Many pet owners are aware that kibble and canned dog food may not be the best for their dogs’ health. My own dogs are on a raw diet, primarily due to the presence of glycotoxins. Glycotoxins, or Advanced Glycation End-products (AGEs), are compounds that form when a fat or protein reacts with sugar, a process known as glycation.
These glycotoxins are not only produced within the body but also ingested through a diet rich in highly-processed and heat-treated foods. The Maillard reaction, responsible for the browning of food, is a common source of AGEs. They are linked to various health issues such as obesity, diabetes, food allergies, poor gut health, heart disease, hardening of arteries, kidney failure, Alzheimer’s, Parkinson’s, and certain cancers. High-temperature cooking processes, like those used in making extruded dry dog food and wet canned food, contribute to the formation of AGEs. This suggests that the same compounds causing diseases in humans are also harming our dogs. Another source of AGEs is endogenous, produced as byproducts from food breakdown within the body, especially when there’s a high intake of carbohydrates. Kibble, being up to 60% processed carbs, can significantly increase AGEs in a dog’s body, potentially causing damage and inflammation. Chronic inflammation is a major factor in many age-related chronic diseases in dogs. The complexity of glycotoxin names, such as carboxymethyl lysine (CML) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, often leads to their neglect in pet food discussions. However, understanding and addressing glycotoxins in dog food is crucial for maintaining the health and longevity of our pets.But when pet food is tested for glycotoxins, it’s usually only for one or two compounds at a time. This can massively downplay the issue. For instance, studies may only test for acrylamide, a human carcinogen. Studies suggest that acrylamide in mass-produced canned and dry food exists at around.02 to 0.40 mg per kg dry matter. The pet industry then deduced that anything below 7 mg acrylamide/kg dry matter is probably “harmless”. How they arrived at this conclusion when the long-term safety is still unproven is anybody’s guess. The emphasis here is on the word “probably”. Also, as acrylamide stays in the tissues, is eating it daily for years really safe?
Pet food research often tests for just one or two advanced glycation end products (AGEs) and then concludes (with limited or no evidence) that it exists in “safe amounts”. While we are highly skeptical of that claim, the bigger issue is what about the tens, if not hundreds, of other AGEs that also exist in heat-processed dog food? A doctoral dissertation in 2020 was one of the few studies to actually measure AGEs in four different kinds of dog food. Predictably, canned food had the highest levels, probably because canned food is cooked at the highest temperatures. Extruded dry dog food (kibble) followed closely with high AGE levels. Dehydrated food had very little; predictably, raw food had the least disease-causing glycotoxins. Other findings include the following: Dogs eating extruded dry food may take in more acrylamide than adult humans. Despite it being labeled at supposedly “safe” levels, this is still worrying. In older dogs, AGEs build up in the brain’s neurons and in the heart’s left ventricle. This may play a role in senior heart disease and dementia. In three recorded cases, dogs with high levels of AGEs in their system developed hard arteries. Pets are estimated to eat up to five times more heterocyclic amines daily in dry and canned pet food than humans. In rat studies, heterocyclic amines are linked to leukemia, breast cancer, and gut, liver, and lung tumors. Other AGEs that show up in much higher levels in dog and cat food than in human food include carboxymethyl lysine (CML), fructose lysine, and hydroxymethylfurfural. CML plays a large role in liver and kidney disorders, as well as diabetes and aging. Fructolysine is connected to diabetes too. When fructolysine oxidizes, it turns into CML, meaning that there is probably more CML in dog food than we think, causing more free radicals and inflammation in the body. One study tested pets eating different kinds of pet foods tested for carboxymethyl lysine (CML), carboxymethyl lysine (CEL), and lysinoalanine (LAL). Predictably, it found that the more heat-processed their food was, the more of these AGEs were in the dogs’ system. All of these are specifically linked to kidney failure. Is it any wonder that about 1 in 10 dogs suffer from renal disease? So far, while the pet food industry can’t deny that glycotoxins exist in pet food, they can point to the lack of research on it as a reason to shrug it off.We don’t know exactly how dogs absorb, break down, or excrete glycotoxins in their food. There aren’t enough long-term studies linking doggy dementia to CML in dog food, so it’s easy to say evidence doesn’t exist. However, a study shows CML accumulates in older dogs’ brains. Common sense tells us if glycotoxins cause havoc in the human body, they will affect dogs too. In fact, dogs probably have a lower tolerance for AGEs than humans. Dogs and cats deal with toxins differently than humans. For example, humans can handle toxins in foods like grapes, raisins, chocolate, and onions that are toxic to dogs. This is because humans evolved to break down and excrete these compounds safely. Meanwhile, dogs evolved to eat meat and didn’t evolve to metabolize compounds in a raisin. As humans evolved to eat more carbohydrates, our blood sugar levels respond to high-carbohydrate meals. Massive spikes in blood sugar may not be good for our health, but it shows our bodies are more capable of processing carbohydrates. This suggests we are probably more capable of eliminating AGEs from our body. Scientists think we began eating cooked foods between 1.8 million and 400,000 years ago. This gave us time to get better at getting rid of glycotoxins from our food. But dogs only became domesticated around 30,000 years ago, so they haven’t evolved to deal with processed carbohydrates. There is good reason to believe dogs are more sensitive and vulnerable to glycotoxins in food than humans. How To Reduce AGEs/Glycotoxins In Your Dog? Feeding your dog a balanced raw diet is the number one way to reduce dietary glycotoxins. But there are other things you can do. According to the Anti-A.G.E’s Foundation, you can give your dog as much exercise as possible depending on his physical ability. Physical activity reduces all the macronutrients in the body that form glycotoxins. If you cook dog food, cook it at low temperatures, such as with a slow cooker. Use a thermometer to check the heat is as low as possible. Or buy freeze-dried, dehydrated, or air-dried food if raw feeding is not available. Freeze-dried food is not processed with heat and retains the nutrients of raw food. Dehydrated or air dried foods are dried at low temperatures but do suffer some nutrient loss from heat. Final thoughts: Dry kibble is bad for dogs for many reasons, such as synthetic additives, low-quality nutrients, aflatoxins, and more. But glycotoxins are the main reason I don’t feed my dogs heat-processed foods. As they are linked to almost every disease, from dementia to cancer, canned or dry dog food is not a good investment in a dog’s long-term health.
The Maillard reaction’s impact on pet food processing and its effects on nutritive value and pet health have been extensively studied. Van Rooijen et al. (2013) provided insights into this reaction’s influence on pet food, while Beynen (n.d.) specifically addressed the presence of acrylamide in pet food.
Palaseweenun et al. (2021) investigated the effects of four differently processed diets on various health markers in healthy dogs, including plasma levels of Advanced Glycation End Products (AGEs), serum levels of Receptor for Advanced Glycation End Products (RAGE), serum and urine metabolome, and fecal microbiome. Further studies have highlighted the urinary excretion of AGEs in dogs and cats, as reported by Hagen-Plantinga et al. (2021), and the distribution of AGEs in cerebellar neurons of dogs by Weber et al. (1998). Chiers et al. (2010) also noted the accumulation of AGEs in canine atherosclerosis.
