For more than 50 years now, there has been only one drug around to combat the immediate and longer-term effects of menopause: estrogen.

The plusses of estrogen are extraordinary — reduced hot flashes, less vaginal dryness, lower levels of “bad” and higher levels of “good” cholsterol, reduced risk of osteoporosis, cardiovascular disease and maybe even Alzheimer’s. Not to mention better mood and intellectual function, at least for some women.

But the minus is a frightening one: a possible 30 to 40 percent increase in the risk of breast cancer. That’s not huge if you’re at normal risk to start with, but it’s big enough that many women say “No, thanks,” even though the lifetime risk of dying of cardiovascular disease is six times higher than the risk of dying of breast cancer.

At long last, there may soon be an option for women trying to juggle the risks and benefits of estrogen therapy. It’s called raloxifene, the first of the “designer estrogens” that manufacturers are racing to bring to market.

On Thursday, an advisory panel of the US Food and Drug Administration will consider whether to recommend approval of raloxifene as a way to prevent one post-menopausal problem, osteoporosis. If it passes that hurdle, the FDA will probably approve it for marketing soon.

But like Premarin — the 40-cents a day pill used by most American women who take estrogen supplements — raloxifene, whose price has not yet been set, falls well short of the ideal.

The big advantage, researchers say, is that it seems not to stimulate breast tissue, as estrogen does. In fact, if early studies are correct, raloxifene may actually lower the risk of breast cancer.

That’s probably because, like its chemical cousin tamoxifen, which is already being marketed to treat breast cancer and is being studied as a way to prevent it in high risk women, raloxifene acts like estrogen in some tissues, but in others like an estrogen blocker. Estrogen is known to promote some breast tumors.

Moreover, unlike both estrogen and tamoxifen, raloxifene does not seem to stimulate uterine tissue, which means it does not cause bleeding and may not raise the risk of uterine cancer. (To offset the increased risk among women taking estrogen, doctors often prescribe another hormone, progesterone.)

Like estrogen, raloxifene also prevents bone loss, though not as powerfully. In studies of 12,000 women in 25 countries, raloxifene increased bone mineral density by 2 to 3 percent, according to Eli Lilly, the manufacturer, though it’s too soon to tell whether this translates into fewer broken bones.

The big drawback to raloxifene is that it does nothing for hot flashes, the main reason many women start taking estrogen around age 50. In some women, raloxifene actually triggers them. It also does nothing to combat vaginal dryness and doesn’t boost good cholesterol as much as estrogen. Perhaps most important, raloxifene has only been studied for three years, versus decades for Premarin, which is made by Wyeth-Ayerst.

“Many view this as a wonder drug,” says Dr. Nananda Col, an internist at New England Medical Center who has analyzed the risks and benefits of estrogen. “But I am very cautious.”

Raloxifene “has a lot of promise, but we don’t have concrete information on long-term risks and benefits,” she says, adding that some drugs initially thought to be safe, like the fen-phen diet pills, later turn out not to be.

On the other hand, it’s progress “just to have any alternative to estrogen,” says Dr. Bruce Kessel, a reproductive endocrinologist at Beth Israel Deaconess Medical Center who also advocates diet and exercise to keep the heart and bones healthy.

Dr. Isaac Schiff, chief of obstetrics and gynecology at Massachusetts General Hospital, agrees. “I believe this is a big step forward, but it’s not necessarily going to be the last agent we come to,” he says.

Currently, Pfizer Inc. is working on one new drug called droxolifene, Wyeth-Ayerst on something they call TSE-424, and SmithKline Beecham on idoxifene.

As with all designer estrogens — or SERMS, selective estrogen receptor modulators — the goal is to concoct a drug that prevents hot flashes, vaginal dryness, osteoporosis, heart disease, and possibly Alzheimer’s, but does not raise breast cancer risk. Unfortunately, nothing in the pipeline so far can do all this.

And because raloxifene, to be marketed under the name EVISTA, does not reduce hot flashes, estrogen will likely remain the drug of choice for women in the immediate throes of menopause.

“Raloxifene isn’t a substitute for estrogen for menopausal symptoms. That’s not what this is all about,” says V. Craig Jordan, director of breast cancer research programs at the Robert H. Lurie Cancer Center at Northwestern University Medical School in Chicago and a consultant to Eli Lilly.

But after a few months or years on estrogen, when hot flashes naturally abate and the reason for taking estrogen becomes prevention of heart disease and osteoporosis, it might make sense to switch to raloxifene, says Kessel, who is about to start a study on the new drug.

“If you’re taking estrogen for osteoporosis and you’re concerned about breast cancer, I would make the switch,” adds Schiff in Boston, though he notes that women should always taper off estrogen slowly and under a doctor’s supervision.

And raloxifene “would be a good initial choice for a woman who has no hot flashes and is concerned about osteoporosis,” says Dr. Ethel Siris, a raloxifene investigator for Eli Lilly and director of the osteoporosis program at Columbia Presbyterian Medical Center in New York.

Another option for such women, she and others note, is Fosamax, an already approved drug that prevents osteoporosis but has none of the other risks or benefits of estrogen.

What has people most excited about raloxifene is its apparent lack of effect on breast tissue.

