Spoiler alert, no food does. Some foods may help, but the one for your dog (or cat) is unlikely to come from a magazine article or a ‘best of’ list. 

There’s a lot of disingenuous marketing in the pet industry. Many brands claim their product(s) have the fix to whatever ails your pet. However, and I want you to read this: if, indeed, any one product was the antidote to a specific issue, or disease, it would be the standard of care. In fact, if it was really that good, and improved the situation so dramatically then that company would file a patent, and have invested large sums of money into clinical trials with the goal of having that product approved as a drug.

Now think about this: we don’t see pet food or supplement companies doing that, right?  No, we do not. Because we don’t see them doing this, they are also unable to make claims that their product ‘cures’, ‘treats’, ‘mitigates’, or ‘prevents’ disease. They are also not allowed to imply this, and doing so makes the folks over at the FDA and FTC cranky.

I’ve been in this industry about 15 years now, and it saddens me to report that most pet food and supplement companies spend more money on marketing than they invest into research and safety. So when a “Best Dog Food for Allergies” or a “Best Overall” food you see on social media from a ‘news’ outlet I want you to think twice.

A company could NOT say this about their own product without triggering regulatory compliance violations. So, a loophole becomes getting that product positioned in a ‘best of’ list by a journalist, in one form or another.

As a pet parent, you already do the work – much more than you would probably like to admit. You read the labels, articles, dove way deeper to a place on Reddit than you wish you knew existed. You’ve probably switched foods two or three times this year chasing an itch, or smell, or stomach that won’t settle, and we know it’s not cheap. So for some a headline or top ten list that seemingly did research feels like relief. But for pets with a longstanding issues it can just be another lap around the same block.

Screenshot of email received June 21, 2026

A rep for a pet food company (that we don’t carry) recently and rather enthusiastically emailed me a recent Forbes article asserting that this particular brand was “Best Dog Food for Allergies Overall.” Now aside from the blatant loophole of avoiding making drug claims, they further stepped in it by saying ‘this type of third-party validation can be a powerful tool for your staff when helping customers find the right food for sensitive dogs.”

Screenshot of article published on June 12, 2026. Date retrieved July 21, 2026. https://www.forbes.com/sites/forbes-personal-shopper/article/best-dog-food-for-allergies/

Now, aside from the fact that my team or I would NEVER use a news article to help a customer pick a food, there is a lot to unpack in such a short email. It is my opinion that marketing this food as “best for allergies” even if the company did not make the claim themselves, borders on making a drug claim because they are implying that the food treats a disease (allergies). Not great. Also claiming that a newspaper article is ‘third-party validation’ is an extreme overreach. As a scientist third-party mean that the information is unbiased and scientific – and this article is neither considering the journalist is speaking from her personal experience with the food and her pet.

Inevitably I also got this forwarded to me by several friends and customers, with something to the effect of “is this legit?”. Fair question for the average pet owner. Infuriating question for someone like me, and the team at NPP.

What does the list mean?

For someone like me, I usually just roll past these headlines and roll my eyes. However, I think it’s a great example for me to highlight how these come to exist. If you scroll past the initial headline and hero imagery, Forbes tells you how they constructed this newest article. It’s a combination of staff picks, general vet commentary about limited-ingredient diets (which has no legal definition by the way), ingredient considerations, and customer feedback. As mentioned, the top pick leans on one writer feeding it to her own dog and having a great experience. I’m genuinely happy for her, however, if you know anything about me you’ll have heard me say what works for one dog will not always work for the next.

At the end of the day, this article is providing recommendations based on opinion and popularity. It’s not a scientific test. No lab work. There is no validation. No feeding trial on dogs with confirmed allergies. No laboratory tests that measure any health biomarkers. No head-to-head comparison against other foods on the market – or anything you could measure and repeat. And it certainly doesn’t tell you what worked for a dog like yours…that my friends is by design.

“Third-party validation” is a real thing. This isn’t it.

I already mentioned this, but it’s worth repeating. Validation has rules. The people validating in a situation like this should be independent from the brand. The method used should not only be written down, but transparently shared so someone else can repeat the workflow and see if they get the same results. Repeating the test, and getting the same (or highly similar) results would be true validation.

In other words, product vetting should be measured against a known and meaningful standard. Then, other experts should be double checking the work again before it’s published (this is called peer review).

So to be clear, a “best of” article clears none of that. Lifestyle writers from any media outlet, personal preferences, lists without standards, or those lacking outside review shouldn’t ever be a benchmark for picking a pets food, supplement (or yours for that matter).

Somebody gets paid, usually…

In most cases, but maybe not all, articles often earn the publisher a commission when you click and buy. The FTC regulates those links because they bend recommendations. No brand paid for the coverage, but this model still rewards big, easy-to-link brands, which describes every product on this particular list. In others, products may be part of ‘best of’ lists in one form or another in the form of what we like to call ‘Advertorials’. Advertorials are when brands pay journalists to write about their product in a positive light. These are really just long form ads made out to look like genuine journal articles, but are not. Take that for what you will.

For the record, we don’t take money from brands to write about products. We also don’t rank brands from this angle since there is no product that is best for every pet, and doing so would be disingenuous. We hold that line because the alternative is the exact thing this article is about.

Your dog’s allergies are a disease

Food reactions in dogs are a clinical condition, and the research on them is boring in the way good evidence usually is.

Among dogs seen by a vet for any reason, food-related skin reactions run about 1 to 2 percent. In other words: food allergies are RARE. The most common culprit are environmental allergens. Things like pollens, mites, fleas, and dander from other pets (it’s true – pets can even be allergic to human dander)!

Food can help dogs and cats that suffer from environmental allergies, however it’s not a magic bullet. These dogs usually require lifelong management, medicated shampoos, gut health consideration (probiotics, digestive enzymes), Omega 3’s (at the right dose), medicated baths (remove the allergens & kill yeast overgrowth), and a combination of prescription drugs in addition to special diet consideration. Allergic dermatitis is incredibly itchy, and can be painful when not well managed.

Most articles also ignore the fact that the only proven way to confirm a food allergy is an elimination diet. This means feeding one novel or hydrolyzed protein for eight to twelve weeks, then reintroduce the old food and watch for the signs to come back (Gaschen & Merchant, 2011). These can’t be determined or figured out by reading an ingredient panels. Even blood or saliva “allergy testing,” doesn’t reliably diagnose food allergies. And a lot of dogs that look like food-allergy dogs have environmental allergies instead. More common. Completely different plan.

How do you know if a food is good for allergies?

Peer-reviewed studies that run the elimination-then-rechallenge feeding protocol on defined groups of dogs would earn the right for a company to say their food is ‘good for allergies’. However, in today’s marketplace I don’t think that is even necessary. I would be happy with a company completing third party testing to ensure that their foods at least meet minimum nutrient requirements, are free of pathogens and contaminants and that they do not release their product into the marketplace until they receive that third party validation back… (see what I did there?) None of that built the Forbes list. That’s not a shot at the writer, it’s just the fact of the matter.

Dose of reality…

You don’t have to become a nutrition researcher to feed your dog well. That’s our job. Our team includes veterinary technicians with real clinical experience, and our guidance is grounded in research-level training and the actual studies, not the press release.

Food isn’t just food, it’s a tool you can use alongside many other tools. But it’s important to individualize the approach to the animal in front of you. Two dogs the same size (or even same litter) can need different things.

We don’t diagnose, treat, or replace veterinary care. We provide nutrition education and product guidance, and we work with your vet, especially when a true elimination trial is on the table.

References

1. Forbes Vetted. “Best Dog Food For Allergies 2026.” https://www.forbes.com/sites/forbes-personal-shopper/article/best-dog-food-for-allergies/
2. Olivry T, Mueller RS. Critically appraised topic on adverse food reactions of companion animals (3): prevalence of cutaneous adverse food reactions in dogs and cats. BMC Vet Res. 2017;13:51. PMID 28202060. https://doi.org/10.1186/s12917-017-0973-z
3. Mueller RS, Olivry T, Prélaud P. Critically appraised topic on adverse food reactions of companion animals (2): common food allergen sources in dogs and cats. BMC Vet Res. 2016;12:9. PMID 26753610. https://doi.org/10.1186/s12917-016-0633-8
4. Mueller RS, Olivry T. Critically appraised topic on adverse food reactions of companion animals (6): prevalence of noncutaneous manifestations of adverse food reactions in dogs and cats. BMC Vet Res. 2018;14:341. PMID 30419909. https://doi.org/10.1186/s12917-018-1656-0
5. Gaschen FP, Merchant SR. Adverse food reactions in dogs and cats. Vet Clin North Am Small Anim Pract. 2011;41(2):361-79. PMID 21486641. https://doi.org/10.1016/j.cvsm.2011.02.005
6. Freeman L, Becvarova I, Cave N, et al. WSAVA Nutritional Assessment Guidelines. J Small Anim Pract. 2011;52(7):385-96. PMID 21649660. https://doi.org/10.1111/j.1748-5827.2011.01079.x
7. WSAVA Global Nutrition Committee. Global Nutrition Guidelines. https://wsava.org/global-guidelines/global-nutrition-guidelines/
8. Pet Nutrition Alliance. Manufacturer transparency resources. https://petnutritionalliance.org/
9. Federal Trade Commission. Disclosures 101 for Social Media Influencers. https://www.ftc.gov/business-guidance/resources/disclosures-101-social-media-influencers

Right now, the industry is getting it wrong. 

Ingredients matter. Quality matters. That’s not up for debate. But something has gone seriously off track in how we evaluate dog and cat food, and the people getting it wrong are often the ones who care the most.

When a formula changes, what’s the first question people ask?

• Does it have fillers?
• Are there by-products

What nobody asks:

• What changed in the nutrient profile?
• Did digestibility shift?
• Are there any measurable differences in how dogs are actually doing on the food?

These questions are missing from every conversation. And that absence is doing real harm.

The List of Ingredients

When we’re talking about kibble or canned diets, we are talking about processed food. Some ingredients are processed multiple times. Processing, which includes grinding, cutting, drying, fractionating, heating, and pressure, changes the structure, digestibility, and nutrient availability of nutrients supplied by ingredients. Sometimes in a positive way, sometimes not. That is not opinion. That is established food science.

A kibble is not a list of raw ingredients. It is a formulated, processed diet designed to deliver nutrients in a specific way, and that process is complex and nearly impossible to genuinely simplify. Yet that is exactly what the industry keeps trying to do.

Two foods with similar ingredient lists can have markedly different nutrient profiles, digestibility, and biological outcomes depending on formulation, processing, and nutrient balancing. Conversely, foods with very different ingredient lists can deliver nearly identical nutritional profiles. What complicates this further, is the bioavailability of the nutrients supplied by these foods, or in other words if the pet can use those nutrients or not. This is why companion animal nutrition evaluates diets on nutrient composition and performance, not ingredient appearance alone. When we reduce evaluation to labels, we ignore the actual formulation work that determines how a diet functions in the animal.

“Filler” Is a Marketing Term. Not a Scientific One.

“Filler” and “by-product” are not scientific or regulatory classifications. They have no legal definitions. They are marketing terms, and they have been so thoroughly adopted by the independent retail channel that we now deploy them as if they constitute clinical evidence of poor nutrition. They do not.

Ingredients like starches and fibers that get reflexively dismissed as “fillers” are frequently included for defined functional reasons: stool quality, fermentation, energy delivery, and overall gastrointestinal function. In plain language, they help deliver nutrients the body needs, and without them there are health consequences. That doesn’t automatically make them ideal in every context, but it also doesn’t make them meaningless, inherently low quality, or a filler.

Take beet pulp for example. It is a moderately fermentable fiber used because it reliably supports stool consistency and colonic health. It is well-studied. It has a defined, functional role in processed pet food. The same fiber category shows up in boutique kibbles and raw toppers under names like chicory root, inulin, and pumpkin, where it gets called a prebiotic or a digestive support ingredient. The ingredient optics are just different. Is it the first ingredient I’d reach for when building a species-appropriate fresh food diet from scratch? No. But calling it a filler is not just imprecise. It is wrong. And communicating ingredients like this to pet parents as nutritional evidence of a food’s decline is a problem.

Ingredient lists also do not reflect dose, proportion, or functional contribution. An ingredient included at a physiologically meaningful level is very different from one included for label appeal, yet both appear identically on a panel. Without understanding inclusion rates and functional intent, it is not possible to determine the role an ingredient is playing in the diet. This is a fundamental limitation of label-based evaluation that is never acknowledged.

Facts About Formulation

One of the most overlooked aspects in pet nutrition is that diets are not simply collections of ingredients, but instead formulated systems. Formulation becomes more important as ingredient complexity increases. For example, whole food inclusions can introduce variability in nutrient composition, bioavailability, and balance, particularly after processing. Without careful formulation and post-processing validation, diets can miss targets for essential nutrients despite appearing high quality on paper.

This is well recognized in both human and veterinary nutrition, where nutrient adequacy, not ingredient identity, is the standard for evaluating a diet. If these outcomes are not being considered, the evaluation is incomplete regardless of how the ingredient list reads.

