indicating the positive association between ACEs

and FMS, in addition to greater FMS symptomatology when mediated by self-

silencing.

Findings may help improve the evaluation and treatment of individuals with

FMS based on their unique psychological constructs around sustaining relationships.

6
2. Introduction

The aim of the research explores whether characteristics of silencing the self

enhances fibromyalgic symptoms in those who have suffered childhood trauma.

Review of the literature reveals many studies and meta-analyses that suggest

an aetiological (causal) relationship between childhood trauma and fibromyalgia

(Häuser et al., 2011; Olivieri et al., 2012; Van Houdenhove & Luyten, 2006; Van

Houdenhove, Luyten & Egle, 2009; Varinen et al., 2017), however, there has been

no specific study that looks at the role of self-silencing as a possible mediating factor

between adverse childhood experiences (ACEs) and the symptoms of Fibromyalgia

syndrome (FMS).

Fibromyalgia is a syndrome with a global mean prevalence of 2.7 percent

(Queiroz, 2013). It is characterised by chronic, severe musculoskeletal tenderness

and pain, including sleep and mood disorders and ‘fibrofog’, a word utilised by FMS

patients to describe the typical cognitive dysfunction they feel (Borchers & Gershwin,

2015). Additional functional symptoms include chronic fatigue, disrupted sleep

patterns, headaches, migraines, Irritable Bowel Syndrome (IBS; abdominal pain

accompanied by constipation, diarrhoea or both) cognitive difficulties (memory and

concentration) and depression (Queiroz, 2013) and is known as a functional disorder

due to the lack of detectable pathology under medical examination. The symptoms

can be debilitating and prognosis is generally poor (Hvidberg et al., 2015) with some

patients rejecting the limited treatment options available, such as prescribed

medications (Chambers et al., 2006). As a result, functional disorders like FMS can

have a considerable economic impact on healthcare systems and patients

themselves (Skaer, 2014).

7
 Increasing evidence suggests a central sensitivity syndrome (CSS) is

responsible for functional disorders such as FMS. The central nervous system

becomes hyper-aroused and oversensitive to the processing and transmission of

pain. This in turn leads to chronic pain due to the elaboration of painful and non-

painful stimuli (Clauw, 2015, Yunus, 2015). Stress has been implicated as a possible

contributor to the pathogenesis (onset) of CSS in genetically predisposed individuals

and studies suggest those with FMS have found functional abnormalities in the

hypothalamic-pituitary adrenal axis (HPA) and autonomic nervous system linked to

abnormal stress level reactivity (Martinez-Lavin, 2007; Woda, Picard & Dutheil,

2016) However, our understanding of the pathogenesis and aetiology of FMS is not

fully complete as research has struggled to explain whether symptoms are biological

(ie. disease) or psychological in origin.

Two further explanations arise from the psychological and the biological

model in that functional disorders should be labelled one (a bodily distress system)

and many (eg. FMS, IBS, Chronic fatigue syndrome [CFS]). From the psychological

viewpoint, one explanation is the lumper hypothesis (Melidis, Denham & Hyland,

2017) which suggests that functional disorders are a category of mental illness that

can be explained via psychological theories and are therefore considered as somatic

disorders (mental distress leads to bodily distress) needing psychiatric or

psychological intervention (Barksy & Borus, 1999). The psychological and psychiatric

theories include somatization and cognitive hypotheses (illness-related cognitions

precipitate maladaptive behaviours). From this perspective the theories can explain

the psychological pathogenesis and comorbidities of psychological disorders that

predicts one type of functional disorder which varies along many dimensions

(Wessely et al., 1999). However, the second explanation or splitter hypothesis

8
suggests functional disorders like FMS are examples of diseases that are yet to be

identified. Indeed, biologically there are immunological, endocrinal and neurological

differences that have been and continue to be discovered in patients with functional

disorders and those that are healthy (Cleare, 2003; Fukudo, 2013; Hornig et al.,

2015; Woolf, 2011), but they do not consistently differ between functional disorders.

Despite this failure, there is hope that a specific psychological illness

(psychopathology) will be uncovered for each functional disorder (Woolf, 2011). In

summary, the splitter and lumper hypotheses are both evidenced through

symptomatology with the literature supporting a general consensus in favour of an

integration of both splitter and lumper hypotheses and as such, an integration of

psychological and biological disease processes (Kanaan et al., 2007; Lacourt et al.,

2013).

Two network theories have aided the interpretation of data supporting splitter

and lumper hypotheses. One is symptom network theory (SNT) based on the

assumption that symptoms are part of a causal network whereby one symptom

causes another, ie. a kind of domino effect. One example could be anxiety leading to

sleep problems which then causes fatigue followed by depression. There is a

rationale behind SNT where one psychological symptom causes another especially

in mental illness where SNT is used extensively (Borsboom & Cramer, 2013; Nuijten

et al., 2016). However, it is harder to apply SNT in the case of functional disorders

where the psychological symptoms coexist alongside somatic symptoms of disorders

like FMS (Scolnik et al., 2016).

Adaptive Network Theory (ANT; Hyland, 2017) is the second model which

proposes a new paradigm comprised of biological and psychological, neurological

and immunological mechanisms within a network of emergent properties.

9
 2.1 Adaptive Network Theory

ANT works on the assumption that symptom clusters are caused by

biological mechanisms and these different mechanisms lead to different groups of

symptoms (Hyland, 2017). In other words, the ANT proposes that repeated failure of

the individual to respond to chronic stress by behaviour-inhibiting symptoms or ‘stop

signals’ leads to the formation of functional disorders. Stop signals change the

control system by inhibiting behaviours through creation of psychological symptoms

such as fatigue, pain, nausea and depression. The stop signal production and the

symptoms arising as a consequence are adaptive in changing the behaviour of the

individual so they reduce activity and allow regeneration. Ignoring the stop signals

causes them to potentiate, resulting in functional disorders (Hyland, 2017). Mounting

evidence demonstrates a sustained stress response can lead to the presentation of

somatic symptoms such as chronic fatigue and pain (Hyland 2002; 2011; Kemeny,

2009). Furthermore, ANT suggests a spectrum of disorders as opposed to distinct

functional disorders due to the polysymptomatic nature of FMS, CFS and IBS.

Thus, the two network models comprised of SNT and ANT illustrate the

covariation and specificity of symptomatology in functional disorders. However, ANT

resolves some of the questions unanswered by SNT by explaining the covariation of

the somatic symptoms of functional disorders (Melidis et al., 2018). It has previously

been used to explain diseases (Hyland, 1999; Hyland 2001a), CFS (Hyland 2001b)

and FMS (Hyland 2002), and is reinforced by evidence that risk factors, including

biological and psychological variables related with these disorders are those

predicted by the theory. As a result, ANT is potentially the better model when

describing symptomatology of disorders like FMS.

10
 Regarding the aetiology of functional disorders like FMS, there is a growing

body of statistical evidence that suggests traumatic experiences in childhood can

have a direct effect on FMS symptomatology in adulthood (Hauser et al., 2011; Lee,

2010; Olivieri et al., 2012).

