Monday, April 30, 2012

Zip Code as Important as Genetic Code in Childhood Obesity

The original heading on this article -- reproduced above -- is a vast exaggeration.  What was actually found was an assembly of mostly non-significant (>.05) relationships.  And it was actually found that the environment around you had NO EFFECT on adults.  It was only among children that some connection was observed.

Comparing Seattle and San Diego strikes me as a bit bizarre and creating large difficulties for control. I haven't bothered to look it up but as far as I am aware,  San Diego has a much higher proportion of blacks and Hispanics than Seattle does.  So how do you control for ethnicity?  You could say, "We will look at whites only" but the whites in the two places might not be comparable.  Due to the well known "white flight" phenomenon, many of the whites in San Diego might be "left behind" people in various ways.

I also believe that San Diego has America's largest population of retired admirals but although that is unlikely to have affected the results below, it is another warning that the populations of the two cities might be non comparable in a number of ways.

And even if we accept that the controls were adequate what do the results mean?  How does "neighborhood" exert its effect?  I doubt that the neighborhood itself does anything.  But maybe people who live in nicer areas send their kids out to exercise of various sorts more.  It may be an exercise effect rather than a neighborhood effect that we are looking at.  That it is something like that is suggested by the fact that the environment had no effect on adult obesity

Nearly 18 percent of U.S. school-aged children and adolescents are obese, as the rate of childhood obesity has more than tripled in the past 30 years. The prevalence of obesity puts children at greater risk of developing heart disease, type 2 diabetes, stroke and other illnesses, and of suffering severe obesity as adults. New study results indicate that where a child lives, including factors such as the neighborhood's walkability, proximity to higher quality parks, and access to healthy food, has an important effect on obesity rates. Researchers found that children living in neighborhoods with favorable neighborhood environment attributes had 59 percent lower odds of being obese.

"Obesogenic Neighborhood Environments, Child and Parent Obesity: The Neighborhood Impact on Kids Study" was published in a special theme issue of the American Journal of Preventive Medicine. Led by Brian Saelens, PhD, of Seattle Children's Research Institute, this is among the first neighborhood environment studies to look at a combination of nutrition and physical activity environments and to assess children and their parents. It is also among the largest studies of its kind to use objective geographic information system (GIS) data to examine the physical activity and healthy food option attributes of a neighborhood related to obesity.

Researchers used GIS to assess Seattle and San Diego area neighborhoods' nutrition and physical activity environments. Nutrition environments were defined based on supermarket availability and concentration of fast food restaurants. Physical activity environments were defined based on environmental factors related to neighborhood walkability and at least one park with more or better amenities for children. Kids that lived in neighborhoods that were poorer in physical activity and nutrition environment had the highest rates of obesity -- almost 16 percent -- in the study. This figure is similar to the national average. On the flip side, only eight percent of children were obese in neighborhoods where physical activity and nutrition environments were positive.

"People think of childhood obesity and immediately think about an individual's physical activity and nutrition behaviors, but they do not necessarily equate obesity with where people live," said Dr. Saelens, who is also a professor of pediatrics at the University of Washington. "Everyone from parents to policymakers should pay more attention to zip codes because they could have a big impact on weight."

Fast food may not be as easy to come by in the Seattle area, based on the study. There were 3,474 fast food locations in San Diego County, as compared to 1,660 in King County, Wash. On a county-level block group average basis, San Diego had 2.0 fast food locations per block group, and King County had 1.1.

Numerous national health organizations have identified neighborhood environment and built environment, including healthy food and physical activity opportunities, as important factors in childhood obesity, including the Institute of Medicine and the Centers for Disease Control and Prevention. "Our data support recommendations from these groups that we need to change our environments to make them more supportive of physical activity and nutrition," said Saelens.


Salad growers find that salad is good for you

With such a tiny sample (10) this is PR, not science.  It is amazing what academic journals will print these days.  As long as it serves the antioxidant religion, I guess ....

Researchers have found that antioxidant-rich watercress can alleviate the natural stress put on our body by a workout. And they found that participants with no watercress in their system who ate the leafy vegetable just two hours before high level exercise still experienced the same level of protection.

Though regular moderate exercise is known to be good for us, the increased demand on our bodies can cause damage to our DNA.

According to a new study from scientists at Edinburgh Napier University and the University of Ulster, eating watercress can prevent some of the damage caused by high intensity exercise and help maximise the benefits of a tough workout.  The study findings have now been published in the British Journal of Nutrition.

Study leader Dr Mark Fogarty, from Edinburgh Napier's School of Life, Sport and Social Sciences, said: "Although we are all aware of how good exercise can be for our bodies, pounding the treadmill, lifting weights, or doing high-levels of training can take its toll. The increased demand on the body for energy can create a build-up of free radicals which can damage our DNA.

"What we've found is that consuming a relatively small amount of watercress each day can help raise the levels of important antioxidant vitamins which may help protect our bodies, and allow us to enjoy the rewards of keeping fit. It's an interesting step forward in sports nutrition development and research."

Ten healthy men, aged on average of 23 years, participated in the study. For eight weeks they were given 85 grams of watercress -- a small bag -- and asked to participate in high-level exercise on the treadmill. An eight week study with no watercress consumption was carried out to act as a control.

The scientists also tested whether the protection properties of watercress were affected by the regularity of consumption.

Dr Fogarty said: "We put participants through short bursts of intense exercise and found that those who had not eaten watercress were found to have more DNA damage than those that did not. What was also fascinating is that the effect of eating watercress was not reliant on an accumulative build-up in our bodies. Those that ate the vegetable just two hours before exercise experienced the same benefits as those who had consumed the vegetable for eight weeks."

The study was sponsored by Vitacress Salads, one of Europe's growers of watercress.


Sunday, April 29, 2012

Regularly eating strawberries and blueberries may stave off mental decline by more than two years

Some proper caution about interpreting the results expressed below

Eating blueberries and strawberries may stave off mental decline in later life, claim researchers.

They found brain ageing could be delayed by up to two and a half years in elderly women regularly eating high amounts of the berries.  The findings come from an ongoing study of nurses which involves only women, but may also apply to men.

Experts believe the benefits are derived from the high content of flavonoids in berry fruits, antioxidant compounds found in plants which can protect against a wide range of diseases.

The US research team used data from the Nurses' Health Study, involving 121,700 female, registered nurses between the ages of 30 and 55 who completed health and lifestyle questionnaires beginning in 1976.  Since 1980 participants were surveyed every four years regarding their frequency of food consumption.

Between 1995 and 2001, cognitive function was measured in 16,010 women over the age of 70 years, at 2-year intervals, says a report in the Annals of Neurology journal.

The findings suggest increased consumption of blueberries and strawberries slows cognitive decline in older women.  Those who had higher berry intake delayed cognitive aging by up to 2.5 years.

The authors warn they cannot rule out the possibility that women who eat more berries also have other healthy habits, such as exercising more, which may play a part in the overall findings.

However, they found a greater intake of anthocyanidins and total flavonoids was also associated with less cognitive deterioration.

Experts believe that stress and inflammation contribute to cognitive impairment and that increasing consumption of flavonoids could mitigate the harmful effects.

Brain cells are particularly sensitive to free radicals, destructive groups of atoms made as a by-product of metabolism that can damage cell membranes and DNA.

Antioxidants help to neutralise free radicals, Dr Elizabeth Devore with Brigham and Women's Hospital and Harvard Medical School in Boston, Massachusetts, said `Our study examined whether greater intake of berries could slow rates of cognitive decline.  `We provide the first epidemiologic evidence that berries may slow progression of cognitive decline in elderly women.

`Our findings have significant public health implications as increasing berry intake is a fairly simple dietary modification to test cognition protection in older adults.'

Derek Hill, CEO of IXICO and Professor of Medical Imaging Sciences, University College London, said: `Later this year, two major drug trials targeting the proteins in the brain associated with Alzheimer's Disease will announce their results. Many experts fear these drugs will be added to the long list of potential dementia treatments that fail to demonstrate conclusively that they slow cognitive decline.

`This latest research suggesting that a diet high on berries can slow cognitive decline in the elderly population is therefore especially welcome.  `It is a large and well-designed study that significantly strengthens the evidence that changes to diet may be able to delay onset of dementia symptoms.

`This suggests that we can take further steps to tackling the scourge of dementia in society while we await the arrival of effective new medicines.'

Dr Eric Karran, Director of Research at Alzheimer's Research UK, said: `Population studies like this can provide useful clues about the effects of lifestyle and diet on cognition, but we must be sensible when interpreting the results. The study suggests a link between eating berries and slower cognitive decline, but there could be many factors at play.

`It is not possible to say whether the increased consumption of berries resulted in an increased, beneficial level of flavonoid antioxidants in the brain.  `Further research will be needed to conclude whether antioxidants in berries are beneficial in the brain and we can't assume that simply eating berries could protect against cognitive aging or dementia.

`Previous evidence has shown that eating fruit as part of a healthy diet in midlife could help to reduce our risk of dementia and so eating a healthy balanced diet is something we should all be thinking about.  `With 820,000 people in the UK living with dementia, there is an urgent need to understand more about how to reduce the risk.'

Carol Brayne, Professor of Public Health Medicine, University of Cambridge, said: `Broccoli, blueberries, Mediterranean diet, is very difficult indeed to be sure that this is not residual confounding as these kinds of dietary patterns are associated with many other positive attributes, which themselves are associated with healthier ageing.

`Blueberries have been of interest for many years and it's certainly worth further investigation, but for definitive evidence we have to await well designed trials as this is another observational study.'

The range of consumption in the study was women eating less than one serving of blueberries a month, between one and 3 servings a month and more than one serving a week, and from less than one serving of strawberries a week to more than two a week.


Can beetroot make runners unbeatable? Chemicals released by the backed vegetable help boost athletes' performance

There have been other reports to this effect and since performance-enhancing driugs are well-known, it is not particularly surprising that some may occur naturally

It seems a most unlikely performance booster but new research suggests beetroot could be the secret to track success at this year's Olympics.

