By Jessica Snyder Sachs, as originally appeared in National Wildlife

ON A MISTY MORNING IN SPRING 2008, federal biologist Jack Jeffrey was leading a class of middle schoolers up the eastern slope of Mauna Kea, beneath the towering koa and 'ōhi'a trees of Hakalau Forest National Wildlife Refuge on the Big Island of Hawai'i. The students had just spent two days in Hakalau's greenhouse, tending seedlings of endangered plants being readied for planting in the upper areas of the refuge's nearly 33,000 acres, which stretch from 2,500 to 6,500 feet above sea level.

The reward for their hard work was a morning birding adventure in the refuge, an ideal spot for such an outing. The U.S. government established Hakalau in 1985 specifically to protect 14 species of Hawaiian birds, most of them endangered, in one of the island's last large remnants of upland rain forest. During the next two decades, refuge staff and volunteers would expand this forest by around 5,000 acres by restoring mountaintop habitat that cattle grazing had devastated.

As was Jeffrey's habit, he led his young visitors to a cluster of small, candelabra-shaped trees, their upward-curving branches ending in sprays of strap-shaped leaves. Jeffrey liked to use this grove of flowering lobeliads as a backdrop for his talk on the 19 years of restoration efforts that followed the plant's rediscovery in the refuge in 1989.

Most North American gardeners know lobeliads as small flowering herbs commonly used in window boxes. But some 13 million years ago, one or more lobeliad relatives somehow reached the shores of Hawai'i. From these first colonists a spectacular array of 125 species evolved to include many flowering bushes and trees--none of them found anywhere else on Earth. Among their unique features, many Hawaiian lobeliads evolved long tubular blossoms and fleshy fruit designed to be pollinated and dispersed by Hawaiian birds, many of which likewise are found nowhere else.

But like much of Hawai'i's unique flora, many of its lobeliads were decimated by pigs-first introduced by Polynesians-and by cattle, sheep and goats presented by 18th-century European explorers as gifts to Hawaiian royalty. Today many native lobeliads are extinct or cling to survival in precarious perches such as cliffs, out of the reach of these voracious grazing animals.

The grove where Jeffrey took his visitors was the refuge's most mature planting of the endangered lobeliad Clermontia lindseyana. Nearby were plantings of its even rarer cousins: Clermontia pyrularia and Cyanea shipmanii. Each of these species' serendipitous rediscovery in and around Hakalau had been followed by years of hit-and-miss efforts to learn how to hand-pollinate its blossoms, germinate its seeds and find the right ecological niche for the plant to thrive, Jeffrey explained. Germination, for example, proved almost impossible for one species until a colleague had the idea of feeding the seeds to the critically endangered 'alalā, or Hawaiian crow, once an important forest-seed disperser that survives now only in captivity. The experiment worked, and the partially digested seeds produced hundreds of seedlings. Since then, refuge staff have planted these seeds across Hakalau's higher slopes to produce today's mature groves.

The hope, Jeffrey explained, was that the groves would attract Hakalau's population of 'i'iwi, a crimson honeycreeper whose long, sickle-shaped bill perfectly matches the trees' blossoms. When an 'i'iwi reaches through the tubular flower to get its nectar, the bird collects a smudge of pollen on its forehead and transfers the pollen to the next blossom it visits. By contrast, common birds such as the 'amakihi simply punch holes in the base of lobeliad flowers to steal nectar without pollinating the plants.

As Hakalau refuge supports one of the last healthy populations of 'i'iwi (around 100,000 birds), hopes were high that this ancient symbiotic relationship could be restored. But year after year, 'i'iwi ignored the plants, Jeffrey told the students. "They've forgotten their ancient nectar source." And without pollination, there was little hope for completing the second half of the plants' natural reproductive cycle: the dispersal of their seeds by the refuge's population of 'ōma'o, or Hawai'i thrush.

As a result, the aging groves of lobeliad plantings were gradually dying off instead of spreading. "So there I was, deep into my 'woe is me' speech," Jeffrey recalls, "when I see these kids start to grin. They're looking right past me, their eyes big as saucers, and I'm thinking, 'Hey, this is serious stuff I'm telling you!'"

The students' teacher pointed over Jeffrey's shoulder. "Look, Jack," she whispered. The biologist turned to see an 'i'iwi insert its long bill into a curving lobeliad blossom and then into another and yet a third before flying away.

Partners in Evolution

Hawai'i is home to around 1,000 species of flowering plants that arose during millions of years of isolation and coevolution with the islands' native animals. More than 60 percent of these plants depend on birds for pollination, seed dispersal or both. And some of the most spectacular coevolved adaptations have taken place between native lobeliads and honeycreepers such as the 'i'iwi. "If Darwin had explored Hawai'i instead of the Galápagos, he might not have needed all those years to work out his theory of evolution," says University of Hawai'i ecologist Jonathan Price, referring to the striking match between native blossoms and beaks.

Tragically, two centuries of land development and a deluge of introduced animals--from disease-carrying mosquitoes to landscape-ravaging livestock--have wrought an ecological holocaust. Though the state of Hawai'i represents just 0.2 percent of the U.S. land area, it accounts for around

75 percent of the nation's plant and bird extinctions. Currently, more than 400  Hawaiian plant and animal species are listed as threatened or endangered by the U.S. Fish and Wildlife Service--nearly all found in the wild only on this small island chain.

At least half of Hawai'i's native birds (71 species) have become extinct since the arrival of Europeans, and half of all survivors are endangered, the 'akeke'e (Kaua'i 'ākepa) and 'akikiki (Kaua'i creeper) being the most recently listed. One of the greatest threats is the rapid spread of nonnative diseases such as bird pox and avian malaria, carried by nonnative mosquitoes that breed in the mud wallows created by nonnative pigs and in the hollowed-out trunks of tree ferns, which are knocked down and eaten by the pigs.

"So many bird pollinators, including the 'i'iwi, have largely disappeared from lower elevations," says Marjorie Ziegler, executive director of the Conservation Council for Hawai'i. "Upper-elevation forests at Hakalau--currently too cool for breeding mosquitoes--are essential to the survival of native forest birds." Yet as climate change drives temperatures up, she adds, mosquitoes likewise are expanding their range into higher elevations.

