Friday, December 4, 2009

Detecting skin cancer at an earlier stage

Detection of skin cancer is usually done by the eye alone. Now Israeli researchers have developed a new device that can detect cancerous tumors at an earlier stage.

Sunbathers are particularly at risk of developing skin cancer if they don't protect their skin from the sun.

Researchers in Israel are developing a new device that can detect cancerous skin tumors, including melanomas that aren't visible to the naked eye, at an earlier stage of the disease.

The Optical Spectro-Polarimetric Imaging (OSPI) instrument, developed at Ben-Gurion University of the Negev (BGU), reveals new textures of lesions that have never been seen before - including melanoma in patients who were diagnosed with various skin lesions and were awaiting surgery for their removal. The instrument diagnosed 73 types of lesions, some of them cancerous.

More than one million cases of skin cancer are diagnosed in the US every year according to the American Cancer Society. Of the 11,590 deaths due to skin cancer in 2009, some 8,650 will be due to melanoma, the most serious and dangerous type of skin cancer.

Today, dermatologists and plastic surgeons typically diagnose skin tumors with the naked eye and only rarely use a dermatoscope - a magnifying tool that allows tumors to be examined in detail.

Skin cancer and beyond

Cancerous mole detection is usually done by looking for one or more telltale visible symptoms: if the mole is asymmetrical; if it's outline is blurred or irregular; if it has multiple colors; if it is larger than five millimeters in diameter; and if stands up above the skin.

The OSPI biosensor, however, uses safe, infrared wavelengths and LC devices to measure tumor characteristics, including contours and spread, identifying tumors at an earlier stage.

"This is an exciting preliminary development since the initial testing shows that we can now identify microscopic tumors in the biological layers of the skin," explains Prof. Ibrahim Abdulahim, who is head of the BGU Electro-Optical Unit in the Faculty of Engineering Sciences and is leading the research group.

"As we continue to develop the OSPI, we also see an opportunity to use this technology for detecting other types of cancerous growths."

Abdulahim is supervising this research with Ph.D candidate Ofir Aharon and MS.c student Avner Safrani. He is also collaborating with BGU Prof. Lior Rosenberg and Dr. Ofer Arnon from the Department of Plastic Surgery at Soroka University Medical Center.

Wednesday, December 2, 2009

5+ Foods to Fight the Flu

Keep your digestive system happy. When the digestive system is healthy it is able to breakdown and access nutrients from the foods you eat, it is better able to get rid of toxicity, and process “bad” bugs such as bacteria & viruses

ChicagoHealers.com Practitioner Dr. Helen Lee offers the following free flu-fighting foods:

Ginger: The volatile oils in ginger warm the body, helping the body to sweat, break a fever and eliminate toxins. Ginger also stimulates mucous release. Ginger is also a metabolic enhancer and the warming also helps with nausea, is a great digestive aid, lung and chest decongesting, and a body cleansing herb. Add fresh ginger to your food or in tea, or eat alone. Ginger tea (especially combined with honey) helps too sooth the throat.

Garlic: Garlic has allicin as an active ingredient giving it antiviral and antibacterial properties. Garlic cleans your liver (which cleans your blood) since your blood cycles through your liver every three minutes. So thereby stimulating the white blood cells and in turn boosting the immune system. An onion garlic syrup can help with mucous release.

Honey: Honey acts as a natural antibiotic with antiseptic properties. There are vitamins such as B-complexes, C, D, E, minerals enzymes and propolis. The propolis in honey boosts the immune system, disables viruses and fights infections. Furthermore, pediatric studies have shown that honey is more effective than cough syrup because it coats the throat better. Locally grown honey is best for seasonal allergies, asthma and respiratory conditions because you are treating with the irritants that are common to your area. Take a tablespoon 4 times per day, taken straight or in tea.

Cayenne: Cayenne pepper has a high vitamin C content making it a natural choice for a cold, as well as vitamin A, B, calcium and potassium. Cayenne also increases the circulation in the body. You may take in capsule form taking 2 – 40,000 heat units (950mg), or liquid 4 drops of the 200,000 heat units. Place a few drops in water and gargle with it every 15-30 minutes to make a sore throat disappear.

“Good” Bacteria: Increase “good” bacteria such as acidophilus and bifidus which can be found yogurt or kefir.

Go Green: Eat dark leafy green vegetables like kale, swiss chard, and spinach provides vitamins B12, folic acid, potassium, vitamins A, C & K which supports a healthy immune system.

Acid and Alkaline: Keep your internal acid/alkaline chemistry balanced by squeezing a half lemon into a cup of hot water to break up congestion, stimulate digestion, and create an alkaline or healing pH chemistry in the body

Wednesday, November 25, 2009

Reconstructive memory

The term 'Rashomon effect' is often used by psychologists in situations where observers give different accounts of the same event,and describes the effect of subjective perceptions on recollection. The phenomenon is named after a 1950 film by the great Japanese director Akira Kurosawa. It was with Rashomon that Western cinema-goers discovered both Kurosawa and Japanese film in general - the film won the Golden Lion at the Venice Film Festival in 1951, as well as the Academy Award for Best Foreign Language film the following year.

Rashomon is an adaptation of two short stories by Akutagawa Ryunosuke. Set in the 12th century, the film depicts the trial of a notorious bandit called Tajomaru (played by Kurosawa's frequent collaborator Toshiro Mifune), who is alleged to have raped a woman and killed her samurai husband. In flashbacks, the incident is recalled by four different witnesses - a woodcutter, a priest, the perpetrator and, via a medium, the murder victim. Each of the testimonies is equally plausible, yet all four are in mutual contradiction with each other.

The film is an examinantion of human nature and the nature of reality. It compels the viewer to seek the truth. Each testimony is influenced by the intentions, experiences and self-perceptions of the witness. They all tell their own 'truth', but it is distorted by their past and by their future. Under Kurosawa's masterful direction, the characters start off happy in the knowledge that they know exactly what happened between the samaurai, his wife and the bandit. One by one, each character begins to doubt their own account of the incident. In the end, both the cast and the viewer are left in a state of confusion and bewilderment.
The idea that we do not remember things as they actually happened is usually attributed to Sir Frederick Bartlett (1886-1969), who spent much of his professional career at Cambridge University, where he became head of the psychology department. He describes the process of memory in his classic 1932 book, Remembering: A Study in Experimental and Social Psychology:

Remembering is not a completely independent function, entirely distinct from perceiving, imaging, or even from constructive thinking, but it has intimate relations with them all...One's memory of an event reflects a blend of information contained in specific traces encoded at the time it occurred, plus inferences based on knowledge, expectations, beliefs, and attitudes derived from other sources.

According to Bartlett, memories are organized within the historical and cultural frameworks (which Bartlett called 'schemata') of the individual, and the process of remembering involves the retrieval of information which has been unknowingly altered in order that it is compatible with pre-existing knowledge.

Bartlett's ideas about how memory works came to him during a game of Chinese whispers, in which a short story is relayed through a chain of people, each of whom makes minor retrieval errors, such that the final retelling may be completely different from the original. One of his experiments involved asking subjects to read a Native American folk story called The War of the Ghosts, and then recall it several times, sometimes up to a year later. He chose it because the cultural context in which it is set was unfamiliar to the participants in his experiments.

Bartlett found that upon recall, the subjects altered the narrative of the story to make it fit in with their existing schemata. Participants omitted information they regarded as irrelevant, changed the emphasis to points they considered to be significant, and rationalized the parts that did not make sense, to make the story more comprehensible to themselves. In other words, memory is reconstructive rather that reproductive.

Although Remembering was largely ignored upon its publication, it is today highly influential. Elizabeth Loftus, a professor of psychology and law at the University of California, Irvine, has devoted her career to studying the reconstructive nature of memory in relation to eyewitness testimony.

Loftus is concerned mainly with how the recollections of eyewitnesses can be deliberately manipulated by misinformation. In extreme cases, this can lead to completely false memories of events that did not take place. One of Loftus's more famous studies addresses the use of 'leading' questions in the courtroom. In the study, students were shown film clips of a car accident, and then asked a question about the accident. Those asked "About how fast were the cars going when they smashed into each other?" gave answers which averaged about 39 mph, whereas those asked "About how fast were the cars going when they contacted each other?" gave answers with an average speed of 32 mph.

Loftus's research, like that of Bartlett's, shows that our memories are quite often not as accurate as we would like to think they are. The knowledge that memory is to some extent confabulation has very serious implications for the use in the courtroom of eyewitness testimonies, because if eyewitness testimonies can be unreliable, then the validity of criminal convictions based upon them is open to question.

As well as confabulating the past, the brain also envisages events that have not yet occurred. The process of anticipating oneself attending a future event probably involves drawing on past experiences to generate a 'simulation' of the future event. Daniel Schacter argues that this 'episodic-future' thinking is entirely dependent on reconstructive memory:

...future events are not exact replicas of past events, and a memory system that simply stored rote records would not be well-suited to simulating future events. A system built according to constructive principles may be a better tool for the job: it can draw on the elements and gist of the past, and extract, recombine and reassemble them into imaginary events that never occurred in that exact form. Such a system will occasionally produce memory errors, but it also provides considerable flexibility.

Most of the evidence that reconstructive memory may be essential for envisioning future events comes from amnesic patients who also have difficulties picturing themselves in the future, and now there is also some experimental evidence. For example, recent functional neuroimaging studies show that some of the brain regions that are activated when recalling a personal memory - the posterior cingulate gyrus, parahippocampal gyrus and left occipital lobe - are also active when thinking about a future event.

Amnesia in the movies

Despite occuring only rarely, amnesia (or memory loss) has featured often in Hollywood films for almost a century. By 1926, at least 10 silent films which used amnesia as a plot device had been made; more recent productions, such as 50 First Dates and Eternal Sunshine of the Spotless Mind, are therefore part of a well established tradition.

