The Problem with Education

An education teaches you what to think, not how to think. For instance, if a doctor has studied one way to do something he will resist anything new even if it makes more sense. For example, it took ten years before doctors would accept the idea that stomach ulcers were caused by bacteria, 200 years to stop the practice of bleeding. When we consider that a great deal of their ongoing education is supplied by drug reps, I fear things will only get worse.

The Perfect Therapist

Oh, the comfort, the inexpressible comfort of feeling safe with a person, having neither to weigh thoughts nor measure words, but pouring them all out, just as they are, chaff and grain together, certain that a faithful hand will take and sift them, keep what is worth keeping, and with a breath of kindness blow the rest away.
-- Dinah Craik

A Good Session

Relapse or Withdrawal Reaction

When someone stops taking a drug they have used for some time, and then seem to get ill again, is it a withdrawal reaction or is it relapse? Has the user actually become ill again, or are drug withdrawal symptoms making them seem (and feel) ill?
The confusion goes back a long way and is found with many drugs, especially sedatives and hypnotics. It partly explains the failure to spot dependence on benzodiazepines (eg Valium/diazepam), for many years. BDZs were usually prescribed for anxiety and stress - so if people felt anxious and stressed when they tried to stop taking them, it was easy to conclude that the drugs worked and were worth taking. World-wide, billions of prescriptions had been written before it was officially recognised that this compounded the dependence, worsening symptoms on withdrawal. The BDZs didn't really go on working at all.
Apart from this, the problem was that the powers-that-be didn't want to know, and went to some lengths to deny the problem could exist. Leading experts from government and industry produced large amounts of lack of evidence to show that dependence was non-existent or rare. Problems were seen as exceptions to the rule, and often attributed to patients with 'dependence-prone personalities', or to sensational reporting by the media. The first serious warnings about benzodiazepine dependence started to appear only after legal action began.
Tranter & Healy (1998) find there is strong evidence that a discontinuation syndrome exists(re: neuroleptics), though nothing like enough to be able to pinpoint how much of a problem it is.
They reached this conclusion after reviewing much evidence on different fronts, including a review of studies in which neuroleptic drugs had been used to treat non-psychiatric states. These are revealing because, if "psychiatric" symptoms appear when a drug is discontinued, they must be true withdrawal symptoms (as there cannot be relapse). The authors point, for example, to long-neglected evidence from the 1960s, when chlorpromazine (the archetypal neuroleptic drug) was used experimentally to treat TB.
Its conclusions mean that the long-term effectiveness of neuroleptics may need to be thoroughly re-evaluated. If withdrawal symptoms have invariably been interpreted as evidence of relapse, the effectiveness of these drugs would have been greatly overestimated over the years

http://www.socialaudit.org.uk/5106-988.htm

The issue was addressed in the Archives of General Psychiatry by an extensive review of neuroleptic withdrawal studies conducted in the last 35 years, accompanied by invited assessment and commentary from 11 clinical researchers. Patricia Gilbert, M.D., and others, of the department of psychiatry at the University of California, San Diego and the San Diego Veterans Affairs Medical Center, found a cumulative relapse rate of 53 percent among 4,365 patients with schizophrenia within a mean follow-up period of 9.7 months after medication was withdrawn; compared to 16 percent who relapse while maintained on antipsychotics (Gilbert and others 1995).
While medication withdrawal was associated with a high risk for relapse, the reviewers found its desirability affirmed by the nearly 50 percent of patients who remained stable off medication for observation periods of more than 10 months. They suggested that for a substantial proportion of cases, however, slow tapering to the lowest effective dose, which may be zero for selected patients, is a more prudent target than complete drug withdrawal.
The researchers cited a study not included in their review (Green and others 1992) which found that a slowly tapered medication regimen over an eight-week period produced relapses in only 8 percent of patients over a six-month follow-up, in comparison to 50 percent who relapsed with more rapid withdrawal over two weeks. Another cited recent study (Smith 1994) achieved an approximate 60 percent reduction in required neuroleptic dosing with accompanied improvement in psychopathologic symptoms in 16 chronically psychotic schizophrenic patients hospitalized for a mean of 11.5 years. Their dose was very slowly reduced by one-fifth to one-third every one or two months as clinical condition allowed.
The two studies did find that medication maintenance tended to reduce likelihood of relapse, although a substantial number of patients receiving medication (46 percent) still relapsed within a two-year follow-up period.

http://www.psychiatrictimes.com/p950633.html

To dispense neuroleptics to the prison population to reduce aggressiveness and then to let them out to the community while they abruptly withdraw from the antipsychotics and go psychotic is unconscionable and is in essence manufacturing insanity.

