Cancer cells under a microscope. Colored stains
mark different compartments in the cell. The nucleus is
red and lysosomes (which break down waste) are purple.
(Image: Carolin Zehetmeier, Morphosys AG, Germany)

Dr. Susan Love thinks breast cancer researchers need to get over their addiction to rodents.

America’s most famous breast cancer surgeon started treating women some 30 years ago. “And we’re still doing the same thing we did when I started,” she told a crowd in San Francisco last month at the Sage Bionetworks conference, aimed at transforming biomedical research.

“Surgery radiation, chemotherapy, hormones, and now we’ve added a little bit of targeted therapies,” said Love, a clinical professor of surgery at UCLA. “We never subtract anything, mind you, we only add things on top. And our results are about the same.”

Although breast cancer incidence and mortality have decreased since 1998, by 1.3% and 2% respectively, more than 200,000 women will be diagnosed with breast cancer this year and more than 40,000 will die from it. Nearly 110 women die from breast cancer every day.

Experts think earlier detection and better treatments account for the decline in deaths, but screening carries risks. With mass screening comes overdiagnosis—that is, diagnosing a condition that would not prove symptomatic or fatal—and with overdiagnosis comes overtreatment and other potential harms (see video below). Screening technology can’t distinguish between aggressive and harmless tumors, which can shrink or even disappear on their own. Overdiagnosis will likely just increase as imaging technology finds smaller and smaller tumors.

Medical experts acknowledged in an editorial in the Annals of Internal Medicine last month that it’s time to recognize overdiagnosis as a serious problem. Most patient-education materials don’t even mention overdiagnosis and most women aren’t aware of the possibility, the authors said. As they pointed out, and any woman knows, “the impact of a cancer diagnosis lasts a lifetime.”

It’s hard to think of a physician who’s done more to acknowledge the trauma of breast cancer than the author of the best-selling “Dr. Susan Love’s Breast Book,” now in its fifth edition.

That book, along with Love's early refusal to accept the oxymoronic (emphasis on moronic) “early detection is your best prevention” mantra of mainstream cancer and advocacy organizations, won her a place of honor among frustrated breast cancer activists, who know all too well that if you can diagnose cancer, you haven't prevented it. Detecting it, by definition, means it's there.

The surgical tools used on breast cancer
patients in the 18th century look gruesome, but
aren't really so far removed from the "slash, burn
and poison" approach to breast cancer today.
(Illustration: Louis-Jacques Goussier)

Activists have long pushed researchers to shift their focus from treatments and cures to true prevention.

Despite $4 billion spent on breast cancer research, researchers still don’t know what causes it or how to prevent it. Yet Love believes that the tools exist to “eradicate breast cancer within our lifetime” if we ask the right questions.

And for decades, Love has helped shine the spotlight on causes, not cures, to spare women from that dreaded diagnosis. But that goal will remain elusive, she believes, as long as researchers keep studying the disease in rodents. That’s because mice and rats don’t get breast cancer. Researchers have to give it to them.

So she’s been trying to wean researchers off rodents. “I can say this is a good study, you could do that in women, and they say, ‘Let me tell you about my rats.’ ”

Yet researchers can learn valuable insights into the origins of disease by comparing people with an illness to matched cohorts of healthy people, as the legendary Nurses’ Health Study has demonstrated for heart disease, diabetes and other conditions.

Finding the causes and, ultimately, how to prevent breast cancer requires a radical shift in thinking, Love said. And that means that at least some researchers have to give up their rats and mice and start working with the people who get the disease.

Researchers used to tell Love that even if they did want to study women, they didn’t know how to find them. But she knew that was the easy part. So for more than three years, the Dr. Susan Love Research Foundation has been recruiting an online "army of women" with a target of enrolling “one million women and a few good men.”

Dr. Susan Love spoke at the Sage Bionetworks conference in San Francisco last month. The Seattle-based nonprofit is dedicated to “moving beyond the current medical information system and its rewards.”

“Scientists come to us with studies that need people, and we e-blast them out to everybody in the army,” Love said.

So far, they’ve recruited 365,000 women for about 60 studies. Seven in 10 of the women don’t have breast cancer, but are "altruistic,” Love said. They’re willing to undergo unpleasant procedures to help researchers figure out root causes. In one study, women in the control group had to endure a sigmoidoscopy and a biopsy. And Love got more enrollees than researchers could use.

By the end of this summer, the foundation will be launching its own Health of Women Study. The large online breast cancer cohort study will follow women with and without a diagnosis to identify new risk factors. It will also follow breast cancer survivors to identify factors that predict long-term survival and consequences of different therapies.

