In Lifespan, Sinclair insists that aging is not a law of nature but a choice. There doesn’t have to be an upward limit to the human lifespan.
Why do we Age?
In any case, why do we age? If you don’t know, that’s okay. Many biologists don’t either. Doctors who specialize in aging (gerontologists) often don’t ask why we age but seek to treat the consequences.
It’s not just aging. In the 1960’s, even the fight against cancer was a fight against its symptoms. Until the second half of the twentieth century, it was accepted that organisms grow old and die for the benefit of species, an idea that dates back to Aristotle. Even modern people such as Elon Musk argue that old age hinders creative thinking and progress, and that death occurs for the good of humanity.
But Sinclair thinks this idea is totally false.
When it comes to longevity, individuals look out for themselves. Driven by their selfish genes, they try to breed for as long and as fast as they can – so long as it doesn’t kill them. In the 1950s, J. S. Haldane, Peter Medawar, and George C. Williams proposed important ideas about why we age. Humans, driven by their selfish genes, will press on and try to breed for as long and as fast as they can as long as it doesn’t kill them.
If our genes never want to die, why don’t we live forever? The three biologists argued that the forces of natural selection are strong when we are young but decline once we hit 40 because we’ve likely replicated our selfish genes enough to ensure their survival. Eventually, the forces of natural selection hit zero, the genes move on. We don’t.
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Disposable Soma Hypothesis
Kirkwood’s theory of evolution is that organisms evolve to a point that lies somewhere between two very different lifestyles: breed fast and die young, or breed slowly and maintain your soma, or body. But a creature cannot breed fast and maintain a healthy and robust body – there isn’t enough energy to do both. Stated another way, any line of creature with a mutation that caused it to live fast soon ran out of resources and was thus deleted from the gene pool.
If you are a small prey animal, you will need to pass down your genetic material quickly. Gene combinations that promoted longevity did not stick around since your ancestors were unlikely to evade predation for long. But if you are on top of the food chain, your genes benefited from building a longer lasting body that could breed for decades. But in return, you could only afford to raise a couple of fledglings a year.
Claude Channon was an electrical engineer from MIT. He was disturbed by the problem of information loss. Having lived through the second World War, he knew that introducing “noise” into analog transmission could cost lives. After the war, he wrote a short but profound scientific paper called “The Mathematical Theory of Communication” on how to preserve information, which many consider the foundation of Information Theory.
This may be the one paper that propelled us into the digital, wireless world in which we now live. Shannon wanted to improve the robustness of electronic and radio communications between two points. More important than that, he discovered how to preserve and restore information, and Sinclair thinks this could be applied to aging.
It is unflattering to know that we may be the biological equivalent of an old DVD player, but this is good news. Information can be recovered from a scratched DVD. The same kind of process can reverse aging. Cloning proves that our cells retain their youthful digital information even when we are old. To become young again, we simply need to find polish to remove the scratches.
The Information Theory of Aging
“Longevity genes” are genes that have shown the ability to extend both average and maximum lifespans in many organisms. These genes don’t just make life longer, they make it healthier, which is why they’re called “vitality genes”. Together, these genes form a surveillance network within our bodies. They communicate with one another between cells and between organs by releasing proteins and chemicals.
Descended from gene B in M. superstes, sirtuins are enzymes that remove acetyl tags from histones and other proteins. These critical epigenetic regulators sit at the very top of cellular control systems. They have evolved to require a molecule called nicotinamide adenine dinucleotide, or NAD.
Sirtuins prevent cell death and boost mitochondria, the power packs of the cell. Activating them can improve DNA repair, boost memory, increase exercise endurance, and keep mice thin, regardless of what they eat.
Sirtuins are turning out to be more amenable to manipulation than many other longevity genes. They are, it would appear, one of the first dominos in the magnificent Rube Goldberg machine of life. The key to understanding how our genetic material protects itself during times of adversity.
TOR, or target of rapamycin, is a gene that regulates growth and metabolism. Like sirtuins, It can signal cells in stress to hunker down and improve survival by boosting activities such as DNA repair and digesting old proteins. Two other well studied genes perform similar roles, mTOR and mTOR2, also have been proven manipulable.
Hormesis
Complementing these approaches are hormesis-mimicking molecules. Drugs in development and at least two drugs on the market can turn on the body’s defenses without creating any damage. It’s like making a prank call to the Pentagon. The troops and the Army Corps of Engineers are sent out, but there’s no war. In this way, we can mimic the benefits of exercise and intermittent fasting with a single pill.
