The Action Of Animal Models

This increases level provides the sense of satisfaction which obese people lack. An increase in serotonin ( a hormone in the brain) eventually leads to weight loss. The combination of a decrease in caloric intake along with the excess production of serotonin by redux is what causes some to lose body weight. This redux treatment is associated with a loss of appetite and may slow gastric emptying.

Bailer et al (1970) compared serotonin activity in recovering anorexia suffers and healthy controls. They found significantly higher activity in the women that were recovering from anorexia, the highest levels found in those women with the highest anxiety levels. This also provides support for AN having a biological cause, in this case an imbalance of neurotransmitters.

With an estimated 9.3% of Americans currently living with major depression or bipolar disorder, according to the NIMH, the safety of antidepressant drugs is at the forefront of many pharmaceutical discussions. At present, the most common drugs used to treat the debilitating lethargy, anxiety, and fatigue often associated with major depression fall into three key categories based upon mechanism of action: SSRIs, Tricyclics, and MAOIs. Since major depression and bipolar disorder are characterized by imbalances of certain chemicals within the brain, prescription medications are often the best way of relieving the symptoms of these disorders. As with any medication, antidepressants carry risks of side-effects, which usually relate to the drug

For as long as antidepressants have been curbing symptoms of mental health disorders, they have also brought their users adverse effects. Monoamine oxidase inhibitors, the first generation of antidepressant medications, were the primary antidepressant utilized between the 1950s and 1970s (Goldberg). Significant side effects of MAOIs include dizziness, high blood pressure, loss of sexual desire and weight gain (Goldberg). Most critically, MAOIs interacted with many other medications (Goldberg). These downsides led to the development of antidepressants with fewer interactions. The result was selective serotonin reuptake inhibitors—the most commonly prescribed antidepressants today (Fink). In a sample survey, 55 percent of individuals reported at least one adverse side effect within the first three months of taking a SSRI (Hirsch). The most common side effects include sexual dysfunction, insomnia, drowsiness, weight gain, dizziness, headache and anxiety (Hirsch). While SSRIs have been shown to reduce risk of suicide

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

Impaired serotonin function has clearly demonstrated to be linked to clinical depression, because low levels of serotonin may negatively affect mechanisms involved in maintaining recovery from depression. However, there is evidence the serotonin pathways may not directly influence mood but may be important mechanisms in depression due to an indirect consequence of shifts in autonomic emotional responses, i.e., the impaired function may simply cause emotional responses to become unstable contributing to depression. Therefore, Prozac, which acts as an inhibitor of the mechanism that reduces serotonin, can help to reduce this emotional imbalance. However, serotonin alone is often not sufficient in treating depression, as there are many mechanisms involved that are associated with depression.

Walker, F. R. (2013). A critical review of the mechanism of action for the selective serotonin reuptake inhibitors: Do these drugs possess anti-inflammatory properties and how relevant is this in the treatment of depression? Neuropharmacology, 67, 304.

Depression being an affective mood disorder is a serious global public health issue with over 350 million sufferers worldwide8,10,11. Although it is described with feelings of low mood, inadequacy, guilt, low self-worth, loss of motivation, interest, pleasure and concentration; it is also associated with a functional deficit of the monoamine transmitters (serotonin and noradrenaline) in certain brain regions such as amygdala, hippocampus and prefrontal cortex6,10. It can also induce biological symptoms like retardation of thought and action as well as sleep disturbances, loss of appetite and libido and if left untreated, it can eventually lead to disability8,11. Therefore, the pharmacotherapy plays a crucial role in the treatment of depression.

three groups.Monoamine oxidase inhibitor (MAOI) medicines block the monoamine oxidase enzyme (MAO) from destroying monoamine neurotransmitters, which allows them to accumulate, alleviating depression. Serotonin selective reuptake inhibitor (SSRI) medications block the serotonin reuptake pump, allowing the serotonin neurotransmitter to remain and accumulate in the receptor for longer. Speaking of serotonin specifically, depression has been related to a deficiency of the 5-hydroxytryptamine (serotonin) neurotransmitter as evidenced by the concentrations of the

γ-lipotropin is literally the same as the first fifty-six amino acid sequences of it. Lipotropin has also, under its name used for the practice of peptide supplementation (Anti-Obesity Drug-9604 (AOD-9604)), been used to combat weight problems. Lipotropin inhibits lipogenesis (prevents the transformation of fatty food materials into body fat) and stimulates lipolysis (the breakdown or destruction of fat). Psychologically speaking, weight gain is a contributing factor to many depressive episodes (and frequently vice versa). “It’s a chicken and the egg phenomenon,” says psychologist Leslie Heinberg, PhD (who directs the Bariatric and Metabolic Institute at the Cleveland Clinic) in an interview by WebMD. “But we do know that depression has lots of symptoms that can worsen obesity - appetite disturbances, lack of energy, lack of motivation to do

Fluoxetine is also known as Prozac, common antidepressant drug (1). It works as selective, competitive reversible antagonist of serotonin receptor that prevent reuptake of serotonin from synapse (2). Due to selectivity, little effect on other neurotransmitters, such as dopamine and noradrenaline. It increase the concentration of serotonin at the synapse and serotonergic neuronal transmission strength, and it triggers negative feedback loop of serotonin, which reduce the conversion of tryptophan to serotonin (3). Fluoxetine does not display species difference, but effect as antidepressant is depend on the dose thought out number of studies. Fluoxetine is administrated as tablets with usual starting dose of fluoxetine is 20mg per day, and it

Depression has become a chronic illness throughout society. The illness not only is a psychological hazard. The sedentary symptoms create physical infirmity. For many years studies and research have influenced the use of antidepressant medications as treatment for depression. Much money and time has been spent in promoting the ideas of chemically assisted happiness. Yet, a much inexpensive alternative to the treatment of depression is ignored by the medical community. Changes in eating habits, physical activity, like an increase in exercise, and natural supplements have shown a more positive outlook. The possibility of being able to avoid the use of medications and changing lifestyle habits is

Fluvoxamineis an antidepressant which functions pharmacologically as a selective serotonin reuptake inhibitor. Serotonin, also known as 5-hydroxytryptamine(5-HT), is amonoamine neurotransmitter with various physiological functions such as mood, appetite, andsleep[1].

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).

Major depression, in itself, is a debilitating mental disorder that negatively impacts most or all aspects of a sufferer’s life and often times can even lead to suicide. Just to give a few numbers, at least 1 million people worldwide every year take their own life (Hawton and Heeringen 1372-81), half of which are caused by the possession and improper or unsuccessful treatment of major depression (Chehil and Kutcher 30-33). In light of these dark statistics, the benefits and limitations of the main treatments for major depression, antidepressants and psychotherapy, are not only worth investigation, but with thousands of lives on line, vital to the human race. However, to take it further, there is much to be said of human