Literature Discussed: "Metabolomic profiling in dogs with dilated cardiomyopathy eating non-traditional or traditional diets and in healthy controls" Smith, C.E., Parnell, L.D., Lai, CQ. et al. Sci Rep 12, 22585 (2022). https://doi.org/10.1038/s41598-022-26322-8
Key Takeaway: While the exact causal dietary components have not been identified, this research identified metabolic differences between dogs with diet-associated and primary DCM, strongly supporting a difference in mechanism for the two disease processes.
Funding: Nestlé Purina PetCare, Tufts Springboard, and the Barkley Fund. This work was also funded in part by United States Department of Agriculture Project Number 8050-51000-107-00D
This study analyzed samples from 75 dogs: 38 dogs with DCM and 12 healthy dogs eating diets that were grain-free or contained pulse legumes or potatoes in the first 10 ingredients (NT diets) and 8 dogs with DCM and 17 healthy dogs eating grain-inclusive diets without pulse legumes or potatoes in the first 10 ingredients (T diets). At 9-month follow-up, 20 of 37 NT DCM dogs were alive to be re-analyzed, compared to 2 of 8 T DCM dogs. Several analyses were performed.
Dogs were compared for metabolites based on disease status, irrespective of diet. Dogs were also compared based on diet, irrespective of disease status. Those two sets were compared to assess potential relationships between diet and DCM. Several compounds were identified that were higher in both groups, some of which changed or decreased significantly following diet change. Analysis to determine the predictive nature of these compounds found 86 and 87% predictive accuracy for DCM status and diet respectively. Authors also compared pathways and findings to previous metabolic research on DCM. The study identified several pathways for further investigation of disease mechanism.
In comparing of pathways between groups, researches noted very little overlap between primary DCM cases and diet-associated DCM cases, suggesting that the causal mechanism of disease is likely to be very different in these instances.
Based on their findings, the authors hypothesize that a nutrient or compound excess, rather than a deficiency, underlies the diet-associated cases of current interest.
The authors recognize several limitations and discuss them (and the reasons for them) in the study. For example, the group of dogs with DCM eating "traditional" diets was smaller, but not unexpectedly, because many dogs being diagnosed with DCM are eating non-traditional diets. The authors discuss the potentially confounding role of breed, and also acknowledge that the diet-groupings are less than ideal, but necessary in the absence of an identified causative ingredient or compound. Authors end, "These findings have the potential to identify therapeutic targets to prevent or delay DCM progression, and validate the application of canine DCM as a spontaneous animal model for human DCM."