Indeed, virtually all of Hawai'i's wildlife faces the triple threat of invasive species, climate change and habitat destruction, says Bruce Stein, NWF's director of climate change adaptation and a lobeliad expert. The Federation recently adopted a special resolution recognizing the biodiversity conservation challenges facing Hawai'i and urging the federal government to increase funding for species recovery and habitat protection, strengthen measures to prevent further introduction and spread of invasive species, and collaborate with the state government to address climate change in its wildlife-action plans.

For many of Hawai'i's most spectacular plants and birds, hopes of recovery hinge on re-establishing age-old ecological partnerships such as that between the 'i'iwi and native lobeliads. But some of these symbiotic relationships are known or inferred only from historical records. Recently, Price and his students at the University of Hawai'i began harnessing technology to clarify some of these ancient relationships.

"We've photographed the rarest of our flowers and scanned in images of possible pollinators," he says. The team recently made its first positive match. It involved Kokia drynariodes, a tree of which there is just a handful of individuals in the wild (on the island of Hawai'i). Though most closely related to cotton, the tree sports giant red blossoms that resemble oversized hibiscus flowers.

"We knew it must have catered to a very long-billed pollinator," Price says. And in fact, overlaying images on a computer revealed a hand-in-glove match with the kioea, a giant honeyeater and the largest of Hawai'i's bird pollinators. "It was almost magical," Price says of the overlay of bill and blossom. "Like we were seeing this interaction emerge from the mists of time." For tragically, the kioea is known only from museum specimens, having gone extinct in the mid-1800s.

The search continues for matches between surviving Hawaiian birds and the rare plants they may have forgotten. The information could be used to guide replanting efforts like those at Hakalau. At present, the 'i'iwi is looking like the lynchpin for a number of endangered flowering trees, Price says. "The dilemma is that we don't have large populations of 'i'iwi outside places like Hakalau."

Already, such grim realities have inspired some of the world's most audacious conservation measures: Field botanists such as Kenneth Wood of Hawai'i's National Tropical Botanical Garden are renowned for rappelling down vertical cliffs to use pipe cleaners to hand-pollinate endangered plants clinging to existence out of the reach of feral goats, pigs and cattle.

Completing the Cycle

At Hakalau in fall 2010, Jeffrey was leading a group of college students to his favorite patch of C. lindseyana, telling the story of how the middle schoolers had looked over his shoulder to witness the plant's historic reunion with the 'i'iwi. Soon after, 'i'iwi also rediscovered the other two endangered lobeliad species planted by refuge staff.

"I was relating how exciting it had been to see the pollination," Jeffrey recalls, "but that I was sad to be retiring soon without seeing the seed dispersed by the 'ōma'o to complete the cycle." A whirr of wings interrupted Jeffrey's lament. Looking up, he and the students saw a plump brown bird launch itself out of the bushes. Yes, an 'ōma'o.

"I'm thinking, 'Can this really be happening?'" Jeffrey recalls. He rushed into the grove that the bird had just exited and examined the lobeliad's small, round, green-yellow fruits. Several bore the 'ōma'o's distinctive triangular bill marks, exposing the bright orange seed pulp inside. "It was true!" Jeffrey says. "We had shown that 'if you plant it, they will come!'"

Three months later, Jack Jeffrey retired a happy man--or at least a hopeful one.

Jessica Snyder Sachs is a New Jersey-based writer and frequent contributor.

A DOSE OF DIVERSITY

Scientists are discovering that species extinctions fuel the rise and spread of infectious diseases and hinder medical research

ON A RECENT AFTERNOON, Laura Shappell followed a slender deer trail into a thicket of invasive Japanese knotweed. The plants towered over her head, and their deer-trampled stalks crunched under her boots as she vanished into the mass of pale green leaves. "If I'm not out in 10 minutes, send help," she called back.

A graduate student at Rutgers University, Shappell is a member of a research team exploring the link between biodiversity and human disease. Read more in the August issue of National Wildlife.

A rare form of black bear--that is actually white--faces threats to its survival in its British Columbia habitat

FROM THE DOCK of British Columbia's Hartley Bay, guide Marvin Robinson looks across the waters of the Douglass Channel to Gribbell Island. The 96-square-mile island--thickly forested in hemlock, cedar and fir--is home to the world's highest concentration of the rare "spirit bear"--a pale color variant of the American black bear. Long revered by the First Nations of British Columbia, scientists dubbed it the Kermode bear in 1905 after one of the first scientists to study the species, Francis Kermode. ... READ MORE at NATIONAL WILDLIFE.

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Copyright Jessica Snyder Sachs, as first published in Parenting

Ann Wood's* son Daniel almost died when he was 2 - from a snack. At first, Wood hadn't been worried when she'd called home from work and her babysitter mentioned that Daniel had just thrown up after eating an almond butter sandwich. "These things happen," she'd reassured her babysitter. "Just keep an eye on him." When Wood called back 15 minutes later, though, Daniel had developed diarrhea. When she called a third time, as she rushed home to their New Jersey suburb, he was struggling for breath. "Call 911 right now!" she instructed.

As Daniel emerged from an ambulance at the hospital, his face was covered with large red welts. The paramedics had found him in anaphylactic shock, which meant that his throat was swelling shut and his blood pressure was plummeting toward zero. They brought him back with injections of the stimulant pinephrine and an inflammation-squelching steroid. The next day, Wood and her husband learned that Daniel's reaction was from a life-threatening food allergy to peanuts, a trace amount of which had likely cross-contaminated the almond butter.

Now in second grade, Daniel isn't the only one of his friends with food allergies. Five kids in his grade carry EpiPens, the prefilled syringes that contain enough epinephrine to reverse a severe allergic reaction. And his grade is hardly unique. In the U.S., about 1 in 12 children under 3 have food allergies, and around 150 die each year because of them. Outside the U.S., the problem is no less serious; the incidence of food allergies in kids around the world has at least doubled over the last decade.

"The increase seems to be part of a general rise in allergies of all kinds," says Scott Sicherer, M.D., a pediatric allergist at New York's Mount Sinai School of Medicine and author of Understanding and Managing Your Child's Food Allergies. 

