12/23/16

Listening to Antidepressants

Prozac took the U.S. by storm when the FDA approved it in 1987. It also had a similarly radical effect on the thinking of a forty year-old psychiatrist named Peter Kramer. In the Introduction of his now classic book, Listening to Prozac, Kramer described how people became “better than well” with Prozac and how they and he began to “listen” to what Prozac told them. Kramer said it “transformed my views about what makes people the way they are.” But even by 1993, when Listening to Prozac was published, the stories of violence and suicide after taking the first SSRI antidepressant were circulating as well.

Toxic Psychiatry by another psychiatrist named Peter Breggin, was published two years earlier and documented reports of suicidal behavior in both the popular press and the professional literature. “Suicidal Behavior Tied to Drug,” was published on February 7, 1991 in The New York Times. The article said two cases of suicidal behavior and fantasies (with no prior history) were reported in The New England Journal of Medicine that same day. Eli Lilly was facing more than 50 lawsuits at the time and of course denied that there was any scientific merit to the claim the medication could prompt suicidal or violent acts. The year before, “Emergence of Intense Suicidal Preoccupation During Fluoxetine Treatment,” was published in the February 1990 issue of The American Journal of Psychiatry. Its abstract read:

Six depressed patients free of recent serious suicidal ideation developed intense, violent suicidal preoccupation after 2-7 weeks of fluoxetine treatment. This state persisted for as little as 3 days to as long as 3 months after discontinuation of fluoxetine. None of these patients had ever experienced a similar state during treatment with any other psychotropic drug.

Breggin also seems to have predicted the rise of what is now called “treatment resistant depression” with SSRIs. He said: “If Prozac can indeed alleviate depression by making more serotonin available in the brain, then with time it may produce incurable depression by making the brain relatively unresponsive to any amount of serotonin.” In Talking Back to Prozac in 1995, Breggin “blew the whistle” on the newer antidepressants and antidepressant-induced violence, suicide and mania. Finally in 2004 the FDA finally required black box warnings to be placed on the newer antidepressants, warning of the potential for the increased risk of suicidal thoughts and behavior in children and adolescents.

Yes, Dr. Kramer did say as far back as Listening to Prozac that the chemical imbalance theory (the amine hypothesis) was at least incomplete and perhaps false. But then Kramer published Against Depression in 2005, arguing that the socio-economic costs of depression were so large, that modern societies should strive to eradicate it as they did with smallpox. On his blog in 2008 he argued that the chemical imbalance theory was prematurely declared dead, even though “the neurotransmitter theory is incomplete and not fully proven.” He asserted that since 1993 the evidence for it had been steadily growing.

Jonathan Leo and Jeffrey Lacasse did an in depth critique of the evidence Dr. Kramer used to support the chemical imbalance theory. They noted several qualifications used when scientists discuss the biological basis of mood with other scientists. “Yet, in the popular press all these qualifications disappear and instead the public is inundated with declarations about ‘chemical imbalances causing mental illness.’” They said there were two different discussions going on about the theory—a simple, straightforward one in the media and advertisements, but a tenuous nuanced one in scientific circles. In scientific circles, the discussion was about the appropriateness of using the chemical imbalance theory with patients and not so much about the strength of the theory.

In the late 1990s, Irving Kirsch decided to research the placebo effect with the newer (SSRIs and SNRIs) antidepressants. He began with the assumption that there actually was a therapeutic effect with antidepressants, but he wanted to assess the placebo effect: “I was not particularly interested in the drug effect. I assumed that antidepressants were effective.” He was surprised to discover how small the drug effect was. Seventy-five percent of the improvement in the drug group also occurred with people who were given placebo pills with no active ingredient in them.

Critics of his findings said the meta-analysis he and his co-author had done was biased; that they had an unrepresentative sample of clinical trials. So Kirsch and three others replicated the original study with the identical data set used by the pharmaceutical companies for the FDA approval of six of the new generation antidepressants at the time. These six accounted for the bulk of antidepressant prescriptions being written at the time, 2002. “In the data sent to us by the FDA, only 43% of the trials showed a statistically significant benefit of drug over placebo. The remaining 57% were failed or negative trials.” The results here were that 82% of the response to antidepressants was due to the placebo effect.

Kirsch again did a replication in 2008 with a larger number of clinical trials and again found the 82% placebo effect. In both analyses, the mean difference between drug and placebo was less than two points (1.8) on the HAM-D depression scale, used in all the FDA clinical trials for antidepressants at the time. The difference was clinically insignificant. In other words, these miniscule differences were too small to be observable in a normal clinical setting with someone who was depressed. Others, including the FDA, have repeatedly replicated their results. The above history can be found in a 2014 article by Irving Kirsch, “Antidepressants and the Placebo Effect,” or in his 2010 book, The Emperor’s New Drugs. There he speculated:

Antidepressants may be nothing more than active placebos, producing side effects through chemical means and therapeutic effects through psychological means.

Twenty-three years after Listening to Prozac, Peter Kramer published his latest book, Ordinarily Well: The Case for Antidepressants. According to Jonathan Rosen, who wrote “The Assault on Antidepressants” for The Atlantic, Kramer said he believed in the utility of antidepressants, despite their flaws. He not only sought to make a case for antidepressants, he also tried to make a case for psychiatry as “a humanistic science that bridges the impersonal ideals of the laboratory and the pragmatic exigencies of clinical intervention.”

In a book review of Ordinarily Well for The New York Times, Jennifer Senior referred to the original Kirsch research and said Kramer was wary of these studies because they flew in the face of his clinical experience. Indicating that when his own patients asked if their improved mood could be due to a placebo effect, “Dr. Kramer’s answer is an unequivocal no.” And Ordinarily Well attempted to prove his belief. Senior indicated Kramer argued that Kirsch deliberately “’seemed to cull studies in which antidepressants underperformed,’ and treated some drugs as placebos even though they may have had antidepressant effects.” Either Senior or Kramer was unaware of, or failed to mention the above-described replications done by Kirsch and others. She did point out how Kramer used meta-analyses to make his own points, but failed to acknowledge that fact. Another area of concern for Kramer was the mechanism for recruiting subjects for clinical trials.

He is particularly devastating on the subject of recruiting test subjects. One of the most damning chapters features an unnamed facility where antidepressant trials are frequently conducted. Many of the participants are unemployed or underemployed — lonely, dispossessed and eager for the money. Suddenly, they’re getting paid, interacting with others and receiving the careful attention of doctors and nurses. “Even on placebo,” Dr. Kramer writes, “these patients ought to get better.”

There is an indication that evidence-based medicine has some flaws; and that the gold standard of meta-analysis can be undermined by flawed analysis, especially in psychiatric drug research. And there really is a problem with recruiting clinical trials subjects; and sometimes with the methodologies used by researchers in those clinical trials. But remember that if Kramer’s concerns are accepted (and I think they should be), then the newer antidepressants were approved using questionable scientific methods and an unreliable approval process. See “Evidence-Based Treatment … Lacks Evidence.”

If that is the case, where is the protection that FDA approval of pharmaceuticals is supposed to provide? And why aren’t more people pressing for regulatory reform of the FDA clinical trial process? If we accept Kramer’s arguments, we should also acknowledge that the clinical trials used for FDA approval of SSRIs were invalid. Kramer’s rationale for dismissing the evidence for the placebo effect with antidepressants also calls into question the methods used for their approval—and many of the studies afterwards touting their continued effectiveness.

A recent review article by Andrews et al., “Is Serotonin a Downer or an Upper?” challenged the assumptions of the therapeutic effects of SSRIs. “Although the idea that a single neurochemical is the cause of depression is now considered simplistic, the low serotonin hypothesis still lies at the foundation of most research on depression.” The authors noted how many types of depression seem to correspond to higher levels of serotonin, not lower ones. They proposed a radical new way of understanding the role of serotonin in the brain, according to Shannon Peters in, “How Do Antidepressant Really ‘Work’?” They suggest that serotonin coordinates metabolic processes with the storage, mobilization, distribution, production and utilization of energy resources.

Under this theory, there are higher levels of serotonin when there is a need to redistribute limited energy resources. “Serotonin cannot be simply described as an ‘upper’ or a ‘downer’; its symptomatic effects depend on the organism’s state,” write the authors.

When listening to antidepressants, we hear a history of effectiveness that can’t be clearly attributed to the therapeutic effect of the drugs. Expectation or placebo plays a significant role in whether or not these drugs will help an individual “overcome” their depression. Peter Kramer continues to hold on to a narrative that the chemical properties of SSRIs actually do help some depressed individuals, with “little of the benefit coming from the classical placebo effect.” But in debunking the science used to affirm the antidepressant placebo effect, he also calls into question the methods used to approve those same SSRIs in the first place.

What about Peter Breggin? He’s still around and critiquing the use of other classes of psychiatric drugs as well as antidepressants. He was recently the expert witness in a 2016 court case, awarding $11.9 million in a Paxil suicide malpractice case. He has a video series on YouTube, “Simple Truths About Psychiatry,” which is also linked on his website: breggin.com. There is plenty of additional material there to support the ineffectiveness and danger of antidepressants. In 2011, Dr. Breggin was the expert witness in a court case where Prozac was found to be a contributing factor to the murder of a teenager by his friend. “This was the first criminal case in North America where a judge has specifically found that an antidepressant was the cause of a murder.”

