We are all attracted to sites like this one because we are inherently interested in the health and well-being of our pets. The question is how much of the control of our pet’s health lies in our hands. We are bombarded with premium pet foods and supplements, all of which purport “better health” for our pets. Which diets do we choose? Many of us are vehement advocates of feeding our dogs raw, and avoid commercial diets altogether. We angst over whether to vaccinate. Which vaccines are necessary, how many doses of those necessary vaccines bestow immunity, and for how long does immunity last? Is neutering really the “healthy” choice for our pets? If so, when?
We think about these topics because we want our pets to achieve optimal health. There are clearly examples where making the right choices with vaccination, spay and neuter, and diet can clearly bestow benefits. For example, by keeping male dogs intact we can help prevent obesity, cranial cruciate rupture, and debatably, certain types of cancer. Nutrition clearly can help to control food allergy, obesity, dental disease. Limiting over-vaccination can lessen the chances of certain immune-mediated disorders and vaccine related sarcomas. But is it in our power to actually bestow longevity upon our pets? Can we make our pets live longer? At the end of the day, shouldn’t that be the ultimate goal? The answer may surprise and perhaps disappoint you.
First, it is helpful to reflect on some of the factors that determine longevity. How do our pets die? We can divide up causes of death into categories. Congenital malformations, dystocia (trouble with birthing), poor nursing and fading syndromes, exposure to infectious disease in unvaccinated puppies and kittens with under-developed immune systems, and inherited breed-related disorders, all contribute to early death, and thus lower overall species life expectancy. Most of these aforementioned causes of early death are not that common, and we have made great strides to lessen their occurrence. Proper vaccination against diseases like parvovirus and panleukopenia, proper nutrition for puppies who won’t suckle, identifying and not breeding animals with known genetic diseases, are all examples where we have made strides to lessen the incidence of infant mortality.
Accidental deaths also occur and thus lower overall species life expectancy. Anesthetic deaths, vaccine-related deaths, hit by cars (HBC), cats with high rise syndrome (cats jumping out of windows) are all examples of this. These too, are fortunately, rare. We can have a limited role in preventing accidents and have done so. Removing harmful toys from the market, not over-vaccinating, recognizing common household and dietary toxins (xylitol gum, chocolate, grapes, certain household plants etc.) all can help minimize these incidences. Proponents of spay and neuter would argue that spaying and neutering will cut down on wandering, dog fights, and HBC’s. The pros and cons of spaying and neutering are discussed in many articles on this site.
Metabolic disease, including cancer, are common causes of death amongst geriatric patients. Suffice it to say that we have made some strides over the years in treating these diseases. I think that it is also fair to say that while we have made great strides in treating and managing metabolic disease, we do face challenges. Simple economics limits both the research and development of various treatments used in humans, and access to some of the treatments that are currently available.
When we are discussing species life expectancy, we are not simply looking at all of the diseases that eventually kill us, but we are also examining the programmed life expectancy of a particular species. Why is it that elephants live 60-70 years, tortoises, 100 years, and gerbils, 7 years? What is it that programs us to age, and to subsequently die of old age? This process of deterioration with age is called senescence.
Cellular senescence is the process where cells in the body stop dividing. This occurs due to telomere (the end caps of genes) shortening. The telomere is responsible for repairing damaged DNA; and when it is shortened, cells lose their ability to repair themselves. Subsequently, they become more susceptible to oxidative damage and cancer expression. Organismal senescence is the aging of the whole animal. To what degree the two are related is an area of intense research. In organismal senescence, there is a disruption in the body’s ability to maintain homeostasis. Homeostasis is the animal’s ability to main stable internal conditions for things like pH and temperature when faced with varying external conditions. There becomes a general susceptibility to age-related diseases. There is always a cause of death. We don’t simply “die of old age”, but we become susceptible to organ dysfunction, lose our ability to deal with harsh environments, repair mutations and to fight cancer. There is an abundance of research into drugs and other therapies that focus on delaying senescence. A recent 60 Minutes special featured one scientist who predicted that within 30 years, we will be able to manipulate the genome’s ability to repair itself, and increase life expectancy in humans to 200 years! This obviously is a bold statement; but if true, it raises a host of ethical dilemmas.
