Evidence Update: Does Dry Food Increase the Risk of Diabetes in Cats?

A perennial question in veterinary nutrition is the relative pros and cons of dry commercial diets. In particular, pet owners and vets alike have a lot of questions about the nutritional value and potential risks of dry food for cats. The argument is often made by proponents of alternative diets that, as obligate carnivores, cat cannot utilize the carbohydrates in commercial diets and, in fact, these contribute to disease. There is no question that cats are carnivores, and it is reasonable to suppose plant foods may not be nutritionally ideal for them. However, the naturalistic fallacy, that says whatever happens in nature is somehow perfect and ideal, is also at play in this issue. And there is evidence that properly prepared plant foods can contribute to a healthy diet for cats, though it seems that strictly vegetarian diets are unlikely to meet all of a cat’s nutritional needs.

As for the role of dry commercial foods in disease, there is very little evidence to go on, despite the widespread, often inflexible opinions many people have on the subject. About five years ago, I reported on an expert consensus document put out by the American College of Veterinary internal Medicine (ACVIM), which addressed this question. Here were the conclusions of that group of experts:

  1. Are dietary carbohydrates an essential or required nutrient for cats?
    Answer- No. Based on a good quality and quantity of evidence, most cats do not require dietary carbohydrates. There are some simple sugars in feline milk, so it is possible that nursing kittens may require these but no clear deficiency has been demonstrated.
  2. Can cats effectively utilize dietary carbohydrates for energy and nutrition?
    Answer- Yes. Based on a good quality and quantity of evidence, cats can effectively digest, absorb, and utilize dietary carbohydrates.
  3. Do dietary carbohydrates in the diet cause obesity?
    Answer- No. The cause of obesity in almost all cats is excessive calorie intake irrespective of whether the calories come from protein, fat, or carbohydrate. In fact, low carbohydrate foods may be more likely to lead to obesity if they are higher in fat than regular diets.
  4. Do dietary carbohydrates contribute to the development of diabetes?
    Answer- The consensus was that they do not, however the research evidence is very limited and not always consistent. The consensus was that even if carbohydrates do play a role as a risk factor for diabetes, this is dwarfed by the much more important factor of obesity.
  5. Are low-carbohydrate diets useful in the management of feline diabetes?
    Answer-Maybe. The evidence is limited and conflicting, and the committee did not achieve a consensus.

I have generally encouraged clients to feed their cats canned rather than dry food when possible because there is at least some reasonable theoretical argument for doing so. However, in the absence of strong evidence, I do not make a crusade out of this as some vets do.

Recently, a new study was published addressing one aspect of this issue, the potential association of diet with the occurrence of diabetes in cats. The theory is sometimes advanced that the carbohydrates in dry diets encourage obesity and create stress on the pancreas, the organ which produces insulin, and that this increases the risk of diabetes for cats eating such diets. Again, there has not so far been much actual evidence that this theory is correct, but the new study does contribute some. As always, the study has strengths and weaknesses which influence how much weight we should give the results and conclusions.

M. € Ohlund, A. Egenvall, T. Fall, H. Hansson-Hamlin, H. R€ocklinsberg, and B.S. Holst. Environmental Risk Factors for Diabetes Mellitus in Cats. Journal of Veterinary Internal Medicine. online early view January, 2017

The study was a case-control design. This means that a database of cats (in this case, those covered by a Swedish pet insurance program) was analyzed to identify cats with diabetes (cases) and those that were as similar as possible in other respects but did not develop diabetes (controls), and any available lifestyle information was compared to see what occurred more often in the cases than the controls, and vice versa. This can identify factors associated with the occurrence of diabetes.

It is important to recognize up front that such studies cannot establish causal relationships, and they are subject to a variety of sources of error, some of which I will discuss relevant to this particular study. They are a useful tool, however, for identifying potential risk factors for disease.

The first issue is the population of cats involved. Cats in Sweden who are covered by health insurance could differ in a variety of relevant ways from other populations of cats. Any associations found for such cats may or may not apply to, say, indoor cats in San Francisco or barn cats in Texas.

