The Power of Suggestion: What We Expect Influences Our Behavior, for Better or Worse

A lucky rabbit foot. A glass of wine. A pill. What do these things all have in common? Their effects -- whether we do well on a test, whether we mingle at the cocktail party, whether we feel better -- all depend on the power of suggestion.

In a new article, psychological scientists Maryanne Garry and Robert Michael of Victoria University of Wellington, along with Irving Kirsch of Harvard Medical School and Plymouth University, delve into the phenomenon of suggestion, exploring the intriguing relationship between suggestion, cognition, and behavior. The article is published in the June issue of Current Directions in Psychological Science, a journal of the Association for Psychological Science.

Over their research careers, Garry and Kirsch have both studied the effects of suggestion on cognition and behavior. Kirsch focused mostly on suggestion in clinical psychology, while Garry, whose work is supported by the Marsden Fund of New Zealand, was interested in the effects of suggestion on human memory. When the two got to talking, "we realized that the effects of suggestion are wider and often more surprising than many people might otherwise think," says Garry.

Across many studies, research has shown that deliberate suggestion can influence how people perform on learning and memory tasks, which products they prefer, and how they respond to supplements and medicines, which accounts for the well-known placebo effect.

But what can explain the powerful and pervasive effect that suggestion has in our lives? The answer lies in our 'response expectancies,' or the ways in which we anticipate our responses in various situations. These expectancies set us up for automatic responses that actively influence how we get to the outcome we expect. Once we anticipate a specific outcome will occur, our subsequent thoughts and behaviors will actually help to bring that outcome to fruition.

So, if a normally shy person expects that a glass of wine or two will help him loosen up at a cocktail party, he will probably feel less inhibited, approach more people, and get involved in more conversations over the course of the party. Even though he may give credit to the wine, it is clear that his expectations of how the wine would make him feel played a major role.

But it's not just deliberate suggestion that influences our thoughts and behaviors -- suggestions that are not deliberate can have the very same effects. As the authors point out, "simply observing people or otherwise making them feel special can be suggestive," a phenomenon termed the Hawthorne effect. As a result, people might work harder, or stick to a task for longer. And this case is more worrying, says Garry, "because although we might then give credit to some new drug or treatment, we don't realize that we are the ones who are actually wielding the influence."

It is for precisely this reason that the issue of unintentional suggestion has important implications for academic researchers. "In the scientific community, we need to be aware of -- and control for -- the suggestions we communicate to subjects," says Garry. The authors note that some recent failures to replicate previous research findings may ultimately be explained by such unintentional suggestion. "Recent research suggests that some of psychological science's most intriguing findings may be driven, at least in part, by suggestion and expectancies," Garry observes. "For example, a scientist who knows what the hypothesis of an experiment is might unwittingly lead subjects to produce the hypothesized effect -- for reasons that have nothing to do with the experiment itself."

And the unintended effects of suggestion aren't just restricted to the laboratory -- they cut across many real world domains, including the fields of medicine, education, and criminal justice. For example, converging evidence on eyewitness identification procedures demonstrates that the rate of false identifications is significantly higher when lineups are conducted by people who know who the suspect is than when the lineups are conducted by people who don't.

While research has provided clear evidence for the phenomenon of suggestion, there is still much more to learn about the underlying relationship between suggestion, cognition, and behavior. As the authors point out, researchers still don't know where the boundaries and limitations of these effects lie. "And, if a 'real' treatment and a 'suggestion' lead to a similar outcome, what differentiates between the two?" says Garry. Understanding these issues has important real world implications. "If we can harness the power of suggestion, we can improve people's lives."

Source: Association for Psychological Science [June 06, 2012]

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Statistical Model Attempting to Estimate Level of Alcohol Consumption That Is 'Optimal' for Health

Cutting the amount we drink to just over half a unit a day could save 4,600 lives a year in England, according to a modelling study by Oxford University researchers published in the journal BMJ Open.

Half a unit of alcohol is as little as a quarter of a glass of wine, or a quarter of a pint [Credit: © G.G. Lattek / Fotolia]

Scientists have carried out a complex analysis in an attempt to determine the "optimal" level of alcohol consumption that is associated with the lowest rates of chronic disease in the UK. They conclude that the intake of about one-half of a typical drink per day would result in the healthiest outcomes, and the authors conclude that the recommended alcohol intake for the UK should be reduced from the current advised level of drinking.

Half a unit of alcohol is as little as a quarter of a glass of wine, or a quarter of a pint. That's much lower than current government recommendations of between 3 to 4 units a day for men and 2-3 units for women.

The researchers set out to find the optimum daily amount of alcohol that would see fewest deaths across England from a whole range of diseases connected to drink. Previous studies have often looked at the separate effects of alcohol on heart disease, liver disease or cancers in isolation.

'Although there is good evidence that moderate alcohol consumption protects against heart disease, when all of the chronic disease risks are balanced against each other, the optimal consumption level is much lower than many people believe,' says lead author Dr Melanie Nichols of the BHF Health Promotion Research Group in the Department of Public Health at Oxford University.

The team used a mathematical model to assess what impact changing average alcohol consumption would have on deaths from 11 conditions known to be at least partially linked to drink.

These included coronary heart disease, stroke, high blood pressure, diabetes, cirrhosis of the liver, epilepsy, and five cancers. Over 170,000 people in England died from these 11 conditions in 2006, and ill health linked to alcohol is estimated to cost the NHS in England £3.3 billion every year.

The researchers used information from the 2006 General Household Survey on levels of alcohol consumption among adults in England. They combined this with the disease risks for differing levels of alcohol consumption as established in large analyses of published research.

They found that just over half a unit of alcohol a day was the optimal level of consumption among current drinkers.

They calculate this level of drinking would prevent around 4,579 premature deaths, or around 3% of all deaths from the 11 conditions.

The number of deaths from heart disease would increase by 843, but this would be more than offset by around 2,600 fewer cancer deaths and almost 3,000 fewer liver cirrhosis deaths.

'Moderating your alcohol consumption overall, and avoiding heavy-drinking episodes, is one of several things, alongside a healthy diet and regular physical activity, that you can do to reduce your risk of dying early of chronic diseases,' says Dr Nichols.

