John Kanzius hopes his machine using radio waves will one day represent a significant advance in treating cancer.
John Kanzius (CBS)
The Hidden Power of Radio Waves
………To Cure Cancer?
The Kanzius Machine: A Cancer Cure?
(CBS) What if we told you that a guy with no background in science or medicine-not even a college degree-has come up with what may be one of the most promising breakthroughs in cancer research in years?
Well it’s true, and if you think it sounds improbable, consider this: he did it with his wife’s pie pans and hot dogs.
His name is John Kanzius, and he’s a former businessman and radio technician who built a radio wave machine that has cancer researchers so enthusiastic about its potential they’re pouring money and effort into testing it out.
Here’s the important part: if clinical trials pan out-and there’s still a long way to go-the Kanzius machine will zap cancer cells all through your body without the need for drugs or surgery and without side effects. None at all. At least that’s the idea.
The last thing John Kanzius thought he’d ever do was try to cure cancer. A former radio and television executive from Pennsylvania, he came to Florida to enjoy his retirement.
“I have no business being in the cancer business. It’s not something that a layman like me should be in, it should be left to doctors and research people,” he told correspondent Lesley Stahl.
“But sometimes it takes an outsider,” Stahl remarked.
“Sometimes it just – maybe you get lucky,” Kanzius replied.
It was the worst kind of luck that gave Kanzius the idea to use radio waves to kill cancer cells: six years ago, he was diagnosed with terminal leukemia and since then has undergone 36 rounds of toxic chemotherapy. But it wasn’t his own condition that motivated him, it was looking into the hollow eyes of sick children on the cancer ward at M.D. Anderson Cancer Center in Houston.
“I saw the smiles of youth and saw their spirits were broken. And you could see that they were sort of asking, ‘Why can’t they do something for me?'” Kanzius told Stahl.
“So they started to haunt you. The children,” Stahl asked.
“Their faces. I still remember them holding on their Teddy bears and so forth,” he replied. “And shortly after that I started my own chemotherapy, my third round of chemotherapy.”
Kanzius told Stahl the chemotherapy made him very sick and that he couldn’t sleep at night. “And I said, ‘There’s gotta be a better way to treat cancer.'”
It was during one of those sleepless nights that the light bulb went off. When he was young, Kanzius was one of those kids who built radios from scratch, so he knew the hidden power of radio waves. Sick from chemo, he got out of bed, went to the kitchen, and started to build a radio wave machine.
“Started looking in the cupboard and I saw pie pans and I said, ‘These are perfect. I can modify these,'” he recalled.
His wife Marianne woke up that night to a lot of banging and clamoring. “I was concerned truthfully that he had lost it,” she told Stahl.
“She felt sorry for me,” Kanzius added.
“I did,” Marianne Kanzius acknowledged. “And I had mentioned to him, ‘Honey, the doctors can’t-you know, find an answer to cancer. How can you think that you can?'”
That’s what 60 Minutes wanted to know, so Stahl went to his garage laboratory to find out.
Here’s how it works: one box sends radio waves over to the other, creating enough energy to activate gas in a fluorescent light. Kanzius put his hand in the field to demonstrate that radio waves are harmless to humans.
“So right from the beginning you’re trying to show that radio waves could activate gas and not harm the human-anything else,” Stahl remarked. “‘Cause you’re looking for some kind of a treatment with no side effects, that’s what’s in your head.”
“No side effects,” Kanzius replied.
But how could he focus the radio waves to destroy cancer cells?
“That was the next $64,000 question,” Kanzius said.
The answer would cost much more than that. Kanzius spent about $200,000 just to have a more advanced version of his machine built. He knew that metal heats up when it’s exposed to high-powered radio waves. So what if a tumor was injected with some kind of metal, and zapped with a focused beam of radio waves? Would the metal heat up and kill the cancer cells, but leave the area around them unharmed? He did his first test with hot dogs.
“I’m going to inject it with some copper sulfate,” Kanzius explained, demonstrating the machine. “And I’m going to take the probe right at the injection site.”
Kanzius placed the hot dog in his radio wave machine, and Stahl watched to see if the temperature would rise in that one area where the metal solution was and nowhere else.
“And when I saw it start to go up I said, ‘Eureka, I’ve done it,'” Kanzius remembered. “And I said, ‘God, I gotta shut this off and see whether it’s still cold down below.’ So I shut it off, took my probe, went down here where it wasn’t injected. And the temperature dropped back down. And I said, ‘God, maybe I got something here.'”
Kanzius thought he had found a way attack cancer cells without the collateral damage caused by chemotherapy and radiation. Today, his invention is in the laboratories of two major research centers – the University of Pittsburgh and M.D. Anderson, where Dr. Steven Curley, a liver cancer surgeon, is testing it.
“This technology may allow us to treat just about any kind of cancer you can imagine,” Dr. Curley told Stahl. “I’ve gotta tell you, in 20 years of research this is the most exciting thing that I’ve encountered.”
That’s because Kanzius impressed Curley with another remarkable idea: to combine the radio waves from his device with something cutting edge – space age nanoparticles made of metal or carbon. They are so small that thousands of them can fit in a single cancer cell. Because they’re metallic, Kanzius was hoping his radio waves would them heat up and kill the cancer.
“If these nanoparticles work then we truly have something huge here,” Kanzius told Stahl.
Enter Rick Smalley, another cancer patient at M.D. Anderson and the man who won the Nobel Prize for discovering nanoparticles made from carbon. As luck would have it, Dr. Curley was called in one day to examine Smalley. Before leaving, he asked him for some of his nanoparticles.
“I proceeded to tell him what I wanted to do and that I thought they would heat. He looked at me with sort of a studied long look and didn’t say anything. And then he looked at me and said, ‘It won’t work,'” Curley remembered. “And just laughed and said, ‘Well, look, I’ll give you some. But don’t be too disappointed.'”
So Dr. Curley brought a vial of those precious nanoparticles to John Kanzius.
And on an August day in 2005, Curley and Kanzius put them to the test. Would the metallic nanoparticles heat up enough to kill cancer?
“So we take the nanoparticles, we put ’em in the radio field. And in about 15 seconds, they’re boiling and heating and Steve Curley couldn’t contain himself. He called Rick Smalley and he said, ‘Rick, you’re not going to believe this. He just blew the smithereens out of your nanoparticles,'” Kanzius recalled.
Smalley’s response? “The only thing that I got out of him after this pause was, “Holy s…,'” Curley recalled.
Not long after that day, Smalley died of lymphoma. Once a skeptic, he had become one of Kanzius’ biggest supporters.
“He didn’t expect it, but he embraced it to his death bed when he told Dr. Curley this will change medicine forever. Don’t stop, no matter what you do,” Kanzius told Stahl.