Ask ‘Un-spin-able’ Questions

If a food has genuinely declined in quality, that is a serious claim. It should be supported by something measurable:

• Changes in nutrient adequacy
• Shifts in digestibility
• Safety concerns backed by data
• Clinical outcomes

Without that, what we have is a store philosophy being communicated as nutritional evidence. Those are not the same thing. Conflating them is where this industry keeps losing the credibility it needs with the veterinarians and scientists who should be its allies.

Digestibility: The Forgotten Variable

Not all nutrients that are listed are utilized. Digestibility determines how much of a nutrient is absorbed and available to the animal, and this can vary significantly between ingredients and processing methods.

A diet with a cleaner ingredient list but lower digestibility may deliver fewer usable amino acids or available energy than a more processed diet with an optimized formulation. In clinical settings, highly digestible diets are often prioritized for gastrointestinal disease, recovery, and performance, not because of how the ingredient list reads, but because of how efficiently the animal can use the nutrients provided.

Without considering digestibility, ingredient-based judgments are incomplete.

The Questions We Should Ask

If we are genuinely concerned about the long-term health impact of processed diets, and there are real reasons to be, there are far more scientifically meaningful questions to be asking than whether an ingredient is labeled a by-product.

Advanced glycation end products (AGEs). These compounds form during high-heat processing, including the extrusion process used to produce kibble. Extrusion exposes ingredients to high temperature and pressure, conditions known to drive Maillard reactions and the formation of these compounds. In human nutrition, AGEs have been associated with inflammation and metabolic dysfunction. In dogs, emerging work is beginning to explore similar pathways. Yet these factors are rarely part of how foods are evaluated at the consumer level, despite being a direct consequence of processing itself.

Acrylamide. Also formed during high-heat processing, and with established health risks in human nutrition. Likewise, these are rarely discussed in the pet food retail context.

Antinutritional factors. Ingredients perceived as clean or whole are not inherently superior if they are not processed appropriately. Legumes and certain grains can contain compounds such as phytates, lectins, and protease inhibitors, which can interfere with mineral absorption and protein digestion if not addressed. In human nutrition, these are well-characterized concerns mitigated through soaking, fermenting, or cooking. In pet food, extrusion reduces some of these compounds, but not always uniformly. This raises a more meaningful question than what is on the label: how were these ingredients processed, and did that processing optimize or limit nutrient availability?

These are the questions that would move the needle on long-term pet health outcomes. They are also the questions almost entirely absent from the conversation at the consumer level, the retail level, and in a lot of influencer-driven content that passes itself off as ‘nutrition education’.

The Uncomfortable Reality for the Fresh Food Camp

I am in the fresh food camp. But there is a persistent assumption in this space that whole food or minimally processed ingredients inherently lead to better nutrition, and that assumption warrants more examination than it recieves.

We’ve swung from one extreme to another. For years, the mainstream commercial pet food establishment dismissed ingredient quality entirely. The backlash was warranted. Ingredients do matter. But we overcorrected. We started treating the ingredient list as the whole story, layered marketing language on top of it, and then communicated that to pet parents as if it were grounded in nutrition science. We built a framework where whole food automatically means better and by-product automatically means bad, without any serious consideration of food science, processing effects, formulation complexity, or measurable outcomes.

And then we used that framework to tell people their pets’ food was no longer good.

Flattening that distinction with the word “filler” doesn’t protect pets. It creates confusion, erodes trust, and generates an enormous amount of unnecessary churn for pet parents who are genuinely trying to do right by their animals.

Imagine If We Asked Different Questions?

Focusing on ingredient perception ignores one of the most practical and measurable indicators of diet quality: how the animal performs on the food. Stool quality, body condition, coat quality, and gastrointestinal tolerance are not subjective preferences. These are reflections of how well a diet is being digested and utilized.

Dogs and cats don’t respond to ingredient stories and philosophies. They respond to what the diet does in the body and how processing affects that. In clinical and research settings, outcome variables like digestibility, tolerance, metabolic response, and long-term health markers are the standard for evaluating diet performance. If a diet supports stable body condition, consistent stool quality, and overall health, that reflects functional adequacy regardless of whether the ingredient list aligns with a particular narrative.

Without incorporating outcomes, diet evaluation remains theoretical rather than physiological.

My View:

I am not a champion of ultra-processed food. The evidence for minimally processed and fresh diets, when properly formulated, is compelling and growing. I think we should be moving pet parents in that direction when we can and meeting them where they are when we can’t.

But I am not going to tell a pet parent their dog’s food is no longer good without evidence. I am not going to call beet pulp a filler because it makes for a cleaner story. And I am not going to let this industry keep making pet parents feel guilty or confused about feeding their dogs a properly formulated, nutrient-adequate processed diet because we decided that an ingredient list is more important than actual nutritional outcomes.

None of this is an argument against caring about ingredients. It is an argument for using them correctly. Ingredients are part of the picture. But in processed diets, they are not the whole picture, and in many cases, they are not the most informative part.

The question has to shift from what’s in the food? to what does the food do? Until it does, we will keep generating confusion, eroding trust, and sending pet parents on an endless loop of switching foods based on rhetoric instead of evidence.

That is not advocacy. That is the opposite of it.

This is Part 2 of a two-part series. Part 1 covered how the diet-DCM narrative was built: the FDA investigation, the data quality problems, the reporting bias, and the Hill’s lawsuit. This article covers what the peer-reviewed science shows, why the “switch back to grains” recommendation has its own problems, and what all of this means for how you feed your dog.

What the Peer-Reviewed Literature Says

The research base on DCM and diet is real, contested, and far more nuanced than either camp acknowledges. Here is a fair accounting of where it stands.

The ‘Golden Retriever’ Studies

Golden Retrievers became a focal point of the grain-free diet and diet-associated cardiomyopathy (DCM) investigation for a specific reason. That is they have a documented predisposition to taurine-deficient DCM, which notably has been recognized in the veterinary literature since at least the mid-1990s (Kramer, Kittleson et al. 1995). In one report from 2005, a reversible taurine-deficient dilated cardiomyopathy was described in five related Goldens, with marked improvement after taurine supplementation. This was not the typical course for hereditary (primary) DCM (Bélanger, Ouellet et al. 2005). Subsequently, this finding deservingly attracted more research attention. Work following initial investigations demonstrated that Goldens are over-represented in taurine-deficient DCM case series and that many affected dogs improve when diet is changed and taurine is supplemented (Kaplan, Stern et al. 2018). This is a notable difference from the primary hereditary DCM seen in breeds like Dobermans, Great Danes, or Irish Wolfhounds, where disease does not improve with taurine supplementation (O’Grady and O’Sullivan 2004).

In 2018, Kaplan and colleagues published a multicenter prospective observational study describing 24 Golden Retrievers with taurine-deficient DCM and 52 healthy Goldens (Kaplan, Stern et al. 2018). Certain diets and diet characteristics were associated with taurine deficiency, and most affected dogs showed echocardiographic and clinical improvement after a combination of interventions: diet change, taurine and L-carnitine supplementation, and standard heart-failure medications. This strengthened the case that Goldens can develop taurine-responsive DCM linked to diet. However, because multiple treatments were introduced simultaneously, the study cannot isolate the specific contribution of diet change from taurine supplementation and cardiac drugs.

In 2020, the same group published a higher-profile study in PLOS ONE evaluating 86 apparently healthy Golden Retrievers fed “traditional” (grain-inclusive, large-manufacturer) versus “non-traditional” (grain-free, legume-heavy, small-manufacturer) diets (Ontiveros, Whelchel et al. 2020). Dogs in the non-traditional group had, on average, lower taurine concentrations and more frequent echocardiographic changes consistent with subclinical DCM.

Later that year, in September 2020, PLOS ONE issued an ‘Expression of Concern’ for this paper (Ontiveros, Whelchel et al. 2020), citing undisclosed conflicts of interest. The conflicts of interest included co-authors’ ties to a commercial amino acid laboratory that captured data for the study, in addition to substantial heterogeneity between diet groups in factors independently associated with DCM risk. After review by an independent statistical expert, the journal issued a formal correction in August 2023. Those editors concluded that between-group heterogeneity was a “substantial concern” and that conclusions linking diet group to echocardiographic abnormalities were “not well-supported” given the study design. Consequently, the authors corrected article, substantially softening its original claims.

Before the ‘Expression of Concern’ and correction, this paper was frequently cited as strong prospective evidence of a grain-free/taurine/DCM link. The more appropriate interpretation of this study that it is hypothesis-generating – at best. This is because it is a notably confounded observational study that raises legitimate questions but is not a reliable standalone basis for definitive clinical recommendations.

The 18-Month Randomized, Double-Blind Trial

On the other end of the evidence spectrum is an 18-month randomized, parallel-group, double-blind study published in the Journal of Animal Science (JAS) evaluating 60 healthy adult dogs being fed four diets with different ingredient profiles (Morris, Stiers et al. 2025). Diets included grain-free with potatoes and peas, grain-inclusive with peas and pea fiber, grain-inclusive without peas or potatoes, and grain-free with potatoes only. Researchers assessed echocardiographic parameters, whole blood and plasma taurine, urinary taurine, and cardiac biomarkers (troponin-I, NT-proBNP) at 6, 12, and 18 months.

The study found no clinically significant changes or between-group differences in cardiac biomarkers, and whole blood and plasma taurine remained within normal ranges and were unaffected by diet assignment (Morris, Stiers et al. 2025). This is as close to a controlled experiment as can be ethically conducted in healthy dogs. It stands as one of the strongest pieces of evidence that properly formulated grain-free diets (even those containing peas/potatoes) do not predictably induce DCM or meaningful cardiac biomarker changes over 18 months. On the other hand, it does not exonerate every commercial grain-free product, nor does it address dogs with pre-existing cardiac or metabolic risk factors, nor does it answer questions beyond an 18 month period. But it directly challenges the blanket clinical narrative that grain-free diets are inherently cardiotoxic.

The Irish Wolfhound Study (Coppinger et al. 2024)

In a 2024 retrospective study of 97 apparently healthy Irish Wolfhounds (Coppinger, Freeman et al. 2024). This breed is documented to have a well-recognized hereditary cardiomyopathy. Coppinger and colleagues compared dogs eating high-pulse diets to those eating low-pulse diets. Results showed no significant differences in echocardiographic measurements between groups, but dogs in the high-pulse group had a significantly higher prevalence of ventricular premature complexes (VPCs) on a 1-minute ECG strip (17% versus 2%). VPCs are a potential early marker of cardiac electrical instability and can precede more serious arrhythmias in some breeds.

The finding is noteable as it involves apparently healthy dogs in a genetically predisposed breed, focused on an arrhythmic endpoint that may precede overt DCM. At the same time, the study is retrospective, limited to one predisposed breed, and based on short ECG strips rather than confirmed cardiomyopathy. It is not a straight line from “legumes cause heart failure,” but a signal that justifies prospective, breed-stratified research. It is also worth noting that senior authors include Drs. Freeman and Rush, who are named defendants in the KetoNatural v. Hill’s litigation; readers can weigh that conflict of interest accordingly.

Owens et al. (2023) Cross-Sectional Study

A 2023 prospective cross-sectional study of 46 healthy client-owned dogs compared those eating traditional grain-inclusive diets to those eating nontraditional, legume-heavy diets (Owens, LeBlanc et al. 2023). Dogs in the nontraditional group had lower indices of systolic function and larger left ventricular volumes, although the authors emphasized these values generally remained within established reference intervals. There were no significant differences in cardiac biomarkers (NT-proBNP or cardiac troponin I) or whole blood/plasma taurine between groups. 

These results may provide some evidence that legume-heavy diets may be associated with subtle subclinical echocardiographic differences in some dogs. However, the small sample size, cross-sectional design, and absence of biomarker differences limit how far those findings can be taken in clinical decision-making. This means, these results from 46 dogs cannot and should not be extrapolated across the entire canine population.

The 2020 BSM Partners Literature Review

A June 2020 review in the Journal of Animal Science examined more than 150 published studies on canine DCM and its potential causes (McCauley, Clark et al. 2020). The authors concluded that the available literature did not support a definitive causal link between grain-free or legume-rich diets and DCM, arguing that the BEG framework lacked scientific rigor and that FDA case data were too incomplete and biased to support firm conclusions.

This review does not function as proof that the dietary DCM issue was fabricated. It’s important to emphasize that many of the limitations it highlights in case-series data are real, and that the issue is very real for a subset of dogs. Nevertheless, this study should be weighed with the same critical scrutiny applied to any industry-funded work.

Not surprisingly, the review attracted criticism from some veterinary commentators who argue that it selectively emphasizes methodological flaws in studies supporting a diet association and may understate the clinical significance of reported improvement following diet change and supplementation (SkeptVet 2021). A conflict-of-interest concern also arose in this study as well. BSM Partners, which funded and conducted the work, provides formulation and consulting services to pet food companies including one or more brands that appeared on the FDA’s most-reported list. Nonetheless, the journal issued a clarification regarding the authors’ employment and BSM’s industry role.