My Theory of What Causes Crazy

The current treatment is to restrict the amount of dopamine available to the brain. This theory is 50 years old and all the treatments are variations of the same song. When LSD was discovered and seen to cause psychosis, researchers for a short time theorized that serotonin excess might be the problem, but they rejected the idea because amphetamines could also cause psychosis and that chemical was dopamine related and reassured them that their old treatments were effective. Hallucinogens affect the central nervous system by disrupting the neurotransmitter serotonin that serves as a filter of unimportant information from incoming sensory stimuli.

Researchers feel dopamine is a chemical messenger (whose effects can be mimicked by amphetamine and cocaine) that makes us happy - it is the pleasure chemical. Temporary elevation of dopamine levels often leads to an improvement in mood, alertness, improved libido, improved memory functions and perhaps even an enhancement in verbal fluency and creativity. It is the neurotransmitter that helps produce feelings of satisfaction and pleasure. Schizophrenics not in the throes of psychosis are said to be experiencing the negative symptoms: apathy, lack of emotion, poor or nonexistant social functioning, disorganized thoughts, difficulty concentrating and/or following instructions, difficulty completing tasks, and memory problems. The neuroleptics cut off the dopamine supply and then psychiatrists say the natural results of the deprivation are a symptom of the disease. One of the leading researchers of schizophrenia, Dr. Daniel R. Weinberger (Chief of the Clinical Brain Disorders Branch, Division of Intramural Research Programs, at the National Institute of Mental Health, National Institutes of Health. whose papers were cited a total of 2413 times, making him the second-most-cited scientist of the 1990s in schizophrenia) explains that there is too little dopamine in the prefrontal cortex in schizophrenia which then causes too much to be produced in the mesolimbic areas. This doesn't make sense to me - in no other part of the body can excess and deficiency coexist.

Sleep Disorders
Serotonin is daily moderated by melatonin which is produced when we sleep. Robert Whitaker, author of Mad in America is currently interviewing recovered schizophrenics and he says absolutely every single case admits to a period of sleeplessness prior to a psychic break. Mind Freedom, an organization of mental health survivors, has interviewed people and the sleep problem is recounted multiple times.

There is an episode of Star Trek in which the crew of the Enterprise was deprived of REM sleep because of some freaky space glitch. As a consequence of being dream deprived, they began to hallucinate when they were awake. Scientists like John Lilly and Jean Houston have proven this does indeed occur.

Small doses of sleep deprivation are familiar to everyone. The most common symptoms of sleep deprivation are inattention, staring, trembling hands, drooping eyelids, increased pain sensitivity and a reduced sense of well-being. Extreme sleep deprivation can lead to a seemingly psychotic state of paranoia and hallucinations in otherwise healthy people. Curiously, sleeping problems occur in almost all people with mental disorders, including those with Alzheimer's disease, depression and schizophrenia.

Animal studies show that sleep and dreaming (REM) sleep are necessary for survival. For example, while rats normally live for two to three years, those deprived of rapid eye movement (REM) sleep survive only about 5 weeks on average and rats deprived of all sleep stages live only about 3 weeks. Sleep deprived rats also develop abnormally low body temperatures and sores on their tail and paws. Scientists (H.P.Roffwarg, J.N. Muzio, W.C. Dement, 1966, Science 152, 604) feel that REM sleep must play an essential role in the development of the central nervous system because developing babies require proportionately greater amounts of REM sleep than a developed adult. In fact the brains of infant rats show significant abnormal development if they are deprived of REM sleep.

