Category Archives: Nutrition

Why is my Dog Fat?

The hormone insulin regulates carbohydrate, fat, and protein metabolism by partitioning ingested calories for either use or storage.

When blood glucose levels rise, usually due to carbohydrates in the diet, the pancreas secretes insulin to partition the glucose out of the bloodstream and into muscle, liver and fat cells. Muscles and the liver store a limited amount of this glucose as glycogen. Once filled, they become insulin resistant, meaning insulin no longer partitions glucose into them.

When all muscles and the liver become insulin resistant, superfluous glucose gets partitioned to fat cells, or adipocytes, through a series of chemical reactions that converts the glucose into triglycerides. Unlike muscle cells, adipocytes typically can store much more fat than muscle cells can store glycogen.

Once the adipocytes do, however, become insulin resistant, the pancreas responds by secreting even more insulin as an attempt to get glucose out of the bloodstream, thus starting a negative feedback loop: increased insulin, insulin resistance, and fat deposits. At this point both obesity and, often, diabetes begin. Moreover, as long as insulin remains high, it acts like a lock preventing these fat deposits from being tapped for energy. If your dog is overweight, this process is why.

That a hormone drives obesity, not the conventionally understood caloric imbalance caused by gluttony and sloth, should not come as any surprise. When a dog is a growing puppy, she is obviously consuming more calories than she is burning: she is growing. Hormones – principally growth hormone – drive this growth. When her adipocytes grow, hormones – principally insulin – drive this growth as well. Hormones regulate all growth. None of this is controverted and can be read in any introductory biochemistry textbook.

Moreover, a growing body of research demonstrates that elevated insulin correlates strongly with many chronic diseases such as cancer, hypothyroidism, diabetes, arthritis, and many others.[1] This indicates that many chronic diseases may be rooted in diet.

In short, hormones drive obesity and may drive many chronic diseases. Anything that raises your dog’s insulin will, at a minimum, likely cause his fat tissue eventually to grow. Carbohydrates do this. Since we already know that dogs are carnivores, replacing carbohydrates in the diet with healthy meat makes biological sense.


[1] See for example:  Weeth, LP, et.al. 2007. “Prevalence of Obese Dogs in a Population of Dogs With Cancer.” American Journal of Veterinary Research. Apr. (68)4: 389-98. (https://www.avma.org/News/Journals/Collections/Documents/ajvr_68_4_389.pdf);

Tvarijonaviciute, A., et. al. 2012. “Obesity-Related Metabolic Dysfunction in Dogs: A Comparison with Human Metabolic Syndrome.” BMC Veterinary Research. Aug. (8): 147-55. (http://bmcvetres.biomedcentral.com/articles/10.1186/1746-6148-8-147147);

Lund, EM, et al. 2007. “Prevalence and Risk Factors for Obesity in Adult Dogs from Private US Veterinary Practices.” International Journal of Applied Research in Veterinary Medicine. 4(2): 177-86. (http://www.jarvm.com/articles/Vol4Iss2/Lund.pdf).

Carnivore or Omnivore?

To determine how to feed our dogs we must first determine their natural diet. Although a body of research exists that claims dogs’ omnivorous disposition, it ignores the evolutionary and biological evidence that underscores dogs’ carnivorous nature.

The evolution of the domestic dog hints at dogs’ carnivorousness.  Humans domesticated dogs between 27,000 and 40,000 years ago.[1]   Anywhere within this range is not enough time for dogs to have evolved away from a carnivorous diet.  Similarly, this range coincides  with prehistoric humans — that is humans before the agricultural revolution, which began roughly 12,000 years ago.[2] Dogs therefore evolved for more than half of their existence alongside hunter-gatherers, who primarily ate meat, not agriculturists.

This evolutionary evidence reconciles with important genetic and anatomical clues. Domestic dogs share approximately 99.8% of their DNA with wolves and 96% with coyotes.[3] Both wolves and coyotes are carnivores.[4] Dogs fall in between them genetically. Anyone wanting to prove that dogs are not carnivores would need to discover how they are excepted from this spectrum. Outside of a few, very narrow, examples[5], no one has done so.

The anatomy and biology of dogs also underscores their carnivorous disposition. Dogs have the same digestive systems as their feral, carnivorous, cousins.[6] Dogs also share a number of other traits primarily unique to carnivores: panting, instead of sweating, to cool; lapping, instead of sipping, to drink; producing their own vitamin C, instead of consuming it; and, claws in lieu of hands or hooves.[7] Despite these overwhelming physical and behavioral signs, a number of researchers argue over the debatable position  that since dogs can digest carbohydrates, they must be omnivorous.[8]

This analysis, however, not only assumes that digestibility of a food alone determines its appropriateness in a diet, but also ignores the metabolic efficiency of that food once digested. Certain foods can be both digestible and biologically inappropriate. Such foods can lead to persistent hormonal imbalances that drive chronic conditions. Recent research shows that most chronic diseases in dogs such as kidney, liver and cardiovascular disease, as well as diabetes and arthritis, to name a few, cluster around obesity.[9]

If your dog isn’t obese, he or she is much more likely to be healthy.[10] Dogs fed a carnivorous diet do not become obese.[11] Lean dogs metabolize their food efficiently because they do not have unnaturally high levels of the hormone insulin constantly circulating through their bloodstreams.[12] Grains and sugars, though arguably digestible, are metabolically inefficient for dogs and raise insulin, thus driving obesity and illness.

