As US health secretary, Robert F. Kennedy Jr. has drawn a lot of attention for promoting pseudoscience and disproven theories, especially on vaccines. He is using that playbook on another major public health issue: gun violence, which remains the leading cause of death for kids in America. When it comes to school shootings and other mass shootings, here’s what RFK Jr. wants you to believe: It’s not the guns, he argues, it’s the pills.
The fringe theory that antidepressants can cause people to turn violent has been around for decades, focused primarily on selective serotonin reuptake inhibitors, or SSRIs, which are the most common class of these drugs. But extensive research by mental health and violence prevention experts has found no credible evidence that antidepressants cause or contribute to mass shootings.
The generalized claim that SSRIs can make people violent—and that they supposedly gave rise to the shootings epidemic—traces in part to an unscientific anti-Prozac campaign in the 1990s from the Church of Scientology and gained some traction in online forums after the Columbine High School massacre in 1999. Disgraced conspiracy theorist Alex Jones, who helped create a miasma of lies claiming that the 2012 mass shooting at Sandy Hook Elementary School was faked, has also peddled the theory.
Proponents of the SSRI theory use anecdotal, often unconfirmed details about shooters’ health histories to argue causation. But multiple studies from experts in psychiatry, law enforcement, and public health show that the theory has no merit. Data on shooters spanning more than a decade from the FBI’s Behavioral Analysis Unit has been used specifically to examine the claim that psychiatric drugs are at the root of school shootings; independent researchers concluded from the FBI data that “most school shooters were not previously treated with psychotropic medications—and even when they were, no direct or causal association was found.”
This is patently false. Placebos work, medicine demonstrably works better.
The original claims that antidepressants don’t work better than placebos was originally reported on 24 years ago after some analysis said they were equally effective, however the trials used to measure these outcomes weren’t at all designed to mimic how antidepressants are actually used.
For example, you wouldn’t judge a cancer treatment by how well it reduced a tumor in 1 week of taking the medicine, if the medicine is meant to be taken for 6 months, would you? Nor would you judge a drug’s ability to eliminate cancer if it doesn’t work for one patient, and doctor’s recommend a different drug that does end up working, but the drug still works for others?
That’s what these reviews did.
Unlike how actual antidepressants are prescribed (many people have no success with their first antidepressants, switch to others later on that do work better), these studies just gave participants the one, in isolation, without the ability to switch to the new drug from another one that didn’t work. This means that participants were statistically likely to have the highest possible chance of that drug not working first try, whereas in the real world, drugs like that would be prescribed to people as an alternative, or a second attempt, where it is known to be more likely to be effective.
On top of that, they were only measured for a limited period. As previously mentioned, you wouldn’t judge a cancer treatment over a fraction of its intended use cycle, so why would you do that with antidepressants? The drug trials only measured usage at a single dose, for a set period of time, without long-term follow-ups.
Studies done even just a few years afterwards demonstrated actual correlations between antidepressants and placebos far different from the picture being painted, showing that antidepressants have an effect larger than placebos, (https://pubmed.ncbi.nlm.nih.gov/19588448/) and even more recent analyses of broader swaths of scientific studies on the topic still shows them to be more effective than placebo. (https://www.nature.com/articles/s41386-024-02044-5)
You say that, but those were double blind clinical trials.
It is pretty safe to presume these drugs are virtually worthless, that the companies pulling BILLIONS a year now from this perverted follow up studies to get it approved. The fda is led by former drug company officials and let the research firms stroke the follow up studies through.
1 percent better than placebo in double blind trials run by the firms they hired if anything is slanted to favour the drugs. Trusting their follow up, and excuses, is beyond ignorant of the way things are these decades.
Yes. They were trials done to one of the highest standards we have for assessing the outcomes of drugs. Double blind studies help to prevent the biases you seem to think that type of study causes. Do you know how these studies even work or why we do them?
The FDA does not control if these papers get published or not, as PubMed has nothing to do with the FDA, and the FDA has no say in how follow-up studies are done on patients using already-approved drugs on the market.
Did you not even look at the resources I sent? Here’s the core piece I think you really need to actually pay attention to:
The
1.24and1.28are the relative risk ratios for treatment with meds, vs placebo. Essentially 1.24 means 24%, 1.28 means 28%. Those percentages being… the likelihood the treatment would treat the underlying symptoms, relative to a placebo.24% and 28% are not 1%.
The companies making these drugs did not hire these researchers. The closest thing they have to influence on their research is funding a conference-focused group that does outreach and education for researchers, which in turn derives only a portion of its funding from one drug manufacturer. (which you would know if you looked at the paper itself and read the clearly visible conflict of interest statement that all good researchers publish with their papers)
I don’t know about you, but if I’m a large group of independent researchers, I’m not going to collectively entirely fabricate fourteen studies over many years, fabricate the analysis in a metanalysis of those works, then publish it with my name attached… because I get to attend a conference for free sometimes and get pitched medical tools???
This isn’t justifiable criticism of the pharmaceutical industry, this is just anti pharmaceutical industry sentiment packaged in whatever words sound bad enough to you regardless of what is observably in reality. I have my problems with the pharmaceutical industry too, but that doesn’t mean I go around saying “all drugs are fake and you should just inject liquefied cilantro” or something crazy like that, since just because something is bad doesn’t mean that every possible bad thing that could be done, is being done.