Some research links lying with such facial and bodily cues as increased pupil size and lip pressing but not with blinking or posture.

By RACHEL ADELSON
July 2004, Vol 35, No. 7
Print version: page 70

Telling a little white lie may on occasion soothe ruffled social feathers, but covering up a murder plot or withholding information on terrorist cells can devastate individuals and society at large. Yet detecting deception often stumps the most experienced police officers, judges, customs officials and other forensic professionals. Research has shown that even agents from the FBI, CIA and Drug Enforcement Agency don’t do much better than chance in telling liars from truth-tellers.
For example, a recent, as yet unpublished meta-analysis of 253 studies of people distinguishing truths from lies revealed overall accuracy was just 53 percent–not much better than flipping a coin, note the authors, psychologists Charles Bond, PhD, of Texas Christian University, and Bella DePaulo, PhD, of the University of California, Santa Barbara.
Spotting the sneaks can be tough. Polygraph tests- so-called “lie detectors”–are typically based on detecting autonomic reactions and are considered unreliable (see “The polygraph in doubt”). That’s why psychologists have been cataloging clues to deception–such as facial expressions, body language and linguistics–to help hook the dishonest. From this research, psychologists are developing new detection tools such as software to analyze facial expressions and writing style.
They’re also training law-enforcement experts. One psychologist doing this is Paul Ekman, PhD, an emeritus psychology professor at the University of California Medical School, San Francisco, who’s studied deception for some 40 years. As part of the Oakland, Calif.-based Institute for Analytic Interviewing, he teaches interviewing skills to everyone from airport security guards to counter-terrorism agents, foreign-service officers and police interrogators, including officials from the CIA, FBI and other such federal agencies.
Mark Frank, PhD, a Rutgers University associate professor of communications, and Ekman are now gathering data on the demeanor and physiology of a large sample of people who tell “high-stakes” lies–for which they could lose money, their spouse, their reputation, their freedom or their life. Ekman says the findings from this new data set should provide “an awful lot [to the field]. I think there’ll be a giant leap.”
Deception cues debated
Are appearances deceiving? The evidence is mixed. DePaulo and co-author Wendy Morris, a psychology graduate student at the University of Virginia, conducted a meta-analysis into the possible predictors of deception for “Deception Detection in Forensic Contexts” (forthcoming from Cambridge University Press). They warn readers that detecting deception is an inexact science, but note an association between lying and increased pupil size, an indicator of tension and concentration. Second, they find that people listening to liars think they seem more nervous than truth-tellers, perhaps because their voices are pitched higher. And liars are more likely than truth-tellers to press their lips together. On the other hand, they note, liars don’t appear to be more fidgety, nor do they blink more or have less-relaxed posture. According to DePaulo and Morris, only when liars are more highly motivated–when the stakes are higher–do they seem unusually still and make notably less eye contact with listeners.
Also investigating bodily deception cues–particularly facial ones–are Ekman and his associates, who in 1978 published the Facial Action Coding System (FACS), which, when combined with voice and speech measures, reaches detection accuracy rates of up to 90 percent, Ekman claims. He and his colleagues are now automating the FACS for use in law enforcement. Meanwhile, they’re trying to raise the accuracy rate even higher.
Of the FACS Ekman says, “We get our biggest payoff from face and voice cues when dealing with lies about emotions at the moment. We add cues from gestures and words when it comes to lies about beliefs and actions, such as crimes.” Ekman and his colleagues do not reveal or publish each validated sign of deception for a very practical reason: They don’t want to tip off the wrong people.
Ekman, through close study, learned that “micro-expressions” lasting less than one-fifth of a second may leak emotions someone wants to conceal, such as anger or guilt. At the same time, signs of emotion aren’t necessarily signs of guilt. An innocent person may be apprehensive and appear guilty, Ekman points out.
He says, “You must use lying as a last interpretation and rule out everything else that’s possible.”
To tell the truth
Facial expressions aren’t the only clue. Because deception is a social act involving language, researchers are also studying liars’ verbal and written output to find distinctive patterns.
DePaulo and Morris say that liars take longer to start answering questions than truth-tellers–but when they have time to plan, liars actually start their answers more quickly than truth-tellers. And they talk less. On the whole, to other people, liars seem more negative–more nervous and complaining, and less cooperative–than truth-tellers, they say.
The content of conversations can be another tip-off. DePaulo and Morris report that liars seem to withhold information, either from guilt or to make it easier to get their stories straight.
“Liars’ answers sound more discrepant and ambivalent, the structure of their stories is less logical, and their stories sound less plausible,” they say. Liars also use fewer hand movements to illustrate their actions but are more likely to repeat words and phrases, they add.
At the University of Texas at Austin, psychology professor James Pennebaker, PhD, and his associates have developed computer software, known as Linguistic Inquiry and Word Count (LIWC), that analyzes written content and can, with some accuracy, predict whether someone is lying. Pennebaker says deception appears to carry three primary written markers:
Fewer first-person pronouns. Liars avoid statements of ownership, distance themselves from their stories and avoid taking responsibility for their behavior, he says.
More negative emotion words, such as hate, worthless and sad. Liars, notes Pennebaker, are generally more anxious and sometimes feel guilty.
Fewer exclusionary words, such as except, but or nor–words that indicate that writers distinguish what they did from what they did not do. Liars seem to have a problem with this complexity, and it shows in their writing.
The LIWC software–published by Lawrence Erlbaum–has been significantly more effective than human judges in correctly identifying deceptive or truthful writing samples, with an average accuracy rate of 67 percent as opposed to 52 percent. The samples were typed in five-minute sessions by participants who were asked to write–as persuasively as possible–truthful and deceptive essays about their views on abortion. They had given their true views, making it possible to know when they were lying.
At New Mexico State University, psychology doctoral student Gary Bond and his colleagues replicated the accuracy rates of LIWC in the field, analyzing the transcribed speech of felons jailed in New Mexico, Kansas and Mississippi and asked to tell the truth or lie about a video they had just seen. What’s more, truthful statements again had fewer negative emotion words and more self-referencing and exclusive words than false statements.
Human lie detectors
Computer programs aren’t the only methods of detecting lies. Some scientists believe that people–such as law-enforcement officers–can be trained to recognize liars through behavioral clues.
In June, APA teamed up with the FBI and the National Institute of Justice on a comprehensive workshop for top law enforcers on the use of intuition. Experts presented the latest research on detecting deception and related psychological topics such as bias and event memory. Ekman thinks such behavioral training may help authorities spot subtle cues that they might miss because they deal with so many liars.
There are no signs of lying per se, but rather signs of thinking too much when a reply should not require thought, or of emotions that don’t fit what is being spoken, he says. “We train people to look for ‘hot spots,’ where they’re not getting a full account,” he explains.
His Institute for Analytic Interviewing trains people to detect deception in the context of research findings on personality, memory and more. For example, Ekman says that skilled interrogators build rapport with suspects: “People will tell their story if they think you’re being open-minded.”
Meanwhile, Ekman has teamed with psychologist Maureen O’Sullivan, PhD, of the University of San Francisco, the lead investigator on a study of the hard-to-find, very small fraction of emotionally intelligent people who can very accurately distinguish deceptiveness from truthfulness. Some of them use the demeanor and vocal clues mentioned in this article, but others base their judgments on behaviors and word usage that no researcher has previously identified, O’Sullivan explains.
Can psychologists learn from these divining rods to train less-sensitive people? Ekman thinks more research is needed. O’Sullivan speculates that it could work only for those with some core skill: “Not everyone can be an Olympic athlete,” she explains. “Agencies should identify people with basic talent and train them.”
Shedding more light on the matter is Frank of Rutgers, who, with Tom Feeley, PhD, of the University at Buffalo of the State University of New York communication department, recently examined the research on training in the detection of deception.
“It showed that although the training methods used by most researchers were clearly inferior [such as just 10 to 15 minutes of training], there was still a significant–if weak–training effect. So we speculated that if training were done properly, it could work considerably better,” says Frank.
Psychology could have a lot to offer, write DePaulo and Morris in their forthcoming book chapter: “Good human lie detectors, if there are such persons, are likely to be good intuitive psychologists. They would figure out how a person might think or feel if lying in a particular situation, then look for behavioral indications of those thoughts or feelings.”
In the end, detecting deception is all about honesty. Ekman concludes, “It’s much harder to find the truth than to find a lie. A good lie-catcher is good at identifying truthfulness.”
Rachel Adelson is a writer in Raleigh, N.C.

Full story at Gratiot County Herald via Breakfast Links.