Scientists have discovered athletes who eat baked beetroot before a race run faster than their rivals.

The purple root vegetable contains high levels of chemicals called nitrates, which have been shown to boost exercise performance.

Researchers at St Louis University in the US recruited 11 fit and healthy men and women and got them to twice run five kilometres on a treadmill.

Before the first run, the volunteers consumed a portion of baked beetroot just over an hour before hitting the treadmill.

Before the second run, they ate an equivalent amount of cranberry relish, chosen because it has a similar calorific content to beetroot but without the same nitrate levels.

The results, published in the Journal of the Academy of Nutrition and Dietetics, showed that after eating the cranberry relish, the runners averaged a speed of 11.9 kilometres per hour, or 7.3mph.

But after scoffing beetroot, their average speed went up to 12.3 kilometres per hour, around 7.6mph.

Researchers said runners appear to be able to maintain their speed for longer if they have eaten the vegetable.  In a report on their findings, they said: `During the last 1.1 miles of the run, speed was five per cent faster in the beetroot trial.  `Consumption of nitrate-rich, whole beetroot improves running performance in healthy adults.'

The findings support earlier research, published in 2009, by British scientists which suggested drinking beetroot juice could have a powerful effect on stamina and endurance, as well as lower blood pressure.

The researchers, from the University of Exeter and the Peninsula Medical School, also in Exter, recruited eight healthy young men to complete a series of cycling tests.

They took them twice - after drinking beetroot juice once a day for six days and after drinking blackcurrant cordial.

When tasked with cycling at an easy pace, the men used less oxygen after drinking beetroot, suggesting their muscles were able to do the same amount of work while spending less energy.

When they were asked to cycle for as long as they could before stopping, the beetroot juice allowed them to pedal an extra minute-and-a-half before running out of energy.

This 16 per cent increase in endurance could mean someone who normally runs out of steam after jogging for an hour would be able to keep going for an extra ten minutes.

It is thought nitrates lead to the blood vessels widening, improving oxygen supply to the muscles.


Saturday, April 28, 2012

Now even the NYT recognizes that "food deserts" are just an elite myth

People who like fast food will eat fast food;  people who like taking drugs will take drugs.  And there's nothing government can do about it.  It must be a bitter pill to Leftists to see that there are limits to what government can do

It has become an article of faith among some policy makers and advocates, including Michelle Obama, that poor urban neighborhoods are food deserts, bereft of fresh fruits and vegetables.

But two new studies have found something unexpected. Such neighborhoods not only have more fast food restaurants and convenience stores than more affluent ones, but more grocery stores, supermarkets and full-service restaurants, too. And there is no relationship between the type of food being sold in a neighborhood and obesity among its children and adolescents.

Within a couple of miles of almost any urban neighborhood, "you can get basically any type of food," said Roland Sturm of the RAND Corporation, lead author of one of the studies. "Maybe we should call it a food swamp rather than a desert," he said.

Some experts say these new findings raise questions about the effectiveness of efforts to combat the obesity epidemic simply by improving access to healthy foods. Despite campaigns to get Americans to exercise more and eat healthier foods, obesity rates have not budged over the past decade, according to recently released federal data.

"It is always easy to advocate for more grocery stores," said Kelly D. Brownell, director of Yale University's Rudd Center for Food Policy and Obesity, who was not involved in the studies. "But if you are looking for what you hope will change obesity, healthy food access is probably just wishful thinking."

Advocates have long called for more supermarkets in poor neighborhoods and questioned the quality of the food that is available. And Mrs. Obama has made elimination of food deserts an element of her broader campaign against childhood obesity, Let's Move, winning praise from Democrats and even some Republicans, and denunciations from conservative commentators and bloggers who have cited it as yet another example of the nanny state.

Speaking in October on the South Side of Chicago, she said that in too many neighborhoods "if people want to buy a head of lettuce or salad or some fruit for their kid's lunch, they have to take two or three buses, maybe pay for a taxicab, in order to do it."
Mrs. Obama has also advocated getting schools to serve healthier lunches and communities to build more playgrounds.

Her office referred questions about the food deserts issue to the Department of Agriculture. A spokesman there, Justin DeJong, said by e-mail that fighting obesity requires "a comprehensive response." The federal effort, he added, includes not just improving access to healthy foods but also improving food in schools, increasing physical education time, and educating people on the importance of healthy diets.

Some researchers and advocates say that further investigation is still needed on whether grocery stores and chain supermarkets in poor neighborhoods are selling produce that is too costly and of poor quality. "Not all grocery stores are equal," said John Weidman, deputy executive director of the Food Trust, an advocacy group in Philadelphia.

It was difficult to design a study that could rigorously answer the questions: Do poor urban neighborhoods lack places to buy fresh produce and is that contributing to obesity? But Helen Lee of the Public Policy Institute of California, a nonprofit, nonpartisan research organization, found a way. For data on where children lived and went to school and how much they weighed, she used a federal study of 8,000 children. For data on the location of food establishments, she used a data set that compiled all the businesses in the nation and included their sizes and locations.
"I knew where the children lived, so let's take the middle of that neighborhood," Dr. Lee said. "What is the nearest grocery store? What is the nearest convenience store?"

She used census tracts to define neighborhoods because they tend to have economically homogeneous populations. Poor neighborhoods, Dr. Lee found, had nearly twice as many fast food restaurants and convenience stores as wealthier ones, and they had more than three times as many corner stores per square mile. But they also had nearly twice as many supermarkets and large-scale grocers per square mile. Her study, financed by the institute, was published in the March issue of Social Science and Medicine.

Dr. Sturm's study, published in February in The American Journal of Preventive Medicine, had a different design. With financing from the National Institutes of Health, he used data on the self-reported heights, weights, and diets of more than 13,000 California children and teenagers in the California Health Interview Survey. The survey included the students' addresses and the addresses of their schools. He used a different data set to see what food outlets were nearby. Dr. Sturm found no relationship between what type of food students said they ate, what they weighed, and the type of food within a mile and a half of their homes.

He has also completed a national study of middle school students, with the same result - no consistent relationship between what the students ate and the type of food nearby. Living close to supermarkets or grocers did not make students thin and living close to fast food outlets did not make them fat. The study will be published soon in Public Health.


The Assault on Food

 John Stossel

Instinct tells us to fear poison. If our ancestors were not cautious about what they put in their mouths, they would not have survived long enough to produce us.

Unfortunately, a side effect of that cautious impulse is that whenever someone claims that some chemical -- or food ingredient, like fat -- is a menace, we are primed to believe it. That makes it easy for government to leap in and play the role of protector.

But for every study that says X is bad for you, another study disagrees. How is a layman to decide? I used to take consumer activists' word for it. Heck, they want to save the world, while industry just wants to get rich. Now I know better. The activists want money, too -- and fame.

To arbitrate, it's intuitive to turn to government -- except ... government scientists have conflicts, too.

Who becomes a regulator except people who want to regulate? Some come from activist groups that hate industry. Some come from industry and want to convert their government job into a higher-paying industry job. Some just want attention. They know that saying, "X will kill you," gets more attention than saying that X is probably safe.

I don't suggest that we ignore the experts and eat like pigs. But the scientific question should not overshadow the more fundamental issue. Who should decide what you can eat: you? Or the state? Should government decide what we may eat, any more than it decides where we live or how long our hair will be? The Food Police claim that they just want to help us make informed choices. But that's not all they want to do. They try to get government to force us to make healthy choices.

The moral issue of force versus persuasion applies even if all the progressives' ideas about nutrition are correct. Even if I would be better off eating no fat and salt, that would not justify forcing restaurants to stop serving me those things. Either we live in a free society or we don't.

It is no coincidence that the push for more food regulation came at a time when Congress obsessed about the rising cost of medical care. When government pays for your health care, it will inevitably be drawn into regulating your personal life. First, politicians promise to pay. Then, they propose to control you.

Where does it stop? If we must control diet to balance the government's budget, will the health squad next ban skydiving and extramarital sex? How about another try at Prohibition?

Government attracts do-gooders and meddlers who believe that, as Mark Twain put it, "Nothing so needs reforming as other people's habits." Or, as Twain's spiritual descendant, H.L. Mencken, said about Puritanism, government health officials seem to have "the haunting fear that someone, somewhere, may be happy."

Often the Food Police strike an innocent pose, claiming that they just want to give people information. Information is good. But it's not free. Mandated calorie signs in restaurants cost money. Those costs are passed on to consumers, and the endless parade of calorie counts and warning labels make us numb to more important warnings -- like, "This Coffee Is Scalding Hot."

It's not as if dietary information isn't already available. Health and diet websites abound. Talk shows routinely discuss the latest books on diet and nutrition. TV diet gurus are celebrities. That's enough. We have information. We don't need government force.

Let the marketplace of diet ideas flourish. Let claim meet counterclaim, but let's not let government put its very heavy thumb on one side of the scale.

The assumption behind so much of government's policy regarding food (and everything else) is that everything good should be encouraged by law and everything bad should be discouraged.

But since everything is arguably helpful or harmful, this is a formula for totalitarianism.

Thomas Hobbes assumed an all-powerful government was necessary to protect us from violence. He called it Leviathan. But he never imagined Leviathan would plan our dinners.


Friday, April 27, 2012

The VIOXX hysteria

There is a ridiculous article here which claims, in effect, that the executives of Merck & Co should have been hanged, drawn and quartered for releasing the anti-arthritis drug Vioxx.

It is all rather water under the bridge now so I won't go into great detail but but I believe Vioxx was unfairly impugned and should still be available to the many people it helped.

The attack on it was underpinned by a practice that I have often criticized on this blog:  Looking at relative risk to the exclusion of absolute  risk.  If the absolute risk is tiny, the relative risk seems of only academic interest to me.  There are risks in everything we do so something that has only a tiny absolute risk attached to it should be one of our better options in life, it seems to me.