In a review published in the British Medical Journal in 2004, clinical neuropsychologist Sallie Baxendale of the Institute of Neurology in London points out that cinematic depictions of amnesia are consistenly inaccurate, and usually "bear no relation whatsoever to any authentic neurological or psychiatric condition".

In her review, Baxendale examines common misconceptions of amnesia found in the cinema, and suggests that knowledge of them can guide clinicians when informing patients and their relatives about diagnoses. She also points out several exceptional films which depict amnesic syndromes accurately.

In the romantic comedy 50 First Dates (2004), Adam Sandler plays veterinarian Henry Roth, who falls for Lucy Whitmore (played by Drew Barrymore) after meeting her in a cafe one morning. The two hit it off, and arrange to meet again. The following day, Roth returns to the café to meet her, but she claims to have no recollection of him. As he leaves, the owner of the café takes him to one side, and explains that Whitmore "lost her short-term memory" after a "terrible car accident". We also learn that she can form new memories during the day, which are then wiped clean during her sleep, so that she wakes up to a "clean slate" every morning.
50 First Dates propagates a number of misconceptions which are common in the films which refer to amnesia. Whitmore's amnesia is the result of a head injury incurred in the car accident; other amnesic characters may lose their memory after being assaulted, or bumping their head in some other way. In reality, memory loss rarely occurs following a head injury; it is most often caused by stroke, brain infection or neurosurgery. The idea that new memories are wiped clean at night is also unrealistic, and unlike any documented amnesic syndrome.

In many cases of cinematic amnesia, head injuries lead to loss of memory of earlier events (retrograde amnesia), but the character usually goes on to lead an otherwise normal life. Real patients who incur brain damage usually suffer from anterograde amnesia - they lose the ability to form new memories, but their memories of events that occured before the amnesia often remain intact. Often they lose memories of many important aspects of their lives - of loved ones and daily routines - and so day-to-day functioning is affected severely.

Amnesic film characters often undergo personality changes or a loss of identity. This confuses amnesia with a poorly-understood condition called dissociative fugue. It also blurs the distinction between the causes of the different amnesic syndromes, as the characters experience psychiatric symptoms, which in reality do not have an organic cause, which are attributed to neurological damage.
Personality changes after a head injury can be seen in the 1987 film Overboard, starring Goldie Hawn and Kurt Russell. Hawn plays a rich and spoilt socialite who loses here memory after bumping her head when falling from her yacht. The character then undergoes a sudden transformation - she becomes warm-hearted and loving and is duped into raising the children of Russel's character as her own. Her memory loss, like that of most other characters, is readly reversible - towards the end of the film, it is cured by another bump on the head. In others, the memories return when they see a familiar object or person. Both of these scenarios are equally implausible.

Memento (2000) is a rare example of a film which depicts amnesia accurately. It is apparently inspired in part by the case of Henry Molaison (H.M.), the famous amnesic who died last December. Guy Pearce plays Leonard, who suffers severe anterograde amnesia after sustaining a head injury in an attack in which his wife is killed. Unlike most amnesic characters, Leonard retains his identity and the memories of events that occurred before the attack, but loses all ability to form new memories. The film's fragmented narrative powerfully depicts how difficult everyday life would be for a severely amnesic patient - Leonard spends much of the film frantically scribbling scraps of information on pieces of paper and, once he has estalished something to be a fact, has it tattooed onto his body.

Another accurate depiction of amnesia is found in the CGI-animated film Finding Nemo (2003). One of the characters, a reef fish called Dory, has a profound memory deficit which, to frustration of her peers, prevents her from learning or retaining any new information, remembering names, or knowing where she is going. As a result, she gets lost when left alone and is often found in a state of confusion. The exact origin of Dory's impairment is not mentioned in the film, but her memory loss accurately reflects the difficulties faced by amnesic patients and those who know them.
Realistic amnesic characters are few and far between in the cinema. Baxendale refers to only one other film, called Se Quien Eres (I Know Who You Are, 2000), containing an accurate depiction of amnesia, in the form of a patient with Korsakoff's Syndrome, the amnesic syndrome condition associated with chronic alcoholism. However, Columbia Pictures announced last month it has acquired the rights to make a film about the life of H.M., based on a book which is to be written by Susanne Corkin, the MIT researcher who worked with him for 4 years.

On a related subject is Rashomon (1950), Akira Kurosawa's masterful examination of the reconstructive nature memory Rashomon depicts a crime as seen from the perspective of four eyewitnesses. As each gives their testimony, the same event is described in four radically different ways. Each of the testimonies contradicts the others, and each of the witnesses initially insists that their version of the event is the right one. Then, as they consider each others' descriptions, something which at first seemed clear becomes utterly confusing, as all the characters and the audience begin to question the accuracy of their own memories.

Monday, November 23, 2009

* Hands-on Tech: Double Amputee Gets Mind-Controlled Arms

When Christian Kandlbauer lost both of his arms in a work accident in 2005, he thought he’d lost his independence. But thanks to amazing advances in prosthesis technology, he now has two high-tech prosthetic arms that allow him to function in many of the ways he did before his accident – and they’re controlled by his thoughts. The arms, developed in a joint venture between the Otto Bock health care company and the Medical University of Vienna, were fitted in 2007. But before they could go on, Kandlbauer had to undergo a complex procedure to re-wire the nerves in his arm stumps, a procedure that only three surgeons in the world can perform. The nerves that used to control his arms were moved to his chest to allow him to control his new bionic arms via electronic sensors.



Now, Kandlbauer moves his new arms the way he moved his old ones: he activates “muscle” movement with impulses from his brain. The prosthetic arms aren’t quite as articulate as natural arms, but they have seven degrees of movement as opposed to the three degrees of movement offered by conventional prostheses. And four years after losing his arms, Kandlbauer was able to achieve one of his biggest goals: he passed his driving test. He’s now able to drive himself around with the help of a modified vehicle, thanks to his high-tech arms.When Christian Kandlbauer lost both of his arms in a work accident in 2005, he thought he’d lost his independence. But thanks to amazing advances in prosthesis technology, he now has two high-tech prosthetic arms that allow him to function in many of the ways he did before his accident – and they’re controlled by his thoughts. The arms, developed in a joint venture between the Otto Bock health care company and the Medical University of Vienna, were fitted in 2007. But before they could go on, Kandlbauer had to undergo a complex procedure to re-wire the nerves in his arm stumps, a procedure that only three surgeons in the world can perform. The nerves that used to control his arms were moved to his chest to allow him to control his new bionic arms via electronic sensors.





Tuesday, November 17, 2009

A new antidepressant really turns women on

To all the men (and women) I've ever heard complain about the female libido, it's time to take the batteries out of your high-tech remote-control sex toys.

Flibanserin appears to be a highly effective libido booster in women who report low sexual desire, three new trials find.

Flibanserin, a drug originally designed to fight depression, turns out to be an ineffective antidepressant but a highly effective libido booster in women who report low sex drives, according to results pooled from three separate clinical trials. (It's long been thought that antidepressants suppress sex drives, so it makes its own strange sense that a poor antidepressant might not have the same suppressing effect.)

"It's essentially a Viagra-like drug for women in that diminished desire or libido is the most common feminine sexual problem, like erectile dysfunction is in men," reports John Thorp Jr., a principal investigator in the studies and the McAllister distinguished professor of obstetrics and gynecology at the University of North Carolina at Chapel Hill School of Medicine.

It's not terribly surprising that flibanserin was not originally designed to boost the female libido, since this is a notoriously complicated task compared to the notoriously uncomplicated approach in men of simply regulating blood flow. More surprising is that these are purported to be the first trials ever to test a female libido therapy in the brain; one would think that all the scoffing women do about men thinking with their "other" heads would indicate women's tendency to do that sort of thinking with the head that sits on their shoulders.

Hypoactive sexual desire disorder, a bulky arrangement of syllables that risks causing the very thing it names, affects anywhere from 9 percent to 26 percent of women in the U.S., studies show. But that doesn't mean you should throw away those high-tech sex toys and run to your local pharmacy; flibanserin is still an investigational drug, available only to those women who've agreed to participate in clinical trials.

The trial results were presented by principal investigator Elaine E. Jolly from the University of Ottawa in Canada on Monday at the Congress of the European Society for Sexual Medicine in Lyon, France.

All three trials were funded by Boehringer Ingelheim Pharmaceuticals, a manufacturer of flibanserin. That means until further studies are done without BIP funding, these results should be viewed with a level of skepticism; developing the first successful female libido booster could be a way for the company that designed such a poor antidepressant to save face.

That brings me to a final point: since women who do not suffer from hypoactive sexual desire disorder might be just the type to enjoy such things as sex toys and libido boosters recreationally (some women take Viagra for fun), one wonders what effect, if any, flibanserin will have on them.

Saturday, November 14, 2009

The Best Exercises for Healthy Bones

By GRETCHEN REYNOLDS
Digital Images/Getty Images

Several weeks ago, The Journal of the American Medical Association published a study that should give pause to anyone who plans to live a long and independent life. The study looked at the incidence of hip fractures among older Americans and the mortality rates associated with them. Although the number of hip fractures has declined in recent decades, the study found that the 12-month mortality rate associated with the injury still hovers at more than 20 percent, meaning that, in the year after fracturing a hip, about one in five people over age 65 will die.
Phys Ed

Meanwhile, another group of articles, published this month as a special section of Medicine & Science in Sports & Exercise, the journal of the American College of Sports Medicine, underscore why that statistic should be relevant even to active people who are years, or decades, away from eligibility for Medicare. The articles detailed a continuing controversy within the field of sports science about exactly how exercise works on bone and why sometimes, apparently, it doesn’t.

“There was a time, not so long ago,” when most researchers assumed “that any and all activity would be beneficial for bone health,” says Dr. Daniel W. Barry, an assistant professor of medicine at the University of Colorado, at Denver, and a researcher who has studied the bones of the elderly and of athletes. Then came a raft of unexpected findings, some showing that competitive swimmers had lower-than-anticipated bone density, others that, as an earlier Phys Ed column pointed out, competitive cyclists sometimes had fragile bones and, finally, some studies suggesting, to the surprise of many researchers, that weight lifting did not necessarily strengthen bones much. In one representative study from a few years ago, researchers found no significant differences in the spine or neck-bone densities of young women who did resistance-style exercise training (not heavy weight lifting) and a similar group who did not.

