Our Longevity Diet

Scientists have argued for some time now on exactly what mechanism drives aging and death. Two different predominant theories have been competing for the past thirty years: Bust vs. Rust.

The bust-down theory claims that genes are responsible for senescence, and after a roughly fixed time span they trigger cells to break down and cease repairing themselves. Evidence in support of this genetically driven model are the observations that certain species are long-lived, while others die young. Also, among humans, longevity has been seen to run in families. The problem with this theory is that it implies the typical age-span for a species is the result of biological evolution, yet much aging (at least among species such as humans) occurs after reproduction stops. Explaining a mechanism by which a feature can evolve when it does not affect reproductive success has been difficult.

The rust theory, on the other hand, suggests we just wear out. Disease, toxins, and especially free-radical oxidation damage, gradually accumulates until the body is no longer able to repair itself. Evidence in support of this theory includes the observation that calorie restriction (CR) and intermittent fasting (IF) can greatly extend the lifespan of study animals. The best available evidence suggests that these practices may improve the repair mechanisms in the body, hence holding off aging for a while.

But while CR and IF have been shown to extend life by as much as 50% or more, the animals in these studies still die. Clearly, these methods slow the aging process, but do not stop it. Thus many researchers came to believe that a combination of the two theories was probably more-nearly correct. Aging is affected by the environmental factors of the ‘rust’ theory, but the ultimate limits are genetically programmed.

Earlier research has shown that it is possible to greatly extend the lifespan of fruit-flies through  a kind of selective breeding program that controls what age the flies are allowed to reproduce at. Now another study has identified the exact genetic mechanism for aging in flatworms. According to that report:

Comparing young worms to old worms, Kim’s team discovered age-related shifts in levels of three transcription factors, the molecular switches that turn genes on and off. These shifts trigger genetic pathways that transform young worms into geezers.

As part of the research, they exposed some of the worms to environmental stresses such as heat, free-radicals, radiation and disease, and then measured the activity of the elt-3 transcription factor, which they found to be the controlling chemical in aging. None of the stress factors induced changes in elt-3 levels. The researchers conclude that genetically controlled changes in elt-3 are largely responsible for aging in the worms.

If confirmed in other animals, this shifts the balance back in favor of a strongly genetic source for aging, but it also provides a chemical target and pathway for interfering with the aging process. As with most research in this field, it is still way too early to tell — but we see progress is being made.

So far as our personal Intermittent Fasting regime is concerned — we never really expected it would help us live much longer than normal, since we started too late in life to reap the full benefits. At best we can hope for an extra 10% (i.e. living to 88 rather than 80). Our main motivation is the evidence that for those remaining years we are likely to be much healthier under the IF lifestyle than otherwise.