Seresto Flea & Tick Collars: The New Satanic Panic?

Like many vets around the country, I’ve had a sudden wave of panicked calls and emails from clients about a dramatic article that appeared in USA Today yesterday. The article essentially claims that the Seresto flea and tick collar is injuring and killing huge numbers of dogs and some humans. Despite all the weaselly linguistic tricks to imply neutrality and plausible deniability if called out on making this accusation, no reasonable person could read this article and not get the message that this product is deadly and that the EPA is callously ignoring the danger, likely because they are in the pocket of Big Pesticide. 

This article is an example of the horrifyingly bad journalism that we see all too often concerning the safety of pet healthcare products. It is full of anecdote and innuendo and guilt-by-association, but devoid of the kind of actual data that might tell us whether the fear the author wants to incite is justified. As veterinarians, we have all been through this before. The web sites, Facebook pages, sloppy journalism, and even lawsuits claiming the pets are being harmed by Rimadyl and other NSAIDs, and TrifexisFebreezeSwiffer, and of course vaccines are a fact of life for anyone in pet health professions. 

It is easy to blame a particular product or treatment for something bad that happens to our pets. We naturally search for explanations when our companions are sick, and we tend to fixate on concrete things we can see and touch and potential causes we are primed to be suspicious of. Both reports of the real dangers of some pesticides, industrial chemicals, and medicines as well as the irrational demonization of all of these by opponents of mainstream medicine have implanted an automatic anxiety about the safety of such products in all of our minds. 

When a pet falls ill suddenly, we look around for a reason. The food or medicine or vaccines or pest control products we may be using come readily to mind. Invisible viruses and bacteria, internal causes inside the body that we can’t see, and other common but intangible causes are less noticeable, and so less likely to be blamed. This availability bias is a classic psychological quirk that impedes our ability to accurately assess risk and identify the causes of undesirable events. It’s why we are more afraid of airplanes and sharks than cars and mosquitoes, even though the former are a lot less likely to hurt us than the latter.

Finally, there is an unfortunate tendency in the media to shock and disturb rather than inform, which this article illustrates. Such media coverage can easily lead to excessive and inappropriate panic about risks that are smaller than made to appear in the media or even entirely unreal. The Satanic Abuse panic of the 1980s is a classic illustration of this. Hysterical and dramatic reporting of individual claims that people had been ritually abused by Satan worshippers went from fringe publications to mainstream media. Despite years of widespread coverage and the ruining of people’s lives by unfounded allegations, hard evidence never emerged to substantiate these claims. While some individuals undoubtedly did experience abuse of some kind, the media generated both a fictional cause to blame and a surge of unreliable anecdotes by presenting the initial reports in a melodramatic and irresponsible way. Sadly, finding and fixing the really dangers behind such claims was only hampered by this media coverage, and the same is often true of health scares such as those I mentioned earlier.

The Claims
Before we try to answer the question whether or not the Seresto collar is safe for our dogs, let’s look at the claims of this article and what they are based on. The writer begins, as usual in these kinds of scare pieces, with a heartbreaking anecdote of a pet dying. The owner believes this death was caused by the flea and tick collar she used, and the writer of the article jumps right from that to the claim that this product has been  “linked to hundreds of pet deaths, tens of thousands of injured animals and hundreds of harmed humans.” The emotional setup here is clear, and the message that the product is dangerous probably doesn’t require any actual evidence for most people at this point. But the author does provide a link to support this claim. So what is that about?

The link is to a collection of reports on the EPA web site of illnesses and deaths in dogs using the Seresto collar. Seems pretty damning, doesn’t it? Here’s the trouble: Those numbers are simply collections of spontaneous reports made to the agency. Zero investigation has been done to show the reports are accurate or that there really is a connection between the product and the events described. The purpose of such reporting sites is to create a place for people to raise concerns. Agencies in charge of various public health areas collect and monitoring these spontaneous reports for signals suspicious for a problem that merits investigation. If a pattern is seen that suggests there might be a safety issue, the agency can investigate to determine if there is a real concern or not.

This is what happened with the issue of grain-free diets and heart disease that I have written about several times. The FDA saw a change in the number of reports received and began an investigation. Two years later, the nature of any association between these diets and the disease is still being studied, and their role, if any, in causing heart disease is still unclear. The fact that people reported their observations about heart disease and what they were feeding their dogs isn’t proof of a causal role, just a collection of anecdotes that may or may not signal a real problem. Rigorous scientific investigation is how we find out if health products are causing harm, not simply accepting every scary anecdote as true. 

The same issue has come up innumerable times over many years with regard to vaccines and the Vaccine Adverse Event Reporting System (VAERS), managed y the CDC and the FDA. VAERS collects unsubstantiated anecdotal reports about possible harm from vaccines. Despite the overwhelming evidence for the safety of vaccination in general and most vaccines in common use, these reports are frequently cited by antivaccine activists to “prove” that vaccines are causing tremendous harm. One doctor actually submitted a report that a vaccine caused him to turn into the Incredible Hulk, and this report would still be in the VAERS database if he had not allowed the government to delete it.

Such databases are useful surveillance tools that can provide early signals of real problems, but they are also full of uncorroborated and inaccurate reports and speculation. They are not reliable evidence for a causal role of any product or medicine in harm done to people or animals. This, again, requires appropriate scientific investigation.

What else does this article rely on to support the clear claim that Seresto collars are killing dogs and injuring people? There are several strategies at play here. One is the use of unrelated cases of harm from pesticides to poison the well and imply that claims about the dangers of Seresto must be true since other pesticides have caused harm. The fact that claims have been made about harm from other pesticides (some true and some also unproven) aren’t relevant at all to the question of whether Seresto is safe or not, but they exacerbate the general anxiety or fear about pesticides to strengthen the reader’s willingness to accept negative claims about it. Clever rhetorical technique, I suppose, but not a legitimate form of argument that leads to the truth.

The citation of experts is also used to suggest Seresto is unsafe and the EPA is failing to protect the public. Quotes are provided from a “senior scientist… who has a doctorate in cell and developmental biology” at an environmental watchdog group and a “retired EPA employee… who worked as both a scientist and communications officer.” Noticeably absent from the expertise consulted is anyone with a specialty in veterinary toxicology or parasitology. Since assessing the safety and effectiveness of parasite control methods and the impact of toxins on veterinary patients is the central area of expertise for people in these fields, such individuals would have been far more likely to have relevant and informed opinions on the scientific question of whether or not Seresto is safe. Not including them is a pretty transparent technique for building a one-sided argument. I have heard from two veterinary toxicologists, a parasitologist, and a veterinarian with a national poison control center, and none of them found the allegations of widespread serious harm from the Seresto collar credible. Hopefully, people with appropriate expertise will weigh in on this issue publicly soon. 

The Science
So is there scientific evidence and, if so, what does it tell us? There are published studies and reviews of the safety of both active ingredients in Seresto, imidacloprid and flurmethrin, as well as studies of the combination in the product itself. As usual, these provide a much more nuanced picture of the risks and benefits. It would be implausible and unreasonable to claim that no dog had ever experienced adverse effects from this or any other parasite preventative. As I point out forcefully and often, no medical intervention that does anything at all is without risks, so the important issue is understanding what the risks and benefits actually are and how they compare.

Imidacloprid is a common pesticide that has been used and studied extensively for decades. This EPA document provides a relative recent overview of the available evidence. Research in dogs and cats has shown extremely low risk, and this product has been used extensively for many years without any consistent or reliable evidence of the kinds of extreme harm depicted in this article. As always, some adverse effects from excessive or inappropriate use or in unusually susceptible individuals can occur, but overall there is nothing in the evidence concerning imidacloprid to justify the level of anxiety directed at Seresto in this piece.

The other ingredient, flumethrin, is a synthetic pyrethroid pesticide, a class that has also been studied and used extensively for a long time in dogs. Cats are especially sensitive to this class of agents, and they are not typically recommended for this species, but dogs are much less likely to experience adverse effects when pyrethroids are used properly. Those cases of harm that do occur are typically associated with improper dosing. Studies of flumethrin in dogshave found limited evidence of toxicity at doses well above recommended use for parasite prevention.

More importantly,  there is published research evidence investigating the use of the combination of these ingredients in the Seresto collar. These have shown some adverse effects, but nothing even approaching the kind of common and devastating effects suggested by this article:

Stanneck 2012

In cats, a total of 28 events were suspected to be related to study medication… 23 in the [Seresto] (9.0%) and 5 in the control group (5.6%) [using a different parasite collar]. This difference was not statistically significant (p > 0.4; Fisher’s exact test). [These events were] were generally mild dermal reactions (alopecia, pruritus, mild contact dermatitis).

In dogs, in the [Seresto] group 3 events (alopecia, hair coloration, dermatitis) and in the [control] group 4 events (alopecia, flea infestation, pruritus, aggressive behaviour towards a collar wearing animal) were scored as being related to the study medication. The difference between the two groups was not statistically significant (P > 0.16; Fisher’s exact test)

Krudewagen 2015

Small Non-Controlled Clinical Safety Study
No clinically relevant adverse event related to der- mal or systemic safety occurred and no abnormalities concerning general health were noticed during the course of the study. 

Controlled safety studies – Seresto®/ Advocate®
All dogs tolerated the treatment well. Two out of 51 treated dogs showed transient skin alterations in the region of collar application, namely a crusty spot (approx. 1 cm diameter) on one day, respectively a moderate erythema of small (< 1 cm) to medium size (1 – 4cm) for about two days. Further findings in the treated group that were considered unlikely to be treatment related were conjunctivitis and a congested nasolacrimal duct in one dog, and a hot spot in the tail region of the same dog that showed erythema in the collar region. In the control group one dog also showed wounds and crusts in the neck region. No further clinical signs were present. 