Education funding is being slashed left and right, and in states like Michigan that have been feeling the big hurt for a long time, that isn’t surprising since there’s only so much money going around, right? Well, Nathan Bootz, a school superintendent wrote a letter to the governor of Michigan requesting that his school be turned into a prison where the state’s funding shortage isn’t having quite the impact it’s having on his schools.

Dear Governor Snyder,
In these tough economic times, schools are hurting. And yes, everyone in Michigan is hurting right now financially, but why aren’t we protecting schools? Schools are the one place on Earth that people look to to “fix” what is wrong with society by educating our youth and preparing them to take on the issues that society has created.
One solution I believe we must do is take a look at our corrections system in Michigan. We rank nationally at the top in the number of people we incarcerate. We also spend the most money per prisoner annually than any other state in the union. Now, I like to be at the top of lists, but this is one ranking that I don’t believe Michigan wants to be on top of.
Consider the life of a Michigan prisoner. They get three square meals a day. Access to free health care. Internet. Cable television. Access to a library. A weight room. Computer lab. They can earn a degree. A roof over their heads. Clothing. Everything we just listed we DO NOT provide to our school children.
This is why I’m proposing to make my school a prison. The State of Michigan spends annually somewhere between $30,000 and $40,000 per prisoner, yet we are struggling to provide schools with $7,000 per student. I guess we need to treat our students like they are prisoners, with equal funding. Please give my students three meals a day. Please give my children access to free health care. Please provide my school district Internet access and computers. Please put books in my library. Please give my students a weight room so we can be big and strong. We provide all of these things to prisoners because they have constitutional rights. What about the rights of youth, our future?!
Please provide for my students in my school district the same way we provide for a prisoner. It’s the least we can do to prepare our students for the future…by giving our schools the resources necessary to keep our students OUT of prison.

Respectfully submitted,
Nathan Bootz, Superintendent,
Ithaca Public Schools

By BENEDICT CAREY / New York Times
Published: May 21, 2011

Between unresolved family conflicts, relationship struggles and his mixed-race identity, James Puckett had enough on his mind in college that he sought professional help. But after bouncing from one therapist to another, he still felt stuck. Stuart Hill
At the American Counseling Association’s annual conference in March, women predominated, as they do in the profession. “They were all female, and they did give me some comfort,” said Mr. Puckett, 30, who works for a domestic-abuse program in Wisconsin. “But I was getting the same rhetoric about changing my behavior without any challenge to see the bigger picture of what was behind these very male coping reactions, like putting your hand through a wall.”
He decided to seek out a male therapist instead, and found that there were few of them. “I’m just glad I ended up with the person I did,” said Mr. Puckett, who is no longer in therapy, “because for me it made all the difference.”

Researchers began tracking the “feminization” of mental health care more than a generation ago, when women started to outnumber men in fields like psychology and counseling. Today the takeover is almost complete.
Men earn only one in five of all master’s degrees awarded in psychology, down from half in the 1970s. They account for less than 10 percent of social workers under the age of 34, according to a recent survey. And their numbers have dwindled among professional counselors — to 10 percent of the American Counseling Association’s membership today from 30 percent in 1982 — and appear to be declining among marriage and family therapists.
Some college psychology programs cannot even attract male applicants, much less students. And at many therapists’ conferences, attendees with salt-and-pepper beards wander the hallways as lonely as peaceniks at a gun fair.
The result, many therapists argue, is that the profession is at risk of losing its appeal for a large group of sufferers — most of them men — who would like to receive therapy but prefer to start with a male therapist.
“There’s a way in which a guy grows up that he knows some things that women don’t know, and vice versa,” said David Moultrup, a psychotherapist in Belmont, Mass. “But that male viewpoint has been so devalued in the course of empowering little girls for the past 40 or 50 years that it is now all but lost in talk therapy. Society needs to have the choice, and the choice is being taken away.”
The reasons for the shift are economic as well as cultural, most people in these professions agree. Managed care took a bite out of therapists’ incomes in the 1990s. Psychiatry, the most male-dominated corner of therapy, increasingly turned to drug treatments. And as women entered the work force in greater numbers, they proved to be more drawn to the talking cure than men — in giving the treatment as well as in receiving it.
“Usually women get blamed when a profession loses status, but in this case the trend started first, and men just evacuated,” said Dorothy Cantor, a former president of American Psychological Association who conducted a landmark study of gender and psychology in 1995. “Women moved up into the field and took their place.”

The impact of this gender switch on the value of therapy is negligible, studies suggest. A good therapist is a good therapist, male or female, and a mediocre one is a mediocre one. Shared experience may even be an impediment, in some cases: therapists often caution students against assuming that they have special insight into person’s problems just because they have something in common.
Still, perception is all important when it comes to seeking help for the very first time. In a recent study among 266 college men, Ronald F. Levant, a psychologist at the University of Akron, found that a man’s willingness to seek therapy was directly related to how strongly he agreed with traditionally male assumptions, like “I can usually handle whatever comes my way.” Such a man on the fence about seeking treatment could be discouraged by the prospect of talking to a woman.

Many men like this believe that only another man can help them, and it doesn’t matter whether that’s true or not,” Dr. Levant said. “What’s important is what the client believes.”
Both male therapists and men who have been in treatment agree that there are certain topics that — at least initially, all things being equal — are best discussed within gender. Sex is one, they say. And some men are far less ashamed about affairs when speaking to another man.
Aggression is another. Many men grow up in a world of hostile body language and real physical violence that is almost entirely invisible to women. A bar fight that sounds traumatic to a female therapist may be no more than a good night out for a man. Likewise, a stare-down in the sandbox that looks vanishingly trivial from a distance may lie like a poisoned well in the stream of the unconscious.
In some men’s groups he used to run, Dr. Levant passed out index cards and had each participant write down the one thing he was most ashamed of, that he was reluctant to admit to himself, much less to anyone else. “I would get things like, ‘I backed down from a fight in junior high school,’ ” he said, “and these were mostly middle-aged, married guys.”

In just the past few years, psychologists have identified a number of issues that are, in effect, male versions of the gender-identity issues that so many mothers face in the work force: the self-doubt of being a stay-at-home father, the tension between being a provider and being a father, even male post-partum depression.
“In the same way that there is something very personal about being a mother, something very important to female identity, the experience of fathering is also very powerful,” said Aaron Rochlen, a psychologist at the University of Texas, Austin. “And some men, I think, prefer to talk about that — the joy of being a father, the stress, how it’s impacting them — with a therapist who’s had the same experience,” from the same point of view.
If they can find one, that is. “I remember when I started training, I looked around and realized that for the first time in my life, I was an endangered minority,” said Ryan McKelley, a psychologist at the University of Wisconsin, La Crosse. “Now I tell my male students, if you’re interested in clinical care, you can write your own ticket. You’ll be hired immediately.”

Scientific American
By Sarah Graham | June 28, 2005

The word “hypnosis” tends to conjure up images of subjects partaking in silly activities they might not otherwise agree to. But over the past few decades, scientific study of hypnosis has begun to identify how the approach can work to alter processes such as memory and pain perception. According to a new report, hypnotic suggestions regulate activity in certain regions of the brain and can help it manage cognitive conflicts.

A well-known example of cognitive conflict involves a person trying to name the color of ink used to print letters that spell out a different color. For example, the word “blue” spelled out in red ink. It usually takes subjects longer to read out such a list than it does to read a list of color names written in matching colored inks. In previous work, Amir Raz and his colleagues at the Weill Medical College of Cornell University had illustrated that hypnosis could be used to reduce this conflict in highly hypnotizable individuals. In the new work, they used functional magnetic resonance imaging (fMRI) and readings from scalp electrodes to monitor brain activity while subjects completed the ink-naming task.

The researchers also gave the subjects a posthypnotic suggestion to interpret the colored words as gibberish, which presumably would allow them to focus more on the color of the ink instead of reading the word. Highly hypnotizable individuals had better accuracy and quicker reaction times compared to those previously identified as being less responsive to hypnosis. The imaging data indicated that the hypnotizable subjects showed reduced brain activity in both visual areas and the anterior cingulate cortex, which is involved in conflict monitoring. Thus, the authors conclude, the results “illuminate how suggestion affects cognitive control by modulating activity in specific brain areas.”

Controlling parents tend to have children who are academically above average but depressed.

Scientific American
By Charles Q. Choi | April 15, 2011 | 6

All parents struggle to find the right balance between encouragement and discipline when it comes to raising their kids. This past winter Yale University law professor Amy Chua drew roars of protest when she asserted in her book, Battle Hymn of the Tiger Mother, that successful parenting entails controlling most aspects of a child’s life, from prohibiting playdates and sleepovers to screaming at children for getting grades lower than an A. What does research say about this style of child-rearing?

