Our latest search for bliss in a bottle: Prozac. How does it work and just what does it do? How many additional problems does Prozac, as a possible solution to depression, create for society and for the individual patient and his family?
Let’s dispel a widely spread myth here in the beginning, which is that “Prozac ‘stimulates’ the body’s own production of serotonin”, thereby helping to balance the brain chemistry. Although this is the understanding of many patients and some practitioners even suffer from this mistaken perception, the fact is that Prozac ABSOLUTELY does not stimulate the production of serotonin!
Serotonin is the neurotransmitter that is believed to affect depression. Serotonin does affect the mood center of the brain.
If you ask a professional, preferably one who has done clinical trials involving Prozac, just how the drug does work and what the theory is behind what Prozac was designed to do, they prozac and alcohol will attempt an explanation, but always end with, “Actually we really don’t know what Prozac does or how it works within the brain.”
Their explanation generally goes like this: Prozac is “designed” to prevent the re-uptake of serotonin into the brain by binding to the cell receptors and the pre-synaptic cell membranes that serotonin passes through within the brain, thereby blocking the serotonin so that it cannot pass through into the blood stream where it is quickly inactivated or metabolized.
The theory is that this binding effect of Prozac will raise the level of serotonin by holding it in the brain and not allowing it to be expelled by the body. Yet we know from animal studies that in the initial administration Prozac causes the brain to shut down it’s own production of serotonin, thereby lowering the level of serotonin and low levels have been detected in those committing violent or aggressive acts. (We have no research to verify just how long this shutting down of serotonin production continues. It appears to be at least the first two to three weeks.)
This would indicate the necessity for extreme caution, specifically in the initial stages of Prozac use. Dr. Peter Breggin, one of the top psychiatrists in the country whose practice is in Bethesda, Maryland, stated that, “This (shutting down of the serotonin production) should have set off red flags at Eli Lilly.”
One can deduct from this information that we do not know at any one given moment during the patient’s use of Prozac if it is causing an increase or decrease in the serotonin level of the patient. A blood test can be taken to determine the blood serotonin levels, but what indication that is of the level of serotonin within the brain itself, we cannot be sure.
A brain biopsy is the most accurate test for measurement of brain serotonin levels, but it is hardly convenient, comfortable, inexpensive, or advisable!
Another important fact to consider is that nobody knows just how Prozac works in the brain or how any anti-depressant works within the brain itself.
Although brain wave patterns give us a direct indication of what is happening with the neurotransmitter action within the brain and Prozac is designed to directly affect the neurotransmitter, serotonin, it is not even common practice to check brain wave patterns through EEG’s to see what might be happening to the brain.
Wouldn’t a patient want to know that? The author would STRONGLY encourage any patient using Prozac or any antidepressant to have EEG’s taken to see how the drug is affecting the neurotransmitters within the brain.
One giant flaw in this theory of raising serotonin levels is that apparently depression can be caused by either high serotonin levels or low serotonin levels.
Since Prozac is designed only to raise the serotonin level (if, in fact, it is actually raising, rather than lowering serotonin) and does not have the capability to actually balance the serotonin level, what might that do to someone who is suffering depression because of high levels of this neurotransmitter? Autistic children generally have either abnormally high or low serotonin levels.
And it is interesting to note that many of the adverse emotional side effects reported by ex-Prozac users are very similar to behavior noted in autistic patients. Recent studies have been done on the possibilities of serotonin levels being directly related to those behaviors considered classically autistic.
Prozac is a highly protein binding drug (94%) thus blocking primarily serotonin in the brain for extended periods. We should question whether or not this binding aspect also inhibits the brain from utilizing the serotonin which is blocked in this manner.
Yet Prozac binds also to other proteins or toxins in the blood, making them too large to be broken down and expelled readily by the body. This protein binding aspect of Prozac is the reason why mixing the drug with other anti-depressants can be so dangerous.
