Wednesday, May 26, 2010

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).


Anonymous said...

well, your comments on the effects of ingesting AGEs defy a boatload of good science that show that AGEs have a major role in cellular disease...

...the damage accumulates during our lives - meaning that the damage is not evident until after we pass our reproductive years...

...even elementary logic would tell you that natural selection (evolution) would not be a factor in our tolerance of AGEs or cigarette smoke, for that matter...

I'm sure your recipe's very nice - but please don't offer health advice unless you can provide some convincing evidence...

by the way, a low-AGE diet can reverse the complications of type II diabetes - why do you think that is?

Ned Kock said...

Are you referring to endogenous (as in hemoglobin glycation) or exogenous (as in charred meat) AGEs?

If you are referring to exogenous AGEs, I would have to look at the "boatload" of scientific evidence you refer to.

Give me some links, or references, and I'll be happy to take a look at them. I'll even edit the post if I'm convinced by the evidence.

Michael Barker said...

I wish I had saved this article for you on food from pigs. It was put out by Michigan State University's Ag school, which is considered the premier Ag school in the world. What they were talking about is the wonderful taste of pork when it is raised, more or less, free.

Pork loin, I always brine because it lacks fat. I place it in a bag with salt, seasonings and water then store it in the freezer. I wash it off well and then grill it. Wonderfull!

Anonymous said...

with pleasure:

Journal of Gerontology: Medical Sciences:
Jaime Uribarri, Weijing Cai, Melpomeni Peppa, Susan Goodman, Luigi Ferrucci, Gary Striker, and Helen Vlassara
Circulating Glycotoxins and Dietary Advanced Glycation Endproducts: Two Links to Inflammatory Response, Oxidative Stress, and Aging

Journal of Gerontology: MEDICAL SCIENCES - Article:
Richard D. Semba, Emily J. Nicklett, and Luigi Ferrucci
Does Accumulation of Advanced Glycation End Products Contribute to the Aging Phenotype?

Josephine M. Forbes, Louis Teo Loon Yee, Vicki Thallas, Markus Lassila, Riccardo Candido, Karin A. Jandeleit-Dahm, Merlin C. Thomas, Wendy C. Burns, Elizabeth K. Deemer, Susan R. Thorpe, Mark E. Cooper, and Terri J. Allen
Advanced Glycation End Product Interventions Reduce Diabetes-Accelerated Atherosclerosis
Diabetes July 2004 53:1813-1823; doi:10.2337/diabetes.53.7.1813
May 27, 2010 10:18 PM

Ned Kock said...

Hi Michael.

Yes, and those free-ranging pigs are likely the ones that make up the bulk of the diet of the longest-living people in the world today:

I like the tenderloin grilled as well. I'll try that preparation sometime soon. Thanks!

Ned Kock said...

Thanks for the refs. I will be reviewing them soon, at least the abstracts, as a start:

Circulating Glycotoxins and Dietary Advanced Glycation Endproducts: Two Links to Inflammatory Response, Oxidative Stress, and Aging

Does Accumulation of Advanced Glycation End Products Contribute to the Aging Phenotype?

Advanced Glycation End Product Interventions Reduce Diabetes-Accelerated Atherosclerosis

I do have references that go against the notion that ingested AGEs are a problem, as long as the GI tract is healthy. But I don't like to ignore evidence that is contradictory to my beliefs.

Getting to the truth is a higher priority for me than the appearance of being right.

Ned Kock said...

Okay, thanks again for the refs. Here is my take on them:

*** Circulating Glycotoxins and Dietary Advanced Glycation Endproducts: Two Links to Inflammatory Response, Oxidative Stress, and Aging

This one I like, because of the fact that they controlled for caloric intake: "The consumption of dietary AGEs, but not of calories, correlated independently with circulating AGEs (CML: r = 0.415, p =.0001 and MG: r = 0.282, p =.002) as well as with high sensitivity C-reactive protein (hsCRP) (r = 0.200, p =.042)."

*** Does Accumulation of Advanced Glycation End Products Contribute to the Aging Phenotype?

This meta-analysis does not look very convincing to me. Their main conclusion is that: " Exposure to AGEs can be reduced by restriction of dietary intake of AGEs and drug treatment with AGE inhibitors and AGE breakers." Yet, the case made for dietary intake is weak at best.

*** Advanced Glycation End Product Interventions Reduce Diabetes-Accelerated Atherosclerosis

This one tells us nothing about dietary AGEs: "... mice [...] were randomized (n = 20) to receive for 20 weeks no treatment, the AGE cross-link breaker ALT-711, or the inhibitor of AGE formation aminoguanidine (AG)." They concluded that: "Diabetes-associated accumulation of AGEs in aortas and plasma and decreases in skin collagen solubility were ameliorated by both treatments ..." But, of course, diabetes is strongly related to endogenous AGE formation.

So, I will look into the "Circulating Glycotoxins ..." paper further, assuming I can get the full-text version, and post a comment here. Hopefully soon.