“It is clear that you don’t stimulate breast cell growth with raloxifene,” Siris says, adding that preliminary data suggest there may even be “a decreased risk of breast cancer, but we don’t want to overly excite people.”

In fact, when Jordan, the Chicago researcher, studied the mammograms of thousands of women taking raloxifene or a placebo in research studies, he found “about half as many women develop breast cancer on raloxifene as on placebo over a two-year period.”

Jordan and other researchers caution that longer studies are needed. With estrogen, for instance, the increased risk of breast cancer shows up only after five or more years of use.

Another unanswered question is what effect raloxifene and its chemical cousins may have on the brain. Some scientists hypothesize that estrogen has a positive effect, which might be why women on estrogen may be less susceptible to Alzheimer’s disease. If raloxifene acts as an anti-estrogen (or estrogen blocker) in the brain as it does in the breast, it would theoretically have no such protective effect.

Figuring out precisely why the same drug boosts estrogen in some tissues yet blocks it in others is big puzzle itself, especially now that scientists know there are at least two distinct types of estrogen receptors, molecules in cells with which estrogen and estrogen-like drugs interact.

But many researchers believe that even before all these answers are in, many women may turn to raloxifen if it gets FDA approval.

That would be good news for women. And there might even be a silver lining for Wyeth-Ayerst, which makes more than $1 billion a year worldwide selling Premarin, until now without competition.

“Raloxifene will have a niche,” according to the company’s party line, “but it will not replace Premarin. It will broaden the market.”

Three weeks ago, an international team of scientists, armed with radar and a somewhat grisly plan, huddled in front of seven grave markers near a church in the tiny Norwegian coal mining village of Longyearbyen, population 1,400.

The light was winter dim, as it always is this time of year in the archipelago that Americans call Spitsbergen, less than 800 miles from the North Pole.

The Norwegians call it Svalbard, and it is the kind of place people describe as godforsaken yet starkly beautiful, where the wind from the polar ice cap is so hard “you could lean against it,” as one scientist put it last week. The temperature these days is 10 degrees Fahrenheit, and the permafrost – the layer of earth that never thaws – is close to the surface.

It is, in other words, a perfect place for quick-freezing things, like the bodies of seven young coal miners who died during the “Spanish flu” pandemic in 1918 and were buried in graves dug by dynamite, so records from the coal mining company suggest.

The 1918 flu – which killed 20 to 40 million people worldwide – was infamous for attacking the young and strong as well as the weak and old and for causing so much fluid to accumulate in the lungs that victims died by drowning. But the virus also vanished within days of causing infection, often leaving no trace as the delicate strands of its RNA simply disintegrated in the body.

That has meant that modern scientists have not been able to get their hands on the virus, much less figure out why the 1918 strain was so deadly or indentify mutations in the ever-evolving microbe that might be equally deadly in the future. That knowledge could prevent another devastating epidemic.

But viruses, or pieces of them, may still lurk in frozen tissue, so the scientists reason that if the bodies of the miners froze quickly and remained so for the nearly 80 years since, they might be able to find them.

The scientists are hoping to get permission to dig up the bodies next fall and extract tissue samples to look for the virus. The samples would be flown out to be studied in so-called P-4 laboratories in England and the United States, facilities built to prevent even the tiniest, most deadly organisms from escaping.

Any 1918 virus that still exists is probably inactive, but there is always a theoretical chance that some samples could be infectious, says Dr. Charles Smith, a pathologist at Toronto’s Hospital for Sick Children and a member of the expedition, though he adds, “I haven’t met anyone who thinks it’s a realistic possibility.”

The idea of digging up bodies to look for the 1918 flu virus is not new. Army researchers did just that in a secret mission to Alaska in the 1950s. But those bodies had not been buried in permafrost and were so decomposed that no virus was found.

The new effort is led by Kirsty Duncan, a 30-year-old gymnast-turned-climatologist at Windsor University in Ontario. Duncan, who still runs 10 miles and does 1,000 situps a day, according to a colleague, did not return phone calls from the Globe.

Other team members also declined to speak on the record, saying they had agreed on a self-imposed “news blackout.”

But a team spokesman in Oslo confirmed to The Associated Press last week that the team had spent five days using radar to determine the depth of the bodies. And Nils Lorentsen, editor of the weekly Svaldbard Posten, which has a staff of four and a circulation of 2,600, said in a telephone interview that he had accompanied the researchers to the graveyard.

He also said the bodies turned out to be buried one meter down, well into the permafrost, which starts a half meter from the surface.

That means the digging will probably go forward next year, a project Lorentsen said villagers deemed “okay” at a town meeting with the scientists on Oct. 11 at UNIS, the Longyearbyen branch of the Norwegian university system.

Final permission to exhume the bodies would have to come from the Norwegian ministries of health and cultural heritage, said an expedition member who spoke on condition he not be named.

For nearly 80 years, scientists have been fascinated – and horrified – by the ferocity of the virus that caused the Spanish flu, which despite its name is thought to have appeared first in Kansas. The virus killed 642,000 Americans over a two-year period at the end of World War I, says Dr. Keiji Fukuda, chief of the influenza branch of the epidemiology section of the Centers for Disease Control and Prevention.

That’s more Americans than were killed in World War I, World War II, the Korean War and the Vietnam War combined – and it could happen again, if the right, or wrong, combination of genes pops up in another mutation in the influenza family.

