One year ago, researchers at the National Cancer Institute published a paper that linked Chronic Fatigue Syndrome with an obscure retrovirus known as XMRV. The article caused a stir because 4% of the supposedly healthy people in the study were infected with the virus. That could mean nearly 12 million Americans are infected with a poorly understood virus that potentially causes a poorly understood disease.

There has followed a mad dash to commercialize a blood test for XMRV, since arguably, the nation’s blood supply needs to be screened for the virus. Unfortunately, progress on this endeavor has been slow.

Like HIV-the virus that causes AIDS-XMRV is a retrovirus. XMRV has also been associated with prostate cancer, although no one really knows whether the virus causes diseases of any kind in humans.

Labs involved the effort to develop an XMRV blood test include those at the CDC and the National Cancer Institute, as well private sector programs at Roche, Abbott and Gen-Probe.

Scientists at Abbott are working with the Cleveland Clinic and Emory University. They have created unequivocally positive blood samples from monkeys that were deliberately infected with XMRV. The infected monkeys produced antibodies to 3 proteins on the surface of the virus, but blood levels of these antibodies became undetectabe within weeks after the infection. Tests based on these antibodies can therefore generate false negative results. False negative results can also be caused by the unusually long delay between the time the monkeys were infected with the virus and the time the antibodies appeared.

Even if these issues can be overcome and the antibody test subsequently proven to be useful on human blood, there would remain additional challenges in commercializing the test. For example, the elapsed time between when the blood is obtained and when it is tested could impact test results.

“When there is a new agent that we don’t know a lot about, it’s always a process,” Michael Busch lamented in an interview with the Wall Street Journal. Bush is the director of San Francisco’s Blood Systems Research Institute and a participant in the working group tasked by the Feds to study the potential impact of XMRV on the nation’s blood supply.

Final Thought: It’s hard to criticize a proactive effort to commercialize a blood test for a virus that could be contaminating our nation’s blood supply, but it sure would be nice to know that XMRV actually causes human disease, and that it actually can be transmitted through a blood transfusion. #CartBeforeTheHorse?

Last month, scientists reported that Truvada, Gilead’s once-a-day pill that is normally used to treat HIV infection, can be used to prevent HIV infection as well.

The report appeared in the New England Journal of Medicine. In the study, nearly 2,500 HIV-negative gay and bisexual men were randomized to receive either Truvada or a placebo. Study participants who received the anti-retroviral pill were 44% less likely to become HIV-positive during the 15 month follow-up than folks in the control group. The risk reduction was 73% among men who managed to take the pill every day or nearly every day.

The study results “represent a major advance in HIV research,” Kevin Fenton, the CDC’s HIV/AIDS czar told the Wall Street Journal. Even President Obama was moved to comment that the study, and those like it “could mark the beginning of a new era in HIV prevention.”

Truvada contains 2 drugs produced by Gilead: tenofovir and emtricitabine. Both drugs are reverse transcriptase inhibitors, which block replication of the AIDS virus in the human body. Normally, Truvada is combined with 2 other drugs to create a cocktail for the treatment of AIDS. This is the first time Truvada has been tested for its ability to prevent infection in the first place.

Gay and bisexual men comprise nearly half of the one million-or-so people who are HIV positive in this country. They are 44 times more likely to be HIV positive than other men.

Despite the apparently good news about Truvada, many public health officials raised concerns that people would not take the drug every day or fail to use condoms in a mistaken belief that the drug is, by itself, enough to prevent HIV infection. There were good reasons for this concern. Men in the study whose adherence to the once-a-day regimen was less than 90% experienced only a 21% reduction in infection risk.

It’s also not clear that Truvada will be similarly effective in IV-drug abusers or heterosexuals, since HIV enters the body via different routes in these people. Studies of Truvada’s prophylactic efficacy in these groups are underway.

The CDC plans to release guidelines for using Truvada to prevent HIV/AIDs in the near future. The drug hasn’t been approved for this purpose by the FDA, but physicians can prescribe drugs for off-label uses if they want.

