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Unstudied though these products often are, their performance is akin to that of any placebo—it might have an effect. Stem-cell activating and resveratrol-laden age-management nostrums may not help prevent visible signs of aging, but it doesn’t really matter if they work. What matters is that consumers believe they will work. Hopes for creaselessness are bolstered into faith by hypnotic ad copy in fashion magazines: hydroxy acids have exfoliatory antioxidant powers. Kinetin causes humectant agents to remain on the skin longer. Hyaluronic acid’s renewing properties are legion. Copper peptides are where it’s at. You mean you aren’t yet taking the age-decelerating coenzyme Q10?
Marketers often use scientific-sounding jargon, but a 2011 study of wrinkle-reduction creams found that “at best the products had a small effect, and not on everyone.” In other tests, those that sell for inflated prices were outperformed by no-name moisturizers. Double-blind trials show that about 20 percent of participants’ wrinkles can be improved slightly to moderately after six months of serums, while about 12 percent of participants’ wrinkles improve simply when taking placebos.
That hasn’t stopped women from risking delirious sums on the off chance they might shrink a wrinkle. The cost of a 16.5 oz. jar of Crème de la Mer (which bioferments the curative powers of the sea into a light-and-sound-wave-treated elixir users are encouraged to “apply day and night—for a lifetime”) is $1,900. Carita’s “infinitely rare antiaging formula” Diamant de Beauté, containing pulverized diamonds (which obviously makes facial skin last forever), costs $600 for 1.7 ounces. Ads for SK-II, one of the priciest beauty brands in the world, tell of a Japanese monk crafting the cream’s secret formula, a nutrient-rich fluid called Pitera: “After many experiments, he discovered a liquid that seemed to defy aging.”
But even if it “seems” to, that doesn’t mean it “does.” Clinique Youth Surge Night cream claims to suspend age and interrupt time by building on sirtuin technology to “virtually slow the signs of aging.” But sirtuin technology, as I would soon learn, remains uncertain at best.
“Younger-acting skin leads to younger-looking skin,” claim ads for Olay Professional Pro-X Age Repair Lotion, which signals the moisture barrier to perform “more like it did when it was younger.” Pro-X research is based on “one of the great scientific achievements,” explains Olay’s website: the sequencing of the human genome. Its efficacy is “proven,” explain advertisements. But according to some consumer testers, using it on half of one’s face while using a vastly cheaper cream on the other leads to no noticeable difference. Other testers, though, report favorable results.
Beyond their logic-stretching promotional slogans, nothing much supports the claims made by most antiwrinkle eye-cream manufacturers. Some evidence suggests that compounds called retinoids may have an effect on photo-aged skin, which has suffered prolonged exposure to UV radiation. A study funded by UK chemist Boots found that their own No7 Protect & Perfect Intense Beauty Serum benefits users with sun-damaged skin who apply it for at least a year. (Since the study was made public, sales have skyrocketed: a bottle of the product is bought every eight seconds at Target.) Regardless of efficacy, we spend billions on cosmetic wrinkle-reduction treatments every year. Even young people are getting in on it: in 2011, Walmart announced a new line of cosmetics with antiaging properties aimed at eight- to twelve-year-olds.
While cosmetic skin creams can contain heavy metals and other toxins, they aren’t as dangerous as the use of human growth hormone (HGH), whose use as an antiaging remedy or for age-related problems is not authorized by the FDA. Covertly used by pro athletes and bodybuilders, there’s a false perception that HGH can make people younger. On the contrary: the misuse of growth hormone has been shown to cause organ malfunctions and tumor formation in test species, as well as an “increased probability of early death,” the most perfectly ironic side effect to a remedy hyped as having life-extending qualities. (Things haven’t changed much since the time of the Han dynasty.)
