This University College London news release describes a complex piece of research that combines cell cultures, human volunteers, a theory that enzymatic proteins called matrix metalloproteinase (MMP) inhibitors are involved in forming threat memories inherent in PTSD, and that a common antibiotic may prevent their formation by blocking the enzymes.
The fact that the research was a theoretical proof-of concept is buried deep in the release so readers might think, based on the headline and earlier paragraphs alone, that the evidence is stronger than it is.
The published research article describes some of the uncertainties involved in biopsychological investigations in animal models and people, but the release doesn’t mention any of them, nor does it include any meaningful numbers to describe the benefits. It does raise the issue of the practicality of using drugs to prevent PTSD since no one can predict when a traumatic event will occur.
The search for the neurochemical and biological roots of PTSD and other kinds of crippling anxieties is a scientific challenge for good reason. The human “mind” is difficult to access; animal models are notoriously unreliable; and experiments on people designed to induce, evoke, or otherwise probe such trauma may be unethical.
The work described here may indeed be an important early step in understanding the role of signaling pathways outside of nerve cells in creating PTSD, and of novel strategies using an already widely available set of drugs to sabotage that role. But a lot more research will be needed to affirm the idea and a release on the research should make that point very clear and very high up in the text.
When and if the blocking of a conditioned fear response by a drug is proven, who would want to take a long term drug in case a terrible event befalls them in the future? That would be taking “preventive medicine” to a whole new level.
The release makes no mention of costs. It could have addressed cost through information about the relatively inexpensive antibiotic used in the study or by mentioning the social and economic costs of those afflicted with PTSD.
Even though the research is called a “proof of concept,” we think if it’s not too soon to issue a news release it shouldn’t be too early to include cost implications.
It’s not clear from the release how statistically strong the results are. The release notes that volunteers taking the antibiotic had a 60% lower fear response in the first session compared to those who took the placebo, “suggesting that the fear memory was significantly suppressed by the drug.” But that number is an average response rate in the treated group and we’d like to see some actual numbers — the number of responses and the range of responses — to assess how many people were helped and to what degree.
The article published in Molecular Psychiatry also reports only the approximate percentage of study volunteers who experienced a reduced reaction to the fear marker, so there are no absolute numbers that could be taken from the study and used in the news release. However, communications staff and journalists are the eyes and ears for readers and it behooves them to seek clarity from the authors of research.
One of the investigators is quoted acknowledging the challenges inherent in using drugs like doxycycline to prevent PTSD, but there is no mention in the release about the many serious adverse side effects and drug interactions that come with the use of tetracycline antibiotics.
Doxycycline has been tried long-term for aortic aneurysms (as a matrix metalloproteinase or MMP inhibitor, the same reason it was tried here) and as an antibiotic for acne, recurrent urinary infections and other conditions. Although generally considered safe to use, over a long term it can cause allergic rashes, antibiotic resistance, changes in friendly gut bacteria, possible weight gain and other problems.
While the release explains that the subjects were all healthy volunteers and that the study was a randomized, placebo-controlled, double-blind trial involving computer simulation, it doesn’t give us much information about the strengths and weaknesses of the research. The primary outcome the researchers sought to measure — startle response — was never really described.
The release doesn’t engage in disease mongering. It provides some context about what PTSD is and what causes it.
Some context about the rate of PTSD in certain populations (e.g. combat veterans, terrorist attack survivors, children of war) and methods currently used to prevent or treat the condition might also have been helpful to include.
The release notes the funding sources and the study stated that there were no conflicts of interest.
The release doesn’t mention any of the other treatment strategies for PTSD or show how this drug might compare with them.
One other drug that’s been studied for its use in the blocking of learning conditioned fear is the beta blocking blood pressure drug propanolol.
The release notes that “more realistic models” of clinical PTSD are needed and any testing of doxycycline in those models is years away.
The release claims novelty through this statement by the study author: “We have demonstrated a proof-of-principle for an entirely new treatment strategy for PTSD,” explains Professor Bach. “The theory is based on the recent discovery that our brains need proteins outside nerve cells, called matrix enzymes, to form memories.”
However, the current study is not the first to identify a drug that may block fear learning, as noted above under the “alternatives” criteria.
The release doesn’t include any sensational, unjustifiable language.