While it's not clear what's behind this disturbing trend, many experts think it may have to do with the so-called Hygiene Hypothesis: that modern life - with its lack of exposure to the "germiness" of infiltered water, dirt, and animals - can leave people's immune systems prone to overreact to harmless substances. The result: Even something as innocent-seeming as a peanut can cause the body's defenses to go into overdrive. As overactive immune cells release histamine and other inflammatory chemicals, they produce symptoms such as hives, itching, diarrhea, and in severe cases, life-threatening anaphylaxis. 

While regular exposure to relatively harmless bacteria might help make us less allergy-prone, no medical expert would advocate going back to the days of rampant cholera and intestinal parasites. So where does that leave us? Fortunately, there are steps you can take to reduce your child's risk of developing food allergies, and ways to handle them if they arise.

 
A Family Affair

The first thing you'll want to figure out is your family's allergy history. "The more people in your family who have allergies, the greater the risk your child will have one," says Dr. Sicherer.

Kathleen Murray-Lyons, of Townsend, Delaware, has allergies and asthma, so her pediatrician suggested special measures to decrease her 1-year-old son James's chances of food allergies. He recommended she delay introducing James to certain foods that are common allergens, such as nuts and eggs, and offer even low-allergenic foods, like carrots and rice, only gradually and one at a time. (See What to Introduce When). "So far, so good," says Murray-Lyons.

Another tactic doctors recommend: Wait to introduce any solids to your baby until after 6 months (as opposed to 4 months), since studies have found that this significantly decreases the risk of your child developing food allergies. As for what you should eat if you're breastfeeding, studies are mixed as to whether it's helpful to eliminate allergenic foods from your diet. Talk to your doctor about your particular case.

How to Recognize and Respond

Figuring out that your child has a food allergy can be half the battle. Leslie Norman-Harris of Woolwich Township, New Jersey, recalls the night her daughter, Camryn, 4, ate a mouthful of rice with shrimp.

"When she told us her mouth felt itchy, my husband and I looked at 
each other and said, 'Uh-oh.'" Fortunately the symptoms subsided, but they knew not to give Camryn any more shrimp.

Other symptoms (which almost always appear a few minutes after eating the offending food):

Nausea

Vomiting

Diarrhea

Itching (throat, mouth, eyes, skin, and/or ears)

Lip swelling

Rash (hives or a flare-up of eczema)

Throat tightness (trouble swallowing or breathing)

Tongue swelling that obstructs the mouth

Chest pain

Dizziness

Sudden paleness or blueness, unconsciousness, and/or a faint pulse

 
For a mild allergic reaction, such as stomach upset or a rash, watch your child carefully in case she gets worse, and call your doctor. To relieve discomfort, you can give her a weight-appropriate dose of an antihistamine such as Benadryl or its generic equivalent (diphenhydramine).

If your child has a severe allergic reaction (like throat tightness, lip swelling, or unconsciousness), call 911. She may need an injection of epinephrine. Later, talk with your doctor about whether you should keep epinephrine on hand. 

Testing and Treatment

If you think your child has a food allergy, see your doctor, who may recommend a pediatric allergist. He'll likely perform one of two tests: the classic skin-prick, which entails scratching a small amount of the allergen into the skin and watching for a reaction, or a blood test that screens for allergy-related antibodies.

But know that allergy tests are far from perfect, says Hugh Sampson, M.D., director of the Jaffee Food Allergy Institute at Mount Sinai School of Medicine. It's possible to have an allergy that doesn't show up on a test, or for a test to show that your child is mildly allergic to a certain food even though he can eat it without a problem. Bottom line: Diagnostic tests are best used to help confirm a suspected allergy, rather than to go fishing for possible ones.

Another alternative for determining food allergies is simply to talk about your child's symptoms with your doctor. Dr. Sampson, for example, says he looks for common patterns. Does the child always develop symptoms within minutes of having a particular food? Is it a food known to provoke allergies? If the answers are yes, then you may be dealing with a food allergy.

Once you know your child is allergic to a food, the best thing to do is avoid it entirely. (Allergy shots, while often effective for respiratory allergies, aren't usually used to treat food allergies because there's a greater risk of a dangerous reaction.) If your child does accidentally eat the wrong thing, the best line of defense is to follow your doctor's emergency plan, which will likely include relieving symptoms with an antihistamine or an emergency shot of epinephrine, depending on how severe the symptoms are.

Several promising treatments are now being studied. Most involve "immunizing" a person against the food allergen by injecting a modified version of it together with a substance that tells the immune system to "back off," or treat it as harmless. If these treatments pan out, they may become available as soon as 2010.

Avoiding Allergens

Steering clear of allergenic foods can be one of the toughest jobs a mom can take on. Fortunately, as of January 2006, the Food and Drug Administration requires all food labels to state if ingredients include any protein derived from one of the eight major allergenic foods. But you still need to be vigilant about reading the fine print on labels, which can contain surprises.

"Who would ever have thought that baby-food meats would have dairy in them?" says Jennie Oko of Westmont, Illinois, who has became an ingredient detective ever since her son Matthew, 3, was diagnosed with a dairy allergy as a baby.

Next: Make Your Child Food Smart

Not only do you need to be careful about keeping problem foods out of your house, you also need to teach your child to steer clear of them in other settings. "You don't want to scare him," Dr. Sicherer cautions. Just calmly explain, "Mommy and Daddy don't want you to feel sick, so it's important that you take food only from us and Grandma."

Dr. Sicherer even suggests role-playing together - for instance, by pretending to be a visitor offering him a cookie. If he starts to accept it, say something like "Uh-oh. Remember what we talked about - visitor doesn't know about your allergies."

You'll also need to get used to explaining your child's dietary restrictions when you eat out. A recent survey found that restaurant workers generally don't realize that something as small as a cross-contaminated serving spoon or frying pan could trigger a severe reaction.

"I Want What They're Having!"

For young children, not being allowed to eat what other kids do can be upsetting. When Sabrina Sciarrotta was 18 months, "she was so eager to have everything her big sister, Julia, had," recalls her mom, Monica, of Brea, California. "But while Julia was fine with dairy, Sabrina got headaches and broke out in rashes." To avoid a conflict, Sciarrotta now doles out Julia's yogurt and milk only when Sabrina is napping.

There will inevitably be times, though - at birthday parties, for instance - when your child can't ignore her limitations. Get in the 

habit of sending your child to such events with "safe" food alternatives. At school, be sure to explain her food allergy to her teachers and the nurse. If your child has a severe allergy, see if her school will even send notes home to her classmates' parents, explaining that certain foods shouldn't be sent in for sharing.