She adds: 'We are not telling people what to do, we are just giving them the best balanced information about the different health effects of alcohol consumption, so that they can make an informed decision about how much to drink.

'People who justify their drinking with the idea that it is good for heart disease should also consider how alcohol is increasing their risk of other chronic diseases. A couple of pints or a couple of glasses of wine per day is not a healthy option.'

Although this study in BMJ Open did not look at patterns of drinking, Dr Nichols says: 'Regardless of your average intake, if you want to have the best possible health, it is also very important to avoid episodes of heavy drinking ("binge drinking") as there is very clear evidence that this will increase your risks of many diseases, as well as your risk of injuries.'

Source: University of Oxford [June 06, 2012]

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To Quit Smoking, Try Eating More Veggies and Fruits

If you're trying to quit smoking, eating more fruits and vegetables may help you quit and stay tobacco-free for longer, according to a new study published online by University at Buffalo public health researchers.

If you're trying to quit smoking, eating more fruits and vegetables may help you quit and stay tobacco-free for longer [Credit: © taviphoto / Fotolia]

The paper, in the journal Nicotine and Tobacco Research, is the first longitudinal study on the relationship between fruit and vegetable consumption and smoking cessation.

The authors, from UB's School of Public Health and Health Professions, surveyed 1,000 smokers aged 25 and older from around the country, using random-digit dialing telephone interviews. They followed up with the respondents fourteen months later, asking them if they had abstained from tobacco use during the previous month.

"Other studies have taken a snapshot approach, asking smokers and nonsmokers about their diets," says Gary A. Giovino, PhD, chair of the Department of Community Health and Health Behavior at UB. "We knew from our previous work that people who were abstinent from cigarettes for less than six months consumed more fruits and vegetables than those who still smoked. What we didn't know was whether recent quitters increased their fruit and vegetable consumption or if smokers who ate more fruits and vegetables were more likely to quit."

The UB study found that smokers who consumed the most fruit and vegetables were three times more likely to be tobacco-free for at least 30 days at follow-up 14 months later than those consuming the lowest amount of fruits and vegetables. These findings persisted even when adjustments were made to take into account age, gender, race/ethnicity, education, household income and health orientation.

They also found that smokers with higher fruit and vegetable consumption smoked fewer cigarettes per day, waited longer to smoke their first cigarette of the day and scored lower on a common test of nicotine dependence.

"We may have identified a new tool that can help people quit smoking," says Jeffrey P. Haibach, MPH, first author on the paper and graduate research assistant in the UB Department of Community Health and Health Behavior. "Granted, this is just an observational study, but improving one's diet may facilitate quitting."

Several explanations are possible, such as less nicotine dependence for people who consume a lot of fruits and vegetables or the fact that higher fiber consumption from fruits and vegetables make people feel fuller.

"It is also possible that fruits and vegetables give people more of a feeling of satiety or fullness so that they feel less of a need to smoke, since smokers sometimes confuse hunger with an urge to smoke," explains Haibach.

And unlike some foods which are known to enhance the taste of tobacco, such as meats, caffeinated beverages and alcohol, fruits and vegetables do not enhance the taste of tobacco.

"Foods like fruit and vegetables may actually worsen the taste of cigarettes," says Haibach.

While smoking rates in the U.S. continue to decline, Giovino notes, the rate of that decline has slowed during the past decade or so. "Nineteen percent of Americans still smoke cigarettes, but most of them want to quit," he says.

Haibach adds: "It's possible that an improved diet could be an important item to add to the list of measures to help smokers quit. We certainly need to continue efforts to encourage people to quit and help them succeed, including proven approaches like quitlines, policies such as tobacco tax increases and smoke-free laws, and effective media campaigns."

The UB researchers caution that more research is needed to determine if these findings replicate and if they do, to identify the mechanisms that explain how fruit and vegetable consumption may help smokers quit. They also see a need for research on other dietary components and smoking cessation.

Gregory G. Homish, PhD, assistant professor in the UB Department of Community Health and Health Behavior, also is a co-author.

Funding was provided by the Robert Wood Johnson Foundation and LegacyA®.

Source: University at Buffalo [June 06, 2012]

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Are You a Facebook Addict?

Are you a social media enthusiast or simply a Facebook addict? Researchers from Norway have developed a new instrument to measure Facebook addiction, the Bergen Facebook Addiction Scale.

More and more people get addicted to social media, such as Facebook. Researchers at University of Bergen have created a scale to measure Facebook addiction [Credit: Colourbox]

"The use of Facebook has increased rapidly. We are dealing with a subdivision of Internet addiction connected to social media," Doctor of Psychology Cecilie Schou Andreassen says about the study, which is the first of its kind worldwide.

Andreassen heads the research project “Facebook Addiction” at the University of Bergen (UiB). An article about the results has just been published in the renowned journal Psychological Reports. She has clear views as to why some people develop Facebook dependency.

"It occurs more regularly among younger than older users. We have also found that people who are anxious and socially insecure use Facebook more than those with lower scores on those traits, probably because those who are anxious find it easier to communicate via social media than face-to-face," Andreassen says.

People who are organised and more ambitious tend to be less at risk from Facebook addiction. They will often use social media as an integral part of work and networking.

"Our research also indicates that women are more at risk of developing Facebook addiction, probably due to the social nature of Facebook," Andreassen says.

According to Andreassen, the research also shows that Facebook addiction was related to extraversion. People with high scores on the new scale further tend to have a somewhat delayed sleep-wake rhythm.

Six warning signs

As Facebook has become as ubiquitous as television in our everyday lives, it is becoming increasingly difficult for many people to know if they are addicted to social media. Andreassen’s study shows that the symptoms of Facebook addiction resemble those of drug addiction, alcohol addiction, and chemical substance addiction.

The Bergen Facebook Addiction Scale is based on six basic criteria, where all items are scored on the following scale: (1) Very rarely, (2) Rarely, (3) Sometimes, (4) Often, and (5) Very often:
 

• You spend a lot of time thinking about Facebook or plan use of Facebook.

