Hypertensive men recognize anger more often than any other emotion


Hypertension is a disease. However, in the majority of cases, there is no clear medical explanation, referred to as “essential hypertension”. Could psychological factors play a role?

In this context, Konstanz biological health psychologists Alisa Auer and Professor Petra Wirtz conducted a study in male participants over several years together with colleagues from Konstanz (Germany) and Switzerland.

The researchers wanted to better understand the psychobiosocial mechanisms in hypertension, since previous work in this area has left many questions open.

In an article published in the Annals of Behavioral Medicine on 22nd March 2022, they show that compared to a healthy control group, men with essential hypertension more often recognized angry expressions when they looked into the faces of others.

In addition, this anger recognition bias seems to contribute to blood pressure increases over time if someone tends to frequently and intensively experience anger. This tendency is called “trait anger”.

Recognition of mixed emotions

In their study in 145 hypertensive and normotensive men, researchers presented different pictures of people who were angry. However, the pictures did not just display anger alone, but combined anger with one of three other emotions: fear, happiness, and sadness. The background for this approach is that, in everyday life, people’s faces rarely show just one emotion.

Mixed emotions are more prevalent. Each of the computer-morphed pictures showed two emotions with varying affect intensities. Participants were asked which emotion they saw in the pictures.

“Hypertensive men recognized anger more often than any other emotion,” Alisa Auer says. “So, they overrated anger displayed in other people’s faces as compared to our healthy control group.”

Petra Wirtz adds: “Overrating anger displayed by other persons seems to affect whether high ‘trait anger’ contributes to blood pressure increases over time.”

Hence, interpersonal factors seem to play a role in essential hypertension. The expectation of associations between hypertension and social aspects was one of the reasons why the study was supported by the Cluster of Excellence “Centre for the Advanced Study of Collective Behaviour”.

Improving treatment of essential hypertension

Auer and Wirtz hope that their results will be examined and confirmed by other researchers. “Then, a next step would be to offer people with essential hypertension a more targeted support,” says Alisa Auer, who is currently completing her doctorate in Psychology. Auer is thinking of “therapeutic treatments that address a person’s perception of social environments in order to protect them from other people´s anger.”

Such therapeutic interventions would be important, because blood pressure lowering medication only treats the consequences of hypertension, but does not address potential causes. In addition, hypertension is one of the major risk factors for cardiovascular disease. In 2020, as in previous years, the Federal Statistical Office (Destatis) listed cardiovascular disease as the leading cause of death in Germany.

“338,001 deaths, or more than one third of all deaths (34%), can be attributed to cardiovascular disease,” Destatis reports in a press release.

Cardiovascular disease is especially deadly for older people: 93% of those who died of cardiovascular disease were 65 years or older.

What about women? The researchers hope that future studies will include women. Since women may possibly differ in their emotion recognition from men and as fewer women suffer from hypertension, the study initially focused on men.

Components of anger
Arousal: autonomic and stress reactivity to provocation

Throughout evolution, anger has had an adaptive role in survival with its fundamental involvement in the fight-or-flight reaction to threat detection (Berkowitz and Harmon-Jones, 2004). As such, physiological responses that share phylogenetically similar mechanisms with other mammals constitute the experience of arousal. Consistent with Selye’s (1976) stress model for example, the body increases autonomic arousal in response to a stressor. In this context, stress reactivity is the subjective perception of uncontrollability or unpredictability that is expressed in quality and degree of the response to provoking elements (e.g., perceived threat to physical safety) (Koolhaas et al., 2011).

Autonomic arousal, indicated by a raised heart rate and muscle tone, altered posture and facial expression due to adrenaline release, all serve as arousal displays of anger (Stemmler and Wacker, 2010). Not surprisingly, the circumplex model of emotion, which charts feelings on dimensions of valence and arousal, places anger in the high arousal and negative valence category of basic emotions (Russell, 1980).

Although fear shares feeling components with anger, such as autonomic arousal to threat, the organism is motivated to withdraw and flee under fear (unless escape is not possible). Unlike fear, anger is characterized by ‘approach’ motivations, and if confrontation is deemed the best course of action, can help mobilize optimal physiological and cognitive support for action tendencies that promote confronting threat and provocation. Thus, perhaps initial arousal to threat or provocation develops into fear or anger depending on context and personality or trait tendencies.

Cognition: the role of anger in biasing attention and cognition

Autonomic arousal during anger feelings is relatively short lived, whereas frequent experiences of anger and thoughts about the provoking situation (i.e., anger rumination) enables the persistence of negative emotions . During a state of anger and perhaps more so during repeated and enduring bouts of anger rumination, attention becomes narrowed and intensely focused toward the source of the provocation (Alia-Klein et al., 2018; Gable et al., 2015a).