Any woman over 18 can register online or with a mobile phone. (Men are welcome, too.)

Love’s study will let participants suggest questions they’d
like to see tested, because she thinks you don’t
need a PhD to come up with a good idea.

She told her San Francisco audience that early theories about the cause of human papillomavirus (HPV) came from observations of people who knew a man whose wife died of cervical cancer, and who then married a second woman who died of the same cancer. “They said, well maybe it’s the guy.”

“And then we figured out it was sexually transmitted, then we figured out it was a virus and now we have a vaccine.”

Potentially, Love reminds us, “Everybody is a patient.” She thinks eliminating disease is something we should all do together.

“”

We've taken another baby step away from the current one size fits all health care system.

We may finally be at the threshold of the age of personalized medicine. In a recent study, scientists were able to predict that a man was at a higher risk for developing Type 2 diabetes and over a two-year period tracked his health as he developed the disease. And even better, because they caught it so early, they were able to stave off the diabetes with lifestyle changes. This man’s glucose levels have returned to normal.

Wow. This story highlights the promise of at least one aspect of personalized medicine. By looking at someone’s DNA, you can predict what might go wrong with someone and so keep an eye out for early symptoms. Or maybe even start out with the right lifestyle changes that will keep the disease from developing in the first place.

This study also showed that intensely studying a single person can yield potential benefits for lots of other people. The researchers saw that just before the test subject’s glucose levels spiked, he had a viral infection. No one was really looking for viruses that trigger Type 2 diabetes in people. Now they will. (Keep in mind we don’t yet know if the two are connected or if it was just a coincidence.)

The study also points to the obstacles we still need to overcome to realize the full potential of personalized medicine. The top ones I could think of off the top of my head are our own ignorance, the inconvenience, the expense, and our lack of willpower.

The researchers were able to predict an increased risk for diabetes as well as an increased risk for high triglycerides but very little else. There is certainly more information lurking in his DNA…we just don’t understand our DNA well enough to tease it out yet.

Soon your treatments will be tailored for you based on at least partly on what's in your DNA.

Another related issue is whether we actually do know enough to make good predictions or if we just got lucky here. In other words, was his developing Type 2 diabetes a coincidence or was he really at a higher risk for getting it? He didn’t have any classic risk factors but given that so many people in the U.S. have the disease, it could have been chance. Doing many more studies on lots of different people should give us some idea about how predictive our DNA really is right now.

Besides our still sketchy knowledge, we also have to deal with the expense and inconvenience of this form of personalized medicine. The test subject had over twenty blood draws over a two year period that each looked at tens of thousands of different things. Not many people would put up with so many blood draws. And the expense of looking at all those different molecules is prohibitively expensive.

A better knowledge of our risks can help with the second point. Once we understand our DNA better and so know what are most likely risks are, we’ll be able to test for fewer molecules which should make the whole thing more affordable. This may also solve the first problem too.

Maybe in the future we’ll look at few enough molecules or the tests will be sensitive enough to get the information we need from a simple finger prick. Then we’d all be like folks with diabetes, self testing our blood on a regular basis. And hopefully in the more distant future, we’ll have some sort of implant that reads the information for us automatically without the need for a blood draw.

All of these are technical hurdles that will almost certainly be overcome at some point. The last obstacle, though, is much more difficult. It deals with human nature.

One reason this is such a powerful story is that the test subject was able to get his glucose under control without the use of medicines. This is not only good for him but it suggests that this form of personalized medicine may prove to be cost effective sooner rather than later. Keeping his Type 2 diabetes at bay will probably save tons of money over his life time. Perhaps even enough to justify the cost of his testing.

But to control his glucose levels, he had to make radical changes to his diet and exercise regime. He had to eat a whole lot less sugar and fat and exercise a lot more. Sound familiar?

Everyone should be doing this stuff anyway but most of us don’t. Will we have the willpower to realize the full potential of personalized medicine? Or will things pretty much stay the same except with more frequent scolding from our doctors?

Of course, catching a disease early and getting patients their medications early when it could do the most good is obviously wonderful too. Just not as cost effective.

What a visit to the doctor in the near future might look like.

Photograph courtesy of EuroMagic via Creative Commons

My nephew is one of the 6 million children in the United States with food allergies. He has a severe nut allergy, requiring an epinephrine (adrenaline) injection and immediate trip to the emergency room after contact with someone whose touched or eaten nuts. His rapid onset of life-threatening symptoms includes swelling of the throat, difficulty breathing, and hives. He isn’t alone. The number of children with peanut allergies has tripled in the last decade. Every three minutes a food allergy reaction sends someone to the emergency room and every 6 minutes the reaction is one of life-threatening anaphylaxis.