Blood hematology and clinical chemistry 
No clinically relevant changes were detected for any parameter in the dog or cat study.

There are neither dermal nor systemic safety issues with the particular combination of the three actives imidacloprid, flumethrin and moxidectin in adult cats and dogs…

There is also research evidence showing that this product is effective in reducing flea and tick infestations, which can have the benefits of reducing allergy symptoms and protecting dogs against infectious diseases (and 23) spread by these parasites. These benefits have to be weighed against any potential harm. 

Finally, in terms of safety the available data has been evaluated by public agencies in many countries and found not to support claims of significant health risks. While the article accuses the EPA of a gross failure and dereliction of duty in not acting aggressively on the anecdotal reports it has received, as I pointed out earlier, such reports appear with many healthcare products, and these often turn out not to be accurate. It is possible that the risk here has been underestimated, but the burden of showing that with hard evidence remains on those making the claim.

One more issue that this article ignores is the subject of knockoff or lookalike products. Unfortunately, if a veterinary product is successful, it is common for other companies to make products that appear similar but have different ingredients in order to capture some of this market. It is also not unusual for fake replicas of a brand-name product to be produced in some countries and sold online as if they were the original product. These knockoffs have not passed the regulatory safety testing required of properly approved products. They may very well be less safe, and this can confound efforts to assess the accuracy of adverse event reports for these products. Such fake Seresto collars have made their way into the market, and it is possible some reports of harm may involve these rather than the original product.

Bottom Line
So what’s the bottom line? Is Seresto a perfectly safe and effective parasite preventative or a poison decimating the dog populations? The truth, of course, is between these extremes. There are undoubtedly some risks to this product, and it is possible that they are greater than has so far appeared in the scientific literature. The research done on this product has mostly come from companies and investigators with a financial interest in it, and that always raises some concern about the potential for bias in the data. On the other hand, such concern doesn’t somehow make collections of unsubstantiated anecdotes a reliable source of data. The fact that some people think Seresto has harmed them or their dogs is not, alone, evidence that it has. 

I don’t personally recommend Seresto for my patients because I find other parasite preventatives more convenient to use. I do have clients using it, and some doctors at my practice do prescribe it, and none of us have seen the kind of terrible effects depicted in this article. That is, of course, only more anecdote, but before we panic because of scary stories, it is worth remembering that there are many veterinarians and pet owners who have not had any negative experience with this product. 

I hope that additional research shows that the concerns raised in this article are unfounded, but if it turns out the risks are greater than we currently realize, that will be important information. Unfortunately, rigorous scientific investigation takes time; a lot more time and work that sensationalist medial reporting. My hope is that reasonable people will respond to this latest example of poor-quality reporting in a reasonable way. We likely should take a careful, objective look at the safety data for this product, and perhaps conduct further research if warranted. We should not panic and blame every bad thing that happens to us or our dogs on the latest media bogeyman. 

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Are NSAID Pain Relievers Dangerous for Your Dog?

One of the most common and useful class of medications available to veterinarians are the non-steroidal anti-inflammatories (NSAIDs). These treat pain and inflammation, and the evidence for their safety and effectiveness is robust (12). Like all medications that have any meaningful benefits, NSAIDs do have potential side effects. However, these are well-characterized, and in most cases with proper dosing and monitoring, NSAIDs can be used safely to treat pain in dogs and in cats.

Unfortunately, NSAIDs are also one of the most heavily demonized medications available, particularly by those who are critical of  science-based medical therapies or promote alternative medicine approaches. Despite the evidence for the safety of NSAIDs, and the successful use of these drugs to reduce suffering in tens of thousands of pets, some critics would have us believe they are pure poison and inevitably cause injury or death. The many alternatives recommended often have little or no evidence to show they are as safe or as effective as NSAIDs. The reality is that there are few other oral pain medications that have been demonstrated to work safely in dogs and cats, and the push for alternatives to NSAIDs has often led to widespread use of drugs that either don’t work (e.g. tramadol) or that we haven’t yet tested adequately to know if they work or not (e.g. CBD, gabapentin). 

I have reported on the safety and efficacy of NSAIDs several times in the past. It is clear from abundant studies that these drugs are very effective for pain, certainly the best oral analgesic we have for dogs and often a good choice for cats as well (34567). In terms of safety, one review found that the rate of adverse events was very low, with no significant difference in the rate of adverse events between the NSAID and placebo when placebos were used. Out of 1589 dogs in the studies reviewed, only 1 experience a severe reaction requiring hospitalization for treatment.

A more recent systematic review found that adverse effects were reported at rates from 0% to as high as 37.5% of dogs. However, the drugs, study characteristics, and patient populations different widely, so it was not possible to directly compare particular drugs or studies. 

Interestingly, when the highest quality studies were considered (randomized, placebo-controlled clinical trials), no difference in adverse effects was detected between dogs receiving NSAIDs and those on placebo. Though it is clear that such side effects do, of course, occur in some dogs on NSAIDs, and while real clinical patients are likely to respond differently than research subjects, this at least suggests that worries about common and severe harm from these medications are not justified.

Other evidence, including trials used to gain FDA approval, show that dogs on NSAIDs can experience minor problems, such as self-limiting vomiting and diarrhea, or potentially more severe problems such as stomach bleeding, worsening of pre-existing kidney disease, or liver failure. However, the rates of these problems are extremely low, and they must be balanced against the life-limiting pain caused by arthritis, the clear efficacy of NSAIDs in relieving this pain, and the great deal of uncertainty about the safety or benefit of alternative treatments.

There has recently been an increase in concerns about NSAID safety, instigated in part by Dr. Karen Becker, a prominent advocate for alternative therapies whom I have discussed here many times, and Rodney Habib, a social media influencer who misrepresents himself as a pet health expert. This centers on a new study that seems, at first glance, to support the notion that NSAIDs are dangerous and commonly cause patient harm. However, the reality is, as always, more complex and nuanced.

Mabry, K., Hill, T. and Tolbert, M. K. (2021) ‘Prevalence of gastrointestinal lesions in dogs chronically treated with nonsteroidal anti-inflammatory drugs.’, Journal of veterinary internal medicine. J Vet Intern Med. doi: 10.1111/jvim.16057.

This study involved comparing the findings of video capsule endoscopy (VCE) in dogs taking NSAIDs with dogs not on these medications and looking for signs of injury to the lining of the stomach or intestines. VCE is a procedure in which a dog swallows a very small automated camera that takes pictures of the gastrointestinal tract as it passes through and is eventually retrieved from the feces. It is a relatively new procedure, and while it is a useful way to visualize the GI tract, there is limited information available on what is normal or abnormal in different patient populations.

The study compared VCE images from 12 dogs who had been taking an NSAID for at least 30 days with the findings from 11 dogs evaluated for gastrointestinal disease who were not on this kind of medication. Two investigators assessed the pictures taken for signs of erosions, small defects in the lining of either the stomach or small intestines. NSAIDs can cause these erosions, as well as deeper and more serious lesions known as ulcers, so it would not be surprising to see some in a through look at the inside of the GI tract, and this is what the study found.

Of the 12 dogs on NSAIDs, 9 (75%) had erosions in the stomach and 6 (50%) in the small intestine, with 83% of the dogs having erosions identified in one or the other part of the system. This was compared to 3/11 (27%) of the control dogs not taking NSAIDs who had erosions on VCE examination. This finding might be disturbing if we could conclude that this means NSAIDs are harming 83% of the patients taking them. This is not however an appropriate conclusion, nor is it what the authors of the study are claiming.

The most important thing to bear in mind when looking at this study is that none of the dogs taking NSAIDs had any clinical symptoms associated with the medicine. No vomiting, no weight loss, no diarrhea, no loss of appetite, absolutely no sign that the erosions seen on VCE had any meaningful effects. This contrasts from the very real orthopedic pain these dogs had, which is why they were taking NSAIDs in the first place. 

Apart from the important fact that the erosions seen by VCE didn’t cause any apparent symptoms, there are some other reasons to be skeptical of the significance of these findings. The dogs taking NSAIDs were not evaluated prior to starting the medications, so it is unknown how many of them might have already had erosions not related to the drugs. Almost 30% of the dogs not taking NSAIDs also had erosions on VCE, so it is likely that some of the dogs in the NSAID group would have had them before starting the medication. This is also a very small study, and there were differences in the breeds and health status of the dogs in the two groups that limit our ability to generalize the results to other patient populations.

The authors of the study were clearly aware of the limitations of the findings and also the potential for misinterpretation and misuse of their results. They state very clearly in the paper:

The clinical relevance of our findings is unclear, and we do not recommend withholding NSAIDs if dogs require pain control, or that all NSAIDs be administered concurrently with gastroprotectants. Lesions were subclinical in all dogs, and none were known to later develop clinical signs of ulceration…Ultimately, the presence of lesions might not have clinical relevance if none of the affected dogs ever go on to develop clinical signs of ulceration.

While it is worth investigating the issue of asymptomatic GI tract erosions associated with NSAIDs and identifying when these might cause actual clinical symptoms, how we might prevent them, and other ways in which this technique could help us make NSAID use even safer, this study does not undermine the already robust evidence that NSAID use in dogs and cats has significant benefit and rarely causes serious harm. Discontinuing NSAID treatment to avoid lesions detectable only by VCE and which caused no symptoms would mean taking away effective pain treatment for no clinical benefit, and this is not in the best interests of these dogs. 

