by Michio Kaku
But is this really possible?
Anyone who has lived in the north during wintertime knows that fish and frogs can be frozen solid in the ice, and that when spring comes and the ice melts, they will emerge as if nothing happened.
Normally, we would expect the freezing process to kill these animals. As you lower the temperature of blood, ice crystals begin to grow and expand both within the cells, eventually rupturing the cell wall, and also outside the cells, potentially squeezing and crushing them. Mother Nature solves this problem using a simple solution: antifreeze. During winter, we put antifreeze in our cars in order to lower the freezing point of water. In the same way, Mother Nature uses glucose as an antifreeze, thereby lowering the freezing point of blood. So although the animal is frozen in a block of ice, the blood in its veins is still liquid and can still perform basic bodily functions.
For humans this high concentration of glucose in our bodies would be toxic and would kill us. So scientists have experimented with other kinds of chemical antifreezes in a process they call vitrification, which involves using a combination of chemicals to lower the freezing point so that ice crystals do not form. Although it sounds intriguing, the results have been disappointing so far. Vitrification often has adverse side effects. The chemicals used in the labs are often poisonous and can be lethal. To date, no one has ever been frozen solid, then thawed out, and lived to tell about it. So we are a long way from effectively achieving suspended animation. (This hasn’t stopped entrepreneurs from prematurely advertising this as a way to cheat death. They claim that people with fatal illnesses can have their bodies frozen, for a hefty fee, and then be revived decades later, when their diseases can be cured. However, there is absolutely no experimental proof that this process works.) Scientists hope that in time, these technical questions might be solved.
So on paper, suspended animation may be the ideal way to solve many of the problems of long-term voyages. Although it is not a practical option today, in the future it might be one of the chief methods of surviving interstellar missions.
However, there is one problem with suspended animation. If there is an unexpected emergency, such as an asteroid impact, then humans may be required to fix the damage. Robots may be activated to make the initial repairs, but, if the emergency is severe enough, human experience and judgment will be required. This might mean that some of the passengers who are engineers may have to be revived, but this last-minute option could be fatal if it takes too long to revive the engineers and human intervention is required immediately. This is the weak point in an interstellar voyage using suspended animation. It may be that a small multigenerational society of engineers would have to be kept awake and ready during the entire voyage.
SEND IN THE CLONES
Yet another proposal to colonize the galaxy is to send embryos containing our DNA into space, in the hopes that one day they may be revived at some distant destination. Or we could send the DNA code itself, to eventually be used to create new humans. (This was the method mentioned in the movie Man of Steel. Although Superman’s home planet, Krypton, had exploded, the Kryptonians were advanced enough to sequence the DNA of the entire Kryptonian population before the planet blew up. The plan was that this information could be sent to a planet like Earth, and then the DNA sequence could be used to create clones of the original Kryptonians. The only problem was that this might involve taking over the Earth and getting rid of humans, who are unfortunately in the way.)
There are advantages to the cloning approach. Instead of having gigantic starships containing huge artificial Earth-like environments and life support systems, this would only involve transplanting DNA. Even large tanks of human embryos could easily fit inside a standard rocket ship. Not surprisingly, science fiction writers have imagined that this happened aeons ago, when some prehuman species might have spread their DNA in our sector of the galaxy, making possible the rise of humanity.
There are, however, several drawbacks to this proposal. At present, no human has ever been cloned. In fact, no primate has ever been successfully cloned either. The technology is not yet advanced enough to create human clones, although it might be accomplished in the future. If so, robots might be designed to create and take care of these clones.
More important, reviving human clones might create creatures genetically identical to us, but they won’t have our memories or personality. They will be a blank slate. At present, the ability to send a person’s entire memory and personality in this way is far beyond our capabilities. Again, this requires a technology that will take decades or centuries to create, if it’s possible at all.
But rather than being frozen or cloned, perhaps another way one can journey to the stars is to slow down or even stop the aging process.
SEARCH FOR IMMORTALITY
The search for eternal life is one of the oldest themes in all of human literature. It goes back to the Epic of Gilgamesh, written nearly five thousand years ago. The poem chronicles the exploits of a Sumerian warrior on a noble quest. Along the way, he has many adventures and encounters, including one with a Noah-like individual who witnessed the Great Flood. The goal of this long journey is to find the secret of immortality. In the Bible, God banished Adam and Eve from the Garden of Eden after they disobeyed Him and ate from the tree of knowledge. God was angry because they might use this knowledge to become immortal.
Humanity has been obsessed with immortality for ages. For much of human history infants died in childbirth, and the lucky ones who survived often lived in a state of near starvation. Epidemics would spread like wildfire because people often threw their kitchen garbage out the window. Sanitation as we know it did not exist, so villages and cities reeked. Hospitals, if they existed at all, were places for the poor to die. They were warehouses for destitute, poverty-stricken patients, since the rich could afford to have private physicians. But the rich were also victims of disease, and their private doctors were little more than quacks. (One midwestern doctor kept a diary of his daily visits to patients. He confessed that there were only two items in his black bag that actually worked. Everything else was snake oil. What actually worked was the hacksaw to cut off injured and diseased limbs, and morphine to dull the pain of amputation.)