Researchers readily admit that they don’t fully understand why some exercise is good for bones and some just isn’t. As the articles in this month’s Medicine & Science in Sports & Exercise make clear, scientists actually seem to be becoming less certain about how exercise affects bone. Until fairly recently, many thought that the pounding or impact that you get from running, for instance, deformed the bone slightly. It bowed in response to the forces moving up the leg from the ground, stretching the various bone cells and forcing them to adapt, usually by adding cells, which made the bone denser. This, by the way, is how muscle adapts to exercise. But many scientists now think that that process doesn’t apply to bones. “If you stretch bone cells” in a Petri dish, says Alexander G. Robling, an assistant professor in the department of anatomy and cell biology at Indiana University School of Medicine and the author of an article in Medicine & Science in Sports & Exercise, “you have to stretch them so far to get a response that the bone would break.”

So he and many other researchers now maintain that bone receives the message to strengthen itself in response to exercise by a different means. He says that during certain types of exercise, the bone bends, but this doesn’t stretch cells; it squeezes fluids from one part of the bone matrix to another. The extra fluid inspires the cells bathed with it to respond by adding denser bone.
Related


Why should it matter what kind of message bones are receiving? Because, Professor Robling and others say, only certain types of exercise adequately bend bones and move the fluid to the necessary bone cells. An emerging scientific consensus seems to be, he says, that “large forces released in a relatively big burst” are probably crucial. The bone, he says, “needs a loud signal, coming fast.” For most of us, weight lifting isn’t explosive enough to stimulate such bone bending. Neither is swimming. Running can be, although for unknown reasons, it doesn’t seem to stimulate bone building in some people. Surprisingly, brisk walking has been found to be effective at increasing bone density in older women, Dr. Barry says. But it must be truly brisk. “The faster the pace,” he says — and presumably the greater the bending within the bones — the lower the risk that a person will fracture a bone.

There seems to be a plateau, however, that has also surprised and confounded some researchers. Too much endurance exercise, it appears, may reduce bone density. In one small study completed by Dr. Barry and his colleagues, competitive cyclists lost bone density over the course of a long training season. Dr. Barry says that it’s possible, but not yet proved, that exercise that is too prolonged or intense may lead to excessive calcium loss through sweat. The body’s endocrine system may interpret this loss of calcium as serious enough to warrant leaching the mineral from bone. Dr. Barry is in the middle of a long-term study to determine whether supplementing with calcium-fortified chews before and after exercise reduces the bone-thinning response in competitive cyclists. He expects results in a year or so.

In the meantime, the current state-of-the-science message about exercise and bone building may be that, silly as it sounds, the best exercise is to simply jump up and down, for as long as the downstairs neighbor will tolerate. “Jumping is great, if your bones are strong enough to begin with,” Dr. Barry says. “You probably don’t need to do a lot either.” (If you have any history of fractures or a family history of osteoporosis, check with a physician before jumping.) In studies in Japan, having mice jump up and land 40 times during a week increased their bone density significantly after 24 weeks, a gain they maintained by hopping up and down only about 20 or 30 times each week after that.

If hopping seems an undignified exercise regimen, bear in mind that it has one additional benefit: It tends to aid in balance, which may be as important as bone strength in keeping fractures at bay. Most of the time, Dr. Barry says, “fragile bones don’t matter, from a clinical standpoint, if you don’t fall down.

Monday, November 9, 2009

The Peril of Palatability

A former FDA chief sounds the alarm about dangerously delicious food.

The End of Overeating: Taking Control of the Insatiable American Diet, by David A. Kessler, Emmaus, Pa.: Rodale Books, 320 pages, $25.95

According to The Washington Post, David Kessler’s research for The End of Overeating included late-night forays into the trash bins behind Chili’s restaurants across California. From the chain’s garbage he retrieved ingredient boxes with nutritional labels that revealed the secret of dishes such as Southwestern Eggrolls and Boneless Shanghai Wings. It turned out they “were bathed in salt, fat and sugars.”

Kessler could have saved considerable time and trouble by paying a Chili’s employee to write down this information for him. Or by visiting the Chili’s website, which provides numbers for the calories, fat, saturated fat, carbohydrates, protein, fiber, and sodium in the company’s food. Or simply by assuming that food promoted as a mouth-watering yet affordable indulgence probably has a lot of fat, salt, and sugar in it. But as The End of Overeating more than amply demonstrates, Kessler is the sort of crusader who spares no effort to uncover the obvious.

Kessler, a professor at the University of California at San Francisco’s medical school, grabbed headlines as head of the Food and Drug Administration under Bill Clinton by taking on Big Tobacco. In this book he mounts an assault on Big Food, but the results are even feebler than his unsuccessful effort to regulate cigarettes without statutory authority. He combines banal observations, dressed up as scientific insights and revelations of corporate misdeeds, with presumptuous advice that overgeneralizes from his own troubled relationship with food.

Kessler urges readers to eschew pasta, French fries, bacon cheeseburgers, candy, and other “hyperpalatable” foods that he and some people he interviewed for the book have trouble consuming in moderation. Kessler wants us to know he is powerless over chocolate-chip cookies and “those fried dumplings at the San Francisco airport.” Using himself and several similarly voracious acquaintances as models, he argues that “conditioned hypereating” is largely responsible for the “obesity epidemic.” He exhorts its victims to resist the machinations of the food industry, “the manipulator of the consumers’ minds and desires” (in the words of a “high-level food industry executive”).

Kessler fearlessly accuses major restaurant chains of a crime they brag about, relying on unnamed “insiders” to reveal that comestible pushers such as Cinnabon and The Cheesecake Factory deliberately make their food delicious—or, as he breathlessly puts it, “design food specifically to be highly hedonic.” Kessler certainly has the goods on the corporate conspiracy to serve people food they like. “We come up with craveable flavors, and the consumers come back, even days later,” a “research chef at Chili’s” confesses to him. Kessler also reveals that Nabisco lures Oreo eaters through a dastardly combination of sweet white filling and crunchy, bittersweet chocolate wafers, achieving “what’s called dynamic contrast.” Or maybe it’s “what the industry calls ‘dynamic novelty,’ ” as Kessler claims in another Oreo discussion elsewhere in the book. Either way, it’s so good it must be bad.

Not only do these sneaky bastards create irresistible food; they then turn around and tell people about it. “With its ability to create superstimuli, coupled with its marketing prowess, the industry has cracked the code of conditioned hypereating and learned exactly how to manipulate our eating behavior,” Kessler writes. “It has figured out the programming that gets us to pursue the food it wants to sell.”

If Kessler hadn’t been so distracted by that plateful of chocolate-chip cookies, perhaps he would have noticed the contradiction between his description of how the food industry goes to great lengths to give consumers exactly what they want and his claim that it arbitrarily decides what products it wants to sell, then uses marketing magic to create a demand for them. The only way to deal with such logic-defying nefariousness, he suggests, is to regulate advertising and require restaurants to nag their customers with conspicuous calorie counts. He also encourages readers to “feel angry at the marketing and advertising techniques designed to get you to eat more, at the huge portion sizes served at restaurants, and at the layered and loaded food you encounter everywhere.” It’s all about “reframing seemingly well-meaning acts as hostile ones.” Thinking back on all those times my mother offered me a second helping, I now realize how much she hates me.

Kessler’s discussion of the science behind his theory of conditioned hypereating is at least as enlightening as his economic analysis of the food industry. “Palatable foods arouse our appetite,” one expert tells him. “They act as an incentive to eat.” Once he’s made sure we know what palatable means, Kessler tries to explain why some foods have this quality. It turns out that palatable foods affect neurotransmitter levels, stimulate “the pleasure center,” and activate “the body’s reward system.” Since the same could be said of pretty much everything that people enjoy, this observation is not very illuminating. It falls into the same true-but-dull category as Kessler’s discovery that “people get fat because they eat more than people who are lean.”

Kessler’s neurological reductionism gives him an excuse to talk about rat studies and MRI scans, but it does not have much explanatory power. “The food we ate for comfort has left its mark on the brain, creating a void that will need to be filled the next time we are cued,” he writes. “The result is a spiral of wanting.” Since all experiences leave a “mark on the brain,” what does this really tell us about why some people eat a few potato chips and stop, while others finish the bag and look for more in the cupboard?

It’s not clear what percentage of the population reacts to food the way Kessler and his hypereating friends do. The government says two-thirds of Americans are “overweight,” but that does not mean they routinely engage in the out-of-control gorging that Kessler describes. Then again, Kessler says “overeating is not the sole province of the overweight,” since thin people can scarf down big bowls of ice cream or M&Ms but compensate by exercising more. It does not make much sense to claim that people who burn all the calories they consume are overeating—unless, like Kessler, you’re promoting a trademarked treatment for overeating called Food Rehab™.

According to The Washington Post, “Kessler estimates that about 15 percent of the population is not affected” by conditioned hypereating, meaning 85 percent is. That seems inconsistent not only with everyday experience but with Kessler’s own analysis of questionnaire data from the Reno Diet Heart Study. He says “one-third of the study population scored high” on one or more of three factors—“loss of control over eating,” “lack of feeling satisfied by food,” and “preoccupation with food”—that characterize the syndrome he typifies.

Yet the section of the book where Kessler describes his Food Rehab™ method seems to be aimed at a general audience, which is like expecting all drinkers to follow the 12 Steps of Alcoholics Anonymous. “I don’t offer a one-size-fits-all technique,” Kessler claims, adding that “few foods will be totally out of bounds.” Yet he lays down some pretty categorical-sounding imperatives. “Neither sugar nor refined carbohydrates that behave much like sugar in the body, such as white flours and pasta, belong in the diet in significant amounts,” he writes, calling for “a diet based largely on lean protein and whole grains or legumes, supplemented with fruits and nonstarchy vegetables.” For everyone? Just for hypereaters? Maybe both, because by this point Kessler seems to have convinced himself that his impulsive, gluttonous reaction to tasty food is a universal trait.