• You feel an urge to use Facebook more and more.

• You use Facebook in order to forget about personal problems.

• You have tried to cut down on the use of Facebook without success.

• You become restless or troubled if you are prohibited from using Facebook.

• You use Facebook so much that it has had a negative impact on your job/studies.

Andreassen’s study shows that scoring “often” or “always” on at least four of the seven items may suggest that you are addicted to Facebook.

About the Scale

In January 2011, 423 students – 227 women and 196 men – participated in tests for the Bergen Facebook Addiction Scale. The scale can facilitate treatment research, clinical assessment and can be used for the estimation of Facebook addiction prevalence in the general population worldwide.

The Bergen Facebook Addiction Scale has been developed at the Faculty of Psychology, University of Bergen in collaboration with the Bergen Clinics Foundation, Norway. The researchers involved are also working with instruments measuring other addictions, such as the recently introduced Bergen Work Addiction Scale.

Author: Sverre Ole Dronen | Source: University of Bergen [May 07, 2012]

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Cocaine and the Teen Brain: New Insights Into Addiction

When first exposed to cocaine, the adolescent brain launches a strong defensive reaction designed to minimize the drug's effects, Yale and other scientists have found. Now two new studies by a Yale team identify key genes that regulate this response and show that interfering with this reaction dramatically increases a mouse's sensitivity to cocaine. 

The findings may help explain why risk of drug abuse and addiction increase so dramatically when cocaine use begins during teenage years. 

The results were published in the Feb. 14 and Feb. 21 issues of the Journal of Neuroscience. 

Researchers including those at Yale have shown that vulnerability to cocaine is much higher in adolescence, when the brain is shifting from an explosive and plastic growth phase to more settled and refined neural connections characteristic of adults. Past studies at Yale have shown that the neurons and their synaptic connections in adolescence change shape when first exposed to cocaine through molecular pathway regulated by the gene integrin beta1, which is crucial to the development of the nervous system of vertebrates. 

"This suggests that these structural changes observed are probably protective of the neurocircuitry, an effort of the neuron to protect itself when first exposed to cocaine," said Anthony Koleske, professor of molecular biophysics and biochemistry and of neurobiology and senior author of both papers. 

In the latest study, Yale researchers report when they knocked out this pathway, mice needed approximately three times less cocaine to induce behavioral changes than mice with an intact pathway. 

The research suggests that the relative strength of the integrin beta1 pathway among individuals may explain why some cocaine users end up addicted to the drug while others escape its worst effects, Koleske theorized. 

"If you were to become totally desensitized to cocaine, there is no reason to seek the drug," he said. 

Koleske and Jane R. Taylor, professor of psychiatry and psychology and an author of the Feb. 14 paper, are teaming up with other Yale researchers to look for other genes that may play a role in protecting the brain from effects of cocaine and other drugs of abuse. 

Shannon Gourley, now of Emory University who worked with Koleske and Taylor, is lead author on the Feb. 14 paper detailing how the structural response to cocaine protects against cocaine sensitivity. Anastasia Oleveska and Michael S. Warren are other Yale authors on this paper. Warren and William D. Bradley of Yale are co-lead authors of the latest Neuroscience paper describing the role for integrin beta 1 in the control of adolescent synapse and dendrite refinement and stability. Yu-Chih Lin, Mark A. Simpson, Charles A. Greer are other Yale-affiliated authors. 

Author: Bill Hathaway | Source: Yale University [February 21, 2012]

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Smoking Zaps Healthy Bacteria In the Mouth

According to a new study, smoking causes the body to turn against its own helpful bacteria, leaving smokers more vulnerable to disease. 

Despite the daily disturbance of brushing and flossing, the mouth of a healthy person contains a stable ecosystem of healthy bacteria. New research shows that the mouth of a smoker is a much more chaotic, diverse ecosystem -- and is much more susceptible to invasion by harmful bacteria. 

As a group, smokers suffer from higher rates of oral diseases -- especially gum disease -- than do nonsmokers, which is a challenge for dentists, according to Purnima Kumar, assistant professor of periodontology at Ohio State University. She and her colleagues are involved in a multi-study investigation of the role the body's microbial communities play in preventing oral disease. 

"The smoker's mouth kicks out the good bacteria, and the pathogens are called in," said Kumar. "So they're allowed to proliferate much more quickly than they would in a non-smoking environment." 

The results suggest that dentists may have to offer more aggressive treatment for smokers and would have good reason to suggest quitting smoking, Kumar said. 

"A few hours after you're born, bacteria start forming communities called biofilms in your mouth," said Kumar. "Your body learns to live with them, because for most people, healthy biofilms keep the bad bacteria away." 

She likens a healthy biofilm to a lush, green lawn of grass. "When you change the dynamics of what goes into the lawn, like too much water or too little fertilizer," she said, "you get some of the grass dying, and weeds moving in." For smokers, the "weeds" are problem bacteria known to cause disease. 

In a new study, Kumar's team looked at how these bacterial ecosystems regrow after being wiped away. For 15 healthy nonsmokers and 15 healthy smokers, the researchers took samples of oral biofilms one, two, four and seven days after professional cleaning. 

The researchers were looking for two things when they swabbed subjects' gums. First, they wanted to see which bacteria were present by analyzing DNA signatures found in dental plaque. They also monitored whether the subjects' bodies were treating the bacteria as a threat. If so, the swab would show higher levels of cytokines, compounds the body produces to fight infection. 

The results of the study were published in the journal Infection and Immunity. 

"When you compare a smoker and nonsmoker, there's a distinct difference," said Kumar. "The first thing you notice is that the basic 'lawn,' which would normally contain thriving populations made of a just few types of helpful bacteria, is absent in smokers." 

The team found that for nonsmokers, bacterial communities regain a similar balance of species to the communities that were scraped away during cleaning. Disease-associated bacteria are largely absent, and low levels of cytokines show that the body is not treating the helpful biofilms as a threat. 

"By contrast," said Kumar, "smokers start getting colonized by pathogens -- bacteria that we know are harmful -- within 24 hours. It takes longer for smokers to form a stable microbial community, and when they do, it's a pathogen-rich community." 

