Major depressive disorder is one of the most common mental disorders, with a 12-month prevalence of 6.7% of adults in the United States (NIMH). There is no definite etiology of depression, but several risk factors have been identified. Functional and structural changes in the brain have also been explored. The most common treatment for depression is the use of drugs that act on monoamine transmitters, including norepinephrine, dopamine, and serotonin. Decreases in these transmitters, especially serotonin, were hypothesized to play an important role in the cause of depression (Breedlove & Watson, 2013). The serotonin hypothesis led to the development of selective-serotonin reuptake inhibitors (SSRIs), which increase the amount of serotonin in the brain. Further research suggests that the serotonin hypothesis is not entirely accurate and the neurobiology of depression is much more complex. The “chemical imbalance” explanation of depression may not reflect the full range of causes and may be given greater credibility by patients and doctors than is supported by evidence based research.
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).
Biological Theories. The monoamine neurotransmitters—norepinephrine, dopamine, serotonin, histamine—are the main focus of theories regarding the cause of depression. However, the focus is not on a single neurotransmitter but on the “studying neurobehavioral systems, neural circuits, more intricate neuroregulatory mechanisms” (Kaplan Sadock 531).
Neurotransmitter Systems. The study of monoamines in relation to MDD has been at the forefront for the majority of the time that the subject itself has been under research. With a particular focus on serotonin (but also norepinephrine and dopamine), these studies find that the rate of serotonin synthesis is often low in depressed patients (Rosa-Neto et al., 2004). Interpretation of serotonin levels may however become problematic, because it can be concluded that: depression may cause a low synthesis of serotonin; a low synthesis of serotonin may cause depression; or that another third process may cause both a low synthesis of serotonin and depression simultaneously. There is little doubt that a decrease in serotonin plays a key role in MDD but the notion of whether the neurotransmitter’s absence is a mechanism that is uniquely responsible, or merely a
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
Serotonin is a chemical generated by the human body which works as a neurotransmitter, it is also referred to as 5-hydroxytryptamine (5-HT). Biochemical theories over time suggest that a decreased level of serotonin is a major contributing factor in depression. According to Jacobsen, Medvedev, and Caron
The leading theory explaining the biology of depression is the monoamine hypothesis of depression. (Stahl, 3) This theory suggests that depression is caused by a deficiency in one or another of the three neurotransmitters: serotonin, norepinephrine and dopamine. The theory was formulated after the accidental discovery of the original drugs for depression and psychosis, much in the same way Fleming discovered penicilin.
The cause of Clinical depression has long been a mystery to physicians and researchers. Many different theories have been proposed, but no conclusive evidence has been put forth. However, most of what we know about depression stems from the results of certain drugs which have been successful in treating the clinically depressed. These anti--depressants have led to the assumption that depression is most likely due to a chemical imbalance (of neurotransmitters) which somehow leads to the symptoms of depression. To try and write a paper on all the theories of depression would be endless, as would be a study on all the different types of
Through my research I wanted to learn about exactly what anti-depressants do chemically . I also wanted to determine what role genetics, heredity, environment, and biological factors play in depression. Though I was not able to answer all of these questions, I learned a lot about depression and even developed some theories of my own. For a long time, I have thought of some forms of depression as a weakness. I truly believed that in many cases it could be controlled by the depressed person themself. I also felt that environmental and personal factors played were the basis for depression. However, through what we have learned in class and from my research, I have come to realize that this theory is not completely true. Mood is a generalized control mechanism like sleep. Eating also exhibits many characteristics of generalized control mechanisms. Mood can be affected by sensory input and the I-function, but it is also autonomous in that it can vary independent of sensory input. This internal variation is pharmacologically dependent. Changes in a persons pharmacological makeup can cause mood changes, sleep disturbances, and even depression. The I-function influences mood manipulation but cannot determine mood. Though you may want to be in a good mood, make a conscious effort to think RhappyS thoughts, and may not have serious stressors in your life, you may still suffer clinical depression as a result of a chemical imbalance in your system. Depression can be physical and
In neurotransmitter dysfunction, the biological approach to depression explains low levels of the neurotransmitter serotonin. This has been linked with many forms of dysfunctional behaviour such as anxiety, excessive anger, poor social functioning and other mood disorders.