Although children often out-grow their allergies to milk, egg, wheat and soy, this is occurring more slowly than in previous decades. Allergies to peanuts, tree nuts, fish or shellfish are generally lifelong allergies.

A food allergy reaction is a learned response, meaning that our bodies learn to overreact to particular food proteins. In this process, the IgE antibody, that is suppose to fight off infections, instead recognizes certain food proteins as abnormal invaders. The IgE antibody tells the body to release histamines and other chemicals that can cause a progressive and sometimes life-threatening reaction (see animated explanation).

Unfortunately there is no cure for food allergies. Unlike other allergies, there aren’t any proven treatments for food allergies either. The only solution has been to avoid the allergy-triggering food. In the case of accidental exposure, antihistamines are taken for mild reactions or epinephrine shots and a trip to the hospital are critical for more severe reactions.

However, promising food allergy therapies are now under study – recently moving from laboratory and animal testing into human clinical trials. The goal is to persuade patients’ immune systems that food allergens aren’t serious threats.

Early clinical trial results have shown promise for three experimental treatments:

• Oral Immunotherapy: Under close medical supervision, patients swallow tiny but increasingly larger amounts of the allergy-triggering food in order to build up immunity. It is being tested for peanut, egg and milk allergies.

• Sublingual Immunotherapy: Liquid containing allergy-triggering food proteins is placed under the tongue, where it is quickly absorbed into the bloodstream. It is being tested for a variety of food allergies.

• Food Allergy Herbal Formula-2 (FAHF-2): Patients take pills comprised of a nine-herb formula that is based on traditional Chinese medicine. This therapy alters the global immune response, rather than that of a single allergen, so it could treat patients allergic to multiple foods. It is being tested for peanut, tree nut, fish and shellfish allergies.

In addition, scientists are trying to understand how food allergies develop in order to help prevent them. For instance, recent studies indicate that early skin exposure to a food protein leads to allergic sensitization, but early oral exposure to a food allergen induces tolerance.

These new studies should give hope to the 15 million people in the United States with food allergies. In order to help educate people about food allergies, the fourteenth annual Food Allergy Awareness Week is May 13-19.

Lorena Ramos, 14, is a patient at the Healthy Hearts clinic at Children's Hospital Oakland. Credit: Gabriela Quirós.

One in six kids in the United States is obese, a condition that doubles their risk of heart disease. Castro Valley teenager Lorena Ramos has been overweight since she was a small child. Now, with the help of her mother and the Healthy Hearts clinic at Children’s Hospital Oakland, she’s fighting to exercise, eat healthily and drop weight. Will she succeed? Watch our story to find out.

The staff at the Healthy Hearts clinic had useful advice for parents. Here's a list I came up with.

7 Things I Learned About How to Help Your Kid Keep a Healthy Weight:

1. Serve appropriate portions.

“Half of your plate should be fruits and/or vegetables, a quarter of your plate is your protein, and the remaining quarter is your whole grains – things like rice or pasta,” said Dr. Lydia Tinajero-Deck, co-director of the Healthy Hearts clinic.

The portion of whole grains should be about the size of a fist, she said. This can sometimes be surprising for kids and parents used to covering their plate with rice or pasta and placing the protein or veggies on top. A serving of meat should be about the size of the palm of a hand.

2. Try to have some meatless meals.

Marin County cardiologist Dean Ornish found in the mid-80s that a low-fat vegetarian diet, together with stress management and exercise, could reverse heart disease. But during our interview, he repeated over and over again that it’s not all or nothing – you don’t have to go vegan to be healthy.

Watch this 5-minute video for more heart-health tips from Dr. Ornish:

3. If you and your family go vegetarian, make sure you don’t eat too much cheese.

“A lot of times, especially with our teen girls on a vegetarian diet, there’s a compensation with extra cheese,” said Dr. June Tester, co-director of the Healthy Hearts clinic, “and they end up actually, ironically, introducing a lot more saturated fat.”

4. Lobby for more and better physical education in schools, healthier school lunches and summer programs for kids.

“I wish for kids to play for an hour every day at school. It will help them academically as well as help their little bodies not gain so much weight,” said Dr. Tinajero-Deck. “And we can feed kids a lot better in schools. Oh, my goodness, we can do so much better.”

After Dr. Tinajero-Deck suggested to a group of dietitians at the Oakland Unified School District that milk or water were better choices than juice for breakfast, they went ahead and modified their menu.