Outgrowing Food Allergies

The good news is that many children's food allergies go away by age 5. In fact, milk, egg, wheat, and soy allergies disappear nearly 85 percent of the time. So if your child has sworn off, say, soy for several years, ask the doctor if it's a good idea to reintroduce it to him again. She may suggest repeat allergy tests under medical supervision.

While you're still dealing with food allergies, however, remember that "life should not be viewed as a mine field," says Dr. Sicherer. Wood agrees: "We try to protect Daniel while letting him live a normal life."

Allergy - or intolerance?

Many people use the terms "food allergy" and "food intolerance" interchangeably, but they're very different things. An allergic reaction involves a misguided immune response to an otherwise harmless substance. The result is runaway inflammation, which produces the rashes, itchiness, and swelling typical of allergies.

An intolerance results when a child (or adult) lacks one or more digestive enzymes needed to break down a food ingredient. Gas, bloating, and an achy stomach are the hallmark symptoms. (Lactose, or milk sugar, is by far the most common offender.) An intolerance can cause serious stomach pain but, fortunately, isn't life threatening.

* Name has been changed for privacy, at the request of the family.

Jessica Snyder Sachs is the author of Good Germs, Bad Germs: Health and Survival in a Bacterial World (Hill & Wang/FSG).

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By Jessica Snyder Sachs

If you're religious about what really matters, you can take shortcuts with the rest. Check out our guide to being a sensible slacker.

1. Work Out 5 Days a Week?

It's not your imagination: Our bodies simply become higher maintenance after 40. Indulgences of food or drink are quicker to take revenge. Muscles require more maintenance. Screening tests become more important. So there's a lot to remember -- and yet the wellness precautions keep coming, with new dos and don'ts every passing year. Can anyone do it all?

Actually, no. And if you try, say experts, you may end up throwing in the towel on some of the essentials, as well as what's helpful but optional. So find out where you can settle for good enough and still enjoy great health.

Rule 1: Work out 30 to 60 minutes a day, five days a week. 
The Midlife Shortcut: Catch up when you miss workouts.

To reduce the risk of heart disease, cancer, and osteoporosis -- all big concerns for women over 40 -- experts urge us to exercise at least 30 minutes a day, five days a week (and for maximum health benefits, make that an hour rather than half an hour). But daily workouts can be difficult to fit into a life crammed with work and family responsibilities. Then there's the knee and joint pain that many women experience after years of pounding their way through "healthful" exercise.

Why there's wiggle room: The cumulative hours -- the total time you clock each week -- is what really counts. In fact, the weekend warrior has gotten a bad rap, says exercise physiologist Jane Roy, PhD, of the University of Alabama at Birmingham. If you're too busy Monday through Friday, weekends are a great time for getting in two or more hours of enjoyable exercise a day. You can catch up by spending a weekend morning or afternoon playing tennis with girlfriends, taking back-to-back aerobic and Pilates classes, or going for a long walk or run.

Then, during the week, concentrate on interspersing sedentary activities such as computer work with small but frequent movement breaks, Roy adds.

2. Get a Pap Smear Yearly?

Rule 2: Get a Pap smear every year.
The Midlife Shortcut: Get tested every two to three years.

Sexually active women under 40 should be tested every year, but women over 40 can stretch it out to once every two to three years once they've had three or more normal results in a row, as long as they're in a long-term, mutually monogamous relationship or are not sexually active, and they're still getting annual pelvic exams.

Why there's wiggle room: When a woman is either not having sex or always has it with the same person (and that person is not having it with anyone else), she's not being exposed to new strains of the human papillomavirus, explains gynecologist Stacy Tessler Lindau, MD, of the University of Chicago Medical Center.

The majority of people who have ever been sexually active have been exposed to one or more strains of HPV. Most women clear the symptoms of the virus within a few months. But in a small minority, the infection causes cells to become precancerous over the course of several years. These are the abnormalities that show up on Pap tests.

What that means is the risk of precancerous changes (and ultimately cervical cancer) becomes very low once women pass through this latency period without being exposed anew by having sex with someone different. Even if you don't have a new partner, says Lindau, "You can be exposed to new sexual partners through your own sexual partner." That's why your relationship has to be mutually monogamous; if you're not sure it is, continue to be tested every year.

3. Eat 5 Servings of Veggies a Day?

Rule 3: Eat your veggies: five servings a day.
The Midlife Shortcut: Aim to include veggies in most meals.

Five servings a day add up to a heck of a lot of vegetables. Using USDA food guide serving sizes, you'd need to swallow up to 17 cups of salad or solid veggies a week to meet that goal -- that on top of the four daily servings of fruit you're supposed to get.

Admittedly, as the over-40 metabolism slows, substituting produce for higher-calorie foods and snacks can help with weight control. But as our lives grow exponentially busier, getting down all those veggies can become overwhelming.

"Five servings a day remains an admirable goal," says registered dietitian Christine Gerbstadt, MD, of the American Dietetic Association. And she argues that meeting it can be a lot easier than you think. "Potatoes count," she notes. "Just don't make it french fries every day." You can also add salsa, tomato sauce, or any kind of bean to the list.

But she's also willing to compromise. "A decent daily plan is to include some vegetables in most meals, then concentrate on rounding out the rest of your diet by pumping up the fibrous whole grains and healthy fats."

Why there's wiggle room: If you look at the big nutrition picture and aim for moderate goals, success may encourage you to surpass your quota. But if you don't hit the mark every single day, Gerbstadt says, you can get by with a daily multivitamin -- that will ensure you get the vitamins and minerals that are naturally abundant in fresh vegetables.

4. Brush After Every Meal?

Rule 4: Brush after every meal. 
The Midlife Shortcut: Put down the toothbrush and grab some gum.

Or a toothpick. Or gum. Or a glass of water. It's not necessary to brush your teeth after every meal if you do something else to remove the food debris.

Why there's wiggle room: Brushing when you get up and before you go to bed is just fine, according to Edmond Hewlett, DDS, of the UCLA School of Dentistry. In fact, Hewlett says it's a bad idea to brush right after consuming acidic foods or beverages such as wine, orange juice, and most soft drinks. "The acidity slightly softens tooth enamel," he explains. So habitually brushing right after eating these foods can contribute to tooth sensitivity and cavities.

