How to Reduce Depression by Dieting - Coursework Example

Depression and Diet and Depression and Dieting In order to reduce depression and fight off lethargy and apathy, it is important to regularly eat adequately. Having insufficient meals is sometimes referred to as under-nutrition. Under-nutrition is usually a result of inadequate food intake, dietary imbalances, and deficiencies of specific nutrients. Not eating regularly can have a severe consequence on an individual’s health and wellbeing, as well as quality of life. The impacts that inadequate eating can have on the general health and wellbeing range from reduced quality of life and ability of working, to taking care of oneself. In addition, undernourished patients also have more GP visits and hospital admissions (Marks et al, 2012, pp.4-7). Depressed patients who do not eat sufficiently are chronically underweight and thus susceptible to acute illnesses. One of the reasons for which people do not eat adequately is depression. However, the consequences of not eating regularly are far and wide. The y include: weight loss, impaired immune system, which eventually slows wound healing and increase the risk of pressure sores, vitamin deficiency, muscle wasting and weakness, impaired respiratory or cardiac function and mobility and unfit dentures. Eventually, the patient may be more depressed than usual, culminating in general lethargy and sluggishness (Abbott Nutrition, 2012, pp.7-9). To reduce malnutrition, patients should be motivated to eat and drink normal foods. Once they eat regular meals, they will acquire strength to reduce apathy and general body weakness quickly. Should the patients fail to gain weight owing to their poor appetite, food and drinks can be enriched thus providing them with more calories and proteins (Gill, 2012, pp.2-7). The quantity of food usually remains constant. For instance, a double cream or cheese may be mixed with soups and mashed potatoes and vaporized milk may be mixed with jellies. Further, the patient may consult a dietician. Nutritional enhancements or sip feeds may also be suggested. Be that as it may, this should serve as a last resort since real food must be the better option (Dyball and Rock, 2011, pp. 16-18). Adrenal fatigue is the avenue through which respiratory infections, allergies, asthma, rhinitis, fibromyalgia, frequent colds, hypoglycemia and diabetes II attack the human body. The ability to undertake laborious activities such as sex, and add metabolism supporting muscles in order to burn fat and live healthily, is highly influenced by adrenals. The adrenal glands rest above the kidneys next to the spine and right beneath the last rib. Their location is strategic because they play a vital role in allowing for a rapid response to hormonal messages (Loge, 2012, pp.1-7). Every activity that we engage in, including drinking tea and sugar, brings about hormonal rise in our system (Palmer Family Chiropatic, 2011, pp.1-2). The hormones signaled by the adrenal glands highly influences the utilization of carbohydrates and fats, the translation of fats and proteins into energy, the spreading of stored fats especially around the waistlines, blood sugar peaks and valleys, as well as healthy cardiovascular and gastrointestinal operation(Loge, 2012, pp.1-7). Further, the adrenal glands oversee and control the anti-inflammatory and anti-oxidant hormones to lower allergic reactions to alcohol, drugs food and environmental allergies (The Institute for Functional Medicine, 2012, pp.1-2). Thus every single stressor, if not properly managed, lowers healthy adrenal function. Depression can be a major cause of adrenal fatigue (Loge, 2012, pp.1-7). High sugar intake heightens inflammation, weakens immune system, feeds pathogenic bacteria in a patient’s gut, and is linked to cardiovascular diseases, diabetes and depression. When carbohydrates like sugar are consumed excessively, the body disintegrates them into glucose (Metagenics, 2011, pp.1-15). Then, boosted by insulin, blood sugar gets into body cells and generates energy. Whenever excessive glucose is produced from a highly sugary diet, insulin is produced in surplus, resulting in inflammation, increased blood triglycerides as well as high blood pressure (Miller, 2010, pp.13-50). Insulin signals the human body to pile up extra glucose in form of body fats, resulting in energy deficiency for supporting the normal demands on body muscles and the brain. High sugar intake thus increases fatigue. Hypothyroidism is a condition in which the thyroid glands fail to generate adequate thyroid hormone. In the absence of this hormone, the human body cannot operate normally, leading to poor growth, fatigue, slow speech, dry thick skin, insufficient energy, weight loss and increased sensitivity to cold environment. Thyroid drugs regulate hypothyroidism but do not cure it. They