Juvenile delinquency and glass ceilings caused by first names? Hmmm….

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Why Curly is a stooge and Justin a golden boy

Among the wealth of research on the importance of given names, a new study correlates first names with criminal behaviour
MICHAEL VALPY | From Monday’s Globe and Mail | June 9, 2008 at 4:44 AM EDT

A Jarrit by any other name might be a brain surgeon.

But unlike Michaels, Matthews and Christophers, he is more likely to be a juvenile delinquent.

Ditto for an Art, a Curly and a Thurmond.

This is the finding of two economists from Pennsylvania’s Shippensburg University presented at Canada’s annual Congress of the Humanities and Social Sciences held this year at the University of British Columbia.

While other researchers have studied the ties between first names and socio-economic status, the work of David Kalist and Daniel Lee is believed to be the first attempt to correlate first names with criminal behaviour.

The researchers tabulated the name frequency of all males born in one unidentified state between 1987 and 1991 then compared the list (dubbed the Popularity Name Index - PNI) with the names of all males in the state’s juvenile delinquency database between 1997 and 2005 -when the males born in 1987-91 had entered their teens.

Prof. Lee explained in an interview that a specific name in itself didn’t propel its bearer toward delinquency.

Rather, a name suggested the presence of a set of background factors, such as poverty and broken families, that predisposed a young male to delinquency.

The researchers looked at the PNI of whites and blacks separately to take into account the higher proportion of blacks with low socio-economic status. They also chose a state with a large multicultural city.

They found that the more popular the name, the less likely its bearer was to get into trouble with the law.

Thus Michaels sparkled with a PNI of 100.

But a misstep on the path of life was more likely for an Alec, Ernest, Ivan, Kareem, Malcolm, Preston and Tyrell, each with a PNI of 1. And at the very bottom of the list were the Arts, Curlys and Jarrits with a PNI of 0.

“We show that unpopular names are associated with juveniles who live in … female-headed households or households without two parents,” write Prof. Kalist and Prof. Lee. “In addition, juvenile delinquents with unpopular names are more likely to reside in counties with lower socio-economic status.”

Their paper points in passing to a wealth of research by other scholars on first names.

Research by U.S. academics Saka Aura and Gregory Hess says that women with diminutive sounding names that end in an “ee” sound - Kathy as opposed to Kate - may face more glass ceilings in the work force.

They report that more popular names, with fewer syllables, standardized spellings, fewer beginnings with vowels and endings with “oh” sounds, are linked to better lifetime outcomes -and in large part are the legacy of parents with a high level of education.

U.S. sociologists Stanley Lieberson and Eleanor Bell found that the most significant impact on naming was the education level of the mother. They cite the example of Allison, a name rarely given by mothers without high-school education but frequently given by mothers with 17 or more years of schooling.

One study shows that boys with names most commonly given to girls - shades of Johnny Cash’s A Boy Named Sue - are more likely to be disruptive in school.

On the other hand, said Prof. Lee, girls with boy-sounding names have been found to do better at math.

Call your daughter Bruce and you may have an Einstein.

Popularity contest
Researchers at Pennsylvania’s Shippensburg University found that men with more popular names tended to get in less trouble. Culled from a data base of more than 15,000 names in one U.S. state, here were the most and least popular names for boys.

LEAST POPULAR
Amram, Arrington, Art, Chevin, Curly, Emmert, Hareed, Jarrit, Kameren, Kimmel, Lan, Mercedes, Nevada, Preslin, Syrus, Tareel, Thurmond, Trevonne, Welton, Weylen.

MOST POPULAR
Andrew, Anthony, Brandon, Brian, Christopher, Daniel, David, James, John, Joseph, Joshua, Justin, Kevin, Matthew, Michael, Nicholas, Robert, Ryan, William, Zachary.

Our “anecdotal” brain sucks up all the sensational news a media (vying for higher ad revenues) can muster.  This results in some skewed gut feelings of what we should be afraid of.

Wired’s book review of Dan Gardner’s The Science of Fear includes a quiz that is worth taking.

“All models are wrong, but some are useful” — I love that quote. For me it highlights the raison d’etre of science: to predict and therefore to increase control. I don’t agree with the article that theories and models will become obsolete, but it is time to add some new tools to the set of predicting tools we already have.  And use the most useful ones.

