High-heat cooking will AGE you, if you eat food deep-fried with industrial vegetable oils

As I said before on this blog, I am yet to be convinced that grilled meat is truly unhealthy in the absence of leaky gut problems. I am referring here to high heat cooking-induced Maillard reactions (browning) and the resulting advanced glycation endproducts (AGEs). Whenever you cook a food in high heat, to the point of browning it, you generate a Maillard reaction. Searing and roasting meat usually leads to that.

Elevated levels of serum AGEs presumably accelerate the aging process in humans. This is supported by research with uncontrolled diabetics, who seem to have elevated levels of serum AGEs. In fact, a widely used measure in the treatment of diabetes, the HbA1c (or percentage of glycated hemoglobin), is actually a measure of endogenous AGE formation. (Endogenous = generated by our own bodies.)

Still, evidence that a person with an uncompromised gut can cause serum levels of AGEs to go up significantly by eating AGEs is weak, and evidence that any related serum AGE increases lead the average person to develop health problems is pretty much nonexistent. The human body can handle AGEs, as long as their concentration is not too high. We cannot forget that a healthy HbA1c in humans is about 5 percent; meaning that AGEs are created and dealt with by our bodies. A healthy HbA1c in humans is not 0 percent.

Thanks again to Justin for sending me the full text version of the Birlouez-Aragon et al. (2010) article, which is partially reviewed here. See this post and the comments under it for some background on this discussion. The article is unequivocally titled: “A diet based on high-heat-treated foods promotes risk factors for diabetes mellitus and cardiovascular diseases.”

This article is recent, and has already been cited by news agencies and bloggers as providing “definitive” evidence that high-heat cooking is bad for one’s health. Interestingly, quite a few of those citations are in connection with high-heat cooking of meat, which is not even the focus of the article.

In fact, the Birlouez-Aragon et al. (2010) article provides no evidence that high-heat cooking of meat leads to AGEing in humans. If anything, the article points at the use of industrial vegetable oils for cooking as the main problem. And we know already that industrial vegetable oils are not healthy, whether you cook with them or drink them cold by the tablespoon.

But there are a number of good things about this article. For example, the authors summarize past research on AGEs. They focus on MRPs, which are “Maillard reaction products”. One of the summary statements supports what I have said on this blog before:

"The few human intervention trials […] that reported on health effects of dietary MRPs have all focused on patients with diabetes or renal failure."

That is, there is no evidence from human studies that dietary AGEs cause health problems outside the context of preexisting conditions that themselves seem to be associated with endogenous AGE production. To that I would add that gut permeability may also be a problem, as in celiacs ingesting large amounts of AGEs.

As you can see from the quote below, the authors decided to focus their investigation on a particular type of AGE, namely CML or carboxymethyllysine.

"...we decided to specifically quantify CML, as a well-accepted MRP indicator ..."

As I noted in my comments under this post (the oven roasted pork tenderloin post), one particular type of diet seems to lead to high serum CML levels – a vegetarian diet.

So let us see what the authors studied:

"... we conducted a randomized, crossover, intervention trial to clarify whether a habitual diet containing high-heat-treated foods, such as deep-fried potatoes, cookies, brown crusted bread, or fried meat, could promote risk factors of type 2 diabetes or cardiovascular diseases in healthy people."

Well, “deep-fried potatoes” is a red flag, don’t you think? They don’t say what oil was used for deep-frying, but I bet it was not coconut or olive oil. Cheap industrial vegetable oils (corn, safflower etc.) are the ones normally used (and re-used) for deep-frying. This is in part because these oils are cheap, and in part because they have high “smoke points” (the temperature at which the oil begins to generate smoke).

Let us see what else the authors say about the dietary conditions they compared:

"The STD was prepared by using conventional techniques such as grilling, frying, and roasting and contained industrial food known to be highly cooked, such as extruded corn flakes, coffee, dry cookies, and well-baked bread with brown crust. In contrast, the STMD comprised some raw food and foods that were cooked with steam techniques only. In addition, convenience products were chosen according to the minimal process applied (ie, steamed corn flakes, tea, sponge cakes, and mildly baked bread) ..."

The STD diet was the one with high-heat preparation of foods; in the STMD diet the foods were all steam-cooked at relatively low temperatures. Clearly these diets were mostly of plant-based foods, and of the unhealthy kind!

