A few days ago, Dr. Patricia McConnell was good enough to review Dogs, Dog Food, and Dogma on her blog. Her review is thoughtful, overwhelmingly positive, and very kind (she even gives major kudos to Kody!). However, I believe that she also mischaracterizes some of what I’ve written in the book.
So earlier today I took the time to write a response to Dr. McConnell. It’s currently awaiting moderation on her blog.
I thought y’all might be interested to see it, in order to better understand what I have and haven’t argued for in Dogs, Dog Food, and Dogma. So please go visit Dr. McConnell’s blog to read her original review and then check out my response (as reprinted below):
I’m the author of Dogs, Dog Food, and Dogma. I’m writing in response to Dr. McConnell’s thoughtful review in order to clarify a couple of issues raised therein, lest prospective readers get the wrong idea about my book.
The first is the suggestion (from Ms. Case as much as from Dr. McConnell) that the process by which dogs metabolize carbohydrates is not well-understood by the scientific community. As Dr. McConnell writes above, “we don’t yet have much research on how these foods are metabolized in dogs (as Linda Case reminds us), but it seems reasonable to speculate that high glycemic foods might have the same [fattening] effect on dogs.”
I do not believe that I am speculating when I describe the process by which dogs metabolize carbohydrates. I believe I am describing something that is a matter of scientific consensus. As the many studies cited in the endnotes to my book show, this process has been studied for several decades, to the point where the body of research supporting it is discussed at length in both the NRC’s “Nutrient Requirements of Dogs and Cats” as well as all major veterinary nutrition textbooks, notably including the one edited by Ms. Case.
At a high level, that process can be described in four steps: (1) dietary carbohydrates are broken-down into glucose during digestion; (2) some carbs (“complex” ones) are broken-down more slowly than others (“simple” or “high-glycemic” ones); (3) the amount of the glucose in the bloodstream is the primary determinant of the amount of insulin secreted by the pancreas; i.e., high blood sugar begets heavy insulin secretion; (4) insulin’s job is to dispose of blood glucose, and one of the primary ways it does this job is by causing fat cells to absorb the substance; this is, literally, what it means for a dog to “get fatter.”
I’m open to being convinced otherwise, but I am not aware of any aspect of the foregoing process that is a matter of speculation. Indeed, the only novel thing that my book does with this topic is link it to the substantial body of evidence (at least six recent peer-reviewed studies) showing that dogs and cats fed high-carbohydrate diets in fact do get significantly fatter (or stay fatter) than those fed lower-carbohydrate diets, precisely as we should expect.
The second thing I wish to explain is that I don’t believe obesity is the sole cause of canine cancer. In Dr. McConnell words, DDD “focuses exclusively on fat as THE problem related to our dog’s health, and not on all the other factors, including environmental influences like herbicides and other chemicals like BPA in canned dog food. Not to mention the known influence of genetic risk factors.” (Emphasis hers.) But I don’t believe this is an entirely accurate characterization of my work.
It was not my intention to write a book arguing that fat is the only cause of cancer. As I explain at the very beginning of the book, body condition is clearly just one of many factors that influences whether a dog develops cancer:
“Recent research has indisputably shown that one’s genetic makeup can increase (sometimes dramatically) the likelihood of developing one or more cancers.”
“[G]enes are just one of many factors that have been shown to influence cancer risk.”
However, as Dr. McConnell noted, mine is a book about canine obesity — its biological causes, its sociological causes, its consequences, what it actually means to be obese — and not one about canine cancer. The links between the two topics are discussed, but those topics fill only 10% of the book’s pages, at most. I believe that the broader topic of obesity is one that warrants a book-length examination because, unlike genetics, adiposity is a cancer risk factor that can be readily controlled by pet owners. If we want to minimize the likelihood that our dogs develop cancer, body condition is something we can control. Genetics is not.
There are, of course, other environmental factors (beyond nutrition) that influence cancer risk. Including plenty that we can control in much the same way that we can control body condition. If you blow cigarette smoke in your dog’s face every day, the animal is quite likely to develop lung cancer at some point.
But unlike many other environmental factors, (1) obesity is stunningly pervasive and (2) there is a particularly robust body of scientific evidence that helps us understand the links between obesity and cancer (both the statistical relationship and HOW one is related to the other at the cellular level).
Is it the case that an environmental “chemical soup” is also contributing to America’s canine cancer epidemic? Perhaps. But, while this sounds reasonable, at present the body of scientific evidence proving it to be so pales in comparison to the science linking obesity and cancer. (Indeed, while I’m pretty ignorant about BPA, I know that large swaths of the leading veterinary nutrition texts are devoted to obesity and I’m not aware of a single one that even mentions BPA.) And I wanted to tell readers what we actually know, not what sounds reasonable. America’s leading veterinary nutritionists have written things like obesity is “the number one chronic health concern in our canine companions.” But there are few, if any, peer-reviewed papers making a similarly strong case against the “chemical soup.” Until there are, that remains largely a reasonable-sounding hypothesis.
(Moreover, I’m not so sure that the case again BPA sounds all that reasonable in the first instance. If BPA from canned dog foods is playing such a significant role in fueling America’s canine cancer epidemic, how come cancer is the leading cause of death among dogs in America today while fewer than 10% of dog-owners feed their pets any kind of canned food product? A topic for another day.)
I hope this helps to clarify some of what I’ve written. I very much welcome further debate on these matters (and any other scientific issues raised by my book). Between this blog, my blog, and Ms. Case’s blog, we have ample resources for respectful, professional public debate. And, given the stakes, it is a debate certainly worth having.
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