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WIRED MAGAZINE: 16.07

The End of Theory: The Data Deluge Makes the Scientific Method Obsolete

By Chris Anderson 06.23.08

The recent medical controversy over whether vaccinations cause autism reveals a habit of human cognition—thinking anecdotally comes naturally, whereas thinking scientifically does not.
On the one side are scientists who have been unable to find any causal link between the symptoms of autism and the vaccine preservative thimerosal, which in the body breaks down into ethylmercury, the culprit du jour for autism’s cause. On the other side are parents who noticed that shortly after having their children vaccinated autistic symptoms began to appear. These anecdotal associations are so powerful that they cause people to ignore contrary evidence: ethylmercury is expelled from the body quickly (unlike its chemical cousin methylmercury) and therefore cannot accumulate in the brain long enough to cause damage. And in any case, autism continues to be diagnosed in children born after thimerosal was removed from most vaccines in 1999; today trace amounts exist in only a few.

The reason for this cognitive disconnect is that we have evolved brains that pay attention to anecdotes because false positives (believing there is a connection between A and B when there is not) are usually harmless, whereas false negatives (believing there is no connection between A and B when there is) may take you out of the gene pool. Our brains are belief engines that employ association learning to seek and find patterns. Superstition and belief in magic are millions of years old, whereas science, with its methods of controlling for intervening variables to circumvent false positives, is only a few hundred years old. So it is that any medical huckster promising that A will cure B has only to advertise a handful of successful anecdotes in the form of testimonials.

Take wheatgrass juice … if you can stomach it. The claims for its curative powers are bottomless. According to the Natural Medicines Comprehensive Database (the “bible” of natural medicines: www.naturaldatabase.com), wheatgrass is “used therapeutically for increasing hemoglobin production, improving blood sugar disorders such as diabetes, preventing tooth decay, improving wound healing, and preventing bacterial infections.” And that’s not all. “It is also used orally for common cold, cough and bronchitis, fever and colds, inflammation of mouth and pharynx, tendency to infection, gout, liver disorders, ulcerative colitis, cancer, rheumatic pain, and chronic skin problems.”

The alleged salubrious effects of wheatgrass were promoted in the 1940s by a Lithuanian immigrant to Boston named Ann Wigmore, a holistic health practitioner who was inspired by the biblical story of King Nebuchadnezzar, recounted in Daniel 4:33, in which “he was driven from men, and did eat grass as oxen, and his body was wet with the dew of heaven, till his hairs were grown like eagles’ feathers, and his nails like birds’ claws.” Wigmore also noted that dogs and cats eat grass when they are ill and feel better after regurgitation, which gave her the idea of the wheatgrass detox. Because we have fewer stomachs than cows do, she hatched the idea of blending freshly cut wheatgrass into juice form for easier digestion—through either orifice—a practice still employed today. She believed that the enzymes and chlorophyll in wheatgrass constitute its healing powers.

According to William T. Jarvis, a retired professor of public health at the Loma Linda University School of Medicine and founder of the National Council against Health Fraud (www.ncahf.org), this is all baloney: “Enzymes are complex protein molecules produced by living organisms exclusively for their own use in promoting chemical reactions. Orally ingested enzymes are digested in the stomach and have no enzymatic activity in the eater.” Jarvis adds, “The fact that grass-eating animals are not spared from cancer, despite their large intake of fresh chlorophyll, seems to have been lost on Wigmore. In fact, chlorophyll cannot ‘detoxify the body’ because it is not absorbed.”

I tried wheatgrass juice at the Oh Happy Days natural food store in Altadena, Calif., as part of an investigation for the pilot episode of Skeptologists, a series we hope to sell to a television network (where another biblical phrase is apropos: “Many are called, but few are chosen”). My co-stars—Kirsten Sanford, who has a Ph.D. in physiology and is now a science journalist, and Steven Novella, director of general neurology at the Yale School of Medicine—also imbibed. If a picture is worth a thousand words, I will double this essay’s length by sharing the above snapshot.

Note: This article was originally printed with the title, “Wheatgrass Juice and Folk Medicine”.

Key points in this article: sleeping allows us to learn. It cements our memories, but also culls them, keeping the ones that are emotionally related. Our brains also solve problems/discover patterns while we sleep. We need about 6 hours of continuous sleep to achieve this, both slow-wave and REM.

Scientific American Mind - August 7, 2008

How Snoozing Makes You Smarter

During slumber, our brain engages in data analysis, from strengthening memories to solving problems

By Robert Stickgold and Jeffrey M. Ellenbogen

Neuroeconomics

Do economists need brains?

A new school of economists is controversially turning to neuroscience to improve the dismal science

FOR all the undoubted wit of their neuroscience-inspired concept album, “Heavy Mental”—songs include “Mind-Body Problem” and “All in a Nut”—The Amygdaloids are unlikely to loom large in the annals of rock and roll. Yet when the history of economics is finally written, Joseph LeDoux, the New York band’s singer-guitarist, may deserve at least a footnote. In 1996 Mr LeDoux, who by day is a professor of neuroscience at New York University, published a book, “The Emotional Brain: The Mysterious Underpinnings of Emotional Life”, that helped to inspire what is today one of the liveliest and most controversial areas of economic research: neuroeconomics.

