Evidence Update: Flame Retardants (PBDEs) and Hyperthyroidism in Cats

The words “chemical” and “toxin” are among the most popular and misused words in the alternative medicine lexicon. They are often more a vague code for “evil spirits” rather than a specific reference to true environmental health hazards, and they are frequently used to frighten people into avoiding conventional medical therapies or employing unproven or quack treatments. “Toxins” are often more an ideological shibboleth than a useful scientific concept.

That said, there are unquestionably real environmental compounds that cause disease. Many of these have been identified by meticulous and rigorous scientific research. Undoubtedly some remain unidentified, quietly increasing our risk of illness without our knowledge. The trick is knowing what is truly dangerous, to whom, in what form, at what time, and so on. The details matter. If we waste our time avoiding and being afraid of the wrong things, or everything, we aren’t focusing our efforts effectively at identifying and controlling true environmental risks. Science, not scare tactics, is the best way to deal with the problem of environmental toxins.

Which brings me to a recent article which has added a bit of information to an ongoing debate about an all-too-common disease, feline hyperthyroidism.

Jessica Norrgran, Bernt Jones, Anders Bignert, Ioannis Athanassiadis, and Åke Bergman. Higher PBDE Serum Concentrations May Be Associated with Feline Hyperthyroidism in Swedish Cats. Environ. Sci. Technol., 2015, 49 (8), pp 5107–5114

Hyperthyroidism is the most common glandular disease in cats. It involves an excess of thyroid hormone produced by a benign tumor of the thyroid gland. The consensus is that the disease is much more common than it was a few decades ago, though there are not reliable numbers and, as always, it’s not completely clear the degree to which more cases are actually occurring versus more cases being diagnosed since we’ve discovered the disease and started testing for it readily. It is, in any case, a significant cause of illness, and though it is very treatable, it causes a great deal of discomfort for cats and expense and worry for their owners.

The problem of hyperthyroidism is especially frustrating because we do not know precisely why cats get the tumors that cause it, or why it appears to have become more common. Whenever there is this sort of uncertainty, the door is wide open for theories, from the plausible to the ridiculous, and there is little basis on which to discriminate among them. Lots of theories have been proposed for the cause of feline hyperthyroidism, and the fact that no single one has been confirmed suggests that multiple risk factors and causal pathways are involved. However, environmental contaminates are considered a significant potential risk factor, and this study adds some support to the concerns previously expressed about one in particular, polybrominated diphenyl ethers (PBDEs).

The authors selected blood samples from cats seen at a Swedish university and measured the levels of 11 different PBDEs and related compounds. These levels were compared with those found in humans in Sweden as well as between cats with and without diagnosed hyperthyroidism. They found higher levels overall in cats than in humans, higher levels of 4 of these compounds in cats with hyperthyroidism, and different patterns of the relative amounts of the different chemicals in cats compared to humans and in hyperthyroid and normal cats. Other compounds did not differ between the two groups of cats. And one compound was found in all of the cats despite having been banned over a decade previously in Europe and not having been detected in house dust or human blood since.

The authors are careful to point out that these data cannot be used to confirm that PBDEs cause hyperthyroidism because there are a number of potential sources of error that are not controlled for in this kind of study. Much more extensive data exist in humans, and yet it is still not clear what role, if any, these chemicals play in causing thyroid disease. Nevertheless, showing that at least in a small number of cats those with thyroid disease appear to have higher levels of PBDEs that those without does suggest some relationship, and further study is certainly warranted to sort out the details.

Research has suggested a relationship between PBDEs, in the environment and possibly in cat food, and the appearance of hyperthyroidism in cats before, though not all studies have found evidence to support this hypothesis. It seems likely that multiple factors are involved, including environmental, genetic, and possibly nutritional variables.