Replacing NSAIDs with other treatments that have far less evidence to show safety and effectiveness is also not a reasonable response to these findings. Dr. Becker and others frequently recommend unproven supplements and alternative therapies for pain that have not been shown to work. The assumption that these treatments are safer than NSAIDs or can partially or fully replace these medications is simply another unproven claim, a roll of the dice based on opinion, anecdote, and little or no reliable scientific evidence.

The goal of all medical treatment is to maximize patient well-being and minimize risk, though such risk can never be completely eliminated. At this time, the evidence is clear that NSAIDs are still the most effective oral pain reliever we have for dogs and cats, and their risks when properly used are small compared to their benefits. Other and better treatments are certainly need, and these will eventually be developed through the slow, rigorous process of scientific research. It is unfortunate that some vets and other proponents of alternative therapies will use these findings to frighten pet owners and encourage them to reduce their use of proven safe and effective pain relief in favor of untested or unrpoven alternatives.

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Why do Dogs get Old? Some Basic Theories of Aging.

Dogs’ lives are too short. Their only fault, really.

Agnes Sligh Turnbull

The question of why our dogs have to get old can be primarily a rhetorical one, expressing our dismay at the process. It can also be a philosophical question, which is how it has most often been treated historically. Aging and death have long been viewed as intrinsic and inevitable features of human and canine existence, to be accepted or raged against and to be explained mostly in metaphysical terms. Whether the changes of aging are seen as an unavoidable playing out of the mechanisms of an impersonal universe or as a necessary journey designed for us by a benevolent creature, metaphysical explanations serve to address our feelings about getting old and our longing for meaning, not the mechanisms of the process. 

Proximate and Ultimate Causes
When we view the question of why we and our animal companions age as a scientific one, the emphasis shifts to understanding the process itself more than the purpose or meaning of it. Science often frames explanations of biological phenomena in terms of ultimate and proximate causes. Ultimate causes answer the question of “why,” though not necessarily from a teleological perspective (that is, with a view to explaining the purpose of the phenomenon). The ultimate explanation for biological processes, like aging, tend to involve the conditions that lead to the existence of the process we are interested in, often emphasizing the evolutionary forces favoring its development. Proximate causes are more an answer to the question “how.” They focus on the detailed mechanisms involved rather than why these mechanisms have taken the particular form they have. 

A simple example of the difference between ultimate and proximate explanations might be the difference in body size between male and female mammals and how this varies between species. Male dogs, for example, are only slightly larger than females, while adult male elephant seals are nearly three times as large as females. The proximate explanations or mechanisms for these differences might have to do with the timing of growth and development, the influence of sex-specific hormones, and other physiologic mechanism. If, for example, males continue growing for a longer period of time, they might on average end up larger than females simply because of an overall longer growth period. If male elephant seals have a growth period and rate of growth that are relatively longer and faster than those of male dogs compared with the females of each species, this would explain why male elephant seals are so much larger than female seals while male dogs are only a little bigger than female dogs.

Ultimate explanations for these size differences, however, would be evolutionary explanations for why they came to exist. Sexual selection theory, for example, argues that the degree of difference in size between males and females has to do with the importance of physical competition between males for the chance to mate. Most male elephant seals never get to mate, but the biggest and strongest can monopolize large groups of females, so only the genes of the largest males make it to the next generation. This leads to evolutionary pressure for greater and greater size in males, without having much effect on the size of females. In dogs, however, one male doesn’t monopolize mating to nearly the same degree, and the advantages of being bigger than other males are less, while the disadvantages (such as needing more food) push against the evolution of greater size. There are other possible explanations for this particular difference, but this illustrates the general difference between proximate and ultimate explanations in biology.

We can apply this same approach to answering the question of why and how our dogs age. Let’s start with some potential theories about the ultimate explanations for aging. Why can’t dogs simply live forever without changing? Or why don’t they live 150-200 years like some tortoises do, or at least as long as we do? 

Ultimate Theories of Aging
Programmed Senescence
One early idea was that evolution favored aging and death of one generation as a way to “make room” for the next. If animals stayed young forever and never died, then their world would get crowded, food and other resources would become insufficient, and the species at a whole might be threatened with extinction. This certainly sounds like a realistic concern given the effect we humans are having on our world as we increase our numbers and our lifespan! However, the problem with this idea is that evolution doesn’t have a way of working towards the “good of the group.” Evolution happens because of differences in reproductive success between individuals within a population. If one big elephant seal fathers a lot of babies and none of the smaller males get to breed, then the next generation of males will have the genes for being big, not small. If this means there isn’t enough food and all the males starve, well, natural selection doesn’t have a way to take that into account.

Antagonistic Pleiotropy and the Disposable Soma
From an evolutionary perspective, a better explanations is that aging is the result of adaptations that have benefits for the young, leading to more reproductive success and the spread of those genes, but that also have costs later in life. Say, for example, small bull elephant seals need less food than larger males, and they are less likely to be caught and eaten by sharks than their more visible and slower comrades. Maybe the really big males even get cancers relatively early in life because the growth hormones that make them so big also stimulate abnormal tumor growth. As a result, small males might live longer than big males and be less likely to get cancer. We might think that evolution would favor this, since it’s obvious a “healthier” set of adaptations that leads to a longer, healthier life. 

However, the fact remains that the big males get to father a lot more baby seals than the little guys. This means that the genes that make them big have an advantage and dominate the next generation, even though they come along with greater risk of an early death from starvation, predation, and cancer. This is a hypothetical example of the concept of antagonistic pleiotropy. Genes that convey a reproductive advantage early in life are favored by evolution, and tend to persist, even though they lead to harm and maybe a shorter, sicker life in the long run than competing genes.  Such a mechanism might explain why organisms have evolved “imperfectly” to age and die. 

The is related to the concept of the disposable soma (“soma” being the Greek word for “body” and referring to all the cells other than the “germ cells” involved in making offspring). This theory suggests that animals have limited resources, such as energy and the raw materials for making and repairing body tissues. These resources can be used to grow and create the soma, or they can be used to reproduce. There is a tradeoff between these activities, and the optimal balance depends on the specific circumstances of a particular species. Some animals may live in unstable and unpredictable environments. The most effective evolutionary strategy in this situation might be to hurry up and have as many offspring as possible as fast as possible. Doing so takes energy away from growth and maintenance of the body, so you might age fast and die young, but you’d leave a lot of offspring (and genes!) behind. If you waited around and spent a lot of your energy of keeping yourself healthy, you’d have fewer offspring and if the unstable environment suddenly killed you off, you wouldn’t have maximized your reproduction very effectively.

Other species live in more stable and predictable circumstances, and this favors a slower approach to life. Individual humans don’t typically have hundreds or thousands of babies, but we spend a lot of time and energy looking after the few we do have to make sure they survive to grow up and reproduce in turn. This strategy works if the environment gives us a chance to stick around a while, but it requires spending more energy and resources on keeping ourselves alive and healthy so we can put in the necessary investment in our limited number of offspring. This theory helps explain differences in the lifespan of different species in terms of their evolutionary history and reproductive strategies. 

These are only simplified versions of some of the more prominent ultimate theories, but they give a flavor for the way aging biology attempts to explain the apparent “flaws” of aging and death in terms of the operation of evolution and natural selection. Such explanations do not, however, give us much opportunity to intervene and influence lifespan and healthspan. If our pattern of aging is fixed by our evolutionary history, then isn’t it fundamentally unalterable? 

This is where proximate explanations of aging come in. The detailed mechanisms of how age-associated changes in health occur is where we can look for opportunities to influence the processes and improve lifespan and healthspan.

Proximate Theories of Aging
This is an enormous subject that has developed over decades and is still the focus of copious and fast-paced research. The devil in medical science is always in the details, and the details are legion and complex in the field of aging biology. In future posts I hope to explore specific mechanisms and potential anti-aging interventions, but for now I will start with a simplified summary of some of the more prominent ideas about how we and our dogs age.

Wear and Tear 
Most of us think of aging as the accumulation of physical damage over time, the gradual effects of wear-and-tear on the body. There is an idea that turns up periodically each of us had a predetermined and limited number of heartbeats, and when we used them up, we would die. If true, this theory would suggest we should do everything we can to conserve our hearbetas and minimize our activity. (This is often associated with the astronaut Neil Armstrong, who was mistakenlyclaimed to have said “I believe that every human has a finite number of heartbeats.  I don’t intend to waste any of mine running around doing exercises.”) 

The reality, as usual, is more complicated. It turns out that slower hear rates are often associated with lifespan, both between and within species. Hamsters have much shorter lifespan than humans, and also a much faster heart rate (c.f. this page for comparisons of heart rate and life expectancy between species). There is also evidence that higher resting heart rates in humans predict a higher risk of death than lower heart rates. However, this is not because faster heart rates use up a fixed number of possible heartbeats. The relationship between body size, metabolic rate, and lifespan between species is complicated and not always consistent. And within humans, slower hear rates are a function of better physical condition (among other factors), which reduces risk of death. It turns out that temporarily speeding up your heart during exercise leads to a lower resting heart rate and better health, so there is no excuse to avoid working out in order to “save” your heartbeats!

Other examples of the physical wear-and-tear hypothesis have turned out to be equally unreliable. Arthritis in joints isn’t just caused by use, and again people who exercise often have better joint health for longer than people who use their joints less because they are more sedentary. We can’t explain aging as just physical parts wearing out with use.

