Essay Sample on Mental Health and Depression

Introduction

Mental disorders are common conditions that affect people in today's society. However, individuals believe that mental illnesses are rare and cannot change people how people behave. Approximately 54 million Americans suffer from one form of psychiatric conditions in a given year (Behavioral Health Barometer North Carolina, 2015). One of the most common mental disorders is depression. This topic is essential because I am a youth advocate and passionate about issues affecting the youths in the community. Therefore, I was prompted to conduct this research on depression because of the rising number of depression cases in my community and across the world. Unfortunately, 80% of the troubled teenagers who have the mental condition have no access or are exposed to insufficient treatment (Behavioral Health Barometer North Carolina, 2015). Additionally, most Americans who suffer from mental illnesses do not have access to care. About 56% of the adults who experience mental disorders do not receive treatment and research indicate that the country has a shortage of mental health workforce (Gartlehner et al., 2017). Overcoming Major Depressive Disorder (MDD) require collaborative assistance from health providers, patients, and close relatives or friends of the victims because it helps avoids relapses and recurrence of the condition.

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Major Depressive Disorder (MDD) is a mental condition classified as a prolonged sadness that affects both adults and children. The victims experience feelings of intense sadness, worthless in society, helpless, and hopeless. Consequently, the condition affects the victims' body, thoughts, and moods and it is capable of interfering with daily life, normal functioning, and leads to pain for both the victims and the people who care about them. The condition is harder to spot in children compared to adults. Moreover, MDD exists in different forms, and all have different symptoms. The major MDD include psychotic depression, postpartum depression, and seasonal affective disorder (CCNC Adults Depression Toolkit for Primary Care, 2015). Scientists are divided on the characterization and definitions of the various forms of depression. However, they believe that the solution to the disorder is medications as prescribed by health providers or therapy.

Pathophysiology

The pathophysiology of depression remains elusive, and this has undermined the drug development against the condition. There exist various theories on the pathogenesis of depression, and most of these concepts are based on the measurement of indirect markers, neuroimaging techniques, and post-mortem studies (Kimmel et al., 2018). For decades, when investigating the disease, researchers focused on depression pharmacotherapy, and a resultant explanation for the underlying pathology was based on the brain monoamine neurotransmitters, and this was after the discovery of iproniazid and imipramine as an antidepressant.

Neural Circuitry of Depression

Functional and structural studies indicate abnormalities in some areas of the brain which are responsible for controlling and regulating mood, executive function, and reward response. Results from various scientific studies suggest that neuroimaging and post-mortem studies have morphological changes that are illustrated by reductions in the glial density in the prefrontal cortex and hippocampus and the grey-matter volume. These regions are the ones that have received the most attention in animal studies on depression (Gartlehner et al., 2017). The reduction in hippocampus function could potentially be responsible for the hypercortisolemia that is witnessed in depression conditions because it is believed that it has an inhibitory effect on the hypothalamic-pituitary-adrenal (HPA) axis.

The other factors that are responsible for the pathogenesis of depression include the mesolimbic dopamine system which entails the nucleus accumbens popularly referred to as (NAc) and the ventral tegmental area (VTA). These two brain regions mediate the reward response pleasurable stimuli such as drugs, food, and sex (Kimmel et al., 2017). Therefore, the lack of pleasure symptom that is common in people suffering from depression can be considered as a dysfunction in the brain reward circuit.

Stress Response Circuits

Hyperactivity of the HPA axis and chronic stress contribute immensely to depression and in recurrence after complete remission. Patients with elevated levels of corticosteroids experience structural brain abnormalities. The brain structure that is affected during this process is the amygdala. This area of the brain is responsible for regulating emotional reactivity and stress response. Moreover, chronic administration of the corticosteroids leads to a decrease in the size of the hippocampus. This area of the brain is useful because it exerts an inhibitory signal to the HPA axis (CCNC Adults Depression Toolkit for Primary Care, 2015). Though there is a lack of complete research on how behavioural stress leads to depression, chronic stress can alter the expression of genes that regulate antioxidant systems. The systems include catalase, glutathione reductase, superoxide dismutases, NADPH oxidase, and glutathione peroxidase. During animal research, studies indicate that treatment with glucocorticoids leads to an elevation in the level of reactive oxygen species both in vitro and the brains of the mammals that were being investigated. The process further down-regulates various antioxidant enzymes and induce depression-like tendencies (CCNC Adults Depression Toolkit for Primary Care, 2015).

