The Role of Stress, Anxiety, and Depression Essays

The Role of Stress, Anxiety, and Depression Essays The Role of Stress, Anxiety, and Depression Paper The Role of Stress, Anxiety, and Depression Paper Human cells are the smallest structures capable of maintaining life and reproducing. They compose all living things, from single-celled plants to multibillion-celled animals. The human body, which is made up of numerous cells, begins as a single newly fertilized cell. Almost all human cells are microscopic in size. To give you an idea of how small a cell is, one average sized adult body, according to one estimate, consists of 100 trillion cells. The brain cells that create brain activity are called neurons. â€Å"The neuron (nerve cell) is the information-processing and information-transmitting element of the nervous system† (Carlson, 2007 p. 30). The brain and spinal cord are made up of many cells, including neurons and glial cells. Neurons are cells that send and receive electro-chemical signals to and from the brain and nervous system. There are about 100 billion neurons in the brain. There are many more glial cells; they provide support functions for the neurons, and are far more numerous than neurons. Structure of Brain Cells Each of the neurons has a cell body. â€Å"The soma (cell body) contains the nucleus and much of the machinery that provides for the life processes of the cell and its shape varies considerably in different kinds of neurons† (Carlson, 2007 p. 30). However, there are two kinds of fibers: axons and dendrites. Axons are â€Å"the long, thin cylindrical structure that conveys information from the soma of a neuron to its terminal buttons† (Carlson, 2007 p. 30). Dendrites are â€Å"a branched, treelike structure attached to the soma of a neuron; receives information from the terminal buttons of other neurons† (Carlson, 2007 p. 30). Each neuron has one axon along The Role of Stress, Anxiety, and Depression 4 which it sends electrical impulses to other neurons. Each neuron has a variable number of dendrites which have many branches. The axon from one neuron is attached to the dendrites of other neurons. The point at which they attach is called the synapse. The synapse is the â€Å"junction between the terminal button of an axon and the membrane of another neuron† (Carlson, 2007 p. 30). Furthermore, dendrites bring information to the cell body and axons take information away from the cell body. This is the process of thinking (Cohen, Kessler Gordon, 1988). A Map of the Brain Corpus callosum – Band of nerves between two hemispheres of the brain. Thalamus – Switching station for information going into the brain Basal ganglia – Control movement and cognitive functions Hypothalamus – Regulates sex hormones, blood pressure and body temperature Pituitary gland – Produces hormones; influences hormone production in other glands Amygdala – Regulates heartbeat; orders flight-or-flight reactions Hippocampus – Critical to long-term memory function Cerebellum – Coordinates movement How Nerve Signals Travel Carlson, (2007) states nerve signal proceeds in the following manner: 1. An electrical impulse is generated in the body of a neuron (nerve cell). The Role of Stress, Anxiety, and Depression 5 2. The impulse travels down the axon to an axon terminal (nerve ending). 3. At the axon terminal the impulse triggers the release of neurotransmitters. 4. Neurotransmitters are chemicals that enable a nerve impulse to jump across the synapse (the gap between nerve cells) at the axon terminal. 5. Once across the synapse, some neurotransmitters trigger the receiver cell; others prevent it from firing. Role of Brain in Mental Illness The belief that the mind plays an important role in physical illness goes back to the earliest days of medicine. From the time of the ancient Greeks to the beginning of the 20th century, it was generally accepted by both physician and patient that the mind can affect the course of illness, and it seemed natural to apply this concept in medical treatments of disease. Chemicals produced by immune cells signal the brain, and the brain in turn sends chemical signals to restrain the immune system. These same chemical signals also affect behavior and the response to stress. Disruption of this communication network in any way, whether inherited or through drugs, toxic substances or surgery exacerbates the diseases that these systems guard against: infectious, inflammatory, autoimmune, and associated mood disorders (Robert Sapolsky, 1998). The brain’s stress response system is activated in threatening situations. The immune system responds automatically to pathogens and foreign molecules. These two response systems are the body’s principle means for maintaining an internal steady state called homeostasis. A substantial proportion of human cellular machinery is dedicated to maintaining it. When The Role of Stress, Anxiety, and Depression 6 homeostasis is disturbed or threatened, a repertoire of molecular, cellular and behavioral responses comes into play. These responses attempt to counteract the disturbing forces in order to reestablish a steady state. They can be specific to the foreign invader or