Suppressing the Passion of Anxiety Overwhelm with Drugs
The next gene to be identified for a psychiatric illness may be for panic disorder, Dr. James C. Ballenger said at a symposium for members of Congress and their staffs. - Clinical Psychiatry News, November 1988From the U.S. Congress to the American public, psychiatry's marketing strategy for the 1990s aims at people who feel anxious. It has become an axiom within modern economics that advertising actually creates consumer needs. By targeting people suffering from anxiety, psychiatry should be able to generate an unlimited demand for its drugs. Prescriptions for one class of these drugs, the benzodiazepines, already are estimated at nearly one hundred million a year in the United States, for a cost of about $500 million. Some estimates place the total cost at $800 million or more.
This chapter will give special attention to two minor(1) tranquilizers that have drawn considerable publicity. One is BuSpar (buspirone), whose potentially damaging effects have been largely ignored, even in the psychiatric literature. The other is Xanax (alprazolam), one of the most intensively marketed and yet dangerous drugs in psychiatry. Then chapter 15 will focus on the political campaign that made Xanax so successful.
Unlike most of the drugs discussed in this book, the minor tranquilizers are highly sought after. Even without doctors pushing them, people would want them. Indeed, they are actively sold illegally on the street. This is not surprising, since people often resort to taking anything that promises even temporary relief from anxiety. Millions drink alcohol, smoke cigarettes, and use marijuana, opiates, and other street drugs. Others eat excessively, exercise compulsively, work to exhaustion, watch TV endlessly, escape into books, relentlessly pursue sex, and overindulge any number of otherwise harmless habits in an attempt to escape their tensions and apprehensions. In chapter 10 we saw that obsessions, compulsions, and phobias also can be seen as efforts to control anxiety. Overall, psychiatric interventions play a relatively minor role in humanity's never-ending struggle to deal with anxiety.
The Minor Tranquilizers and Other Sedative-Hypnotics
Among psychiatric medications for the treatment of anxiety, the most commonly used are the minor tranquilizers, starting in 1957 with the introduction of Librium (chlordiazepoxide). In the 1970s the minor tranquilizer Valium (diazepam) topped the charts as the most widely prescribed drug in America, to be replaced by Xanax in 1986. Most of the minor tranquilizers belong to the group called benzodiazepines and are closely related chemically to Librium, Valium, and Xanax. They differ mostly in their duration of action and in the dosage required to achieve the same effect. They have nearly identical clinical effects.
The benzodiazepine minor tranquilizers include Xanax, Valium, Librium, Tranxene (clorazepate), Paxipam (halazepam),
Centrax or Verstran (prazepam), Klonopin (formerly Clonopin) (clonazepam), Dalmane (flurazepam), Serax (oxazepam),
Ativan (lorazepam), Restoril (temazepam), and Halcion (triazolam).
Sleeping medications also have tranquilizing effects. These include Doriden (glutethimide), Noludar (methyprylon), Placidyl (ethchlorvynol), and Noctec, Somnos, or Beta-Chlor (chloral hydrate), and the various barbiturates, including Seconal (secobarbital), Luminal (phenobarbital), Butibel (butabarbital), Amytal (amobarbital), Nembutal (pentobarbital), and Tuinal (amobarbital and secobarbital).
All of these drugs have the potential for abuse and addiction. Since all have a calming or sedative effect, people addicted to these "downers" use many of them interchangeably, depending on what is available, often mixing them with alcohol. The minor tranquilizers and alcohol make a very dangerous, frequently lethal, combination.
BuSpar, the most recent addition to the minor tranquilizers, is being promoted as nonsedative, nonaddictive, and relatively safe.
The Most Widely Used Psychiatric Drugs
According to FDA data reported by Carlene Baum and her associates in the February 1988 Medical Care, there was a dramatic decline in the use of minor tranquilizers and other antianxiety drugs, from a peak of 103 million prescriptions in 1975 to 67 million in 1981 in the United States. There are no complete totals available for recent years, but the APA's task force report, Benzodiazepine Dependence, Toxicity and Abuse (1990), estimates that annual prescriptions for benzodiazepines have leveled off since the mid-1980s at about 61 million.
The minor tranquilizers, now led by Xanax, remain by far the most commonly prescribed psychiatric medications. In some countries, such as France, the use of these agents continues to escalate.
Most minor tranquilizer prescriptions - 65 percent - were for women in 1984. However, women predominate in all psychiatric drug categories. Thirty-five percent of all patients were sixty years of age or older.
Are the Minor Tranquilizers Something New?
Because of the popularity surrounding the minor tranquilizers, we tend to think that they represent something very new and radically different among drugs; but I recall my medical school professor of psychopharmacology reminding us in 1960 that the sedative attributes of minor tranquilizers differ little from those of the barbiturates, such as phenobarbital. He said, however, that he hesitated to tell this to practicing physicians, because their faith in drugs helped their patients benefit from them. Like most biopsychiatrists, he raised no concerns about encouraging people to have more faith in a pill than in themselves.
Even before the barbiturates, there were sedative and hypnotic drugs, many of which are still in use today. People used them, sometimes got short-term relief from them, and sometimes became addicted to them. Chloral hydrate (Noctec) and paraidehyde (Paral) are among them. Earlier, the highly toxic bromides had their day. And before them, opiates were freely dispensed in private practice and in mental hospitals.