By the way, Truvada costs just under $1,000 per month in the US. Also of note, the scientists responsible for the so-called Prep trial covered here are continuing to follow enrollees to look for drug resistance and long-term side effects. It’s something to keep in mind as the dust settles on this exciting finding.

Scientists know that our perceptions about taste and texture drive our food preferences. They know quite a lot about the role of taste in this regard, and the results of some recent experiments have shed new light on the role of texture as well, particularly as it relates to foods containing starch.

Starch is a major component of potatoes, rice, corn, wheat and the enormous variety of foods derived from them. It is also added to many other products from maple syrup to pudding. In fact starch accounts for 40-60% of the calorie content in the average Western diet, and more than that in many Asian and third-world diets. 

Humans begin digesting starch in the mouth, where the salivary glands secrete an enzyme known as amylase. This enzyme breaks down starch and other complex carbohydrates into simpler sugar molecules which end-up being absorbed from the small intestine into the bloodstream.

For years, scientists knew that people’s DNA contains between 2 and 15 copies of AMY1, the gene that codes for amylase. Recently, Abigail Mandel and colleagues at the Monell Chemical Senses Center in Philadelphia hypothesized that the number of copies of the AMY1 gene that a person has might impact the speed with which that person breaks down starch in his or her diet. This in turn might affect the way that person perceives the texture of starchy foods, and ultimately his or her preferences for that food.

To test their theory, Mandel’s team determined the number of AMY1 genes and the amount and activity of salivary amylase in 62 healthy volunteers. Sure enough, the team found that people with more AMY1 genes produced more salivary amylase. Then, the team asked the volunteers to swish-and-swirl starch-containing solutions in their mouths and rate the “runniness” of these solutions after 60 seconds. The high-amylase producers found the solutions to be “more runny” than the low amylase producers.

So what, you ask? Well, Mandel’s team believes this finding helps explain why people experience starch-containing foods as creamy vs. slimy, or sticky vs. watery. In the case of ice cream and hard chocolate for example, Mandel’s team had shown in a separate study that people who really dig these treats seem to be particularly enthralled by creamy sensations that start off as “solid” and then subsequently melt away in the mouth.

“We all have had the experience of liking a food that someone else complains is too tacky, or slippery, or gritty, or pulpy,” Breslin explained to the Wall Street Journal. “This is why a given line of product often comes in different textural forms,” like orange juice with and without pulp, he added.

Of course, an abundance of salivary amylase is just a part of a much larger food preference story. Scientists have, for example, identified another gene that renders bitter tastes more intense and shown that people who have this gene tend not to consume bitter-tasting vegetables like kale and spinach. And learned phenomena also play a role: people who don’t initially like scotch for example, can wind up enjoying it with “practice.”

Breslin’s amylase study appears in PLoS ONE.

Nearly 300,000 people per year in the US collapse suddenly and die as a result of cardiac arrest, in which a heart attack or something else causes the heart to cease pumping blood effectively. The condition is fatal in minutes unless afflicted individuals receive cardiopulmonary resuscitation.

The vexing public health problem with cardiac arrest is that many witnesses hesitate to administer CPR because they don’t want to get involved with the “mouth-to-mouth” part of the process. Some won’t do it because they are grossed-out by vomitus that may be in the patient’s mouth. Others worry that they might catch an infectious disease from the patient. Tens of thousands of lives are lost each year because of this hesitation.

That’s why the results of a new study by Bentley Bobrow and colleagues at the Arizona Department of Health Services were a cause for celebration after being released last week. The results of the study showed that cardiac arrest patients that received only chest compressions (not mouth-to-mouth) from witnesses had higher survival rates than patients who received CPR the old fashioned way (compressions plus mouth-to-mouth).

The study was published in the Journal of American Medical Association. It included 4,415 adults that sustained cardiac arrest between 2005 and 2009. In the study, survival rates (measured at hospital discharge) were 13.3% in the chest compressions only group, 7.8% in patients that received conventional CPR, and 5.2% for those who received no CPR.

