The truth is that you can get started on a fantastic fitness regimen in only an hour a week. Further, a focused writer can create a novel in a year in only an hour a day. And gigantic strides can be made toward stress relief in only five minutes a day. THAT is the playing field: give yourself five minutes, and you can cut your stress in half. Give yourself an hour a week, and you can have health and fitness. An hour a day can jump-start a career.

1) Five Minutes a day. Five times a day, for just sixty seconds, stop and breathe slowly and deeply from your belly. Go to a local yoga or Tai Chi school and ask to learn a relaxation breathing technique. If you can’t find one, then slow down, get quiet, and feel your heartbeat for sixty seconds. Do this every three hours for sixty seconds, and you will halve your stress levels.

2) An hour a week. Three times a week, perform twenty minutes of the right body-weight or weight exercises. Hindu Squats and Hindu Pushups are wonderful whole-body exercises. Do a Google search for them, and you’ll find multiple sites on the Internet selling or giving away the information for free. For faster results, use “Kettlebell” style whole-body weight exercises. These exercise tools look like little cannon-balls with handles, and they are used in a variety of swinging and yoga-like moves that are unbelievably efficient for developing strength, endurance, flexibility, power and athleticism, all at the same time. You can even use an ordinary dumbbell in the beginning. Again, do a Google search, and you’ll find the information, often for free!

3) An Hour a day. This is what I call the “Golden Hour.” You need to accept the idea that one hour out of every day belongs to you. Not your job, not your husband or wife, or your kids—it belongs to you. During this time, if you plan it properly, you can exercise, practice your art, meditate, read—whatever. If you are a writer, I’d suggest that Monday, Wednesday, and Friday, you “flow”—just create rough draft, with no attempt to edit it. Tuesday, Thursday, and Saturday you do your editing, polishing the work you did the previous day. If you learn to focus properly, there is no reason in the world you can’t learn to produce 1000 words of rough draft in an hour. That’s enough to produce a novel a year, in just an hour a day.

The “Golden Hour” is a goal, one that might take you a year or two to work toward. But if you will just start with five minutes a day, and a commitment to an hour a week…working TOWARD an hour a day, you have placed your feet on the road toward peace of mind, a healthy body, and a happy heart: a tiny investment for a gigantic reward.

About the Author: NY Times Bestselling Writer Steven Barnes has published over three million words, and is the creator of Lifewriting, the first high-performance system for writers (www.lifewrite.com). He combines this with Scott Sonnon's break-through technology to create The Path, a radical mind-body success system that provides all basic fitness and meditation requirements in only one Golden Hour a week! Join us in Los Angeles on June 24th. Learn more at www.Rmax.tv

www.lifewrite.com

Steven Barnes is a NY Times bestselling author, personal performance coach, and martial artist who has written for The Twilight Zone, The Outer Limits, and Stargate SG-1. He has lectured on story and human consciousness at UCLA, Mensa, the Smithsonian Institute, and USC. Steve created the Lifewriting system of high-performance living for writers and readers. www.lifewrite.com

"I've had three heart attacks, two heart surgeries. I have chronic headaches, chronic upper respiratory infections. I get pneumonia two or three times a year," she said. "I have chronic fatigue, joint aches, muscle aches. I have a rash that migrates all over my body."

Sterry figures the initial symptoms began in Saudi Arabia in September of 1991 while she was serving with the National Guard. Three years later, after completing her tour of duty and coming back home, the symptoms were still there, but much more severe.

State Sen. Gayle Slossberg said one of the sources of the diseases may be depleted uranium. She was one of those who helped pass legislation last year setting up a health registry in Connecticut, strictly to keep records on our military personnel.

"We'll know where they've served, what they've done, what the scope of the job was," she said. "We'll be able to identify to some extent what they've been exposed to and what their symptoms are."

But it will come too late for David Leighton, of Naugatuck, a Marine who served in Saudi Arabia in Desert Storm. When he came home, the symptoms he had had for quite some time would not go away.

His mother, Gail Leighton, said that for the next 15 years, she saw her once vital and vibrant son slowly dying before her eyes.

"You would have had to have been there during the journey and see him in bed and sweating and in agony," she said.

She said her son was a patriot, that his dad had been a Marine. She said the federal government did not believe that those coming back became sick because of the conditions in which they served.

"That was the hardest part, I think, more than anything, to have the DOD, the Department of Defense, and the VA spending so much time and energy trying to deny and discount and discredit some of the people who were doing research."

State Veterans Commissioner Linda Schwartz told NBC 30 that making the connection between battlefield exposures and diseases has been a long, ongoing process.

She said the use of depleted uranium has to be studied because, as she put it, we're sending our best people into battle and their well-being must be the top priority.

Behind the Fetal Cell Research

For those of you who want to know a little more about these fetal cells, I should say, first: Dr. Kirby Johnson works at the Tupper Research Center (supported by Mr. Tupper of Tupperware fame, for those of you who like sealed plastic containers) at Tufts University.

