Posts tagged neuroscience

ScienceDaily (June 7, 2012) — A study led by Karolinska Institutet in Sweden reports for the first time the positive effects of an active vaccine against Alzheimer’s disease. The new vaccine, CAD106, can prove a breakthrough in the search for a cure for this seriously debilitating dementia disease. The study is published in the scientific journal Lancet Neurology.

A study led by Karolinska Institutet in Sweden reports for the first time the positive effects of an active vaccine against Alzheimer’s disease. (Credit: © Tyler Olson / Fotolia)

Alzheimer’s disease is a complex neurological dementia disease that is the cause of much human suffering and a great cost to society. According to the World Health Organisation, dementia is the fastest growing global health epidemic of our age. The prevailing hypothesis about its cause involves APP (amyloid precursor protein), a protein that resides in the outer membrane of nerve cells and that, instead of being broken down, form a harmful substance called beta-amyloid, which accumulates as plaques and kills brain cells.

There is currently no cure for Alzheimer’s disease, and the medicines in use can only mitigate the symptoms. In the hunt for a cure, scientists are following several avenues of attack, of which vaccination is currently the most popular. The first human vaccination study, which was done almost a decade ago, revealed too many adverse reactions and was discontinued. The vaccine used in that study activated certain white blood cells (T cells), which started to attack the body’s own brain tissue.

The new treatment, which is presented in Lancet Neurology, involves active immunisation, using a type of vaccine designed to trigger the body’s immune defence against beta-amyloid. In this second clinical trial on humans, the vaccine was modified to affect only the harmful beta-amyloid. The researchers found that 80 per cent of the patients involved in the trials developed their own protective antibodies against beta-amyloid without suffering any side-effects over the three years of the study. The researchers believe that this suggests that the CAD106 vaccine is a tolerable treatment for patients with mild to moderate Alzheimer’s. Larger trials must now be conducted to confirm the CAD106 vaccine’s efficacy.

Source: Science Daily

ScienceDaily (June 7, 2012) — Researchers at Columbia University Medical Center (CUMC) have identified a brain receptor that appears to play a central role in regulating appetite. The findings, published June 7 in the online edition of Cell, could lead to new drugs for preventing or treating obesity.

"We’ve identified a receptor that is intimately involved in regulating food intake," said study leader Domenico Accili, MD, professor of Medicine at CUMC. "What is especially encouraging is that this receptor is belongs to a class of receptors that turn out to be good targets for drug development, making it a highly ‘druggable’ target. In fact, several existing medications already seem to interact with this receptor. So, it’s possible that we could have new drugs for obesity sooner rather than later."

In their search for new targets for obesity therapies, scientists have focused on the hypothalamus, a tiny brain structure that regulates appetite. Numerous studies suggest that the regulatory mechanism is concentrated in neurons that express a neuropeptide, or brain modulator, called AgRP. But the specific factors that influence AgRP expression are not known.

The CUMC researchers found new clues to appetite control by tracing the actions of insulin and leptin. Both hormones are involved in maintaining the body’s energy balance, and both are known to inhibit AgRP. “Surprisingly, blocking either the insulin or leptin signaling pathway has little effect on appetite,” says Dr. Accili. “We hypothesized that both pathways have to be blocked simultaneously in order to influence feeding behavior.”

To test their hypothesis, the researchers created a strain of mice whose AgRP neurons lack a protein that is integral to both insulin and leptin signaling. As the researchers hypothesized, removing this protein — Fox01 — had a profound effect on the animals’ appetite. “Mice that lack Fox01 ate less and were leaner than normal mice,” said lead author Hongxia Ren, PhD, associate research scientist in Medicine. “In addition, the Fox01-deficient mice had better glucose balance and leptin and insulin sensitivity — all signs of a healthier metabolism.”

Since Fox01 is a poor drug target, the researchers searched for other ways to inhibit the action of this protein. Using gene-expression profiling, they found a gene that is highly expressed in mice with normal AgRP neurons but is effectively silenced in mice with Fox01-deficient neurons. That gene is Gpr17 (for G-protein coupled receptor 17), which produces a cell-surface receptor called Gpr17.

To confirm that the receptor is involved in appetite control, the researchers injected a Gpr17 activator into normal mice, and their appetite increased. Conversely, when the mice were given a Gpr17 inhibitor, their appetite decreased. Similar injections had no effect on Fox01-deficient mice.

According to Dr. Accili, there are several reasons why Gpr17, which is also found in humans, would be a good target for anti-obesity medications. Since Grp17 is part of the so-called G-protein-coupled receptor family, it is highly druggable. About a third of all existing drugs work through G-protein-coupled receptors. In addition, the receptor is abundant in AgRP neurons but not in other neurons, which should limit unwanted drug side effects.