Influenza viruses that affect humans are made up of the single-stranded genetic material RNA and come in one of two main types, A or B, said Dr. John J. Treanor, an infectious disease specialist at the University of Rochester Medical Center.

The B type does not cause worldwide pandemics. But the A type, including the Spanish flu virus, does, probably because it infects not just people but waterfowl, chickens, pigs, horses, seals, and whales.

Both A and B flu viruses are constantly mutating. Usually, the mutations are minor, a process called antigenic drift that results in small changes in the two major proteins on the virus’ surface, hemagglutinin and neuraminidase. Though small, these changes are big enough that if you are vaccinated against the flu or become infected one year, the antibodies you make probably won’t protect you against the new strains a year later.

But sometimes the mutations are huge, a process called antigenic shift, rather than drift. Scientists think this often occurs when a flu virus from a bird and one from a human simultaneously infect a pig.

The two viruses combine and swap genetic material inside pig lung cells and the result is a new, virulent virus, says Treanor, adding that this occurs every 10 to 20 years – including in 1957 and 1968, pandemic flu years.

Last summer, scientists were alarmed that a terrible pandemic might be brewing when a 3-year-old child in Hong Kong died of an influenza A virus that appeared to have come directly from birds, without going through a pig host. But so far, no other humans have been found to be infected with this virus.

For a while, scientists thought the deadly 1918 flu virus might also have jumped directly from birds to people. But last March, researchers at the Armed Forces Institute of Pathology in Washington, D.C., led by pathologist Jeffrey K. Taubenberger, reported in the journal Science that they had deciphered a small part of the 1918 virus and found that it had adapted to growth in mammals.

The group had access to a unique asset, said Ann Reid,a research biologist at the institute – millions of tissue samples from as long ago as the Civil War preserved in parafin.

The team searched the archives for samples from people who had died quickly in 1918 – fast enough that traces of the elusive virus might not have disappeared. They found more than a dozen such samples and examined them under the microscope.

They hit pay dirt with one, from a 21-year-old Army private who died at the height of the pandemic. Using a technique called PCR, or polymerase chain reaction, the researchers amplified the sample until they had enough to try to determine the exact sequence, or genetic code, of the viral RNA.

So far, they have identified more than 7 percent of the virus’s genetic makeup, said Reid, adding that the Armed Forces team is now collaborating with the Spitsbergen group.

But “we still haven’t found the smoking gun,” she said, meaning that the bits of virus already studied provide no clue as to why the 1918 virus was so lethal. But the work is still proceeding, and the final clue may come from the little churchyard in Longyearbyen.

“There is competition between the Longyearbyen group and those working on parafin samples in warmer climes,” said one researcher working on the Norwegian project. “But I don’t care who wins, because if the viral fragments are found and decoded, the winner is humanity as a whole.”

Protect yourself

The best way to protect yourself against influenza, which leads to the death of 20,000 Americans a year, is to get a flu shot. But if you do get sick, anti-viral drugs can help.

So far, only two are on the market, amantadine and rimantadine. Both work only against Type A influenza, the more serious type, and both have side effects that can make them unsuitable for some people. Two newer drugs under study are Zanamivir (GS167) and a competitor called GS4104, both of which work against Type A and Type B strains.

Zanamivir reduces symptoms if taken early, according to a study published in September in the New England Journal of Medicine.

It works by blocking an enzyme called neuraminidase that the virus needs to spread, says Dr. John J. Treanor of the University of Rochester Medical Center, one of the authors. The drug, inhaled or taken as a nasal spray, was tested in 262 adult flu patients in more than 60 medical centers in the United States and Europe. It cut the duration of flu by about a day, and in patients with fever, by three days.

Zanamivir is being developed by Glaxo Wellcome, for whom several of the researchers, including Treanor, have consulted.

The other drug, GS4104, also a neuraminidase blocker, is under study by F. Hoffmann-LaRoche Ltd. and Gilead Sciences, Inc.

In a study of 80 people with the flu, the researchers reported in September, the pill decreased the duration of symptoms by 50 percent. In another study, the drug prevented flu in all 37 volunteers who took it after being deliberated infected with the virus.

New vaccines are also in the works, among them a DNA-based product being studied in Tennessee and at the University of Massachusetts Medical Center.

As for this year’s flu season, scientists are expecting no surprises, says Dr. Susan Lett, director of immunization at the state Department of Public Health. But if you haven’t gotten your shot, you should – they’re 70 to 90 percent effective.

If you do get the flu, you can ask your doctor about anti-flu drugs. But in most cases, you’ll probably be told to try the old standby stuff – rest, fluids and acetaminophen (not aspirin, which can cause Reye syndrome in kids with the flu.)

Information on where to get flu shots is available from your local Board of Health, or check with your doctor or health plan.

A few weeks ago, a 35-year-old Connecticut man was stunned by his diagnosis – scleroderma – and even more surprised by his doctor’s advice: Whatever you do, don’t check the Internet.

“It’s not just that there’s misinformation out there,” Dr. Ann Semolic an internist in Willimantic, says she told the frightened young man. “It’s that there are 100 different ways any disease can play out, but you will just have one. Let’s not worry about the other 99.”

