The Impact of Depression on an Elderly Persons Well-Being - Literature review Example

The Impact of Depression on an Elderly Person’s Well-Being by 0 INTRODUCTION The population worldwide of older people from the age 65 and up will dramatically rise in the coming years, reaching around 600 million in the next few years to around nearly two billion by 2050 (Chen et al., 2009). Moreover, in many developed countries, almost 25% of their populations will be older than 65 turn some population pyramids upside down (Chen et al., 2009). Therefore, at the same time that the population ages, demands on health services will increase because of greater morbidity and mortality compared to younger adults (Chen et al., 2009). Similarly, it also cannot be denied that immunosenescence will also be an increasing trend as well, which means that as the population ages, their immune systems ages as well. Nevertheless, part of the upcoming escalation of immunosenescence in the coming years is actually allegedly due to depression that appears to accompany a significant number of older individuals (Chen et al., 2009) and the negative effects that this psychological disorder has on the body, particularly on the immune system. 2.0 DEFINITIONS 2.1 Old People Currently the elderly are considered to be those aged 65 or above, and represent the population mostly born after the war and is referred to the baby boomer generation (Desquilbet et al., 2009). 2.2 Immune Status of the Elderly The immune status of the elderly is their ability to protect themselves from diseases, many of which they have become susceptible to as a result of their aging immune system (Desquilbet et al., 2009). There is no doubt that depression is of significant concern among some of the aging population and is considered to be due to isolation with the increase of single households, increasing lack of mobility, poor health, and economic status invariably due to living on a fixed income in an unstable economic environment (Desquilbet et al., 2009). the cause of impaired immunity in the elderly is considered by some due to depression (Gold & Irwin, 2009; Dantzer, 2009; Blume et al., 2011; Weiskopf et al., 2009; Haase & Rink, 2009; Leonard, 2010; Dowlati et al., 2010; Stewart et al., 2009; Grippo & Johnson, 2009; Irwin & Cole, 2011; & Kop et al., 2010) whereas other studies (Capuron &Miller, 2011; Silverman et al., 2010; Gimeno et al., 2009; Bull et al., 2009; Khairova et al., 2009; & Elderkin-Thompson et al., 2012) state that it is the inflammatory responses of the immune system that trigger depression. 2.3 T-Cells Function T-cells are a subset of lymphocytes that undergo the final stage of their development in the thymus gland (Desquilbet et al., 2009). They continue that very effective immune response always involves the activation of a T-cell. 2.4 Depression Depression is the psychological disorder where a person may experience a particular lack of interest and pleasure in certain everyday activities (Desquilbet et al., 2009). They continue that signs and symptoms of depression include significant weight loss or gain, lack of energy, insomnia, excessive sleeping, feelings of worthlessness, excessive guilt or frequent thoughts of suicide or death but most significantly inability or lack of interest in activities of daily living (ADL) (Desquilbet et al., 2009). 2.0 THE IMPACT OF DEPRESSION ON THE OLDER PERSON’S WELL-BEING AND IMMUNE SYSTEM 2.1 Immune System Changes The aging of the immune system, or what is termed as immunosenescence, is closely related to stressors that accumulate becoming chronic stress (Bauer et al., 2009). What is specifically affected by chronic stress is the key allostatic systems involved in the way organisms adapt to the changes in the environment, particularly as they are implicated in the aging process (Bauer et al., 2009). Specifically, chronic stressed older people increase the speed of the process of aging because of an increase in the exposure of their tissues to cortisol (Bauer et al., 2009). In the same way, cortisol, which is the hormone implicated in immune dysfunction, is increased in depressed individuals, therefore there is a tendency for the same hormone to invade the tissues and hasten their aging (Bauer et al., 2009). A study by Gold and Irwin (2009) also showed that patients with major depressive disorder have marked alterations in their immunological markers, thus a proof that depression produces negative immune system changes. These alterations in immunological markers actually include increases in inflammation caused by proinflammatory cytokine activity (Gold & Irwin, 2009). Moreover, there is a high possibility for the inflammation to also occur in the central nervous system (Gold & Irwin, 2009). Overall, the point by Gold and Irwin (2009) is that depression and major depressive disorders cause alterations or changes in several aspects of the body’s immunity that may therefore contribute to the development of many other illnesses as well as the exacerbation of many others already in situ. This is the reason why the aggressive management of depression and major depressive disorders is actually the key to the improvement of disease outcome and the prevention of the development of a disease (Gold & Irwin, 2009). Similarly, Kolmann et al. (2012) stated that any change in the immune development in the very old is usually brought