Source: Science Daily

ScienceDaily (June 7, 2012) — Increasing the spacing between characters and words in a text improves the speed and quality of dyslexic children’s reading, without prior training. They read 20% faster on average and make half as many errors. This is the conclusion reached by a French-Italian research team, jointly headed by Johannes Ziegler of the Laboratoire de Psychologie Cognitive (CNRS/Aix-Marseille Université).

Increasing the spacing between characters and words in a text improves the speed and quality of dyslexic children’s reading, without prior training. (Credit: © Johannes Ziegler, courtesy CNRS)

These results were published 4 June 2012 in the Proceedings of the National Academy of Science (PNAS). In parallel, the team has developed an iPad/iPhone application, available under the name “DYS.” It allows both parents and children to modify the spacing between letters and thus test the benefits of these changes on reading. This will enable researchers to collect large-scale, real time data, which they will then analyze and study.

Dyslexia is a learning disability that impairs an individual’s capacity to read and is linked to difficulty in identifying letters, syllables and words — despite suitable schooling and in the absence of intellectual or sensorial deficiencies. Dyslexia, which often causes writing problems, affects on average one child in every class and 5% of the world’s population.

In this study, the researchers tested the effects of letter spacing on the reading ability of 54 dyslexic Italian and 40 dyslexic French children aged between 8 and 14 years. The children had to read a text composed of 24 sentences, in which the spacing was either normal or wider than usual. The results showed that wider spacing enabled the children to improve their reading both in terms of speed and precision. On average, they read 20% faster and made half as many errors. This progress could stem from the fact that dyslexic children are particularly sensitive to “perceptual crowding,” in other words the visual masking of each individual letter by those surrounding it. The results of this study show that this crowding effect may be reduced by spacing letters apart.

This finding opens interesting perspectives in the field of dyslexia treatment techniques. Indeed, reading better means reading more — yet it takes one year for a dyslexic child to read what a “normal reader” reads in two days. This is because reading can be “torture” for dyslexic children, whose decoding difficulties cause to stumble, putting them off reading on a regular basis. The researchers have found a simple and efficient “trick” that helps these children break the vicious circle and correctly read more words in less time.

An iPad/iPhone application known as “DYS” has been developed in parallel with these research results by Stéphane Dufau, CNRS research engineer at the Laboratoire de Psychologie Cognitive. Available initially in French and English and downloadable free of charge from Apple Store, it enables both parents and children to adjust the spacing between letters and to test the benefits of such modifications on reading. The researchers for their part hope to be able to collect large-scale data that will allow them to quantify and analyze whether optimal spacing exists as a function of the subject’s age and reading level.

Download available: http://itunes.apple.com/us/app/dys-help-people-with-dyslexia/id529867852?mt=8

Source: Science Daily

ScienceDaily (June 6, 2012) — Even when brain injury is so subtle that it can only be detected by an ultra-sensitive imaging test, the injury might predispose soldiers in combat to post-traumatic stress disorder, according to a University of Rochester Medical Center study.

The research is important for physicians who are caring for troops in the years following deployment, as they try to untangle the symptom overlap between PTSD and mild traumatic brain injury (mild TBI) and provide the appropriate treatment. Until now, the nature of the interaction between TBI and PTSD was unclear. URMC researchers believe they are the first to find an association that can be demonstrated with advanced imaging techniques.

The study is published online by the Journal of Head Trauma Rehabilitation.

"Most people believe that, to a large extent, chronic stress from intense combat experiences triggers PTSD. Our study adds more information by suggesting that a physical force such as exposure to a bomb blast also may play a role in the genesis the syndrome," said lead author Jeffrey J. Bazarian, M.D., M.P.H., associate professor of Emergency Medicine at URMC, and a member of the 2007 Institute of Medicine committee that investigated brain injuries among war veterans.

By 2008 it was estimated that 320,000 troops suffered concussions in Iraq and Afghanistan. Bazarian’s research involved 52 war veterans from western New York who served in combat areas between 2001 and 2008. Approximately four years after their final tour of duty, researchers asked each veteran about PTSD symptoms, blast exposures, mild concussions, and combat experiences.

Researchers measured combat stress in the study participants with a standard Walter Reed Institute of Research Combat Experiences Survey, which asks about the intensity of deployment duties (such as handling or uncovering remains), exposure to explosive devices, vehicle accidents, falls or assaults, and events such as being ambushed or knowing someone who was seriously injured or killed. The investigators also performed standard MRI testing, as well as a more sensitive test called diffusion tensor imaging, or DTI. The latter has been used to detect axonal injury, a type of neuronal damage that occurs during a concussion.