Anyway, I will comment here only on the one big study that was most used to condem Vioxx.  The VIGOR study compared Vioxx with an accepted "safe" drug in its class: Naproxen.

And it found that using  Vioxx raised the absolute risk of a heart attack by one third of one percent -- from .01 to .04%  I would have interpreted that finding as showing that both drugs were low risk with only trivial differences between them but medical researchers love their relative risk statistics.  Without a heavy focus on RR, most of their findings would be trivial so RR is almost a religion with them. 

So they treated these essentially trivial results in a most frightening way: saying that Vioxx was FOUR TIMES as likely to give you heart attacks as its alternative.  And if you ignore that all the risks involved were tiny, that does sound alarming.  In fact, however, it was the usual medical research practice of making mountains out of molehills.  My recommendation from the data would have been that VIOXX is safe, except perhaps for  people with known heart problems

But that's not all.  While the heart attack rate  with Vioxx was elevated, the overall mortality was not!  In other words, Vioxx was not more likely to kill you than its control.  It may have led to a few more heart attacks but it REDUCED your risk of dying from other causes.  So even in relative risk terms it is a safe drug.  When you're dead you're dead.  It does not matter what you died of -- so overall mortality should have been the dominant criterion for evaluating Vioxx.  That it was essentially ignored just shows how hysterical people can get about drug companies.  They pick on trivialities to bring down what they hate as "Big Pharma".

Merck was unfairly persecuted by small minds and Vioxx should still be available to those it helped.  Arthritis is a most disabling condition and for some people Vioxx gave better relief than other drugs in its classs.

I could go on and discuss the other nitpicking associated with the VIGOR study but Humpty Dumpty is now well and truly off his wall so I see no point in going further.  I do however feel very sorry for the people at Merck and also sorry for the people who were   denied the chance to continue with something that was best for their disability.  Vioxx would not have once been so widely used without it being a very helpful drug.

LOL!  Health supplements 'could cause cancer': Study finds some products may increase chance of getting disease

Is the anti-oxidant religion fading at last?

Millions of people who take dietary supplements to ward off cancer may be toying with a ‘two-edged sword’ that might do them harm, experts have warned.

People were being misled by ‘messages from supplement manufactures’ stressing the health benefits of their products, including cancer prevention, according to a team of U.S. scientists.  They said there was no good evidence that supplement pills and capsules reduced the risk of cancer in healthy individuals.

They pointed out that antioxidants such as beta carotene, and vitamins C and E might even have biological effects that promote cancer.

Antioxidants are believed to counter the destructive effects of rogue oxygen molecules called free radicals.  Oxidative stress by free radicals, which attack cell membranes, proteins and DNA, has been linked to cancer and heart disease.

But the U.S. authors, writing in the Journal of the National Cancer Institute, argue that the supposed benefits of antioxidant supplements are largely a myth.

The panel of five experts, led by Dr Maria Elena Martinez, from the University of California at San Diego, wrote: ‘Undoubtedly, use is driven by a common belief that supplements can improve health and protect against disease, and that at worst, they are harmless.  ‘However, the assumption that any dietary supplement is safe under all circumstances and in all quantities is no longer empirically reasonable.’

Health supplements are booming in the U.S., with annual sales estimated at £18.6 billion, said the scientists, who assessed the evidence relating to several supplements including antioxidants, folic acid, vitamin D and calcium.

A number of animal, laboratory and observational studies had appeared to show that dietary supplements could lower cancer risk, they said.  However, these findings were not confirmed by the ‘gold-standard’ in evidence-based medicine, randomised controlled trials (RCTs).

Only a small number of RCTs had been carried out to test the effectiveness of dietary supplements, said the experts - and several of these had reported increased risks.

‘Supplementation by exogenous anti-oxidants may well be a two-edged sword,’ the scientists wrote. ‘These compounds could, in vivo (outside the laboratory), serve as pro-oxidants or interfere with any number of protective processes such as apoptosis induction.’ Apoptosis, or programmed cell death, causes malfunctioning cells effectively to ‘commit suicide’.

Experimental studies had shown that different tissues with different cancer-triggering pathways may not respond the same way to a particular nutrient.  ‘In fact, a nutrient may be associated with protection in one tissue and harm in another,’ said the experts.

They added that supplement users were ‘sometimes quick to discredit caution’ and distrustful of mainstream science which they suspected of being corrupted by links to the drug industry.

Users may also assume the supplements they bought to be as well regulated as over-the-counter medications.

‘These beliefs underscore the need for efforts by scientists and government officials to encourage the public to make prudent decisions based on sound evidence with respect to use of dietary supplements for cancer prevention,’ the scientists concluded.


Thursday, April 26, 2012

Now pizza gets the nod

A finding in laboratory glassware only

It may not be the most obvious of health foods, but pizza could be good for you, research suggests.  Scientists have found that oregano, a seasoning commonly used in pizza and other Italian food, has the potential to become a powerful weapon against prostate cancer.

A medicine inspired by it could have  fewer side-effects than existing treatments, which can cause problems from incontinence to impotence.  Prostate cancer is the most common cancer in British men, affecting 37,000 a year and killing more than 10,000.

Researchers from Long Island University, New York, studied carvacrol, a chemical in oregano. Added to prostate cancer cells in the lab, it rapidly wiped them out. Left for four days, almost all the cells were killed, the Experimental Biology conference in San Diego heard.  Tests showed it triggered the cells to kill themselves.

The oregano chemical could now be used itself as a treatment against cancer, or as the blueprint for an even more powerful drug.  Experts warned, though, that when oregano is eaten, it could be that carvacrol is digested  before it can do any good.

Researcher Supriya Bavadekar, a pharmacologist, said: `Some researchers have previously shown that eating pizza may cut down cancer risk.  `This effect has been mostly attributed to lycopene, a substance found in tomato sauce, but we now feel that even the oregano seasoning may play role.'

Lycopene, the pigment that gives tomatoes their read colour is credited with a host of health benefits, including warding off cancer and cutting the risk of heart disease.

Dr Bavadekar said: `If the study continues to yield positive results, this super-spice may present a very promising therapy for patients with prostate cancer.  `A significant advantage is that oregano is commonly used in food. We expect this to translate into a decreased risk of severe toxic effects.  `But this study is at a very preliminary stage and further experiments need to be conducted to get a better idea of uses in the clinic.'

Possibilities include using carvacrol itself or using it as the blueprint for an even more powerful treatment.

Others stressed that it is too early for men to start stocking up on pizza.  Margaret Rayman, a Surrey University professor of nutritional medicine who has compiled a cookbook of recipes designed to keep prostate cancer at bay said that much more work needs to be done.

For instance, any oregano-inspired treatment would have to be much less harmful to healthy cells than cancerous ones.


Another vote for chocolate

I must say that "chocolate is good for you" findings are common.  Note however that only dark chocolate -- which most people don't like much -- gets the nod

It has long been suggested  that dark chocolate is good for your heart.  Now a study has confirmed that eating it in moderate quantities does indeed lower blood sugar and cholesterol levels.

The research team set out to test the direct effect of eating chocolate which is a source of several substances that scientists think might impart important health benefits.

Chocolate contains compounds called 'flavanols' that appear to play a variety of bodily roles including those related to their potent antioxidant and anti-inflammatory actions.

Researchers at San Diego State University in the U.S. asked 31 people to eat a 50g bar of either regular dark chocolate, dark chocolate that had been overheated, or white chocolate, for 15 days.

When compared to the white chocolate group, those eating either form of dark chocolate were later found to have lower blood glucose and lower levels of `bad' blood lipids.

The researchers concluded that dark chocolate may reduce the risk of cardiovascular disease by improving blood glucose levels and lipid profiles.

However, they warned that although habitual dark chocolate consumption may benefit health by reducing the risk of heart disease, it must be eaten in moderation because it can easily increase daily amounts of saturated fat and calories.

A spokesman for the research team said: `We had great compliance with our study subjects because everybody wanted to eat chocolate.  `We actually had to tell them not to eat more than 50g a day.'

Now the researchers are planning follow-up studies involving more people and a longer duration of chocolate consumption.  The results will be presented at the Experimental Biology 2012 meeting in San Diego.


Wednesday, April 25, 2012

EPA human experiments debunk notion of ‘killer’ air pollution: Agency hides exculpatory results

A lesson in not trusting official science.  They may be the biggest liars of all

The U.S. Environmental Protection Agency has conducted air pollution experiments on live human subjects that discredit its claims that fine particulate matter kills people. obtained the explosive and heretofore undisclosed results through the Freedom of Information Act (FOIA) and reveal them here for the first time.


Last September, broke the news that EPA researchers had reported in Environmental Health Perspectives the case study of a woman who allegedly suffered atrial fibrillation after being exposed to concentrated airborne fine particulate matter (PM2.5) in an experimental setting.

After disposing of the EPA’s effort to link the woman’s atrial fibrillation with her exposure to PM2.5, we commented:

    It’s also worth asking whether this is the only study subject that the EPA has studied. Are there others? What were their results? Do we only get to hear about the one result that could possibly be twisted to fit the EPA agenda?

To answer this question, we filed a Freedom of Information Act request with the agency to see if we could get answers those questions.

Result and Analysis of the FOIA Request.

This data sheet shows the following:

    EPA has been conducting air pollution effects tests on human subjects since at least January 2010.

    By the time the EPA researchers had published their September 2011 report in Environmental Health Perspectives, they had conducted 41 such tests.

    Of the 41 human experiments, clinical effects were reported by the EPA in only two study subjects. Both of these are controversial. One is the case study reported in Environmental Health Perspectives, which has been previously debunked. The other study subject flagged by the EPA researchers as experiencing a clinical effect (“a short episode of an elevated heart rate during exposure”), in fact, denied feeling any effects.