The other major concern is that the data consisted entirely of owners’ answers to a questionnaire, not medical records. That means that the study relied on owners correctly remembering medications their cats had been given, characterizing their diet history and eating habits, and reporting other lifestyle details that were then analyzed for associations with the occurrence of diabetes. Studies of human patients and their caregivers and family members show that our memories of such things are often highly unreliable and influenced by the very factors such studies are trying to evaluate. Owners whose cats have developed diabetes are likely to remember their cats’ medical and dietary histories differently than those whose cats don’t have this disease, and this can influence the associations seen in the data.

The authors are, of course, aware of and openly address these limitations:

Limitations of our study are mainly related to the study design, especially the problems with dietary recall bias and the difficulties for owners to accurately assess their cat’s body condition. Owners of diabetic cats can be more prone to remember events preceding the cat’s diagnosis of DM [diabetes] because of a recall bias, causing a type I error. They can also have more knowledge about DM and be more aware of the risk factors for disease, which might influence their responses. For example, owners of diabetic cats are more likely to be aware of their cat’s body condition, and also of the dangers of obesity. Moreover, owners of diabetic cats are asked about circumstances the year preceding their pet’s diagnosis of DM, which can be several years back in time. This differs from the control group, whose replies refer to the last year in the cat’s life, in general more recently.

Such limitations do not, of course, invalidate the research. All research has some sources of error that cannot be perfectly controlled. This is why consistency in findings across studies by different investigators and using different designs is crucial to arriving at an accurate understanding. However, we always need to incorporate an awareness of these sources of error into our interpretation of research studies and try not to blindly rely on the results of any one.

And what were the results of this study? A number of factors were associated with either a greater or lesser risk of diabetes. Breed and sex and previous use of corticosteroid medications were factors that have been associated with diabetes in other studies and were in this research as well. With regard to medication, however, no details about type of steroid, dose, or frequency were available, and the association relied entirely on owner memory, so this is not a particularly useful finding in terms of guiding the use of such medications.

There were some associations with diet and diabetes, but these were complex and not entirely clear. Partly, this is because obesity is a well-established risk factor for diabetes, and the association between type of diet and occurrence of diabetes seems to vary with body weight (again, with both diet and body weight determines solely by owner memory and judgment). Here is one example from the paper.

The only association that is statistically significant (the confidence interval does not include 1) is the comparison of dry food and wet food only in cats of normal weight. A couple of others are close, but it is impossible to tell if these would achieve statistical significance under different circumstances. The more important question, however, is do the pattern of results make sense? If dry food increases the risk of diabetes, shouldn’t this be the case for cats of all body weights? Of is the role of obesity so great that it swamps any effect of diet, so diet only shows up as a risk factor in cats of normal weight? The authors are very reasonable and circumspect in how they address these findings, and they are clearly aware that the implications of these results need to be sorted out in the context of the existing literature and, ideally, through further research.

The association of DM risk with dry food diet in normal weight cats is to our knowledge previously not reported, and it has earlier been proposed that the proportion of dry food in the diet might not be a risk factor for DM. However, because cats are obligate carnivores, whose natural diet consists mainly of protein- rich animal prey, it has been hypothesized that a high carbohydrate diet such as commercial dry food might put an increased demand on the cat’s insulin secretion, thereby predisposing them to the development of DM….

In our study, an effect of type of diet was found only in cats with a normal body condition, suggesting that for overweight cats, the risk of the obesity per se is more important than the type of diet….

Our results should be interpreted with caution, as the macronutrient content in food given to cats in our study is unknown, although a typical commercial dry diet generally contains more carbohydrates than a typical wet diet. It is also possible that the difference between dry and wet food detected in our study might relate to a protein effect rather than a carbohydrate effect, as it is not possible to alter one macronutrient without another.

The study also found some associations suggesting being indoors might increase the risk of diabetes. However, this involves a number of potential confounding factors, and only one of these was directly evaluated. Obviously, if obesity is a known risk factor and indoors cats are more likely to be obese, due perhaps to constant access to food or lower levels of activity, then being indoors would be associated with diabetes without being directly causal. Indoor cats kept lean would not be at higher risk just because they are indoors in obesity is the intervening condition.

In this study, the results were presented only in terms of the interaction between indoor status and activity level (again,  reported by owners, who may well not characterize their cats’ levels of activity accurately; who sits home and monitors their cat’s activity all day, and who sees what their cat is doing when it is outside all the time?). Cats reported to have moderate or low levels of activity seemed less likely to have diabetes if allowed outdoors, whereas outdoor access did not seem associated with diabetes in cats reported to be active.