“Anybody can do hands-only CPR by pushing hard and pushing fast in the center of a person’s chest,” Michael Sayre, an associate professor at Ohio State University and a CPR expert told the Wall Street Journal.

Responding quickly to the findings, the American Heart Association modified its CPR recommendations. The new recommendations call for adults to emphasize chest compressions rather than mouth-to-mouth resuscitation. The AHA recommendations can be seen here.

Note that when kids are found unresponsive, they do indeed need mouth-to-mouth resuscitation since the causes for the condition in kids is usually respiratory, not cardiac.

Most people know that cigarette smoking causes lung cancer and cardiovascular disease. Now, as if anyone needed another reason to kick the habit, a new study has shown that heavy smoking in middle-age is associated with an increased risk of Alzheimer’s disease and other forms of dementia as well.

To reach these conclusions, Minna Rusanen, Rachel Whitmer and colleagues at Kaiser Permanente identified 21,000 patients that had completed a cigarette smoking survey between 1978 and 1985, and then tracked down diagnoses that had been entered into their medical records between 1994 and 2008.

It turned out that nearly 5,400 people (25%) from the original cohort were diagnosed with dementia, including 1,100 people that developed Alzheimer’s disease and another 400 that developed vascular dementia. After adjusting for a host of possibly confounding factors, Rusanen’s group found that people who reported smoking at least 2 packs of cigarettes per day on that initial survey were 2.15 times more likely than non-smokers to develop dementia from all causes, 2.5 times more likely to develop Alzheimer’s disease, and 2.7 times more likely to develop vascular dementia during follow-up.

The deleterious impact of smoking grew with increasing cigarette consumption. Thus, people who smoked “only” 1-2 packs per day had 1.4 times the risk of all-cause dementia. And former smokers—those who said they’d quit at the time of the initial survey—were not at increased risk for dementia.

“It’s a pretty clear picture that heavy smoking … elevates your risk of dementia,” said Whitmer, who works at Kaiser Permanente’s research division in Oakland. “If you are a heavy smoker and you’re lucky enough to make it to old age, you’re not in the clear. You’re still at risk for dementia.”

The study confirms the results of recent clinical trials on the relationship between cigarette consumption and Alzheimer’s disease. An interesting historical note is that older studies had actually suggested that smoking reduced the risk of cognitive impairment and dementia in elderly folks. Most scientists have discounted these older studies because many of the heavy smokers in those studies ended up dying before they had a chance to develop Alzheimer’s disease; that’s a phenomenon which could have biased the results.

The write-up of the current study appears in the Archives of Internal Medicine.

It’s hard to know whether Clint Eastwood’s new movie, Hereafter, prompted a recent surge in interest concerning near-death experiences, or whether the flick simply tapped into the surge. Regardless, an otherworldly 15 million American adults claim to have had a near-death experience, according to the results of 1997 survey. That number might be a lot higher now that automatic external defibrillators have become commonplace.
 
It’s also hard to know what to make of these claims from a scientific standpoint, but there’s no denying that near-death experiences are described in stunningly similar ways by people with diverse cultural, ethnic, and religious backgrounds, and across all age groups, right down to toddlers.

People typically describe a near-death experience as a sensation of floating above one’s body, and/or moving through a tunnel towards a light. Often, there are associated feelings profound of joy and peace, and visions of past experiences or deceased acquaintances. The experience usually ends with a realization that it’s not time to die, and a return to one’s injured or failing body.

Some people who’ve experienced the phenomenon and then manage to recover their health undergo personality changes that they attribute to the experience. Others, as is the case with the lovely French reporter played by Cecile de France in Hereafter, become convinced there is an afterlife.

What have scientists learned about the physiologic underpinnings of near-death experiences? The answer, as you might guess, is not much.

