“Processed dog food contributes to Cancer” – Fact.

Due to my stance on this matter, as logical as it may seem, I get quite a substantial amount of abuse. I get accusations of lying for profit, trying to report my Facebook page, leaving negative reviews of my business and even trying to shut it down.

All because I speak a relatively simple truth. Here is how processed food diets contribute to cancer.

Improve the diet, reduce the chances of disease.

It’s called epigenetics, the way we look after ourselves or our dogs affects gene expression and how healthy we are. The evidence for the power and simple truth of epigenetics is shown in plenty of animal model studies. (1, 2, 3, 4, 5)

Epigenetics (modifying gene expression) means a capability to reduce hereditary or genetic links to disease and has been shown possible with nutrition in these animal studies (6, 7, 8, 9, 10, 11, 12). This is called nutrigenomics and it’s why I make breed homemade dog food recipes. Each breed is different and is genetically more predisposed to one issue or another.

The Wrong diet contributes to Cancer.

Going back to cancer, this means that even if your dog has an increased probability of cancer due to breed type or just bad luck through genetics, you can reduce the probability of this disease through a specific homemade diet.

Cancer is a part of life and it affects not only humans, but molluscs, fish, reptiles, birds and mammals. However, genetically caused cancers are relatively rare. In fact extremely, this figure shows the role of genes and environment in the development of cancer. This is the human breakdown, but that is neither here nor there. The study of naturally occurring cancers in the domestic dog provides an appropriate model in the understanding, diagnosing and managing of cancer in humans [13,14,15,16].

This is extremely important. Dogs and humans are exceptional models of cancers for each other because they naturally develop the same cancers (21). Indeed, dog tumours are histologically similar to human tumours and respond similarly to conventional therapies (22). Conventional therapies like prevention in the form of lifestyle change, with epigenetics and with diet.

Processed dog food contributes to cancer.

This is a relatively simple concept to wrap ones head around and is backed up by mass of studies highlighting how chronic inflammation, obesity and calorie excess negatively effects DNA, increasing DNA damage, which increases the risk of cancers. (17)

Processed dry dog food and wet tinned food is made with ingredients so low quality it’s illegal to serve to humans, void of any fresh food ingredients, inappropriately balanced with macronutrients, packed with unnatural, dangerous additives that when heated become carcinogenic and engineered to last for over 2 years without refrigeration.

To say that processed food is not killing dogs, is wrong.

80% of dogs eat kibble. 70% of dogs are obese and these obese dogs die two years younger than healthy dogs (18).  The overwhelming parallel, driving why 47% of dogs die from cancer (Veterinary Cancer Society) is this mass spread of dangerously low quality and totally inappropriate processed food diets that we serve to our dogs every single day.

Researchers from the University of Helsinki conducted an experiment where dogs that ate processed foods or kibble for their whole lives, were weaned onto raw food for 3 months. These dogs showed an 81% decrease in disease markers in their bloodstream. Conversely dogs that had eaten raw food their whole life, were weaned onto kibble for 3 months and they showed an increase in disease markers of 353%. 

Improve the diet, reduce the chances of disease.

The fact that only 5–10% of all cancer cases are due to genetic flaws and that the remaining 90–95% are due to environment and lifestyle factor offers major opportunities for preventing cancer (20).

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References:

1.     Aagaard-Tillery KM, Grove K, Bishop J, Ke X, Fu Q, et al. 2008. Developmental origins of disease and determinants of chromatin structure: maternal diet modifies the primate fetal epigenome. J. Mol. Endocrinol. 41:91–102

2.     Schaible TD, Harris RA, Dowd SE, Smith CW, Kellermayer R. 2011. Maternal methyl-donor supplementation induces prolonged murine offspring colitis susceptibility in association with mucosal epigenetic and microbiomic changes. Hum. Mol. Genet. 20(9):1687–96

3.     Strakovsky RS, Zhang X, Zhou D, Pan Y-X. 2011. Gestational high fat diet programs hepatic phos- phoenolpyruvate carboxykinase gene expression and histone modification in neonatal offspring rats. J. Physiol. 589(Pt. 11):2707–17

4.     Wang L, Zhang H, Zhou J, Liu Y, Yang Y, et al. 2014. Betaine attenuates hepatic steatosis by reducing methylation of the MTTP promoter and elevating genomic methylation in mice fed a high-fat diet. J. Nutr. Biochem. 25(3):329–36