5. Give your kid the gift of movement.

“Jumping rope 5 to 10 minutes, four days a week, is great exercise,” said Tess Barbieri, the exercise physiologist at the Healthy Hearts clinic. “You get a lot of bang for your buck.” She also recommends things as simple as bouncing a ball back and forth, or tossing bean bags and skipping to retrieve them.

6. Help your child find their life-long exercise.

Some kids like to ride a bike or rollerblade; others prefer to go on a walk with their friends. The important thing is to get moving and to make moving a habit.

“You really have to teach kids at a young age that movement is just a part of their lives,” said Dr. Tinajero-Deck.

7. Find someone for your kid to exercise with.

Sometimes kids won’t exercise with a parent. Or parents don’t have time (imagine that!).

“Try to figure out who’s going to be that motivator for your kid,” said Dr. Tinajero-Deck. “Maybe a best friend.”

You can also find out more about obesity prevention in a related post from KQED's State of Health blog, Lessons Learned from the War on Smoking, Applied to Obesity.

Just 30 years ago, doctors could only watch patients as they suffered their heart attacks. As many as 20 percent of them ended up dying. Now, by rushing patients to the operating table and opening their blocked arteries while their heart attacks are underway, they’re able to save all but 5 percent of those who make it to the hospital.

This success is the result of a national campaign by the American Heart Association, the American College of Cardiology and other groups to reduce the time it takes for the hospital to move a heart attack patient from the hospital door to the operating table. Among healthcare personnel, this is known as “door-to-balloon” time. The balloon refers to the stents cardiologists inflate inside heart attack patients’ coronary arteries to remove the clots blocking blood flow to their heart and causing their heart muscle to die.

Cardiologist Agustin Argenal was able to bring down the time it takes heart attack patients at John Muir Medical Center, Concord, to get from the hospital door to the operating table. Credit: Gabriela Quirós.

“Time is muscle,” said Dr. Agustin Argenal, former chief of John Muir’s catheterization lab, where heart attack patients are treated. “The longer that an artery is blocked, and thereby heart muscle is deprived of oxygen and blood flow, the more muscle is damaged and actually dies.”

At John Muir Medical Center in Concord, door-to-balloon time is usually under an hour, compared to the campaign’s national target of 90 minutes, said nurse Pam Lavering, coordinator for the hospital’s chest pain centers in Concord and Walnut Creek. In 2007, the hospital’s Concord campus averaged 94-minute door-to-balloon times. In the first quarter of 2012, the average was 48 minutes, said Lavering.

Dr. Argenal helped reduce John Muir’s door-to-balloon times by having paramedics diagnose heart attacks in the field, instead of waiting until patients arrived in the emergency room.

“Historically, the emergency room would evaluate the patient,” said Argenal. “If they were having a heart attack, a cardiologist would be called. A lot of time was wasted.”

Today, paramedics call the emergency room to let them know that they’re bringing in a heart attack patient; the emergency room calls the cardiologist and the rest of the team, and the patient is taken directly into the catheterization lab as soon as they arrive at the hospital. That way, a doctor can start removing the blockage in the patient’s arteries as soon as possible, said Dr. Argenal.

The last remaining challenge to getting patients onto the operating table as soon as possible is getting them to recognize that they’re having a heart attack and calling 911, he said. He offered some tips to help the public recognize heart attack symptoms.

7 Things You Might Not Know About Heart Attack Symptoms:

1. The most common symptoms are quite varied.

The most common symptoms of a heart attack are chest tightness associated with breathlessness and perspiration; arm discomfort – classically the left arm, but it can be in both arms, and heaviness, numbness or tightness in the arms. Neck discomfort, jaw discomfort and even upper back discomfort can be symptoms too.

2. People having a heart attack often don’t realize they’re having one.

“That’s a really major issue,” said Dr. Argenal. “So if patients could possibly recognize the symptoms, although they may not seem to be cardiac, and call 911, I think more lives would be saved.”

3. People often confuse their heart attacks with indigestion, muscle skeleton pain and sore muscles.

4. Even if you're in doubt, the best thing to do is to call 911.

“The key thing is to get to a place where the physicians can get blood tests and do an EKG,” said Dr. Argenal. “Those kinds of things really help us differentiate between something that may be innocent, and something that may be life-threatening.”

An EKG or electrocardiogram is a test by which doctors can determine the electrical output of the heart. Beating heart cells have unique electrical properties that make them similar to brain cells. These properties help them beat in unison to pump blood throughout the body. An EKG can detect areas in the heart that are being injured during a heart attack, which makes it a good diagnostic tool.

Ambulances are equipped with devices to perform electrocardiograms, which is why it's key to call 911 if you suspect you're having a heart attack. Driving yourself to the hospital can waste precious time and lead to more heart damage, or death.

