Depression and Antidepressants
Specifically the serotonergic hypothesis and the action of Prozac
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
…show more content…
The pertinent findings will be explained, and their implications on future anti-depressants will be addressed.
Many clinical studies have been used to suggest a role for serotonin in the propensity for depression or suicidal tendencies. Most of these studies measured the level of serotonin in the CSF in certain individuals. Results established a link between reduced serotonin neurotransmission and aggression, impulsivity, depression, and suicidal tendencies. Other data, using markers in presynaptic and postsynaptic serotonergic neurons have shown that reduction in serotonin neurotransmission is a biochemical "risk factor" for suicide (1).
Other clinical studies have implicated fluoxetine’s effects on serotonin neurotransmitters, based on the fact that serotonin is synthesized from the essential amino acid tryptophan. Patients taking fluoxetine who were in remission from major depression were given a special diet which was tryptophan-free. This rapidly decreased plasma serotonin levels, and after a short period of time (as little as 30 minutes) many of the patients began to have signs of specific depressive symptoms. Later, the reappearance of more general depressive symptoms were observed in a majority of the patients. Thus it was shown that fluoxetine has a profound effect on the neurotransmitter serotonin, and decreased
Chronic intake, the delayed onset of action, drug resistance and numerous side effects force the researchers to look for the new, safe antidepressant strategies (1, 2) with rapid onset and longer time of action.
Depression has always been a mystery to us; throughout time, we have tried to figure out what causes depression and how to cure it. In the 17th century, a British clergy and scholar named Robert Burton wrote a book called The Anatomy of Melancholy. He believed that depression or melancholy is produced by an excess of black
Thus far, I have learned about the pros and cons to using medication in treatment with clients. In addition, I have seen first hand the benefits of implementing medications in client’s treatment plan. From my understanding, Depression is one of the most prevalent illnesses in the world. Because of this fact it is important that we understand and explore all the implications surrounding the use and efficacy for treatment. In order to treat our clients with the best care possible, we as therapist should be educated on the types of medications for depression, the impact they have on the body, and their efficacy of improving symptoms and overall functioning. In this paper I will explore three articles about antidepressants and their efficacy for treating clients with depression. In addition, I will provide my overall reaction to the studies and the material provided for the efficacy of antidepressants for treating depression.
In order to be able to treat a person with depression effectively, doctors have to sort out what kind of role the narcotics may play in the depression. If the feelings of depression is simply a part of a withdrawal due to a narcotic and are only something temporary, it is very unlikely that a antidepressant will be of any benefit. Antidepressants take a bare minimum of two to three weeks to begin working. The most effective treatment in such a case would be to try and help the person at hand to get their drug use under control or stop entirely. Both taking drugs and the withdrawal process may produce depressive symptoms themselves, makingit very difficult to know what it is that’s exactly going on, if it even seems that the depression led to taking drugs in the first place. As a result, It’s extremely vital to the treatment of the individual that the problem with narcotics is sorted out so that is will be possible to further judge whether antidepressants or other treatments used for depression will be needed. This, of course, does not mean it’s
In Issue 13 of Taking Sides, the controversial question Have Antidepressant Drugs Proven to be Effective is analyzed. Psychiatrist Peter D. Kramer argues in this issue that antidepressant drugs "can transform depressed patients into happy people with almost no side effects" (p.212). On the contrary, professors of psychology Seymour Fisher and Roger P. Greenburg "claim that the studies that demonstrate the effectiveness of antidepressants are seriously flawed" (p.212). Kramer's agreement with the statement above is due mostly to the testing he did with his patient Tess and antidepressant drugs. However Fisher and Greenberg disagree with the statement mainly because of the bias drug studies that
Selective serotonin reuptake inhibitors are utilized for their ability to reversibly block the reuptake of serotonin in the synaptic cleft. In order to understand the importance of these drugs, it is crucial to review the various regions of the brains that are influenced by serotonin and the implications of impaired functioning. A dysfunction in the hypothalamus region of the brain might lead to weight or appetite changes. Sleep disturbances are characterized by a dysfunction in the hypothalamus as well, along with the thalamus, basal forebrain, and prefrontal cortex. Thoughts of suicide and perceived feelings of guilt or worthlessness are associated with a dysfunction in the brain regions connected to our emotional well-being, including the amygdala, ventromedial prefrontal cortex, and orbitofrontal cortex. Psychomotor agitation is linked