“There’s no evidence that intrusiveness is appropriate in any culture we’ve been to before, including China,” says psychologist Brian K. Barber of the University of Tennessee Knoxville. To learn more about how psychological control might vary across the world, Barber and his colleagues interviewed 120 adolescents from five different cultures, including Costa Rica, Thailand and South Africa, and then surveyed another 2,100. Their findings, which they recently submitted to the Journal of Adolescence, suggest that some of the behavior described in Chua’s book, such as insulting kids (she once called her daughter “garbage”), invalidating their feelings and violating their privacy, correlated with children’s depression and antisocial behavior, a finding that matches past research.

Barber distinguishes “authoritarian” households—those that are overly coercive—from “authoritative” households, where strictness is accompanied by warmth and encouragement of self-direction. In a prior study of more than 20,000 U.S. high schoolers, Laurence Steinberg of Temple University and his colleagues found that children raised in authoritative households were typically psychologically healthy, whereas those raised in authoritarian ones had elevated anxiety and depression. Notably kids from both households got comparably good grades, suggesting tiger mothering isn’t necessary for excellence after all.

A new study finds that alcoholic mice more readily form Pavlovian associations with addictive substances. Similar subconscious memories may haunt recovering addicts

By Nina Bai | April 27, 2011 | 11
Scientific American

Memory Maker: Long-term alcohol abuse can increase the “plasticity of synaptic plasticity,” leaving the brain more vulnerable to other addictions.
Image: flickr/swanksalot

Recovering addicts are often told to avoid the people, places, and things connected with their addiction—tried-and-true advice that may be gaining support from neuroscience. A view widely accepted among addiction researchers is that drug abuse can cause the brain to form persistent, enduring associations between a drug and the environment in which it is purchased and consumed. These mental ties represent a subconscious form of learning and contribute to the tenacious grip of addictions.

“There’s a growing consensus in the addiction field that addiction is a learning and memory disorder. We learn behavior associated with these drugs too well.” says Hitoshi Morikawa, a neurobiologist at the University of Texas at Austin. New research from Morikawa’s lab, published April 6 in the Journal of Neuroscience, found that repeated use of alcohol can make the brain more susceptible to forming reward-based associations. Mice given a weeklong binge of alcohol were more likely to remember the environment in which they later received cocaine. In human addicts similar associations could explain why certain environments are apt to trigger relapse.

Pavlovian memories
Addictive drugs cause dopamine neurons, which synthesize and store the neurotransmitter dopamine, to release it, signaling to other brain areas to take note of the context surrounding the drug—the better to replicate the experience in the future. “We can think of those neurons that release dopamine as ‘teachers’ that tell other brain areas, the ‘students,’ to learn the associations surrounding rewards such as food, sex and addictive drugs,” Morikawa explains. In essence, alcohol and other addictive drugs help the “teachers” teach better.

Morikawa emphasizes that the study does not show that alcohol improves “conscious” forms of learning and memory—a fact that could be corroborated by many a college freshman. Indeed, alcohol use is known to cause both acute and lasting damage to cognitive function.

The type of learning that alcohol and other addictive drugs may promote is best described as “subconscious” reward-based conditioning, much like the classic example of Pavlov’s dog. Just as the dog learns to associate the sound of a bell with food (a reward), a person may similarly associate a particular street corner in his hometown with cocaine use. After much repetition the dog salivates at the sound of a bell, and a cocaine addict craves a hit when he returns to the old hangout. The new insight from Morikawa’s work is that alcoholics may be more vulnerable to reward-based conditioning—meaning they would learn new cravings sooner.

Earlier work by Morikawa’s lab, also on mice, showed that repeated amphetamine use has a similar positive effect on reward-based conditioning. Morikawa expects likewise from other addictive drugs, such as opiates and nicotine—the common thread: increased dopamine levels.

All forms of learning and memory rely on synaptic plasticity, the ability of the brain to tweak the connections between neurons. These connections, or synapses, can be strengthened by a process known as long-term potentiation (LTP), which largely depends on the flow of calcium ions into and out of neurons. Morikawa’s work suggests that repeated dopamine release somehow boosts the chances of LTP in the brain’s reward pathways, although the molecular details are not yet clear.

Mice in booze camp
In the new study, performed on adolescent male mice, ethanol alcohol exposure seemed to enhance synaptic plasticity in the ventral tegmental area (VTA), a part of the brain that plays a critical role in the reward pathway. The VTA contains dopamine neurons whose axons extend to many other regions of the brain.

Researchers injected the mice with two grams of ethanol per kilogram of body weight three times daily for seven days. In humans this would be comparable to binge drinking, or blood alcohol levels roughly two to three times that of the U.S. legal driving limit of 0.08 percent, Morikawa says. Control mice underwent the same regimen but with injections of saline.

After one day of rest, mice were tested for “conditioned place preference,” a common measure of reward-based conditioning. Mice were allowed to explore what resembles a long, narrow shoe box, consisting of two distinctive compartments, one with a mesh floor and white walls, the other with a grid floor and black walls. The mice initially showed no preference for either decor, splitting their time evenly between the two compartments. Each animal was then given a reward—a cocaine injection—in one of the compartments and subsequently confined to that compartment for 30 minutes.

After two cocaine injections the mice were again allowed to freely explore the compartments. The mice that had a week of saline injections increased their stay in the compartment where they had received cocaine by 7 percent. But the mice that had a week of ethanol injections—the “hard-drinkers”—lingered in their cocaine compartments much longer, increasing their time there by 14 percent. One week of heavy alcohol intake had increased the mice’s ability to remember the context of a rewarding experience. The heightened potential for synaptic plasticity was temporary, lasting between a week and a month after ethanol injections stopped, according to the researchers.

They also observed these changes on a neuronal level by studying slices of VTA taken from sacrificed mice. By repeatedly stimulating neurons with electrodes, researchers were able to induce LTP, the strengthening of synapses. Neurons taken from ethanol-injected mice showed on average more than twice as much LTP than neurons from saline-injected mice.

Differences and details
A 2005 study of ethanol exposure in mice did not find enhancement of synaptic plasticity. But Anthony Riley, a psychologist at American University and co-author of the 2005 study, was not surprised by the new findings. The mice in the earlier study were given significantly less alcohol, were of a different breed, and were adult mice. “[Morikawa's team] trained and tested their animals during adolescence, a period associated with greater reinforcing effects of drugs. The parameters are dramatically different—that likely accounts for the difference in results,” Riley says.

How does steady alcohol use encourage neurons to link up? The molecular mechanisms are complex and still somewhat speculative, Morikawa says, but it begins with the flood of dopamine caused by alcohol use. Autoreceptors on dopamine neurons sense the dopamine being released. Chronic activation of these autoreceptors revs up the activity of protein kinase A (PKA). PKA phosphorylates IP3 receptors located on cell membranes, inducing them to release intracellular stores of calcium ions. The flow of calcium ions eases communication between neurons, promoting LTP along the reward pathway.

Riley says this biochemical interpretation requires further confirmation, such as challenging part of the proposed mechanism to see if the effect is blocked: “That is needed for them to talk of a causal role in their effect.”

From mice to men
Larry Zweifel, a pharmacologist at the University of Washington in Seattle who was not involved in Morikawa’s or Riley’s work, says that the new research shows that drug abuse can change the brain by “strengthening the capacity of neurons in the reward circuit to be strengthened, in effect setting up a positive feedback loop to drive persistent drug seeking.”

If the thought of binge-drinking teenagers getting hooked on cocaine is stressing you out, Morikawa has more bad news. “People frequently drink to relieve daily stress, but that might actually provide an ideal setting to get hooked up to alcohol-associated stimuli and behavior very effectively,” he says. When brain slices were bathed in a stress hormone, IP3-induced calcium signaling also increased. In fact, compared with ethanol, which enhances synaptic plasticity only after long-term use, “stress can do the same job more rapidly,” Morikawa says.

It doesn’t take a neuroscientist to know that avoiding temptations from a drug-addled past is a good idea, so why go to all the trouble of studying alcoholic mice? By understanding the basic mechanisms of drug addiction in animal models, “we can extrapolate these findings to develop selective therapies to reverse the pathophysiological changes associated with compulsive drug-seeking,” Zweifel says.

Morikawa puts it in more straightforward terms: “The goal is not simple—we are talking about erasing certain memories without affecting others—but I believe it is an attainable goal,” he says.

