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Denial and Cardiovascular Health

Denial is psychological coping strategy that allows people to engage in behavior with little conscious awareness of the consequences (Allan and Scheidt, 1996). A review by Sirous (1992) traced 21 empirical studies on denial in coronary heart disease (CHD) published in the past 25 years and concluded that denial has a long-term negative effect on cardiovascular outcome (Allan and Scheidt, 1996). However, cardiac denial is a complex phenomenon. It appears that certain types of denial might be beneficial, while others might be very detrimental to cardiovascular health. This review of the scientific literature will discuss what is currently known about denial as a possible psychosocial risk factor for CHD. In the process, methods of assessment of denial and resulting methodological problems will be discussed, as well as evidence which is helping coronary-prone behavior researchers to better distinguish between dangerous and harmless, or even beneficial, uses of the basic defense mechanism of denial.

How is denial assessed?

A number of scales have been created in attempts to accurately assess and quantify denial and have been used in multiple clinical trials (Levine et al., 1987; Ramanaiah et al., 1977; Yanagida et al., 1981; Jamner and Schwartz, 1986). There is no standard measurement of denial, but the best-known scale assessing cardiac denial is that of Hackett and Cassem (Hackett and Cassem, 1974). According to Fields, 1989, their scale originated from a 1964 study by Olin and Hackett which “noted that myocardial infarction patients would go to extremes to attribute chest pain to causes other than the heart. From this study, Hackett and Cassem developed an interview technique consisting of a few structured questions, such as “What did you feel caused your chest pain?” The interviewers rated patients on a 31-item scale that indicates behavior typically seen in patients who deny major illness. This denial scale significantly distinguished three groups that they labeled as major, partial, and minimal deniers. Interrater reliability and comparisons with clinical observers have been consistently significant (Hackett and Cassem, 1974).” However, according to Dracup et al., 1995, there is still no evidence related to the reliability and validity of this rating scale.

Since no standard well-validated measure of denial exists, when comparing studies investigating the relationship between denial and cardiovascular health, it is a rarity that two studies using an identical method of assessment of denial will be observed. Many of these assessments of denial have not been sufficiently tested in reliability and validity. Therefore caution must be taken in placing too much weight on data from any group of studies until consistent results have been obtained using a variety of measures of denial, each with acceptable levels of validity and reliability.

The Early Stages of Myocardial Infarction and Denial

As previously mentioned, it appears that only certain types of denial, or denial at certain critical points in time, appear to be detrimental to cardiovascular health. Among the greatest of dangers to cardiovascular health that denial may present is the denial of a possible cardiac event. Denial is one of the first adaptive behaviors or mechanisms that an individual uses during the stress-producing event of an acute episode of chest pain (Hackett and Cassem, 1982). The key question to be answered is whether denial of a cardiac event in order to allay fear, anxiety, or other unpleasant emotions directly leads to a greater time delay in seeking medical help. The individual who delays seeking medical treatment risks increased myocardial damage, morbidity, and mortality (Allan and Scheidt, 1996). Since the mid-1980’s, several large-scale studies have demonstrated that thrombolytic therapy can significantly reduce mortality from acute myocardial infarction (AMI)(Kennedy et al., 1985; Marder and Sherry, 1988; Simoons et al., 1985; White et al., 1987; Yusuf et al., 1985). The benefits of thrombolytic therapy are directly related to the interval between the onset of symptoms and the administration of the drug. The shorter the interval, the better the outcome (Dracup et al., 1995). In previous studies it has been shown that a large part of the total time for a patient to come under coronary care is taken up by the patientUs decision to ask for medical help, the so-called patient delay (Goldstein et al., 1972; Simon et al., 1972; Colling et al., 1976; Rawles and Haites, 1988; Wielgosz et al.,1988; Leitch et al., 1989). Patient delay is defined as the time between the start of complaints from an AMI and the moment the patient or significant other calls for medical help (Bleeker et al., 1995).

The significance of denial in relation to patient delay has not been assessed thoroughly. Wielgosz and Nolan(1991) pointed out that denial has not been definitively linked with patient delay. Two studies(Wielgosz and Nolan, 1988; Hackett and Cassem, 1969) found no significant relationship between denial and patient delay. A more recent study (Bleeker et al., 1995), however, found that denying patients waited longer before looking for medical help. Bleeker et al., 1995 suggest that the use of different operationalizations and instruments may be the cause of these conflicting findings. Additionally, only one of four dimensions of the Denial questionnaire (Trijsburg et al., 1987; Trijsburg et al., 1989), resentment, was robustly related to patient delay. Conflicting findings will only be resolved through future research, and as a result, denial has yet to definitively linked with patient delay.