Alcohol Competes with Minor Tranquilizers
To divest the minor tranquilizers of their medical mystique we need only recall that alcohol was prescribed for generations by doctors as a sedative for anxious patients. As recently as 1943, Torald Sollmann's classic text A Manual of Psychopharmacology professed:
A certain amount of alcohol, varying for individuals, may be taken occasionally or even daily without demonstrable permanently injurious effects. The relaxation, the easing of strain, of maladjustments, of excessive self-consciousness, of excessive inhibitions, indeed the euphoria, may sometimes be beneficial.... (P. 718)Sollmann goes on to warn about the disadvantages and dangers of alcohol use, but then he reassures the reader:
On the other hand, the moderate use of alcohol is often blamed for shortened duration of life and for various physical injuries, without adequate data, or on the basis of effects that are produced only by very large quantities. (P. 718)Obviously many people still consider alcohol the tranquilizer of choice, but I am not arguing that doctors should prescribe whiskey or gin. I don't think they should, Nor do I think they should so cavalierly prescribe the other sedative or tranquilizing drugs. I want to emphasize that there is nothing unique or medically sacrosanct about the current drugs commonly prescribed for anxiety. The drugs possess a number of dangerous qualities, many of them similar to the properties of alcohol.
Sedative-Hypnotics and Central Nervous System Depression
All of the commonly used minor tranquilizers - with the possible exception of BuSpar - are central nervous system depressants very similar to alcohol and barbiturates in their clinical effects. Along with alcohol and barbiturates, they are classified as sedative-hypnotics, meaning that they produce relaxation (sedation) at lower doses and sleep (hypnosis) and eventually coma at higher ones. It is important to grasp the principle that minor tranquilizers are central nervous system depressants - and, in particular, sedative-hypnotics - because this classification removes the mystery surrounding these "tranquilizers." The so-called antianxiety effect is merely an early stage of central nervous system depression - sedation . The basic clinical effect on the mind cannot be distinguished from alcohol or barbiturates.
It should be emphasized again that all minor tranquilizers combine with each other or with other central nervous system depressants - such as barbiturates, antidepressants, neuroleptics, lithium, and alcohol - with a potentially fatal result. While they can be lethal when taken alone, they are especially dangerous in combination with these other drugs. A large percentage of drug-related emergency room visits involve minor tranquilizers.
All of the minor tranquilizers impair mental alertness and physical coordination and can dangerously compromise mechanical performance, such as automobile driving.
At low doses the minor tranquilizers are sufficiently potent to impact noticeably on the brain waves on routine EEGS, especially in the frontal lobe region. However, they do not typically have the lobotomizing impact epitomized by the neuroleptics.
Addiction, Tolerance, and Withdrawal Symptoms
All hypnotic-sedatives, including the minor tranquilizers, are habit-forming and addictive and can produce withdrawal symptoms or an abstinence syndrome when they are stopped. In the extreme, the abstinence syndrome can cause life-threatening neurological reactions, including fever, psychosis, and seizures. Less severe withdrawal symptoms include increased heart rate and lowered blood pressure; shakiness; loss of appetite; muscle cramps; impairment of memory, concentration, and orientation; abnormal sounds in the ears and blurred vision; and insomnia, agitation, anxiety, panic, and derealization. Obvious withdrawal symptoms typically last two to four weeks. Subtle ones can last months.
Consistent with the principle that the minor tranquilizers differ little in their clinical effect from other sedatives, the Xanax write-up in the 1991 PDR acknowledges that withdrawal symptoms are "similar in character to those noted with barbiturates and alcohol."
Studies of Xanax (see ahead) show that most patients develop withdrawal symptoms during routine treatment lasting only eight weeks. Tolerance, or the need for increasing doses to achieve the same psychoactive effect, is the underlying physical mechanism of addiction. Within two to four weeks, tolerance can develop to the sedative effect of minor tranquilizers taken at night for sleep. This again warns against the use of these drugs for more than a few days at a time.
The short-acting benzodiazepines can produce especially severe withdrawal symptoms, because the drug is cleared from the body at a relatively rapid rate. These include Xanax, Halcion, Ativan, Restoril, and Serax.(2) However, according to expert Louis Fabre in a February 1991 interview with me, tightness of binding to receptors is probably more indicative of addictive potential, and the most tightly binding are Xanax, Halcion, Ativan, and Klonopin.
Individuals who take only one pill daily for sleep or anxiety are not exempt from withdrawal problems. In my private practice during the last few years I have worked with several people who were unable to stop taking a once-a-day standard dose of Xanax, Ativan, Klonopin, or other minor tranquilizers. In each case, the attempt to stop the medication led to a disturbing degree of anxiety or insomnia within twenty-four hours. The problem seemed to be caused by rebound anxiety or rebound insomnia (see ahead).
In a personal communication in late December 1990, internist John Steinberg confirmed that patients taking one Xanax tablet each day for several weeks can become addicted. Steinberg is medical director of the Chemical Dependency Program at the Greater Baltimore Medical Center and president of the Maryland Society of Addiction Medicine. He points to research that Xanax and other short-acting benzodiazepines can cause a reactive hyperactivity of the receptors that they block. The hyperactive receptors then require one or more doses of Xanax each day or they produce anxiety and emotional discomfort. Steinberg calls the impact of Xanax "a fundamental change in the homeostasis of the brain." After the patient stops taking the Xanax, according to Steinberg, it takes the brain six to eighteen months to recover. Xanax patients should be warned, he says, that it can take a long time to get over painful withdrawal symptoms. Since doctors frequently don't realize this, they, too, are likely to be confused and to continue the drug in the hope of "treating" the patient's drug-induced anxiety and tension.
