Critical Psychiatry Textbook, Chapter 8: Depression and Mania (Affective Disorders) (Part Nine)

Editor’s Note: Over the next several months, Mad in America is publishing a serialized version of Peter Gøtzsche’s book, Critical Psychiatry Textbook. In this blog, he describes more harms caused by depression pills, including akathisia and its connection to homicide, as well as dementia and sexual dysfunction. Each Monday, a new section of the book is published, and all chapters are archived here.

More about SSRIs and SNRIs causing homicide

Some critical psychiatrists believe that the suicide risk has been better documented than the homicide risk. Perhaps so, but the main reason is that SSRIs and SNRIs cause suicide much more commonly than they cause homicide, which is therefore more difficult to prove.

The evidence, which I have described in detail in another book,^7:103 is nonetheless overwhelming.^{2,6,7,21,401,402}

The main mechanisms of action are that depression pills can cause akathisia, emotional blunting and psychosis. Many people who have committed homicide were, by all objective and subjective measures, completely normal before the act, with no precipitating factors; they had akathisia; and they returned to their normal personality when they came off the offending drug.^135,402

There are numerous reports in the literature and on websites that people of all ages have killed other people or came close to it after having experienced akathisia. Many of these people were healthy and had been prescribed the drug for non-disease-related reasons, e.g. for fun, stress, distress, insomnia, worry, harassment at work, family problems, or economic problems.^2,6,277,402

In many cases, the treatment provided by the psychiatrists constituted medical malpractice and contributed directly to the violent actions. I was an expert witness in a double homicide case in Holland in 2016^255:114 and emphasized in my written statement that professional malpractice played a crucial role. A mother had killed her two children while she had indisputable symptoms of akathisia on paroxetine but her pleas for help were ignored. After three months on the drug, the mother became suicidal but instead of withdrawing it, her psychiatrist advised continued use.

The mother told two people about nightmares where she slit her children’s throats (which she ultimately did, and also tried to commit suicide). Two days prior to the homicides, she reported to her “supervisor” that she was ill and told several people that she was not feeling well. She also went to her family doctor (who had prescribed paroxetine) with her complaints and visited her company doctor, who dismissed her. Finally, she contacted her psychologist, who did not have time for her.

It was a gruesome story. She was not herself, which a forensic psychiatrist confirmed three days after the homicides. And her doctors continued to harm her. They stopped paroxetine abruptly when she was in the psychiatric penitentiary six months after the homicides, causing serious harm that persisted for five months. She got a long jail sentence but questions were raised in parliament about whether the judicial system in Holland was too harsh. Indeed. She should have been freed for reason of drug-induced insanity.

The expert for the prosecution, Anton Loonen, did not have any good arguments against my testimony, which included a criticism of his own report to the court. In the middle of the proceedings, he suddenly handed over a document to the court where he had written in Dutch that he suspected I suffered from a mental disorder that made me seriously disinhibited and advised that I should be examined by a doctor in order to protect myself from myself. This was the third time I had been “diagnosed” by someone with a psychiatric background who did not know me and had not examined me but had some grudge against me.

Another example of medical malpractice is a 26-year-old woman who tried to kill her two children on two occasions.^7:105,402 She was prescribed paroxetine for stress but experienced an episode of rage and attempted suicide and then stopped taking the drug. Despite this, she was prescribed paroxetine again two years later and was reassured about its safety. This time she experienced intense restlessness, surges of rage and anger, panic attacks, impulsive spending sprees, and constant suicidal ideation. She overdosed and was admitted to hospital where the paroxetine dose was increased.

She tried to kill herself again and was diagnosed with an “adjustment disorder.” She was switched to venlafaxine, and after each dose increase, she was unable to get out of bed (akinesia). Her mental state deteriorated and violent outbursts and suicidal ideation became frequent and severe. Unable to stay in one place, she drove several hundred miles with her children and tried to kill them and herself by car exhaust. A few days later she tried to kill her children and herself again.