Researchers suggest that healthy people need not only an adequate amount but also the right kind of sleep just like they need an adequate amount of proper exercise. In adults non-rapid eye movement (NREM) and rapid eye movement (REM) sleep alternate cyclically throughout the night beginning with NREM sleep which lasts about 80 minutes followed by REM sleep which lasts about 10 minutes. Theorists suspect that REM sleep relaxes the mind and NREM sleep relaxes the body, and that most remembered dreams occur during REM sleep. It is during REM sleep that most brain areas show greatly increased blood flow, almost uniformly greater than 50% above the waking level and as great as nearly 200%. Brain temperatures rise during REM sleep. There are nerve cells in our brains which fire five to ten times more frequently during certain sleep stages than during wakefulness and it is likely that dreams are responsible for maintaining the central nervous system throughout the lifespan.

Incidentally, REM sleep also stimulates the brain regions used in learning. In an experiment, people taught a skill and then deprived of NREM sleep could recall what they had learned after sleeping while people deprived of REM sleep could not.

Sleeping patterns change in adolescence. Beginning in early adolescence there is a gradual decline in delta wave sleep. The decline may represent one of the earliest known indicators of the aging of the central nervous system and may be relevant to the appearance of schizophrenia in early adulthood. Sleeplessness and stress often go hand in hand.

Sleep is controlled by the conversion of serotonin to melatonin. The pineal gland located deep in the center of the brain stores serotonin that is chemically converted to melatonin and the melatonin is converted back to serotonin in daily cycles that determine the body clock. If melatonin is not produced, the serotonin goes into overload and causes psychosis.

Many people who take the over-the-counter melatonin have commented on an increase in the vividness and frequency of dream activity and have noted an increase in dream recall. Loss of dream recall is known to be a symptom in other problems. Researchers have found that 80% of depressed patients cannot recall dreams. It has been found that alcohol suppresses REM sleep, causing the body to make up this loss of REM by carrying it over to the waking stage. In an advanced stage, this waking stage hallucination may be the cause of delirium tremens. Researchers have found that people deprived on REM sleep for one night will have more REM dreams the following night. Perhaps our bodies quota of hallucinations must be supplied one way or another. "Dreaming permits each and every one of us to be quietly and safely insane every night of our lives." -William Dement

Psychotic episodes are the most frightening to the general public and of the most concern to psychiatrists. Psychosis is actually not so very uncommon and there are lots of medical and psychiatric causes of hallucinations besides schizophrenia. Some common causes include the following:

*Pellagra, which is the deficiency disease caused by a severe lack of niacin in the diet also is characterized by dementia.
*B-12 deficiency which also causes insomnia
*Fever, which can occur with almost any infection, frequently produces hallucinations in children and the elderly
*Intoxication or withdrawal from such drugs as amphetamines, LSD, cocaine/crack, heroin, psilocybin (magic mushrooms), PCP and alcohol
*Delirium or dementia
*Sensory deprivation such as blindness or deafness
*Lack of sleep and disruption of circadian rhythms
*Severe medical illness including liver failure, kidney failure, and brain cancer
*Various prescription drug reactions: Lariam, the commercial name for the anti-malarial drug mefloquine, withdrawal from excessive doses of barbiturates (sedative drugs commonly prescribed as sleeping pills), PCP used as human anaesthesia,Aldomet, Benadryl, Catapres, Celebrex, Cipro, Dexatrim, Elavil, Halcion, Inderal, Lanoxin, Procanbid, Sonata, Tagamet, Ultracet, Valium, Vioxx and withdrawal from neuroleptics

If schizophrenia were excess dopamine, the sufferer would be animated and the hallucinations would be glorious and euphoric rather than usually frightening. The current excess dopamine idea came about because the hallucinations were similar to amphetamine psychosis - amphetamines increase dopamine, hence dopamine is the problem. But who sleeps less than a "speed freak" thus creating an imbalance of serotonin/melatonin? The soporific effects of the antipsychotics is the reason they may appear to be effective; however, unfortunately the antipsychotics cause irreversible brain damage and frequent Parkinson's disease.

