Can Your Beliefs Impact Your Health and Well-Being?
The Chicago Social Brain Network
People have many sources of information, knowledge, and understanding. We consider the most common of these to be empirically acquired—learned facts, relations, associations, and perceptual and motor skills. Such learned associations serve as powerful determinants of thought and behavior. But other sources of information and knowledge also affect our interaction with the environment, including reflex-like (constitutionally endowed) circuits that are independent of explicit learning. Examples include central networks for pain withdrawal, hunger circuits for the ingestion of essential nutrients, social affiliation networks, and neural systems that promote maternal bonding. Each of these sources of information or knowledge can impact thoughts and beliefs, and thoughts and beliefs can impact behaviors and other bodily functions.
[A] Maori woman who, having eaten some fruit, was told that it had been taken from a tabooed place; she exclaimed that the sanctity of the chief had been profaned and that his spirit would kill her.... The next day...she was dead....1
I have seen a strong young man die...the same day he was tapued (tabooed); the victims die under it as though their strength ran out as water1
A superstition is a belief based not on reason or knowledge, but on legend, magical thinking, or other nonrational basis. Beliefs color the way we perceive the world; they direct and shape our actions and define our personalities. Beliefs are powerful determinants of action. A useful illustration of the power of beliefs comes from the parable of the Sultan (who had studied psychology) and his “lie-detecting” donkey. Lore has it that the Sultan was missing a valuable vase from his estate and suspected that one of his servants had stolen the piece. To identify the culprit, the Sultan gathered his servants in front of a dark room in which a donkey was tied and then asked each of his servants if they had stolen the item. Each said, “No.” The Sultan explained that inside the room was a magical donkey, specially trained to detect liars, who would bray when slapped by someone who had lied. The servants were sent into the room, one by one, and were instructed to close the door, slap the donkey, and return. “When the donkey brays,” the Sultan loudly proclaimed, “I will have my culprit.” The first servant was sent into the room and returned shortly thereafter—tremendously relieved, as the donkey had not brayed. One by one, the remaining servants entered the room and returned. The donkey had not brayed and all the servants looked quite relaxed. The Sultan was sanguine—he knew this donkey never brayed under any circumstances. The Sultan asked the servants to show him their hands. He then pointed to one of them and declared, “We have our thief,” instructing the guards to take him away. How had he identified the culprit? Rather than relying on a magical donkey, the Sultan, who was a student of psychology, took a more rational approach. Understanding the impact of beliefs on behavior, the Sultan had surreptitiously infiltrated powdered charcoal into the donkey’s hair. When the servants slapped the donkey, the charcoal marked their hands—with the exception of the guilty servant, who had not slapped the donkey, out of a belief and associated fear that the donkey could detect a liar.
Power of Beliefs
Beliefs may be potent determinants of behavior, but can they kill? And if so, how? How can these invisible, intangible entities impact health? In a now classic article published in the American Anthropologist in 1942, Walter Cannon, a leading Harvard physiologist and expert on the autonomic nervous system, proposed an answer.1 Investigating phenomena such as voodoo practices of the Haitians and “bone-pointing” among Australian aborigines, Cannon found that a common feature among the victims of such rituals was a strong belief in the curse and an associated morbid fear of the outcome. That fear, he argued, could trigger a “fight-or-flight reaction” (a phrase he had earlier coined), characterized by powerful and exaggerated activation of the sympathetic nervous system. The resulting vascular constriction diminishes blood flow to critical tissues (ischemia), with consequent hypoxia (decreased oxygen) and disturbances in normal metabolism and cellular function. These reactions may be exacerbated by the lack of food and water as the victim “pines away.” Cannon argued that these reactions could become life-threatening—fulfilling the gruesome legacy of the ritual—based on a belief in the supernatural, the veracity of which is largely irrelevant. More relevant is the emotion triggered by the belief, specious as it may be.