work by reversing the symptoms of hypothyroidism. They are also used to cretinism autoimmune hypothyroidism and goiter (US Food and Drugs Association, 2012, pp. 1-36). Antidepressants treat depression, anxiety disorder, obsessive compulsive disorder, as well as panic attacks. They work by raising the level of serotonin, a substance in the human brain that assists in maintaining mental balance (Paterson and Bilsker, 2012, pp.3-72). One of the examples of antidepressants includes phenelzine. Alcoholic drinks are not recommended when a patient is on antidepressants (US Food and Drugs Association, 2012, pp. 1-36). This is because many alcoholic drinks, including tap beer, have trramine. Others include red wine, liqueurs and sherry. Tyramine can also be found in alcohol-free foodstuffs and reduced alcohol beer. Tyramine reacts with the antidepressants, making them ineffective in the body. Additionally, alcohol can worsen the side effects brought by the antidepressants (US Food and Drugs Association, 2012, pp. 1-36). Alcohol use, as a central nervous system depressant, has been found to have a severe complication for depressed patients, who take it to change their moods. Alcohol should generally be avoided when undergoing treatment against depression owing to several reasons. To begin with its initial anti-anxiety impact, alcohol can bring about increased feeling of anxiety or depression, which is counter-productive to the treatments being administered. Alcohol can cause a depressed mood that persists for several weeks, even after quitting it. Finally, in combination with antidepressants, alcohol can worsen the side effects of drugs (Shelton and Duckworth, 2012, pp.1-28). Worse still, it may render the antidepressants less effective (National Collaboration Center for Mental Health, 2006, pp.1-76). It also lowers inhibition, thereby heightening the risk of suicide (Mitchell et al, 2013, pp.1-131). Depressed patients are advised not to consume caffeine especially when they are on antidepressants. Caffeine has many negative effects on the gastrointestinal tract. The substance relaxes the lower oesophageal sphincter and may predispose to gastro-oesophagael reflux complication. It also brings about hypersecretion, which is linked to susceptibility to ulceration. Caffeine consumption has also been associated with anxiety disorder, sleep disorder and eating disorder. There is a probable link of caffeine with schizophrenia. It is irrefutable that caffeine causes insomnia. This lowers slow-wave sleep in the beginning of the sleep cycle (Jaberi, Hardwick and Winston, 2014, pp.432-439). Caffeine raises episodes of wakefulness. Increased consumption of the substance in the late evening can lengthen the period of time taken before being carried away by sleep. Among the elderly, the use of drugs harboring caffeine is also linked to an increased risk of difficulty falling asleep (Harbottle, 2013, pp.1-16). Medical experiences indicate that individuals with eating disorders like anorexia nervosa and bulimia nervosa usually take in large amounts of drinks containing caffeine, driven by the thought that caffeine speeds up metabolic rates and suppresses appetite. For anorexia nervosa patients who are already susceptible to cardiac arrthymias, the stimulant effect of caffeine on the heart may be risky (Centre for Addiction and Mental Health, 2005, pp.2-11). Overconsumption of caffeine may also lead to osteoporosis, common among the anorexia nervosa patients (Jaberi, Hardwick and Winston, 2014, pp.432-439). Medical experts have found that there exists an interconnection between adenosine A2 receptors and the doperminergic system in the human brain. Since adenosine inhibits dopaminergic neurotransmission, blockage of A2A receptors by caffeine may increase dopaminergic activity, thereby exacerbating psychotic symptoms. Clinically, the symptoms of caffeine intoxication can imitate those of psychosis, or be confused with the side effects of medication. Caffeine cessation causes tiredness or fatigue and dizziness, which may be confused with the side effects of psychotropic drugs (Jaberi, Hardwick and Winston, 2014, pp.432-439). All metals at high concentrations are potentially poisonous to the human body, irrespective of whether they are biologically essential at moderate levels. Metal toxicity manifests itself in the form of inhibition of growth or metabolic activity (Vilar-Rojas et al, 2010, p.1371). Human beings exposed to metals for a long time can have harmful effects. For instance, Chromium exposure has been linked to genotoxicity and carcinogenicity (Aykin-Burns, Gurer-Orchan and Ercal, 2001, pp.529-539). Toxic metals, like lead, calcium and mercury are widely found in our environment. Human beings are constantly exposed to these elements from many sources, such as contaminated water, air or food (Adams, 