Results showed that 30 of the 52 New York veterans suffered at least one mild traumatic brain injury, and seven reported having more than one. Sixty percent of the veterans were exposed to one or more explosive blasts.

All 52 veterans had one or more PTSD symptoms, and 15 met the formal criteria for PTSD, which is a devastating psychiatric illness. The severity of veterans’ PTSD symptoms correlated with the amount of axonal injury seen on the DTI scans.

In addition, five of the 52 veterans showed abnormalities on standard MRI scans, and their PTSD severity was much worse than the 46 veterans with normal MRIs.

Interestingly, PTSD severity did not correlate with the clinical diagnosis of mild TBI. This suggests that subtle brain injury can occur without producing the loss of consciousness or amnesia that is typically associated with diagnosis of mild TBI, and that this injury may make a person more vulnerable to psychiatric illness when coupled with extreme chronic stress.

"Based on our results, it looks like the only way to detect this injury is with DTI/MRI," Bazarian said. "While it may not be feasible due to costs and limited availability of some neuro-imaging tests to screen thousands of service members for brain injury, our study highlights the pressing need to develop simpler tests that are accurate and practical, that correlate with brain injury."

Source: Science Daily

ScienceDaily (June 6, 2012) — Psychoactive medications in water affect the gene expression profiles of fathead minnows in a way that mimics the gene expression patterns associated with autism spectrum disorder in genetically susceptible humans, according to research published June 6 in the open access journal PLoS ONE. These results suggest a potential environmental trigger for autism spectrum disorder in this vulnerable population, the authors write.

The researchers, led by Michael A. Thomas of Idaho State University, exposed the fish to three psychoactive pharmaceuticals — fluoxetine, a selective serotonin reuptake inhibitor, or SSR1; venlafaxine, a serotonin-norepinephrine reuptake inhibitor, and carbamazepine, used to control seizures — at concentrations comparable to the highest estimated environmental levels.

They found that the only gene expression patterns affected were those associated with idiopathic autism spectrum disorders, caused by genetic susceptibility interacting with unknown environmental triggers. These results suggest that exposure to environmental psychoactive pharmaceuticals may play a role in the development of autism spectrum disorder in genetically predisposed individuals.

Lead researcher Michael A. Thomas remarks, “While others have envisioned a causal role for psychotropic drugs in idiopathic autism, we were astonished to find evidence that this might occur at very low dosages, such as those found in aquatic systems.”

Source: Science Daily

ScienceDaily (June 6, 2012) — An Indiana University biologist has shown that natural variation in measures of the brain’s ability to process steroid hormones predicts functional variation in aggressive behavior.

Researchers studied the behaviors of free-living dark-eyed juncos during breeding season to measure variations in aggressiveness. (Credit: Image courtesy of Indiana University)

The new work led by Kimberly A. Rosvall, a postdoctoral fellow and assistant research scientist in the IU Bloomington College of Arts and Sciences’ Department of Biology, has found strong and significant relationships between aggressive behavior in free-living birds and the abundance of messenger RNA in behaviorally relevant brain areas for three major sex steroid processing molecules: androgen receptor, estrogen receptor and aromatase.

"Individual variation is the raw material of evolution, and in this study we report that free-living birds vary in aggression and that more aggressive individuals express higher levels of genes related to testosterone processing in the brain," she said. "We’ve long hypothesized that the brain’s ability to process steroids may account for individual differences in hormone-mediated behaviors, but direct demonstrations are rare, particularly in unmanipulated or free-living animals."

Rosvall said the study shows that aggression is strongly predicted by individual variation in gene expression of the molecules that initiate the genomic effects of testosterone. The new work, “Neural sensitivity to sex steroids predicts individual differences in aggression: implications for behavioral evolution,” was published June 6 in Proceedings of The Royal Society B.

The findings are among the first to show that individual variation in neural gene expression for three major sex steroid processing molecules predicts individual variation in aggressiveness in both sexes in nature, results that should have broad implications for understanding the mechanisms by which aggressive behavior may evolve.

"On the one hand, we have lots of evidence to suggest that testosterone is important in the evolution of all kinds of traits," Rosvall noted. "On the other hand, we know that individual variation is a requirement for natural selection, but individual variation in testosterone does not always predict behavior. This conundrum has led to debate among researchers about how hormone-mediated traits evolve."

To find such strong relationships between behavior and individual variation in the expression of genes related to hormone-processing is exciting because it tells scientists that evolution could shape behavior via changes in the expression of these genes, as well as via changes in testosterone levels themselves.

