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Nutritional Cardiomyopathy: Still A Major Problem In Dogs

Staff holding pet

Though the case numbers have reduced in the past few years, the emergency and cardiology departments at MVES and OPVES are still seeing too many dogs develop life-ending complications of dilated cardiomyopathy (DCM) secondary to their diets, termed “nutritional cardiomyopathy”. Following is a summary of strategies to recognize potentially problematic diets, detect cardiac changes associated with nutritional deficiency/excess, and recommendations for the varying stages of the disease.


Some dogs develop dilated cardiomyopathy secondary to receiving long-term boutique canine diets.


Implicated diets have been empirically labeled “boutique”, representing smaller brand diets that do not undergo feeding trials in dogs before making it to the shelf.

Implicated diets are almost always grain-free

Many manufactures replace grains with legumes and their associated pulses (peas, lentils, beans); many grain-free diets have high concentrations of legumes/pulses as a result. Recent evidence supports that the high concentrations of these products may be the actual nutritional problem that leads to nutritional cardiomyopathy rather than the lack of grains itself.

Some cardiologists report development of nutritional cardiomyopathy with diets that contain grain but have high concentrations of these products (I have seen one such case).

Some dog food companies have moved the large “GRAIN-FREE” label from the front of the bag to a smaller label on the back of the bag (or no label at all) after the initial backlash a few years prior rather than changing the diet formulation itself. Check the label carefully and read the ingredient list.

Nearly all implicated diets will include a nutritional adequacy statement from the Association of American Feed Control Officials (AAFCO); this does not mean the diet is excluded from the risk of nutritional cardiomyopathy.

Nearly all implicated and non-implicated canine diets include taurine in the ingredients; having taurine in the diet (or extra supplementation beyond what is in the diet) does not prevent nutritional cardiomyopathy associated with grain-free diets.

Recent evidence suggests the risk of significant cardiomyopathy does not occur until consistent 1.5 – 2 years of eating such a diet, but the duration of feeding is incredibly variable between affected dogs (1).

A recent study found differences in metabolites between implicated diets and "standard" diets, finding some interesting differences that could point toward potential causes for development of heart disease (2).

Lower concentrations of B vitamins, cofactors in taurine and carnitine synthesis, was found in implicated diets. HOWEVER, blood-concentrations of taurine are most typically normal in affected dogs.

Higher concentrations of amino-acid related compounds, betaines, and xenobiotics/plant-based compounds were found in implicated diets. Some of these compounds have been implicated to interfere with carnitine transport and bioavailability in cardiac tissue in human studies. Genetic disruption of such transport has been connected to huamn patients with DCM.

There is still a lot we don’t know about what causes this nutritional cardiomyopathy in dogs, which is frustrating for us and our clients alike; ongoing research is searching for more answers, but many details regarding the association between these diets and DCM will likely remain unknown.


Any dog of any breed of any sex of any ageare at risk, though most are greater than 2 years of age due to length of time needed to develop cardiac changes.

Clearly not every dog eating a grain-free diet long term develops DCM. There are undoubtedly patient-specific factors (genetic and/or environmental factors) that cause some to develop problems and not others. As of yet, this appears to be very unpredictable.

Breeds with genetic predisposition to primary DCM (Dobermans, great Danes, etc.), Pitbulls and related breeds, and golden retrievers seem particularly at risk for nutritional cardiomyopathy development for reasons that are not yet clear.

Blood taurine concentrations (which are used as a surrogate for myocardial taurine concentrations and is perhaps a fallacy) are typically normal in dogs with grain-free diet nutritional cardiomyopathy unless the dog is of a breed known to be at risk of taurine deficiency (golden retrievers, Cocker spaniels).

As of yet, no clear evidence of cats developing nutritional cardiomyopathy with grain-free diets is reported; some cardiologists have recently reported anecdotal increases in cat cases of DCM with grain-free diets as a common denominator (I have yet to recognize this association in practice).


Dilated cardiomyopathy characterized by progressive reduction in ventricular systolic function (contractility), leading to progressive cardiac chamber dilation and associated wall thinning. These changes are often undetectable by owners and on physical examination until severe.

Once severe, congestive heart failure (CHF) can develop, primarily manifesting as cardiogenic pulmonary edema with associated clinical signs of tachypnea, dyspnea, and new onset cough.

Right-sided congestive heart failure is also possible (ascites, pleural effusion), but is less common

Arrhythmias, including supraventricular and ventricular ectopic beats, are possible with severe cardiac changes. Severe, life-threatening arrhythmias such as atrial fibrillation and ventricular tachycardia are possible.

We have seen dogs die or be euthanized because of these complications due to lack of recognition of the problem until it is too late.

Dogs with nutritional cardiomyopathy have the capacity for improvement in the heart’s structure and function; this contrasts with primary (genetic) DCM, where progressive worsening is inevitable. However, the more severe the cardiac changes/damage at the time of diagnosis, the lower the capacity for improvement.

TL;DR: mildly affected dogs can improve back to normal hearts with diet change and can live a normal life. Severely affected dogs are left with permanent hemodynamically significant cardiac changes that typically lead to life-ending complications of heart disease.