Chewing sugarless gum has other benefits besides removing food residue. It also increases saliva, which contains minerals that help replace the enamel lost to acidic food and acid-producing mouth bacteria. That's particularly important after age 40, when your natural saliva production starts to decrease. And if the gum contains xylitol, you'll get an added bonus: This sugar substitute inhibits the growth of cavity-causing tooth bacteria.

5. Sleep for 8 Hours?

Rule 5: Eight hours of sleep every night -- no sleeping in. 
The Midlife Shortcut: Sleep late on weekends.

Yes, the human body does need eight hours of sound sleep each night, says Joanne Getsy, MD, of Drexel University College of Medicine, in Philadelphia. "It's a fallacy that you need less sleep as you get older," she says. "You don't need less; you simply get less." Anyone dealing with hot flashes and sleep disturbances knows this too well. But whereas many experts insist that "catch-up sleep" isn't as good as the real thing, Getsy says there's room for deviating from your normal wakeup and going-to-bed times.

Why there's wiggle room: "The aim should be to pay back your sleep debt as soon as you can," Getsy says. Specifically, she recommends scheduling twice-a-week catch-up nights. "Pick one weeknight and one weekend night, and don't plan anything on those evenings," she advises. "Let them be your nights to recover." Daytime napping is okay too, she adds: "Just keep it under an hour so it doesn't interfere with a solid night's sleep."

As for sleep-bingeing on weekends, Getsy advises staying in bed as late as you like on Saturday. Then on Sunday, split the difference between when you'd like to get up and when you have to get up on Monday. That will help ease you back into your weekday schedule.

Even better news: Getsy says that when it comes to sleep debt, it's okay to pay back less than you borrowed. Usually one full night's sleep is enough to make up for a couple of shortchanged ones, she says. "If you feel better in the morning, you've slept enough."

6. Lift Weights 3 Times a Week?

Rule 6: Lift weights three times a week.
The Midlife Shortcut: Try for one or two sessions a week.

On top of encouraging us to meet aerobic exercise quotas, the health gurus tell us to get to the gym and pump iron at least three days a week. Strength training is especially important after menopause, at which point a woman's body tends to lose both muscle mass and bone strength.

"When you make the muscle grow, you strengthen the bone that's attached to it," explains Felicia Cosman, MD, of the National Osteoporosis Foundation. Aerobic exercise such as jogging works only about 20 percent of muscle fibers, she says, while strength training with weights engages up to 90 percent.

Why there's wiggle room: There's no magic number as to how often you need to strength train. Aim for regularity, Cosman says, even if it's just twice a week. Nor do you have to schlep to a gym. "Weight machines and free weights are good," Cosman says, "but so are equipment-free Pilates and yoga moves, and push-ups."

7. Do a Breast Self-Exam?

Rule 7: Do a breast self-exam every month.
The Midlife Shortcut: Do it often enough to notice changes.

We came of age being trained to search for lumps every month. The mandate feels even more compelling now, given how greatly the incidence of breast cancer increases after 40.

As it turns out, however, there's little evidence that obsessively examining yourself really helps women catch more life-threatening lumps.

Why there's wiggle room: After years of urging women to perform monthly self-exams, the American Cancer Society recently deemed them optional. But what's still important, says ACS spokesperson Debbie Saslow, PhD, is that women become familiar with how their breasts feel and what's normal for them. "For a lot of women, that's still a monthly exam. For others, it's the occasional self-exam or simply paying attention when getting dressed or showering."

Where Not to Cheat

Here's where our health gurus draw the line. Follow these three rules, they say, as scrupulously as you can.

Keep Moving 
Yes, you get brownie points for working out on weekends, but you lose out on lots of benefits if you just sit in a chair the rest of the week, says Jane Roy, PhD, of the University of Alabama at Birmingham. So get up for a stretch break at least once an hour at work (you could walk down the hall to talk to a colleague instead of sending an e-mail), and a few times a day, catch some fresh air with a quick five-minute stroll outside.

If you need extra motivation, consider this: Five one-minute stretch breaks over the course of a day burn just 15 to 20 calories. But over the course of a year, that adds up to over two pounds of fat.

Get a Mammogram Every Year 
When cancer strikes women in their 40s, the tumors tend to be aggressive, which means fast-growing -- so the early detection offered by mammograms is crucial, says the American Cancer Society's Debbie Saslow. After menopause, women tend to have slower-growing cancers, she adds, but the incidence increases. "So going longer than a year just isn't worth the risk," she says.

Maintain a Healthy Weight 
Overweight women are more likely to develop heart disease, diabetes, and many types of cancer than normal-weight women are.

In fact, a recent analysis estimates that 20 percent of all cancer deaths in American women are linked to excess weight. In general, cancer rates increase when a woman's body mass index exceeds 25, says Colleen Doyle of the American Cancer Society. The risk rises more dramatically when the BMI passes 30. Abdominal fat appears to be closely associated with postmenopausal breast cancer and cancers of the colon and pancreas. And some experts say that the risk increases when a woman's waistline exceeds 32 inches.

Originally published in MORE magazine, February 2009.

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Copyright Jessica Snyder Sachs

Originally published in Discover magazine, March 2008

Rogue genetic snippets spread antibiotic resistance all over the environment.

On a bright winter morning high in the Colorado Rockies, a slight young woman in oversize hip boots sidles up to a gap of open water in the icy Cache la Poudre River. Heather Storteboom, a 25-year-old graduate student at nearby Colorado State University, is prospecting for clues to an invisible killer.

Storteboom snaps on a pair of latex gloves and stretches over the frozen ledge to fill a sterile plastic jug with water. Then, setting the container aside, she swings her rubber-clad legs into the stream. "Ahh, no leaks," she says, standing upright. She pulls out a clean trowel and attempts to collect some bottom sediment; in the rapid current, it takes a half dozen tries to fill the small vial she will take back to the DNA laboratory of her adviser, environmental engineer Amy Pruden. As Storteboom packs to leave, a curious hiker approaches. "What were you collecting?" he asks. "Antibiotic resistance genes," she answers.