Genetic Vulnerability and Environmental Interaction

Depression is a result of a complex gene-environmental interaction that can alter an individual response to stressful life situations. The gene polymorphism is not responsible for causing depression, and studies indicate that genetic factors can make a group of individuals susceptible to depression because the factors increases their vulnerability to stressful environmental factors. Scientists have focused more on allelic variation in the promoter region of the gene encoding the serotonin transporter (5- HTT). The promoter region of the serotonin transporter (5 -HTT) gene (5- HTTLPR) contains a functional polymorphism resulting in a long or short variant in the promoter region upstream of the transcription starting site (CCNC Adults Depression Toolkit for Primary Care, 2015). The short allele of the 5-HTT puts carriers at a higher risk of developing depression in response to stressful life conditions because of the low-activity. The short allele of further leads to adverse outcomes after antidepressant non-pharmacological and pharmacological treatments.

The tryptophan hydroxylase (TPH) which is a rate-limiting enzyme in serotonin biosynthesis is encoded by two distinct genes, that is, Tph2 and Tphl. The two genes play a vital role in the pathogenesis of depressive disorders. Moreover, single nucleotide polymorphisms on the Tph2 gene further leads to increased incidences of major depressive disorders. Functional polymorphism produces a valine to methionine substitution at the codon 66. This happens in the pro-BDNF region, and their presence in the BDNF gene leads to a detrimental effect on intracellular trafficking activity-dependent secretion. The process influences hippocampal function, brain morphology, and episodic memory (CCNC Adults Depression Toolkit for Primary Care, 2015). Healthy people with the BDNF Met variant have a smaller hippocampus volume and low emotional stability. Moreover, research indicates that complex interaction that exists between the polymorphisms in gene encoding 5- HTT and BDNF can result in a depressed phenotype.

Neuropeptides

Studies indicate that neuropeptides takes part in the modulation of stress-related moods and traits. This achieved by acting on the neurokinin type-1 receptors (NK- 1). The condition is enhanced by elevated CSF SP which is considered to be one of the neuropeptides that widely spread distribution in the brain and further its co-localization with 5-HT and NE neurons. Depressed patients have elevated CSF SP concentrations after exposure to stressful stimuli. Moreover, the central administration of the SP induces a stress response in humans (CCNC Adults Depression Toolkit for Primary Care, 2015). The process is supported by the antidepressant activity of NK-1 antagonists.

Hormones

The main hormones that trigger in depression include thyroid hormones, estrogen, and vasopressin. The thyroid hormones assist in the development of the brain, maturation, and further promote neurogenesis in the specific hippocampus. The imbalance of these hormones is implicated in the pathophysiology of psychiatric and neurodegenerative conditions. Additionally, the hypothyroidism may lead to depressive behaviours that area be to impair hippocampal neurogenesis which resolved with hormone replacements (Ciesielski et al., 1994). Research further indicates that thyroid hormone can lead to an increase in serotonergic neurotransmission that supports the analysis that TH supplementation is beneficial in managing refractory cases of depression. Additionally, estrogen can enhance mood by increasing the rates of degradation of MAO and intraneuronal 5- HT transport (Kimmel et al., 2018). The process results in an overall increase in the 5- HT availability in the synapse. Moreover, the serotonergic neurotransmission has a modulatory effect on hippocampal neurogenesis, BDNF signalling, and HPA axis function in women. The arginine vasopressin popularly referred to as (AVP) is a hypothalamic hormone that can influence critical symptoms that are pertinent to MDD. The level of arginine vasopressin is elevated in patients who suffer from depression. Moreover, the AVP can regulate stress response which may lead to depression. This occurs because AVP can synergize with the CRF and influence the release of ACTH (Ciesielski et al., 1994).

Standard of Practice

According to 2015 statistics, about 593,000 adults aged 18 or above with any mental illness (the figure represents 48.2% of all the adults with any mental illness in North Carolina), per year from 2010 to 2014 have received mental health treatment or counselling within the prior to the commissioning of the survey (CCNC Adults Depression Toolkit for Primary Care, 2015). The key recommendations for assessing, diagnosing, and managing major depressive disorder are screening for MDD with the assistance of the 'two quick questions' method. Later the health providers are required to use the Patient Health Questionnaire to help in diagnosing and monitoring the patient's condition. Moreover, people who suffer from MDD are prone to suicide. Thus providers should access the suicide risk in all patients that show signs of depression. After that, providers should use the available options for non-pharmacological and pharmacological interventions which exist as short, medium, and long-term assistance (Furr et al., 2001). After the process, patients are expected to continue for at least six months after remission and treatment to recover occupational and social functioning.

Screening

During the screening and assessment of patients with symptoms for MDD, the two quick question method is typically used. The questions are based on the condition and behaviours for the past one month. Therefore, patients are asked if in the past one month:

• They have lost pleasure or interest in things they usually liked to do.
• They have felt low, sad, down, hopeless, or depressed.

If the answer to any of the above questions is a YES, then the patients require a more detailed assessment (Behavior Health Barometer North Carolina, 2015). A comprehensive evaluat...