The following quote, from the results, pretty much tells us that the high omega-6 content of industrial oils used for deep frying was likely to be a major confounder, if not the main culprit:

"... substantial differences in the plasma fatty acid profile with higher plasma concentrations of long-chain omega-3 fatty acids […] and lower concentrations of omega-6 fatty acids […] were analyzed in the STMD group compared with in the STD group."

That is, the high-heat cooking group had higher plasma concentrations of omega-6 fats, which is what you would expect from a group consuming a large amount of industrial vegetable oils. One single tablespoon per day is already a large amount; these folks were probably consuming more than that.

Perhaps a better title for this study would have been: “A diet based on foods deep-fried in industrial vegetable oils promotes risk factors for diabetes mellitus and cardiovascular diseases.”

This study doesn’t even get close to indicting charred meat as a major source of serum AGEs. But it is not an exception among studies that many claim to do so.

Reference

H Birlouez-Aragon, I., Saavedra, G., Tessier, F.J., Galinier, A., Ait-Ameur, L., Lacoste, F., Niamba, C.-N., Alt, N., Somoza, V., & Lecerf, J.-M. (2010). A diet based on high-heat-treated foods promotes risk factors for diabetes mellitus and cardiovascular diseases. The American Journal of Clinical Nutrition, 91(5), 1220-1226.

Slow-cooked meat: Round steak, not grilled, but slow-cooked in a frying pan

I am yet to be convinced that grilled meat is truly unhealthy in the absence of leaky gut problems. I am referring here to high heat cooking-induced Maillard reactions and the resulting advanced glycation endproducts (AGEs). If you are interested, see this post and the comments under it, where I looked into some references provided by an anonymous commenter. In short, I am more concerned about endogenous (i.e., inside the body) formation of AGEs than with exogenous (e.g., dietary) intake.

Still, the other day I had to improvise when cooking meat, and used a cooking method that is considered by many to be fairly healthy – slow-cooking at a low temperature. I seasoned a few pieces of beef tenderloin (filet mignon) for the grill, but it started raining, so I decided to slow-cook them in a frying pan with water and some olive oil. After about 1 hour of slow-cooking, and somewhat to my surprise, they tasted more delicious than grilled!

I have since been using this method more and more, with all types of cuts of meat. It is great for round steak and top sirloin, for example, as well as cuts that come with bone. The pieces of meat come off the bone very easily, are soft, and taste great. So does much of the marrow. You also end up with a delicious sauce. Almost any cut of beef end up very soft when slow-cooked, even cuts that would normally come out from a grill a bit hard. Below is a simple recipe, for round steak (a.k.a. eye round).

- Prepare some dry seasoning powder by mixing sea salt, black pepper, dried garlic bits, chili powder, and a small amount of cayenne pepper.
- Season the round steak pieces at least 2 hours prior to placing them in the pan.
- Add a bit of water and olive oil to one or more frying pans. Two frying pans may be needed, depending on their size and the amount of meat.
- Place the round steak pieces in the frying pan, and add more water, almost to the point of covering them.
- Cook on low fire covered for 2-3 hours.

Since you will be cooking with low fire, the water will probably not evaporate completely even after 3 h. Nevertheless it is a good idea to check it every 15-30 min to make sure that this is the case, because in dry weather the water may evaporate rather fast. The water around the cuts should slowly turn into a fatty and delicious sauce, which you can pour on the meat when serving, to add flavor. The photos below show seasoned round steak pieces in a frying pan before cooking, and some cooked pieces served with sweet potatoes, orange pieces and a nectarine.

A 100 g portion will have about 34 g of protein. (A 100 g portion is a bit less than 4 oz, cooked.) The amount of fat will depend on how trimmed the cuts are. Like most beef cuts, the fat will be primarily saturated and monounsatured (both very healthy), with approximately equal amounts of each. It will provide good amounts of the following vitamins and minerals: iron, niacin, phosphorus, potassium, zinc, selenium, vitamin B6, and vitamin B12.

Oven roasted meat: Pork tenderloin

This cut of pork is the equivalent in the pig of the filet mignon in cattle. It is just as soft, and lean too. A 100 g portion of roasted pork tenderloin will have about 22 g of protein, and 6 g of fat. Most of the fat will be monounsaturated and saturated, and some polyunsaturated. The latter will contain about 450 mg of omega-6 and 15 mg of omega-3 fats in it.