We are now much closer to having a map of the complete sequence of our DNA. As of 2022 (after the release of this book), the human genome has been fully mapped. But we still won’t be able to find an aging gene. We have only found genes that impact the symptoms of aging, and longevity genes that control the body’s defenses against aging and help slow aging through various interventions. But unlike the oncogenes that were discovered in the 1970s that have been useful in the battle against cancer, we haven’t found a single gene that causes aging. And we won’t. Our genes did not evolve to cause aging.
Over time, we accumulate DNA damage from the sun or an X-ray. Smoking accelerates the aging clock and makes you more likely to die than a nonsmoker (15 years earlier, on average). That is why we have fought it with legislation, taxes, and public health campaigns. We have done the same for cancer, investing billions of dollars’ worth of research. We know that aging makes you more likely to die, but we have accepted it as fate.
Consider this: though smoking increases the risk of getting cancer fivefold, being 50 years old increases your cancer risk a hundredfold. By the age of 70, it is a thousandfold.
Fasting
Blue Zones are areas where longevity is the highest.
There is ultimately no best diet for humans because of our differences. But we are similar enough to have commonalities. More vegies, less meat; fresh food, no processed food.
After twenty-five years of researching aging and having read thousands of scientific papers, if there is one piece of advice I can offer, one surefire way to stay healthy longer, one thing you can do to maximize your lifespan right now, it’s this: eat less.
Not malnutrition. Not starvation. These are not pathways to more years, let alone better years. But fasting—allowing our bodies to exist in a state of want, more often than most of us allow in our privileged world of plenty—is unquestionably good for our health and longevity.
CR (caloric restriction) works to extend the lifespan of mice, even when initiated at 19 months of age, the equivalent of a 60- to 65-year-old human, but the earlier the mice start on CR, the greater the lifespan extension.
What these and other animal studies tell us is that it’s hard to “age out” of the longevity benefits of calorie restriction, but it’s probably better to start earlier than later, perhaps after age 40, when things really start to go downhill, molecularly speaking.
If you’re interested in a long and healthy life, your diet probably needs to look a lot more like a rabbit’s lunch than a lion’s dinner. When we substitute animal protein with more plant protein, studies have shown, all-cause mortality falls significantly.
Exercise
We need to induce some physical adversity, too. If that doesn’t happen, we miss a key opportunity to trigger our survival circuits further.
When researchers studied the telomeres in the blood cells of thousands of adults with all sorts of different exercise habits, they saw a striking correlation: those who exercised more had longer telomeres.
And according to one study funded by the Centers for Disease Control and Prevention and published in 2017, individuals who exercise more—the equivalent of at least a half hour of jogging five days a week—have telomeres that appear to be nearly a decade younger than those who live a more sedentary life.
But why would exercising delay the erosion of telomeres? Exercise, by definition, is the application of stress to our bodies. It raises NAD levels, which in turn activates the survival network, which turns up energy production and forces muscles to grow extra oxygen-carrying capillaries. The longevity regulators AMPK, mTOR, and sirtuins are all modulated in the right direction by exercise, irrespective of caloric intake, building new blood vessels, improving heart and lung health, making people stronger, and, yes, extending telomeres.
Even about ten minutes of moderate exercise a day added years to their lives.35 35There is a difference between a leisurely walk and a brisk run, however. To engage our longevity genes fully, intensity does matter. Mayo Clinic researchers studying the effects of different types of exercise on different age groups found that although many forms of exercise have positive health effects, it’s high-intensity interval training (HIIT)—the sort that significantly raises your heart and respiration rates—that engages the greatest number of health-promoting genes, and more of them in older exercisers.
Cold
Cold activates longevity genes.
As with most things in life, it’s probably best to change your lifestyle when you are young, because making brown fat becomes harder as you get older. If you choose to expose yourself to the cold, moderation will be key. Similar to fasting, the greatest benefits are likely to come for those who get close to, but not beyond, the edge. Hypothermia is not good for our health. Neither is frostbite. But goose bumps, chattering teeth, and shivering arms aren’t dangerous conditions.
Heat
A more convincing study followed a group of more than 2,300 middle-aged men from eastern Finland for more than twenty years.
Those who used a sauna with great frequency—up to seven times a week—enjoyed a twofold drop in heart disease, fatal hearts attacks, and all-cause mortality events over those who heat bathed once per week. And there’s a lot of extra damage to be had out there.
Smoking
Cigarettes, for starters. There aren’t many legal vices out there that are worse for your epigenome than the deadly concoction of thousands of chemicals smokers put into their bodies every day. There’s a reason why smokers seem to age faster: they do age faster. The DNA damage that results from smoking keeps the DNA repair crews working overtime, and likely the result is the epigenetic instability that causes aging. And al