Many detoxification beds are occupied by patients addicted to minor tranquilizers and even more by those who are cross-addicted with alcohol and other drugs. Steinberg says that Xanax is "by far and away" the worst offender and that it definitely causes addiction without being mixed with other sedatives.
Steinberg estimates that one in ten patients receiving Xanax will become addicted.(3) Based on an estimated fifteen million people receiving Xanax each year in the United States, Steinberg concludes that 1.5 million Xanax addicts are produced each year.
Rebound Anxiety and Insomnia
Rebound anxiety is one of the common reactions to withdrawal or to dose reduction of a minor tranquilizer . As with most psychiatric drugs, the use of the medication eventually causes an increase of the very symptoms that the drug is supposed to ameliorate, and thus rebound anxiety can lead to a false diagnosis of chronic anxiety disorder. As noted in the American Psychiatric Press Textbook of Psychiatry, long-term treatment can be erroneously maintained or reinstated when drug-induced rebound anxiety occurs. Addiction is the ultimate outcome.
Some experts, such as John Steinberg, disagree with my assertion that there is no difference between a tranquilizing and a sedative effect. They suspect that in addition to the obvious sedation, minor tranquilizers probably also produce a specific inhibition of anxiety. If true, this means that they also cause a specific rebound anxiety as the blocked receptors become hyperactive.
Rebound insomnia also results from taking most sleeping medications, because the brain reacts against the central nervous system (CNS) depressant effects by becoming more aroused or alert. Medications for sleep generally should not be taken for more than a day or two at a time.
Addiction Can Go Unnoticed
Seriously addicted patients may show no outward signs to their family or physicians until accidentally removed from the medication - for example, following surgery or during a medical emergency. Their withdrawal symptoms may then be wholly misinterpreted as an aspect of some other disorder or as a psychological problem. Marked withdrawal symptoms, including persistent rebound anxiety, can begin as much as five to seven days after stopping the medication and can last up to a month.
The minor tranquilizers can produce paradoxical reactions - acute agitation, confusion, disorientation, anxiety, and aggression - especially in children, adults with brain disease, and the elderly. The Xanax report in the 1991 PDR states, "As with all benzodiazepines, paradoxical reactions such as stimulation, agitation, rage, increased muscle spasticity, sleep disturbances, hallucinations and other adverse behavioral effects may occur in rare instances and in a random fashion."
In nursing homes the medications may seem to help the insomnia of an elderly patient for a night or two, only to produce generalized brain dysfunction as the medication accumulates in the system. The agitated patient may then be mistakenly overdosed with further medication, perhaps a neuroleptic. According to Rober( Hales and Stuart Yudofsky's Textbook of Neuropsychiatry (1987), the "routine" prescription of these medications in nursing homes and hospitals "should be avoided," especially for anything but brief periods of insomnia related to a particularly difficult or stressful situation.
As in response to alcohol, some people more readily lose their self-control and become violent when taking minor tranquilizers. There are frequent references to this in the literature, including cases of murder under the influence of minor tranquilizers. Partly because of this disinhibiting effect, the drugs cannot be used effectively for purposes of controlling behavior within institutions.
Halcion has been especially implicated in causing aggressive and suicidal behavior, as well as delirium, hallucinations, and seizures.
Memory Dysfunction from Minor Tranquilizers
Recently there has been much-publicized concern about Halcion producing amnesia for events prior to the taking of the drug. However, this has long been an unheralded problem with minor tranquilizers in general. Years ago I recall noticing that patients who mixed alcohol with Valium the night before a psychotherapy session sometimes would have severe black-out spells and could not recall much of the prior evening. It is well known that the intravenous infusion of benzodiazepines, such as Valium or Ativan, typically produces a similar amnesia for the several hours surrounding the infusion. While this may be a benefit in forgetting the painful effects of surgery, it becomes a potentially serious problem in the routine use of the minor tranquilizers for anxiety or sleep disorders and can interfere with psychotherapy, studying, learning anything new, or recalling previously retained memories .
Long-Term Effects on Mental Function from the Minor Tranquilizers
Despite the obvious need for concern, few studies have attempted to measure the impact of long-term minor tranquilizer usage on overall mental function. Susan Golombok and her colleagues from the Institute of Psychiatry in London published "Cognitive Impairment in Long-Term Benzodiazepine Users" in the 1988 Psychological Medicine. Using a variety of neuropsychological tests to evaluate the impact of minor tranquilizers on cognitive function in patients who were administered the medication for at least one year, they found chronic impairment in measures of visual-spatial ability and attention span.