And they haven’t stopped. They’ve already shown that the Kanzius machine can heat nanoparticles and cook cancer to death in animals. Dr. Curley with rabbits, and in Pittsburgh, Dr. David Geller demonstrated to 60 Minutes how he used nanoparticles, made from gold, to kill liver cancer cells grown in rats.
“Now what we’re going to do is inject the nanoparticles,” Dr. Geller explained. “Directly into the tumor.”
In the study the rats, anesthetized to keep them still, were exposed to the Kanzius radio waves. Dr. Geller later examined their tumors under a microscope.
“What you can see is that cells are starting to fall apart. You see white spaces in between them. The body of the cell is shrinking, the cells are starting to die,” Geller pointed out.
“And can you tell from this whether the area surrounding the tumor had any destruction?” Stahl asked.
“Grossly inspecting the animal, we did not see not see any damage to the surrounding tissue,” Geller said.
So far, the Kanzius method has only been applied to solid, localized tumors in animals. The ultimate goal is to treat cancer that has metastasized or spread to other parts of the body. Those undetectable rogue cells are what most often kill people with cancer and the trick is finding them.
“If we can’t target the microscopic cells this is not going to be a cure,” Curley said.
That’s why Curley is trying to use special molecules that are programmed to target cancer cells and attach nanoparticles to them.
He showed Stahl an animation of how he hopes the targeting will work in people one day, with a simple injection of gold nanoparticles into the bloodstream.
“What we’re seeing here is an example of a gold nanoparticle in this case with an antibody on it, so the antibody would be the targeting molecule,” Curley explained. “You can see it is tiny compared to a normal red blood cell just imagine all of these billions of these gold nanoparticles circulating through the body and then once they get into the blood vessels going to the tumor, these nanoparticles would go through and bind on the surface of the cell.”
“The cancer cell. It wouldn’t bind on a normal cell,” Stahl observed.
“That’s right, they would bind only to the cancer cell. Now here’s the nanoparticles in the cell, here comes John’s radio frequency treatment. The cells get hot and they’re destroyed,” Curley said.
“Gosh, it does look like one of those science fiction movies,” Stahl remarked.
“Right now it is a little science fiction,” Curley agreed. “We’re not quite to the real time yet, but it’s got a lot of promise.”
Even if all goes well in the lab, it’ll be at least another four years before human trials can start. But John Kanzius says he’s afraid he doesn’t have that much time. So to help speed up the research, he’s been raising millions of dollars and getting press coverage about his invention.
“Now I can’t count the number of times the journalistic community, has done stories on a cancer cure,” Stahl said. “I did one in 1973. …How many times have we seen these things work in the Petri dish, work with animals. And then you get them into humans and they don’t work.”
“Dozens,” Curley replied.
But if this one does work, it most likely won’t be developed in time to help the man who invented it. John Kanzius may have the option of a bone marrow transplant that could buy him more time, but after six years of chemo it would be another grueling ordeal.
“Did you ever say, ‘I’m not going to do this anymore. I’m not going to put myself through it,’?” Stahl asked.
“Yes. I said that-only about a year and a half ago,” Kanzius replied. “I changed my mind because I think with all the research that’s going on with the institutions, that maybe, I’d like to be around for the first patient to get treated and just have a smile.”
“Oh my God,” Stahl said.
“And then I don’t care anymore,” Kanzius replied.
Harvard Medical School – Neck pain is no stranger to many of us. Doctors estimate that seven out of 10 people will be troubled by neck pain at some point in their lives. For one in 20 sufferers, the discomfort can significantly limit the ability to work and play. Surprisingly, movement may be the key to relieving neck pain.
If you’re like many people, you’ve never lifted weights in your life and you may wonder why start now? As you age, muscle tissue and strength dwindles, but weight or strength training can reverse this process. It can also lighten your heart’s workload, boost levels of good cholesterol, help prevent and treat diabetes, ease stiffness from arthritis, lead to weight loss, and improve your mobility. While it’s clear that there are plenty of reasons to include strength training in your routine, you may not know where to start.
Strength training can relieve chronic neck pain
Most of us are troubled by neck pain at some point in our lives. The most common culprit is overuse or misuse of muscles and ligaments. Today’s computer-dominated workplace can be especially tough on necks, because so many of us sit for long periods with shoulders slumped and heads extended toward monitors.
Considerable study has been devoted to the treatment of chronic neck pain. The choices include medications, chiropractic manipulation, electrical nerve stimulation, massage, and various forms of exercise. Results so far have been inconsistent and difficult to compare, and the quality of research has been uneven. Still, there’s mounting evidence that certain exercises designed to strengthen neck muscles can help break longstanding cycles of neck pain.
A randomized trial has found that women with work-related neck pain experienced significant and long-lasting relief by regularly practicing five specific neck muscle–strengthening exercises. General fitness workouts, by contrast, reduced the pain only slightly. Results were published in the January 2008 issue of Arthritis Care and Research.
Danish scientists at the National Research Center for the Working Environment in Copenhagen recruited women engaged in repetitive work, mostly at computer keyboards, at banks, post offices, administrative offices, and an industrial facility. All complained of neck pain lasting more than a month during the previous year. They were eligible for the study if physical examinations showed they had trapezius myalgia — chronic pain and tightness in the muscles that run down the back of the neck and fan out toward the shoulders.
Participants were divided randomly into three groups. One group received strength training focused on neck and shoulder muscles. The second group received general fitness training, which consisted of riding an exercise bike without holding onto the handlebars. The third group was given only health counseling. The two exercise groups worked out for 20 minutes three times a week for 10 weeks.
The women rated pain intensity in the trapezius muscles immediately before and immediately after each training session and two hours after each workout. The strength training group experienced a 75% decrease in pain, on average, during the intervention as well as during a 10-week follow-up period involving no workouts. General fitness training resulted in only a short-term decrease in pain that was too small to be considered clinically important, although the researchers did suggest that even a little reduction in pain severity could encourage people to give exercise a try. There was no improvement in the health counseling group.
This study isn’t the final word on relieving chronic neck pain. The number of participants (48) was small, and most of the women were under age 60. The results may not apply to women who are older or have conditions that limit their ability to strength train. Still, the findings suggest that performing specific muscle-strengthening exercises may be a helpful strategy for many women with chronic neck pain. (The researchers have investigated the effectiveness of each exercise with electromyography, which measures muscle-generated electrical activity. Results will be published in the journal Physical Therapy.)
Five Exercises (check with your doctor before beginning any new exercise regime)
Strength training in the Danish study consisted of five exercises that involved the use of hand weights to strengthen neck and shoulder muscles. Three times a week (Mondays, Wednesdays, and Fridays), for 20 minutes per session, participants performed three of the five exercises, doing three sets of eight to 12 repetitions (each set lasting 25 to 35 seconds) for each exercise. The exercises changed from session to session but always included dumbbell shrugs. The weight load was gradually increased during the study, roughly doubling in 10 weeks.