a particular stress, or they can be generalized and nonspecific when the threat to homeostasis exceeds a certain threshold. The adaptive responses may themselves turn into stressors capable of producing disease. The immune system’s job is to bar foreign pathogens from the body and to recognize and destroy those that penetrate its shield (Rubin Staddon, 1999). The immune system must also neutralize potentially dangerous toxins; facilitate repair of damaged or worn tissues, and dispose of abnormal cells. Its responses are so powerful that they require constant regulation to ensure that they are neither excessive nor indiscriminate and yet remain effective. When the immune system escapes regulation, autoimmune and inflammatory diseases or immune deficiency syndromes result. The central nervous and immune systems, however, are more similar than different in their modes of receiving, recognizing and integrating various signals and in their structural design for accomplishing these tasks. Both the central nervous system and the immune system possess â€Å"sensory† elements (Rubin Staddon, 1999), which receive information from the environment and other parts of the body; and motor elements, which carry out an appropriate response. Both systems also rely on chemical mediators for communication. Electrical signals along nerve pathways, for instance, are converted to chemical signals at the synapses between neurons. The chemical messengers produced by immune cells communicate not only with other The Role of Stress, Anxiety, and Depression 7 parts of the immune system but also with the brain and nerves (Robert Sapolsky, 1998). Chemicals released by nerve cells can act as signals to immune cells. Hormones from the body travel to the brain in the bloodstream, and the brain itself makes hormones. Indeed, the brain is perhaps the most prolific endocrine organ in the body and produces many hormones that act both on the brain and on the tissues throughout the body. A key hormone shared by the central nervous and immune systems is corticotrophin-releasing hormone (CRH); produced in the hypothalamus and several other brain regions, it unites the stress and immune responses (Science, 2001). The hypothalamus releases CRH into a specialized bloodstream circuit that conveys the hormone to the pituitary gland, which lies just beneath the brain. CRH causes the pituitary to release adrenocorticotropin hormone (ACTH into the bloodstream, which stimulates the adrenal glands to produce cortisol, the best-known stress hormone. Cortisol is a steroid hormone that increases the rate and strength of heart contractions, sensitizes blood vessels to the actions of norepinephrine, an adrenaline like hormone, and affects many metabolic functions as well as actions that help the body meet a stressful situation (Gerrig Zimbardo, 2002). In addition, cortisol is a potent immunoregulator and anti-inflammatory agent. It plays a crucial role in preventing the immune system from overreacting to injuries and damaging tissues. Furthermore, cortisol inhibits the release of CRH by the hypothalamus which also keeps this component of stress response under control (Rubin Staddon, 1999). Thus, CRH and cortisol directly link the body’s brain regulated stress response and its immune response. The Role of Stress, Anxiety, and Depression 8 CRH-secreting neurons of the hypothalamus send fibers to regions in the brain stem that help to regulate the sympathetic nervous system, as well as to another brain stem area called the locus ceruleus. The sympathetic nervous system, which mobilizes the body during stress, also innervates immune organs, such as the thymus, lymph nodes and spleen, and helps to control inflammatory responses throughout the body. Stimulation of the locus ceruleus leads to behavioral arousal, fear and enhanced vigilance (Rubin Staddon, 1999). Perhaps even more important for the induction of fear related behaviors is the amygdala, where inputs from the sensory regions of the brain are charged as stressful or not. CRH-secreting neurons in the central nucleus of the amygdala send fibers to the hypothalamus, the locus ceruleus, and to other parts of the brain stem. These CRH-secreting neurons are targets of messengers released by immune cells during an immune response (Rubin Staddon, 1999). Cytokines is the more general term for biological molecules that many different kinds of cells use to communicate. Each cytokine is a distinct protein molecule, encoded by a separate gene that targets a particular cell type. A cytokine can either stimulate or inhibit a response depending on the presence of other cytokines or other stimuli and the current state of metabolic activity (Science, 2001). This flexibility allows the immune system to take the most appropriate actions to stabilize the local cellular environment arid to maintain homeostasis. Activation of the brain by cytokines from the peripheral parts of the body induces behaviors of the stress response, such as anxiety and cautious avoidance that keep an individual out of harm’s way until full healing occurs. Anyone who has experienced lethargy and excess The Role of Stress, Anxiety, and Depression 9 