5.     Wolff GL, Kodell RL, Moore SR, Cooney CA. 1998. Maternal epigenetics and methyl supplements affect agouti gene expression in Avy/a mice. FASEB J. 12(11):949–57

6.     GeZJ,LuoSM,LinF,LiangQX,HuangL,etal.2014.DNAmethylationinoocytesandliveroffemale mice and their offspring: effects of high-fat-diet-induced obesity. Environ. Health Perspect. 122:159–64

7.     GlierMB,NgaiYF,SulistyoningrumDC,AleliunasRE,BottiglieriT,DevlinAM.2013.Tissue-specific relationship of S-adenosylhomocysteine with allele-specific H19/Igf2 methylation and imprinting in mice

8.     Huang Y, Khor TO, Shu L, Saw CL-L, Wu T-Y, et al. 2012. A γ-tocopherol-rich mixture of toco- pherols maintains Nrf2 expression in prostate tumors of TRAMP mice via epigenetic inhibition of CpG methylation. J. Nutr. 142:818–23

9.     Leclerc D, Le ́vesque N, Cao Y, Deng L, Wu Q, et al. 2013. Genes with aberrant expression in murine preneoplastic intestine show epigenetic and expression changes in normal mucosa of colon cancer patients. Cancer Prev. Res. 6(11):1171–81

10.  Schwenk RW, Jonas W, Ernst SB, Kammel A, Ja ̈hnert M, Schu ̈rmann A. 2013. Diet-dependent alterations of hepatic Scd1 expression are accompanied by differences in promoter methylation. Horm. Metab. Res. 45(11):786–94

11.  Vucetic Z, Carlin JL, Totoki K, Reyes TM. 2012. Epigenetic dysregulation of the dopamine system in diet-induced obesity. J. Neurochem. 120(6):891–98

12.  Wang L, Zhang H, Zhou J, Liu Y, Yang Y, et al. 2014. Betaine attenuates hepatic steatosis by reducing methylation of the MTTP promoter and elevating genomic methylation in mice fed a high-fat diet. J. Nutr. Biochem. 25(3):329–36

13.  Khanna C et al. 2006 The dog as a cancer model. Nat. Biotechnol. 24, 1065–1066. (doi:10.1038/ nbt0906-1065b)

14.  Rowell JL, McCarthy DO, Alvarez CE. 2011 Dog models of naturally occurring cancer. Trends Mol. Med. 17, 380–388. (doi:10.1016/j.molmed.2011. 02.004)

15.  Nat. Biotechnol. 24, 1065–1066. (doi:10.1038/ nbt0906-1065b)

16.  Rowell JL, McCarthy DO, Alvarez CE. 2011 Dog models of naturally occurring cancer. Trends Mol. Med. 17, 380–388. (doi:10.1016/j.molmed.2011. 02.004)

17.  Pelham JT, Irwin PJ, Kay PH. Genomic hypomethylation in neoplastic cells from dogs with malignant lymphoproliferative disorders. Res Vet Sci (2003) 74:101–4. doi: 10.1016/S0034-5288(02)00179-0

18.  https://bsava.com/position-statement/obesity/

19.  FerlayJ,SoerjomataramI,ErvikM,DikshitR,EserS,etal.2012.Cancerincidenceandmortalityworldwide: IARC CancerBase No. 11. GLOBOCAN 2012 v1.1, accessed on Jan. 23, 2015, Int. Agency Res. Cancer, Lyon, Fr. http://globocan.iarc.fr

20.  Anand, P., Kunnumakara, A.B., Sundaram, C., Harikumar, K.B., Tharakan, S.T., Lai, O.S., Sung, B. and Aggarwal, B.B., 2008. Cancer is a preventable disease that requires major lifestyle changes. Pharmaceutical research, 25(9), pp.2097-2116.

21.  Tamburini, B.A. et al. (2009) Gene expression profiles of sporadic canine hemangiosarcoma are uniquely associated with breed. PLoS ONE 4, e5549

22.  Paoloni, M. and Khanna, C. (2008) Translation of new cancer treatments from pet dogs to humans. Nat. Rev. Cancer 8, 147–156