It is worth noting that BSM Partners is one company in the pet food industry, among others, that provides formulation and technical support that many smaller boutique companies choose not to use. These smaller companies sometimes underestimate or dismiss the need for formal nutrition expertise, robust validation, and true transparency. In that sense, BSM is attempting to solve the very problem that the DCM investigation indirectly highlighted: the lack of rigorous formulation and published nutritional data behind many commercial diets.

Two 2025 Narrative Reviews with Different Conclusions

A broad 2025 review examined grain-free diets across multiple health dimensions including DCM, allergies, glycemic response, and mycotoxin exposure (Zhang, Ji et al. 2025). For DCM specifically, the evidence was characterized as mixed: FDA data and case series suggest a possible association, but several studies including controlled trials found no association. The overall conclusion was that nutritional adequacy, balance, and individualized assessment matter more than the presence or absence of grain. This is the more measured of the two reviews.

A second 2025 narrative review focused narrowly on diet as a predisposing factor for DCM (Mornard, Brasileiro et al. 2025). It characterizes the cumulative findings as suggesting a strong link between nontraditional, legume-rich diets and DCM, It noted larger left ventricular diameters, reduced systolic function, and more frequent ventricular premature complexes in dogs on such diets. Importantly, this review does not prominently address the methodological criticisms of the case-series literature or the null findings from controlled trials.

The fact that two peer-reviewed narrative reviews published in the same year, drawing on largely the same underlying literature, reached different characterizations reflects a larger point. It highlights a genuine divide in how researchers are currently weighing this evidence, and is exactly why a single headline or a single study citation cannot give you the full picture.

Taurine: The Leading Hypothesis and Its Limits

Taurine deficiency has been a nutritionally established cause of DCM in cats since at least the 1980s (Hayes 1982, Pion, Kittleson et al. 1987, Pion, Kittleson et al. 1992). In cats, taurine is an essential amino acid that must be obtained from diet. At the time, this was a breakthrough that led to mandatory taurine supplementation of commercial cat food and largely eliminated the problem in that species (Pion, Kittleson et al. 1992). The hypothesis that a parallel mechanism might operate in some dog breeds is plausible and supported by evidence in specific contexts, particularly Golden Retrievers, who have a documented predisposition to taurine-deficient DCM.

Dogs can synthesize their own taurine from methionine and cysteine, and therefore taurine was not historically considered essential or required at a minimum level in commercial pet foods (Hand, Thatcher et al. 2010). Since the most abundant dietary source of taurine is muscle meat, the assumption was that commercial foods with animal protein would supply enough (Spitze, Wong et al. 2003). However, breed-specific differences, genetic factors, and health status mean that some dogs may require dietary taurine. Inflammatory states are also relevant here: taurine plays a role in immune cell function and modulating oxidative stress, and chronic inflammation can increase taurine demand and utilization. A dog with underlying gut inflammation, systemic inflammatory burden, or dysbiosis may have elevated taurine requirements that dietary intake alone does not meet, independent of diet type. As a result, taurine should be considered conditionally essential in canine nutrition multiple studies demonstrate several factors that may render endogenous synthesis insufficient, leading to taurine‑deficient DCM in some dogs (Li and Wu 2023), regardless of diet type.

What taurine deficiency does not explain is that many dogs reported to have diet-associated DCM have normal blood taurine concentrations (McCauley, Clark et al. 2020). This finding has been replicated across multiple studies and is not contested. If simple systemic taurine depletion were the primary driver, we would expect to see deficiency consistently. We do not. The current mechanistic thinking is considerably more complex: interactions between dietary fiber fractions, bile acid cycling, sulfur amino acid bioavailability, gut microbiota composition, and breed-specific metabolic differences may all contribute to functional taurine insufficiency at the tissue level even when blood taurine appears normal (Ko, Backus et al. 2007, Ko and Fascetti 2016, Donadelli, Pezzali et al. 2020, Quilliam, Ren et al. 2021).

This means taurine status is not a single number to measure once and interpret in isolation. It is a dynamic metabolic state influenced by diet composition, body condition, gut function, and breed genetics. Assessing whether any given dog is “taurine sufficient” is considerably more complicated than a single blood draw suggests. The leap from “some affected dogs have low taurine” to “grain-free diets cause taurine deficiency” happened much faster than the underlying science justified.

Why Taurine Measurement Is More Complicated Than a Blood Draw

The finding that many dogs with diet-associated DCM had normal blood taurine concentrations has been interpreted in two directions: by some as evidence that taurine is not involved, and by others as evidence that the measurement is inadequate. The second interpretation is better supported by what we know about taurine physiology.

Both whole blood and plasma taurine concentrations reflect recent dietary intake and short-term metabolic flux more than they reflect tissue taurine stores (Tôrres, Biourge et al. 2022). The relationship between circulating taurine concentrations and cardiac muscle taurine concentrations in dogs is poorly characterized, and the data are limited. A dog can have circulating taurine within the laboratory reference interval while having suboptimal taurine availability at the tissue level, particularly under conditions of increased biosynthetic demand or impaired recycling. Studies reporting normal blood taurine in affected dogs are not exonerating taurine as a mechanistic contributor, but rather this is exposure of a measurement gap. Reference interval-based blood taurine testing was developed in a different clinical context and was not validated as a tool for ruling out functional taurine insufficiency in the context of a complex dietary exposure question. Using it as though it has shaped the interpretation of a substantial portion of this literature.

“Grain-Free” Is a Marketing Category, Not a Nutritional Mechanism

This is a point that gets lost in almost every public discussion of this topic.

“Grain-free” is a marketing designation, not a nutrient profile. Two products can carry the same label and have nothing else in common. One may be formulated by a board-certified veterinary nutritionist and/or PhD/MS nutritionist, with documented amino acid (protein) bioavailability, third-party AAFCO nutrient profile verification, and published feeding trial data. Another may come from a company with no in-house nutrition expertise, legume fractions dominating the first five ingredients, no feeding trial history, and no published data on sulfur amino acid adequacy. The label tells you what is not in the bag. It also tells you nothing about whether the formulation is sound, whether protein quality has been characterized and verified, or whether the amino acid profile supporting taurine synthesis has ever been measured.

The BEG framework was coined to describe a cluster of characteristics that often appeared together in implicated products. These were small manufacturers, novel proteins, high legume inclusion, and absence of AAFCO feeding trial data. It bundles multiple independent variables under one label. “Grain-free” was the most marketable part of that label, so it became the shorthand. The mechanism, to the extent one exists, almost certainly has nothing to do with the absence of grain and everything to do with specific ingredient composition, processing quality, level of processing, and nutritional completeness.

Grain-inclusive diets are not automatically safe or well-formulated. The ironic part to this entire story is that the real transparency gap is not limited to small or boutique manufacturers. Some veterinary brands, including Hill’s, Purina, and Royal Canin, do not have (or at least won’t provide) AAFCO feeding trial substantiation for every formula in their lineup. More concerning, none of these brands publicly provide a full analyzed AAFCO nutrient profile for their products when asked, even on the veterinary level. They publish guaranteed minimums and maximums which are the floor and ceiling required by law. These are not the real analyzed values that would allow a nutritionist, veterinarian, or informed consumer to evaluate what a dog is actually consuming. A guaranteed minimum for crude protein tells you nothing about amino acid profile, sulfur amino acid (taurine) bioavailability, or whether the formulation has ever been assessed for taurine precursor adequacy. That information usually does exist internally. It is simply not shared under the guise of ‘proprietary or intellectual’ reasoning.

This matters because the entire premise of the “reputable company” qualifier embedded in the Tufts reporting protocol, and implied throughout the BEG framework, rested on the assumption that major brands represent a nutritionally characterized, validated, and verifiable baseline. That assumption is false. As of this writing, the only companies willing to provide that level of data transparency would themselves be classified as BEG, which may just be the most ironic part about this whole story. Regardless, the DCM investigation, whatever its methodological limitations, was never a legitimate basis for treating grain inclusion or brand size as proxies for nutritional rigor. Those are marketing variables. The relevant variable is data transparency. It is not brand recognition, not ingredient composition, and not market share.

What the “Switch Back to Grains” Narrative Gets Wrong

The diet-associated DCM narrative that grain-inclusive diets are the safer default, rests on a framing assumption that has gone largely unexamined. That is conventional grain-inclusive dry dog food represents a well-characterized, safe baseline against which grain-free diets should be evaluated. That assumption was never tested, and therefore has not been proven.

Agricultural Contaminants: The Risk That Doesn’t Get Discussed

Grains are agricultural commodities, and they carry the contamination profile of agricultural commodities. Mycotoxins which include aflatoxins, deoxynivalenol, and fumonisins  are produced by mold species that colonize corn, wheat, and other grain crops both in the field and in storage (Macías-Montes, Rial-Berriel et al. 2020). Aflatoxin contamination in corn-based pet foods has caused documented mass fatality events in dogs, with multiple FDA-reported outbreaks over the past two decades (PFI 2011, FDA 2021). Pesticide and herbicide residues represent an additional consideration, particularly for crops with well-established high agricultural chemical exposure profiles (Macías-Montes, Luzardo et al. 2025). These are regulatory-documented, recurring risks associated with specific grain ingredients. Risks that were never meaningfully incorporated into the diet-DCM narrative as a plausible contributing factor or alternative health concern. That omission is not a minor oversight. It reflects a framework that treated grain inclusion as inherently protective while leaving its actual contamination burden unexamined.

Digestibility, Bile Acid Cycling, and What We Don’t Yet Know

Not all grains are equivalent in how dogs process them, and this matters for the taurine hypothesis specifically. Certain grain fractions, particularly insoluble fiber components, are poorly fermented or digested in the canine gastrointestinal tract (Sunvold, Fahey et al. 1995, de Godoy, Kerr et al. 2013). Impaired digestibility has implications for bile acid cycling: when bile acids are excreted in feces rather than recirculated, the body’s demand for taurine synthesis increases (Donadelli, Pezzali et al. 2020). If specific grain fiber fractions are contributing to bile acid loss, then a grain-inclusive diet is not categorically protective in the way the clinical messaging implied.

This is not a settled question. The literature characterizing the bile acid and taurine metabolic effects of specific grain fractions in dogs is thin. Recommending a return to grain-inclusive diets as the evidence-based safer choice requires evidence that those diets are, in fact, safer along this specific metabolic pathway. That evidence does not robustly exist.

After Extrusion, the Label Tells You Less Than You Think

When starch-based ingredients are processed through high-temperature, high-pressure extrusion, which is how most dry pet food is manufactured, starch granules gelatinize (Perry, Valach et al. 2022). The degree of gelatinization, and consequently the glycemic and digestive behavior of the finished product, is driven substantially by processing conditions rather than the identity of the starch source. A well-formulated kibble built on rice or oatmeal and a well-formulated kibble built on potato or peas are not nutritionally equivalent in every respect, but the structural differences between them at the point of canine digestion are considerably smaller than ingredient list comparisons suggest. The name on the label identifies the source; it does not fully describe what the dog’s gastrointestinal tract encounters.

Adding Grains to a Complete Diet Is Not a Solution

Some owners have reported their veterinarian advising them to add cooked grains such as rice or pasta to a grain‑free diet as a way to reduce perceived diet‑associated DCM risk, rather than changing the underlying formulation (Annonymous 2025). This deserves direct challenge. A complete and balanced commercial diet is formulated to deliver specific macronutrient ratios, amino acid profiles, and micronutrient targets per calorie consumed. Adding calorie-dense, low-protein carbohydrate sources dilutes protein density, distorts the amino acid balance, which includes the sulfur-containing amino acid precursors relevant to taurine synthesis, and contributes to caloric excess without proportional nutritional return. If impaired taurine recycling is the mechanism of concern, reducing the dietary protein fraction and increasing carbohydrate load is not consistent with addressing that mechanism. It is the kind of reductive clinical translation that occurs when a hypothesis moves into practice faster than the evidence justifies.

Pet Food Processing Chemistry Questions

The diet-associated DCM investigation focused narrowly on ingredient category as the variable of concern. It did not ask what happens to food during manufacturing, or more specifically the thermal processing of pet food. The thermal processing conditions required to produce dry pet food at commercial scale generate a predictable suite of bioactive compounds with documented physiological consequences (van Rooijen, Bosch et al. 2014, Oba, Hwisa et al. 2022, Bridglalsingh, Archer-Hartmann et al. 2024, Xiong, Li et al. 2024). The only question is not what goes into the bag. Other questions about byproducts of the manufacturing process, and what lifetime exposure to those outputs does to the animal consuming them are also important.

One of these byproducts, advanced glycation end products (AGEs) are formed when reducing sugars react non-enzymatically with proteins, lipids, or nucleic acids under heat. The reaction pathway is the Maillard reaction, and it is not incidental to pet food manufacturing, rather it is intrinsic to it. High-temperature extrusion generates well-characterized AGE species including Nε-carboxymethyllysine (CML) and Nε-carboxyethyllysine (CEL) at concentrations that substantially exceed what is found in minimally processed food. This is not a grain-free problem or a grain-inclusive problem. It is a processed food problem.