Deficiencies cause the human body many more problems than excess. The diseases of rickets, scurvy, beri–beri, pellagra, hypothyroidism, immune deficiencies and diabetes are all diseases in which the body does not manufacture enough of an essential element. Even the "excess cholesterol causes heart attacks" theory has come into question:

When I say “heart attack” what are your first thoughts in terms of causes? A good bet is that you will consider cholesterol levels, and immediately after that, diet. After a bit more thought, you might want to add stress induced by a job with too much pressure and responsibility, and finally—just maybe—you will consider the possibility of a genetic predisposition. These are all the causes we hear from the media are associated with heart disease, and indubitably there is a lot of research to back these claims up. However, and most astoundingly, research available since the 1960s and repeated several times since, also shows that all the above factors are actually minor causes of heart disease. The best single predictor of heart problems is indeed stress, but of an entirely different and still widely ignored type: the stress that comes not from doing too much or being under self-imposed pressure, but from being ordered around with little or no control over your destiny.

A study conducted among 17,000 British civil servants (and before that on a million employees of Bell Telephones in the 1960s) clearly shows that the status of a person’s job is the most reliable predictor of heart attack, more than obesity, smoking or high blood pressure (though these count as well, so don’t rush to get that triple cheeseburger just yet). High cholesterol is also a risk factor, but only in people that are genetically predisposed to it. It seems that your heart is by and large at the mercy of the size of your pay check.

The studies linking the pecking order on the job with heart problems found that what happens is that being ordered around diminishes your sense of control over your life, which causes stress mediated by the release of the hormone cortisol. High levels of cortisol not only create problems for your coronary arteries, but depress your immune response, so that you are also more likely to fall prey to an infection—which is not helped by the fact that the rise in cortisol is accompanied by a decrease in serotonin(ed note: did he mean melatonin?), meaning that you don’t sleep very well and you never feel rested.

Researchers have been able to explode another myth related to heart attacks: the idea that it is a disease of the rich, suffered by CEOs because of the high pressure they experience on their job for prolonged periods of time and the associated responsibilities of such a situation. Well, if you are a CEO and are planning on using that as an excuse to raise your bonus this year, forget it. While there are exceptions, the heart attack rate in this category is actually much lower than the population at large, presumably because these people are actually very much in control of what they are doing, since they are everybody else’s boss (and even when they “fail” they get to retire with a few extra million dollars in their bank accounts). This category becomes at risk—rather ironically—only after retirement, possibly because their new “relaxed” life style is actually associated with very little control. Taking it easy for someone used to issue orders and be in charge can be fatal, literally.

Human beings are primates, and evolutionary theory teaches us to expect something similar in our inter-specific cousins. Sure enough, studies on baboons have shown an increase in stress level and production of cortisol in males that join a new troop, because when they do so they find themselves at the bottom of the pecking order, with little control over availability of food and mates. The same is true for monkeys studied in zoos, where researchers found a nice inverse relationship between pecking order and the furring up of arties. Next time you see a monkey or ape, remember to empathize with their working conditions.

Amazingly, you can even demonstrate the effect experimentally on humans by dividing people into two groups, giving them the same tasks, but ordering around one group and empowering the other with self decision making. The latter group experiences lower levels of stress hormones, blood pressure and heart rate. - Dr. Massimo Pigliucci

Sometimes medicine takes a 180 degree turn such as the findings that giving too much liquid to distance runners may prove fatal or that bacteria causes stomach ulcers. "It is an observable fact that psychiatry, unlike any legitimate science, is a discipline in which two dissertations so incompatible that for either one to be valid the other must be incompetent nonsense can both be awarded Ph.D.s by the same department of the same university in the same year." William R. Harwood, Book reviewer on Amazon.

I once saw a program where the lecturer held up a five year old copy of the New England Journal of Medicine and said something to the effect that "we no longer believe 60% of what was printed here." How is it that the psychiatry business still keeps trying to ram that same round peg into that square hole after 50 years of dopamine suppression that continues to fail to fix the problem? Or would mild sedatives, removal from a stressful environment and a sleeping pill be less profitable than lifelong drugging?

Too true

Actually I believe this is true. That is why the psychiatric community loves the "chemical imbalance" thing.