about by changes in the composition of the microbiome of the small intestine, implying that problems with immune development may be traced to physical or physiological causes. Therefore, although this particular study did not particularly mention that depression among the elderly can cause immune system degradation, it clearly implies that an old person’s immune system will somehow naturally deteriorate. Moreover, according to Dantzer (2009), the presence or occurrence of major depressive symptoms is associated with an increase in the circulating levels of proinflammatory cytokines, particularly interleukin-6. This means that the occurrence of depression may always be associated with these inflammatory biomolecules despite having an unclear cause and effect relationship. Blume et al. (2011), on the other hand, clearly recognized that depression is something that promotes both immune suppression and prevents immune activation. Therefore, the mere occurrence of depression is accompanied by the rise in the number of inflammatory markers such as IL-6, TNFα and CRP, as well as markers of impaired cellular immunity which include the decreased cytotoxicity of the NK cell (Blume et al., 2011). According to Weiskopf et al. (2009), the decline in the immune function among the elderly will occur regardless of whether there is an associated depression. They highlight that susceptibility to infection and vulnerability to diseases, as well as deaths from common diseases such as pneumonia and influenza, represent the sixth leading cause of death among the elderly in the United States of America and other developed countries, among those aged 65 or older. The explanation for this is that immunity declines in terms of function as one naturally gets older, with or without depression. According to Haase and Rink (2009), regarding immunosenescence, one study states that with zinc deficiency among elderly people is not uncommon due to a combination of lack of the trace mineral in their diet and decreased absorption from the intestine, which is required for optimal immune function. As the occurrence of depression is often associated with decrease in the levels of zinc in the human body system, it is then therefore believed that depression can naturally trigger the impairment of the immune system and the decrease of the T helper type 2 cells (Haase & Rink, 2009). They conclude that there is no stopping the decline of the T helper type 2 cells (Th2), decrease of response to vaccination and continual impairment of innate immune cells. Moreover, according to Leonard (2010), in order to reinforce the claim of this paper, it is both anxiety and depression as well as stressful situations that actually cause changes in the immune system of the patient. Moreover, the increase in the proinflammatory cytokines and the hypercortisolaemia that is brought about by stress and chronic states of depression usually trigger a series of biomolecular changes in the patient including the conversion of glucocorticoids and proinflammatory cytokines to convert tryptophan to kynurenine, resulting in the decrease of the levels of serotonin found in the brain. Serotonin is a neurotransmitter that functions to produce feelings of happiness and well-being (Leonard, 2010). This then leads to formation of neurotoxins, which then increase the chances of the apoptosis of the neurons, oligodendroglia and astrocytes (Leonard, 2010). Such apoptosis will then eventually leading to malfunctioning of the nervous system. Additionally, Leonard (2010) also suggests that this inflammatory response to apoptosis of these parts of the nervous system as well as the exclusive action of the proinflammatory cytokines is the one that damages the immune system. These results support the study by Dowlati et al. (2010), which states that significantly higher amounts of the particular proinflammatory cytokines TNF-α and IL-6 usually appear during depression, and that, it is these proinflammatory cytokines that actually lower the immune system. According to Silverman et al. (2010), psychosocial factors such as depression, anxiety and sleep disorders actually correlate with chronic or central fatigue. Furthermore, they continue such fatigue, which is also apparent in individuals suffering from chronic diseases such as psychiatric disorders, neurologic disorders, cancer, fibromyalgia, chronic fatigue syndrome, systemic lupus erythematosus, multiple sclerosis, cardiorespiratory diseases, myasthenia gravis, and particular autoimmune diseases such as rheumatoid arthritis. Such information correlates that a particular psychosocial factor like depression can actually trigger the body to experience chronic fatigue, and that this chronic fatigue will then produce the physiological and physical changes in the body that may trigger certain diseases. However, correlations between the psychosocial factors and central fatigue, as well those between central fatigue and certain diseases, are actually merely correlations. The most important thing is to determine the causal connection among these things. In fact, according to Stewart et al. (2009), the directionality of the depression-inflammation connection is actually “unclear.” Thus, it is possible that certain changes in the immune system or a particular external cause may trigger the inflammatory process that will produce a state of depression in the