Hailed as a medical miracle by many and a dangerous psychoactive drug by others, Prozac is perhaps the most controversial drug ever marketed. Developed by Eli Lilly and Company, Prozac was launched in the United States in 1987 after fifteen years of clinical research. It has quickly become the most widely prescribed (and most profitable) antidepressant drug. Despite the tremendous publicity, Prozac is not a panacea for depression. In fact, it is no more effective than other antidepressants, including drugs that have been around since the 1950s. Prozac may not be more effective, but it is more expensive. The monthly cost for Prozac can range between $50 and $200 depending upon dosage while by comparison the monthly cost is around $7 for a generic tricyclic antidepressant. Detailed clinical studies indicate that roughly one-third of patients with depression will either not be helped by Prozac and other anti depressant drugs or will be unable to tolerate its side effects.
Why is Prozac so popular? The media has played a major role by publishing articles labeling Prozac as a major breakthrough in the treatment of depression. The public, hungry for information on this miracle "happy pill," kept psychiatrist Peter Kramer's pro-Prozac book, Listening to Prozac, on the New York Times best-seller list for nearly four months. In Kramer's book he advocated the use of Prozac for "cosmetic psychopharmacology" or as a "personality pill" in helping a normal person develop a more "socially rewarding personality." According to Dr. Kramer, "Prozac seems to fire confidence to the habitually timid, to make the sensitive brash, to lend the introvert the social skills of a salesman." Of course Dr. Kramer also points out that not all patients respond this way.
Another reason for its widespread popularity is that Prozac, as well as other antidepressant drugs, fits nicely into the dominant theoretical model of depression -- the "biogenic amine" hypothesis. This model focuses more on biochemical factors in the brain causing depression rather than psychological factors. Perhaps the main reason this model is so popular is that it is a better fit for drug therapy. According to the biogenic amine hypothesis, depression is due to a biochemical deficiency characterized by imbalances of amino acids, which form neurotransmitters known as monoamines. Monoamines include serotonin, melatonin, dopamine, and norepinephrine.
Environmental, nutritional, psychological, and genetic factors can all lead to an imbalance in the monoamines, which might result in depression. Monoamine neurotransmitters are released by brain cells to carry a chemical message by binding to receptor sites on neighboring brain cells. Almost as soon as the monoamine is released, enzymes are at work that will either breakdown the monoamine or work to uptake the monoamine back into the brain cell. Different antidepressant drugs act by increasing different monoamines in the brain by blocking either the re-uptake or the breakdown or by enhancing the effect of a specific monoamine.
It is interesting to note that the monoamines are manufactured from dietary amino acids, the building block molecules of proteins. For example, the amino acid tryptophan serves as the precursor to serotonin and melatonin, while phenylalanine and tyrosine are precursors to dopamine, epinephrine, and norepinephrine. These amino acids have proven to be effective natural antidepressants and are discussed in chapter 9.
How Does Prozac Work?
Prozac works by specifically inhibiting the re-uptake of serotonin at the nerve endings in the brain. As a result more serotonin is likely to bind to receptor sites on brain cells and transmit the serotonin signal. Serotonin is a very important neurotransmitter. It is the brain's own natural antidepressant and tranquilizer. A decrease in serotonin function is thought to be a major cause of depression, anxiety, and insomnia.
Prozac and several other drugs (e.g., Effexor, Paxil, and Zoloft) are technically classified as a "selective serotonin re-uptake inhibitor" (SSRI). Other antidepressant drugs are classified according to their chemical structure and/or mechanism of action. Tricyclic drugs such as amitriptyline (Elavil, Endep) are also thought to inhibit the re-uptake of serotonin, but they are less selective than the newer drugs in that they also inhibit the re-uptake of norepinephrine. Monoamine oxidase inhibitors, such as phenelzine (Nardil) and tranylcypromine (Parnate), inhibit an enzyme (MAO type A) responsible for the breakdown of all monoamines; as a result levels of all monoamines are increased. Two other drugs, bupropion (Wellbutrin) and trazodone (Desyrel), are classified as miscellaneous antidepressants, although trazodone has exhibited selective serotonin re-uptake inhibition, and bupropion has been shown to inhibit the re-uptake of both serotonin and epinephrine.
Prozac and other antidepressants typically require at least a two-week period before any effects are observed.