We don’t know exactly how hormones affect us. Preliminary results of a six-year, $45 million National Institutes of Health study of testosterone therapy among elderly men will be available in 2015. In the meantime, HGH and other supposedly age-defying hormones remain procurable online, as do books such as Grow Young with HGH: The Amazing Medically Proven Plan to Reverse Aging, by Dr. Ronald Klatz, MD, DO, “a world recognized authority on preventive medicine and advanced biotechnologies.” Klatz is the president of the American Academy of Anti-Aging Medicine (A4M), an organization whose position statement is that “Aging is no longer inevitable.”
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We’ve tried to explain the causes of growing old in many ways. One of the twentieth century’s most discussed theories of aging is the oxidative model. In the post–World War II years, a chemist and biogerontologist named Denham Harman suggested that aging is caused by cellular exposure to oxygen. This basic concept has obvious appeal based on a causal truth: air makes things age. Just as it causes a cut apple to brown or uncorked wine to oxidize, it weakens our mitochondria. Hence the notion that if we could only prevent oxygen from invading our molecular structure, we could prevent aging.
Antioxidants—the phytonutrients found in colorful fruits and vegetables—seem to protect the body from free radicals, the intercellular equivalent of terrorists. But nobody knows for sure. Numerous other experiments have given rise to doubts that oxidative damage is the main cause of aging. Antioxidant-based vitamin supplements may not limit bodily oxidative damage or even influence aging whatsoever. We can’t say. The answer is blowing in the mitochondrial wind. But the dearth of evidence hasn’t prevented this idea from being accepted as a proven fact, especially among canny marketers.
“In simple language, we don’t get old, we rust from oxygen,” announced Dr. Harry B. Demopoulos in 1989. An occasional actor with a baroque comb-over, Demopoulos was among the first to theorize that consuming antioxidants might slow aging. His company, Health Maintenance, Inc., supplied Hollywood celebrities with a patented blend of vitamins, generating an estimated $10 million in 1990. Since then, sales of antioxidant superfruits such as açaí and blueberries have soared.
In 2002, UC Berkeley’s Dr. Bruce Ames, a winner of the US National Medal of Science, launched a product called Juvenon whose antioxidant supplements have the tagline “Stay Young.” Another company, Eukarion, joined the fray, licensing its discoveries to Estée Lauder. The excitement over Eukarion slowed when the mania for free radicals started fading.
Today antioxidant superfoods are available at most supermarkets, in a multitude of forms. Consuming them won’t make us live longer, although they may make us healthier. “Antioxidants haven’t extended life—that whole idea is out the window,” one senior researcher at the US Department of Health & Human Services’ National Institute on Aging told me. “Things we thought we understood we realized we don’t. The simple ideas just don’t work. There is so much we don’t know.”
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Cynthia Kenyon is a molecular biologist at UC San Francisco whose findings appear to contradict what we assume we know about aging. Her genetic work on roundworms called C. elegans has demonstrated that they can be made to live four times longer than normal. “That’s not immortal,” she concedes. “That’s not to say that you couldn’t. But we haven’t.” She feels confident that her discoveries will translate into human applications. On her website, she has posted a special section for nonscientists in which she explains her views: “We don’t know yet, but to me it seems possible that a fountain of youth, made of molecules and not simply dreams, will someday be a reality.”
Her position is precisely the opposite of another UCSF scientist, Leonard Hayflick, an evolutionary biologist and anatomist who has spent his career working with cells and debunking false scientific claims about immortality. He’s best known for positing the Hayflick limit—that somatic cells can only divide a certain number of times, after which they senesce and die. (Previous to his demonstration o
f this phenomenon, cell populations were thought to be immortal.) The biological cause of aging, Hayflick says, “is the same as the cause of nonbiological aging—it’s the second law of thermodynamics.” Everything, he asserts, eventually breaks down, collapses, and falls apart. That’s the nature of entropy; and entropy is a fact of nature. “Let’s take something infinitely simpler than your body and mine: automobiles,” says Hayflick. “Even if you put the car in a garage and don’t use it, it won’t stand there forever. Eventually, it will age and disintegrate. This is an inevitable law of physics.”
