The Oates Journal (ISSN: 1098-1446) is a publication of the Wayne E. Oates Institute addressing issues related to spirituality, ethics, and healing from the perspective of pastoral care and counseling.

At the core of our being, we are not alone when we invest our faith in the One who stands by us and gives us courage and comradeship through adversity. Convictions That Give You Confidence by Wayne E. Oates "We dedicate this paper to the memory of Wayne E. Oates, our friend, pastor, mentor, and colleague. He taught us to give "bare attention" to the common events of life. He believed in the sacredness of the simple everyday acts of humankind. He saw the connectedness of reality and made a place for students of our disciplines. We have addressed sadness as if we might have been discussing it with Wayne.” Introduction

Sadness is a dynamic we encounter on the spiritual journey of life described by Lewis Sherill (1959) as the "struggle of the soul." For Sherrill, the religious and spiritual development of the individual takes place as we go through the crises of life from infancy to death. The struggle of the soul leads to integration of one's understanding of God into daily life. How we accept and deal with sadness is essential to our psychological, physical and spiritual development and wellbeing. In this paper we address sadness as one of the negative aspects of the struggle of the soul.

Sadness is a common, troublesome feeling; a negative affect that is felt as unpleasant and observed by others as a sign of distress. Its range of intensity is from slight to deep and its severity from mild to extreme. In this article, our purposes are to: (1) mention briefly the origin and changing use of the word, sadness, (2) describe its development during childhood and look at its neurobiological basis, (3) present the clinical significance of sadness in grief, depression and especially dysthymia; and (4) discuss some treatment considerations.

According to the Oxford English Dictionary (1961), the word, sadness, has an Anglo-Saxon derivation. It first appeared in our language about the year 1000 and has had a number of interesting meanings. Until the mid 1400's, it meant steadiness or heaviness and had mainly a positive connotation. However, about the middle of the 15th century, Chaucer used it to describe a morose condition. Until the middle of the 18th century, it was used to mean sturdiness, seriousness, and/or heaviness. In the 18th century, Descartes (1644), whose philosophy is centered on the famous premise: "I think, therefore, I am", considered it to be one of the six primitive emotions; the remaining five were admiration, desire, love, joy, and hate. With the flowering of the Romantic Movement in the literature (especially poetry), music, and art of Western Society in the 18th century, sadness was used increasingly to refer to a sorrowful countenance or disposition. Consistent with the 18th century, the Judeo-Christian Scriptures describe sadness as an affective response; for example, in Job 9:27, he states: "I will put off my sad countenance." (Oxford Annotated Bible, 1962) In his poem, "The Rime of the Ancient Mariner", Coleridge (1782) wrote the now familiar words "He awoke a sadder but wiser man." (Coleridge, 1973) But, some of the old usage has remained, at least until about 30 years ago. In rural Eastern Kentucky some of the housewives referred to the bread they baked as being "sad" when it had not risen and was heavy.

Sadness as a Negative Affect

The word sadness often is used interchangeably with the term emotion. We tend to stick with the somewhat more scientific view that emotion refers to the cognitive and somatic changes that accompany a predominant feeling as well as to the feeling, whereas affect refers primarily to the feeling-tone that accompanies memories, thoughts, or actions. Thus, sadness is one of the negative affects, a primary component of disappointment, lowered mood, loss, grief, and the various depressive conditions.

Although many of the standard textbooks in psychiatry do not even list the word, sadness, in their indices, more attention than in the past is being given to the negative affects, mainly sadness, anger, and fear. The interest in sadness extends from studies of infants and children in nurseries and schools, to the elderly in nursing homes. We think that much of that interest has been fueled by the marked increase in depressive illnesses evidenced by the results of epidemiologic and related studies. (Schwab, 1970)

Origins and Functions of Sadness

In depth understanding of the affects and emotions requires increased knowledge of their evolutionary origins and functions. According to Randolph Nesse (1998), they are "special states" that have been shaped by natural selection to "adjust various aspects of the organism to give it a selective advantage in the face of adaptive challenges. The affects have been designed, especially, to maximize reproductive success (not happiness)". Also, to understand an affect, such as sadness in an evolutionary and ethological sense as well as sociobiologically, we need to look at some of the unique characteristics of human beings and their development. Harlow (1996) emphasized that the human newborn, unlike other primates, does not cling. Consequently, attachment, which is essential for survival, is dependent on seeing, touching, and being touched by the mother or maternal object. Her not being felt or seen obviously can mean doom. The perception of possible loss of the mother and thus of survival calls forth a primordial reaction, the affect, sadness, which thus is basically an interpersonal and a social affect.