But what about those of us who reject Kessler’s ethic of rigidly ordered abstemiousness, which replaces hypereating with hypervigilance? Consider celebrity chef and food writer Anthony Bourdain, who supplied a blurb for this book (“disturbing, thought-provoking, and important”) that suggests he hasn’t read it. As anyone who watches No Reservations, Bourdain’s show on the Travel Channel, can attest, his attitude toward food is about as far from Kessler’s as it’s possible to get. While Kessler says we should be wary of delicious dishes, Bourdain conspicuously consumes all manner of fatty, salty, calorie-packed food in large quantities without apology (and nevertheless keeps a trim figure). Bourdain’s fans see a man who relishes life and refuses to sacrifice pleasure on the altar of health. Kessler presumably would see a victim of conditioned hypereating who desperately needs a course of Food Rehab™.

Friday, November 6, 2009

Israeli scientists find stroke drug could help cure cancer

By Ofri Ilani, Haaretz Correspondent
Tags: cancer, Tel Aviv University

Israeli scientists have identified a substance that can kill cancerous cells without harming healthy ones, paving the way for more effective cancer treatment.
The findings by researchers at Tel Aviv University and Sheba Medical Center, Tel Hashomer, were published in the current issue of the international peer-reviewed journal Breast Cancer Research.
"We actually found the Achilles heel of the cancer cell," said Prof. Malka Cohen-Armon from Tel Aviv University, who headed the research team. "As soon as you can target cancerous cells without killing healthy ones, you can produce medications that would cause a lot less suffering to the patient. We can even give a much more aggressive treatment without worrying about harming healthy tissues."
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The substance identified by the researchers, which delays cell proliferation in healthy and cancerous cells, is a component of a drug developed a decade ago to preserve nerve cells and prevent them from dying after a stroke.
But while the drug causes the rapid death of cancer cells, healthy cells activate a mechanism that overcomes the delay in proliferation within hours, and those cells continue to proliferate exactly like cells not exposed to the substance.
Cohen-Armon said the drug's effectiveness in treating cancer cells was discovered accidentally.
"I'm not even a cancer researcher," she said. "But two years ago an article we published on various functions in the cell got me interested in cancer cells."
She said the scientists involved in the discovery - who include doctoral student Asher Castiel and Professor Shai Izraeli's research group at the Sheba Cancer Research Center - haven't figured out why the drug affects the cells the way it does.
"We don't even fully understand why this is happening, but we see cancerous cells die and healthy cells overcome this obstacle," said Cohen-Armon. "They somehow find a way to proliferate even in the presence of the substance."
She said the drug was tested on several types of cancer, but so far only the breast cancer tests results have been published.
The experiment has been carried out on female mice, which were injected with human cancerous cells. The substance was gradually released over two weeks. The mice that weren't treated with the substance developed malignant tumors - but in those that got the treatment, the substance either prevented or significantly stalled the development of the cancerous cells.
The experiments did not find any changes in the behavior of the mice treated with the substance.
One of the obstacles to applying the discovery to all forms of cancer is that the medicine is registered as a patent of an American pharmaceutical company. Tel Aviv University's technology transfer company, Ramot, has secured a usage patent enabling it to develop the drug to treat only breast cancer.
The future development of the drug depends on the goodwill of the American company, or on another company developing a similar substance.
"We really want to develop this drug, but there are some completely non-scientific obstacles," Cohen-Armon said. "I hope the research doesn't fade away because of that."

Tuesday, September 29, 2009

Blind patient sees again with eye tooth


A 60-year-old woman blind for nine years has regained useful vision following a rare operation in Miami in which surgeons removed one of her teeth, drilled a hole in it, inserted a plastic lens into the hole and implanted the tooth-lens combination into her eye.

Thursday, September 24, 2009

Experimental HIV Vaccine Raises Hopes

BANGKOK -- For the first time, an experimental vaccine has prevented infection with the AIDS virus, a watershed event in the deadly epidemic and a surprising result. Recent failures led many scientists to think such a vaccine might never be possible.

The vaccine cut the risk of becoming infected with HIV by more than 31% in the world's largest AIDS vaccine trial of more than 16,000 volunteers in Thailand, researchers announced Thursday in Bangkok.

Even though the benefit is modest, "it's the first evidence that we could have a safe and effective preventive vaccine," Col. Jerome Kim said in a telephone interview. He helped lead the study for the U.S. Army, which sponsored it with the National Institute of Allergy and Infectious Diseases.

The institute's director, Anthony Fauci, warned that this is "not the end of the road," but said he was surprised and very pleased by the outcome.

"It gives me cautious optimism about the possibility of improving this result" and developing a more effective HIV vaccine, Dr. Fauci said in a telephone interview. "This is something that we can do."

Even a marginally helpful vaccine could have a big impact. Every day, 7,500 people world-wide are newly infected with HIV and two million died of AIDS in 2007, the U.N. agency UNAIDS estimates.

"Today marks an historic milestone," said Mitchell Warren, executive director of the AIDS Vaccine Advocacy Coalition, an international group that has worked toward developing a vaccine.
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* Researchers' statement | Study info

"It will take time and resources to fully analyze and understand the data, but there is little doubt that this finding will energize and redirect the AIDS vaccine field," he said in a statement.

The Thailand Ministry of Public Health conducted the study, which used strains of HIV common in Thailand. Whether such a vaccine would work against other strains in the U.S., Africa or elsewhere in the world is unknown, scientists stressed.

The study actually tested a two-vaccine combo in a "prime-boost" approach, where the first one primes the immune system to attack HIV and the second one strengthens the response.

They are ALVAC, from Sanofi Pasteur, the vaccine division of French drug maker Sanofi-Aventis; and AIDSVAX, originally developed by VaxGen Inc. and now held by Global Solutions for Infectious Diseases, a nonprofit founded by some former VaxGen employees.

ALVAC uses canarypox, a bird virus altered so it can't cause human disease, to ferry synthetic versions of three HIV genes into the body. AIDSVAX contains a genetically engineered version of a protein on HIV's surface. The vaccines are not made from whole virus -- dead or alive -- and can't cause HIV.

Neither vaccine in the study prevented HIV infection when tested individually in earlier trials, and dozens of scientists had called the new one futile when it began in 2003.

"I really didn't have high hopes at all that we would see a positive result," Fauci confessed.

The results proved the skeptics wrong.

"The combination is stronger than each of the individual members," said the Army's Col. Kim.

The study tested the combo in HIV-negative Thai men and women ages 18 to 30 at average risk of becoming infected. Half received four "priming" doses of ALVAC and two "boost" doses of AIDSVAX over six months. The others received dummy shots. No one knew who got what until the study ended.

All were given condoms, counseling and treatment for any sexually transmitted infections, and were tested every six months for HIV. Any who became infected were given free treatment with antiviral medicines. Participants were followed for three years after vaccination ended.

According to the results: New infections occurred in 51 of the 8,197 given vaccine and in 74 of the 8,198 who received dummy shots. That worked out to a 31% lower risk of infection for the vaccine group.

The vaccine had no effect on levels of HIV in the blood of those who did become infected. That had been another goal of the study -- seeing whether the vaccine could limit damage to the immune system and help keep infected people from developing full-blown AIDS.

That result is "one of the most important and intriguing findings of this trial," Dr. Fauci said. It suggests that the signs scientists have been using to gauge whether a vaccine was actually giving protection may not be valid.

"It is conceivable that we haven't even identified yet" what really shows immunity, which is both "important and humbling" after decades of vaccine research, Dr. Fauci added.

Details of the $105 million study will be given at a vaccine conference in Paris in October.

This is the third big vaccine trial since 1983, when HIV was identified as the cause of AIDS. In 2007, Merck & Co. stopped a study of its experimental vaccine after seeing it did not prevent HIV infection. Later analysis suggested the vaccine might even raise the risk of infection in certain men. The vaccine itself didn't cause infection. In 2003, AIDSVAX flunked two large trials, the first late-stage tests of any AIDS vaccine at the time.

It is unclear whether vaccine makers will seek to license the two-vaccine combo in Thailand. Before the trial began, the U.S. Food and Drug Administration said other studies would be needed before the vaccine could be considered for U.S. licensing.

Also unclear is whether Thai volunteers who received dummy shots will now be offered the vaccine. Researchers had said they would do so if the vaccine showed clear benefit, defined as reducing the risk of infection by at least 50%.

Those issues, plus how to proceed with future studies, will be discussed among the governments, study sponsors and companies involved in the trial, Kim said. Scientists want to know how long will protection last, whether booster shots will be needed, and whether the vaccine helps prevent infection in gay men and injection drug users, since it was tested mostly in heterosexuals in the Thai trial.

The study was done in Thailand because U.S. Army scientists did pivotal research in that country when the AIDS epidemic emerged there, isolating virus strains and providing genetic information on them to vaccine makers. The Thai government also strongly supported the idea of doing the study.

Tuesday, July 28, 2009

Cure for radiation sickness found?

Exclusive: Dramatic discovery by Jewish-American scientists could change world; anti-radiation medication proves effective, safe in tests. Further experiments to be fast tracked, FDA approval possible within 1-2 years
Ronen Bergman


The ground-breaking medication, developed by Professor Andrei Gudkov – Chief Scientific Officer at Cleveland BioLabs - may have far-reaching implications on the balance of power in the world, as states capable of providing their citizens with protection against radiation will enjoy a significant strategic advantage vis-à-vis their rivals.

For Israel, the discovery marks a particularly dramatic development that could deeply affect the main issue on the defense establishment's agenda: Protection against a nuclear attack by Iran or against "dirty bomb" attacks by terror groups.

