A couple of years ago, I wrote about the proposed connection between a collection of once-common flame retardant chemicals (PBDEs) and hyperthyroidism in cats. While the notion of “toxins” as the cause of disease is often a vague and ill-founded idea promoted by advocates of alternative medicine, there are certainly some environmental toxins that clearly cause disease, and it is important that we be vigilant in evaluating and eliminating these. The case for PBDEs as the cause of hyperthyroidism rests primarily on three points:
- PBDEs came into common use at about the same general time as hyperthyroidism, once unheard of in cats, became a relatively common disease.
- There are laboratory studies supporting the potential influence of PBDEs on the thyroid hormone system in multiple species.
- There are some associations between PBDE levels and the occurrence of thyroid disease in cats, though not all studies consistently show this.
The hypothesis that PBDEs may play a causal role in feline hyperthyroidism is plausible and supported by some evidence, though there are also other hypotheses with similar support, and it seems likely that multiple causal factors are involved.
The subject has gotten a lot of attention recently due to an article in the New York Times which discusses the problem of hyperthyroidism in cats and the possible role of PBDEs. The article is pretty reasonable and balanced in its discussion of the subject, but it is easy to miss the nuance and take away the message that PBDEs are definitely the major culprit in this disease.
Given the renewed interest in the subject generated by this article, I thought I’d take another look at the literature and see if there was any new evidence on the subject. I found a nice study from 2016 which certainly doesn’t solve the question once and for all but which does add some additional information.
Guo WeiHong; Gardner, S.; Yen, S.; Petreas, M.; Park JuneSoo. Temporal changes of PBDE levels in California house cats and a link to cat hyperthyroidism. Environmental Science & Technology, 2016, 50, 3, pp 1510-1518
This study looked at a relative small number of cats (22 total: 11 each with and without hyperthyroidism). The investigators measured PBDE levels, as well as levels of several other environmental toxins as a control, and compared the levels between cats with thyroid disease and those without as well as between two time periods: 2008-2010 and 2012-2013. This latter comparison was done to evaluate changes in PBDE levels over time. These compounds were banned in 2004, and PBDE levels have been declining in humans as a result, so the hope was they would be declining in cats as well.
The results did, encouragingly, show that PBDE levels have been declining, though cats still have much higher levels than humans (probably because they are more likely to ingest dust from the environment, in the process of grooming themselves). They did also find higher levels in cats with thyroid disease than in those without, which might support the idea that PBDEs are part of the cause of this condition. However, they also found higher levels of the unrelated environmental toxins in hyperthyroid cats compared with normal cats. One of the features of hyperthyroidism is that cats lose weight quickly. This weight loss can lead to an increase in blood levels of many compounds since the same amount of the substances are present in a now smaller cat. Therefore, it isn’t entirely clear if the higher PBDE levels in hyperthyroid cats reflect its role in causing the disease or simply the fact that these cats have lost weight rapidly while the healthy cats have not.
The bottom line form this study is that, as in the past, there appears to be some association between PBDEs and hyperthyroidism in cats, but it is not as simple as saying PBDEs are the sole cause of the condition. It is also encouraging that PBDE levels appear to be declining in cats, as in humans, due to the gradual elimination of PBDE use following the 2004 ban. If PBDEs are, in fact, an important factor in causing hyperthyroidism, we should expect the incidence of this disease to decline as a result. If the incidence does not decline, then we will have to keep looking for other risk factors.