sleepiness during an illness will recognize this set of responses as â€Å"sickness behavior† (Carson, Butcher, Mineka, 2000). Brain and Depression Although the role of the stress response in inflammatory disease in humans is more difficult to prove, there is growing evidence that a wide variety of such diseases are associated with impairment of the HPA axis and lower levels of CRH secretion, which ultimately results in a hyperactive immune system. Furthermore, patients with a mood disorder called atypical depression also have a blunted stress response and impaired CRH function, which leads to lethargy, fatigue, increased sleep and increased eating that often results in weight gain. A deficiency of CRH could contribute to lethargy in patients with chronic fatigue syndrome. Injection of CRH into these patients causes a delayed and blunted ACTH secretion by the HPA axis. That same response is also seen in patients whose hypothalamus has been injured or who have a tumor (Dobbs, 2006). Also, fatigue and hyperactivity of the immune response are associated with cortisol deficiency, which occurs when CRH secretion decreases. The hormone levels and responses in patients with fatigue syndromes suggest, but do not prove, that their HPA axis functions are impaired, resulting in a decrease in CRH and cortisol secretion and an increase in immune system activity. Together these findings indicate that human illness characterized by fatigue and hyperim unity could possibly be treated by drugs that mimic CRH actions in the brain (Dobbs, 2006). The Role of Stress, Anxiety, and Depression 10 When it comes to the chemistry of the human brain, dopamine and serotonin are the reigning stars. Like other neurotransmitters, they trigger and modulate the electrical signals that nerve cells use to communicate. In comparison, the chemicals called trace amines are considered mere bit players. Now, a study reveals that people have genes that encode cell surface proteins dedicated to responding to trace amines (Kowalski, 1999). Trace amines, so named because they’re present at low concentrations in the human brain, drew considerable interest in the 1960’s. They turned out to be the key neurotransmitters in insect brains, but interest in the chemicals waned when scientists failed to find dedicated receptors in vertebrates. The low concentrations of trace amines and their rapid turnover in the brain also made them difficult to study. Meanwhile, scientists identified receptors for dopamine and serotonin, which led to the development of crucial drugs (Kowalski, 1999). The trace amines, which include tryamine, betaphenylethylamine (beta-PEA), tryptamine, and octopamine, continued to draw some attention. Studies showed that diets rich in these chemicals can elevate a person’s blood pressure and trigger Imipramines in patients taking antidepressants know as MAO inhibitors. The reason for this is that unlike axons, there are no voltage-activated ion channels in the cell membrane of dendrites, so the electrical signal cannot regenerate itself. Instead, it gets smaller and smaller as it travels from the synapse to the cell body (Kowalski, 1999). Brain and Anxiety The classic form of depression, melancholia, is actually not a state of inactivation and suppression of thought and feeling; rather it presents as an organized state of anxiety. The The Role of Stress, Anxiety, and Depression 11 anxiety of melancholia is chiefly about the self. Melancholic patients feel impoverished and defective and often express hopelessness about the prospects for their unworthy selves in either love or work. The anxious hyper-arousal of melancholic patients also manifests as a pervasive sense of vulnerability (Carver Scheier, 2000). Many studies have been conducted on patients with major depression to determine whether the excessive level of cortisol associated with depression correlates with suppressed immune responses. Some have found a correlation between hypercortisolism and immunosuppressant; other have not. Because depression can have a variety of mental and biochemical causes, only some depressed patients may be immunosuppressed (Goldstein Dekker, 2001). The excessive secretion of cortisol in melancholic patients is predominantly the result of hyper secretion of CRH, caused by a defect in or above the hypothalamus. Thus, the clinical and biochemical manifestations of melancholia reflect a generalized stress response that has escaped the usual counter regulation, remaining stuck in the on position. The effects of tricyclic antidepressant drugs on components of the stress response support the concept that melancholia is associated with a chronic stress response. In rats, regular, but not acute, administration of the tricyclic antidepressant Imipramine significantly lowers the levels of CRH precursors in the hypothalamus (Jeanette, Webster Esther, 2002). Imipramine given for two months to healthy people with normal cortisol levels causes a gradual and sustained decrease in CRH secretion and other HPA axis functions, indicating that down regulation of important The Role of Stress, Anxiety, and Depression 12 components of the stress response is an intrinsic effect