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The relationship of medication to psychotherapy has been debated endlessly. Although it would be difficult to find a psychoanalytically trained psychiatrist who never prescribes medication or a psychopharmacologist who never recommends therapy, it is nonetheless true that most psychiatrists fall on one side or the other of this great divide. Either they passionately believe that psychotherapy (or another form of talk therapy) is die preferred treatment, or they believe, that medication should generally come first.

The issue is particularly important in terms of the treatment of depression. Few would argue the importance of medication for illnesses such as schizophrenia or severe manic depression. But people often feel different about depression, especially if it is mild or moderate. Increasingly few professionals question die necessity of medication in cases of moderate to severe depression. However, there is still a tendency, to blame the victims, to believe that if they will only get themselves together, confront their issues, and deal forthrightly with their fears either in treatment or by themselves, they would feel less depressed— without medication. Medication, in this sense, is seen as a weak second choice to be made only when therapy has failed.

Certainly there are times when therapy is all that is required, and in those instances it can be very effective, arming patients with much-needed support and hard-won insights and helping; them drop destructive old behaviors and substitute constructive new ones.

But often that doesn’t happen. There are too many patients who, after years of weekly or twice-weekly appointments, are still struggling with depression. And even when the therapy has been declared successful and the depression appears to have exited forever, it is merely dormant, awaiting its biological cue for spontaneous recurrence. In an enormous percentage of patients, depression returns.

It doesn’t have to. For an extraordinarily large number of patients who are now being given psychotherapy alone for various forms of depression, overt or hidden, Prozac or another antidepressant is the treatment of choice and should be given either in conjunction with psychotherapy or instead of it. Ideally, medication should be accompanied by some form of psychotherapy especially in the first three or four months. But if it is necessary to pick either medication or therapy, the choice is clear. Medication can return a depressed patient to a normal emotional state by eliminating symptoms, including the urge to commit suicide. If the patient wants to enter psychotherapy in addition to taking medication, so much the better, a number of studies have now demonstrated that patients recovering from acute episodes of major depression do better when they are receiving both therapy and an antidepressant drug than they do with medication alone.

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The most exaggerated claim that has been made for Prozac, acknowledging that most psychiatric clinicians and researchers agree on its superb antidepressant effects, is that it can also dramatically alter personality in people without an underlying diagnosable clinical or subclinical depression. According to this popular notion, people who are simply unhappy or don’t like themselves can, by taking a Prozac pill, become outgoing, assertive, sociable, and confident: new personalities with altered inner selves, creations of the dubious field of “cosmetic psychopharmacology.”

Most people, who are helped by Prozac, whether they were only mildly or seriously depressed, just return to their former, non-depressed selves. But some people do seem to undergo a rapid and remarkable metamorphosis. This phenomenon is understandable if one is armed with a full knowledge of the patient’s family history and genetic background. The signs that enable one to predict who these hyperresponders might be are all degrees of moodswing, ranging from the subtle highs and lows on one end of the bipolar spectrum to full-blown manic depression, along with what geneticists call behavioral equivalents of manic depression in the family history which have been shown scientifically to include alcoholism and drug abuse, suicide, gambling, sociopathy, as well as the less commonly recognized behaviors associated with manic excess such as compulsive buying of things not needed, promiscuity, nonstop socializing, excess telephoning without purpose, and finally, workaholism. Depressed patients whose personal or family histories show these tendencies, even in their most subtle, hardly recognizable forms, are the candidates who become Prozac hyperresponders.

Among these hyperresponders (no more than 10% of those taking Prozac), there are basically three types that scientifics classify clinically, according to the patient’s predepressive behavior, and genetically, according to the family history:

• Hyperthymic respondent are patients with depression, ranging from minimal to major, who become energetic, outgoing, assertive, efficient, able to organize and prioritize, and more often than not, able to correct the imbalances in their personal and professional lives once the depression has lifted. After taking Prozac, their depression and anxiety disappear. To all outward appearances, their personalities have changed positively. They feel great, and for good reason. They are their old, energetic, sociable—hyperthymic—selves.

• Hypomanic responders go one step beyond the hyperthymic. These depressives develop even more energy on Prozac, need very little sleep, and tend to work and socialize compulsively, often very successfully. Family, friends, and peers at the office who notice their rapid accomplishments and non-stop activities may respond at first with admiration but later with a feeling that something is not quite right, and they may describe these hyperresponders as wired or slightly crazy. Extremely demanding, impatient, and unreasonable, these patients are prone to sudden, intense enthusiasm, irritation that may turn into bursts of anger, and lack of judgment in areas as varied as money management (they overextend themselves financially and often commit fraud), sexuality, driving recklessly, and excesses of all kinds. The hypo-manic response to Prozac can be both positive and negative. When a patient on Prozac begins to show signs of hypomania, it can become serious and the dose should be immediately lowered or discontinued. The patient may need lithium, but by this time, many have quit treatment only to take a plane to Monte Carlo or Las Vegas.