Beliefs and emotions have consequences, both behavioral and physiological. A recent example comes from contemporary medical literature. There is now a well-documented condition, sometimes triggered by something as innocuous as a spousal argument or a surprise birthday party, that entails the hallmark clinical and physiological features of a heart attack, including chest pain, abnormalities on the electrocardiogram, and elevated cardiac enzymes (reflecting damaged heart muscle).2 The condition has variously been termed takotsubo cardiomyopathy, left-ventricular apical ballooning, myocardial stunning, stress cardiomyopathy, or, in the more vernacular parlance of The New York Times, broken heart syndrome (prompted by a medical review that was published just before Valentine’s Day). In general accord with the speculation of Cannon, broken heart syndrome appears to be triggered by an exaggerated autonomic nervous system response, characterized by sympathetic activation and high levels of the stress hormone epinephrine (adrenalin).3 It is important to note in these cases that psychological states, as mild as they may be, are able to induce a clear and demonstrable organ pathology.
Physiological abnormalities or dysfunctions underlie medical conditions and, indeed, constitute the defining features of disease states. An important question, however, is how those dysfunctions come to be. Disease develops in many ways—traumatic injuries, biotic infections, degenerative conditions, and the list goes on. The fields of psychophysiology, psychosomatic or behavioral medicine, and health psychology are particularly concerned with how psychological and behavioral factors impact physiological systems and, therefore, health. Of particular interest are those psychological dimensions that uniquely impact physiology.
An example comes from the study of Herpes Simplex viral infections. Herpes Simplex viruses (HSV) are responsible for cold sores (HSV type I) and genital herpes (HSV type II). Once contracted, herpes virus infections generally remain for life, although they are characterized by periodic eruptions and remissions. During the latter, the immune system effectively dampens viral activity, and the virus retreats to an essentially dormant state. Although multiple factors likely contribute to the reactivation of HSV, one trigger appears to be stress—the defacing cold sore that erupts, for example, just before the prom or an important date. Ohio State researchers sought an animal model of this reactivation so the underlying links and mediators could be studied. Try as they might, however, the research group was unable to reactivate HSV infections in mice with standard laboratory stressors such as restraint stress or shock. In a collaborative effort, we pointed out that the stressors that lead to HSV reactivation in humans were often of a social nature. Indeed, for both humans and mice, social relations are central to happiness, adaptation, and even survival. In light of this, a social stressor was introduced into the project (changing the housing groupings and thus disrupting established social relations). The social stress, not physical stressors, resulted in significant HSV reactivation.4Psychological factors, in this case a specific social psychological variable, uniquely impacted an important aspect of viral immunity. This early finding led to a series of studies that have elucidated physiological pathways that mediate the relationship among social stress, immune function, and HSV reactivation. But what is it that makes social stress unique and distinct from physical stressors?
We have identified a probable general contributor to the differences between lower-level physical or homeostatic challenges and higher-level psychological and social stressors. Basic homeostatic reflexes—reflexes that keep in balance various critical bodily processes, such as blood pressure, body temperature, and blood sugar—are largely hard-wired and organized at relatively low levels of the nervous system, such as the brainstem and spinal cord. An example comes from autonomic nervous system regulation of cardiovascular function. The sympathetic division of the autonomic nervous system is an activational, energy-mobilization system that comes into play in the face of adaptive challenges. Sympathetic activation increases heart rate and results in peripheral vasoconstriction, both of which tend to increase blood pressure. In contrast, the parasympathetic division is an energy-conserving, deactivational brake that generally opposes the sympathetic system, yielding decreases in heart rate and blood pressure. The baroreceptor heart rate reflex is a homeostatic reflex that functions to maintain blood pressure within homeostatic limits. Unique pressure-sensitive receptors in the heart and large arteries detect changes in blood pressure, and a decrease in blood pressure triggers the baroreceptor heart rate reflex, increasing sympathetic activity and reciprocally decreasing parasympathetic tone. Both effects serve to increase heart rate (and thus cardiac output) and constrict arteries throughout the body, thereby restoring the pressure perturbation. In basic reflexes, the two autonomic branches are generally regulated in this reciprocal fashion and thus synergistically amplify the effects of the other. This is a useful mechanism to adjust to severe adaptive challenges, such as a decrease in blood pressure and compromised circulation.