Gudkov's discovery may also have immense implications for cancer patients by enabling doctors to better protect patients against radiation. Should the new medication enable cancer patients to be treated with more powerful radiation, our ability to fight the disease could greatly improve.

Dramatic test results
The process that led up to the medical innovation dates back to 2003, when Professor Gudkov came up with the idea of using protein produced in bacteria found in the intestine to protect cells from radiation.

Gudkov recounted an experiment he held with two groups of mice.

"We exposed both groups to lethal radioactive radiation," he said. "All the mice in the control group died within a short period of time. A few days later, when I approached the cage with the mice that received the protein, I could see that they're ok, that they're alive. They survived. It's hard to describe the joy all of us felt. We realized that finally, after so many years and so many experiments and frustrations, we made a breakthrough that may save the lives of millions."

Prof. Gudkov published the findings of the protein experiment in Science, the world's leading scientific journal; however, the discovery of the medication was kept secret until now, while Gudkov and his associated waited for the results of two series of critical tests examining the medication's effectiveness and safety.

The first series of tests included experiments on more than 650 monkeys. Each test featured two groups of monkeys exposed to radiation, but only one group was given the medication. The radiation dosage was equal to the highest dosage sustained by humans as result of the Chernobyl mishap.

The experiment's results were dramatic: 70% of the monkeys that did not receive the cure died, while the ones that survived suffered from the various maladies associated with lethal nuclear radiation. However, the group that did receive the anti-radiation shot saw almost all monkeys survive, most of them without any side-effects. The tests showed that injecting the medication between 24 hours before the exposure to 72 hours following the exposure achieves similar results.

Another test on humans, who were given the drug without being exposed to radiation, showed that the medication does not have side-effects and is safe. Prof. Gudkov's company now needs to expand the safety tests, a process expected to be completed by mid-2010 via a shortened test track approved for bio-defense drugs. Should experiments continue at the current rate, the medication is estimated to be approved for use by the FDA within a year or two.

'Stable, safe, and easy to inject'
The company's subcontractor in Europe is already prepared to embark on mass production. Meanwhile, emergency regulations in Israel allow the government to purchase drugs on short notice, even if they are still in the process of being approved. Notably, the medication in question is not a vaccine, but rather, a preventative drug administered via one or several shots.

The medication works by suppressing the "suicide mechanism" of cells hit by radiation, while enabling them to recover from the radiation-induced damages that prompted them to activate the suicide mechanism in the first place.

Prof. Gudkov heads a group of Jewish-American scientists and has cooperated with an Israeli researcher and Israeli investors. A large part of the revolutionary medication's development process was funded by the US Defense and Health departments, which thus far earmarked $40 million to the project. About two weeks ago, the US Defense Department announced that in light of the successful tests, it will continue to fund the project.


The Israeli scientist involved in the research, Dr. Elena Feinstein, made Aliyah to Israel in 1985 and for many years served as a cancer researcher at the Weizmann Institute of Science. Dr. Feinstein met Prof. Gudkov while they worked together in Moscow and was among the founders of the company, serving as its deputy director for some time.

Today, Feinstein works for an Israel company engaged in cancer research and continues to cooperate with Gudkov. Referring to the innovative medication, she says: "Both its effectiveness and safety had been proven. It is stable, safe, and easy to inject."

Both Feinstein and Gudkov stress that the innovative drug does not provide 100% protection against radioactive damage. However, should the discovery announced by the scientists meet all the required tests and permits, it may change the 21st Century.

Friday, June 12, 2009

David Kessler "The End of Overeating."


David Kessler visits Google's Mountain View, CA headquarters to discuss his book "The End of Overeating." This event took place on May 28, 2009, as part of the Authors@Google series.

Before we can begin to address America's eating epidemic, we need to understand WHY we have such difficulty controlling what we eat. Kessler spent the past seven years meeting with top scientists, physicians, psychologists, and food industry insiders, and conducting his own research to reveal how specific foods produced by giant food corporations and restaurant chains ("Big Food") feed our desire to eat by stimulating the brain with an infinite variety of diabolical combinations of salt, fat and sugar. People of all ages are being set up for a lifetime of food obsession due to the ever-present availability of foods laden with salt, fat and sugar. It is no wonder that millions of Americans are gaining weight and getting sick. The End of Overeating provides a highly readable and indispensable picture of the problems we face and offers solutions for how to fight them and regain control.

David Kessler, MD, served as commissioner of the US Food and Drug Administration. Dr. Kessler, a pediatrician, has been dean of the medical schools at Yale and the UCSF. He is the father of two grown children and lives with his wife in California.

Thursday, June 11, 2009

Health Officials Declare Flu Pandemic

GENEVA -- The World Health Organization declared an H1N1 flu pandemic Thursday -- the first global flu epidemic in 41 years -- as infections in the United States, Europe, Australia, South America and elsewhere climbed to nearly 30,000 cases.
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The long-awaited pandemic announcement is scientific confirmation that a new flu virus has emerged and is quickly circling the globe. WHO will now ask drugmakers to speed up production of an H1N1 flu vaccine. The declaration will also prompt governments to devote more money toward efforts to contain the virus.

WHO chief Dr. Margaret Chan made the announcement Thursday after the U.N. agency held an emergency meeting with flu experts. Dr. Chan said she was moving the world to phase 6 -- the agency's highest alert level -- which means a pandemic, or global epidemic, is under way.

"The world is moving into the early days of its first influenza pandemic in the 21st century," Dr. Chan told reporters. "The (H1N1 flu) virus is now unstoppable."

On Thursday, WHO said 74 countries had reported 28,774 cases of H1N1 flu, including 144 deaths. Chan described the virus as "moderate." According to WHO's pandemic criteria, a global outbreak has begun when a new flu virus begins spreading in two world regions.

The agency has stressed that most cases are mild and require no treatment, but the fear is that a rash of new infections could overwhelm hospitals and health authorities -- especially in poorer countries.

Still, about half of the people who have died from H1N1 flu were previously young and healthy -- people who are not usually susceptible to flu. H1N1 flu is also crowding out regular flu viruses. Both features are typical of pandemic flu viruses.

The last pandemic -- the Hong Kong flu of 1968 -- killed about 1 million people. Ordinary flu kills about 250,000 to 500,000 people each year.

H1N1 flu is also continuing to spread during the start of summer in the northern hemisphere. Normally, flu viruses disappear with warm weather, but H1N1 flu is proving to be resilient.

The decision might have been made much earlier if WHO had more accurate information about H1N1 flu's rising sweep through Europe. Dr. Chan said she called the emergency meeting with flu experts after concerns were raised that some countries like Britain were not accurately reporting their cases.
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After Thursday's meeting, Dr. Chan said the experts agreed there was wider spread of H1N1 flu than what was being reported.

Dr. Chan would not say which country tipped the world into the pandemic, but said all countries and experts were agreed that it was time to declare a global outbreak.

WHO said it was now recommending that flu vaccine makers start making H1N1 flu vaccine. Drug giant GlaxoSmithKline PLC said they could start large-scale production of pandemic vaccine in July but that it would take several months before large quantities would be available.

The pandemic declaration will require all countries, including the dozens that haven't yet reported any cases, to launch pandemic-prevention plans.

Peter Cordingley, a spokesman for the WHO based in Manila, noted that the term pandemic was "a measure of the spread of the virus, not the severity of the virus." The virus's effects are moderate at the moment, he noted. "But it's still going to infect an awful lot of people."

Nearly half the world's confirmed cases, or 13,217, are in the U.S., including 27 deaths, according to the WHO.

In Australia, the number of the new disease, also known as swine flu, has more than tripled in the past week, reaching 1,263 on Thursday, when three new cases were confirmed in the state of Tasmania. It recorded its first case of the disease on May 9.

"Australia catches our eye particularly not because of the number of cases but because of strong evidence of community transmission," particularly in the southern state of Victoria and its capital, Melbourne, said Mr. Cordingley. He said the WHO is also focusing on similar evidence in the U.K., Spain, Japan and Chile.

More than 1,000 Australia's swine flu cases are in Victoria, which has been hit by the cold temperatures and dry conditions that flu viruses thrive in.
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Victorians now account for around 3.6% of total confirmed cases globally, and authorities are struggling to understand exactly why the virus has taken such a hold in the state, Victoria's acting chief health officer, Rosemary Lester, said Thursday.

"Perhaps we may never have a definitive answer on that," Lester told Australian Broadcasting Corp. radio. "We do know that we have had an extensive testing regime so we have uncovered a lot of cases that were there to be uncovered. And because the disease is so mild in the majority of people, that allowed it to spread undetected," she said.

Cases detected so far have been relatively mild, with no deaths from the virus yet recorded in the country. The majority of sufferers in Australia have been aged between five and 18, but the virus continues to strike healthy adults including several professional Rugby League players who competed in an interstate match in Victoria's capital, Melbourne, last week.

Those players were quarantined from their clubs, and earlier this week, authorities canceled a major swim meet due to be held in Melbourne. Victoria is on a higher level of alert than other Australian states.

On the streets of Melbourne there is little evidence of major concern among the city's nearly four million residents. Shops, bars and cafes -- while affected by the economic slowdown -- are still busy, and the city's public transport has shown no signs of reduced patronage.

Schools in the nation are no longer being closed if a student is reported as having the virus, although authorities have requested that school aged children at risk from the virus stay home for seven days.

In contrast, Hong Kong's government on Thursday ordered the closure of all nurseries, kindergartens and primary schools for two weeks after a dozen students at one school tested positive for swine flu.

Australian health authorities have stopped testing every suspected case of the virus -- drawing some condemnation from critics -- and Victoria is now focusing treatment on those most vulnerable to viral infections, such as the very old or very young.

New York City health officials say three more people have died from swine flu, bringing the city's total to 15. One victim was a child under the age of 5, one was a person between 5 to 24 years old, and another was between 30 to 39 years old.