This reported effect was most probably due to some pre-existing condition or other stressor given the low-level of PM2.5 to which the study subject was exposed. Certainly the EPA has no reason to believe that was not the case or that the alleged heart rate jump was due to the PM2.5 exposure.

    The other 39 study subjects were exposed to PM2.5 levels up to 21 times greater (i.e, up to 750 μg/m3) than the EPA’s own permissible exposure limit for PM2.5 on a 24-hour basis (i.e, 35 μg/m3). All reported exposures among the 39 study subjects were greater than the EPA’s 24-hour PM2.5 standard. Seven study subjects were exposed to levels 10 times greater than the EPA’s 24-hour PM2.5 standard. No clinical effects were reported for any of these exposures.


There are at least three points to be made in light of this discovery.

1. The experimental results provide no evidence that ultra-high exposures to PM2.5 kill.

EPA administrator Lisa Jackson testified to Congress last September that,

    [Airborne] particulate matter causes premature death. It doesn’t make you sick. It’s directly causal to dying sooner than you should.

These experiment results — produced by EPA’s own researchers — in no way support Jackson’s assertion.

2. The experimental results invalidate EPA’s cost-benefit analyses for its CSAPR and MATS rulemakings.

The EPA justified the multibillion dollar costs of its Cross-State Air Pollution Rule (CSAPR) and its Mercury Air Toxics Standard (MATS) largely on the basis that the rules would prevent thousands of premature deaths from PM2.5, thereby purportedly providing tens of billions of dollars in monetized health benefits from “lives saved.”

But ambient levels of PM2.5 are typically far below the PM2.5 levels to which subjects were exposed in this EPA experiment. We reported earlier that the EPA’s 24-hour PM2.5 of 35 μg/m3 was exceeded only about 0.0096% of the time in the U.S. during 2009.

Moreover, the EPA experiment provides no evidence that PM2.5, even at very high exposures, causes any health effects, let alone premature death.

3. EPA and its researchers have heretofore failed to disclose to the public these significant results.

Finally, there is the matter of the ethics and perhaps even the legality of the conduct of the EPA and its researchers.

The EPA’s experimental data on PM2.5 clearly paint a quite different picture than that provided by the September 2011 report in Environmental Health Perspectives and the agency’s recent PM2.5-related regulations (i.e., CSAPR and MATS).

The EPA researchers failed to mention the results from the other 40 human experiments in their Environmental Health Perspectives report. At the very least, their failure to disclose their own contrary results raises serious ethical concerns.

As an agency, the EPA failed to disclose these stunning results in its CSAPR and MATS rulemakings. This ought to raise concerns about the legal bases for these rulemakings. More than simply ignoring its own negative data, the agency seems to have actually hid them from public view.


In addition to these EPA-conducted experiments, there is other compelling data that casts doubt on the EPA’s claim that PM2.5 causes premature mortality, including historic air pollution data, current Chinese experience with air quality and the study “Fine Particulate Air Pollution and Total Mortality Among Elderly Californians, 1973–2002.”

The results of’s FOIA request add to this growing body of evidence.

Given the significant actual costs of the EPA’s PM2.5-related regulations on society, it is incumbent upon Congress to conduct a thorough investigation of the agency and its PM2.5 claims.


Fertility drugs 'more than double the chances of children developing leukaemia'

This is ridiculous.  IVF mothers are treated with ovary stimulating drugs too and yet they were found to have no increased risk.  It makes no sense.  It has to be a random result

Fertility drugs can more than double the chances of children born to mothers who struggle to get pregnant developing leukaemia, a study has shown.

Children were 2.6 times more likely to become ill with acute lymphoblastic leukaemia (ALL), the most common type of childhood leukaemia, if their mothers had been treated with ovary-stimulating drugs.

They had a 2.3-fold increased risk of suffering the rarer form of the disease, acute myeloid leukaemia (AML).

Children conceived naturally after their mothers waited more than a year to get pregnant had a 50 per cent greater-than-normal likelihood of developing ALL.

But no heightened risk of childhood leukaemia was associated either with in-vitro fertilisation (IVF) or artificial insemination.

The French scientists cannot yet fully explain their findings, the first to show a specific link between use of fertility drugs and childhood leukaemia.

Study leader Dr Jeremie Rudant, from the Centre for Research in Epidemiology and Population Health at the French research institute INSERM in Villejuif, Paris, said: 'It has always been hypothesised that assisted reproductive technologies may be involved in the onset of childhood cancer as they involve repeated treatment at the time of conception and or manipulation of the sperm and egg. And it is now established that a majority of acute leukaemia have a pre-natal (pre-birth) origin.

'The findings indicate that more research is now needed to investigate more closely the link between specific types of fertility drugs and what role the underlying causes of infertility may play in the potential development of childhood leukaemia.'

Dr Rudant presented the results at the Childhood Cancer 2012 conference in London, hosted by the charity Children with Cancer UK.

A total of 2,445 French children and their mothers took part in the study, comprising 764 children who had been diagnosed with leukaemia and 1,681 who were free of the disease.

Mothers were asked if they had taken more than a year to conceive a child, and questioned about the treatments they had received.

Around 44,000 cycles of fertility treatment are carried out each year in the UK.  Use of fertility technology is increasing worldwide. In the UK, 1.8 per cent of all live births in 2007 followed fertility treatment, compared with just 0.5 per cent in 1992.

Despite a significant increase in risk, the actual number of children developing leukaemia after their mothers undergo fertility treatment remains very small.  Just 400 cases of childhood leukaemia are diagnosed each year in the UK, three-quarters of which are ALL.  ALL can affect children of any age but is most common between the ages of one and four. It is also more likely to affect boys than girls.

Dr Rudant said: 'Previous studies have suggested a link between infertility treatments and acute childhood leukaemia but there haven't been many studies, most of them have been small and they focused either on IVF or hormonal treatment. Our study was much larger and it's the first time that a specific increased risk linked to fertility drugs has been found.'


Tuesday, April 24, 2012

Avocados  tackle dangerous molecules -- in yeasts

The "antioxidant" religion again

Avocados could be a weapon in the fight against ageing and disease, say scientists.  Oil from the fruit was shown in tests to combat free radicals – dangerous molecules said to have a hand in everything from ageing to heart disease and cancer.

These are particularly common inside mitochondria, the tiny powerhouses in our cells that turn the food we eat into energy.

Many ‘antioxidant’ chemicals in vegetables and fruits such as carrots and tomatoes can mop up free radicals – but they can’t make their way inside mitochondria.

Those in avocados can, the American Society for Biochemistry and Molecular Biology’s annual conference heard. Researcher Christian Cortes-Rojo said: ‘The problem is that the antioxidants in [other] substances are unable to enter mitochondria.

‘So free radicals go on damaging mitochondria, causing energy production to stop and the cell to collapse and die.  ‘An analogy would be that, during an oil spill, if we cleaned only the spilled oil instead of fixing the perforation where oil is escaping, then the oil would go on spilling, and fish would die anyway.’

Unstable free radicals are natural waste products of metabolism but may be generated in greater numbers due to factors such as pollution, tobacco smoke and radiation.  They wreak havoc in the body, triggering chain reactions that destroy cell membranes, proteins and even DNA.

The phenomenon is one of the prime drivers of ageing and believed to play a major role in damage to arteries and cancer.

The researchers found avocado oil allowed yeast cells to survive exposure to high concentrations of iron – an element that produces ‘huge amounts’ of free radicals.

‘We’ll need to confirm that what has been observed in yeasts could occur in higher organisms, such as humans,’ said Mr Cortes-Rojo, from the University Michoacana de San Nicolas de Hidalgo  in Mexico.

Avocado oil is similar in composition to olive oil, consumption of which is associated with unusually low levels of chronic disease in some Mediterranean countries, and Mr Cortes-Rojo said his discovery could mean avocado oil becoming ‘the olive oil of the Americas’.

Previous research conducted in Mexico, the world’s largest avocado producer, has shown that the fruit lowers blood levels of cholesterol, and certain fats linked to diabetes.


Some old quackery  lives on in a modern  psychiatric  guise

In 1861 Samuel A. Cartwright, an American physician, described a mental illness he called “drapetomania.” As Wikipedia points out, the term derived from drapetes, Greek for “runaway [slave],” and mania for madness or frenzy.

Thus Cartwright defined drapetomania as “the disease causing negroes to run away [from captivity].”

“[I]ts diagnostic symptom, the absconding from service, is well known to our planters and overseers,” Cartwright wrote in a much-distributed paper delivered before the Medical Association of Louisiana. Yet this disorder was “unknown to our medical authorities.”

Cartwright thought slave owners caused the illness by making “themselves too familiar with [slaves], treating them as equals.”  Drapetomania could also be induced “if [the master] abuses the power which God has given him over his fellow-man, by being cruel to him, or punishing him in anger, or by neglecting to protect him from the wanton abuses of his fellow-servants and all others, or by denying him the usual comforts and necessaries of life.”

He had ideas about proper prevention and treatment:

[I]f his master or overseer be kind and gracious in his hearing towards him, without condescension, and at the sane [sic] time ministers to his physical wants, and protects him from abuses, the negro is spell-bound, and cannot run away. . . .

If any one or more of them, at any time, are inclined to raise their heads to a level with their master or overseer, humanity and their own good requires that they should be punished until they fall into that submissive state which was intended for them to occupy in all after-time. . . . They have only to be kept in that state, and treated like children, with care, kindness, attention and humanity, to prevent and cure them from running away. [Emphasis added.]

Dysaethesia Too

The identification of drapetomania is not Cartwright’s only achievement. He also “discovered” “dysaethesia aethiopica, or hebetude of mind and obtuse sensibility of body—a disease peculiar to negroes—called by overseers, ‘rascality.’” Unlike drapetomania, dysatheisa afflicted mainly free blacks. “The disease is the natural offspring of negro liberty–the liberty to be idle, to wallow in filth, and to indulge in improper food and drinks.”