This was an intensive program and study participants were carefully supervised. So before you embark on a similar regimen, consult a physical therapist or exercise specialist who can help design a program for your needs and make sure that you’re doing the exercises correctly. In the exercises pictured here, the starting weights in parentheses are those used in the study. For each exercise, you should start with a weight that allows a maximum of eight to 12 repetitions.
1) Dumbbell shrug
Stand straight with your feet shoulder-width apart and your knees slightly bent. Hold a weight in each hand, and allow your arms to hang down at your sides, with your palms facing your body. Shrug your shoulders upward, contracting the upper trapezius muscle, hold for one count, and lower. Repeat eight to 12 times per set. (Starting weight: 17 to 26 pounds.)
2) One-arm row
Stand with your left knee on a flat bench and your right foot on the floor. Hold a weight in your right hand. Bend your torso forward, placing your left hand on the bench for support. Allow the weighted hand to hang down toward the floor. Pull the weight up until your upper arm is parallel with your back, pause, and then lower it. Repeat eight to 12 times per set. Switch to the left side, and repeat. (Starting weight: 13 to 22 pounds.)
3) Upright row
Stand straight with your feet shoulder-width apart. Hold the weights down in front of your thighs, with your palms facing your body. Slowly bring the weights straight up, as if you were zipping up a jacket. Slowly lower the weights to their original position. Repeat eight to 12 times per set. (Starting weight: 4 to 11 pounds.)
4) Reverse fly
Lie on a bench at a 45-degree angle. Hold a weight in each hand and allow your arms to extend down toward the floor. Keeping your elbows slightly bent, lift the weights up and out to the side to about shoulder level. Slowly lower the weights. Repeat eight to 12 times per set. (Starting weight: 2 to 6 pounds.)
5) Lateral raise
Stand straight with your feet shoulder-width apart and your knees slightly bent. Lift your arms up to the sides until they are parallel with the floor. Your elbows should be slightly bent. Slowly lower your arms. Repeat eight to 12 times per set. (Starting weight: 4 to 9 pounds.)
For more information on strength training, order Special Health Report, Strength and Power Training, at www.health.harvard.edu/SPT.
Click here to read about Arno’s riveting war time experience as a young adult.
This article was taken from the UW Medicine magazine for alumni of the University of Washington School of Medicine, Fall 2002, Volume 25, No. 2.
This exerpt was taken from an article by Clement A. Finch, M.D., titled
Arno Motulsky came to the UW in 1953 as an instructor in hematology, having trained with Karl Singer in Chicago at Michael Reese Hospital and with William Crosby at Walter Reed Army Graduate School. Because of Motulsky’s interest in hereditary hemolytic anemias and genetic disorders in general, the suggestion by Department of Medicine chair Robert Williams that he spend more time in genetics fell on responsive ears. After a year at the Galton Laboratory of University College in London under Lionel Penrose, Motulsky returned in 1957 to build a division of medical genetics. This preceded the establishment of the Department of Genetics in UW’s College of Arts and Sciences by three years. Several division members later obtained joint appointments with this department.
In 1967 the division obtained a program-project grant on gene action, and in 1972 NIH funded a broadly based center. Subsequent research in human and medical genetics has been far-ranging, consistent with the many interests of Motulsky and other faculty members. UW researchers carried out population studies in many parts of the world on malaria-dependent red cell traits, with emphasis on G6PD (glucose 6-phosphate dehydrogenase). Stanley Gartler used the G6PD enzyme system to study tumor origin, which led to the demonstration by Philip Fialkow that several hematological malignancies are clonal in origin.
Motulsky performed the first successful bone marrow transplantation in an experimental animal model to eradicate an inherited red cell disease (hereditary spherocytosis in deer mice). A post-doctoral fellow, Joe Goldstein, pioneered studies on the role of genetic hyperlipidemia in coronary artery disease. Later, as a faculty member of the University of Texas at Dallas/Southwestern, Goldstein won a Nobel prize for the discovery of a cell receptor for low density lipoprotein and its influence on cholesterol metabolism. Recent studies on fetal hemoglobin production by George Stamatoyannopoulos uncovered the mechanism for the developmental switch to adult hemoglobin that may lead to a treatment for sickle cell anemia. Such research has attracted investigators from this country and abroad and has helped popularize genetics as an important basic and applied science.
The principal theme of the work of Dr. Motulsky is the role of heredity-environment interactions in the pathogenesis of disease. Dr. Motulsky introduced the concept of genetically determined drug reactions (pharmacogenetics) and worked extensively on several pharmacogenetic traits. Current emphasis deals with the extension of pharmacogenetics to other environmental agents (ecogenetics) in conjunction with the UW center on ecogenetics. Previous studies on the frequency and genetics of hyperlipidemia in populations of patients with coronary heart disease led to the definition of the role of various genetic hyperlipidemias in coronary heart disease. Dr. Motulsky’s current work in this field focuses on the study of lipid-related genes and is being carried out at genetic and population genetic levels. Other work deals with the genetics of homocysteine elevations as a risk factor in arteriosclerotic vascular disease and polymorphisms for MT hydrofolate reductase and the role of folic acid in regulating homocysteine levels. Another aspect of Dr. Motulsky’s work is on the molecular genetics of color vision genes. Much heterogeneity was found in the molecular make-up of color vision pigment genes in individuals with normal and with defective color vision. The psychophysical perception of color is correlated with molecular gene arrangement.
By Claudia Dreifus, The New York Times – Among scientists, 84-year-old Arno Motulsky is known as the “father of pharmacogenomics.” In 1957, Dr. Motulsky, a medical doctor and researcher at the University of Washington, published an article reporting that two drugs had negative interactions with enzymes produced by certain human genes. Might this be true of other pharmaceuticals, Dr. Motulsky wondered? His question set off a revolution in research. Dr. Motulsky, who grew up Jewish in Nazi Germany, barely made his way out of wartime Europe and to safety in America.
Q. IN 1939 YOU BOARDED AN OCEAN LINER FROM HAMBURG TO CUBA WITH YOUR MOTHER, BROTHER AND SISTER. DID YOU EVER GET THERE?
A. We got as far as Havana harbor. Our ship was the S. S. St. Louis. The Cuban government had canceled the transit permits of most of the passengers — nearly a thousand refugees. We could not disembark.
Q. YOU MUST HAVE BEEN TERRIFIED.
A. I was 15. At that age, one tends to be optimistic. Many of the older men, they’d been in concentration camps and they had a better sense of what could happen. For days, appeals went out to the U.S. government to take us in. Then the Cubans ordered the St. Louis out of Havana harbor. The captain — who was a decent sort — sailed the ship up the Florida coast, hoping something would change. You could see Miami. Eventually, the St. Louis turned around for Europe. Our family was given asylum by Belgium. After a year in Brussels, we got our visas for America, but before we could leave, the country was overrun by the German Army.