AGEs are not inert. They cross-link collagen and elastin, reducing tissue compliance in load-bearing structures including the myocardium (Wasim, Mahmood et al. 2022). They activate the receptor RAGE, triggering inflammatory signaling, oxidative stress, and endothelial dysfunction. Chronic RAGE activation has been associated with fibrosis, impaired cardiac contractility, and vascular stiffening in human and animal models (Hooshiar, Esmaili et al. 2022). The cardiac implications of lifetime AGE exposure in dogs have not been studied. That is the point.

AGEs are not the only concern. Acrylamide is a probable human carcinogen whose metabolite glycidamide is genotoxic (Perera, Hewavitharana et al. 2021). It forms predictably from asparagine and reducing sugars above 120°C, meaning starchy kibble of any formulation is a reliable source. High-temperature protein processing generates heterocyclic amines. Lipid oxidation produces malondialdehyde and 4-hydroxynonenal, both of which modify proteins and DNA and compound the AGE burden. Furans and oxidized lipid polymers accumulate in rendered fat fractions and persist in the finished product. None of these are manufacturing defects. They are predictable outputs of the thermal conditions required to produce pet food at commercial scale.

None of these compounds appeared in the FDA’s diet-associated DCM investigation. None were weighed against the speculative legume association when veterinary organizations recommended returning to conventional grain-inclusive kibble. The processing chemistry of conventional dry pet food escaped scrutiny not because it was demonstrated safe, but because it was the historical norm. Historical norm is not the same as demonstrated safety. That asymmetry is a scientific problem this field has not yet addressed.

What Adequate Evidence Would Actually Look Like

The diet-associated DCM literature has generated substantial noise. It has not generated a study that could settle the question it raised. It is worth being honest about why. The answer is because the study that would actually answer this question is not merely difficult. It may be practically and ethically impossible to execute.

A properly designed interventional study would require, at minimum:

• Randomized diet assignment with standardized formulations and fully documented ingredient sourcing.
• Cardiologist-confirmed echocardiographic endpoints, evaluated blinded to diet group, across follow-up periods long enough to capture a disease that typically develops over years, not weeks or months.
• Whole blood taurine measured alongside tissue-level assessment, because circulating taurine and cardiac muscle taurine do not reliably correlate.
• Pharmaceutical and supplementation interventions withheld or rigorously controlled, which is where the ethical problem becomes unavoidable. If a dog develops echocardiographic changes consistent with DCM during the study period, withholding pimobendan or other medications known to improve outcomes is not ethically defensible.

The study design that would generate clean causal data cannot be run in dogs with any reasonable ethical framework.

Sample size requirements compound the problem. DCM occurs in under 0.5% of non-predisposed dogs. Detecting a dietary effect on a condition with that background prevalence requires enrollment numbers that no single institution can feasibly support. And the breed question adds another layer:

• A study powered to detect an effect in the general dog population would almost certainly miss breed-specific metabolic vulnerabilities.
• A breed-specific study cannot be generalized to the broader population.

These are not the same question, and they cannot be answered by the same study. What this means in practice is that the evidentiary standard used to reshape clinical guidelines and consumer behavior in 2018, a voluntary case series filtered through a biased reporting protocol, was not a temporary gap waiting to be filled by better research. It reflects a genuine structural constraint on what this field can produce. The question was raised with epidemiological tools that cannot establish causation. The study design that could establish causation faces ethical and logistical barriers that have not been resolved. That is the honest state of the science, and the public deserves to have it described plainly.

What the Evidence Supports and Doesn’t

What Appears to Be Real

• Some dogs diagnosed with DCM have been eating certain grain-free, legume-rich diets at the time of diagnosis. A subset of those dogs have shown echocardiographic and clinical improvement after a combination of interventions that usually includes diet change, taurine and L-carnitine supplementation, and standard cardiac medications. The clinical cases and improvements are real; what is not clear is how much of that improvement is specifically attributable to diet.
• In breeds with an existing genetic predisposition to cardiomyopathy, including Irish Wolfhounds and possibly Golden Retrievers, high-pulse or nontraditional dietary patterns are associated with measurable differences in cardiac risk markers such as ventricular premature complexes and subtle changes in systolic function in some cross-sectional studies, although most values often remain within reference intervals and causality has not been established.
• Taurine status is a meaningful variable in at least some dogs, particularly Golden Retrievers and certain spaniels, and can interact with diet composition in ways that affect risk of taurine-responsive DCM. However, many suspected diet-associated DCM cases have normal circulating taurine, so taurine deficiency cannot explain all of them.
• Reversal or improvement of cardiac changes following intervention is documented in a subset of dogs with suspected diet-associated or taurine-deficient DCM. That pattern of improvement is more consistent with a nutritional or secondary process than with classic hereditary DCM. However, because diet, supplementation, and medications are typically changed together, the specific contribution of diet alone remains uncertain.

What Is Not Established

• A definitive causal mechanism. Taurine deficiency explains some cases; it does not explain all of them. The alternative hypotheses which is that fiber-mediated bile acid interference with taurine recycling, antinutritional factors in legumes, compromised amino acid bioavailability, microbiome-mediated effects remain speculative, with some having more plausibility than others.
• That “grain-free” as a category increases DCM risk compared to all other properly formulated, tested diets. The 18-month RCT did not find this. The FDA did not conclude this. The best reading of the literature is that specific formulation profiles in some grain-free products, but not grain-free itself, may be risk-modifying in susceptible dogs.
• That the initial FDA case database was representative of the true population of DCM cases in grain-free-fed dogs, given the documented reporting protocol at Tufts and the surge in reports following public announcement.

How NorthPoint Pets Approaches This

NPP sells raw diets, fresh diets, freeze-dried diets, and grain-free kibble alongside grain-inclusive options. We also work closely with veterinarians across a range of diet and health conversations. We have some financial stake in how this question is answered, but truthfully, we carry products on both sides of this debate and our business doesn’t hinge on the outcome. What we do have a stake in is giving clients an accurate read on the evidence, because that’s the foundation the rest of what we do is built on. So rather than a position statement, what follows is an honest accounting of what the science shows and where it genuinely falls short.

• We do not tell clients that grain-free diets cause DCM. The evidence does not justify that level of certainty.
• We do not tell clients that grain-free diets are automatically safe. Formulation quality, ingredient sourcing, amino acid bioavailability, and batch consistency vary enormously across grain-free products, as they do across all commercial pet foods.
• We evaluate products on evidence of nutritional competence: AAFCO data, manufacturer transparency about analyzed nutrient levels, amino acid profile data, company nutrition expertise, and track record. These criteria apply regardless of whether a food contains grain.
• For high-risk breeds like Dobermans, Great Danes, Irish Wolfhounds, Golden Retrievers we recommend discussing targeted monitoring with your veterinarian: taurine assessment (ideally with breed-specific reference intervals), baseline echocardiography, and awareness of early DCM symptoms. The diet question is part of that conversation, not a substitute for clinical assessment.
• We don’t manage diet choices based on marketing labels. “Grain-free,” “ancient grains,” “ancestral,” “wild-inspired” because none of these terms carry nutritional meaning that can be evaluated without looking at the actual analyzed nutrient data behind them.

Bottom line for your dog: DCM is real. Diet-related DCM is real in a subset of dogs. The evidence for “grain-free as a category causes DCM” is not strong, and the data collection that drove the public narrative had documented methodological problems. The honest answer, which no one in this conversation has commercial incentive to give you, is that we don’t fully understand the mechanism yet, the risk is real but narrower than headlines suggested, and diet quality is a more meaningful variable than the presence or absence of grain.

If you want to work through your dog’s specific diet, risk factors, and what monitoring might be appropriate, that’s exactly the kind of conversation we’re built for at NorthPoint Pets.

The information in this article is for educational and informational purposes only and is not a substitute for individualized veterinary medical advice, diagnosis, or treatment. Always consult your veterinarian or a board- certified specialist regarding your pet’s specific health needs, diagnostic testing, and dietary recommendations. Never disregard professional veterinary advice or delay seeking it because of something you have read here.

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A federal class action against major pet food brands was certified in January 2026. A new peer-reviewed study on PFAS contamination in pet food in February of 2026. Seven states have new chemical restrictions taking effect this year. Your social feed is probably full of alarming headlines.

Before you overhaul your pet’s diet, read this.

You may have heard the term “forever chemicals”, referring to a broad family of synthetic compounds that don’t break down in the environment or in the body. The name likely sounds familiar because these chemicals are genuinely everywhere. Teflon, or PTFE, used in non-stick cookware. PFOS, the active compound in Scotchgard and firefighting foam. Fluorotelomer sulfonates in floor coatings, cleaning products, and waxes. Related compounds in stain-resistant rugs and fabrics, food packaging, clothing, makeup, dental floss. Because they are so pervasive in our homes and daily lives, they are also in our water supply, our food supply, and, as a growing body of research now confirms, in our pets. The concern is legitimate, the science is real and developing, and the media coverage is making it nearly impossible to respond to any of it proportionately. That’s what this piece is for.

What Are PFAS? A Brief, Precise Overview

PFAS stands for per- and polyfluoroalkyl substances (1). This is not one chemical, but a family of more than 12,000 synthetic compounds that share a common structural feature: a carbon-fluorine (C-F) bond (2). The C-F bond is one of the strongest in organic chemistry. That strength is exactly why PFAS were so commercially useful since it gives them the ability to resist heat, oil, water, and grease. However, this is also the reason why they are so environmentally persistent. They do not break down under ordinary environmental conditions. Hence being termed “forever chemicals.”

PFAS were first developed in the 1940s and found their way into an enormous range of applications: non-stick cookware coatings, waterproof fabrics, firefighting foam (AFFF), food packaging grease-proofing, carpet and furniture stain treatments, dental floss coatings, and industrial processes across dozens of sectors. Their ubiquity means that by now, detectable PFAS concentrations have been found in virtually every corner of the global environment including Arctic ice cores, remote mountain lakes, rainwater, topsoil, wildlife on every continent, and the blood of nearly every person tested.

Within the PFAS family, the most studied, and the most concerning, are two specific long-chain compounds:

1. PFOA (perfluorooctanoic acid) was the primary ingredient in Teflon manufacturing for decades and was central to the 3M and DuPont contamination cases that shaped the modern regulatory landscape. It is classified as a Group 1 human carcinogen by the International Agency for Research on Cancer (IARC).
2. PFOS (perfluorooctane sulfonic acid) was the active compound in Scotchgard and in AFFF firefighting foam. It is one of the most persistent PFAS known, has been detected in blood samples globally, and is regulated under the Stockholm Convention on persistent organic pollutants.

Both PFOA and PFOS have been phased out of production by U.S. manufacturers. PFOA largely by 2015, PFOS by 2002, however because they do not degrade, legacy contamination persists in soil, water, wildlife, and human and animal tissues. Many manufacturers replaced these long-chain compounds with shorter-chain variants or alternative fluorinated chemicals. Although, this may not negate risk of their predecessors since it’s possible they also carry their own concerns and are far less studied (2).

Where PFAS Come From: It’s Not Just the Food Bowl

This is the single most important context point to establish before any discussion of PFAS in pet food, and it is the one most consistently omitted from consumer-facing coverage.

Pets, particularly indoor dogs and cats, are exposed to PFAS from multiple simultaneous routes (3). Food is one of them. It is not the only one, and in many household environments it may not even be the primary one.

Indoor Environments

Stain-resistant carpeting and upholstered furniture treated with PFAS-based products shed these chemicals into household dust. Dogs are in close contact with flooring surfaces for most of their waking hours and ingest house dust at higher rates than humans through grooming and floor-sniffing behavior. Research published in the American Journal of Veterinary Research found that serum PFAS profiles in companion dogs closely mirror those of their human owners, suggesting shared indoor exposure routes including water, dust, and PFAS-treated textiles are primary contributors (3).

Drinking Water

PFAS contamination in municipal and private well water is widespread, particularly in areas near military bases, industrial sites, or locations where AFFF foam was historically used. The EPA established Maximum Contaminant Levels for six PFAS in drinking water in April 2024. Pets drink from the same water sources as their owners, often at higher volume relative to body weight.

Household Products

Non-stick cookware, waterproof outerwear stored in the home, treated textiles, certain dental floss products, and some cleaning agents contribute to the ambient PFAS load in indoor environments. Dogs exposed to homes with high levels of treated textiles or flooring show correspondingly higher serum PFAS concentrations than dogs in less-treated environments.

Food Packaging

Grease-resistant food packaging which has historically been a major dietary PFAS exposure route for humans has been a focus of both regulatory action and litigation. The FDA announced in February 2024 that PFAS-based grease-proofing agents for paper and paperboard food packaging are no longer being sold for food-contact use in the United States and reaffirmed this again in January 2025 (4). This action was intended to eliminate the primary authorized dietary exposure source from food contact surfaces. The key word is “authorized” legacy packaging, imported products, and non-paper packaging materials operate under different frameworks.

The relevance to pet food: the active litigation is about packaging migration is a contested scientific question about whether PFAS from bag coatings migrates into the kibble or wet food inside. It is not about PFAS inherently present in the ingredients themselves. That distinction matters enormously and will be revisited in the litigation section below.