Cognitive scientist Matthew Schulkind knows “earworms” inside and out—especially those spawned by the Wiggles.
by Shannon Sweeney
From the Brain special issue; published online March 26, 2009

If you can’t recall your mother’s birthday but can readily belt out all the lyrics to “Piano Man,” welcome to the club. Music and melody seem to have a unique place in memory, Amherst College cognitive scientist Matthew Schulkind suggests. His studies with older adults explore why pop songs grab hold of our memories—and whether music could help dementia patients reconnect with lost knowledge.

Why is it so easy to sing along with old Top 40 songs when it’s so hard to remember things you actually tried to learn, like French verbs or algebra?
To a certain extent, musical memory is procedural rather than declarative. Declarative memory is your memory for facts, like the Spanish word for dog. Procedural memory is your memory for skills, such as how to hit a tennis ball. This doesn’t take conscious thought. Once you start the swing, it just happens. Similarly, once you get a song started, you don’t have to think about what comes next. You hear the first few notes of a song, and it just comes pouring out.

Can older people really remember tunes from childhood as if it were yesterday?
That’s exactly what I expected to happen. I thought I would get older adults into the lab, play them these songs, and they would be crying and singing along with them. Instead, they said things like, “Well, that sort of sounds familiar, but I’m not really sure.” That surprised me.

One man heard about three notes of a song called “Sh-Boom” by the Crew Cuts and knew it immediately. He sang the entire song from start to finish. He knew it was released in 1954. He knew the B side of the single. He knew all kinds of things about the song. It turns out it was released the day after he was married, and that’s what the hotel band played every night on his honeymoon.

I think there are a small number of songs that you do have a special relationship with. When you hear them, you’re carried back to that time and place. Because these experiences are powerful, I think people tend to overestimate how frequently they happen.

What about “earworms,” the songs that get stuck in our heads?
This seems to be a universal phenomenon. People typically like what gets stuck in their heads, yet it’s a very unpleasant experience. A song stuck in your head will seem to plague you for hours. The simpler the song, the more likely it is to get stuck in your head—like the Wiggles. Fortunately, my kids are phasing out of the Wiggles’ music. It’s brutally catchy!

There are lots of instances where people can’t get rid of thoughts. It’s much easier to distract yourself from unwanted thoughts—just do your taxes, no problem. But doing your taxes won’t help get an unwanted melody to go away, which might suggest that the brain areas that support musical recall are different from the brain areas that support other kinds of memory.

Can music bring back lost memories?
In a study I did with dementia patients, I wanted to know if music might help people retrieve information stored in long-term memory. The fundamental question for this dementia study was, is information available somewhere in there that people just can’t get to? In one experiment, we found that listening to music increased the likelihood of patients’ remembering famous faces or the names associated with those faces. It wasn’t that the music took them back to an earlier decade; it had a general effect on their ability to retrieve other information, suggesting that at least some of the deficits observed in dementia involve an inability to recover information.

Why do pop songs evoke the past so clearly?
People stop paying attention to pop music as they get older. Also, pop songs come and go. People listen to jazz and classical music over and over, but no one’s listening to Adam and the Ants anymore. If I hear an Adam and the Ants song, it’s like, “Oh, I haven’t heard that song in a long time.” I think it’s the simplicity of pop music. It makes it more likely to get saved. The simpler the pattern, the easier it will be to pour right back out.Shannon Sweeney

THE STUDY “Oxytocin Increases Generosity in Humans,” by Paul Zak et al., published in the November 2007 issue of PLoS ONE.

THE QUESTION What drives us to be charitable to strangers when it is costly to ourselves? Researchers investigated the role that the hormone oxytocin plays in regulating our generous behavior.

THE METHOD Produced naturally during sexual arousal and childbirth, oxytocin has long been linked to social behaviors. By binding to brain regions associated with emotion, the hormone helps parents bond with children and increases trust. Adding a twist to this story, neuroeconomist Paul Zak of Claremont Graduate University proposed that oxytocin might also play a role in material generosity by promoting the ability to empathize with others.
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To test his hypothesis, Zak focused on monetary transfers. He rounded up 68 male participants (women were excluded because oxytocin increases the risk of miscarriage) and administered oxytocin to half of them through a nasal inhaler. The other half inhaled only salt water. Then participants were paired randomly and identified only by a number via computer, a setup that prevented them from identifying each other or talking at all.

In a first round of trials, subjects were told that one of each pair would receive $10 but would need to offer his partner a share. If the partner accepted the offer, they would divide the money as proposed by the other partner. But if the subject rejected the offer—which might happen if the offer seemed too stingy—neither person would get anything. Prior to learning which role he would assume (giver or receiver), each participant was asked to decide on personal courses of action—if doling out the money, how much would he give, and if receiving, what was the minimum offer he would accept? “We used this strategy to force people to take another’s perspective,” Zak explains. The money was real, and players received cash at the end in accordance with these rules.

In a second round, the same people were paired, but this time the receiving partner had no say over the offer: He had to accept it, no matter what it was.

THE RESULTS In the first part of the study, oxytocin made no difference whatsoever in the minimum offer a partner was willing to accept: It was $2.97, on average, regardless of whether he received the hormone or a placebo.

But when it came to the actual generosity of giving, oxytocin mattered a lot. Those inhaling the hormone offered an average of $4.86 compared with $4.03 for those who inhaled saline. In fact, those who received oxytocin were so giving that they actually left the lab with about 5 percent less money than their placebo counterparts.

Results were different in the second trial, where recipients had to accept the offer no matter what. With no possibility of rejection, offers were lower overall ($3.68 on average), and there was no statistical difference between the oxytocin and placebo groups. In other words, oxytocin had no effect.

THE MEANING Since oxytocin increased the level of giving only in the first transaction—in which the partner’s response mattered—Zak concludes that the hormone’s effect is specific, altering generosity only when we have to think about others’ feelings. “When something drives us emotionally, when we feel connected to other people, that’s when we open our wallets,” he says.

Should you worry about casinos or charities spritzing this stuff in the air to make you spend or give more? “The answer is no,” Zak says. “You have to get a lot in your nose to get it into your brain. You would know you were getting it up your nose.” The larger danger is manipulation of our empathy (video) and generosity through heart-wrenching images or narratives that cause the natural release of oxytocin to the brain.

Part of the motivation behind investigations like this one, Zak says, is that “as we become aware of these unconscious processes, we have better control over them.” But we would not want to override oxytocin’s effects. By increasing empathy, he says, oxytocin “makes us bind together as a species. All kinds of daily transactions require that people spend just a little bit of their time and resources to help someone out. I think society as we know it couldn’t exist without that.”

Stats Behind the study
• Donors in the United States gave $295 billion to charities
in 2006.
• Nearly $223 billion of that came from individuals.
• Who got the money? A third went to religious congregations, and 14 percent went to education. Foundations and human services organizations received more than 10 percent each. Cultural organizations and international affairs groups received 4 percent each.
• The average person in the United States gave away 2.2 percent of after-tax income in 2005.
• That same year, 65 million Americans donated time to charities.
• 96 percent of volunteers said “feeling compassion toward other people” motivated them to give their time.
• Previous research by Zak and his colleagues suggests that because estrogen increases the number of oxytocin receptors, in countries where people consume larger amounts of plant-based estrogens (found in foods such as nuts, soy products, and legumes), average trust levels are higher.

A psychologist says secret corporate documents show how ineffective the drugs really are. //   by Ben Harder – published online October 10, 2008

THE STUDY
“Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration” by Irving Kirsch et al., published online on February 26 in PLoS Medicine.

THE QUESTION
Irving Kirsch no longer sends patients to seek out antidepressants. “As a clinical psychologist,” he says, “I used to refer patients to colleagues who were psychiatrists to get these medications.” But his research over the years has soured him on the drugs, suggesting they work only marginally better in the average patient than a placebo pill. Kirsch recently analyzed the numbers behind a multitude of studies to answer the question: Do antidepressants work?

THE METHODS
For the analysis, Kirsch and his colleagues were reluctant to rely solely on published drug trials. Those that get published, other researchers have found, tend to show medications in a more positive light than trials that go unpublished. To circumvent that influence, known as “publication bias,” Kirsch’s team used the Freedom of Information Act (FOIA) to solicit records from the Food and Drug Administration. That gave them access to data from all manufacturer-sponsored trials of the six antidepressants approved between 1987 and 1999—including some trials the manufacturers had never published.
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Even then, the data did not reflect everything the researchers would have liked to know. For two of the drugs, for example, there was no indication as to how much the average patient’s symptoms improved during treatment. So the researchers ignored those drugs and focused on the other four—fluoxetine (Prozac), paroxetine (Paxil), venlafaxine (Effexor), and nefazodone (formerly sold in the United States as Serzone). In all, they analyzed 35 trials, each of which involved a group of patients who took a placebo and at least one group who took one of those four antidepressants. Kirsch’s team considered how sick each group of patients had been before treatment, how much they improved during treatment, and whether they’d gotten a real drug or an inert pill.