There’s more discussion of Irving Kirsch and the placebo effect here on my website. Start with: “Dirty Little Secret” or do a search of the website for his name.

10/18/16

Dancing with the Devil

I once knew a woman who had an anxiety disorder. She also abused benzodiazepines. She was able to conjure up a panic attack in a doctor’s office and walk out with a prescription for the benzo of her choice. At one time, she had four concurrent prescriptions for these anti-anxiety medications. Another person I know of has a ten-year history of using benzodiazepines at close to the maximum recommended dose. When he had an unexpected short-term hospital stay, the treating physicians were reluctant to continue prescribing benodiazepines at such a high level while he was in the hospital. When he returned home, in case his medical issue resulted in another unexpected stay, he put together an emergency hospital kit with various things—including extra benzodiazepines.

A study published in the American Journal of Public Health in April of 2016 found that benzodiazepines were the second most common drug in prescription overdose deaths for 2013. Given the common knowledge of the potential dangers of benzodiazepines and people becoming more aware of opioids, Marcus Bachhuber and a team of researchers thought that their study would show a steady of declining pattern for prescribing benzodiazepines. But they found exactly the opposite. Between 1999 and 2013 there was an increase of 30% among adult Americans who filled a benzodiazepine prescription. In addition, the amount of medication within a prescription doubled over the same time period.

Bachhuber was quoted by CNN as saying the study’s findings were very concerning. The risk of overdose and death from benzodiazepines alone is said to be generally lower in otherwise healthy adults. But in combination with other drugs like alcohol or opioids, they can be lethal.

Future research should examine the roles of these potential mechanisms to identify effective policy interventions to improve benzodiazepine safety. In particular, as underscored by several recent reports, interventions to reduce concurrent use of opioid analgesics or alcohol with benzodiazepines are needed.

The overdose problem with benzos has been overshadowed by the problems with prescription opioids. Writing for CNN, Carina Storrs said: “The current study could help shine a light on the problem of benzodiazepine abuse and overdose.” Dr. Gary Reisfield, a professor of psychiatry at the University of Florida, referred to the problem with benozdiazepines as a “shadow epidemic”:

Much attention has been paid to the explosion of prescription opioid prescribing and the associated morbidity and mortality. Much less attention has been paid to the shadow epidemic of benzodiazepine prescribing and its consequences.

A 2015 study by Jones and McAninch found that emergency department visits and overdose deaths involving opioids and benzodiazepines increased significantly between 2004 and 2011. Overdose deaths from combining the two classes of drugs rose each year from 18% in 2004 to 31% in 2011. This rate increased faster than the percentages of people filling prescriptions and the quantity of pills in the prescriptions.

As Dr. Indra Cidambi wrote in “Are We Ignoring an Escalating Benzodiazepine Epidemic?”, she observed with increasing alarm the rising rate of concurrent use/abuse of benzos among opiate users. She pointed to two possible factors driving this trend. First, some opiate abusers use benzos to “spike” the euphoria from their opiates. Second, patients often receive their prescriptions from two different physicians. She said that it is “notoriously difficult” for doctors to refuse to prescribe these two medications.

Unfortunately, and ironically, pain and anxiety are neither verifiable nor quantifiable through medical testing! Consequently, self-reported symptoms by patients are the sole basis on which prescriptions for these medications are written, enabling individuals addicted to these medications to obtain them fairly easily.

Dr. Cidambi recommended the establishment of a national database for physicians to verify whether or not a patient has been prescribed one of these medications before prescribing or filling a prescription for the other. Second, she said physicians should develop limited, short-term treatment plans from the beginning to treat noncancerous pain with opiates and anxiety with benzodiazepines.

Studies have shown the decreasing efficacy of long-term treatment for pain with opioid medications, and evidence-based treatment protocols for benzodiazepines clearly indicate that long-term use of benzodiazepines is not recommended.

In “Benzos: A Dance with the Devil,” Psychiatrist Kelly Brogan described some of her work helping patients taper off of benzodiazepines. A woman who had been placed on Remeron (an antidepressant) and Klonopin (a benzodiazepine) for eight years said of her original prescriber: “He never once told me there might be an issue with taking these meds long-term. In fact, he told me I probably needed them after I tried stopping them cold turkey and felt so sick I thought I was dying.” Brogan said no one ever discussed with this woman or her patients the true risks, benefits and alternatives to psychiatric medications like benzodiazepines, “perhaps because we as clinicians are not told the full story in our training.”

She went on to quote from a paper by another psychiatrist, Peter Breggin, on the risks of benzodiazepines, which include: cognitive dysfunction that can range from short-term memory impairment and confusion to delirium; “disinhibition or loss of impulse control, with violence toward self or others, as well as agitation, psychosis, paranoia and depression.” There can also be severe withdrawal symptoms, ranging from anxiety and insomnia to psychosis and seizures after abruptly stopping long-term larger doses. The person can re-experience their pre-drug symptoms as they taper. These so-called rebound symptoms of anxiety, insomnia and others serious emotional reactions can be more intense than they were before drug treatment began. And don’t forget dependency or abuse.

Psychiatrist Allen Frances, the former chair of the DSM-IV, recently wrote: “Yes, Benzos Are Bad for You.” He introduced his article by saying that he was going to say some very negative things about benzodiazepines in the hope that doctors think twice before prescribing them and patients are discouraged from taking them. Benzos were wonder drugs in the 1960s. Anyone remember the 1966 song, “Mother’s Little Helper,” by the Rolling Stones? These drugs were reputed to be safe, and so were used for a variety of “ills,” such as anxiety, alcohol use disorders (yes, really), to take the edge off of agitation in dementia, and to help people sleep. “Initially we were pretty oblivious to the risk of addiction.” So benzodiazepines quickly became the most prescribed medications in America.

A second craze began in the 1980s with the release of Xanax. Frances said the dose to treat panic disorder was “dangerously close” to the dose leading to addiction. “This should have scared off everyone from using Xanax, but it didn’t.” It remains a best seller, with its own “brand” that now leads to fentanyl be pressed into counterfeit Xanax pills. See “Buyer Beware Drugs” and Paul Gaita’s article on fake Xanax laced with fentanyl.

The real wonder of the benzos is that sales continue to boom, despite their having so little utility and no push from pharma marketeering (because patents have run out – thereby decreasing costs and profits.) Between 1996 and 2013, the percentage of people in the U.S. using benzos jumped more than one-third from an already remarkable 4.1 to 5.6 percent. Especially troubling is that benzo use is ridiculously high (nearly one out of ten) in the elderly, the group most likely to be harmed by them.

Frances said the beneficial uses of benzodiazepines can be counted on the fingers of one hand: short-term agitation in psychosis, mania and depression; catatonia; “as needed” use for times of special stress, like fear of flying, or for sleep. While they should be used very short term, in real life most people take them long term—“in doses high enough to be addicting, and for the wrong reasons. . . . Benzos are very easy to get on, almost impossible to get off.”

In addition to the harm from overdoses, Frances described the painful and dangerous withdrawal symptoms, which he said are a “beast.” Common symptoms are irritability, insomnia, tremors, distractibility, sweating and confusion. “The anxiety and panic experienced by people stopping benzos is usually much worse than the anxiety and panic that initially led to their use.” Concurrent use or abuse of alcohol or other drugs, like opioids, complicates withdrawal even further.

The most insidious issues with benzos for Frances, is how they effect brain functioning. Especially with the elderly, ongoing benzo use can be devastating. Many elderly begin their downward spiral to death and disability from falls—that happen from their benzo use! He said: “If you meet an elderly patient who seems dopey, confused, has memory loss, slurred speech, and poor balance, your first thought should be benzo side effects — not Alzheimer’s disease or dementia.” See “Sedating Seniors” for more information on this topic. It’s been over 30 years since he last prescribed a benzo for anxiety.

The tough question is what to recommend for those many unfortunates already suffering the tyranny of benzo addiction. Should they stay the course to avoid the rigors and risks of withdrawal or should they make the great effort to detox? This is an individual decision that can’t be forced on someone. But the longer you are on them, the harder it gets to stop, and the cognitive side effects of benzos create more and more dysfunction as your brain ages. The best bet is to stick with a determined effort to detox, however long and difficult, under close medical supervision. On a hopeful note, some of the happiest people I have known are those who have overcome their dependence on benzos.

So it was encouraging to see that the FDA will require class-wide changes in drug labeling to bring attention to the dangers of combining opioids and benzodiazepines. The changes will include boxed warnings on nearly 400 products with information on the risks of combining these medications. The FDA Commissioner, Robert Califf said: “It is nothing short of a public health crisis when you see a substantial increase of avoidable overdose and death related to two widely used drug classes being taken together.” He implored health care professionals to carefully and thoroughly evaluate on a patient-by-patient basis whether the benefits outweigh the risks when using these drug classes together.

Used alone or in conjunction with opiates, benzodiazepines are potentially lethal and addictive. A too sudden withdrawal from benzodiazepines can be fatal, where the same is rarely true with opiates. They work quickly and effectively for anxiety and sleep problems and yet they can have a multitude of side effects, including addiction. Did I say they are addictive? Using benzodiazepines has become a dance with the devil for too many unsuspecting individuals … those that are still alive to regret it, that is.

This article previously appeared on the addiction and recovery website “The Fix” under the title of “Dangerous Dance.”

