Advanced Glycation End-products, AGEs, are a diverse collection of compounds that have been associated with endothelial dysfunction, cataracts, kidney disease, and atherosclerosis in both animal models and human studies. Not all involve glycation nor glucose, but the catch-all name has stuck.
There are a number of actively-held theories of aging, such as the idea that aging is the result of accumulated products of oxidative injury; a genetically pre-programmed script of declining hormones and other phenomena; genetic “mis-reading” that results in disordered gene expression, debris, and uncontrolled cell proliferation (e.g., cancer); among others.
One of the fascinating theories of aging is, cutely, the AGEing theory of aging, i.e., the accumulation of AGE debris in various tissues. Such AGEs have been recovered in lenses from the eyes, atherosclerotic plaque in arteries, kidney and liver tissue, even brain tissue of people with Alzheimer’s dementia. AGEs perform no known useful physiologic function: They are relatively inert once formed (especially polymeric AGEs), they do not participate in communication, they make no contribution of significance. They simply gum up the works–debris. (AGEs are to health as the USDA food pyramid is to dietary advice: material for the junkyard.)
There are two general ways to develop AGEs:
1) Endogenous–High blood glucose (any blood sugar above 100 mg/dl) will permit glycation of the various proteins of the body. The higher the blood glucose, the more glycation will proceed. Glycation also occurs at low velocity at blood glucose levels below 100 mg/dl, though this would therefore represent the “normal,” expected rate of glycation. Endogenous glycation explains why people with diabetes appear to age and develop all the phenomena of aging faster than non-diabetics (kidney disease, eye diseases, atherosclerosis, dementia, etc.). Hemoglobin A1c, HbA1c, is a readily-obtainable blood test that can show how enthusiastically you have been glycating proteins (hemoglobin, in this case) over the last 2 to 3 months.
A low-carbohydrate diet is the nutritional path that limits endogenous glycation leading to AGE formation. Restricting the most obnoxious carbohydrates, the ones that increase blood sugar the most, such as wheat, cornstarch, rice starch, potato starch, tapioca starch, and sucrose, will limit endogenous AGE formation.
2) Exogenous–AGEs (here especially is where the “AGE” label is misleading, since many other reactions besides glycation lead to such compounds) are formed with cooking at high temperatures, especially meats and animal products. Therefore, a rare steak will have far less than a well-done steak. A thoroughly baked piece of salmon will have greater AGE content than sashimi.
The forms of cooking that increase AGE content the most: roasting,deep-frying, and barbecuing. Temperatures of 350 degrees Fahrenheit and greater increase AGE formation.
Therefore, cooking foods at lower temperature (e.g., baking, sauteeing, or boiling), eating meats rare whenever possible (not chicken or pork, of course), eating raw foods whenever possible (e.g., nuts) are all strategies that limit exogenous AGE exposure. And minimize or avoid butter use, if we are to believe the data that suggest that it contains the highest exogenous AGE content of any known food.
If we connect the dots and limit exposure to both endogenous and exogenous AGEs, we will therefore not trigger this collection of debris that is likely associated with disease and aging. So following a low-AGE diet may also be an anti-aging strategy.
The New Track Your Plaque Diet, soon to be released on the Track Your Plaque website, has incorporated strategies to limit both endogenous as well as exogenous AGEs.
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Dear Dr Davis,
I know your opinion against butter, but disagree, based on a lifelong experience, as a skin chronic healed by milkfats and (land)animal fats.
For the first 40 years of my life I was never free of allergic reactions and imflammated skin symptoms. Raw food helped not, vegetables and salads helped not, and the official healthy lifestyle helped not either. 10 years ago, when the stsart of Zonish lowcarb (much like your style) finally helped me incredibly much… Yet my skin has healed fully only after I switched to very, very buttery and egg-yolky diet close to Jan Kwasniewski.
I live far up North, but have no symptoms of vitamin D deficiency, in spite of not eating the pills and not having much sun for the better part of the year. Furthermore, I cannot eat fish, and do no longer supplement with fish oil either, due to problems induced by it. Yet my skin has never been as good as now, fully without irritation or other symptoms. And unlike my frends and colleagues, I no longer seem to catch seasonal colds, either.
So far the only thing I can blame for the last few years of well-being is increased use of milkfat and non-muscle parts of animals (fat, marrow, liver and skin collagen). Of these the milkfats make up a major part of the daily calories, often more than 50 E%.
I'm interested to hear your thought on possible causes, which make this butter strategy work the best of all that we've ever tried; both for myself and for others in our family
With regards,
LeenaS
I am a Type 2 Diabetic with normal blood sugar who takes -0- drugs and -0- insulin.
I experienced tremendous benefits from going low carb primal. I won't detail them here but I have not been sick in 20 mos.
This summer I performed a one week dairy fast (I'd been off milk for almost a year) and then added back butter.
Butter was very inflammatory. I no longer eat it. Clarified butter or Ghee and Cheese are not inflammatory and I eat it occasionally.
So for me, I agree with butter.
Anonymous, thanks for the info on sausage. I buy raw sausage and I'm careful to avoid over-cooking any meat, mostly because it gets like shoe leather.
Another question: is cream high in AGEs? Does the churning action required for butter contribute to oxidation or AGEs?
What's the consensus on carnosine ? I've read some articles claiming it helps with AGE factors.
Dr. Davis, it's fine to have data on a diet that contains AGEs, but where's the data on a diet that avoids AGEs? Where is the justification for adopting such a diet? Avoiding something leads to adopting something else. What will that be? You can't predict. Nobody can predict. This is the danger of advising to avoid something just like that was the danger of advising to avoid saturated fat and pretty much all animal fat altogether in one big swoop.