Cartwright, I dare say, was a quack, ever ready to ascribe to disease behavior he found disturbing. A far more informative discussion of the conduct of slaves can be found in Thaddeus Russell’s fascinating book, A Renegade History of the United States.

Have things changed much since Cartwright’s day? You decide.

The current edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) list Oppositional Defiant Disorder (ODD) under “disorders usually first diagnosed infancy, childhood, or adolescence.”  According to the manual:

"The essential feature of Oppositional Defiant Disorder is a recurrent pattern of negativistic, defiant, disobedient, and hostile behavior toward authority figures that persist for at least six months. It is characterized by the frequent occurrence of at least four of the following behaviors: losing temper, arguing with adults, actively defying or refusing to comply with the requests or rules of adults, deliberately doing things that will annoy other people, blaming others for his or her own mistakes or misbehavior, being touchy or easily annoyed by others, being angry and resentful, or being spiteful and vindictive."

Marked on a Curve

In diagnosing this disorder, children are marked on a curve. “To qualify for [ODD], the behaviors must occur more frequently than is typically observed in individuals of comparable age and developmental level” (emphasis added). The behaviors must also be seen to impair “social, academic, and occupational functioning.”

The parallel with drapetomania is ominous. Children, after all, are in a form of captivity and as they get older may naturally resent having decisions made for them. They may especially dislike being confined most days in stifling government institutions allegedly dedicated to education (“public schools”). Some may rebel, becoming vexatious to the authorities.

Is that really a mental, or brain, disorder? PubMed Health, a website of the National Institutes of Health, discusses treatment and prevention in ways that suggest the answer is no. “The best treatment for the child is to talk with a mental health professional in individual and possibly family therapy. The parents should also learn how to manage the child’s behavior” (emphasis added), it says, adding, “Medications may also be helpful.”

As for prevention, it says, “Be consistent about rules and consequences at home. Don’t make punishments too harsh or inconsistent. Model the right behaviors for your child. Abuse and neglect increase the chances that this condition will occur.”

Strange Illness

It seems strange that an illness can be treated by talk and prevented by good parenting. And how was four arrived at as the minimum number of behaviors before diagnosis? Or six months as the minimum period? Odd, indeed.

While ODD is discussed with reference to children, one suspects it wouldn’t take much to extend it to adults who “have trouble with authority.” Surely one is not cured merely with the passing of adolescence. Adults are increasingly subject to oppressive government decision-making almost as much as children. Soviet psychiatry readily found this disorder in dissidents. Let’s not forget that the alliance of psychiatry and State permits people innocent of any crime to be confined and/or drugged against their will.

So we must ask: Do we have a disease here or rather what Thomas Szasz, the libertarian critic of “the therapeutic state,” calls “the medicalization of everyday life.” (Szasz’s chief concern is commonly thought to be psychiatry, but in fact it is freedom and self-responsibility. See my “Szasz in One Lesson.”)

It seems that the common denominator of what are called mental (or brain) disorders is behavior that bothers others which those others wish to control. Why assume such behavior is illness? Isn’t this rather a category mistake? Why stigmatize a rebellious child with an ODD “diagnosis”? (Let’s not forget what psychiatry not long ago regarded as illness and abetted control of.)


In our scientific age, many people find scientism, the application of the concepts and techniques of the hard sciences to persons and economic/social phenomena, comforting. In truth it is dehumanization in the name of health.

Szasz, a prolific author who celebrated his 92nd birthday earlier this week, writes:

"People do not have to be told that malaria and melanoma are diseases. They know they are. But people have to be told, and are told over and over again, that alcoholism and depression are diseases. Why? Because people know that they are not diseases, that mental illnesses are not “like other illnesses,” that mental hospitals are not like other hospitals, that the business of psychiatry is control and coercion, not care or cure. Accordingly, medicalizers engage in a never-ending task of “educating” people that nondiseases are diseases."

No one believes drapetomania is a disease anymore. Slaves had a good reason to run away. We all have reasons–not diseases–for “running away.”


Monday, April 23, 2012

Positive Feelings May Help Protect Cardiovascular Health

Or maybe good health gives you positive feelings

Over the last few decades numerous studies have shown negative states, such as depression, anger, anxiety, and hostility, to be detrimental to cardiovascular health. Less is known about how positive psychological characteristics are related to heart health. In the first and largest systematic review on this topic to date, Harvard School of Public Health (HSPH) researchers found that positive psychological well-being appears to reduce the risk of heart attacks, strokes and other cardiovascular events.

The American Heart Association reports more than 2,200 Americans die of cardiovascular disease (CVD) each day, an average of one death every 39 seconds. Stroke accounts for about one of every 18 U.S. deaths.

"The absence of the negative is not the same thing as the presence of the positive. We found that factors such as optimism, life satisfaction, and happiness are associated with reduced risk of CVD regardless of such factors as a person's age, socioeconomic status, smoking status, or body weight," said lead author Julia Boehm, research fellow in the Department of Society, Human Development, and Health at HSPH. "For example, the most optimistic individuals had an approximately 50% reduced risk of experiencing an initial cardiovascular event compared to their less optimistic peers," she said.

In a review of more than 200 studies published in two major scientific databases, Boehm and senior author Laura Kubzansky, associate professor of society, human development, and health at HSPH, found there are psychological assets, like optimism and positive emotion, that afford protection against cardiovascular disease. It also appears that these factors slow the progression of disease.

To further understand how psychological well-being and CVD might be related, Boehm and Kubzansky also investigated well-being's association with cardiovascular-related health behaviors and biological markers. They found that individuals with a sense of well-being engaged in healthier behaviors such as exercising, eating a balanced diet, and getting sufficient sleep. In addition, greater well-being was related to better biological function, such as lower blood pressure, healthier lipid (blood fat) profiles, and normal body weight.

If future research continues to indicate that higher levels of satisfaction, optimism, and happiness come before cardiovascular health, this has strong implications for the design of prevention and intervention strategies. "These findings suggest that an emphasis on bolstering psychological strengths rather than simply mitigating psychological deficits may improve cardiovascular health," Kuzbansky said.


How to do better in your exams: Drinking a glass of water can boost your results by a grade

I doubt that the drink did anything.  Taking a drink into an exam may however indicate forethought -- and forethought may mean that they have studied more too

Forget expensive private tutors and brain-boosting vitamins. The key to  exam success could be as simple as a glass of water.  Students who took a drink into the exam hall did up to 10 per cent better than those who did not - the difference between a grade.

Although it is unclear why a drink should help, one theory is that information flows more freely between brain cells when they are well hydrated.  Researchers said that drinking water may also calm nerves, while those who became thirsty during test time could be more easily distracted.

The study, which looked at hundreds of university students, compared whether they took a drink - such as water, coffee or cola - into the exam with their final marks.

The students' overall academic ability was then factored in, to ensure that the results were not skewed by the possibility that smarter students are also more thirsty.

Those who arrived armed with drinks did around 5 per cent better on average. But the improvement was even more marked among those just starting out at university, whose results improved by as much as  10 per cent - the difference between being awarded a first-class degree and a 2.1, the annual conference of the British Psychological Society's heard.

The type of drink did not change the results, meaning the students' performance could not be put down to caffeine or sugar.

Researcher Chris Pawson, from the University of East London, said: 'The results imply that the simple act of bringing water into an exam was linked to an improvement in  the students' grades.' Dr Mark Gardner, of Westminster University, added that it was not clear why the greatest improvement was seen in new students.

However, it could be they were the most anxious, or having newly left home were more prone to wild nights out and so in greater need of hydration.

Earlier research from the University of East London has shown that children aged between seven and nine who drank water did better on tests of visual attention and memory.


Sunday, April 22, 2012

Cancer chemical alert over crisps and coffee as Food Standards Agency identifies 13 at-risk products

The old acrylamide scare pops up again.  It was a hot topic in California in 2005.   I don't think I need  to add anything  beyond what I said in 2007

Food firms have been warned about the presence of a cancer-risk chemical in everyday products ranging from crisps and chips to instant coffee and ginger biscuits.

A biscuit designed for babies and toddlers has also been caught up in the alert.

Experts are even warning families to  only lightly toast their bread at home, as the chemical, called acrylamide, is more likely to form the longer and darker foods cook.

A study by the Food Standards Agency has identified 13 products containing raised levels of the chemical. In each case, officials at the local council where the supplier is based have been told to notify them.

Acrylamide, which is still being investigated by scientists, is a cooking by-product associated with frying, baking, roasting or toasting foods at very high temperatures, usually greater than 120c.

The FSA insists its findings raise no immediate risk to the public and there is no need for people to change their diet.

However, it is putting pressure on all food companies to reduce acrylamide levels because long-term consumption could increase the risk of cancer. Its official advice is also that families should ensure bread and chips they eat are only toasted or baked to the 'lightest colour possible'.

The FSA said its study of levels of acrylamide and furan – another cancer-risk chemical – is used to identify which firms need to take action. Acrylamide is formed by a reaction between natural components in food as it cooks.

In reality it has probably been in the diet for as long as man has fried, roasted or toasted food. Manufacturers including Heinz and McVitie's have already responded by changing their recipes.

But others, including Nestle, makers of Nescafe, say it is impossible to do so without harming the flavour and quality of their products. It added: 'There is currently no scientific evidence to suggest any particular product has any negative impact on health in the context of acrylamide exposure.'

The FSA is required by the EU and the European Food Safety Authority to carry out the annual tests. It looked at 248 samples, from chips sold by fast-food outlets to supermarket own-label and big brand ranges. In 13 cases levels were above  the 'indicative value' – a trigger point to tell the firm it should examine its production process.

European watchdogs have been putting pressure on food manufacturers to reduce acrylamide for almost a decade. In 2002 Swedish studies revealed high levels formed during the frying or baking of potato or cereal products.

The FSA said: 'This raised worldwide public concern because studies in laboratory animals suggest acrylamide has the potential to cause cancer in humans by interacting with the DNA in cells.

