Question: Covid-19 Assignment Just over a year ago, the Covid-19 (Coronavirus) disease was declared a pandemic. Across the p

Anxiety, Depression, and Anger: Core Components of Negative Affect in Medical Populations

Ephrem Fernandez and Robert D. Kerns

NEGATIVE AFFECT

Within psychology, the term ‘affect’ has evolved out of restricted usages within psy- choanalysis and clinical psychiatry into a general term that refers to any kind of subjec- tive feeling (Tomkins, 1962). Imposed with a metaphor from chemistry, affect is now regarded as either positive or negative in valence, the former implying pleasant feelings and the latter implying unpleasant feelings. Other terms used interchangeably with negative affect are ‘dysphoria’ and ‘distress’, though sometimes the words ‘stress’ and ‘suffering’ are also used to loosely suggest negative affect. The main point of consensus is that negative affect refers to any form of subjective feeling that is experienced as unpleasant in quality. Such unpleasantness can also vary quantitatively, that is, on a dimension of intensity. This common property of affect (be it positive or negative) is also labeled as activation or arousal.

Various types of negative affect have appeared in the diagnostic criteria for psychi- atric disorders (e.g. schizophrenia, post-trau- matic disorder, borderline personality disorder, obsessive-compulsive disorder) partly because ‘distress’ is regarded as one of the associated features of all mental disorders (American Psychiatric Association, 2000). Yet people with somatic complaints of med- ical disease have rarely been examined for clinically significant levels of negative affect. This is probably an outcome of the mind–body dualism that has infused the health sciences for centuries. In this chapter, we report on some of the recent findings that do point to a spectrum of negative affect in medical populations. Supported by theoreti- cal foundations and empirical data, we direct our attention to three specific types of nega- tive affect: anger, fear, and sadness, or their clinical equivalents of anger, anxiety, and depression, respectively. This, we call the core of negative affect (CONA). With refer- ence to medical populations, we focus on the

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three highly prevalent ailments in developed as well as developing countries of the world: cardiovascular disease (CVD), cancer, and HIV/AIDS. Furthermore, we draw parallels between the CONA as manifested in these populations and CONA as already researched in one population: patients who suffer from pain.

ANXIETY, DEPRESSION, AND ANGER

Anxiety and depression have often been studied as twin features of negative affect, but more recently, anger has been introduced as a close relative to form a new triad of neg- ative affect. Barlow (1991) made a bridge between the experimental psychology of emotions and the clinical psychology of emotional disorders, by postulating how fear, sadness, and anger lie at the root of anxiety, depression, and anger disorders. Spielberger et al. (1995) grouped depression, anxiety, and anger under the label of ‘emotional vital signs’, a construct later echoed by Ghosh and Puja (2004). Examining pain patients as a ‘test population’, Fernandez et al. (1999) and Fernandez (2002) showed that there is ample empirical evidence to position anxiety, depression, and anger within the core of negative affect.

Vital signs

The idea of emotional vital signs was origi- nally spun out of Spielberger’s view that anx- iety was analogous with heart rate, anger with blood pressure, and depression with fever. The analogy may not be perfect since the term ‘vital signs’ as used in medicine refers to objective signs that the systems of the body (required to keep a person alive) are in working order or normal. When measured values for respiration, heart rate, blood pres- sure, and temperature are zero, the person is evidently dead; when they reach a certain norm for the species, the organism is essentially

alive and well. In the case of anxiety, depres- sion, and anger, zero values would point to healthy emotional functioning, while high values, though not necessarily a sign that life is threatened, do raise concerns for the well- being of oneself or others. Profound depres- sion could forebode suicidality, extreme anger could potentiate acts of destruction, and high-grade fear could be crippling or dis- abling. In that sense, if one were to select three affective types as indices of a person’s emotional health, anxiety, depression, and anger would probably be the most appropriate choices.