Golombok and her coworkers were unable to follow up with tests after drug termination. However, these findings of chronic brain dysfunction raise a serious concern about possible permanency. The investigators comment:
It is impossible to determine how long it is safe for a patient to continue to take benzodiazepines, or at what dose, before cognitive ability will begin to deteriorate. Nevertheless, it is clear from the inspection of our data that taking a low dose for a short time has little effect, while a high intake is almost always certainly harmful. (P. 371)The test results indicate that "these patients are not functioning well in everyday life," while they remain unaware of their impairment:
This is in line with clinical evidence that patients who withdraw from their medication often report improved concentration and increased sensory appreciation and that only after withdrawal do they realize that they have been functioning below par. . . . It appears, therefore, that not only are long-term benzodiazepine users at risk of dependence, but that cognitive impairment also represents a very real hazard. (P. 373)It cannot be overemphasized that brain-disabling treatments render patients less able to evaluate their own dysfunction. The Golombok study is exceedingly important from the viewpoint of the patient who wishes to avoid brain dysfunction and from the viewpoint of the ethical physician who wishes to avoid causing it in his or her patients.(4)
If doctors wish to prescribe minor tranquilizers or if patients want to take them, it would be prudent to follow the advice of The New Harvard Guide to Psychiatry (I 988): "The main usefulness of the antianxiety agents is in general medicine in the short-term treatment of relatively transient forms of anxiety, fear, and tension" (p. 524).
Brain Shrinkage from Long-Term Minor Tranquilizer Use
An even more terrifying specter haunts the long-term use of minor tranquilizers - the possibility of brain atrophy. Although rarely mentioned in establishment books or reviews, in their letter to the editor in the July 1989 Archives of General Psychiatry, Isaac Marks and his ten colleagues summarize the as yet brief literature: "The cerebral ventricular enlargement reported in patients with anxiety/panic disorders who were long-term benzodiazepine users could be due to the disorder or to other factors rather than to the drugs, but wisdom advises caution" (p. 669). In fact, the cerebral ventricular enlargement - the equivalent of atrophy of the brain - is most likely due to the drugs. C. Schmauss and J-C. Kreig in "Enlargement of Cerebrospinal Fluid Spaces in Long-Term Benzodiazepine Abusers" in the 1987 Biological Medicine found that il our data suggest that the increase in the VBRs [ventricular enlargement] is dose-dependent on long-term BDZ [benzodiazepine] medication" (p. 873).
I mentioned the studies on brain atrophy to one expert who replied that although he had not heard of them, he was not surprised. "The minor tranquilizers are like alcohol," he observed, "and alcohol when used long-term causes brain shrinkage." He asked to remain anonymous for fear of offending other drug experts.
BuSpar - the Latest Miracle Tranquilizer
While the 1989 Treatments of Psychiatric Disorders by the APA task force notes that the clinical advantages of BuSpar have not been proven, BuSpar has become the latest fad tranquilizer.
BuSpar, unlike the other minor tranquilizers, is said to have a relatively low potential for abuse, addiction, and withdrawal symptoms. It is slow to take effect, often requiring weeks, and produces a lesser frequency of nervousness, restlessness, headache, and dizziness. That's the "book" on BuSpar, but there are reasons to be skeptical, and even concerned, about its use.
BuSpar, unlike other minor tranquilizers, affects the dopamine receptors, blocking their activity. The possibility of tardive dyskinesia - that untreatable and usually permanent neurological disorder - immediately comes to mind. As discussed in chapter 4, suppression of dopamine activity by neuroleptics frequently causes permanent dopamine hyperreactivity, resulting in tardive dyskinesia. While the mode of dopamine inhibition by BuSpar differs from that of the neuroleptics, the impact is sufficiently similar to raise red flags.
Even the manufacturer, Mead Johnson, shows concern about the drug's impact on dopamine receptors and warns in the 1990 PDR about the possible danger of neurological reactions similar to those caused by the neuroleptics, specifically including tardive dyskinesia. Cases of tardive dyskinesia from BuSpar have not yet been reported; but remember, it took twenty years before doctors and pharmaceutical firms recognized neuroleptic-induced tardive dyskinesia. Mead Johnson itself states: "Generally, long-term sequelae of any drug's use can be identified only after several years of marketing."
With a rare exception, the psychiatric establishment isn't showing any concern. I found no mention of the possibility of permanent neurological problems from BuSpar in the relevant section of most of the recently published psychiatric textbooks.
Despite the fact that all minor tranquilizers have been implicated in abuse and addiction, the most current textbooks of psychiatry dismiss or fail to mention this possibility in regard to BuSpar. Yet it is common knowledge in the profession that apparently nonaddictive medications have turned out to be addictive soon after hitting the market and the streets. Darvon, for example, was widely marketed as a harmless analgesic and later turned out to be addictive. Indeed, initially the minor tranquilizers Valium and Librium were promoted as relatively safe in regard to potential abuse, until the FDA, despite legal resistance from Hoffman-La Roche, placed curbs in them.
Xanax - Approved for Panic Disorder - click on the link for the full report about the nature and dangers of Xanax.
Is There Any "Therapeutic Role" for the Minor Tranquilizers?
Don't people have a right to escape anxiety at times? To use shortcuts if necessary, including sedative drugs? Yes, they surely do. But should doctors encourage this approach to life? I don't think so, except under the most limited circumstances. Because people cannot obtain minor tranquilizers without a doctor's prescription, I don't fault physicians who occasionally prescribe them to help patients get through a difficult few days or to get a good night's sleep; but their usefulness for more than a few days is highly questionable. Even the prodrug literature has not been able to show a beneficial impact beyond a few weeks, when tolerance and withdrawal symptoms develop.