In discussing the extraordinary rapidity of change in neonatal development during the first few years of life, Stella Chess (1969) pointed out that there is a "steady progression of demands upon the growing organism for increasing socialization" (pp. 125-136). Clinically, sadness was observed by Spitz (1946) in his now classical studies of infants in foundling homes who were deprived of mothering. Their sadness often was followed by infantile anaclitic depression, characterized by severe emotional and physical withdrawal, a sunken-faced apathy, a general loss of well-being, and an apparent "giving-up" equivalent to hopelessness. Spitz's longitudinal study was the basis for the description of the syndrome, "hospitalism" (p. 2). Thus, Nesse (1998) maintains that we can consider such basic negative affects as anxiety and sadness, like pain, to be defenses that have evolved, and need to be thought of "in terms of relationship strategies and social emotions (which offer great promise for psychotherapy)" (pp. 397-415).

Thus sadness is a negative affect that evolves as a marker in response to adaptive challenges during human development from infancy to adulthood.

The Neurobiology of Sadness

Some of the significant advances in knowledge of the neurobiological basis for and the physiological concomitants of the affects are illustrated by the results of W.A. Brown and colleagues' research (Brown, Sirota, Niaura, et al., 1993, pp. 458-467). They reported associations between endocrine changes and subjective ratings of induced sadness or elation. Serum cortisol levels were found to increase equally during induced sadness or elation. Also, growth hormone levels along with heart rate and blood pressure tended to increase with elation. Thus, sadness and elation were associated with definite endocrine correlates.

In 1995, Mark S. George and his colleagues, reported that transient sadness significantly activated limbic and paralimbic brain structures as well as the brainstem, thalamus, and the caudate/putamen, as measured by changes in regional cerebral blood flow (rCBF) during experimental positron emission tomography (PET) scanning (George, Ketter, Parekh, et al., 1995, pp. 341-351). In contrast, with transient happiness there were no areas of increased activity but there was a wide reduction of rCBF, especially in the right prefrontal and bilateral temporal-parietal regions. The findings were considered to have both theoretical and clinical implications for greater understanding of the neural substrates of the normal and the pathological emotions, especially anxiety and mood disorders as well as sadness.

Moreover, in a recent study, George and his colleagues reported "gender differences in rCBF during transient self-induced sadness or happiness"(George, Ketter, Parekh, et al., 1999, pp. 859-871). Their major finding was that "women activated a significantly larger portion of the limbic system in transient sadness than did men." We question whether the larger activated limbic system in females is associated with the bonding essential to the mother-infant attachment and the historic view of women as being capable of greater emotionality than men. In his comment on gender differences, J. C. Ballenger (1998) noted that George and his colleagues' study was remarkable and had attracted the attention of the national media.

The most exciting and apparently the most definitive new neurobiological findings are centered on the major role of the amygdala in the development of the negative affects, including sadness. A study of a person whose amygdala had been destroyed by disease revealed that it has a central role in discerning human social signals. The person could not perceive fear in others' expressions but had no difficulty recognizing the smiles of happiness. In 1995 J.L. McGaugh and colleagues at the University of California, Irvine, "pinpointed the amygdala as the site where adrenaline and other hormones affect memory" (McGaugh, Cahill, Parent, et al., 1995, p. 205). Also, a number of studies have determined that it "plays a central role in the onset of clinical depression...(and) even appears to cement recollection of charged events more firmly in the mind by linking emotions to long-term memories." Leslie Brothers at UCLA stated that the findings "make it very clear that the amygdala is involved in receiving social signals in humans" (Brothers, 1990, pp.81-91). Antonio Damasio and his colleagues maintained that the ongoing research provides "important evidence that the mind and the body evolved together, with primary emotions becoming a separate and integral part of the brain because they play such an important role in survival" (Damasio, 1998, pp. 57-71). For example, Hotz (1995) emphasizes that the amygdala is connected to the other parts of the brain that elaborate the primordial "fight-or-flight" reflexes.

The increased understanding of the neurobiology of sadness is important in as much as the cultural, economic and religious beliefs are the social signals received by the brain and play a role in the development of sadness as an affect.