It holds them in the blood stream for a longer period of time and increases the dosage of those drugs within the blood. Prozac can raise the level of tricyclic anti-depressants and MAOs (Monoamine Oxidase Inhibitors) to toxic levels quickly.
All of this binding to body proteins would cause excess stress to be placed on the organs involved in metabolizing and elimination, the liver, pancreas, etc. Those patients having the extremely adverse effects right away tend to be those with pancreatic and liver weaknesses or a past history of diseases affecting those organs, including a past history of excessive alcohol usage.
Eli Lilly states in their clinical pharmacology warnings on the product that “Fluoxetine (Prozac) is extensively metabolized in the liver. As might be predicted from it’s primary source of metabolism, liver impairment can affect the elimination of fluoxetine.
This suggests that the use of fluoxetine in patients with liver disease must be approached with caution. If fluoxetine is administered to patients with liver disease, a lower or less frequent dose should be used.”
A frightening observation is that one of the more frequent complaints of adverse reactions made to the FDA about Prozac is impaired liver function. If a patient is taking a drug that impairs the organ that is essential in controlling the amount of medication the body retains in the blood, how safe can the drug be? Once the liver function is impaired, Prozac will rapidly accumulate within the body to toxic levels.
With the combination of fluoxetine (Prozac) and alcohol or other drugs or excessive intake of processed sugars or the inability of the body to maintain balanced blood sugar levels the liver would go into overload and not be able to function normally.
This would create much higher levels of Prozac in the blood, thus producing the “nightmarish” results we are witnessing from this drug. It would give us an explanation of why patients and families report that the suicidal or homicidal impulses came on suddenly, without warning.
Who knows how long their liver will be able to control the level of Prozac in their blood? Patients should be aware of this aspect of Prozac and realize that they are playing Russian Roulette with not only their own lives but the lives of those with whom they associate.
The most recent pharmaceutical product warnings on Prozac (May 1990) mention the possibility of the use of this drug causing diabetes, hypoglycemia and pancreatitis. The harm caused to the pancreas may be causing an imbalance in the blood sugar levels which in turn causes a compulsive desire for excesses in alcohol (See information on Prozac – alcohol connection in the next chapter.), processed sugars and other stimulants – all of which impair liver function.
The impaired liver function then raises the level of Prozac in the system to dangerous heights and the vicious cycle of this drug becomes self-propelling!
Because of the undue stress placed upon the pancreas, even to the point of pushing the once healthy pancreas into malfunction, causing the excessive craving for stimulants that would then impair liver function, and because of the high incidence reports to the FDA of liver impairment as a reaction to Prozac, we should question anyone’s ability, no matter how healthy, to withstand the effects of this drug over a prolonged period of usage.
The length of time involved before the adverse side effects begin to appear would only demonstrate the strength of the patient’s constitution to withstand those effects.
The PDR (Physicians’ Desk Reference) states, “The effectiveness of Prozac in long-term use, that is for more than 5 to 6 weeks, has not been systematically evaluated in controlled trials. Therefore, the physician who elects to use Prozac for extended periods should periodically re-evaluate the long-term usefulness of the drug for the individual patient.”
The wide majority of patients on Prozac have been on the drug for far more than 5 or 6 weeks and few have been “periodically re-evaluated”, as most doctors see no need because of the sales pitch never mentioning details such as side effects. And apparently the importance of consistent re-evaluation has not been stressed to the prescribing physician because close monitoring of Prozac is rare.
Unfortunately the attitude of the majority of the medical community, after being persuaded by pharmaceutical reps that Prozac has few side effects, is “This is a wonderful new drug with no side effects. Here, try it. You will feel great.” The patient rarely even gets the “call me in the morning” on this one! The doctor often says, “Here is your prescription for the next year.
Unless YOU notice any problems, we will see you then.” In this way he puts the responsibility on the patient and removes it from himself. If the drug did not alter the mind and impair one’s judgement, that might be a rational statement to make, but few ex-Prozac patients will claim to have been capable of judging whether or not they were having problems with this drug.