2.2 Adverse Childhood Experiences

The aetiology of FMS has recently been linked to and is gaining momentum

regarding the concept of a genetic vulnerability within certain populations more

predisposed to developing FMS as a result of specific environmental triggers (Ablin,

Neumann & Buskila, 2008; Borchers & Gershwin, 2015; Yunus, 2007). Triggers

which have been highlighted as precipitating the onset of FMS include chronic

infection, physical and psychological trauma (Buskila, 2009; Yunus, 2007).

The ACE study (Felitti et al., 1998) of 17,000 adults found strong evidence of

the negative effects of Adverse Childhood Experiences (ACEs) or trauma on health,

with results indicating a significant relationship between the number of ACEs

reported and the number of negative health problems and behaviours (eg. smoking,

obesity, sexually transmitted diseases and drug/alcohol abuse) in adulthood.

Norman et al’s. (2012) review on the health consequences of childhood abuse

concluded that children who have suffered physical and emotional abuse or neglect

experience changes to their neurobiological development making them more

susceptible to psychological, physical, cognitive, social and emotional challenges.

Patients with FMS who reported ACEs have high allostatic load scores ie. a

physiological measure of wear and tear (Imbierowicz & Egle, 2003),

immune/inflammatory disorders (Danese et al., 2007), disruption to normal daily

cortisol systems, (Weissbecker et al., 2006), HPA (Hypothalamic-pituitary-adrenal)

axis dysfunction which regulates stress hormones such as cortisol (Calis et al.,

11
2004), as well as long term endocrinal (hormonal) regulation (Yeung, Davis, &

Ciaramataro, 2016). In addition, Afari et al’s. (2014) meta-analysis found individuals

who have experienced traumatic childhoods are 2.7 times more likely to be

diagnosed with a functional somatic syndrome. These findings are robust against

publication bias and poor study quality that had previously been cited as confounding

factors by Häuser et al.’s (2011) meta-analysis. Moreover, Lee (2010) and Olivieri et

al. (2012) show significant associations between ACEs and pathogenesis of FMS,

thereby adding to the evidence that childhood abuse and FMS have a significant

relationship. It is important to add the caveat of ACEs being one factor in the

complex aetiology of FMS (Jones, 2014) nevertheless, there is strong evidence to

suggest that trauma is involved in the development of FMS in a significant number of

patients (Yavne et al., 2018).

Lastly, childhood trauma has been shown to act as a predictor for FMS and in

relationship to depression in adulthood (Olivieri, 2012). Depression has also been

strongly associated with the construct of self-silencing whereby individuals silence

their thoughts and feelings from their partners (Duarte & Thompson, 1999;

Thompson, 1995).

2.3 Silencing the Self

Silencing the self theory was developed through Jack’s (1991) longitudinal

work with women who were clinically depressed. Jack (1991) conceptualised the

theory of silencing the self as a relational strategy where women ‘silence certain

thoughts, feelings, and actions (Jack & Dill, 1992, p.98). As a result, cognitive

schemas are constructed which concern how women create and sustain safe and

intimate relationships (Jack, 1991). Jack (1991) suggests that self-silencing in

females is evoked by environmental elements that direct socially acceptable

12
feminine behaviour. This can lead to women ‘silencing’ or suppressing specific

thoughts, feelings and behaviours from their romantic partners due to fear of conflict

within the relationship or loss of the relationship. By negating their own needs and

desires, self -silencing contributes to lowering self-esteem, loss of sense of self, and

ultimately depression (Jack, 1991).

The psychometric scale was developed to measure the construct of self-

silencing, and is comprised of four subscales which measure the central dimensions

hypothesised to consider the dynamics of depression. These are Externalised Self

Perception (ESP), Care as Self Sacrifice (CASS), Silencing the Self (STS), and the

Divided Self (DS; Jack & Dill, 1992). However, it is of note that the factor structure

which is based on the four factor oblique structure varies across studies (Cramer &

Thoms, 2003; Jack & Dill, 1992; Stevens & Galvin, 1995). Cramer & Thoms (2003)

as an example, found that two of the factors; ESP and DS identified within their

female sample collapsed into a single factor for the male sample. In addition, other

studies use just the global self-silencing scores without the four factors (Ali, Oatley &

Turner, 2002; Besser & Flett, 2003) or have removed some of the questions within

the factors entirely due to recommendations for scale revision (Stevens & Galvin,

1995).

For the first factor, women who score highly on the silencing the self scale

(STSS) are likely to have an externalised self-perception whereby they are more

disposed to evaluate themselves based on the perception of others.

The second and third factors are linked to women’s interpersonal behaviour.

The women engage on the act of inhibiting or silencing their voice in relationships

and tend to evolve from three different fears which are seen as the impetus behind

self-silencing.

13
 1. Fearing the destruction of their security and that of their children. In

relationships where the woman is financially reliant on their partner, the

choice to self-silence is the preferable option when compared with divorce

or suicide.

2. Women who feel worthless or unlovable will tend to self-silence in an

attempt to mask their true self and thus protect themselves from potential

relationship breakdown.

3. Women who fear that their feelings are wrong and that by giving voice to

those feelings they open themselves to rejection by others.

The third subscale of care as self-sacrifice explores the different way in which

self-silencing women understand care. They are more likely to measure and define

care in relation to the self-sacrifice they make in a relationship. As a result of the

devalued position of women in society, women make some attempt to match their

worth by making personal sacrifices.

The final subscale of STSS is related to the phenomenology of depression

whereby women experience a ‘divided self’. In other words there is a separation

between the external ‘false self’, (the self outwardly portrayed that conforms to the

partner’s views and needs) and the ‘inner self’ (the concealed self that wants to

leave or experiences high levels of suppressed anger and hostility against their

situation). The external self tries to comply with societal expectations of female

goodness as the resentment and anger builds internally due to unfulfilled needs. As

a result of the divided self, women experience a disconnection from themselves

along with a lack of relational intimacy with their partners (Jack, 1991).

There is continued discourse surrounding the definition of whether self-

silencing is actually a personality trait as Jack (1991) asserts that traditional cultural

14
perceptions of femininity and female social behaviour are social constructs, leading

to specific internal cognitive schemas in women and therefore cannot be termed as a

static trait. Seeley (2003) goes further arguing that self-silencing is influenced by

personality traits and the level of self-silencing is determined not only by

environmental and cultural factors but also by the self-silencing individual’s

temperament moderated by the romantic partner’s temperament. From this

perspective, it can then be argued it is temperament that is also fundamental in how

much an individual will self-silence. Temperament has shown itself to be fairly stable

within individual differences of behaviour displayed from early childhood in humans

(Buss & Plomin, 1984; Chess & Thomas, 1977) and is determined to a high degree

by biological factors such as heritability (Buss & Plomin, 1984).

In addition, associations exist within personality trait vulnerabilities showing

high levels of socially prescribed perfectionism in those who self-silence whereby

they may suffer from chronic stress that can impact health (Besser et al., 2010).

Chronic stress stems from a sense of inferiority and self-reproach which arises from

the unrealistic and idealistic standards that the self-silencing individual uses to judge

the self (Besser et al., 2010; Jack, 1999). In addition, chronic stress is already

implicated as a major factor for FMS with raised cortisol levels (Weissbecker et al.,

2006) and dysfunction within the HPA axis which regulates cortisol (Calis et al.,

2004). Indeed, individuals with Chronic Fatigue Syndrome, who are overwhelmed

with unexplainable fatigue, share many comorbidities with FMS (Clauw,

& Chrousos,1997), and are more likely to put others first, judge themselves by

external standards and present as outwardly compliant in social situations whilst

feeling internally hostile (Hambrook et al., 2011). Furthermore, the functional

15
disorder of Irritable Bowel Syndrome is significantly correlated with a high score for

self-silencing, self-blame and emotional abuse (Ali et al., 2000).