Accumulated Damage
However, some aspects of the physical wear-and-tear idea do carry over into more nuanced and complex theories of aging. We do accumulate damage on a cellular and molecular level over time, and our body can only do so much to repair that damage. The balance between damage of critical components and their repair and replacement likely is part of the loss of function we and our dogs experience as we age. I hope to explore more detailed aspects of this theory in the future. Some of the proposed examples of the types of damage that accrue over time include: mutations in DNA, methylation of DNA and effects of this on gene expression, telomere shortening, oxidative damage to cells and mitochondria, cross-linking and glycosylation or aberrant folding of proteins, and the persistence of nonfunctional or dysfunctional senescent cells within specific tissues. These are all examples of accumulation of damage over time that overwhelms repair systems and leads to the loss of resilience and function associated with age. This can be thought of, in some sense, as a wear-and-tear phenomenon, though not in the strict physical sense of the original idea.

Neuroendocrine Hypotheses
Another theory for how aging works is that changes in various complex and interrelated hormonal systems that control many bodily functions are the core mechanisms behind the physical and functional decline seen in aging. Organs such as the hypothalamus and the pituitary in the brain, the testes and ovaries, the adrenal glands, and others are all connected with the nervous system in an intricate web of feedback relationships that regulate hormones and most physiologic activities. Over time, these systems may come out of balance or certain elements may falter or fail, and this leads to the generalized functional losses associated with aging. There is no question that the neuroendocrine axis is a critical component of the aging process, but there isn’t yet strong evidence for a single master switch or mechanism that cane explain all the features of aging. 

Other Theories
There is research evidence to support a role in aging for many other processes, including free radicals and oxidative damage, mitochondrial dysfunction and a decrease in total energy available to power bodily functions, epigenetic factors and changes in gene expression, and others. There is clearly also a connection, in humans at least, between behavior and aging. Lack of physical activity, poor nutrition, smoking and other toxin exposures, social isolation, and many other behavioral factors influence how our bodies and our abilities change with time. There is less evidence in dogs, of course, but so much of the basic biology of living and of aging are shared between human and dogs, it is likely that behavioral factors are important for healthy aging in our canine companions as well.

As I go forward on this journey into the field of aging biology, I hope to explore many of the specific theories of aging in more detail and look at the strength of evidence for particular testable hypotheses. Of course, the long view is focused on what do these theories allow us to do to influence aging, in our dogs and in ourselves? Having finally come to a mechanistic, scientific perspective on aging as a biological process like any other, we are making great progress in understanding how it works. This opens the door to therapies that can extend life and health. 

The concept of a magical fountain of youth is, of course, mythical and not practically useful. Proponents of alternative and pseudoscientific health practices have long claimed to have answers to the problem of aging. Simplistic interpretations, or misinterpretations, of scientific aging research and unjustifiable extrapolation from theories and weak preliminary evidence to clinical interventions and panaceas are the bread and butter of alternative medicine, and these are all part of unscientific approaches to aging. From exuberant claims for the benefits of antioxidant supplements and foods, to wild assertions about how to prevent or reverse mitochondrial damage, to many other unfounded claims, pseudoscience flourishes on the margins of the aging biology world as it does in so many areas of cutting edge science. My goal, as always, is to follow the evidence, complex, nuanced, and even sometimes unsatisfying or disappointing as it may be. The only reliable path to improvement in health for our pets, in aging as in all other areas of medicine, is through rigorous scientific research. 

I think there is reason for optimism about the potential to develop therapies that extend lifespan and healthspan in our dogs. Talk of “curing aging” isn’t reasonable or responsible, but the idea that aging is incomprehensible and immutable is also unjustified. We have already been tremendously successful at extending the length of our lives, and those of our pets, by reducing the risks of death associated with many causes, from infectious disease to trauma to cancer. We have also had success in extending the productive, functional portion of our life, though this has not kept pace with the increase in lifespan, and it is more common for pets and humans to experience prolonged periods of declining health and function at the end of life. My hope is that we will continue making progress extending life and will bring our ability to extend health up to speed to match this progress. As always, let me know what specific questions you have about aging science in dogs and cats, and I will do my best to answer them here.

Posted in Aging Science | Leave a comment

Why do Dogs get Old? A New Adventure for the SkeptVet.

Most of us fortunate enough to be blessed with dogs in our lives have had to confront one great limitation in our canine companions-they don’t live as long as we do. Watching bright-eyed, bouncy puppies evolve slowly into creaky, grey-faced old dogs is a painful privilege. 

The experience often prompts us to ask “Why?” Why do our beloved dogs have to get old? This is mostly a rhetorical question; more an expression of frustration and regret than a real desire for more information. But while aging, and the loss of comfort and function that typically accompany it, may seem inevitable, it is not incomprehensible. More and more we are learning that aging is a biological process, shaped by evolutionary and guided by internal and external forces that can be understood and manipulated. Immortality for our canine friends may be only a dream, but the more we understand how dogs age, as a species and as individuals, the more we realize there is real hope we may be able to influence how this aging happens, and how our pets experience it.

As with most subjects in science, we shouldn’t really talk about the causes of aging until we have defined the term itself. That is, however, more difficult than it seems. While we think of aging as a universal characteristic of living things, there is actually tremendous variability in how species, and individuals within a species, change physically over time. From the mayfly that lives only a day to tortoises that can live nearly 200 years, animal species vary dramatically in maximum lifespan. 

Even within a species, some individuals age faster than others. The longest-living individual dogs have been documented at close to 30 years of age, but most of our canine companions don’t enjoy nearly so much time. Surveys suggest average lifespan can vary from about 6 years in some breeds to 15 years or more in others. 

Though it is counterintuitive, time alone turns out to be a poor predictor of aging as a biological process. We can see in our own species that some people may be greying or balding in their thirties while others have full, pigmented hair into their seventies or longer. There are individuals with debilitating arthritis, or other conditions typically thought of as age-related, in early middle age, and then individuals running marathons in their eighties. Aging does happen over time, but many factors besides the passage of time determine how we age. 

There is no universally accepted definition of aging. Most scientists studying the phenomenon agree that aging consists of changes, usually deleterious, that occur in individuals over time. These changes often involve the loss of function and an increase in the risk of death. Depending on the specific theory for why aging happens one holds, aging can be seen as the accumulation of damage or the shifting in balance between degradation and production or repair of critical components in the body. Some theories emphasize environmental influences on health and the role of random chance in causing changes in function. Others focus on the role of evolution and how different species have evolved strategies for survival and reproduction that affect longevity. All major approaches to the biology of aging agree, however, that there are specific mechanisms behind the changes we experience as we get older, and that these mechanisms can be understood and potentially altered to influence longevity and health.

Understanding why some breeds and individuals live longer and healthier lives than others is key to understanding aging and how we can influence it. Death may be inevitable for all living things, but research is showing us that the determinants of both lifespan (how long we live) and healthspan (how long we stay healthy) are flexible and can be understood and influenced like other biological phenomena.

My interest in this area has grown over time. As a clinician, many of the most important health conditions I treat, and many of the problems that are life-limiting for my patients, are related to aging. Arthritis pain, loss of muscle strength, and loss of nerve function and coordination are extremely common in older dogs, especially those of larger breeds. These changes frequently have severe negative effects on quality of life, leading to euthanasia. One of my own dogs was in great overall health at 16 years old, which is unusual for a large breed. Unfortunately, progressive arthritis related to age and to congenital dysplasia of several joints eventually left him unable to stand and walk independently, and I ultimately had to let him go because of this, even though he was happy and healthy in every other way. 

Cancer is another age-related health problem that I see often in practice. It is one of the leading causes of death in dogs. While there are some identifiable genetic and environmental triggers, the risk of cancer rises dramatically with age. Many of the factors that trigger cancer or protect against it change with age, so even very different types of cancer are connected by underlying mechanisms of aging. Understanding these mechanisms can provide us with tools to prevent many common health problems that might otherwise seem unrelated.

On a personal level, of course, I experience aging like everyone else, in my family members and myself. As a scientist and healthcare professional, I have always been interested in the science of preventing and retarding age-associated health problems, and that interest naturally sharpens as I and those I know get older!

I have recently had an exciting opportunity to get more directly involved in helping to understand aging and its effects on our canine companions. After several months as a consultant, I have joined the team at Loyal for Dogs, also known as Cellular Longevity. This is a small startup company focused on understanding the biology of aging in dogs and developing therapies to reduce age-associated health problems.

Working with Loyal has been a great opportunity for me to learn about aging science. My focus as a clinician has been on prevention and  treatment of specific health problems, but less on the common pathways of aging that lead to many of these problems. While I have always practiced preventative medicine, emphasizing with clients the importance of maintaining a healthy weight through proper nutrition and exercise, preventing infectious and parasitic disease through vaccines and other science-based tools, and using what we know about specific risk factors for particular diseases to monitor and detect and treat these as effectively as possible, I haven’t focused as much on the basic science concerning the common mechanisms triggering many age-related diseases. So far, the learning curve has been steep!

As in the past, my goal here is to share what I learn to help pet owners understand the health challenges they may face, the scientific evidence concerning these, and the choices they have available to them. When I pursued my training in acupuncture, I shared the experience through this blog. I have created a new post category for Aging Science, and as I learn about this field, I hope to share more about the subject here. As a result, readers are likely to see an increased in content on the subject of aging biology.

This new opportunity has not, of course, replaced all of my other work. I am still active as a clinician in the same practice I have worked at for over 16 years. I am still involved in promoting evidence-based veterinary medicine (EBVM), and still actively writing about EBVM and science-based pet health in my Veterinary Practice News column and elsewhere. And, of course, I will still be here, following developments in science-based medicine, challenging pseudoscience, and trying to help pet owners navigate claims about alternative therapies for pets. 

Since this is my first involvement with a company that is developing, and will perhaps one day be selling, medical therapies for pets, the question will inevitably arise whether this work represents a conflict of interest or somehow undermines my independence as the SkeptVet. People who dislike my critique of specific ideas or medical practices have always resorted to the Pharma Shill Gambit. It is always easier to reject an argument or evidence against one’s claims by dismissing it as “biased” rather than engaging with the argument and evidence directly. In the past, it was easy for me to say that since I had no connections with industry, financial or otherwise, such a claim was not only a fallacious argument but clearly irrelevant. 

