'Worry' Spot in Brain Found

(HealthDay News) -- Stanford researchers report that worrying about something before it happens might do more than just create knots in your stomach.

They found that people who seemed to have higher levels of "anticipatory worry" -- judged by brain scans of activity in a part of the brain known as the anterior insula -- did better in a financial game, said study author Gregory Samanez-Larkin, a psychology graduate student at Stanford.

If the anterior insula was more active, the subjects had "a higher fidelity when it comes to making economic decisions," said Samanez-Larkin. "They were better at predicting what might happen." These volunteers learned to avoid losses when playing the same game months later, he noted.

"I wouldn't call it intelligence," he said. Instead, "it's a sort of expertise."

The anterior insula is a region buried deep inside the brain that's considered an artifact of humans' reptilian heritage. "At the very basic level, it has something to do with sensing danger or monitoring danger," explained Rajesh Miranda, an associate professor at Texas A & M Health Science Center.

But researchers haven't spent too much time on that region, because they prefer brain regions that are easier to access and understand, he said.

In the new study, Samanez-Larkin and colleagues recruited 23 subjects to play a financial game while scanners measured their brain activity. Eight to 10 months later, the subjects returned and played a similar game, although their brains weren't scanned.

The researchers then tried to find links between the brain scans and how the subjects performed in the games. "We looked in the brain for readings that were active while people were anticipating losses" in the game, Samanez-Larkin said.

The results were published in the April issue of Psychological Science.

Miranda said the study doesn't add much to existing knowledge. "It seems like it deals essentially with what's been known," he said.

Still, expanded knowledge about that particular brain region could lead to better treatments for anxiety and help researchers predict who might do a better job of handling stress, Miranda said.

Samanez-Larkin said the research could also be used to detect people who are most likely to get too many credit cards and fall into debt or fall victim to scams, because they aren't adept at processing financial information. "You could identify people who are susceptible to things like this and try to help them," he said.

More information
Check out images of various brain regions at brainexplorer.org.

One-Third of Dementia Cases Laid to Small Blood Vessel Damage

(HealthDay News) -- Small blood vessel damage caused by hypertension and diabetes may be among the leading causes of dementia, according to new research.

The findings provide an additional reason to control these common conditions, according to Dr. Thomas Montine of the University of Washington, who was to present the study Sunday at Experimental Biology 2008 in San Diego.

The autopsied brains of a third of men and women with dementia or cognitive decline showed evidence of small vessel damage -- a cumulative injury that can result from multiple small strokes caused by hypertension and diabetes. The strokes are often so small that the person notices nothing until the cumulative effect reaches critical mass, the researchers said.

Meanwhile, 45 percent of the risk for dementia was associated with pathologic changes of Alzheimer's disease. Another 10 percent risk was linked to Lewy bodies, which are neocortical structural changes that indicate a degenerative brain disease known as Lewy Body Dementia, a possible variant of Alzheimer's and/or Parkinson's disease, the study found.

The finding about small vessel disease challenges conventional wisdom and conclusions from most autopsy studies of brain aging and dementia, Montine said in a prepared statement.

The broader population sample on which the autopsy study was based may be reason for the differing results, he said. Most previous research had focused on participants in Alzheimer's disease center studies, or was limited to one gender, ethnic or professional group. The individuals in the new study were part of a large managed care program and representative of the Seattle urban and suburban area they came from: white, Asian, African-American and Hispanic, with a range of educational and professional levels.

In the study, which ran from 1994 to 2006, some participants suffered cognitive impairment and dementia, while others did not. Roughly a third of all 3,400 participants died, and autopsies were performed on the 221 who had given permission for this to be done.

More information
The American Heart Association has more about controlling high blood pressure.

Compulsive Gamblers Don't Learn From Their Mistakes

(HealthDay News) -- A form of mental rigidity that leads to compulsive behavior may explain why gambling addicts can't stop trying their luck even when they're on a losing streak, a new Italian study suggests.

It's not known what causes compulsive gambling, but it's been suggested that environmental factors and genetic predisposition play a role, affecting chemical signals in the brain, said researcher Donatella Marazziti and colleagues at the University of Pisa.

They conducted a series of neuropsychological tests on 15 male and five female pathological gamblers in an attempt to identify areas of the brain associated with the disorder. The results of the tests, which assessed problem-solving abilities, were compared to a group of healthy people.