The core

In using the word ‘core’ to refer to the group of three negative affects, we do not imply anything that resides deep within the individ- ual. These subjective feelings are not neces- sarily hidden as part of an individual’s inner life. In fact, they are quite open to observa- tion and measurement. It is their ubiquity and functional significance that earns them mem- bership within the core of negative affect. This kind of pervasiveness and importance is also captured in the common adage that depression is the common cold of psychiatry, the notion in much of psychology that anxiety is inherent in neuroses if not in our very exis- tence as humans, and the vast and recurrent media coverage of acts of anger and rage.

Evolutionary roots

The clinical syndromes of anxiety, depres- sion, and anger are rooted in fear, sadness, and anger, respectively. These three discrete emotions play a primordial and universal role in the defense against aversive stimuli. Fear, for instance, is regarded as the most basic of all emotions because it motivates escape or avoidance from predators or other insur- mountable threats, thereby being crucial for survival. As Marks puts it ‘Fear is a vital evolutionary legacy … Without fear, few

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would survive long under natural conditions’ (1987: 3). Anger is a twin emotion of fear in the defense against aversive stimuli. Thus Walter Cannon (1929) coined the term ‘fight or flight’ to refer to the twin options of fleeing out of fear or fighting out of anger during an emergency. Inasmuch as anger mobilizes the organism to retaliate in the face of provocation or assault, it promotes survival.

Surprisingly omitted from evolutionary accounts of basic emotion is sadness. This emotion may be viewed as a third option in the repertoire of responses toward threat or attack. When escape is not possible, when retaliation is not feasible, and the prospect of defeat is looming, then sadness is the emo- tion that arises in the service of the next most appropriate response of yielding or submission. A variant of it is what Seligman and colleagues term ‘learned helplessness’ (Peterson et al., 1993; Seligman, 1972). Buerki and Adler simply call it ‘giving up’ in order to conserve resources:

If a person has experienced certain situations, in which fight or flight was impossible or of no avail, he or she might react with conservation–with- drawal when exposed anew … Conservation–with- drawal is primarily a biological reaction pattern, the counterpart of Cannon’s fight–flight reaction. Both reaction patterns are directed toward adapta- tion to stressful situations. They are aimed at self- protection and self-preservation. Fight–flight attempts to reach its goal by engaging, conserva- tion–withdrawal by disengaging and saving of energy. (2005: 5–6)

In the face of an overwhelming offensive, fighting would be a waste of resources if not an acceleration toward death. Similarly, when fighting or fleeing are not viable options in the face of overwhelming adver- sity, the emotion is likely to be sorrow and dejection which primes the individual to yield or surrender.

Physiological mechanisms

It has been portrayed that certain emotions have biochemical commonalities such as hormones and neurotransmitters (serotonin,

dopamine), and involve the same brain struc- tures. The evidence for this has been highly conflicting and no attempt will be made to review these findings here. Besides, it is not necessary to show biochemical specificity to justify the existence of different emotions or to show biochemical commonality to argue for the similarity of emotions.

What is relatively clear is that anger and fear involve the hypothalamic–pituitary axis in order to mobilize the organism toward vig- orous action of fight or flight. However, sym- pathetic reactivity is not only the result of negative affect but can be even greater during positive affect (Heponiemi et al., 2006). Also, depression is the one component of negative affect that is least likely to involve sympathetic activation, and that makes sense because the goal in depression is not one of action as much as inaction.

Recently, Ryff et al. (2006) found that anxiety and anger had more in common with regard to biological correlates. Women with an average age of 74 years old completed psychometric tests of anxiety, depression, and anger in addition to providing urine and blood samples on multiple occasions. It was found that traits of anxiety were negatively associated with systolic blood pressure (SBP) and positively associated with glyco- sylated hemoglobin. Traits of anger were inversely correlated with SBP and positively associated with glycosylated hemoglobin. Depression did not have any significant asso- ciations with the above biological correlates but was positively associated with weight.

