This post may contain affiliate links.
The following is an article written by Joseph Powell that shares his thoughts on the cause of dilated cardiomyopathy in dogs. This article was shared on Keep the Tail Wagging with his permission and has been reviewed/approved by a holistic veterinarian. If you have an issue with the thoughts shared in this article, Mr. Powell shares his email address at the end and welcomes further discussion. This post is an Opinion Piece and not meant to diagnose or treat heart issues in dogs or humans.
When Joseph Powell approached me about posting his thoughts on DCM, I was excited because, after our Facebook Live (video is below), I felt like I finally had an understanding of what was going on – which is basically, no one really knows WHAT's happening. There are many reasons dogs are being diagnosed with DCM and Joseph shares his theories on one possible cause. Is he right? I don't know. But it does make sense and it inspires me to continue educating myself because despite being a raw feeder, I know my dogs aren't immune from a future DCM diagnosis.
So, after reading, I'd love to know your thoughts. Do you agree? Disagree? And if you think Joe has missed the point, please explain because we're here to learn. Thanks!
Ok, Ok, I’m sorry. That is not a fun title, but we need to talk about this. It’s time to say the emperor has no clothes. We are trying to pin Dilated Cardiomyopathy (DCM) on just about anything that won’t cost pet food manufacturers any moola, money, cash, Benjamin’s. This world revolves around money, and we can trace almost all motivation back to the almighty dollar.
Big Pet Food is taking a page directly out of Big Tabacco’s playbook. There are a few articles (so-called “studies”) out there that claim to point to a correlation between Boutique, Exotic, or Grain-Free (BEG) pet foods and DCM. Let’s be clear though: no relationship exists! There is no real scientific evidence for their claims—none, zip, nada.
These types of studies are called gray studies. They’re usually sponsored by the folks making the cashola, all to muddy up the subject just enough to cause doubt so you will just go on spending your greenbacks with them.
Big Tabacco has used this technique very effectively for the last 50 years or so. You know…“It’s the couch’s fault your house caught on fire, not the cigarette” argument. This is why your couch is now full of fire-resistant material. The idea is to blame something/anything other than their product. I call it the “find a new villain technique.”
Many veterinarians (not all) and other experts in this arena use the term DCM as a catch-all to describe all heart disease (cardiac failure) in dogs. There are many forms of heart disease in our dogs:
- DCM [Dilated Cardiomyopathy]
- Hypertrophic Cardiomyopathy
- Restrictive Cardiomyopathy
- Congestive Heart Failure
- Myocardial Infarction
- Cardiomyopathy caused by Pulmonary Hypertension
However, the strict definition of DCM is a thinning and stretching of the heart muscle. But in order to break it down for you, and for the sake of this paper, we’re going to put these issues into two categories.
1. Thin, weak, overstretched cardiac muscle. Dilated Cardiomyopathy (DCM)
2. Thickening of the heart wall muscle, Hypertrophic Cardiomyopathy (HCM)
I already hear you asking: “But, but, but, what about my dog and DCM?”
Ok, let’s get to it.
DCM/HCM is simply (although truthfully, there is nothing simple about it) a stretching and/or thickening of the heart wall, which is a muscle. When heart muscle is overstretched, weakened and thin this is classic DCM. Take a pair of nylon running shorts (Ok, stop picturing me in running shorts, it’s not a pretty sight). You can stretch them to a given distance and they will bounce back, but if you over-stretch them they will never regain the old shape again, which is the same for the heart.
You can also think of a person with large plugs in [gauges] their earlobes. Once you remove the plugs the earlobes don’t bounce back, right? They stay stretched out. Stretch the heart wall muscle of the left ventricle beyond its abilities to regain elasticity and EF drops precipitously.
There are potentially a number of causes for this stretching.
- First, a congenital defect could cause a weak and underdeveloped cardiac muscle that eventually dilates. This is much like stepping on a balloon and stretching out the balloon wall.
- There can also be a nutrient deficiency causing poor development of the heart muscle (maybe a taurine deficiency).
- The heart muscle can also stretch in response to an increase in pressure in the arteries that the heart must pump against.