Kenyon, on the other hand, starts speeches by rejecting such reasoning as old-fashioned. “In the past,” she states, “we thought you wear out, like an old car.” Her colleague the MIT molecular biologist Lenny Guarente, who studied stress in yeast and found that certain genes express themselves in those that live longest, puts it this way: “The wear-and-tear theory is best viewed as a laudable initial attempt to come to grips with the problem, but is not a serious scientific theory; the problem is that people turn out to be more complex than Chevys.” The difference between inanimate objects and biological organisms, the two point out, is that living systems have self-repairing mechanisms. True, Hayflick and his peers concede, but our body can repair itself only for so long. “Aging occurs because the complex biological molecules of which we are all composed become dysfunctional over time as the energy necessary to keep them structurally sound diminishes,” explains Hayflick. As we age, the defense and maintenance programs that protect us when young gradually stop working.
What if we could find a way of activating such genetic pathways later in life? Scientists have done so with worms, yeast, fruit flies, and mice. The names for these longevity genes are usually technical: SIR2, InR, p66Shc, fos, chico, age-I. (One exception is the recently discovered fruit-fly gene INDY, which stands for “I’m Not Dead Yet.”) The results are indisputable, but interpreting them is another issue altogether. “When single genes are changed, animals that should be old stay young,” Guarente and Kenyon summarized in a Nature article about genetic perturbations that increase life span in simple animals. “On this basis we begin to think of aging as a disease that can be cured, or at least postponed.” Of course, not everyone agrees with their conclusion. It’s certainly a leap to go from genuine genetic findings to speculation that aging in humans is a curable disease.
If anything certain can be gleaned from the current public argument between evolutionary and experimental biologists, it’s how limited the scientific understanding of our aging actually is. The deepest researchers in the world today still don’t know whether there’s a universal biological process behind aging. One side, composed mainly of experimental genetic biologists with ties to pharmaceutical companies, believes that we will be able to manipulate longevity genes in all species. They hope to translate the findings they’ve made on a molecular level into human-ready medicines. On the other side, evolutionary biologists don’t think we’ll ever have the ability to intervene in fundamental human aging. For the rest of us, seeing aging as a disease or not is a personal choice.
Ending aging is for now as elusive as ending time, but scientists have found aging research to be fantastically rewarding financially. In 2008, GlaxoSmithKline paid $720 million for the rights to exploit pharmaceutical drugs based on the genetic pathways uncovered by Guarente and his graduate students. “What we’re working toward is a drug that gives the benefit of exercise and diet without having to exercise and diet,” explained Sirtris’s cofounder David Sinclair, in a statement that neatly encapsulates the contemporary American dream.
Their findings remain inconclusive, at least in human medicine. GSK executives defended their expenditure as high risk—a shot in the dark with the possibility of a high return. Their inferences may prove to be useful, but an inference is not something meant to be believed; it’s meant to be tested. Once the testing is further along, we’ll know more about whether aging genes can be affected in humans.
“I doubt that aging can be reversed,” says Hayflick. “Aging is a random, stochastic process that occurs after reproductive maturation and results from the loss of molecular fidelity.” Guarente, Kenyon, and fellow experimental researchers contend that the genes they’ve isolated have the power to keep an animal’s “natural defense and repair activities going strong regardless of age.” As they wrote in Scientific American, these genes, in lab species, can “dramatically enhance the organism’s health and extend its life span. In essence, they represent the opposite of aging genes—longevity genes.” Heady, but such hopes always have been.
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In both biology and reality, the end begins at the cellular level. Without exception, flora and fauna consist of cells. Our bodies are made up of trillions of cells doing what cells do best, which is making replicas of themselves. Then they die.
For most of history, life consisted of unicellular organisms popping around. To this day, the majority of creatures on earth are single-celled. When a single-celled organism such as a bacterium or a protozoan reproduces through binary fission, what was one becomes two. In some cases, such as division in a yeast or E. coli, clearly a younger cell and an older cell result from each fission. The young one gets all new parts, and the older one gradually senesces. And on it goes.