Mental Illness on the rise

SS: Your research also shows that there is a real increase in people who have a severe mental disorder. Now, this seems counterintuitive, but is it true that you believe much of this increase is caused by the overuse of some of the new generations of psychiatric drugs?
RW: Yes, exactly. I looked at the number of the so-called severely disabled mentally ill -- people who aren't working or who are somehow dysfunctional because of mental illness. So I wanted to chart through history the percentage of the population who are considered the disabled mentally ill.

Now, by 1903, we see that roughly 1 out of every 500 people in the United States is hospitalized for mental illness. By 1955, at the start of the modern era of psychiatric drugs, roughly one out of every 300 people was disabled by mental illness. Now, let's go to 1987, the end of the first generation of antipsychotic drugs; and from 1987 forward we get the modern psychiatric drugs. From 1955 to 1987, during this first era of psychiatric drugs -- the antipsychotic drugs Thorazine and Haldol and the tricyclic antidepressants (such as Elavil and Anafranil) -- we saw the number of disabled mentally ill increase four-fold, to the point where roughly one out of every 75 persons are deemed disabled mentally ill.

Now, there was a shift in how we cared for the disabled mentally ill between 1955 and 1987. In 1955, we were hospitalizing them. Then, by 1987, we had gone through social change, and we were now placing people in shelters, nursing homes, and some sort of community care, and gave them either SSI or SSDI payments for mental disability. In 1987, we started getting these supposedly better, second-generation psychiatric drugs like Prozac and the other selective serotonin re-uptake inhibitor (SSRI) antidepressants. Shortly after that, we get the new, atypical antipsychotic drugs like Zyprexa (olanzapine), Clozaril and Risperdal.

What's happened since 1987? Well, the disability rate has continued to increase until it's now one in every 50 Americans. Think about that: One in every 50 Americans disabled by mental illness today. And it's still increasing. The number of mentally disabled people in the United States has been increasing at the rate of 150,000 people per year since 1987. That's an increase every day over the last 17 years of 410 people per day newly disabled by mental illness.

SS: So that leads to the obvious question. If psychiatry has introduced these so-called wonder drugs like Prozac and Zoloft and Zyprexa, why is the incidence of mental illness going up dramatically?
RW: That's exactly it. This is a scientific question. We have a form of care where we're using these drugs in an ever more expansive manner, and supposedly we have better drugs and they're the cornerstone of our care, so we should see decreasing disability rates. That's what your expectation would be.

Instead, from 1987 until the present, we saw an increase in the number of mentally disabled people from 3.3 million people to 5.7 million people in the United States. In that time, our spending on psychiatric drugs increased to an amazing degree. Combined spending on antipsychotic drugs and antidepressants jumped from around $500 million in 1986 to nearly $20 billion in 2004. So we raise the question: Is the use of these drugs somehow actually fueling this increase in the number of the disabled mentally ill?

When you look at the research literature, you find a clear pattern of outcomes with all these drugs -- you see it with the antipsychotics, the antidepressants, the anti-anxiety drugs and the stimulants like Ritalin used to treat ADHD. All these drugs may curb a target symptom slightly more effectively than a placebo does for a short period of time, say six weeks. An antidepressant may ameliorate the symptoms of depression better than a placebo over the short term.

What you find with every class of these psychiatric drugs is a worsening of the target symptom of depression or psychosis or anxiety over the long term, compared to placebo-treated patients. So even on the target symptoms, there's greater chronicity and greater severity of symptoms. And you see a fairly significant percentage of patients where new and more severe psychiatric symptoms are triggered by the drug itself.

SS: New psychiatric symptoms created by the very drugs people are told will help them recover?
RW: Absolutely. The most obvious case is with the antidepressants. A certain percentage of people placed on the SSRIs because they have some form of depression will suffer either a manic or psychotic attack -- drug-induced. This is well recognized. So now, instead of just dealing with depression, they're dealing with mania or psychotic symptoms. And once they have a drug-induced manic episode, what happens? They go to an emergency room, and at that point they're newly diagnosed. They're now said to be bipolar and they're given an antipsychotic to go along with the antidepressant; and, at that point, they're moving down the path to chronic disability.

SS: Modern psychiatry claims that these psychiatric drugs correct pathological brain chemistry. Is there any evidence to back up their claim that abnormal brain chemistry is the culprit in schizophrenia and depression?
RW: This is the key thing everyone needs to understand. It really is the answer that unlocks this mystery of why the drugs would have this long-term problematic effect. Start with schizophrenia. They hypothesize that these drugs work by correcting an imbalance of the neurotransmitter dopamine in the brain.