We’ll get back to this in a minute.
Let’s talk about the thickening (Hypertrophic Cardiomyopathy) of the cardiac muscle first.
Bigger muscles are better, right? (I have been trying to build big guns to impress my wife for over twenty-five years now.) So yes, bigger muscles can lead to increased force and therefore improved performance, but a muscle needs to be able to elongate (stretch) before it can apply force.
Think about being in a straight-jacket for an extreme example. You have the same muscles, but you just can’t elongate those muscles to apply force. Make sense?
Or think about the classic muscle-bound bodybuilder. They have huge muscles, but they can’t apply as much force as you would think someone with that size muscle should be able to produce (don’t get mad at me, body builders…I’m just jealous). Imagine a big, built bodybuilder with huge biceps, chest, and forearms. They can’t bend their arms very well due to the enlarged muscles. Same thing with the heart. When the heart muscle (usually the left ventricle because it must pump to the entire body) thickens (and enlarges), it loses its ability to stretch or elongate and therefore cannot produce enough force to pump oxygenated blood to the body. We call this ejection fraction (EF), or the amount of blood the heart can eject in one contraction.
In humans, this decrease in EF is usually caused by a blockage in the cardiac blood flow causing damage to the heart muscle; this results in a significant decrease in EF. This is the classic heart attack, also known as a Myocardial Infarction (MI). This often results in a condition called congestive heart failure (CHF). I have treated hundreds of these patients over the years and the prognosis is never great.
In our furry four-legged friends, the issue is they don’t complain of chest pain, don’t call 911, and don’t get rushed off to the nearest ER to get the blood clot removed. They endure the pain, we don’t detect the heart attack, and damage to the heart muscle ensues. This damage decreases the heart’s ability to pump (EF). Many times, the heart muscle develops scar tissue and thickening (HCM) from the lack of oxygenated blood flow. In the DCM animal, a weak overstretched heart cannot withstand this decrease in oxygen feeding the muscle. Over time, the damaged heart can’t supply enough blood to the body and the animal succumbs.
There are some potential genetic issues going on here as there are some specific breeds that are at higher risk for DCM/HCM. It also seems that large breed dogs have much higher incidents of both. That said, being genetically predisposed to an issue (DCM/HCM) is not usually the causative factor in whether your dog acquires that particular disease.
In my humble opinion, there are three factors influencing cardiomyopathy in dogs. Let’s refer to them collectively as EOP.
- Excessive workload (HCM or DCM) of the left ventricle from pumping against excessive pressure in the vasculature, therefore producing a stretching of the heart muscle or a compensatory growth (adaptive response.)
- Overgrowth (HCM) of the heart wall muscle (left ventricle) due to hyperinsulinemia, IGF, MTOR stimulation and heart wall damage.
- Poor perfusion (MI) of the heart muscle and body due to vascular damage and inflammation.
All three factors are strongly influenced by diet. Dogs are carnivores and therefore don’t eat many carbohydrates in their wild environment (they don’t do much farming and cultivating). When we feed carbs to dogs (dog food manufacturers love carbs because they are extremely cheap and stable), and they, much like humans, have a subsequent insulin response, and the circulating insulin spikes well beyond what would be normal levels. This increase in circulating insulin can stay elevated for long periods of time, causing hyperinsulinemia and insulin resistance. All kibble is bound by carbs; adding carbs is the only way to produce shelf-stable dry bits. However, you need to be careful: wet, raw, or fresh food can still have carbs added (usually to decrease cost).
Hyperinsulinemia causes an inflammatory response throughout the body. It could be argued that the sugar (carbs) cause the inflammation, but that is really a chicken or the egg argument. This inflammation causes a very complex lesion, clotting, and atherosclerotic cascade in the vasculature. The blood vessels get swollen (just like your ankle does when you injure it). When the blood vessels swell, the inside of the vessels get smaller and the residual pressure that the heart must pump against increases the workload of the heart exponentially. The heart wall will then stretch (DCM) in response to these high vascular pressures, just like in our balloon example earlier. Step on the balloon, and the balloon will grow bigger, stretching and weakening the wall of the balloon. In the long run, this can also cause an adaptive response to an increased workload increasing the size of the heart wall muscle (HCM). Remember, cardiomyopathy is an enlarged heart.
