Dietary sugars, microbial acids and dental/gut disease – a deeper dive.

A look at how dietary sugars can negatively effect the dental and gut health of your patients.

Since as early as 1912, research has shown that in dogs, excessive quantities of glucose within their diet, together with meat, can lead to a variety of negative health consequences. For example, increased calcium oxalate crystal formation in the kidneys that are microscopically present in urine, which coincides with mucous gastritis.3 When excessive sugar is present in an animal’s diet, one of the waste products from microbial sugar fermentation is oxalic acid.5-6 Research from over the past 7 years shows that organic acids, like oxalic acid, can be produced by specific species of the dog’s oral and gut microbiomes that are linked to inflammation and chronic inflammatory diseases, such as periodontal disease. These organic acid fermentation products impact the canine’s local and systemic physiology. But, dietary sugars can effect both cats and dogs, and result in changes within their overall dental and gut health.

From mouth to gut: the effect of dietary sugars on pets

When a cat or dog is over-exposed to dietary sugars (complex and simple sugars), such as rice, fruits, and honey, the structure and microbial composition of the biofilms that exist on the tooth surface and subgingivally are significantly different.9,10 In a study on domestic and feral cats, domestic cats that ate commercial cat food had more calculus than feral cats who ate live prey.8 In our research, domestic cats on a commercial diet also have thicker plaque, (known to microbiologists as extracellular polymeric matrix, that contains extracellular polymeric substances, or EPS) with a course tartar and have more fungal species and a higher burden of C. acnes and Peptostreptococcus and Streptococcus spp than feral cats, which likely have a more diverse diet.

The EPS can be of a protective or pathogenic nature to the host, the nature of which is particularly influenced by diet. Diet influences the kinds of metabolic waste products produced by the oral microbiome and the identity of the microbes that inhabit the microbiome, and what kind of EPS they make. EPS examples made when sugar is available in the diet are oxalic acid, lactic acid, propionic acid, acetic acid and many others. The presence of these organic acids embedded in the plaque creates microenvironments that can reach as low as 3.8-5.5 pH, which induces local inflammation in the subgingiva and local areas of demineralization of the enamel, but also fosters the growth of acid-tolerant bacteria such as Enterococcus faecalis, Streptococcus spp and fungi.11 These microbes tend to be associated with inflammation and slowing the wound healing process, which is a significant problem in animals with periodontal disease and irritable bowel – two common gut-related inflammatory processes driven by sugars in the diet.12

 This transition from neutral or basic conditions in the mouth and lower gut to acidic conditions have a narrowing effect on the microbiome, also known as dysbiosis, which decreases the microbial diversity and constricts the kinds of waste products to an over-abundance of EPS of a pathogenic nature. A graphic description of the process is presented in Figure 1.

A graphic description of the process of dietary sugar break down
Figure 1. Dietary grains, fruit and simple sugars’ effect on the oral microbiome and pathogenic factors that transition a mouth from healthy to diseased. Starches present in many commercial diets and treats are rapidly broken down in the mouth and gut by microbial hydrolases to make simple sugars. These simple sugars drive the growth and development of disease-associated microbes through sugar fermentation pathways, builds large amounts of plaque/extracellular polymeric matrix that is comprised of EPS, which include organic acids and pathogenic factors that induce localized inflammation and tissue damage, if the sugar sources persist. This also has a direct effect on survival and persistence of harmful microbes that are overgrown, causing dysbiosis. Figure adapted from [13]

Preventive measures

Simple things that can be done to help dogs’ and cats’ upper and lower guts are:

  • Restrict commercial diets with carbohydrates to only a day or two a week. Things like chickpeas, sweet potatoes, potatoes, rice, wheat, corn, honey, are quickly converted to simple sugars by oral and lower gut microbes, which can lead to inflammatory waste products.
  • Limit treats and chews. Most commercial treats and chews have binding agents that are modified starches, which are very quickly converted to simple sugars.
  • Opt for products whose major ingredients are protein – to steer the metabolic activity of the microbes towards an alkaline-producing profile. The alkaline-producing profile will counterbalance the inflammatory acids produced by harmful dental bacteria.

References

  1. Mosenthal HO. 1911. Observations of the succus entericus. Exp. Med. 13(3):319-27.
  2. Grey EG. 1916. An experimental study of the effect of chole-cystgastrostomy on gastric acidity. Exp. Med. 23(1):15-24.
  3. King JH, Moyle RD, Haupt WC. 1912. Studies in glycosuria: second paper: glycosuria following anesthesia produced by the intravenous injection of ether. Exp. Med. 16(2):178-93.
  4. Marine D. 1914. Observations on tetany in dogs: relation of the parathyroids to the thyroid; relation of tetany to age, amount of parathyroid tissue removed, accessory parathyroids, pregnancy, lactation, rickets, sulphur, and diet; relation of parathyroids to sugar tolerance; effect of calcium salts. Exp. Med. 19(1):89-105.
  5. Hegedus DD, Rimmer SR. 2005. Sclerotinia sclerotiorum: When “to be or not to be” a pathogen? FEMS Microbiol Letters. 251(2):177-184.
  6. Li Z, Tongshuo B, Dai L, Wang F, Tao J, Meng S, Hu Y, Wang S, Hu S. 2016. A study of organic acid production in contrasts between two phosphate solubilizing fungi: Penicillium oxalicum and Aspergillus niger. Scientific Reports. (6):25313.
  7. Watson AD. 1994. Diet and periodontal disease in dogs and cats. Vet. J. 71(10):313-318.
  8. Clarke DE, Cameron A. 1998. Relationship between diet, dental calculus and periodontal disease in domestic and feral cats in Australia. Vet. J. 76(10):690-693.
  9. Takahashi N, Nyvad B. 2011. The role of bacteria in the caries process: ecological perspectives. Dent. Res. 90(3):294-303.
  10. Pitts NB, et al. 2017. Dental caries. Rev. Dis. Primers. 3:17030.
  11. Svensater G, Larsson UB, Greif EC, Cvitkovitch DG, Hamilton IR. 1997. Acid tolerance response and survival by oral bacteria. Oral Microbiol. Immunol. 12(5):266-73.
  12. Chong KK, Tay WH, Janela B, Yong AM, Liew TH, Madden L, Keogh D, Barkham TM, Ginhoux F, Becker DL, Kline KA. 2017. Enterococcus faecalis modulates immune activation and slows healing during wound infection. Infect. Dis. 216(12):1644-1654.
  13. Bowen WH, Burne RA, Wu H, Koo H. 2017. Oral biofilms: pathogens, matrix and polymicrobial interactions in microenvironments. Trends Microbiol. 26(3):229-242.
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Emily Stein, Ph.D. founded Primal Health (TEEF for Life) in 2017 to focus on improving the dental health of both humans and animals by producing oral microbiome modulation products. She has spent 12 years developing Selective Microbial Metabolism Regulation Technology (SMMRT™) at Primal Therapies, Inc., which is focused on using metabolic influencers to re-engineer disease-causing bacterial biofilms into those that are health-promoting, to decrease inflammation and to improve outcomes. Prior to that, she spent 7 years as a research fellow at Stanford University in Rheumatology and Immunology focused on the neuro-endocrine-immune axis in autoimmune and chronic inflammatory diseases. She holds a Ph.D. in Microbiology from the University of California at Berkeley where she studied inter- and intra-cellular signaling pathways involved in stress response and community development in bacteria and received her B.S. in Microbiology and Immunology at the University of Iowa where she studied the interaction between M. tuberculosis and innate immune cells.

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