Kory Eggert
Morgan
Psychology 321
5 October 1998
Anti Depressants: Selective Serotonin Receptor Inhibitors
Anti depressants are prescribed to treat a variety of
depressive disorders. Some of the most common of these
disorders are: seasonal affective disorder, summer
depression, unipolar depression, and bipolar depression.
Depression is the most common serious psychiatric
disorder. It leads to high rates of morbidity and
incalculable economic losses, and it can be fatal.
The lifetime risk of clinically significant depression
is greater than one in ten (Baldessarini 4).
The following research is intended to provide a
clearer picture of depression, and some pertinant
information about its treatments. Some areas of this
project focus solely on Prozac and research related to this
drug. Prozac is used here only as an example,
represenative of many other possible treatments for this
disorder.
One of the most important aspects of the
antidepressant it how it works and why. The type of anti
depressant that we will be discussing is known as a
Selective Serotonin Receptor Inhibitor (SSRI). Some
examples of these medicines are Prozac and Paxil. They
work by helping to correct the chemical imbalance in the
brain that is causing the depression. Such drugs are known
to increase the brain's supply of a neurotransmitter called
serotonin.
"Serotonin is an indolamine transmitter substance"
(Carlson 610). It is this synaptic transmitter that plays
a key role in the effectiveness of anti depressant drugs.
"Most drugs that affect behavior do so by affecting
synaptic transmission" (Carlson 94). These drugs that
block or inhibit the postsynaptic effects are called
antagonists. SSRIs selectively block the uptake of
serotonin, and the initial selective effects on either
noradrenergic or serotonergic neurons can produce the
antidepressant effect.
As mentioned above, the synaptic transmitter involved
in the antidepressant effect of SSRIs is serotonin. The
SSRI treatments use "a drug that inhibits the re of
serotonin without affecting the reuptake of other
neurotransmitters" (Carlson 527). However, as an aside,
depression is also strongly associated with other
neurotransmitters as well. These would include epinephrine
and norepinephrine. "Anti depressants increase the levels
of these chemicals by interfering with the enzymes that
eliminate them from the synapses, a process called reuptake
inhibition" (Carlson 527).
Studies are ongoing in this area as in all others, and
the above information reflects the lack thereof readily
available. Much progress has been made in the field of
depression and its treatment since the 1950s. At the same
time, however, much is still yet to be known. What I have
mentioned I have done so as only a partial represenative of
a much larger picture. There is much more to be known
about SSRIs, such as side affects, and physiological
changes in the body. In the following section of our
report we will elaborate on the side effects of SSRIs, and
then discuss the inhibitory potential changes.
Works Cited
"An Introduction to Anti Depressant Medications." 15
Sept.1998Online posting.
http://www.depression.com/anti/anti 01 antidepressants.htm.
Baldessarini, Ross J. Biomedical Aspects of Depression.
USA: American Psychiatric Press, 1983.
Carlson, Neil R. Physiology of Behavior. Needham Heights:
Allyn and Bacon, 1998.
Prozac. Advertisement. Pamphlet Dec. 1995.
Prozac Side Effects
By Deborah Briggs
With twenty years of research behind it, many of
Prozac=s long term side effects are now known. Prozac has
few side effects when compared to other antidepressent
drugs. These may include dry mouth, rash, sweating,
constipation, insomnia, restlessness, altered appetite and
weight, nausea, tension headaches, fatigue, drowsiness,
dizziness and memory loss. These are usually Short term
side effects that normally go away within one to two weeks
after taking the drug. However, Prozac is especially long
acting. Its extended half life in the body can be a
pharmacologic disadvantage; if a patient experiences a side
effect of Prozac, such as nausea or headache, the
medication will not wash out for many days, and the side
effects may persist for the whole of that time, even though
the patient has stopped taking medicine.
In US placebo controlled trials for depression, out of
1,728 patients treated with Prozac, twelve to sixteen
percent reported anxiety, nervousness, or insomnia compared
to seven to nine percent of 975 patients treated with
placebo.
In US placebo controlled clinical trials for obsessive
compulsive disorder, insomnia was reported in twenty eight
percent of 266 patients treated with Prozac and twenty two
percent of 89 patients treated with placebo. Anxiety was
reported in fourteen percent of patients treated Prozac and
seven percent of patients treated with placebo.
In US placebo controlled clinical trials for bulimia
nervosa, insomnia was reported in thirty three percent of
450 patients treated with Prozac and thirteen percent of
267 patients treated with placebo.
In US placebo controlled clinical trials for
depression, eleven percent of patients treated with Prozac
and two percent of patients treated with placebo reported
anorexia.
In US placebo controlled clinical trials for OCD,
seventeen percent of patients treated with Prozac and ten
percent of patients treated with placebo reported anorexia.
Significant weight loss in underweight depressed or
bulimic patients may be an undesirable result of treatment
with Prozac.
Only rarely have patients discontinued treatment with
Prozac because of weight loss. However, weight change
should be monitored during therapy.