This is an interesting finding, but incomplete and in need of a lot more direct study to find the direct and modifiable risk factors involved. (Not to mention the question of whether the overall health and longevity of cats is better when kept indoors or allowed outdoors. Even if indoor-only cats are at greater risk for diabetes, they may be healthier overall and live longer than outdoor cats because they are protected from infectious disease, parasites, trauma, and predation.)

Undoubtedly, some anti-vaccine activists will make much of the association seen between vaccination and diabetes in this study. However, there are many reasons to be skeptical of this association. Apart from all the study limitations already noted, there is no plausible mechanism by which vaccines could lead to diabetes (unlike, say, obesity or dry food), the vast majority fo the cats were vaccinated (93%), and this seems more likely to be a spurious associated confounded by the fact that cat owners who take their pet to the doctor more often are both more likely to have them vaccinated and more likely to have diabetes diagnosed than owners who don’t see the vet much and tend not to pay for vaccines or diagnostic tests. Here’s what the authors say about this issue:

An association with an increased risk of DM was seen in fully vaccinated cats compared with unvaccinated cats, but the proportion of unvaccinated cats in the study population was low (7%). There are no supporting evidence that vaccines cause DM in cats, and the association detected in our study should not be interpreted to support a decision not to routinely vaccinate cats. The finding can be explained by diabetic cats having had more visits to a veterinarian than control cats, and can also refer to a recall bias because owners of diabetic cats could be more aware of their cat’s health and vaccination status than owners of healthy cats.

Bottom Line
Overall, this study is a preliminary step in looking for lifestyle factors that might increase the risk of diabetes in cats. It is plausible that dry foods, for example, could be a risk factor, and this study makes more focused investigation of that hypothesis clearly worthwhile. However, there are a lot of limitations to the study and unanswered questions, so this study clearly cannot be taken to prove any such causal relationship. It also appears to show an association between vaccination and diabetes, and this is almost certainly a spurious relationship caused by uncontrolled confounding and other study limitations, which illustrates why these results have to be taken with a grain of salt, or perhaps even a few grains.

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4 Responses to Evidence Update: Does Dry Food Increase the Risk of Diabetes in Cats?

  1. Aign0r says:

    Hi, first I have to say I love your blog, you have some very good content. I am also a veterinarian trying to be as evidence based as possible, though when it comes to nutrition particularly I have troubles coming to peace with some of the research coming from Veterinary nutritional researchers. My distrust comes mostly from the influence I know pet food industry has on veterinarians in general, and is additionally fed by all the recent developments in research of human nutriton, and how for 50 years we’ve been lied (I say lied because we now know sugar industry bought scientist to push their agenda) that sugar is great and fat is bad, when it turns to be other way around. Don’t get me wrong I’m not against dry food, I’ve had 20 cats in my lifetime and many more fosters that ended up adopted by someone else and all of them ate kibble almost exclusively, and none of them had any issues, what so ever let alone diabetes. However I can’t wrap my head around something the us vets do every day which is give contrary advice to human nutritional science, which I think we’ll agree is far more advanced, especially regarding refined and processed foods. Almost every modern nutritional guideline tells us to avoid processed foods like the plague, but we do exact opposite for our patients.
    I would really like to hear your thoughts on these issues, I’ll understand if you don’t want to speculate publicly about this given that contents of your blog are some the least speculative I’ve ever seen. But if you’d like to share your thoughts on this with me hit me up on email, I’d like to hear opinion from someone as thoughtful as you are.
    Keep up the good work, really appreciate your work!

  2. skeptvet says:

    Thanks for the comment and very good question. I’m happy to speculate, so long as I make it clear that’s all I’m doing here. 🙂

    One problem with your question, I think, is the definition of “processed food.” In human nutrition, this refers to packaged convenience foods and fast food, which are designed and marketed to appeal in terms of taste, appearance, and so on, and which are not intended to be nutritionally balanced or healthy as the predominant food source. Fresh fruits and vegetables, whole grains, reasonable amounts of lean meat and other animal products, fish, etc are recommended as a healthier diet because there is good evidence this diet actually is healthier. There is also, unfortunately, good evidence that simply telling people this doesn’t bring about healthy eating habits. We are evolutionarily primed to seek sugar, salt, fat, and other foods that were scarce in the environment in which our species evolved and which, now, are all too plentiful. The trick for humans, is finding a way to make people eat a nutritionally balanced diet that limits the very things we find most appealing in foods, and we haven’t found a very effective way to do this yet.