THE RESULTS
Just as one would hope, taking an antidepressant typically improved a person’s depressive symptoms, the trials showed. But so did taking a placebo. In fact, the overall difference between medication and placebo was so small that it was “clinically insignificant” for all but the most depressed patients, Kirsch says, a point that was consistent with his past findings. Moreover, antidepressant therapy improved symptoms by the same degree in both mildly and moderately ill patients. “There seems little evidence to support the prescription of antidepressant medication to any but the most severely depressed patients,” says Kirsch, “unless alternative treatments have failed to provide benefit.”

THE MEANING
In the end, the researchers found that most patients who take antidepressants may glean little from them other than a placebo effect. However, the initial severity of a patient’s depression did influence the placebo effect. Placebos seem to help very depressed patients less than they help those with moderate symptoms. As a result, says Kirsch, antidepressants proved substantially more effective than placebos in—and only in—trials involving the most down-and-out patients. Blair Johnson, a social psychologist at the University of Connecticut in Storrs and co-author, recommends that doctors look at all of the alternative therapies—including psychotherapy, exercise, light therapy, omega-3 fatty acid supplements, and various others—first for all but the most depressed patients.

SECOND OPINION
Even if the drugs are effective, you would expect these results because the majority of depressed patients do not get better on the first antidepressant they are prescribed, say numerous critics including members of the pharmaceutical industry and physicians. Darrel Regier, the American Psychiatric Association’s director of research, says this is probably why so many patients did not improve significantly. If the unresponsive patients had been tested on two or three antidepressants back-to-back, say critics of this analysis, then more improvement would have been seen.

Moreover, critics say a study like Kirsch’s should focus on how many individual patients improve with treatment, not whether the average improvement is clinically significant. By averaging outcomes, the study dilutes some patients’ large improvements with others’ unchanged symptoms. “That’s true,” says Kirsch, but if some people improve more than the average, he says, some must improve less—or even be harmed. “Medications have side effects,” he says. “One of the side effects [of antidepressants] is increased risk of suicide.”

STATS BEHIND THE STUDY
• Kirsch’s team found that symptoms of SSRI-treated patients improved, on average, by 9.6 points on an index called the Hamilton Rating Scale for Depression. The average improvement of patients getting a placebo was over 80 percent as effective.

• More prescriptions are dispensed for antidepressants—232.7 million nationwide in 2007—than for drugs of any other type, according to the data firm, IMS Health.

• U.S. sales of antidepressants totaled $11.9 billion in 2007, IMS Health reports.

• A 2006 trial aiming to treat depression with various drugs found that two out of three depressed patients ultimately received a drug that helped put their illness in remission. In that trial, 37 percent of patients went into remission on the first antidepressant they tried, 31 percent on a second drug, 14 percent on a third, and 13 percent on a fourth.

• An increase in SSRI sales by one pill per capita per year is associated with a 5 percent drop in suicides nationwide, according to 2007 working paper by the National Bureau of Economic Research.

• It takes $20,000 worth of SSRI pills to prevent one suicide, the NBER found.
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Lustig is a specialist on pediatric hormone disorders and the leading expert in childhood obesity at the University of California, San Francisco, School of Medicine, which is one of the best medical schools in the country. He published his first paper on childhood obesity a dozen years ago, and he has been treating patients and doing research on the disorder ever since.

The viral success of his lecture, though, has little to do with Lustig’s impressive credentials and far more with the persuasive case he makes that sugar is a “toxin” or a “poison,” terms he uses together 13 times through the course of the lecture, in addition to the five references to sugar as merely “evil.” And by “sugar,” Lustig means not only the white granulated stuff that we put in coffee and sprinkle on cereal — technically known as sucrose — but also high-fructose corn syrup, which has already become without Lustig’s help what he calls “the most demonized additive known to man.”

It doesn’t hurt Lustig’s cause that he is a compelling public speaker. His critics argue that what makes him compelling is his practice of taking suggestive evidence and insisting that it’s incontrovertible. Lustig certainly doesn’t dabble in shades of gray. Sugar is not just an empty calorie, he says; its effect on us is much more insidious. “It’s not about the calories,” he says. “It has nothing to do with the calories. It’s a poison by itself.”

If Lustig is right, then our excessive consumption of sugar is the primary reason that the numbers of obese and diabetic Americans have skyrocketed in the past 30 years. But his argument implies more than that. If Lustig is right, it would mean that sugar is also the likely dietary cause of several other chronic ailments widely considered to be diseases of Western lifestyles — heart disease, hypertension and many common cancers among them.

The number of viewers Lustig has attracted suggests that people are paying attention to his argument. When I set out to interview public health authorities and researchers for this article, they would often initiate the interview with some variation of the comment “surely you’ve spoken to Robert Lustig,” not because Lustig has done any of the key research on sugar himself, which he hasn’t, but because he’s willing to insist publicly and unambiguously, when most researchers are not, that sugar is a toxic substance that people abuse. In Lustig’s view, sugar should be thought of, like cigarettes and alcohol, as something that’s killing us.

This brings us to the salient question: Can sugar possibly be as bad as Lustig says it is?

It’s one thing to suggest, as most nutritionists will, that a healthful diet includes more fruits and vegetables, and maybe less fat, red meat and salt, or less of everything. It’s entirely different to claim that one particularly cherished aspect of our diet might not just be an unhealthful indulgence but actually be toxic, that when you bake your children a birthday cake or give them lemonade on a hot summer day, you may be doing them more harm than good, despite all the love that goes with it. Suggesting that sugar might kill us is what zealots do. But Lustig, who has genuine expertise, has accumulated and synthesized a mass of evidence, which he finds compelling enough to convict sugar. His critics consider that evidence insufficient, but there’s no way to know who might be right, or what must be done to find out, without discussing it.

If I didn’t buy this argument myself, I wouldn’t be writing about it here. And I also have a disclaimer to acknowledge. I’ve spent much of the last decade doing journalistic research on diet and chronic disease — some of the more contrarian findings, on dietary fat, appeared in this magazine —– and I have come to conclusions similar to Lustig’s.

The history of the debate over the health effects of sugar has gone on far longer than you might imagine. It is littered with erroneous statements and conclusions because even the supposed authorities had no true understanding of what they were talking about. They didn’t know, quite literally, what they meant by the word “sugar” and therefore what the implications were.

So let’s start by clarifying a few issues, beginning with Lustig’s use of the word “sugar” to mean both sucrose — beet and cane sugar, whether white or brown — and high-fructose corn syrup. This is a critical point, particularly because high-fructose corn syrup has indeed become “the flashpoint for everybody’s distrust of processed foods,” says Marion Nestle, a New York University nutritionist and the author of “Food Politics.”

This development is recent and borders on humorous. In the early 1980s, high-fructose corn syrup replaced sugar in sodas and other products in part because refined sugar then had the reputation as a generally noxious nutrient. (“Villain in Disguise?” asked a headline in this paper in 1977, before answering in the affirmative.) High-fructose corn syrup was portrayed by the food industry as a healthful alternative, and that’s how the public perceived it. It was also cheaper than sugar, which didn’t hurt its commercial prospects. Now the tide is rolling the other way, and refined sugar is making a commercial comeback as the supposedly healthful alternative to this noxious corn-syrup stuff. “Industry after industry is replacing their product with sucrose and advertising it as such — ‘No High-Fructose Corn Syrup,’ ” Nestle notes.

But marketing aside, the two sweeteners are effectively identical in their biological effects. “High-fructose corn syrup, sugar — no difference,” is how Lustig put it in a lecture that I attended in San Francisco last December. “The point is they’re each bad — equally bad, equally poisonous.”

Refined sugar (that is, sucrose) is made up of a molecule of the carbohydrate glucose, bonded to a molecule of the carbohydrate fructose — a 50-50 mixture of the two. The fructose, which is almost twice as sweet as glucose, is what distinguishes sugar from other carbohydrate-rich foods like bread or potatoes that break down upon digestion to glucose alone. The more fructose in a substance, the sweeter it will be. High-fructose corn syrup, as it is most commonly consumed, is 55 percent fructose, and the remaining 45 percent is nearly all glucose. It was first marketed in the late 1970s and was created to be indistinguishable from refined sugar when used in soft drinks. Because each of these sugars ends up as glucose and fructose in our guts, our bodies react the same way to both, and the physiological effects are identical. In a 2010 review of the relevant science, Luc Tappy, a researcher at the University of Lausanne in Switzerland who is considered by biochemists who study fructose to be the world’s foremost authority on the subject, said there was “not the single hint” that H.F.C.S. was more deleterious than other sources of sugar.