Let it be noted that in the above studies, the stated
frequencies represent the proportion of individuals who
experienced, at least once, a treatment emergent event if it
occurred for the first time or worsened while receiving therapy
following baseline evaluation. Events that were reported during
therapy were not necessarily caused by it.
There are other side effects that remain for the time Prozac
is taken and usually subside when the patient is no longer taking
Prozac.
A change in sexual function is one common complaint. Usually
the dysfunction is in difficulty achieving orgasm, more noticeably
in men but in women as well.
Thoughts of suicide is another reported side effect of
Prozac and even though some patients considered suicide before
taking Prozac, many reported that their self-destructive drive was
more persistent and more intense. Studies show that two
effects of overstimulation, akathisia and agitation, are
experienced by some people who take Prozac. Akathisia is a need
to move about such as pacing, or the need to stand up. The person
can feel anxious or irritable and can feel extreme agitation.
Akathisia is related to a breakdown in the ability to control
impulses. It has been associated with violent and suicidal acts
in a number of reports and studies. A person=s nervousness may
reach a psychotic level when the overstimulation of the nervous
system is severe. People can become extremely depressed,
paranoid, suicidal and dangerous to others. It has been estimated
in a 1989 report in the Journal of Clinical Psychiatry that the
actual share of Prozac users who suffer from akathisia is between
ten and twenty five percent.
More rarely, Prozac has been associated with damage of one
sort or another to almost every body system and organ from
arrhythmia of the heart to inflammation of the liver to
dysfunction of the thyroid gland. Prozac is relatively safe, but
no drug is risk free. Prozac is not addictive and there is no
known withdrawal syndrome, but people who have experienced a good
response to it are often leery about coming off medication out of
fear that they will return to their old way of feeling and
behaving. Psychotherapeutic drugs can sometimes cause tardive
neurological disorders, which may appear years after a drug is
discontinued; and questions have been raised whether Prozac can
cause such syndromes. Prozac has been around too briefly for
anyone to know all of its long-term effects.
References:
Kramer, Peter D. Listening to Prozac. Viking, 1993.
Go Ask Alice!: Prozac Side Effects (Online) Available:
www.goaskalice.columbia.edu./0817.html [1998, August 28]
Prozac, Part 1. The Dangers of Prozac: part 1. (Online)
Avaliable: www.garynull.com/Documents/prozac1.htm [1998,
September 01]
Dista Products Company. Division of Eli Lilly and Company.
Phamplet 60FL88400
Martha Carneal
Morgan
Psychology 321
5 October 1998
Inhibitory Potential Changes and Body Changes
Fluoxetine is most commonly known as Prozac. The effects on
the body are as varied as the types of depression.
Prozac is known as an SSRI type of anti depressant. SSRI
stands for Selective Serotonin Re uptake Inhibitor. The function
of Prozac is to inhibit the ability of the neuro receptor from
depleting the level of Serotonin available for the synapse to use.
Depression usually occurs when Serotonin levels are relatively
low. By inhibiting the re uptake of Serotonin, the levels of
Serotonin stabilize. The process usually takes two to three weeks
in most studies (Physiology of Behavior, sixth edition, p.110)
Research on the effects of Prozac is an ongoing process. The
American Journal of Psychiatry offers advice to individuals who
appear to do well on Prozac. Researchers have found that when
treated for twelve weeks, people whose depressive symptoms remit
should continue treatment with Fluoxetine for at least an
additional twenty six weeks to minimize the risk of relapse (Am J
Psychiatry 1998; 155: 1247 through 1253)
As stated earlier, one of the side effects of using
Fluoxetine as an antidepressant can, for some individuals, be
insomnia. A study from the American Journal of Psychiatry showed
results of a test where individuals with major depressive disorder
were given a combination of Fluoxetine and Melatonin. "No
particular side effects were noted from the combination of
Fluoxetine and slow release Melatonin." The conclusion in this
study was that this "combination"..."should be investigated
further."(Am J Psychiatry 1998; 155: 1119 through 1121)
The use of Fluoxetine and other second generation
antidepressants have become more popular because of less side
effects associated with them. However, the Dista Products Company
reports that Fluoxetine should be discontinued for at least 5
weeks before starting a Monoamine Oxidase Inhibitor because
Fluoxetine stays in the body for so long. Fluoxetine can be
started as a treatment only 14 days after discontinued use of an
MAOI.
Research on the effects of Prozac is still relatively new and
should be followed closely. Researchers have not come to a full
understanding of how exactly the brain works and why some people
are affected in certain ways as opposed to how others are affected
by treatment. As with most medications, before discontinuance of
this type of drug, it is best to have a physician aid in the
process. It is not recommended to stop this medication all at
once.
There is still more research material on the subject of
antidepressants and the functions of the brain. It is best to
conclude that so far all we know is that Prozac works real well on
some individuals with little side effects, and that it is one of
the better known Selective Serotonin Re uptake Inhibitors.
As an overall summary on the subject of antidepressants,
it is amazing that there is so much information on these drugs and
yet as with quantum mechanics, the research continues. The brain,
although very small by comparison to the rest of the body, is one
of the most complex subjects in psychology.
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This page last edited October 7, 1998
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