Minor tranquilizers, like any sedative, can be harmful in the long run not only because they are habit-forming and addictive, but because they cover up anxiety by suppressing the capacity of the brain to generate feelings. The brain, as usual, tries to overcome the suppression and reacts in ways we cannot begin to predict or fully comprehend. As we have seen, drug-induced rebound anxiety is one common effect.
The drugged individual with a suppressed and confused anxiety signal system lives under a considerable handicap. At the least, feelings are pushed down, and with that, self-awareness is muted. More seriously, as the brain reacts against the drug, natural anxiety responses are muted but abnormal rebound anxiety reactions begin to flare up.
What about people who are so overwhelmed by anxiety that they cannot cope at all?
Without drugs, severely anxious patients often can be helped rather quickly to overcome the worst of their anguish (see chapter 10). Over a longer period they can learn new approaches to living relatively free of anxiety.
But success in psychotherapy is not guaranteed. Failure may result from a faulty delivery of therapy or from a poorly motivated client, or from a bad "chemistry" between client and therapist. Whatever the cause of the failure, what about drugs as an alternative?
I would rather urge a client to try another therapist, or several other therapists, as well as other approaches, such as group therapy, self-help groups, self-help books, self-hypnosis, relaxation techniques, deep massage, or meditation and other spiritual exercises, rather than to turn to drugs.
Improvement while on drugs is rarely a psychologically clean affair; the improvement almost always leaves an aftermath of persistent personal helplessness. The individual is unable to say with confidence, "I overcame my anxiety and I know how I did it." There is always the lingering suspicion that "the drugs did it."
Even prescribing medications on an occasional basis can interfere with and undermine the real work of psychotherapy.
After a session, a client called me in the evening to request a telephone prescription for a few minor tranquilizers.
"What's up?" I asked.
"Sorry to bother you, Peter. I can't sleep. I just want something to sleep
"How come you didn't bring it up in the session today'?" I asked.
"Hey, Doc, you were hardly listening to me today. You seemed in another world yourself"
In an instant I knew he was right. I'd received distressing news by telephone moments before his session, and without realizing it at the time, I hadn't shaken off the effect.
"Thanks for telling me," I said. "if you can come in tomorrow morning, I'll give you a free session to make up for it."
"It's a deal. And forget the drugs. Good-night."
If I had readily acquiesced to the request for a prescription, the patient's real feelings never would have surfaced. Giving drugs runs the risk of distracting from the work of psychotherapy, not only for the client but for the therapist.
Scientific Studies of Efficacy
By now, I hope, the reader will approach the question of "scientific studies" in psychiatry with a large measure of skepticism, and even cynicism. In regard to the minor tranquilizers, there are some blanket endorsements, such as this one from the American Psychiatric Press's Textbook of Psychiatry: "The efficacy of the benzodiazepines in the treatment of anxiety, including the symptoms of worry, psychic anxiety, and somatic symptoms (gastrointestinal and cardiovascular), has been clearly and repeatedly demonstrated in many well-controlled studies" (p. 810). On the other hand, there is a detailed review of the literature by Ronald Lipman in Seymour Fisher and Roger Greenberg's The Limits of Biological Treatments for Psychological Distress (1989). Lipman finds that, except for the very short-term treatment of generalized anxiety, there is little evidence for the efficacy of these medications. Most reviews suggest that use should be short term and that long-term use is generally dangerous and unwarranted.
Authority and Helplessness
That the drugs encourage helplessness and dependency on the physician seems apparent. In The New Harvard Guide to Psychiatry, two of the nation's leading psychopharmacologists, Ross Baldessarini and Jonathan Cole, make these observations:
Favorable patient response to antianxiety agents has been associated with lack of psychological sophistication and inability to express unhappiness verbally in terms of intrapsychic or interpersonal conflict; a favorable response also tends to occur in patients with passive and almost magical expectations of the physician. An enthusiastic, charismatic presentation of the medication and its sedative effects by the physician also seems to help. (P. 524)When drugs are of questionable efficacy and possess serious drawbacks, such as the potential for addiction, one must wonder whether informed consent is incompatible with an "enthusiastic, charismatic presentation.
The antidepressant Anafranil (clomipramine) was approved by the FDA for use in obsessive-compulsive behavior in January 1990. Except for the addition of a chloride radical, this drug is identical in chemical structure to the old-fashioned tricyclic antidepressant Tofranil. It has received a great deal of media hype, including TV specials. Lipman's review indicates that it is of marginal value. Moreover, a 1987 study by W.O. Montiero and others in the British Journal of Psychiatry shows a very high rate of interference with orgasm. It can cause a variety of side effects, including dry mouth, sedation, difficulty urinating, weight gain, dizziness, seizures, as well as others that are typical of tricyclic antidepressants (see chapter 8).
The use of beta blockers is routine in certain cardiovascular diseases, but it is more speculative in the treatment of anxiety, based largely on the inhibition of the cardiovascular symptoms associated with anxiety, especially increased heart rate and palpitations. These medications also can have a sedativelike effect, dampening emotional responsiveness. My patients who have withdrawn from them sometimes feel considerably more clearheaded. Beta blockers are known to cause depression and, rarely, hallucinations, and may combine adversely with other drugs, including lithium. They can cause memory impairment.
Beta blockers - beta-adrenergic blocking agents - include propranolol (Inderal, Detensol, Novopranol), nadolol (Corgard), metoprolol (Lopressor, Betaloc), oxprenolol (Trasicor), timolol (Blocadren) and acebutolol (Sectral).