'The Agency believes exposure to such chemicals should be as low as reasonably practicable.'

The latest survey found 'an upward trend' in acrylamide levels in processed cereal-based baby foods, excluding rusks. Importantly however, the FSA said this did not mean parents should stop giving these products to youngsters.

The Food and Drink Federation,  which represents manufacturers,  said members are 'ensuring levels are as low as reasonably achievable'.

Heinz changed its Banana Biscotti recipe this year to reduce acrylamide to trace levels. United Biscuits, which makes McVitie's Gingernuts, said it has cut acrylamide by 70 per cent. The firm also pledged to cut levels in its McCoy’s crisps.


Scientists Regenerate Damaged Mouse Hearts by Transforming Scar Tissue Into Beating Heart Muscle

This sounds like REALLY good news

Scientists at the Gladstone Institutes just announced a research breakthrough in mice that one day may help doctors restore hearts damaged by heart attacks -- by converting scar-forming cardiac cells into beating heart muscle.

These scientists previously transformed such cells into cardiac muscle-like cells in petri dishes. But Gladstone postdoctoral scholar Li Qian, PhD, along with researchers in the laboratory of Deepak Srivastava, MD, has now accomplished this transformation in living animals -- and with even greater success. The results, which may have broad human-health implications, are described in the latest issue of Nature, available online April 18.

Cardiovascular disease is the world's leading cause of death. Annually in the United States alone, the nearly 1 million Americans who survive a heart attack are left with failing hearts that can no longer beat at full capacity.

"The damage from a heart attack is typically permanent because heart-muscle cells -- deprived of oxygen during the attack -- die and scar tissue forms," said Dr. Srivastava, who directs cardiovascular and stem cell research at Gladstone, an independent and nonprofit biomedical-research institution. "But our experiments in mice are a proof of concept that we can reprogram non-beating cells directly into fully functional, beating heart cells -- offering an innovative and less invasive way to restore heart function after a heart attack."

In laboratory experiments with mice that had experienced a heart attack, Drs. Qian and Srivastava delivered three genes that normally guide embryonic heart development -- together known as GMT -- directly into the damaged region. Within a month, non-beating cells that normally form scar tissue transformed into beating heart-muscle cells. Within three months, the hearts were beating even stronger and pumping more blood.

"These findings could have a significant impact on heart-failure patients -- whose damaged hearts make it difficult for them to engage in normal activities like walking up a flight of stairs," said Dr. Qian, who is also a California Institute for Regenerative Medicine postdoctoral scholar and a Roddenberry Fellow. "This research may result in a much-needed alternative to heart transplants -- for which donors are extremely limited. And because we are reprogramming cells directly in the heart, we eliminate the need to surgically implant cells that were created in a petri dish."

"Our next goal is to replicate these experiments and test their safety in larger mammals, such as pigs, before considering clinical trials in humans," added Dr. Srivastava, who is also a professor at the University of California, San Francisco (UCSF), with which Gladstone is affiliated. "We hope that our research will lay the foundation for initiating cardiac repair soon after a heart attack -- perhaps even when the patient arrives in the emergency room."

This research builds on the groundbreaking cell-reprogramming work of another Gladstone scientist and UCSF professor of anatomy, Shinya Yamanaka, MD, PhD. Dr. Yamanaka's 2007 discovery of a way to turn adult human skin cells into cells that act like embryonic stem cells has radically advanced the fields of cell biology and stem cell research. But these new Gladstone experiments go further by both completing the experiments directly in live hearts and by employing a technique called "direct reprogramming." Direct reprogramming could revolutionize the field of regenerative medicine, as it lets scientists transform one adult cell type into another without first having to revert back to the stem cell state. In the future, Gladstone scientists hope to use direct reprogramming not only to treat heart failure, but also for spinal cord injury and devastating illnesses such as Alzheimer's and Parkinson's disease.


Saturday, April 21, 2012

Bucky Balls Could Double Your Lifespan

Generalizing about lifespans from a short-lived species (rats)to a long lived species (humans) is intrinsically dubious.  We  may already have some equivalent of whatever helped the rats below

Buckminster fullerene molecules, the naturally occurring spheres made up of 60 carbon atoms, have long been suspected to have biological benefits. Now, a study that set out to establish if they were toxic when administered orally has proven quite the opposite-they almost doubled the lifespan of the rats that they were fed to.

The experiments, which were carried out at the Universite Paris Sud, France, set out to assess what adverse reactions might be caused by ingesting Bucky balls orally. To do that, they fed three groups of rats differently. Along with their normal diet, one group was held as a control; a second was fed olive oil; and a third group was fed olive oil doped with a 0.8 mg/ml concentration of Buckminster fullerene.

The results, which appear in Biomaterials, took the researchers by surprise. The control group had a median lifespan of 22 months, and the olive oil group one of 26 months. But the Bucky ball group? They stuck it out for 42 months. That's almost double the control group.

The researchers have established that the effect is mediated by a reduction in oxidative stress-an imbalance in living cells that contributes to ageing. To say these results are important is an understatement: the desire to live longer runs strong in many of us, and it's a feat scientists have been hoping to achieve for centuries.

But while it's a remarkable finding, it's worth remembering that it's just a single study. It's going to take a hell of a lot more work before the scientific community is completely convinced that we should all be splashing Bucky-enriched olive oil on our salads, that's for sure.


Prenatal exposure to inner-city air pollution among NYC minorities  is linked to childhood obesity, claims study

Silly me!  I would have thought that air pollution would be rather bad anywhere in Northern Manhattan or the South Bronx but apparently there are variations.

Generally speaking poorer people live in more polluted areas and poor people are more likely to be obese but the authors  are obviously so used to that criticism that they have in this study attempted to correct for that by controlling for maternal receipt of public assistance

So maybe the air in some parts of NYC really is polluted enough to be bad for you

A study of pregnant women and their children in New York City has provided clinical evidence that links environmental pollution with childhood obesity.

The most up-to-date statistics show that 17 per cent of children in the U.S. are obese, and that figure rises to 25 per cent in built-up, inner-city neighborhoods.

While poor diet and lack of exercise are still the major contributors to the national epidemic, this new evidence suggest that air pollution can play a role.

Columbia University's Mailman School of Public Health conducted the study of expecting mothers in New York, and found that those exposed to higher concentrations of airborne chemicals were more than twice as likely to have children who were obese by the age of seven.

The burning of coal, diesel, oil and gas - as well as other substances, such as tobacco - produce chemicals called polycyclic aromatic hydrocarbons (PAH).

The school's report, published in the American Journal of Epidemiology, and its lead author - Dr Andrew Rundle - said: 'Obesity is a complex disease with multiple risk factors. It isn't just the result of individual choices like diet and exercise.'

Dr Rundle, a professor of epidemiology, added: 'For many people - who don't have the resources to buy healthy food or don't have the time to exercise - prenatal exposure to air pollution may tip the scales, making them even more susceptible to obesity.'

Researchers recruited 702 non-smoking pregnant women through prenatal clinics at New York Presbyterian Hospital and Harlem Hospital.

The women were selected between the ages of 18 and 35, and identified themselves as either African-American or Dominican. They lived in areas in Northern Manhattan or the South Bronx, which are predominantly low-income areas.

Children of women exposed to high levels of PAH during pregnancy were nearly twice as likely (1.79 times) to be obese at age five, and more than twice as likely (2.26 times) to be obese at age seven, compared with children of mothers with lower levels of exposure.

The seven-year-olds whose mothers were in the highest exposure group had, on average, 2.4lb more fat mass than children of mothers with the least exposure.

Previous research from Columbia University found that prenatal exposure to PAH can negatively affect childhood IQs and is linked to anxiety, depression and attention problems in young children.

PAH also disrupt the body's endocrine system and are known carcinogens.  But Dr Rundle said there are ways to reduce PAH exposure.  Certain fuels release more of the chemicals than others, and efforts in New York City to take diesel buses off the streets and retrofit oil furnaces so they burn cleaner fuel was already starting to help.


Association of Childhood Obesity With Maternal Exposure to Ambient Air Polycyclic Aromatic Hydrocarbons During Pregnancy

By Andrew Rundle et al.


There are concerns that prenatal exposure to endocrine-disrupting chemicals increases children’s risk of obesity. African-American and Hispanic children born in the Bronx or Northern Manhattan, New York (1998–2006), whose mothers underwent personal air monitoring for polycyclic aromatic hydrocarbon (PAH) exposure during pregnancy, were followed up to ages 5 (n = 422) and 7 (n = 341) years. At age 5 years, 21% of the children were obese, as were 25% of those followed to age 7 years.

After adjustment for child’s sex, age at measurement, ethnicity, and birth weight and maternal receipt of public assistance and prepregnancy obesity, higher prenatal PAH exposures were significantly associated with higher childhood body size.

In adjusted analyses, compared with children of mothers in the lowest tertile of PAH exposure, children of mothers in the highest exposure tertile had a 0.39-unit higher body mass index z score (95% confidence interval (CI): 0.08, 0.70) and a relative risk of 1.79 (95% CI: 1.09, 2.96) for obesity at age 5 years, and they had a 0.30-unit higher body mass index z score (95% CI: 0.01, 0.59), a 1.93-unit higher percentage of body fat (95% CI: 0.33, 3.54), and a relative risk of 2.26 (95% CI: 1.28, 4.00) for obesity at age 7 years. The data indicate that prenatal exposure to PAHs is associated with obesity in childhood.


Friday, April 20, 2012

IVF problems?

There seems to be a certain desperation to find something wrong with IVF.   It was heavily opposed by the medical profession in its early days.  And the Pope thinks it is immoral, of course.  Sadly for the ghouls, however, the incidence of medical problems among IVF-conceived children is in fact very low. 