(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)
Depression is a serious mental disorder that may be displayed by major episodes of sadness, restlessness, and loss of interest. Depression has several symptoms such as excessive sleep, increased or loss of appetite, aches, cramps, insomnia, and fatigue. It can affect anyone of all ages and may not be recognizable for those who are experiencing it. A medication called anti-depressants helps treat depression by altering the serotonin receptors levels. There are several types of anti-depressant medications such as Abilify, Celexa, Aplenzin, Asendin, and many more. There are individuals that may argue that anti-depressants are an over-prescribed medications. They believe that this medication can affect the patient’s mental status and inhibit self-control with this addictive drug. On the other hand, the opposition may argue that anti-depressants are not overly prescribed and that it should not be problematic because it is an accessible, helpful, and a quicker treatment. The debate of whether anti-depressants are an over-prescribed medication has been an ongoing controversial issue as evidenced by statements of supporters and those in opposition.
The typical description of a disease would be something that causes unwanted effects on the body; however, mental illnesses show few physical symptoms and cause problems that outsiders can rarely see. Major Depressive Disorder (MDD), to be specific, is a complex disorder that occurs when a person has five of the following symptoms: a depressed mood, diminished pleasure, weight loss or gain, insomnia, lethargy, problems with concentrating, fatigue, feeling worthless, or having thoughts of suicide (Myers 3). While MDD is chronic, depression is the infrequent counterpart. The official etiology of depression is important because it is widespread and is becoming increasingly more common. Knowing why an illness occurs, in theory, can help physicians
Many people with mild to moderate depression can be successfully treated with psychotherapy and other non medical interventions such as bright light; exercise; relaxation techniques; eliminating the use of substances like recreational drugs, alcohol and caffeine; getting regular sleep; eating a balanced diet; and stress reduction. But when these interventions have been tried and failed, or when a patient's depression is severe enough to interfere with their ability to function in their work, relationships, and self-care, doctors will recommend antidepressant medications as well. There are several different classes of antidepressants to choose from, including older medications called monoamine oxidase inhibitors (MAOIs) and tricyclics; selective serotonin reuptake inhibitors (SSRIs); norepinephrine and serotonin reuptake inhibitors; and others. Despite the differences in these medications' effects on neurotransmitters, chemical properties, side effects, and pharmaceutical company advertising, they all are EQUALLY EFFECTIVE in treating depression. The choice between them, therefore, is made on the basis of other factors. When deciding which antidepressants may be best for a given patient, a doctor should take into consideration several factors. The first is the patient's history. If a patient has
Not only do Prozac and other SSRIs provide results for those suffering from depression, they manage to have other purposes. Prozac succeeds in reducing symptoms of major depressive disorder such as suicidal ideation, depressed mood, worthlessness and loss of energy. SSRI antidepressants “have better overall safety and tolerability than older antidepressants” and allowed patients to take the medication for longer (SSRI Antidepressant Medications: Adverse Effects and Tolerability). Not only could they help people experiencing the side effects of tricyclic antidepressants, but they could also be prescribed to children and the elderly (SSRI Antidepressant Medications: Adverse Effects and Tolerability). This lead to “more patients now [being] successfully treated for depression than ever before” (SSRI Antidepressant Medications: Adverse Effects and Tolerability). The new discoveries continued pouring in as researchers linked SSRI antidepressants to increased abstinence for people trying to quit smoking and effectiveness in eliminating symptoms of panic disorder (Elevated positive mood: A mixed blessing for abstinence, Panic disorder and suicidal behavior: A follow-up study of patients treated with cognitive therapy and SSRIs in Hungary). A Hungarian study using SSRIs was able to eliminate symptoms of panic disorder in 38.5% of participants and significantly reduce their suicidal ideation and behaviour (Panic disorder and suicidal behavior: A follow-up study of patients treated with cognitive therapy and SSRIs in Hungary). Furthermore, multiple studies have been conducting showing a negative relationship between smoking and the use of SSRI antidepressants, specifically for patients with generally low positive mood (Elevated positive mood: A mixed blessing for abstinence, Multicenter trial of fluoxetine as an adjunct to behavioral smoking cessation treatment.). SSRI antidepressants