People think that if information “comes over a $ 2,000 machine, it’s got to be reliable,” she says. “But that’s not necessarily true.”

Some patients are helped enormously by information they find on the Net, she adds, citing a woman with panic disorder who returned reassured after cruising the Net. But others wind up scared, confused and misled.

“You have to learn to be a good judge of information,” agrees Dr. Bruce Karlin, a primary care physician in Worcester whose concern led him to attend a recent conference on Internet health information at MIT.

“I want patients to bring me the information” they find on the Net, he says. “I’ll be glad to referee.”

The exploding world of medicine online is a vast “place,” with an estimated 10,000 to 25,000 web sites devoted to health matters, and more coming along all the time.

About 40 percent of people who cruise the Net “do so for health information at one point or another,” says Dr. Helga E. Rippen, a physician-engineer who runs a health information think tank in McLean, Va.

Yet the quality of the information ranges from the impeccable to the intolerable, says a growing group of Net watchers like Rippen who are working to give consumers better tools to assess medical advice online.

On Friday, for instance, Rippen’s think tank, the Health Information Technology Institute, will host a “summit” at which several dozen specialists will hammer out guidelines to help distinguish solid advice from schlock.

Last month, a World Health Organization group met in Geneva to study the problem of illegal, cross-border prescription drug sales on the Net and general problems of information about medical products touted online. One group trying to coordinate all these efforts is Internet Healthcare Coalition, which incorporated in August.

And there’s the Health on the Net Foundation in Geneva (www.hon.ch), which has developed a self-policing system complete with a seal of approval, called HON, for web sites to display as evidence their information is solid. But the system is purely voluntary.

The very appeal of the Net, of course, is that it is utterly democratic – anyone from the most elite researcher to the greediest shyster to the most desperate patient can say anything she wants.

There’s no tedious peer review of data before it goes public, as there is in medical journals. No standards of accuracy and fairness. No way to ensure that all sides get equal time. All that’s fine, even with many of those concerned with bad information.

In other words, you’re on your own in the medical maze.

Well, not totally. The folks now slaving to create consumer guidelines have some good ideas to help you evaluate health information online. So caveat surfer, and here goes:

Authorship, or who wrote this stuff?

“If the author or person publishing this information doesn’t give you basic identifiers and credentials, you should be suspicious,” says Bill Silberg, editorial director for medical news and new media at the Journal of the American Medical Association. In April, JAMA published its own suggested guidelines for evaluating health information online.

You can also answer the “whodunit” question by clicking on “about us” on many web site home pages, says Deb Falk, vice president of Mediconsult.com, a group that combs medical journals and rewrites articles for a lay audience on the Net.

Attribution.

Web sites should clearly list sources for information. If it comes from an authoritative publication such as the New England Journal of Medicine (www.nejm.org) or JAMA (www.ama-assn.org/jama), for instance, you can trust the data has been vetted by experts. They’re not always right, of course, and new research comes along regularly to shake up the prevailing wisdom, but they’re not likely to be off-the-wall. The same goes for many other journals, such as those in big data bases like Medline.

Information from major medical centers and government agencies such as the National Institutes of Health is considered reliable. Pharmaceutical companies offer valuable information, but remember that they’re selling products.

You can get some clues from the language of the Net itself. Sites with a “.com” after their name are commercial. Those with “.edu” are educational, those marked “.org” are nonprofits, those with “.gov” are governmental and those with “.mil” are military. Knowing that begins to give you some idea what their agenda might be. Those marked “.net” are providers directly involved with Internet operations. Some sites are also marked with a country code.

But it gets tricky. You can start out on a reputable site, then click on a “link” to a site with much shakier information, so keep track of the web addresses.

Disclosure.

Ideally, people who put information on the Net tell you about any financial or ethical conflicts of interest. But they may not, and hidden agendas may be subtle. A group for patients with a disease may shape its message to exclude other viewpoints. It’s also a red flag if somebody explains the basics, then suggests only one treatment.

Timeliness.

Check the date that the information was posted on the site and see if it has been updated. Newspapers, TV networks and medical journals constantly update information. Not all web sites do.

Anecdotal information.

The Net puts you in touch with two things, “data and people, and a lot of times, people can be more useful,” says Dr. Tom Ferguson, author of “Health Online,” a book about finding health information and support groups electronically.

People with a newly diagnosed problem often start out looking for disease information, but wind up using the Net to stay in touch with others in the same boat, Ferguson says.

This can be helpful and frightening. Through “chat rooms” and online discussion groups, you can find great information and support. You may also read stories that scare or depress you. The bottom line is that anecdotes, while emotionally powerful, tell you about only one person’s experience.

Studies, the good, the bad and the confusing.

It takes a sophisticated eye to read a study carefully, especially to notice what information is not there.

At first glance, you may not see that the study involved only a handful of people. Or that that there was no control group, or that the study was not “double blind,” meaning doctors and patients weren’t told who was getting, say, a real drug and who, a placebo.

You may also not notice whether the study was done retrospectively, that is, by asking patients to recall events or by looking at records. In general, a study is more convincing if researchers follow patients and recorded what happens as treatment goes along.

And it can be easy, especially if a study tells you what you desperately want to hear, to be taken in by a site that touts one study but fails to note studies that reached different conclusions.

Target audience.