Q. WERE YOU THEN INTERNED?
A. Yes, I was sent to a succession of camps in France. Though conditions were bad — hunger, typhoid — I always tried to know what was going on. I always tried to get a hold of newspapers, which was very difficult.
After many months, the Vichy French moved those internees with the possibility to emigrate to a special camp near Marseilles. We were allowed to visit consulates in the city. I spent much time at the American consulate, pleading for a renewal of my now-expired visa.
That came through right before my 18th birthday. So 10 days before I turned 18, I crossed into Spain. From there I went to Lisbon and eventually Chicago, where my father was. If my visa had taken any longer, I wouldn’t be here today because Franco had barred males over 18 from transiting through Spain; I would have ended up in Auschwitz, like most of the people I left behind.
Q. WHAT BECAME OF YOUR MOTHER AND SIBLINGS?
A. For two years, there was no news. In Brussels, they’d gotten orders to be “resettled in the East.” With the help of Belgian friends, they illegally crossed into Switzerland. We didn’t see them until 1946.
Q. HOW DID YOU BECOME A DOCTOR? THAT COULDN’T HAVE BEEN EASY FOR A PENNILESS REFUGEE KID.
A. I had a great piece of luck. When I was 20, I was drafted! The Army needed doctors for the war. They put me into a special program, where they sent me to Yale and later to medical school.
Q. HOW DID GENETICS BECOME YOUR SPECIALTY?
A. While at Michael Reese Hospital in Chicago, I met the hematologist Dr. Karl Singer, and he had all these modern ways of studying blood. That interested me. Because there are hereditary blood diseases, I soon became interested the genetic aspect of hematology.
Q. YOUR OBSERVATION IN 1957 ABOUT THE INTERACTIONS BETWEEN THE ENZYMES PRODUCED BY GENES AND SOME DRUGS — DOES IT PLEASE YOU TO SEE HOW IMPORTANT IT HAS BECOME?
A. Yes, because at first the idea was not well accepted. I remember going to an important pharmaceutical executive and I said, “I found a new way to find out about drug reactions.” And he kissed me off: “Drug reactions?”
Things also moved slowly for a long time because it was hard to test for this. But now, with the new DNA testing, you can do many things faster and better. And with the modern computerized genomics, you can even test for reactions to many different enzymes, all at the same time.
On the other hand, I think the promise of pharmacogenetics is sometimes overhyped. There are people who think we’ll be able to solve almost everything with an individualized prescription. We need more research, which will be expensive.
Q. WILL HEALTH INSURANCE PAY FOR DNA TESTING AND CUSTOM PHARMACEUTICALS?
A. That’s a problem. On the hopeful side, people say it may soon be possible to sequence a person’s genome for $1,000. Once they figure out low-cost ways to sequence the genome, the price of personalized medicine will come down.
Still, one shouldn’t be misled. What we know about the genome today is not enough for all the miracles many expect from this field. There’s a lot about what regulates the genes and how they interact that we still need to understand. We won’t have the answers by tomorrow.
Q. AT 84, YOU’RE STILL WORKING. WHAT ARE YOU TACKLING IN YOUR LABORATORY?
A. One project I’m very excited about relates to human color vision. About 8 percent of males have inherited red-green color blindness. This is caused by hereditary abnormalities in color sensitive pigments of the retinal cones in the back of the eyes, which are actually part of the brain. Our laboratory found that one-half of males with normal color vision had the amino acid alanine in their red pigment, while the other half all carried the amino acid serine, at the same site. This finding means that the same exact red color is perceived as a different type of red, depending on a person’s genetic makeup.
Q. WHAT’S THE POINT OF KNOWING THIS?
A. It’s exciting to learn that because of heredity, different people can see the same thing differently. I think this may prove useful in studying more complex brain functions. If this were 20 years ago, I’d focus on neurogenetics. What’s going on in the brain, that’s the last frontier.
Q. DO THE EXPERIENCES OF YOUR CHILDHOOD HAVE AN IMPACT ON YOUR LIFE AND WORK TODAY?
A. I often think about it. Whenever something good happens, I say to myself, “Look, you almost didn’t live to experience this.” When I see pictures from Africa, I think: “That could be me. I was once a refugee.”
- Drought in Africa reduced the world population into small, isolated groups, study says
- Separate study says number of humans may have fallen to 2,000
- Analysis: Humans banded together again in Stone Age, increased in numbers
Migrations out of Africa appear to have begun about 60,000 years ago
WASHINGTON (AP) — Human beings may have had a brush with extinction 70,000 years ago, an extensive genetic study suggests.
Geneticist Spencer Wells, says the study tells “truly an epic drama.”
The human population at that time was reduced to small isolated groups in Africa, apparently because of drought, according to an analysis released Thursday.
The report notes that a separate study by researchers at Stanford University estimated that the number of early humans may have shrunk as low as 2,000 before numbers began to expand again in the early Stone Age.
“This study illustrates the extraordinary power of genetics to reveal insights into some of the key events in our species’ history,” said Spencer Wells, National Geographic Society explorer in residence.
“Tiny bands of early humans, forced apart by harsh environmental conditions, coming back from the brink to reunite and populate the world. Truly an epic drama, written in our DNA.”
Wells is director of the Genographic Project, launched in 2005 to study anthropology using genetics. The report was published in the American Journal of Human Genetics.
Studies using mitochondrial DNA, which is passed down through mothers, have traced modern humans to a single “mitochondrial Eve,” who lived in Africa about 200,000 years ago.
The migrations of humans out of Africa to populate the rest of the world appear to have begun about 60,000 years ago, but little has been known about humans between Eve and that dispersal.
The new study looks at the mitochondrial DNA of the Khoi and San people in South Africa, who appear to have diverged from other people between 90,000 and 150,000 years ago.
The researchers led by Doron Behar of Rambam Medical Center in Haifa, Israel, and Saharon Rosset of IBM T.J. Watson Research Center in Yorktown Heights, New York, and Tel Aviv University concluded that humans separated into small populations before the Stone Age, when they came back together and began to increase in numbers and spread to other areas.
Eastern Africa experienced a series of severe droughts between 135,000 and 90,000 years ago, and researchers said this climatological shift may have contributed to the population changes, dividing into small, isolated groups that developed independently.
Paleontologist Meave Leakey, a Genographic adviser, asked, “Who would have thought that as recently as 70,000 years ago, extremes of climate had reduced our population to such small numbers that we were on the very edge of extinction?”
Today, more than 6.6 billion people inhabit the globe, according to the U.S. Census Bureau.
The research was funded by the National Geographic Society, IBM, the Waitt Family Foundation, the Seaver Family Foundation, Family Tree DNA and Arizona Research Labs.