But the guy writing below reports   that there was a a different average of vascular indicators among IVF kids.  So he  drew the usual non-sequitur that IVF CAUSED that problerm.  That mothers who turn to IVF often have other health problems he seems to overlook.  The problem he identified could simply be a normal genetic transmission, in other words. Just a few such children in the sample could be skewing the average of the whole sample

IVF (In Vitro Fertilisation) has brought the miracle of childbirth to hundreds of thousands; indeed it is now estimated that 1 per cent to 3 per cent of all births in developed nations involve IVF.

There have already been some health problems documented in IVF offspring. There is an approximately 20 per cent to 30 per cent increase in the risk of major malformations in IVF babies. However, the absolute risks of such outcomes is low.

Of greater concern would be any significant increase in the risk of the common cardiovascular diseases, such as heart attack or stroke.

A recent scientific study from Switzerland has found significant abnormalities in the blood vessels in the body and lungs of 12-year-old children who were born through IVF (published in Circulation this month). The investigators assessed 65 IVF and 50 non-IVF children, and found significant adverse changes in their developing blood vessels.

The study included the careful examination of relevant control groups. By doing this, the authors found that the problems observed were likely caused by events that influenced the embryo when "in the test tube". Other research has recently also found elevated blood pressure and blood sugar levels in IVF offspring.

Can environmental exposures so early in life actually alter the risk of later heart disease?

In 1992, we conducted research that found that abnormalities could be seen in the blood vessels of high-risk children. In 2005, we found increased blood vessel thickening in newborns with low birth weight, showing that even foetal events could potentially influence cardiovascular health in later life. It now seems that even the environment of the embryo might also influence heart-disease risk in adulthood.

Do children born from IVF need to be treated differently, from a health point of view? It is very important for IVF parents and children not to be unduly alarmed by these preliminary findings, mainly based on a single study of only 65 children. It would seem prudent for IVF children to lead a "heart-healthy" lifestyle of no smoking, sensible diet, regular exercise and occasional check-ups by their GPs.


Systemic and Pulmonary Vascular Dysfunction in Children Conceived by Assisted Reproductive Technologies

By Urs Scherrer, MD et al.


Background—Assisted reproductive technology (ART) involves the manipulation of early embryos at a time when they may be particularly vulnerable to external disturbances. Environmental influences during the embryonic and fetal development influence the individual's susceptibility to cardiovascular disease, raising concerns about the potential consequences of ART on the long-term health of the offspring.

Methods and Results—We assessed systemic (flow-mediated dilation of the brachial artery, pulse-wave velocity, and carotid intima-media thickness) and pulmonary (pulmonary artery pressure at high altitude by Doppler echocardiography) vascular function in 65 healthy children born after ART and 57 control children. Flow-mediated dilation of the brachial artery was 25% smaller in ART than in control children (6.7±1.6% versus 8.6±1.7%; P<0.0001), whereas endothelium-independent vasodilation was similar in the 2 groups. Carotid-femoral pulse-wave velocity was significantly (P<0.001) faster and carotid intima-media thickness was significantly (P<0.0001) greater in children conceived by ART than in control children. The systolic pulmonary artery pressure at high altitude (3450 m) was 30% higher (P<0.001) in ART than in control children. Vascular function was normal in children conceived naturally during hormonal stimulation of ovulation and in siblings of ART children who were conceived naturally.

Conclusions—Healthy children conceived by ART display generalized vascular dysfunction. This problem does not appear to be related to parental factors but to the ART procedure itself.


Gum disease 'does not cause heart trouble': Any link 'coincidental', say scientists

A quite amazing degree of epidemiological realism below

The belief that gum disease can lead to heart attacks and strokes is unfounded, experts said yesterday.

A panel of 13 U.S. scientists insisted there was no evidence for a causal link between bad gums and cardiovascular disease.

They reviewed 500 articles in scientific journals and concluded that while people with gum disease may be at greater risk of heart and artery problems, the association is probably coincidental.

Both conditions shared common risk factors, such as smoking, and both produced similar inflammation markers.  Those common factors could help explain why diseases of the blood vessels and mouth can occur in tandem.

Research has shown that people with gum disease are almost twice as likely to suffer from coronary artery disease as those without gum disease.

'Much of the literature is conflicting, but if there was a strong causative link, we would likely know that by now,' said Professor Peter Lockhart, co-chairman of the expert panel and chairman of oral medicine at the Carolinas Medical Centre in Charlotte, North Carolina. 'There's a lot of confusion out there.'

He cited coincidental lifestyle factors. 'We already know that some people are less proactive about their cardiovascular health.

'Individuals who do not pay attention to the very powerful and well-proven risk factors, like smoking, diabetes or high blood pressure, may not pay close attention to their oral health either.'

Professor Lockhart added: 'The message sent out by some in healthcare professions that heart attack and stroke are directly linked to gum disease can distort the facts, alarm patients and perhaps shift the focus on prevention away from well-known risk factors for these diseases.'

Only a large, long-term study could prove that dental disease caused heart disease, but there was no likelihood of such an investigation in the near future.

'It's most important to let patients know what we know now, and what we don't know,' said Professor Lockhart. The panel spelled out their views in a scientific statement published in the American Heart Association journal Circulation.

A number of theories have been suggested to explain the association between gum and heart disease. One is that mouth bacteria attach to fatty deposits in arteries and trigger blood clots. Another is that they are a source of inflammation,  which leads to a thickening of artery walls.

But the experts writing in Circulation said statements that imply a cause and effect relationship between gum and heart and artery disease were 'unwarranted' at this time.

Natasha Stewart, of the British Heart Foundation, said: 'Maintaining good oral hygiene, as well as a healthy diet, avoiding smoking and taking part in  regular physical activity, are essential for good health including protecting your heart and gums.'

Professor Nairn Wilson, from the British Dental Association, said: 'One thing we can say with confidence is keeping your teeth and gums healthy by brushing your teeth twice a day with a fluoride toothpaste, restricting sugary foods to meal times and visiting the dentist regularly makes an important contribution to oral health and general well-being.'


Thursday, April 19, 2012

BOOK REVIEW of The Obesity Epidemic by Zoe Harcombe (Columbus Publishing Ltd 328 pp £20)

Reviewed by Dr. Alick Dowling

This masterly fully-referenced comprehensive survey of the field in 136,000 words demolishes current advice. Those who absorb her message reject misguided policy from World Health Authorities.

The author, an experienced nutritionist is brave to challenge, not only the current `consensus' of the medical establishment, but also that shared by her fellow nutritionists and dieticians, that `cholesterol' is responsible for heart attacks and strokes. `I regularly attend obesity conferences where I am a lone and unwelcome voice in amongst an overwhelming majority of dieticians.' (p 272)

I knew nothing about her book until Feb 2012 (though published in 2010) when Zoe Harcombe featured on I wrote to her:

"How refreshing to see a nutritionist writing sense about fats. I admire your sensible response to Dr Malcolm Kendrick's 'The Great Cholesterol Con'. To put my cards on the table: I am a long-retired GP born in 1920 who reviewed his book for the Bristol MedChi website (also on John Ray's blog "Food & Health Skeptic".  See here). This mentions my booklet 'Enjoy Eating Less', a copy of which I would be happy to send you as it might interest you as we have written on the same subject"

We exchanged copies.

As a member of 'thincs' (The International Network of Cholesterol Sceptics), Harcombe admires Malcolm Kendrick's The Great Cholesterol Con, agrees that Cholesterol is not responsible for heart attacks and nor are statins the answer to a non-existent problem.

In turn Kendrick supports Harcombe: Switching from high fat to high carbohydrate could be the single greatest cause of the recent obesity epidemic. Kendrick does not exclude other causes.

Having read (and re-read!) her full text (hoping to review it for the Bristol Medchi site) I realized table 1 on p 2 reveals an anomaly, which I missed at the first reading, not discussed by Harcombe.

This table shows that between 1966 and 1982 UK percentages of overweight and obese rose from 14% to 44% for men, from 11% to 26% for women. This was long before the wrong advice was substituted in 1983, when the percentages started the even sharper rise vividly described by Harcombe.

What happened in the late 70s/early 80s before Harcombe's obesity epidemic took off? The alternative suspect is Portion size!

Nearly 50 years ago, large portion sizes, associated with affluence in developed countries, was then the predominant cause of obesity. With our 6 children age 14 to 5, we visited New York in 1964 (en route to Edmonton in Canada to stay with our Canadian/Polish brother-in-law and their family of 6 children). We saw for the first time enormous portion sizes and widespread obesity, obvious then in New York, noticeable in Canada, but then rare in the UK.

This was nearly 2 decades before the 1983 wrong medical advice was given to switch from fats to high carbohydrate, which Harcombe denotes as the beginning of the obesity epidemic.

Large-sized portions in the past were confined to the affluent, for example the Edwardian penchant for enormous meals. Only after WWII did such affluence spread to a wider society. The early clear signs from Table 2 towards the `epidemic' of obesity were later fuelled by bad medical advice.

For the overweight it is common sense that food portions return to `normal' levels. Eating less is one way to do this, and accepted as sensible, though difficult, by most of the obese. Advising `eating less' was shorthand for reducing portion size for those with a weight problem. If eating too much of almost anything, not just processed food, can cause obesity, it is commonsense to recommend those affected to eat less.

Her writing style is humorous and clear. Her book is not easy reading because much of the material is technical, especially when she has to deal with the complexities of the cholesterol controversy and the arguments used to maintain the `consensus' that `fats' and cholesterol are bad for us. She is to be congratulated for her success in surmounting these difficulties.

Many other factors complicate individual problems. Harcombe recognizes a strong genetic factor, why some people are never likely to be thin. She has three dietary tips:

1) Eat real food,

2) Eat three meals a day & don't snack,

3) Manage carbohydrates for weight problems.

She deplores all processed food. I am more relaxed. Small quantities of carefully chosen processed food don't need to be totally banned. Our versatile digestive system is robust enough to deal with processed foods, unless overwhelmed by sheer quantity.