The Net serves everybody – researchers as well as people who know more about their cars than their bodies – so look for sites that neither talk down to you nor leave you in the technobabble dust.

Some sites do an excellent job at this, including the National Cancer Institute’s site (wwwicic.nci.nih.gov/). Once at the site, you can choose information written for patients, health professionals or researchers. One strategy is to start at the patient level, then work your way up later on, if you still want to know more after you’re more comfortable with your diagnosis and the information you’ve already digested.

Tattling.

The Net can be self-correcting. If you find something misleading, tell your friends, the webmaster who posted the bad information or a higher authority, if you can figure out who that is.

The US Food and Drug Administration, for instance, is charged with making sure pharmaceutical manufacturers make only approved claims for products on package labels and in advertisements. If you spot an improper claim, tell the FDA (www.fda.gov) about it.

The Internet Healthcare Coalition (www.ihc.net) is also working with drug makers, publishers and others to improve health information online, says John Mack, the IHC president.

Don’t fly solo.

Just as you use the Net to amplify what your health care professional has told you, use that person to help evaluate what you learn on the Net.

If it sounds too good to be true, it probably is.

Examples abound here, but here’s one. The California-based Wine Institute has barraged reporters and Net surfers of late with blurbs on the seemingly-endless virtues of the grape.

But when the Center for Science in the Public Interest, a watchdog group in Washington, took a close look at the site (www.wineinstitute.org), it found what it called “propaganda” that was “disguised as objective information based on recent research,” including claims that booze may help with everything from a cold to pancreatic cancer.

All of which means you have to use common sense.  Or, as Ferguson, the “Health Online” author, puts it, “You can’t check your brain at the door.”

In a Sept. 29 column on hypochondria, the citation of a newly-released book was left out due to lack of space. That book is “Phantom Illness – Recognizing, Understanding and Overcoming Hypochondria,” by Carla Cantor with Dr. Brian A. Fallon; published by Houghton Mifflin.

Things should have been blissful for Carla Cantor, a New Jersey freelance writer who had just had her second child.

But soon after her son’s birth in 1990, Cantor, now 42, began experiencing bad pains in her wrist. Doctors suggested cortisone shots, wrist splints, not nursing the baby. Nothing helped.

As her pain spiraled out of control, so did her panic – and symptoms, which soon included hair loss and sun allergies.

With the doctors seemingly stumped, Cantor began her own research – and soon became panicked that she had systemic lupus erythematosus, an often debilitating autoimmune disease.

One night, feeling “so distraught I didn’t know what to do,” Cantor rushed to an emergency room, where doctors still couldn’t find a cause for her distress. She wound up spending the night – on the psychiatric ward.

In a sense, that night was a first step toward recovery for Cantor, who hopes her book on hypochondria, just out in paperback, may help others living in daily dread of disease.

As a culture, we seem to have managed, slowly, to destigmatize cancer, even to take away some of the misplaced shame over psychological problems like anxiety and depression. At least we seem able to talk more openly about such things now.

But hypochondriacs – who may constitute 6 to 12 percent of those who visit doctors – still get no respect.

Worry too much, or too loudly, about your health when doctors can find nothing very wrong, and many people – including those in the white coats – assume you’re faking it, hopelessly neurotic, or just looking for attention.

Wrong, say psychiatrists who study those who “somatize” excessively, or express emotional distress via bodily symptoms.

Many people who have health worries out of proportion to their medical condition are depressed or have underlying panic or anxiety problems, says Dr. Arthur Barsky, director of psychosomatic research at Brigham and Women’s Hospital.

Increasingly, researchers suspect some may have a version of obsessive-compulsive disorder, says Dr. Brian A. Fallon, Cantor’s co-author and a researcher at the New York State Psychiatric Institute.

And the more researchers understand about the inner workings of these patients, the more they are finding treatments that help.

In a small pilot study, for instance, Fallon found that the antidepressant drug Prozac helped 70 percent of patients, though he says it takes high doses – 60 to 80 milligrams a day, not the 20 to 40 mg used for depression. (Don’t increase your dose of Prozac or similar drugs on your own – for one thing, these medications can transiently increase anxiety and agitation.)

Fallon’s preliminary findings are so promising that the National Institute of Mental Health recently awarded him a $ 500,000 grant to do a bigger placebo-controlled study.

And non-drug therapies may help, too, says Barsky, who also has an NIMH grant to study 180 people to see if cognitive-behavioral therapy can teach them to worry less.

There’s no question that, on top of their misery – and hypochondriacs really feel the symptoms they express – these suffering souls carry an extra burden of stigma, probably because other people tend to ridicule or distance themselves from problems they don’t understand, says Dr. Ken Duckworth, a Massachusetts Mental Health Center psychiatrist.

To be sure, some people really do feign illness – the so-called malingerers and those with Munchausen’s syndrome. These folks know they’re not sick and fake symptoms to get attention or, in the case of some drug addicts, to get painkillers.

But people with hypochondria and so-called somatization disorder are quite different – they really fear they’re sick.

It’s normal to “somatize” at times, or have unexplained symptoms that prompt a medical visit – a mole that might be melanoma, a memory lapse that might be Alzheimer’s.

And it makes sense to check such things out. In fact, reassuring the worried well is a large and appropriate part of what doctors do; an estimated 50 percent of primary care visits are by people who turn out to have nothing seriously wrong.