Hyperinsulinemia also stimulates Insulin Growth Factor (IGF or IGF1), and IGF stimulates this thing we call MTOR (Mammalian Target Of Rapamycin). So why do we care? Well, MTOR is a nutrient sensor that, when stimulated, copies cells. In short, it tells the body to build more cells. MTOR is great when we are young and growing (i.e. puppies) or when we are trying to build muscle, but not so great if we don’t want to overbuild heart muscle (also terrible if we are reproducing cancer cells.) So too much MTOR stimulation and/or too often builds too much heart muscle (HCM), especially if we are overtaxing that heart muscle because it must work against increased pressure.
There may be role for MTOR stimulation in the DCM animal in an attempt to build the heart muscle, but that stimulation should not come from insulin and carbs.
On top of the inflammation and MTOR stimulation, hyperinsulinemia causes the body to turn carbs/sugar to fat and send it to be stored. This converted sugar/fat is abrasive to the walls of the blood vessels, and it abrades the inside of the blood vessel. Think of a bottle brush cleaning out the inside of a long skinny balloon. It is going to scratch and cause damage to the inner walls of the balloon. When you damage a vessel wall, the body sends cholesterol to go fix the injury. Soon you have cholesterol-laden plaque that builds up inside the vessel further narrowing it. Consequently, it will increase the workload of the heart and decrease the oxygenated blood supply to that very same heart muscle.
By the way, cholesterol is not the bad guy here. It is just trying to repair the damage caused by the carbs and hyperinsulinemia. Cholesterol is high when there is a lot of damage to the blood vessels. Saying cholesterol is bad is like saying firefighters are bad because they are always around when there are fires. Get it?
“Ok…then carbs are bad and protein is good,” you say?
Not so fast! Protein is not an angel in this process. Dogs have a ZERO (yes, ZERO!) carbohydrate requirement. Dogs can live without carbs and be perfectly healthy, but they must have protein to survive. So, we must give them protein, but (it’s always the BUT that gets you) if you feed excessive amounts of protein, it goes through a process of gluconeogenesis (the protein turns to sugar) which stimulates IGF and insulin and well, we’re back to all the issues we talked about earlier.
The other issue with protein is that it’s a stimulator of MTOR, and MTOR tells the body, “Hey, we have plenty of building blocks, so let’s build stuff.” Consequently, we build more cardiac muscle cells, which also contributes to the problem in HCM. Your animals should consume protein, so what is the answer? You have to read to the end to find out. Lol. (I don’t know if I can write lol in an article, but what the heck.)
As mentioned above, we discussed genetic issues and the problem of large breed dogs having a higher rate of DCM/HCM. We need to look at the fact that the larger an animal, the more MTOR stimulation they have. They must grow more cells than smaller animals. So, the fact that larger animals are more susceptible to HCM makes sense in a high MTOR stimulation environment.
Ok, Ok, Ok, I hear you say…“I’ve got it! FAT! Just give them fat and no carbs and no protein.”
You are correct…sort of. Fats are good and necessary and do not contribute to any of the issues above. Fats do not contribute to hyperinsulinemia, inflammation, MTOR stimulation, or vascular damage but (there is that BUT again), if you heat fats they oxidize (or rust). These oxidized fats cause a whole slew of cellular issues, not the least of which is inflammation, and there you go again down that pathway. By the way, the high heat processing of proteins doesn’t do us any favors either, not to mention that heating any macronutrient quickly removes much of the beneficial nutrient content.
While we are talking about heating proteins (most kibbles are heated four separate times) we should address the taurine deficiency issue here. Taurine is an amino acid and therefore derived from protein. Taurine deficiency in cats causing DCM is real and has been largely solved by the addition of taurine and the taurine precursors methionine and cystine to cat foods. After we identified taurine-deficiency issues in cats, the next logical step was to assume that taurine was the problem with dogs. While we shouldn’t discard all related taurine deficiency research, it doesn’t appear that this is the answer to our issues with DCM/HCM.
