IntechOpen

Home > Books > Stress-Related Disorders

Open access peer-reviewed chapter

Stress-induced Anger and Hypertension: An Evaluation of the Effects of Homeopathic Treatment

Written By

Leena S. Bagadia and Arun More

Submitted: 05 January 2022 Reviewed: 21 March 2022 Published: 05 June 2022

DOI: 10.5772/intechopen.104589

Stress-Related Disorders IntechOpen
Stress-Related Disorders Edited by Emilio Ovuga

From the Edited Volume

Stress-Related Disorders

Edited by Emilio Ovuga

Book Details Order Print

Chapter metrics overview

353 Chapter Downloads

View Full Metrics
Advertisement

Abstract

Excessive pressure or demand on an individual resulting in adverse reaction affecting mentally and physically is termed “stress.” Chronic stress has been assumed as a risk factor for hypertension which constitutes an important public health issue. According to the latest data, it affects 30% of the world population. Hypertension (HTN) rates are not decreasing despite improved detection and treatments. People experiencing increased anger, anxiety, depression brought on by globalization, and stress leading to high-risk behaviors are increasing many folds. There is the possibility that blood pressure (BP) may positively correlate with anger variables leading to essential hypertension (EHT). Homeopathy considers the human being having an integrated mind and body. It works holistically, helping the patient cope with environmental and psychosocial changes. The following research is one such example. It was conducted on 172 patients (108 males and 64 females) randomized and divided into intervention and control groups. The intervention group was administered individualized homeopathic treatment. We found that most EHT patients, especially those with a family history of HTN, suppress their anger and hostile impulses. Most appropriate homoeopathic medicine lessens anger and thereby has a reduction in elevated BP. Also, it relieves associated ailments.

Keywords

  • essential hypertension
  • anger-state
  • trait
  • STAXI-2

1. Introduction

Despite the common acceptance that psychological stress causes disease, the biomedical populace remains skeptical of this outcome. Stress contributes to many disease processes. Exposures to chronic stress are considered the most deleterious as it leads to everlasting distortion in the emotional, physiological, and behavioral reverberation that accelerates susceptibility to and course of disease like essential hypertension. It is now well established that the total variability in the aetiology of HTN cannot be solely explained by physiological, genetic, and lifestyle factors. Several physiological and behavioural mechanisms are suggested to explain the link between psychological stress, hypertension, and cardiovascular diseases (CVD). The hypothalamus–pituitary–adrenal axis and the sympathetic nervous system are activated by psychological stress, due to which hemodynamic and hormonal responses are generated [1]. Mimicking chronic stress by experimentally elevating glucocorticoids within the brain produces enhanced adrenocorticotropic hormone (ACTH) responses [2]. It increases both baseline arterial blood pressure [3] and blood pressure and heart responses to an acute novel stressor [4], as seen in many animal studies. There is a vast body of documentation to support the role of psychosocial factors as the primary risk for HTN [5, 6, 7]. As a result, national HTN guidelines recommend psychosocial intervention as a means to prevent or delay the onset of HTN [8, 9, 10].

Hypertension (HTN) is a rapidly pervasive condition observed in different parts of the world. It brings about a variety of chronic conditions in the human body [11] without apparently noticeable symptoms and hence is often called a silent killer [12]. It affects the overall body functioning and human life in various ways. Untreated patients with HTN have an average life expectancy between 50 and 60 years, compared with 71 years for the population at large.

What causes essential hypertension is still unknown. The intensity and duration of exposure to chronic stressors are presumed to be important determinants of risk. Effects of acute stressors on blood pressure (BP) have been demonstrated, but ongoing exposure to stress may be more plausibly linked to sustained BP elevations and hypertension incidence [5]. The effects of chronic stress in several domains are being investigated, including work-related stress, relationship stress, low socioeconomic status (SES). The adrenal gland is a major site that coordinates the stress response via the hypothalamic-pituitary–adrenal axis and the sympathetic-adrenal system. There is a fight or flight response to the stress stimulus. Due to which catecholamines are released from the adrenal medulla, they function in the neurohormonal regulation of blood pressure and have a well-established link to hypertension.

The psychological status of an individual greatly affects his physical condition. Hypertension is among the seven psychosomatic diseases for which mental aetiologies were proposed in the 1950s [13]. Studies conducted during the last decade have reported significant relationships between HT and psychological factors such as anger, anxiety, and depression. Usually, as individuals experience stress, they activate the sympathetic nervous system and the hypothalamic-pituitary–adrenal–cortical axis system. As a result of this activation, catecholamines (e.g., epinephrine and norepinephrine) and glucocorticoids (e.g., cortisol) are released, contributing to increases in blood pressure and heart rate [14]. Although the exact mechanism that explains the relationship between cardiovascular reactivity (CVR) and high blood pressure (and the subsequent development of coronary artery disease) is still under debate, research has focused on releasing catecholamines and glucocorticoids [15]. Early research in this field investigated trait anger and whether it was related to overall increased physiological reactivity [14]. These researchers assumed physiological reactivity was a person-based trait associated with a constellation of emotional, cognitive, and behavioural anger reactions. Anger could contribute to the elevation of BP directly through the psychophysiological activation and indirectly by facilitating the emergence of a coping style that contributes to the maintenance of elevated BP [16, 17, 18].

Also, anger and hostility are associated with adverse lifestyle behaviour, such as excess alcohol consumption and smoking, higher BMI values, and increased total energy intake [19], which are recognized as critical behavioural risk factors for HT and cardiovascular diseases.

Advertisement

2. Risk factors for hypertension

2.1 Non-modifiable

2.1.1 Age

The prevalence of hypertension is reported to increase with age linearly [20, 21, 22].

2.1.2 Genetic

Positive family history is commonly found in hypertensive patients, with the heritability varying between 35% and 50% in most studies [17, 23]. Family history of hypertension doubles the risk of developing hypertension [24] independent of other risk factors, such as weight, age, and smoking status.

2.1.3 Gender

Gender is also a critical social determinant of Health to which global forums have increasingly drawn attention. Gender encompasses various practices, beliefs, roles, opportunities, and constraints, shaping men's and women's Health differently. In both men and women, the subjective experience of psychophysiological wellbeing significantly correlates with cardiovascular risk factors [25]. It seems that men must defend their status more often than women. The effects of job strain on BP tend to be stronger among men than women [26].

2.2 Modifiable

2.2.1 Behavioural

Excess alcohol consumption and smoking, higher BMI values, and increased total energy intake [19] are recognized as critical behavioural risk factors for HT.

2.2.2 Deprivation and socioeconomic status

Epidemiologic studies consistently demonstrate graded associations between SES and risk of hypertension, cardiovascular disease, and mortality [27, 28, 29]. Low SES is associated with hypertension-related BP patterns, including reduced nocturnal BP dipping [24] and delayed BP recovery following laboratory stress [30].

2.2.3 Type of job

Employed men are healthier than their unemployed counterparts even after adjusting for low income and low educational attainment [31]. The same holds for women [32], although employment does not affect all women in the same way [33].

2.2.4 Job strain

Psychosocial stress was defined under four domains: social, work, financial, and environment. Women and young adults reported higher psychological stress levels, particularly at work, which raised age-and sex-related job strain issues with high demand and low control (Figure 1) [34, 35].

Figure 1.

Karasek job strain model.

Modifying effect of suppressed anger on the relationship between job stress and hypertension were studied by Cottington et al. [36], and they found that high blood pressure was markedly associated with self-reporting of ambiguous job future, disappointment with colleagues, and advancements in ranks among employees who suppress their anger. These findings advocate that anger expression, a coping mechanism, maybe an important factor that can modify the relation between occupational stress and essential hypertension.

Advertisement

3. Anger

Anger is the most basic emotion varying from mild irritation to intense fury in response to feeling threatened or hurt.

It has three components:

  • Physical – fight or flight response.

  • Cognitive – angry thoughts.

  • Behavioural – anger expressed verbally, physically, or just withdrawal.

Unfortunately, anger is also poorly understood in current diagnostic practices. For example, in DSM V, there are no Axis I disorders that directly address the emotion of anger, unlike anxiety and mood disorders.