In the late 1990s a generation of academic economists had their eyes opened by Mr LeDoux’s and other accounts of how studies of the brain using recently developed techniques such as magnetic resonance imaging (MRI) showed that different bits of the old grey matter are associated with different sorts of emotional and decision-making activity. The amygdalas are an example. Neuroscientists have shown that these almond-shaped clusters of neurons deep inside the medial temporal lobes play a key role in the formation of emotional responses such as fear.

These new neuroeconomists saw that it might be possible to move economics away from its simplified model of rational, self-interested, utility-maximising decision-making. Instead of hypothesising about Homo economicus, they could base their research on what actually goes on inside the head of Homo sapiens.

The dismal science had already been edging in that direction thanks to behavioural economics. Since the 1980s researchers in this branch of the discipline had used insights from psychology to develop more “realistic” models of individual decision-making, in which people often did things that were not in their best interests. But neuroeconomics had the potential, some believed, to go further and to embed economics in the chemical processes taking place in the brain.

Early successes for neuroeconomists came from using neuroscience to shed light on some of the apparent flaws in H. economicus noted by the behaviouralists. One much-cited example is the “ultimatum game”, in which one player proposes a division of a sum of money between himself and a second player. The other player must either accept or reject the offer. If he rejects it, neither gets a penny.

According to standard economic theory, as long as the first player offers the second any money at all, his proposal will be accepted, because the second player prefers something to nothing. In experiments, however, behavioural economists found that the second player often turned down low offers—perhaps, they suggested, to punish the first player for proposing an unfair split.

Neuroeconomists have tried to explain this seemingly irrational behaviour by using an “active MRI”. In MRIs used in medicine the patient simply lies still during the procedure; in active MRIs, participants are expected to answer economic questions while blood flows in the brain are scrutinised to see where activity is going on while decisions are made. They found that rejecting a low offer in the ultimatum game tended to be associated with high levels of activity in the dorsal stratium, a part of the brain that neuroscience suggests is involved in reward and punishment decisions, providing some support to the behavioural theories.

As well as the ultimatum game, neuroeconomists have focused on such issues as people’s reasons for trusting one another, apparently irrational risk-taking, the relative valuation of short- and long-term costs and benefits, altruistic or charitable behaviour, and addiction. Releases of dopamine, the brain’s pleasure chemical, may indicate economic utility or value, they say. There is also growing interest in new evidence from neuroscience that tentatively suggests that two conditions of the brain compete in decision-making: a cold, objective state and a hot, emotional state in which the ability to make sensible trade-offs disappears. The potential interactions between these two brain states are ideal subjects for economic modelling.

Already, neuroeconomics is giving many economists a dopamine rush. For example, Colin Camerer of the California Institute of Technology, a leading centre of research in neuroeconomics, believes that incorporating insights from neuroscience could transform economics, by providing a much better understanding of everything from people’s reactions to advertising to decisions to go on strike.

At the same time, Mr Camerer thinks economics has the potential to improve neuroscience, for instance by introducing neuroscientists to sophisticated game theory. “The neuroscientist’s idea of a game is rock, paper, scissors, which is zero-sum, whereas economists have focused on strategic games that produce gains through collaboration.” Herbert Gintis of the Sante Fe Institute has even higher hopes that breakthroughs in neuroscience will help bring about the integration of all the behavioural sciences—economics, psychology, anthropology, sociology, political science and biology relating to human and animal behaviour—around a common, brain-based model of how people take decisions.

However, not everyone is convinced. The fiercest attack on neuroeconomics, and indeed behavioural economics, has come from two economists at Princeton University, Faruk Gul and Wolfgang Pesendorfer. In an article in 2005, “The Case for Mindless Economics”, they argued that neuroscience could not transform economics because what goes on inside the brain is irrelevant to the discipline. What matters are the decisions people take—in the jargon, their “revealed preferences”—not the process by which they reach them. For the purposes of understanding how society copes with the consequences of those decisions, the assumption of rational utility-maximisation works just fine.

But today’s neuroeconomists are not the first dismal scientists to dream of peering inside the human brain. In 1881, a few years after William Jevons argued that the functioning of the brain’s black box would not be known, Francis Edgeworth proposed the creation of a “hedonimeter”, which would measure the utility that each individual gained from his decisions. “From moment to moment the hedonimeter varies; the delicate index now flickering with the flutter of the passions, now steadied by intellectual activity, low sunk whole hours in the neighbourhood of zero, or momentarily springing up towards infinity,” he wrote, poetically for an economist.