of Imipramine (Goldstein Dekker, 2001). Brain and Stress Stress not only is personal but is perceived through the prism of social interactions. These interactions can either add to or lessen psychological stress and affect our hormonal responses to it, which in turn can alter immune responses. For instance, in humans, loneliness is associated with a â€Å"threat,† or adrenaline-like pattern of activation of the stress response and high blood pressure, whereas exercising is associated with a â€Å"challenge† pattern of high blood flow and cardiac output (Sternberg, 2001). Studies have shown that people exposed to chronic social stresses for more than two months have increased susceptibility to the common cold. The popular belief that stress exacerbates inflammatory illness and that relaxation or removal of stress ameliorates it may indeed have a basis in fact. The interactions of the stress and immune systems and the hormonal responses they have in common could explain how conscious attempts to tone down responsively to stress could affect immune responses. How much of the response to stress is genetically determined and how much can be consciously controlled is not known. The set point of the stress response is to some extent genetically determined (Sternberg, 2001). In addition, factors in early development, learning, and later experiences contribute to differences in stress responsiveness. An event that is physiologically highly stressful to one individual may be much less or so to another, depending on the sum of each person’s genetic tendency to hormonal reactivity and their previous The Role of Stress, Anxiety, and Depression 13 experience. In my opinion, the degree to which stress could precipitate or exacerbate disease would then depend not only on the intensity and duration of the stressful stimulus but also on the person’s ability and learned perception of the event as stressful and on the set point of the stress system. Psychological stress can affect an individual’s susceptibility to infectious diseases. The regulation of the immune system by the neuro-hormonal stress system provides a biological basis for understanding how stress might affect these diseases. Thus stress hormones released from the brain, cortisol from the adrenal glands, and nerve chemicals, such as norepinephrine and epinephrine released from nerve endings, all modify the ability of immune cells to fight infectious agents and foreign molecules (Mayer Saper, 2000). There is evidence that stress does affect human immune responses to viruses and bacteria. In studies with volunteers given a standard dose of the common cold virus rhinovirus, individuals who are simultaneously exposed to stress show more viral particles and produce more mucus than do not stressed individuals (Jeanette, Webster Esther, 2002). Stress and the Role of Social Support in Bereavement; A Theoretical Analysis According to cognitive stress theories, critical life events such as bereavement are stressful because they require major readjustments. The intensity of stress created by a life event depends on the extent to which the perceived demands of the situation tax or exceed an individual’s coping resources, given that failure to cope leads to important negative consequences. Stress theory provides the theoretical underpinning for the â€Å"buffering model,† The Role of Stress, Anxiety, and Depression 14 which suggests that high levels of social support protect the individual against the deleterious impact of stress on health (Lazarus Folkman, 1984). According to Cohen and Willis (1985), there are two ways in which social support can buffer the individual against the negative impact of the stress experience. First, support can intervene between the stressful event and a stress reaction by attenuating or preventing a stress appraisal response. Second, adequate support may intervene between the experience of stress and the onset of the pathological response by eliminating the stress reaction or by directly influencing physiological processes. Whereas these two pathways reduce the individual’s vulnerability to the impact of the stressful event, however a third way in which social support may affect individual stress response, namely, by aiding in recovery. Thus, social support may also help individuals to recover more readily from the impact of the stressful life event. The Deficit Model of Partner Loss was developed as an application to cognitive stress theory to bereavement. On the basis of the interactional definition of stress, the deficit model offers an analysis of the situational demands characteristic of widowhood and of the coping resources needed to deal with these demands. Marital bereavement marks the end of a close mutual relationship, and the loss of a partner is likely to result in a number of deficits in areas in which the spouse had previously been able to rely on the partner. The Deficit Model suggests that the loss of a partner leads to deficits in areas that can broadly be characterized as loss of instrumental support, loss of validational support, loss of emotional support, and the loss of social contact support. The Deficit Model postulates