The fact that I do now have such a connection will undoubtedly embolden such attacks and, in the minds of some, render the last 20 years of my career as a vet and science advocate meaningless. People with such a view are likely so closed-minded and unreachable already, that arguing about the issue would be unproductive. However, I will at least point out that while questions about my objectivity may be perfectly reasonable when I make claims about any therapies Loyal may produce, or about anti-aging therapies and other subjects directly related to my work there, they aren’t a legitimate objection to every argument I make. 

Loyal has no control or influence over my work as a clinician or a science communicator, apart from my legal obligation not to give away any proprietary information about their products. No one has even suggested they want to influence what I say as the SkeptVet or in my other advocacy channels. There is no reason for Loyal to care what I say about homeopathy, raw diets, acupuncture, or any of the many other subjects I routinely address since these have no bearing at all on the company’s goals or business interests. My efforts to promote science-based medicine and reduce the harm of veterinary pseudoscience will continue unabated.

I hope my adventure learning about why our dogs age and what we can do about it will be as exciting, interesting, and perhaps useful to you as it is to me. I welcome any questions or suggestions for specific topics in this area. Some of the most interesting subjects I have learned about over the more than 10 years I have been writing this blog have come from you, so keep it up!

Posted in Aging Science | 2 Comments

Evidence Update: Discouraging News for CBD & Arthritis in Dogs

I have been tracking the growing body of evidence concerning veterinary uses of CBD since 2018, and it is an exciting and fast-changing field. While there has only been a little clinical trial research in dogs and cats, there have been a couple of encouraging papers looking at CBD for treatment of canine arthritis. 

A 2018 study looked at 16 dogs taking either 2 mg/kg of CBD or a placebo twice daily and evaluated subjectively by blinded owners and veterinarians. The owner measures showed improvements in pain and function, while the veterinarian measures showed improvement in pain but not function.

A second study in 2020 evaluated 20 dogs in four groups: high-dose CBD (50mg/day), low-dose CBD (20mg/day), liposomally encapsulated CBD, and placebo.  Generally, owner and veterinarian subjective measures improved for the high-dose and liposomally encapsulated CBD groups and not for low-dose CBD or placebo, though there was some variation. 

These studies are small and have some significant limitations, but as preliminary evidence, they are encouraging, and I have been hopeful that eventually the data will be robust supporting the use of CBD for arthritis pain in dogs. However, a new study has dampened that hope somewhat.

Mejia, S. et al. (2021) ‘Evaluation of the Effect of Cannabidiol on Naturally Occurring Osteoarthritis-Associated Pain: A Pilot Study in Dogs.’, Journal of the American Animal Hospital Association. J Am Anim Hosp Assoc. doi: 10.5326/JAAHA-MS-7119.

In this study, 23 dogs were randomly assigned to begin treatment with 2.5 mg/kg twice daily of hemp oil with CBD or hemp oil without CBD, and then were crossed over to the other treatment after 6 weeks. Any effects were assessed by activity counts (essentially Fitbits for dogs), weight bearing using a pressure mat, and evaluation of gait by a blinded veterinarian.

Blood testing showed that dogs on the placebo had no measurable CBD or THC in their blood while dogs getting the active treatment had both. Unfortunately, no difference between the treatment and placebo was identified by any of the measures evaluated. As is common in studies of CBD, a few dogs had elevations of liver enzymes without apparent clinical symptoms on the drug, and a couple experienced vomiting when taking it, one of whom had serious enough symptoms to be removed from the study. A small placebo effect was detected by one measure of effect, but not by the others.

As always, individual studies are almost never the definitive word on any medical question. Just as the previous studies were encouraging but by no means absolute proof that CBD is helpful for arthritis in dogs, this study is discouraging, but it does not close the book on CBD as an arthritis treatment. There are several possible explanations for the lack of an effect in this study. The most obvious is that CBD doesn’t help dogs with arthritis, and that is certainly a possibility. However, it is also possible that no effect was seen because of the specific product or dose used, the lack of a washout period between CBD and placebo, the effects of other chemicals in the hemp oil or other treatments the dogs were receiving, or issues with the measurement tools used. 

The presence of adverse effects (vomiting and liver enzyme elevations) as well as the difference seen in blood CBD levels and the presence of some caregiver placebo effects are all good signs in that they indicate the study was using a treatment with significant biological effects and measurement tools that could distinguish, at least in part, between placebo effects and true treatment effects. Studies that show no adverse effects and no placebo effects raise a red flag that there may be something wrong with their methods or the treatment being tested.

This study also raises the issue of the Decline Effect. This is a phenomenon in science in which early research into a novel idea tends to show strongly positive findings. However, as more studies are done by a greater variety of scientists, the size of the effect tends to decline, sometimes to zero. This likely represents both the influence of bias in early studies caused by enthusiasm of scientists for their own new hypotheses and a gradual improvement in methods and reduction in overall positive bias as the scientific community studies new ideas over a period of time. 

It may be that the different findings of individual studies looking at CBD as a treatment for arthritis in dogs result from specific differences in study methods or the CBD products used. Or it may be that we are seeing the beginnings of the Decline Effect in action, and that there will turn out to be little benefit to this treatment, or less than we initially thought. The most important thing is that we continue to study the issue, refining our hypotheses and methods as we go along. This path provides the best chance of finding the real value, if any, of CBD for our arthritis canine companions.

Posted in Herbs and Supplements | 3 Comments

Plant-based vs Meat-based Diets for Cats: Which is Healthier?

It hasn’t been very long since I last wrote about vegetarian diets for pets, but a new study is out that touches on the issue, so I thought it was time for an update. 

Dodd, S. A. S. et al. (2021) ‘A cross-sectional study of owner-reported health in Canadian and American cats fed meat- and plant-based diets’, BMC Veterinary Research. BioMed Central, 17(1), p. 53. doi: 10.1186/s12917-021-02754-8.

This study specifically addresses vegetarian diets for cats, so let’s start with the conclusions from my most recent article on the subject:

Cats have been more lightly touched by domestication and artificial selection than dogs, and they are clearly still obligate carnivores.34,35 This does not mean they are healthiest when fed only raw birds and small mammals, and in fact the evidence indicates this is not the safest or healthiest diet for domestic cats.36,37 However, domestication has had limited effects on the physiology of cats, and their dietary requirements are unlikely to be effectively met by plant-only diets. The need for preformed vitamin A, taurine and other specific amino acids lacking in plant-based foods, and other specific and known dietary requirements of cats makes it unlikely that long-term feeding of vegan diets will support good health in this species.35,38

There are few studies evaluating the health effects of plant-based diets on cats. Some research on cats fed commercial vegetarian diets by their owners have found deficiencies in some nutrients in some cats, but the evidence is limited and of low quality, so no robust conclusions can be drawn.9,39–41

This new study appears to suggest that the jury is in and that plant-based food for cats has no health risks and may even have health benefits. Here are some of the key results:

* No differences in reported lifespan were detected between diet types. 

* Fewer cats fed plant-based diets reported to have gastrointestinal and hepatic disorders. 

* Cats fed plant-based diets were reported to have more ideal body condition scores than cats fed a meat-based diet.

* More owners of cats fed plant-based diets reported their cat to be in very good health. 

However, even the authors recognize that these findings don’t just the general conclusion that vegetarian diets are safe or health for cats. Here is their more measured assessment:

Cat owner perception of the health and wellness of cats does not appear to be adversely affected by being fed a plant-based diet. Contrary to expectations, owners perceived no body system or disorder to be at particular risk when feeding a plant-based diet to cats. This study collected information from cat owners and is subject to bias, as well as methodological limitations. Further research is warranted to determine if these results are replicable in a prospective investigation.

The key point here is that this study didn’t actually evaluate the effect of plant-based vs. meat-based diets on health or longevity in cats. What the study evaluated was the perceptions of owners about their cats’ diet and health. The difference is crucial. 

The study was essentially an online survey distributed through a pet store and cat-centered social media. The owners surveyed were those who voluntarily chose to go to the web site and fill out the survey. This already introduces a selection bias since the people willing and able to do this differ in various ways from the rest of the population. People who respond to web surveys, for example, are younger, whiter, and richer, than people who are more likely to respond to mail or phone surveys. And people tend to respond to surveys when they have a higher level of interest in the subject than the average person. Surveys touching on unconventional diet and medical beliefs tend to be biased towards people with the strongest feelings on these issues, which biases the results.

The other major problem with such a sample is that the health status of the cats was determined entirely based on the opinions and reports of owners. No medical evaluation or records were involved. Owners, however, are neither medical professionals nor objective about their cats’ health, and they are likely to report their beliefs, which often doesn’t line up with the reality. 

For example, 55% of cats in the study were reported to be a health weight. However, previous research has shown that owner assessment of body condition is inaccurate and tends to underestimate weight in overweight cats. People who fed a plant-based diets were much more likely to report that their cats were a healthy weight (71% compared with 54% of those on meat-based diets) and less likely to report they were overweight (22% compared with 34% of those on meat-based diets). Proponents of plant-based diets will likely conclude that this means such diets lead to a healthier weight than meat-based diets. This is possible, but it isn’t a conclusion we can reach based on this survey. All we can say is that owners who choose to feed a plant-based diet believe their cats are a healthier weight than owners who feed meat-based diets. Since plant-based diets are fed to a small minority of cats (only 18% in this survey, which likely overestimated the true popularity), the people who feed these diets must choose to do so based on pre-existing beliefs about their health value. Such individuals already believe these diets are healthier, and they are likely to see and report what is consistent with these beliefs, whether or not it is the reality of their cats’ condition.