Anger as such is a natural emotion, but if it increases, it can cause devastating effects upon the body and most conspicuously upon the heart [37]. It is observed that healthy persons may also occasionally have a conspicuous boost in their blood pressure occasionally when they are angry [38, 39] explain that anger is an arousing state with feelings varying from slight irritation to intense fury or rage. It is reported that anger-arousing situations also become an important contributing factor for increased blood pressure [17]. Historically, its roots back to 1939, when Alexander identified the suppression of anger as a major cause of HTN and further investigated its lethal outcomes in the human body. The reactivity hypothesis describes that individuals prone to HTN react to environmental stress with intense anger [23]. In an earlier study on people with HTN [24] reports that blood pressure rises remarkably during anger states. The association of anger with HTN has been confirmed by many researchers [40, 41], and is a well-established risk factor for CHD [40, 42] further augmenting the association between HTN and cardiovascular diseases.

Figure 2.

Proposed biological and behavioral pathways linking psychological factors to an increased risk of incident essential hypertension [41].

Anger is an important variable in essential hypertension. Cardiovascular reactivity to stress in which a recurrent pattern of exaggerated sympathetic nervous system activity is proposed to up-regulate basal blood pressure levels over time.

The neurohormonal model shows that psychological characteristics may predispose to CVR and hypertension development by altering the central nervous system control of baroreceptor function, opioid activity, and neurotransmitter levels. Unresolvable anger causes prolonged sympathetic nervous system over-activity. Anxiety and guilt of consequences of expressing anger results in suppression of anger. In vulnerable individuals, neural mediation of repetitive high BP episodes causes structural adjustments in arterioles culminating in sustained hypertension. Anger could be contributing to the elevation of BP directly through psychophysiological activation via the HPA axis and indirectly by facilitating the emergence of a coping style that contributes to the maintenance of elevated BP (Figure 2).

According to Addotta [43] anger comes from the reptilian part of our body, known as the amygdala, an almond-shaped structure located just above the hypothalamus, one on each side. They consist of several nerves connected to various parts of the brain, such as the neocortex and the visual cortex. Amygdala is an excellent indicator of threats. Its primary purpose is emotional and social processing. One can react to a threat before the prefrontal cortex, responsible for the brain's thoughts and judgments, can assess the rationality of the reaction. The amygdala is responsible for the brain to react to a threat or fear before the prefrontal cortex can consider the consequences. Resilient people can make rapid recoveries from stress, with their prefrontal cortex working to calm the amygdala. However, the brain cannot release itself out of an emotional rut; and, the body is flooded with the cascade of cortisol or stress hormones ("Effects of Anger,", para. 18).

Before one feels anger, a primary emotion is felt. It can be a feeling of fear, offense, disrespect, force, entrapment, or pressure. When the primary emotions become too intense, the secondary emotion of anger is experienced.

In some cases, minor irritation can trigger full-blown anger within a shorter period. According to Dr. Sietse d Boer of the University of Groningen, "serotonin deficiency appears to be related to pathological, violent forms of aggressiveness, but not to the normal aggressive behaviour that animals and humans use to adapt to everyday survival" (as cited in Society for Neuroscience, 2007, para. 19).

Anger can assemble psychological resources for corrective action. Uncontrolled anger can negatively affect personal and social wellbeing. Many philosophers and writers have cautioned against the spontaneous, wild fits of rage, but they disagree on anger's intrinsic value. Coping with anger has been addressed in the writings of the earliest philosophers up to modern times. Most notable being Bhagvad Geeta in its Chapter 2, Verse 63, says:

क्रोधाद्भवति सम्मोह: सम्मोहात्स्मृतिविभ्रम: |स्मृतिभ्रंशाद् बुद्धिनाशो बुद्धिनाशात्प्रणश्यति || Meaning: Anger distorts thought & perception leading to errors in reasoning which results in damage & destruction [44].

Modern psychologists and psychiatrists have also pointed out the harmful effects of suppressing anger.

Anger is a predominant feeling expressed behaviorally, cognitively, and physiologically when a person consciously chooses to stop the threatening behaviour of another outside force immediately [45].

3.1 Concept and assessment of anger

Anger is a universal emotion. It has long been recognized as a significant constituent of human life since long. Individuals face many problems in their daily lives and solve them [46]. While solving these problems, they exhibit different emotional and behavioral reactions, and anger is one of them. Anger is one of the basic emotions felt by almost everyone at times. Simultaneously, it can be suggested that it is one of the most interesting and least understood feelings [47].

Kassinove and Tafrate [48] asserted that anger is often a learned emotion. They believe that anger is partly an inborn quality but mostly modeled from family and the surrounding environment. However, people learn from the social environment about what and when they will get angry and the kind of behaviors they will exhibit [49, 50, 51, 52].

Anger is a multidimensional construct that consists of physiological (general sympathetic arousal, hormone/neurotransmitter function), cognitive (irrational beliefs, automatic thoughts, inflammatory imagery), phenomenological (subjective awareness and labeling of angry feelings), and behavioral (facial expressions, verbal/behavioral anger expression strategies) variables [53, 54, 55]

3.2 Anger expression/anger subcategories

Spielberger et al. [56] stated that the expression of anger must be distinguished conceptually and empirically from the experience of anger as an emotional state (S-anger) and individual differences in anger as a personality trait (T-anger).

  1. Anger-In (AX-In): mean anger held in or suppression of angry feelings.

  2. Anger-Out (AX-O): this is defined as the frequency at which angry feelings are expressed in verbally or physically aggressive behavior.

  3. Anger Control (AX-Con): this refers to attempts to control and suppress or mitigate anger expression.

Advertisement

4. Mode of action of homoeopathic medicine

Homeopathy is an over 226-year-old system of complementary and alternative medicine (CAM) developed by the German physician Samuel Hahnemann, MD. This mode of healing is based on distinct principles, comprehensive case history-based clinical findings], noteworthy patient contentment, and an expanding contemporary research database. It deals with the patient holistically and looks at the patient's ailment as a multicausative phenomenon. Dynamic forces that derail need dynamic intervention, and homeopathy provides a solution. It focuses on the patient with hypertension rather than on hypertension itself.

4.1 Essential principles of classical homeopathy

  1. Potentially therapeutic substances must be tested carefully in healthy subjects in order to document their ‘pure’, direct effects on physical as well as mental sphere; this is the basis of the medical matter.

  2. The remedy capable of causing a similar state in a healthy subject causes a counter-reaction in a patient that is stronger than the pathological stimulus of the disease itself.

  3. The disease must be studied as a whole (and not only in terms of its main symptom or pathology but also the state of mind it causes in an individual) in order to ensure that it and the drug interact in a global manner; the choice of the remedy must be based on the complex of individual symptoms rather than on the name of the disease and the organ or system affected.

  4. The dose must be the minimal effective dose and therefore adjusted on the basis of individual sensitivity.

The original method of preparing homeopathic medicines comprises trituration in lactose and/or serial dilution in ethanol–water solutions and succession (vigorous replicated cycles of pounding by hand or standardized mechanical arm pounding on a hard surface) in glass vials containing ethanol–water solutions [37]. This generates "top–down" nanoparticles of the source material. Nanoparticles range in size from 1 nanometer (nm) on a side up to 1000 nm or more. Thus, insoluble substances were converted into effective remedial agents for the first time in the history of western medicine. He also observed that as these potentization methods ascend the scale, the capacity of the drug to produce mental symptoms increased. By potentization, the drug energy is released in a form best suited to restoring the lost harmony through the use of a similar force. The physico-chemical effects of the remedy cease, and it acts at the dynamic level where it follows the rules applicable to the field of dynamics.

Figure 3.

Nanoparticle model for homeopathic remedy action: hormesis, allostatic cross-adaptation, and time-dependent sensitization of the nonlinear stress response mediator network. Global and local healing occur across the person as a self-organized complex adaptive system in response to the individualized remedy serving as personalized hermetic stressor, i.e., holistic nanomedicine: an exogenous nanoparticle stimulating self-amplified, bidirectional adaptive change (see text).