    In veterinary medicine, commercial diets are designed and produced quite differently than human convenience foods. They are specifically designed to be balanced and complete nutrition, and there is a fair bit of research showing they are adequate and able to support a long, healthy life. There is much we don’t know, of course, and there is undoubtedly a risk of bias in industry-funded research. However, the best evidence so far supports these as diets that allow a long, healthy life for many pets.

    Now, are these diets optimal? Who knows? I absolutely believe our existing knowledge is incomplete, and we will undoubtedly continue to improve pet nutrition. It is certainly possible that fresh diets similar to what is recommended for humans (with some significant differences related to our very different evolutionary history and nutritional requirements) may be better than commercial diets. Unlike in humans, however, we don’t yet have any direct evidence to show this is true. And we do know that many homemade diets out there lack nutritional adequacy over the long term. If we tell people to replace commercial diets with homemade diets, might we not end up with most people feeding something inferior to what they do now? We can’t know what exactly to tell them to feed until we have research evidence comparing commercial and fresh diets and looking at long-term health outcomes, as has been done in humans. And we still have to consider the possibility that even if we have a better homemade diet to offer, people might end up feeding diets that are convenient, inexpensive, and not actually healthy or appropriate, as humans often do for ourselves even though we have a pretty good idea what we should be eating.

    Overall, I’m somewhat sympathetic to the hypothesis that fresh diets might be better than existing commercial diets. But I think existing diets are a lot better than critics generally admit, and I think we need to develop evidence-based guidelines for what a healthy homemade diet is before we discourage people from feeding commercial diets for which we do have a lot of evidence to support nutritional adequacy.

  3. Aign0r says:

    Thanks for the replay, my definition was definitely off, since I didn’t consider general definition but what I mean by processed foods, being foods which are full of preservatives, and other additives some of which have been proven to have detrimental health effects on humans, though most of these are usually only found in low quality foods, and my bigger concern with these foods is loss of nutritional value through these processes and storage, since air in a big city probably has more toxins and carcinogens than even the worst kind of processed food available.

    That aside I agree with most of what you wrote, but In my research into human nutrition I have come to believe that “balanced” diet is kind of a red haring, meaning that proper nutrition in humans seems to be highly individual thing. Many people thrive and are healthier on unconventional diets like keto, vegan, even full carnivorous, while others crash and burn on them, and none of these would fit definition of “balanced” diet, not too mention that most dietary recommendations date back to 50s and 60s and haven’t changed since.
    This is a recent finding for me and I’ve been thinking about pet nutrition in the same light, and I haven’t been able to find (maybe i haven’t looked hard enough) who, when, how and in which breeds, determined what “balanced” diet is. Also that longevity study from PURINA didn’t really fill me with confidence… whilst 13,5 years isn’t a bad lifespan for a Labrador, the fact that none of 48 dogs lived longer then that is somewhat worrying to me.
    I feel like we’re being fed bunch of ringers from the industry to keep as at bay and keep selling their products. Especially in light of recent evidence that human food industries have done exactly that in the last 70 years.

  4. skeptvet says:

    Well, I don’t think you are likely to find evidence for what an optimal diet is in particular breeds because I don’t think it exists. It is a very complex subject that requires difficult, lengthy, and expensive research. There is considerable uncertainty about many nutrition issues in humans, and this is with epidemiologic studies in thousands of people lasting decades. Not likely we will ever have the same quality of evidence in our field.

    I would be interested in what specific additives you are concerned about. I certainly haven’t investigated them all, but whenever I have looked into the evidence for specific flavorings or colors or preservatives people are concerned about, I have yet to find convincing evidence of harm. Usually, the concern is a media-based extrapolation from lab animal studies that don’t reflect real-world exposure.

    I think your concerns about the bias in the info we get from industry is valid. However, it begs the question of what information we have that is more reliable. Most of the alternatives recommended to commercial diets are just made up based on the particular ideology or bias of the person inventing the alternative (e.g. BARF), and they have even less reliable evidence to support health claims than exists for commercial diets. It’s a bit of a bind in terms of making specific recommendations to clients.

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