Why Fish-Based Diets Test Higher And What The Headline Is Missing

Breeds with Inherited Copper‑Handling Defects

In February 2026, a peer-reviewed study from Ehime University’s Center for Marine Environmental Studies was published in Environmental Pollution (5). Researchers analyzed 100 commercial pet foods sold in Japan. The study included 48 dog foods, and 52 cat foods, measuring concentrations of 34 PFAS compounds. The study found PFAS were detectable across many products, with fish-based pet foods consistently showing higher concentrations of long-chain PFAS, particularly PFOS, perfluoroundecanoic acid (PFUnDA), and perfluorotridecanoic acid (PFTrDA).

This result is not surprising to anyone with a working knowledge of environmental contaminant chemistry. It is a direct consequence of biomagnification.

How PFAS Accumulate in Aquatic Food Chains

PFAS are proteinophilic. This just simply means they bind to proteins, particularly albumin and fatty acid-binding proteins. Unlike many lipophilic environmental contaminants that concentrate in fat tissue, PFAS concentrate in blood and protein-rich tissues. In aquatic environments, PFAS enter the food chain through contaminated water and sediment, are taken up by plankton and small invertebrates, and increase in concentration at each successive trophic level. This process is called biomagnification. By the time a predatory fish like tuna or salmon has accumulated PFAS across its lifespan, it carries substantially higher concentrations than the water it swims in.

“The ocean often acts as a final sink for many synthetic chemicals,” the lead researcher Kei Nomiyama noted in commentary accompanying the study (5). “PFAS can move and concentrate in aquatic food webs.” Fish used as ingredients are a significant source of PFAS exposure, and this pattern is consistent with what has been observed in human seafood consumption studies as well.

The Critical Caveat: Human Reference Values Applied to Pets

This is where the coverage loses the thread, and where the science requires precision.

The Nomiyama study calculated hazard quotients (HQs) for dogs and cats using the European Food Safety Authority’s (EFSA) tolerable weekly intake thresholds established for humans (5). Several products showed average HQs exceeding 1, which is the threshold that signals potential concern. This is the number the headlines ran with.

What the headlines omitted: EFSA itself, when asked to comment on the study, explicitly stated that its human reference values should not be applied as-is to risk assessments in other species. The researchers agree, and the authors state clearly that “due to the lack of species-specific toxicokinetic information for dogs and cats, the EFSA-based risk characterization presented here should be interpreted as a preliminary assessment.”

No reference doses for PFAS have been established for dogs or cats. The HQ calculations in this study are the best available approximation given current data. This is genuinely useful as a signal that the topic warrants further investigation and species-specific toxicological work. What they are not is a confirmed finding of harm. 

The study also found that while dry foods had higher PFAS concentrations per gram, estimated daily exposure was greater from wet foods due to higher serving volumes. Meat-based products generally showed lower PFAS than fish-based products. Some brands tested at or near non-detectable levels.

Physiology of PFAS Accumulation: How These Chemicals Behave in the Body

PFAS do not behave like most toxicants. They do not accumulate in fat. They bind to albumin and liver fatty acid-binding proteins, concentrating in blood, liver, and kidneys. This protein affinity has several important physiological consequences:

Half-life differences between species. In humans, some PFAS persist in serum for years. For instance, PFOS has an estimated half-life in humans of roughly 4 years; PFOA approximately 3.5 years. In dogs, data we do have suggests that PFAS are cleared far more quickly. Research presented at the 2023 AVMA Convention by Dr. Heather Brake of Michigan State University found that exposed dogs may clear PFAS from the body within eight days to a couple of months, compared to years in humans (3). This species difference is critical when interpreting studies that measure serum PFAS levels in pets as proxies for cumulative dietary or environmental exposure.

Hepatic effects. PFAS exposure is associated with increased liver weight and elevated liver enzymes, including ALT, AST, and GGT, in both rodent models and companion animals. A study by You et al. (2022) analyzed PFAS levels and blood chemistry in police dogs and beagles, finding that specific PFAS compounds were significantly associated with changes in hepatic biomarkers, though the directionality and magnitude varied by PFAS type (6).

Thyroid disruption. Among the most consistent findings in companion animal research is a possible association between long-chain PFAS, particularly PFOS and PFNA, and thyroid function, especially in cats. A 2018 study by Wang et al. examining serum PFAS in Northern California cats found significantly higher concentrations of long-chain perfluorinated carboxylic acids in hyperthyroid cats compared to euthyroid controls, and elevated PFOS levels in hyperthyroid animals specifically (7). Feline hyperthyroidism is among the most common endocrine disorders in older cats. Whether PFAS exposure is a contributor, a correlate, or unrelated to the disease’s prevalence increase over recent decades remains an open research question, certainly not a settled one.

Kidney function. Significant associations between PFAS exposure and kidney function markers have been documented in both dogs and cats. Given that the kidneys are a primary excretion route for PFAS, this is biologically plausible. Causation has not been established.

Maternal transfer. PFAS cross the placenta and are present in milk in both humans and animals. This means developmental and neonatal exposure occurs before any direct dietary exposure, and cumulative lifetime burden begins at conception. For breeding animals, this is a particularly important consideration.

Immunological effects. Decreased vaccine response is among the more consistently documented effects of PFAS in human research, including in children. Whether this translates to clinically meaningful immune suppression in companion animals at typical exposure levels has not been adequately studied.

What the Litigation Actually Found

The legal landscape around PFAS in pet food has moved fast. Understanding what the lawsuits claim, and what courts have and have not established, is essential context.

Jeruchim v. The J.M. Smucker Co. (N.D. Cal., No. 22-cv-6913)

This is the case that generated most of the headlines. In January 2026, U.S. District Judge William H. Orrick certified a class action against J.M. Smucker, covering California consumers who purchased 9Lives, Kibbles ‘n Bits, or Meow Mix between November 2018 and December 2022, over allegations that PFAS in the packaging were not disclosed despite health-based marketing claims like “100% healthy” (8).

Certification is a procedural threshold, not a verdict. It means the case can proceed as a class rather than as individual suits. It is not a finding that PFAS migrated into the food, that any pet was harmed, or that Smucker violated the law. Those questions go to trial, currently scheduled for October 27, 2026 in San Francisco, with summary judgment motions this summer that could narrow or end the case before it gets there.

What the court did find is narrower: that consumers plausibly alleged economic harm, overpayment based on an omission. A reasonable consumer, the court concluded, would not expect a product labeled “100% healthy” to contain packaging with PFAS. That is a consumer protection theory. It is a meaningful legal development. It is not proof of harm.

The plaintiffs’ operative theory that “any prolonged exposure to PFAS is harmful to animals” is a litigation posture designed to establish a class wide common question. It is not a scientific consensus statement, and it cannot be, because the data doesn’t exist to support one. There are no established reference doses for PFAS in dogs or cats. There are no regulatory limits for PFAS in pet food. The same evidentiary gap that makes this a legitimate scientific concern also makes it nearly impossible to prove, or disprove, specific harm in a courtroom. That tension is exactly what the merits trial will have to navigate.

Judge Orrick has been here before. He drew explicitly on his 2021 ruling in Zeiger v. WellPet, where he certified a class over arsenic, lead, and bisphenol in dog food on the same logic: that “any exposure could be harmful” functions as a class wide question even without individualized exposure data. The PFAS case rests on the same legal scaffold. A parallel class action against Nestle Purina over Cat Chow packaging is pending in the same court.

Broader PFAS Packaging Litigation

The Smucker case is part of a broader wave. Nestle Purina faces a similar class action alleging PFAS in Cat Chow packaging, also filed in the Northern District of California. Similar suits have been filed against fast food packaging, microwave popcorn manufacturers, and other food brands. Many of these cases have struggled or been dismissed due to standing challenges, lack of product-specific testing, and the difficulty of proving migration. The Smucker certification is notable precisely because most comparable cases failed at this stage.

The litigation’s central premise, that PFAS in packaging poses a risk through migration into food, is scientifically plausible but unproven. FDA’s January 2025 determination that grease-proofing PFAS are no longer being sold for food contact uses eliminates the primary authorized source going forward. It does not retroactively address legacy packaging or clarify what concentrations, if any, historically migrated into packaged food.

The Regulatory Gap

Federal oversight of PFAS in pet food is essentially nonexistent, and this is not unlike many other contaminants found in commercial pet food. The FDA regulates PFAS in food contact materials for human food, but there are no established maximum contaminant levels for PFAS in pet food ingredients or finished products. AAFCO nutrient profiles, the standard framework for pet food nutritional adequacy, do not address contaminants at all. They are designed to define minimum nutrient requirements, not to set toxicological limits for environmental contaminants. As always, AAFCO compliance is a floor, not a ceiling, and in this case the floor says nothing about PFAS.

At the state level, as of 2026, seven states have new consumer product PFAS restrictions taking effect, covering food packaging, cookware, cosmetics, and other product categories (9). Fourteen states have enacted food packaging PFAS laws of varying scope. Minnesota’s Amara’s Law is among the most comprehensive, with reporting requirements that took effect in 2025 and a phased ban on all consumer products with intentionally added PFAS by 2032. Connecticut, where NorthPoint Pets operates, banned intentionally added PFAS in packaging beginning in 2023. These are meaningful steps, but their reach is narrower than the headlines suggest. They target deliberate use of PFAS in packaging materials. They do not address PFAS entering the food supply through contaminated ingredients, environmental bioaccumulation, or imported products. And without systematic independent testing for compliance, these laws create legal accountability on paper without consistently delivering it in practice. The regulatory infrastructure is catching up to the science, but slowly and unevenly.

Internationally, EFSA has established tolerable weekly intakes for PFAS in humans. Japan’s Pet Food Safety Act, enacted in 2008, does not currently regulate PFAS in pet food. No national regulatory body has established species-specific PFAS reference doses for companion animals.

Where Does This Leave Us? Practical Guidance Without Panic

The honest answer to “what should I do?” is: apply proportionate concern and make targeted adjustments where the evidence is strong enough to act on.

What the evidence supports

Reducing fish-heavy diets as a primary protein source is a reasonable precautionary step given what is known about PFAS bioaccumulation in aquatic food chains, especially for cats consuming fish-based wet food as the bulk of their diet. This does not mean fish is never appropriate or that a fish topper ruins an otherwise varied diet. It means fish-centric feeding patterns carry a higher PFAS load than meat-based alternatives, and that is consistent with the literature.

Addressing water quality matters. If your municipal water supply or well water has known PFAS contamination, this is a significant exposure route for your pet. Filtered water, using activated carbon or reverse osmosis, meaningfully reduces PFAS in drinking water. This is one of the highest-leverage interventions available.

Consider indoor exposure. PFAS-treated carpeting, upholstered furniture, and stain-resistant products are meaningful contributors to household PFAS burden for indoor animals. When replacing flooring or furniture, PFAS-free alternatives exist. Regular wet mopping (which removes dust more effectively than dry vacuuming) reduces the settled dust load.

Monitor routine blood work. Given the association between PFAS exposure and hepatic and thyroid biomarkers, routine monitoring of liver enzymes, kidney values, and thyroid function in older cats and dogs is sound preventive medicine regardless of PFAS concerns. If values are trending in the wrong direction, PFAS exposure is one factor worth investigating alongside others.

What the evidence does not support

Complete elimination of all fish from the diet based on current data is disproportionate. A varied diet with occasional fish-based components does not create the same exposure profile as daily fish-centric feeding.

The assumption that “your pet’s food is making them sick right now.” The research establishes that PFAS are detectable in pet food, that some products show levels that would exceed human reference thresholds, and that PFAS are associated with certain health markers in companion animals. It does not establish that typical commercial pet food, at typical feeding volumes, is causing clinical disease in otherwise healthy animals eating a varied diet.

Switching to homemade or raw diets based on PFAS concerns alone. This introduces a separate set of nutritional risks that are far better documented than the PFAS risks being avoided. Ingredient sourcing matters in homemade diets too, meat from animals raised in contaminated areas carries its own PFAS burden.

The NorthPoint Pets Position

PFAS are a legitimate environmental health concern that deserves serious scientific attention. The coverage they are currently receiving is not serious scientific attention but rather fear-based content that strips away context, misapplies human reference thresholds to animals without noting the species limitation, and buries the packaging-versus-ingredient distinction that is central to the entire legal and scientific debate.

Companion animals are, in the words of PFAS researchers, “sentinels”, as they share our environments, eat from the same ingredient supply chains, and are exposed to the same indoor contamination sources we are (10). That makes them valuable early-warning systems. It also means that PFAS in a pet’s body is usually a reflection of the household environment broadly, not just the food bowl.

There are no PFAS-free diet options for pets. There are no PFAS-free environments. The goal is not zero exposure, that is not achievable. The goal is proportionate reduction of avoidable exposures while keeping nutritional adequacy, digestibility, and overall health optimization at the center of every feeding decision.

AAFCO compliance tells you a diet meets minimum nutrient thresholds. It tells you nothing about contaminant load, ingredient quality, bioavailability, or how a specific animal with specific genetics and history will respond. Individual assessment, actual health monitoring, diet diversity, and relationship with a veterinarian who knows your animal remains the most protective intervention available regardless of what the next alarming headline says.