Although this reciprocal mode of regulation of the autonomic branches has considerable utility and is characteristic of basic reflex organizations, it may not always be optimal. The autonomic nervous system provides the basic support for action and adjustment, and although it figures prominently in survival-related functions, it also provides the basic visceral support for emotional and cognitive operations. It has long been recognized that cognitively demanding tasks elicit greater autonomic activation than is needed to meet the metabolic demands of the tasks. Moreover, ascending neural signals to the brain from visceral organs such as the heart and blood vessels serve to modulate and regulate cognitive activities.5 The notable early psychologist William James proposed that emotion is the experience of somatovisceral sensory feedback. James suggested that we do not run from the bear because we are afraid, but rather we are afraid because we run from the bear.6 Although the strong form of this theory has not been supported, it remains the case that ascending visceral signals can modulate learning, attention, and cortical and cognitive processing.5 The autonomic nervous system is not only for lower-level reflexive adjustments. Indeed, it is increasingly recognized that there is a highly complex, even intricate, interaction between the autonomic nervous system and higher-level brain structures (such as the frontal cortex) involved in human behavior. Importantly, these circuits and their interactions with the autonomic nervous system are highly flexible and are not constrained by the simple organization rules that govern basal functions such as homeostasis and reciprocal control of the autonomic branches. Rather, higher-level systems engage in highly sophisticated “banter” with the autonomic nervous system.
In contrast to the reciprocal control characteristic of autonomic reflexes, higher-level brain circuits exert more flexible control over the autonomic nervous system. This can include the classic reciprocal control pattern but can also include an independent control pattern in which only the sympathetic branch or only the parasympathetic branch of the autonomic nervous system is activated, and a coactive control pattern in which both branches are activated. This greater flexibility in control may have behavioral and health significance.
Beliefs about One’s Relationship with God and Autonomic Functioning
Recently, we used a population-based sample of 50- to 68-year-old adults in the Chicago Health, Aging, and Social Relations Study to examine risk factors for heart attacks—a health outcome known to be influenced by the autonomic nervous system. We were particularly interested in whether spirituality influenced risk for heart attacks. With very few exceptions, everyone in our sample expressed a belief in God. However, individuals differed in how they perceived the quality of their relationship with God, much as individuals differ in how they perceive the quality of their relationships with other people. We defined spirituality as the degree to which a personal relationship with God was believed to offer safety, security, contentment, and love. One observation that emerged from this study was that spirituality was associated with a lower incidence of heart attacks.7 This remained true after ruling out the effects of demographics, health behaviors, body mass index, blood pressure, and other potential explanatory factors. Short of divine intervention, was there a rational explanation for this relationship? We certainly know that psychological factors can impact autonomic control, among other aspects of physiology.
As mentioned earlier, sympathetic activation may have harmful consequences if it is extreme or prolonged. For example, heightened sympathetic activation is known to predict a poorer outcome after a heart attack. In contrast, parasympathetic activity may have beneficial or protective effects. From the perspective of a reciprocal model of autonomic control, high parasympathetic with low sympathetic control would be optimal, whereas high sympathetic with low parasympathetic control would be considered a risk. But we also know that higher-level neurobehavioral systems may not be constrained to reciprocal autonomic controls. Moreover, it has been argued that more autonomic control is better than little control, in that it affords greater capacity for adjustment of visceral functions. Could high levels of parasympathetic control, for example, mitigate the negative effects of sympathetic activation, and perhaps yield an even more advantageous health outcome?
To examine these questions, we developed two quantitative measures of autonomic control.8 The first was a common metric of autonomic balance (Cardiac Autonomic Balance), which represents the relative dominance of the two branches along a single autonomic continuum that ranges from purely parasympathetic control to purely sympathetic control. This metric is consistent with the classical model of reciprocal control, characteristic of reflex processes, in which autonomic balance can be biased toward one of the autonomic branches. High scores indicate sympathetic dominance and low scores indicate parasympathetic dominance. Independent estimates of sympathetic and parasympathetic control were obtained using standard measurement procedures, and the level of parasympathetic control was subtracted from sympathetic control to derive a measure of Cardiac Autonomic Balance. A second metric was designed to capture an alternative mode of autonomic control (Cardiac Autonomic Regulation) that assesses the degree of relative coactivation (rather than reciprocal activation) of both branches. This is a metric that taps into the nonreciprocal regulatory influences of higher neural structures. Cardiac Autonomic Regulation scores were derived by essentially summing activities of the sympathetic and parasympathetic branches to afford a measure of total overall autonomic cardiac control. High scores indicate high activation and low scores indicate low activation of both branches of the autonomic nervous system.