This is “equivalent to neuroeconomics’ brain scan,” notes David Colander, an economist at Middlebury College in Vermont, in an article last year in the Journal of Economic Perspectives, “Edgeworth’s Hedonimeter and the Quest to Measure Utility”. Later economists such as Irving Fisher, Frank Ramsey (who proposed a utility-measuring machine called a “psychogalvanometer”) and Friedrich von Hayek would discuss the role of the complex inner workings of the brain. Hayek cited early advances in neuroscience to explain why each individual has a unique perspective on the world.

The reason why economists in the late 19th century and much of the 20th put the rational utility-maximising individual at the heart of their models was not that they thought that economics should avoid looking into the brain, but because they lacked the technical means to do so, says Mr Colander. “Economics became a deductive science because we didn’t have the tools to gather information inductively. Now, better statistical tools and neuroscience are opening up the possibility that economics can become an abductive science that combines elements of deductive and inductive reasoning.”

The big question now is whether the tools of neuroscience will allow economics to fulfil Edgeworth’s vision—or, if that is too much to ask, at least to be grounded in the physical reality of the brain. Studies in the first decade of neuroeconomics relied heavily on active MRI scans. Economists’ initial excitement at being able to enliven their seminars with pictures of parts of the brain lighting up in response to different experiments (so much more interesting than the usual equations) has led to a recognition of the limits of MRIs. “Curiosity about neuroscience among economists has outstripped what we have to say, for now,” admits Mr Camerer.

A standard MRI identifies activity in too large a section of the brain to support much more than loose correlations. “Blood flow is an indirect measure of what goes on in the head, a blunt instrument,” concedes Kevin McCabe, a neuroeconomist at George Mason University. Increasingly, neuroscientists are looking for clearer answers by analysing individual neurons, which is possible only with invasive techniques—such as sticking a needle into the brain. For economists, this “involves risks that clearly outweigh the benefits,” admits Mr McCabe. Most invasive brain research is carried out on rats and monkeys which, though they have similar dopamine-based incentive systems, lack the decision-making sophistication of most humans.

One new technique being used by some neuroeconomists is transcranial magnetic stimulation, in which a coil held next to the head issues a low-level magnetic pulse that temporarily disrupts activity in a certain part of the brain, to see if that changes the subject’s preferences—for example, for a particular food and how much he is willing to pay for it. However, this tool, too, has only limited applicability, as it cannot get at the central temporal node of the brain where much basic reward activity takes place.

Still, Mr Camerer is confident that neuroeconomics will deliver its first big breakthroughs within five years. Likewise, Mr McCabe sees growing sophistication in neuroeconomic research. For the past four years, a group of leading neuroeconomists and neuroscientists has met to refine questions about the brain and economic behaviour. Researchers trained in both neuroscience and economics are entering the field. They are asking more sophisticated questions than the first generation “spots on brains” experiments, says Mr McCabe, such as “how these spots would change with different economic variables.” He expects that within a few years neuroeconomics will have uncovered enough about the interactions between what goes on in people’s brains and the outside world to start to shape the public-policy agenda—though it is too early to say how.

The success of neuroeconomics need not mean that behavioural economics will inevitably triumph over an economics based on rationality. Indeed, many behavioural economists are extremely pessimistic about the chances that brain studies will deliver any useful insights, points out Mr Camerer with regret.

However, Daniel Kahneman, a Princeton University psychologist who in 2002 won the Nobel prize in economics for his contribution to behavioural economics, is an enthusiastic supporter of the new field. “In many areas of economics, it will dominate, because it works,” says Mr Kahneman.

Even so, “we are nowhere near the demise of traditional neoclassical economics,” he argues. Instead, insights from brain studies may enable orthodox economists to develop a richer definition of rationality. “These traditional economists may be more impressed by brain evidence than evidence from psychology,” he says; “when you talk about biology either in an evolutionary or physical sense, you feel they have greater comfort levels than when you start to talk about psychology.”

In this respect, Mr Kahneman’s Princeton colleagues and neuroscience-bashers may be making a mistake in bundling behavioural economics—soft mind science—and neuroeconomics—hard biology—together. “It is far easier to argue for mindless economics than for brainless economics,” he says.

This article from Discover Magazine includes an eye-opening section on interpretation of clinical research studies and doctors’ understanding of it.

I am passing this article on to my doctor.