He works very closely with Diana Bianchi, chief of genetics at the New England Medical Center in Boston. Bianchi did some of the pioneering research that discovered that moms carry fetal cells in their blood for years and years.

Carol Artlett has a lab at Thomas Jefferson University in Philadelphia and works with Sergio Jimenez there.

There's another fellow, Lee Nelson at the Fred Hutchinson Cancer Research Center in Seattle, who has also studied these cells.

Also, just to be honest and fair, there are more than two hypotheses being investigated by all these scientists.

Yes, there is the "Good Hypothesis": that the cells stay in the mom and try to protect her for the rest of her life.

And yes, there is the "Bad Hypothesis”: that the cells gather at inflammation sites and contribute to mom's autoimmune diseases.

But there is also a third hypothesis: that the cells stay in mom all her life and do… nothing. This is the "Bystander Hypothesis": that the cells float around, hang out, rubberneck when at sites where mom gets ill, but neither help or hurt. This third hypothesis has not been disproved, meaning it's still in contention.

Finally, the big question right now is, can scientists find evidence that fetal cells are actually doing repairs when mom is stricken?

It's not a far-fetched idea. These cells may behave like those famous embryonic cells: They can turn themselves into any cell mom needs.

If she's got a bad heart, they can be healthy heart cells.

Bad lungs? No problem, they can be lung cells. Fetal cells may be the ultimate repairmen (or repairwomen).

A cautionary note: The anecdote I mention in the story, about the 30-year-old woman who has liver trouble and seems to heal herself, is not proof of the Good Hypothesis. There are no published studies that definitively show baby cells floating to, say, a liver cancer site and then turning themselves into healthy liver cells. That's the hunch. That's the theory. But we have no hard data -- not yet.

But everybody I talked to is whispering that something like repair is what they are seeing in mice and in humans. Carol Artlett comes right out and says so in our story.

But so far, it's very, very preliminary, and in her mind -- and everybody else's I talked to -- it's too early to know if baby cells are really repairing moms. They hope so. But hope is not proof and these folks are too professional to get ahead of their evidence.

And finally, I want to thank my friend Jonah Lehrer for suggesting this idea to me; he's a wonderful science reporter and a font of fascinating ideas, which he (stupidly) shares with me. And -- since we're all here sharing -- here's what I'd like to know:

If fetal cells really are helping moms, I wonder if women who have babies (and abortions and miscarriages) tend to live longer than women who do not conceive. After all, the Conceivers have an extra gang (the more conceptions, the bigger the gang) of helpful cells inside.

Maybe there's some measurable consequence. And if the Good Hypothesis turns out to be true and every child leaves a posse of good soldiers in their mothers, then no matter how crummy we are to our moms, we are, willingly or unwillingly, still doing something nice for her -- on the inside.

It was hormones that drew Judith Campisi to study science: her own hormones, that is. “I went to an all-girl Catholic high school,” she laughs, “and I decided I’d had enough of the girls. I wanted to be where the boys were, and the boys were in the sciences.” But it was the excitement of lab life that kept her there. “Science is always challenging, it’s never dull,” says Campisi, now a researcher at the Lawrence Berkeley Labs and the Buck Institute for Age Research.

“She’s an outstanding scientist,” says Art Pardee, Campisi’s postdoctoral advisor, of the Dana-Farber Cancer Institute and Harvard Medical School. In Pardee’s lab, Campisi examined the cell-cycle profiles of cancer cells and their normal counterparts. One experiment involved labeling cells with thymidine to track their replication and then collecting samples for several days. “Judy was a machine,” recalls Estela Medrano of the Baylor College of Medicine in Houston, who worked alongside Campisi at the time. “She brought in her sleeping bag and spent nights working in lab and then slept for a few hours during the day.”

“I have no circadian rhythm,” jokes Campisi, who still has no problem laboring through the wee hours when there’s work to be done. Her diligence has paid off. “Her career has been sprinkled with one key paper after another,” says Ron DePinho, also at Dana-Farber. A large portion of those papers focus on an exploration of cellular senescence, a condition in which aged cells cease to divide. Campisi was the first to identify an enzyme marker unique to senescent cells, a discovery she used to show that these replicatively exhausted cells accumulate in aging organisms, including humans. “Judy really is one of the first to bring rigorous biological thinking to the phenomenology of aging,” says DePinho. “She thinks on the molecular, cellular, and organismal levels and is able to integrate all that information to clarify and address important questions in aging.”


HEEDING THE HAYFLICK LIMIT

Following her stint in Pardee’s lab, Campisi took her studies of the molecular underpinnings of cancer to nearby Boston University, where she’d accepted a position as an assistant professor. There she was approached by fellow faculty members Rich Miller and Barbara Gilchrist. Miller was hoping to study T cell changes with age, while Gilchrist was studying aging skin. They proposed that Campisi study senescence. “They said there’s this weird phenomenon where [cultured] human cells divide for a certain amount of time and then stop. And some people think that has to do with aging.”