The Biology of Anxiety
The biological basis for anxiety overwhelm is so flimsy that one recent textbook, The New Harvard Guide to Psychiatry, gives it only a paragraph and labels the exclusively biological approach "an extreme theoretical position that falls to take psychological facts into account. " The American Psychiatric Press Textbook of Psychiatry does discuss various biological hypotheses as "promising," but it endorses none in particular. The 1989 Comprehensive Textbook of Psychiatry makes clear that the data are preliminary, conclusions are tentative, and no biological cause for anxiety has been determined. Each textbook devotes much more space to psychological explanations. Nonetheless, biopsychiatrists have staked out a biology of anxiety in the popular press and mass market books.
On April 28, 1990, NIMH director Lewis Judd told the Southern California Psychiatric Society that anxiety is now known to be a genetic and biological disorder.
Inspired by NIMH, a flurry of newspaper and 'TV feature stories in recent years have reported that infusions of lactic acid produce anxiety in panic-prone individuals, presumably suggesting a similar mechanism within the body. One national TV news expose show displayed no skepticism whatsoever when a lactate infusion experiment showed a woman having a panic attack on cue.
Infusions of lactic acid sometimes can produce heart palpitations and probably other feelings of uneasiness, similar to those during an anxiety attack, leading an individual to feel as if he or she is getting anxious; but there is no evidence that the production of lactate in the body has anything to do with causing anxiety.
When I wrote a review and analysis entitled "The Psychophysiology of Anxiety," published in the December 1964 Journal of Nervous and Mental Disease,(5) I pointed out that even an infusion of adrenaline by itself cannot produce anxiety. People who fear anxiety may develop anxiety in response to infusions of adrenaline, while people who do not fear anxiety will observe merely that their hearts are pounding or that their hands are trembling. Large doses of adrenaline, injected into asthmatic patients during medical emergencies, typically produce relief of anxiety, because the patient anticipates or experiences relief of the asthma attack. In the lactate experiments, the panic-prone individuals probably reacted with anxiety to the experimental situation and to cardiac symptoms produced by the lactate. Perhaps they also were fulfilling the expectations of the experimenters in front of the TV cameras.
The Biology of Obsessions and Compulsions
As already described, obsessions and compulsions usually are classified among anxiety disorders, although they can occur in response to guilt and shame as well.
Judith Rapoport, chief of child psychiatry at NIMH and the author of The Boy Who Wouldn't Stop Washing (1989), strongly supports the biological viewpoint. In an interview in the March 13, 1989, People magazine Rapoport says of obsessive-compulsive disorder (OCD), "It is like a short circuit in the brain. . . . " There are, of course, no short circuits in the brain. Its "circuitry" cannot be compared to house wiring.
In the March 1989 Scientific American Rapoport argues that obsessions and compulsions are caused by a defect in the basal ganglia and frontal lobes. By now the words frontal lobe and basal ganglia may be familiar to the reader (chapter 4). Rapoport would have contributed equally to our knowledge had she said, "I believe the brain has something to do with the mind and therefore with obsessions and compulsions."
In her book The Boy Who Wouldn't Stop Washing, Rapoport suggests that Anafranil has been found effective in treating some obsessive-compulsive behavior - a conclusion we have already seen challenged. Since Anafranil affects serotonin metabolism, Rapoport further suggests that serotonin is involved in the biology of obsessions and compulsions.
But brain cells using serotonin are found in all regions of the brain, especially in the emotion-regulating limbic system and frontal lobes. Of course, serotonin is involved in the obsessive-compulsive process. It's involved in every mental and emotional process (see the discussion of Prozac in chapter 8).
Besides, as already discussed, it's impossible to reason backward from a drug effect to a brain defect. Psychoactive drugs, from alcohol to neuroleptics, exert their impact on normal brain function. Their calming or suppressive effects on emotions have nothing to do with any prior brain abnormality.
Studies that show abnormalities on brain scans in people diagnosed as obsessive-compulsive suffer from all of the problems discussed in regard to schizophrenia (see chapter 4). Most of the patients are severely emotionally handicapped, often with severe depression, and therefore have been treated with a variety of drugs, including antidepressants and neuroleptics. It is most likely that findings of pathology, often located in the striatum, are the result of antidepressant or neuroleptic treatment, or of polydrug therapy with a variety of agents.
Reviving the Menace of Psychosurgery
Speaking of lobotomy, Rapoport says in her book, "I have yet to send a patient for such treatment, but the success of these operations fascinates me because the procedures sever connections in parts of the brain that our brain-imaging studies find abnormal in OCD. This is another clue to the biology of this sickness" (The Boy Who Wouldn't Stop Washing, P. 16).(6) Of course, it's no clue at all; lobotomy is a nonspecific blunting operation (see chapter 3). It also was used on "schizophrenic" people, depressed people, violent people, sexually aggressive criminals, people with chronic pain, alcoholics, and dying cancer patients. And it will blunt animals as well as people.