In 1900, the official life expectancy in the United States was forty-nine. But two revolutions added decades to that number. First, sanitation improved, which gave us clean water and waste removal and helped to eliminate some of the worst epidemics and plagues, adding about fifteen years to our life expectancy.
The next revolution was in medicine. We often take for granted that our ancestors lived in mortal fear of a bestiary of ancient diseases (like tuberculosis, smallpox, measles, polio, whooping cough, and so on). In the postwar era these diseases were largely conquered by antibiotics and vaccines, adding another ten years to our life expectancy. During this time, the reputation of hospitals changed significantly. They became places where real cures for diseases were dispensed.
So can modern science now unlock the secrets of the aging process, slowing down or even stopping the clock, increasing life expectancy to an almost limitless degree?
This is an ancient quest, but what is new is that it has now gained the attention of some of the richest people on the planet. In fact, there is an influx of Silicon Valley entrepreneurs investing millions to defeat the aging process. Not content to wire up the world, their next goal is to live forever. Sergey Brin, the cofounder of Google, hopes to do nothing less than “cure death.” And Calico, led by Brin, may eventually dump billions into a partnership with the pharmaceutical company AbbVie to tackle the problem. Larry Ellison, cofounder of Oracle, thinks that accepting mortality is “incomprehensible.” Peter Thiel, the cofounder of PayPal, wants to live to a modest 120 years, while Russian internet tycoon Dmitry Itskov wants to live to 10,000 years. With the support of people like Brin and technological innovations, we may finally be able to use the full force of modern science to unlock this age-old mystery and extend our life span.
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Recently, scientists have revealed some of the deepest secrets of the aging process. After centuries of false starts, there are now a few reliable, testable theories that seem promising. These involve caloric restriction, telomerase, and age genes.
Of these, one and only one method has proven to extend the life span of animals, sometimes even doubling it. It is called caloric restriction, or severely limiting the intake of calories in an animal’s diet.
On average, animals that eat 30 percent fewer calories live 30 percent longer. This has been amply demonstrated with yeast cells, worms, insects, mice and rats, dogs and cats, and now primates. In fact, it is the only method that is universally accepted by scientists to alter the life span of all animals that have been tested so far. (The only important animal that has not yet been tested is humans.)
The theory is that animals in the wild naturally live in a state of near starvation. These animals use their limited resources to reproduce during times of plenty, but during hard times they enter a state of near hibernation to conserve their resources and live past the famine. Feeding animals less food triggers the second biological response and they live longer.
One problem with caloric restriction, however, is that these animals become lethargic, sluggish, and lose interest in sex. And most humans would balk at the prospect of eating 30 percent fewer calories. So the pharmaceutical industry would like to find the chemicals that govern this process and harness the power of caloric restriction without its glaring side effects.
Recently, a promising chemical called resveratrol has been isolated. Resveratrol, found in red wine, helps to activate the sirtuin molecule, which has been shown to slow down the oxidation process, a principle component in aging, and therefore it may help protect the body from age-related molecular damage.
I once interviewed Leonard P. Guarente, the MIT researcher who was one of the first to show the link between these chemicals and the aging process. He was surprised at the number of food faddists who have latched onto it as a fountain of youth. He doubted this was the case but left open the possibility that if the true cure for aging was ever found, resveratrol and these chemicals may play some role. He even cofounded a company, Elysium Health, to explore these possibilities.
Another clue to the cause of aging might be telomerase, which helps to regulate our biological clock. Every time a cell divides, the tips of the chromosomes, called telomeres, get a bit shorter. Eventually, after approximately fifty to sixty divisions, the telomeres become so short that they disappear and the chromosome begins to fall apart, so the cell enters a state of senescence and no longer functions correctly. Thus there is a limit to how many times a cell can divide, called the Hayflick limit. (I once interviewed Dr. Leonard Hayflick, who laughed when asked if the Hayflick limit can somehow be reversed to give us the cure for death. He was extremely skeptical. He realized that this biological limit was fundamental to the aging process, but its consequences are still being studied, and because aging is a complex biochemical process involving many different pathways, we are a long way from being able to alter that limit in humans.)
Nobel laureate Elizabeth Blackburn is more optimistic and says, “Every sign, including genetics, says there’s some causality [between telomeres] and the nasty things that happen with aging.” She notes that there is a direct link between shortened telomeres and certain diseases. For example, if you have shortened telomeres—if your telomeres are in the bottom third of the population in terms of length—then your risk of cardiovascular disease is 40 percent greater. “Telomere shortening,” she concludes, “seems to underlie the risks for the diseases that kill you…heart disease, diabetes, cancer, even Alzheimer’s.”