As such, anger narrows attentional scope (Gable et al., 2015b), often compromising the efficiency of cognitive processing and decision making (Garfinkel et al., 2016). It is suggested that learned bias toward engaging anger in response to stressors can develop as a function of associative network connections across feelings, thoughts, memories and physiological and expressive motor reactions (Berkowitz and Harmon-Jones, 2004). The rapid unfolding of emotional information through this network promotes rapid interpretations and causal cognitive attributions of the provocation, which facilitate enhancement of anger (Maoz et al., 2017). In a recent theory of human anger, the authors expand on the unique cognitive elements of anger (Sell, 2006, 2011; Sell et al., 2017, 2009). The recalibrational theory holds that anger evolved in humans to bargain for better treatment, as in evolutionary biology and game theory approaches. Since humans rely on language and cognition to bargain, the recalibrational studies and theory rely on the correct assumption that substantial attentional and cognitive resources are diverted toward the source of interpersonal conflict, with such processes mediated by interactions between prefrontal (PFC) and subcortical brain networks, often with opposing activations (Siever, 2008). Thus, it is interesting to understand the mechanisms behind failure in recalibration, when anger is no longer helpful in negotiation and therefore needs regulation Hortensius et al., 2016.

Anger regulation: low road from provocation to reactive aggression

Some theories argue that regulatory processes are activated at the initiation of anger experiences, or at later appraisal stages. However, most agree that processes involved in anger regulation occur at different stages of anger escalation, depending on a multitude of factors (LeDoux, 1990), including the degree of emotion regulation capacity (Siever, 2008). The anger regulation strategy of reappraisal depends on one’s ability to distance the self from the provocation or to re-evaluation of the provocation as less threatening or frustrating than it is initially perceived. This capacity is sometimes also referred to as anger control (Spielberger, 1988) and it can serve to reduce the intensity of anger and prevent escalation to maladaptive behaviors (Szasz et al., 2011).

Because cognitive reappraisal and other higher-level anger management training heavily rely on intact intellectual and executive functioning (Ochsner and Gross, 2008), patients suffering from intellectual disabilities or neurodevelopmental disorders can show frequent loss of control. Even with intact intelligence and despite the availability of cognitive strategies as reappraisal, high levels of arousal and stress reactivity induced during anger can challenge the ability to constrain its expression.

In particular, uncontrollable anger situations may trigger a ‘low road’ of activation (e.g., with minimal mediation by higher-order cognition), rapidly leading to anger displays and aggression. Some argue that intense frustration triggers anger leading to reactive aggression in animals when there is high level of danger and the threat is very close (Blair, 2012). In humans, whether stemming from frustration or from perceived threat, anger often requires some degree of regulation.

However, the inhibiting effects of PFC recruitment during such times of intense and negatively valenced approach emotion may be greatly weakened or circumvented (Alia-Klein et al., 2009). This concept of a low road is adapted from fear studies, which have found that a specific fear response reflects an automatic process that does not even require conscious recognition of the feared stimulus (Ohman, 2005; Carr, 2015; Ledoux, 1996).

Thus fear reactions (and anger as well) are partly managed by ancient brain systems, primarily the amygdala, that may act relatively independently of the later emerging higher cognitions (LeDoux, 1996; Rosen and Schulkin, 1998). Notably, the use of psychoactive substances such as alcohol can escalate feelings of anger and facilitate the low road to rapid aggressive responses (Parrott et al., 2003). Sleep restriction also intensifies anger perhaps by reducing tolerance for provocation (Krizan and Hisler, 2019).

Physiological and behavioral displays of anger

Anger signals are recognized in humans, especially the facial and bodily expressions that exaggerate perceptions of physical strength and fighting ability analogous to animals that bare their fangs (Ekman, 1973). Indeed, facial displays of anger often include jaw-clenching, indicating readiness to attack. Face displays of anger are already functional at six months of age and may demonstrate cross-cultural uniformity in its basic elements.

As an example, congenitally blind children produce normative anger facial expressions. However, it should be noted that although anger displays are part of a universal species-typical system evolved by natural selection, these are partly calibrated by cultural variation (Clark-Polner et al., 2017; Potegal and Novaco, 2010). Linguistic expressions are also part of the human display of anger. Anger prosody of sound and tone as well as angry language indicating escalation are used as a communication of anger in humans (see section on linguistic expressions). Together, these facial, bodily, and language displays (raising the voice, pounding on table, shaking a fist, breaking something, physically assaulting) allow for a rapid exchange of information about the ability to inflict costs on the provocateur(s).