The city health department says a telephone poll of over 1,000 residents found nearly 7% had flu-like symptoms in April and May. That suggests more than half a million New Yorkers were ill.
—Lyndal McFarland in Melbourne, Peter Stein in Hong Kong and the Associated Press contributed to this article.

Monday, June 8, 2009

Swine Flu Is Way Worse Than Expected

When we began writing about the impending swine flu pandemic, many readers thought we were buying into some kind of government created panic. Our view was exactly the opposite: the government was understating the risks of swine flu, worried that a "panic" would hurt the economy. Mainstream media sources started by being "responsible" and under-reporting the risks in the US, bought into the panic for a week or so, then quietly dropped the story.

The story of swine flu has now effectively dropped out of public discussion. In fact, when it is discussed it usually as a critique of health authorities for needlessly creating a scare.

Once again, however, this is exactly backwards. Swine flu has not turned out to be a non-event. It is not more confined than intially feared. Indeed, the official risk models of swine flu dramatically underestimated how widespread it has become.

As the New York Times reports, two rival supercomputer teams made projections about the swine flu epidemic. One said that swine flu would hit 2,000 people by the end of May. Another said the number would be 25 percent higher: 2,500. (The innumerate editors of the New York Times call these estimate "surprisingly similar," but that's not important for now.)

In fact, the Centers for Disease Control and Prevention estimate that by the end of May there were upwards of 100,000 cases of swine flu in the country. So much for the models that told us the risks weren't so big.

Saturday, June 6, 2009

Chagas Disease: A Century Later

Chagas Disease: A Century Later

By Kara Rogers on Health

In 1909 Brazilian physician Carlos Chagas discovered American trypanosomiasis, better known as Chagas disease. In the 100 years since, there have been two drugs developed that can cure the disease and a lot learned about how it can be prevented. Yet, it affects between 8 and 11 million people in the Americas and Caribbean. So instead of celebrating a centennial marked by successful control or elimination of Chagas, researchers and public health officials are calling for assistance, especially increased government and private funding.

Chagas has fallen unceremoniously into the pile of neglected tropical diseases, a group of human afflictions that thrive in the poorest and most destitute rural and urban regions of the world. The urgency with which health organizations have had to respond to diseases like malaria and AIDS has overshadowed Chagas, which is endemic to Mexico and countries in Central and South America. There are roughly 50,000 new cases of Chagas diagnosed annually in these places, and at the rate that its incidence appears to be increasing, there is concern that in the Americas and Caribbean the disease actually may be as prevalent as or even more so than malaria.

Chagas is a vector-borne disease, and thus it involves a carrier (vector), a parasite, and a mechanism of transmission to humans. The carrier is a bloodsucking insect known as the kissing bug, or barber beetle, because its favorite place to bite an unsuspecting victim is the face. The kissing bug attacks at night and is most commonly found in poorly constructed or dilapidated houses that have cracks in their walls or roofs, which serve as entry points for the bugs. Trypanosomas cruzi.

The parasite that causes Chagas disease is Trypanosomas cruzi, a protozoan that has a flagellum to propel it from place to place. When a kissing bug bites its victim, it deposits the infectious parasite in its feces. The victim scratches the bite and rubs the feces into the wound, thereby facilitating the entry of the parasite into nearby cells. Once inside a cell, the parasite matures and multiplies. The organisms eventually burst out of the cell and into the bloodstream. They then travel to and infect various tissues, though they seem to have an affinity for muscle cells and neuroglia, cells that function to support neurons.

Chagas is a frightening and sometimes unpredictable disease. It is characterized by acute and chronic stages, both of which may be silent, meaning that obvious symptoms do not always manifest. Acute disease in which there are no or only very mild symptoms often goes undiagnosed and therefore untreated. As a result, the parasite remains in the body, setting the stage for chronic disease, which can take one or more decades to develop and is often fatal. Chronic disease often appears in the form of heart abnormalities, which may lead to sudden cardiac death or heart failure, or in the form of gastrointestinal disease, which arises due to the parasitic destruction of nerve cells.

Only two drugs—nifurtimox and benznidazole—are effective for the treatment of Chagas, and they are useful only in the acute stage of disease, when they can cure infection. If treatment is delayed or if infection persists, the chance for ridding the body completely of parasites drops significantly. More importantly, however, Chagas can be prevented in the first place. Improving the construction of houses, spraying insecticides, using bed nets, and improving basic hygiene can stop kissing bugs from getting into houses and transmitting the disease.

Prevention and proper treatment are the most practical ways to break the cycle of infection from insect to human to insect. These approaches also can reduce the likelihood that people migrating from one place to another will carry the parasite with them. But delivering the needed preventative, educational, and therapeutic resources to affected regions requires money and people. Researchers and health workers hope that their efforts this year will draw attention to Chagas. After all, a century has passed. Perhaps it is time to bring this otherwise preventable disease under control.

Sunday, May 31, 2009

Are Cancer Drugs Worth The Money?

Matthew Herper and Robert Langreth 05.30.09, 4:15 PM ET

ORLANDO - At the annual meeting of the American Society for Clinical Oncology, giant banners with pictures of heroic cancer patients proclaim doctors are "Personalizing Cancer Care."

But many companies seem to be maximizing cancer profit instead. Big drug companies are making big money off smaller and smaller improvements in cancer care. Newfangled cancer drugs can cost $50,000 a year, and that doesn’t mean they will add a year to the patient’s life--you might spend $50,000 for a year and extend the patient's life by only weeks.

The numbers would look better if drug companies did a better job of targeting drugs at the patients most likely to benefit. But that targeting has occurred in only a few scattered examples.

The skyrocketing costs for limited benefit are leading some experts to worry about whether the medical system has the right incentives.

"We are wasting a lot of resources treating people with treatments they don't need," says Otis Brawley, chief medical officer at the American Cancer Society. Novartis, Wyeth and Pfizer all sell very expensive cancer pills. "We would like to believe that cost should be no object, but that is not reality," says Leonard Saltz, a colon-cancer expert at Memorial Sloan-Kettering Cancer Center.

The poster child for high-cost cancer drugs is Roche's Avastin. The drug has $4.8 billion in sales and is approved to treat breast, colon, lung and brain cancer. It was first approved in 2004 after research showed it could extend survival in advanced colon-cancer patients by five months.

The hope was that further studies of Avastin in other types of cancer or in earlier stages of the disease would show even greater survival benefits. But they haven’t. In several breast-cancer trials--including a new one being presented at the meeting this weekend--Avastin slowed the progression of disease but did not extend patient survival at all. But doctors still use the drug in treating breast cancer because they figure it helps symptoms, even if patients don’t live longer. Avastin costs up to $55,000 a year.

In another major study presented at the meeting, Avastin failed to prevent colon cancer from recurring after surgery. In the first year of treatment, more patients who got Avastin remained free of detectable cancer. But after a year, the drug was stopped, and by the end of the study, the apparent initial benefit had faded completely.

Historically, the goal of therapy in early-stage cancer has been to increase the cure rate. But results hint that Avastin may not be curing anyone--it may suppress microscopic cancer deposits without killing them by preventing the growth of their blood vessels. The doctor who conducted the trial, Norman Wolmark of Allegheny General Hospital, is talking about testing Avastin for twice as long in order to get an effect, but that may not be enough. To make a difference in early-stage disease, "the patient may need very, very long-term or even permanent treatment with Avastin," says Saltz. "It gets phenomenally expensive."

Roche says the hints of efficacy support Avastin's future prospects. "It is a validation of the fact that Avastin has a role in early-stage disease," says William Burns, head of Roche's pharmaceuticals division. He forecasts Avastin could still reach sales of $8 billion by 2012 or 2013, even without use in earlier stages of cancer. "With Herceptin, we have learned that it is a drug to start with and stay with" at multiple stages of disease, says Burns, referring to the company's targeted breast cancer drug. "We are start[ing] to piece together exactly the same journey for Avastin."

Burns says the company will consider altering its ongoing trials of Avastin in early-stage breast and lung cancer to include longer-term Avastin use.

Roche is also combining other expensive drugs with Avastin. One study at the meeting showed that adding Tarceva, from OSI Pharmaceuticals and Roche, delayed by one month the median time it takes lung tumors to grow. While it is not yet possible to tell whether there is an effect on survival, the results were statistically significant and financially momentous. U.S. sales of Tarceva were $457 million last year. "We estimate we have the potential for at least $500 million in new [U.S.] business from this study," says OSI Chief Executive Colin Goddard.

One problem is that doctors have no idea which patients are likely to benefit from Avastin, so they give it to everyone in hopes that a few will benefit. Another strategy might be to amp up the search for blood-test results that could predict whether a patient will respond to Avastin, says Angela DeMichele, an oncologist at the University of Pennsylvania whose research focuses on breast cancer. There are clues as to how patients most likely to benefit from Avastin might be identified, she says, but these avenues haven't been pursued yet. "We're still treating people in an unselected way," DeMichele says.

"Avastin is probably not a targeted therapy, as far as I am concerned," says MD Anderson Cancer Center breast cancer expert Franciso Esteva.

Drugs like Tarceva and AstraZeneca's Iressa, which is no longer used in the U.S., work best in patients whose tumors have a mutation in the gene for the epidermal growth factor receptor (EGFR), which is involved in cell growth. In another lung cancer study, Tarceva only slightly delayed the median progression in the overall group of patients, but the small subset of patients with EGFR mutations in their tumors had a tenfold lower risk of the tumor progressing when they took Tarceva.

Since Iressa, AstraZeneca has made a point of pairing drugs with diagnostic work. But it didn’t with Zactima. This experimental drug delayed the progression of lung cancer by three weeks to 17 weeks. Although promising--and viewed as one of AstraZeneca’s most important new products--it has not been paired with a test. Doctors hope for a greater benefit if it is used in earlier stages of the disease.

One of the most impressive results was not from a fancy new therapy at all. Alimta, a more traditional chemotherapy pill sold by Eli Lilly, didn't just slow tumor progression but also increased survival for patients with non-small-cell lung cancer by a median 2.8 months, extending survival to 13.4 months.