Harcombe thought my `advice and book would have been invaluable before the obesity epidemic took hold'. It is still relevant and helps those readers who are prepared to limit their food intake.

Harcombe had the misfortune to be involved in the Minnesota Starvation scheme in her teens (p 42 & 54). It is probable this has influenced her attitude to hunger, and that a neural pathway `remembers' it for her as an addiction to food. For most people in the affluent world hunger is not something to be feared.

James le Fanu, not mentioned by Harcombe, should be remembered for his early championing of Kendrick's book in the Telegraph (18/3/2007, 25/3/07, 1/4/07, 8/4/07) when he described `taking a statin holiday'. He was attacked by a cardiologist (Weissberg) as naive for being taken in by someone like Kendrick.

To return to the book: The Obesity Epidemic: the excellent Contents Page shows the structure and how well the material is organized. The Index is not as complete as expected, with no mention of metabolic rate. In contrast the 399 footnotes with valuable references are separated by Chapters, after the Index.

The research needed to analyze these - many needed hours of computation - is most impressive. They rebut those who question the author's competence to pronounce on technical matters. The Glossary and Abbreviations are useful; the Appendix has 4 rather technical pages, presumably needed to complement the footnotes.

After the Introduction (pp 12) the content is divided into 4 parts, these subdivided into 16 Chapters. The book ends with a brief Summary (p 280-285).

1: General principle: Eat less/do more. This has 4 relatively brief chapters 1-4 (pp 13-44) Chapter 4 (pp 37-42) explains the Minnesota `Starvation Experiment' May 1944 when 200 conscientious objectors volunteered to starve as an alternative to call-up; Harcombe unwittingly as a teenager (p 42) had a similar experience.

2: The Calorie Formulae (p 46-51): - To lose one pound of fat." 3 chapters 5-7 (pp 52-79) all devoted to `calories'

3: The Diet Advice The bulk of the book (pp 87-231) with a short `What should we eat' survey (p 82-86) followed by the Chapters 8-14. Chapter 8, the major one is devoted to Cholesterol, including a Pre-amble and a `Post-amble' the latter being an eloquent summary why Cholesterol should be regarded as a `good thing'. See the end of this review for a clinching argument.

Chapter 9 (pp 126-136) details how and why medical advice was changed in 1983 for the worse as mentioned above. Denis Burkitt (p 136) is rebuked for recommending fibre to be in our diet. However he did not do so for nutritional reasons, but to help to eliminate abdominal problems, which it did. I remember hearing him on this subject.

Medical advice then for irritable bowel and colitis was to `rest' the colon by starvation, which made painful abdominal cramps worse. Patients soon learnt to ignore such advice, just as now many refuse to take statins.

Chapter 10 "What is our current advice, a short account" (pp 137-152) is followed by Chapter 11 "Have we reviewed the U turn" (pp 153-166). Chapter 12 "Eat Less Fat" (pp 167-191) contrasts with Chapter 13 ("Base your meals on starchy foods" (pp 192-211). The last Chapter of this section 14 "Do More" (pp 212-231), is a controversial one about exercise.

4: How can we stop The Obesity Epidemic (p 232-235). 2 Final Chapters 15 & 16 (p 236-273). Chapter 15 was the most stressful and difficult to write (p 258); it comes over as a challenge to her tenacity in seeking answers from obstructive officials. The final Chapter 16, which is devoted to the question of how to organize obesity management without impinging on freedom to choose, raises more questions than it answers. The summary at the end rounds off her advice.

To summarize: Harcombe and I are both outside the present Health Adviser's `consensus' on the evils of cholesterol. Many other contributors in the `obesity' field are also in this position.

When will the medical establishment realize their vulnerability to being sued for ignoring the increasingly known dangers of statins? Many victims will be eager to initiate actions. The web makes this a likely prospect.

Harcombe is trenchant about Bariatric Surgery: (p 271) I have not proposed bariatric surgery as a solution, because a fundamental premise of this book is that we need to remember why we eat.

Campbell-McBride calls the gut the second brain of the body. Do we have full and certain knowledge of what will happen long term by surgically altering our digestive tract in such drastic ways? She goes on to describe a victim who was unable to eat lamb because he knew he could not digest it, but who was able to eat bread, potato and pastries and was gaining weight at a steady pace.

She has 2 footnotes on this subject, 379 and 380, referring to A study on the economic impact of bariatric surgery from The American Journal of Managed Care and The Association for the Study of Obesity Annual Conference, Liverpool (June 2009) respectively.

Since then there have been unexpected research developments involving recently identified hormones PYY and ghrelin that control respectively sensations of fullness and hunger. These control body weight by `talking' from the gut to the brain (see Campbell McBride above).

Dr Carel Le Roux (Imperial College & King's College London) believes that bariatric surgery has a powerful and unexpected side effect: it can re-balance the hormones so the patient would `stop thinking like a fat person and think and behave like a thin one'.

It remains to be seen whether this is substantiated but if it is there must surely be a less radical procedure than bariatric surgery to do this `re-balancing', for example via pills or injections. Research into `discordant identical twins' who have different weights, presumably due to these hormones being `unbalanced' is part of this ongoing research in the field of epigenetics.

For those who still have a lingering doubt that Cholesterol must still be an evil substance, as many doctors and dieticians still believe, despite the arguments presented here and in her book, and for readers who find the complexities of the saturated and unsaturated fats, and the idiotic subdivisions of `good' and `bad' cholesterol too difficult to comprehend, a final word from Harcombe, might convince or at least comfort by its common-sense explanation that as cholesterol is made by the body it is unlikely to be something that is harmful or will kill us. (p 123).

Human breast milk contains significant quantities of cholesterol.. . . It would not do so if cholesterol were in any way a harmful substance. (p 124).
See also Addiction to food: A relevant review of Theodore Dalrymple's book Junk Medicine subtitled Doctors, Lies and the Addiction Bureaucracy

Received via email from the author

Crooked medical research

A Sharp Rise in Retractions Prompts Calls for Reform

In the fall of 2010, Dr. Ferric C. Fang made an unsettling discovery. Dr. Fang, who is editor in chief of the journal Infection and Immunity, found that one of his authors had doctored several papers.

It was a new experience for him. "Prior to that time," he said in an interview, "Infection and Immunity had only retracted nine articles over a 40-year period."    The journal wound up retracting six of the papers from the author, Naoki Mori of the University of the Ryukyus in Japan. And it soon became clear that Infection and Immunity was hardly the only victim of Dr. Mori's misconduct. Since then, other scientific journals have retracted two dozen of his papers, according to the watchdog blog Retraction Watch. "Nobody had noticed the whole thing was rotten," said Dr. Fang, who is a professor at the University of Washington School of Medicine.

Dr. Fang became curious how far the rot extended. To find out, he teamed up with a fellow editor at the journal, Dr. Arturo Casadevall of the Albert Einstein College of Medicine in New York. And before long they reached a troubling conclusion: not only that retractions were rising at an alarming rate, but that retractions were just a manifestation of a much more profound problem - "a symptom of a dysfunctional scientific climate," as Dr. Fang put it.

Dr. Casadevall, now editor in chief of the journal mBio, said he feared that science had turned into a winner-take-all game with perverse incentives that lead scientists to cut corners and, in some cases, commit acts of misconduct.   "This is a tremendous threat," he said.

Last month, in a pair of editorials in Infection and Immunity, the two editors issued a plea for fundamental reforms. They also presented their concerns at the March 27 meeting of the National Academies of Sciences committee on science, technology and the law.

Members of the committee agreed with their assessment. "I think this is really coming to a head," said Dr. Roberta B. Ness, dean of the University of Texas School of Public Health. And Dr. David Korn of Harvard Medical School agreed that "there are problems all through the system."

No one claims that science was ever free of misconduct or bad research. Indeed, the scientific method itself is intended to overcome mistakes and misdeeds. When scientists make a new discovery, others review the research skeptically before it is published. And once it is, the scientific community can try to replicate the results to see if they hold up.

But critics like Dr. Fang and Dr. Casadevall argue that science has changed in some worrying ways in recent decades - especially biomedical research, which consumes a larger and larger share of government science spending.

In October 2011, for example, the journal Nature reported that published retractions had increased tenfold over the past decade, while the number of published papers had increased by just 44 percent. In 2010 The Journal of Medical Ethics published a study finding the new raft of recent retractions was a mix of misconduct and honest scientific mistakes.

Several factors are at play here, scientists say. One may be that because journals are now online, bad papers are simply reaching a wider audience, making it more likely that errors will be spotted. "You can sit at your laptop and pull a lot of different papers together," Dr. Fang said.

But other forces are more pernicious. To survive professionally, scientists feel the need to publish as many papers as possible, and to get them into high-profile journals. And sometimes they cut corners or even commit misconduct to get there.

To measure this claim, Dr. Fang and Dr. Casadevall looked at the rate of retractions in 17 journals from 2001 to 2010 and compared it with the journals' "impact factor," a score based on how often their papers are cited by scientists. The higher a journal's impact factor, the two editors found, the higher its retraction rate.

The highest "retraction index" in the study went to one of the world's leading medical journals, The New England Journal of Medicine. In a statement for this article, it questioned the study's methodology, noting that it considered only papers with abstracts, which are included in a small fraction of studies published in each issue. "Because our denominator was low, the index was high," the statement said.

Monica M. Bradford, executive editor of the journal Science, suggested that the extra attention high-impact journals get might be part of the reason for their higher rate of retraction. "Papers making the most dramatic advances will be subject to the most scrutiny," she said.

Dr. Fang says that may well be true, but adds that it cuts both ways - that the scramble to publish in high-impact journals may be leading to more and more errors. Each year, every laboratory produces a new crop of Ph.D.'s, who must compete for a small number of jobs, and the competition is getting fiercer. In 1973, more than half of biologists had a tenure-track job within six years of getting a Ph.D. By 2006 the figure was down to 15 percent.