The action of homoeopathic remedy on a living organism (Figure 3) [57]

Fundamental research in basic science indicates that authentically-prepared homeopathic medicines:

  1. contain calculable source nanoparticles (NPs) and/or silica nanoparticles with adsorbed original materials [57, 58, 59, 60], which are compositely dispersed in colloidal solution;

  2. act by regulating the biological function of the allostatic stress response network [61, 62], including cytokines, oxidative stress, and heat shock proteins [63, 64], as well as immune, endocrine, metabolic, autonomic, and central nervous system functions [65, 66];

  3. evoke biphasic actions on the adaptive plasticity of living systems [67, 68, 69, 70, 71] via organism-dependent, endogenously amplified, rather than agent-dependent pharmacological effects [72]. The effects of homeopathic remedy nanoparticles involve state- and time-dependent adaptive changes [63, 64, 73, 74, 75, 76] within the complex adaptive organism [75, 76, 77, 78]. The main clinical outcome is

  4. improvement in intrinsic resilience to future environmental stressors and recovery back to normal healthy homeostatic operating [79]. The disease resolves as an indirect result of changing the system dynamics that had supported its initial development [78, 80], rather than as a downright consequence of suppressing end-organ symptoms.

The action of homoeopathic medicines can be explained with the help of the biopsychosocial model. The biopsychosocial model reflects the development of illness through the complex interaction of biological factors (genetic, infections, trauma, nutrition, etc.), psychological factors (mood, personality, emotional turmoil, negative thinking, etc.), and social factors (cultural, socioeconomic, technological, etc.) [81]. According to the biopsychosocial model, individuals as per their present state and personal history, respond differently to one and the same substance. Homeopathy is the pioneer of personalized medicine where the patient's complete data of health issues is considered for a precisely aimed therapy. The homoeopath considers the case a disease phenomenon that is a modification in the whole individual from his original state of health. It is the totality of alterations that comprises all the patient's mental, physical, and psychological changes.

The prescription of a homoeopath is based on the totality of the symptoms, which includes patient's life span, counting past illnesses, family history, constitution and temperament, and peculiar symptoms of the present illnesses. A patient's portrait is created on this base, and this disease partite is correlated with a remedy picture. When these two portraits match, a homeopathic response is established, and the body shall make efforts to cure the illness. It is called the similia principle. The fundamental law of homoeopathy is based on nature’s law of “Like cures like,” also known as the “Law of similars.” According to this law, the prescribed homeopathic medicine faces very little resistance as the patient exhibits an enhanced susceptibility to it (Figure 4).

Figure 4.

Application of the law of similia in homeopathy.

Modern anti-hypertensive drugs are not always well-tolerated due to their many harmful side effects [82]. They have the inconvenience of drug treatment despite its unchallenged efficacy [83, 84]; side effects [85] and difficulties with drug compliance occur in up to 70% of the patients [86]. They have no impact on depression, general psychopathology, and quality of life scores compared to those who use only a dietary program [87]. Such drugs do not have any effect on reducing the anger of hypertensive patients. Homeopathic medicines do not have unwanted side effects [88].

This research studies the relationship between essential hypertension (EHT), higher levels of negative emotion such as high trait anger and perceived stress, and their homeopathic treatment. This anger research has mainly explored the experience and expression of anger. The purpose of this study is to ascertain the efficacy of a homeopathic similimum in treating anger and thereby controlling EHT. Homeopathic treatment is much more cost-effective, has no adverse effects, and improves the quality of life, making it more readily accepted.

Advertisement

5. Materials and methods

This trial was randomized, placebo-controlled, comparative, and open-label conducted at an urban and a rural charitable homoeopathic hospital and a plastic factory. About 1187 adults were screened for hypertension. They were asked about the history of hypertension as well. We found 303 patients with either history of hypertension or were detected with hypertension during screening on BP measurements. The screening was carried out at a rural and an urban charitable hospital and a plastic factory. Secondary hypertension was ruled out among these 303 hypertensive patients by checking routine blood biochemistry, Ultrasonography (USG), electrocardiogram (ECG), and x-ray chest. However, eight patients were found to have secondary causes like renal artery stenosis, Conn's syndrome, coarctation of the aorta; these patients were excluded from moving into the study. One-hundred and seventy-two patients (108 males and 64 females) between 18 and 65 years who gave their informed, voluntary consent were enrolled in the study as per the approval from the ethics committee of Dr. M.L. Dhawale Memorial Homoeopathic Institute's approval. By simple randomization, they were allocated their respective groups, i.e., placebo and intervention groups. More than 50% of patients in both groups were on Antihypertensives prescribed by the physician at the beginning of the study.

All the patients were given necessary lifestyle management advice, also suggested a dietary approach to stop hypertension (DASH diet) [89] and regular exercises. Thorough homeopathic case-taking was done, and the STAXI-2 scale was applied at the beginning and after a 6-months study period to measure the change in anger for all the patients. Every 2 weeks, these patients were followed up for subjective criteria like anger, anger episodes, fights, and moods. Also, objective criteria were assessed like BP, pulse rate, physical complaints. Regular follow-up was done every 2 weeks to check all the patients' subjective and objective parameters.

Data were entered in MS Excel and then transferred to SPSS SW V. 21 for analysis. The quantitative data were represented as mean ± SD & compared using Student's t-test. In addition, a Pearson correlation test was performed to find correlations between variables.

5.1 STAXI-2

Spielberger’s State-Trait Anger Expression Inventory-2 (STAXI-2) is a measure of anger experience and expression used to assess aggression and violence, given the close association between anger dysregulation and aggressive and violent behavior. The STAXI-2 is one of the most widely used measures in clinical and research settings (Table 1) [56].

STAXI-2 scale/subscaleDescription of scale/subscale
1State anger (S-Ang)Measures the intensity of angry feelings and the extent to which a person feels like expressing anger at a particular time
AFeeling angry (S-Ang/F)Measures the intensity of the angry feelings the person is currently experiencing
BFeel like expressing anger verbally (S-Ang/V)Measures the intensity of current feelings related to the verbal expression of anger
CFeel like expressing anger physically (S-Ang/P)Measures the intensity of current feelings related to the physical expression of anger
2Trait anger (T-Ang)Measures how often angry feelings are experienced over time
AAngry temperament (T-Ang/T)Measures the disposition to experience anger without specific provocation
BAngry reaction (T-Ang/R)Measures the frequency that angry feelings are experienced in situations that involve frustration and/or negative evaluations
3Anger expression-out (AX-O)Measures how often angry feelings are expressed in verbally or physically aggressive behaviour
4Anger expression-in (AX-I)Measures how often angry feelings are experienced but not expressed (suppressed)
5Anger control-out (AC-O)Measures how often a person controls the outward expression of angry feelings
6Anger control-in (AC-I)Measures how often a person attempts to control angry feelings by calming down or cooling off
7Anger expression index (AX Index)Provides a general index of anger expression based on responses to the AX-O, AX-I, AC-O, & AC-I items

Table 1.

Brief overview of the STAXI-2 scales and subscales.

It calculates the experience and expression of anger and is a 57-item self-report questionnaire. It consists of six scales and an anger expression index. It is a widely used scale for assessment, with the following dimensions:

  1. State anger (S-Ang): the intensity of angry feelings at the time of completion;

  2. Trait anger (T-Ang): a disposition to experience anger;

  3. Anger Expression-Out (Ax-O): the expression of angry feelings out;

  4. Anger Expression-In (AX-I): the suppression of angry feelings;

  5. Anger Control-Out (AC-O): the prevention of anger expression toward other people or objects;

  6. Anger Control-In (AC-I): the control of suppressed anger and

  7. Anger Expression Index (AX-index): an overall index of the frequency of anger expression, regardless of direction.

Advertisement

6. Results

The maximum number of patients was 36–50 years. Seventy-eight out of 171 (46%) patients belonged to this age group in this study.

It has been noticed that hypertensive men reported more anger than hypertensive women. It is a randomized trial, and a separate analysis of anger between men and women has not been attempted. However, these findings were observed.

Sixty-four participants (28 females and 36 males) out of 171 had a positive family history of hypertension. Furthermore, it was observed that people with a family history of hypertension were more likely to suppress their anger.