“When I presented the idea to her, she looked at me as though I was crazy,” recalls Miller, now at the University of Michigan, Ann Arbor. Campisi felt that replicative senescence – first observed in cultured human cells by Leonard Hayflick, then at the Wistar Institute – had nothing to do with aging. “Barbara and I agreed with her,” says Miller. “But we told her to pretend it had something to do with aging for the duration of the site visit.” Even if senescence did not drive the aging of tissues or organisms, they reasoned, it might provide a powerful mechanism for the prevention of cancer: A cell that won’t proliferate cannot form a tumor or become malignant and colonize other tissues.

“That sounded fascinating,” says Campisi, who chose to play along. That decision would change the course of her career. “We got the grant,” says Miller, and Campisi turned her attention to senescence. “And the more she got into it, the more she became convinced that we had all been wrong,” says Miller, “that [senescence] had something to do with aging after all.” Perhaps the strongest evidence, published when Campisi moved to the West Coast, was her demonstration that senescent cells not only exist in vivo but also accumulate in aging tissue. What’s more, she and her colleagues have found that in culture, these nonreplicating cells are far from inert. They produce a plethora of unpleasant proteins that can, among other things, destroy the structural integrity of the tissue that surrounds them.

The ultimate experiment, however, has yet to be conducted. “The critical test would be to create an organism in which you prevent senescent cells from accumulating,” says Campisi. She and her colleagues are working on devising a system to do that test. They are developing a mouse in which an inducible promoter allows them to activate a gene that will selectively eliminate senescent cells.

Whether senescent cells contribute to aging, notes Miller, “is the kind of scientific question that most people in the field decided not to pay attention to and hoped others would stop asking.” But Campisi thrives on attacking such puzzles. Take, for example, the observation that mouse cells and human cells behave differently in culture. Normal human fibroblasts divide maybe 50 or 60 times before they senesce; mouse cells, on the other hand, divide 5 or 10 times and then either die or become transformed.

“People had known about that phenomenon for 20 years and sort of ignored it,” says Miller. Campisi investigated and found that mouse cells are more sensitive to oxidative damage than human cells and that the oxygen concentration used in the typical incubator (about 20%) is more than mouse cells can handle. The observation raises a tantalizing possibility, says Campisi: “One of the reasons why mice live so much shorter and develop cancer much more readily than humans is because they’re much more oxygen sensitive.”


THE CANCER CONNECTION

At the same time, Campisi has also done more extensive work to shore up the connection between senescence and cancer. In experiments in tissue culture and in mice, she finds that proteins produced by senescent fibroblasts, including proteases, growth factors, and even molecules that promote angiogenesis can fuel malignancy, encouraging premalignant cells to become fully cancerous and form tumors that can kill an animal. “That was a very important observation,” notes DePinho. “Advancing age is, far and away, the most important of all carcinogens, and understanding why that is has been one of the central questions in the aging field.”

In addition to confronting such questions, Campisi spends a good deal of her time mentoring young scientists and advising friends and colleagues. “I always rely on Judy when I have something to publish,” says Medrano. “I get her opinion about our ideas and ask if we were rigorous enough before I submit the paper.”

Campisi offered career advice to Gordon Lithgow, now her neighbor at the Buck Institute, when he met her in a cab as a postdoc attending an aging conference. “Judy was one of my heroes, and she couldn’t have been nicer,” he says. “It was amazing to have someone you held in such high regard trying to get to know your science and where you want to go with it.” And it wasn’t just Lithgow. “She’s incredibly supportive of junior scientists,” he says, particularly those who’ve trained in her lab.

Campisi not only allows postdocs to take their projects with them when they set up their own labs, a situation that former postdoc Pierre-Yves Desprez found “amazing,” but she also continues to offer all sorts of support. When Desprez was setting up his lab at the California Pacific Medical Center in San Francisco, he often called Campisi to talk through problems or ask for advice. “Even if she was saturated with work,” he says, “she never told me ‘No, I don’t have time.’ Never.”

When Junko Oshima, another former postdoc, was trying to clone the gene responsible for Werner syndrome, Campisi sent cell lines and a cDNA library. “Today you can make a cDNA library with a kit. But in those days, 15 years ago, building a cDNA library was itself a project,” says Oshima, now at the University of Washington in Seattle. “When I found that gene, the first person I phoned was Judy,” she says. “To this day she’s like my mother. I think a lot of people feel that way. She takes care of people very well after they leave.”

In her spare time, Campisi jets off to meetings, where she harvests information to share with her colleagues and collaborators. “She always comes back with tasty tidbits,” says Lithgow. “She just loves the science so much and doesn’t like to see people wasting their time because of lack of knowledge.”

Being a “major node in this information network,” says Lithgow, helps Campisi to navigate her way through the complicated matrix of molecular and cellular interactions that drive organismal aging, a task that is likely to keep her busy for years to come. “It’s a mistake to imagine that the process is so simple that we’re going to find the aging gene or the aging pathway or the magic bullet to postpone all aging,” says Campisi. “But I wouldn’t be working on aging if I thought it was so hopelessly complex that we’ll never understand it.”