Despite Jack and Dill’s (1992) hypothesis that women self-silence more than

men, more recent research has indicated the reverse with men self-silencing more

than women, particularly as a divided self or through externalised self-perception

(Cramer & Thoms, 2003). It has been suggested that there are different reasons for

men self-silencing as they may use it to maintain power in the relationship by self-

concealment to their partner, (Page et al., 1996) or because they lack the emotional

vocabulary that is more typical to women, to express their emotional or relational

needs (Gratch, 1995). The results showing higher levels of self-silencing in men

have important implications for Jack’s (1991) model and theories of gendered

depression. Further research is needed in this area to explore how gender roles,

motivation and temperaments may mediate the relationship between self-silencing

and depression in men and women. Regardless, it is important to note that

psychometric investigations generally support the reliability and validity of the STSS

when used with males and females equally (Cramer & Thoms, 2003).

In summary there is enough evidence to suggest that self-silencing may have

a mediating potential with increased FMS symptomology when combined with ACEs.

Hypotheses: Individuals with high ACE scores will report a greater incidence

of FMS symptoms. When mediated by those with high STSS scores, FMS

symptoms will be further enhanced.

The hypotheses are expected in the FMS sample and student sample.

However, it is expected that the students will present with a lower level of

symptomatology in comparison .

16
3. Methods

3.1. Participants

A purposive sample of seventy three male and female patient participants (4

men, 69 women, Mage= 46.63, SD= 12.57) were approached through Fibromyalgia

UK who advertised the study to their members via their magazine.

Eighty control participants, all women (Mage= 21.54, SD= 3.92) were students

accessed through Plymouth University’s online participation system and were offered

0.5 points for their participation in the study. They confirmed they were ≥18 years old

and were asked at the end of the questionnaire if they had had a formal medical

diagnosis of either FMS, IBS or CFS.

3.2. Materials and Procedures

Ethical approval for the project was granted by the University of Plymouth

Ethics Board and Cornwall Council Ethics Board.

The participants were provided with a hyperlink where they logged on, read

the brief (Appendix A) and consented to their participation in the online

questionnaire. The study was accessible online from 7/10/19 to 28/02/20 for the FMS

sample and between 25/03/19 and 17/05/19 for the student sample.

The participants were not needed for the remainder of the study after completion of

the questionnaires and were accordingly debriefed (Appendix B). Their data was

anonymised through participant self-generation of a unique ID code.

All of the participants were required to complete three short self-report online

questionnaires:

17
 General Symptom Questionnaire (GSQ65; Hyland & Sodergren, 1998). The

GSQ65 consists of a list of 65 symptoms, grouped into 11 symptom clusters which

were previously obtained through a machine learning procedure (Melidis et al.,

2017). In principal they are differentiated by physical or mental symptoms (Table 1).

Two clusters were removed for this analysis, being made up of just one

symptom each – frequent urination and tinnitus. Both are low frequency and low

severity symptoms and have been omitted in previous research for this reason

(Melidis et al., 2017).

The GSQ65 was designed to be used with functional disorders such as IBS,

FMS or CFS. Self-report ratings are obtained through a 6 point frequency scale of

how often these symptoms are experienced from 0 = never or almost never, 1 = less

than 3 or 4 times a year, 2 = every month or so, 3 = every week or so, 4 = more than

once a week, 5= every day, with a maximum score of 390 and good internal

consistency (α = 0.98).

Table 1
Symptom Clusters and Diagnostic Category (Melidis et al., 2017)
Cluster number and Symptoms
diagnostic category
1. Fatigue/cognitive Fatigue for no reason; Fatigue increasing the
day after you are active; Easily feel too
hot/sweating; Difficulty getting to sleep; Waking
up often at night

2. Hypothalamic/ Nightmares/night terrors; Head cold, sore throat

pituitary/adrenal or ‘flu; Mouth ulcers (sores in mouth); Cold
sores(on or near lips); Skin rash; Boils or
pimples on face or body; Twitching of eyelid;
Twitching other than eyelid; Choking
sensations; Loss of voice; Double vision

3. Limbic System Chest pain; Heartburn; Nausea for no reason;

Very vivid dreams; Racing heart; Feeling faint;
Feeling very ill for no reason

4. Atopy Thirsty all the time; Blocked nose; Running

nose; Itchy skin; Itchy eyes

18
 5. Central sensitisation Pain in legs and arms (which is not due to hard
exercise); Pain moving from one place of body
to another on different days; Backpain;
Sensitive or tender skin; Pain increasing the day
after you are active; More clumsy than others;
Sensitivity to bright lights; Sensitivity to noise

6. Gastric Headaches; Stomach pain; Diarrhoea;

Constipation; Bloating of the stomach; Intolerant
to some food

7. Mood Depression; Feeling anxious for no reason;

Irritable; Jittery. Easily startled, often worried

8. Micro-capillary Easily feel too cold; Very cold hands or feet

9. Small nerve fibre Swollen, painful joints; Fatigue increasing after

a cold or sore throat; Hands tremble or shake;
Face flushes; Cramps in leg, foot or bottom;
Numbness/tingling/pins and needles

ACE questionnaire (Felitti et al., 1998). Ten questions make up this

dichotomous survey which retrospectively measures forms of neglect, abuse and

family dysfunctions. Answers are given as either Yes or No with individuals being

assigned a score from 0 to 10 depending on the number of questions positively

answered. Example questions include, ‘Did a parent or other adult in the household

often swear at you, insult you, put you down, or humiliate you or act in a way that

made you afraid that you might be physically hurt?’ and ‘Did you live with anyone

who was a problem drinker or alcoholic or who used street drugs?’

Silencing the Self Scale (STSS: Jack, & Dill, 1992). This is a 31-item Likert

measure designed to access certain schemas regarding the formation and

preservation of close relationships. These schemas are represented by questions

grouped into four subscales made up of Externalised Self Perception (ESP; 6 items)

e.g, ‘I tend to judge myself by how I think other people see me’ Care as Self Sacrifice

(CASS; 9 items) e.g., ‘In a close relationship, my responsibility is to make the other

19
person happy’ Silencing the Self (STS; 9 items) e.g., ‘I don't speak my feelings in an

intimate relationship when I know they will cause disagreement’ and Divided Self

(DS; 7 items) e.g., ‘I feel I have to act in a certain way to please my partner’. Self-

report ratings are obtained through a 5 point scale of how strongly the respondent

agrees or disagrees with the question, anchors being 1 = Strongly disagree, 2 =

Somewhat disagree, 3 = Neither agree nor disagree, 4 = Somewhat agree 5 =

Strongly agree. The subscales showed adequate reliability with the present sample:

ESP α = 0.77, CASS α = 0.74, STS α = 0.88, DS α = 0.87.