Smokers also have higher levels of cytokines, indicating that the body is mounting defenses against infection. Clinically, this immune response takes the form of red, swollen gums -- called gingivitis -- that can lead to the irreversible bone loss of periodontitis. 

In smokers, however, the body is not just trying to fight off harmful bacteria. The types of cytokines in smokers' gum swabs showed the researchers that smokers' bodies were treating even healthy bacteria as threatening. 

Although they do not yet understand the mechanisms behind these results, Kumar and her team suspect that smoking is confusing the normal communication that goes on between healthy bacterial communities and their human hosts. 

Practically speaking, these findings have clear implications for patient care, according to Kumar. 

"It has to drive how we treat the smoking population," she said. "They need a more aggressive form of treatment, because even after a professional cleaning, they're still at a very high risk for getting these pathogens back in their mouths right away. 

"Dentists don't often talk to their patients about smoking cessation," she continued. "These results show that dentists should take a really active role in helping patients to get the support they need to quit." 

For Kumar, who is a practicing periodontist as well as a teaching professor, doing research has changed how she treats her patients. "I tell them about our studies, about the bacteria and the host response, and I say, 'Hey -- I'm really scared for you.' Patients have been more willing to listen, and two actually quit." 

Kumar's collaborators include Chad Matthews and Vinayak Joshi of Ohio State's College of Dentistry as well as Marko de Jager and Marcelo Aspiras of Philips Oral Healthcare. The research was sponsored by a grant from Philips Oral Healthcare. 

Author: Maureen Langlois | Source: Ohio State University [February 15, 2012]

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Moderate marijuana use doesn’t damage lung function

Occasional and low cumulative marijuana use is not associated with adverse effects on pulmonary function, a new study has found. 

Exposure to tobacco smoke causes lung damage with clinical consequences that include respiratory symptoms, chronic obstructive pulmonary disease, and lung cancer. 

Mark J. Pletcher and his colleagues from the University of California examined associations between marijuana, both current and lifetime exposure, and pulmonary function. 

The Coronary Artery Risk Development in Young Adults (CARDIA) study is a longitudinal study collecting repeated measurements of pulmonary function and smoking over 20 years (March 1985-August 2006) in a group of 5,115 men and women in 4 U. S. cities. 

Lifetime exposure to marijuana joints was expressed in joint-years, with 1 joint-year of exposure equivalent to smoking 365 joints or filled pipe bowls. Lung function was assessed by the measurements of forced expiratory volume in the first second of expiration (FEV1) and forced vital capacity (FVC), with lower measures corresponding to poorer lung function. 

More than half of participants reported current marijuana smoking, tobacco smoking, or both at 1 or more examinations. The median intensity of tobacco use in tobacco smokers was substantially higher - 8-9 cigarettes per day, than the median intensity of marijuana use in marijuana smokers -2-3 episodes in the last 30 days. 

In fully adjusted models that considered 4-level categorizations of current and lifetime exposure to tobacco and marijuana, tobacco smoking was associated with a lower FEV1 and current smoking with a lower FVC. 

In contrast, exposure to marijuana was associated with higher FVC and lifetime exposure with higher FEV1. At low lifetime exposure levels, increasing marijuana use was associated with an increase in both FEV1 and FVC. 

"With up to 7 joint-years of life-time exposure e. g., 1 joint a day for 7 years or 1 joint/week for 49 years, we found no evidence that increasing exposure to marijuana adversely affects pulmonary function," the researchers said. 

At more than 10 joint-years of lifetime exposure, there was a nonsignificant decline in FEV1, but there was a significant decline in FEV1 at more than 20 episodes of marijuana use per month. 

"Marijuana may have beneficial effects on pain control, appetite, mood, and management of other chronic symptoms. Our findings suggest that occasional use of marijuana for these or other purposes may not be associated with adverse consequences on pulmonary function," they said. 

"It is more difficult to estimate the potential effects of regular heavy use, because this pattern of use is relatively rare in our study sample; however, our findings do suggest an accelerated decline in pulmonary function with heavy use and a resulting need for caution and moderation when marijuana use is considered," the researchers added. 

The study has been recently published in JAMA. 

Source: Top News [January 11, 2012]

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Study evaluates effects of marijuana ingredients on brain functioning during visual stimuli

Different ingredients in marijuana appear to affect regions of the brain differently during brain processing functions involving responses to certain visual stimuli and tasks, according to a report in the January issue of Archives of General Psychiatry, one of the JAMA/Archives journals. 

Sagnik Bhattacharyya, M.B.B.S., M.D., Ph.D, at the Institute of Psychiatry, King's College in London, and colleagues studied 15 healthy men, who were occasional marijuana users, to examine the effects of Δ9-tetrahydrocannabinol (Δ9-THC) and cannabidiol (CBD) on regional brain function during salience processing, which is how people perceive things around them. 

The authors used functional MRI images to study each participant on three occasions after administration of Δ9-THC, CBD or placebo. Study participants performed a visual oddball task of pressing buttons according to the direction arrows on a screen were pointing, as a measure of attentional salience processing. 

"Pairwise comparisons revealed that Δ9-THC significantly increased the severity of psychotic symptoms compared with placebo and CBD whereas there was no significant difference between the CBD and placebo conditions," the authors conclude. 

Δ9-THC had a greater effect than placebo on reaction time to nonsalient relative to salient stimuli. This was associated with modulation of both prefrontal and striatal function by Δ9-THC, augmenting (increasing) activation in the former region and attenuating (weakening) it in the latter. 

"Moreover, in the present study, the magnitude of Δ9-THC's effect on response times to nonsalient stimuli was correlated with its effect on activation in the right caudate, the region where the physiological effect of Δ9-THC was linked to its induction of psychotic symptoms," the authors write. 

They conclude that "collectively, these observations suggest that Δ9-THC may increase the aberrant attribution of salience and induce psychotic symptoms through its effects on the striatum and lateral prefrontal cortex." 

When the effects of CBD were contrasted with Δ9-THC and placebo with respect to the visual task there was a "significant effect" in the left caudate with CBD augmenting (increasing) the response and Δ9-THC attenuating (weakening) it. 