This table shows the analysis of different variables done at the end of the study period—6 months. As seen in this table depicting the intervention arm—except state anger & its subgroups, all other anger variables & systolic and diastolic BP have a statistically significant reduction with the p-value <0.001 with a 95% confidence interval (Table 2).

GroupMeanStd. deviationStd. error meanMean difference95% confidence interval of the differenceP-value
LowerUpper
S_ang_diffT4.729.5051.0252.062−0.4144.5390.102
C2.666.6290.719
S_ang_F_diffT3.7712.6691.3662.756−0.8356.3460.132
C1.0111.0481.198
S_Ang_V_diffT3.819.4441.0181.202−1.4193.8240.367
C2.617.8380.850
S_ang_P_diffT4.0010.9931.1852.188−0.5514.9270.117
C1.816.5800.714
T_Ang_diffT13.638.6090.9288.9936.47311.5120.000
C4.648.0660.875
T_Ang_T_diffT11.169.4831.0237.5634.93710.1890.000
C3.607.8240.849
diff_T_Ang_RT16.009.2390.9969.1066.36211.850.000
C6.898.9310.969
Diff_AX_OT11.8411.6991.2627.724.49210.9470.000
C4.129.5591.037
Diff_AX_IT11.7210.1251.0928.2625.59810.9260.000
C3.467.2730.789
Diff_AC_OT9.0512.3621.333−7.988−11.125−4.8510.000
C1.067.9080.858
Diff_AC_IT13.9112.0431.29910.7547.66413.8450.000
C3.158.0020.868
Diff_AX_IndexT13.9112.0431.29910.7547.66413.8450.000
C3.158.0020.868
Diff_SBPT31.2014.8391.60920.47416.29924.6480.000
C10.7312.5381.368
Diff_DBPT18.1216.1511.74212.818.35217.2690.000
C5.3113.2201.434

Table 2.

Change in variables in both groups w.r.t. anger after 6-months study period (Test used: unpaired t-test).

This slide shows the values in both arms at the end of the study period. The values in the intervention arm show a much greater reduction in the values of all the variables compared to the control arm.

In both arms, the patients who were on standard antihypertensive treatment (AHT), in the control arm, 98% of patients continued with the same dose of their medicines at the end of the study period. However, standard AHT was stopped completely in the intervention group in 33% of patients. And in 28% of patients, the dose of AHT was reduced.

At the end of the study period, in both the arms, the patients who were not on standard AHT, in the control arm, 16% patients had to be prescribed standard AHT. Whereas in the intervention arm, the BP of all patients was maintained on the indicated homoeopathic medicine.

No statistical difference was found in rural and urban participants in both control and intervention arms with respect to anger and blood pressure variables (Tables 3 and 4).

Group statistics—Control group
ResidenceNMeanStd. deviationStd. error meantSig. (2-tailed)95% confidence interval of the difference
LowerUpper
S_ang_diffU442.005.1040.769−0.9490.346−4.2291.498
R413.377.9551.242
S_ang_F_diffU440.5510.4981.583−0.4010.689−5.7613.827
R411.5111.7201.830
S_Ang_V_diffU441.685.9600.899−1.1350.260−5.3061.450
R413.619.4261.472
S_ang_P_diffU440.643.6290.547−1.7260.088−5.2450.371
R413.078.5801.340
T_Ang_diffU444.008.2861.249−0.7500.455−4.8092.175
R415.327.8691.229
T_Ang_T_diffU443.147.8991.191−0.5640.575−4.3532.431
R414.107.8101.220
diff_T_Ang_RU445.958.2911.250−1.0050.318−5.8031.908
R417.909.5701.495
Diff_AX_OU443.098.6101.298−1.0260.308−6.2541.997
R415.2210.4771.636
Diff_AX_IU443.365.8790.886−0.1240.901−3.3562.961
R413.568.5971.343
Diff_AC_OU44−0.777.0901.0690.3440.732−2.8394.025
R41−1.378.7801.371
Diff_AC_IU442.776.9711.051−0.4520.653−4.2602.683
R413.569.0501.413
Diff_AX_IndexU442.776.9711.051−0.4520.653−4.2602.683
R413.569.0501.413
Diff_sys_BPU4410.9110.4651.5780.1390.889−5.0985.866
R4010.5314.6202.312
Diff_dia_BPU446.168.2711.2470.6140.541−3.9607.498
R414.3917.0822.668

Table 3.

To check if there is a significant difference in anger variables in the control group based on residence (rural/urban) of participants.

ResidenceNMeanStd. deviationStd. error meantSig. (2-tailed)Mean difference95% confidence interval of the difference
LowerUpper
S_ang_diffU484.4610.0571.452−0.2860.775−0.594−4.7213.532
R385.058.8801.441
S_ang_F_diffU482.0814.5102.094−1.3930.167−3.811−9.2521.629
R385.899.6421.564
S_Ang_V_diffU483.6710.1341.463−0.1620.872−0.333−4.4353.768
R384.008.6241.399
S_ang_P_diffU484.2112.1291.7510.1960.8450.471−4.3025.245
R383.749.5201.544
T_Ang_diffU4813.799.4551.3650.1970.8440.371−3.3684.109
R3813.427.5251.221
T_Ang_T_diffU4811.9210.3881.4990.8270.4111.706−2.3965.809
R3810.218.2371.336
diff_T_Ang_RU4815.1710.1881.471−0.9390.350−1.886−5.8782.106
R3817.057.8881.280
Diff_AX_OU4811.4611.4171.648−0.3360.738−0.857−5.9364.221
R3812.3212.1841.976
Diff_AX_IU4811.7110.4621.510−0.0130.990−0.029−4.4264.369
R3811.749.8221.593
Diff_AC_OU48−7.7513.0961.8901.0940.2772.934−2.3988.266
R38−10.6811.3261.837
Diff_AC_IU4812.4212.8361.853−1.2950.199−3.373−8.5521.807
R3815.7910.8331.757
Diff_AX_IndexU4812.4212.8361.853−1.2950.199−3.373−8.5521.807
R3815.7910.8331.757
Diff_sys_BPU4733.4314.7642.1541.5510.1254.978−1.40711.364
R3828.4514.6562.377
Diff_dia_BPU4818.6018.2522.6340.3130.7551.104−5.9078.116
R3817.5013.2442.148

Table 4.

To check if there is a significant difference in anger variables in the treatment group based on residence (rural/urban) of participants.

The family history of hypertension was analyzed in female participants of the study, as shown in the above table, and it has been correlated with various anger components (Table 5).

F/H of HTMeanStandard deviationStandard error meantSig. (2-tailed)Mean difference95% confidence interval of the difference
LowerUpper
S_ang_diff0.004.919.0531.530−0.1930.848−0.493−5.6044.617
1.005.4111.0642.129
S_ang_F_diff0.001.0317.0492.882−1.2820.205−4.749−12.1572.658
1.005.7810.1121.946
S_Ang_V_diff0.004.2310.1381.7140.0580.9540.154−5.1715.48
1.004.0710.7202.063
S_ang_P_diff0.002.918.9361.510−0.9270.358−2.715−8.5763.146
1.005.6314.0552.705
T_Ang_diff0.007.147.9451.343−2.5140.015−6.116−10.982−1.251
1.0013.2611.2062.157
T_Ang_T_diff0.005.897.9551.345−2.5720.013−6.114−10.869−1.359
1.0012.0010.7702.073
diff_T_Ang_R0.009.607.9971.352−1.9380.057−4.993−10.1460.16
1.0014.5912.2392.355
Diff_AX_O0.005.3110.2201.728−1.7110.092−4.315−9.360.729
1.009.639.3321.796
Diff_AX_I0.004.577.7701.313−2.1430.036−5.206−10.067−0.346
1.009.7811.3452.183
Diff_AC_O0.00−1.839.7901.6553.0440.0037.9492.72513.173
1.00−9.7810.7032.060
Diff_AC_I0.004.6911.0291.864−3.070.003−8.425−13.916−2.935
1.0013.1110.2931.981
Diff_AX_Index0.004.6911.0291.864−3.070.003−8.425−13.916−2.935
1.0013.1110.2931.981

Table 5.

Comparison of positive and negative F/H of HT in control and treatment groups: (females).