The team measured natural variation in aggressiveness toward the same sexes in male and female free-living dark-eyed juncos (Junco hyemalis) early in the breeding season. The dark-eyed junco is a North American sparrow that is well studied with respect to hormones, behavior and sex differences. By comparing individual differences in aggressiveness (flyovers or songs directed at intruders) to circulating levels of testosterone and to neural gene expression for the three major sex steroid processing molecules, the researchers were able to quantify measures of sensitivity to testosterone in socially relevant brain areas: the hypothalamus, the ventromedial telencephalon and the right posterior telencephalon.

Their results suggest selection could shape the evolution of aggression through changes in the expression of androgen receptor, estrogen receptor and aromatase in both males and females, to some degree independently of circulating levels of testosterone. They found, for example, that males that sing more songs at an intruder have more mRNA for aromatase and estrogen receptor in the posterior telencephalon, and also that males and females that dive-bomb an intruder more frequently have more androgen receptor, estrogen receptor and aromatase mRNA in brain tissues including the medial amygdala, an area of the brain that’s known to control aggression in rodents and other birds. mRNA are single-stranded copies of genes that are translated into protein molecules.

The work reveals there is ample variation in hormone signal and in gene expression on which selection may act to affect aggressiveness. It also establishes a prerequisite for the evolution of testosterone-mediated characteristics through changes in localized gene expression for the key molecules that process sex steroids, and suggests that trait evolution can occur with some degree of independence from circulating testosterone levels.

"Researchers have thought this was probably the case for about a hundred years, based on a lot of really important work that uses experimental manipulations like castration or hormone replacement," Rosvall said. "But very few people have looked to see if individuals actually do vary in expression of these genes, and whether this individual variation means anything, in terms of an animal’s behavior. Our work shows that it does."

The new insights into how neuroendocrine mechanisms of aggression may be modified as populations diverge into species also offer opportunities for future research, including trying to determine whether genes that are up- or down-regulated in response to environmental stimuli may be the same genes that contribute to the evolution of certain traits and characteristics.

Source: Science Daily

ScienceDaily (June 6, 2012) — New pictures from the University of Iowa show what it looks like when a person runs out of patience and loses self-control.

Brain activity when people exert self-control. (Credit: Image courtesy of University of Iowa)

A study by University of Iowa neuroscientist and neuro-marketing expert William Hedgcock confirms previous studies that show self-control is a finite commodity that is depleted by use. Once the pool has dried up, we’re less likely to keep our cool the next time we’re faced with a situation that requires self-control.

But Hedgcock’s study is the first to actually show it happening in the brain using fMRI images that scan people as they perform self-control tasks. The images show the anterior cingulate cortex (ACC) — the part of the brain that recognizes a situation in which self-control is needed and says, “Heads up, there are multiple responses to this situation and some might not be good” — fires with equal intensity throughout the task.

However, the dorsolateral prefrontal cortex (DLPFC) — the part of the brain that manages self-control and says, “I really want to do the dumb thing, but I should overcome that impulse and do the smart thing” — fires with less intensity after prior exertion of self-control.

He said that loss of activity in the DLPFC might be the person’s self-control draining away. The stable activity in the ACC suggests people have no problem recognizing a temptation. Although they keep fighting, they have a harder and harder time not giving in.

Which would explain why someone who works very hard not to take seconds of lasagna at dinner winds up taking two pieces of cake at desert. The study could also modify previous thinking that considered self-control to be like a muscle. Hedgcock says his images seem to suggest that it’s like a pool that can be drained by use then replenished through time in a lower conflict environment, away from temptations that require its use.

The researchers gathered their images by placing subjects in an MRI scanner and then had them perform two self-control tasks — the first involved ignoring words that flashed on a computer screen, while the second involved choosing preferred options. The study found the subjects had a harder time exerting self-control on the second task, a phenomenon called “regulatory depletion.” Hedgcock says that the subjects’ DLPFCs were less active during the second self-control task, suggesting it was harder for the subjects to overcome their initial response.

Hedgcock says the study is an important step in trying to determine a clearer definition of self-control and to figure out why people do things they know aren’t good for them. One possible implication is crafting better programs to help people who are trying to break addictions to things like food, shopping, drugs, or alcohol. Some therapies now help people break addictions by focusing at the conflict recognition stage and encouraging the person to avoid situations where that conflict arises. For instance, an alcoholic should stay away from places where alcohol is served.

But Hedgcock says his study suggests new therapies might be designed by focusing on the implementation stage instead. For instance, he says dieters sometimes offer to pay a friend if they fail to implement control by eating too much food, or the wrong kind of food. That penalty adds a real consequence to their failure to implement control and increases their odds of choosing a healthier alternative.