If we can't eat fat, we must eat sugar. There's no other alternative. If we can't eat meat, we must eat some other form of protein. What will that be, soy, wheat, any other grain, legumes? If we can't eat meat, we must eat some other form of those essential nutrients like B12 and EFAs. But where can we get such a high quality source of those nutrients but in animal flesh? The quick answer is nowhere.
When you advise to avoid AGEs without giving us a safety threshold, the safe course is to avoid all AGEs, not just a little bit. When you give a safety threshold, it doesn't matter because the substance has been declared bad entirely anyway so the safe course is the same.
We can see this with animal fat and pretty much any kind of fat. Fat is bad, so any fat is bad, so less fat is good or better, but no fat is best. That's how it works in spite of having some form of safety threshold we can abide by like say 10g of saturated fat per day maximum. Why is that? The safety threshold is declared as a maximum with no minimum.
So tell us Dr. Davis, what is the maximum and the minimum amount of AGEs you advise we eat? But more relevant to the discussion, how can we find out exactly how much AGEs is in the food we eat every day so that we can make an informed decision on exactly how much AGEs we eat every day? Is there a tool that will allow me to find that out? The point is that even if you give us a precise number on how much AGEs we can and cannot eat, we can't even control how much AGEs we eat. Accordingly, the best course of action is to avoid all AGEs and not just a little bit just to be safe because the contention is that lots of AGEs is worse than none.
With endogenous AGEs production due to high blood glucose and other simple sugars like fructose, the problem is much simpler. That's because this AGEs aspect of sugars is merely the last installment of How Sugars Kill Us Slowly. We already know that sugars kill us slowly and we already know just how much of it will do it and how long it will take and etc. But until you find out exactly how much exogenous AGEs we must avoid and exactly how much we can get away with and how to measure the AGEs in the food we eat, this problem will remain unresolved and unresolvable.
In other words, the best course of action with exogenous AGEs is to just ignore them outright. After all, we've been ignoring them outright for the past couple million years without so much trouble.
Bill,
Butter is high in AGEs? Wow – why? What about Ghee?
Do you know what the AGEs are in smoked meats like smoked trout?
Does the canning process increases ages as in canned wild caught salmon?
Hi, Fred-
I believe that smoked fish tend to be moderately high in exogenous AGEs.
One of the difficulties with quantification of AGEs in foods is we have limited data on the AGE content of various foods. It's not like grams fats or carbohydrates listed in plain sight on the label.
I find the AGE conversation a fascinating new potential insight into helping us decide how to best manage food choices, as well as food preparation.
As with all new ideas, it will cause upheaval in preconceived notions.
Given some of the previous blog posts, the largest preconceived notion might be yours toward butter. So, it's no big deal if you aren't up to the challenge of defending what you posted. That's okay. Trying to be coy about it, not so much.
Count me as a skeptic on this one.
Very good review on AGEs. Dr. Davis is 100% right to be concerned.
http://biomedgerontology.oxfordjournals.org/content/65A/9/963.full#ref-109
Chris Masterjohn has the skinny on AGEs in butter:
The Daily Lipid: Is Butter High in AGEs?
People are confusing exogeneous AGEs which are generally harmless compared to the dangerous endogenous AGEs.
Endogenous AGEs are created by proteins in our bodies reacting with reducing sugars. Practically the only sources of dietary reducing sugars are fructose (table sugar, HFCS) and cooked starches. The obvious solution is to eat far more meat and butter and drastically reduce carbohydrates.
Humans have been eating cooked food for 1.8 million years and are very well adapted to them. The novel foods in the human diet are large quantities of plant proteins, starches and sugars.
I'm surprised you think kale and spinach are so wonderful. Renowned toxicologist Dr Bruce Ames says that there are considerable amounts of natural toxins and carcinogens present in all food plants.
http://www.fortfreedom.org/n16.htm
Any potential benefits from eating kale is likely to be due to hormesis.
In fact there is absolutely nil direct scientific evidence that eating fruit and vegetable has any health benefits whatseover. The benefits of vegetables have only been found in a few poorly designed population studies. Any observed 'benefits' of eating vegetables are probably just due to confounding variables – people who eat vegetables smoke less, drink less alcohol, are more active and eat less sugar and junk foods.
Gary Taubes is skeptical of the claims about exogenous AGES
http://www.healthcentral.com/diabetes/c/36758/17729/gary-taubes
Hi Apra,
In 'The Diet Delusion' Gary Taubes says that the natural diet of humans is almost purely carnivore with a few berries. Taubes studied physics at Harvard and aerospace engineering at Stanford before becoming a journalist. Because he was properly trained in using rigorous scientific methods he can readily see the flaws in nutrition research.
I've read the sole paper that lists butter as a high-AGE food: "Advanced Glycoxidation End Products in Commonly Consumed Foods" (2004, Journal of the American Dietetic Association, via Google Scholar cache).
The data is in Table 1, which refers to "foods prepared by standard cooking methods" (these include frying), but the table says nothing specific about how the butter was processed. I am willing to bet that the butter in question had been treated at high temperature (maybe used in frying).
Consider these values:
Milk, cow, whole …. 0.05 kU/mL
Butter ………….. 265 kU/g
Expecting high AGEs in uncooked butter — over 5000 times the level in milk! — would make little sense.
Would you consider revising your post in light of this?
The data table lists butter as 100 gm serving, or over 3 ounces (23,000 – 26,000). In the serving size database, the amount of AGEs normalize a bit, at 1100 – 1300. I wish they had done organic vs commercial butters, but maybe next time we can see that data. No surprise on pan fried bacon at 91,577 for 3 ounces and 11,905 for the serving size (2 slices is the norm). As with all foods, moderation. And thank you for your blog – it is very informative!