Photograph by Becky Hale
Current Projects: The Genographic Project
Spencer Wells is a leading population geneticist and director of the Genographic Project from National Geographic and IBM. His fascination with the past has led the scientist, author, and documentary filmmaker to the farthest reaches of the globe in search of human populations who hold the history of humankind in their DNA. By studying humankind’s family tree he hopes to close the gaps in our knowledge of human migration.
A National Geographic Explorer-in-Residence, Wells is spearheading the Genographic Project, calling it “a dream come true.” His hope is that the project, which builds on Wells’s earlier work (featured in his book and television program, The Journey of Man) and is being conducted in collaboration with other scientists around the world, will capture an invaluable genetic snapshot of humanity before modern-day influences erase it forever.
Wells’s own journey of discovery began as a child whose zeal for history and biology led him to the University of Texas, where he enrolled at age 16, majored in biology, and graduated Phi Beta Kappa three years later. He then pursued his Ph.D. at Harvard University under the tutelage of distinguished evolutionary geneticist Richard Lewontin. Beginning in 1994, Wells conducted postdoctoral training at Stanford University’s School of Medicine with famed geneticist Luca Cavalli-Sforza, considered the “father of anthropological genetics.” It was there that Wells became committed to studying genetic diversity in indigenous populations and unraveling age-old mysteries about early human migration.
Wells’s field studies began in earnest in 1996 with his survey of Central Asia. In 1998 Wells and his colleagues expanded their study to include some 25,000 miles (40,000 kilometers) of Asia and the former Soviet republics. His landmark research findings led to advances in the understanding of the male Y chromosome and its ability to trace ancestral human migration. Wells then returned to academia where, at Oxford University, he served as director of the Population Genetics Research Group of the Wellcome Trust Centre for Human Genetics at Oxford.
Following a stint as head of research for a Massachusetts-based biotechnology company, Wells made the decision in 2001 to focus on communicating scientific discovery through books and documentary films. From that was born The Journey of Man: A Genetic Odyssey, an award-winning book and documentary that aired on PBS in the U.S. and National Geographic Channel internationally. Written and presented by Wells, the film chronicled his globe-circling, DNA-gathering expeditions in 2001-02 and laid the groundwork for the Genographic Project.
Since the Genographic Project began, Wells’s work has taken him to over three dozen countries, including Chad, Tajikistan, Morocco, Papua New Guinea, and French Polynesia, and he recently published his second book, Deep Ancestry: Inside the Genographic Project. He lives with his wife, a documentary filmmaker, in Washington, D.C.
Spencer Wells is risking life and limb to collect DNA from the most isolated, remote peoples on the planet. Five years, 100,000 samples, and 40 million dollars later, he’ll have a new road map to human history.
By Michael Shnayerson
WALKING THROUGH TIME: Spencer Wells, accompanied by a party of Bushmen, treks across a dry watering hole in northern Namibia.
Spencer Wells knows exactly where he wants to go next: the Tibesti mountains. He wants to fly to Libya, now that it’s open to Westerners again, then hail a camel caravan across the Libyan desert to Chad, where the seven inactive volcanoes of the Tibesti rise 11,000 feet (3,353 meters) from the central Sahara: a private world of crags and chasms seldom seen by more than a handful of outsiders. Like any intrepid traveler, he’s unfazed by the prospect of deadly North African windstorms and burning desert heat. The land mines near the border of Libya and Chad do pose a problem, but local guides can thread a path. As for the fierce and isolated Tubu, who’ve ruled the Tibesti long enough for Herodotus to have named them the Troglodytes, they’re the real payoff. Wells wants to learn their oral history, how their ancestors exacted tribute from traders passing to and from the Middle East, and what this crossroads reveals about one of Earth’s earliest cultures on the continent where all human life began. Then he wants to stick a cheek swab into each of their mouths to collect a generous gob of DNA-rich saliva.
Wells, 36, is a population geneticist using science in global pursuit of the greatest story not yet told: the story of how humankind traveled from its origins in Africa to populate the planet. The most telling clues lie with isolated, indigenous tribes like the Tubu, for their DNA remains, in a sense, the purest. Their unique genetic markers, characteristic mutations in a defined sequence of DNA, are like flags waving from the place their ancestors have inhabited for thousands of years—the starting point for ancient migrations. Any venturesome Tubu who crossed the Sahara to see the outlying world, and propagated in the process, passed on one or another of those genetic markers to his or her offspring. Any traveler who came through the Tibesti and intermarried did the same. Wells might take a cheek swab from an investment banker in Boston and find that same genetic marker: proof that one of those Tubu created a family line that leads, in some circuitous way, over continents and generations, from the Tibesti to an oak-paneled office in Back Bay. It’s in the hope of tracing myriad journeys such as this that Wells, a newly named National Geographic Explorer-in-Residence, is undertaking one of the most ambitious and expensive research adventures in the National Geographic Society’s 117-year history: the grandly named Genographic Project.
At a cost of 40 million dollars over five years, the brunt of it borne by National Geographic, IBM, and the Waitt Family Foundation, the Genographic Project under Wells’s direction is establishing 11 DNA-sampling centers around the world, with the goal of collecting 100,000 cheek swabs or blood samples from mostly indigenous peoples like the Tubu. A sense of urgency infuses the project: Year by year, at an ever quickening rate, the outside world is crowding in on, and at the same time absorbing, indigenous peoples. A Tubu who moves to Paris will still have the genetic markers that distinguish him as a Tubu, but the geographical context for his markers will be gone. As for the Tubu who remain in the Tibesti mountains, they may marry more with outsiders as modern technology makes contact more likely. Generation by generation, tracing the last routes of historical migration of such isolated people grows that much harder. Wells wants to map as many routes as he can while their geographical origins are relatively intact.
Wells has a nifty and novel idea to help fund and publicize the project. “We’re taking this directly to the people,” he declares. “Because in addition to doing this work with indigenous populations, we’re going to be offering for sale to the public, in the developed world mostly, the opportunity to do this cheek-swab test to see how they fit into the family tree.” For about a hundred dollars, a contributor gets his or her very own cheek-swab kit along with a map of migratory routes, as Wells has charted them thus far, that is like an explorer’s parchment map of the New World. “Because these participation kits are totally anonymous, there’s no way anyone can find out anything about your history except you,” Wells says. “Once the results are ready, you can access the Web site (www.nationalgeographic.com/genographic
) for extensive details about genetics, archaeology, history, and the context for genetic variation. Your sample, if you choose, can be put into our database, so that it adds to this increasing data set about genetic variation all over the world. But when you purchase your cheek-swab kit, you’re also funding research, and part of the money will be channeled back to taking samples from the 100,000 people.”
