We appreciate that there is a need to get a reader’s attention with the title of any document, including news releases. This headline grabs readers with the suggestion that lithium “reduces side effects of most common treatment for Parkinson’s disease,” a statement that’s simply not supported as no humans with Parkinson’s disease were studied. Treating mice with an induced form of the disease is not the same as treating actual people with Parkinson’s disease. Having said that, the release recovers quickly — in the very first sentence — to clarify that the research was done in mice, which is commendable. The release also includes some useful caveats regarding the quality of evidence and what additional research needs to be done before lithium can be considered a viable option in humans. A bit more information about the actual research findings and potential harms of lithium would have been helpful.
Parkinson’s disease is primarily a disease of the late middle-aged and elderly population. At the moment there are between 500,000 and 1,500,000 people in the US with the disease and approximately 60,000 are diagnosed annually. Although there are now numerous innovative approaches to managing symptoms, dopamine replacement therapy is the dominant treatment. As noted in the news release, the effects of dopamine replacement on the classic symptoms of Parkinson’s are frequently replaced by a set of equally crippling movement disorders. An inexpensive and low-risk solution for the treatment related movement disorders would be a welcomed option for sufferers of the disease and their families
After a misleading headline, the release establishes quickly that the research is in mice and that clinical trials haven’t been performed. And at this early stage of development, the cost of treatment is not an issue. So we rule this Not Applicable. Having said that, if lithium augmentation of carbidopa/levodopa did indeed work in humans, the low cost of lithium is a distinct advantage to patients.
We aren’t really provided with much in the way of information here — the number of animals involved or how they measured the actual improvement in abnormal movements or what the results were. One of the researchers talks about “significant behavioral improvement,” but is that “significant” only in a statistical sense or something that would be noticeable to an average person? We are also told, “lithium boosted the expression of tyrosine hydroxylase which increases dopamine synthesis via the inhibition of calpain-1, an enzyme that normally reduces dopamine synthesis” but without really informing the reader with why this is important. We are also told about findings from two earlier studies, “We clearly saw a prevention of the motor difficulties we would expect to see in the animals,” said Andersen. “The treatment also protected the area of the brain that is normally damaged by Parkinson’s.” It would have been helpful to have some numbers here, or a more thorough description of what the study actually showed.
The news release is silent on the issue of the potential for toxicity with lithium augmentation. Although the research was conducted in mice, the researchers did note the potential for toxicity in their publication, “…in a few reported cases lithium treat- ment was suggested to be detrimental to PD patients and to cause side effects…” Since lithium is also used in the treatment of psychiatric disorders, it’s possible the release could have pulled from the literature on this use to discuss potential side effects.
On its own, the headline of this news release is misleading: “Low-dose lithium reduces side effects from most common treatment for Parkinson’s disease.” Any reader would take this to mean that we’re talking about humans with Parkinson’s disease, when the research was done in mice with an induced form of the disease. That being said, we applaud the release for clarifying in the very first sentence that we’re talking about mice — something that’s not often done in news releases. We also think the excellent comments of Dr. Simon provided some clarity and placed the study into the right context. “This study suggests potential therapeutic benefit in PD…..One caveat is that other agents that have shown clear efficacy in this model of PD have subsequently failed to show benefit in clinical studies in PD (e.g. CoQ10, creatine, and pioglitazone). However, this study provides additional evidence on top of prior work from Dr. Andersen’s lab and others that lithium may have therapeutic potential in PD, which is a hypothesis that should be tested in clinical trials,” So, although the headline alone would be given an unsatisfactory rating, the immediate and extensive clarifications about the quality of evidence saved the day.
The release notes that Parkinson’s disease is diagnosed in 60,000 new people each year, a figure which is supported by the NIH. It would have been helpful to state one’s lifetime risk of developing the disease, to help put this number in context.
The funding source for the research is clearly identified in the release. However, we are not advised that the Buck Institute and the two senior authors of the paper filed a patent application for low-dose lithium in Parkinsons (US20130017274 A1).
Although levodopa/carbidopa is the main approach to treatment, other drugs are available that are not mentioned. In addition to medical therapy, deep brain stimulation is also available at most academic medical centers.
The release makes it clear that lithium is currently available and used for psychiatric illness. Given that the drug is available, it’s conceivable that desperate patients will seek treatment with lithium based on these findings — which is why it’s all the more important to carefully qualify the results in the headline.
It is clear that the use of lithium for this purpose is new. The release also establishes that there was previous research leading up to the study.
The headline of the release cannot be justified on the basis of the information provided or by the results of the study itself.