AFFECTIVE FORM

As pointed out earlier, research has resound- ingly demonstrated that affect can be charac- terized in terms of valence and intensity. In other words, it can be distinguished qualita- tively as well as quantitatively. Being high in affective arousal says nothing about whether the person is elated or upset, just as being low in emotional arousal leaves open the

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possibility that the person may be gloomy or just glad. In addition to valence and intensity, affect can also be described in terms of form. By this we mean that affect (which we intro- duced as a general term) can assume differ- ent configurations depending on its patterns of occurrence.

State versus trait

One binary distinction, now popular in psy- chology, is between affect as a momentary state versus affect as an enduring trait. Thus, the anger a person experiences can be qualified in terms of whether it is a passing event or a habitual occurrence. Most of the effort in making this distinction is credited to Spielberger and colleagues who first pub- lished the state–trait anxiety scale (STAI; Spielberger et al., 1977), then the state– trait anger expression inventory (STAXI; Spielberger, 1988), and more recently, the state–trait depression scale (STDS; Krohne et al., 2002). In doing so, they have proposed that affective quality be distinguished according to whether it is a state happening ‘right now’ or a trait that is present ‘most of the time’. This mirrors the dichotomy between situational and dispositional aspects of behavior that have been the subject of much discussion by personality theorists and behaviorists.

Emotion, mood, temperament

The state–trait dichotomy was certainly an advancement upon vernacular labels for affect, and it soon caught on as a practice in psychological research to describe both state and trait when assessing anxiety, anger, or depression. However, the state–trait instru- ments are limited by some ambiguities (Fernandez, 2002). Asking subjects to report how they feel ‘right now’ still leaves unclear the distinction between emotion and mood, both of which may be present at a point in time and hence get subsumed under ‘state’.

Similarly, asking how a person ‘feels gener- ally’ may elicit answers that could pertain to either mood or trait because both mood and trait share the property of taking up more time. Clearly, the domain that is most obscured by the state–trait distinction of affect is mood.

A further improvement would be to refine the dichotomy into a trichotomy which allows for any affective quality to assume the form of an emotional episode, a mood state, or a temperamental trend (Table 32.1). The first of these three forms represents a rela- tively sharp and short-lived change in affec- tive intensity, the second represents a medium-term duration of affect, and the third represents the recurrent frequency of a par- ticular affect. These in turn correspond to the phasic, tonic, and cyclic properties of all affect. Emotion occurs as an episode and is therefore phasic, mood persists and is there- fore tonic, and temperament is the recurrence of a particular emotion and therefore has a cyclic quality.

These three different forms of any affec- tive quality are sometimes reflected by the semantic variations within many languages. In English for example, when a person becomes angry, that condition may be labeled anger or fury; when the anger persists for an extended time, the person may be said to be in a ‘crabby’ or irritable’ mood, whereas one who is habitually angry may be deemed a hostile or fractious person (Table 32.1). Language, however, turns out to be a crude instrument for labeling affect because of numerous individual differences in word

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Table 32.1 Emotion, mood, and temperament forms of affect

Affective form Affective quality Emotion Mood Temperament Fear Afraid Anxious Nervous Anger Angry Irritable/ Hostile

irascible Sadness Sad Depressive/ Melancholic

dysthymic

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usage and the fact that any single language has its fair share of gaps and redundancies in labeling phenomena.

CORE OF NEGATIVE AFFECT (CONA) IN MEDICAL POPULATIONS

In our present review of the research on anger, fear, and sadness in medical popula- tions, it was not always possible to clearly delineate what was emotion from what was mood-related, or temperament but we do regard this tripartite form of affect as a nec- essary frame of reference for future research in this field. Another obstacle to firm conclu- sions in this endeavor was the uncertainty of the exact role or influence played by each affective type within each medical condition. As in the context of pain, affect could be a precipitant, a predisposing factor, an aggra- vator, a perpetuating factor, a consequence, or just a correlate (Fernandez, 2002). With regard to the last of these, it would also help to know if we are referring to co- occurrence, covariance, or equivalence between two variables. This is another pro- posed extension of our methodological approach to studying affect in illness, even though past literature may not lend itself to such a level of discrimination.