00, negative family history; 1.00, positive family history.

The result suggests that women with a positive family history of hypertension scored higher on trait anger and angry temperament. Still, they tended to suppress their outward expression of anger than participants with negative F/H of HT. It correlates with higher blood pressure values. In expressing anger, cultural standards define what is appropriate and appear to determine such expressions' physiological consequences.

In the group analysis of male participants in the study, as shown in the above table, the results suggest that even men with a positive family history of hypertension have higher trait anger and anger temperament. Still, they tend to suppress their outward expression of anger compared to participants with negative F/H of HT. Besides, they try to resolve their anger by calming down or cooling off (Table 6).

fam_histMeanStandard deviationStandard error meanSig. (2-tailed)Mean differenceStd. error difference95% confidence interval of the difference
LowerUpper
S_ang_diff0.002.035.9900.7370.110−2.2621.405−5.0480.523
1.004.298.5271.332
S_ang_F_diff0.001.067.5100.9240.262−2.3052.043−6.3561.746
1.003.3713.6192.127
S_Ang/V_diff0.002.036.7620.8320.233−1.8231.520−4.8371.191
1.003.858.8931.389
S_ang_P_diff0.001.676.5870.8110.287−1.6021.495−4.5671.364
1.003.278.8291.379
T_Ang_diff0.007.039.6281.1850.012−4.6281.806−8.208−1.048
1.0011.668.1111.267
T_Ang_T_diff0.004.948.8911.0940.012−4.6701.818−8.276−1.065
1.009.619.5421.490
diff_T_Ang/R0.009.8810.8641.3370.081−3.5362.006−7.5130.441
1.0013.418.6751.355
Diff_AX_O0.006.8213.0701.6090.093−4.0602.395−8.8090.689
1.0010.8810.1591.587
Diff_AX_I0.006.8510.3661.2760.130−2.9561.935−6.7930.880
1.009.808.6001.343
Diff_AC_O0.00−3.2710.8851.3400.0554.3372.234−0.0938.767
1.00−7.6111.7831.840
Diff_AC_I0.006.5511.7071.4410.022−5.3082.286−9.840−0.776
1.0011.8511.1391.740
Diff_AX_Index0.006.5511.7071.4410.022−5.3082.286−9.840−0.776
1.0011.8511.1391.740

Table 6.

Comparison of positive and negative F/H of HT in control and treatment groups: (males).

Table of associated illnesses these participants suffered from (Table 7):

NumberAssociated illnessNo. of patientsTotal %
1Alcoholism42.34
2Allergic dermatitis63.51
3Allergic rhinitis42.34
4Acid-peptic disorder3419.88
5Benign paroxysmal postural vertigo10.6
6Cholelithiasis21.17
7Chronic obstructive pulmonary disease63.51
8Chronic suppurative otitis media10.6
9Climacteric complaints63.51
10Dysthymia42.34
11Diabetes mellitus3621.05
12Dyslipidaemia63.51
13Epilepsy21.17
14Fibromyalgia127.02
15Frozen shoulder42.34
16Generalised anxiety disorder84.68
17Hypothyroidism127.02
18Hyperthyroidism10.6
19Hyperuricaemia84.68
20Irritable bowel syndrome21.17
21Malnutrition42.34
22Menstrual irregularities127.02
23Migraine21.17
24Obesity42.34
25Osteo-arthritis knees84.68
26Psoriasis21.17
27Rheumatoid arthritis42.34
28Urolithiasis63.51
29Urinary tract infection—recurrent21.17
30Vitiligo21.17

Table 7.

Associated illnesses seen in patients along with essential hypertension.

It shows the list of associated ailments these patients had along with EHT.

At the end of the study period:

About 89% of patients had relief in the symptoms of their comorbidities in the treatment group with the curative effect of the similimum, but 73% of patients' symptoms of associated illnesses were status quo in the control arm.

A Pearson's correlation test was done to determine whether there is a linear correlation between anger variables and systolic and diastolic BP. Unfortunately, in this study (like many others in the past), we could not find a significant correlation (Table 8).

Table 8.

Post-test correlations between variables in TREATMENT group.

Correlation of variables in each group.

Advertisement

7. Discussion

The predictive importance of stress resulting in anger was seen only in the subgroup of participants with high genetic susceptibility to hypertension, defined as having one or more hypertensive parents. It is also important to emphasize that although a family history of hypertension was an important predictor of alterations in BP status on its own, high trait anger greatly potentiated this increased risk of developing elevated BP.

High-stress responsivity itself may have a possible genetic basis. In addition, there is a possible lack of generalizability to older persons because the sample was restricted to 18–65 years. It indicates that any adverse effects of increased life stress or decreased stress buffers would be most evident among those who are both high-stress responders and have a genetic susceptibility to hypertension and heart disease.

This study was conducted at charitable hospitals and in a plastics factory, where patients belonged to the low-income group. Hence, only 18% of patients had middle or high SES. Although employment itself does not seem to be a risk factor, there is some evidence that the combination of jobs and a family may increase hypertension and CHD incidence in women. In two studies, the Framingham study [90, 91] and the Minnesota Heart Survey, [92] working women reported greater levels of stress than working men or homemakers. A similar observation was found in the female participants in the present study. Many study participants were rotational factory shift workers, including working days, afternoon, and night shifts. Blood pressure elevation effects appear to be mainly mediated by maladaptive or unhealthy coping behaviors such as excessive consumption (food, cigarettes or bidis, gutka, and alcohol) and physical inactivity. These inconclusive results may have resulted partly from lifestyle differences in the study populations and have been strongly influenced by different perceptions of overwork and stress. It was found that psychological stress was associated with age, sex, and socioeconomic status. In addition, higher stress levels at work were found but lower levels of financial stress among persons with high versus low levels of income or education in both men and women. It was observed that blood pressure was explicitly related to job control (lower control linked to higher pressure) and perceived stress on the job. Participants with higher socioeconomic status and women were more stressed by low job control than men and people with lower socioeconomic status (SES). Women and young adults reported higher psychological stress levels, particularly at work, which raised age-and sex-related job strain issues with high demand and low control at work [34, 35].

A correlation between anger and hypertension (Table 8) was examined. The finding that none of the anger measures was associated with resting BP in this study is consistent with literature reviews on anger and hypertension [93, 94, 95]. In addition, previous reviews have found only low and inconsistent associations between trait anger and HT [96, 97, 98].

All homeopathic medicines alter the state of mind and disposition in their peculiar way [99]. Therefore, the changes in the patient's state of mind and disposition must be considered and matched with the particular homeopathic remedy that can produce a similar state in a healthy human being. As a result, permanent relief from the disease can occur. Furthermore, this ability to make distinctions among patients and superficially similar disease processes – that is, to "individualize" every case – is the natural result of the concern for the whole person, which lies at the core of homeopathic practice."

The study results also showed a reduction in anger in the control group, which was statistically significant but not as much as the reduction of anger variables in the treatment group, suggesting rapport building, up-front collaborative agenda-setting, and acknowledging social and emotional concerns as done during homeopathic case taking may help improve quality of care and efficiency. The consultation process's therapeutic benefits on health outcomes in conventional medicine and CAM have been depicted in various studies [78, 80]. These contextual effects include not the treatment's active components but are inherent within the whole treatment package such as the doctor–patient relationship, rapport-building and relationship maintenance, empathic response to social and emotional cues and mindfulness [100, 101, 102, 103, 104, 105]). Research into homeopathic consultation has identified contextual factors such as empathy and empowerment [106], which may mediate the homeopathic therapeutic effect. Homeopathy consultations involve a complete exploration of the patient's emotional, spiritual, and physical wellbeing to enable the whole person's treatment, not just the illness.

Our consultation process was standardized in that specific topics were covered (e.g., detailed clinical history, current symptoms and medication, assessment of emotional and mental states, etc.) to identify the relevant information to prescribe. The consultations' content varied between patients and between consultations; homeopathic intervention was individualized and patient-centered and led by the patient's narratives.

