Health Celebrates Life – Gaining An Edge On Age

This special piece of content is devoted to youthful aging, meaning how to be as alert and able during the second half of life as during the first. There has never been a time like this in science, when so many brilliant minds are working to unravel the mysteries of why our biological clocks wind down and what can be done to slow that decline. In the following paragraphs I bring you a report from the front lines of Aging Research, with tips from the experts on what you can do today to put more in life in your future years. What better way for Health to celebrate its own Longevity than to start you on the Road to Rejuvenation!

Consider Two Established Numbers: The Life Span of our species, the maximum time any human can stay alive, has been estimated at 115 years. Our Life Expectancy, the average length of time Americans really live, is only 75 years. The distinction is important because people generally believe that life span has increased dramatically throughout history, when it hasn’t. Great Strides have been made in life expectancy, however. During the Roman Empire, life expectancy was a mere 22 years. But life span then was pretty much what it is today – somewhere around 115 years.

Life expectancy has continued to increase because we have eliminated or learned to treat so many fatal childhood ailments and because we now cope so much better with infectious diseases. But the ancients who made it past these roadblocks had as good a chance as we moderns of inching towards 115 – and as little chance of going beyond.

While scientists work feverishly to increase longevity, much of the public is ambivalent. To many, longer life means additional decrepitude. Dr. Roy Walford, Professor of Pathology at the University of California, Los Angeles, School of Medicine and a leading expert in dietary restriction, is well aware of this prejudice. “People are afraid of increasing life span because they think it means just adding old years onto old. But we’re talking about keeping people younger longer.” Indeed, the goal of longevity research is to extend youthfulness as well as life itself.

But it may not be turning out that way. That’s the view of Dr. Jacob Brody, an epidemiologist who is Dean of the School of Public Health at The University of Illinois in Chicago. Brody comes at you with scary statistics. “Today in Sweden,” he says, “Only 18 percent of all deaths occur in those under 65 years old. That will be true throughout the rest of the developed world by coming decade.” Good news? Not really, says Brody. “Dying will occur later and later, that will give people time to get nonfatal, age dependent diseases.” What we should strive for, according to Brody, is “Active Life Expectancy – years one lives free of any illness and at full function.” Right now, he claims, for every four months tacked onto human life expectancy, only one month will be lived independently at full function.

Brody points out that though we’ve added 25 years to the life expectancy of women in this century, the age of menopause hasn’t been affected. He suggests a two-pronged approach to postponing nonfatal, Age-dependent Conditions: Studying the effects of behavior change, such as regular exercise and a healthy diet, against these conditions; and more basic research to answer questions such as, why do people’s eyes begin to deteriorate at age 40?

Aging is a basic mechanism that brings our species to its knees. If you don’t think this piece of content applies to you because you’re too young – well, if you’re old enough to read health articles, you’re probably already aging. Some scientists say we begin to age soon after puberty. Edward L/ Schneider, Director of the Buck Center for Research in Aging, a privately supported center has a more radical view. “Aging starts somewhere around conception,” he likes to say. Whenever it starts, aging is a problem for more than the elderly. Now for the good news, we’re starting to make headway.


Do Our Bodies Wear Out, Or Are Our Genes Preset To Self-Destruct?

While a breakthrough drug or therapy to extend life remains a far-off fantasy, scientists are making headway tracking down clues to another mystery: Why do we age? What is it that builds up, goes awry or is depleted, causing the changes in physiology that we interpret as aging?

It is unlikely that these researchers will stumble on some magical potion or secret of perpetual youth, but they may make discoveries that will allow our biological functions to run more efficiently and avoid breakdowns. Their findings may slow some aging processes.

Scientists from the Soviet Union to California are testing various theories, taking care to separate what is cause and what is merely effect. Some of the so-called causes of aging put forth by researchers today may turn out to be only superficial signs of a more important mechanism tomorrow. It would be silly, for instance, to say that gray hair causes aging. Someday, when more is known about the processes of senescence, the following ideas may be absurd

The Tired Refrigerator Hypothesis

Scientists prefer to call this the “stochastic” theory. A more dignified name, but essentially this hypothesis holds that our bodies are like any major appliance and they wear out. (A stochastic system is a random system, one that breaks down by chance, like an old refrigerator.) This very popular theory comes in many forms and is easy for the layperson to grasp: The body is like a Volkswagen; the clutch goes, the head gasket warps and eventually it dies in a pool of oil. There’s only one problem: Human beings are neither appliances nor automobiles. On the positive side, we have cells that replicate and refrigerators do not. On the negative side, sure, cars wear out, but we can intervene quite effectively to extend their maximum life spans, something we can’t do with humans. The average life expectancy of an automobile is somewhere around eight years or 100,000 miles. Yet my neighbor has a ’32 Ford in mint condition that runs like a top. All it takes is perfect maintenance. A 1932 Ford on the road today is equivalent to a 534-year-old human, since it has exceeded life expectancy for its species by more than seven rimes.