Storteboom and Pruden are at the leading edge of an international forensic investigation into a potentially colossal new health threat: DNA pollution. Specifically, the researchers are seeking out snippets of rogue genetic material that transforms annoying bacteria into unstoppable supergerms, immune to many or all modern antibiotics. Over the past 60 years, genes for antibiotic resistance have gone from rare to commonplace in the microbes that routinely infect our bodies. The newly resistant strains have been implicated in some 90,000 potentially fatal infections a year in the United States, higher than the number of automobile and homicide deaths combined.

Among the most frightening of the emerging pathogens is invasive MRSA, or methicillin-resistant Staphylococcus aureus. Outbreaks of MRSA in public schools recently made headlines, but that is just the tip of the iceberg. Researchers estimate that invasive MRSA kills more than 18,000 Americans a year, more than AIDS, and the problem is growing rapidly. MRSA caused just 2 percent of staph infections in 1974; in the last few years, that figure has reached nearly 65 percent. Most reported staph infections stem from MRSA born and bred in our antibiotic-drenched hospitals and nursing homes. But about 15 percent now involve strains that arose in the general community.

It is not just MRSA that is causing concern; antibiotic resistance in general is spreading alarmingly. A 2003 study of the mouths of healthy kindergartners found that 97 percent harbored bacteria with genes for resistance to four out of six tested antibiotics. In all, resistant microbes made up around 15 percent of the children's oral bacteria, even though none of the children had taken antibiotics in the previous three months. Such resistance genes are rare to nonexistent in specimens of human tissue and body fluid taken 60 years ago, before the use of antibiotics became widespread.

In part, modern medicine is paying the price for its own success. "Antibiotics may be the most powerful evolutionary force seen on this planet in billions of years," says Tufts University microbiologist Stuart Levy, author of The Antibiotic Paradox: How the Misuse of Antibiotics Destroys Their Curative Powers. By their nature, antibiotics support the rise of any bug that can shrug off their effects, by conveniently eliminating the susceptible competition.

But the rapid rise of bacterial genes for drug resistance stems from more than lucky mutation, Levy adds. The vast majority of these genes show a complexity that could have been achieved only over millions of years. Rather than rising anew in each species, the genes spread via the microbial equivalent of sexual promiscuity. Bacteria swap genes, not only among their own kind but also between widely divergent species, Levy explains. Bacteria can even scavenge the naked DNA that spills from their dead compatriots out into the environment.

The result is a microbial arms-smuggling network with a global reach. Over the past 50 years, virtually every known kind of disease-causing bacterium has acquired genes to survive some or all of the drugs that once proved effective against it. Analysis of a strain of vancomycin-resistant enterococcus, a potentially lethal bug that has invaded many hospitals, reveals that more than one-quarter of its genome-including virtually all its antibiotic-thwarting genes-is made up of foreign DNA. One of the newest banes of U.S. medical centers, a supervirulent and multidrug-resistant strain of Acinetobacter baumannii, likewise appears to have picked up most of its resistance in gene swaps with other species.

So where in Hades did this devilishly clever DNA come from? The ultimate source may lie in the dirt beneath our feet.

For the past decade, Gerry Wright has been trying to understand the rise of drug resistance by combing through the world's richest natural source of resistance-enabling DNA: a clod of dirt. As the head of McMaster University's antibiotic research center in Hamilton, Ontario, Wright has the most tricked-out laboratory a drug designer could want, complete with a $15 million high-speed screening facility for simultaneously testing potential drugs against hundreds of bacterial targets. Yet he says his technology pales in comparison with the elegant antibiotic-making abilities he finds encoded in soil bacteria. The vast majority of the antibiotics stocking our pharmacy shelves-from old standards like tetracycline to antibiotics of last resort like vancomycin and, most recently, daptomycin-are derived from soil organisms.

Biologists assume that soil organisms make antibiotics to beat back the microbial competition and to establish their territory, Wright says, although the chemicals may also serve other, less-understood functions. Whatever the case, Wright and his students began combing through the DNA of soil microbes like streptomyces to better understand their impressive antibiotic-making powers. In doing so the researchers stumbled upon three resistance genes embedded in the DNA that Streptomyces toyocaensis uses to produce the antibiotic teicoplanin. While Wright was not surprised that the bug would carry such genes as antidotes to its own weaponry, he was startled to see that the antidote genes were nearly identical to the resistance genes in vancomycin-resistant enterococcus (VRE), the scourge of American and European hospitals.

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"Yet here they were in a soil organism, in the exact same orientation as you find in the genome of VRE," Wright says. "That sure gave us a head-slap moment. If only we had done this experiment 15 years ago, when vancomycin came into widespread use, we might have understood exactly what kind of resistance mechanisms would follow the drug into our clinics and hospitals." If nothing else, that foreknowledge might have prepared doctors for the inevitable resistance they would encounter soon after vancomycin was broadly prescribed.

Wright wondered what else he might find in a shovelful of dirt. So he handed out plastic bags to students departing on break, telling them to bring back soil samples. Over two years his lab amassed a collection that spanned the continent. It even included a thawed slice of tundra mailed by Wright's brother, a provincial policeman stationed on the northern Ontario-Manitoba border.

By 2005 Wright's team had combed through the genes of nearly 500 streptomyces strains and species, many never before identified. Every one proved resistant to multiple antibiotics, not just their own signature chemicals. On average, each could neutralize seven or eight drugs, and many could shrug off 14 or 15. In all, the researchers found resistance to every one of the 21 antibiotics they tested, including Ketek and Zyvox, two synthetic new drugs.

"These genes clearly didn't jump directly from streptomyces into disease-causing bacteria," Wright says. He had noted subtle variations between the resistance genes he pulled out of soil organisms and their doppelgangers in disease-causing bacteria. As in a game of telephone, each time a gene gets passed from one microbe to another, slight differences develop that reflect the DNA dialect of its new host. The resistance genes bedeviling doctors had evidently passed through many intermediaries on their way from soil to critically ill patients.

Wright suspects that the antibiotic-drenched environment of commercial livestock operations is prime ground for such transfer. "You've got the genes encoding for resistance in the soil beneath these operations," he says, "and we know that the majority of the antibiotics animals consume get excreted intact." In other words, the antibiotics fuel the rise of resistant bacteria both in the animals' guts and in the dirt beneath their hooves, with ample opportunity for cross-contamination.