In other cases, there appears to be no distinction between the progeny and the original cell. The two fission products are effectively clones. There are two ways of describing what happens here: the parent cell either dies while becoming two identical offspring, or it gives birth to an identical replica of itself that will also divide again at the same moment as the parent. Whether the initial cell dies into twins or gives birth to itself, both definitions are valid, and they both showcase the limits of language to explain natural processes.
When cells started getting specialized in order to aggregate into more complex organisms, they became two distinct types of cells: germinal cells and somatic cells. Our soma cells constitute the majority of our body. Our germ cells are those in our gametes—the female ova and the male spermatozoa. Somatic cells age and can replicate a finite number of times (known as the Hayflick limit). Germinal, or reproductive, cells, however, have the capacity to keep on dividing more or less continually. They contain the hereditary information in DNA that is passed on through subsequent generations.
A benefit of ovigerous sexual reproduction is greater complexity for the entire species. Each descendant obtains a bit of both parents’ germ cells. This form of ever-radiating genetic diversity is a defense against potential threats. Even if a large swath of the species gets wiped out by a genetic invasion, some part of the population is likely to be immune. But when species do go extinct, their genetic code disappears. Species are not immortal; nor can what’s lost be re-created.
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The mysteries of the cell may one day reveal something about aging that we don’t as yet understand. For example, just as certain single-celled organisms are capable of regenerating themselves seemingly endlessly, so can cancerous cells. The replicative capacity of a normal cell is finite; cancer cells are simply normal cells that mutate and, for some reason, begin to proliferate continually. The cell buildup is what’s called a tumor. Within each of us, stem cells also have the ability to make apparently limitless copies of themselves, but they are usually quiescent, active only in youth or in a medical emergency.
Cancer cells, stem cells, and unicellular organisms that experience unstoppable growth are spoken of as having cellular immortality. This does not mean they are indestructible. They are not undying. When a host body dies of cancer, the uncontrollable cancer cells die with it. So-called immortal cells can keep dividing in the correct medium (as with the cells of Henrietta Lacks, known as HeLa cells), but obviously they perish if taken out of that culture. Cellular immortality doesn’t mean we can orchestrate the immortalization of life-forms.
In the nineteenth century, August Weismann, author of Upon the Eternal Duration of Life, wrote of how imm
ense numbers of organisms “do not die.” Our somatic cells perish, he conceded, but germ cells are “potentially immortal” as they can transfer themselves into a new individual. Even though we die, if we have children, our genetic information outlives us.
Just as cells make copies of themselves, our bodies evolved to live long enough to reproduce. We reach our peak in our twenties and start going downhill in our thirties and forties. In our postreproductive period, many of the exact same genetic processes that contributed important and valuable functions in our youth start to have harmful effects. This phenomenon, technically known as antagonistic pleiotropy, is one of the biggest obstacles to solving the aging riddle. Genes involved in cancer or Alzheimer’s are also those that promote healthy growth earlier on. Aging-related illnesses are the price we pay for living to eighty.
Immortalists make much of how certain jellyfish, sponges, corals, and deep-sea creatures appear not to senesce. That these creatures lack nervous systems or memory isn’t an issue. They “don’t age,” prolongevists say. They “may be practically immortal.” Yet as slowly or imperceptibly as they age, they die when killed. Some of them can sprout new limblets if the conditions are favorable or bud body parts, but that doesn’t mean they are eternal.
The freshwater hydra is a tiny, brainless organism with fascinating regenerative capabilities. Even if much of it is killed, it can spring back to health, giving the impression of imperishability. Imagine a three-millimeter-long tube topped with dreadlocks. The hydra is often compared to a fountain, its body a jet of water that shoots into a splash of tentacles. The tube is made up of cells that seem to be both germinal and somatic. As the tube’s old cells age, die, and are sloughed off, new ones are generated. Being hermaphroditic, a hydra can bud off some of those cells into entirely new hydra. It can also rebuild itself from almost any bit of its body. Still, as amazing as it is, it isn’t immortal. It’s a simple organism whose body cells are also germinal cells. Take it out of water and it perishes.
Book of Immortality Page 31