The number of animals with DCM/HCM that have a taurine deficiency is relatively the same as ones that do not. This may be partially in part to the fact that we lump all cardiomyopathies into the same bucket and are not doing a good job of teasing out which cardiac disease is correlating to taurine deficiencies. You wouldn’t think on face value that HCM animals would have taurine deficiencies. Why did cats have a taurine deficiency? In my opinion, if you high heat process your protein sources (kibble or cooked food) then the quality of the proteins decreases respectively and…yep, you just might have a taurine deficiency issue and DCM. If we want to cover this base for our dogs, let’s use quality protein sources AND let’s not heat process them. If we can’t afford quality raw protein sources, then a taurine supplement may be helpful.
“Ok, then I give up!” I hear you yell. “I’m just never gonna feed my dog ever again!” Not so fast. Here is a summary of the issues:
- Too many carbs for dogs, which don’t eat carbs in the wild. (No, they have not adapted in the last 100 years, and grain-free doesn’t mean carb-free. In fact, grain-free pet foods commonly have more carbs than grain-based foods.)
- Too much protein, or protein too often, stimulates MTOR, gluconeogenesis, and inflammation.
- Oxidized proteins cause loss of nutrients, and amino acids (taurine) and oxidized fats from high heat processing cause inflammation, vascular and cellular damage.
So, here’s what science suggests we do:
- Get rid of the carbs and feed a fresh food diet without added carbs as fillers. If you do feed any carbs, your animal should get a direct benefit from that carb, i.e. antioxidants, vitamins, minerals, fiber, etc.
- Do not overfeed protein. Protein should be fed in an amount to maintain quality muscle mass. Some suggest feeding protein at 0.75-1.0 grams per pound of body weight. The less you heat or process protein, the less protein you must feed to maintain quality muscle mass. *
- Feed once a day to allow MTOR stimulation to happen only once a day. Dogs don’t eat three times a day in the wild. They make a kill, gorge themselves and then do not eat for several days. Feeding multiple times a day is stimulating MTOR every time they eat. Consequently, cells (good cells and bad cells) are reproducing multiple times a day. Also, each time you give your dog a food treat, MTOR is firing up and making cells, so don’t treat your dog as it creates the same issues. *
- Only feed fats and proteins that have not been heat-processed. A fresh, raw balanced diet is best. How many dogs do you see cooking their food in the wild? Exactly.
- Make sure your animal gets plenty of exercise and activity, as it helps burn any sugar/carbs circulating in the bloodstream and helps decrease insulin activity.
*Recommendations #2 and #3 should not be followed with puppies or animals under 18 months of age.
So, is your dog going to get DCM or HCM?
If you continue to feed carbohydrate-laden foods that are high heat processed with oxidized fats and proteins, overfeed proteins, and feed/treat them too often, then the probability of heart issues is significantly higher. But we have options. Let’s take those options and improve our animals’ health and decrease the chances that a devastating disease strikes our furry friends.
Just a quick note: If your animal has been clearly diagnosed with DCM and not HCM, then there may be a role for feeding smaller amounts of quality protein multiple times a day to stimulate MTOR more often (without stimulating IGF and insulin) to give the heart the building blocks it needs. There is also some emerging information that ketones improve EF and cardiac efficiency and therefore may be beneficial in both DCM and HCM animals. If the body is using carbs for fuel, it will not make ketones, but if the body gets the correct amount of protein and fat, it will produce its own ketones.
Don’t let the junk pet food manufacturers (McDonald's of pet food) sell you that DCM/HCM is an issue of taurine, boutique pet food manufactures or a lack of grains in your pet’s diet. We should look at all possible issues, but we should start with a good foundation first. It might be correct to say that I got my ONE abdominal muscle in the middle of my tummy from a vitamin C deficiency, but I would suspect it was the all the pizza, fast food, and soda I have consumed over the years. Go figure. Manufacturers always want to add something to solve an issue and never want to remove something. You can’t sell something you remove or take away. In the 1800’s we had issues of deficiencies in our diets. In 2019 we have issues of excess! The problem is they can’t sell you more of something you are already buying too much of. How will they increase market share?