Recently, scientists have been experimenting with telomerase, the enzyme discovered by Blackburn and her colleagues that prevents the telomeres from shortening. It can, in some sense, “stop the clock.” When bathed in telomerase, skin cells can divide indefinitely, far beyond the Hayflick limit. I once interviewed Dr. Michael D. West, then of the Geron Corporation, who experiments with telomerase and claims that he can “immortalize” a skin cell in the lab so that it lives indefinitely. (This has added a new verb to the English language: “to immortalize.”) The skin cells in his lab can divide hundreds of times, not just fifty or sixty.
But it should be pointed out that telomerase has to be regulated very carefully, because cancer cells are also immortal and they use telomerase to attain that immortality. In fact, one of the things that separates cancer cells from normal ones is that they live forever and reproduce without limit, eventually creating the tumors that can kill you. So cancer may be an unwanted byproduct of using telomerase.
GENETICS OF AGING
Yet another possibility for defeating aging is through gene manipulation.
The fact that aging is heavily influenced by our genes is readily apparent. Butterflies, after they emerge from the cocoon, live only for a few days or weeks. Mice studied in laboratories usually live only about two years or so. Dogs age about seven times faster than humans and live a little more than ten years.
In looking at the animal kingdom, we also find animals that live so long that their life span is difficult to measure. In 2016, in the journal Science, researchers reported that the Greenland shark has an average life span of 272 years, surpassing the 200-year life span of the bowhead whale, making it the longest-lived vertebrate. They calculated the age of these sharks by analyzing the layers of tissue in their eyes, which grow with time, layer for layer, like an onion. They even found one shark that was 392 years old and another that might be as old as 512.
So different species with different genetic makeup vary widely in life expectancy, but even among humans, with our almost identical genes, studies have consistently shown that twins and close relatives have similar life expectancies and that people chosen at random vary far more widely.
So if aging is at least partially governed by genes, the key is to isolate those genes that control it. There are several avenues of approach.
A promising one is to analyze the genes of young people and then compare these genes with those of the old. By comparing the two sets using a computer, one can rapidly isolate where most of the genetic damage caused by aging takes place.
For example, aging in a car takes place mainly in the engine, where the oxidation and wear and tear take the greatest toll. The “engines” of a cell are the mitochondria. That’s where sugars are oxidized to extract energy. A careful analysis of the DNA within the mitochondria indicates that errors are indeed concentrated here. The hope is that one day scientists might use the cells’ own repair mechanisms to reverse the buildup of errors in the mitochondria and therefore prolong the cells’ useful life.
Thomas Perls of Boston University analyzed the genes of centenarians, on the assumption that some people are genetically disposed to live longer, and identified 281 markers for genes that seem to slow down the aging process and somehow make these centenarians less vulnerable to disease.
The mechanism of aging is slowly being revealed, and many scientists are cautiously optimistic that it might be controllable sometime in the coming decades. Their research shows that aging, apparently, is nothing but the accumulation of errors in our DNA and our cells, and perhaps one day we can arrest or even reverse this damage. (In fact, some Harvard professors are so optimistic about their research that they have even set up companies in hopes of capitalizing on the advanced aging research being done in their labs.)
So the fact that our genes play an important role in how long we live is indisputable. The problem arises in identifying which genes are involved in this process, separating out environmental effects, and altering these genes.
CONTROVERSIAL AGING THEORIES
One of the oldest of myths concerning aging is that you can achieve eternal youth by drinking the blood or consuming the soul of the young, as if youth can be transferred from one person to another, as in the vampire legend. The succubus is a beautiful mythical creature who re
mains eternally youthful because when she kisses you, she sucks the youth from your body.
Modern research indicates there might be a kernel of truth to this idea. In 1956, Clive M. McCay of Cornell University sewed the blood vessels of two rats together, one old and decrepit and the other young and vigorous. He was astonished to find that the old mouse started to look younger, while the reverse happened to the young mouse.
Decades later, in 2014, Amy Wagers at Harvard University reexamined this experiment. Much to her surprise, she found the same rejuvenation effect among mice. She then isolated a protein called GDF11 that seems to underlie this process. These results were so remarkable that Science magazine chose it as one of the ten breakthroughs of the year. But in the years since this astonishing claim, other groups have tried to duplicate this research, with mixed results. It remains unclear whether GDF11 will be a valuable weapon in the quest to fight aging.
Another controversy involves the human growth hormone (HGH), which has created an enormous fad, but its effectiveness in preventing aging is based on very few reliable studies. In 2017, a major study on more than eight hundred subjects by the University of Haifa in Israel found evidence of the opposite effect, that HGH might actually decrease a person’s life expectancy. Furthermore, another study indicates that a genetic mutation that results in a reduced HGH level may lengthen the human life span, so the effect of HGH may backfire.
These studies teach us a lesson. In the past, wild claims concerning aging often faded when analyzed carefully, but today researchers demand that all results be testable, reproducible, and falsifiable, the hallmark of true science.