Wonder Drugs That Can Kill

06.20.2008

Modern pharmaceutical “breakthroughs” sometimes do more harm than good.

by Jeanne Lenzer

Phil Brewer thought he knew exactly what to do when the ambulance crew wheeled a well-dressed man in his late sixties into the emergency department. What he didn’t know: He was about to be involved in a series of events that would kill his patient. Brewer, then an assistant professor of emergency medicine at Yale School of Medicine, had been alerted by the crew that the man, Sanders Tenant (a pseudonym), had suddenly begun to talk gibberish while dining out with his family. Then his right arm and leg had gone weak.

Brewer suspected an acute stroke, but first he had to rule out conditions that can masquerade as a stroke, such as low blood sugar, a seizure, a brain tumor, and migraine headache. He had only minutes to make the correct diagnosis. Then the gathering medical team would decide whether to use a new stroke treatment that had recently been approved, a clot-buster known as tPA. Brewer called in a neurologist and the stroke team. After a CAT scan of the patient’s brain showed no sign of bleeding (something that would prevent the use of a clot-buster), the decision was made: Yes, use tPA. Despite following each step of the established protocol for this new treatment, Brewer experienced the unthinkable—his patient’s death. Tenant suffered a massive brain hemorrhage and died, not from his stroke but from effects of tPA, the drug that was meant to save him.

When we go to the doctor, we assume that the drugs he or she prescribes have been carefully tested to make sure they are both safe and effective. Most times they are. Yet sometimes the drugs cause more problems than they solve. Adverse drug reactions kill tens of thousands of people annually; one widely cited study published in the Journal of the American Medical Association (JAMA) in 1998 puts the number at more than 100,000. Recently a series of drug recalls have pulled back the curtain to show how the media, the public, and some doctors can misinterpret medical studies or take them out of context in ways that make medical treatments look safer and more effective than they actually are.

To a greater degree than ever before, powerful forces in the marketplace are impacting the quality, use, and safety of prescription medications. Drug manufacturers are spending more to promote their products while being subjected to tighter regulation and greater pressure for financial returns. The media are talking up each new “miracle cure” in headlines and television segments. Doctors have to navigate a tangle of administrative and medical concerns, one physician noting that “if you have a patient in your office, you can’t say, ‘Oh, I’m going to look at the drug company’s online database about Zyprexa.’ Most doctors don’t even know the databases exist. But even if they did, the next thing you know, three or four hours have gone by and you’ve missed all the patients waiting to see you.” Insurance companies and even the stock market play a role too. And consumers, increasingly subject to pharmaceutical advertising, are routinely urged to demand the best and the newest for their health. All together, this is a perfect storm for prescription drug problems.

How often do today’s medical “breakthroughs” become tomorrow’s discredited science? John P. A. Ioannidis, an epidemiologist at Tufts University School of Medicine in Boston and the University of Ioannina School of Medicine in Greece, studied the question. He examined the most-cited clinical studies published in the top three medical journals between 1990 and 2000 to see how well researchers’ initial claims held up against subsequent research. His findings, published in JAMA, show that the key claims of nearly one-third (14 out of 49) of the original research studies he examined were either false or exaggerated. Small study size, design flaws, publication bias (failure to publish negative results or duplication of positive results), drug-industry influence, and the play of chance were among the problems Ioannidis found that caused false or exaggerated claims.

Studies can be designed and interpreted in ways that make even ineffective drugs seem like lifesavers, says Curt Furberg, a well-known cardiovascular epidemiologist and former chief of the clinical trials branch at the National Heart, Lung, and Blood Institute in Bethesda, Maryland. Furberg, a tall, square-faced man with a Swedish accent, wants more objectivity in medical research. “We need more publicly funded studies,” he says, adding that manufacturer-sponsored research tends to minimize risks and exaggerate benefits.

A score of studies support his opinion. Among them is a 2003 analysis by Cary P. Gross, an associate professor of medicine at Yale School of Medicine, that was published in JAMA. In his survey, one study found that industry-sponsored research was positive 87 percent of the time compared with 65 percent positive for research that was not industry sponsored. According to Gross, the evidence was overwhelming that “industry sponsorship was likely to yield pro-industry results.” A 2006 analysis published in the American Journal of Psychiatry found that 90 percent of manufacturer-sponsored studies of antipsychotic drugs led to claims that the study drug was as good as, or superior to, every other drug in its class. Shannon Brownlee, an award-winning medical writer based in Washington, D.C., ascribed this to the “Lake Wobegon effect,” which renders every drug “above average.”