  1. Disease correlates of chronic anger
    The enduring propensity to anger feelings is characterized as high trait anger in the literature (Spielberger, 1988; Gan et al., 2016). Trait anger has been related to chronic disease and negative consequences to one’s own health, wellbeing and social support (Johnson, 1990; Phillips et al., 2006; Williams, 2010). In fact, disproportionate and pathological manifestations of anger are a cross-diagnostic feature of many psychiatric disorders, and anger is known as an emotion that exacerbates mental health symptoms and complicates psychiatric recovery (for review see, Novaco, 2010). Intermittent explosive disorder (IED) is perhaps the only disorder in the Diagnostic and Statistical Manual (American Psychiatric Association, 2013) for which repeated manifestations of anger is its core feature (Coccaro, 2000). Lifetime and 12-month prevalence estimates of IED are 7.3% and 3.9%, and most persons diagnosed with the disorder display a mean of 43 lifetime attacks of anger and aggressive behavior (Kessler et al., 2006). Problematic and chronic anger is also a prominent feature in oppositional defiant disorder, bipolar disorder, and borderline personality disorder, to name a few (for review see, Fernandez and Johnson, 2016).

Importantly, these detrimental manifestations of anger do not only express themselves in psychiatric symptoms but also may result in chronic diseases of the heart and digestive and immune systems, due at least in part to the chronic arousal and hypervigilance associated with anger experiences, combined with the high cognitive and physiological resources needed to downregulate such chronic anger (Johnson, 1990). Several pathways linking anger to chronic disease states have been explored in studies. First, anger may influence health status and disease processes through its effects on inflammation.

Anger has been associated with increased circulating inflammatory and coagulation markers, such as interleukin-6 (IL-6), a pro-inflammatory cytokine, and fibrinogen (Carroll et al., 2011). Specifically, both trait anger and outward displays of anger (e.g., yelling, slamming doors) have been associated with higher IL-6 and fibrinogen, whereas better anger control (and reappraisal) predicts lower IL-6, at least among women (Boylan and Ryff, 2013). Socioeconomic status, a broad concept including educational attainment, socio-cultural variables, and ethnicity (Boylan et al., 2015), has also been shown to moderate the relationship between anger and inflammation.

Second, chronic and acute episodes of anger can be detrimental to the cardiovascular system and is considered the most robust personality-related predictor of cardiovascular disease (Russell et al., 2016). The risk of cardiovascular events following outbursts of anger has been examined in a meta-analysis (Mostofsky et al., 2014): based on the totality of the evidence, in the 2 h following episodes of anger there is a significant risk of myocardial infarction, acute coronary syndrome, ischaemic and haemorrhagic stroke, and arrhythmia among individuals at risk of a cardiovascular event.

However, the impact of anger outbursts may be modified by trait anger, since individuals with an angry temperament, showing chronically high levels of physiological arousal and stress reactivity, and persons with traits characterized by anger (i.e., Type A personality) are considered coronary-prone. Experiences of competitiveness and angry, hostile and distrusting dispositions require higher levels of vigilance, resulting in prolonged neurohormonal activation conducive to atherosclerosis and coronary disease (Pollock et al., 2017). It has been shown that sympathetic effects and increased cardiac output prevail in the context of harassment or personalized recall of anger events.

Thus, the persistent and pervasive action of physiological arousal sustained by the emotion of anger can well explain the consistent relationship between anger, cardiovascular disease (Cox et al., 2017; Siegman, 1993) and hypertension (Harburg et al., 1991). Indeed, several studies have shown that high levels of both expressed and suppressed anger predict risk for hypertension and stroke across cultures (Kitayama et al., 2015), as well as increase the risk of recurrent cardiac events and earlier mortality among patients with previous coronary heart disease (Russell et al., 2016).

Third, anger has been associated with motility, functional gastrointestinal disorders, and to visceral and pain hypersensitivity, as shown for other negative emotions. For example, anger control and suppression, consisting of cognitive and behavioral efforts to restrain angry feelings, are associated with prolonged gastric emptying, and a delayed gut transit (Bennett et al., 2000; Evans et al., 1996; Zoccali et al., 2006).

These effects, likely mediated by the corticotropin-releasing factor, which is involved in the central stress response, are probably a way to prevent digestion during a stressful period when energy is better spent on defense. In contrast, gastric hyperemia and increased secretion have been reported during states of acute anger and aggressive behavior (Drossman, 1998).

For example, patients with irritable bowel syndrome have been shown to display increased anger, as well as colonic motor activity and decreased antral motor activity, during experimental anger-provoking conditions compared to healthy controls (Welgan et al., 2000). When classified according to the predominant bowel habit alteration as constipation or diarrhea predominant, different profiles of irritable bowel syndrome have been extracted which differ along the dimensions of anger, depression and anxiety (Muscatello et al., 20162010, 2014, 2016).

reference link :https://www.sciencedirect.com/science/article/pii/S0149763419302167

Original Research: Closed access.
Do Hypertensive Men Spy With an Angry Little Eye? Anger Recognition in Men With Essential Hypertension – Cross-sectional and Prospective Findings” by Alisa Auer et al. Annals of Behavioral Medicine


Please enter your comment!
Please enter your name here

Questo sito usa Akismet per ridurre lo spam. Scopri come i tuoi dati vengono elaborati.