In some countries, including the United States, about 10% of the entire population is in treatment with depression pills. This is a tragedy. These drugs do not have relevant effects on depression; they increase the risk of suicide and violence; and they make it more difficult for patients to live normal lives (1). They should therefore be avoided. We have been fooled by the drug industry, corrupt doctors on industry payroll, and by our drug regulators (1).
Surely, many patients and doctors believe the pills are helpful, but they cannot know this, because people tend to become much better with time even if they are not treated (1). This is why we need placebo-controlled trials to find out what the drugs do to people. Unfortunately, virtually all trials are flawed, exaggerate the benefits of the drugs, and underestimate their harms (1).
Cold turkey in the placebo group
Virtually all patients in the trials are already on a drug similar to the one being tested against placebo. Therefore, as the drugs are addictive, some of the patients will get abstinence symptoms (usually called withdrawal symptoms) when randomized to placebo, even if a wash-out period before randomization is introduced (1). These abstinence symptoms are very similar to those patients experience when they try to stop benzodiazepines. It is no wonder that new drugs outperform the placebo in patients who have experienced harm as a result of cold turkey effects.
To find out how long patients need to continue taking drugs, so-called maintenance (withdrawal) studies have been carried out, but such studies also are compromised by cold turkey effects. Leading psychiatrists don’t understand this, or they pretend they don’t. Most interpret the maintenance studies of depression pills to mean that these drugs are very effective at preventing new episodes of depression and that patients should therefore continue taking the drugs for years or even for life.
Lack of blinding
Because of the conspicuous side effects of the drugs, quite a few patients (and their doctors) know who is on the drug and who is on placebo (1). It does not take much unblinding in a trial before the small differences recorded can be explained purely through the bias in the outcome assessment on a subjective rating scale (1).
The smallest effect that can be perceived as an improvement on the Hamilton Depression Rating Scale is 5 to 6, but flawed trials attain only approximately 3 (1). Several meta-analyses have found that the effect is larger if the patients are severely depressed, but the reported effects are small and below what is clinically relevant for all severities of depression (2). Further, it is likely just a mathematical artifact that the effect seems to be slightly larger in severe depression (3). The bias caused by the lack of blinding will be greater when the baseline score for depression severity is larger.
The small effects of depression pills measured in flawed trials disappear if the placebo contains atropine, which has similar side effects to the pills—e.g., dry mouth (4).
A score on a rating scale says very little or nothing about how well a patient is functioning. According to the American Psychiatric Association, major depression is present when the patient exhibits five or more of nine possible symptoms that “cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.” Given how the disorder is defined, it makes no sense that no effectiveness trials have used these stated outcomes (1).
Since these drugs have purely symptomatic effects, one highly relevant outcome is the patients’ conclusions as they weigh any benefits they have experienced against the harms, which they do when deciding whether to continue the trials to the end or drop out. Based on almost 70,000 pages of unpublished reports from drug regulators, we found that 12% more patients dropped out on a drug than on placebo, which means it is better to get placebo than a drug (5). It is remarkable that people preferred placebo even though some were harmed due to cold turkey effects.
We also wanted to study quality of life in the trials but discovered that even the clinical study reports were grossly unreliable (5). The degree of selective reporting within these reports was astounding, and drug regulators had done absolutely nothing to request the missing data from the drug companies, even though these reports are used in getting drugs approved.
There is no doubt that these drugs negatively impact the quality of patients’ lives, and we know, for example, that half of the patients experience disturbances to their sex life after starting the drugs (1).
Depression pills are also far more dangerous than people know. We found that they double the occurrence of events that can lead to suicide and violence in healthy adult volunteers (6); they increase aggression in children and adolescents by a factor of 2 to 3 (7)—an important finding considering the many school shootings where the killers were on depression pills; and they increase the risk of suicide and violence by four to five times in middle-aged women with stress urinary incontinence (8). Also, twice as many women experienced a core or potential psychotic event (8).
I have described the dirty tricks and scientific dishonesty involved when drug companies and leading psychiatrists try convincing us that these drugs protect against suicide and other forms of violence (1). Even the FDA was forced to give in when it admitted in 2007, at least indirectly, that depression pills can cause suicide and madness at any age (1, 9).
There is no doubt that the massive use of depression pills is harmful. In all countries where this relationship has been examined, the sharp rise in disability pensions due to psychiatric disorders has coincided with the rise of psychiatric drug usage (10), and depression pills are those which are used the most by far. This is not what one would expect if the drugs were helpful.
As these pills cannot cure anyone, it is immensely misleading to call them antidepressants, suggesting they are as effective as antibiotics for infections.
Professor Peter C. Gøtzsche, MD, co-founded the Cochrane Collaboration. He has published more than 70 papers in the top five general medical journals and six books, most recently, Death of a Whistleblower and Cochrane’s Moral Collapse. He recently launched the new Institute for Scientific Freedom with the goal of preserving honesty and integrity in science.
- Gøtzsche PC. Deadly psychiatry and organised denial. Copenhagen: People’s Press, 2015.
- Jakobsen JC, Katakam KK, Schou A, et al. Selective serotonin reuptake inhibitors versus placebo in patients with major depressive disorder. A systematic review with meta-analysis and Trial Sequential Analysis. BMC Psychiatry (2017): 17-58.
- Gøtzsche PC, Gøtzsche PK. Cognitive behavioural therapy halves the risk of repeated suicide attempts: systematic review. J R Soc Med. 110(2017): 404-10.
- Moncrieff J, Wessely S, Hardy R. Active placebos versus antidepressants for depression. Cochrane Database Syst Rev. 1(2004): CD003012.
- Sharma T. Effects of selective serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake inhibitors (SNRIs) on suicidality, violence, and quality of life. Ph.D. thesis, defended 23 April 2019 at the University of Copenhagen. Available here.
- Bielefeldt AØ, Danborg PB, Gøtzsche PC. Precursors to suicidality and violence on antidepressants: systematic review of trials in adult healthy volunteers. J R Soc Med. 109(2016): 381-92.
- Sharma T, Guski LS, Freund N, et al. Suicidality and aggression during antidepressant treatment: systematic review and meta-analyses based on clinical study reports. BMJ 352(2016): i65.
- Maund E, Guski LS, Gøtzsche PC. Considering benefits and harms of duloxetine for treatment of stress urinary incontinence: a meta-analysis of clinical study reports. CMAJ 189(2017): E194-203.
- FDA. Antidepressant use in children, adolescents, and adults. Available here.
- Whitaker R. Anatomy of an epidemic. New York: Broadway Books, 2015.