Furberg’s efforts to debunk overly enthusiastic interpretations of medical studies have led to occasional clashes with his colleagues. In 2004 the U.S. Food and Drug Administration (FDA) was preparing to hold hearings on the safety of painkillers known as COX-2 inhibitors, including Vioxx, which David Graham, an official in the FDA’s Office of Drug Safety, said may have caused an estimated 39,000 to 60,000 heart-attack deaths in just five years. At the time, Furberg was a member of the FDA Advisory Committee on Drug Safety and Risk Management. But after he told The New York Times that the COX-2 inhibitor Bextra also caused heart attacks, the agency made a surprising move: It removed Furberg from the advisory panel. Sandra Kweder, acting director of the Office of New Drugs, Center for Drug Evaluation and Research at the FDA, told a reporter that Furberg’s comments showed he could not be objective. Furberg now asks, “If bias was a concern, why did they allow 10 advisory members with ties to the manufacturers to be seated?” He was reinstated to the panel two days later and vindicated when the FDA announced that it had asked Pfizer to voluntarily withdraw Bextra from the market.

Nothing pisses me off more than deliberately misleading advertising. Want to eat healthier and buy whole grain products? Good luck — this article explains why no one knows how much whole grain there is in some products.

From Business Week:
July 23, 2008, 12:01AM EST

How Whole Is Whole Grain?

A settlement between Sara Lee and the Center for Science in the Public Interest may lead to more accurate claims about whole grains on food labels

by Pallavi Gogoi

Hundreds of bread and cereal brands claim to be “whole grain.” But how many are “wholly” made from whole grain?

Thanks to some fancy footwork by food companies, that distinction eludes most consumers. However, the difference now has tripped up one of the big food companies, Sara Lee (SLE), as well. On July 21, Sara Lee agreed to change the labels on its popular Soft & Smooth bread to make clear it is made of just 30% whole grains. That is part of a settlement with the Washington (D.C.)-based consumer advocacy group the Center for Science in the Public Interest. The group had threatened to sue Sara Lee in December, saying that the “whole grain goodness” sign splashed on Soft & Smooth packaging was misleading because the bread was made primarily of refined white flour.

“The food industry’s term ‘made with whole grain’ is actually code for made with very little or some whole grain,” says Bonnie Liebman, director of nutrition at the Center for Science in the Public Interest.

Grains for Good Health

Sara Lee spokeswoman Sara Matheu says the company had been considering the new labels as early as last fall even before meeting with the advocacy group. “We adamantly deny allegations made by CSPI,” she says. “We are proud of the 10g of whole grains per serving this transitional bread offers our consumers.…The blend of whole wheat and enriched wheat flour is designed to help consumers increase their consumption of whole-grain breads without a radical change in taste and consistency.”

The dispute points up the growing popularity of whole-grain breads and cereals. The whole-grains drumbeat started in the U.S. after 2001, when concerns over increasing obesity rates grew, and dieticians and nutritionists began looking for ways to improve Americans’ diets. In 2003, an Agriculture Dept. analysis found that Americans were consuming an average of 10 servings of grain a day, but just a little over one serving of that was whole grain.

Since then, many studies have found that whole grains are good for health (among other things, the high-fiber content benefits the digestive tract). A study released in February by a team of researchers at Pennsylvania State University found that diets with high amounts of whole grains help achieve weight loss and reduce the risk of chronic diseases such as diabetes and cardiovascular disease, and even lower blood pressure. “Whole grains are known to benefit the digestive system, and they also contain vitamins and minerals, which are lost when they are refined,” says Marion Nestle, professor of nutrition at New York University and author of several books, including Food Politics and What to Eat.

The food industry has responded with a plethora of new products that contain at least some whole grain.

Cocoa Puffs with Fiber

Consumer products researcher Mintel reports that new food products claiming to be made with “whole grains” more than doubled, to 361, in 2005, when they were recommended in dietary guidelines from the USDA. Whole-grain products rose to 633 in 2007. Another 492 such products have been launched just in the first half of this year, with breakfast cereals and baked goods topping the list.

Of course, how many of those products are made wholly from whole grain is anybody’s guess.

“The food industry is notorious for making nutrition claims even when reality is far removed from the appearance, and whole grains is a classic example,” says Kelly Brownell, director of the Rudd Center for Food Policy & Obesity at Yale University. “Sara Lee, General Mills (GIS), and others will make small changes in the food and make them appear to be big.”

In 2004, General Mills, maker of such popular cereals as Cheerios, Cocoa Puffs, and Lucky Charms, said it was converting its entire cereal lineup to whole grain—a claim it now makes in its ads. But few if any of the cereals are 100% made of whole grain. In some cases, the cereals consist mostly of refined flour. “After that, Cocoa Puffs went from zero grams of fiber per serving to 1g of fiber—that’s how small the change was,” says NYU’s Nestle.