2007, pp.1-28). Recent surveys reveal that transition metals act as catalysts in the oxidative reactions of biological macromolecules, thus the toxicities linked to these metals might be attributed to oxidative tissue damage (Shacter, 2000, pp.307-326). Redox-active metals like chromium, copper and iron, go through redox cycling, while redox inactive metals like lead, mercury and cadmium deplete cell’s major antioxidants, especially the thiol-constituting enzymes and antioxidants (Aykin-Burns, Gurer-Orchan and Ercal, 2001, pp.529-539). Both redox-active and redox-inactive metals may speed up the production of reactive oxygen species like hydroxyl radicals, superoxide radicals or hydrogen peroxide. Increased production of reactive oxygen species can overpower the human cell’s intrinsic antioxidant defenses, thereby leading to a complication commonly referred to as oxidation stress. Cells suffering from oxidative stress show various dysfunctions due to lesions caused by reactive oxygen species to DNA, lipids and proteins (Cronin, Morris and Vako, 2005, pp.1161-1208). Following high metal toxicity, it is important for a patient to administer antioxidant food supplements, which are mostly found in proteins (Felice et al, 2010, pp.435-442). Proteins have for a long time been viewed as principle target for oxidants due to their abundance in biological systems. Proteins like albumin have significant antioxidant activity (Varsha et al, 2010, pp.94-99). Thus for plasma known to be continually exposed to oxidative stress, eating food rich with proteins can help reduce metal toxicity (Danyal et al, 2006, pp.67-97). Chronic depression is normally associated with activation of the inflammatory response. Antidepressants stimulate an anti-inflammatory response independent of the antidepressant activity. C-reactive protein was the earliest acute-phase protein to be described, having the capacity of precipitating the somatic C-polysaccharide of streptococcus pneumonia. Being a hypersensitive systemic marker of tissue damage and inflammation, it is generated through hepatocytes majorly under transcriptional control through pro-inflammatory cytokine interleukin 6. The main factor dictating the circulation of C-reactive proteins is the synthesis rate (O’Brien et al., 2006, pp. 449-482). Generally, its production rises speedily in reaction to a pathological stimulus. However, it rapidly lowers following resolution of a particular stimulus. Severe depression has also been found to be associated with the stimulation of the inflammatory response. These changes may take the form of rise in the number of leucocytes, whether monocytes or neutrophils (O’Brien et al., 2006, pp. 449-482). Positive acute-phase proteins like C-reactive ones often increase, while negative acute-phase proteins such as albumin drops. This acute-phase reaction constitutes an integral part of the inflammatory response. It is meant for enabling protein mobilization, so as to reduce tissue damage and activate repair. It is now clear that depression is linked to chronic, low-grade inflammatory response as well as stimulation of cell-mediated immunity. It is also associated with the activation of the compensatory anti-inflammatory reflex system. This always go hand in hand with increased oxidative and nitrosative stress, that has a hand in neuroprogression in the disorder (Berk et al., 2013, pp.2-16). Nutrition is a major factor that influences inflammation. In particular, low-levels of Vitamin D, especially 25-hydrocyvitamin D, are rampant among Western populations. This makes it the most prevalent deficient state. Vitamin D receptors are usually expressed in major brain areas. It has an important role in the circadian rhythms and sleep, influences glucocorticoids and the neuronal development and cell proliferation in the growth of the brain and embryogenesis. Further, deficiency in Vitamin D has been linked to a broad range of severe complications, ranging from osteoporosis to cancer (Berk et al., 2013, pp.2-16). References Abbott Nutrition., 2012. Malnutrition in the Community and Hospital Setting. The Patients Association, [e-journal], pp.7-9. Available at: < http://www.patients-association .com > [Accessed 26 May 2014] Adams, B.J., 2007. Summary of Biomedical Treatments for Autism. ARI Publication, [e- journal], 40, pp. 1-28. Available at: < http://www.autism.asu.edu >[Accessed 26 May 2014] Aykin-Burns, N., Gurer-Orhan, H., and Ercal, N., 2001. Toxic Metals and Oxidative Stress Part 1: Mechanisms Involved in Metal Induced Oxidative Damage. Current Topics in Medicinal Chemistry, [e-journal] 1, pp.529-539. Available at: < http://www.umr.edu > [Accessed 26 May 2014] Berk et al., 2013. So Depression is an Inflammatory Disease, but where does the Inflammation Come from? BMC Medicine, [e-journal] 11, pp. 2-16. 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