(Happy hour is a new series of science related posts, focusing on a single topic, in the style of a casual weekend discussion with friends in a bar).
When in India, I had a number of Jain friends, and visited their houses often, or Jain temples occasionally. There I've encountered a number of Jain ascetics and teachers, many of whom were old. Very old, often in their eighties or older, but perfectly healthy and active. Given their tradition of extreme austerity, plenty of fasts, and a typical meal (eaten once a day) of one chappati and some greens, their extreme longevity struck me.
A number of us have also read about the Okinawans in Japan. This region has the highest life expectancy in the world, with Okinawan seniors living well in to their eighties (with centenarians a dime a dozen). They also have a fifth the heart disease, and a fourth the breast or prostate cancer than Americans.
One thing they have in common with Jains is their lean (though not nearly as austere) diet, and their tendency to follow the Confucian adage of eating until your stomach is 80 % full.
I’ve seen some of this in my own family as well, with my grandpa, and some other folks of his generation. An old uncle of mine (who lived well in to his eighties, as did my grandpa) used to cup his tiny palm, and say “this much of rice in a meal is enough”, and then cup both his palms and say “but you should eat so much vegetable”. Observing weekly fasts was also routine.
The one thing in common here is calorific restriction. This is sometimes easily confused with malnutrition, but is not. Calorific restriction is just restricting the number of calories consumed daily. And these folks apparently live very long. But this is just anecdotal evidence. Is there any science behind this?
Interestingly, this effect was first noticed studies in the eighties, and since then a number of studies in rodents have shown this quite clearly. Reduction of calorific intake by 30-50% resulted in a substantial increase in lifespan, as well as a big reduction in the incidence of age related diseases, a much better resistance to toxins and stresses, and better maintenance of function late in to life. This also included delayed onset of diseases like cancer, diabetes or arthrosclerosis. So it wasn’t just eating less and live longer, but it was eating less and living longer and better.
But for most of this time we didn’t have a real clue about what was going on in the body. Surprisingly, our first real detailed molecular understanding of calorific restriction leading to longer lives came from the humble yeast. Apparently, it’s more useful than just in making beer, bread or wine. Scientists can actually measure how old a yeast is by just measuring the number of mother cell divisions. In their studies, they identified a specific gene, called SIR2 that played a critical role in ensuring this longevity. This is where the power of yeast genetics came in to play. You can knock-out a gene (delete it completely) in yeast very easily, and the yeast strains where this gene was knocked-out lived, but did not show any beneficial effects of calorific restriction. But clearly, the effects of calorific restriction included the activation of various different pathways and processes in the body, which did not seem connected at all with this gene. It seems now that this gene is actually important in maintaining over-all appropriate gene expression. And, this gene is also present in us mammals (where it’s called SIRT1).
The yeast studies gave us plenty of clues on what might happen in mammals, and yes, us. All our cells have little organelles called a Mitochondria. These are the “energy plants” of the cells, where the primary source of energy we use, ATP, is synthesized (using glucose and other substances). Now clearly, logic has it that calorific restriction will have some effect on the mitochondria, since this is where most of the energy we use is produced. So research would definitely try to see how mitochondria function was affected by calorific restriction. Some excellent recent work has tried to pin it down to a few specific processes.
Now, adipose tissue is where most fat is stored. Most of the adipose tissue is white, and called white adipose tissue. This stuff serves as heat insulation, mechanical cushioning and importantly, a source of energy, when energy intake is not equal to output. What researchers have recently observed is that in white adipose tissue, there is a BIG increase in mitochondrial biogenesis (i.e. more mitochondria) in calorie-restricted mice. This means much better and more mitochondrial function. What they also saw was that in mice lacking another specific gene, eNOS (which synthesizes a gas, Nitric Oxide, which then activates a very important pathway that leads to many effects, calorific restriction did not increase mitochondria at all. And, they showed that this eNOS gene in mice regulated the original important gene, SIRT1.
We’re now slowly beginning to understand molecular pathways by which calorific restriction leads to longer, healthier lives.
So if any one says, “lean, mean, fighting machine”, you should take the statement more seriously.