Surveying the last five years of published research, we set out to find studies of CVD, cancer, and HIV/AIDS in which all three core components of negative affect had been investigated. The product was a handful of studies quite divergent in terms of their design and their hypotheses. Nevertheless, these studies mark the beginnings of a new line of enquiry into the CONA and they are therefore the subject of review in the accom- panying section.

Cardiovascular disease (CVD)

In an extensive narrative review of CONA in coronary heart disease (CHD), Suls and

Bunde (2005) reported (1) evidence for depression in the development (precipitation) of CHD; (2) some evidence for depression leading to disease progression (exacerbation) in CHD; (3) evidence for anxiety in the development of CHD; (4) meager evidence for anxiety in the progression of CHD; (5) some evidence for hostility in the deve- lopment of CHD; and (6) minimal evidence of hostility in the progression of CHD. This means that anxiety, depression, and anger are primarily precipitants rather than aggravators of CHD. This is only in partial agreement with the findings on pain, where anxiety is a definitely a precipitator, depression is largely a consequence, and anger is at least a corre- late of pain. Suls and Bunde do not comment on the relative or collective effects of the triad of emotions on CHD because of insuffi- cient research on all three affective qualities within the same samples.

Mixed results in the review by Suls and Bunde may be due to methodologically diverse studies – especially the use of different meas- ures of affect across studies. Also, Suls and Bunde relied on significance levels rather than effect sizes to reach their inferences. Their interpretations that anxiety and depression (but not anger) are related to increased CHD risk in healthy samples may be re-evaluated on close inspection of their data as summarized in Table 32.2. As shown in the table, the actual percentage of studies reporting significant rela- tionships between affect and development of CHD never deviated far from chance levels nor did it differ appreciably across the three affec- tive types: 53% for depression, 42% for anxi- ety, and 48% for anger (Table 32.2). The role of depression as an aggravator of existing CHD is unclear due to what the authors identified as negative significant effects. Unfortunately, the exact number of negative significant effects was not specified. Other than that, the percentage of studies reporting significant aggravation of CHD by affect is remarkably similar: 29% for anxiety, and 27% for anger. Despite these findings, the role of anger (relative to its CONA counterparts) is seemingly understated in the etiology of CHD.

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It must also be pointed out that Suls and Bunde used measures of anger expression as predictors of CHD prognosis, when alterna- tively anger inhibition has also been impli- cated in CHD (Brosschot and Thayer, 1998; Magai et al., 2003; Smith and MacKenzie, 2006). The suppression or internalization of anger may demand greater cognitive effort and involve vagal mechanisms that increase the risk of cardiovascular deterioration. Given that many of the studies reported used the STAXI to assess anger, a distinction could have been made between internalized and externalized anger.

A subsequent study by Kubzansky et al. (2006) appeared in response to the limitations of previous research in which anxiety, depres- sion, and anger had been measured either singly or else as parts of a broader construct. The authors proposed a measure of general distress common to anxiety, depression, and anger in addition to orthogonal measures that were termed ‘iso-anxiety’, ‘iso-depression’, and ‘iso-anger’, respectively. They turned to the MMPI-2 which has 72 items that make up three content scales for measuring anxiety, depression, and anger, respectively. Responses to these 72 items were extracted from a

sample of 1,306 men who had completed the MMPI-2, and these data were subsequently analyzed using principal factor analysis with orthogonal varimax rotation. Based on this, three near-orthogonal scales were created for measuring the three corresponding affective types. Additionally, a fourth ‘general distress’ scale was constructed to include items that loaded equally strongly on more than one factor. The same sample of men was followed up for an average of 11 years at which point the MMPI-2 was re-administered. Data were analyzed in terms of multivariate-adjusted rel- ative risks of CHD for those highest versus lowest on each of the scales. Results showed a strong association between general distress and the incidence of CHD. Iso-anxiety was significantly associated with CHD outcomes, especially for myocardial infarction; iso-anger was associated primarily with angina pectoris; and iso-depression was not significantly asso- ciated with any CHD outcome. The authors concluded that their results call for an appreci- ation of the shared as well as unique contribu- tions of negative emotions in the development of CHD.

