Open any conventional magazine, or, listen to ‘health experts’, and they’ll tell you to eat a little less than you usually would, to eat less fat and carbohydrates, and, to make sure you get enough protein. With the exception of the recommendation for a higher protein intake (a topic for another day!), these are generally good recommendations for health. Calorie restriction (CR) is well documented to reduce disease risk and to extend lifespan in a variety of organisms. Similarly, a reduced fat and carbohydrate intake have been shown to decrease risk for obesity and heart disease.
But, there’s another variable that is not at all considered in the health discussion, and they are a group of molecules known as advanced glycation end products (AGE). AGE products are formed as a result of the heat-induced binding of sugar to protein, fat or nucleic acids (DNA or RNA). The common way to identify AGE products in food is the browning effect-deep-frying, broiling, roasting, and grilling each produce a temperature that is sufficient to greatly increase AGE product formation, relative to either raw or boiled food. For example, broiled or fried chicken breast contains ~6-fold more of one particular type of AGE product (carboxy-methyl-lysine, CML), relative to boiling. Processed foods such as pasteurized dairy products, cheeses, sausages, processed meats and commercial breakfast cereals also contain significant amounts of AGE products. For example, processed American cheese has a greater amount of CML than fried, roasted or broiled chicken breast. Similarly, butter (on a per gram basis) has ~4-fold more CML than broiled or fried chicken breast, and ~20-fold more than boiled chicken breast (Goldberg et al. 2004).
The importance of dietary AGE products is that they have been shown to be related to a reduced lifespan in mice. Cai et al. (2007) quantified the amount of CML found in the mouse diet, and then created mouse food with half of this amount. They then fed the normal diet and the low-CML containing diet to 2 separate (but of the same genetic background) mice. The low-CML diet was sufficient to significantly extend median and maximal lifespan by 15% and 6%, respectively. Translated into human lifespan, these results would be indicative of an increase in average lifespan from 75 to 85 years! No difference in food intake was observed when comparing the 2 groups-from this it can be concluded that the lifespan extending effect of the low-CML diet was not related to a reduction in calorie intake. In addition, diet composition-total calories, protein, fat and carbohydrate content of the two different diets were identical.
As mentioned earlier, calorie restriction is the gold standard in terms of minimizing disease risk and extending longevity in a variety of organisms, including worms, flies, mice, dogs and monkeys. Because CR mice eat less than controls, the possibility exists that they also eat a lower amount of AGE products, and is one possible explanation for the reduction in disease risk and extended longevity associated with a CR diet. To address this possibility, Cai et al. (2008) quantified the amount of AGE products that CR-fed mice consumed, and then increased this amount to either equal to or greater than what mice on a regular diet ate. In terms of lifespan, mice on a low AGE product, low calorie diet were found to have increased average and maximal lifespan, relative to mice on a regular, ad libitum diet. However, CR-fed mice whose food contained an amount of AGE products that was equivalent to or than greater mice on a regular diet lived shorter than CR-fed mice at all measured time points, and had a lifespan that was almost equivalent to mice that ate a regular diet. These data suggest that if you eat less calories than normal, you will live longer, but, if your lower-calorie diet is poor in quality (i.e. high in AGE products), you will lose the lifespan extending effect of CR.
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