Sanofi's Breast Cancer Bet

Sanofi's Breast Cancer Bet
Robert Langreth and Matthew Herper 05.31.09, 1:50 PM ET

ORLANDO, Fla. -- North Carolina resident Terri M. Allen noticed two strange pimple-like bumps on her scalp in June 2007. When she finally got them checked out, her worst fears were confirmed. Her breast cancer that had been removed in 2005 had returned with a vengeance, spreading to her sternum, hipbone and both lungs. Worse, she had a particularly nasty form called triple negative that doesn't respond to several standard treatments.

"I thought I was not going to make it," says Allen, now 54. Then her doctor told her about an experimental drug from Sanofi-Aventis that is looking promising in patients with her form of cancer. She started taking the drug along with chemo in March 2008. Within three months the tumors had virtually disappeared. "This is incredible to me," says Allen, who remains on the Sanofi drug and in remission. "I have no side effects and a completely normal standard of life."

Allen is among the first to benefit from a new class of drugs that aim at a weak spot in certain breast and ovarian cancers: limitations in their inability to repair DNA damage. While not cures, the drugs, called PARP inhibitors, may work well in triple negative breast cancers, about 15% of cases. They also show promise in patients with cancer due to inherited mutations in the BRCA1 and BRCA2 genes.

PARP inhibitors are among the few hot new drugs being highlighted at an otherwise sleepy meeting of the American Society of Clinical Oncology in Orlando. In a trial on 116 triple negative patients, patients who got the Sanofi parp drug lived 3.5 months longer than those who just got standard cell-killing chemotherapy regimens. "It is a big deal," says study leader Joyce O'Shaughnessy of the Baylor Charles A. Sammons Cancer Center. "We don't see survival advantages very often in [advanced] breast cancer." Adds Eric Winer, a breast cancer expert at the Dana-Farber Cancer Institute: "This is one of the most exciting results we have seen in a long time" for these patients. Triple negative cancers aren't responsive to standard hormone therapy or the drug Herceptin.

Sanofi-Aventis Chief Executive Christopher Viehbacher hopes that the drug will reinvigorate his company's cancer franchise. Sanofi sells some of the world's most used chemotherapy drugs, but has never made a name in the newer targeted drugs that are mainstays for Roche, Eli Lilly and Novartis. The PARP drug could help change this. Sanofi got the drug with its $500 million acquisition of BiPar Sciences, a biotech firm with only 18 employees that Sanofi bought earlier this year.

"This is a first-in-class drug, so it puts us back in the game of really innovative medicine," says Viehbacher. "There are other PARP inhibitors out there, but for the moment we've been able to stay in the lead." Parp stands for poly (ADP-ribose) polymerase.

Sanofi's biggest competition is AstraZeneca. It has tested its drug in an even narrower group of patients, women with inherited mutations in the BRCA1 or BRCA2 genes. (About 5% of breast cancer patients, including Allen, have one of these mutations.) Two small studies at the meeting found that the AstraZeneca's drug helped shrink 41% of breast cancer patients with the mutations and also helped ovarian cancer patients, without the need for chemotherapy.

One patient it helped is 70-year-old Los Angeles resident Barbara Shellow. She started on the AstraZeneca PARP inhibitor for her advanced ovarian cancer in July 2007, and her tumors quickly shrank. She has now gone 18 months without a relapse. "The drug has been a miracle for me," she says. Larger trials will be needed to confirm the benefits of both drugs before they can be approved.

If AstraZeneca or Sanofi had tested their drugs on all breast cancer patients, they likely would not have worked, as most breast tumors probably aren't being driven by aberrant DNA repair. "One of the key things is to match the cancer drug to the right patient population," says Alan Ashworth at the Institute of Cancer Research in London, who did an early experiment showing that patients with BRCA mutations might be susceptible to PARP blockers.

Many tumor types besides breast and ovarian may have DNA repair defects. A problem is there is no good test yet to determine which tumors have such defects. Researchers are furiously working to find one, says Ashworth.

"Getting at the molecular defects that are driving cancer is the only way to intelligently apply targeted therapy," says William Audeh, an oncologist at Cedars-Sinai Medical Center in Los Angeles who is testing the AstraZeneca drug. He says researchers need to start treating patients based on what mutations lie hidden inside their tumors, instead of based on what part of the body the tumor is in.

Tuesday, May 26, 2009

Top 5 Cholesterol Myths

Even if you think you know everything there is to know about cholesterol, there may be a few more surprises in store. Check out these common myths about high cholesterol; find out who’s most likely to have it, what types of food can cause it, and why—sometimes—cholesterol isn’t a bad word.

By Health.com

Myth 1: Americans have the highest cholesterol in the world

One of the world’s enduring stereotypes is the fat American with cholesterol-clogged arteries who is a Big Mac or two away from a heart attack. As a nation, we could certainly use some slimming down, but when it comes to cholesterol levels we are solidly middle-of-the-road.

According to 2005 World Health Organization statistics, American men rank 83rd in the world in average total cholesterol, and American women rank 81st; in both cases, the average number is 197 mg/dL, just below the Borderline-High Risk category. That is very respectable compared to the top-ranked countries: In Colombia the average cholesterol among men is a dangerous 244, while the women in Israel, Libya, Norway, and Uruguay are locked in a four-way tie at 232.

Myth 2: Eggs are evil

It’s true that eggs have a lot of dietary cholesterol—upwards of 200 mg, which is more than two-thirds of the American Heart Association’s recommended limit of 300 mg a day. But dietary cholesterol isn’t nearly as dangerous as was once thought. Only some of the cholesterol in food ends up as cholesterol in your bloodstream, and if your dietary cholesterol intake rises, your body compensates by producing less cholesterol of its own.

While you don’t want to overdo it, eating an egg or two a few times a week isn’t dangerous. In fact, eggs are an excellent source of protein and contain unsaturated fat, a so-called good fat.

Myth 3: Kids can’t have high cholesterol

Most people think high cholesterol is a problem that’s strictly for the middle-aged. But guess what? Research has shown that atherosclerosis—the narrowing of the arteries that leads to heart attacks—can start as early as age eight. In July 2008, the American Academy of Pediatrics released guidelines on kids and cholesterol that recommended that children who are overweight, have hypertension, or have a family history of heart disease have their cholesterol tested as young as two years of age.

Children with high cholesterol should be on a diet that restricts saturated fat to 7% of calories and no more than 200 mg per day of dietary cholesterol, according to the guidelines. Fiber supplements and more exercise are also recommended.

While the guidelines prompted a bit of an outcry from parents worried that doctors would be pushing cholesterol-lowering drugs for kids, a new study suggests that less than 1% of adolescents aged 12 to 17 would be considered candidates for medication.

Myth 4: Food is heart-healthy if it says “0 mg cholesterol”

The Cholesterol portion of the nutritional label refers to dietary cholesterol, which is only one of the things found in food that can cause your cholesterol to go sky-high. (A bigger contributor to elevated cholesterol? A high-fat diet.) It’s also believed to be the least important. Saturated fat (found in animal foods and dairy products) and trans fats (found in packaged foods) appear to have a far greater impact on low-density lipoprotein (LDL), the so-called bad cholesterol that causes atherosclerosis, than dietary cholesterol.

Myth 5: Cholesterol is always a bad thing

When most people hear “cholesterol” they think “bad.” Like most things in life, the reality is more complex. High cholesterol can be dangerous, but cholesterol itself is essential to various bodily processes, from insulating nerve cells in the brain to providing structure for cell membranes. That’s why your body makes the white, waxy substance (about 75% of the cholesterol in your blood is made by the liver and cells elsewhere in your body).

The role of cholesterol in heart disease is often misunderstood. Cholesterol is carried through the bloodstream by low-density and high-density lipoproteins (LDL and HDL). LDL, known as bad cholesterol, and not the cholesterol it carries per se, is responsible for atherosclerosis.

Sunday, May 24, 2009

WU engineers develop ultrasound cell phone




William D. Richard (left) takes an ultrasound probe of colleague David Zar's carotid artery with a low-power imaging device he designed.
(David Kilper/WUSTL Photo)
By Liz Stoever
ST. LOUIS POST-DISPATCH
05/18/2009

Everyone knows cell phones can pinpoint your location by GPS signals, record photos and video, browse the Internet and keep your schedule. They even can make phone calls.

But now, thanks to engineers at Washington University, cell phones can scan your insides.

Computer engineers David Zar and David Richard have invented a combination ultrasound and high-end smart phone — a super-portable device to scan the body using sound waves.

The new device, adapted from existing portable ultrasounds, will provide a cheaper and more portable alternative to ultrasounds typically limited to hospitals.


In a world where 70 percent of the population does not have access to medical imaging, Zar said, he and his partner expect the device to permanently change the current medical and global computer landscape.

"Twenty-first century medicine is defined by medical imaging," Zar said. "But it's typically not used."
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Although ultrasounds are very practical, they can be difficult to use because the machines are large, old and shared, Zar said. With the cell phone ultrasound, doctors can use it more often.

"This fits in a coat pocket and the whole thing can start up in 10 to 15 seconds," Zar said.

The device also allows patients with diseases such as Duchenne muscular dystrophy to do ultrasounds at home and send information to any centralized unit in the world for a diagnosis.

The device's mobility will also be helpful in developing countries where hospitals are far, but cell phone towers may be more abundant.

Everyone, not just medical professionals, can purchase the ultrasound device from California-based Interson Corp., the manufacturer, in about a month. While ultrasounds are relatively safe, Zar said frequent use can be problematic, and he does not recommend it to pregnant mothers.

Zar and Richard received a $100,000 grant from the Microsoft Corp. in 2008 as part of its larger project to make health care mobile in remote areas. Microsoft External Research has funded approximately $2 million dollars toward projects using cell phones for health care.