It should also be noted that independent investigations have shown that acute outbursts

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Table 32.2 Number of studies showing affective influences on coronary heart disease (CHD), based on Suls and Bunde (2005)

Significance of effect Marginal or select

Direction of effects Significant significant Non-significance Total Depression → CHD 10 7 2 19 Depression ↑ CHD 24 5 15 44 Anxiety → CHD 5 3 3 12 or 11 Anxiety ↑ CHD 4 1 9 14 Anger → CHD

Cynical hostility 5 2 4 11 Trait anger 1 1 1 3 Anger expression 5 2 2 9 ∑ 11 5 7 23

Anger ↑ CHD Cynical hostility 1 0 5 6 Trait anger 1 1 1 3 Anger expression 2 0 4 6 ∑ 4 1 10 15

→ Precipitating factor ↑ Exacerbating factor

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of anger, fear, and sadness can trigger heart attacks (Carroll et al., 2002; Kamarck and Jennings, 1991; Lear and Kloner, 1996; Mittleman et al., 1995). However, cardiovas- cular reactivity is not only the result of nega- tive affect and can be even greater during intensely positive affect (Heponiemi et al. 2006). By implication, it is the sudden inten- sification of arousal during emotion that seems to be a precipitating factor in cardiac incidents. In the long term, anger, depres- sion, and anxiety may also encourage other unhealthy behaviors (e.g. smoking) that increase the risk of CHD (Smith and Ruiz, 2002).

The role of multiple affective qualities in cardiac incidents is also reflected in the rela- tively new construct called vital exhaustion (VE). As conceptualized by its originator, this includes irritability, demoralization, and fatigue (Appels, 1990; Appels and Mulder, 1988a, 1988b). Here, elements of anger and sadness are combined with fatigue. The anger seems to be internalized rather than externalized in people with this condition (Bages et al., 1999). VE seems to overlap partially with the type A personality which is characterized as a pattern of hostility, impa- tience, and competitiveness (Rosenman et al., 1975). It is quite possible that the fatigue and depression of VE may actually be a byproduct of (prolonged) type A-related behavior. In terms of life events, sustained job stress/conflict, unemployment, and bereavement have been known to culminate in VE (Falger and Schouten, 1992).

Whatever its bases, VE was initially regarded as a precipitator of myocardial infarction (Appels, 1990). It has also been shown to be associated with angina pectoris (Appels and Mulder, 1988a) and cardiac events following angioplasty (Kop, 1995). It is not a stretch to find the depressive and anergic elements of VE following serious cardiac incidents.

It bears mentioning that both the type A and VE constructs have had their share of mixed results in their relationship to CVD (e.g. Miller et al., 1991). This is not surprising

given the curious admixture of somatic, affective, and behavioral features within these constructs. Nonetheless, what is common to both constructs is a role of affect, even though VE emphasizes depression and type A emphasizes anger. Yet other psycho- logical investigations have revealed a part played by anxiety in CVD (e.g. Barger and Sydeman, 2005; Herrmann-Lingen and Buss, 2007). In sum, it pays to go in search of all three of these core affective qualities, keep- ing in mind that each may enter the picture through a different pathway, namely as precipitator, exacerbator, consequence, or perpetuator of CVD.

Cancer

Almost opposite to the anger-prone type A personality that is implicated in CHD, a personality prone to repressing negative emo- tions was articulated (Temoshok, 1987). Such non-expression of negative affect was sus- pected as a factor in the etiology of cancer. It came to be known as the type C personality.