individual. It is also equally possible that depression itself triggers certain biomolecular changes that will cause an impairment in the immune system and at the same time trigger inflammatory processes. However, based on the study by Stewart et al. (2009), it seems that the direction involving depression and the immune system is clear. Nevertheless, according to the research by Stewart et al. (2009), recent evidence shows that depressive symptoms precede and augment certain inflammatory processes which are relevant to coronary artery disease among older adults who are healthy. The researchers have also concluded that there is a great possibility that depression leads to inflammation, and that this inflammation will then trigger mechanisms that contribute to cardiovascular risk. According to Grippo and Johnson (2009), depression actually brings about a disruption in the functions of norepinephrine and dopamine. There is also a corresponding increase in norepinephrine levels, and this particular increase seems to lead to elevated risks of congestive heart failure in patients with depression. Irwin and Cole (2011) stated that certain social and environmental conditions like a low socio-economic status, the death of a spouse, or social isolation will most likely lead to an increased risk of infectious disease. This increased risk to acquire a disease is actually most probably due to the insufficient expression of certain immune response genes. Moreover, with or without depression, certain social and environmental conditions can actually cause inflammations in the human body related to the cardiovascular, neurodegenerative, neoplastic, and autoimmune diseases. This may also be attributed to the increase in the levels of certain hormones that inhibit antiviral genes and thus naturally activate specific pro-inflammatory genes. The evidence for this psychological connection between social, environmental and personal problems and the deterioration of the immune system is actually a result of the frequency of cases that demonstrate this trend. In fact, this may happen with or without depression. However, with depression, there is a general tendency for the patient to develop unexplained fatigue or sleep impairment. This then results in the production of certain inflammatory cytokines as depression naturally involves high levels of inflammation on the biomolecular level. According to a study by Kop et al. (2010), depression is actually directly associated with an autonomic nervous system dysfunction, thus this explains the increase in the inflammation markers. Moreover, this also makes depression a trigger for an increase in the risk for cardiovascular disease. However, based on the results of other studies, the connection between depression and the immune system is slightly reversed, since it is the impairment of the immune system due to stress that actually produces the necessary biochemical changes in the body in order for depression to occur. The specific biomolecular connection between the immune system and the production of proinflammatory cytokines is that the former can trigger the latter. These cytokines will then influence the central nervous system and interact with a cytokine network in the brain in order to produce specific negative changes in the individual (Capuron & Miller, 2011). It is therefore the action of the immune system that triggers depression. The question, however, is what triggers the immune system to produce such changes, and one study stated that it could be certain bacterial or viral infections (Silverman et al., 2010). In the same way, Gimeno et al. (2009) found has concluded that direction of association between inflammatory markers and depression is from the former to the latter. Therefore, it is the inflammatory markers that bring about the cognitive symptoms of depression. The above findings also agree with those of Bull et al. (2009) which has concluded that depression and fatigue are usually most likely the side effects of a treatment involving interferon-α. The reason is that this particular treatment involves the inflammatory response system and the serotonergic system of the autonomic nervous systems. In short, it is the nervous system that actually triggers depression and fatigue, and not the other way around. This is basically the same as the findings of Khairova et al. (2009) which concluded that inflammatory cytokines as well as certain hormonal changes in the body brought about by social, bacterial or viral stimuli may actually lead to the occurrence of severe mood disorders including depression. Moreover, the release of C-reactive protein and interleukin-6 will more or less trigger the occurrence of depression, and this is common among the elderly (Elderkin-Thompson et al., 2012). Nevertheless, according to Pasco et al. (2010), because of several conflicting results from those above, the true cause-effect relationship is still not clear between the release of inflammatory cytokines involving immune system activation and the occurrence of depression. 3.0 CONCLUSIONS Based on a number of studies, depression may actually weaken the immune system of older people as this particular psychological disorder may actually trigger the release of inflammatory cytokines and many other biochemicals that will degrade the immune system. 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