But if your fears are constant and extreme, despite the lack of detectable disease, or if they’re out of proportion to your medical state, it’s time to ask what’s really going on.

For instance, if you repeatedly focus on a symptom and demand that somebody take care of you and even operate on you right away, you may have somatization disorder, says Dr. Charles Ford, a University of Alabama psychiatrist. Such people often worry more about getting rid of the immediate symptom than what the symptom may mean.

If you don’t care so much about your immediate pain or symptoms but are terrified they mean you have a fatal illness, you may be a hypochondriac, especially if you find yourself poring over medical books, cruising the Internet, and demanding endless, often expensive tests. Another clue is if you can’t stay reassured by good news, or you develop a scary new symptom as soon as you let go of an old one.

“These people suffer,” says Barsky. “It is as if they had cancer. They die every day.”

They also cost the health care industry an estimated $ 30 billion a year, say Fallon and Cantor, now director of publications at New York University Medical Center.

To address both their suffering and the economic costs, sometimes derided as “frequent fliers” or medical “addicts,” many health plans offer special programs.

Harvard Pilgrim Health Care, for instance, has a six-week course for those who have unexplained physical complaints or trouble coping with a diagnosed medical condition. It costs $ 88 for members and $ 140 for nonmembers.

The program is designed as an adjunct to other treatments, including psychotherapy, says psychiatrist Dr. Steven Locke, chief of behavioral medicine at Harvard Pilgrim.

But the program also cuts down on medical visits for those who take it, from an average of 11.6 a year before the course to 6.5 afterward, a savings of $ 428 a year per patient.

The program works by helping people “develop the capacity for awareness of recurrent behavior patterns” and change those that are counterproductive, adds Dr. Matthew Budd, an internist who designed the Harvard program and now runs a health care consulting company in Cambridge.

Procter & Gamble Co., which markets the Harvard course to managed care plans nationwide, clearly buys that. P&G won’t give specifics but says it is “very encouraged by early results.”

But others take a more cautious view. Education helps if ignorance is the problem, but it can’t substitute for needed therapy, says James Wrich, CEO of J. Wrich & Associates in Chicago, a firm that reviews efficiency for health care systems.

And there are other ways to save money and allay fears. One way is to offer more medical visits, not fewer, and to schedule them every few weeks, says Ford, the Alabama psychiatrist. “If they know they have an appointment scheduled, they’re less likely to need emergency room visits, which are more costly.”

But you don’t have to wait for your doctor or health plan to step in. If you think you freak out too much about health, you can try focusing on things other than your symptoms.

In one study, some people who had their teeth pulled were asked to rate their pain every 20 minutes, while others were only asked two hours later. Those who were asked to pay more attention to their pain reported more of it, notes Barsky.

And you don’t have to make medical woes the center of your identity. In one study, Barsky’s team interviewed people in a clinic, asking them to describe themselves.

People who were not hypochondriacs spoke of being teachers, fathers, of hobbies – even if they had cancer. Those who were hypochondriacs described themselves first and foremost as patients.

It can, of course, be tough to face up to that tendency in oneself, as Carla Cantor knows. But it can also be liberating. Cantor now believes that her fears stem from a car accident years ago in which she was driving and a friend was killed.

Today, she takes an antidepressant and has come to see her recovery as like that of an alcoholic: “You always have to be aware that you can relapse and that help is available. And to realize you’re not alone.”

Where to learn more

You might want to read:

• “Phantom Illness – Recognizing, Understanding and Overcoming Hypochondria;” by Carla Cantor with Brian A. Fallon, M.D.; Houghton Mifflin Co.
• “Hypochondria – Woeful Imaginings;” by Susan Baur; the University of California press.

Brian Dube was 14 when severe acne first struck.

“It was pretty bad,” says Dube of his initiation into the blotchy hell that virtually all teenagers experience to some degree just before and during puberty. But a five-month course of the potent drug Accutane worked miracles.

“My face was very, very clear” for years, says Dube, who is on leave from Bristol Community College and working as a mental health counsellor in New Bedford.

Then, this year, his acne flared again. For a young man of 24 who prides himself on being “pretty well-dressed,” it’s distressing, he says, to wind up again with “ugly things on your face.”

In his case, the acne came back in late winter. But for many young people, acne flares up in the fall in a paroxysm of perversity – just when classes, jobs, sports and romances begin anew and the urge to put one’s best face forward is strongest.

Dermatologists don’t know why this is, but they do have educated guesses – and some increasingly good ways to treat it.

Some think that exposure to the sun’s ultraviolet rays in the summer may make acne better – an effect that would clearly lessen as the days get shorter.

But several large studies have shown that UV doesn’t do much except camouflage blotches, says Dr. Robert Stern, vice-chairman of the dermatology department at Beth Israel Deaconess Medical Center. A summer tan, in other words, may simply make red pimples and other signs of acne less noticeable.

Others, among them Dr. Nancy M. Satur, a dermatologist at Scripps Memorial HospitalsCQ in Encinitas, Calif., suspect that acne flares up in the fall because dry, dead cells caused by summer sun exposure begin shedding and clogging up pores.

Still others suspect it’s mostly stress – the body’s hormonal response to the onslaught of intellectual, physical and emotional demands that come with this time of new beginnings.