At the APA's annual meeting, reported in the July 1989 Clinical Psychiatric News, Rapoport again raised the possibility of psychosurgery. Going directly to the public in her People magazine interview, she describes a man who was lobotomized in 1960:
The procedure is far less common today and would only be considered if every other possible treatment had failed. It cured his OCD, but unfortunately, because the surgery was not as sophisticated 20 years ago as it is now, he suffered personality changes and began pinching young women and urinating in the street.So the chief of child psychiatry at NIMH, in professional and public forums, is lending credence to lobotomy, albeit only if "every other possible treatment had failed." That's how lobotomy has always been promoted; but since there are so many "failures" in psychiatry, there will be no shortage of victims available for lobotomy. As documented in chapter 3, her remark that the brain-mutilating surgery is relatively safe nowadays is simply not true.
The promotion of psychosurgery for obsessive-compulsive disorders seems to be taking hold. It rears up in some textbooks and most recently in the April 1990 Harvard Medical School Health Letter. Michael Jenike, director of the Obsessive-Compulsive Disorder Clinic and Research Unit at the Massachusetts General Hospital, speaks highly of psychosurgery, specifically an operation called cingulotomy, which electrically melts nerve connections to the frontal lobes. He says, "There is a growing body of evidence that these people will benefit from a precisely localized brain surgery." He does not hint at the inevitable damage to the brain and mind.
I have followed the cingulotomy operations performed at the Massachusetts General Hospital for twenty years.(7) Indeed, the main surgeon, H. T. Ballantine, recently retired after performing hundreds of them, mostly on women. He did not limit himself to so-called obsessive-compulsives, but even operated on a patient with chronic back pain. There is nothing new about these operations, and they have always been reported in the literature by the surgeons as virtually harmless. Psychosurgeon Ballantine actually claims that his operations had no effect on the mind, adverse or otherwise. As if talking about a subtle intervention that did not coagulate brain tissue with hot electrodes, he opines that the operation corrected biochemical imbalances.
I have now interviewed and studied the records of five of Ballantine's psychosurgery patients as well as patients operated on by other surgeons. All of the patients have lobotomy syndromes, with disabling degrees of mental dysfunction. Of Ballantine's patients, the four who can speak are very bitter about what was done to them. Since the operation, the one who no longer can speak has displayed fear of every doctor who comes near her. She was reduced to a state of severe, chronic mental deterioration (dementia) following the psychosurgery.
I am concerned about so many recent public remarks in favor of psychosurgery by high-ranking psychiatrists. It seems aimed at laying the groundwork for resuming psychosurgery in full force at NIMH, Harvard, and elsewhere. This would reverse the accomplishments of the past decade, which brought most psychosurgery in the country to a halt.
Children and Their Parents
Rapoport's radical biological theories will appeal to those who cannot bear to face their own self-destructive mental processes. Her views also wi 'II appeal to some parents who don't wish to believe that they have had anything to do with their offsprings' problems. In her book, Rapoport announces with emphasis a "great piece of news" for parents and sufferers alike: "It May Not Be Your Fault That You Or Your Child Has Obsessive-Compulsive Disorder!" (p. 39). This is great news only if you'd rather not take any personal responsibility for your own problems or those of your children.
In the next two chapters we shall see how far psychiatry has gone in blaming child-victims for their own problems while exonerating parents, schools, and other authorities. Unfortunately, Rapoport's views are part of an overall NIMH strategy that aligns itself with the parents and custodians rather than with the patients themselves, who are often in conflict with their parents and custodians. It is very dangerous when physicians fall to ally themselves with their patients, and it is even more dangerous when they ally themselves with the parents of mental patients. Too often these parents are angry and frustrated with their offspring.
Obsessions and Compulsions in Brain-Damaged People
There is a relationship between brain disease and increased obsessions and compulsions, but it's the opposite of the one suggested by contemporary biopsychiatrists. Since the early work of Kurt Goldstein (for example, Human Nature, published in 1944), clinicians have observed that patients develop obsessive-compulsive tendencies after they have been brain-damaged by war injuries, auto accidents, and psychiatric treatments, such as lobotomy. I also have seen it happen after electroshock. Faced with increased helplessness in dealing with the world, the brain injured person attempts to control inner anxiety and the outer environment alike with repetitive rituals. Everything must be put in the right place, no routines may be changed, plans must be reviewed again and again, simple ideas must be repeated over and over, reassurance about irrational worries will be asked for endlessly.
It's unlikely that the obsessive-compulsive behavior is directly caused by the injury. More likely it is a psychological defense aimed at increasing the individual's sense of security in the face of reduced mental function. This is confirmed by the fact that heavy reliance on obsessions and compulsions can be seen at both ends of the age spectrum, in childhood and in old age. A small child getting ready for bed often needs a fixed ritual with no deviations in order to handle bedtime without too much anxiety or insomnia. Many young children go through periods of time when everything in their room must be in its proper place before going to bed. Similarly, the elderly become more set in their routines and more focused on controlling small details of their daily activities: when and what they eat, when they go to the bathroom, when they visit with people, what they watch on TV or read, when they go to bed, how they arrange their possessions. Often their communications become compulsively repetitive.
In the normal childhood, there's no reason to believe that brain damage or malfunction plays any role in the frequent tendency toward obsessions and compulsions. In old age, the loss of mental acuity and other physical infirmities affecting the mind and the body increase the individual's sense of helplessness and dependence, encouraging reliance on obsessions and compulsions to give a semblance of control over one's life.