A recent study found expected survival time of 465 days for dogs that experienced CHF secondary to nutritional cardiomyopathy. This is better than the 6 – 9 month expected survival for dogs with CHF secondary to genetic DCM, but still terrible when considering many nutritional cardiomyopathy dogs are diagnosed as young adults.


Early detection of potentially problematic diets is imperative.

Avoid grain-free diets unless there is a medical reason for their use

Grain allergies are relatively rare in dogs

If grain-free diet is required for medical reasons or if client refuses to change, make sure concentrations of legumes/pulses are not high

Clear recommendations for this are not available given the wide variety of concentrations and the limited information gained from ingredient lists on food packaging. Typically, avoidance of pea, lentils, and beans (and their associated products) within the first 5 ingredients on the food label is recommended.

Consultation with a veterinary nutritionist is strongly recommended if home-prepared diets are fed.


Obtain information on current diet and diet history for every patient

It is highly recommended to provide an intake diet history form for client to complete, as verbal questioning often neglects diet history.

Recommend transition to grain-inclusive diet without high concentrations of legumes/pulses for ALL dogs, ideally from a pet food manufacturer that utilizes feeding trials (Hill’s, Iams, Purina, Royal Canin, etc.), unless there is a medical reason to avoid such diets. Gradual diet change is recommended to avoid gastrointestinal upset.

There is no "one-size fits all" diet for dogs. Different dogs in differential life stages have different nutritional needs. There is no single "best" dog food.

If avoidance of commercial dog foods is preferred and home-cooked is desired, recommend consultation with a veterinary nutritionist ( or use of, a homemade dog food formulating tool managed by board-certified veterinary nutritionists.

Blood taurine measurement and taurine and L-carnitine supplementation are likely unnecessary (but unlikely to be harmful), except for breeds with known predisposition to taurine deficiency (golden retrievers, Cocker spaniels).

If patient has received boutique brand grain-free (+/- high concentrations of legumes/pulses) diet for 2+ years, and…

Is asymptomatic with no physical exam abnormalities:

Change diet.

Recommend screening for substantial structural cardiac changes via thoracic radiographs and/or serum NT-proBNP measurement.

Start pimobendan (~0.25mg/kg PO q12hr) and refer to cardiologist for echocardiogram if radiographic cardiomegaly and/or elevated NT-proBNP.

No treatment or referral necessary without abnormalities; prognosis is likely excellent even if reduced systolic function were found on echo.

Is asymptomatic but has a heart murmur, arrhythmias, or other cardiovascular abnormalities on examination:

Change diet.

Same as above, except referral is recommended even without radiograph or NT-proBNP abnormalities to investigate the cause of the murmur/arrhythmias. In-house ECG is recommended for any case with appreciable arrhythmia on auscultation.

Other heart disease, separate from diet, could also be to blame, especially in predisposed breeds (myxomatous mitral valve disease in older small breed dogs, for example). Radiographs and NT-proBNP alone are unable to differentiate between different heart diseases.

Has symptoms potentially associated with CHF or other complications of heart disease:

Recommend screening for CHF and for substantial structural cardiac changes via thoracic radiographs and/or ECG.

Start treatment if CHF present; consider emergency referral to MVES/OPVES for stabilization if findings are severe (CHF, rapid AFIB, severe ventricular arrhythmias, syncope)

Change diet.

MVES Cardiology is always available for remote consultation to answer additional questions regarding this topic or others. References are available upon request.


Walker AL, DeFrancesco TC, Bonagura JD, et al. Association of diet with clinical outcomes in dogs with dilated cardiomyopathy and congestive heart failure. J Vet Cardiol. 2022 Apr;40:99-109. doi: 10.1016/j.jvc.2021.02.001. Epub 2021 Feb 18. PMID: 33741312.

Smith, C.E., Parnell, L.D., Lai, CQ. et al. Investigation of diets associated with dilated cardiomyopathy in dogs using foodomics analysis. Sci Rep 11, 15881 (2021).

Adin D, DeFrancesco TC, Keene B, et al. Echocardiographic phenotype of canine dilated cardiomyopathy differs based on diet type. J Vet Cardiol 2019;21:1-9.

Adin D, Freeman LM, Stepien R, et al. Effect of diet type on circulating taurine concentrations, cardiac biomarkers, and echocardiograms in four dog breeds. J Vet Intern Med 2021;35:771-779.

Freid KJ, Freeman LM, Rush JE, et al. Retrospective study of dilated cardiomyopathy in dogs. J Vet Intern Med 2021;35:58-67.

Kaplan JL, Stern JA, Fascetti AJ, et al. Taurine deficiency and dilated cardiomyopathy in golden retrievers fed commercial diets. PLoS One 2018;13(12


There is no doubt that published scientific evidence to support what I see in the hospital on a daily basis is limited at this time; though many factors play a role in this, it is important to remember that this problem was recognized only a few years prior (2018) and research takes time to plan, perform, and publish. I have no doubt that more and more scientific publications are on the way to help shed more light on this problem. This "deficiency" is not a legitimate reason to ignore the current association between implicated diets and heart disease in dogs; this is a very real problem even if we don't have all of the answers yet.

Shane Murphy, DVM, DACVIM (Cardiology)

Board-certified Veterinary Cardiologist

Mission Veterinary Emergency & Specialty