Depression And Its Effects On An Individual 's Life Essay

Depression is a mental health disorder that can be characterized by loss of interest of once enjoyable activities, and a persistent mood of depression (MacGill, 2017). As previously stated earlier in this paper, hundreds of millions suffer from this debilitating mental disorder on a global scale and is extremely prevalent in today’s society. According to MacGill, those individuals suffering from depression often times have symptoms consisting of feelings of loneliness, worthlessness, apathy, or depressed moods and tend to have a difficult time doing things or getting out of bed (2017). Other symptoms that arrive with depression can also include irritability, anxiety, isolation, lethargic tendencies, suicidal thoughts, appetite loss, and weight gain or loss. There are numerous causes of depression, according to MacGill, ranging from genetics, environmental factors, traumatic events, psychological and psychosocial problems, drugs and drug abuse, having had a major depressive disorder, or a change in neurotransmitter levels (2017). Serotonin, a neurotransmitter that results in a happy feeling, is typically found in highly reduced levels in those who suffer from depression which usually leads to said person being diagnosed SRIs (serotonin reuptake inhibitors) as a form of treatment and is usually prescribed

In Gary Greenberg's Manufacturing Depression: The Secret History of a Modern Disease, he takes an in depth look at the history behind depression, antidepressants, and how we have come to recognize and accept depression as a biochemical disease. When analyzing this book we can see that depression itself, whether it be a disease that is biochemically manifested or not, is deeply integrated into our society in a variety of ways as many aspects of society associated with depression have specific functions that are integral for society to function properly as a whole.

Background: Major depression remains one of the most detrimental mental disorders without precise pathogenesis and effective treatment.

The pertinent findings will be explained, and their implications on future anti-depressants will be addressed.

This affects the the brain-derived neurotrophic factor (BDNF)- a crucial factor in the neurobiology of depression. The hippocampus is rich in BDNF, which is related in neuronal growth, survival and maturation, as well as arborization and synaptic plasticity in the adult brain. Stress suppresses BDNF synthesis in the hippocampus showing low concentrations in depressed patients, correlating with the severity of the depression. The use of antidepressant drugs increase its synthesis and signalling in the hippocampus and PFC. In a post-mortem study of depressed patients at the time of death, there were significant differences between the BDNF concentrations in treated and untreated patients. Antidepressants work by balancing neurotransmitters that affect mood and emotion. The use of antidepressants and going to therapy are the most effective ways to treating depression. Weight gain and the feeling of mental numbness is a side effect of antidepressants. Depression can be prevented. Daily exercise, having strong relationships,and watching alcohol intake are ways to prevent depression. Depression is a long term,recurrent condition often taking a chronic course. It is associated with significant morbidity, comorbidity and mortality (suicide and physical illness). In order to achieve and maintain optimum brain function and reduce the risk of recurrence, antidepressant drug treatment full remission is

This report will focus on the effects and memory of therapeutic and off label drugs. A study shown by Star*D gives insight to the first exposure to a patient taking antidepressant, that only 28% to 33% will go into complete remission. Total remission of depressive symptoms is now the aim of current modern antidepressant psychopharmacology (Rosse, Richard MD 2007). Research has shown that mostly all the market available antidepressant users are very effective in treating depression. It has been proven to in fact elevate the patient’s mood and help retake interest in everyday life. Aside other frustrations such as poor sleep and concentration and loss of care for sleep this drug has been effective. Antidepressants have also been successfully

The linkage of serotonin to depression has been known for the past five years. From numerous studies, the most concrete evidence of this connection is the decreased concentration of serotonin metabolites like 5-HIAA (5-hydroxyindole acetic acid) in the cerebrospinal fluid and brain tissues of depressed people. If depression, as suggested, is a result of decreased levels of serotonin in the brain, pharmaceutical agents that can reverse this effect should be helpful in treating depressed patients. Therefore, the primary targets of various antidepressant medications are serotonin transports of the brain. Since serotonin is activated when released by neurons into the synapse, antidepressants function at the synapse to enhance serotonin activity. Normally, serotonin's actions in the synapse are terminated by its being taken back into the neuron then releases it at which point "it is either recycled for reuse as a transmitter or broken down into its metabolic by products and transported out of the brain." As a result, antidepressants work to increase serotonin levels at the synapse by blocking serotonin reuptake (2).

The basic pathophysiology of major depressive disorder has not been clearly explained. Current evidence suggests a complex interaction between the availability of the neurotransmitter, receptor regulation, and sensitivity underlying the affective symptoms.