The saturated fat is good for you. The omega-6-to-omega-3 ratio is not a great one, but a 100 g portion will have a small absolute amount of omega-6 fats, which can be easily offset with some omega-3 from seafood or a small amount of fish oil. Pork tenderloin is easy to find in supermarkets, and is much less expensive than filet mignon, even though it is a relatively expensive cut of meat.

Below are the before and after photos of a roasted pork tenderloin we prepared and ate recently; a simple recipe follows the photos. This type of cooking leads to a Maillard reaction, which is clear from the browning of the meat and around it on the casserole. I am not too concerned; more about this after the recipe.

Below is the simple recipe. The roasted pork pieces come off easily after the roasting is done, and almost melt in the mouth!

- Make about 10 holes on 2 lbs of pork tenderloin, and add chopped garlic pieces into each of them.
- Pour about a cup of salsa evenly over the pork tenderloin pieces.
- Cover roasting container (casserole in photos) with aluminum foil to preserve moisture.
- Preheat over to 375 degrees Fahrenheit.
- Roast the pork tenderloin for about 3 hours.

Now back to the Maillard reaction. When it happens inside the body, it is a step in the formation of advanced glycation endproducts (AGEs), which is not very good, as AGEs are believed to cause accelerated aging. However, the evidence that cooked meat is unhealthy, in the absence of leaky gut problems, is very slim. There are many hypothesized causes of the leaky gut syndrome, one of which is consumption of refined wheat products.

Our Paleolithic ancestors must have eaten charred meat on a regular basis, so it does not make much evolutionary sense to think that eating roasted meat leads to accelerated aging through the ingestion of AGEs. It is possible that eating charred meat caused health problems for our ancestors, and they threw their meat in the fire and then ate it charred anyway. Perhaps the health problems caused by charring were offset by the benefits of killing parasites living in meat with the heat of fire.

This is an open issue that needs much more research. Based on most of the research I have seen so far, eating roasted meat is not even in the same universe, in terms of the health problems that it can possibly generate, as is eating foods rich in refined carbohydrates and sugars (e.g., white bread, bagels, pasta, and non-diet sodas).

Ketosis, methylglyoxal, and accelerated aging: Probably more fiction than fact

This is a follow up on this post. Just to recap, an interesting hypothesis has been around for quite some time about a possible negative effect of ketosis. This hypothesis argues that ketosis leads to the production of an organic compound called methylglyoxal, which is believed to be a powerful agent in the formation of advanced glycation endproducts (AGEs).

In vitro research, and research with animals (e.g., mice and cows), indeed suggests negative short-term effects of increased ketosis-induced methylglyoxal production. These studies typically deal with what appears to be severe ketosis, not the mild type induced in healthy people by very low carbohydrate diets.

However, the bulk of methylglyoxal is produced via glycolysis, a multi-step metabolic process that uses sugar to produce the body’s main energy currency – adenosine triphosphate (ATP). Ketosis is a state whereby ketones are used as a source of energy instead of glucose.

(Ketones also provide an energy source that is distinct from lipoprotein-bound fatty acids and albumin-bound free fat acids. Those fatty acids appear to be preferred vehicles for the use of dietary or body fat as a source of energy. Yet it seems that small amounts of ketones are almost always present in the blood, even if they do not show up in the urine.)

Thus it follows that ketosis is associated with reduced glycolysis and, consequently, reduced methylglyoxal production, since the bulk of this substance (i.e., methylglyoxal) is produced through glycolysis.

So, how can one argue that ketosis is “a recipe for accelerated AGEing”?

One guess is that ketosis is being confused with ketoacidosis, a pathological condition in which the level of circulating ketones can be as much as 40 to 80 times that found in ketosis. De Grey (2007) refers to “diabetic patients” when he talks about this possibility (i.e., the connection with accelerated AGEing), and ketoacidosis is an unfortunately common condition among those with uncontrolled diabetes.

A gentle body massage is relaxing, and thus health-promoting. Add 40 times to the pressure, and the massage will become a form of physical torture; certainly unhealthy. That does not mean that a gentle body massage is unhealthy.

Interestingly, ketoacidosis often happens together with hyperglycemia, so at least part of the damage associated with ketoacidosis is likely to be caused by high blood sugar levels. Ketosis, on the other hand, is not associated with hyperglycemia.

Finally, if ketosis led to accelerated AGEing to the same extent as, or worse than, chronic hyperglycemia does, where is the long-term evidence?

