Moving onward and deeper into the protein debate, I find myself now at the methionine sub debate. As if the protein conundrum couldn’t get anymore complex. I now realize I am searching for a holy grail in the nutritional world. This protein debate has existed for decades in some form or fashion. How much protein and from what sources sounds like an innocent enough question, but that is about where the innocence of the issue stops. Sometimes I feel like I am running circles, and have to remind myself that I am not going to find a pointed answer but will have to pick my gradient value from an ever fluctuating gray scale.
On to Methionine: Let’s start with a simple inquiry.
Methionine is classified as an essential amino acid, which means this is an amino acid we do not synthesize inside our bodies but must consume from external sources. Methionine has become a popular topic within the life extension community since some studies found a potential link to methionine restriction and longer life span. This aspect with or with out IGF-1 levels, could also help to explain the reason behind increased life spans of protein restricted rodents, and possibly contribute to the CR effect.
Notice how I say, “contribute to the CR effect”. I have observed many articles and forum discussions in various places looking for an alternate but equal approach to CRON. Whether a supplement or a lesser intense form of dietary manipulation, I see people looking for an different way to increase longevity. To date, only CR has shown drastic life extension possiblities, but the mechanism is not in any way fully understood. So, all my protein (and sub topic) questioning falls under the CRON scope. I’m am trying to learn what dietary manipulations my be in part responsible for the CR effect. But I have once again digressed, back to methionine and some studies:
This study sought to investigate a possible mechanism behind increased longevity as a result of a reduction in energy intake. For this experiment, two main groups of rats were observed. One group (the control) was fed a purified diet containing 0.86% L-methionine, and the other was fed a purified diet containing 0.17% L-methionine.The researchers noted that in previous methionine studies, the low Met group naturally consumed fewer calories, so the researchers also observed food intake amounts for all groups.
Observations:
* Rats fed the low Met diet starting at 4-6 weeks in age experienced both longer median life span (1059days vs 818 days), and longer max life span (1252 days vs 1116 days).
* Rats fed the low Met diet failed to grow after 42 days of age.
* Food intake for the low Met group was observed to decline. During the first 2mo, 10% less was consumed, 12% less at 3mo, and 24.5% less by 24mo of age. To help compensate for this possible skewing results, the researchers also fed a low Met group a more energy dense food to observe intake.
* The rats in the energy dense low Met group consumed the same about of ration (I’m assuming from a weight perspective, thus more calories), but still failed to gain weight during their 3rd month and body weights were approximately the same as the regular low Met group.
* They researchers also limited the food of the 0.86% Met group to mimic the reduced intake of the low Met group, and observed an initial lag in growth. However, the differences were not significant past the 2nd month.
The researchers conclude that the restriction of this single dietary component can prolong life. Also, the researches say that because they gave unrestricted access to food for both groups, their study can not be called energy restricted in the traditional sense despite the lower energy intake by the low Met group. They note that while food intake was lower for the low Met group, the intake in relation to body weight was actually greater (note: this is observed in CR too). The researchers continue to say that because of this, the term restriction can not be applied (but if that is the case, then restriction can not be applied to CR either). They also conclude that lowering energy intake in the normal Met group had no affect on longevity based on unimpaired growth because they argue that life span increases are only seen when growth is limited.
NOTES/ISSUES: One problem is that this study started all rats on this diet from a young age. CRON in humans begins in adulthood, and often dietary manipulation in youth (for people and animals) can have adverse effects or effects that would not be strongly observed (if at all) if the diet was started in adulthood. Another issue is the low level of Met is almost impossible to reach in a human diet even with veganism, and the level of overall protein was not reduced. For a human to eat a low Met diet, protein would almost have to be reduced in some fashion. Finally, I don’t think there was enough consideration given to the lowered energy intake factor. How can the diets be identical with “only one” component being reduced (Met) if the rats also don’t eat as much; the experiment now becomes a two variable experiment. I do feel that there is some merit to lowering Met in relation to life span, but please don’t muddle the data and then make bold confident claims. IMO, this study shows there is likely an association with Met and increased life span, but to what extent (and effect) we could apply this to a human diet has yet to be understood.
First note I only have access to this abstract. The researchers note that CRON decreases the aging rate and mitochondrial ROS (MitROS) production and oxidative stress in rat tissues, and these traits are also observed in long lived species. They continue to say that with 80% Met restriction, MitROS production and oxidative stress was lowered and thus appeared to play a large role in the lowered oxidative stress and MitROS production observed in CRON. They suggest that lowering Met reduces oxidative stress by decreasing the sensitivity of proteins to damage and lowering the rate of MitROS produciton, and seems to be responsible for the similar observations in CRON.
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I want to go ahead and make my statements for this topic. While research does suggest a strong correlation between methionine reduction and increased lifespan, the practically as well as potential negative consequences are still unknown for humans. Since the Met results were obtained without a reduction in total protein and only reduction of the individual amino acid, the observations suggest that some of the protein restriction results are directly related to lower Met. Even though Met studies showed a greater lifespan increase than PR studies, do not forget that the mice in the Met studies did eat less on a low Met diet, so some effects of CR may have compounded the results.
My own perspective is Met reduction is not to be ignored, but I do not intend on strictly attempting to reduce my Met intake. One reason for this laissez faire approach is because with CR, my intake of Met is reduced already. So, unless I eat all my protein from egg whites or eat tons of brazil nuts, my Met levels will be fairly low. Since this by no means is the only possible mechanism behind CR, it is not conducive to risk the larger goal for one detail of the picture.