09/20/16

Appalling Silence on ECT

Kenny was put on antidepressants at the age of 14 because he was struggling in a difficult family situation. His symptoms became worse. The psychiatrist added another drug with again worsening symptoms. At one point, he was taking six different psychiatric drugs. Kenny was eventually told his depression was “treatment resistant” and needed electroshock therapy. “The risks were downplayed.” He was given 30 rounds of ECT and went from a high school honor student to having to be retaught how to tie his shoes. Wait, there’s more!

Kenny lost all memories of childhood and all memories of high school. He says it’s an identity crisis. He suffered severe headaches for a year and a half after the shocks and had to see a cardiologist because ECT left him with heart arrhythmia. Testing by a neurologist, done six months after the shocks, showed a loss of 50 IQ points compared to his high school IQ. Kenny still suffers from night terrors about the shocks.

Dr. Langemann’s article on “Shock Therapy” for the Huffington Post also referred to a biomedical engineer who said the “brief pulse” of ECT is actually a series of several hundred pulses, and not a single pulse. These pulses overstimulate brain cells, causing rapid random firing, intentionally causing a Grand Mal seizure. “The current causes overheating inside the brain and the electric field can tear holes in the cells (which causes the cells to die).” She noted that a conservative estimate is that 100,000 patients per year receive ECT.

Incredibly, ECT has never been through the standard clinical trial process to prove its safety or efficacy. Although the FDA has had the authority to regulate medical devices since 1976, it disregarded ECT machines because they’ve been in widespread use since the 1950s, according to STAT News in “Psychiatric Shock Therapy.” The FDA placed ECT machines in the class III (high risk) category where they have remained since that time. But in December of 2015, the FDA made public a draft document proposing to reclassify ECT machines as a class II (low risk) device. Before the public comment period ended in late March of 2016, the FDA had received 2,040 comments on its draft rule. The agency has not set a timetable for issuing its final ruling.

While the proposed regulations would indicate that ECT was “safe and effective” and only moderately risky for adults, it would only be approved for adults with severe depression who haven’t responded to medication or other therapies. It would remain classified as a high risk (class III) for psychiatric conditions other than major depression and for children and adolescents. There would be new requirements as well. Doctors would have to warn patients of the side effects of ECT, which include confusion and memory loss; and that long-term safety for ECT is not proven.

Psychiatrists warn that that these new regulations could lead to insurers not covering ECT and doctors not recommending it for younger patients and those with conditions like schizophrenia, bipolar disorder and catatonia. (They say it like that’s a bad thing) Charles Kellner, a professor of psychiatry at the Icahn School of Medicine said, “Its use for these indications is widespread, even ubiquitous, and to deny the extensive evidence in support of that is indefensible.” Supporters say ECT has come a long way since it was portrayed in “One Flew Over the Cuckoo’s Nest.” Patients get anesthesia and sedatives to minimize pain and muscle spasms, so they are less likely to hurt themselves during the ECT seizure. “Ultra-brief pulse therapy delivers a fraction of the electricity used in the past.” However, as noted above, this claim is disputed. See “The Frankenstein Monster of ECT” and “Is ECT Brain Disabling?” on this website.

Writing for GlobalResearch, Dr. Gary Kohls described ECT “therapy” sessions as: “sub-lethal electrocutions of the brain that reliably produces seizures and coma.” He noted that the perceived improvement with ECT is often because of the frequent short-term and long-term memory loss that occurs with shock treatment. “The patient may no longer remember the traumatizing interpersonal/sexual/social/ psychological/spiritual conflicts that previously made them feel sad, nervous, depressed, anxious or hopeless.” He lamented that studies show physicians reach for their prescription pad within minutes of most clinic encounters. “Time is money.”

Dr. Kohls then quoted excerpts from the testimony of Leonard Roy Frank before the Mental Health Committee of the New York State Assembly in 2001. Mr. Frank was a psychiatric survivor and activist who personally experienced 35 ECT procedures and 50 insulin coma treatments. The transcript of his testimony can be read here in its entirety. He said:

This was the most painful and humiliating experience of my life. My memory for the three preceding years was gone. The wipeout in my mind was like a path cut across a heavily chalked blackboard with a wet eraser. Afterwards I didn’t know that John F. Kennedy was president although he had been elected three years earlier. There were also big chunks of memory loss for events and periods spanning my entire life; my high school and college education was effectively destroyed. I felt that every part of me was less than what it had been.

Frank then elaborated on some of the adverse effects from ECT. With regard to memory loss, he indicated that the APA downplays memory loss, saying most patients actually report improved memory; and only a minority of patients report problems with memory loss. He said the vast majority of individuals he has talked to reported moderate-to-severe amnesia going back two years and more from the time they received ECT. His own experience was noted above.

Quoting the 2001 APA Task Report on ECT, Frank noted where a reasonable ECT-related mortality rate was suggested to be 1 per 10,000 patients. However, some studies show the ECT death rate is about one in 200. This rate may not still be accurate, as an increasing number of the elderly are being electro shocked. “Statistics based on California’s mandated ECT reporting system indicate that upwards of 50 percent of all ECT patients are 60 years of age and older.”

Frank described what he referred to as “the myth of informed consent.” While outright force is seldom used, “genuine informed consent is never obtained” because ECT specialists minimize the procedure’s nature and effects to candidates and their families; and because of the implicit coercion that can be brought to play. There is a lack of accountability with psychiatry. It was a “Teflon” profession, meaning what little criticism there is doesn’t stick. “Psychiatrists routinely carry out brutal acts of inhumanity and no one calls them on it — not the courts, not the government, not the people.”

Electroshock could never have become a major psychiatric procedure without the active collusion and silent acquiescence of tens of thousands of psychiatrists. Many of them know better; all of them should know better. The active and passive cooperation of the media has also played an essential role in expanding the use of electroshock. Amidst a barrage of propaganda from the psychiatric profession, the media passes on the claims of ECT proponents almost without challenge. The occasional critical articles are one-shot affairs, with no follow-up, which the public quickly forgets. With so much controversy surrounding this procedure, one would think that some investigative reporters would key on to the story. But it’s happened only rarely up to now. And the silence continues to drown out the voices of those who need to be heard. I’m reminded of Martin Luther King’s 1963 “Letter from Birmingham City Jail,” in which he wrote: “We shall have to repent in this generation not merely for the vitriolic words and actions of the bad people, but for the appalling silence of the good people.”

Psychiatrist Peter Breggin has advocated against ECT for decades. You can watch an 11-minute video he did called, “Electroshock is Brain Trauma.” He indicated the 100,000 per year estimate for ECT was based on data he gathered in 1979 for his book critical of shock treatment. He said today every large city has several places that do shock treatment. “It’s extremely remunerative.”

Dr. Lagemann indicated that standard treatment is 9 to 12 shocks, at a cost of $2,000 to $2,500 each. When you do the math, you come up with a minimum income of $1.8 billion (9 x 100,000 x $2,000 = $1.8 billion). About half the cost is covered by Medicare. Mr. Frank indicated that in 2001, psychiatrists specializing in shock treatment earned $300,000-$500,000 a year compared to other psychiatrists whose mean annual income was $150,000.

What’s wrong with shock treatment? How does it work? It’s not as mysterious as the advocates make out. Shock works by passing an electric current through one or both frontal lobes of the brain, producing an electrical lobotomy. The electricity also passes through the memory centers of the temporal lobe, causing additional devastation. Finally, the current passes throughout the brain and that, along with the severe seizures that result, causes widespread brain dysfunction and damage. Some patients initially become euphoric from the damage, whereupon the shock doctor notes approvingly, “mood elevated.” All patients eventually become apathetic and indifferent, and unable to resist, whereupon the doctor notes with finality about the outcome, “no longer complaining.”

Dr. Breggin said the only reason that modern shock doctors don’t talk about ECT as damaging the brain is because he publicized and documented how it was in his book, Electroshock: Its Brain-Disabling Effects. He noted that when ECT treatment is done, it results in a period of coma. “How could a blow to the brain with electricity so severe it causes a coma, and you’re not harmed by it?” Very often the EEG brain waves flat line—that’s temporary brain death. The person wakes up completely disoriented. The longer the treatment continues, the more past memory the person loses.

The STAT News article noted where a woman who had 66 ECT treatments between 1996 and 2010 to treat depression left such holes in her memory that she couldn’t recall her wedding day or the birth of her children. Her 28-year marriage ended, ““because I couldn’t remember that relationship, and without those memories, I had no emotional connection.”

Dr. Breggin created a free website about shock treatment: ECT Resources Center. Among its documents is a simple introductory statement and brochure for widespread distribution. There are also PDFs of more than 100 scientific articles on issues with ECT. He urged people to do everything they can to stop someone they know getting ECT, because they will never be the same afterward.

As of September 1^st, there has not been an announcement of what the FDA plans to do with ECT. But when the FDA announced it was soliciting comments of the proposed regulatory changes, the American Psychiatric Association created a form letter for psychiatrists to “take the lead in expressing their views” regarding the role of ECT in clinical practice and treating major depressive disorder. See “Time is Now to Support the ECT Reclassification Effort.” The letter asserted that ECT was an important treatment option for some people with severe mental health conditions. “Your proposed reclassification will greatly improve access to safe, effective treatment for individuals with serious and persistent psychiatric disorders.” You can download and read a copy of the form letter in the above link. I wonder how many of the 2,040 comments were APA form letters from psychiatrists?