For a man just weeks from the public announcement of this global gambit, Wells is forgivably a bit tense on an early spring day in his fourth-floor office at National Geographic’s Washington, D.C., headquarters. Ruddy and fit—a whole lot more fit than your typical laboratory-bound scientist—he radiates a steely cool, like a field marshal on the eve of battle. The inevitable layman’s queries about genetics elicit crisp details about mitochondrial DNA and Y chromosomes in gleaming, perfectly formed paragraphs. Most of us talk in analog; Wells is digital. Only a framed picture on the shelf suggests that not all goes according to plan. Wells’s two young daughters are with their mother in Geneva; a divorce is under way. For ten years of fieldwork around the world, Wells is paying a human toll.
To Wells, the Genographic Project is a perfect double helix of history and science, the origins of which trace, for him, to a university science lab in Lubbock, Texas, which became a second home when he was all of nine years old. That was when Wells’s mother, a professor at Texas Tech University’s medical school, took time off to earn a Ph.D. in biology and let her son hang out while she performed her experiments. The same year, 1979, Wells was also strongly influenced by English polymath James Burke’s ten-part television series Connections, with its anecdotal braiding of science and history. After earning a B.S. in biology at 19, Phi Beta Kappa, from the University of Texas at Austin, Wells took his own Ph.D. at Harvard University in evolutionary genetics—the historical side of the science, as he says—and studied fruit flies with world-renowned population geneticist Richard Lewontin.
Fruit flies had served as an ideal test case since the early 20th century, when Thomas Hunt Morgan used them in his Fly Room at Columbia University to show how chromosomes worked, to prove that chromosomes were made up of genes, and to show how genes were passed down. But at the end of the day, Wells says, “I’m not that interested in fruit fly history. But I am interested in human population history. I wanted to apply some of those methods to human history.”
“What I appreciate about Spencer is that he is not the kind of scientist who is only interested in his favorite molecule or DNA mutation,” says fellow geneticist and Genographic Project coordinator Lluis Quintana-Murci of the Pasteur Institute in Paris. “Many scientists tend to be closed off in their little rooms. He always had much broader interests—human biology and history. And he uses genetics as a tool to unravel the past.”
For that, Wells went to Stanford University to work with the “grand old man” of human population genetics, Luca Cavalli-Sforza, who is now a chairman of the Genographic Advisory Board. He wanted to learn what the bold new field of genome sequencing—identifying every gene in a living thing and mapping its relation to every other gene—could do for tracing human history.
For years, scientists had studied blood for genealogical clues. Blood characteristics suggested the different cultures of a family tree. But blood was little help for telling when a Middle Eastern people, say, might have migrated to western Europe and intermarried. What the scientists needed, Wells says, was a clock.
That clock came in the form of DNA. The seemingly endless ribbons of DNA found in human hair, saliva, blood—any cell in the body—are made up of three billion individual units, known as A, C, G, and T. Subtle variations in that sequence are what genetically distinguish one person from another. As incredibly able as the human system is at replicating each unique sequence from one generation to the next, a small number of variations, or mutations, do occasionally crop up. By analyzing specific regions of the DNA, comparing the results to known reference sequences, and identifying differences that are anthropologically significant, geneticists are able to track mutations.
“They’re like spelling mistakes,” Wells says. “Imagine you’re copying a very long document, and occasionally you’ll put an A where there should be a C. And that mistake has been translated down through the generations, and more mistakes have accumulated. So the longer the lineage has been in existence, the more mistakes the sequence is going to have. And if you know the rate at which those mistakes occur, you can actually estimate how long this individual has been evolving since that origin, how long his DNA has been accumulating changes.”
Initially Cavalli-Sforza’s team focused on something called mitochondrial DNA—a good choice because it appears frequently in the cell, so it’s easy to find and track. “It’s effectively the remnant of a bacteria that became engulfed by the cell about a billion years ago,” Wells explains. “And all higher organisms have these structures in their cells.” As Cavalli-Sforza’s group knew, mitochondrial DNA is inherited strictly maternally. A mother passes it to her son, but the son can’t pass it on. Only from mother to daughter does it keep descending, generation to generation. In most African tribes, women did the traveling, mostly to find mates, while the men stayed put. So the story that mitochondrial DNA told was only half of the story. Cavalli-Sforza’s geneticists needed a piece of male DNA they could study to prove their theory of African origins and migration. That was when the team’s researchers began studying variations in the Y chromosome, which is passed down from fathers to sons and had, up until then, been a maddeningly inscrutable bit of DNA.
By studying how mutations had accumulated in both mitochondrial DNA and Y chromosomes and determining the rate at which those mutations occur—like counting tree rings—the geneticists made a dramatic conclusion: The populations with the greatest number of mutations were in sub-Saharan Africa. They had the oldest living lineages, which meant they were, beyond the shadow of a genealogical doubt, directly related to the earliest of our traceable ancestors. Their DNA marked the spot where humankind began.
Archaeology had suggested this, of course. But what the geneticists saw from their DNA sequencing of current-day Africans is that their ancestors appeared to have lived as the only humans on Earth as recently as 60,000 years ago. That was when they started migrating, taking their genetic mutations with them, and passing them down. Why did they leave when they did? Because 10,000 years before that, one of the Pleistocene epoch’s worst cold snaps nearly drove humankind to extinction, and these were the survivors, whose better brains made them more adaptable.
If Steven Spielberg were making the movie, a fur-garbed posse of these plucky migrants—the first adventure travelers!—would set off together at dawn across the savanna, covering miles each day in search of fresh prey. In fact, the “Great Leap Forward,” as anthropologist Jared Diamond puts it (in a facetious borrow from Mao Zedong), probably occurred less than 10,000 years ago. The intellectual leap, Diamond and Wells contend, came first: A few children born with higher intelligence and better communication skills, capable of fashioning better tools, passed their superior genes to offspring who came to dominate their clans.
Smarter humans learned to hunt certain species. As those species migrated a few miles every year or so, or died out on the clan’s home turf, the hunters pursued them. Drought accelerated these trends by causing animals to disperse more widely. Eventually, a few migrants reached the Indian Ocean and adopted a fishing life. Little by little, they migrated north up Africa’s east coast. Some traversed the Red Sea—perhaps on simple log rafts. Others headed farther north to the Mediterranean. By 45,000 years ago, as garbage dumps from the time attest, hunters with relatively sophisticated tools were ensconced on the Mediterranean’s shores, engaged in art and other shows of complex culture, and curious about the unknown lands that lay before them in every direction.
Wells wanted DNA samples to fill in this tantalizingly sketchy picture of humankind’s origins. Where had the first of those migrating Africans gone? What routes had they taken, in just tens of thousands of years, to populate the rest of the world?
Following different routes out of Africa, successive waves of early humans migrated into new territories, eventually populating the entire globe save Antarctica. This map shows this complex web of migrations in their broadest strokes. Maps by Joyce Pendola.