Ned Kock said...

I spoke too soon regarding the "Circulating Glycotoxins ..." paper. I started reviewing it with an open mind. I am holding back here, as I know how hard it is to do empirical research, but I am very, very disappointed.

For starters, the statistics look quite suspicious to me. Some of the resuts appear to be based on unstable beta coefficients and related estimates. Take a look at Table 2, for example:

How on earth a beta = 0.002 would lead to a P = .009!? This is a beta coefficient that is very close to zero, the lowest in the entire table, and it is statistically significant!?

Plus, the other b = 0.002 in the table is statistically insignificant; at least one would expect similar P values for similar beta coefficients, if reliable statistical methods are being used.

Even stranger are the stats for what really mattes, the multiple regressions linking dietary AGEs and serum AGEs. They have two types of serum AGEs as dependent variables, which they call serum CML and MG. Look at Table 4:

They have a beta = 0.204, with a P = .002 for dietary AGE intake and serum CML, which is statistically significant. Okay.

But, for serum MG the beta = 0.015 and the P = .001!? That is, a much, much lower beta coefficient leading to an even more statistically significant relationship!

My guess is that reviewers looked at these results and questioned the stats, which may be why the authors state that: "The Kolmogorov–Smirnov goodness-of-fit test was used to test for normal distribution." But they don't report the results of the Kolmogorov–Smirnov goodness-of-fit test.

Besides, have these authors ever heard about robust statistical methods (as used in WarpPLS; see They use ANOVA and T tests. C'mon, statistical methods have evolved over the years, in part to avoid these types of problems!

Now, for the final, and most damning issue if this is a paper that is supposed to indict charred meat as a major contributor to serum AGEs.

Note that they find a significant association between dieatary AGEs and one type of serum AGE - serum CML. This is in Table 4.

But what is CML? It is carboxymethyl-lysine. And what kind of diet leads to particularly high serum CML levels? A vegetarian diet:

Richard Nikoley said...

Looks good, Ned.

Here's another version which can be done on the BBQ or oven. In this case, I stuff whole cloves of garlic & rosemary and then make a sauce with lots of parprika.

Be sure and click on the final photo for a hi-res closeup.

Michael Barker said...

Richard, you have me salivating. I'm going to give that a go.

I've never payed much attention to anything on ingested AGEs. Humans have been grilling meat for thousands of years. It is so ubiquitous amongst the human population, it could be said that we are driven to this behaviour. The research I would love to see would be about what attracts us so much to grilled meat. It has to be feeding some system.

Ned Kock said...

Thanks Richard. That looks awesome!

Ned Kock said...

Hi Michael.

Very good point. We know that it kills parasites, and some argue that denatured protein resulting from cooking is more easily digestible.

But I'd like to see some targeted research. Maybe there is some out there.

Ned Kock said...

Michael, I have just remembered this book (I hope Blogger doesn't cut off the link), which I think gets very close to answering your question:

Ned Kock said...

Blogger cut off the link. Well, the title of the book is:

Catching Fire: How Cooking Made Us Human

Anonymous said...

Hunter gatherers tend to slow cook their meat otherwise it's as tough as rubber. The Paleolithic Diet and Its Modern Implications: An Interview with Loren Cordain
Mammoth "luau-style"

Anonymous said...

Thanks for your thoughtful comments and review of the citations I provided. These were just a quick grab of papers that reference the subject (dietary AGEs). I apologize for my snippy tone in my initial response, but I'm hopeful I can point you toward an ongoing consideration of the potential impacts of all the MRPs on ageing.

I still find the connection between Paleolithism and ageing to be a bit wierdly unscientific - unless I'm mistaken, ageing wasn't an issue for Paleoliths. Once we outlive our fecundity - we move outside of selection pressures.

I love pork - tenderloin is a great cut - low in fat. I eat a low MRP diet and have lost more than 30 lbs without calorie restriction. I am not a raw foodist but restrict my cooking to low-temperature methods.

A low-AGE/MRP diet has had a phenominally positive impact in my overall health - just anecdotal evidence, I know - but at age 60 I have a 34 inch waist, optimal cholesterol, BP 112/62. All of this has happened over the past 7 months. Food for thought?

Ned Kock said...

Yours results are very positive, but aren't they due to other factors? For example, a reduction or removal of refined carbohydrates and sugars from one's diet will also have significant health benefits, for most people.

I am open to evidence, but it has to be convincing. Looking at empirical research is practically all I do in this blog.

Selective pressures among our ancestors were definitely reduced post-reproductive age, but there are some things to consider. For example, men can have children at very advanced ages. Also, and this is particularly important, human infants are rather vulnerable. So ancestral parents and grandparents had to look after them. That generated selection pressure for survival at older ages.

There are a few interesting things about evolution that are not so obvious. One is that a very small selection pressure can lead traits to evolve fast - e.g., in a few hundred years, not the millions of years that many think are necessary:

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