Clock Of Aging Theory

A much more intriguing, and more modern, concept is that there’s a genetic program somewhere in the body that dictates how fast (and in what manner) each of us will age and die. It has yet to be found, but some researchers speculate that this DNA clock might be contained in each cell, perhaps in a supergene, while others believe it resides in the brain. In fact, people have been aging and dying like clockwork for many millennia, so it’s not too farfetched to believe that a hard-wired mechanism controls this genetic process.

Error Catastrophe

This theory takes many forms, but it’s basically a cross between the stochastic and clock of aging concepts. The basic idea is that the genetic code that controls the production of the cells’ proteins goes awry. There are two ways of looking at this: Either wear and tear damages the genetic machinery and causes these errors (stochastic theory) or, for some reason, the “errors” are built in to the gentic code (the clock of aging theory).

The error catastrophe theory has been “pretty much demolished,” according to Dr. Robert N. Butler, Brookdale professor of geriatrics at Mt. Sinai School of Medicine in New York City, as old cells now appear to do as well as young cells when it comes to protein production. It was a very useful theory for many years, however, as it spurred scientists to study the whole area of proteins and genetic error.

The Smudged Xerox Hypothesis

This one was dreamed up by the noted gerontologist Alex Comfort, better known for his book The Joy of Sex (Pocket Books, 1987). Think of it in this way: Take a page of Health magazine and photocopy it. Then photocopy your photocopy. Now make a photocopy of the second photocopy, and so on. By the 50th copy, you will have a blurry mess. Likewise with cells, says Comfort. Every time they replicate, the new copy of DNA gets more and more smudged. Comfort reportedly has since pulled away from this notion, which in fact is a variation on error catastrophe.

The Autoimmune Hypothesis

When the immune system rebels, responses may be as trivial as hay fever, as painful as rheumatoid arthritis or as deadly as lupus. In this theory, aging and death are part of one, big autoimmune disease, in which the immune system becomes confused and starts attacking the body’s own cells.

Suite Genes

A person’s fate depends on whole families, or “suites,” of genes, say some experts. “Unless all members are perfect, you won’t live as long or as well as you should,” says Joan Smith-Sonneborn, who chairs the program on aging and human development at the University of Wyoming in Laramie.

Smith-Sonneborn’s experiments show that there may be a way to clean up accumulated DNA damage in imperfect genes. Many years ago, she made a landmark discovery in aging research when she bombarded single-cell organisms called paramecia with ultraviolet light, then shoved them under black light. The dark was known to trigger an enzyme that repaired the DNA damage caused by sunlight. What Smith-Sonneborn discovered was that these paramecia lived 50 percent longer than untreated paramecia did.

Free Radicals

It’s the trendiest idea around, but in reality, the free-radical theory is simply an elegant variation on the stochastic theory. Namely, there are chemical agents called free radicals that wear down our bodies.

The Glycation Hypothesis

Another hot theory holds that blood sugar interacts with proteins manufactured by the body’s cells and distorts the genetic information. Furthering this notion is the fact that diabetics who have difficulty metabolizing sugars often contract age-related diseases such as cataracts and atherosclerosis while they are still relatively young. Edward J. Masoro of the University of Texas Health Science Center at San Antonio recently found that long-lived rats in dietary-restriction experiments have low blood glucose, thus bolstering the glycation (from the word glucose) hypothesis even more.

The Death Hormone

Let’s finish up with a fun theory. It goes something like this: There’s one part of us that lives forever – DNA, the master molecule of heredity. Human DNA doesn’t want to die, so it keeps the species alive as best it can and is passed from generation to generation.

Individuals, however, are expendable. Because a species must mutate or change to keep pace with a changing environment, and because this evolution is slow, it’s in that species’ best interests to turn over generations as quickly as possible so that favorable mutations will show up in the gene pool.

This is the thinking behind the rather wild theory that there is a “death hormone,” a substance, possibly secreted by the pituitary gland, which ages us and eventually kills us. For if we lived too long, we would hold up the process of evolution.


Alongside researchers working to untangle the mystery of why we age are practical-minded scientists concentrating on how to interfere with those processes under scrutiny. Two promising life-extenders involve food: on the one hand, eating more of certain substances to “clean up” cellular breakdown; on the other, eating less to prolong life.

