I'm sure you all know by now that restricting the amino acid methionine in the diet provides many of the health and longevity benefits of calorie restriction - in mice, at least. This is only the case for methionine, not any of the other essential amino acids that must be obtained through diet, and the resulting changes in biochemistry are not exactly the same as calorie restriction. This suggests that, for example, the loss of visceral fat associated with calorie restriction also plays an important role in extended healthspan and longevity.
Per recent research, it looks like too much methionine is a bad thing - biochemical measures of damage and good operation that are improved by lowering methionine intake are instead made worse when methionine is supplemented in the diet. This worsened set of metabolic processes occurs in addition to any further unpleasant effects produced by the visceral fat tissue most of us would gain in boosting our methionine intake the easy way - by eating more.
Methionine restriction without energy restriction increases, like caloric restriction, maximum longevity in rodents. Previous studies have shown that methionine restriction strongly decreases mitochondrial reactive oxygen species (ROS) production and oxidative damage to mitochondrial DNA, lowers membrane unsaturation, and decreases five different markers of protein oxidation in rat heart and liver mitochondria. It is unknown whether methionine supplementation in the diet can induce opposite changes, which is also interesting because excessive dietary methionine is [damaging to the liver] and induces cardiovascular alterations.
Because the detailed mechanisms of methionine-related [liver demaage] and cardiovascular toxicity are poorly understood and today many Western human populations consume levels of dietary protein (and thus, methionine) 2-3.3 fold higher than the average adult requirement, in the present experiment we analyze the effect of a methionine supplemented diet on mitochondrial ROS production and oxidative damage in the rat liver and heart mitochondria.
It was found that methionine supplementation increased mitochondrial ROS generation and percent free radical leak in rat liver mitochondria but not in rat heart. In agreement with these data oxidative damage to mitochondrial DNA increased only in rat liver, but no changes were observed in five different markers of protein oxidation in both organs. ... These results show that methionine supplementation in the diet specifically increases mitochondrial ROS production and mitochondrial DNA oxidative damage in rat liver mitochondria offering a plausible mechanism for its [ability to cause liver damage].
Less oxidative damage should be taken as better, although it's not always that simple; in some circumstances a little oxidative damage can spur the body to better repair and prevention efforts in the future. Here, however, more oxidative damage is a bad thing. You'll recall the role of mitochondrial reactive oxygen species (ROS) in the damage of aging per the mitochondrial free radical theory of aging - increased damage to mitochondria and increased production of mitochondrial ROS are not good for long term health.
The lesson to take away from this - as for many other related research results - is that diet affects your long term prospects for health and degenerative aging on a sliding scale that is measured in calories and methionine intake. More calories and more methionine is worse for you. Fewer calories and less methionine, assuming you're still obtaining the optimum level of required nutrients, is better for you.
Gomez, J., Caro, P., Sanchez, I., Naudi, A., Jove, M., Portero-Otin, M., Lopez-Torres, M., Pamplona, R., & Barja, G. (2009). Effect of methionine dietary supplementation on mitochondrial oxygen radical generation and oxidative DNA damage in rat liver and heart Journal of Bioenergetics and Biomembranes DOI: 10.1007/s10863-009-9229-3