The same sorts of biases create a problem for all of the other measures of health assessed in this study. Again, it didn’t really evaluate diet and health, only diet and owner beliefs about health. As the authors suggest, prospective, blinded, randomized feeding studies would be needed to allow any strong conclusions about whether or not plant-based diets are safe and healthy for cats.

References
9. Knight A, Leitsberger M, Knight A, Leitsberger M. Vegetarian versus Meat-Based Diets for Companion Animals. Animals. 2016;6(9):57. doi:10.3390/ani6090057

34.     MacDonald ML, Rogers QR, Morris JG. Nutrition of the Domestic Cat, a Mammalian Carnivore. Annu Rev Nutr. 1984;4(1):521-562. doi:10.1146/annurev.nu.04.070184.002513

35.      Morris JG. Idiosyncratic nutrient requirements of cats appear to be diet-induced evolutionary adaptations. Nutr Res Rev. 2002;15(01):153. doi:10.1079/NRR200238

36.      Glasgow A, Caver N, Marks S, Pedersen N. Role of Diet in the Health of the Feline Intestinal Tract and in Inflammatory Bowel Disease.; 2002. http://www.vetmed.ucdavis.edu/ccah/530-752-7295. Accessed December 28, 2018.

37.      Schlesinger DP, Joffe DJ. Raw food diets in companion animals: a critical review. Can Vet J = La Rev Vet Can. 2011;52(1):50-54. http://www.ncbi.nlm.nih.gov/pubmed/21461207. Accessed October 27, 2018.

38.      Weeth L, Chandler M. Vegetarian Diets. Clin Br. 2015;(January):61-63. https://www.cliniciansbrief.com/article/vegetarian-diets. Accessed April 29, 2019.

39.      Leon A, Bain SA, Levick WR. Hypokalaemic episodic polymyopathy in cats fed a vegetarian diet. Aust Vet J. 1992;69(10):249-254. http://www.ncbi.nlm.nih.gov/pubmed/1359869. Accessed April 29, 2019.

40.      Wakefield L, Michel KE. Taurine And Cobalamin Status of Cats Fed Vegetarian Diets. J Anim Physiol Anim Nutr (Berl). 2005;89(11-12):427-428. doi:10.1111/j.1439-0396.2005.00611_2.x

41.      Gray CM, Sellon RK, Freeman LM. Nutritional adequacy of two vegan diets for cats. J Am Vet Med Assoc. 2004;225(11):1670-1675. http://www.ncbi.nlm.nih.gov/pubmed/15626215. Accessed April 29, 2019.

Posted in Nutrition | 12 Comments

Diet-Associated Dilated Cardiomyopathy (DCM) in Dogs: What Do We Know So Far?

I have been following the controversy, and the research, on diet-associated dilated cardiomyopathy (DCM) in dogs since the issue was first addressed by the FDA in 2018. I recently had a chance to talk with Andy Roark on his Cone of Shame podcast about the subject, and I will share that when it is available. In the meantime, I wanted to post an update on the subject and also collect all of my reporting and the main sources of evidence in one place. 

This is a complex subject, and a great example of the scientific process. An observation (an apparent increase in the number of dogs not usually vulnerable to DCM developing the disease while eating grain-free or other non-traditional diets) led to a hypothesis (some component of these diets was causing DCM in these dogs). Clinicians and researchers and members of the pet food industry have all weighed in on the subject with a variety of perspectives and interpretations of the facts. The evidence is still limited, and no definitive, science-based conclusion has emerged. 

While the evidence is developed, we are able to watch not only the scientific process in action but also the influence of ego, personal bias, financial bias, and other human factors that so often influence how we approach understanding new ideas and problems in medicine. This can shed light on both the strengths and weaknesses of veterinary research and medicine.

Just to start with clarity, I will give you the bottom line as I see it:

Bottom Line

  1. Some dogs of breeds not known to be genetically prone to DCM have developed this disease.
  2. Many of these dogs have been eating diets that are grain-free or that contain pulses and legumes (e.g. peas, lentils, etc.).
  3. Many of these dogs have experienced partial or complete recovery with diet change, supplementation of taurine of other nutrients, and a variety of common treatments for heart disease. This is encouraging since genetic DCM is usually not very responsive to treatment and is typically fatal.
  4. There is uncertainty and disagreement about key facts, including
    1. Whether or not the incidence of DCM is increasing
    2. Whether or not more dogs of breeds not usually prone to DCM are getting the disease
    3. If diet is truly the main cause of DCM in these dogs
    4. What features of diets associated with DCM may be responsible for the disease 
    5. What the role of taurine is in diet-associated DCM
    6. How diet and genetics and other unidentified factors may interact to produce DCM
  5. No one on either “side” of the debate believes we have sufficient evidence to definitively answer these questions, and more research is ongoing
  6. The process of understanding this complex issue will take years and will likely lead to an understanding more nuanced and complicated than the simplest versions of current theories
  7. Economic interests significantly complicate the scientific process of understanding any relationship between diet and DCM. Because the concerns and potential changes in diet they might suggest entail an economic cost to some individuals and companies, this increases concerns about confirmation bias and funding bias in all of the debates and research around this subject.

What Should Dog Owners Do?
While there is still significant uncertainty, it is reasonable to be concerned that diets which are grain-free or contain legumes in the top 5-10 ingredients may put some dogs at greater risk of developing DCM. There are no proven health benefits to these diets, so even with uncertainty about the level of risks, it is not unreasonable to consider avoiding these diets, especially if you have a dog of a breed reported as experiencing diet-associated DCM (e.g. golden retrievers, Irish wolfhounds, American Cocker spaniels, Newfoundlands, St. Bernards). This may turn out to be an unnecessary precaution, but the limited evidence suggests potential risks may be greater than hypothesized benefits.

If you are feeding a diet with no grains or with legumes or a diet that has been listed by the FDA as potentially associated with DCM, it is reasonable to have your dog screened for DCM and taurine deficiency by your veterinarian.

If you have a dog with DCM, regardless of breed, it is reasonable to consider changing to a diet containing grains and supplementing taurine along with any other treatments recommended by your veterinarian. There is some evidence that these actions may improve the chances or survival and even recovery in some dogs.

My Posts and Articles on Diet-associated DCM

Grain-free Diets and Heart Disease in Dogs
August, 2018

FDA Webinar Discussing Dietary Risk Factors for Dilated Cardiomyopathy
September, 2018

Evidence Update: Grain-free and other “BEG” Diets Associated with Heart Disease in Dogs
December, 2018

FDA Update on Grain-free Diets and Heart Disease in Dogs
June, 2019

Column in VPN about Diet-associated DCM and the McCauley et al. Review
September, 2020

The Latest on Dietary Risk Factors for Dilated Cardiomyopathy (DCM) & Misleading Media Spin by Grain-free Diet Manufacturers
November, 2020

Other Relevant Publications

Early 2000s to 2017
Grain-free diets began to grow in popularity due to claims they might reduce food allergies (which are still unproven) and in response to “gluten-phobia” and other cultural factors. These diets went from uncommon to a large share of the dog food market.

FDA Announcement 2018
The FDA had received a steady trickle of reports of DCM in dogs for some time (~1-2/year, total of 13 from 2014-2017). Then the saw a spike in reports in the first half of 2018 (16 cases). Most of these dogs (>/= 90%) were eating grain-free diets. This led to a public announcement in July, 2018 letting veterinarians and pet owners know about the case reports and encouraging awareness and reporting of the disease. This led, naturally, to an increase in reports. Some have argued that this introduced a sampling bias and that the reason there are more reported cases is not because there truly are more cases but because there is more awareness and concern about the issue. There is likely some truth to this, however it is important to remember that the spike in reports predated the FDAs first public announcement, and that the only way we ever find out about relatively uncommon diseases is through encouraging surveillance and reporting.

The FDA made additional announcements in February, 2019 and June, 2019. These were both followed by an increase in reports, but reports did continue between announcements. The FDA also has indicated that reports of DCM in dogs are down significantly in 2020, but that reports of all conditions have decreased due to the COVID pandemic.

Kaplan et al., December 2018
Kaplan JL, Stern JA, Fascetti AJ, Larsen JA, Skolnik H, et al. (2018) Taurine deficiency and dilated cardiomyopathy in golden retrievers fed commercial diets. PLOS ONE 13(12): e0209112. 

This study evaluated 24 Golden retrievers with DCM to investigate possible dietary causes and the role of taurine. 11 of these dogs were in congestive heart failure. Many of these dogs were eating grain-free diets or diets containing legumes, and 15/24 were eating ACANA, one of the brands later identified by the FDA as common to many of the cases. These dogs appeared to have low taurine levels compared with healthy golden retrievers, but “normal” taurine levels, in general and for specific breeds, have not been clearly established. There was a correlation between the ACANA diet and taurine level, but no correlation with the other diets. 22/23 dogs were eating lower calorie levels than predicted for their body size, which has fed some theories that one element of the problem may be relative deficiency in protein or taurine precursors in individual dogs who tend to eat less than typical dogs their size.

All dogs were treated with standard therapies for heart disease as well as taurine supplementation. Some also received other supplements (e.g. l-carnitine), and 21/24 changed diets. Of these 7 changed to diets containing grains, 4 to different grain-free diets. Almost all the dogs improved, and of those in congestive heart failure, 5/11 were able to discontinue their diuretic therapy completely, and 4 were able to reduce the dose of this medicine. Only one dog failed to improve.