The question, then, isn’t whether high-fructose corn syrup is worse than sugar; it’s what do they do to us, and how do they do it? The conventional wisdom has long been that the worst that can be said about sugars of any kind is that they cause tooth decay and represent “empty calories” that we eat in excess because they taste so good.

By this logic, sugar-sweetened beverages (or H.F.C.S.-sweetened beverages, as the Sugar Association prefers they are called) are bad for us not because there’s anything particularly toxic about the sugar they contain but just because people consume too many of them.

Those organizations that now advise us to cut down on our sugar consumption — the Department of Agriculture, for instance, in its recent Dietary Guidelines for Americans, or the American Heart Association in guidelines released in September 2009 (of which Lustig was a co-author) — do so for this reason. Refined sugar and H.F.C.S. don’t come with any protein, vitamins, minerals, antioxidants or fiber, and so they either displace other more nutritious elements of our diet or are eaten over and above what we need to sustain our weight, and this is why we get fatter.

Whether the empty-calories argument is true, it’s certainly convenient. It allows everyone to assign blame for obesity and, by extension, diabetes — two conditions so intimately linked that some authorities have taken to calling them “diabesity” — to overeating of all foods, or underexercising, because a calorie is a calorie. “This isn’t about demonizing any industry,” as Michelle Obama said about her Let’s Move program to combat the epidemic of childhood obesity. Instead it’s about getting us — or our children — to move more and eat less, reduce our portion sizes, cut back on snacks.

Lustig’s argument, however, is not about the consumption of empty calories — and biochemists have made the same case previously, though not so publicly. It is that sugar has unique characteristics, specifically in the way the human body metabolizes the fructose in it, that may make it singularly harmful, at least if consumed in sufficient quantities.

The phrase Lustig uses when he describes this concept is “isocaloric but not isometabolic.” This means we can eat 100 calories of glucose (from a potato or bread or other starch) or 100 calories of sugar (half glucose and half fructose), and they will be metabolized differently and have a different effect on the body. The calories are the same, but the metabolic consequences are quite different.

The fructose component of sugar and H.F.C.S. is metabolized primarily by the liver, while the glucose from sugar and starches is metabolized by every cell in the body. Consuming sugar (fructose and glucose) means more work for the liver than if you consumed the same number of calories of starch (glucose). And if you take that sugar in liquid form — soda or fruit juices — the fructose and glucose will hit the liver more quickly than if you consume them, say, in an apple (or several apples, to get what researchers would call the equivalent dose of sugar). The speed with which the liver has to do its work will also affect how it metabolizes the fructose and glucose.

In animals, or at least in laboratory rats and mice, it’s clear that if the fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat. This apparently induces a condition known as insulin resistance, which is now considered the fundamental problem in obesity, and the underlying defect in heart disease and in the type of diabetes, type 2, that is common to obese and overweight individuals. It might also be the underlying defect in many cancers.

If what happens in laboratory rodents also happens in humans, and if we are eating enough sugar to make it happen, then we are in trouble.

The last time an agency of the federal government looked into the question of sugar and health in any detail was in 2005, in a report by the Institute of Medicine, a branch of the National Academies. The authors of the report acknowledged that plenty of evidence suggested that sugar could increase the risk of heart disease and diabetes — even raising LDL cholesterol, known as the “bad cholesterol”—– but did not consider the research to be definitive. There was enough ambiguity, they concluded, that they couldn’t even set an upper limit on how much sugar constitutes too much. Referring back to the 2005 report, an Institute of Medicine report released last fall reiterated, “There is a lack of scientific agreement about the amount of sugars that can be consumed in a healthy diet.” This was the same conclusion that the Food and Drug Administration came to when it last assessed the sugar question, back in 1986. The F.D.A. report was perceived as an exoneration of sugar, and that perception influenced the treatment of sugar in the landmark reports on diet and health that came after.

The Sugar Association and the Corn Refiners Association have also portrayed the 1986 F.D.A. report as clearing sugar of nutritional crimes, but what it concluded was actually something else entirely. To be precise, the F.D.A. reviewers said that other than its contribution to calories, “no conclusive evidence on sugars demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.” This is another way of saying that the evidence by no means refuted the kinds of claims that Lustig is making now and other researchers were making then, just that it wasn’t definitive or unambiguous.

What we have to keep in mind, says Walter Glinsmann, the F.D.A. administrator who was the primary author on the 1986 report and who now is an adviser to the Corn Refiners Association, is that sugar and high-fructose corn syrup might be toxic, as Lustig argues, but so might any substance if it’s consumed in ways or in quantities that are unnatural for humans. The question is always at what dose does a substance go from being harmless to harmful? How much do we have to consume before this happens?

When Glinsmann and his F.D.A. co-authors decided no conclusive evidence demonstrated harm at the levels of sugar then being consumed, they estimated those levels at 40 pounds per person per year beyond what we might get naturally in fruits and vegetables — 40 pounds per person per year of “added sugars” as nutritionists now call them. This is 200 calories per day of sugar, which is less than the amount in a can and a half of Coca-Cola or two cups of apple juice. If that’s indeed all we consume, most nutritionists today would be delighted, including Lustig.

But 40 pounds per year happened to be 35 pounds less than what Department of Agriculture analysts said we were consuming at the time — 75 pounds per person per year — and the U.S.D.A. estimates are typically considered to be the most reliable. By the early 2000s, according to the U.S.D.A., we had increased our consumption to more than 90 pounds per person per year.

That this increase happened to coincide with the current epidemics of obesity and diabetes is one reason that it’s tempting to blame sugars — sucrose and high-fructose corn syrup — for the problem. In 1980, roughly one in seven Americans was obese, and almost six million were diabetic, and the obesity rates, at least, hadn’t changed significantly in the 20 years previously. By the early 2000s, when sugar consumption peaked, one in every three Americans was obese, and 14 million were diabetic.

This correlation between sugar consumption and diabetes is what defense attorneys call circumstantial evidence. It’s more compelling than it otherwise might be, though, because the last time sugar consumption jumped markedly in this country, it was also associated with a diabetes epidemic.

In the early 20th century, many of the leading authorities on diabetes in North America and Europe (including Frederick Banting, who shared the 1923 Nobel Prize for the discovery of insulin) suspected that sugar causes diabetes based on the observation that the disease was rare in populations that didn’t consume refined sugar and widespread in those that did. In 1924, Haven Emerson, director of the institute of public health at Columbia University, reported that diabetes deaths in New York City had increased as much as 15-fold since the Civil War years, and that deaths increased as much as fourfold in some U.S. cities between 1900 and 1920 alone. This coincided, he noted, with an equally significant increase in sugar consumption — almost doubling from 1890 to the early 1920s — with the birth and subsequent growth of the candy and soft-drink industries.

Emerson’s argument was countered by Elliott Joslin, a leading authority on diabetes, and Joslin won out. But his argument was fundamentally flawed. Simply put, it went like this: The Japanese eat lots of rice, and Japanese diabetics are few and far between; rice is mostly carbohydrate, which suggests that sugar, also a carbohydrate, does not cause diabetes. But sugar and rice are not identical merely because they’re both carbohydrates. Joslin could not know at the time that the fructose content of sugar affects how we metabolize it.

Joslin was also unaware that the Japanese ate little sugar. In the early 1960s, the Japanese were eating as little sugar as Americans were a century earlier, maybe less, which means that the Japanese experience could have been used to support the idea that sugar causes diabetes. Still, with Joslin arguing in edition after edition of his seminal textbook that sugar played no role in diabetes, it eventually took on the aura of undisputed truth.

Until Lustig came along, the last time an academic forcefully put forward the sugar-as-toxin thesis was in the 1970s, when John Yudkin, a leading authority on nutrition in the United Kingdom, published a polemic on sugar called “Sweet and Dangerous.” Through the 1960s Yudkin did a series of experiments feeding sugar and starch to rodents, chickens, rabbits, pigs and college students. He found that the sugar invariably raised blood levels of triglycerides (a technical term for fat), which was then, as now, considered a risk factor for heart disease. Sugar also raised insulin levels in Yudkin’s experiments, which linked sugar directly to type 2 diabetes. Few in the medical community took Yudkin’s ideas seriously, largely because he was also arguing that dietary fat and saturated fat were harmless. This set Yudkin’s sugar hypothesis directly against the growing acceptance of the idea, prominent to this day, that dietary fat was the cause of heart disease, a notion championed by the University of Minnesota nutritionist Ancel Keys.