The theory was that people with schizophrenia had overactive dopamine systems; and these drugs, by blocking dopamine in the brain, fixed that chemical imbalance. Therefore, you get the metaphor that they're like insulin is for diabetes; they're fixing an abnormality. With the antidepressants, the theory was that people with depression had too low levels of serotonin; the drugs upped the levels of serotonin in the brain and therefore they're balancing the brain chemistry.

First of all, those theories never arose from investigations into what was actually happening to people. Rather, they would find out that antipsychotics blocked dopamine and so they theorized that people had overactive dopamine systems. Same with the antidepressants. They found that antidepressants upped the levels of serotonin; therefore, they theorized that people with depression must have low levels of serotonin.

But here is the thing that one wishes all of America would know and wishes psychiatry would come clean on: They've never been able to find that people with schizophrenia have overactive dopamine systems. They've never been able to find that people with depression have underactive serotonin systems. They've never found consistently that any of these disorders are associated with any chemical imbalance in the brain. The story that people with mental disorders have known chemical imbalances -- that's a lie. We don't know that at all. It's just something that they say to help sell the drugs and help sell the biological model of mental disorders.

But the kicker is this. We do know, in fact, that these drugs perturb how these chemical messengers work in the brain. The real paradigm is: People diagnosed with mental disorders have no known problem with their neurotransmitter systems; and these drugs perturb the normal function of neurotransmitters.

SS: So rather than fixing a chemical imbalance, these widely prescribed drugs distort the brain chemistry and make it pathological.
RW: Absolutely. Stephen Hyman, a well-known neuroscientist and the former director of the National Institute of Mental Health, wrote a paper in 1996 that looked at how psychiatric drugs affect the brain. He wrote that all these drugs create perturbations in neurotransmitter functions. And he notes that the brain, in response to this drug from the outside, alters its normal functions and goes through a series of compensatory adaptations.

In other words, it tries to adapt to the fact that an antipsychotic drug is blocking normal dopamine functions. Or in the case of antidepressants, it tries to compensate for the fact that you're blocking a normal reuptake of serotonin. The way it does this is to adapt in the opposite way. So, if you're blocking dopamine in the brain, the brain tries to put out more dopamine and it actually increases the number of dopamine receptors. So a person placed on antipsychotic drugs will end up with an abnormally high number of dopamine receptors in the brain.

If you give someone an antidepressant, and that tries to keep serotonin levels too high in the brain, it does exactly the opposite. It stops producing as much serotonin as it normally does and it reduces the number of serotonin receptors in the brain. So someone who is on an antidepressant, after a time ends up with an abnormally low level of serotonin receptors in the brain. And here's what Hyman concluded about this: After these changes happened, the patient's brain is functioning in a way that is "qualitatively as well as quantitatively different from the normal state." So what Stephen Hyman, former head of the NIMH, has done is present a paradigm for how these drugs affect the brain that shows that they're inducing a pathological state.

SS: So the paradox is there's no evidence for modern psychiatry's claim that there is any pathological biochemical imbalance in the brain that causes mental illness, but if you treat people with these new wonder drugs, that is what creates a pathological imbalance?
RW: Yes, these drugs disrupt normal brain chemistry. That's the real paradox here. And the real tragedy is, that even as we peddle these drugs as chemical balancers, chemical fixers, in truth we're doing precisely the opposite. We're taking a brain that has no known abnormal brain chemistry, and by placing people on the drugs, we're perturbing that normal chemistry. Here's how Barry Jacobs, a Princeton neuroscientist, describes what happens to a person given an SSRI antidepressant. "These drugs," he said, "alter the level of synaptic transmission beyond the physiologic range achieved under normal environmental biological conditions. Thus, any behavioral or physiologic change produced under these conditions might more appropriately be considered pathologic rather than reflective of the normal biological role of serotonin."

Psychiatric Drugs: An Assault on the Human Condition
Street Spirit Interview with Robert Whitaker
Interview by Terry Messman