This study supports the hypothesis that in golden retrievers diet-associated taurine deficiency can lead to DCM which can be improved or even cured with diet change and medical therapy. However, the small number of dogs and the great variation in their management and nutrition is a weakness of the study, and it is not conclusive. Nor does this study say much about DCM in other breeds or in dogs who are not taurine deficient.

Adin et al 2018
Darcy Adin, Teresa C. De Francesco, Bruce Keene, Sandra Tou, Kathryn Meurs, Clarke Atkins, Brent Aona, Kari Kurtz, Lara Barron, Korinn Saker. Echocardiographic phenotype of canine dilated cardiomyopathy differs based on diet type.J Vet Cardiol. 2019;21:1-9.

Though published in 2019, this study was reported at the ACVIM Forum in 2018 and was referred to in some of the early papers discussing diet-associated DCM. It was a retrospective study of dogs with DCM and a known diet history seen between 2015 and 2018. The main finding was that dogs on grain-free diets tended to have more severe changes in their hearts on ultrasound than dogs on diets containing grains. Most of these dogs did not have taurine deficiency. 7/48 dogs improved with diet change (6 of these also got taurine supplementation).

This study doesn’t address a number of the key issues in the controversy, but it does show that taurine deficiency is not the only mechanism by which diet might be causing DCM and that breeds other than golden retrievers are affected.

Freeman et al Dec., 2018
Freeman LM, Stern JA, Fries R, Adin DB, Rush JE. Diet-associated dilated cardiomyopathy in dogs: what do we know? J Am Vet Med Assoc. 2018 Dec 1;253(11):1390-1394. doi: 10.2460/javma.253.11.1390.

This was a commentary summarizing the research findings and hypotheses to that point. The authors reported a subjective impression among cardiologists they surveyed that DCM was being seen more often and more commonly in breeds not previously known to be susceptible to it. Many of these dogs were on nontraditional diets, including diets that were grain free, that contained legumes/pulses, that had unusual protein sources, or that were made be relatively new and small companies. These were called BEG diets as a shorthand (boutique manufacturers, exotic protein, grain free). This acronym has generated a great deal of rancor in the pet food industry. 

The authors were explicit about the fact that there was insufficient data to show these observations were even correct, much less that there was a causal relationship between specific aspects of BEG diets and DCM. The paper was intended to start, not finish, a conversation and research effort to understand the initial observations and hypotheses.

FDA Feb 2019 Announcement
At this point, the FDA detailed the case reports they had received. The agency indicated that 294 cases had been reported, 90% of which were being fed grain-free diets, mostly containing lentils, and that the other diets involved were often vegetarian diets.

FDA June 2019 Announcement
In this announcement, the FDA detailed the breeds and specific brands of food included in the reports the agency had received to that date. This generated a great deal of controversy from industry, especially as the market share of some brands and grain-free diets declined noticeably after the announcement. Despite the uncertainties about the causal role of diet in DCM, the fact that certain brands predominate in these reports is a legitimate piece of data and cause for concern. While the FDA has tried to be very politic about not blaming specific manufacturers or products or ingredients for diet-associated DCM, it is obliged to make this information available so that appropriate investigations can be carried out.

Similarly, the overrepresentation of relatively rare protein sources, such as kangaroo, in the diets associated with these cases raises a legitimate question about the potential role of such proteins in this disease. The amino acid profile and bioavailability of uncommon protein sources is not as well-characterized as those of common proteins such as beef, chicken, and pork, and until this research is done, it is reasonable to ask whether such sources might have relevant deficiencies. More recent reporting by the FDA, though, has not found consistent associations between protein source and DCM, even as the association between legumes and grain-free diets has remained strong.

McCauley et al 2020
McCauley SR, Clark SD, Quest BW, Streeter RM, Oxford EM. Review of canine dilated cardiomyopathy in the wake of diet-associated concerns. J Anim Sci. 2020;98(6).

This is a comprehensive narrative review of DCM and various known and potential causes. I have written about this paper in detail elsewhere. It is a useful contribution to the discussion, and it makes several important points about the limitations of existing research evidence:

  • the studies include few subjects
  • there is variable representation of breeds with different genetic predispositions to DCM 
  • diet and health histories are often incomplete

These limitations preclude any definitive conclusion regarding a causal relationship between BEG diets and DCM. In emphasizing that additional research is needed to clarify the role of diet in DCM, the review authors agree with the authors of the papers proposing the hypothesis.

However, the authors of this review also chose not to address other information relevant to evaluating the hypothesis, including:

  • patients with DCM from breeds not previously thought to be predisposed to the disease are disproportionately represented among cases fed BEG diets
  • a large proportion of diets associated with DCM cases were produced by small manufacturers or contained uncommon protein sources even though such diets are a small fraction of those on the market

The authors make several strong statements that go beyond a factual critique of the existing evidence:

The use of the acronym BEG and its association w/ DCM are without merit because there is no definitive evidence in the literature.

This exhaustive review of the literature provides support that eliminates the pet food characteristics that have been implicated to have a subjective association with DCM.

Unfortunately, the arguments made in this paper are undercut by the failure of the authors to disclose up front that several of them are employed by companies producing grain-free diets or by BSM, a nutrition consulting firm that does business with such companies. Since the publication of this review, BSM has accepted a grant from a pulse manufacturer and active opponent of the BEG diet hypothesis to study the issue.

These conflicts of interest do not necessarily invalidate the authors’ points, but they do remind us that financial bias is a relevant concern in debates about scientific issues, especially when the evidence is preliminary and uncertain. 

Ontiveros et al May, 2020
Ontiveros ES, Whelchel BD, Yu J, et al. Development of plasma and whole blood taurine reference ranges and identification of dietary features associated with taurine deficiency and dilated cardiomyopathy in golden retrievers: A prospective, observational study. Staffieri F, ed. PLoS One. 2020;15(5):e0233206. doi:10.1371/journal.pone.0233206

This study evaluated taurine levels in 86 golden retrievers eating traditional dry dog foods (contains grains, no legumes other than soy and no potatoes in the top 5 ingredients, manufactured by a large company) or nontraditional diets (kibble or raw diet with no grains, legumes or potatoes, or made by a small company). 

Taurine levels were found to be lower in dogs on the nontraditional diets. These dogs were also more likely to have ultrasound findings suggestive of DCM. A number of methodological concerns and potential conflicts of interest have been raised about the study, some acknowledged and others disputed by the authors.

KSU Virtual Conference, Sept. 2020
The FDA organized a virtual conference on the subject of diet-associated DCM through Kansas State University. Many of the presentations are available there, though not all. 

The FDA provided updated statistics on the case reports received (1100 canine cases as of July, 2020 from all 50 states and Canada) and preliminary data on a sibset of cases analyzed by theVeterinary Laboratory & Investigation Response Network (Vet-LIRN). 

 Of 150 cases reported between 1/2018 to 4/2019, 107/121 recovered fully or partially. All of the dogs who recovered fully had changed diets, and many had received taurine, pimobendan, and other treatments. Full recovery took 7-13 months.

Consistent with previous reports, 90% or more of the diets fed before the DCM diagnosis were grain free and had legumes high in the ingredient list. The protein sources in the diets fed to these cases were varied, and no consistent association was seen.

Representatives from BSM also made several presentations at the symposium supporting several claims:

  • There is no actual increase in DCM associated with increasing popularity of grain-free diets
  • There is no change in the breeds being diagnosed with DCM, and most are still breeds with known genetic predispositions
  • Only fasted plasma taurine levels have been shown to correlate with taurine level sin heart muscle, so the methods used to measure  taurine in other studies may not be reliable
  • There is no evidence that small pet food manufacturers have lesser quality control than larger companies or are disproportionately represented among cases of DCM reported to the FDA

Data from a survey of cardiology practices that was presented by BSM at the conference was subsequently published as a preprint for a journal article still undergoing peer review:

Quest B, Clark SD, Garimella S, Konie A, Leach SB, Oxford EM. Incidence of canine dilated cardiomyopathy, breed and age distributions, and grain-free diet sales in the United States from 2000-2019: A retrospective survey. bioRxiv. September 2020:2020.09.27.315770. doi:10.1101/2020.09.27.315770

Pezzali et al, January, 2020
Pezzali JG, Acuff HL, Henry W, Alexander C, Swanson KS, Aldrich CG. Effects of different carbohydrate sources on taurine status in healthy Beagle dogs. J Anim Sci. 2020;98(2). doi:10.1093/jas/skaa010

In this lab study, 12 Beagles were fed diets with grains or diets without grains and utilizing potatoes, peas, or tapioca starch as a carbohydrate source. Taurine levels did not differ between the groups. The relevance of this for other breeds, other diets, and DCM in dogs without taurine deficiency are unclear.

Donadelli et al, July, 2020
Donadelli RA, Pezzali JG, Oba PM, et al. A commercial grain-free diet does not decrease plasma amino acids and taurine status but increases bile acid excretion when fed to Labrador RetrieversTransl Anim Sci. 2020;4(3). doi:10.1093/tas/txaa141

In this lab study, 8 Labrador retrievers were fed an ACANA grain-free diet for 26 weeks and their taurine levels were measured. No decline in taurine was seen. The relevance of this for other breeds, other diets, and DCM in dogs without taurine deficiency are unclear.

Freid Nov 2020
Freid KJ, Freeman LM, Rush JE, et al. Retrospective study of dilated cardiomyopathy in dogs. J Vet Intern Med. December 2020.

This study looked at medical records of dogs diagnosed with DCM at the Tufts Veterinary School between 2014 and 2018. Data from 71 dogs were analyzed, and 56/72 were eating nontraditional diets (grain-free, containing pulses, or manufactured by a company not meeting international industry standards). Dogs in the two diet categories were similar in most ways, though dogs on nontraditional diets were more likely to be in congestive heart failure when diagnosed. Taurine was only measured in a few dogs, most in the nontraditional diet group, and was only low in a couple of them. The study also reported an increase in the number of DCM cases seen at the hospital, and this began in 2016, before the first FDA announcement about diet-associated DCM in 2018.