General Mills spokeswoman Heidi Geller says all the company’s cereals contain at least 8g of whole grain in each serving, with its flagship Cheerios containing 23g of whole grain. Cocoa Puffs contain 10g, and Honey Nut Cheerios, 14g. However, Geller couldn’t provide the percentage of whole wheat vs. processed wheat in General Mills’ cereals. The USDA recommends the consumption of 48g of whole grain per day.

Massaging the Marketing

So why don’t food companies just make their products with whole grains? For one thing, white flour is easier to bake and has a longer shelf life since it doesn’t spoil quickly, says Nestle. Then there are the obvious differences in consumer preferences: Processed flour is lighter and softer than whole wheat. “If consumers want it, only the 100% whole grain counts as the real thing,” says Nestle.

The government, for its part, is very aware of how misleading some marketing claims can be. In a statement drafted in 2006, the Food & Drug Administration recognized that consumers could be confused by unqualified “whole grain” claims for products that contain a mixture of whole grain and refined grain.

The FDA stated that manufacturers could make factual statements about the amount of whole grain in a product, including claims such as “10g of whole grains,” or percentage claims such as “100% whole grain,” as long as they were true.

Manufacturers have gotten around that by stating that their products are “made with whole grain,” without saying exactly how much. “It’s obviously not untruthful to say that a product is made with whole grain,” says William Hallman, associate professor and director of the Food Policy Institute at Rutgers University in New Jersey. “But the question is whether it’s substantial enough to make a difference.”

Gogoi is a contributing writer for BusinessWeek.com.

If you want to control your blood sugar level (and possibly even lose weight), vinegar is your friend. And if you want to avoid cancer-causing damage by meat, red wine (or fruit in general) will neutralize some of the nasties before it even gets into your bloodstream. So start your meal with a vinaigrette salad; have some wine with your meat and fruit for dessert.

Here are the two articles supporting the above.

=======================================================

A Spoonful of Vinegar Helps the Sugar Go Down

on Tuesday, February 08 @ 14:57:23 CST

2 tablespoons of vinegar before a meal even as part of a vinaigrette salad dressing—will dramatically reduce the spike in blood concentrations of insulin and glucose that come after a meal.

A Spoonful of Vinegar Helps the Sugar Go Down
Carol Johnston is a professor of nutrition at Arizona State University’s East campus. When she started developing menus to help prevent and control diabetes, she began with a high-protein, low-carbohydrate diet. The diet worked amazingly well, but it involved major changes from the way people usually eat. Johnston feared they would give up and start downing Twinkies in no time. She wondered if there was an alternative.

Johnston struck gold while reading through some older studies on diabetes. Actually, she struck vinegar.

Her studies indicate that 2 tablespoons of vinegar before a meal—perhaps, as part of a vinaigrette salad dressing—will dramatically reduce the spike in blood concentrations of insulin and glucose that come after a meal. In people with type 2 diabetes, these spikes can be excessive and can foster complications, including heart disease

In Johnston’s initial study, about one-third of the 29 volunteers had been diagnosed with type 2 diabetes, another third had signs that they could become diabetic, and the rest were healthy. The scientists gave each participant the vinegar dose or a placebo to drink immediately before they ate a high-carbohydrate breakfast consisting of orange juice, a bagel, and butter. A week later, each volunteer came back for the opposite premeal treatment and then the same breakfast. After both meals, the researchers sampled blood from the participants.

Although all three groups in the study had better blood readings after meals begun with vinegar cocktails, the people with signs of future diabetes—prediabetic symptoms—reaped the biggest gains. For instance, vinegar cut their blood-glucose rise in the first hour after a meal by about half, compared with readings after a placebo premeal drink.
In contrast, blood-glucose concentrations were only about 25 percent better after people with diabetes drank vinegar. In addition, people with prediabetic symptoms ended up with lower blood glucose than even healthy volunteers, after both groups drank vinegar.

In these tests, vinegar had an effect on volunteers’ blood comparable to what might be expected from antidiabetes drugs, such as metformin, the researchers reported January in Diabetes Care. A follow-up study has now turned up an added—and totally unexpected—benefit from vinegar: moderate weight loss.

Both findings should come as welcome news during this season when sweet and caloric treats taunt diabetics, who face true health risks from indulging in too many carbs.

Johnston was looking for possible diet modifications that would make meals less risky for people with diabetes. While reviewing research published earlier by others, she ran across reports from about 2 decades ago that suggesting that vinegar limits glucose and insulin spikes in a person’s blood after a meal.