We will continue tracking this research as it develops. The 2026 Nomiyama study is the first of what will be many. Nonetheless, species-specific toxicokinetic data are urgently needed, regulatory frameworks are lagging, and the litigation will push disclosure requirements forward. When the science moves, we will move with it.

Not sure what’s right for your dog? Our team at NorthPoint Pets specializes in personalized nutrition guidance based on your dog’s unique needs—not trends or fear-based marketing. Stop in or talk with us today.

REFERENCES

1. Buck RC, Franklin J, Berger U, Conder JM, Cousins IT, de Voogt P, et al. Perfluoroalkyl and polyfluoroalkyl substances in the environment: Terminology, classification, and origins. Integrated Environmental Assessment and Management. 2011;7(4):513-41.
2. Kwiatkowski CF, Andrews DQ, Birnbaum LS, Bruton TA, DeWitt JC, Knappe DRU, et al. Scientific Basis for Managing PFAS as a Chemical Class. Environ Sci Technol Lett. 2020;7(8):532-43.
3. Brake HD, Wilkins MJ, Kaneene JB. Per- and polyfluoroalkyl substances: using comparative medicine to understand exposure and adverse health outcomes in people and their pets. Am J Vet Res. 2023;84(7).
4. Administration USFaD. Per- and Polyfluoroalkyl Substances (PFAS) 19 December 2025 [Available from: https://www.fda.gov/food/environmental-contaminants-food/and-polyfluoroalkyl-substances-pfas.
5. Nomiyama K, Sato A, Tanoue R, Saeki K, Ikenaka Y, Mizukawa H. Widespread PFAS contamination in pet food: Dietary sources and health risks to companion animals. Environ Pollut. 2026;395:127779.
6. You D, Chang X, Guo L, Xie W, Huang S, Li X, et al. Per- and polyfluoroalkyl substances (PFASs) in the blood of police and Beagle dogs from Harbin, China: Concentrations and associations with hematological parameters. Chemosphere. 2022;299:134367.
7. Wang M, Guo W, Gardner S, Petreas M, Park JS. Per- and polyfluoroalkyl substances in Northern California cats: Temporal comparison and a possible link to cat hyperthyroidism. Environ Toxicol Chem. 2018;37(10):2523-9.
8. Atkins D. Smucker Pet Food Buyers Win Cert. In PFAS Disclosure Fight. Law360. 2026 January 22.
9. Tomlinson H, Giambrone B. States Continue to Address PFAS in U.S. Food and Water Supply 2025 [updated July 25, 2025. Available from: https://www.astho.org/communications/blog/2025/states-continue-addressing-pfas-in-food-and-water/.
10. Rock KD, Polera ME, Guillette TC, Starnes HM, Dean K, Watters M, et al. Domestic Dogs and Horses as Sentinels of Per- and Polyfluoroalkyl Substance Exposure and Associated Health Biomarkers in Gray’s Creek North Carolina. Environ Sci Technol. 2023;57(26):9567-79.

Recent social media posts warn that “millions of dogs are in imminent danger” from copper in commercial pet food. Those posts are tapping into a real scientific debate, but they often miss critical nuance: copper is essential, some dogs are clearly being harmed by excess copper, and at the same time we genuinely do not know the optimal copper range for every dog.  Here we will walk through what we do know from peer‑reviewed research, where the uncertainty lies, and how pet owners can make informed decisions without the panic and fear‑mongering driven by social media.

1. Copper Is Essential and a “Goldilocks” Nutrient

Copper is an essential trace mineral involved in many everyday body functions: using iron to make healthy red blood cells, building strong bones and joints, keeping the immune system working, and protecting cells from damage. Dogs cannot synthesize copper on their own, so they must obtain it from food. Too little copper can lead to anemia, weak bones and connective tissue, poor growth, and changes in coat color or quality. A key point is that trying to avoid copper altogether is not a solution. Fortunately, true copper deficiency is rare in dogs eating “complete and balanced” diets that meet basic nutritional standards.

Copper works by enabling many enzymatic “worker proteins” to function properly. It acts like a key that turns certain enzymes “on,” supporting energy production, iron utilization, healthy connective tissues, normal pigmentation, and antioxidant protection. When copper is insufficient, these systems begin to struggle; when it is excessive, the liver can become overwhelmed by stored copper.

Copper is also a redox‑active metal, meaning that at high concentrations it can drive oxidative injury, inflammation, scarring (fibrosis), and eventually cirrhosis. In dogs, cirrhosis is an end‑stage liver change that can result from many chronic liver diseases; one important subset involves copper‑associated hepatopathy (CAH), also called copper‑associated chronic hepatitis.

Because too little is problematic and too much can be damaging, copper is best thought of as a “Goldilocks nutrient”: not too little, not too much, but a just‑right amount for that individual dog. Genetics, liver health, and the rest of the diet can all shift where that “just right” range falls. This factor is one of the many reasons nutrition is far more nuanced than “more is always better” or “less is always safer.” This complexity also explains why setting a single strict upper limit for copper that fits every breed and every dog is genuinely difficult. The fact is that some individuals may need more copper to support essential body processes, while others with copper‑handling defects can be harmed by amounts that are perfectly safe for most dogs.

2. What the Research Actually Shows

Rising Hepatic Copper Over Time

Over the past 30–40 years, multiple biopsy‑based studies have documented a clear upward trend in liver copper concentrations in dogs. Critically, this is not limited to breeds historically considered at risk for CAH; it is a broader, population‑level finding confirmed across several peer‑reviewed publications:

• In a 546‑dog archive spanning 1982–2015, median hepatic copper concentrations roughly doubled between the 1980s and the late 2000s. In the same study, the proportion of dogs with markedly increased copper (>1,000 μg/g dry weight) increased approximately threefold (1).
• A large pathology series of 4,559 dogs published in 2022 found that half of all liver samples had copper concentrations above 400 ppm (the upper end of many reference ranges), and 19% exceeded 1,000 ppm. Higher copper was associated with more severe inflammation and necrosis, and with certain breeds (Doberman Pinscher, Labrador Retriever, West Highland White Terrier) (2).
• A 2025 comparative review linking canine CAH to human Wilson disease highlighted that copper accumulation is now recognized across a broader range of breeds than the classic Bedlington Terrier — underscoring both genetic and environmental (dietary) contributors (3).

These are not fringe findings. They come from multiple institutions and journals and consistently show that more dogs have higher hepatic copper than in past decades.

Limitations of the Biopsy Data

That said, (warning, this is a little technical, but important) the biopsy data we have come primarily from referral hospitals and pathology archives. This means samples are biased toward dogs sick enough to be biopsied and not a random sampling of the general pet dog population. 

Additional technical factors matter too. For example, copper distribution across the liver tissue is often uneven (e.g., centrilobular vs. periportal). This means that the site and size of the biopsy can affect the measured concentration. The method of which the copper is measured can also give varied results. For example, histologic stains such as rhodanine are useful for semi‑quantitative (not exact measurements) screening but can under‑ or over‑estimate copper compared with other methods with true quantitative assays (AAS/ICP‑MS). 

Together, these factors show just how complicated this problem is, but that investigating it is also complicated, and nuance. We do know that the documented rise in hepatic copper is a real signal, but it does not directly tell us the true prevalence of copper‑associated disease in the general dog population.

3. Breed‑Specific and Individual Risk

Breeds with Inherited Copper‑Handling Defects

Several breeds carry a markedly increased risk of CAH due to inherited defects in hepatocellular (liver) copper handling and biliary excretion. Bedlington Terriers are the classic example: an autosomal recessive deletion in the COMMD1 gene impairs copper excretion, leading to extreme hepatic copper accumulation (often >10,000 μg/g dry weight) and progressive hepatitis and cirrhosis if untreated. Even within this breed, genetic testing and selective breeding have reduced but not eliminated disease prevalence, and additional ATP7B variants have been described in some affected dogs.

Other breeds showing a strong association with abnormally high hepatic copper and copper‑associated chronic hepatitis include:

• Labrador Retrievers
• Doberman Pinschers
• West Highland White Terriers
• Dalmatians
• Welsh Corgis
• Cavalier King Charles Spaniels

In Labradors and Dobermans, familial clustering and centrilobular copper accumulation patterns support a heritable defect in copper metabolism, likely involving variants in copper transporters such as ATP7A/ATP7B or related regulators which interact with environmental (dietary) copper exposure. Notably, some breeds such as Bloodhounds may have lower‑than‑expected hepatic copper, emphasizing that both genetic susceptibility and diet shape individual risk (5)

Why One Cutoff Doesn’t Fit All Breeds

Historical and more recent data both show that median “normal” hepatic copper is not identical across breeds. Studies have reported significantly different mean liver copper concentrations in Doberman Pinschers, Cocker Spaniels, Keeshonds, and West Highland White Terriers compared with mixed‑breed dogs; West Highland White Terriers in particular show a very wide, continuous range of values. This has led investigators to question whether a single numeric upper limit of normal (e.g., 400 ppm or 1,000 ppm dry weight) is appropriate for all breeds, versus moving toward risk‑stratified thresholds that consider breed, age, lesion pattern, and clinical context. Current cutoffs are pragmatic rather than biologically universal.

4. Primary vs. Secondary Copper Accumulation

Copper‑associated hepatopathy is classically described as a primary storage disease in which copper itself is the main driver of hepatocellular injury, inflammation, and fibrosis. However, excess hepatic copper can also accumulate secondarily in many chronic liver diseases that impair bile flow or hepatocellular function, including cholestatic disorders and chronic hepatitis of other causes. In such cases, copper may exacerbate damage but is not necessarily the initiating cause.

Distinguishing primary CAH from secondary copper accumulation based on a single biopsy can be challenging. This is why most hepatologists emphasize integrating quantitative copper measurements, lesion pattern and distribution, clinical history, and when available genetic information before labeling a case as “primary copper‑associated hepatopathy.”

5. Diagnosis Requires More Than a Blood Panel

Serum ALT, ALP, bile acids, and ultrasound can suggest liver disease, but they cannot reliably distinguish copper‑associated hepatopathy from other hepatopathies, nor can they quantify hepatic copper burden. The current diagnostic gold standard for CAH is histopathologic evaluation of a liver biopsy combined with quantitative measurement of hepatic copper on a separate sample from the same liver.

Rhodanine staining on biopsy or cytology can screen for increased copper and correlates moderately with quantitative values, but it does not replace a true numerical copper concentration when treatment decisions (such as chelation therapy and strict dietary restriction) are being made. Repeat biopsies with quantitative copper can be useful to monitor treatment response in severely affected dogs, because serum liver enzymes alone may lag or incompletely reflect changes in hepatic copper stores.

6. Is Diet to Blame? What We Know and Don’t Know

Evidence Supporting a Dietary Contribution

Several lines of evidence implicate diet as a contributing factor. The temporal increase in hepatic copper coincides with regulatory and formulation changes that increased dietary copper and its bioavailability (for example, greater use of highly bioavailable copper chelates and supplements, and reduction of dietary antagonists such as certain fibers and minerals) (4). In dogs with copper‑associated liver disease, low‑copper diets and copper chelation can reduce hepatic copper and improve clinical outcomes, implying that ongoing dietary intake is driving the accumulation. A 2021 JAVMA viewpoint by Center et al. argued that copper content in many commercial dog foods appears to exceed biological requirements for some dogs and may surpass tolerance in copper‑sensitive individuals, and called for AAFCO to re‑establish a maximum copper concentration in its nutrient profiles (4).

What We Still Don’t Know

These data are not “smoking gun” controlled trials in which normal dogs are fed different copper levels for years and prospectively tracked for liver disease. This is because those studies do not exist. Other variables influence risk: genetics, nutrient interactions, copper in the water source, environmental exposures, chronic hepatitis of other causes, and overall liver health. In many dogs, copper accumulation may be one important piece of a multifactorial puzzle rather than the sole cause of disease. It is more accurate to say that diet is a plausible and likely contributor, but not the only one. Focusing on a single cause risks oversimplifying a genuinely complex disease process.

Image retrieved February 25, 2026 via @happytrailswagntails Instagram feed. It should be noted that this account has paid partnerships and/or affiliate links with multiple pet food brands that do not third‑party test for copper prior to releasing each lot into the marketplace, and do not provide those reports publicly.

7. AAFCO, Copper, and the Limits of Minimum Standards

As we emphasize consistently at NorthPoint, AAFCO nutrient profiles are designed to define minimum levels to prevent overt deficiency. These profiles are not designed to define optimal intake for every nutrient, breed, or life stage. Copper is a textbook example of that gap.

AAFCO’s Dog Food Nutrient Profiles currently specify minimum copper requirements but do not include a numeric maximum for adult maintenance diets. In their 2021 paper, Center et al. proposed a range of 0.9–1.1 mg Cu per 1,000 kcal and urged AAFCO to re‑establish a maximum and restrict supplemental sources to copper oxide (4). In response, AAFCO convened an expert panel to review the literature; the panel acknowledged the rising hepatic copper data but concluded there were insufficient controlled toxicity data to set a scientifically defensible maximum that would apply to all dogs.