Nobody knows how long free-floating DNA might persist in the water.

A 2001 study by University of Illinois microbiologist Roderick Mackie documented this flow. When he looked for tetracycline resistance genes in groundwater downstream from pig farms, he also found the genes in local soil organisms like Microbacterium and Pseudomonas, which normally do not contain them. Since then, Mackie has found that soil bacteria around conventional pig farms, which use antibiotics, carry 100 to 1,000 times more resistance genes than do the same bacteria around organic farms.

"These animal operations are real hot spots," he says. "They're glowing red in the concentrations and intensity of these genes." More worrisome, perhaps, is that Mackie pulled more resistance genes from his deepest test wells, suggesting that the genes percolated down toward the drinking water supplies used by surrounding communities.

An even more direct conduit into the environment may be the common practice of irrigating fields with wastewater from livestock lagoons. About three years ago, David Graham, a University of Kansas environmental engineer, was puzzled in the fall by a dramatic spike in resistance genes in a pond on a Kansas feedlot he was studying. "We didn't know what was going on until I talked with a large-animal researcher," he recalls. At the end of the summer, feedlots receive newly weaned calves from outlying ranches. To prevent the young animals from importing infections, the feedlot operators were giving them five-day "shock doses" of antibiotics. "Their attitude had been, cows are big animals, they're pretty tough, so you give them 10 times what they need," Graham says.

The operators cut back on the drugs when Graham showed them that they were coating the next season's alfalfa crop with highly drug-resistant bacteria. "Essentially, they were feeding resistance genes back to their animals," Graham says. "Once they realized that, they started being much more conscious. They still used antibiotics, but more discriminately."

While livestock operations are an obvious source of antibiotic resistance, humans also take a lot of antibiotics-and their waste is another contamination stream. Bacteria make up about one-third of the solid matter in human stool, and Scott Weber, of the State University of New York at Buffalo, studies what happens to the antibiotic resistance genes our nation flushes down its toilets.

Conventional sewage treatment skims off solids for landfill disposal, then feeds the liquid waste to sewage-degrading bacteria. The end result is around 5 billion pounds of bacteria-rich slurry, or waste sludge, each year. Around 35 percent of this is incinerated or put in a landfill. Close to 65 percent is recycled as fertilizer, much of it ending up on croplands.

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Weber is now investigating how fertilizer derived from human sewage may contribute to the spread of antibiotic-resistant genes. "We've done a good job designing our treatment plants to reduce conventional contaminants," he says. "Unfortunately, no one has been thinking of DNA as a contaminant." In fact, sewage treatment methods used at the country's 18,000-odd wastewater plants could actually affect the resistance genes that enter their systems.

Every tested strain in a dirt sample proved resistant to multiple antibiotics.

Most treatment plants, Weber explains, gorge a relatively small number of sludge bacteria with all the liquid waste they can eat. The result, he found, is a spike in antibiotic-resistant organisms. "We don't know exactly why," he says, "but our findings have raised an even more important question." Is the jump in resistance genes coming from a population explosion in the resistant enteric, or intestinal, bacteria coming into the sewage plant? Or is it coming from sewage-digesting sludge bacteria that are taking up the genes from incoming bacteria? The answer is important because sludge bacteria are much more likely to thrive and spread their resistance genes once the sludge is discharged into rivers (in treated wastewater) and onto crop fields (as slurried fertilizer).

Weber predicts that follow-up studies will show the resistance genes have indeed made the jump to sludge bacteria. On a hopeful note, he has shown that an alternative method of sewage processing seems to decrease the prevalence of bacterial drug resistance. In this process, the sludge remains inside the treatment plant longer, allowing dramatically higher concentrations of bacteria to develop. For reasons that are not yet clear, this method slows the increase of drug-resistant bacteria. It also produces less sludge for disposal. Unfortunately, the process is expensive.

Drying sewage sludge into pellets-which kills the sludge bacteria-is another way to contain resistance genes, though it may still leave DNA intact. But few municipal sewage plants want the extra expense of drying the sludge, and so it is instead exported "live" in tanker trucks that spray the wet slurry onto crop fields, along roadsides, and into forests.

Trolling the waters and sediments of the Cache la Poudre, Storteboom and Pruden are collecting solid evidence to support suspicions that both livestock operations and human sewage are major players in the dramatic rise of resistance genes in our environment and our bodies. Specifically, they have found unnaturally high levels of antibiotic resistance genes in sediments where the river comes into contact with treated municipal wastewater effluent and farm irrigation runoff as it flows 126 miles from Rocky Mountain National Park through Fort Collins and across Colorado's eastern plain, home to some of the country's most densely packed livestock operations.

"Over the course of the river, we saw the concentration of resistance genes increase by several orders of magnitude," Pruden says, "far more than could ever be accounted for by chance alone." Pruden's team likewise found dangerous genes in the water headed from local treatment plants toward household taps.

Presumably, most of these genes reside inside live bacteria, but a microbe doesn't have to be alive to share its dangerous DNA. As microbiologists have pointed out, bacteria are known to scavenge genes from the spilled DNA of their dead.

"There's a lot of interest in whether there's naked DNA in there," Pruden says of the Poudre's waters. "Current treatment of drinking water is aimed at killing bacteria, not eliminating their DNA." Nobody even knows exactly how long such free-floating DNA might persist.

All this makes resistance genes a uniquely troubling sort of pollution. "At least when you pollute a site with something like atrazine," a pesticide, "you can be assured that it will eventually decay," says Graham, the Kansas environmental engineer, who began his research career tracking chemical pollutants like toxic herbicides. "When you contaminate a site with resistance genes, those genes can be transferred into environmental organisms and actually increase the concentration of contamination."

Taken together, these findings drive home the urgency of efforts to reduce flagrant antibiotic overuse that fuels the spread of resistance, whether on the farm, in the home, or in the hospital.

For years the livestock pharmaceutical industry has played down its role in the rise of antibiotic resistance. "We approached this problem many years ago and have seen all kinds of studies, and there isn't anything definitive to say that antibiotics in livestock cause harm to people," says Richard Carnevale, vice president of regulatory and scientific affairs at the Animal Health Institute, which represents the manufacturers of animal drugs, including those for livestock. "Antimicrobial resistance has all kinds of sources, people to animals as well as animals to people."