Given the lengthy patient delay that is usually reported, it remains tempting to identify denial as an important psychological response that significantly increases delay time (Dracup et al., 1995). According to Dracup et al., 1995, “two methodological problems make it difficult to understand the role of denial in patient delay time. The first is that all data related to the patient’s decision process must, of necessity, be collected retrospectively. Denial is a transitory coping mechanism that is difficult to evaluate after the fact. Investigators can ask patients how serious they thought their symptoms were or if they labeled their symptoms as cardiac in origin, but in the end it is impossible to assess the degree to which the patient used denial to ward off anxiety.” Secondly, the lack of an appropriate psychometric instrument to measure denial presents a large methodological problem. Previous studies which have not found a relationship between denial and patient delay (Wielgosz et al., 1988; Schmidt and Borsch, 1990; Hackett et al., 1968; Hackett and Cassem, 1969) may relate more to the inherent difficulty in measuring denial than to the lack of such a relationship (Dracup et al., 1995).

Hospitalization and Recovery from AMI and Denial

Once under coronary care, denial appears to play a different role in AMI patient outcome. Several studies have found AMI patients with high denial levels had superior outcomes during the first three days of recovery (Prince et al., 1982; Levine et al., 1987; Lazarus, 1983). During the first three days of hospitalization, arrhythmias, tachycardia, strong anxiety, and elevated blood pressure levels all increase mortality. In the coronary care unit setting, patients with strong denial experience fewer of these problems, perhaps because of less adrenergic nervous system stimulation (Fields, 1989). Levine et al.(1987) followed 30 men for 1 year post-MI and reported that individuals with high scores on a denial scale spent fewer days in intensive care and had fewer signs of cardiac dysfunction while in the hospital in comparison with those who had low scores.

However, once post-MI patients have been discharged from the hospital setting, this same study (Levine et al., 1987) suggests that denial switches from an adaptive behavior to a maladaptive behavior. After 1 year, high deniers were more non-compliant with treatment recommendations and required more days of re-hospitalization. Further support that denial of illness leads to problems once removed from the hospital setting comes from a recent prospective study by Julkunen and Saarinen, 1994. Using return to work 1 year following MI as a MI recovery outcome variable, they found that denial of illness was the best single psychological predictor of return to work. Denial of illness, assessed using a subscale of the Coping with Illness Scale (Julkunen, 1989; Saarinen, 1992) which was developed specifically for CHD patients, was more strongly correlated to return to work than work stress, anxiety, Type A, anger-out, or depression measures. Specifically, denial of illness had a -0.32 correlation with return to work (p<0.001). Numerous other studies also support that prolonged denial leads to ignorance of necessary activity restrictions, refusal to appreciate the seriousness of the illness, or failure to take prescribed medications needed to recover (Gentry and Haney, 1975; Douglas and Druss, 1987; Fields, 1989; McKenday and Logan, 1982; Scalzi and Burke, 1982; Viswanathan and Vizner, 1984).

Denial of Emotions, CHD, and CHD risk factors

There is also reason to believe that denial is not only a danger to individuals who are either in the early stages of AMI or in the process of out-of-hospital recovery from AMI. Prolonged denial of negative emotions and problems may substantially increase the risk of developing CHD. Denial of problems has been significantly positively correlated (p<0.01) with CHD somatic risk factors, such as LDL cholesterol, body mass index, and triceps skinfold, in 15 year old girls (Keltikangas and Jokinen, 1989). Similarly, denial of problems has been significantly positively correlated (p<0.01) with LDL cholesterol and total cholesterol in 12 year old girls (Keltikangas and Jokinen, 1989). It should be noted that significant correlation between denial and these CHD risk factors were not observed in 12, 15, and 18 year old boys, or 18 year old girls (Keltikangas and Jokinen, 1989).

Grossarth-Maticek and colleagues provide much stronger evidence that prolonged repression and denial of emotions may greatly increase the risk for CHD (Grossarth et al., 1985). According to a review of psychosocial risk factors for CHD by Kabat-Zinn, 1992: They “investigated the relationship between a number of psychosocial and personality factors and the incidence of and mortality from heart disease. In a 10-year prospective study in Yugoslavia of approximately 1400 people, they found that an 11-item questionnaire assessing rationality-antiemotionality, or repression and denial of emotions, was the best single predictor of the subsequent development of CHD. The relative risk for CHD was ten times greater for those who scored high on this scale compared to those who scored lower.

Rationality-antiemotionality was a stronger predictor of heart disease than the traditional CHD risk factors in this study (smoking levels).”

Does Denial Play a Role in the Development of High Blood Pressure, Exaggerated Blood Pressure Reactivity, or High Stress Levels?

Several studies have investigated whether or not hypertensives tend to be less self-disclosing and more likely than normotensives to use denial to blot out negative affect, neurotic conflicts, or awareness of psychiatric disorder.