That’s all I’ve got for now. Remember, it is just my humble opinion. I am not a vet, I don’t play one on TV and this isn’t medical advice (I think I covered all needed disclaimers, lol). For full transparency, I own a raw pet food company that my wife and I started after we lost our third dog to cancer and needed to find a solution to the cancer issue [that serves an area of Southern California]. Feel free to contact me if you have any questions or if I can help in any way.
~ Joe Powell, Joe@vibrantk9.com
About Joseph Powell (Author)
- Joe has been in pre-hospital emergency medicine for over 35 years. Joe is the EMS Chief for the City of Rialto Fire Department.
- He has been published in the Journal of Emergency Medical Services and in the Western Journal of Emergency Medicine multiple times.
- He owns 2 US patents that he wrote.
- Joe started a study 5 years ago at his fire department on cardiac survivability in CPR patients. Due to his ongoing study, he has one of, if not the highest cardiac arrest survival rates in the entire world. Joe lectures on the study along with heart, cardiac issues and cardiac arrest survival across the US and internationally.
- Joe has lectured in 6 countries, and many cities in the US in the last few years teaching his equation for cardiac arrest and survival in a CPR status.
Additional Reading on DCM in Dogs
As you know, when it comes to learning about the health of our dogs, we seek information for more than one source. I appreciate Joe Powell for sharing his opinion on a possible cause of DCM in dogs. After sharing this article, one individual was kind enough to share more reading.
What I'm finding are more experts (veterinarians experienced in heart issues) who state that (1) DCM is not just related to dogs fed a grain-free diet, (2) “Most dogs being diagnosed with DCM do not have low taurine levels.” ~ Dr. Lisa Freeman, and (3) dogs fed a raw diet have been diagnosed with DCM too.
- ‘BEG’ pet food and DCM, part 2: Is veterinary bias at play?, Ryan Yamka
- Grain-Free Diets and DCM, The Raw Feeding Community
- Bad Science and Big Business are Behind the Biggest Pet Food Story in a Decade, Daniel Schulof of KetoNatural Pet Foods
- It’s Not Just Grain-Free: An Update on Diet-Associated Dilated Cardiomyopathy, Dr. Lisa Freeman*
- Echocardiographic Phenotype of Canine Dilated Cardiomyopathy Differs Based on Diet Type, Journal of Veterinarian Cardiology
*It's important to know that Dr. Freeman has worked for several large dry dog food companies and while those companies may not be providing the funding on studies she's involved with about DCM, I feel that full disclosure is important. I would also disclose if she had worked for raw food companies.
“Dr. Freeman has received research funding or provided sponsored lectures or consulting services for Royal Canin, Nestlé Purina PetCare, and Hill’s Pet Nutrition.”Source: Scopus Preview/American Journal of Veterinary Research
Other Blog Posts I've Written on DCM and Grain-Free Diets
- Did a Grain-Free Diet Base Mix Harm My Raw Fed Dog? (Dr. Becker and Rodney Habib speak with Dr. Gundry)
- Rodney Habib Recommends Purina Pro Plan?
Raw-Friedly, Integrative Veterinarians
There are a lot of people who are recommending various resources and groups to help us learn about DCM and not all of the resources/groups are raw-feeder-friendly. Therefore, I feel that it's important that I share qualified, integrative veterinarians who are raw-friendly and won't insist that you switch to a diet of dry dog food if this isn't your wish for your dog.
Dr. Alinovi is the veterinarian who helped me make the decision to transition to raw which saved the life of one of my dogs. She also helped me transition to DIY raw feeding, which saved me money and made it easier for me to control the ingredients and feed a balanced diet (I balance to NRC, not AAFCO – which is for kibble and not raw/holistic friendly, see Susan Thixton of Truth About Pet Food to learn more).
Dr. Coger hosts the annual Healthy Dog Expo, offers meal formulation consultations, and has been a wealth of knowledge as I’ve traversed this journey of learning how to raise my dogs naturally. Dr. Coger also reviews nutrient analysis testing, including the one I do for my four dogs.