This release focuses on a recently-published study in rats with high blood pressure that are at risk of heart failure, a condition in which the heart does not pump blood as efficiently as it should. The study’s findings suggest treating the animals with a low dose of the thyroid hormone triiodothyronine (T3) improved cardiac health in the rats. Specifically, the study focused on diastolic heart failure, in which the left ventricle of the heart does not fill with blood properly, limiting the amount of blood pumped through the body with each heartbeat. The release mentions right in the headline that the study involved animals, and it does a good job of highlighting that much work needs to be done before the work done in rats may lead to clinical use in humans. The release could have done a better job describing the known risks associated with this hormone and describing the benefits observed in the study.
Heart failure is a big deal. According to the CDC, more than 5 million people in the United States are diagnosed with heart failure and — in 2009 — heart failure was a contributing factor in one out of every nine deaths in the U.S. The CDC also notes that heart failure costs the U.S. an estimated $32 billion each year in missed work and treatment costs. Because of its prevalence, health impact and economic impact, any new advances in treatment that could ameliorate health risks associated with heart failure are certainly of interest.
This release is reporting on work done in an animal model, far removed from clinical use in humans. As such, it would be virtually impossible to tell readers precisely how much potential treatment might cost consumers. And so we won’t ding the story for not including a discussion of costs — we’ll rate this Not Applicable.
That being said, it wouldn’t have been difficult to discuss costs in general. T3 is not a new drug. For example, combinations of T3 and thyroxine (another thyroid hormone) are prescribed to patients with hypothyroidism or thyroid cancer. The release could have mentioned that versions of T3 are already on the market and discussed cost at least in general terms. Is it relatively inexpensive? Expensive?
The release refers to “encouraging cardiac improvements” and says “cardiac health improved,” but those benefits are not quantified. The release also tells readers that “T3 treatment inhibited the major cause of stiffening of the heart in hypertension” and “overall improvement in…heart function.” But it doesn’t tell readers what this means. How much improvement was there? And what, exactly, was improving?
We recognize that this issue would have been difficult to address, since the paper itself does not provide specifics on these benefits. But we maintain a high standard, and the researchers could have been prodded to provide answers. It would have been nice at the least to have some sense of how the changes compared with those observed other studies.
The release does not adequately discuss potential harms. Thyroid hormone treatment for other conditions, such as hypothyroidism, has been around for years. And, in those cases, it’s known that such treatment can cause side effects such as heart palpitations and insomnia. But there are other risks as well, which the release itself points out in a very roundabout way. The release says that the study’s lead author “has long argued that medical opinion on thyroid treatment for patients with heart disease is largely shaped by outdated studies that used toxic doses of thyroid hormones.” This sentence manages to highlight that there can be significant risks associated with the use of thyroid hormones (the “toxic doses” reference), but it isn’t clear what these risks are, and it’s not made clear that there may be risks (even lesser risks) associated with the undefined “low-dose” applications of thyroid hormone used in this study.
First, let’s give kudos to the release for clearly stating in the headline and lead sentence that this was an animal study. News releases almost never take that simple step to clarify what kind of evidence we’re talking about. So that alone merits a Satisfactory rating here.
Of course, we can quibble with the release’s description of the study. It tells readers “aging female rats with hypertension progressing to heart failure were treated for one year (half their lifetime) with a low oral dose of the active form of thyroid hormone, T3.” But how large was the study? Did they examine 3 rats? 30? 300? Was there a control group? Did the researchers vary dosage across the experimental group? What is a “low” dose?
But this is a minor concern in the description of a study about rats.
The release does not mention either how the study was funded or whether there were conflicts of interest for the authors. The study was funded by the National Heart, Lung, and Blood Institute, and there don’t appear to be any conflicts of interest — but it’s important to tell readers that.
There are many heart failure treatment options, from surgery to drugs. But most of those treatment options, such as angiotensin-converting enzyme (ACE) inhibitors, target systolic heart failure specifically. There are currently no effective treatments for diastolic heart failure, and the release tells readers this.(Diastolic heart failure happens when the left ventricle doesn’t let in enough blood; systolic heart failure occurs when the left ventricle doesn’t squeeze hard enough to push out sufficient blood.)
The release does an excellent job of making clear that this was an animal model study and that clinical trials have not yet been approved for this treatment technique — meaning that this work is at least years away from widespread clinical use.
The release does a good job of placing the new study into context, and articulating what sets the most recent study apart. The release notes that the lead author has published on 32 animal studies that looked at links between thyroid hormone levels and heart health, and offers some discussion of at least two of these other studies and why they’re relevant. The release also mentions other studies in the field (though it refers to them as “outdated”.
The release makes very clear that this was an animal study, from the headline through the body of the text. It also puts the work into context, and uses cautious language when describing effects (e.g., “encouraging cardiac improvements”).
Systematic, Criteria-Driven
Fascinating case study in medical journalism... https://twitter.com/garyschwitzer/status/1547278045781819395
.@garyschwitzer nails it, again.
It doesn't have to be this way.
This: https://twitter.com/garyschwitzer/status/1547278045781819395
Someone please fund Health News Review again. Goodness knows we need a health news watchdog more than ever. https://twitter.com/garyschwitzer/status/1547278045781819395
Comments (1)
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A Martin Gerdes, PhD
October 23, 2015 at 4:15 pmThis was my study and I would like to comment further. A 1950 study showed reduced mortality in three patient groups with ischemic heart disease who were treated with Armour thyroid (T3 and T4). Unfortunately, there was never a good followup to this study. Key subsequent studies used overdoses of thyroid analogs rather than actual thyroid hormones. The current rat study related to the news release is one in a series of experiments designed to answer what I believe is the most important question in this field. It is assumed that thyroid hormones are too dangerous to give to heart patients due to possible arrhythmias from overdosing. Is that true or is there actually a therapeutic window? In a series of experiments examining T3 treatment of diabetic cardiomyopathy (NY Weltman, Mol Med 2014), hypertension (current study in Am J Physiol), and myocardial infarction (paper submitted), we have used oral T3 doses ranging from 0.03 to 0.08 micrograms/ mL in drinking water. The 0.03 dose completely prevented diabetic cardiomyopathy, the 0.04 dose (current study) was effective in hypertensive rats, and the 0.08 study produced dramatic improvements after myocardial infarction (paper submitted). On the 0.08 dose, some of the rats began to show a slight increase in heart rate so this dose was at the upper limit. Overall, our cumulative studies show a therapeutic window between 0.02 and 0.08 with remarkable benefits. In each case, T3 safely restored normal hormone values in the heart. For the first time, these studies suggest a therapeutic window to safely restore depressed cardiac tissue T3 levels (a condition that by itself can cause heart failure) with remarkable benefits. This potential window should be explored in patients. I think we now know enough to conduct clinical trials in people with diagnosable borderline or overt low thyroid function using very low and safe doses of T3. These animal studies suggest that ~3 times the effective dose would be needed to produce overtreatment. Since thyroid hormones improve contractile function, cardiac relaxation, coronary blood flow, reduce fibrosis, improved gene expression, and also appear to inhibit arrhythmias, it is certainly worth exploring the possibilities in a select group of patients with heart diseases leading to failure. I predict that restoring normal thyroid hormone balance in heart patients will become common practice in the not so distant future. We need to do the human studies correctly to know for sure.
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