Finally, proponents of the omnivorous dog ignore the observation that dogs fed carnivorously are on balance much healthier than dogs fed omnivorously. Common sense dictates that whatever diet produces the healthiest dogs is the natural diet of dogs – the starting point of our inquiry. But the science alone obviates the need for common sense.


[1] Skoglund, P., E. Ersmark, E. Palkopoulou, L. Dalén. 2015. “Ancient Wolf Genome Reveals An Early Divergence of Domestic Dog Ancestors and Admixture Into High-Latitude Breeds”. Current Biology. Jun. 25(11): 1515–19. (http://www.cell.com/current-biology/abstract/S0960-9822(15)00432-7).

[2] See generally, Diamond, J. 1999. Guns, Germs, and Steel: The Fates of Human Societies. (New York: Norton).

[3] Wright, R.K. 1993. “Molecular Evolution of the Dog Family.” Trends Genet. Jun. 9(6): 218-224. (http://www.sciencedirect.com/science/article/pii/016895259390122X).

[4] Landry, S.M., H.J. Van Kruiningen. 1979. “Food Habits of Feral Carnivores: A Review of Stomach Content Analysis.” Journal of the American Animal Hospital Association. Nov./Dec. Vol. 15: 775.

[5] See, for example, Axelsson E., et al. 2013.   “The Genomic Signature of Dog Domestication Reveals Adaptation to a Starch-Rich Diet.” Nature. (495): 360-364. (http://www.nature.com/nature/journal/v495/n7441/full/nature11837.html).

[6]Strong carnassial teeth, simple stomachs of great digestive capability, thickly muscled esophaguses, stomachs, and intestines, residual cecae, and simple non-sacculated colons.

[7]Roberts, W.C. 2000. “Twenty Questions on Atherosclerosis.” Proceedings (Baylor University. Medical Center). Apr. (13)20: 139–143.

[8] Axelsson, et. al.

[9] See, for example:

German A.J., S.L. Holden, T. Bissot, R.M. Hackett, and V. Biourge. 2007.“Dietary Energy Restriction and Successful Weight Loss in Obese Client-Owned Dogs.”Journal of Veterinary Internal Medicine. Nov./Dec. 21(6): 1174–80. (http://www.ncbi.nlm.nih.gov/pubmed/18196722).

Hansen, R.A., et. al. 2008. “Fish Oil Decreases Matrix Metalloproteinases in Knee Synovia of Dogs With Inflammatory Joint Disease.” Journal of Nutritional Biochemistry. Feb. 19(2): 101-8. (http://www.ncbi.nlm.nih.gov/pubmed/17531456).

Jeusette I.C., E.T. Lhoest, L.P. Istasse, and M.O. Diez. 2005.“Influence of Obesity on Plasma Lipid and Lipoprotein Concentrations in Dogs.”American Journal of Veterinary Research. Jan. 66(1): 81–6. (http://www.ncbi.nlm.nih.gov/pubmed/15691040).

Kealy R.D., D.F. Lawler, J.M. Ballam, S.L. Mantz, and D.N Biery, E.H. Greeley, G. Lust, M. Segre, G.K. Smith, and H.D. Stowe. 2002.“Effects of Diet Restriction on Life Span and Age-Related Changes in Dogs.” Journal of the American Veterinary Medical Association. May 220(9): 1315–20.   (http://www.ncbi.nlm.nih.gov/pubmed/11991408).

Rawitscher, R.E., W.S. Gardner, and W.H. Muller, Jr. 1973. “Experimental Canine Coronary Atherosclerosis.” Annals of Surgery. Mar. 177(3): 357-61. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1355540/pdf/annsurg00253-0109.pdf)

Tvarijonaviciute et al. 2012. “Obesity-Related Metabolic Dysfunction in Dogs: A Comparison with Human Metabolic Syndrome.” BMC Veterinary Research. Aug. (8): 147-55. http://www.biomedcentral.com/1746-6148/8/147.;

Tvarijonaviciute et al.   2013. “Effect of Weight Loss in Obese Dogs on Indicators of Renal Function or Disease.” Journal of Veterinary Internal Medicine. Jan./Feb. (27)1: 31-8. (http://onlinelibrary.wiley.com/doi/10.1111/jvim.12029/full).

Weeth, L.P, et al. 2007.“Prevalence of Obese Dogs in a Population of Dogs With Cancer.” American Journal of Veterinary Research. 68(4): 389-98.

Yamka R.M., K.G. Friesen, and N.Z. Frantz. 2006. ”Identification of Canine Markers Related to Obesity and the Effects of Weight Loss on the Markers of Interest.” International Journal of Applied Research in Veterinary Medicine. 4(4): 282–92.

[10] Ibid.

[11] Rothwell, N.J., and M.J. Stock. 1981. “Thermogenesis: Comparative and Evolutionary Considerations.” In Cioffo, James, and Van Itallie, eds., 1981, 335-44.

[12] See, for example:

Berson, S.A. and R.S. Yalow. “Insulin ‘Antagonists’ and Insulin Resistance.” In Diabetes Mellitus: Theory and Practice, ed. M. Ellenberg and H Rifkin (New York: McGraw-Hill), 388-423. (1970).

Gordon, E.S. 1970. “Metabolic Aspects of Obesity.” Advances in Metabolic Disorders. 4: 229– 96.

Gordon, E.S. 1970 1969. “The Metabolic Importance of Obesity.” In Symposium on Foods: Carbohydrates and Their Roles, ed. H. W. Schultz. Westport, Conn.: Avi Publishing, 322– 46.

Taubes, G. 2007. Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight-Control, and Disease. (New York: Random House), 178-185.