2. Prozac and depression 2
Abstract
Depression patients receive different treatments for their condition; one of the most famous is the
prescription of Prozac. It is said that Prozac’s effect on the neurotransmitter, Serotonin, is to
credit for the results seen in these patients. However, it remains an unexplored possibility that in
humans the true antidepressant effect comes from the rehabilitation of shrunken and unhealthy
neurons. This paper proposes that this possibility be looked into, due to the improbability of the
SSRI’s effect on depression patients based on logic.
3. Prozac and depression 3
Major Depressive Disorder is a mental disorder that is characterized by a dominant low
mood. Major Depressive Disorder, more commonly referred to as clinical depression, is a big
problem in our modern society with increasing numbers. Clinical depression patients exhibit
certain signs or symptoms that include: feelings of hopelessness or helplessness, self-loathing,
loss of interest in daily activities, appetite or weight changes, sleep changes, concentration
problems and loss of energy, among others.
Up until now the most accepted cause of Major Depressive Disorder, biologically
speaking has been placed in the reuptake of the neurotransmitter, Serotonin. Serotonin affects
different things: mood, sleep, sex drive, attention, pain and appetite, making it a very attractive
possibility when it comes to depression, because it accounts for the symptoms. Serotonergic
neurons are found at the top of the spinal cord and have axons which project to different parts of
the brain and body. For much time, this has been assumed to be behind depression, and the
prescribed solution to these patients has been the use of an anti-depressant, an SSRI.
Prozac, a very famous anti-depressant, has been named an SSRI (selective serotonin
reuptake inhibitor) because of the effect that it has on this neurotransmitter. What it does is
prevent the reuptake of Serotonin by neurons, making sure that it passes from neuron to neuron.
The effect of these pills on the neurotransmission is immediate, and yet the effect isn’t seen until
a week later. Why is that? There in lies the possibility that this effect isn’t what is causing the
antidepressant effect in these patients, also in the fact that the reverse of Prozac’s work has no
effect on people, the impulse of Serotonin uptake does not cause depression in a normal person
so to speak.
4. Prozac and depression 4
But if this isn’t what is causing the antidepressant effect then what is? Well, there are two
possibilities, there is the possibility of a placebo effect and then there is the possibility that will
be discussed further: the rehabilitation of shrunken and unhealthy neurons via Prozac.
Prozac or Fluoxetine Hydrochloride contains certain trophic factors, which are like
nutrients for neurons. These molecules allow neurons to feed, grow and flourish, an effect called
BDNF (brain derived neurotrophic factors). This however, has only been tested on rodent
subjects, though it is very likely to work the same way in humans. This is where my proposal
comes into play.
Were I to get the necessary permissions from the IRB to work with human subjects I
would require six selected psychologists with multiple clinical depression patients. I would ask
these psychologists to send a notice to all their patients to see who would be interested in
participating in this experiment. Out of the candidates that are willing, I will choose the
necessary twenty with similar characteristics such as the level of depression and inciting
incidents. These patients will be evaluated by a different psychologist to examine their state of
mind and their emotional state before the experiment; they will also undergo an fMRI scan. This
will show us the level of depression we are dealing with and the neural activity that pertains to it.
Ten of the patients will receive a dosage of 20mg of Prozac and the other ten will serve as
a control group receiving a placebo. This will be for the effects of the placebo effect hypothesis.
The patients will be reevaluated a day after the initial dosage, both psychologically and
biologically, meaning with psycho evaluation and fMRI. The patients will take their dosage
every day for a week, and be reevaluated the same way after that week has passed.
The expected results are that the majority of the control group will still feel depressed and
show no change in neural activity. On the other hand in the experimental group, what is expected
5. Prozac and depression 5
based on the hypothesis is that neural activity will be more active after the week has passed
which implies healthier neurons due to the trophic factors in Prozac, proving my hypothesis.
Were it to happen this way, this would lead to further study. For example, the possibility
that exercise can replace antidepressants in clinical depression patients will be a future study.
6. Prozac and depression 6
References
Phelps, Jim. (2005) How mood affects the brain. PsychEducation.org.
http://www.psycheducation.org/mechanism/9TrophicFactors.htm
Rosling, Claire. Serotonin as a neurotransmitter. University of Bristol.
http://www.chm.bris.ac.uk/motm/serotonin/serotonin%20as%20a%20neurotransmitter.htm
Saisan, Joana. Understanding Depression. HelpGuide.org.
http://www.helpguide.org/mental/depression_signs_types_diagnosis_treatment.htm#authors
(4/20/2009) Prozac. Rxlist.com. http://www.rxlist.com/prozac-drug.htm
Multum, Cener. (05/14/2009) Prozac. Drugs.com. http://www.drugs.com/prozac.html
Lehrer, Jonah. (06/06/2008) Head Fake. Boston.com. http://www.boston.com/bostonglobe/ideas/
articles/2008/07/06/head_fake/
