I'll just jump straight into today's topic: AGEs and methionine. If you feel like you have no clue about what I'm saying here, please go check the first part of this post, which was published last week. One thing's for sure, though! We're discussing serious matters, like longevity-promoting diets and nutritional problem-makers, aka those compounds that we cannot realistically eliminate from our diets, but which we should really try to keep an eye on. So, as A's go first...
Advanced glycation end-products (AGEs)
Glycation is a metabolic process in which a sugar molecule attaches itself to a protein or lipid molecule, impairing its function. In plain English, we'd probably call this hijacking. Glycation is usually followed by all sorts of reactions that culminate in the production of advanced glycation end-products or AGEs. Such an appropriate name, as AGEs have been associated with many age-related chronic diseases, like cardiovascular diseases, cancer or Alzheimer's. Interestingly enough, glycation can be formed both outside, as well as inside of our bodies.
Exogenous glycation is produced by cooking proteins or fats at high temperatures and/or for a long time. Think about grilling meat, baking cakes or roasting chicken. On the other hand, endogenous glycation occurs after the absorption of simple sugars in the bloodstream. That is, after dessert. If by now you don't hate glycation as much as I do, do not forget about wrinkles. Skin proteins like collagen and elastin are also threatened by sugar molecules and their glycation potential.
In order to optimize your diet it would be preferable to monitor your AGE intake. Here is a table that lists the AGE content of 549 foods, based on carboxymethyllysine content and which might come in handy for grocery shopping and cooking.
Methionine
Methionine is an amino acid whose dietary restriction has been associated with several health benefits, including an overall life span extension. Here is an excerpt from a study conducted in 2003 on the effects of methionine restriction (MR) in rats.
MR has repeatedly resulted in life span extension comparable to that seen in energy restricted animals. In one of our typical studies using Fischer 344 rats, MR resulted in a 42% increase in mean survival and a 44% increase in maximal longevity (Fig. 1). While living longer, animals on MR grow significantly less (Fig. 2), and consume more food when food intake is expressed on a per body mass basis. This latter observation has led to some controversy, since when expressed on a per animal basis, MR rats, being smaller, consume slightly less food per animal than their C-fed counterparts. This has left open the possibility that the effect of methionine restriction on life span is secondary to a restriction of caloric intake, and not due to methionine deficiency. In order to examine the
proposition that MR might be an effect secondary to CR, we have pair-fed rats, so that animals consumed control diet in the same quantity as consumed by methionine restricted rats. Since animals fed in this way will consume exactly the same energy levels regardless of which diet they consume, this would exclude caloric intake as an explanation for the MR effect. When C rats were fed in quantities equivalent to that consumed by MR animals they consumed all of the food offered, and there was a modest reduction in weight gain relative to ad libitum fed C animals. However, there was no prolongation of life span (Fig. 3) associated with the slightly reduced food intake and body size (Fig. 4), indicating that life span extension associated with restricted methionine intake is not primarily due to reduced energy consumption.
(J. A. Zimmerman, V. Malloy, R. Krajcik, N. Orentreich, 'Nutritional Control of Aging', Experimental Gerontology, 2003, Jan-Feb: 47-52.)
Furthermore, the effects of a methionine deficient diet on glucose, T4, IGF-1 and insulin levels have been depicted in a 2005 study on mice.
A diet deficient in the amino acid methionine has previously been shown to extend lifespan in several stocks of inbred rats. We report here that a methionine -deficient (Meth-R) diet also increases maximal lifespan in (BALB/cJ x C57BL/6 J)F1 mice. Compared with controls, Meth-R mice have significantly lower levels of serum IGF-I, insulin, glucose and thyroid hormone. Meth-R mice also have higher levels of liver mRNA for MIF (macrophage migration inhibition factor), known to be higher in several other mouse models of extended longevity. Meth-R mice are significantly slower to develop lens turbidity and to show age-related changes in T-cell subsets. They are also dramatically more resistant to oxidative liver cell injury induced by injection of toxic doses of acetaminophen. The spectrum of terminal illnesses in the Meth-R group is similar to that seen in control mice. Studies of the cellular and molecular biology of methionine-deprived mice may, in parallel to studies of calorie-restricted mice, provide insights into the way in which nutritional factors modulate longevity and late-life illnesses.
(R.A. Miller, G. Buehner, Y. Chang, J. M. Harper, R. Sigler, M. Smith-Wheelock, Methionine-deficient diet extends mouse lifespan, slows immune and lens aging, alters glucose, T4, IGF-I and insulin levels, and increases hepatocyte MIF levels and stress resistance, Aging Cell, 2005 Jun:119-25)
You can check the methionine content of a large number of food products at this link.
Finding your path through the valley of calories, glycemic indexes and loads, AGEs and methionine is not easy, but, in time and with the right amount of determination, it will eventually work out for you and for the goals that you have set for yourselves. The good part is that it's not rocket science. The bad part is that it might be even more demanding than that. But, in the end, what matters is that you stay true to yourselves and if living a long healthy life is what you care about, then reviewing these lists every now and then might be one of the tools to help you reach just that!
