Neuropsychiatric Disorders Such as Depression - Literature review Example

Inflammation and Depression Introduction Inflammation is widely considered as a cause of various diseases including neuropsychiatric disorders such as depression. According to Miller et al (2009), increased inflammation as a result of inflammatory biomarkers such as cytokines leads to depression by accessing the brain and interacting with all pathophysiologic domains associated with depression. Inflammation affects depression-causing domains including neuroendocrine function, neural plasticity and neurotransmitter metabolism. Psychosocial stress is also considered to be a stimulating factor for inflammation; it stimulates inflammatory signaling materials such as nuclear factor kappa B. Patients with depression disorders associated with inflammation are also considered to be resistant to treatment. The best mechanism of reducing stress would therefore be inhibiting inflammatory cytokines that cause depression as well as their signaling pathways. Inhibiting those cytokines will improve depressed mood and increase response to treatment via antidepressant medication. Therefore, there is a positive relationship between inflammation and depression so that if inflammation increases, depression also increases. Inflammation and Lifestyle Various factors have specific implications on depression; and most of these factors are associated with inflammation. Most of those factors are associated with lifestyle and include poor diet, physical inactivity, dental cares, sleep, smoking, and obesity. Causes of inflammation mediate for the pathway to risk and depression. Most of these factors may lead to psychiatric disorders including bipolar disorder, schizophrenia and stress disorder. These factors are also amenable to preventive and therapeutic interventions. Diet is one of the lifestyle factors that influence stress disorders. There has been a change in dietary habits across the world over the past few decades. Diet involving nutrient-based foods, high fiber content and unsaturated fatty acids is now being replaced with dietary patterns comprising saturated fats and high levels of sugar. Berk et al (2013) suggest that change in diet affects depression. For instance, clinical depression may be caused by low lycopene contents in food and low availability of selenium in groundwater. According to Berk et al (2013), inflammation is an important aspect used to explain the consistent relationship between dietary patterns and depression. Poor quality of diet impacts negatively on immune functioning, increases systemic inflammation, and consequentially increases the levels of depression. Inflammation can be reduced through the consumption of fiber-rich foods including grains. Grain foods have beta-glucans which improve immune functioning and decrease the chances or levels of inflammation (Berk et al, 2013). As a result, this leads to low levels of depression. Exercise is also considered as an important factor affecting depression. Scientific evidence shows that exercise is an important strategy for treating depression. Exercise can be practiced as a habit in order to protect the body against incursion by depressive illnesses. Effects of inactive childhood are replicated with higher risk of depression during adulthood. The effect of exercise on the level of depression can be identified through its effects on inflammation (Bower et al, 2003). Inflammatory cytokines and reactive oxygen species are generated by acute exercise; consequentially damage muscle cells and cause inflammation and pain. Regular exercise decreases systemic inflation through homeostatic adaptation. It also leads to the reduction of leptin which is usually associated with high levels of depression (Bower et al, 2003). This shows that inflammation plays a crucial role in mood improvements through exercise. Sedentary behaviour is also an important influence of inflammation. It is a risk factor affecting various physical health conditions including depression. Sedentary behaviour causes cardiovascular risk and adiposity. Obesity is a consequence of lifestyle which is associated with chronic physical health problems. Berk et al (2013) suggest that there is a relationship between obesity and depression. Increased obesity leads to higher depression and high depression increases the risk of developing obesity. The relationship between inflammation and depression can be explained through obesity because obesity is considered as a state of inflammation. Fat cells contain inflammatory cytokines in large numbers. These cytokines are involved in fat metabolism which causes obesity. There are also other factors that cause obesity-related inflammation including high levels of fatty acids, leptin, and oxidative stress. Studies show that obesity leads to the alteration of inflammatory cytokines; hence causing increased in depression. Patients experiencing depression often exhibit cigarette smoking habits. Berk et al (2013) suggest that smoking leads to depression and depression increases smoking tendencies. Cigarette smoking influences depression through inflammatory pathways. Cigarette smoking causes systemic inflammatory immune responses which in turn lead to depression. Berk et al (2013) suggest that cigarette smoke contains several chemicals such as metals, tars and radicals which cause inflammatory response and lead to increased levels of O&NS. Pro-inflammatory cytokines are also caused by cigarette smoking, and they represent similar effects as those experienced by depressed patients. Depressed smokers often experience higher levels of inflammatory responses than non-depressed smokers. Brain Functions and Inflammation Depression is also related to inflammation through brain functioning. Miller et al (2009) claim that inflammatory cytokines contribute to depression through brain functioning. In this case, cytokines enter the brain and interact with pathophysiologic domains related to depression such as neural plasticity, neuroendocrine function, and neurotransmitter metabolism (Quan and Banks, 2007). However, it is still unclear whether inflammatory responses in the central nervous system originate from in the periphery or whether stress induces inflammatory responses from the brain. Miller et al (2009) argue that such an unresolved issue will hinder the use of therapeutic responses that involve the brain. Considering the fact that inflammatory cytokines are large polypeptides, examination on animals have been carried out to determine the mechanisms through which signals of cytokines reach the brain. During the movement of cytokine signals to the brain, there are various pathways including passage of cytokine through blood-brain-barrier leaky regions. Other pathways of the cytokine to the brain include: active transport through saturable molecules, endothelial cell activation in the cerebral vasculature, and binding of cytokines to peripheral nerve