07/1/16

Misleading Info on ADHD

Three Swedish researchers did a study on the information published online by the National Institute of Mental Health (NIMH) on ADHD. What is intriguing about their study is that they were looking at how the NIMH document sought to persuade its readers to take action to address their child’s ADHD problem. They suggested there was a circular argument wherein ADHD was defined according to the presence of certain behaviors, which the diagnostic label of ADHD was said to explain. They also pointed out how ADHD is presented as legitimate medical disorder, despite the fact that “diagnostic criteria are subjectively interpreted from the behavior of the child.”

The authors, Erlandsson, Lundun and Punzi, linked this Easy-to-Read NIMH document on ADHD in their study. However, their citations appear to be from this NIMH document, “What is Attention Deficit Hyperactivity Disorder (ADHD, ADD)?” They noted where the image of ADHD as a legitimate medical disorder was established by the first sentence of the article, “ADHD is one of the most common childhood disorders [and can continue through adolescence and adulthood].” This is word-for-word in the latter article, where the Easy-to-Read one is slightly different: “ADHD is a common mental disorder that begins in childhood and can continue through adolescence and adulthood.” The bracketed phrase was not quoted by Erlandsson, Lundun and Punzi, possibly because they were looking at ADHD in children; or when they examined the document in October of 2015, it wasn’t there.

Erlandsson et al. noted how the repeated use of the term “disorder” (at least 15 times) and a number of references to brain imaging and brain chemicals gave the impression of a chronic, long-term disability. The rhetoric is clearly suggestive that ADHD is a brain disorder. And yet, because symptoms vary from person to person, the ‘disorder’ can be difficult to diagnose. The so-called ‘key behaviors of ADHD’ are also found in all children—inattention, hyperactivity, and impulsivity. “But for children with ADHD, these behaviors are more severe and occur more often.” They have to be present for at least six months, and be present to a degree “that is greater than other children of the same age.” Erlandsson et al. said:

In fact, as shown in the document, there are no biological markers, environmentally defined categories, or objective tests to distinguish “ADHD” as a discrete condition. Rather, diagnostic criteria are subjectively interpreted from the behavior of the child: “No single test can diagnose a child having ADHD. Instead, a licensed health professional needs to gather information about the child, and his or her behavior and environment.” Professionals as well as teachers and parents are involved in the evaluation and examination process, and subsequently in the diagnostic process.

There is a clear bias in presenting ADHD as a biomedical problem. While saying scientists aren’t sure what causes ADHD, NIMH then said many studies suggest genes play a large role. Twin studies show ADHD runs in families. “Children with ADHD who carry a particular version of a certain gene have thinner brain tissue in the areas of the brain associated with attention.” But the differences were not permanent and as the children with this gene grew up, the brain developed to a normal level of thickness and the ADHD symptoms improved. As Erlandsson et al. commented: “The biomedical discourse assumes that there is a consensus among professionals on how to interpret the behaviors of the child, which means that pharmacological treatment is the preferred intervention.” But this is not the case.

In “ADHD: an Imbalance of Fire over Water or a Case of the Fidgets?” I reviewed several different sources questioning whether ADHD was a biochemical disorder. Psychiatrist Peter Breggin said the search for a genetic and biological cause for ADHD would never succeed because the researchers are looking in the wrong place. Neurologist Fred Baughman said:

Despite regular pronouncements that its biologic roots have been discovered, no proof of a definite physical or chemical abnormality is ever found. All such research and all such claims … have been a sham, meant to create illusions of science and disease while proving nothing.

The NIMH material also did not mention there was a lack of consensus on the safety of using medication to treat children. Rather, medication is said to be a safe treatment: “Under medical supervision, stimulant medications are considered safe.” The potential for substance abuse or dependence is downplayed, saying: “there is little evidence of this.” ADHD stimulants are classified as Schedule II controlled substances, which have “a high potential for abuse, with use potentially leading to severe psychological or physical dependence.” See “ADHD: an Imbalance of Fire over Water or a Case of the Fidgets?” for more information on ADHD medications and addiction.

The consequences of a biomedical view of ADHD were addressed in a recent study by the CDC of ADHD treatment among children between 2 and 5 years of age. While the American Academy of Pediatrics and other organizations recommend behavior therapy ahead of stimulant medication for children under 5, only 53% of children had received behavior therapy in the year prior to the survey, while 47% had received stimulant medication during the previous week. Between 75% and 78.5% of children aged 2-5 with ADHD received one or more ADHD medications.

ADHD is a highly prevalent condition that can lead to poor health and social outcomes. Despite 2007 and 2011 guidelines recommending behavior therapy as first-line treatment for children aged <6 years with ADHD, during 2008–2014 only about half of children aged 2–5 years with ADHD received psychological services. To effectively mitigate impairments associated with ADHD and minimize risks associated with ADHD medications, it is important to increase the percentage of young children with ADHD who receive evidence-based psychological services, especially parent training in behavior therapy.

Around 30% of children aged 3-5 experienced adverse effects from ADHD medications. The most common ones were appetite suppression and sleep problems. But other commonly reported side effects were: abdominal pain, emotional outbursts, irritability, lack of alertness, repetitive behaviors and thoughts, social withdrawal, and irritability when the medication wears off. In one large study, of methylphenidate (Ritalin or Concerta) over 10% of children 3-5 had to stop treatment because of adverse effects. They were also 20% lower for height and 55% lower for weight. Anne Schuchat, the CDC’s Principle Deputy Director, said:

We are still learning about potential side effects of long-term use of ADHD medicine on young children. Until we know more, the recommendation is to refer parents for training in behavior therapy for children under 6 years of age with ADHD.

We recognize that these are not easy treatment decisions for parents to make. We know that behavior therapy is effective, and the skills they learn through behavior therapy can help the whole family be successful. Building these skills in parents and children both empowers families and helps young children with ADHD live up to their full potential.

An article in The Washington Post, “CDC Warns that Americans May Be Overmedicating Youngest Children with ADHD,” addressed this concern as well. The long-term effects of the drugs of choice for treating ADHD, Adderall and Ritalin, were not well studied. An estimated 2 million of the 6 million children diagnosed with ADHD were so labeled between the ages of 2 and 5. While ADHD medications don’t work for everyone, in many cases they take effect almost immediately. In contrast, behavior therapy can take several months to have an impact. However, it can be long lasting; and has no side effects.

06/21/16

Now There’s Chewable Speed

Do you have a difficult time giving your child ADHD medication? Not that you don’t want them to take it—you do. But they don’t like the taste; or they have problems swallowing pills; or they just don’t like how it makes them feel. Or maybe you’re an adult who chronically forgets to take your medication in the morning. You don’t want to carry a prescription bottle around with you. People may wonder why you are popping pills in the middle of the day. Now there is an ADHD medication that is right for you! It’s chewable and comes in fruit flavors too!

Okay, the paragraph above was a tad satirical, but it is entirely true in what it said about ADHD medication. In mid-May of 2016, Adzenys, a chewable, fruity form of amphetamine became available. As STAT reported, Adzenys XR-ODT was approved by the FDA in January of 2016 by the FDA for patients six and older. The CEO of Neos Therapeutics said they were “launching now at full speed.” They want to get “ahead of back-to-school season.”

Vipin Garg, the CEO of Neos, said the new quick-dissolving formula will help “harried mothers” get their children medicated faster in the morning before school. And if adults forget to take their pill at breakfast, they can “pop a tablet” on the way to work—it comes in a blister pack, not in a pill bottle. “You go to a pharmacy, and everything is in gummy bear format. . . . Why would that be the case if there wasn’t a need for this?” Garg sees the dissolving tabs as part of a trend to make medications more pleasant to take.

All that adds up to a booming market. Sales for ADHD medications were at $4.7 billion in 2006, had nearly tripled to $12.7 billion by last year, and are projected to grow to $17.5 billion by 2020, according to a 2015 report from market research firm IBISWorld.

Adzenys is not alone as a chewable ADHD medication. In December of 2015, one month ahead of Adzenys, the FDA approved QuilliChew for Pfizer. Similar to Adzenys, it is an extended release tablet and was approved for patients six and older. The tablet is even scored, so it can be easily halved to individualize the needs of the patient taking it. The active ingredient in QuilliChew is methylphenidate hydrochloride.

Ann Childress, the president of the Center for Psychiatry and Behavioral Medicine in Las Vegas, was quoted by Medscape as saying: “As a physician, it is important to have treatment choices for patients with ADHD and their caregivers. QuilliChew ER extended-release chewable tablets give healthcare providers an additional treatment option to meet their patients’ needs.”

Dr. Childress was a paid consultant and spokesperson for Pfizer according to ProPublica. Between August 2013 and December of 2014 she received $25,911 for “consulting”, “promotional speaking/other” “travel and lodging” by Pfizer for activities related to Quillivant XR. Looking at the archived data on ProPublica, she has had a speaking, consulting and research relationship with Pfizer for several years. She has also been paid $17,998 during the same time period for consulting and other activities by Shire, which makes Vyvanse, another ADHD medication.