Somewhere between 80,000 and 50,000 years ago, Africa saved Homo sapiens from extinction. Charting the DNA shared by more than six billion people, a population geneticist—and director of the Genographic Project—suggests what humanity “owes” its first home.
by Spencer Wells
Guest editor Bono as a toddler, circa 1961, with maps showing the migrations of his matrilineal (top) and patrilineal ancestors (middle), based on analysis of his DNA. His father’s ancestors were among the first modern humans to enter Europe. Courtesy of the Hewson family.
Do you think you know who you are? Maybe Irish, Italian, Jewish, Chinese, or one of the dozens of other hyphenated Americans that make up the United States melting pot? Think deeper—beyond the past few hundred years. Back beyond genealogy, where everyone loses track of his or her ancestry—back in that dark, mysterious realm we call prehistory. What if I told you every single person in America—every single person on earth—is African? With a small scrape of cells from the inside of anyone’s cheek, the science of genetics can even prove it.
Here’s how it works. The human genome, the blueprint that describes how to make another version of you, is huge. It’s composed of billions of sub-units called nucleotides, repeated in a long, linear code that contains all of your biological information. Skin color, hair type, the way you metabolize milk: it’s all in there. You got your DNA from your parents, who got it from theirs, and so on, for millions of generations to the very beginning of life on earth. If you go far enough back, your genome connects you with bacteria, butterflies, and barracuda—the great chain of being linked together through DNA.
What about humanity, though? What about creatures you would recognize as being like you if they were peering over your shoulder right now? It turns out that every person alive today can trace his or her ancestry back to Africa. Everyone’s DNA tells a story of a journey from an African homeland to wherever you live. You may be from Cambodia or County Cork, but you are carrying a map inside your genome that describes the wanderings of your ancestors as they moved from the savannas of Africa to wherever your family came from most recently. This is thanks to genetic markers—tiny changes that arise rarely and spontaneously as our DNA is copied and passed down through the generations—which serve to unite people on ever older branches of the human family tree. If you share a marker with someone, you share an ancestor with him or her at some point in the past: the person whose DNA first had the marker that defines your shared lineage. These markers can be traced to relatively specific times and places as humans moved across the globe. The farther back in time and the closer to Africa we get, the more markers we all share.
What set these migrations in motion? Climate change—today’s big threat—seems to have had a long history of tormenting our species. Around 70,000 years ago it was getting very nippy in the northern part of the globe, with ice sheets bearing down on Seattle and New York; this was the last Ice Age. At that time, though, our species, Homo sapiens, was still limited to Africa; we were very much homebodies. But the encroaching Ice Age, perhaps coupled with the eruption of a super-volcano named Toba, in Sumatra, dried out the tropics and nearly decimated the early human population. While Homo sapiens can be traced to around 200,000 years ago in the fossil record, it is remarkably difficult to find an archaeological record of our species between 80,000 and 50,000 years ago, and genetic data suggest that the population eventually dwindled to as few as 2,000 individuals. Yes, 2,000—fewer than fit into many symphony halls. We were on the brink of extinction.
And then something happened. It began slowly, with only a few hints of the explosion to come: The first stirrings were art—tangible evidence of advanced, abstract thought—and a significant improvement in the types of tools humans made. Then, around 50,000 years ago, all hell broke loose. The human population began to expand, first in Africa, then leaving the homeland to spread into Eurasia. Within a couple of thousand years we had reached Australia, walking along the coast of South Asia. A slightly later wave of expansion into the Middle East, around 45,000 years ago, was aided by a brief damp period in the Sahara. Within 15,000 years of the exodus from Africa our species had entered Europe, defeating the Neanderthals in the process. (Neanderthals are distant cousins, not ancestors; our evolutionary lineages have been separate for more than 500,000 years.) We had also populated Asia, learning to live in frigid temperatures not unlike those on the Moon, and around 15,000 years ago we walked across a short-lived, icy land bridge to enter the Americas—the first hominids ever to set foot on the continents of the Western Hemisphere. Along the way we kept adapting to new climates, in some cases lost our dark tropical skin pigmentation, developed different languages, and generated the complex tapestry of human diversity we see around the world today, from Africa to Iceland to Tierra del Fuego. But the thing that set it all in motion, the thing that saved us from extinction, happened first in Africa. Some anthropologists call it the Great Leap Forward, and it marked the true origin of our species—the time when we started to behave like humans.
Africa gave us the tool we needed, in the form of a powerful, abstract mind, to take on the world (and eventually to decode the markers in our DNA that make it possible to track our amazing journeys). Perhaps just a few small genetic mutations that appeared around 50,000 years ago gave humans the amazing minds we use to make sense of the confusing and challenging world around us. Using our incredible capacity to put abstract musing into practice, we have managed to populate every continent on earth, in the process increasing the size of our population from a paltry few thousand to more than six billion. Now, 50 millennia after that first spark, times have changed. A huge number of things have contributed to Africa’s relative decline on the world stage, perhaps most important geography. As Jared Diamond describes in his masterly book Guns, Germs, and Steel, Eurasia, with its East-West axis, allowed the rapid latitudinal diffusion of ideas and tools that would give its populations a huge advantage after the initial leap out of Africa. Couple that with the results of colonial exploitation over the past five centuries, and Africa, despite many strengths and resources, is once again in need, as it was 70,000 years ago. This time, though, things are different.
The world population that was spawned in Africa now has the power to save it. We are all alive today because of what happened to a small group of hungry Africans around 50,000 years ago. As their good sons and daughters, those of us who left, whether long ago or more recently, surely have a moral imperative to use our gifts to support our cousins who stayed. It’s the least we can do for the continent that saved us all thousands of years ago.
For more about the Genographic Project, visit nationalgeographic.com.
Dr. Spencer Wells is explorer-in-residence at the National Geographic Society and the director of the Genographic Project.
American Institute For Cancer Research
Calls on Americans to Slash Red Meat Consumption
Typical US “Meat-and-Potatoes” Eating Pattern Increases Risk, Say Cancer Experts
What about processed meat?
The AICR Expert Report found that processed red meat (like ham, sausage, bacon and cold cuts) raises risk for colorectal cancer by 42 percent for every 3.5 ounces (100 g) eaten per day, an even greater increase than that associated with regular red meat.
In fact, although evidence suggests it is possible to eat as much as 18 ounces of red meat per week without increasing risk, the AICR report found no such “safe zone” for processed meat.
That’s why the AICR Expert Panel advises avoiding processed meat. Enjoy it on special occasions – a ham at Easter, a hot dog at a ballgame – but making it part of your everyday diet is not a good idea.
April 2008, WASHINGTON, D.C. – Experts at the American Institute for Cancer Research (AICR) say Americans can’t afford to wait any longer to make a cancer-protective shift in their eating habits. The evidence linking red meat to colon cancer is now so strong it should prompt a nationwide reduction in red meat consumption, they said.