"These effects suggest that CBD may also influence the effect of cannabis use on salience processing – and hence psychotic symptoms – by having an opposite effect, enhancing the appropriate response to salient stimuli," the authors wrote. 

Source: JAMA and Archives Journals [January 02, 2012]

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Researchers Create Healthier Cigarette

From a health care perspective, the best cigarette is no cigarette, but for the millions of people who try to quit smoking every year, researchers from Cornell University may have found a way to make cigarette smoking less toxic. 

Using natural antioxidant extracts in cigarette filters, the researchers were able to demonstrate that lycopene and grape seed extract drastically reduced the amount of cancer-causing free radicals passing through the filter. The research will be the 1500th article published in the ground-breaking Journal of Visualized Experiments (JoVE), the only peer-reviewed, PubMed indexed video-journal. 

"The implications of this technique can help reduce the hazardous effects of tobacco smoke," said Dr. Boris Dzilkovski, who co-authored the paper, "because free radicals are a major group of carcinogens." 

Scientists have tried to make safer cigarettes in the past. Haemoglobin (which transports oxygen in red blood cells) and activated carbon have been shown to reduce free-radicals in cigarette smoke by up to 90 percent, but because of the cost, the combination has not been successfully introduced to the market. 

JoVE Content Director, Dr. Aaron Kolski-Andreaco, is very excited to be publishing this article as the journal’s landmark 1500th article. 

"Practically, this research could lead to an alternative type of cigarette filter with a free radical scavenging additive," said Kolski-Andreaco. "It could lead to a less harmful cigarette." 

To watch the full video article, please click here: http://www.jove.com/video/3406/a-protocol-for-detecting-and-scavenging-gas-phase-free-radicals-in-mainstream-cigarette-smoke. 

Source: Journal of Visualized Experiments [January 01, 2012]

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One trait has huge impact on whether alcohol makes you aggressive

Drinking enough alcohol to become intoxicated increases aggression significantly in people who have one particular personality trait, according to new research. But people without that trait don't get any more aggressive when drunk than they would when they're sober. That trait is the ability to consider the future consequences of current actions. 

"People who focus on the here and now, without thinking about the impact on the future, are more aggressive than others when they are sober, but the effect is magnified greatly when they're drunk," said Brad Bushman, lead author of the study and professor of communication and psychology at Ohio State University. 

"If you carefully consider the consequences of your actions, it is unlikely getting drunk is going to make you any more aggressive than you usually are." 

Peter Giancola, professor of psychology, at the University of Kentucky, co-authored the paper with Bushman and led the experiments used in the study. Other co-authors were Dominic Parrott, associate professor of psychology at of Georgia State University and Robert Roth, associate professor of psychiatry, at Dartmouth Medical School. Their results appear online in the Journal of Experimental Social Psychology and will be published in a future print edition. 

Bushman said it makes sense that alcohol would make present-focused people more aggressive. 

"Alcohol has a myopic effect -- it narrows your attention to what is important to you right now. That may be dangerous to someone who already has that tendency to ignore the future consequences of their actions and who is placed in a hostile situation." 

The study involved 495 adults, with an average age of 23, who were social drinkers. Before participating, the participants were screened for any past or present drug, alcohol and psychiatric-related problems. Women were tested to ensure they weren't pregnant. 

All participants completed the "Consideration of Future Consequences scale." They indicated how much they agreed with statements like "I only act to satisfy immediate concerns, figuring the future will take care of itself." Scores on this measure determined how much participants were present-focused or future-focused. 

Half the participants were put in the alcohol group, where they received alcohol mixed with orange juice at a 1:5 ratio. The other half were given orange juice with just a tiny bit of alcohol. The rims of the glasses were also sprayed with alcohol so that they thought they were consuming a full alcoholic beverage. 

Participants in the alcohol group had a mean blood alcohol level of 0.095 just before aggression was measured and 0.105 following, meaning they were legally drunk and that their alcohol levels were rising during the measurement of their aggressive behavior. 

Those in the placebo group had mean blood alcohol levels that didn't exceed 0.015, meaning they had very little alcohol in their systems and were well below standards of intoxication. 

The aggression measure used in this study was developed in 1967 to test aggressiveness through the use of harmless but somewhat painful electric shocks. The researchers measured the participants' threshold to the electric shock pain before the experiment began to ensure that no one received a shock that exceeded what they could take. 

Each of the participants was told that he or she was competing with a same-sex opponent in a computer-based speed reaction test, with the winner delivering an electrical shock to the loser. The winner determined the intensity and the length of the shock delivered to the loser. 

In actuality, there was no opponent. There were 34 trials, and the participant "won" half of them (randomly determined). Each time they "lost," the participants received electric shocks that increased in length and intensity over the course of the trials, and the researchers measured if they retaliated in kind. 

"The participants were led to believe they were dealing with a real jerk who got more and more nasty as the experiment continued," Bushman said. "We tried to mimic what happens in real life, in that the aggression escalated as time went on." 

Results were clear, Bushman said. 

"The less people thought about the future, the more likely they were to retaliate, but especially when they were drunk. People who were present-focused and drunk shocked their opponents longer and harder than anyone else in the study," he said. 

"Alcohol didn't have much effect on the aggressiveness of people who were future-focused." 

Men were more aggressive than women overall, but the effects of alcohol and personality were similar in both sexes. In other words, women who were present-focused were still much more aggressive when drunk than were women who were future-focused, just like men. 

Bushman said the results should serve as a warning to people who live only in the moment without thinking too much about the future. 

"If you're that kind of person, you really should watch your drinking. Combining alcohol with a focus on the present can be a recipe for disaster." 

Source: Ohio State University [December 19, 2011]

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Making Big Tobacco pay smokers' health bills: lessons from the United States

Reports that Nicola Roxon plans to encourage state governments to consider legal action to recover around A$31 billion in smoking-related health-care costs from the tobacco industry highlight the incoming attorney-general’s commendable commitment to reducing the impact of smoking-related illness and mortality. 