Shire recently applied to the FDA to be allowed to bring a chewable Vyvanse to market. On April 14, 2016 Shire announced they had submitted a new drug application to the FDA for a chewable tablet version of Vyvanse for individuals who may have problems swallowing or opening a capsule. The existing Vyvanse capsules can be swallowed whole or opened so that the medication can be mixed into food or water. “Vyvanse chewable tablets will offer an additional administration option for patients.” The proposed indications for chewable Vyvanse would be the same as the existing uses for Vyvanse capsules—ADHD and Binge Eating Disorder. By the way, sales for Vyvanse more than doubled between 2010 and 2014, from $986 million to $2.1 billion.

Opinions are mixed on the new chewable formulas, according to STAT. Dr. Ben Biermann, an assistant professor of psychiatry at the University of Michigan, thought there was nothing revolutionary about Adzenys. “It’s simply another delivery mechanism for a medication that already exists and has widespread use.” On the other hand, Dr. Mukund Gnanadesikna, a child and adolescent psychiatrist in Napa, California, thought it was a recipe for people to request it and then sell it: ““I’m not a big fan of controlled substances that come in forms that can be easily abused — and certainly a chewable drug falls into that category.”

Both Adzenys and Vyvanse are amphetamines, as is Adderall. Quillivant and Quillichew are methylphenidate, as are Concerta and Ritalin. All ADHD stimulants are Schedule II controlled substances, meaning they have a high potential for abuse and dependence. And there are multiple potential issues when using stimulants. Here are some of the precautions noted on the Adzenys-XR-ODT medication guide: serious cardiovascular reactions including sudden death, stroke and myocardial infarction; adverse psychiatric reactions such as psychosis or mania. Other adverse reactions can include insomnia, loss of appetite, nervousness, weight loss, and agitation.

The existing and potential harm to children from stimulant medications like Adzenys and Quillichew are well documented and described by Dr. Peter Breggin on his website, breggin.com. He said too many children grow up believing they are inherently defective. The latest scientific literature indicates the potential consequences of boys aged 7-9, who were given a diagnosis of mild hyperactivity in the 1970s and treated with Ritalin. Those boys have much higher rates of early death, atrophy of the brain, suicide, psychiatric hospitalization incarceration and drug addiction than a control group of children from the same time period.

Breggin gave multiple reasons for these potentially dreadful outcomes, including the misinterpretation of adverse effects like depression, anxiety, agitation, insomnia psychosis and aggression. Instead of seeing these as adverse drug reactions, they are viewed disorders that were “unmasked” by the stimulants, which leads to further prescriptions to deal with these newly uncovered mental disorders. Embedded in his linked page are several videos he has done that explain the harmful effects and method of action of stimulants; the negative effects of diagnosing children with ADHD; and the long term consequences to children using stimulants like Ritalin.

There is more information available on the problems with ADHD medications and ADHD diagnosis on this website. Try “A Drug in Search of a Disorder”, “Pseudoscience with Vyvanse?” or “ADHD: An Imbalance of Fire over Water or a Case of the Fidgets?” Also try a search of “ADHD.”

06/10/16

Psych Drugs and Violence

A man began taking Zoloft because of some anxiety over whether he could cope with high school students as a student teacher. By the second day on Zoloft, he was having delusions. By day three, he believed aliens were hiding in the normal bodies of people all around him. He thought the alien leader had taken over his wife’s body. On the seventh day of Zoloft, he became certain that he had to kill the alien inside his wife to save himself and the world. So he drove their car full speed into a road barrier, unbuckling her seatbelt just before the crash. Finding her lying on the ground and alive after the wreck, he began to bang her head against the concrete and choke her. His wife survived, but their marriage did not.

A psychiatrist with a successful practice was stressed because of difficulties that ended up with him taking another psychiatrist to court. She in turn sued his son, who was involved in the business. He prescribed himself Prozac hoping to relieve some of his tension and raise his spirits, but that didn’t help. He sought out treatment from another psychiatrist who treated him with more antidepressants, which led to further deterioration. Eventually he was placed on Luvox—the same antidepressant one of the Columbine shooters was taking. He became increasingly incensed at the psychiatrist who countersued his son and attacked her with a tack hammer.

These are just two of the case studies described by psychiatrist Peter Breggin in his book, Medication Madness. However, you don’t have to read it to find further examples. Read about the speculation after the Sandy Hook shootings about Adam Lanza. Or read this 2010 article by Moore, Glenmullen and Furberg, “Prescription Drugs Associated with Reports of Violence Toward Others.” Thirty-one different drugs met the study’s criteria for a disproportionate association with violence. The drugs included 11 antidepressants, 5 hypnotic/sedatives, 3 ADHD drugs and varenicline (Chantix). “SSRI Stories” describes over 6,000 stories where it seems prescription drugs (primarily SSRIs) were linked to adverse outcomes, including violence. Also look at “Drugs, Violence and Revolution” or “Smoke and Mirrors” on this website.

These data provide new evidence that acts of violence towards others are a genuine and serious adverse drug event that is associated with a relatively small group of drugs. Varenicline, which increases the availability of dopamine, and serotonin reuptake inhibitors were the most strongly and consistently implicated drugs. Prospective studies to evaluate systematically this side effect are needed to establish the incidence, confirm differences among drugs and identify additional common features.

Several years ago I attended a conference and heard a presentation by Yolande Lucire on her research into the association of violence and psychiatric medications. At the time I found her presentation both fascinating and concerning in that she thought she had identified a biomedical association between antidepressant medications and some perpetrators of violence. Could there actually be medical evidence of an association between antidepressants and violence? But I didn’t hear anything more about this finding, despite the parade of case studies and anecdotes like those above that did suggest a connection. Then I saw where she was the coauthor of an article in the April 2016 issue of Forensic and Legal Medicine, describing a forensic investigation of three individuals who committed homicide, two of which also intended suicide while taking antidepressants.

The article by Eikelenboom-Schieveld, Lucire and Fogleman was a forensic investigation of three cases they believed to be instances of antidepressant-induced akathisia-related homicide. They suggested that mutations in the CYP450-encoding genes of these individuals contributed to problems metabolizing psychiatric medications and were thus contributing factors to their homicides. The cytochrome P450 family of enzymes is responsible for metabolizing most of the drugs used in psychiatry. “These individuals also had diminishing mutations in the CYP450 family of metabolizing enzymes and all were taking medicines that further decreased metabolism by inhibition.”

None of the three individuals knew they were supposed to take their medication regularly or how to stop taking it safely; and none of them improved on the medications. In addition, none of the prescribers recognized their complaints as adverse drug reactions. Nor were they aware of any impending danger from their patients. Interviews with the individuals indicated they had struggled with akathisia (agitation or distress), confusion, delirium, euphoria, extreme anxiety, obsessive preoccupation with aggression, and an incomplete recall of events. Impulses to kill were acted on without warning. Upon recovery, they all saw their actions as out of character. Their beliefs and behaviors horrified them.

They were all prescribed medications that interacted with one another and one person combined these with alcohol. The drug-to-drug interactions further decreased their metabolizing capacity and increased their risk for adverse events by prolonging the half-life of the medications and raising their blood levels.

Fast-changing levels of psychotropic substances, up or down, can cause behavioural changes, as the neurotransmitters in the brain react to reach some equilibrium. This phenomenon makes starting and stopping medication the most dangerous times for suicide and violence, but both can happen at any time, with stress, provocation, dose change, addition or subtraction of a medication. These toxic responses to antidepressants may occur early or later in treatment.

When reading this paper, I saw that Dr. Lucire had previously published an article in 2011 on anti-depressant-induced akathisia-related homicide and the CYP450 genes. In Lucire and Crotty they found that CYP450 allele frequencies were higher in those individuals who had experienced akathisia/serotonin toxicity after taking psychiatric medications. They presented ten cases whose the use of antidepressants had not mitigated their distress. Every person’s emotional reaction worsened while their treating physician attempted a “trial and error” method of increasing doses and then changing to another antidepressant when the previous one did not work.

The symptoms of antidepressant drug toxicity were not recognized as such by the subjects or their physicians. In many cases, the dosage of the antidepressant was increased while other medications were given to address the side effects Frequently the adverse effects were compounded.

In some cases the violence ensued from changes occasioned by withdrawal and polypharmacy. In all of these cases, the subjects were put into a state of drug-induced toxicity manifesting as akathisia, which resolved only upon discontinuation of the antidepressant drugs.

This paper has detailed and substantiated in specific terms how the metabolism of each of the antidepressant drugs used by the subjects would have been seriously impaired both before and at the time they committed or attempted homicide. They were experiencing severe reported side effects, adverse drug reactions due to impaired metabolism complicated by drug–drug interactions against a background of variant CYP450 alleles.

Eikelenboom-Schieveld, Lucire and Fogleman concluded that CYP450 was an important factor for determining who could tolerate a drug or combination of drugs from who could not. “Testing for cytochrome P450 identifies those at risk for such adverse drug reactions.” They hoped that as awareness of the biological causes of these disastrous side effects became more known, justice would be better served for both the victims and perpetrators of akathisia-related violence. “The medicalization of common human distress has resulted in a very large population getting medication that may do more harm than good by causing suicides, homicides and the mental states that lead up to them.”