Selective Serotonin Reuptake Inhibitors (SSRIs) are currently one of the most controversial groups of medicines, with fluoxetine, more commonly known by its brand name Prozac, at the head of the controversy. Opponents of the use of SSRI medications as a successful and safe method for treating depression and related disorders assert that the actions of the drug are an unnatural and a dangerous form of tampering with our neurochemistry. Not only are these medications incredibly safe in almost all cases, they are actually an unnatural method of modifying an already disordered, natural sequence of chemicals in the brain, and therefore are not a form of tampering, but are a method for fixing
The history of antidepressants began with isoniazid, which was an anti-tuberculosis medication. This came after finding that the medication had euphoric effects on the patients taking it. The drug had a mood altering side effect which later became the primary effect for depression and was a basis for synthesis of generations of new antidepressants (Indian J Psychiatry, 2011). Antidepressants are psychiatric medications given to patients with depressive disorders to alleviate symptoms (MNT, 2012). Neurotransmitters in the brain can cause changes in mood and behavior, antidepressants can help correct these chemical imbalances. Many psychiatric conditions can be treated with antidepressants including anxiety disorders and dysthymia. According to medicalnewstoday.com, there were 13.3 million people using antidepressants in 1996 by 2010 that number jumped to 23.3 million. The website goes on to say they believe the increase in antidepressant use can be credited to a higher need for mental health treatments, campaigns promoting mental health care being more widespread and mental health treatments becoming more widely accepted. In the years since the antidepressant age came to be many new antidepressants have been made, the Royal College of Psychiatrist say there are at least thirty different kinds of antidepressants, all of which can be divided into five main types.
Common types of medication include POM (prescription only medication) which can be obtained from a pharmacist only if prescribed by a doctor. These could include anti-depressants which are very common. Anti-depressants work by selecting receptors in the brain and controls levels of serotonin. They come under the group 'SSRIS' (selective serotonin reuptake inhibitors). Over the counter medicines (OTC) may include things like paracetamol or ibuprofen, which are everyday painkillers. Something like paracetamol inhibits the production of pain and inflammation-causing chemicals called prostaglandins.
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).
(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)
for serotonin to bind between depressed people who respond to SSRI’s and those who don’t. The
Serotonin syndrome is a potentially lethal disorder triggered by excessive serotonergic bustle in the nervous system, it depicts as mental status vicissitudes, autonomic unsteadiness, and neuromuscular hyperactivity (Volpi-Abadie, Kaye, & Kaye, 2013). According to Volpi-Abadie, Kaye, and Kaye (2013), serotonin syndrome could happen amid individuals utilizing multiple serotonergic drugs or amid individuals with substantial exposure to a sole serotonin augmenting drug, the diagnosis is usually made with the utilization of Hunter Serotonin Toxicity Criteria or the Sternbach’s criteria. The diagnosis of Serotonin syndrome diagnosis necessitate the existence of one or more of the classical traits, namely inducible clones with
Like dopamine, serotonin also has some physical factors as well, it is known to impact a person’s mood, hunger, sleep, and arousal (Myers & Dewall, 2015). Since serotonin makes us happy, it is obvious how it affects these things, if we’re not happy, we’re going to be in a bad mood, which will affect our eating and sleeping habits, and our arousal because we won’t have much of a sexual drive. Since serotonin make us happy, its easy to imagine that not enough of it would leave us sad. People that are depressed have low levels of serotonin being released and being transferred through out their body compared to non-depressed people (Parsey, et al., 2006). When serotonin isn’t being released enough, or as much as it should be it really affects how happy we are and can put us into serious states of depression. Medications for depression often times are meant to help with releasing more serotonin into the body, giving the depreesed patient more of this “liquid happiness”. Serotonin can also be linked to bulimia and eating disorders. It is thought that dieting and binge eating can result in the decreasing of serotonin in the brain, which could be a reason why patients who are suffering from bulimia nervosa have very low levels of serotonin (Serotonin Function in Bulimia Nervosa, 2004). When we aren’t feeling happy, it could cause us to harm our bodies, even though we don’t realize what we are doing. When our serotonin levels are low, our health is at serious risk. When serotonin levels are low in our body, it causes these mental illnesses. Serotonin is not all to blame, but it certainly plays a role in the development of these
are happy when they achieve something or saddened when they fail a test or lose