The Starvation Principle

It’s the only method that actually increases life span (presently it stands at 115), and it has worked every time it has been tried in the past 60 years. It’s called dietary restriction, and it means dieting each day of one’s life. Oh yes, and there’s a catch: We don’t know yet whether it works on humans.

Take a mouse, as gerontologist Roy Walford of the University of California, Los Angeles, had done many times, and gave it about half the food a mouse usually eats. Then wait. By 36 months, a normally fed mouse will be dead, for that’s the maximum life span of the species. But the dieting mouse will keep on going… and going, until 54 months. We’re talking about increased life span, not just life expectancy. Normally mice in the best health under the best of conditions can’t break 36 months, but the under-fed rodents live on average, 50 percent longer.

Ronald W. Hart had the most ambitious study of dietary restriction. Leaving nothing to chance, he had nearly 200,000 lab animals in life-extending experiments at the National Center for Toxicological Research (NCTR) in Jefferson, Arkanas. Of these, 25,000 mice were living on a diet that’s about 60 percent the normal ration of lab chow – though it’s fortified to provide the same vitamins and minerals. About 95 percent of the restricted mice live 35 months or longer. Only 25 percent of the controlled mice make it that far. Said Hart, “We see no cancer in restricted mice [at the 35-month period].

“What’s interesting,” he continued, “is that any layperson can tell the difference between the restricted animals and those on the ‘buffet’ diet. The former are the happiest centenarians – in the mouse sense – I’ve ever seen. The ones on the buffet are either limping or dead.”

Why Does Caloric Restriction Work?

No one knows, though many theories exist. Some researchers maintain that it simply wards off disease because the organism takes in fewer toxins. Others suspect it reduces the number of free radicals or increases the number of enzymes and nutrients that scavenge on free radicals. Walford said it might influence biomarkers of aging in the immune system or increase the DNA repair capacity of cells.

The more immediate, and unanswered, question is whether dietary restriction increases life span in people. No one has yet done such a scientific study, but there is anecdotal evidence.

The Japanese island of Okinawa, for example, is a de facto dietary-restriction experiment in that Okinawans eat from 20 to 40 percent less food than other Japanese, a people not known for stuffing themselves. The result: Okinawa boats about 20 times the number of centenarians found in the rest of the world.

Extrapolating from the animal data, Walford believed we could increase our life span to 170 or 180 years if we ate like his lab animals. In fact, he found the evidence so compelling, he ate like a mouse himself. At 65, he took in a mere 1,650 calories per day, even though he regularly jog, swim and pump iron.

If you want to try this yourself, Walford recommended you first determine your “setpoint,” what you weigh when you’re neither overeating nor undereating. For most people, that’s what you weighed in your 20s, assuming you weren’t too fat or skinny. Once you’ve established that, lose weight very gradually, taking as long as four to six years to reduce it to 10 to 25 percent below setpoint (rapid weight loss is dangerous). Walford weighed 155 pounds from age 20 until 60. Next 5 years i.e. until 65, he shed 20 pounds and expected to break the 115-year barrier.

Incidentally, don’t expect to live to 180 by starting dietary restriction now, said Walford, because that life span is based on beginning the regimen shortly after weaning. In fact, Walford would recommend against putting children on the diet because it could retard their growth. However, even if begun after adolescence, one could still expect to boost life span to age 140 or thereabouts. (For more on dietary restriction, you can refer Walford’s The 120-Year Diet.)

Lean Dangers: Another pioneer in the field of dietary restriction, Edward J. Masoro, former chairperson of the department of physiology at the University of Texas Health Science Center at San Antonio, had misgivings about the technique. “I have no problem with Roy’s regimen,” he said, “but I don’t think the layman is in a position to set his own regimen. People can take the diet to extremes, and it could do great damage.”

On the other hand, Hart thought that a lifetime of dietary restriction is considerably safer than most short-term diets. “Roy’s diet is well thought-out and well balanced,” he said, “though it’s more severe than I think is necessary.”

Actually, an unexpected danger was revealed by Hart’s experiments at NCTR, where lab animals are monitored around the clock. At certain times during the day, the mice’s body temperatures drop several degrees, and, unable to shiver or otherwise respond to cold temperatures because their dieting robs them of the fuel their muscles need, the animals suddenly die. Does that mean dietary restriction should only be followed by Los Angelinos such as Walford (who favors sabbaticals in India or tropical jungles) and avoided by those in colder climes? Not really, said Hart: “One of the nice things about being human is that you can put on clothes.” He also notes that restricted animals survive heat stress better than normal rodents do.