Dogs were treated with a variety of different medications for their heart disease. Some received taurine supplementation (almost all in the nontraditional diet group), and about 55% in the nontraditional diet group had their diet changed while only 49% of those in the other group changed foods. Dogs eating a nontraditional diet that had a diet change lived significantly longer than dogs who did not. The authors concluded:

The underlying cause of diet-associated DCM remains unknown but is being actively investigated by the FDA and several researchers. Diet-associated deficiencies, toxins, or a multifactorial etiology (eg, nutritional, other environmental factors, genetics) remains possible explanations. The underlying cause of diet-associated DCM remains unknown but is being actively investigated by the FDA and several researchers. Diet-associated deficiencies, toxins, or a multifactorial etiology (eg, nutritional, other environmental factors, genetics) remains possible explanations. The underlying cause of diet-associated DCM remains unknown but is being actively investigated by the FDA and several researchers.

 

Posted in Nutrition | 2 Comments

Raw Pet Foods & The Death of Expertise

One of the more enlightening, and terrifying, books to come out in the last 5 years is Tom Nichols’ The Death of Expertise. In clear prose, with cogent argument and substantiating evidence, the author makes the case that the proliferation of misconceptions, delusions, and bizarrely wrong beliefs about the world in every domain, from science to politics, reflects powerful and pervasive elements of American culture. Access to accurate information is easier than ever, yet misinformation thrives. The problem is not that the truth isn’t available to us, it’s that we actively reject it. In Nichols’ words,

These are dangerous times. Never have so many people had so much access to so much knowledge and yet have been so resistant to learning anything.

[The real problem is] we’re proud of not knowing things. Americans have reached a point where ignorance, especially of anything related to public policy, is an actual virtue. To reject the advice of experts is to assert autonomy, a way for Americans to insulate their increasingly fragile egos from ever being told they’re wrong about anything…It is a new Declaration of Independence: No longer do we hold these truths to be self-evident, we hold all truths to be self-evident, even the ones that aren’t true. All things are knowable and every opinion on any subject is as good as any other.

This is a phenomenon I have wrestled with for many years in my efforts to promote science-based veterinary medicine. Giving people facts and evidence is not sufficient because, as Nichols says, “When feelings matter more than rationality or facts, education is a doomed enterprise.” Believers and promoters of pseudoscience in medicine are armored by feelings and conviction against any inconvenient facts or evidence. And the average pet owner is at a disadvantage since they can’t always judge the relative merits of scientific claims or data for themselves, and they are left deciding which source of information to trust or, in the worst case, simply choosing to believe the claim that best fits their pre-existing world view.

A recent survey of pet owners investigating attitudes about raw and commercial coked pet diets illustrates this death of expertise quite starkly. 

Empert-Gallegos A, Hill S, Yam PS. Insights into dog owner perspectives on risks, benefits, and nutritional value of raw diets compared to commercial cooked dietsPeerJ. 2020;8:e10383. doi:10.7717/peerj.10383

The facts are clear and not seriously questioned by actual experts, including veterinary nutritionists and most mainstream veterinarians. Raw diets have no proven benefits and any claimed for them are based on pure anecdote or theory. Raw diets do, however, have clearly established risks, including causing potentially deadly food-borne illness and often being nutritionally inadequate. The evidence to support these facts can be found in the many posts I have written on this subject.

Unfortunately, these facts are inconvenient for people who choose to feed such diets, and their reaction to being confronted with them is simply to redefine themselves as the “real experts.” Among owners feeding conventional cooked diets, 78% felt their veterinarian had a high level of knowledge about nutrition (4 or 5 on a 5-point scale). In this age when anyone can declare themselves an expert based on an internet search or some other informal way of investigating a subject, 65% of owners feeding cooked diets rated themselves as highly knowledgeable about pet nutrition, at the same level of knowledge, in fact, as their veterinarian. It is pretty unlikely that a majority of these owners have degrees in animal health or have taken formal instruction in animal nutrition, so this is a pretty unreasonable assessment. But it gets worse.

Of the raw feeders, 86% declared themselves highly knowledgeable (4-5 out of 5) while only 45% of them credited their veterinarian with this level of expertise. Raw feeders are no more likely than other pet owners to have degrees in animal health or nutrition, but they do have stronger feelings about the subject and are more likely to have investigated web sites or books for the general public making nutrition claims. These owners, whose beliefs are the least consistent with the facts, have the greatest confidence in their own knowledge and the least confidence in the expertise of actual veterinary professionals. This is unlikely to lead to good feeding choices or the best outcomes for pets.

The irrationality behind this false sense of expertise is illustrated by other findings in this study. Raw feeders rated commercial and homemade raw diets as more nutritious and safer than commercial cooked diets, both beliefs inconsistent with the facts. These owners likely imagine they have some special knowledge or insight into the “real truth” about pet food that owners feeding cooked diets, or even veterinarians, lack. This insight was not evidence, however, in their free-text answers to questions about the reasons for feeding raw diets, which included many vague references to unproven health benefits and terms consistent with unscientific beliefs about nutrition, such as “natural,” “processed,” “chemicals” and so on. 

These owners clearly believe strongly that raw diets are healthier than cooked diets, but the strength of this belief, and the confidence in their own expertise in the subject, are based on misinformation and falsehoods. As Mulder would say, “The Truth is Out There,” along with the evidence to support it. But truth and facts aren’t nearly as effective at generating belief as the vapid handwaving and passionate proselytizing of raw food advocates. Ultimately, if people choose belief and feelings over science and expertise, they can maintain any belief regardless of the facts. Raw feeding, like so many other alternative veterinary practices, is just one more illustration of this pervasive and malignant cultural problem.

Posted in Nutrition | 8 Comments

Neutering and Aggression in Dogs

I have written extensively about the positive and negative effects of neutering dogs for many years. This is an area of great controversy and rapidly advancing research. There is no simple relationship between neutering or age at neutering and health. Neutering itself changes many aspects of an animal’s physiology, and some of these changes have beneficial effects while others have harmful effects. The breed and genetic makeup of an animal, the age at which it is neutered, the environment in which it lives, and many other factors all work together to influence health, and the simplistic notion that neutering is “good” or “bad” for all dogs is simply untrue.

I recently found an interesting study examining the relationship between neutering and aggressive behavior in dogs which illustrates this complexity.

Farhoody P, Mallawaarachchi I, Tarwater PM, Serpell JA, Duffy DL, Zink C. Aggression toward Familiar People, Strangers, and Conspecifics in Gonadectomized and Intact DogsFront Vet Sci. 2018;5:18. 

It has traditionally been assumed, by dog owners and many veterinarians, that neutering reduces aggression, at least in males. The research to date, however, has been far from clear. Some studies support this idea, others show no effect of neutering on aggressive behavior, and some find neutering can increase aggression. The sex of the dog and the age at which it is neutered all play a role as well. While there likely is some relationship between neuter status and behavior, including aggression, behavior is a tremendously complex product of a multitude of factors, and what relationships there is between this and neutering is unlikely to be simple or universal.

This study approached the question in an interesting way. By looking through data collected in the past on thousands of animals using a behavioral questionnaire that has been widely used and is well-validated, they selected a huge population of dogs for which the details of neutering and also of aggressive behavior patterns were known. This has the advantage of a large enough s ample size to allow robust statistical comparisons. However, such a retrospective design has a lot of limitations, including the inability to acquire and consider relevant information that might not have been recorded in the survey and potential bias in the population of animals included. This was not a study population selected in an unbiased fashion specifically for the project but a database of voluntary responses to an online behavior questionnaire. People likely to fill out such a questionnaire, and their dogs, are likely different in meaningful ways from people not choosing to do so.

The researchers used mathematical techniques to compare the rates of different types of aggressive behavior (directed towards familiar people, directed towards unfamiliar people, and directed towards other dogs) with information about neutering and other factors (sex, age, weight, etc.). When all of the variables considered in the study were included in the model, no relationship was found between neutering at any age and any type of aggression.

When a different model was used to consider only a limited subset of the variables considered, the only relationship found was a small increase in the odds of aggression towards strangers among dogs neutered between 7 and 12 months of age.

The real-world significance of these findings is not completely clear. The authors emphasize that the results don’t support the assumption that neutering reduces aggression since neutered dogs were not significantly less aggressive than intact dogs. Of course, the other way to frame the findings is that the results suggest neutering has no effect on aggression either way, so aggressive behavior shouldn’t be a major consideration in decisions about neutering. The finding that aggression towards strangers was more common in dogs neutered between 7 and 12 months of age is likely a statistical fluke, and though the authors propose some possible hypotheses for it, they admit it is difficult to explain.

The study did not consider breed, which likely plays a significant role in some kinds of aggression based on previous studies. It also did not consider owner factors, which clearly influence both the behavior and the neuter status of dogs. It has always been an open question whether aggression by certain breeds or by intact dogs might have more to do with the owners who choose the breed and decide whether or not to neuter than with the neutering or breed per se. This study does not help clarify that question.

Overall, this is an interesting but not definitive contribution to the subject of how neutering might affect behavior. It undermines the traditional and simplistic notion that neutering prevents aggression, and it suggests that there are many factors influencing aggressive behavior in dogs and neutering is only one and likely not the most important.

Posted in General | 3 Comments

Five Most Dangerous Alternative Therapies for Pets- From SkeptVet TV

Posted in SkeptVet TV | 7 Comments