The panel’s review of older toxicity studies suggested that the no‑observed‑adverse‑effect level could fall somewhere between roughly 28–31 mg and 112–124 mg Cu per 1,000 kcal. It’s important to emphasize that this is an extremely wide range reflecting limited data. The panel argued that selecting a single number would be somewhat arbitrary and might falsely reassure consumers that any diet below that value is “safe” for all dogs.

In parallel, the AAFCO Copper Claim Workgroup reviewed whether to allow label claims about copper content and concluded that “low copper” wording could easily mislead consumers into thinking a food is below minimum requirements or inherently safer for all dogs. The workgroup explored a voluntary “controlled copper” claim tied to specific upper limits (e.g., 15 mg/kg dry matter and 3.75 mg/1,000 kcal), but even this was contentious. Some members and industry groups argued these values are not proven to benefit dogs with or at risk for CAH, and raised concerns that manufacturers might cluster around the new target range in ways that are not ideal for all life stages.

For comparison, the European body FEDIAF does set a maximum of approximately 28 mg/kg dry matter. However, notably this limit is driven largely by environmental concerns about copper excretion rather than canine health endpoints.

These regulatory decisions highlight how much of the nutritional conversation is built on incomplete evidence and differing priorities. Copper illustrates why “AAFCO‑compliant” should be viewed as a baseline, not a guarantee of optimal or ideal nutrition for every individual dog.

8. How Serious Is the Risk for the Average Dog?

The social media claim that “millions of dogs are in imminent danger” goes beyond what the available evidence supports. Pathology archives do show more dogs with higher hepatic copper, but CAH represents a subset of all liver disease cases. Importantly, not every dog with elevated liver copper develops clinical disease.

As one large study suggested, roughly one‑third of dogs with chronic hepatitis have copper‑associated disease. While this is significant, it not universal (2). The remaining two‑thirds have other variables at play that appear to be larger drivers in that subset. This underscores the need for more research to understand those factors and how to mitigate individual risks. Many dogs with high hepatic copper are clinically normal at the time of biopsy; some may never progress, while others may decompensate later.

The concern is real, especially for at‑risk breeds and dogs with unexplained liver enzyme elevations. However, this is more accurately described as a growing, under‑recognized chronic liver disease problem rather than an acute poisoning crisis for every dog eating commercial food. Individual assessment and management are far more valuable than mass alarm.

9. Practical Take‑Home Points

Copper is essential, but a “Goldilocks” nutrient. Too little is harmful; too much over time can damage the liver in susceptible dogs.

Liver copper levels in dogs have increased over recent decades. Histopathology archives document higher median hepatic copper and more dogs with very high levels compared with the 1980s.

Diet is likely one contributor, but not the only one. Genetics, overall liver health, nutrient interactions, and copper bioavailability all play roles.

AAFCO profiles protect against overt deficiency, not necessarily against long‑term, low‑grade excess in every dog. There is currently no AAFCO maximum for copper in dog food, and experts disagree on where that maximum should be.

We still lack high‑quality data on optimal copper levels for different dogs and life stages. That uncertainty is exactly why some specialists are calling for more conservative targets and greater transparency about copper content and sources in commercial diets.

What Pet Parents Can Do Right Now

• Work with a veterinarian to monitor liver enzymes in at‑risk breeds (e.g., Labs, Dobermans, Westies) or dogs with chronic GI or hepatic signs.
• If copper‑associated disease is diagnosed or strongly suspected, use diets formulated to be lower in copper alongside appropriate medical management — or work with a Board‑Certified Veterinary Nutritionist to formulate a homemade diet tailored to individual needs.
• Avoid assuming that “more copper” or “more of any trace mineral” is better simply because a label exceeds AAFCO minimums.

For us at NorthPoint, this topic is a powerful illustration of why “complete and balanced” based on AAFCO minimums is the bare minimum benchmark and not the finish line. We simply do not have definitive, long‑term data defining optimal levels for many nutrients across diverse dog populations living modern lifestyles and eating a wide variety of commercial diets. This means nutrition must be approached individually rather than by seeking the “perfect” or “best” product. Individual needs change over time, and as pet parents, acknowledging our pets’ unique risks and needs helps us avoid the many fear‑based marketing tactics that exist in today’s marketplace.

Not sure what’s right for your dog?
Our team at NorthPoint Pets specializes in personalized nutrition guidance based on your dog’s unique needs—not trends or fear-based marketing. Stop in or talk with us today.

REFERENCES

1. Strickland JM, Buchweitz JP, Smedley RC, Olstad KJ, Schultz RS, Oliver NB, et al. Hepatic copper concentrations in 546 dogs (1982–2015). J Vet Intern Med. 2018;32(6):1943–50.
2. Ullal TV, Lakin S, Gallagher B, Sbardellati N, Abdo Z, Twedt DC. Demographic and histopathologic features of dogs with abnormally high concentrations of hepatic copper. Journal of Veterinary Internal Medicine. 2022;36(6):2016–27.
3. Ullal T, Choi EA, Gui D, Medici V. Comparative review of copper‑associated chronic hepatitis in dogs and Wilson disease in humans. Frontiers in Veterinary Science. 2025;Volume 12.
4. Center SA, Richter KP, Twedt DC, Wakshlag JJ, Watson PJ, Webster CRL. Is it time to reconsider current guidelines for copper content in commercial dog foods? J Am Vet Med Assoc. 2021;258(4):357–64.
5. Dirksen K, Fieten H. Canine Copper‑Associated Hepatitis. Vet Clin North Am Small Anim Pract. 2017;47(3):631–44.

THE SHORT VERSION:

“Grain-free food causes heart disease in dogs” became a clinical talking
point. It was never what the data showed. Seven years later, the FDA closed its
investigation without establishing causality, a $2.6 billion lawsuit has raised serious questions about how that investigation was triggered, and the peer-reviewed literature remains genuinely contested. This article covers how the narrative was built: the investigation, the data quality problems, and the legal aftermath. Part 2 covers what the peer-reviewed science actually shows and what it means for your dog.

In June 2018, before the FDA’s first public alert, Dr. Lisa Freeman published a Petfoodology blog post titled “A broken heart: Risk of heart disease in boutique or grain-free diets and exotic ingredients.” This post warned about a possible connection between grain-free diets and dilated cardiomyopathy (DCM) (Freeman 2018) . In the prior year, a small group of academic veterinarians had begun reporting a trend they felt warranted further investigation. Cardiologist Joshua Stern at UC Davis was seeing an apparent cluster of Golden Retrievers with DCM, low taurine, and similar grain-free diets, while Lisa Freeman and colleagues at Tufts were observing DCM in dogs eating BEG diets (Wood 2018).

Between January and July 2018, prior to formal announcement of an investigation, the FDA received 25 case reports of DCM that mentioned a possible diet link. Of those 25 reports, seven came from Freeman’s group at Tufts. Internally, Tufts had circulated guidance instructing its clinicians to report DCM cases to the FDA only if the dog was eating a BEG or non-“reputable” diet. This means that grain-inclusive diets from major brands were not reported by design, even though cases existed.

In July 2018, the FDA announced it was investigating a potential link between certain dog food diets and DCM (Adminstration 2018) . Within months, the story had simplified dramatically: veterinarians warned clients off grain-free diets, brands lost market share by the hundreds of millions of dollars, and a generation of dog owners began associating peas and lentils with cardiac death.

That narrative was reinforced on December 1, 2018, when a commentary article by Freeman and colleagues titled “Diet-associated dilated cardiomyopathy in dogs: what do we know?” was published in the Journal of the American Veterinary Medical Association (JAVMA) (Freeman, Stern et al. 2018) . This was published as a viewpoint piece, not a peer-reviewed original study, but was frequently cited and shared as though it were primary evidence.

In a November 2018 Petfoodology update titled “It’s Not Just Grain‑Free: An Update on Diet Associated Dilated Cardiomyopathy,” Freeman re‑framed the concern around boutique, exotic, grain‑free (BEG) diets, argued that most diet‑associated DCM cases in her hospital were eating such diets (Freeman 2018) . She recommended that owners switch to diets from large, “well‑established” manufacturers using common ingredients including grains, despite acknowledging that the underlying cause of diet‑associated DCM was still unknown.

Combined with the Petfoodology blogs and the FDA alert, the JAVMA and Petfoodology blogs effectively functioned as a de facto position statement for the veterinary profession. This narrative ballooned and solidified quickly, spreading far beyond what the underlying evidence could support. This article walks through what the data and investigation record actually show. This included the parts obscured by both the alarm camp and the grain-free advocacy camp, neither of which has given pet owners the complete picture.

Then in June 2019, the FDA took the unusual step of publishing the names of 16 pet food brands that appeared most frequently in its adverse-event reports, while still stating that it had not established causation (Administration 2022) . Naming brands at this early signal-detection stage implied a level of certainty the data did not support, and media coverage amplified the brand list while largely stripping away the caveats.

What Is DCM?

DCM is a disease in which the heart muscle weakens and the chambers enlarge, reducing the heart’s ability to pump blood effectively (Tidholm and Jönsson 2005) . Over time, untreated DCM can progress to congestive heart failure, arrhythmia, or sudden death. It is the second most common form of heart disease in dogs (McCauley, Clark et al. 2020) . DCM has two clinically distinct categories. Primary or hereditary DCM is genetically driven and disproportionately affects certain large and giant breeds (e.g. Doberman Pinschers, Great Danes, Boxers, Irish Wolfhounds and Golden Retrievers). Athough it’s important to know that DCM has not been widely studied across most breeds (O’Grady and O’Sullivan 2004) . In fact, the natural history of the disease has been described in greatest detail in Doberman Pinschers, where longitudinal and genetic studies show a very high lifetime prevalence and a well-defined progression from occult disease to heart failure. For most other affected breeds, available data on true incidence, age of onset, and typical progression are much more limited and thus extrapolated at least in part from Doberman Pincher data.

Secondary DCM, the kind at the center of this debate, develops because of something else. This could be an infection, a medication, a toxin, a nutritional problem, a combination of these, or even another factor we are not aware of. What separates secondary DCM from primary DCM is that can improve or resolve when the underlying cause is corrected; hereditary DCM does not. This is clinically important and tends to get lost in public discussions. When someone says “we
see lots of heart disease in dogs on grain-free diets,” that could reflect primary hereditary DCM that would have occurred regardless of diet, secondary DCM, or something else entirely. Diet type alone is not a diagnosis.

Clinically, DCM describes how the heart looks and behaves. It does not describe why it ended up that way (O’Grady and O’Sullivan 2004) . Multiple different processes can produce the same dilated, poorly contracting heart: inherited myocardial disease, chronic tachycardia, myocarditis, endocrine disease such as hypothyroidism, certain toxins, and in some cases specific nutrient deficiencies like taurine. In many dogs, especially in general practice, the underlying cause is never definitively identified, because the tests required (e.g. myocardial biopsy, extensive infectious and metabolic workups) are rarely performed. That uncertainty is part of why it is so easy to over-attribute DCM to whatever risk factor is most visible at the time.

How the FDA Investigation Started — and Their Data Quality

The FDA’s investigation formally launched in July 2018 after an unusual cluster of DCM cases was observed in dog breeds not typically prone to the disease. The common thread reported by the investigating veterinarians: the dogs were eating diets labeled “grain-free,” many of which were high in peas, lentils, or other pulses. The FDA began soliciting reports from veterinary professionals and, by December 2022, had collected 1,382 canine DCM case reports. At first
pass, more than 90% from dogs eating grain-free diets, 93% from dogs eating diets containing peas and/or lentils.

That sounds damning. But the data collection methodology has since come under serious scrutiny. Let’s look at why.

The Tufts Reporting Protocol

Among the earliest and most prominent contributors to the FDA’s diet-associated DCM case pool was Dr. Lisa Freeman of Tufts University’s Cummings School of Veterinary Medicine. FDA adverse-event records obtained under the Freedom of Information Act show that Tufts clinicians submitted 7 of the first 25 diet-linked DCM cases that informed the agency’s initial July 2018 communication (Santoro 2022) . In the same FOIA production, a June 2018 internal protocol from Tufts instructed veterinarians to report DCM cases to the FDA “if patient is eating any diet besides those made by well-known, reputable companies or if eating a BEG diet”. This means that dogs eating grain-inclusive diets from major manufacturers were, by design, not reported from this institution.

What we can say with confidence is that the early data submitted to the FDA were not a representative sample of all dogs with DCM. They were a selected subset, shaped by an internal reporting rule that favored one kind of answer over others.

The Surge After Public Announcement

The FDA made its investigation public in July 2018, and case reports surged immediately. Between 2014 and mid-2018, the FDA received only a handful of DCM reports per year (Administration 2022) . However, after the announcement, that number jumped into the hundreds annually, before tapering off. This is a well-described phenomenon in pharmacovigilance: publicizing a suspected link dramatically increases reports of that link, because veterinarians who previously would not have associated diet with DCM began actively looking for and reporting cases that fit the new narrative.

For context, there are an estimated 87 million dogs in the U.S. as of 2025 (Association 2025). Scientific literature sugges that somewhere between 0.05–1.1% of the canine population is living with DCM at any given time (Fioretti and Carri 1988, Sisson, Thomas et al. 1995) .Based on this, simple math estimates approximately 435,000 to 957,000 dogs living with DCM in the U.S. at any given time. And these numbers are before diet enters the picture. Reporting bias does
not mean those dogs were not sick, rather it means the data cannot tell us whether they were sick because of what they ate.