The findings confirm previous work demonstrating that therapeutic benefits arise from inquiries within the homeopathic interview which includes communication skills, empathy, hopefulness, enablement, and narrative competence [82, 83, 84]. Homeopathic consultation necessitates a detailed understanding of the patient and is a unique and personalized approach. Therefore, the placebo effects of the homeopathic consultation may be specific to this therapy, possibly dependent on the process of the collaborative and highly individualized consultation imperative to find a homeopathic remedy and the associated symbolic meaning response for that patient [102].

During regular follow-ups every 2 weeks, there was no adverse reaction reported to homeopathic medicine in any study participants in the intervention group, proving the safety of the individualized medicine prescribed to the patients.

Advertisement

8. Conclusion

  1. The results suggest the usefulness of the individualized homoeopathic treatment in the management of anger and the EHT in the population.

  2. During regular follow-ups every 2 weeks, no adverse reaction to the homoeopathic medicine was found in any intervention group study participants, proving the safety of the individualized medicine prescribed to the patients.

  3. STAXI-2 instrument was successfully used to measure the various anger variables in the study participants.

    It was found that all the variables in both the groups were statistically not significantly different except the trait anger (T-Ang), angry temperament (T-Ang/T), and angry reaction (T-Ang/R), which were higher in the treatment group in comparison with the control group.

  4. Convincing evidence did not emerge for the existence of strong linear relationships between anger and blood pressure.

  5. A significant correlation between high blood pressure and suppressed anger was found in male and female participants with a positive family history of HTN.

  6. The study results also showed a reduction of anger in the control group, which was statistically significant but not as much as the reduction of the anger variables in the treatment group, suggesting rapport building, up-front collaborative agenda-setting, and acknowledging social and emotional concerns as done during homoeopathic case taking might help improve quality of care and efficiency.

Advertisement

9. Limitations and future directions

  1. Study needs replication with a larger sample size over a longer duration.

  2. Presence of "Social desirability bias" – cannot be denied in a self-reporting scale-like STAXI-2.

  3. Ambulatory BP monitoring is not used, so there can be misdiagnosed cases of white-coat hypertension or cases of masked HT that could have been missed.

  4. Lack of generalizability to population older than 65 years of age.

  5. Anger variables were not analysed separately for man and women as this being a randomized controlled trial, the number of male and female participants was unequal.