20
4.0 Results

4.1 Data Analysis

These statistics were computed using IBM® SPSS version 16.0 after the data

had been organised and transposed from Microsoft® Excel. The aim was to examine

whether the association between ACEs and FMS symptoms was influenced by self-

silencing. Partial correlations were first computed between these variables,

controlling for the effects of a clinical diagnosis. Next, regression analysis was

conducted with FMS symptoms as the dependent variable to determine whether

variance in this factor was accounted for by self-silencing over and above that of

ACEs. Lastly, the mediating effects of self-silencing was tested using Model 4 of the

PROCESS procedure (Hayes, 2018). PROCESS is a macro extension which utilises

tools for mediation into a single, user-friendly command file.

Table 2
Means and standard deviations measured by diagnosis
Measure Diagnosis No diagnosis F(1, 150)
M SD M SD
Symptoms 4.07 0.89 2.91 0.75 8.69**
ACE 3.01 2.31 1.96 1.92 3.05*
STSS Measures
ESP 22.50 5.17 21.11 4.60 1.75*
CASS 31.84 6.74 28.33 6.11 3.36*
STS 28.75 7.48 23.03 7.28 4.79**
DS 29.94 7.80 16.45 6.25 11.75**
*
p < .01
**
p < .001.

Means and standard deviations for the study variables are presented

separately for those with an FMS diagnosis and those without in Table 2. Scores on

FMS symptoms, ACEs and silencing the self subscales were compared using t-tests.

21
An independent t-test showed that the difference between conditions was significant

with higher symptomatology, ACEs and STS subscales recorded for those with an

FMS diagnosis. The size of this effect was strong and significant for symptoms and

the divided self with smaller significant effects recorded for silencing the self, ACEs

and care as self sacrifice. There was no significant effect for ESP.

4.2 Correlational Analysis

Table 3 presents correlations between measures for the non-diagnostic

sample.

Table 3
Correlations among symptoms, ACEs and silencing the self for non-diagnosis sample
Variables 1 2 3 4 5 6
1. Symptoms —
2. ACE .332** —
STSS subscales

3. Externalised self-perception .450** .330** —

4. Care as self-sacrifice .173 .0.41 .525** —
6. Silencing the self .147 .075 .512** .399** —
7. Divided Self .433** .229 .353** .291* .576** —
*
p < .05 (two-tailed)
**
p < .01

Significant associations were found between FMS symptoms and ACEs. In

addition, symptoms were significantly positively related to externalised self-

perception and the divided self. There was a moderate association between adverse

childhood experiences and externalised self-perception. However, there was no

association between FMS symptoms and care as self-sacrifice and silencing the self.

22
Table 4
Correlations among symptoms, ACEs and silencing the self for diagnosis sample
Variables 1 2 3 4 5 6
1. Symptoms —
2. ACE .427** —
STSS subscales

3. Externalised self-perception .537** .382** —

4. Care as self-sacrifice .372** .334** .606** —
6. Silencing the self .307** .234* .575** .526** —
7. Divided Self .782** .298** .424** .323** .298** —
*
p < .05
**
p < .01

Correlations among variables shown in Table 4 present the diagnostic

sample. Significant positive associations were found between FMS symptoms and

ACEs. Higher levels of FMS symptoms and ACEs were positively associated with

higher levels of self-silencing across all four subscales. Divided self had a strong

positive association with FMS symptoms with moderate associations for symptoms

and externalised self-perception, care as self-sacrifice and silencing the self. There

were moderate positive correlations between ACEs and ESP, CASS and DS

respectively. The association with silencing the self and ACEs was weak through

still significant.

Both tables show positive correlations although the diagnostic sample is

stronger.

An additional correlation analysis was run for the diagnostic sample including

the symptom clusters of Fibromyalgia and their relationship with ACEs and self-

silencing subscales (see Table 5).

23
Table 5
Correlations among ACEs, silencing the self and symptom clusters for diagnosis sample
Variables 1 2 3 4 5 6 7 8 9 10 11 12 13 14

1. ACE -

STS subscales

2. ESP .38** -
3. CASS .33** .61** -

4. STS .23* .58** .53** -

5. DS .30** .42** .32** .30** -

Symptom Clusters
6. C 1 .30** .48** .28* .25* .66** -
7. C 2 .43** .32** .30** .19 .53** .42** -
8. C 3 .36** .43** .31** .25* .70** .62** .73** -
9. C 4 .33** .49** .33** .38** .63** .67** .56** .69** -
10. C 5 .27* .38** .29** .18 .68** .83** .52** .59** .66** -
11.C 6 .33** .32** .23* .07 .65** .26* .53** .67** .39** .39** -
12. C 7 .31** .58** .35** .37** .54** .54** .49** .65** .52** .44** .50** -
13. C 8 .22* .36** .15 .12 .50** .46** .36** .31** .43** ..54** .33** .21 -
14. C 9 .30** .50** .25* .25* .58** .75** .62** .74** ..71** .73**. .48** .66** .35** -

Cluster 1: Fatigue/Cognitive, Cluster 2: HPA axis, Cluster 3: Limbic, Cluster 4: Atopy, Cluster 5: Central
sensitisation, Cluster 6: Gastric, Cluster 7: Mood, Cluster 8: Microcapillary, Cluster 9: Small nerve
fibres.
*
p < .05, **p < .01.

Significant positive correlations were found between ACEs and all symptom

clusters. In addition externalised self-perception and the divided self had moderate to

strong significant positive associations with the symptom clusters. Small nerve fibre

(9) symptoms and mood (7) had the strongest significant associations with ESP

whereas there were strong associations for all clusters and DS particularly with

limbic, central sensitisation, fatigue/cognitive symptoms, gastric and atopy

symptoms. Care as self-sacrifice had moderate significant relationships with

symptoms clusters, namely mood, atopy, limbic and HPA axis symptomatology

respectively but no significant relationship with microcapillary symptoms. Silencing

the self as a subscale had moderate significant associations with atopy and mood

24
but weak non-significant correlations with gastric, microcapillary, central sensitisation

and HPA axis symptomatology.

4.3 Regression analysis

A Hierarchical Multiple Regression (HMR) was run with FMS symptoms as the

dependent variable. Age and sex were included as covariates with sex coded as 1

for female (N = 69) and 0 for male (N = 4). Diagnostic status was coded 1 for

diagnosis and 0 for non-diagnosis. Full results are shown in Table 6.

Table 6
Results of hierarchical multiple regression analysis on FMS symptoms, ACEs and silencing the self.

β t Sig. 95% confidence interval Adj. R2

Lower Upper
1. Symptoms
Age .14 1.55 .12 -.002 .02
Diagnosis .41 4.68 < 0.001 .48 1.18
Sex .07 1.14 .26 -.33 1.23
ACEs .32 5.00 < 0.001 .09 .20 .43
2. Symptoms
Age .05 .73 .47 -.01 .01
Diagnosis .11 1.47 .15 -.08 .52
Sex -.002 -.04 .97 -.62 .60
ACEs .13 2.44 .02 .01 .11
Externalised self-perception .29 4.38 < 0.001 .03 .09
Care as self-sacrifice -.02 -.33 .74 -.02 .02
Silencing the Self -.18 -2.71 .01 -.04 -.01
Divided self .62 8.28 < 0.001 .05 .08 .68

The first linear regression model was significant for ACEs: ΔR2 = .45, F (3,148)

= 29.44, p < .001 with Model 1 explaining 43% of the variance in FMS symptoms

(adjusted R2 = .43). Diagnosis showed an association as would be expected

25
according to the literature (Häuser et al., 2011; Olivieri et al., 2012). However,

neither age nor sex was significant.