Whatever the trigger – and specific foods, including chocolate, have not been proven guilty, though a high fat diet is suspect – the underlying cause of acne is an unhappy combination of hormones, clogged pores and bacteria.

A couple of years before puberty, a hormone made in the adrenal glands called DHEA (dehydroepiandrosterone) begins signalling the sebaceous glands, at the base of hair follicles in the skin, to pump out oil.

DHEA is the same hormone that some people take as a dietary supplement to ward off aging and is tightly enough linked to acne that it’s been dubbed the “acne androgen,” says Dr. Donald Lookingbill, a dermatologist at the Mayo Clinic branch in Jacksonville, Fla.

Once puberty is in full swing, other androgens, or male hormones made in the ovaries and testicles, further stimulate the glands. Though both males and females get acne, boys often get it worse because they have more androgens.

As the oil glands go into overdrive, the ducts through which the oil travels to the skin surface tend to become clogged with a sticky combination of oil and cells shed from inside the duct, says Dr. Barbara Gilchrest, chairman of the dermatology department at Boston University School of Medicine.

The first sign of trouble is a tiny bump at the surface, a whitehead or “closed comedo,” in medical jargon.

If the pore enlarges, the gunk in the duct may oxidize and turn black, creating a blackhead or “open comedo.” (Contrary to widespread belief, blackheads are not caused by dirt or lack of good hygiene.)

Bacteria in the follicle may also start gorging on the oil, or sebum, turning it into a fatty acid that causes inflammation, says Dr. Bonnie Mackool, a Massachusetts General Hospital dermatologist.

The result is an all-too-familiar blotch that most people call a zit or a pimple.

Luckily, there are lots of ways to banish zits, including washing your face – no more than a couple of times a day and without harsh scrubbing – with a non-irritating soap.

You can also minimize the use of “occlusive clothing” – shoulder pads, baseball caps worn backward with the strap on your forehead and tight Spandex garments.

If you spend all day on the phone, try cleaning the receiver. If you habitually rest your chin on your hand, stop.

You should also go easy on hair pomades, which can trigger acne along the hairline. That goes for makeup, too, some say, although many brands now are “noncomedogenic” – less likely to cause acne.

“We are taught by department stores to put something on our skin constantly,” says Gilchrest of BU, but it’s a bad idea. “If you can convince people to stop putting stuff on their face, acne gets better.”

Over-the-counter remedies like Oxy-5, Oxy-10 or Clearasil that contain benzoyl peroxide often help by killing bacteria. Stridex pads, which contain salicylic acid, also help.

But steer clear of harsh scrubbers or cleansing grains – these can actually aggravate acne, dermatologists warn. And resist the temptation to pop your pimples – you can make things worse.

If you try this simple stuff and nothing works, see a dermatologist, who may prescribe topical antibiotics such as erythromycin or clindamycin, or oral antibiotics, usually tetracycline or erythromycin. These often clear up acne, though drug resistance is becoming a problem.

Retin-A, or tretinoin, is another effective prescription medication – it works by keeping follicles from clogging up. A newer form, Retin-A-Micro, works, too, and may be less irritating to the skin. Another retinoid-type drug, Differin, may also help, as may a non-retinoid medication, Azelex, which also fights bacteria.

Women often get improvement with a birth control pill called Ortho-Tricyclin that offsets the androgen hormones that can cause acne. Two other birth control pills, Desogen and Ortho-Cept, also seem to work against acne, although they are not approved for this use.

As a powerful last resort, some people, like Brian Dube, use Accutane, which is widely viewed as the most effective of all acne drugs because it virtually shuts down the sebaceous glands.

But Accutane is highly toxic to a developing fetus, which means any woman of childbearing age who takes it must be on birth control pills to prevent conception.

When acne flared earlier this year, Dube took Accutane again, and, as before, was delighted to see his face clear up dramatically. Now he takes an oral antibiotic and Retin-A to control small breakouts.

“You don’t have to have acne,” he says. “No matter how mild or severe it is, if it’s making you insecure, get it treated.”

Joel Cutler was 8 or 9 when he came down with Crohn’s disease, a “brutal” illness, as he puts it now, that causes incapacitating diarrhea and painful abdominal cramps.

When he was 12, he lived for a year with an ostomy, an artificial opening in the abdomen through which fecal matter empties into a bag. At 15, he spent three months at Children’s Hospital, living solely on intravenous feedings to give his tortured gut a rest and his body a chance to grow.

Today, at 39, he runs a business in Newton, is happily married and delights in his baby daughter. But his Crohn’s still flares up sometimes, and he can’t play golf, go sailing or do anything that keeps him very far from a bathroom.

Yet he is amazingly upbeat and eager to tell the 1 to 2 million Americans with inflammatory bowel disease – a category that includes Crohn’s and ulcerative colitis – that it is time to end the silence about these most private afflictions.

It is also a time, researchers say, for growing hope. While the cause of inflammatory bowel disease is still unknown – genetics seems to play a role; stress probably does not – there are a number of new treatments in the pipeline.

IBD or inflammatory bowel disease – not to be confused with the more common but less serious “irritable bowel syndrome” – is rarely fatal. But as Cutler can attest, it involves an intermittent battle with severe diarrhea and pain that at times can be both physically and psychologically stressful.