What is also interesting is that there is variation in life expectancy, not just between species, but also within the same species. For example, within nature there is, in general, a correlation between size and life expectancy. Larger animals, in general, live longer (compare an elephant to an ant, for example). Why is this same phenomenon not true within the canine species? Smaller dogs have a longer life expectancy than larger dogs. Dr. Cornelia Kraus studied a host of different possible explanations including onset of senescence, faster aging, susceptibility to various types of diseases, etc. She concluded that once larger dogs hit senescence, they age faster and thus die sooner. One potential cause may be the higher levels of growth hormone and IGF-1 during growth in larger dogs.1. Manipulation of these hormones could be worthy of study in promoting longevity, but more research is warranted.
While we are certainly some time away from manipulating genes to alter longevity, are there any things that we can do to increase longevity? How about nutrition? Are there any diets or supplements that have been shown definitively to increase lifespan? Sadly, the only study in veterinary medicine involving diet and longevity was one that demonstrated that calorie restriction led to an increased lifespan in dogs 2. . Perhaps we should worry less about what to feed our dogs, but more on how much to feed them.
What effects does spaying and neutering have on life-expectancy. The benefits of keeping animals intact or of at least delaying spaying and neutering have been described throughout other posts on this blog. Does keeping animals intact increase life expectancy? As of now, there is conflicting data. A study involving 119 Rottweillers with exceptional longevity demonstrated that females that maintained their ovaries, for at least the first 4 years of their life, lived an average of 30% longer than their spayed cohorts. This phenomenon is also seen in humans, where women live longer than men and are more likely to reach 100 years old by a factor of more than 4:1. Possible explanations could include a protective effect of estrogen against oxidative stress and an enhanced immune response. 3. Interestingly, the study also demonstrated that spayed female Rottweilers were more likely to die of cancers like osteosarcoma (bone cancer). While this is another reason to consider not spaying, especially young pups, once these dogs were removed from the study, the association between ovaries and exceptional longevity persisted. Critics of this study cite that there was only one breed represented in the study. Furthermore, there was no indication of whether or not the intact females were bred, and if so how often; there was no indication of genetics or whether the participants in the study were related to each other; and that there was a small sample size of dogs in the study.
In contrast, a retrospective study examined over 40,000 causes of death among sterilized and reproductively intact dogs at American teaching hospitals. They were able to demonstrate that reproduction comes with a cost to the mother. This effect has been demonstrated in a wide range of animal species. The theory is that the energy expended by a mother to create, carry and nurture offspring, in order to pass on her DNA, comes with the cost of shortening her lifespan. They found in this study that sterilization was strongly correlated with increased lifespan. While it decreased risk of death from some causes like infectious disease, it actually increased the risk of death from cancer. 4. While the increased cancer risk was in sterilized animals, it was also supported in the Rottweiler study. The authors of this retrospective study concluded that the increased risk of cancer was simply a reflection of sterilized animals living longer, and thus being more likely to develop cancer. Critics of this study point to the fact that these data were collected at referral hospitals, which are often not reflective of the general population. There was no data as to whether or not the females in the study were bred or not. It is difficult to prove cause and effect through retrospective studies; moreover, the study didn’t specify at what age the sterilized dogs that were sterilized.
As we start to really understand the aging process at the cellular level, moral hazards surface. Would you directly manipulate your pets DNA or supplement him with hormones to make him live longer? At what point are we “playing GOD”? If it were feasible to manipulate your dog to live 50 years, would you do it? Why is that not ethical if tortoises live a lot longer than that? Are there already too many unwanted pets out there at current life expectancies? Certainly increasing life expectancy would exacerbate that problem. Your thoughts and comments below would be appreciated.
1. Kraus, Cornelia, Parvard, Samuel, Promislow, Daniel E.L. The Size-Life Span Trade-off Decomposed: Why Large Dogs Die Young. Am. Nat 2013. Vol 181. 492-505.
2. Kealy, Richard d., Lawler, Dennis F., Ballam, Joan M. Effects of Diet Restriction and lifespan and Age-related Changes in Dogs. Javma Vol 220 (9). 1315-20.
3. Waters, David. Kengeri, Seema. Clever, Beth. Exploring Mechanisms in Sex Differences in Longevity: Lifetime Ovary Exposure and Exceptional Longevity in Dogs. Aging Cell. 2009 December 8 (6): 752-5.
4. Hoffman, Jessica M. Creevy, Kate E., Promislow, Daniel E. Reproductive Capability is Associated With Lifespan and Cause of Death in Companion Dogs. PLOS One April 17, 2013.