Model 2 added the STS subscales to explore any increased variance in

symptoms in comparison with just previous covariates and symptoms. This model

was significantly better than model 1: ΔR2 = .25, F(7,144) = 46.20, p < .001

explaining 69% of the variance in FMS symptoms when ESP, CASS, STS and DS

were included (adjusted R2 = .68). ESP and DS were significant predictors with a

reduced effect of ACEs and diagnosis having no effect on symptoms. The significant

predictors in Model 2 were externalised self-perception and the divided self. There

was no effect of CASS on symptoms whilst STS was negatively significant as

posited previously.

4.4 Mediation analysis

The main objective of the research was to investigate whether self-silencing

subscales mediate the association between ACEs and FMS symptomatology.

Mediation was run using Model 4 from Hayes (2018) PROCESS. ACEs were

included as the x variable and FMS symptoms were the y variable. ESP and DS

were the mediators.

Figure 1 represents the outcome analyses to test for the possible mediating

effects of externalised self-perception and the divided self on the relationship

between ACEs and FMS symptoms.

26
Figure 1
Mediation effects of externalised self-perception and divided self on the direct effect of ACEs on FMS
symptoms. Unstandardized coefficients shown. **p < .01.

Table 7 shows the indirect effects observed. Both externalised self-perception

and divided self show significant positive indirect effects.

Table 7
Indirect effects on the association between ACEs and FMS symptoms observed.

Silencing the self factor Indirect effect 95% confidence interval

(Unstandardized B) Lower Upper
Externalised self-perception .03 .11 .07
Divided self .05 .02 .08

27
5. Discussion

The current study was, to the author’s knowledge the first to examine the

association between adverse childhood experiences and fibromyalgic symptoms

mediated by silencing the self. If there was an association between adverse

childhood experiences and fibromyalgic symptomatology then mediation by silencing

the self should enhance FMS symptoms. Relative to the student sample, analyses

revealed there was a strong positive association between FMS individuals who

reported childhood adversities having symptoms, with externalised self perception

and the divided self as significant predictors for greater symptomatology. Consistent

with the prediction, further mediation analysis showed individuals who had

experienced ACEs and had FMS were more likely to have enhanced

symptomatology if they evaluated themselves based on the perception of others, or if

they presented an outwardly compliant self while inwardly feeling subjectively hostile

and angry. In addition, all individual symptom clusters appeared to be affected by

ACES and a divided self. Overall, the results of this study indicate that individuals

who self silence may experience greater FMS symptomatology.

The current study failed to find a prediction for enhamced FMS symptoms

when the factors of STS or CASS were included. This was already noted as a

potential issue as STS has previously been recommended for some minor scale

revision due to low factor loading (Stevens & Galvin, 1995), with other studies (Flett

et al., 2007; Hambrook et al., 2011) finding that the subscales differ in their

relationship strength depending on the disorder, illness or personality trait studied.

For example. Hambrook and colleagues (2011) found anorexia sufferers had higher

levels of CFS symptoms when they tend to define and measure care in relation to

the amount of self-sacrifice they make in a relationship. The aspect of gender can

28
also affect the results with depressed men tending to score more highly for DS and

ESP (Cramer & Thoms, 2003). However, with only four men in the present study’s

diagnostic sample, the strength of their reports could not be considered as

generalisable across the whole study.

With respect to ACEs and FMS, the current study’s findings were consistent

with previous literature that suggests an aetiological relationship between the two

(Hauser et al., 2011; Olivieri et al., 2012; Van Houdenhove & Luyten, 2006). Indeed

it is already acknowledged that the role of chronic stress from traumatic childhoods

may trigger the onset of FMS (Calis et al., 2004; Weissbecker et al., 2006). Further,

Norman et al’s (2012) review established that neurobiological development changes

occur in children who have experienced physical and emotional abuse which results

in physical, cognitive, social and psychological challenges. As a result the present

study can add to the growing empirical research regarding ACEs and FMS.

The present study was the first to show the mediating effect of ESP and DS

as self silencing factors on FMS symptoms. Similar studies with other functional

disorders have indicated comparable findings, with IBS strongly correlated with self

silencing (Ali et al., 2000) although this was measured using the global score of

STSS. Individuals with CFS, which shares many comorbidities with FMS (such as

fatigue, widespread pain and headaches), are also more likely to judge themselves

by external standards and appear outwardly more compliant in social situations

whilst feeling internally hostile (Hambrook et al., 2011). Whilst IBS and CFS are not

definitively the same, they are both considered functional disorders and share

comorbidities with Fibromyalgia. Thus, the current study could be added to a small

but growing body of empirical evidence that support the psychosocial role that self

silencing may have within the pathology of FMS and other functional disorders.

29
 As chronic stress has been identified as a potential cause of FMS, self-

silencing can act as another factor in enhancing FMS symptoms as the individuals

may be unable to vocalise their stress and anxieties for fear of rejection from their

partners. Besser and colleagues (2010) suggest chronic stress arises from a sense

of inferiority and self reproach due to socially prescribed perfectionism, resulting from

unrealistic and idealistic standards that the self silencing individual uses to judge the

self. As the stress becomes overwhelming the individual may become depressed,

which in turn acts as the potential trigger for FMS onset (Hyland, 2002; 2011,

Kemeny, 2009; Martinez-Lavin, 2007). This would also correspond with Hyland’s

(2017) Adaptive Network Theory as a series of tipping points initiated by ignoring

stop signals and the individual failing to inhibit harm causing behaviours. Indeed,

Hyland (2017) suggests an individual may fail to respond to stop signals as a result

of social and family obligations and therefore continue in an activity despite feeling

pain and fatigue in pursuit of some higher goal, consistent with the construct of self-

silencing.

The current study found strong correlations between ACEs and all nine

symptom clusters which concurs with the concept of sustained stress and trauma as

a major contributory factor to the widespread pain of central sensitisation (Clauw &

Chrousos, 1997), and raised cortisol levels (Weissbecker, et al., 2006) which are all

part of the pathology of FMS. This was in contrast to a review (Tanriverdi et al.,

2007) which found hypocortisolemia (depressed cortisol levels) indicating an

underactive stress response system. However, Calis and colleagues (2004) found

that more than 95% of the patients with FMS in their study had HPA axis dysfunction

which guided their conclusion that dysregulation of the central stress axis leads to

FMS symptom onset. It was further noted that HPA axis dysregulation predisposed

30
individuals to develop stress related disorders in adulthood. Collectively however, the

investigations on HPA axis function in individuals with FMS indicate that ACEs and

sustained activation of the body’s stress response system may be a factor in the

aetiology and progression of the syndrome. In addition, mood as a symptom cluster

was also associated ACEs whereby an individual with FMS will suffer from

depression, anxiety and irritability corresponding with Olivieri (2012) who found

childhood trauma to be a predictor of FMS and depression in adulthood.

Discovering the significant relationships between ACEs and specific FMS

symptom clusters was an interesting result as this perspective has not been

investigated before as far as the author is concerned. However, the mechanisms to

study these relationships were not present in the current study but it is important to

recognise the associations as highlighted by biological literature research exploring

ACEs and FMS, and therefore could be investigated in future research.