AICR’s landmark report, Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective concluded that the scientific evidence linking red meat (beef, pork and lamb) to colorectal cancer is now convincing. Accordingly, the expert panel who authored the report issued a recommendation to limit consumption of red meat to no more than 18 ounces (cooked) per week and avoid processed meat.
Many Americans eat far greater amounts of red meat per week. Consider a person who often chooses eggs with two sausage links (2oz) for breakfast, or a quarter-pound fast food burger (4oz) at lunch, or a pork chop (6oz) or two for dinner. This person is likely to far exceed the recommended 18 ounces per week.
If such a person eats lunch or dinner at restaurants several times a week, it becomes even more difficult to keep consumption in check. Today, many restaurants offer 9 to 12 ounce servings of steak or roast beef and often compete for business by inflating portion sizes even more.
Cancer experts are asking Americans to assess the amount of red meat they typically eat and substitute poultry or fish more often, or simply increase the amount of meatless meals they enjoy in a given week.
“The meat-and-potatoes mindset is slowly killing us,” said AICR Nutrition Advisor, Karen Collins, MS, RD. “We need to break ourselves of the notion that we need a hunk of red meat at every meal.”
Collins noted, however, that some Americans are just a few ounces over the recommended weekly amount. These individual can start eating for lower cancer risk simply by substituting a hearty vegetable chili and salad for a hamburger at lunchtime, or preparing poultry or fish instead of steak for dinner two nights a week.
Report: Risk Rises with Increased Consumption
According to the AICR report’s analysis of the collected evidence, every 3.5 ounces (100 g) of red meat eaten per day increases risk for colorectal cancer by 30 percent.
What is alarming about this increased risk, Collins said, is the real-world impact that 30 percent figure takes on once its effects are felt across the entire population of the world. “Smokers are a subset of people whose chosen habit places them at much higher risk for lung cancer, but this is different. Everybody eats,” she said. “And everybody who eats a diet high in red meat is at a higher risk of colon cancer, whether they know it or not.”
Given the huge number of people involved, the effect of red meat consumption on colon cancer incidence is immense, Collins said. “If there were a drug that was found to increase risk of a disease by 30 percent, it would get pulled off the shelves.”
AICR is not calling for the elimination of meat from US diets. Instead, the cancer experts are urging Americans to recognize that cutting back on how much red meat they eat every week is an important, cancer-protective step.
Awareness of Meat-Cancer Link Surges, But Will U.S. Diets Change?
Prior to release of the AICR expert report in November 2007, only 36 percent of Americans were aware that diets high in red meat are a cause of cancer, according to an AICR telephone survey of 1022 US adults. Upon its publication, the AICR expert report received a great deal of media and scientific attention. It was also the subject of aggressive statements from the meat industry seeking to discredit the recommendation, which raised the report’s public profile even further.
That furor seems to have had a lingering impact on public awareness. Five months after the November release of the report, AICR has resurveyed Americans on their awareness of the red meat-cancer link. According to this follow-up survey of 1,008 US adults, public awareness that red meat is a cause of cancer has jumped by 18 percentage points, to 54 percent.
According to government statistics, a gradual shift away from red meat has been underway in the U.S. for decades. The USDA’s Economic Research Service reports that the average American’s annual consumption of beef has decreased by nearly 14 pounds (224 ounces) since 1970.
That decrease was likely sparked by public education campaigns that focused on the fat content of red meat and the effect it has on health, such as increasing the risk of heart disease. Collins noted that although choosing lean cuts does play a protective role in heart health, diets high in red meat – no matter its fat content – increase risk for colorectal cancer.
AICR’s new brochure The Facts About Red Meat and Processed Meat gives practical, everyday advice for making a cancer-fighting transformation to your diet and provides more information on the science behind the meat-cancer link. The brochure can be read, ordered, or downloaded at www.aicr.org/redmeat. Or call 1-800-843-8114, extension 466, between 9:00 a.m. and 5:00 p.m. ET, Monday through Friday, for a complimentary single copy.
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The American Institute for Cancer Research (AICR) is the cancer charity that fosters research on the relationship of nutrition, physical activity and weight management to cancer risk, interprets the scientific literature and educates the public about the results. It has contributed more than $86 million for innovative research conducted at universities, hospitals and research centers across the country. AICR has published two landmark reports that interpret the accumulated research in the field, and is committed to a process of continuous review. AICR also provides a wide range of educational programs to help millions of Americans learn to make dietary changes for lower cancer risk. Its award-winning New American Plate program is presented in brochures, seminars and on its website, www.aicr.org. AICR is a member of the World Cancer Research Fund International.
3 cups fat-free, reduced-sodium chicken stock or broth
1 small green zucchini squash in 1/2- inch dice
6 thin asparagus stalks, cut in 1/2-inch pieces, tips reserved
1 medium carrot, halved lengthwise and thinly sliced
1 Tbsp. extra-virgin olive oil
1 cup finely chopped Spanish onion
1 cup Arborio rice
2 tsp. lemon juice, preferably fresh
1 small garlic clove, minced
1/2 cup fresh or frozen baby green peas
1/4 cup chopped flat-leaf parsley
1 Tbsp. low-fat yogurt
2 Tbsp. grated Parmigiano-Reggiano cheese
Mrs. Dash for seasoning
- Heat the chicken stock to boiling. Set it aside.
- Place zucchini in a large bowl. Add asparagus and carrots.
- Heat oil in deep saucepan over medium-high heat. Add onion and garlic and saute until translucent, about 2 minutes. Mix in rice until coated with oil and opaque, about 1 minute. Add lemon juice, stirring until rice is almost dry, less than 1 minute. Mix in half the chopped vegetables. Cook one minute.
- Add hot broth, a half-cup at a time, stirring well after each addition. Cook, stirring continually, until rice is almost dry before adding more broth. When most of the broth has been used and rice is almost done but has a hard core, about 15 to 18 minutes, add remaining vegetables and parsley. Add the last of the broth and cook until rice is tender but still al dente, about 3 to 4 minutes. Stir in yogurt and cheese. Season with Mrs. Dash.
- Remove pot from heat. Serve immediately.
1 head cauliflower, broken into small florets
1/2 cup safflower oil
1/2 pound fresh mushrooms, cleaned and sliced
1 to 3 onions, sliced
1/3 cup blanched slivered almonds
2 teaspoons chicken bouillon
1 1/2 tablespoons cornstarch
1 cup water
- Heat one inch of water to a boil in a saucepan over medium-high heat. Add cauliflower florets, and cook covered for 7 to 9 minutes, or until tender. Drain and set aside.
- Pour oil in a large skillet over medium heat. Saute mushrooms, onion, and almonds. Stir in the chicken bouillon. Dissolve the cornstarch in water, and gradually stir into the mushroom mixture. Cook until thickened. Pour the mushroom mixture over the hot cauliflower, and serve.