This release reports on an early study using mice to evaluate the potential usefulness of tandospirone, a drug to treat both the anxiety and depression that follows binge drinking, as well as curb the negative effects on neurogenesis (the growth and development of neurons) that alcohol can cause.
The release states in the second paragraph that this is a mouse study but then several times it suggests that the findings will be applicable in humans. Only human clinical trials can show if this is the case. The release doesn’t quantify any improvements, define any potential harms from the drug, name who funded the work or offer any insights into conflicts of interest. While it mentions the drug is now available in China and Japan, it offers no information on its probable cost if approved for sale in the West.
The release headline doesn’t mention that this study took place in rodents. As a result, some news story headlines are echoing that this drug has been found to reverse brain effects of alcohol, never making it clear that the results apply only to rodents.
Alcoholism is a major challenge to patients, their loved ones and to public health as a whole. Drugs that might positively affect its damage, and perhaps even reverse it — as this release suggests — would be a great benefit. But this release reports only on very preliminary work done in animals which has yet to be shown transferable to human medicine. The release should have offered more specific information and more caveats as to its applicability.
There is no mention within the release as to the cost of this drug, although it is readily available in both China and Japan. Readers have no indication whether the drug is cheap or expensive, an important factor when evaluating its usefulness among those battling binge drinking and alcoholism.
The news release assumes that binge-drinking in selectively-bred rodents and the brain and behavior changes they evidence have some relevance to humans. Quantification of benefits are irrelevant since rodent drinkers are not the same as human drinkers. Some evidence on human benefit is needed.
As to the benefits of using tandospirone in mice, the release provides the following: “….two weeks of daily treatment with the drug tandospirone reversed the effects of 15 weeks of binge-like alcohol consumption on neurogenesis – the ability of the brain to grow and replace neurons (brain cells).” Simply saying it “reversed the effects” or “the drug was effective” isn’t adequate for conveying any potential benefits from the drug’s use.
When it comes to potential harms from using the drug, the release only offers the following: “It is commonly used there [in Asia] and shown to be highly effective in treating general anxiety and well tolerated with limited adverse effects.” What are those limited effects? How often do they occur? Are they greater or lesser than the side effects of other drugs used in curbing heavy drinking?
A caution on the the potential toxicity of the drug if taken with alcohol should have been included.
The release states in the second paragraph that the research was done in adult mice. That, however, is overshadowed by the headline, the lead paragraph, and quotes by the researchers that suggest the findings will automatically transfer to humans — a highly speculative conjecture. While animal studies are essential to discoveries leading to improvements in human medicine, the degree to which their results are duplicated in human trials varies greatly. Stories and releases reporting advances evolving from animal research need to be clear throughout that the findings may — or may not — be replicated in humans. One mention isn’t sufficient.
The release does not appear to commit disease mongering.
The release makes no mention of the funding sources of this research, nor does it provide any information on potential conflicts of interest.
There is no mention in the release as to alternative drugs that are used to treat heavy drinking, although there are some, or any mention of any non-drug approaches to curbing drinking.
The release clarifies that “This drug is relatively new and available only in China and Japan.”
The release points out that the drug is not just meant to curb drinking but is also aimed at both reducing the anxiety and depression which may follow binge drinking, and suggests that it may alter the reduction in neurogenesis that excessive alcohol use can lead to. It’ important to remember that any claims of novelty apply to mice enrolled in this study only.
Related drugs in the same drug class (5-HT1a receptor partial agonist which also include Buspirone (buspar), Abilify (aripiprazole) and Seroquel (quetiapine) have long track records in human disease but no established role in the treatment of alcohol use disorder per se. While the claim may be novel in mice treatment, drugs in this class have already been used to treat anxiety in people with AUD and comorbid anxiety disorder.
The release takes the wrong tack when it suggests that a model of selectively-bred mice exposed to alcohol for two hours every 24 hours has relevance to what it refers to as human “alcoholism.” Without an explanation, the cautious reader should worry that the diagnosis of “alcoholism” in rodents is itself close to disease mongering, without any explanation of the mouse model of disease being validated in humans.
We also found the release’s final quote troubling: “While it could possibly have that effect, it might be able to help reboot the brain and reverse the deficits the alcohol abuse causes — both the inhibition to the brain’s ability to regenerate, and the behavioural consequences that come from what alcohol is doing to the brain, like increases in anxiety and depression.” These are pretty strong claims to be made based only on early studies in mice!
Systematic, Criteria-Driven
With the discontinuation of @HealthNewsRevu, there's a genuine concern that well-written and researched "reality checks" in healthcare are not economically interesting. This should be disconcerting to anyone, and yet I'm only seeing more and more piling into "promising findings"
Thanks for ALL you do and have done, Gary. https://t.co/93K4hzQXZj
Thanks for sharing this with all of us today, @garyschwitzer @HealthNewsRevu
A nice gift.
#healthcare #healthcarenews #journalism #reporting #factsmatter #truthmatters https://t.co/hNHdZDl2rc
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