By Dick Teresi
Author (Dick Teresi) Bio: Dick Teresi is the author or co-author of several books about science and technology, most recently The God Particle and Lost Discoveries: The Ancient Roots of Modern Science, both selected as New York Times Book Review notable books. He has been editor in chief of Science Digest, Longevity, VQ, and Omni, of which he was also a cofounder, and has written for The New York Times, The Wall Street Journal, Smithsonian, The Atlantic, and Discover, among other publications.
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.