5. Doctors sometimes confuse patients’ symptoms with gall bladder disease, stomach upsets or gastritis.

6. Even cardiologists can get confused by their own heart attack symptoms.

“I started with thumb tingling in both hands, and that led to numbness in my arms, and ultimately, after quite some time, discomfort in the chest,” said Dr. Argenal. “But I’m a cardiologist, and I was faked out. So it is difficult for patients.”

7. Women's symptoms can look different than men's.

Women are somewhat more likely than men to experience symptoms like shortness of breath, nausea or vomiting, and back or jaw pain, according to the American Heart Association.

Lorena Ramos, 14, struggles to lose weight.

The show opens with the 14-minute story Childhood Obesity: Kids Fight Back. One in six kids in the United States is obese, a condition that doubles their risk of heart disease. Castro Valley teenager Lorena Ramos, 14, has been overweight since she was a small child. Now, with the help of her mother and the Healthy Hearts clinic at Children’s Hospital Oakland, she’s fighting to exercise, eat healthily and drop weight. Will she succeed?

A heart patient is treated at John Muir Medical Center in Concord.

Rushing to Save Heart Attack Patients tells the story of Arlene Skuba, who survived a heart attack at 72, after doctors at the John Muir Medical Center in Concord rapidly unclogged her arteries. Just 30 years ago, doctors could only watch patients as they suffered their heart attacks. As many as 20 percent of them ended up dying. Now, by opening their blocked arteries while their heart attacks are underway, they save all but 5 percent of those who make it to a hospital.

After being injected with three genes, the hearts of mice who had suffered a heart attack pumped blood normally. All photos by Gabriela Quirós.

The special report’s final 4-minute story, New Hope for Heart Repair, takes us into the future, to a time when a single injection of three genes might be able to repair damaged hearts and give heart attack survivors their quality of life back. We visit the Gladstone Institutes, in San Francisco, and watch as researchers repair tiny mice hearts using the next generation of cell reprogramming.

You can watch each of the three stories individually, as well, by following the links below:

A plate full of edible insects, including bee larvae, grasshoppers and a waterbug native to Thailand.Image courtesy of Sevda Eris/QUEST.

Still, it's a hard sell to convince even intrepid foodies to incorporate edible insects into the culinary rotation. While making this story, Daniella shared with me and the camera crew a dish consisting of fileted strips of Thai waterbug atop cucumber slices. She described this exotic insect's flavor as "this complex kind of a Jolly Rancher soaked in banana peel perfume with a hint of melon and green apple and anchovy."

I can't concur with this florid description of an insect with a face only a mother could love as I missed the opportunity to sample this particular dish. Still, the description offered an opportunity for Daniella to share with me a few of the interesting flavors and textures which recur among the roughly 1700 insects which are thought to be edible. At the time of our filming in late November, Daniella had eaten between 20 to 25 different kinds of edible insects, making her as good of an authority as any I'd encounter within the flavor "galaxy", as she put it, of this unusual cuisine.

"Crickets and things that hop, for instance, grasshoppers – they all have a bit of a nutty flavor," she said, adding that "larvae, for instance, often taste rich and buttery…sort of bacon-y. And then some of the smaller ones taste a little bit like mushrooms."

QUEST Producer Sheraz Sadiq interviews Daniella Martin about her enthusiasm for entomophagy, the practice of eating insects.Image courtesy of Sevda Eris/QUEST.

While making this story, I also had the opportunity to meet Norm Gershenz, the gracious and passionate Executive Director of SaveNature, an NGO dedicated to environmental education and the conservation of diverse habitats around the world, from Namibia to Palau. We filmed with Daniella Martin in his Insect Discovery Lab where the two of them talked about various insects, some of which were edible and some were not, such as the eastern lubber grasshopper. Its bright coloration serves as a warning to would-be predators that it sequesters nasty chemicals, making it an unappetizing meal. Green-colored grasshoppers, on the other hand, are safe to eat, as are mealworms which are the juvenile stage of darkling beetles. The beetles, on the other hand, do not make a tasty morsel.

All my interview subjects were quick to point out that our cultural aversion to the consumption of insects is unusual since 80% of the world's population regularly dines on a smorgasbord of edible bugs. In Mexico, for example, not only were insects eaten among Olmec and Maya civilizations well before the arrival of Spanish conquistadors, to this day, many regions abound with their own particular insect specialties.

This waterbug, which is native to Thailnad, was prepared by entomophagy advocate and educator Daniella Martin.Image courtesy of Sevda Eris/QUEST.