The correlational analysis also indicated significant relationships between self

silencing and certain symptom clusters. It would be expected that the divided self,

being most concerned with the phenomenology of depression (Jack & Dill, 1992)

would have had the strongest relationship with the Mood cluster. However, chest

pain and a racing heart from the Limbic cluster and Central Sensitisation cluster had

the strongest relationships. The concept of the divided self and the split between

external ‘false’ self and what the internal ‘true’ self actually wants may be more

strongly related to Clauw & Chrousos’s (1997) theories of sustained stress being a

key contributory factor to central sensitisation. Again, the mechanisms to study

these relationships further were not present and at first glance appears to show

consistency with the literature and would need further investigation.

31
 5.1 Limitations

There are some limitations of the present study that need to be considered in

the interpretation of the findings. For one, it is important to note that causality can

not be inferred among the variables in the study and as a result it is not possible to

conclude definitively that ACEs precede FMS symptoms. A controlled longitudinal

study would be one way of addressing this issue directly. For instance, an

exploration could establish the timing of the ACEs and their temporal relation to the

onset of symptoms.

Low sample size was another limitation with only 153 participants in total with

73 individuals in the FMS sample. Greater sample size would increase the power

and generalisability of the findings. The present study also used the student

population of Plymouth University who’s mean age was twenty years lower to that of

the FMS participant sample. It could be argued that the student sample is not

representative of the general population however they would have come from a

varied socio-economic demographic thereby mitigating some of the more obvious

issues regarding representativeness.

Lastly, there are limitations generally with psychometric questionnaires and

self-report. Due to questionnaires being completed online and not under controlled

experimental conditions it could be argued that inattentive or random responses

might have skewed the data in addition to social desirability issues. However, as

online platforms are commonly used for psychometric research there is evidence to

suggest that the resulting data is reliable and candid (Woods et al., 2015).

32
 Future research could investigate other psychosocial constructs such as

social support and self-efficacy as variables within the FMS population as these

could show a reduced level of symptomatology.

In addition, further studies are needed in relation to traumatic childhood

adversities and social experiences on epigenetic programming and by taking a

greater look at disease aetiology, progression and outcomes. A viewpoint such as

this is relevant in chronic pain disorders such as FMS where ACEs may be a

significant risk factor for later development of the syndrome.

A more sensitive study exploring the symptom clusters specifically with ACEs

could elicit more detailed findings and understanding through the deconstruction of

the ACE questionnaire and studying the individual adverse childhood experiences

and their aetiological relationship with specific Fibromyalgic clusters.

33
7. References

Ablin, J., Neumann, L., & Buskila, D. (2008). Pathogenesis of fibromyalgia–a

review. Joint Bone Spine, 75(3), 273-279.

Ablin, J. N., Zohar, A. H., Zaraya-Blum, R., & Buskila, D. (2016). Distinctive

personality profiles of fibromyalgia and chronic fatigue syndrome patients. PeerJ, 4,

doi:10.7717/peerj.2421.

Afari, N., Ahumada, S.M., Wright, L.J., Mostoufi, S., Golnari, G., Reis, V., & Cuneo,

J.G. (2014). Psychological trauma and functional somatic syndromes: a systematic

review and meta-analysis. Psychosomatic Medicine, 76, 2–11.

Ali, A., Toner, B. B., Stuckless, N., Gallop, R., Diamant, N. E., Gould, M. I., & Vidins,

E. I. (2000). Emotional abuse, self-blame, and self-silencing in women with irritable

bowel syndrome. Psychosomatic Medicine, 62(1), 76-82.

Barsky, A. J., & Borus, J. F. (1999). Functional somatic syndromes. Annals of

internal medicine, 130(11), 910-921.

Besser, A., Flett, G. L., & Hewitt, P. L. (2010). Silencing the self and personality

vulnerabilities associated with depression. In D.C. Jack & A. Ali (Eds.), Silencing the

self across cultures: Depression and gender in the social world (pp. 285-312). New

York, NY, US: Oxford University Press.

34
Borchers, A. T., & Gershwin, M. E. (2015). Fibromyalgia: a critical and

comprehensive review. Clinical reviews in allergy & immunology, 49(2), 100-151.

Borsboom, D., & Cramer, A. O. (2013). Network analysis: an integrative approach to

the structure of psychopathology. Annual review of clinical psychology, 9, 91-121.

Bowlby, J. (1982). Attachment and loss: retrospect and prospect. American journal of

Orthopsychiatry, 52(4), 664-678.

Burri, A., Lachance, G., & Williams, F. (2015). A discordant monozygotic-twin

approach to potential risk factors for chronic widespread pain in females. Twin

Research and Human Genetics,18, 188-197.

Buskila, D. (2009). Developments in the scientific and clinical understanding of

fibromyalgia. Arthritis research & therapy, 11(5), 242.

Buss, A. H., & Plomin, R. (1984). Theory and measurement of EAS. Temperament:

Early developing personality traits, 84, 104.

Calis, M., Gökçe, C., Ates, F., Ülker, S., Izgi, H. B., Demir, H., ... & Kelestimur, F.

(2004). Investigation of the hypothalamo-pituitary-adrenal axis (HPA) by 1 μg ACTH

test and metyrapone test in patients with primary fibromyalgia syndrome. Journal of

Endocrinological Investigation, 27(1), 42-46.

35
Chambers, D., Bagnall, A. M., Hempel, S., & Forbes, C. (2006). Interventions for the

treatment, management and rehabilitation of patients with chronic fatigue

syndrome/myalgic encephalomyelitis: an updated systematic review. Journal of the

Royal Society of Medicine, 99(10), 506-520.

Chess, S., & Thomas, A. (1977). Temperamental individuality from childhood to

adolescence. Journal of the American Academy of Child Psychiatry, 16(2), 218-226.

Choi, K., Vickers, K., & Tassone, A. (2014). Trait Emotional Intelligence, Anxiety

Sensitivity, and Experiential Avoidance in Stress Reactivity and Their Improvement

Through Psychological Methods. Europe’s Journal of Psychology, 10(2), 376–404.

doi:10.5964/ejop.v10i2.754.

Clauw, D.J., & Chrousos, G.P. (1997). Chronic pain and fatigue syndromes:

overlapping clinical and neuroendocrine features and potential pathogenic

mechanisms. Neuroimmunomodulation, 4, 134–153.

Clauw, D.J. (2015). Fibromyalgia and related conditions. Mayo Clinic Proceedings,

90, 680–692.

Cleare, A. J. (2003). The neuroendocrinology of chronic fatigue syndrome.

Endocrine reviews, 24(2), 236-252.

36
Cooper, A., & Petrides, K. V. (2010). A psychometric analysis of the Trait Emotional

Intelligence Questionnaire-Short Form (TEIQue-SF) using Item Response Theory.

Journal of Personality Assessment, 92, 449-457.

Cramer, K. M., & Thoms, N. (2003). Factor structure of the silencing the self scale in

women and men. Personality and Individual Differences, 35(3), 525-535.

Danese, A., Pariante, C. M., Caspi, A., Taylor, A., & Poulton, R. (2007). Childhood

maltreatment predicts adult inflammation in a life-course study. Proceedings of the

National Academy of Sciences, 104(4), 1319-1324.

