The Best Ways to Cook Meat to Reduce AGE Glycotoxins

Journal articles with titles like, “Extended Lifespan in Mice Exposed to a Low Glycotoxin Diet” exemplify the studies showing lowering dietary AGE intake can improve longevity, whereas increasing AGE intake can impair learning and memory and cut lives short in rodents. In one study, while 76 percent of mice fed a low-AGE diet lived at least 56 weeks, not a single one of the mice fed an AGE-rich diet survived over 44 weeks.

The effect is so great it can even trump calorie restriction. While life-long calorie restriction predictably prolongs the lifespan of mice, feed them high AGE food pellets and they die sooner than mice eating regular diets and do worse in every category tested—inflammation, oxidative stress, insulin resistance, and marked heart and kidney fibrosis, meaning scar tissue buildup. The benefits of reducing food quantity can be obviated by reductions in food quality.

There are numerous human clinical trials showing high-AGE foods can increase inflammation and oxidation, and lowering AGEs in your diet has a bunch of metabolic benefits, but many involve dietary changes that make the AGE contribution difficult to tease out. For example, you can improve the health of people with a quote-unquote “low-AGE diet” by restricting meat intake to once a week, but that only proves the benefit of cutting down on meat consumption, which may or may not have anything to do with AGEs. The solution researchers came up with was to randomize people to oral loads of AGEs directly, or have people change the way they cook the same foods.

Most challenge studies showed the oral AGEs led to an increase in blood AGEs, accompanied by an increase in inflammation and artery dysfunction. Similarly, meta-analyses of randomized controlled trials showed that having people reduce AGE intake by, for example, sticking to the same foods but switching from frying, baking, or grilling, to poaching, stewing, or steaming led to a decrease in inflammation, oxidative stress, and insulin resistance, whereas the reverse led to an increase in inflammation. Interestingly, the decrease in inflammation on low-AGE diets was greater than the increase in inflammation on high-AGE diets, since the so-called “high” AGE diet that was so harmful was actually similar to the average estimated daily intake of AGEs by the general population. Reviewers conclude that a “low AGE diet is a low cost, safe, readily scalable, and easy to implement strategy, which can be used for both prevention and treatment of cardiometabolic risk factors and disease.”

The experiments lasted for up to a year, but even a single meal can do it. A single oral AGE challenge can impair artery function and increase markers of inflammation and oxidative stress within 90 minutes. If you randomized people to a meal of fried or broiled chicken breast and veggies, compared to the same meal, same ingredients—including the oil—but instead steamed or boiled chicken breast with veggies, that single high AGE meal induced a profound impairment of artery function within hours. The steamed or boiled chicken meal still impaired arterial function, but significantly less than when it was fried or broiled. This difference was attributed to AGEs, but there are other heat-generated toxins formed when meat is cooked, such as heterocyclic amines (originating mainly from the creatine in the muscle) that makes absolute attribution impossible.