The legacy of the US Master Settlement Agreement holds significant lessons for policy makers in Australia [Credit: Razvan Caliman]

Such litigation is a potentially powerful way of countering the tobacco industry, but has been largely limited to the United States to date. As part of preliminary work on the proposal, Roxon has brought Matthew Myers, president of the leading US tobacco control organisation, Campaign for Tobacco-Free Kids, to Australia to discuss litigation with state officials. 

Myers, as The Australian points out, advised US attorneys-general during litigation against the tobacco industry in the late 1990s, and played a key role in negotiations that resulted in the controversial 1998 Master Settlement Agreement (MSA). 

While a spokeswoman for Roxon stated that Myers had been brought in to “share his extensive experience in tobacco-related litigation” and that the minister was “heartened by the support of such an esteemed anti-tobacco expert", the MSA has, in fact, had limited impact on the tobacco industry and effectively split the tobacco control community in the United States. 

Probably best known for its requirement that Philip Morris and other leading tobacco corporations make payments of US$246 billion to those states party to the settlement over a 25-year period, the MSA remains controversial within US tobacco control and broader public health circles, and it’s imperative that Australian officials consider the circumstances surrounding its progress carefully. 

The US Master Settlement Agreement 

The MSA was the result of secret negotiations between the tobacco industry, and attorneys-general and members of the tobacco control community including Myers. Critics of the negotiations claim the tobacco industry was on the defensive in the late 1990s – facing a combination of dozens of state lawsuits, damaging insights into its long-standing knowledge of the harms of smoking, and falling stock prices – and that state lawsuits should have been allowed to go to trial. In effect, the negotiations let the industry off the ropes. 

Under the terms of the MSA, the tobacco industry paid US$246 billion, agreed to fund a national initiative to reduce smoking and accepted limited restrictions on advertising. In return, outstanding litigation was dropped by the 46 states party to the settlement, and future state-level litigation was pre-empted. 

The final terms have been described by Allan Brandt, professor of history of medicine at Harvard Medical School and author of the book The Cigarette Century, as “a pale reflection” of earlier proposed settlements. As many had predicted, tobacco corporations passed the costs of the MSA on to consumers through sharp price hikes essentially making the agreement, Brandt contends, little more than a new excise tax on cigarettes. 

Settlement results 

Ostensible marketing restrictions in the agreement contained so many loopholes that spending on cigarette advertising and promotion has, in fact, increased dramatically in the United States since 1998. Not only has the MSA had virtually no impact on tobacco industry income or marketing practice, signatory states have realised little benefit from it. 

And while it may appear impressive, the agreed multi-billion dollar payment was insufficient to cover the costs of treating smoking-related illnesses and, more significantly, there were no assurances included in the settlement that monies received by the states would be dedicated to health-care and tobacco control programs. 

In many cases these funds have disappeared into general revenues, making state politicians reliant on this unexpected income, and effectively making the states partners of the tobacco industry. As Brandt argues, any new legal challenges to the industry have become “threats to the states' cash flow”. 

Australia’s tobacco control legislation is considerably more advanced than that in the United States, so concerns that the MSA does little to curtail industry advertising are largely irrelevant here. But the legacy of the MSA does hold significant lessons for policy makers in this country assessing the advisability of mounting legal action to secure compensation for smoking-related health-care costs. 

Most importantly, the MSA demonstrates that litigation, once launched, will have to be pursued diligently and without recourse to negotiated settlements with the industry. 

The experience of US states also underlines the importance of installing a regulatory mechanism that ensures any monies recovered from the industry are used to underwrite health costs related to tobacco use. Given his central role in the MSA negotiations, Myers' best advice to Australian policy makers may well be about what not to do in future litigation. 

Author: Ross MacKenzie | Source: The Conversation [December 16, 2011]

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Cannabis harms the brain - but that's not the full story

For the first time, scientists have proven that cannabis harms the brain. But the same study challenges previously-held assumptions about use of the drug, showing that some brain irregularities predate drug use. 

Professor Dan Lubman, from Turning Point Alcohol and Drug Centre and Monash University, along with a team of researchers from Melbourne University have conducted a world-first study examining whether these brain abnormalities represent markers of vulnerability to cannabis use. 

“Previous evidence has shown that long-term heavy cannabis use is associated with alterations in regional brain volumes,” Professor Lubman said. 

“Although these changes are frequently attributed to the neurotoxic effects of cannabis, no studies have examined whether structural brain abnormalities are present before the onset of cannabis use until now.” 

To fill this void in present studies, Professor Lubman and his team recruited participants from primary schools in Melbourne, Australia, as part of a larger study examining adolescent emotional development. 

Of the 155 original participants who underwent structural magnetic resonance imaging at age 12, 121 completed a follow-up survey measuring substance use four years later. It was found that by age 16, 28 participants had commenced using cannabis. 

“This is an important developmental period to examine, because although not all individuals who initiate cannabis use during this time will go on to use heavily, early cannabis use has been associated with a range of negative outcomes later in life,” Professor Lubman said. 

Their findings revealed that youth with smaller orbitofrontal cortex (OFC) volumes, part of the frontal lobe of the brain, at age 12 were more likely to have initiated cannabis use by age 16. The volumes of other regions of the brain did not predict later cannabis use. 

“Given the lack of research in this area, we hypothesised that pre-drug use differences would be consistent with the structural abnormalities that have been found in studies of heavy users,” Professor Lubman said. 

“What we found is that only the OFC predicted later cannabis use, suggesting that this particular part of the frontal lobe increases an adolescent’s vulnerability to cannabis use. However, we also found no differences in brain volume in other parts of the brain that we have shown to be abnormal in long-term heavy cannabis users, confirming for the first time, that cannabis use is neurotoxic to these brain areas in humans.” 

The OFC plays a primary role in inhibitory control and reward-based decision making; previous studies of adolescent cannabis users have demonstrated subtle deficits in problem-solving, attention, memory and executive functions. 

“In adult cannabis users, decreased activation of the OFC has been associated with faulty decision-making, suggesting that a reduced ability to weigh the pros and costs of one’s actions might render certain individuals more prone to drug problems,” Professor Lubman said. 