A few research groups had conducted limited follow-up trials. For instance, Johnston points to a 2001 paper in which researchers at Lund University in Sweden evaluated pickles—cucumbers preserved in vinegar—as a dietary supplement to lower the blood-sugar rise in healthy people after a meal. The Swedish team, led by Elin M. Östman, reported that pickles dramatically blunted the blood-sugar spike after a high-carb breakfast. Fresh cukes didn’t.

“I became really intrigued,” Johnston says, because adding vinegar to the diet would be simple “and wouldn’t require counting how many carbs you ate.” At first, she attempted to replicate findings by others, focusing specifically on people with diabetes or prediabetic symptoms.

When these individuals showed clear benefits from vinegar after a single meal, Johnston’ group initiated a trial to evaluate longer-term effects. It also explored vinegar’ effect on cholesterol concentrations in blood. The Arizona State scientists had hypothesized that by preventing digestion of carbs in the stomach, vinegar might cause carbohydrate molecules to instead ferment in the colon, a process that signals the liver to synthesize less cholesterol.

So, in one trial, Johnston had half of the volunteers take a 2-tablespoon dose of vinegar prior to each of two meals daily for 4 weeks. The others were told to avoid vinegar. All were weighed before and after the trial.

As it turns out, cholesterol values didn’t change in either group. To Johnston’ surprise, however, “here was actually about a 2-pound weight loss, on average, over the 4 weeks in the vinegar group.” In fact, unlike the control group, none in the vinegar cohort gained any weight, and a few people lost up to 4 pounds. Average weight remained constant in the group not drinking vinegar.

Johnston would now like to repeat the trial in a larger group of individuals to confirm the finding, but that study is currently on hold.

Why? To no one’s astonishment, the study volunteers didn’t like drinking vinegar straight—even flavored, apple-cider vinegar. Indeed, Johnston says, “I would prefer eating pickled foods or getting . . . vinegar in a salad dressing.”

Now, the scientists are developing a less objectionable, encapsulated form of vinegar and testing its efficacy. Although there are commercially available vinegar dietary supplements, Johnston notes that they “don’t appear to contain acetic acid,” and based on studies by others, she suspects that’s the antidiabetic ingredient in the vinegar.
Diabetes Care Jan, 2005

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Wine and health

Of sommeliers and stomachs

Jul 3rd 2008
From The Economist print edition

Red wine exercises its benefits before it enters the bloodstream

FINE food sings on the palate, but pairing it with the right wine creates a chorus. Among those in the know, the plum, chocolate and spice flavours of Cabernet Sauvignons, Merlots, Pinot Noirs and Sangioveses best accentuate the rich flavours of red meats. Now, however, a group of researchers led by Joseph Kanner of the Hebrew University of Jerusalem has discovered that pairing red wines like these with red meat appears to be more than just a matter of taste. If the two mix in the stomach, compounds in the wine thwart the formation of harmful chemicals that are released when meat is digested.

The idea that red wine is actually good for your health is irresistible to the average tippler. But it appears to be true. In particular, red wines are rich in polyphenols, a group of powerful antioxidants that are thought to protect against cancer and heart disease by destroying molecules that would otherwise damage cells. How the polyphenols in wine exercise their beneficial effects, though, has been mysterious. That is because they do not seem to travel in any quantity from the stomach into the bloodstream.

The answer, Dr Kanner has found, lies in the stomach itself. The digestion of high-fat foods such as red meat releases oxidising toxins. One in particular, called malondialdehyde, is implicated in arteriosclerosis, cancer, diabetes and a host of other serious diseases. Dr Kanner suspected that the key to wine’s protective effect is when, precisely, it is consumed. He hypothesised that if the polyphenols arrive in the stomach at the moment when the fats are releasing malondialdehyde and its kin, then this might stop these toxic materials from getting any farther into the body.

To test this idea, he and his colleagues fed a group of rats one of two meals—either red meat from a turkey (a foodstuff shown by previous research to raise malondialdehyde levels in humans) or such meat mixed with red-wine concentrate. An hour and a half after the rats had eaten, they were killed. Dr Kanner then removed their stomachs and analysed the contents. As he reports in the Journal of Agricultural and Food Chemistry, the wine concentrate did indeed reduce the formation of malondialdehyde. It also cut the level of hydroperoxides, another group of oxidising agents that cause cell damage.

Based on these results, Dr Kanner and his colleagues argue that looking for antioxidants from wine in the bloodstream was a mistake; they do not need to be there to be useful. Their research also suggests that the habit of eating fruit at the end of a meal is a healthy one. Many fruits, too, are rich in polyphenols (wine is, after all, just fermented fruit juice). By treating them as dessert, these fruits arrive in the stomach at the point when meat-digestion is poised to do its worst—nipping the problem in the bud, as it were.