fibers which relay signals of the cytokine to relevant regions in the brain including hypothalamus and the solitary tract nucleus (Quan and Banks, 2007). Inflammatory responses are amplified by relevant cell types which are activated by peripheral cytokine signals that reach the brain. After cytokine reaches the brain, they get involved in the synthesis, release and uptake of neurotransmitters that cause moods, including monoamines (Quan and Banks, 2007). Administering cytokine inducers in humans causes metabolism of norepinephrine and serotonin. Drugs administered on humans are therefore considered as inhibitors of norepinephrine and serotonin reuptake and are likely to affect metabolism of monoamine. As a result, this influences the development of depression in humans – meaning that the depressive behaviour is cytokine-induced through inflammatory responses in the brain. Cytokines also influence inflammation and depression through their impact on hypothalamic-pituitary-adrenal axis (Harvard Health Publications, 2012). Acute administration of cytokine stimulates expression and release of adrenocorticotropic hormone, corticotrophin-releasing hormone and cortisol which are elevated in human beings with depression (Bower et al, 2005). On the other hand, chronic cytokine administration leads to elevation of corticotrophin-releasing hormone or cortisol in humans. It leads to flattening of diurnal cortisol slope and increased levels of evening cortisol. These effects are related to fatigue and depression in humans. Other studies indicate that the brain has a direct effect on the stomach. For instance, a problematic intestine can send signals to the brain, and a troubled brain sends signals to the gut. The stomach or the intestine is therefore the product or cause of stress, depression or anxiety. The reason for this is that the gastrointestinal (GI) system is intimately connected to the brain (Harvard Health Publications, 2012). When a person experiences gastrointestinal upset without any physical cause then it becomes difficult to heal the distressed gut without looking into the role of emotion and stress. This close interaction between the brain and the gut makes a person to become nauseated or feel intestinal pain during moments of distress. In this case, psychology combines with physical factors to cause pain and bowels humans. Stress can therefore cause functional gastrointestinal disorders, inflammation, poor movement and contractions, and susceptibility to infection. Stress can make existing pain even worse through inflammatory responses. How to Reduce Inflammation and Depression It is clear that depression and inflammation are related. Therefore, eliminating or reducing depression requires the reduction of inflammatory responses. One of the most important ways of reducing inflammatory responses is by reducing inflammatory cytokine release because it causes pain and inflammation which results in depression. One way of reducing cytokine is through exercise. Regular exercise decreases systemic inflammation through homeostatic adaptation. Furthermore, fitness and exercise result in reduction of leptin which is a main cause of increased depression. Reduction of obesity also leads to reduction of inflammation and depression. In order to reduce obesity, it is important first to reduce the adipose tissue through calorie restriction. This leads to reduced production of TNFa, IL-8, IL-8 and leptin which are key causes of inflammatory cytokines (Berk et al, 2013). This reduction leads to reduced inflammation and consequentially decreases the level of depression in humans. Smoking can also be a cause of depression. Lifestyle change can be initiated to reduce depression by reducing the level of smoking. Decline in smoking habits causes a reduction in inflammatory responses which would be caused by thousands of chemicals contained in cigarette smoke including tar, metals and free radicals (Berk et al, 2013). Another way of reducing inflammation which would otherwise cause depression is through psychological and brain therapy which will enable the brain to get used to certain circumstances so that they can send positive signals to the gut, which will in turn reduce the inflammation which leads to reduced stress. Evaluation Based on the research from existing literature, it is clear that depression and inflammation are related in some ways. Inflammation which is usually caused by inflammatory cytokines affects depression-causing domains including neuroendocrine function, neural plasticity and neurotransmitter metabolism (Berk et al, 2013). Inflammation affects depression through both lifestyle and brain functions. In terms of lifestyle, various lifestyles such as obesity, smoking, exercise and diet influence the amount of inflammatory cytokine in the body. For instance, an uptake of a lot of fatty acids, sugar and cholesterol foods in the diet can lead to increased inflammatory cytokines which increase inflammation. Various studies indicate that cigarette smoke, obesity, and acute exercise cause risk of depression. Similarly, brain functions are affected by cytokine signals which reach the brain; and they send troublesome messages (inflammatory responses) to the gut which in turn responses with stress and pain. This shows clearly that cytokine is the main cause of inflammation, and it is released in both brain functions and lifestyle. The common impact in both cases is that the inflammatory cytokine leads to inflammation which in turn causes depression. Conclusion From this analysis it is clear that depression and inflammation are positively related so that if inflammation increases, depression also increases. Inflammation which results from increased inflammatory cytokine causes neuroendocrine function, neurotransmitter metabolism and neural plasticity which end up causing depression. The inflammatory cytokine can be caused by both brain functions through the gut and lifestyles such as obesity, diet and smoking. Therefore, depression can be reduced through inhibition of inflammatory cytokines. References list Berk, M., Williams, L.J., Jacka, F.N., O’Neil, A., Pasco, J.A., Moylan, S., Allen, N.B., Stuart, A.L., Hayley, A.C., Byrne, M.L. and Maes, M. (2013). So depression is an inflammatory disease, but where does the inflammation come from? BMC Medicine, 11, 200. Bower, J.E., Ganz P.A., Dickerson, S.S., Petersen, L., Aziz, N., Fahey, J.L. (2005). Diurnal cortisol rhythm and fatigue in breast cancer survivors. Psychoneuroendocrinology, 30, 92–100. Harvard Health Publications (2012). The gut-brain connection. Accessed November 10, 2014 from http://www.health.harvard.edu/Harvard Health Publications/the-gut-brain- connection. Miller, A.H., Maletic, V. and Raison, C.L. (2009). Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression. Biol. Psychiatry, 65(9), 732– 741. Quan, N., Banks, W.A. (2007). Brain-immune communication pathways. Brain Behav Immun., 21, 727–735. Read More