The gamblers did well on all the tests except for the Wisconsin Card Sorting Test (WCST). In this test, the gamblers had great difficulty in finding different ways to solve each problem in the test, while the healthy participants got better with practice.

"Our findings show that in spite of normal intellectual, linguistic and visual-spatial abilities, the pathological gamblers could not learn from their mistakes to look for alternative solutions in the WCST," the study authors wrote.

This suggests that compulsive gamblers have differences in an area of the brain called the prefrontal region, which is involved in problem-solving.

"These differences might provoke a sort of cognitive 'rigidity' that predisposes a person to the development of impulsive or compulsive behavior, leading to pathological gambling," the researchers concluded.

The study was published in the March 26 issue of Clinical Practice and Epidemiology in Mental Health.

More information
The American Academy of Family Physicians has more about problem gambling.

Abdominal Fat Boosts Dementia Risk

(HealthDay News) -- A potbelly in middle age more than triples the risk of senility decades later, according to a large study that pinpoints a new link between obesity and dementia.

"The take-home message is that it's not only what you weigh, but it's where you carry your weight in midlife," said study author Rachel Whitmer, a research scientist with the Kaiser Permanente Division of Research, in Oakland, Calif.

The good news? Lose weight, and you may be able to reduce the increased risk, she said.

Researchers have been tracking the mental fallout of obesity for years. In 2005, Whitmer and her colleagues reported that people who were fatter in middle age were as much as 74 percent more likely to develop dementia as senior citizens.

An estimated 10 million American baby boomers will develop Alzheimer's disease in their lifetime, according to research released earlier this month, while another study found that more than 20 percent of seniors have memory loss not classified as dementia.

In the new study, researchers looked specifically at belly fat, checking to see if it posed a risk in people even if they were otherwise not overweight.

The study examined 6,583 Kaiser Permanente health-care plan members between the ages of 40 and 45 who had their abdominal fat measured in the late 1960s and early 1970s. The researchers followed up to see what happened to them between 1994 and 2006, when they reached their 70s and beyond.

The findings were published in the March 26 online issue of Neurology.

Overall, 16 percent of those studied developed dementia, also known as senility. Researchers found that obese people who had the most abdominal fat in their 40s were 3.6 times more likely to develop dementia than those with the least amount of abdominal fat.

People who were overweight -- a step below obese -- and had large bellies in their 40s were 2.3 times more likely to develop dementia.

Overall, 21 percent of those with high levels of belly fat developed dementia, compared to 15 percent of others, Whitmer said.

The effects of belly fat remained even when researchers adjusted their statistics to take into account the effect of conditions such as stroke and diabetes.

It's still possible that a factor other than abdominal fat may cause the higher rate of dementia. The study doesn't confirm a direct cause-and-effect relationship. Still, the findings suggest that something about abdominal body fat affects the brain independently of cardiovascular disease or diabetes, Whitmer noted.

It's not clear, however, exactly how obesity translates into reduced brain function. It may have something to do with how belly fat surrounds the body's organs and secretes hormones and toxic substances that could disrupt the way the brain functions, Whitmer speculated.

William Thies, vice president of medical and scientific relations with the Alzheimer's Association, said another theory is that the physical presence of belly fat and its compression of abdominal organs could burden the entire body, affecting the brain by increasing blood pressure and cholesterol. However, "whether there's a direct biological link between body fat and Alzheimer's has yet to be established," he said.

Whatever the cause for the connection, all hope is not lost.

"Even with moderate exercise, you can reduce that visceral fat, the fat around the organs," Whitmer said, adding that there's a lot of evidence that the roots of dementia develop years before it becomes obvious, so a change now could spell a big benefit later.

More information
To learn more about proper weight loss, visit the National Women's Health Information Center.

Scientists Spot Biochemical Sign of Depression

(HealthDay News) -- Researchers say they've discovered a biomarker for depression that could lead to a quick lab test to determine whether a particular antidepressant is making headway against the disease.

"This may be a very simple biochemical indicator for depression," said study co-author Mark Rasenick, director of the Interdisciplinary Neuroscience Program at the University of Illinois at Chicago. The test "wouldn't tell you which [medication] to start, but it would tell you if the one you're taking is working."

It may even be possible to use the test to determine whether rounds of psychotherapy are reaping any benefit, he said.

For now, however, such a test is a hypothetical, pending further exploration of the finding reported in the March edition of The Journal of Neuroscience.