The traditional explanation, first promulgated 25 years ago by British neuroscientist Susan Blackmore, was that cerebral oxygen deprivation caused the experience. She noted that astronauts and fighter pilots experience visual disturbances and cognitive abnormalities during high altitude maneuvers in oxygen-poor environments, and their experiences mimic near-death experiences. Alas, a recent study seemed to contradict her theory by showing that people who had near-death experiences actually had higher oxygen levels in their blood than those who did not.

Earlier this year, a study of cardiac-arrest patients in the Journal of Critical Care reported finding high blood levels of carbon dioxide in patients who had near-death experiences. This condition is known to cause hallucinations and out-of-body experiences, even in people who are not on death’s door.

A second study of dying patients in the Journal of Palliative Medicine found that EEG patterns in dying patients revealed a spike in electrical activity just before they passed away. The surge began in one part of the brain and spread in wave-like fashion to other regions. The study authors postulated that such activity could trigger visual and auditory experiences consistent with near-death experiences.

Other scientists have proposed that areas of the brain which control memory could become activated by severe physiologic abnormalities, and that could explain the recollections some people have as a part of their near-death experience. Similar abnormalities could trigger the release of endorphins which could in turn evoke feelings of joy and euphoria.

As for the actual existence of an afterlife, we’ll leave that discussion to others.

Traditional approaches to anorexia nervosa are based on the assumption that parental behaviors—or at least their interactions with afflicted individuals—helped cause or exacerbate the problem. Consistent with this assumption, treatments for the potentially deadly eating disorder typically exclude family members.

But a recent study by scientists at the University of Chicago and Stanford provides strong evidence that parents can play a decisive role in improving outcomes for patients with anorexia.

The study of 121 patients with the condition was published earlier this month in the Archives of General Psychiatry. It focused on the so-called Maudsley model, in which parents are present at each meal until the anorexic child eats.

The Maudsley model was developed in London 2 decades ago. It calls for parents to assume responsibility for mealtimes involving their anorexic child, “making it impossible not to eat,” study author Daniel Le Grange explained to the Wall Street Journal.

The study by Le Grange and his colleagues showed that that anorexia patients who received care according to the Maudsley model were more likely to achieve and maintain a therapeutic weight than those treated using conventional one-on-one interventions with a behavioral therapist.

The relative improvement vs. conventional therapy was present one year after treatment ceased, and increased over time. Thus at the end of the second year post-treatment, almost half the patients receiving family-treatment were in remission, whereas only 23% of the patients in the therapist treatment group were in remission. The difference was statistically significant.

“This is additional evidence that involvement of the family can be a very effective way in helping kids overcome their problems,” said B. Timothy Walsh, a professor of psychiatry at Columbia University Medical Center.

People forget the stir Big Pharma created 16 months ago when it gave Big-Ups to the Big O at a time when he desperately needed passengers to ride the Health Reform Express.

The dust-up took place before Massachusetts produced “Guess Who’s Coming to Dinner” starring Scott Brown, and before Congressional parliamentarians reminded us what reconciliation meant. And it happened before Congress managed to vote 100% along party lines on what was inarguably one of the most important pieces of social legislation in our generation.

But it did happen. In June, 2009, Big Pharma’s main lobbying arm offered the Big O a deal he couldn’t  refuse: “We’ll cut prices on drugs purchased by Medicare by $80 billion over the next 10 years if you don’t push Medicare to import cheap drugs from Canada or direct it to negotiate price cuts with us.”

At the time, the Party of No was aghast! How could Big Pharma do such a thing? John Boehner was so moved by the treasonous behavior, he accused the lobbying group of trying to appease a “bully.”

(Oh c’mon John! Obama? A “bully”?)

Of course all of this is old news especially since Republicans cleaned house in the midterms and are now threatening to repeal and replace the Big O’s health reform law altogether.

Will the purge include a bit of pay-back for Big Pharma? Alas, probably not. There have been no calls for retribution by the Republicans. In fact, many industry insiders believe drug companies might make out just fine in view of the antiregulatory, antigovernment sentiments espoused by the Boehners.