  6. A double-blind, randomized controlled trial without using conventional anti-hypertensives is highly recommended.

References

  1. 1. Inoue N. Stress and atherosclerotic cardiovascular disease. Journal of Atherosclerosis and Thrombosis. 2014;21(5):391-401
  2. 2. Laugero KD, Gomez F, Manalo S, Dallman M. Corticosterone infused intracerbroventricularly inhibits energy storage and stimulates the hypothalamo-pituitary axis in adrenalectomized rats drinking sucrose. Endocrinology. 2002;143:4552-4562
  3. 3. Scheuer DA, Bechtold AG, Shank SS, Akana SF. Glucocorticoids act in the dorsal hindbrain to increase arterial pressure. American Journal of Physiology. 2004;286:H458-H467
  4. 4. Scheuer DA, Bechtold AG. Activation of dorsal hindbrain glucocorticoid receptors enhances the arterial pressure response to acute stress. Journal FASEB. 2004;18:A675-A679
  5. 5. Sparrenberger F et al. Does psychosocial stress cause hypertension? A systematic review of observational studies. Journal of Human Hypertension. 2009;23(1):12-19
  6. 6. Spruill TM. Chronic psychosocial stress and hypertension. Current Hypertension Reports. 2010;12(1):10-16
  7. 7. Steptoe A. Psychosocial factors in the development of hypertension. Annals of Medicine. 2000;32(5):371-375
  8. 8. Chobanian AV et al. Seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure. Hypertension. 2003;42(6):1206-1252
  9. 9. The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. Archives of Internal Medicine. 1997;157(21):2413-2446
  10. 10. The fifth report of the Joint National Committee on detection, evaluation, and treatment of high blood pressure (JNC V). Archives of Internal Medicine. 1993;153(2):154-183
  11. 11. Grimsrud A, Stein DJ, Seedat S, Williams D, Myer L. The association between hypertension, depression and anxiety disorders: Results from a nationally-representative sample of South African adults. South African Medical Journal. 2009;4(5):358-366
  12. 12. Barcelo A. Diabetes and hypertension in the Americas. West Indian Medical Journal. 2000;49:262-265
  13. 13. Shapiro PA. Cardiovascular disorder. In: Sadock BJ, Sadock VA, editors. Kaplan and Sadock's Comprehensive Textbook of Psychiatry Psychosocial Factors Affecting Medical Condition. 8th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2004. pp. 430-2142
  14. 14. Kubzansky LD, Kawachi I. Going to the heart of the matter: Do negative emotions cause coronary heart disease? Journal of Psychosomatic Research. 2000;2000(48):323-337
  15. 15. Pickering TG, Gerin W. Cardiovascular reactivity in the laboratory and the role of behavioural factors in hypertension: A critical review. Annual Behavioural Medicine. 1990;12:3-16
  16. 16. Brosschot JF, Gerin W, Thayer JF. The perseverative cognition hypothesis: A review of worry, prolonged stress-related physiological activation, and health. Journal of Psychosomatic Research. 2006;60(2):113-124
  17. 17. Gerin W, Davidson KW, Christenfeld NJ, Goyal T, Schwartz JE. The role of angry rumination and distraction in blood pressure recovery from emotional arousal. Psychosomatic Medicine. 2006;68(1):64-72
  18. 18. Gerin W, Davidson KW, Schwartz AR, Christenfeld N. The role of emotional regulation in the development of hypertension. In: International Congress Series, Vol. 1241. Elsevier; 2002. pp. 91-97
  19. 19. Ohira T, Hozawa A, Iribarren C, Daviglus ML, Matthews KA, Gross MD, et al. Longitudinal association of serum carotenoids and tocopherols with hostility: The CARDIA Study. American Journal of Epidemiology. 2008;167:42-50
  20. 20. Dash SL, Swain PK, Sundaram KR. Hypertension: Epidemiology in an Indian tribal population. J.A.P.I. 1986;34:567
  21. 21. Kumar P, Chaudhary V. Epidemiological study of hypertension in a rural community of western Rajasthan. Indian Heart Journal. 1991;43(1):43-45
  22. 22. Tuomisto MT. Intra-arterial blood pressure and heart reactivity to behavioural stress in normotensives, borderline and mild hypertensive men. Health Psychology. 1997;16(6):554-565
  23. 23. Light KC. Hypertension and the reactivity hypothesis: The next generation. Psychosomatic Medicine. 2001;63(5):744-746
  24. 24. Landesbergis PA, Schnoall PL, Warren K, Pickering TG, Schwrtz JE. Association between ambulatory blood pressure and alternative formulations of job strain. Scandinavian Journal of Work Environmental Health. 1994;20:349-363
  25. 25. Rose G, Sivik T, Delimar N. Gender, psychological wellbeing, and somatic cardiovascular risk factors: Erratum. Integrative Physiological and Behavioural Science. 1996;31(3):274
  26. 26. Ohlin B, Berglund G, Rosvall M, Nilsson PM. Job strain in men, but not in women, predicts a significant rise in blood pressure after 6.5 years of follow-up. Journal of Hypertension. 2007;25:525-531
  27. 27. Adler NE, Ostrove JM. Socioeconomic status and health: What we know and what we don't. Annals of the New York Academy of Sciences. 1999;896:3-15
  28. 28. Albert MA, Glynn RJ, Buring J, Ridker PM. Impact of traditional and novel risk factors on the relationship between socioeconomic status and incident cardiovascular events. Circulation. 2006;114:2619-2626
  29. 29. Seeman T, Merkin SS, Crimmins E, et al. Education, income and ethnic differences in cumulative biological risk profiles in a national sample of US adults: NHANES III (1988–1994). Social Science and Medicine. 2008;66:72-87
  30. 30. Steptoe A, Marmot M. Psychosocial, haemostatic, and inflammatory correlates of delayed post-stress blood pressure recovery. Psychosomatic Medicine. 2006:531-537
  31. 31. Sorlie PD, Rogot E. Mortality by employment status in the national longitudinal mortality study. American Journal of Epidemiology. 1990;132:983
  32. 32. Adelmann PK, Antonucci TC, Crohan SE, Coleman LM. A causal analysis of employment and health in midlife women. Women Health. 1990;16:5
  33. 33. Repetti RL, Matthews KA, Waldron I. Employment and women's health. American Psychology. 1989;44:1394
  34. 34. de Smet P, Sans S, Dramaix M, Boulenguez C, de Backer G, Ferrario M, et al. Gender and regional differences in perceived job stress across Europe. European Journal of Public Health. 2005;15(5):536-545. DOI: 10.1093/eurpub/cki028
  35. 35. Kidwai R. Demographic factors, social problems, and material amenities as predictors of psychological distress: A cross-sectional study in Karachi, Pakistan. Social Psychiatry and Psychiatric Epidemiology. 2014;49(1):27-39. DOI: 10.1007/s00127-013-0692-0
  36. 36. Cottington EM, Matthews KA, Talbott E, Kuller LH. Occupational stress suppressed anger and hypertension. Psychosomatic Medicine. 1986;48(3):249-260
  37. 37. Williams JE, Nieto FJ, Sanford CP, Couper DJ, Tyroler HA. The association between trait-anger and incident stroke risk: The atherosclerosis risk in communities (ARIC) study. Stroke. 2002;33:13-20
  38. 38. Spielberger CD, Jacobs G, Russell S, Crane R. Assessment of anger: The State-Trait Anger Scale. In: Butcher JN, Spielberger CD, editors. Advances in Personality Assessment (Vol. 2). Hillsdale, NJ: Lawrence Erlbaum; 1983. pp. 161-189
  39. 39. Borteyrou X, Bruchon- Schweitzer M, Spielberger CD. The French adaptation of the STAXI-2. C.D. Spielberger’s State-trait-anger expression inventory. Encephale. 2008;34(3):249-255
  40. 40. Player MS, King DE, Mainous AG, Geesey MA. Psychological factors and progression from pre-hypertension to hypertension or coronary heart disease. Annals of Family Medicine. 2007;5:403-411
  41. 41. Rutledge T, Hogan BE. A quantitative review of prospective evidence linking psychological factors with hypertension development. Psychosomatic Medicine. 2002;64(5):758-766
  42. 42. Borde-Perry WC, Campbell KL, Murtaugh KH, Gidding S, Falkner B. The association between hypertension and other cardiovascular risk factors in young adult African Americans. Journal of Clinical Hypertension. 2002;4(1):17-22
  43. 43. Addotta K. Anger! 2006. Retrieved from: www.kipaddotta.com/mental-health/anger.html
  44. 44. Chapter 2, Verse 63, Bhagwad Geeta
  45. 45. DiGiuseppe R, Tafrate RC. Understanding Anger Disorders. USA: Oxford University Press; 2007
  46. 46. Quinn CA, Rollock D, Vrana SR. A test of Spielberger's state-trait theory of anger with adolescents: Five hypotheses. Emotion. 2014;14(1):74
  47. 47. Kisac I. Universite ogrencilerinin bazi degiskenlere gore surekli ofke ve ofke ifade Duzeyleri [PhD thesis]. Unpublished. Ankara: Hacettepe University Sosyal Bilimler Enstitusu; 1997
  48. 48. Kassinove H, Tafrate RC. Anger management: The Complete Treatment Guidebook for Practitioners. California: Impact Publishers, Inc.; 2002
  49. 49. Dey BK, Rahman A, Bairagi A, Roy K. Stress and anger of rural and urban adolescents. Psychology. 2014:177-184
  50. 50. Naser A, Afshoon F, Mohammadi HR, Tavasoli E, Fard MR, Khalili A. Comparing the dimensions of aggression in adolescent athletes and non-athletes divorced families. European Journal of Experimental Biology. 2014;4(1):452-455
  51. 51. Sharma N, Maqbool M. Relationship between body mass index and anger among graduate students. Indian Journal of Health and Wellbeing. 2014;5(6):723-725
  52. 52. Balkaya F, Sahin NH. Cok Boyutlu ofke olcegi. Turk Psikiyatri Dergisi. 2003;14:192-202
  53. 53. Berkowitz L. Aggression: Its Causes, Consequences, and Control. New York: McGraw-Hill; 1993
  54. 54. Deffenbacher JL. Anger reduction: Issues, assessment, and intervention strategies. In: Siegman AW, Smith TW, editors. Anger, Hostility, and The Heart. Hillsdale, NJ: Erlbaum; 1994. pp. 239-269
  55. 55. Eckhardt CI, Deffenbacher JL. Diagnosis of anger disorders. In: Kassinove H, editor. Anger Disorders: Definition, Diagnosis, and Treatment. Washington, DC: Taylor & Francis; 1995. pp. 27-48
  56. 56. Spielberger CD, Johnson EH, Russell SF, Crane RJ, Jacobs GA, Worden TJ. The experience and expression of anger: Construction and validation of an anger expression scale. In: Chesney MA, Rosenman RH, editors. Anger and Hostility in Cardiovascular and Behavioural Disorders. Washington, DC: Hemisphere; 1985. pp. 5-30