At issue is whether the brain itself shows physical or chemical signs of depression.

The researchers looked at the interaction of neurotransmitters and a protein called Gs alpha. In brain cells, the protein acts like a kind of butler, passing messages from neurotransmitters on the outside and amplifying their messages, Rasenick explained.

When the protein is working properly, it's like a butler whose "hands are just flying, cooking and cleaning at the same time," he said. But when the brain is depressed, "it just sits there in the corner."

In this post-mortem study, the researchers looked at the protein in the brains of 18 depressed people who committed suicide and compared them to the brains of non-depressed people. They found the protein would have worked less effectively in the brain cells of the suicide victims.

The findings raise the prospect of a blood test that would measure within days whether antidepressants are effectively treating depression, Rasenick said.

Now, it can take several weeks for patients and psychiatrists to figure out if an antidepressant is working properly. According to Rasenick, only about 30 percent of depression patients will respond to a specific drug.

"Unfortunately, we have a very poor ability to predict which antidepressant might be more effective for any individual," said Dr. Gregory Simon, a psychiatrist and mental health researcher with Group Health Cooperative in Seattle. "There's a long history of research using patterns of symptoms or biological measures -- chemicals measured in blood or spinal fluid -- to predict response to a particular antidepressant. None of those hoped-for predictors have significant value."

Genetic tests may provide some clues, he said, and the new study suggests there might be another approach. "It would not eliminate trial-and-error, but it would reduce the waiting time with each trial. But it's a long way from a study like this one to a test that's useful to patients and doctors."

Rasenick is hopeful, however, and he said the proposed test could do more than gauge whether drugs are working. It could conceivably measure the effectiveness of talking to a therapist, study co-author Rasenick said, since psychiatrists think psychotherapy has a physical effect on the brain.

Rasenick said more research and money are needed. The study was funded by the U.S. Public Health Service and the American Foundation for Suicide Prevention.

"The next step is to partner with people who are doing large-scale studies on individuals with depression and begin to look at this," he said. "We can begin to get hundreds of people and see if we can confirm that we're right."

More information
Learn more about depression from the National Institute of Mental Health.

Weight-Loss Drug Fights Alcoholic Fatty Liver Disease

(HealthDay News) -- Mice given the weight-loss drug rimonabant became resistant to alcohol's fat-building effects in the liver, which suggests the medication may help fight alcoholic fatty liver in humans, says a U.S. study.

Alcoholism is the leading cause of liver disease in Western societies, according to background information in the study.

Rimonabant, which blocks cannabinoid receptors, is approved for weight loss in several European countries but has not been approved in the United States. Last June, a U.S. Food and Drug Administration panel recommended that rimonabant should not be given the FDA's blessing because of continuing concerns about increased risks for suicidal thoughts among some users.

In this latest study, the researchers found that mice fed a low-fat diet and ethanol showed an increase in the gene encoding the CB1 cannabinoid receptor and in liver levels of an endocannabinoid called 2-arachidonoylglycerol (2-AG). These mice developed fatty livers.

Another group of mice that received the same diet plus rimonabant did not differ from mice fed a control diet. And mice lacking CB1 receptors, either throughout the body or only in the liver, were protected from alcoholic fatty liver.

"What makes these findings particularly interesting from our perspective is that they may have practical implications," said study author George Kunos, of the U.S. National Institute on Alcohol Abuse and Alcoholism. "Treatment of animals with a [cannabinoid receptor] antagonist largely prevented alcohol's effect. It suggests that the development of fatty liver in those who use alcohol could be interfered with, or perhaps reversed, with such treatment."

The findings were published in the March issue of Cell Metabolism.

"Although alcoholic fatty liver is reversible in the early stages by cessation of drinking, this is often not feasible," the study authors wrote. "The present findings suggest that treatment with a CB1 antagonist may slow the development of fatty liver and thus prevent its progression to more severe and irreversible forms of liver disease."

Drugs that selectively act on CB1 receptors found outside of the brain might help fight fatty liver with less risk of side effects such as anxiety and depression, they said.

"Rimonabant has recently been introduced in Europe for the treatment of visceral obesity and the metabolic syndrome, which themselves are known risk factors for [liver disease]. Clinical trials testing the effectiveness of CB1 receptor blockers in the treatment of both alcoholic and nonalcoholic fatty liver and their more severe sequelae may be warranted," the researchers concluded.

More information
The American Liver Foundation has more about fatty liver.