Duarte, L. M., & Thompson, J. M. (1999). Sex differences in self-

silencing. Psychological reports, 85(1), 145-161.

Felitti, V.J., Anda, R.F., Nordenberg, D, Williamson, D.F., Spitz A.M., Edwards, V.K.,

Koss, M.P., & Marks, J.S., (1998). Relationship of childhood abuse and household

dysfunction to many of the leading causes of death in adults: The Adverse Childhood

Experiences (ACE) Study. American Journal of Preventative Medicine, 14(4), 245-

258.

Flett, G. L., Besser, A., Hewitt, P. L., & Davis, R. A. (2007). Perfectionism, silencing

the self, and depression. Personality and Individual Differences, 43(5), 1211-1222.

Fukudo, S. (2013). IBS: Autonomic dysregulation in IBS. Nature Reviews

Gastroenterology & Hepatology, 10(10), 569.

37
Hambrook, D., Oldershaw, A., Rimes, K., Schmidt, U., Tchanturia, K., Treasure, J., &

Chalder, T. (2011). Emotional expression, self-silencing, and distress tolerance in

anorexia nervosa and chronic fatigue syndrome. British Journal of Clinical

Psychology, 50, 310–325. doi: 10.1348/014466510X519215.

Häuser, W., Kosseva, M., Üceyler, N., Klose, P., & Sommer, C. (2011). Emotional,

physical, and sexual abuse in fibromyalgia syndrome: A systematic review with

meta-analysis. Arthritis Care & Research 63, 808–820.

Hornig, M., Montoya, J. G., Klimas, N. G., Levine, S., Felsenstein, D., Bateman, L.,

Petersen, D.L., Gottschalk, S.G., Schultz, A.F., Che, X., & Eddy, M. L. (2015).

Distinct plasma immune signatures in ME/CFS are present early in the course of

illness. Science advances, 1(1), e1400121.

Hvidberg, M. F., Brinth, L. S., Olesen, A. V., Petersen, K. D., & Ehlers, L. (2015). The

health-related quality of life for patients with myalgic encephalomyelitis/chronic

fatigue syndrome (ME/CFS). PloS one, 10(7).

Hyland, M. E., & Sodergren, S. C. (1998). Relationship between lifestyle and minor

health complaints: evidence of two clusters of association. Journal of Nutrition and

Medicine, 8, 233–246.

Hyland, M. (1999). A connectionist theory of asthma. Clinical and Experimental

Allergy, 29(11), 1467-1473.

38
Hyland, M. E. (2001a). A two‐phase network theory of atopy and asthma causation:

a possible solution to the impact of genes, hygiene and air quality. Clinical &

Experimental Allergy, 31(10), 1485-1492.

Hyland, M. E. (2001b). Extended network learning error: A new way of

conceptualising chronic fatigue syndrome. Psychology and Health, 16(3), 273-287.

Hyland, M. E. (2002). The intelligent body and its discontents. Journal of Health

Psychology, 7, 21-32.

Hyland, M. E. (2011). The origins of health and disease. Cambridge: Cambridge

University Press.

Hyland, M.E. (2017). A New Paradigm to Explain Functional Disorders and the

Adaptive Network Theory of Chronic Fatigue Syndrome and Fibromyalgia Syndrome.

In G.B. Sullivan, J. Cresswell, B. Ellis, M. Morgan, & E. Schraube (Eds.). Resistance

and renewal in theoretical psychology. Concord, ON: Captus University Publications.

Imbierowicz, K., & Egle, U. T. (2003). Childhood adversities in patients with

fibromyalgia and somatoform pain disorder. European journal of pain, 7(2), 113-119.

Jack, D.C. (1991). Silencing the self: Women and depression. Cambridge, MA:

Harvard University Press.

39
Jack, D.C., & Dill, D. (1992). The Silencing the Self Scale: Schemas of Intimacy

Associated with Depression in Women. Psychology of Women Quarterly, 16, 97-106.

Kanaan, R. A., Lepine, J. P., & Wessely, S. C. (2007). The association or otherwise

of the functional somatic syndromes. Psychosomatic Medicine, 69(9), 855.

Kemeny, M. E. (2009). Psychobiological responses to social threat: evolution of a

psychological model in psychoneuroimmunology. Brain, Behavior, and Immunity, 23,

1-9.

Kempke, S., Luyten, P., Claes, S., Goossens, L., Bekaert, P., Van Wambeke, P., &

Van Houdenhove, B. (2013). Self-critical perfectionism and its relationship to fatigue

and pain in the daily flow of life in patients with chronic fatigue

syndrome. Psychological Medicine, 43, 995-1002.

doi:10.1017/S0033291712001936.

Lacourt, T., Houtveen, J., & van Doornen, L. (2013). “Functional somatic syndromes,

one or many?”: An answer by cluster analysis. Journal of psychosomatic research,

74(1), 6-11.

Lee, Y. (2010). Fibromyalgia and childhood abuse: Exploration of stress reactivity as

a developmental mediator. Developmental Review, 30, 294-307.

40
Martinez-Lavin, M. (2007). Biology and therapy of fibromyalgia. Stress, the stress

response system, and fibromyalgia. Arthritis Research & Therapy, 9, 216.

https://doi.org/10.1186/ar2146.

Melidis, C., Denham, S. L., & Hyland, M. E. (2018). A test of the adaptive network

explanation of functional disorders using a machine learning analysis of symptoms.

Biosystems, 165, 22-30.

Norman, R. E., Byambaa, M., De, R., Butchart, A., Scott, J., & Vos, T. (2012). The

long-term health consequences of child physical abuse, emotional abuse, and

neglect: a systematic review and meta-analysis. PLoS medicine, 9(11).

Nuijten, M. B., Deserno, M. K., Cramer, A., & Borsboom, D. (2016). Mental disorders

as complex networks: an introduction and overview of a network approach to

psychopathology. Clinical Neuropsychiatry, 13(4), 5.

Olivieri, P., Solitar, B., & Dubois, M. (2012). Childhood risk factors for developing

fibromyalgia. Open Access Rheumatology : Research and Reviews, 4, 109-114.

Queiroz, L.P. (2013). Worldwide epidemiology of fibromyalgia topical collection on

fibromyalgia. Current Pain and Headache Reports, 17, 1-6.

Scolnik, M., Vasta, B., Hart, D. J., Shipley, J. A., McHugh, N. J., & Pauling, J. D.

(2016). Symptoms of Raynaud’s phenomenon (RP) in fibromyalgia syndrome are

similar to those reported in primary RP despite differences in objective assessment

41
of digital microvascular function and morphology. Rheumatology international,

36(10), 1371-1377.

Seeley, E. M. (2003). Two temperaments, one relationship: the interpersonal context

of traits as a predictor of self-silencing. (Doctoral dissertation). Retrieved from

https://scholarworks.umass.edu/theses/2401/.

Skaer, T. L. (2014). Fibromyalgia: disease synopsis, medication cost effectiveness

and economic burden. Pharmacoeconomics, 32(5), 457-466.

Stevens, H. B., & Galvin, S. L. (1995). Structural findings regarding the Silencing the

Self Scale. Psychological reports, 77(1), 11-17.