Monica Martinez, an artist and chef who launched in 2011 the nation's first edible insect food cart, Don Bugito, hails from Mexico and is familiar with some of these regional offerings. In Oaxaca, for example, chapulines, which are roasted grasshoppers seasoned with chile and lime, can readily be found in street markets.

Monica Martinez at the premiere of her edible insect food cart, Don Bugito, at the San Francisco Street Food Festival in August 2011. Image courtesy of Monica Martinez.

Another delicacy, escamoles, which hails from the central Mexican state of Hidalgo, are the eggs of an ant from the genus Liometopum that burrows into the roots of agave and maguey plants. Also found in Hidalgo is the white agave worm which Monica said is prepared by toasting and pan frying this "very juicy" worm and then serving them in tacos.

Escamoles appetizer served at a restaurant in Mexico City. Image courtesy of Eddie Odabachian.

Given the taxonomic similarity between gourmet crustaceans such as shrimp and lobsters and their arthropod cousins, the insects, it is interesting that in the West we turn our nose up at and our shoe often stomping down upon insects.

Brian Fisher, Curator of Entomology at the California Academy of Sciences, regularly visits Madagascar where the population regularly dines on 15 different varieties of insects, including locusts the size of a hot dog. He shared with me an interesting bit of trivia: a former queen of Madagascar had not one but two chefs specializing in insect cuisine.

"Imagine if Michele Obama had two cooks specialize in insects. Would that change the perspective on insects in our society?", he mused. Maybe, although it would probably take much more than the edible seal of approval from the First Lady to get people to throw a few locusts on the grill at the next fourth of July barbecue.

Now, scientists in San Francisco say a more effective treatment might be on the way.

Three months after being injected with three genes, the hearts of mice that had suffered a heart attack pumped as much blood as a normal heart. Credit: Gabriela Quirós, QUEST

The researchers from the Gladstone Institutes, affiliated with the University of California-San Francisco, reported today that using a new genetic technique, they have succeeded for the first time in repairing, from within, the hearts of mice weakened by heart attacks.

“There are a variety of approaches we use right now to help people who are left with damaged hearts,” said Dr. Deepak Srivastava, senior author of the paper and director of cardiovascular research at the Gladstone Institutes, “but none of them actually get to the root of the problem, which is replacing that damaged heart muscle. And that’s where our focus has been.”

The scientists injected three genes into the hearts of research mice that had been given mild heart attacks. Within three months, the genes transformed non-beating cells in the heart into cells that looked and acted just like beating heart muscle cells. These new beating cells restored the heart’s ability to pump blood to the rest of the body.

Human hearts have billions of non-beating cells, which support the beating cells by forming the heart’s structure, Srivastava said. Mice have millions of these support cells too. When a heart attack happens, the support cells rush to the site of the damage and form scar tissue, which preserves the heart’s structure, but doesn’t help it pump blood.

“We’ve found a way to take these support cells that should normally never become muscle, and convert them into new muscle cells that actually integrate with the rest of the heart, contribute to the force that it generates, and allow us to regenerate the heart from within the organ itself,” said Srivastava.

Non-beating heart cells became beating heart cells like these. Credit: Li Qian, Gladstone Institutes

The new research appears in the April 18 online edition of the journal Nature and was led by Li Qian, also from the Gladstone Institutes.

Heart attacks and other heart disease kill 600,000 people each year. Many more survive, yet lead diminished lives. Some 5.7 million people live with damaged hearts that pump less blood, making it difficult for them to climb a flight of stairs or walk across a parking lot.

During a heart attack, clots block one or several coronary arteries and cut off blood flow. By rushing patients to the operating table and unclogging their arteries with catheters and stents, doctors are able to save all but 5 percent of victims who make it to the hospital.

“While we’ve been doing better at saving lives, each time we save a life the patient still loses some of their muscle,” Srivastava said. “So the number of people who are left with damaged hearts is actually growing, even though the number of people who die from heart attacks is getting smaller.”

Treatments for humans could be six to seven years away, he added. The next step will be to test the treatment on pigs. Scientists still need to figure out if cell reprogramming is safe for humans; how to deliver the genes into the heart, and how to produce enough new beating heart cells to repair a human – rather than a mouse – heart.

Nevertheless, the research is drawing the attention of other heart researchers.

“It’s a major discovery and certainly suggests a new approach to treat injury that previously had been thought to be irreversible,” said Dr. Eduardo Marbán, director of the Cedars-Sinai Heart Institute in Los Angeles.

Marbán said it’s been “a long-held dogma” that once scar tissue has formed in the heart, it can’t change into heart muscle. This finding in mice, and recent research by Marbán’s team on a small group of human patients, challenge that belief, he said.