Since the late 1800s people have been experimenting with ketosis-inducing diets, and documenting the results. The Inuit and other groups have adopted ketosis-inducing diets for much longer, although evolution via selection might have played a role in these cases.

No one seems to have lived to be 150 years of age, but where are the reports of conditions akin to those caused by chronic hyperglycemia among the many that went “banting” in a more strict way since the late 1800s?

The arctic explorer Vilhjalmur Stefansson, who is reported to have lived much of his adult life in ketosis, died in 1962, in his early 80s. After reading about his life, few would disagree that he lived a rough life, with long periods without access to medical care. I doubt that Stefansson would have lived that long if he had suffered from untreated diabetes.

Severe ketosis, to the point of large amounts of ketones being present in the urine, may not be a natural state in which our Paleolithic ancestors lived most of the time. In modern humans, even a 24 h water fast, during an already low carbohydrate diet, may not induce ketosis of this type. Milder ketosis states, with slightly elevated concentrations of ketones showing up in blood tests, can be achieved much more easily.

In conclusion, the notion that ketosis causes accelerated aging to the same extent as chronic hyperglycemia seems more like fiction than fact.

Reference:

De Grey, A. (2007). Ending aging: The rejuvenation breakthroughs that could reverse human aging in our lifetime. New York: NY: St. Martin’s Press.

Ketosis, methylglyoxal, and accelerated aging: Fact or fiction?

Ketosis is a state typically associated with very low carbohydrate diets, such as the Atkins diet. In this state, the liver produces ketones based on fat (body fat or dietary fat). Unlike fats, ketones are water soluble and used by many tissues (including brain tissues) as a source of energy.

Unlike glucose and lipoprotein-bound fats (in VLDL, for example), unused ketones cannot be converted back to substances that can be stored by the body. Thus excess ketones are eliminated in the urine; leading to their detection by various tests, e.g., Ketostix tests.

This elimination of unused ketones in the urine is one of the reasons why very low carbohydrate diets are believed to lead to enhanced body fat loss.

From an evolutionary perspective, one could argue that a ketosis state that involves the elimination of ketones in the urine is an inefficient and unnatural emergency mechanism. For our Paleolithic ancestors, dying of starvation was a much bigger problem than dying of obesity complications.

An interesting hypothesis has been around for quite some time about a possible negative effect of ketosis. It goes more or less like this. Ketosis leads to the production of an organic compound called methylglyoxal, which is believed to be a powerful agent of glycation (a misnomer; see note below).

Glycation is a process whereby sugar molecules “stick” to protein or fat molecules, impairing their function. Glycation leads to the formation of advanced glycation endproducts (AGEs), which appear to be associated with a host of diseases, including diabetes, and to be implicated in accelerated aging (or “ageing”, with British spelling).

In short: ketosis leads to the production of methylglyoxal, which leads to the formation of AGEs, which in turn cause diseases and accelerated aging.

Note: Since glycation refers to “sugar” molecules sticking to protein and fats, its use in the context of methylglyoxal is arguably incorrect. Methylglyoxal is not a sugar, but an aldehyde.

One of the strongest indictments of ketosis, in relation to methylglyoxal, is made in a fairly well referenced book by De Grey (2007); the full reference to the book is at the end of this post. De Grey’s book is about aging, and how to stop or at least delay it. Overall, it is an excellent book. Here is some relevant text, from page 173 of the book:

… one established effect of very low-carbohydrate diets of the Atkins type is to bring down both triglyceride levels and the body’s total exposure to carbohydrates, so some advocates have hypothesized that these diets world reduce a person’s AGE burden. Unfortunately, it turns out that the metabolic state that these diets induce (the notorious “ketosis”) has the unfortunate side effect of causing a jump in the production of the oxoaldehyde methylglyoxal, a major precursor of AGEs that is also, ironically, produced within cells of diabetic patients when they are forced to take in more glucose than they can immediately process … methylglyoxal is far more chemically reactive than blood sugar (up to 40,000 times more reactive, in fact), and is known to cause wide-ranging damage in the body, of which AGE cross-links are but one example. This potentially makes the Atkins diet a recipe for accelerated AGEing …

Is this notion that ketosis, through methylglyoxal, can cause accelerated aging fact or fiction?

Sorry, but I need to consult with my guru before I post my answer.

Reference:

De Grey, A. (2007). Ending aging: The rejuvenation breakthroughs that could reverse human aging in our lifetime. New York: NY: St. Martin’s Press.