About 15 other projects are already under way under the grant program and have produced results including a device that also attaches to a cell phone and can help children with autism communicate more effectively through picture-based communication. Another cell phone compatible device monitors heart rhythms and can diagnose heart problems.

Kristin Tolle, senior research program manager at Microsoft External Research, said the mobile health care project is more prominent than others because it can work anywhere in the world.

"We wanted to encourage ideas," she said. "We are really trying to help underserved communities."

Dr. Antonella Quattromani, a cardiologist on staff with DePaul Health Center, who went on a mission to Ecuador in March, said the device would be very practical on her other mission trips to remote areas.

"The quality of the image is good," she said. "It would be really useful."

The only limitation is the cell phone reception needed to send images in some remote areas, Quattromani said.

By next year, however, everyone in the world should have access to a cell phone tower, Tolle said.

Before the device becomes available to developing countries, Zar said they will need help developing training and distribution for the device.

"This is much bigger than two geeks at Washington University can support," Richard said. "We need layers of people between us and the people on the ground in India."

Friday, May 22, 2009

The Obamacare to Come

The Obamacare to Come
Dems’ health-care plans do not provide the reform most Americans seek.

By Michael Tanner

Drip by painful drip, the details of the Democratic health-care-reform plan have been leaking out. And from what we can see so far, it looks like bad news for American taxpayers, health-care providers, and, most important, patients.

The plan would not initially create a government-run, single-payer system such as those in Canada and Britain. Private insurance would still exist, at least for a time. But it would be reduced to little more than a public utility, operating much like the electric company, with the government regulating every aspect of its operation.

It would be mandated both that employers offer coverage and that individuals buy it. A government-run plan, similar to Medicare, would be set up to compete with private insurers. The government would undertake comparative-effectiveness and cost-effectiveness research, and use the results to impose practice guidelines on providers. Private insurance would face a host of new regulations, including a requirement to insure all applicants and a prohibition on pricing premiums on the basis of risk. Subsidies would be extended to help middle earners purchase insurance. And the government would subsidize and manage the development of a national system of electronic medical records.
The net result would be an unprecedented level of government control over one-sixth of the U.S. economy, and over some of the most important, personal, and private decisions in Americans’ lives.

Let’s look at some of the most troubling ideas in detail.

An employer mandate. Employers would be required to insure their workers through a “pay or play” mandate. Those who did not provide “meaningful coverage” for their workers would pay a penalty, equal to some percentage of their payroll, into a national fund that would provide insurance to uncovered workers. Such a mandate is, of course, simply a disguised tax on employment. As Princeton University professor Uwe Reinhardt, the dean of health-care economists, points out, “[That] the fiscal flows triggered by mandate would not flow directly through the public budgets does not detract from the measure’s status of a bona fide tax.” Estimates suggest that an employer mandate could cost 1.6 million jobs over the first five years.

An individual mandate. As is the case with an employer mandate, an individual mandate is essentially a disguised tax. It is also the first in a series of dominoes that will lead to greater government control of the health-care system.

To implement an insurance mandate, the government will have to define what sort of insurance fulfills it. As the CBO puts it, “an individual mandate . . . would require people to purchase a specific service that would have to be heavily regulated by the federal government.” At the very least, deductible levels and lifetime caps will have to be specified, and a minimum-benefits package will likely be spelled out. This means the oft-repeated promise that “if you are happy with your current insurance, you can keep it” is untrue. Millions of Americans who are currently satisfied with their coverage will have to give it up and purchase the insurance the government wants them to have, even if the new insurance is more expensive or covers benefits the buyer does not want.

A “public option.” The government would establish a new universal-health-care program, similar to Medicare, that would compete with private insurance. Regardless of how it is structured or administered, such a plan would have an inherent advantage in the marketplace because it would ultimately be subsidized by taxpayers. It could, for instance, keep its premiums artificially low or offer extra benefits, then turn to the U.S. Treasury to cover any shortfalls. Consumers would naturally be attracted to the lower-cost, higher-benefit government program.
A government program would also have an advantage because its tremendous market presence would allow it to impose much lower reimbursement rates on doctors and hospitals. Government plans such as Medicare and Medicaid traditionally reimburse providers at rates considerably below those of private insurance. Providers recoup the lost income by raising prices for those with private insurance. It is estimated that privately insured patients pay $89 billion annually in additional insurance costs because of cost-shifting from government programs. If the new public option would have similar reimbursement policies, it would result in additional cost-shifting of as much as $36.4 billion annually. Such cost-shifting would force insurers to raise their premiums, making them even less competitive with the taxpayer-subsidized public plan. Lewin Associates estimates that as many as 118.5 million Americans, nearly two out of every three people with insurance, would shift to the government program. The result would be a death spiral for private insurance.

Given that many of the most outspoken advocates of the “public option” have, in the past, supported a government-run single-payer system, it is reasonable to suspect they support a public option precisely because it would squeeze out private insurance and eventually lead to such a system. President Obama himself has said that if he were designing a health-care system from scratch, his preference would be a single-payer system “managed like Canada’s.” He has also said that, while his proposal is a less radical approach, “it may be that we end up transitioning to such a system.”
Comparative- and cost-effectiveness research. In an attempt to control health-care costs, the government would undertake research to determine which health-care procedures and technologies are most effective and, more ominously, cost-effective. Of course, there is a great deal of waste in the U.S. health-care system, and if the government’s goal were simply to provide better information there would be little cause for concern. But there is every reason to believe such research would be used to impose restrictions on how medicine is practiced. For example, some reform advocates have said that when an insurance company fails to comply with government practice guidelines, workers should no longer be able to exempt the value of that company’s plans from their taxable income.

There is no doubt that other countries use comparative-effectiveness research as the basis for rationing. For example, in Great Britain, the National Institute on Clinical Effectiveness makes such decisions, including a controversial determination that certain cancer drugs are “too expensive.” The U.K. government effectively puts a price tag on each citizen’s life — about $44,305 (£30,000) per year, to be exact, under NICE’s guidelines. That’s just a baseline, of course, and, as NICE chairman Michael Rawlins points out, the agency has sometimes approved treatments costing as much as $70,887 (£48,000) per year of extended life. But such treatments are approved only if it can be shown they extend life by at least three months and are used for illnesses that affect fewer than 7,000 new patients per year.

The final health-care-reform bill is likely to include a number of other bad ideas: a host of new insurance regulations that will drive up costs and limit consumer choice (under one leaked proposal, Americans would be limited to a choice of four standardized insurance plans); subsidies for middle-class families (a family of four earning as much as $83,000 per year would receive subsidized care under one proposal); and government preemption of private investment and research into health IT. All of this would come at a cost to taxpayers of at least $1.5 trillion over the next ten years.

The American people are right to demand health-care reform. The current system is broken. But taken individually, most of the ideas currently being considered by Congress would make the problems we face even worse. Taken together, they amount to a complete government takeover of the American health-care system. That is not the type of reform most Americans seek.

— Michael Tanner is a senior fellow at the Cato Institute, author of Leviathan on the Right: How Big Government Conservatism Brought down the Republican Revolution, and co-author of Healthy Competition: What's Holding back Health care and How to Free It.

Thursday, May 14, 2009

Vitamins Found to Curb Exercise Benefits

Vitamins Found to Curb Exercise Benefits
By NICHOLAS WADE

If you exercise to improve your metabolism and prevent diabetes, you may want to avoid antioxidants like vitamins C and E.

That is the message of a surprising new look at the body’s reaction to exercise, reported on Monday by researchers in Germany and Boston.

Exercise is known to have many beneficial effects on health, including on the body’s sensitivity to insulin. “Get more exercise” is often among the first recommendations given by doctors to people at risk of diabetes.

But exercise makes the muscle cells metabolize glucose, by combining its carbon atoms with oxygen and extracting the energy that is released. In the process, some highly reactive oxygen molecules escape and make chemical attacks on anything in sight.

These reactive oxygen compounds are known to damage the body’s tissues. The amount of oxidative damage increases with age, and according to one theory of aging it is a major cause of the body’s decline.

The body has its own defense system for combating oxidative damage, but it does not always do enough. So antioxidants, which mop up the reactive oxygen compounds, may seem like a logical solution.

The researchers, led by Dr. Michael Ristow, a nutritionist at the University of Jena in Germany, tested this proposition by having young men exercise, giving half of them moderate doses of vitamins C and E and measuring sensitivity to insulin as well as indicators of the body’s natural defenses to oxidative damage.

The Jena team found that in the group taking the vitamins there was no improvement in insulin sensitivity and almost no activation of the body’s natural defense mechanism against oxidative damage.

The reason, they suggest, is that the reactive oxygen compounds, inevitable byproducts of exercise, are a natural trigger for both of these responses. The vitamins, by efficiently destroying the reactive oxygen, short-circuit the body’s natural response to exercise.

“If you exercise to promote health, you shouldn’t take large amounts of antioxidants,” Dr. Ristow said. A second message of the study, he said, “is that antioxidants in general cause certain effects that inhibit otherwise positive effects of exercise, dieting and other interventions.” The findings appear in this week’s issue of The Proceedings of the National Academy of Sciences.

The effect of vitamins on exercise and glucose metabolism “is really quite significant,” said Dr. C. Ronald Kahn of the Joslin Diabetes Center in Boston, a co-author of the report. “If people are trying to exercise, this is blocking the effects of insulin on the metabolic response.”

The advice does not apply to fruits and vegetables, Dr. Ristow said; even though they are high in antioxidants, the many other substances they contain presumably outweigh any negative effect.

Dr. Kahn said it might be that reactive oxygen is beneficial in small doses, because it touches off the body’s natural defense system, but harmful in higher doses.

Andrew Shao of the Council for Responsible Nutrition, a trade association of dietary supplement makers, said the new study was well designed but was just one bit of evidence in a complex issue. Most available evidence points to the opposite conclusion, that antioxidants benefit health by reducing oxidative stress, he said.

“I wouldn’t change recommendations for anyone based on one study,” he said. “This is one small piece of the puzzle.”