Insulin
Keeping your insulin levels down is the most accessible path to longevity
We were taught in biology class that insulin regulates our blood sugar. This is true. But long before blood was invented, insulin was the primary hormone regulating lifespan. Insulin was produced in response to satiety, and insulin hastens aging, shortening life span when there is plenty to eat.
Aging is very old, and evolutionary selection is smarter than 20th century biologists are liable to give it credit. Orthodox evolutionary theory says that Darwin’s imperative is simply to generate offspring, as copious and as fast as possible. But it’s been at least a billion years since natural selection figured out that this is a recipe for ecocide, and selection has rewarded behaviors that are far more pro-social.
Part of evolution’s temperance is that animals are evolved to limit their numbers and assure that they don’t outgrow their food supply. You may not know that V. C. Wynne-Edwards was a distinguished, prolific, and eloquent British naturalist whose reputation tanked when he made exactly this claim in 1962. Wynne-Edwards was correct, even if he didn’t have the mathematical models to support his thesis. The mathematicians who knocked him off his pedestal were pedantic theorists who knew nothing of real-world biology.
Anyway — back to insulin.
In 1993, Cynthia Kenyon, working at UC San Francisco, discovered that disabling a single gene could double the lifespan of her lab worms. Of course, she was eager to dig into the genome and discover the purpose of this gene. Result — the gene was named DAF2, and it is the worm’s only insulin receptor. If worms cannot respond to insulin, they live twice as long.
Even before worms, yeast cells have an analog of insulin signaling in a hormone called Sch9, which shortens lifespan in response to perceived high levels of sugar.
The game that evolution has learned to play is to make hay while the sun shines, then hang back in difficult times. When there is plenty of food is when there is danger that the population will grow too rapidly. Reproduction is copious, but lifespans are short. When food is scarce, the optimal strategy is to wait, to extend lifespan so as to ride out the famine, and hold back reproduction until more food is available.
The ancient function of insulin is to invoke the former strategy — short lifespan and copious reproduction. In the absence of insulin, reproduction is curtailed and lifespans are longer.
In lab worms, it is the worm’s primitive nervous system (302 nerves) that makes the decision. How do we know? Again, Kenyon’s well-designed research. She was able to disable the DAF2 gene selectively in different tissues of the same worm. When the genes were disabled in the stomach or the muscles, the worms remembered how to shorten their life span just fine. But when the genes were disabled in the nerve cells, the worms forgot how to shorten their life spans! It’s the best example I know of a “deliberate” adaptation to shorten the length of life for the sake of population regulation, and it’s not something that is arranged automatically through chemical signals, but actually “calculated” by the nerve cells.
Mammals like us
Mice have a hormone called IGF for “insulin-like growth factor”. When this gene is disabled, the mice never reach full size, but they live half again as long as full-size mice. Mice also respond to caloric restriction by expressing less insulin, and they live up to 40% longer. Mice respond to under-feeding with better resistance to disease, enhanced agility and speed, quicker and more reliable neuronal responses. All this is mediated by insulin.
Humans, like most other mammals, lose insulin sensitivity with age. We pump out more insulin to have the same effect on blood sugar. And the insulin makes us age faster.
The bottom line for us is that keeping insulin low is the most available strategy for healthy aging and longer life.
So, why don’t Type I diabetics live a long time? They lack pancreatic iislet cells and are unable to make insulin. The problem is that their blood sugar soars, leading (over time) to peripheral neuropathy, blindness, and (eventually) gangrene.
So we can’t drop insulin to zero, but we can lower our insulin leels by avoiding sugar and starchy foods, and with exercise — especially exercise right before eating. It’s not a ticket to immortality, but the health benefits are robust, and it will add a few years to your life expectancy.



I note your comment about type 1 diabetics but don’t think it’s a very complete explanation. It is possible to replace the insulin lost due to the autoimmune disorder which kills the islet cells and live a healthy life. It used to be said that type 1 diabetics were healthier. I’m speaking as a type 1 diabetic for 48 years now and have no diabetic neuropathy at all. Many type 1 diabetics appear to die of heart disease but I suspect that they have nighttime hypo attacks and have lost their ability to respond by awakening and this causes levels to drop so low that they have a heart attack. It is simply recorded as a heart attack but that is not necessarily the underlying cause. Furthermore many type 1 diabetics are also overweight and insulin resistant so, type 1 and type 2. The medical system just encourages using more and more insulin so the individual becomes more and more obese.
The hungry mice live longer.
Don't eat that first potato chip.
Do difficult things outside every day.
;-/