Sadness: A Component of Grief

In a number of interpersonal situations, sadness is appropriately expressive. But, it can be an emotional reaction to a disappointment or loss, a fundamental component of grief, or a major symptom of clinical depression, even in its extremes of melancholia or psychotic depression. Thus, as a major negative affect, we think of sadness as being on a clinical continuum, beginning with sadness as a common feeling state and extending to pathological grief and then to depression.

In thinking of sadness as being intrinsic to the human condition, and of its being on a clinical as well as an existential continuum, an important early question arises: "When is it pathological or clinically significant?" As we have seen, transient sadness is normal, and, as such, can serve important interpersonal, usually communicative functions. When it is prolonged, too intense, or otherwise excessive in everyday life, however, treatment considerations are necessary. Clinical interventions are especially needed when sadness is described as "painful" and/or interferes with ordinary functioning.

When a person is grieving about the death of a loved one, sadness is usually the dominant affect. Often, it is linked to guilt about what one did or, more often, what one thinks he or she failed to do or did not do it sufficiently or adequately. Three points that need to be addressed are (1) grief is a normal reaction; (2) there is a personal, not necessarily a correct prescribed way to grieve; and (3) it can be evidence of respect for the deceased. Who would want to think that she or he had died and that no one had grieved nor expressed sadness? Would it mean that one had lived a meaningless life, that she or he had not "touched" another human being? However, prolonged and/or intense grief with significant physical and interpersonal complications as well as sadness generally call for psychiatric referral.

Grief can come as a shock-like reaction to catastrophic illness affecting oneself or a loved one or to the terminal illness and death of a family member or companion. In addition to sadness, it brings with it a heightened awareness of one's own personal vulnerability and mortality along with loss and disappointment. Chase Kimball's description of the medical psychotherapy of the grieving process deserves our attention. He sees it as involving four overlapping, often recurring, processes: (1) denial, (2) ventilation of affect, (3) defensiveness, and (4) reconstitution (Kimball, 1975, pp. 608, 641).

Some degree of denial can serve a protective function for the organism. It can be both emotionally and physically deleterious and potentially dangerous to the patient, and is often fraught with difficulties for doctors, nurses, and other caregivers. Meerloo, who called it "the negative illness," considered it the most serious reaction to illness (Meerloo, 1956, pp. 31-43). When a patient is denying an illness, we point out that such denial is a normal initial reaction that serves a useful purpose when, for example, it allows us to accept the illness or death and adjust to it at our own pace and not be a slave to the dictates of "should," others' opinions, or to convention. Then, if the denial (and with patients we use the word repeatedly) persists for an excessively long period of time, it can cause harmful delays in receiving needed medical care and even surgery.

Denial has implications for the doctor-patient relationship. It precludes collaboration, if not agreement about the severity of the illness and cooperation with needed treatments. For example, patients sign out of the hospital against advice or, more commonly, do not adhere to medication regimens.

When working with a patient who is using excessive denial, it is helpful to ascertain its sources. Three common ones are fear, sadness, and other persons' opinions. We need to grasp the extent of the patient's fear and to bear in mind that excessive denial can be indicative of psychological fragility, of his or her deep fears of not being able to maintain emotional stability. Consequently, after firmly labeling the denial, we may not confront it directly but instead we immediately bring up the topics of fear and sadness, use the words redundantly, and avoid euphemisms. The two therapeutic goals are, first, to get the patient to ventilate fears and feelings by encouraging him or her to bring out thoughts and feelings. We ask about possible irrational thoughts which, it is wise to explain, are commonplace at such times. Also, it is helpful to distinguish between thoughts and feelings and persuade the patient to do so.

The second goal is for the doctor, nurse, and other caregivers to provide a meaningful explanation of what is happening, what are the options, and what the expected outcome will be. Words that explain and also communicate care and caring are some of physicians' and nurses' most powerful tools. Seventy-five years ago, Harvard professor, Francis Peabody (1987) reminded all of us that the care of the patient is basically the caring for the patient. Physicians and nurses, as the strong care-giving persons, can become the targets of the grieving person's loss. Of course, in modern managed-care America, the quips about doctors are "We don't care about how much you know, we want to know how much you care."