03/29/16

Tip of the ADHD Iceberg

Stimulant medications prescribed to children with ADHD are known to cause hallucinations and psychotic symptoms. The risk of these adverse events was widely thought to be minimal, but a recent study published in the journal Pediatrics suggests that is not the case. MacKenzie et al. reported that psychotic symptoms were found in 62.5% of youth who had taken stimulants versus 27.4% of individuals who had never taken stimulants. The researchers said this association was still significant even after potential confounding variables were controlled.

Mad in America noted in “ADHD Drugs Linked to Psychotic Symptoms in Children” that clinical trials used to test the safety and efficacy of stimulant medications such as Adderall, Ritalin and Vyvanse estimate that only 1-2% of children on stimulants have such a reaction. MacKenzie et al. suggested these underestimates were partly because researchers often rely upon participants to self-report these symptoms, which leads to significant underreporting. Among the children diagnosed with ADHD in the study, 11 of 17 (65%) treated with stimulants experienced psychotic symptoms, while only 4 (25%) of the 16 who were not treated with stimulants had such symptoms.

The children included in the MacKenzie et al. study had at least one parent with a diagnosis of major depression, bipolar disorder or schizophrenia. However, “the association between stimulants and psychotic symptoms remained consistent after the researchers controlled for other risk factors, age, gender, and parent diagnosis.” The researchers were also able to confirm that the occurrence of the symptoms coincided with the time when the children were actively taking stimulant medications. They concluded:

We report an association between the use of stimulant medication and psychotic symptoms in children and adolescents at familial risk of mental illness. The association of current use of stimulants with current psychotic symptoms and the close temporal relationship between stimulant use and psychotic symptoms in youth who started and stopped stimulants indicated a potential causal relationship. The findings suggest that psychotic symptoms may be relatively common adverse effects of stimulants in youths with a family history of major psychiatric disorders.

In “Psychotic Symptoms in Children on Stimulants,” Dr. Lydia Furman, an Associate Editor for Pediatrics, said the study put a microscope on the subpopulation of children with an ADHD diagnosis, whose risk of psychotic symptoms is substantially higher. She added that the study was just the tip of the iceberg with regard to ADHD diagnosis, stimulant treatment and the risk in adulthood of psychotic disorders or episodes. She cited a study by Moran et al. that demonstrated how adult individuals with psychotic disorders, who were exposed to stimulants in their youth, had a significantly earlier age of onset of psychosis than those who were unexposed.

But Furman seems more interested in seeing ADHD diagnosis as an increased risk factor for adult diagnosis of psychotic disorders, rather than looking at the evidence of how stimulant medications seem to trigger or increase the risk of psychotic symptoms. She commented that an additional body of evidence suggests that ADHD diagnosis in childhood is associated with an increased risk of adult diagnosis of psychotic disorders, and then referenced two studies: Rho et al. and Dalsgaard et al. It wasn’t clear to me from the abstracts that stimulant medication as a confounding variable was controlled for in either study.

Given that the MacKenzie study found the symptoms of psychosis occurred during the active use of stimulant medication, and that the association remained even after the researchers controlled for risk factors including parental diagnosis, it seems the more significant results were that using stimulant medication may trigger hallucination and psychotic symptoms more frequently than has been previously reported.

Cherland and Fitzpatrick reported in a 1999 study, “Psychotic Side Effects of Psychostimulants,” that 6% of children developed psychotic side effects from methylphenidate (Ritalin). They also indicated their findings likely were an underestimate in the prevalence. Significantly, the symptoms stopped as son as the medication was discontinued. No psychotic symptoms were reported among children diagnosed with ADHD who did not receive medication.

Dr. Peter Breggin also reported the danger of ADHD medications triggering symptoms of psychosis in his article for International Journal of Risk & Safety in Medicine. He noted how several studies have compared stimulant-induced psychoses to the symptoms of schizophrenia. Methylphenidate has even been used to experimentally produce or worsen psychotic symptoms in adults diagnosed with schizophrenia. He commented that psychoactive drugs would tend to produce psychosis at a higher rate in children than in adults.

In his “Simple Truths About Psychiatry” series of videos on YouTube (Simple Truth 7 and Simple Truth 8), Dr. Breggin said stimulant drugs don’t fix or cure anything. They actually cause biochemical imbalances in the brain that make children docile, and take away their spontaneity. This adverse effect is then interpreted as a positive effect. I agree with Breggin that these drugs should never be given to children. Ultimately, he asserted that children who are raised on stimulant drugs will never know who they really are. “Since you’re messing up several neurotransmitters in the brain, you’re going to be causing life-long changes in the child’s brain.”

An NIH-funded study by Collins and Clearly found there has been a 43% overall increase in the diagnosis of ADHD since 2003. Among children between the ages of 10 and 14 the increase was 47%, and 52% among adolescents aged 15-17. There were increasing trends for all racial/ethnic groups, most notably among Hispanics, where the increase in ADHD diagnosis was 83% from 2003 to 2011. Dr. Clearly hedged his bet, saying that the reported increase could be a true increase in ADHD or it could be the result of a tendency to over-diagnose the condition. “Additional studies must be done to identify the underlying cause of the increase.”

In the meantime, his advice was for parents to “talk to your doctor.” That is often pharma-speak for “get a prescription.” We may be just beginning to see the tip of the iceberg of consequences from ADHD medications.

03/8/16

Chemical Straightjackets for Children

In a five-minute video, “Stop the Psych Drugging of Children—Now!, Dr. Peter Breggin made some alarming statements about the consequences of several decades of giving children psychiatric drugs. He said we have parents who believe their children are incorrigible. And we have children who grow up thinking they are defective and need psychiatric drugs. Many of the children who started out with a mere ADHD diagnosis when they were younger are growing up to be “career mental patients, taking multiple psychiatric drugs.” In an article he published in the journal Children & Society, Breggin reviewed in more detail many of the concerns he just touched on in his video. Here, I want to look at the growing problem of using antipsychotics with children.

Mad in America reported that a study published in JAMA Psychiatry indicated that the majority of children, adolescents and young adults who are prescribed antipsychotic medications have not been diagnosed with a mental disorder. “Most of the younger children (60.0%), older children (56.7%), adolescents (62.0%), and young adults (67.1%) treated with antipsychotics had no outpatient or inpatient claim that included a mental disorder diagnosis.” Among the children who do have a diagnosis for a mental disorder, many of them are being prescribed antipsychotics off label.

In other words, while antipsychotics are only approved to treat children diagnosed with schizophrenia and bipolar disorder, children with diagnoses like ADHD are being given these powerful drugs to “treat” their behavior problems. In addition, very few of the children receiving antipsychotics also receive psychotherapeutic care. Mark Olfson, the lead author of the study said:

Relatively few of these young people are receiving psychotherapy. We may need to put greater effort into increasing access to psychosocial interventions that can treat symptoms and behaviors that are currently being addressed with antipsychotic medications.

In the same issue of JAMA Psychiatry in which the Olfson et al. article was published, Drs. Carroll and Blader acknowledged in “Antipsychotic Use in Youth Without Psychosis” that the use of antipsychotic medications has been increasing since the mid-1990s. They added this pattern was most pronounced in the U.S. They affirmed evidence suggests that second-generation antipsychotic use was chiefly with children with aggression and behavioral problems, ADHD, and disruptive behavior disorders. “Although antipsychotics are clearly effective for aggressive behaviors … other interventions with lower adverse effect burdens, when implemented adequately, can avert the need for antipsychotic treatment.”

Reporting for the StarTribune, Gail Rosenblum noted that in 2014 20,000 prescriptions for antipsychotic medications were written for children 2 and younger. According to IMS Health, a healthcare data company, that was a 50% increase over the year before. Turn to the article to see a photo of a child playing with Lego-like blocks branded with “Risperdal” at a pediatrician’s office.

IMS found that at least 10,000 children, ages 2 and 3, were prescribed medications such as Adderall to treat attention deficit hyperactivity disorder (ADHD). The protocol falls outside of American Academy of Pediatrics guidelines. Children younger than age 2 received prescriptions for risperidone (commonly known as Risperdal), quetiapine (Seroquel) and the antidepressant Prozac.

In his Children & Society article, Dr. Breggin noted where the so-called second-generation antipsychotics cause the same adverse effects as the older antipsychotics. These adverse effects include: “lobotomy-like indifference and apathy, Parkinsonian symptoms, akathisia, dystonia, tardive dyskinesia, neuroleptic malignant syndrome, gynecomastia [enlarged breasts in men] and other sexual dysfunctions.” Tardive dyskinesia (TD), a movement disorder caused by antipsychotic drugs, is a major threat to children, according to Breggin. TD can effect any muscle functions that are wholly or partially under voluntary control. That includes the face, eyes, tongue, jaw, neck, back, abdomen, and more. Here are two videos of what TD looks like in a child. The first is a girl after she stopped taking her medications, presumably because of the TD. The second one is of another young girl trying to fall asleep.

Even ‘mild’ cases of eye blinking or grimacing can humiliate, stigmatize and isolate a child. More severe cases disable children with painful spasms in the neck and shoulders, abnormal posture and gait, or constant agitated body movements.

Additional concerns with the newer antipsychotics include a potential predisposition to heart disease and early death; weight gain and obesity; elevated blood sugar and diabetes; elevated blood lipids and atherosclerosis, and high blood pressure.