Lieberman and Goldstein (2006) therefore investigated whether the ventilation of anxi- ety, depression, fear, and anger would have an impact on depression and quality of life in patients already diagnosed with breast cancer. The patients engaged in emotional expression through the medium of Internet bulletin boards for a period of about six months. The use of negative emotional words in each of the affective categories was exam- ined in relation to the dependent measures. Regression analyses revealed that anger expression was associated with improved quality of life and reduced depression, thus hinting at the psychodynamic notion of depression as anger turned inward. However, the expression of anxiety or fear was associ- ated with increased depression and reduced quality of life. The expression of sadness was not significantly related to the outcome measures. While these findings by no means show that suppression of negative affect causes cancer, they encourage the view that

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unexpressed anger is related to psychosocial impairment in breast cancer.

More extensive coverage of the research in this area was achieved in a meta-analysis by McKenna et al. (1999). Aggregating effect sizes across 46 studies, they found only a modest relationship between the presence of anxiety, depression, or anger (or their equiva- lent temperaments) and the development of breast cancer. The average effect sizes did not exceed 0.38 even when some of the depend- ent measures were combined into a broader construct of emotional denial/ repression.

A recent prospective study by Tijhuis et al. (2000) attempted to find out cancer incidence and mortality as a function of emotional con- trol of anxiety, depression, and anger. Almost a thousand men born between 1900 and 1920 and living in Zutphen, Netherlands were examined medically for cancer and also interviewed and assessed using the Courtald Emotional Control Scale (CECS) (Watson and Greer, 1983) in 1985, 1990, 1993, and 1995. Focusing on a final sample of 590 men, it was found that from 1985 to 1995, 119 of them were diagnosed with cancer and 71 died of cancer. Descriptive statistics for the sample revealed the highest level of emo- tional control for anxiety (19.2), a slightly lower level for depression (18.4) and a slightly lower level for anger (16.4) with almost equivalent degrees of variability. When Cox proportional hazards models were used to determine effects of emotional con- trol on cancer incidence and mortality, it was found that men within the highest and inter- mediate tertiles of controlled depression had a significantly increased risk of cancer mor- tality even after adjustment for other risk fac- tors such as age, marital status, and SES; this was not the case for men who suppressed anxiety or anger. Control of depression was also significantly related to cancer incidence, but anger control or anxiety control were not. This study is nevertheless informative because it shows that cancer patients are con- sumed not only by the somatic demands of their disease but also by a struggle to control anxiety, anger, and depression even though

only one of these (when controlled) seems to increase the incidence and mortality associated with cancer.

Also using the CECS, an Australian study on breast cancer failed to find any significant associations between cancer outcome and emotional suppression of any kind, before or after controlling for age effects (O’Donnell et al., 2000). Once again, the more important message for our purposes is that the cancer patients did seem to experience components of the core of negative affect, as implied by their scores on emotional control for each of these.

A qualitative illustration of core compo- nents of negative affect in cancer patients is visible in some of the nursing literature. For example, Bowers et al. (2002) mention that even though many women with cervical cancer were depleted of physical energy, they would utter statements such as:

That was once in my mind I was angry. I wanted to get in and get over with as soon as possible and not wait a month. Then I was too weak and tired to display it very much … One day I came home and went to bed. The longer I laid in bed the madder I got. I was screaming to myself. I thought I would call a friend, but I did not want to dump on her so I said I can’t take it anymore and I came downstairs and banged and slammed and got supper. (2002: 144–145)

A further quote by Bowers et al. captures the almost existential anxiety of the cancer patient: ‘There is a reason for everything. I don’t know it is. I don’t know why. I began to think. Get a grip on yourself and find a pur- pose’ (2002: 139). A final quote by Bowers et al. captures the despair/depression of the cancer patient. ‘I guess my life was interest- ing, with so many things, and now it is not. Life is destroyed. It was so good before’ (2002: 145). These anecdotes help remind us of the cognitive appraisals that underlie the statistical data on anxiety, depression, and anger in medical populations.

HIV/AIDS

One of the few recent empirical studies of the CONA in the context of HIV/AIDS was

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conducted by Atwine et al. (2005). In a rural district of southwestern Uganda, 123 chil- dren aged 11–15 years old whose parents …