Although the cell reprogramming research doesn’t involve stem cells, the Gladstone scientists used techniques that were discovered through stem cell research.

The scientists said their work was inspired by the discovery in 2007 that a few genes can transform an adult skin cell into a cell with the properties of a human embryonic stem cell. Researchers have been intensely interested in embryonic stem cells as a possible source of treatments for diseases like Parkinson’s because they can be coaxed to turn into virtually any type of cell in the body. But because embryonic stem cells are plucked from embryos left over from fertility treatments, and require the destruction of these embryos, their study has been controversial.

An alternative to embryonic stem cells came with the skin cell breakthrough five years ago. Then, Dr. Shinya Yamanaka, of the Gladstone Institutes and Kyoto University in Japan, inserted four genes that are present in embryonic stem cells into adult skin cells. The four genes reprogrammed the skin cells to become embryonic-like stem cells.

That led scientists to look for a way to transform one type of adult cell into another type of adult cell without the need to create stem cells at all.

“Yamanaka opened up the idea that adult cells weren’t permanently fixed,” said Srivastava. “That led us to ask whether or not we could convert one of these heart support cells into a heart muscle cell.”

Bypassing the creation of stem cells has several advantages. Though stem cells are versatile, when they’re introduced into the body they can behave as cancer cells and form tumors.

“It’s a dramatic and heady possibility that vindicates for the first time the idea that we might be able to harness truly regenerative medicine,” Marbán said.

Dr. Mina Bissell of LBNL Life Sciences in her laboratory. Photo courtesy of Lawrence Berkeley National Laboratory. © 2010 The Regents of the University of California, Lawrence Berkeley National Laboratory.

The human body is comprised of about ten trillion cells. These cells are constantly bombarded with damaging factors, like radiation from the sun, that cause some of the cells to mutate. Even healthy people produce many genetically impaired cells every day, but our bodies successfully eradicate these cancer-prone cells so the majority of people live cancer-free lives. How is this possible?

We all know that the human body has a highly developed immune system that detects and destroys invading pathogens and tumor cells. Researchers at Lawrence Berkeley National Laboratory (LBNL) have demonstrated that there is also a second line of defense against cancer: neighboring healthy cells.

Dr. Mina Bissell is a Distinguished Scientist with LBNL and one of the world’s leading researchers on breast cancer. Her group recently found that normal breast cells provide an innate defense mechanism against cancer, by secreting interleukin 25 (a protein known to play a key role in the immune response to inflammation) to actively and specifically kill breast cancer cells without harming normal ones.

Overall Bissell’s research has focused on the importance of factors other than genetics in the development of breast cancer, demonstrating the critical role that a breast cell’s microenvironment plays in whether it develops normally or whether it turns cancerous. A cell’s microenvironment includes other surrounding cells, like cancer-killing normal breast cells, and a supporting structure known as the extracellular matrix. This extracellular matrix (ECM) consists of a complex network of fibrous and globular proteins surrounding the breast cell. Bissell has shown that a healthy ECM is critical for a breast cell to function normally. If the ECM is damaged, this can lead to breast cancer.

As Bissell explained to attendees at an American Association for Cancer Research conference in 2009, “No cell is an island. All cells are surrounded by their own unique microenvironment. It is quite clear that the context in which a cell exists determines what that cell can do.”

Surprisingly, Bissell has also demonstrated that malignant breast cancer cells can “revert” back to function like normal breast cells by manipulating their microenvironment. A reverted cell’s genetic makeup (genotype) indicates that it is still cancerous, but the actual observed properties (phenotype) are that of a normal breast cell. Bissell explained at an LBNL lecture, “Clearly the genome is a mess, but we manipulate the cells to make them think they are normal. They revert to a normal phenotype.”

Image courtesy of Friends of Berkeley Lab.

Her studies also imply that there may be a better way to treat breast cancer. Bissell argues that therapies that modulate the microenvironment have the potential to make malignant cells appear normal or to at least help tumor cells remain dormant.

Dr. Bissell will discuss her pivotal breast cancer research at LBNL’s Science at the Theater: Health Detectives upcoming lecture. Four LBNL scientists will explain how they are uncovering the mysteries of disease. This free public lecture will be held at the Berkeley Repertory Theater on April 23 at 7 pm.

View of the Sierra Nevada over Owens Valley from high in the White Mountains. The glories of the high country can be ruined by the body's reaction to the altitude. Photos by Andrew Alden except where noted.

In the medical news this week was a study showing that altitude sickness can be prevented with ordinary ibuprofen. This is interesting for geologists and anyone else who goes to high places. It was particularly so for me, because I served in that research study.