The New York Times published an article by Alan Schwartz, that looked at the growing practice of giving antipsychotics to children under the age of 2. His introductory case illustration was a boy who was first prescribed the antipsychotic Risperdal when he was 18 months of age. His mother indicated that she was never told of the potential risks to her son with Risperdal. “It was just ‘Take this, no big deal,’ like they were Tic Tacs,” said Genesis Rios. The prescribing doctor declined to be interviewed by the NYT.

Cases like that of Andrew Rios, in which children age 2 or younger are prescribed psychiatric medications to address alarmingly violent or withdrawn behavior, are rising rapidly, data shows. Many doctors worry that these drugs, designed for adults and only warily accepted for certain school-age youngsters, are being used to treat children still in cribs despite no published research into their effectiveness and potential health risks for children so young.

Schwartz reported that almost 20,000 prescriptions for antipsychotics such as risperidone (Risperdal) were written for children 2 years old and younger in 2014. This was a 50% jump from the year before. As a side note, prescriptions for the antidepressant fluoxetine (Prozac) rose 23 percent in one year for the same age group. A dozen experts in child psychiatry had never heard of children younger than 3 getting such medication and had difficulty explaining a reason for it. Dr. Martin Drell, a former president of the American Academy of Child and Adolescent Psychiatry said he was “hard pressed to figure out what the rationale would be.” Dr. Ed Tronick, a professor of developmental and brain sciences at the University of Massachusetts said:

I think you simply cannot make anything close to a diagnosis of these types of disorders in children of that age. . . . There’s this very narrow range of what people think the prototype child should look like. Deviations from that lead them to seek out interventions like these. I think it’s just nuts.

The American Academy of Pediatrics and the American Academy of Child and Adolescent Psychiatry have not taken a stand for or against the practice. They have no guidelines or position statements on the use of antidepressant or antipsychotics with children younger than 3. One possible factor in their silence is there are no formal trials in infants and toddlers with these medications. Dr. Mary Gleason a pediatrician and child psychiatrist at Tulane University School of Medicine said children with ages measured in months have brains whose neurological development was occurring at too rapid of a rate—and in still unknown ways—to risk using medications that could profoundly influence that growth. “There are no studies … and I’m not pushing for them,” said Dr. Gleason.

In an article for Psychiatric Services, psychiatrists at Dartmouth expressed concern about the increasing numbers of children being prescribed antipsychotic medications. In an article summarizing the concerns of the authors, Mad in America quoted them as saying:

The crux of the issue is this: Children in the United States have increasingly been prescribed antipsychotic medications despite potentially serious short- and long-term side effects. . . . Yet other efficacious and safer interventions are available. . . . We should be concerned about overuse of antipsychotics for many reasons. Children are inherently vulnerable because their brains and bodies are still developing and may be permanently altered by powerful medications. . . . Their disruptive behaviors are often related to disruptive parenting and stressful environments, which deserve primary attention. Adults may be motivated by the desire to achieve short-term control of behavior rather than to enhance children’s long-term growth and development.

Daviss et al. recommended five changes to reduce the use of antipsychotics in children. First, there is a need for preventive care that addresses socioenvironmental problems. Second, mental health professionals need to become more aware of the dangers of using antipsychotics in children as well as the availability of evidence-based therapies and interventions. Third, clinical guidelines need to be developed along with steps to ensure compliance with those guidelines. Fourth, there should be shared decision making when treating children with these medications. “Clinicians, patients, and parents all need better information on antipsychotics and should all be involved in deciding on appropriate treatment methods.” And fifth, education programs regarding these concerns are needed to reach the agencies and counselors who take care of and support vulnerable children.

Dr. Gleason commented that people are trying to do the best they can with the tools available to them. “There’s a sense of desperation with families of children who are suffering, and the tool that most providers have is the prescription pad.” These children and families deserve better than a choice between trying to cope with the behaviors they see their child struggle with, and using a chemical straitjacket with the potential of long-term cognitive and physiological harm.

02/26/16

Hollow Man Syndrome

On her blog Joanna Moncrieff reflected on a memory she has of a young woman she encountered as a medical student in the 1980s who was confused and frightened when first brought to the hospital. She thought she was being watched and manipulated by evil forces. She believed there was something implanted in her body. Put on an antipsychotic, she became increasingly quiet as the dose was increased. But she also became emotionless, expressionless and physically sluggish. To Joanna, the woman seemed “empty and lifeless compared to what she had been before, although she was less distressed.” This was seen as making her ‘better.’

That reminded me of a young man I knew briefly around the same time who had a psychotic episode, triggered by his heavy use of marijuana. At least, that was his theory. My impression of him after his release from the hospital, where he also began using an antipsychotic, was that his personality had withered; he’d become a hollow man. A few years ago, I met briefly with someone trying to reclaim their thinking ability after taking lithium for over fifteen years. They wanted to cut back on the levels of lithium they were taking. We began working on that plan, but they kept getting caught up in a cognitive eddy of fear that they were going to lose their salvation. Was that psychosis or impaired thinking from the medication?

Another time I was concerned that after a first time manic episode an adolescent would remain on a maintenance dose of an antipsychotic for the rest of his/her life. Over time I convinced the family to transfer care to a psychiatrist willing to taper the teen off the antipsychotic. The person’s dose was initially halved and symptoms of mania emerged within ten to fourteen days of the initial taper. Was that a suppressed bipolar disorder emerging or was it a reaction to too steep an initial taper? The reaction was viewed by the family as a manifestation of the bipolar disorder that had been kept at bay by a low maintenance dose of the antipsychotic. They decided to stop counseling with me.

These and other experiences have led to the several articles I’ve written on the complications and dangers of antipsychotic medications. Reading the thoughts of psychiatrists like Joanna Moncrieff, Peter Breggin, and David Healy and others on Mad in America over the years had an effect as well. I appreciate the approach of Dr. Moncrieff, who said: “There are times when the use of antipsychotic drugs seems to produce just enough suppression that people can put aside their psychotic preoccupations, and re-establish a connection with the outside world.” Yet she can still see where “they produce an artificial state of neurological restriction,” like a chemical straightjacket.

In my view antipsychotic drugs can be useful in suppressing psychotic symptoms, and sometimes, when people are beset by these symptoms on a continual basis, life on long-term drug treatment, even with all its drawbacks, might be preferable to life without it. But most people who experience a psychotic breakdown recover. [Emphasis added] In this situation, antipsychotics are recommended not on the basis that they provide relief from severe symptoms, but because they are said to reduce the risk of relapse.

The Cochrane Collaboration published a review of antipsychotic maintenance treatment for schizophrenia in 2012. Their report was the first systematic review comparing the effects of all antipsychotic drugs to placebo for maintenance treatment. This is standard care after an acute phase of schizophrenia to prevent relapse. (And it seems, if a teenage manic episode is suspected of being a latent bipolar disorder) Not surprisingly, they found that antipsychotics were more efficacious than placebo in preventing relapse, especially at seven to 12 months. But they noted it was rare to find a study that did follow up longer than 12 months.

Randomised controlled trials (RCTs) since the 1950s have consistently shown that antipsychotic drugs effectively reduce relapses and need for hospitalisation. Conversely, they are, as a group, associated with a number of side effects such as movement disorders, weight gain and sedation.

Moncrieff pointed out two additional problems with these kinds of comparisons. First is the fact that they don’t compare people started on long-term medication treatment and people who were drug free in the placebo groups. Rather, the latter group consists of people who are withdrawn from long-term antipsychotics. Usually the taper or withdrawal occurs too quickly, precipitating discontinuation symptoms, like with the teen I described above. “The difference in relapse rates is almost certainly exaggerated in these studies, therefore, especially since relapse is often defined only in terms of a modest deterioration in general condition or symptoms.”

Another problem is there is typically little data in the studies on anything other than the so-called “relapse,” which is too loosely defined in most studies. So global functioning could be worse for people on continuous drug treatment than they would have been without it, even if they did experience a relapse. “Since the data has not been collected, we just don’t know.”

The first problem perpetuates a distorted message of how antipsychotic medications prevent relapse. The second problem means there is no information on whether someone might be better off if they didn’t use medication.

Moncrieff recently published an article in PLOS Medicine that called for a rethinking of antipsychotic maintenance: “Antipsychotic Maintenance Treatment: Time to Rethink?” Her summary points in the article were:

Existing studies of long-term antipsychotic treatment for people with schizophrenia and related conditions are too short and have ignored the impact of discontinuation-related adverse effects.
Recent evidence confirms that antipsychotics have a range of serious adverse effects, including reduction of brain volume.
The first really long-term follow-up of a randomised trial found that patients with first-episode psychosis who had been allocated to a gradual antipsychotic reduction and discontinuation programme had better functioning at seven-year follow-up than those allocated to maintenance treatment, with no increase in relapse.
Further studies with long-term follow-up and a range of outcomes should be conducted on alternatives to antipsychotic maintenance treatment for people with recurrent psychotic conditions.

She described a long-term randomized controlled trial (RCT) by Wunderlink et al. in the Netherlands (in this article as well as in her blog) that confirms how long-term antipsychotic use will impair a person’s ability to function. The study also showed that when you gradually reduce people’s antipsychotics in a supportive manner, they are better off in the long-term.

This study should fundamentally change the way antipsychotics are used. These are not innocuous drugs, and people should be given the opportunity to see if they can manage without them, both during an acute psychotic episode and after recovery from one. If psychiatrists had not forgotten the lessons of the past, and if they had been prepared to acknowledge what they saw the drugs doing with their own eyes, this would have come about long ago.