This is why “we see lots of heart disease in dogs on grain-free diets” is not, by itself, evidence that grain-free diets cause that heart disease. Without standardized diagnostics, case definitions, and a proper denominator, it is impossible to separate background hereditary DCM from any true dietary signal.

The FDA Reports Contextualized

It’s important to keep the scale of the problem in mind. Using conservative estimates, somewhere between 435,000 to 957,000 dogs with DCM in the U.S. at a given time. Considering this the FDA’s reported case pool of 1,382 canine DCM reports since 2018 represents a fraction of a percent of dogs estimated to have DCM, regardless of diet. A voluntary adverse-event reporting system that captures only a tiny fraction of background disease, and that was further filtered at some institutions to exclude grain-inclusive diets from the outset, does not constitute surveillance data. It constitutes a selected case series and those selected case series cannot establish prevalence, incidence, or causation.

Unlike human medicine, which benefits from centralized public-health surveillance systems such as the CDC that track disease trends across large populations, veterinary medicine has no comparable, comprehensive database for canine heart disease. This absence of systematic surveillance makes it much harder to accurately quantify risk, identify true patterns, or distinguish signal from noise when evaluating potential dietary and disease relationships in dogs.

More importantly, something like this is detected in a small, highly selected subset of cases, it is dangerous to extrapolate that signal to the entire dog population. Overgeneralizing from such data can inflate perceived risk, stigmatize entire categories of diets or ingredients, and misdirect research and clinical resources away from the much larger burden of background DCM and other cardiac disease.

This Is What Voluntary Reporting Systems Do

The pattern of the FDA’s DCM reports over time: a low baseline, a sharp surge following the July 2018 announcement, and a subsequent plateau, is not unique to this situation. It closely resembles a well-described artifact of voluntary pharmacovigilance systems known as the Weber effect. This is the tendency for voluntary adverse-event reports to spike after media coverage or regulatory announcements and then taper, regardless of whether the underlying event rate has truly changed. Combined with notoriety bias (the tendency for clinicians and owners to report cases that fit a publicized pattern while overlooking those that do not) and the denominator blindness inherent in a system with no defined reporting population, the shape of the FDA’s DCM data is entirely consistent with a reporting artifact layered on top of a large background burden of disease.

The Reversibility Argument Does Not Mean What It Is Claimed to Mean

One of the most frequently cited pieces of evidence for diet causation is that some dogs improved after switching away from grain-free diets. In most reported cases where clinical improvement was documented, dogs were not simply switched to a different diet and observed. They were simultaneously started on standard cardiac medications which are typically pimobendan, ACE inhibitors, or both. These patients also often received taurine and L-carnitine supplementation. In other words, multiple interventions were introduced at once. When a dog improves under those conditions, attributing that improvement specifically to diet change is not scientifically defensible. The reversibility argument, used throughout the diet- association literature as implicit proof of causation, is hypothesis-generating at best, and even that is a reach. Without controlled data that separates these variables, it cannot carry the evidentiary weight placed on it.

The Diagnosis Problem

Compounding the data collection bias is a data quality problem that received far less attention: the cases themselves were not uniformly diagnosed to the same standard. Dukes-McEwan and colleagues specifically recommended that a DCM diagnosis require echocardiographic evaluation by a veterinary cardiologist to be considered reliable (Dukes-McEwan, Borgarelli et al. 2003) . What’s problematic in this instance is that a meaningful portion of the FDA’s reported cases were submitted by general practitioners. When echocardiographic data were present (most cases did not have this), they were not standardized across submissions.

In some instances, dogs with soft murmurs, dogs with radiographic cardiomegaly but no documented systolic dysfunction, or even dogs eating grain-free diets without any confirmed structural or functional heart disease were all reported under the umbrella of DCM. As a result, findings that would not meet formal diagnostic criteria in a cardiology referral setting were reported as DCM, and any analysis built on the assumption that all reports represent equivalent DCM diagnoses will overstate the problem, especially when this underlying data is unverified or incomplete.

The FDA’s Own Conclusion

On December 23, 2022 which happened to be the Friday before Christmas, the FDA announced that it was ending routine public updates on the investigation (Administration 2022) . The agency’s stated reason: adverse event reports alone do not supply sufficient data to establish a causal relationship. After more than four years and 1,382 case reports, the FDA had not identified a mechanism, had not established causality, had not issued any recalls or dietary prohibitions, and concluded it lacked sufficient scientific basis to take further regulatory action.

Industry Guidance Was Never Retracted

In the period following the FDA’s initial July 2018 announcement, major veterinary
organizations and key opinion leaders which included the World Small Animal Veterinary Veterinary Association (WSAVA) Global Nutrition Committee and American Animal Hospital Association (AAHA)-linked nutrition resources began advising clinicians to avoid grain-free/BEG diets in dogs at risk for, or diagnosed with, DCM. However, these were largely applied to all dogs, and even cats and not ‘at risk’ cases. In fact, these recommendations still appear in many current veterinary and client-facing resources, often presented as practical, evidence-based guidance to clients in the clinic rather than clearly labeled as provisional interpretations of an evolving dataset.

These recommendations have not been systematically revisited considering the FDA’s 2022 decision to stop public updates for lack of causal evidence. They continue to shape practitioner conversations and consumer behavior in ways that no longer fully reflect the state of the evidence. This is how preliminary signals become clinical dogma: the announcement travels fast and wide; the quiet closure does not. The asymmetry between how this investigation opened and how it ended is itself part of the story.

The Hill’s Lawsuit: Allegations and Unanswered Questions

In February 2024, KetoNatural Pet Foods filed a $2.6 billion Lanham Act lawsuit against Hill’s Pet Nutrition (a Colgate-Palmolive subsidiary), the Morris Animal Foundation, the Mark Morris Institute, and veterinary researchers Drs. Lisa Freeman, Joshua Stern, Darcy Adin, Ryan Fries, and John Rush (2024) . The complaint alleges that Hill’s and several associated researchers made false and misleading marketing claims about grain-free diets and DCM to the economic
detriment of competing pet food brands.

The suit claims that Hill’s, facing substantial market share losses as grain-free competitors grew, orchestrated a coordinated campaign to weaponize the FDA’s reporting system. Specific allegations include:

• that Hill’s-affiliated veterinarians selectively submitted grain-free-associated DCM cases to the FDA while withholding cases in dogs eating Hill’s-brand and similar grain-inclusive diets;
• that the resulting data created a distorted picture of the association;
• that Hill’s and its associates then amplified the resulting panic through academic publications, veterinary channel marketing, and social media, allegedly including a private Facebook group used to suppress dissenting perspectives;
• and that the financial result was a near-total reversal of Hill’s market decline, with the company becoming arguably the fastest-growing pet food brand in the country in the years following the investigation.

The suit is built around the Lanham Act, a U.S. statute governing false advertising and unfair competition. The legal theory is that Hill’s and its associates made false and misleading statements about the scientific evidence surrounding grain-free diets, disseminated through marketing materials and academic papers, thereby harming competitors economically.

As of the date of this article, the case is on appeal. In November 2024, the district court granted Hill’s motion to dismiss on legal grounds, holding that many of the challenged statements were not actionable “commercial speech” under the Lanham Act and that the complaint had not adequately pled its claims. KetoNatural has appealed that decision to the Tenth Circuit.

In plain language, the court’s ruling addressed whether the alleged statements could legally be treated as advertising claims. It did not rule on whether the underlying scientific narrative around grain-free diets and DCM was accurate. These are two different things. A controversy that began as a scientific question about diet and heart disease has, at least so far in the courtroom, been decided on the technicalities of marketing law rather than on a full evaluation of the evidence.

What the lawsuit means for your interpretation of the science:

Serious. The FOIA documents describing the Tufts reporting protocol are real. The financial conflicts of interest involving the named researchers and the major grain-inclusive pet food companies (Hill’s, Nestlé Purina, Mars) are documented. The market share data is real.

What it doesn’t mean: The lawsuit does not establish that no dogs have developed DCM on grain-free diets. Clinical cases of diet-associated DCM are real. Dogs got sick, some improved on diet change, and that signal is meaningful regardless of whether Hill’s manipulated the reporting pool. The lawsuit, if it proceeds, will adjudicate commercial law claims — not definitively resolve whether legume-heavy diets contribute to DCM in some dogs.

The honest answer is: both things can be true. The investigation may have been shaped by financial conflicts of interest and biased data collection, AND a real but narrower signal may exist in a subset of susceptible dogs on specific high-legume formulations. These are not mutually exclusive.

Ready to dive deeper? Read Part Two here.

The information in this article is for educational and informational purposes only and is not a substitute for individualized veterinary medical advice, diagnosis, or treatment. Always consult your veterinarian or a board- certified specialist regarding your pet’s specific health needs, diagnostic testing, and dietary recommendations. Never disregard professional veterinary advice or delay seeking it because of something you have read here.

REFERENCES:

(2024). KetoNatural Pet Foods, Inc. v. Hill’s Pet Nutrition, Inc., et al., United States Distruct Court for the District of Kansas.

Association, A. V. M. (2025). “U.S. Pet Ownership Stats.”   Retrieved March 9, 2026, 2026, from https://www.avma.org/resources-tools/reports-statistics/us-pet-ownership-statistics.

Dukes-McEwan, J., M. Borgarelli, A. Tidholm, A. C. Vollmar and J. Häggström (2003). “Proposed guidelines for the diagnosis of canine idiopathic dilated cardiomyopathy.” J Vet Cardiol 5(2): 7-19.

FDA. (2018, July 12, 2018). “Food and Drug Administration, CVM,  Investigating Potential Connection Between Diet and Cases of Canine Heart Disease.”   Retrieved March 9, 2026, 2026, from https://wayback.archive-it.org/7993/20201222194256/https://www.fda.gov/animal-veterinary/cvm-updates/fda-investigating-potential-connection-between-diet-and-cases-canine-heart-disease.

FDA. (2022, December 23, 2022). “Food and Drug Administration, CVM, Investigation into Potential Link between Certain Diets and Canine Dilated Cardiomyopathy.”   Retrieved March 9, 2026, 2026, from https://www.fda.gov/animal-veterinary/outbreaks-and-advisories/fda-investigation-potential-link-between-certain-diets-and-canine-dilated-cardiomyopathy.

Fioretti, M. and E. D. Carri (1988). “Epidemiological survey of dilatative cardiomyopathy in dogs.”

Freeman, L. (2018). “A broken heart: Risk of heart disease in boutique or grain-free diets and exotic ingredients.” Petfoodology https://sites.tufts.edu/petfoodology/2018/06/04/a-broken-heart-risk-of-heart-disease-in-boutique-or-grain-free-diets-and-exotic-ingredients/ 2026.

Freeman, L. (2018). “It’s Not Just Grain-Free: An Update on Diet-Associated Dilated Cardiomyopathy.” Petfoodology https://vetnutrition.tufts.edu/2018/11/dcm-update/ 2021.

Freeman, L. M., J. A. Stern, R. Fries, D. B. Adin and J. E. Rush (2018). “Diet-associated dilated cardiomyopathy in dogs: what do we know?” J Am Vet Med Assoc 253(11): 1390-1394.

McCauley, S. R., S. D. Clark, B. W. Quest, R. M. Streeter and E. M. Oxford (2020). “Review of canine dilated cardiomyopathy in the wake of diet-associated concerns.” J Anim Sci 98(6): skaa155.

O’Grady, M. R. and M. L. O’Sullivan (2004). “Dilated cardiomyopathy: an update.” Veterinary Clinics: Small Animal Practice 34(5): 1187-1207.

Phillips-Donaldson, D. (2020). U.S. pet food market grows 7% despite grain-free decline. Pet Food Industry, Pet Food Industry.

Santoro, H. (2022). “Did Industry Funding Influence an FDA Investigation into Canine Heart Disease and Grain-Free Dog Food?”   Retrieved March 9, 2026, 2026, from https://100r.org/2022/07/did-industry-funding-influence-an-fda-investigation-into-canine-heart-disease-and-grain-free-dog-food/.

Sisson, D., W. Thomas, S. Ettinger and E. Feldman (1995). Textbook of veterinary internal medicine, WB Saunders, Philadelphia, PA.

Soffastaii, M. (2019). “Dog with heart disease showing improvements after switching from grain-free diet.”   Retrieved March 8, 2026, 2026, from https://www.wmar2news.com/matterformallory/dog-with-heart-disease-showing-improvements-after-switching-from-grain-free-diet.

Tidholm, A. and L. Jönsson (2005). “Histologic characterization of canine dilated cardiomyopathy.” Veterinary pathology 42(1): 1-8.

Wood, T. J. (2018, July 19, 2018). “UC David Investigates Link Between Dog Diets and Deadly Heart Disease.”   Retrieved March 9, 2026, 2026, from https://www.vetmed.ucdavis.edu/news/uc-davis-investigates-link-between-dog-diets-and-deadly-heart-disease.