Altitude sickness—a syndrome formally called acute mountain sickness—affects about a quarter of people who ascend from sea level to elevations above 2500 meters, or 8250 feet. The main symptoms are headache, fatigue, nausea, loss of appetite and trouble sleeping. For most victims it goes away in a day or two, but some cases are severe enough to be disabling, and if untreated the brain may sometimes start swelling inside the skull to the point of death.

The best treatment for acute mountain sickness is to move to a lower elevation until the symptoms stop. But that isn't always possible—bad weather may pin you down, for instance. Some people, like search-and-rescue teams or soldiers, simply must carry on. Others, like ski parties or expeditions, are very reluctant to get off schedule. There are prescription drugs for preventing acute mountain sickness, but they have side effects that can be as severe as the condition they're treating. Plus, they need to be taken a day ahead of time—not good for, say, a fire-fighting crew.

So a team of doctors, most of them at Stanford, designed a double-blinded study to test over-the-counter ibuprofen as a preventative. They sent groups of ordinary folks on a two-day summer exercise in the White Mountains, where Stanford maintains high-altitude research facilities. They sent out a call for volunteers. Sounded good to me. I arranged two more nights on the road and made a nice field trip through eastern California out of it.

The study employed 86 people on four separate weekends in the summer of 2010. My group assembled August 20 in Bishop, at the Owens Valley Laboratory, part of the University of California's White Mountain Research Station, and spent the night there at 1240 m (4100 ft). We got up early the next morning.

After breakfast we took our first doses (ibuprofen or placebo, no one knew which), underwent examinations and filled out questionnaires. Among other things, we had our eyeballs ultrasounded.

Photo courtesy Nic Kanaan, MD

Then we drove into the White Mountains and stopped for lunch at the bristlecone pine forest, where I'd never been before. The big snag on the left might be thousands of years old.

Here, at least, it was clear how the range got its name: large areas of dolomite marble. One idea for why bristlecones reach incredible ages here is simply that only dolomite can resist erosion for that long. I thought it was beautiful stuff.

From here, too, the view east over Nevada was immense; range after parallel range marching off to the horizon. Geologists know this as the Basin and Range province, a zone where the crust has stretched westward to one-and-a-half times its original width. The White Mountains, with their southern sister the Inyo Mountains, are the westernmost and highest of these ranges.

Next we parked at a gate at 3545 m (11,630 ft), took another dose, then hiked almost three miles with our backpacks of clothes and bedding to UC's Barcroft Station at 3800 m (12,470 ft).

Photo courtesy Nic Kanaan, MD

I had never hiked at such an altitude before. Walking on level ground was OK, but whenever the path turned uphill my heart and lungs went into overtime and my legs turned to lead. When I couldn't push any more, though, I could pause for just a minute or two and feel fine again. That was uncanny. When the going was good, being there felt at times like floating in the sky.

We left our packs at Barcroft Station and then made one last steep climb to Mount Barcroft's summit, 3975 m (13040 ft). It felt so good to stop, and the view was fantastic. This is looking due west. . .

This wide area of the Owens Valley is a volcanic tableland made up of thick ashflow deposits of the Bishop Tuff; Chidalgo Canyon slashes across it and Lake Crowley in the Long Valley caldera is visible to its rear, in front of the high Sierra.

. . . and this is White Mountain Peak, to the north.

White Mountain Peak is the highest point in the Basin and Range province and the third-highest point in California at 4344 m (14252 ft).

That evening one of the researchers delivered a thorough lecture on acute mountain sickness and other medical issues of high altitudes. It was a peek into the world of adventurers who braved altitudes twice as high as ours, pushing the limits of human capability.

Most of us experienced some of the symptoms of acute mountain sickness, no matter which pills we had taken. We played pool and socialized until bedtime. That's when I noticed how hard it was to sleep; part of it was physiological and part of it was an inability to tolerate snoring.

But I took advantage of the sleepless night by arising before dawn. That was how I managed to witness a rare green flash as the sun first peeked over the Nevada ranges. After that was all downhill: breakfast, a final dose, and a last round of examinations. Then we were free to go. Some of us had plans to tackle White Mountain Peak; mine were to visit the volcanic wonders of Long Valley, at a much more manageable elevation.

And that was it for me until the first paper from the study came out this week in Annals of Emergency Medicine. Ibuprofen, it turned out, works roughly as well as other medicines but is much cheaper to get and easier to take. It won't stop all the symptoms, but it makes a notable difference and may save you from a very bad time. Remember it the next time you hit the high country.