These insiders doubt the GOP would seek to reverse the “doughnut hole” savings for Medicare beneficiaries that was part of the original deal, since that would be panned by senior citizens and why give the Pelosis an issue they can leverage?

Beyond this, Big Pharma believes the GOP might just help them out by reauthorizing the Prescription Drug User Fee Act, which permits drug and device companies to funnel cash to the FDA in order to expedite product reviews. The drug industry claims this process assures new drugs get to market more quickly by assuring the FDA has enough resources to move things along (and want you to ignore those silly consumer advocates who argue such fees could bias the FDA process!).

The impetus to repeal the PDUFA in the first place came from Connecticut Rosa DeLauro and other House Democrats, who are now playing second fiddle to the Boehners. “Consumer groups will be neutered in this discussion,” analyst Ira Loss of Washington Analysis LLC told the Wall Street Journal.

And it didn’t hurt matters that Big Pharma donations, which tilted uncharacteristically toward the Big O in 2008, flowed heavily toward GOP candidates this time ‘round…

Why is it that some people can make life-altering decisions like deciding to get married without hesitation, while others take  hours to decide on trivial matters like whether to buy black or navy blue underwear?

The reason, psychologists tell us, has to do with the amount of ambivalence people have: Do they see the world in black-and-white or in shades of gray?

Although psychologists have just begun to study ambivalence, they already agree that people who tend to be ambivalent in one aspect of their lives tend to be ambivalent in other aspects as well.

It’s unclear why some folks tend to be more ambivalent than others. Personality traits like the need to reach a definitive conclusion for a particular situation tend to drive some towards black-and-white thinking. It also likely that parental influences and cultural aspects play a role. For example, many people in Asian cultures tend to be more comfortable with dualism, the concept that good and bad coexist in all aspects of life from relationships to the workplace. This cultural influence often translates to greater degrees of ambivalence.

Behavioral scientists have shown that ambivalence affects the way people solve problems. Black-and-white thinkers make decisions more quickly but tend to end up in conflict with others more frequently. Ambivalent problem solvers are more capable of feeling empathy and display healthier coping strategies during periods of stress. On the job however, ambivalent employees tend to perform more erratically, consistent with changing feelings about the job.

Though the field of ambivalence research remains in its infancy, there is an evolving consensus that the ability to remain open to different points of view reflects emotional and cognitive maturity: It amounts to “coming to grips with the complexity of the world,” Texas Tech psychologist Jeff Larsen explained to the Wall Street Journal.

Aortic Stenosis (AS) is a condition caused by progressive narrowing of the valve that governs blood flow from the heart to the brain and most other internal organs. About 1.5 million Americans have AS, one-fifth of whom have a severe form that is life-threatening.

Traditionally, the treatment for severe AS involves open heart surgery, an expensive procedure that is associated with its own risks and contraindicated in frail, elderly folks…just the kinds of people that develop the condition in the first place.

Now, scientists have shown that a relatively non-invasive treatment for severe AS may obviate the need for open-heart surgery.

The new approach involves attaching a replacement valve to a catheter, and then threading it through blood vessels to a place where it can serve the role of the malfunctioning valve. 

The replacement valve is produced from cow tissue and is housed within a metal frame. 

A study of the new device was published 2 weeks ago in the New England Journal of Medicine. In the study, a group of elderly patients received the catheter-placed device while others received various other non-surgical interventions.

The one-year mortality rate for people that received the replacement-valve was 31%. This was lower than the 51% mortality observed in controls. Of note, the study also revealed a higher incidence of early strokes (5% vs. 1%) in patients who received the new device. The increased stroke risk was nevertheless deemed “an acceptable price to pay” by Craig Smith, a study co-author.

The study was funded by Edwards Lifesciences, the same company that designed the valve. Several authors have financial ties to the company. Catheter-delivered valves “should be the new standard of care” for patients with severe AS that can’t tolerate open-heart surgery, they concluded. 

Edwards hopes to gain FDA approval for its device in 2011.