Surrey, J. (1985). The “self-in-relation”: A theory of women's

development. Wellesley, MA: Wellesley College, Stone Center for Developmental

Services and Studies.

Tanriverdi, F., Karaca, Z., Unluhizarci, K., & Kelestimur, F. (2007). The

hypothalamo–pituitary–adrenal axis in chronic fatigue syndrome and fibromyalgia

syndrome. Stress, 10(1), 13-25.

Thompson, J. M. (1995). Silencing the self: Depressive symptomatology and close

relationships. Psychology of Women Quarterly, 19(3), 337-353.

42
Van Houdenhove, B., & Luyten, P. (2006). Stress, depression, and fibromyalgia,

Acta Neurologica Belgica, 106, 149-156.

Van Houdenhove, B., Luyten, P., & Egle. U.T. (2009). Stress as a key concept in

chronic widespread pain and fatigue disorders. Journal of Musculoskeletal Pain, 17,

390-399.

Varinen, A., Kosunen, E. Mattila, K., Koskela, T., & Sumanen, M. (2017). The

relationship between childhood adversities and fibromyalgia in the general

population. Journal of Psychosomatic Research, 99, 137-142. doi:

https://doi.org/10.1016/j.jpsychores.2017.06.011.

Weissbecker, I., Floyd, A., Dedert, E., Salmon, P., & Sephton, S. (2006). Childhood

trauma and diurnal cortisol disruption in fibromyalgia

syndrome. Psychoneuroendocrinology, 31(3), 312-324.

Wessely, S., & White, P. D. (2004). There is only one functional somatic syndrome.

The British Journal of Psychiatry, 185(2), 95-96.

Woda, A., Picard, P. & Dutheil, F. (2016). Dysfunctional stress responses in chronic

pain. Psychoneuroendocrinology, 71, 127-135.

http://dx.doi.org/10.1016/j.psyneuen.2016.05.017.

43
Woods, A. T., Velasco, C., Levitan, C. A., Wan, X., & Spence, C. (2015). Conducting

perception research over the internet: a tutorial review. PeerJ, 3,

e1058. https://doi.org/10.7717/peerj.1058.

Woolf, C. J. (2011). Central sensitization: implications for the diagnosis and

treatment of pain. Pain, 152(3), S2-S15.

Yeung, E. W., Davis, M. C., & Ciaramitaro, M. C. (2016). Cortisol Profile Mediates

the Relation Between Childhood Neglect and Pain and Emotional Symptoms among

Patients with Fibromyalgia. Annals of behavioral medicine: a publication of the

Society of Behavioral Medicine, 50, 87-97.

Yunus, M. B. (2007). Fibromyalgia and overlapping disorders: the unifying concept of

central sensitivity syndromes. Seminars in arthritis and rheumatism 36(6), 339-356.

Yunus, M. B. (2008). Central sensitivity syndromes: a new paradigm and group

nosology for fibromyalgia and overlapping conditions, and the related issue of

disease versus illness. Seminars in Arthritis & Rheumatology, 37, 339–352. doi:

https://doi.org/10.1016/j.semarthrit.2007.09.003

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8. Appendices

Appendix A

BRIEF AND CONSENT: THIS WILL APPEAR ONSCREEN

NAME OF STUDY: Self silencing mediates the effect of adverse childhood

experiences and Fibromyalgia symptoms.

PRINCIPAL INVESTIGATOR: Eugenie Walker

SUPERVISOR: Dr Alison Bacon

I am undertaking this research as part of my MSc Psychology dissertation at

Plymouth University under the supervision of Dr Alison Bacon. This project has
been approved by Faculty of Health and Human Sciences Ethics Committee.

For this study, we will be interested to see if there is a relationship between

personality and severity of fibromyalgic symptoms.

The study should not take longer than 10 min in total.

One of the questionnaires will ask you about levels of your fibromyalgic symptoms.
The final questionnaire will also ask if you have encountered negative events in your
early life, for example, family dysfunction or abuse. This is because experiences
such as these can influence empathy. We will present a list of ten experiences and
you will be asked simply to confirm by mouse click whether or not these events
happened to you. Please be assured that you will not be required to give details of
these experiences. The final questionnaire examine’s different aspects of empathy.
These present statements about how you may think, feel or behave. You are asked
to respond in terms of what most closely feels right for you as an individual. Try not
to dwell on the questions too long – the intuitive answer is usually your best

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response. You will be supplied with more detailed instructions for each
questionnaire.

Your participation in this study is voluntary and you may withdraw at any point by
clicking out of the browser. You also have the choice to withdraw at a later date.
You will be provided with instructions on how to withdraw after completion of the
study. Your responses will be stored confidentially, and data will only accessed by
the researchers involved with study. Your name will not be used in any published
report of the study and you will not be identifiable.

If you have any further questions, please contact the researcher now. If not, please
read the declaration below and click the box to signal your consent to take part.

• I am aged 18 years or over

• I have read the details above
• I understand that I am free to withdraw from the research at any stage, and
ask for my data to be destroyed if I wish
• I understand that my anonymity is guaranteed, unless I expressly state
otherwise.
• I understand that the Principal Investigator of this work will have attempted, as
far as possible, to avoid any risks.

I agree to participate in the research.

This is an online study and participants will check a box here to indicate that they
have read the brief and consent to take part. Only when this is done will the
questionnaires be presented.

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 Appendix B

DEBRIEF: THIS WILL BE PRESENTED AFTER THE STUDY ITEMS ARE

COMPLETE

Thank you for taking part in this study. This research investigates the relationship
between personality and fibromyalgic symptoms.

The questionnaires you completed were:

• General Symptom Questionnaire – levels of symptoms measured
• Silencing the Self scale – another scale about understanding and relating to
other people
• ACE questionnaire – ten statements about adverse childhood experiences

I hope you enjoyed taking part in this study and have found it interesting. I will be
happy to answer any further questions you may have. Please be assured that all
data is completely confidential and will only be reported as group statistics. There will
be no association between your name and the data, nor will your name appear in
any publications or presentations of the research.

You have the right to withdraw from the study at any point without incurring penalty.
If you decide to withdraw at a later date, please email the researcher with your
unique ID code generated at the start of the study. This will allow us to identify and
access your anonymised data for withdrawal.

Researcher: Eugenie Walker, eugenie.walker@students.plymouth.ac.uk

If participation in this study has raised any personal issues that you would like to
discuss with someone, you can contact…

For students:
The university’s student counselling service at studentcounselling@plymouth.ac.uk
or phone 01752 587701. This service is based on campus in the Wellbeing Centre

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along with other services which offer support with mental or physical health. They
can also be contacted via their website at: http://www.plymouth.ac.uk/counselling .

For non-students:
The Samaritans for free by phone on 116 123 or via their website at
http://www.samaritans.org . Alternatively, you can contact The Survivors Trust at
http://thesurvivorstrust.org/ or by phone on 0808 801 0818.

Thank you again for taking part.

If you have any concerns about this research, please contact the Principle
Investigator, Eugenie Walker (eugenie.walker@students.plymouth.ac.uk) in the first
instance, or my supervisor Dr Alison Bacon ambacon@plymouth.ac.uk . If you feel
your concern has not been fully addressed, please contact the secretary to the
Faculty of Health and Human Sciences Ethics Committee
hhsethics@plymouth.ac.uk

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