(3) While successful drug therapies which act on neurotransmitters in the brain imply that depression is a neurobiological condition (4), the fact that such medications do not help about 20 percent of depression-sufferers seems to show that not all depression is due to such imbalances. Rather, depression is not caused by one single factor; it is most often caused by many different things. Genetics, biochemical factors, medicines and alcohol, developmental and other external factors, and relationships, marriage and children all have effect on the development of clinical depression. (5) The strongest hypotheses on the pathways to depression are in decreases in the activity of specific neurotransmitters, or the overactivity of certain hormonal systems. (3)

However, the exact mechanism underlying the development of depression and antidepressant action is still elusive. Studies on depression have focused on the interactions between the monoamine neurotransmitters and their reuptake and the receptor proteins. The current antidepressants available by chemical synthesis have a high incidence of dangerous side effects and are inadequate for number of individuals [1].. Accordingly, it is of great significance to research for and develop more effective antidepressants with fewer drawbacks. Other mechanisms of depression development should also be considered, as they might provide potential effective targets should extend New approaches : with rapid onset antidepressants. broader efficacy, and fewer adverse

One of the largest trends in neuroscience in the United States today is the usage of a pharmaceutical treatment option for those suffering from depression. While there are a host of other potential treatment options ranging from psychotherapy to electric convulsion therapy (for the most severely depressed patients), anti-depressant medication is far and away the most popular treatment. In fact, in 2011 more than 1 in 10 Americans over the age of 12 was using a selective serotonin reuptake inhibitor (SSRI) in order to combat their depression (Krystal, 2011). The medical and psychological community has had a raging debate regarding the efficacy of SSRI’s since they became widely prescribed in the late 1990’s. This paper will summarize

Monoamines are neurotransmitters that include serotonin, dopamine, norepinephrine, and epinephrine. Numerous antidepressant drugs increase synaptic levels of serotonin, but they also enhance the levels of the neurotransmitters, norepinephrine and dopamine. In the body there is another monoamine called monoamine oxidase that has the effect of breaking down serotonin and norepinephrine. Therefore, by blocking the effect of the monoamine oxidase, there is a increase of synaptic concentrations of monoamines and te symptoms of depression are relieved. This discovery led to the monoamine hypothesis of depression over 30 years ago, which proposes that the underlying biological basis for depression is a deficiency of central noradrenergic and serotonergic systems and that targeting this neuronal lesion with an antidepressant would tend to restore normal function in depressed patients. A class of drugs known as monoamine oxidase inhibitors (MAOI) have this effect. However, although helpful to many patients, the monoamine theory of depression does’t address othes issues such as why antidepressants can treat panic disorders, OCD etc. and why enhacing monoamine concentrations isn’t always effective in treating depression. (1) (2)

After 30 days of daily reserpine injections, the significant changes in the OFT parameters and hunched back appearance persisted and were similar to those observed after 15 days of reserpine treatment. In addition to the motor deficits, the present depletion in cortical and hippocampal monoamine levels induced by reserpine confirms the development of the rat model of depression, since the central depletion in 5-HT, NE and/or DA have been postulated as the main cause for the pathogenesis of depression (Schechter et al., 2005)

This review article was published recently in 2015 in an international journal called Nutritional Neuroscience. Nutritional Neuroscience first published in 1998 and had an impact factor, in 2015, of 2.616 by Journal citation reports. It reports basic and clinical research on the effects of nutrition on the central and peripheral nervous system. Moreover, the authors consist of a collaborative team involving three different countries and reputable universities consisting of Iran, Australia and Italy. The article at hand discusses the ever-growing epidemiological problem of depression. The WHO Global Burden of Disease estimates depression to be the leading cause of long-term disability by the year 2030. However, the use of antidepressants such as serotonin-reuptake inhibitors and monoamine oxidase inhibitors often involves using multiple drugs, has numerous undesirable side effects and lastly, are marginally effective compared to placebos. As a result, more attention is being given to dietary supplements and their role in attenuating the neurobiological symptoms of depression. The authors have therefore conducted a review of available literature on the probable

The severity of depression has been supported through scientific evidence that indicates that depression has a biological basis in the brain of a depressed person along with psychological and social implications. Whilst there are many catalysts in a person’s life that can be identified as a possible root cause of depression, such as stressful life events or the death of a loved one, the issue is far more complex, as the biological triggers of depression are not as easily expressed, such as faulty mood regulation in the brain, vulnerable genetics in the DNA, and other medical problems. Many things are altered in the brain of the depressed person. Firstly, what most understand to be an imbalance in the levels of chemicals that regulate emotions, is in reality far more elaborate. The true issue surrounding the many chemicals involved inside and outside of the nerve cells that undergo numerous chemical reaction which make up the dynamic system that is responsible for mood, perceptions, and the way one experiences life you experiences life can be altered in different ways that affect how one lives. Along with the brains chemicals, the connections between nerve cells called neurons decrease and deteriorate, meaning the