“These results have important implications for understanding neurobiological predictors of cannabis use, but further research is still needed to understand their relationships with heavier patterns of use in adulthood as well as later abuse of other substances.” 

This research has been published online in Biological Psychiatry, the official journal of the Society of Biological Psychiatry. 

Source: Monash University [December 13, 2011]

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New strain of lab mice mimics human alcohol consumption patterns

A line of laboratory mice developed by a researcher from the School of Science at Indiana University-Purdue University Indianapolis drinks more alcohol than other animal models and consumes it in a fashion similar to humans: choosing alcohol over other options and binge drinking.

Credit: Robin Hutton

Animal models previously available to alcohol abuse and alcoholism researchers do not get as drunk as the new strain, unless alcohol is the only choice of fluids, or alcohol is administered by the experimenter. When given the option, previously bred mouse lines continue to drink water even when they can select alcohol. 

These new mice, selectively bred over 40 generations at the School of Science at IUPUI to prefer alcohol over all other choices, will help researchers explore new aspects of the behavioral and genetic determinants of alcoholism. 

In a study published online ahead of print in the journal Addiction Biology on Nov. 29, senior author Nicholas Grahame, associate professor of psychology in the School of Science at IUPUI, reports on the mice he has bred since 1997. The rodents reach blood-alcohol levels of more than 260 mg/dl of alcohol daily, over three times the equivalent of the human legal driving limit and the approximate consumption level that the severest human alcoholics attain. 

"The free-choice drinking demonstrated by the new mouse line provides a unique opportunity to study the excessive intake that often occurs in alcohol-dependent individuals and to explore the predisposing factors for excessive consumption, as well as the development of physiological, behavioral and toxicological outcomes following alcohol exposure," says Grahame, who is a biopsychologist specializing in alcoholism. 

According to the National Institute on Alcohol Abuse and Alcoholism, part of the National Institutes of Health, an estimated 17.6 million Americans abuse alcohol or are alcohol dependent. Alcohol abuse and alcoholism can be treated but cannot be cured. 

Mice share 80 percent of their genes with humans, so they are an excellent model to study alcoholism, a disease with a strong genetic component. The risk of developing alcoholism is known to be influenced by lifestyle. Animal models allow researchers to employ methods that they are unable to use in humans.

"This line of high-alcohol-seeking mice should be able to give us a better understanding of the basic brain mechanism involved in alcohol consumption as well as greater insight into the toxic effects on the brain, with the goal of developing therapies," said Grahame, whose research focuses on behavioral genetics and behavioral pharmacology. 

As with humans, the mice become intoxicated when the pace of alcohol consumption is faster than the liver can eliminate it. Typically it takes six or seven hours of continuous alcohol drinking for the new strain of mice to reach the highest levels of intoxication. 

Doctoral candidate Liana M. Matson is a co-author of the study. She has conducted research focusing on when the mice drink and determined that they are nocturnal drinkers. This knowledge enabled the mice's blood-alcohol levels to be tested when at their highest level.

 Undergraduate School of Science students Amy Buckingham and Nick Villalta assisted in the research by measuring intake and blood-alcohol levels in the new strain of high-alcohol-seeking mice. In a related study, they analyzed how drunk the mice became by testing how the animals performed on a balance beam.

Development of the mouse line and the Addiction Biology study, "Pharmacologically Relevant Intake During Chronic, Free-Choice Drinking Rhythms in Selectively Bred High Alcohol-Preferring Mice" were funded by NIAAA and the School of Science at IUPUI. 

Source: Indiana University [December 12, 2011]

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Erasing The ‘Memory’ Of Cocaine: A Breakthrough In Treating Addiction

Unlike many other drugs, cocaine does not trigger a physical addiction. It can however cause a psychological one in some 20% of its users, which can push them to lose control over their consumption, and can often lead to dire consequences. 

Hooked on the memory [Credit: andronicusmax]

It is also that psychological addiction that lasts even after rehab, because the brain will forever remember having taken the drug  

Now, neuroscience researchers from Geneva University may have found a way to erase that memory through a new laser technique that they have successfully tested on mice. 

The scientists focused on a part of the nervous system called the “reward circuit.” The main function of this network of brain cells is associating vital behaviors – like eating or reproducing – with feelings of pleasure. Information is transmitted between two different areas of the brain: one holds information on levels of satisfaction, and the other registers the context in which it happened. 

Cocaine abnormally raises levels in the brain of dopamine, a substance responsible for the transmission of information between both parts of the brain. That phenomenon forever marks the brain and explains why even after years of sobriety, a recovering addict can still be tempted by the drug. 

“Take someone who took cocaine in a certain place. Even sober, this person won’t be able to walk by that same place without some of his brain cells getting excited and awakening a desire to take the drug,” says Vincent Pascoli, the lead researcher. 

It is this hidden memory, mixing context and desire to use, that the researchers say can be erased. Working on mice that have ingested cocaine, they infect certain brain cells in a virus that introduces a light-sensitive protein that can be targeted by a laser. With the use of a laser, researchers were able to control brain activity and bring information transmission levels back to normal. 

The process proved a success in the short term, with the mice acting like they’d never taken cocaine in the days following the procedure. The long-term effects have yet to be tested on mice. And of course, the procedure must still be tried on humans. 

Source: Le Temps vya Worldcrunch [December 14, 2011]

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Study IDs new genetic links to impulsivity, alcohol problems in men

Being impulsive can lead us to say things we regret, buy things we really don't need, engage in behaviors that are risky and even develop troublesome addictions. But are different kinds of hastiness and rashness embedded in our DNA? A new study suggests the answer is yes -- especially if you're a man. 

The research, led by University of Nebraska-Lincoln assistant professor of psychology Scott Stoltenberg, found links between impulsivity and a rarely researched gene called NRXN3. The gene plays an important role in brain development and in how neurons function. 

The newly discovered connection, which was more prevalent among men than women in the study, may help explain certain inclinations toward alcohol or drug dependence, Stoltenberg said. 

"Impulsivity is an important underlying mechanism in addiction," he said. "Our finding that NRXN3 is part of the causal pathway toward addiction is an important step in identifying the underlying genetic architecture of this key personality trait." 