In the 50- to 68-year-old adults in our sample, spirituality was found to be associated not only with a lower incidence of a heart attack, but also with a higher level of Cardiac Autonomic Regulation. That is, people who felt a closer relationship with God exhibited higher overall autonomic regulation—both sympathetic and parasympathetic. This was associated, in part, with lesser diminution of parasympathetic control and a greater degree of coactivation. Moreover, Cardiac Autonomic Regulation (but not Cardiac Autonomic Balance) predicted better overall health status and was associated with a lower incidence of a heart attack. Participants who had low Cardiac Autonomic Regulation were more likely to have suffered from a heart attack.
Could higher Cardiac Autonomic Regulation scores explain why spirituality was associated with less risk for a heart attack? That is, could a pattern of autonomic regulation associated with spirituality explain the link between spirituality and a heart attack? To address this question, we conducted statistical tests of these linkages. As we already knew, both spirituality and Cardiac Autonomic Regulation are associated with a lower incidence of a heart attack. When the predictive effects of spirituality were statistically extracted, Cardiac Autonomic Regulation continued to be a significant predictor of a lower incidence of heart attacks. However, when the linkage test was reversed and the effects of Cardiac Autonomic Regulation were extracted, spirituality was no longer a significant predictor. This indicates that Cardiac Autonomic Regulation is a plausible mediator that may explain the relationship between spirituality and heart attacks.
By capturing higher levels of parasympathetic control and the associated autonomic coactivation of the sympathetic and parasympathetic branches, Cardiac Autonomic Regulation provided a critical metric that permitted the study of a previously “invisible” and mysterious link between spirituality and health outcomes. This in no way diminishes the relationship between spirituality and health, but it instead offers an important hypothesis on how spirituality may impact physiology and health status. Spirituality reflects an important aspect of the general domain of sociality and social relationships—a domain heavily influenced by our genetic constitution as a social species. Indeed, the importance of sociality may be more related to beliefs and attitudes about the meaningfulness of relationships than their existence or number. And again, beliefs about social relationships also have real consequences.
Conclusion
Beliefs impact thoughts and actions. This may be reflected in phenomena as diverse as biasing a behavioral disposition (such as slapping a donkey), coloring our perception of the environment, or determining how we perceive the quality of our social (including spiritual) relations. Psychology can impact physiology, and physiology, in turn, can influence our thoughts and emotions. Psychophysiology is the study of these relationships, and it promises to illuminate the intricacies of psychosomatic relations and the previously “invisible” mechanisms that mediate these links. The relations between the mind and the body, the so-called mind-body problem, are complex and still rather obscure. Nevertheless, the mind-body problem is yielding to science, and the problem it poses is progressively diminishing. Among the components of the mind-body problem yielding to rigorous scientific inquiry are the effects of spiritual beliefs, including feelings of closeness to God.
Endnotes
1. W. B. Cannon, “‘Voodoo’ Death,” American Anthropologist 44 (1942): 169–181.
2. I. S. Wittstein, “The Broken Heart Syndrome,” Cleveland Clinic Journal of Medicine 74, Supplement 1 (2007): S17–22.
3. I. S. Wittstein, D. R. Thiemann, J. A. Lima, K. L. Baughman, S. P. Schulman, G. Gerstenblith, K. C. Wu, J. J. Rade, T. J. Bivalacqua, and H. C. Champion, “Neurohumoral Features of Myocardial Stunning Due to Sudden Emotional Stress,” New England Journal of Medicine 352 (2005): 539–548.
4. D. A. Padgett, J. F. Sheridan, J. Dorne, G. G. Berntson, J. Candelora, and R. Glaser, “Social Stress and the Reactivation of Latent Herpes Simplex Virus—Type I,” Proceedings of the National Academy of Sciences 95 (1998): 7231–7235.
5. G. G. Berntson, M. Sarter, and J. T. Cacioppo, “Ascending Visceral Regulation of Cortical Affective Information Processing,” European Journal of Neuroscience 18 (2003): 2103–2109.
6. W. James, “What Is an Emotion?” Mind 9 (1884): 188–205.
7. G. G. Berntson, G. Norman, L. Hawkley, and J. T. Cacioppo, “Spirituality and Autonomic Cardiovascular Control,” Annals of Behavioral Medicine 35 (2008): 198–208.
8. G. G. Berntson, G. J. Norman, L. C. Hawkley, and J. T. Cacioppo, “Cardiac Autonomic Balance vs. Cardiac Regulatory Capacity” Psychophysiology 45 (2008): 643–652.