  57. 57. Bell IR, Koithan M. A model for homeopathic remedy effects: Low dose nanoparticles, allostatic cross-adaptation, and time-dependent sensitization in a complex adaptive system. BMC Complementary and Alternative Medicine. 2012;12(1):1-21
  58. 58. Bhattacharyya SS, Mandal SK, Biswas R, Paul S, Pathak S, Boujedaini N, et al. In vitro studies demonstrate anticancer activity of an alkaloid of the plant Gelsemium sempervirens. Experimental Biology and Medicine (Maywood). 2008;233(12):1591-1601
  59. 59. Chikramane PS, Suresh AK, Bellare JR, Kane SG. Extreme homeopathicdilutions retain starting materials: A nanoparticulate perspective. Homeopathy. 2010;99(4):231-242
  60. 60. Upadhyay RP, Nayak C. Homeopathy emerging as nanomedicine. International Journal of High Dilution Research. 2011;10(37):299-310
  61. 61. Ives JA, Moffett JR, Arun P, Lam D, Todorov TI, Brothers AB, et al. Enzyme stabilization by glass-derived silicates in glass-exposed aqueous solutions. Homeopathy. 2010;99(1):15-24
  62. 62. Karatsoreos IN, McEwen BS. Psychobiological allostasis: Resistance, resilience and vulnerability. Trends in Cognitive Science. 2011;15(12):576-584
  63. 63. McEwen BS. Central effects of stress hormones in health and disease:Understanding the protective and damaging effects of stress and stress mediators. European Journal of Pharmacology. 2008;583(2–3):174-185
  64. 64. Van Wijk R, Wiegant FA. Postconditioning hormesis and the homeopathic Similia principle: Molecular aspects. Human & Experimental Toxicology. 2010;29(7):561-565
  65. 65. Van Wijk R, Wiegant FA. Postconditioning hormesis and the similia principle. Frontiers in Bioscience (Elite Ed). 2011;3:1128-1138
  66. 66. Khuda-Bukhsh AR, Bhattacharyya SS, Paul S, Dutta S, Boujedaini N, Belon P. Modulation of signal proteins: A plausible mechanism to explain how a potentized drug secale cor 30C diluted beyond Avogadro's limit combats skin papilloma in mice. Evidence-Based Complementary and Alternative Medicine. 2011;2011:286320
  67. 67. Bellavite P, Ortolani R, Pontarollo F, Pitari G, Conforti A. Immunology and homeopathy. 5. The rationale of the 'Simile'. Evidence-Based Complementary and Alternative Medicine. 2007;4(2):149-163
  68. 68. Bertani S, Lussignoli S, Andrioli G, Bellavite P, Conforti A. Dual effects of ahomeopathic mineral complex on carrageenan-induced oedema in rats. British Homeopathic Journal. 1999;88(3):101-105
  69. 69. Malarczyk E, Pazdzioch-Czochra M, Graz M, Kochmanska-Rdest J, Jarosz-Wilkolazka A. Nonlinear changes in the activity of the oxygen-dependent demethylase system in Rhodococcus erythropolis cells in the presence of low and very low doses of formaldehyde. Nonlinear Biomedical Physics. 2011;5(1):9
  70. 70. Hyland ME, Lewith GT. Oscillatory effects in a homeopathic clinical trial: An explanation using complexity theory, and implications for clinical practice. Homeopathy. 2002;91(3):145-149
  71. 71. Bell IR, Schwartz GE. Enhancement of adaptive biological effects by nanotechnology preparation methods in homeopathic medicines. Homeopathy. 2015;104(02):123-138
  72. 72. Bell IR, Howerter A, Jackson N, Aickin M, Bootzin RR. Nonlinear dynamical systems effects of homeopathic remedies on multiscale entropy and correlation dimension of slow wave sleep EEG in young adults with histories of coffee-induced insomnia. Homeopathy. 2012;101(3):182-192
  73. 73. Iavicoli I, Calabrese EJ, Nascarella MA. Exposure to nanoparticles and hormesis. Dose Response. 2010;8(4):501-517
  74. 74. Wiegant F, Van Wijk R. The similia principle: Results obtained in a cellular model system. Homeopathy. 2010;99(1):3-14
  75. 75. Bell IR, Howerter A, Jackson N, Brooks AJ, Schwartz GE. Multi-weekresting EEG cordance change patterns from repeated olfactory activation with two constitutionally-salient homeopathic remedies in healthy young adults. The Journal of Alternative and Complementary Medicine. 2012;18(5):445-453
  76. 76. Bellavite P, Signorini A. The Emerging Science of Homeopathy. Complexity, Biodynamics, and Nanopharmacology. 2nd ed. Berkeley: North Atlantic Books; 2002
  77. 77. Bellavite P. Complexity science and homeopathy: A synthetic overview. Homeopathy: The Journal of the Faculty of Homeopathy. 2003;92(4):203-212
  78. 78. Koithan M, Bell IR, Niemeyer K, Pincus D. A complex systems science perspective for whole systems of CAM research. Forsch Komplementar med Klass Naturheilkd. 2012;19(Suppl. 1):7-14
  79. 79. Pincus D, Metten A. Nonlinear dynamics in biopsychosocial resilience. Nonlinear Dynamics, Psychology, and Life Sciences. 2010;14(4):353-380
  80. 80. Bell IR, Koithan M, Pincus D. Research methodological implications of nonlinear dynamical systems models for whole systems of complementary and alternative medicine. Forsch Komplementarmed Klass Naturheilkd. 2012;19(Suppl. 1):15-21
  81. 81. Munir Ahmed R. Handbook of Advanced Teaching of Fundamentals of Homeopathy. Bengaluru: RGUHS; 2017. pp. 69-70
  82. 82. Ahmad S. Homoeopathic Management of Hypertension. New Delhi: B. Jain Publishers (P) Ltd.; 1999 pp. 1, 6, 18-20
  83. 83. Goldstein IB, Shapiro D, Thananopavarn C, Sambhi MP. Comparision of drug and behavioural treatment of essential hypertension. Health Psychology. 1982;1:7-26
  84. 84. Lubrosky L, Crits-Christoph MS, Brady JP, et al. Behavioural versus pharmacological treatments for essential hypertension—A needed comparison. Psychosomatic Medicine. 1982;44:202-213
  85. 85. Wadden TA, Stunkard AJ. Possible dangers in the pharmacological treatment of mild essential hypertension (letter). New England Journal of Medicine. 1982;307:1523-1524
  86. 86. Dunbar JM, Stunkard AJ. Adherence to diet and drug regimens. In: Levy R, Rifkind R, Diennis B, Ernst N, editors. Nutrition, Lipids, and Coronary Heart Disease. New York: Ravn Press; 1979
  87. 87. Dragioti E, Tsartsalis D, Kallikazaros I. Impact of anti-hypertensive medication on psychological status and quality of life in essential hypertension. European Psychiatry. 2015;30:615. DOI: 10.1016/S0924-9338(15)30489-2 Abstracts of the 23rd European Congress of Psychiatry Article: 0615
  88. 88. Digby B. The Homoeopathic Family Guide. ALM Process, Homoeoforce. Bergvlei. 1997. pp. 5, 7
  89. 89. Siervo M, Lara J, Chowdhury S, Ashor A, Oggioni C, Mathers JC. Effects of the dietary approach to stop hypertension (DASH) diet on cardiovascular risk factors: A systematic review and meta-analysis. British Journal of Nutrition. 2015;113(1):1-5
  90. 90. Haynes SG, Feinleib M. Women, work and coronary heart disease: Prospective findings from the Framingham heart study. American Journal of Public Health. 1980;70:133
  91. 91. Haynes SG, Feinleib M, Kannel WB. The relationship of psychosocial factors to coronary heart disease in the Framingham Study III. Eight-year incidence of coronary heart disease. American Journal of Epidemiology. 1980;111:37
  92. 92. Sorensen G, Pirie P, Folsom A, Luepker R, Jacobs D, Gillium R. Sex differences in the relationship between work and health: The Minnesota Heart Survey. Journal of Health and Social Behaviour. 1985, 1985;26:379
  93. 93. Mills J, Schneider RM, Dimsdale JE. Anger assessment and reactivity to stress. Journal of Psychosomatic Research. 1989, 1989;33:379-382
  94. 94. Knight RG, Paulin JM, Wall-Manning HJ. Self reported anger intensity and blood pressure. British Journal of Clinical Psychology. 1987, 1987;26:5-6
  95. 95. Friedman R, Schwartz JE, Schnall PL, Landsbergis PA, Pieper C, Gerin W, et al. Psychological variables in hypertension: Relationship to casual ambulatory blood pressure. Psychosomatic Medicine. 2001, 2001;63:19-31
  96. 96. Suls J, Wan CK, Costa PT. Relationship of trait anger to resting blood pressure: A metaanalysis. Health Psychology. 1995;14:444-456
  97. 97. Jorgensen RS, Johnson BT, Kolodziej ME, Schreer GE. Elevated blood pressure and personality: A meta-analytic review. Psychology Bulletin. 1996;1996(120):293-320
  98. 98. Mann SJ. The mind-body link in ssential hypertension: Time for a new paradigm. Alternative Therapy Health Medicine. 2000, 2000;6:39-45
  99. 99. Hahnemann S. Organon of the Medical Art. 6th ed. Redmond, WA: Birdcage Books; 1843
  100. 100. Di Blasi Z, Harkness E, Ernst E, Georgiou A, Kleijnen J. Influence of context effects on health outcomes: A systematic review. Lancet. 2002;357:757
  101. 101. Walach H. Placebo and placebo effects—A concise review. Focus on Alternative and Complementary Therapies. 2003;8:178-187
  102. 102. Moerman D, Jonas W. Deconstructing the placebo effect and finding the meaning response. Annals of Internal Medicine. 2002;136:471-476
  103. 103. Hyland M. A tale of two therapies: Psychotherapy and complementary and alternative medicine and the human effect. Clinical Medicine. 2005;5:361-367
  104. 104. Mercer SW. Practitioner empathy, patient enablement and health outcomes of patients attending the Glasgow Homeopathic Hospital: A retrospective and prospective comparison. Wiener Medizinische Wochenschrift. 2005;155:498-501
  105. 105. Hartog C. Elements of effective communication rediscoveries from homeopathy. Patient Education and Counceling. 2009;77:172-178
  106. 106. Thompson T, Weiss M. Homeopathy—What are the active ingredients? An exploratory study using the UK Medical Research Council’s framework for the evaluation of complex interventions. BMC Complementary and Alternative Medicine. 2006;6:37

Written By

Leena S. Bagadia and Arun More

Submitted: 05 January 2022 Reviewed: 21 March 2022 Published: 05 June 2022

© 2022 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Continue reading from the same book

View All
Chapter 5 The Influence of Anger and Imagery on the Maintena...

By Tony McHugh and Glen Bates

191 downloads

Chapter 6 Oxidative Stress and Cardiovascular Diseases: The ...

By Imen Ghorbel, Mariem Chaâbane, Awatef Elwej, Fatma...

194 downloads

Chapter 7 Correlates of Mobbing among Medical Residents in a...

By Panagiota Xaplanteri

129 downloads