According a 1989 review of psychosocial variables and hypertension(Sommers-Flanagan and Greenberg, 1989), there were eight such studies from 1979 to 1986. Five of those studies (McLelland, 1979; Drummond, 1982; Cumes, 1983; Svensson and Theorell, 1983; Santonastaso et al., 1984) found elevated blood pressure tended to be associated with less personal disclosure or greater denial of neurotic conflicts, while three found no such relationship (Monk, 1980; Mann, 1984; Cottington et al., 1985). More recent studies have also supported a possible relationship between denial and hypertension. Asymptomatic hypertensives (Knox et al., 1988) , as well as normotensives with a family history of hypertension (Jorgensen and Houston, 1986; Theorell, 1990), seem to express fewer emotions, have a noncomplaining attitude, and lack an ability to differentiate feelings, similar to denial (Karasek, 1990). Although these results are far from conclusive, they do support the existence of a tendency for hypertensives to use denial more frequently than normotensives. However, due to a lack of prospective studies investigating whether denial may play a causative role in the development of hypertension, there is no strong evidence to suggest that denial poses a significant risk to cardiovascular health via increased risk for high blood pressure.

As previously mentioned, normotensives with a positive family history of hypertension (FH+ normotensives) seem to express fewer emotions, have a noncomplaining attitude, and lack an ability to differentiate feelings (Jorgensen and Houston, 1986). FH+ normotensives manifest greater sympathetically driven cardiovascular reactivity to stressors than normotensives with a negative family history(FH-)(Hastrup et al., 1982; Jorgensen and Houston, 1981; Manuck and Proietti, 1982). Furthermore, it appears that a subgroup of these FH+ normotensives characterized by denial and unwillingness to admit to neurotic feelings or aggressiveness may be responsible for the exhibited exaggerated blood pressure reactivity of FH+ normotensives (Jorgensen and Houston, 1986). This subgroup reported little negative affect in response to experimental stressors in which they exhibited exaggerated blood pressure reactivity, which suggests they deny or suppress their feelings. Denial of negative affect in response to experimental stressors and effects on exaggerated blood pressure reactivity have not been sufficiently studied.

In a recent study by Suter et al., 1997, an inverse association between self-perceived stress and systolic blood pressure was found. They suggest that “the inverse association between systolic blood pressure(SBP) and the self-perceived stress reflects a neuroendocrine and biochemical setting characterized by inadequate stress handling associated with a higher fat and alcohol intake and more abdominal fat tissue leading to a higher blood pressure.” They believe their “data suggest that stress denial in combination with abdominal obesity, alcohol consumption, and smoking may be proxy for a high stress level.” Further research is needed investigating whether denial indeed plays an important role in exaggerated blood pressure reactivity or high stress levels.

Social determinants of Denial

There has been remarkably little research on the determinants of denial, particularly social class and job stress. Such factors might shape personality development in childhood. For example, certain parental behavior patterns (i.e., overly strict, critical and demanding of conformity) are more common in low SES households, and may be viewed as a reflection of the parents’ occupational and other life experiences, which are characterized by low control and insecurity. Similarly, an adult’s experience, which might include stressful, low control jobs, may shape their personality development (Kohn and Schooler, 1982). Thus, research on the social determinants of personality measures believed to be associated with illness outcomes needs to be a major priority in future research.


As Sirous (1992) concluded in his review on denial in CHD, denial likely has a long-term negative effect on cardiovascular health. The extent and importance of that negative effect on cardiovascular health is still quite unknown due to methodological problems concerning the assessment of denial. Prompt medical treatment is crucial to the survival of AMI, and denial of cardiac events may be a primary reason for patient delay. However, denial has yet to be definitively linked to patient delay. Further research is needed on the relationship between denial and patient delay, because if such a link exists, dramatic reductions of patient delay might be possible. As a result, thousands of lives per year could be saved by getting AMI patients to the hospital early enough to receive thrombolytic therapy. Although denial may be an adaptive behavior towards the first three days of recovery from AMI, there is strong evidence that prolonged denial of the significance of the illness negatively effects AMI recovery outcome once removed from the hospital setting.

There is also prospective evidence suggesting that prolonged repression and denial of emotions may greatly increase the risk for CHD. Unfortunately, there has been a lack of prospective studies on denial and repression of emotions as a CHD risk factor since the findings by Grossarth et al., 1985. More prospective studies on the cardiovascular effects of denial of emotions are needed to confirm and better understand the findings of Grossarth et al., 1985.

Other studies have found denial to be associated with elevated blood pressure, exaggerated blood pressure (BP) reactivity, and possibly even high stress levels. Once again, due to the lack of prospective evidence on denial as a risk factor for hypertension, BP reactivity, or high stress levels, there is no strong evidence yet for any these hypotheses.

The study of denial as a psychosocial risk factor for CHD has not been studied nearly as thoroughly as other more heavily focused-on psychosocial risk factors, such as hostility, anger, type A behavior pattern, anxiety, or depression. With improvements in the validity and reliability of assessments of denial, and increased attention from coronary-prone researchers, it will be possible to better understand how much of a role that denial plays in effecting cardiovascular health.

Lastly, very little is known about the determinants of denial. Research on the social determinants of personality measures believed to be associated with illness outcomes needs to be a major priority in future research.


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