Interestingly, the temperature-dropping aspect may turn out to be the most valuable piece of evidence ever uncovered on the subject. Perhaps, NCTR researchers are telling themselves, it isn’t the diet but the colder body temperature brought on by the diet that makes the mice beyond the 36-month limit. Indeed, this works for some animals – when their body temperatures cool down significantly, their life span increase.

Similarly, Hart’s mice often drop into a torpor state in their sleep, a condition akin to hibernation. If it’s torpor that turns them into frisky centenarians, maybe someday there will be a pill that will allow humans to cool down at night. Then there will be no more talk about diets – just a pill with your nightcap, a cold bedroom and a 180-year life span.

Free Radicals: Sharks in a Protoplasmic Sea

It was Denham Harman who first suspected the awful truth: Human beings rust. At least that’s the theory.

Back in 1950s, Harman, a chemist turned physician at the University of Nebraska College of Medicine, discovered that radiation caused accelerated aging in lab animals and also created an excess of free radicals in cells. A free radical is an unstable part of a molecule with one or more free, unpaired electrons. A free radical must find another molecule to which to attach itself. Gerontologist Alex Comfort likened one to a convention delegate away from his wife. He called it “a highly reactive chemical agent that will combine with anything that’s around.”

That may be bad news for the cells. It is believed that free radicals trigger a chain reaction that “rusts” the body just as oxygen rusts out the rocker panels on an Oldsmobile. And what helps create free radicals? Here’s the bad news: oxygen. In fact, every breath you take ages you, because oxygen and the everyday process of oxidation involved in metabolism create free radicals and your ultimate destruction. Among other things, free radicals supposedly obfuscate genetic information in each cell.

Let’s stop for a warning. The free radical theory is the trendiest thing going in research today. But though you may have heard the theory presented as gospel, it has not been proven beyond a shadow of a doubt. Many respected researchers believe it, but it is just that – a belief.

Likely Cure. Free radicals are produced by everyday metabolism, but also by a host of other elements: some painkillers and anticancer drugs; burnt material, such as that found on grilled meats or toast; tobacco smoke; even sunlight. What combats them? Harman was aware that antioxidants were used in industry to prevent materials such as leather and rubber from degrading and to keep butter from turning rancid. Now the quest has begun for antioxidants that will keep us from turning rancid. Some likely prospects include vitamin B, C and E, beta carotene, glutathione, selenium, uric acid and food preservatives such as BHT, BHA and propyl gallate. One of the ironic things about the free radical theory is that it flies in the face of previously held beliefs about what constitutes healthy eating. The oft-reviled cereal preservatives BHT and BHA, may in fact preserve humans as well as cornflakes. And people who gave up butter for margarine years ago, in an attempt to avoid cholesterol buildup and heart disease, are now being told that polyunsaturated fats may increase free radical production. Thus the quandary: whether to butter and risk cardiac arrest, or switch to margarine and age every cell. (Refer another article “Ode to Cheez Whiz,” for other dilemmas.)

The most famous antioxidant is SOD, superoxide dismutase, a natural enzyme that neutralizes, or scavenges, free radicals. When SOD was discovered in 1969, it helped prove the existence of free radicals in human cells and boosted the credibility of Harman’s speculations. Further studies by Richard Cutler at the National Institute on Aging showed a positive link between the amount of SOD activity as it related to oxygen consumption in a particular species and its life span, at least in mammals. A gorilla, for instance, lives much longer than a mouse and has more SOD to protect against a given quantity of free radicals. Cutler then discovered that the same correlation held true for other antioxidants. The more vitamin E, beta carotene and so on that a mammal had, the longer it lived.

Vitamin E: The Natural Antioxidant

So what can one do? Eat several boxes of BHT-enhanced cereal a day? Go back to slathering corn with butter? What antioxidants keep a person fresh? The father of free radicals says to stick with the classics: vitamin E and C and beta carotene. Vitamin E is Harman’s favorite; he calls it “the natural antioxidant. It’s in all our membranes.” He cites a study of 5,000 women on the English island of Guernsey: Those with the highest blood levels of vitamin E had the lowest incidence of breast cancer. It’s also being tested against senile dementia, Parkinson’s disease and other age-related disorders. Harman’s says it’s hard to overdose on E.

Before you begin to rustproof yourself, consider some recent experiments in dietary restriction, the only proven method of boosting life span in mammals. Animals on a highly restricted diet increase their longevity dramatically, and free radical advocates have always assumed that low food consumption equaled fewer free radicals – a reasonable assumption. But studies by Masoro and others now show that food restriction does not reduce metabolic rate one whit. No one knows, in fact, why it works. The free radical connection, if any, has yet to be proven.

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