A common assumption at the time was that if one hypothesis was right, then the other was most likely wrong. Either fat caused heart disease by raising cholesterol, or sugar did by raising triglycerides. “The theory that diets high in sugar are an important cause of atherosclerosis and heart disease does not have wide support among experts in the field, who say that fats and cholesterol are the more likely culprits,” as Jane E. Brody wrote in The Times in 1977.

At the time, many of the key observations cited to argue that dietary fat caused heart disease actually support the sugar theory as well. During the Korean War, pathologists doing autopsies on American soldiers killed in battle noticed that many had significant plaques in their arteries, even those who were still teenagers, while the Koreans killed in battle did not. The atherosclerotic plaques in the Americans were attributed to the fact that they ate high-fat diets and the Koreans ate low-fat. But the Americans were also eating high-sugar diets, while the Koreans, like the Japanese, were not.

In 1970, Keys published the results of a landmark study in nutrition known as the Seven Countries Study. Its results were perceived by the medical community and the wider public as compelling evidence that saturated-fat consumption is the best dietary predictor of heart disease. But sugar consumption in the seven countries studied was almost equally predictive. So it was possible that Yudkin was right, and Keys was wrong, or that they could both be right. The evidence has always been able to go either way.

European clinicians tended to side with Yudkin; Americans with Keys. The situation wasn’t helped, as one of Yudkin’s colleagues later told me, by the fact that “there was quite a bit of loathing” between the two nutritionists themselves. In 1971, Keys published an article attacking Yudkin and describing his evidence against sugar as “flimsy indeed.” He treated Yudkin as a figure of scorn, and Yudkin never managed to shake the portrayal.

By the end of the 1970s, any scientist who studied the potentially deleterious effects of sugar in the diet, according to Sheldon Reiser, who did just that at the U.S.D.A.’s Carbohydrate Nutrition Laboratory in Beltsville, Md., and talked about it publicly, was endangering his reputation. “Yudkin was so discredited,” Reiser said to me. “He was ridiculed in a way. And anybody else who said something bad about sucrose, they’d say, ‘He’s just like Yudkin.’ ”

What has changed since then, other than Americans getting fatter and more diabetic? It wasn’t so much that researchers learned anything particularly new about the effects of sugar or high-fructose corn syrup in the human body. Rather the context of the science changed: physicians and medical authorities came to accept the idea that a condition known as metabolic syndrome is a major, if not the major, risk factor for heart disease and diabetes. The Centers for Disease Control and Prevention now estimate that some 75 million Americans have metabolic syndrome. For those who have heart attacks, metabolic syndrome will very likely be the reason.

The first symptom doctors are told to look for in diagnosing metabolic syndrome is an expanding waistline. This means that if you’re overweight, there’s a good chance you have metabolic syndrome, and this is why you’re more likely to have a heart attack or become diabetic (or both) than someone who’s not. Although lean individuals, too, can have metabolic syndrome, and they are at greater risk of heart disease and diabetes than lean individuals without it.

Having metabolic syndrome is another way of saying that the cells in your body are actively ignoring the action of the hormone insulin — a condition known technically as being insulin-resistant. Because insulin resistance and metabolic syndrome still get remarkably little attention in the press (certainly compared with cholesterol), let me explain the basics.

You secrete insulin in response to the foods you eat — particularly the carbohydrates — to keep blood sugar in control after a meal. When your cells are resistant to insulin, your body (your pancreas, to be precise) responds to rising blood sugar by pumping out more and more insulin. Eventually the pancreas can no longer keep up with the demand or it gives in to what diabetologists call “pancreatic exhaustion.” Now your blood sugar will rise out of control, and you’ve got diabetes.

Not everyone with insulin resistance becomes diabetic; some continue to secrete enough insulin to overcome their cells’ resistance to the hormone. But having chronically elevated insulin levels has harmful effects of its own — heart disease, for one. A result is higher triglyceride levels and blood pressure, lower levels of HDL cholesterol (the “good cholesterol”), further worsening the insulin resistance — this is metabolic syndrome.

When physicians assess your risk of heart disease these days, they will take into consideration your LDL cholesterol (the bad kind), but also these symptoms of metabolic syndrome. The idea, according to Scott Grundy, a University of Texas Southwestern Medical Center nutritionist and the chairman of the panel that produced the last edition of the National Cholesterol Education Program guidelines, is that heart attacks 50 years ago might have been caused by high cholesterol — particularly high LDL cholesterol — but since then we’ve all gotten fatter and more diabetic, and now it’s metabolic syndrome that’s the more conspicuous problem.

This raises two obvious questions. The first is what sets off metabolic syndrome to begin with, which is another way of asking, What causes the initial insulin resistance? There are several hypotheses, but researchers who study the mechanisms of insulin resistance now think that a likely cause is the accumulation of fat in the liver. When studies have been done trying to answer this question in humans, says Varman Samuel, who studies insulin resistance at Yale School of Medicine, the correlation between liver fat and insulin resistance in patients, lean or obese, is “remarkably strong.” What it looks like, Samuel says, is that “when you deposit fat in the liver, that’s when you become insulin-resistant.”

That raises the other obvious question: What causes the liver to accumulate fat in humans? A common assumption is that simply getting fatter leads to a fatty liver, but this does not explain fatty liver in lean people. Some of it could be attributed to genetic predisposition. But harking back to Lustig, there’s also the very real possibility that it is caused by sugar.

As it happens, metabolic syndrome and insulin resistance are the reasons that many of the researchers today studying fructose became interested in the subject to begin with. If you want to cause insulin resistance in laboratory rats, says Gerald Reaven, the Stanford University diabetologist who did much of the pioneering work on the subject, feeding them diets that are mostly fructose is an easy way to do it. It’s a “very obvious, very dramatic” effect, Reaven says.

By the early 2000s, researchers studying fructose metabolism had established certain findings unambiguously and had well-established biochemical explanations for what was happening. Feed animals enough pure fructose or enough sugar, and their livers convert the fructose into fat — the saturated fatty acid, palmitate, to be precise, that supposedly gives us heart disease when we eat it, by raising LDL cholesterol. The fat accumulates in the liver, and insulin resistance and metabolic syndrome follow.

Michael Pagliassotti, a Colorado State University biochemist who did many of the relevant animal studies in the late 1990s, says these changes can happen in as little as a week if the animals are fed sugar or fructose in huge amounts — 60 or 70 percent of the calories in their diets. They can take several months if the animals are fed something closer to what humans (in America) actually consume — around 20 percent of the calories in their diet. Stop feeding them the sugar, in either case, and the fatty liver promptly goes away, and with it the insulin resistance.

Similar effects can be shown in humans, although the researchers doing this work typically did the studies with only fructose — as Luc Tappy did in Switzerland or Peter Havel and Kimber Stanhope did at the University of California, Davis — and pure fructose is not the same thing as sugar or high-fructose corn syrup. When Tappy fed his human subjects the equivalent of the fructose in 8 to 10 cans of Coke or Pepsi a day — a “pretty high dose,” he says —– their livers would start to become insulin-resistant, and their triglycerides would go up in just a few days. With lower doses, Tappy says, just as in the animal research, the same effects would appear, but it would take longer, a month or more.

Despite the steady accumulation of research, the evidence can still be criticized as falling far short of conclusive. The studies in rodents aren’t necessarily applicable to humans. And the kinds of studies that Tappy, Havel and Stanhope did — having real people drink beverages sweetened with fructose and comparing the effect with what happens when the same people or others drink beverages sweetened with glucose — aren’t applicable to real human experience, because we never naturally consume pure fructose. We always take it with glucose, in the nearly 50-50 combinations of sugar or high-fructose corn syrup. And then the amount of fructose or sucrose being fed in these studies, to the rodents or the human subjects, has typically been enormous.

This is why the research reviews on the subject invariably conclude that more research is necessary to establish at what dose sugar and high-fructose corn syrup start becoming what Lustig calls toxic. “There is clearly a need for intervention studies,” as Tappy recently phrased it in the technical jargon of the field, “in which the fructose intake of high-fructose consumers is reduced to better delineate the possible pathogenic role of fructose. At present, short-term-intervention studies, however, suggest that a high-fructose intake consisting of soft drinks, sweetened juices or bakery products can increase the risk of metabolic and cardiovascular diseases.”