The point at which grief becomes abnormally prolonged and/or intense requires several considerations. One is cultural. The appropriate length of the period of mourning differs among various cultural and religious groups. In our Anglo-Saxon culture, the usual time for mourning has shortened greatly. In the 20th century, such conventional signs of mourning as a black armband or a wreath on the front door have become almost non-existent. We speculate that such developments have contributed to emotional problems attendant grief's becoming somewhat more severe than in the past. But such sociocultural changes as the prevailing instability of relationships, even the marital and familial, are supervening and are conducive to relatively short mourning periods and to the disappearance of displays of mourning. In psychiatry, the relative inattention given to both bereavement and to grief in DSM-III-R and in DSM-IV (1994) attests to the disinterest in them, although, grief reactions have both psychiatric and medical significance. Also, both anticipatory grief and "anniversary" reactions are commonly overlooked.

Avery Weisman (1985) and his colleagues discuss grief as extending for about one year and, in many cultures, a one-year mourning period was considered essential. In the USA, it is now generally anticipated that the marked sadness, anxiety, and emotional distress of acute grief will begin to wane after about three months. However, some definite symptoms of distress, especially lingering sadness compounded with loneliness and both common and uncommon physical symptoms often persist until the first anniversary reaction has been endured. Thus clinically, attention needs to be given to the intensity and duration of the grieving process. The unattended grief that began as sadness can evolve into complicated grief and serious mental illness.

Diagnostic Considerations

Inasmuch as sadness usually is the dominant affect in grief, unresolved grief, complicated bereavement, and in major depression, the differential diagnosis is often difficult. Some guidelines are as follows:

In addition to medications and supportive interpersonal or cognitive psychotherapy, spiritual counseling and group therapies can be very helpful. When the patient has severe depression, especially melancholic or psychotic, emergency psychiatric hospitalization is usually needed.

The most common overlooked depressive condition in which sadness is the prominent feature probably is dysthymia, often termed neurotic depression, chronic sorrow, or chronic depression. As a clinical condition, dysthymia has been known since the days of Hippocrates in the 5th century B.C.; in Greek, the word, means "ill-humored". Most dysthymic patients complain about being sad most of the time, not being able to enjoy themselves, feeling low self-esteem, having difficulty making decisions, and being fatigued or low in energy. In many cases, the sadness and lack of enjoyment lead to interpersonal difficulties in which their spouses maintain that they are continually irritable and, often the dysthymic patient complains of irritability. After questioning, some of these patients tell that they are abnormally sensitive as well as joyless, negative and irritable. They describe having interpersonal difficulties because they cannot tolerate seemingly normal levels of noise, light, and/or temperature. Moreover, the chronic sadness of dysthymia is frequently accompanied by a generalized pessimism that is disturbingly negativistic. Sometimes, the patient complains of reverse symptomatology, particularly oversleeping and overeating along with anhedonia, lack of motivation, a poor level of general functioning, and "leaden paralysis" (Gruenberg and Goldstein, 1997, p. 1013).

The age of onset of dysthymia generally is the adolescent years, although some dysthymic patients state that they were chronically sad, even in childhood. The official diagnostic criteria require the presence of symptoms for a minimum of two years and the exclusion of major depression although, sometimes major depression is superimposed on dysthymia and the patient then has "double depression" (Keller, Lavori, Endicott, et al., 1983, pp. 689-694). Usually, there is a positive family history of some degree of depression and/or alcoholism. The prevalence of dysthymia is unknown, but has been considered to be as great as 6.4% (Gruenberg and Goldstein, 1997, p. 1014). Often, the outcome is not good. Wells et al. found that, compared with other depressed patients, those with dysthymia "had the worst outcomes and a poorer initial functioning status, as well as the poorest prognosis, even in the absence of major depression" (Wells, Burnham, Rogers, Hays, and Camp, 1992, pp. 788-794; Keller, 1994).

Fortunately, most dysthymic patients respond to treatment with supportive psychotherapies, an exercise program, hormones (thyroid, estrogens, testosterone), and antidepressant medications. Usually a serotonin reuptake inhibitor in moderate dosage for an extended period of time is beneficial and long-term maintenance medication generally is a necessity.

Conclusion

In closing, we emphasize that humanistically, spiritually and clinically, sadness is a normal affect that is related to social interaction. It is a reaction, a marker which serves many purposes. In particular, sadness can be a marker for grief, depression, especially dysthymia and for despair, if not hopelessness.

As Sherrill (1959) has pointed out, sadness can be a marker for spiritual growth, the struggle of the soul, as well as for many of the nodal events in our lives. Our roles and functions are to lessen the distress of sadness by using our skills and caring.

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