Part of that stress occurs because the problems strike so early in life, usually between ages 15 and 40. In fact, many parents only learn that a child has bowel disease when she stops growing because she can’t absorb enough calories.

Parents realize “they haven’t had to buy new clothes, especially new shoes . . . or the child has remained at the same height for a long time,” says Dr. Richard Grand, chief of pediatric gastroenterology at New England Medical Center.

For many teenagers, the only way to resume growing is to insert a tube through the nose and into the stomach at night and pump in a formula of 1,500 to 1,800 calories as they sleep. For adults, who have already attained full height, nighttime feedings are usually not necessary, although they may lose weight and become malnourished during flareups.

It’s not always easy to distinguish between Crohn’s and ulcerative colitis, but it’s worth the time and money to undergo barium X-rays and colonoscopy – in which a doctor examines the lining of the intestine through a tube – because the treatments, especially surgeries, differ depending on which form of inflammatory bowel disease you turn out to have.

In ulcerative colitis, the mucosal lining of the colon (large intestine) is inflamed, perhaps because of a misguided attack by the immune system or an infection. Flareups can be triggered by non-steroidal anti-inflammatory medications like ibuprofen.

Whatever the trigger, the result is that immune cells and chemicals they secrete called cytokines flock to the intestinal lining and damage it. In virtually all cases, ulcerative colitis starts in the rectum and spreads upward, sometimes involving the entire colon.

Over time, this inflammation raises the risk of colon cancer, especially for people with widespread disease. The normal lifetime risk of colon cancer is 5 percent; for those with ulcerative colitis, it’s five times that, says Dr. Mark A. Peppercorn, director of the center for inflammatory bowel disease at Beth Israel Deaconess Medical Center.

Increasingly, though, people with ulcerative colitis have better treatments to choose from. Many, for instance, get relief from so-called 5-ASA drugs such as sulfasalazine. Newer drugs in this class include Asacol, Pentasa and Dipentum.

If these fail, steroids like Prednisone often help, though they have side effects. A drug called budesonide, already on the market in Europe and Canada but not yet approved here, appears to act like Prednisone but with fewer side effects.

And doctors sometimes use even more potent drugs like Imuran (azathioprine) or 6-MP (mercaptopurine), says Dr. Bruce Sands, director of inflammatory bowel disease clinical research at Massachusetts General Hospital.

Some studies suggest that omega-3 fatty acids – available as dietary supplements – may also help, but you have to take quite a bit of this stuff, so check with your doctor first.

Surprisingly, the same nicotine patches that smokers use to kick the habit may work, too. (For unclear reasons, smokers are at lower risk for ulcerative colitis and those who quit have twice the normal risk for two years. But quitting still pays.)

And then there’s surgery, which usually involves removing the entire colon. The result is “you don’t have ulcerative colitis anymore because you don’t have a colon,” says Dr. Kenneth R. Falchuk, a gastroenterologist at Beth Israel Deaconess.

If the colon is removed, surgeons either create a hole in the abdominal wall through which feces exit or they attach the end of the small intestine to the anus and create an internal pouch to collect feces.

People who have the internal pouch go to the bathroom normally, though often five to six times a day – an improvement over the 10 to 20 times a day many had before. In some people, however, the internal pouch itself may become inflamed.

If the problem is Crohn’s disease, parts of both the large and small intestine may be inflamed, and the stomach, esophagus and mouth may be involved, too.

Although some researchers think there may be a link between Crohn’s disease and measles vaccination, this is unproven, and vaccinating kids “is not a serious worry,” says Grand.

Many people with Crohn’s also develop abcesses (pockets of infection) or fistulas – perforations of the intestine that allow feces to travel to the bladder, vagina, abdominal cavity or skin. Strictures, or scar tissue that can create intestinal obstructions, are also common.

In general, extensive surgery is less useful for Crohn’s because the disease tends to recur, although surgery can help with strictures, abcesses and fistulas.

Many of the medications for ulcerative colitis help in Crohn’s disease, too, but there are others as well, including antibiotics and a class of drugs that work on cytokines, the natural substances that act as messengers for the immune system.

Though not on the market yet, a drug called cA2 has yielded “very exciting results” in two-thirds of patients tested, says Peppercorn of Beth Israel Deaconess.

It’s not clear whether cA2 will be equally effective in ulcerative colitis, adds Sands of MGH, but several other drugs, including two cytokine-based drugs, are being studied.

“These are very exciting new drugs,” says Falchuk of Beth Israel Deaconess. “They are not commercially available, but doctors in this area can channel patients to these trials.”

But for people like Cutler who have battled bowel disease for years, it’s not just the new drugs that are exciting. It’s the hope that, as people go public with problems that have historically been shrouded in silence, the stigma will decrease.

“People with these diseases go through long periods of feeling really, really horrible,” says Cutler. But “I honestly and truly believe that in many ways, finding an equibilibrium in life from having a difficult disease has made me stronger.”

To learn more

 For more information about Crohn’s disease and ulcerative colitis, call the Crohn’s & Colitis Foundation of America, Inc.: – 1-800-343-3637 for brochures.

• 1-800-932-2423 for information on support groups
• 617-449-0324 for the Northern New England Chapter.