There were no interacting drugs in her regimen and many of the harms described in the product information for venlafaxine fit well with her experiences, e.g. intentional injury, malaise, suicide attempt, depersonalisation, abnormal thinking, akathisia, apathy, ataxia, CNS stimulation, emotional lability, hostility, manic reaction, psychosis, suicidal ideation, abnormal behaviour, adjustment disorder (which became a psychiatric diagnosis for her, although it was a drug harm), akinesia, increased energy, homicidal ideation, and impulse control difficulties.⁴⁰²

In 2001, for the first time, a jury found a drug firm liable for deaths caused by a depression pill, paroxetine.^7:106 Donald Schell, aged 60, had been taking it for just 48 hours when he shot and killed his wife, his daughter, his granddaughter and himself.⁴⁰³ Central to the case were SmithKline Beecham internal documents showing the company was aware that a small number of people could become agitated or violent from paroxetine but did not warn about it. Company documents stamped “confidential” showed that some volunteers experienced anxiety, nightmares, hallucinations and other harms—definitely caused by the drug—within two days of taking it, and two of the volunteers attempted suicide after 11 and 18 days, respectively.

However, GSK, which took over SmithKline Beecham, lied blatantly. Even in 2011, ten years after the verdict, GSK denied that paroxetine can cause people to commit homicide or suicide and that there are withdrawal problems.⁴⁰⁴

On the internet, there is a collection of media stories of massacres, homicides, suicides, and school and college shootings that involve depression pills and ADHD drugs.⁴⁰⁵

Does the disease or the pills increase the risk of dementia?

Three textbooks warned that depression doubles the risk of dementia,^{17:358,18:126,20:429} and another book noted that some patients with recurrent depression develop dementia.^16:260 We are also told that if the depression is not treated, the risk increases for new depressions and permanent reduction in the ability to concentrate.^{17:358,18:126,18:237}

Only one book had any references to the claim that depression doubles the risk of dementia.^20:429 There were two. The first was to a Danish register study that compared patients admitted to a psychiatric ward with mania or depression with patients who had osteoarthritis or diabetes.⁴⁰⁶ The authors argued that treatment of the two latter conditions was not known to increase the risk of cognitive dysfunction, but they said nothing about the risk with psychiatric drugs. They adjusted their analyses for various confounders and noted that drug abuse and alcohol increased the risk of dementia.

In the discussion section, they quoted another researcher who suggested that treatment for depression might increase the risk of dementia. But the Danish researchers had no data on treatment for their own study. They tried to circumvent this essential problem in a most remarkable way:

“If treatment explained the findings in our studies of an increased risk of developing dementia in affective disorder (hypothesis 1), then this treatment should be given for long periods of time to patients with unipolar or bipolar disorders. Antidepressants are usually only given for short periods in patients with bipolar disorder (Frances et al., 1998), however anxiolytics may often be given to both patient groups for a longer time. As indicated by Jorm, the literature is inconsistent as benzodiazepine use has been associated with cognitive decline (Prince et al., 1998) as well as a lower incidence of Alzheimer’s disease (Fastbom et al., 1998).”

This explanation was misleading, for at least five reasons:

1. There is no evidence that psychiatric drugs need to be given for a long time before they cause dementia.
2. It is misleading to say that depression pills are usually given short-term to patients with bipolar disorder, as 84% of the included patients in their study were not bipolar but had depression.
3. Depression pills are not given for short periods. In 2006, only 20% of the patients in Den-mark who got a prescription for a depression pill were first-time users.¹¹³ Ten years later, 33% of all patients who were prescribed a pill in 2006 had received a new prescription every single year and were still on treatment. And many of them were on treatment also before 2006. I also studied psychosis pills and found the same: 20% first-time users in 2006 and 35% of all users were still on them in 2016. This is iatrogenic harm of epic proportions.
4. The authors wrote that their patients were the most severely affected ones because they had all been hospitalised. Drug usage would therefore be expected to be much more pronounced and long-term in their patients than what I found.
5. Whatever benzodiazepines do to the brain, it is of minor importance in this context because the standard treatments for unipolar and bipolar depression do not include these drugs. They include depression and psychosis pills.

The other study the textbook authors referred to wasn’t any better.⁴⁰⁷ It was a meta-analysis of case-control studies and cohort studies, which didn’t say anything about previous treatments. There wasn’t the slightest hint that the increased risk of dementia could be due to the medication rather than to the depression, although this is far more likely. In contrast to the first study, this possibility was not even considered in the paper.

Poul Videbech, an influential depression researcher who edited one of the textbooks,¹⁸ uncritically quoted this meta-analysis as evidence that depression doubles the risk of dementia.⁴⁰⁸ He added that depression pills can help the brain regenerate. The wishful thinking in psychiatry has no limits, it seems.