For the study, researchers measured impulsivity levels in nearly 450 participants -- 65 percent women, 35 percent men -- via a wide range of tests. Then, they compared those results with DNA samples from each participant. They found that impulsivity was significantly higher in those who regularly used tobacco or who had alcohol or drug problems. 

The results, interestingly, also came down along gender lines. In men, two connections clearly emerged; first, between a particular form of the NRXN3 gene and attentional impulsivity, and second, between another NRXN3 variant and alcohol problems. The connections for women, meanwhile, were much weaker. 

Stoltenberg said the gender-specific results are a rich area for further study. 

"We can't really say what causes these patterns of association to be different in men and women. But our findings will be critical as we continue to improve our understanding of the pathways from specific genes to health-risk behaviors," he said. 

The researchers were interested in impulsivity because the trait can predispose people to any number of behavioral problems -- addictions, behavior control, failing to plan ahead or think through consequences of actions -- and settled on the role of NXRN3 from previous, recent studies. 

While the results add important new evidence to the genetic role in impulsivity and, in turn, its role in substance abuse, researchers were careful to not claim a perfect cause-and-effect relationship. Impulsivity may interact with sensitivity to alcohol, for one example, or anxiety, for another, to create complex pathways to substance use problems in both men and women. 

"If you're working to explain how genes are associated with something like (substance) dependence, you have to connect a lot of dots," Stoltenberg said. "There's a big gap between genes and a substance use disorder. Impulsivity is one factor to such problems -- not the only factor." 

Source: University of Nebraska-Lincoln [November 16, 2011]

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The serotonin system in women's brains is damaged more readily by alcohol

After only four years of problem drinking, a significant decrease in the function of the serotonin system in women's brains can be seen. This is the system that regulates such functions as impulse control and mood. It takes 12 years before a corresponding decrease is seen in men. This is the conclusion of multidisciplinary research carried out at the Department of Psychology and the Sahlgrenska Academy at the University of Gothenburg, Sweden. 

The research group in the multidisciplinary project Gothenburg Alcohol Research Project (GARP) has studied for the first time three of the major neurotransmitter substances in the brain in a single individual. They have studied a group of women and a group of men with alcohol dependence. The results will be published in January 2012 in the journal Alcoholism: Clinical & Experimental Research. 

"We have used what is known as neuroendocrine techniques to show that it is principally the serotonergic system in the brain that is seriously impaired by alcohol. This is the system that regulates impulse control and mood, among other functions", says Kristina Berglund, scientist at the Department of Psychology and representative for the research group. 

Both men and women suffer adverse effects, but the effects arise much more rapidly in women. The results show that the function of women's serotonin system has fallen by 50% after as little as four years with problematic alcohol consumption, while it takes 12 years before the function of men's systems is halved. 

"It is important to note that the damage is just as serious in men and women, but the time courses are different. We still don't know whether the serotonin system can repair itself, but there are research results showing that other damage to the brain can heal after a certain period without alcohol", says Ulf Berggren of the Sahlgrenska Academy, University of Gothenburg.  

Source: University of Gothenburg [November 15, 2011]

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Moderate drinking and cardiovascular health: here comes the beer

Beer could stand up alongside wine regarding positive effects on cardiovascular health. This is the conclusion of a study conducted by Research Laboratories at the Fondazione di Ricerca e Cura "Giovanni Paolo II", in Campobasso, Italy. Both for wine and beer the key is moderate and regular drinking. 

The research, published today on line by the European Journal of Epidemiology, using the statistic approach of meta-analysis, pooled different scientific studies conducted worldwide in previous years to achieve a general result. This way it has been possible to examine data concerning over 200,000 people, for whom alcohol drinking habits were associated with cardiovascular disease. 

Results confirm what was already known about wine: a moderate consumption (approximately two glasses per day for men and one for women) can lower the risk of cardiovascular disease, up to 31% less when comparing to non drinkers. What this research adds are new data on beer. For the first time, in fact, evidence about dose-dependent effect is shown for this beverage. Maximum protection is observed, for a beer containing 5% of alcohol, with a consumption of slightly more than an English pint a day. 

"In our research – explains Simona Costanzo, first author of the paper - we considered wine and beer separately: you first observe a reduction in cardiovascular risk with low to moderate drinking. Then, with an increasing consumption, you can see that the advantage disappears, until the risk gets higher. The interesting part of our research is that, among the studies selected for this meta-analysis, there were 12 in which wine and beer consumption could be compared directly. Using these data we were able to observe that the risk curves for the two beverages are closely overlapping". 

But beer as well as wine, drinkers, should be cautious before toasting too much at these results. "What we are talking about – says Augusto Di Castelnuovo, head of the Statistic Unit of Research Laboratories and a pioneer in alcohol epidemiological studies - is moderate and regular drinking. I think we will never stress enough this concept. Wine or beer are part of a lifestyle. One glass can pair with healthy foods, eaten at proper time, maybe together with family of friends. There is no place for binge drinking or any other form of heavy consumption. 

"The data reported in our meta-analysis – Di Castelnuovo emphasizes- cannot be extrapolated to everybody. In young women still in their fertile age, as an example, alcohol can slightly raise the risk for some kind of cancer. This could counterbalance the positive effect on cardiovascular disease and reduce the overall benefit of alcoholic beverages on health". 

In the similarity between wine and beer regarding positive effects on cardiovascular health there is a still unanswered question: the evidence we are observing derives from alcohol alone or from other substances contained in beverages? Wine and beer are different in composition, except for alcohol, so we could think this is the main player. But they both contain polyphenols, albeit different ones. Researchers at Fondazione "Giovanni Paolo II" underline how this is something to look at more closely in the future. 

"A research like this - comments Giovanni de Gaetano, director of Research Laboratories at Fondazione "Giovanni Paolo II" – is part of a concept that our group strongly pursues: to look at people's real life. Health and disease are conditions deriving from our lifestyle. New therapies, new drugs, are extremely important. But a healthy life, with a strong attitude toward prevention, is the key element of the medicine in the years to come". 

Source: Catholic University - Campobasso [November 15, 2011]

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