Obsessions and compulsions also are apt to occur or to worsen at times of severe stress. People subjected to constant stress, such as athletes, are notorious for their rituals. So are soldiers at the front. In ordinary life, obsessive-compulsive problems rear up when a frightening decision is at hand, such as choosing a new career direction or deciding to get married.
Despite all the hopes for finding a genetic basis of anxiety disorders, none has been demonstrated. A remarkable headline in the December 4, 1987, Psychiatric Times reads GENETIC FINDINGS. The story begins with the statement, "A study in the November Archives of General Psychiatry offers preliminary evidence that panic disorder may be caused by a gene on chromosome 16. " Toward the end of the brief report it is admitted that the finding was "not statistically significant," but that the investigators believe that more research is warranted. Donald Goodwin, in Anxiety (1986), was reduced to pointing to differences in fearfulness among animals and to one unidentified study of identical twins supposedly showing that they have a similar degree of fear of strangers. Some studies do show a familial pattern for certain anxiety problems, but this is not surprising. Psychotherapists typically find that anxious patients have learned their emotional reactions in part, at least, from their parents.
Anxiety sometimes can be temporarily alleviated by a variety of sedative drugs, including minor tranquilizers, barbiturates, opiates, alcohol, and perhaps antidepressants. But the effects are short-lived, with little or no evidence for sustained relief, and the hazards are considerable, including addiction, withdrawal reactions, rebound anxiety, mental dysfunction, and lethality.
Even if these drugs were more effective or safer, should physicians prescribe them for the relief of anxiety? Few psychiatrists would keep a pitcher of martinis at hand in the office to ease the anxiety of their patients; yet most are willing to reach into the drawer for a sample of "alcohol in a pill", the minor tranquilizers. Both alcohol and minor tranquilizers accomplish the same thing - a brief escape from intense feelings by suppressing or sedating normal brain function.
It is understandable that some people want to try to handle their problems through psychiatric or recreational drugs, but should doctors endorse this dangerous and self-defeating avenue as a form of medical treatment? As physicians or psychotherapists we should empower our patients to trust themselves and their capacity to triumph over frightening emotions. We should help them overcome anxiety through self-understanding, improved self-control of their minds and actions, more courageous attitudes, and more successful principles of living.
1. The drugs are called "minor" tranquilizers to distinguish them from "major" tranquilizers, but nowadays the latter are called neuroleptics or antipsychotics. While the minor tranquilizers might now simply be called tranquilizers, that term itself is somewhat misleading. Basically, they are sedatives.
2. A drug-by-drug breakdown of half-lives can be found in the 1989 Comprehensive
3. Steinberg does not use the term addiction loosely. By addiction he means that the patient periodically loses control of his or her drug intake and has a pattern of compulsive use, despite adverse consequences. If Steinberg were merely speaking of habituation, or difficulty stopping the use of the drug, his estimates would be much higher. He considers Xanax "very easily habituating" and observes that people are especially susceptible to the initial "euphoria or disinhibiting effect" that it has in common with alcohol.
4. While insufficiently stressing the problem of memory loss, a discussion and bibliography is presented in the APA task force report, Benzodiazepine Dependence, Toxicity, and Abuse (Washington, D.C.: American Psychiatric Association, 1990).
5. These theoretical formulations on the psychophysiology of anxiety, developed in medical school and published shortly thereafter, have been recently confirmed by David Barlow in Anxiety and Its Disorders (New York: Guilford Press, 1988). He states, "Breggin's general impressions are receiving substantial experimental support, as described below in some detail" (p. 116), and Breggin's "psychobiological model, now over 20 years old, still accommodates the laboratory provocation data to a degree that no unidimensional psychological or biological model can attain" (p. 157; see also p. 152). Barlow does note that details have to be modified in keeping with new data. Also see Peter Breggin, "The Sedative-like Effect of Adrenaline," Archives of General Psychiatry 12: 255-59, 1965.
6. Rapoport also discusses lobotomy on pp. 8-9.
7. My international campaign in the 1970s to stop lobotomy and other forms of psychosurgery is described, albeit from a negative viewpoint, in Rael jean Isaac and Virginia Armat, Madness in the Streets (New York: Free Press, 1990). I have not written extensively about my reform work, but Isaac and Armat, while attempting to defend lobotomy and to portray my efforts in a negative light, devote a chapter to my success in stopping most of the psychiatric surgery performed in the United States.
Peter Breggin's Home Site - Peter R. Breggin, M.D. founded The International Center for the Study of Psychiatry and Psychology (ICSPP) as a nonprofit research and educational network concerned with the impact of mental health theory and practices upon individual well-being, personal freedom, and family and community values. For 25 years ICSPP has been informing the professions, media and the public about the potential dangers of drugs, electroshock, psychosurgery, and the biological theories of psychiatry.
Suggested Reading:Brain-Disabling Treatments in Psychiatry : Drugs, Electroshock, and the Role of the FDA Today! by Peter R. Breggin, M.D.
The Manufacture of Madness : A Comparative Study of the Inquisition and the Mental Health Movements by Thomas S. Szasz, M.D., Professor
Law, Liberty, and Psychiatry : An Inquiry into the Social Uses of Mental Health Practices by Thomas S. Szasz, M.D., Professor
The Limits of Biological Treatments for Psychological Distress by Seymour Fisher and Roger P. Greenberg
Psychiatric Drugs: Hazards to the Brain by Peter R. Breggin, M.D.
Say NO To Psychiatry!
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