• Manic responders are clearly recognizable and are extremely rare. They possess an unreasonable degree of energy and niay go for days on end without sleep, to be followed by collapse into depression and physical exhaustion. They are expansive, grandiose, or paranoid, and filled with unrealistic schemes and theories. They may call the White House, begin^suing everyone around them, or try to buy Trump Tower on Fifth Avenue in New York City. Their minds race, and they may become delusional. Their judgment is disastrous and they are unable to function in the workplace or the home. Many of these people are none to alcoholism as well. Mania requires hos-italization because it evolves quickly into manic psychosis with its complex paranoid systems, hallucinations, and delusions (many of which involve the F.B.I.. the C.l.A, and other institutions). This is an infrequent response to Prozac and other antidepressants, new and old, but when it does occur, it requires emergency hospitalization and treatment. This reaction in most cases can be predicted by the skilled psychopharmacologist and avoided by prior treatment with lithium.

The frequency of this last Prozac hyperresponse has not been adequately studied but I would estimate it to be no more than 1% to 2% of all those taking Prozac, depending on the population being studied. In my clinical experience, the more severe the manic episodes or genetic equivalents in the personal or family history, the more likely one is to get an undesirable hypomanic or manic response with antidepressant agents. When a person comes in with such a family history, even if he or she has never shown signs of hypomanic or manic behavior, the prescribing physician must begin gingerly, with a low dose and weekly monitoring. What you’re hoping for is a normal response—i.e., a lifting of depression—or even a hyperthymic response, which some psychiatrists may call transformation In order for this to happen, the genetic potential has to be there.

But occasionally, a chronically depressed person comes in, quickly becomes a Prozac hyperresponder and yet seems to have no past or family history of manic depression or its equivalents.

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The concept of depression has entered the public’s consciousness so fully that many people today use the word “depressed” in the same way that they might once have described themselves as dejected, discouraged, or simply glum. At the same time, many people who believe they are in a temporary down or think they are reacting in a normal, healthy way to difficult circumstances are in fact clinically depressed and should seek both diagnosis and treatment.

Clinical depression does not simply go away. Depression is worse than unhappiness, more than malaise, and not in the least like a stubborn refusal to “buck up.” “Depression” is a term that can be applied to a collection of disorders, each of which is characterized by a constellation of specific and debilitating symptoms. It is not a monolithic disorder. Just as major (or clinical) depression is riot the same as simply feeling down, major depression is also not the same as minor depression (now categorized by psychiatrists as dysthymia). Likewise, feeling manic is not the same as feeling happy.

The concept of “cure,” so basic for physicians with other specialties, is an elusive one for psychiatrists. Prozac does not cure depression or any other chronic or recurrent illness for which it is prescribed; thus, it is similar to all other psychotropic drugs that alleviate illness but do not cure it. From 75% to 80% of depressed patients have depression that tends to recur.

On the other hand, Prozac and other antidepressants sometimes appear to cure. Perhaps 20% to 25% of the patients whose depression is relieved by Prozac or other medications are never destined to have a recurrence. This does not mean that the illness has been cured by the antidepressant drug, although it certainly looks that way. Rather, the patient was destined through genetics and environment to have only one depressive episode in his or her lifetime.

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What is the total percentage of patients who stop taking Prozac because of the side effects? In clinical trials, 17% of those taking Prozac discontinued treatment, compared to a full 31% of those taking the tricyclic antidepressants.

Does the size of the dose determine the side effects? The incidence of most side effects, including nausea, anxiety, anorexia, diarrhea, insomnia, tremor, and drowsiness, increases with the size of the dose.

What are the most common sedating side effects of Prozac? About 12% of patients taking Prozac (compared to about 24% of these treated with tricyclics) complain of drowsiness, and 4% have reported a feeling of asthenia, or weakness. If the feeling doesn’t go away within a few days, a smaller dose of Prozac should be tried. In addition, in placebo-controlled clinical trials, 4.2% of the 1730 patients taking Prozac complained of fatigue and 1.9% reported feelings of sedation.

Has Prozac been adequately tested for long-term side effects? No, if you define long-term, as being 25 to 30 years. Prozac has only been available since 1987. Most patients who have been on long-term Prozac since then have been on it for a maximum of five to seven years. Not until patients have been adequately observed and tested on Prozac for fifteen to thirty years can one say that the medication has been adequately tested for long-term side effects.

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This phenomenon is not easily explicable but occurs with many medications, both in psychiatry and in general medicine. It is not uncommon to hear that a patient’s first experience with an antidepressant drug was not successful but that the second time it went extremely well.

One possible explanation of this is the so-called placebo effect, present in 10% to 15% of patients. The placebo effect is usually thought of as influencing patients in a positive way: that is, their positive expectations or belief in the doctor may cause them to see immediate improvements even before the drug theoretically is supposed to work. But the placebo effect has a negative side also, for if the patient is worried or even phobic about taking a given drug, the anxiety can produce side effects for which the drug itself is not responsible, and these negative expectations may cause the patient to discontinue the medication prematurely, before it has had a

chance to work. A related issue has to do with the patient’s overall confidence in authorities, in this instance a physician. The more the patient trusts the doctor, the better the reaction to the drug is likely to be.

A second possible explanation has to do with the patient’s metabolism, which may from time to time vary in its fluid and electrolyte balance, either as a result of taking other medications or of changing diet or fluid intake. Or the patient’s metabolism may have simply changed in some way that at first glance is not easily understood by either the patient or the physician.

Finally, the patient may have been given too much of the drug on the first occasion. On the second try, if the drug is given in a much smaller amount, with the dosage being raised gradually, the results may be highly effective, and rewarding.

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