The institute's own data testify to the magnitude of antibiotic use in livestock operations, however. Its members sell an estimated 20 million to 25 million pounds of antibiotics for use in animals each year, much of it to promote growth. (For little-understood reasons, antibiotics speed the growth of young animals, making it cheaper to bring them to slaughter.) The Union of Concerned Scientists and other groups have long urged the United States to follow the European Union, which in 2006 completed its ban on the use of antibiotics for promoting livestock growth. Such a ban remains far more contentious in North America, where the profitability of factory-farm operations depends on getting animals to market in the shortest possible time.

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On the other hand, the success of the E.U.'s ban is less than clear-cut. "The studies show that the E.U.'s curtailing of these compounds in feed has resulted in more sick animals needing higher therapeutic doses," Carnevale says.

"There are cases of that," admits Scott McEwen, a University of Guelph veterinary epidemiologist who advises the Canadian government on the public-health implications of livestock antibiotics. At certain stressful times in a young animal's life, as when it is weaned from its mother, it becomes particularly susceptible to disease. "The lesson," he says, "may be that we would do well by being more selective than a complete ban."

McEwen and many of his colleagues see no harm in using growth-promoting livestock antibiotics known as ionophores. "They have no known use in people, and we see no evidence that they select for resistance to important medical antibiotics," he says. "So why not use them? But if anyone tries to say that we should use such critically important drugs as cephalosporins or fluoroquinolones as growth promoters, that's a no-brainer. Resistance develops quickly, and we've seen the deleterious effects in human health."

A thornier issue is the use of antibiotics to treat sick livestock and prevent the spread of infections through crowded herds and flocks. "Few people would say we should deny antibiotics to sick animals," McEwen says, "and often the only practical way to administer an antibiotic is to give it to the whole group." Some critics have called for restricting certain classes of critically important antibiotics from livestock use, even for treating sick animals. For instance, the FDA is considering approval of cefquinome for respiratory infections in cattle. Cefquinome belongs to a powerful class of antibiotic known as fourth-generation cephalosporins, introduced in the 1990s to combat hospital infections that had grown resistant to older drugs. In the fall of 2006, the FDA's veterinary advisory committee voted against approving cefquinome, citing concerns that resistance to this vital class of drug could spread from bacteria in beef to hospital superbugs that respond to little else. But the agency's recently adopted guidelines make it difficult to deny approval to a new veterinary drug unless it clearly threatens the treatment of a specific foodborne infection in humans. As of press time, the FDA had yet to reach a decision.

Consumers may contribute to the problem of DNA pollution whenever they use antibacterial soaps and cleaning products. These products contain the antibiotic-like chemicals triclosan and triclocarban and send some 2 million to 20 million pounds of the compounds into the sewage stream each year. Triclosan and triclocarban have been shown in the lab to promote resistance to medically important antibiotics. Worse, the compounds do not break down as readily as do traditional antibiotics. Rolf Halden, cofounder of the Center for Water and Health at Johns Hopkins University, has shown that triclosan and triclocarban show up in many waterways that receive treated wastewater-more than half of the nation's rivers and streams. He has found even greater levels of these two chemicals in sewage sludge destined for reuse as crop fertilizer. According to his figures, a typical sewage treatment plant sends more than a ton of triclocarban and a slightly lesser amount of triclosan back into the environment each year.

For consumer antibacterial soaps the solution is simple, Halden says: "Eliminate them. There's no reason to have these chemicals in consumer products." Studies show that household products containing such antibacterials don't prevent the spread of sickness any better than ordinary soap and water. "If there's no benefit, then all we're left with is the risk," Halden says. He notes that many European retailers have already pulled these products from their shelves. "I think it's only a matter of time before they are removed from U.S. shelves as well."

Consumers may contribute to the problem of DNA pollution whenever they use soaps and cleaning products containing antibiotic-like compounds.

Finally, there is the complicated matter of the vast quantity of antibiotics that U.S. doctors prescribe each year: some 3 million pounds, according to the Union of Concerned Scientists. No doctor wants to ignore an opportunity to save a patient from infectious disease, yet much of what is prescribed is probably unnecessary-and all of it feeds the spread of resistance genes in hospitals and apparently throughout the environment.

"Patients come in asking for a particular antibiotic because it made them feel better in the past or they saw it promoted on TV," says Jim King, president of the American Academy of Family Physicians. The right thing to do is to educate the patient, he says, "but that takes time, and sometimes it's easier, though not appropriate, to write the prescription the patient wants."

Curtis Donskey, chief of infection control at Louis Stokes Cleveland VA Medical Center, adds that "a lot of antibiotic overuse comes from the mistaken idea that more is better. Infections are often treated longer than necessary, and multiple antibiotics are given when one would work as well." In truth, his studies show, the longer hospital patients remain on antibiotics, the more likely they are to pick up a multidrug-resistant superbug. The problem appears to lie in the drugs' disruption of a person's protective microflora-the resident bacteria that normally help keep invader microbes at bay. "I think the message is slowly getting through," Donskey says. "I'm seeing the change in attitude."

Meanwhile, Pruden's students at Colorado State keep amassing evidence that will make it difficult for any player-medical, consumer, or agricultural-to shirk accountability for DNA pollution.

Late in the afternoon, Storteboom drives past dairy farms and feedlots, meatpacking plants, and fallow fields, 50 miles downstream from her first DNA sampling site of the day. Leaving her Jeep at the side of the road, she strides past cow patties and fast-food wrappers and scrambles down an eroded embankment of the Cache la Poudre River. She cringes at the sight of two small animal carcasses on the opposite bank, then wades in, steering clear of an eddy of gray scum. "Just gross," she mutters, grateful for her watertight hip boots.

Of course, the invisible genetic pollution is of greater concern. It lends an ironic twist to the river's name. According to local legend, the appellation comes from the hidden stashes (cache) of gunpowder (poudre) that French fur trappers once buried along the banks. Nearly two centuries later, the river's hidden DNA may pose the real threat.

Jessica Snyder Sachs is the author of Good Germs, Bad Germs: Health and Survival in a Bacterial World, published in fall 2007 by Hill & Wang, a division of Farrar, Strauss and Giroux. Her last feature for Discover looked at how antibiotics affect the body's bacterial ecosystem.

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