that social support alleviates the stress of The Role of Stress, Anxiety, and Depression 15 bereavement, but only to the extent to which it helps to replace the deficits created by the loss of a partner (W. Stroebe M. Stroee, 1987; K. Gergen, M. Gergen, 1980, 1982). It follows from the Deficit Model that bereaved individuals are in greater need of social support than married individuals. The model therefore predicts an interaction of social support and marital status on the level of psychological symptoms, such as the buffering effect. However, because it is unlikely that family and friends are able to alleviate completely the deficits caused by the loss of the partner, one would also expect a main effect of marital status on symptomatology. In contrast, attachment theory rejects the notion that supportive friends can compensate for the loss of an attachment figure (Bowlby, 1969; Weiss, 1975). Bowlby (1969) proposed that the attachment figure, unlike other people in the social environment, was uniquely able to foster general feelings of security and that other people could not simply take over this function. He thus goes beyond optimal matching by not only requiring a match between the characteristics of stressful events confronting the individual and the form of social support that is beneficial in this context, but by stating categorically that this type of social support can only be provided by one specific type of person (Cutrona Russell, 1990). Weiss (1975) elaborated these ideas in his relational theory of loneliness, in which he drew a fundamental distinction between emotional and social loneliness and argued that the two types of loneliness cannot compensate for each other: The loneliness of emotional isolation appears in the absence of a close emotional attachment or the reintegration of the one that had been lost. Those experiencing this form of loneliness are apt to experience a sense of utter The Role of Stress, Anxiety, and Depression 16 aloneness, whether or not the companionship of others is in fact accessible (Weiss, 1975). Thus, according to attachment theory, social support from relatives and friends cannot compensate for the major deficit caused by bereavement, namely, the loss of an attachment figure. However, social support should help with a second type of loneliness, namely, the loneliness of social isolation. Social loneliness is associated with the absence of an engaging social network, and this absence can only be remedied by access to such a network. The dominant feeling of this type of loneliness is boredom, together with feelings of marginality (Weiss, 1975). Attachment theory thus suggests that marital status and social support influence well being by distinctly different pathways, with the impact of marital status being mediated by emotional loneliness and the impact of social support by social loneliness. According to this Dual-Path Model, one would predict main effects of marital status and social support on measures of symptomatology, but no interaction. Because each of these main effects is assumed to be mediated by a different type of loneliness, one would further expect marital status to affect emotional but not social loneliness and social support to affect social but not emotional loneliness. Finally, one would expect that control for emotional loneliness should reduce or eliminate the impact of marital status on symptomatology, whereas control for social loneliness should reduce or eliminate the effect of social support on symptom levels. The two major theories of bereavement outcome thus make different and partly contradictory predictions about the role of social support in adjustment to loss. Consistent with popular beliefs about the helpfulness of social support to the bereaved, cognitive stress theory predicts a social support times a marital status interaction on symptomatology constitutes the The Role of Stress, Anxiety, and Depression 17 buffering effect, in addition to a main effect of marital status. In contrast, attachment theory predicts main effects of both marital status and social support on levels of symptoms, but no interaction. It further suggests that these two main effects on symptomatology are mediated by different types of loneliness. These predictions have not yet been addressed by empirical research. Stress and the Role of Social Support in Adjustment to Loss; A Review of the Evidence Guided by stress theory, research on the role of social support in adjustment to loss has focused exclusively on testing the buffering against the main effect model. As Cohen and Wills (1985) argued in their influential review of the literature on the social support, such tests require a factorial design that includes at least two levels of stress and two levels of social support. Furthermore, to test whether social support buffers individuals against the negative impact of the loss of a marital partner, one has to compare the impact of social support in bereaved and married samples. Buffering effects would be reflected by a statistical interaction of social support with marital status on health. In the earlier review of literature on social support and bereavement