This complexity is frustrating, as it prevents identifying a single, simple cause that can be avoided. The bulk of the PBDE exposure is believed to come from ingestion of house dust through self-grooming. PBDEs have been incorporated into a bewildering variety of household items, and while many of these compounds are no longer manufactured or used, it is likely indoor cats will continue to be exposed to them through these sources for some time. However, there are a host of other, and generally more severe, health problems associated with letting cats roam outdoors, so this is not a great solution.

Similarly, there is some concern about PBDE exposure through canned cat food. However, there is also some limited evidence that canned foods are better for cats than kibble in terms of other health risks. And while fresh, homemade diets may be ideal in theory, in practice most owners cannot put the time and energy into making truly nutritionally balanced and safe homemade diet.

If PBDEs are a significant part of the cause for, hopefully further research will clarify their role and give us the detailed information we need to reduce exposure and disease risk. Any action we take on this subject, however, needs to be thoughtful and based on solid data, since making dramatic changes in how we feed or otherwise manage our feline companions without a strong foundation in science will very likely lead us into simply exchanging one set of risks for another.

 

 

 

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6 Responses to Evidence Update: Flame Retardants (PBDEs) and Hyperthyroidism in Cats

  1. v.t. says:

    I thought exposure to PBDE’s were commonly from flooring (carpets) and furniture. And since cats generally live at “ground level” to these items it seems a reasonable “culprit”. Additionally, if some forms of PBDE’s have been banned, cats would remain exposed due to the fact that humans don’t often replace their flooring or furniture for several years.

    Skeptvet, may I respectfully ask, if you feel appropriate, for a slight adjustment to your paragraph about exposure through canned cat food – not all cat owners are aware the current theory is the can’s lining or the pull-top aluminum lid may be suspect- or we’ll be hearing about a conspiracy of manufacturers knowingly adding PBDE’s directly in cat food during production. Yes, if the theory proves to be true through continued research, obviously PBDE’s would leach through to the food, but it’s not the food itself that is contaminated prior to sealing.

  2. skeptvet says:

    Right, the concern about PBDEs in food has centered in the can liners rather than the food itself. However, there is also some concentration of these chemicals as you go up the food chain, and fish are considered another possible source associated with cat food, though as usual the evidence is pretty limited. Obviously, they are not being added deliberately!

  3. v.t. says:

    Ah, good point about the fish, thanks!!

  4. LitterBoxOfHorrors says:

    I’m curious what you think of this site, especially 1) the criticism of the Hill’s y/d diet and 2) radioactive iodine as a “gold standard” for treatment. My brief experience with the Hill’s y/d wasn’t good. (My cats, hyperthyroid or not, don’t like it)

  5. skeptvet says:

    In general, Dr. Pierson and I come to similar conclusions for very different reasons. I agree that most experts consider radioiodine the gold-standard treatment in terms of the overall risk/benefit balance. There is not unanimity, certainly, but I think this is a reasonable claim. It is the therapy I most often recommend, but there are plenty of reasons why it may not be best for individual patients, including cost, concurrent disease, and others.

    I also agree that medications do not alter the underlying disease process, they simply prevent the negative consequences of benign thyroid tumors. These drugs have risks as well as benefits, just as do the other therapies for hyperthyroidism, and sometimes the risks or unintended effects may outweigh the benefits. However, the nonsense about “putting chemicals in your body” is silly and embarrassing in a veterinarian. If she drinks water, she puts a potentially deadly “chemical” in her body. Many cats live healthy, happy lives thanks to medication as treatment for thyroid disease, and the risk/benefit balance has to be evaluated in the overall context of the individual case.

    I agree to some extent with her objections to Y/D, in that long-term safety has not been established and that it can be difficult to implement, especially with concurrent diseases (such as chronic kidney disease) or other cats in the house. It seems a solution in search of a problem given the better options already out there. The issue of carbohydrate and protein content is a reasonable one, though not as clearcut as she makes it seem. However, the “bad ingredients” argument is again nonsense and unscientific.

  6. Art malernee dvm says:

    It amazes me that the cause of the sudden occurrence of this disease can not be identified. I just hope it does not turn out to be the canary in the coal mine for some human cancer.

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