Other harms of depression pills

Other harms of depression pills were also consistently downplayed. One textbook claimed that children may experience mild, often temporary, harms at the start of treatment.^19:294 It is far more important to know about the harms that are not temporary, but there was no information about them. A fact box showed harms that occur in over 10% of the children: fatigue, diarrhoea, nausea, dry mouth, drowsiness, headache, dizziness and insomnia.

One book noted that sexual harms are seen in “some” children.^19:294 Some? The pills disrupt the sex lives in about half of those treated.³⁸³ In a carefully conducted study, 59% of 1022 people who had a normal sex life before they came on a depression pill developed sexual disturbances: 57% experienced decreased libido; 57% had delayed orgasm or ejaculation; 46% no orgasm or ejaculation; and 31% had erectile dysfunction or decreased vaginal lubrication.³⁸³ About 40% of the patients considered their sexual dysfunction unacceptable.

The sexual dysfunction can persist long after the patients came off the offending drug and can become permanent.^409-411 David Healy has described that, in some unpublished phase 1 trials, over half of the healthy volunteers had severe sexual dysfunction that in some cases lasted after treatment stopped.⁴¹⁰ Rats can become permanently sexually impaired after having been exposed to SSRIs early in life,⁴¹² which we have confirmed in our systematic review of animal studies.⁴¹³

In the upside-down world of psychiatry, the pills that destroy your sex life—which, in contrast to their claimed effect on depression, people can surely feel—are called happy pills.

When the patients find out that they will never again be able to have intercourse, e.g. because of impotence, some kill themselves.^{8:170,409,410,414} When I lectured for Australian child psychiatrists in 2015, one of them said he knew three teenagers taking depression pills who had attempted suicide because they couldn’t get an erection the first time they tried to have sex. This is cruel.

About harms, another textbook also mentioned sedation, orthostatic hypotension, cardiac conduction disorders, anticholinergic harms, gastrointestinal harms and serotonin syndrome (which is very dangerous and can be deadly).^16:582

A third textbook, where all the authors are psychiatrists, was different to the two others. It claimed that SSRIs have few harms, which are rarely severe;^18:124 and that they are first and foremost sexual ones: delayed ejaculation, decreased libido, and difficulty in obtaining orgasm.^18:238

This is not true. In drug trials, a severe side effect is one that is incapacitating with inability to work or do usual activity. By this definition, is it a severe harm to be unable to have sex, which is a usual activity for most people. And this incapacity is certainly not rare either.

The companies were also untruthful about this predominant problem. An FDA scientist found out that they had hidden sexual problems by blaming the patients rather than the drug, e.g. female anorgasmia was coded as “Female Genital Disorder.”³⁰⁷ The companies claimed that very few patients become sexually disturbed, e.g. only 1.9% in the registration application for fluoxetine,¹⁷² whereas the true occurrence is 30 times higher.

One textbook noted that depression pills can cause mania,^18:113 which in another book was downplayed to short-term hypomanic episodes that may occasionally be seen in association with depression pills.^16:252

About the prolongation of the QTc interval, we are told that tricyclics can be fatal and that an ECG is therefore needed before starting them (to see if the patient has a genetically determined prolongation of the interval).^18:124 Later, the same book noted that other drugs than tricyclics can cause QTc prolongation in rare cases and that an ECG is recommended if the patient has heart disease, electrolyte disturbances, some other diseases, or is treated with methadone.^18:238 Another textbook only mentioned QT prolongation under tricyclics.^17:660

This is confusing, and it is not true that SSRIs rarely cause QT prolongation. This is what these drugs do, and it has been known for decades.²⁷⁹ I therefore believe that if doctors want to prescribe a depression pill—which they shouldn’t—they should have an ECG taken before, and not only if there are other problems.

Quality of life

Given these drugs’ common and severe harms, we would expect them to decrease the quality of life. However, this was well hidden from public view. We showed in our large systematic review that there is an extreme degree of selective reporting of quality of life not only in the published literature,³²⁶ but even within the clinical study reports of the placebo-controlled trials of depression pills.⁴¹⁵

These drugs likely decrease quality of life. We found that 12% more patients dropped out on drugs than on placebo (P < 0.00001).³⁰¹ The patients weigh any perceived benefit from the pills against their harms when they decide if they want to continue in a study till the planned end, and drop-out for any reason is therefore a highly relevant outcome. The patients prefer to be treated with a placebo!

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To see the list of all references cited, click here.