In simpler language, how much of this stuff do we have to eat or drink, and for how long, before it does to us what it does to laboratory rats? And is that amount more than we’re already consuming?

Unfortunately, we’re unlikely to learn anything conclusive in the near future. As Lustig points out, sugar and high-fructose corn syrup are certainly not “acute toxins” of the kind the F.D.A. typically regulates and the effects of which can be studied over the course of days or months. The question is whether they’re “chronic toxins,” which means “not toxic after one meal, but after 1,000 meals.” This means that what Tappy calls “intervention studies” have to go on for significantly longer than 1,000 meals to be meaningful.

At the moment, the National Institutes of Health are supporting surprisingly few clinical trials related to sugar and high-fructose corn syrup in the U.S. All are small, and none will last more than a few months. Lustig and his colleagues at U.C.S.F. — including Jean-Marc Schwarz, whom Tappy describes as one of the three best fructose biochemists in the world — are doing one of these studies. It will look at what happens when obese teenagers consume no sugar other than what they might get in fruits and vegetables. Another study will do the same with pregnant women to see if their babies are born healthier and leaner.

Only one study in this country, by Havel and Stanhope at the University of California, Davis, is directly addressing the question of how much sugar is required to trigger the symptoms of insulin resistance and metabolic syndrome. Havel and Stanhope are having healthy people drink three sugar- or H.F.C.S.-sweetened beverages a day and then seeing what happens. The catch is that their study subjects go through this three-beverage-a-day routine for only two weeks. That doesn’t seem like a very long time — only 42 meals, not 1,000 — but Havel and Stanhope have been studying fructose since the mid-1990s, and they seem confident that two weeks is sufficient to see if these sugars cause at least some of the symptoms of metabolic syndrome.

So the answer to the question of whether sugar is as bad as Lustig claims is that it certainly could be. It very well may be true that sugar and high-fructose corn syrup, because of the unique way in which we metabolize fructose and at the levels we now consume it, cause fat to accumulate in our livers followed by insulin resistance and metabolic syndrome, and so trigger the process that leads to heart disease, diabetes and obesity. They could indeed be toxic, but they take years to do their damage. It doesn’t happen overnight. Until long-term studies are done, we won’t know for sure.

One more question still needs to be asked, and this is what my wife, who has had to live with my journalistic obsession on this subject, calls the Grinch-trying-to-steal-Christmas problem. What are the chances that sugar is actually worse than Lustig says it is?

One of the diseases that increases in incidence with obesity, diabetes and metabolic syndrome is cancer. This is why I said earlier that insulin resistance may be a fundamental underlying defect in many cancers, as it is in type 2 diabetes and heart disease. The connection between obesity, diabetes and cancer was first reported in 2004 in large population studies by researchers from the World Health Organization’s International Agency for Research on Cancer. It is not controversial. What it means is that you are more likely to get cancer if you’re obese or diabetic than if you’re not, and you’re more likely to get cancer if you have metabolic syndrome than if you don’t.

This goes along with two other observations that have led to the well-accepted idea that some large percentage of cancers are caused by our Western diets and lifestyles. This means they could actually be prevented if we could pinpoint exactly what the problem is and prevent or avoid that.

One observation is that death rates from cancer, like those from diabetes, increased significantly in the second half of the 19th century and the early decades of the 20th. As with diabetes, this observation was accompanied by a vigorous debate about whether those increases could be explained solely by the aging of the population and the use of new diagnostic techniques or whether it was really the incidence of cancer itself that was increasing. “By the 1930s,” as a 1997 report by the World Cancer Research Fund International and the American Institute for Cancer Research explained, “it was apparent that age-adjusted death rates from cancer were rising in the U.S.A.,” which meant that the likelihood of any particular 60-year-old, for instance, dying from cancer was increasing, even if there were indeed more 60-years-olds with each passing year.

The second observation was that malignant cancer, like diabetes, was a relatively rare disease in populations that didn’t eat Western diets, and in some of these populations it appeared to be virtually nonexistent. In the 1950s, malignant cancer among the Inuit, for instance, was still deemed sufficiently rare that physicians working in northern Canada would publish case reports in medical journals when they did diagnose a case.

In 1984, Canadian physicians published an analysis of 30 years of cancer incidence among Inuit in the western and central Arctic. While there had been a “striking increase in the incidence of cancers of modern societies” including lung and cervical cancer, they reported, there were still “conspicuous deficits” in breast-cancer rates. They could not find a single case in an Inuit patient before 1966; they could find only two cases between 1967 and 1980. Since then, as their diet became more like ours, breast cancer incidence has steadily increased among the Inuit, although it’s still significantly lower than it is in other North American ethnic groups. Diabetes rates in the Inuit have also gone from vanishingly low in the mid-20th century to high today.

Now most researchers will agree that the link between Western diet or lifestyle and cancer manifests itself through this association with obesity, diabetes and metabolic syndrome — i.e., insulin resistance. This was the conclusion, for instance, of a 2007 report published by the World Cancer Research Fund and the American Institute for Cancer Research — “Food, Nutrition, Physical Activity and the Prevention of Cancer.”

So how does it work? Cancer researchers now consider that the problem with insulin resistance is that it leads us to secrete more insulin, and insulin (as well as a related hormone known as insulin-like growth factor) actually promotes tumor growth.

As it was explained to me by Craig Thompson, who has done much of this research and is now president of Memorial Sloan-Kettering Cancer Center in New York, the cells of many human cancers come to depend on insulin to provide the fuel (blood sugar) and materials they need to grow and multiply. Insulin and insulin-like growth factor (and related growth factors) also provide the signal, in effect, to do it. The more insulin, the better they do. Some cancers develop mutations that serve the purpose of increasing the influence of insulin on the cell; others take advantage of the elevated insulin levels that are common to metabolic syndrome, obesity and type 2 diabetes. Some do both. Thompson believes that many pre-cancerous cells would never acquire the mutations that turn them into malignant tumors if they weren’t being driven by insulin to take up more and more blood sugar and metabolize it.

What these researchers call elevated insulin (or insulin-like growth factor) signaling appears to be a necessary step in many human cancers, particularly cancers like breast and colon cancer. Lewis Cantley, director of the Cancer Center at Beth Israel Deaconess Medical Center at Harvard Medical School, says that up to 80 percent of all human cancers are driven by either mutations or environmental factors that work to enhance or mimic the effect of insulin on the incipient tumor cells. Cantley is now the leader of one of five scientific “dream teams,” financed by a national coalition called Stand Up to Cancer, to study, in the case of Cantley’s team, precisely this link between a specific insulin-signaling gene (known technically as PI3K) and tumor development in breast and other cancers common to women.

Most of the researchers studying this insulin/cancer link seem concerned primarily with finding a drug that might work to suppress insulin signaling in incipient cancer cells and so, they hope, inhibit or prevent their growth entirely. Many of the experts writing about the insulin/cancer link from a public health perspective — as in the 2007 report from the World Cancer Research Fund and the American Institute for Cancer Research — work from the assumption that chronically elevated insulin levels and insulin resistance are both caused by being fat or by getting fatter. They recommend, as the 2007 report did, that we should all work to be lean and more physically active, and that in turn will help us prevent cancer.

But some researchers will make the case, as Cantley and Thompson do, that if something other than just being fatter is causing insulin resistance to begin with, that’s quite likely the dietary cause of many cancers. If it’s sugar that causes insulin resistance, they say, then the conclusion is hard to avoid that sugar causes cancer — some cancers, at least — radical as this may seem and despite the fact that this suggestion has rarely if ever been voiced before publicly. For just this reason, neither of these men will eat sugar or high-fructose corn syrup, if they can avoid it.

“I have eliminated refined sugar from my diet and eat as little as I possibly can,” Thompson told me, “because I believe ultimately it’s something I can do to decrease my risk of cancer.” Cantley put it this way: “Sugar scares me.”

Sugar scares me too, obviously. I’d like to eat it in moderation. I’d certainly like my two sons to be able to eat it in moderation, to not overconsume it, but I don’t actually know what that means, and I’ve been reporting on this subject and studying it for more than a decade. If sugar just makes us fatter, that’s one thing. We start gaining weight, we eat less of it. But we are also talking about things we can’t see — fatty liver, insulin resistance and all that follows. Officially I’m not supposed to worry because the evidence isn’t conclusive, but I do.

By GARY TAUBES (New York Times)
Published: April 13, 2011
Gary Taubes is a Robert Wood Johnson Foundation independent investigator in health policy and the author of “Why We Get Fat.”