The studies used to justify current clinical practice don’t provide reliable data on the pros and cons of long-term antipsychotic therapy. More research is needed to evaluate the efficacy of a gradual and individualized approach to antipsychotic discontinuation. Assessment of outcomes in addition to relapse is needed. Moncrieff recommended that while we await the results of further long-term discontinuation studies, that we reconsider antipsychotic maintenance treatment as the default strategy for people with recurrent psychotic disorders.

In “Psychiatric Drug-Induced Chronic Brain Impairment,” Peter Breggin described how chronic brain impairment (CBI) from chronic exposure to psychiatric drugs produces effects similar to those from a traumatic brain injury. He drew a parallel of effects between electroshock treatment, closed head injuries from repeated concussions (like what was portrayed in the movie, Concussion), and long exposure to psychiatric drugs:

The brain and its associated mental processes respond in a very similar fashion to injuries from causes as diverse as electroshock treatment closed head injury from repeated sports-induced concussions or TBI in wartime, chronic abuse of alcohol and street drugs, long-term exposure to psychiatric polydrug treatment, and long-term exposure to particular classes of psychiatric drugs including stimulants, benzodiazepines, lithium and antipsychotic drugs.

He said that by recognizing CBI, clinicians can enhance their ability to identify individuals who need to be withdrawn from long-term psychiatric drug treatment. Most patients show signs of recovery from CBI early in the withdrawal process. “Many patients, especially children and teenagers, will experience complete recovery.” With others, recovery could take place gradually; sometimes over years. Even when recovery is incomplete, Breggin said most patients wish to remain on reduced medication or none at all.

The symptoms of this syndrome include (1) Cognitive deficits, often first noticed as short-term memory dysfunction and impaired new learning, and difficulty with attention and concentration; (2) Apathy, indifference or an overall loss of enjoyment and interest in life activities; (3) Affective dysregulation, including emotional lability, loss of empathy and increased irritability; (4) Anosognosia or a lack of self-awareness about these changes in mental function and behavior.

12/2/15

Deep Brain Problems

Danielle Egan opened her article for Mad in America on the adverse effects of deep brain stimulation (DBS) with a quote from a DBS patient named Jim: “I just want the thing out. . . . It could be harming my brain and it’s certainly doing a lot of psychological harm to me. It’s a very real presence and I can feel the wires under my skull and at my neck. After two years of this, I just want to be done with it.” Jim is one of around 272 people worldwide who have had these experimental implants to treat psychiatric disorders such as depression, OCD and Tourette’s syndrome.

Egan has been investigating DBS and writing about individuals who have had the surgery for a number of years. Jim is just one of several people she’s met and interviewed. You can read about several of these individuals on her website under the “neuroscience” heading of her blog. The first DBS surgical procedure for depression occurred in 2003. It has been used and approved previously as a treatment for movement disorders like Parkinson’s. At first, the news about this technique was almost wildly positive. See “Deep Brain Jolts.”

In a 2005 interview for the NPR program “All Things Considered,” Dr. Helen Mayberg, reported that four out of six patients were relieved of intractable depression with her DBS procedure. “At six months, the four patients that responded to this treatment were actually near remission … meaning they weren’t just better, they were well.” Mayberg and her research colleagues reported their finding in the March 2005 issue of Neuron. Reporting on Mayberg’s research for Scientific American, John Horgan attended a lecture she gave in March of 2014 where she was still describing promising results. But according to Horgan, she “buried the lead” by mentioning midway through her talk that a multi-center trial of her method of DBS had been halted by the FDA.

This meant that the FDA suspended the BROADEN trial because it failed a “futility analysis,” meaning it did not appear to have a reasonable chance of improving upon current treatments.

As Egan related in her article, advocates of DBS still have no clear sense of what its mechanism of “therapeutic” action is, even though it has been studied since the 1980s. When treating depression, Mayberg’s method targets an area of the brain known as the subgenual cingulate gyrus (Cg25). In theory, DBS is reversible; so it was thought to be a better way to inhibit brain activity than the permanent lesions of psychosurgery. But so-called “micro-lesions” from the surgery and the DBS implants have been found. Long-term studies of Parkinson’s patients treated with DBS have shown they have DBS-related scar formation in their brains. There have been serious mood, behavior and personality changes documented as well.

These include suicide, depression, apathy, fatigue, mania and serious impulse control issues, such as hypomania, aggression, addiction (to gambling, shopping, drugs, alcohol) and hypersexuality, sometimes resulting in criminal behaviour, including pedophilia.

Because of the area of the brain targeted by DBS treatment for psychiatric disorders, the cerebral cortex, the risks are likely to be more pronounced than with Parkinson’s. Within the cerebral cortex are a variety of cognitive functions, such as learning, sorting and rationalizing input from the inner and outer world. It is also the seat of human personality, with associations to mood, decision-making, impulse control and other behaviors. The Cg25 area is also thought to be linked to self-esteem, motivation, reward-based thoughts and moral decision-making. “Clinical studies have linked tissue damage in the Cg25 with disinhibition, which is associated with frontal lobe brain damage causing poor impulse control.”

Mayberg et al.’s 2005 study did post-operative PET scans showed decreased activity in the Cg25 area, which was believed to be a positive inhibiting effect. But blood flow increased in other areas, especially the brain stem, where mechanisms like heart rate, breathing anxiety and euphoria are regulated. Other studies have shown these blood flow changes to be connected to mania, dementia, psychosis and dissociation.

Returning to Jim, he had no idea that the sponsor of the BROADEN clinical trial he was in terminated it because it failed to reach a benchmark of a 50% response rate as measured by the Hamilton Depression Scale. Beside his cognitive issues, Jim had extreme sleep problems that began about six months post-implant. Eventually he sought out a sleep disorder specialist who diagnosed him with REM Behavior Disorder. This means the brain functions just as it does during consciousness, without the muscle paralysis that come with REM sleep.

“I’d have night terrors and catatonic sleep, like narcolepsy; it would just come over me in the middle of the day and I’d have 20 minutes to get somewhere safe before it took over and knocked me out; my wife couldn’t even wake me up. That happened four or five times per week.”

Eventually Jim returned to his study center to have the device turned off. His thinking began to clear up. His sleep problems almost disappeared. “But I want this thing out.” When he signed up for the trial, his consent from said that DBS was reversible by removing the implant. But when he registered for the followup study, its consent form said: “In some cases the device is not removable.” The complexity of the frontal cortex with its connection with so many other regions of the brain seems to be the reason. The surgeon explained that the leads (wires) from the device may be too tense and “they might have to leave them there.”

Jim had his “explant” surgery, a four-hour surgery instead of a routine one-and-a-half hour outpatient procedure. “I guess the surgeon had to do a bit of prying.” A part of the device that fits into the skull gave the surgeon trouble because bone and tissue had knitted together around it. His head was throbbing; as was the skin around where the pacemaker had been implanted in his chest. I feel like the DBS broke my brain; it broke something in me. . . . But I need to put what happened behind me. I’m just relieved it’s out.”

After John Horgan published his March 2014 story mentioned above, he was contacted by Steve Ogburn, who had also been a patient in the BROADEN trial. He quoted Steve as referring to himself as ‘colatteral damage’ from the study in a May 2014 article. Steve had his surgery at Stanford in November of 2012. He developed severe head pain three months into the study. The leads were 18 inches too long, and had been coiled up in his chest and the top of his head. He could feel them externally. He had “bowstringing” a condition where scar tissue forms around the leads. This has been documented in others DBS cases and can cause permanent complications. He had problems with shoulder and jaw muscle atrophy, spinal accessory nerve palsy and occipital nerve palsy. Steve is pursuing a lawsuit against St. Jude (the medical device company), Stanford University, Stanfords’s IRB (institutional review board), and the neurosurgeon who did the DBS implant. You can watch a 15-minute video of Steve telling his story. A link is embedded in Danielle Egan’s article and in Horgan’s May 2014 article.

In July of 2015 John Horgan reported on a second DBS clinical trial failure, now with the medical device developed by Medtronic. A team from Massachusetts General Hospital led by Darin Dougherty tested 30 subjects with treatment resistant depression; half received DBS and half received a placebo treatment. There was not a significant difference in response rates between the DBS and the placebo subjects. Dougherty said: “The bottom line is that we can’t separate out active treatment from placebo.”

“The Dr. Peter Breggin Hour” podcast for 9.30.15 was a conversation between Peter Breggin and Danielle Egan on many of the issues discussed here and covered in her Mad in America article. The podcast is also available free through iTunes. Egan said in the podcast that after she learned of the original Canadian trial study conducted by Dr. Mayberg (before she went from Canada to Emory University in Atlanta), she tried repeatedly to contact the individuals involved in the Canadian study with no success. It was only in 2015 after Steve Ogburn helped, was she able to interview some of those individuals.

DBS is not going away, despite what is reported here. Emory University published a press release touting the positive results of Mayberg’s continued research with DBS. A woman has a new life, “After three decades of severe depression and trying nearly every treatment, deep brain stimulation helped [her] reclaim her life and regain the ability to feel joy.” Horgan noted that the press release didn’t mention the two failed DBS clinical trials.

Faith Seeking Understanding

Charles Sigler, D.Phil.

Tag: Peter Breggin