up to 1986 (W. Stroebe M. Stroebe, 1987), there were no studies found that satisfied these criteria. In the meantime, a few studies using adequate designs, comparing the impact of levels of social support in bereaved samples to that of married controls, have been published. The results are not unanimous in favor of buffering. Although some do indeed report evidence of buffering (Krause, 1986; Norris Murrell, 1990; Schwarzer, 1992), albeit using measures of social integration or received social support, other do not (Greene Feld, 1989; Murphy, 1988). The Role of Stress, Anxiety, and Depression 18 Krause (1986) studied the impact of life stresses and social support on depressive symptoms in a random sample of 351 individuals older than 65 living in Galveston, Texas. Social support was assessed with a modified version of the Inventory of Socially Supportive Behaviors (ISSB: Barrera, Sandler, Ramsay, 1981). Depressive symptomatology was assessed with the Center for Epidemiology Studies Depression Scale (CES-D; Radloff, 1977). Whereas no buffering effects occurred for the overall indicator of stressful life events, buffering was found for the numerically undefined subgroup of individuals who had been bereaved within the previous year. These buffering effects modified weak bereavement main effects. As part of a larger study of individuals aged 55 and older, Norris and Murrell (1990) obtained interviews of three samples of older adults: 45 persons who had recently lost a spouse, 40 who had lost a parent or child, and 45 who were not bereaved. Depression was assessed with the CES-D. Social support was measured with the Louisville Social Support Scale which consists of two subscales reflecting social integration, or embeddedness in a social network, and expected help. â€Å"Expected help taps the respondents more specific expectations of help in an emergency from family, friends, and community† (Norris Murrell, 1987 p. 431) and appears to reflect aspects of perceived social support. However, expected help had no impact on depression, an ameliorative effect of social embeddedness on depression was reported. The more individuals were embedded in their social networks, the less they were depressed nine months after their loss. This association between social embeddedness and depression was The Role of Stress, Anxiety, and Depression 19 stronger for the widowed sample than for a combined control group consisting of individuals who were either not bereaved or had lost a parent or child. Schwarzer (1992) studied a sample of 248 individuals about the age of 60, of which 152 had lost a family member or a friend within the previous year. Social support was defined in terms of visits by children and family members. The criterion measure in this study was anxiety, assessed with a German version of the State-Trait Personality Inventory (Schwarzer Schwarzer, 1983). When the sample was dichotomized into those who were visited at least every other week and those who received fewer visits, a clear buffering effect was observed, with loss having no impact on anxiety for individuals who received many visits but a strong impact on those who received few visits. One puzzling feature of these studies is that buffering effects were observed for measures of social support that typically do not yield buffering effects. According to Cohen and Wills (1985), buffering effects ought only to be found with measures of perceived social support but not with network measures or scales assessing received social support. In contrast, the above studies report buffering effects with measures of social network (Krause, 1986) or received social support (Norris Murrell, 1990; Schwarzer, 1992). The one study that assessed both social embeddedness and perceived social support did not find any effects for perceived social support (Norris Murrell, 1990). It is plausible that this discrepancy has something to do with the fact that the study included only elderly individuals, a subgroup for whom the needs, provisions, consequences, and perceptions of social support are very different from those of younger groups. The Role of Stress, Anxiety, and Depression 20 Two studies, both using samples of more long term bereaved, did not find buffering effects. In a follow up assessment of 49 family members and close friends of 51 adult disaster victims of the Mount Saint Helens volcano eruption conducted 3 years after the disaster, in which their mental distress was compared with that of a non-bereaved control group, there was no evidence or main or buffering effects (Murphy, 1988). Social support was measured with an index developed by scientists that assesses social embeddedness, as well as perceived social support (Coppel, 1980). Greene and Feld (1989) examined the relationship between social support and well-being in groups of 151 married women and 60 widowed women who had lost their partner within the previous five years. Respondents were drawn from a national sample of women aged 50 and older. Social support was assessed in terms of the number of social support function for which respondents mentioned one or more social supporters. Well-being was measured w