The study might also help people who suffer from a loss of self-control due to birth defect or brain injury.

"If we know why people are losing self-control, it helps us design better interventions to help them maintain control," says Hedgcock, an assistant professor in the Tippie College of Business marketing department and the UI Graduate College’s Interdisciplinary Graduate Program in Neuroscience.

Source: Science Daily

June 6, 2012 by Chris Barncard

Stress may affect brain development in children — altering growth of a specific piece of the brain and abilities associated with it — according to researchers at the University of Wisconsin–Madison.

"There has been a lot of work in animals linking both acute and chronic stress to changes in a part of the brain called the prefrontal cortex, which is involved in complex cognitive abilities like holding on to important information for quick recall and use,” says Jamie Hanson, a UW–Madison psychology graduate student. “We have now found similar associations in humans, and found that more exposure to stress is related to more issues with certain kinds of cognitive processes.”

Children who had experienced more intense and lasting stressful events in their lives posted lower scores on tests of what the researchers refer to as spatial working memory. They had more trouble navigating tests of short-term memory such as finding a token in a series of boxes, according to the study, which will be published in the June 6 issue of the Journal of Neuroscience.

Brain scans revealed that the anterior cingulate, a portion of the prefrontal cortex believed to play key roles in spatial working memory, takes up less space in children with greater exposure to very stressful situations.

"These are subtle differences, but differences related to important cognitive abilities" Hanson says.

But they maybe not irreversible differences.

"We’re not trying to argue that stress permanently scars your brain. We don’t know if and how it is that stress affects the brain," Hanson says. "We only have a snapshot — one MRI scan of each subject — and at this point we don’t understand whether this is just a delay in development or a lasting difference. It could be that, because the brains is very plastic, very able to change, that children who have experienced a great deal of stress catch up in these areas."

The researchers determined stress levels through interviews with children ages 9 to 14 and their parents. The research team, which included UW–Madison psychology professors Richard Davidson and Seth Pollak and their labs, collected expansive biographies of stressful events from slight to severe.

"Instead of focusing in on one specific type of stress, we tried to look at a range of stressors," Hanson says. "We wanted to know as much as we could, and then use all this information to later to get an idea of how challenging and chronic and intense each experience was for the child."

Interestingly, there was little correlation between cumulative life stress and age. That is, children who had several more years of life in which to experience stressful episodes were no more likely than their younger peers to have accumulated a length stress resume. Puberty, on the other hand, typically went hand-in-hand with heavier doses of stress.

The researchers, whose work was funded by the National Institutes of Health, also took note of changes in brain tissue known as white matter and gray matter. In the important brain areas that varied in volume with stress, the white and gray matter volumes were lower in tandem.

White matter, Hanson explained, is like the long-distance wiring of the brain. It connects separated parts of the brain so that they can share information. Gray matter “does the math,” Hanson says. “It takes care of the processing, using the information that gets shared along the white matter connections.”

Gray matter early in development appears to enable flexibility; children can play and excel at many different activities. But as kids age and specialize, gray matter thins. It begins to be “pruned” after puberty, while the amount of white matter grows into adulthood.

"For both gray and white matter, we actually see smaller volumes associated with high stress," Hanson says. "Those kinds of effects across different kinds of tissue, those are the things we would like to study over longer periods of time. Understanding how these areas change can give you a better picture of whether this is just a delay in development or more lasting."

More study could also show the researchers how to help children who have experienced an inordinate amount of stress.

"There are groups around the country doing working memory interventions to try to train or retrain people on this particular cognitive ability and improve performance," Hanson says. "Understanding if and how stress affects these processes could help us know whether there may be similar interventions that could aid children living in stressful conditions, and how this may affect the brain.”

Provided by University of Wisconsin-Madison

Source: medicalxpress.com

June 6, 2012

New research by scientists at the University of North Carolina School of Medicine may have pinpointed an underlying cause of the seizures that affect 90 percent of people with Angelman syndrome (AS), a neurodevelopmental disorder.

This image shows inhibitory neurons (red) and cell bodies (blue) in the cerebral cortex of an Angelman syndrome model mouse. Credit: Philpot Lab, UNC School of Medicine

Published online Thursday June 7, 2012 in the journal Neuron, researchers led by Benjamin D. Philpot, PhD, professor of cell and molecular physiology at UNC, describe how seizures in individuals with AS could be linked to an imbalance in the activity of specific types of brain cells.

"Our study indicates that a common abnormality that may apply to many neurodevelopmental disorders is an imbalance between neuronal excitation and inhibition," Philpot said. This imbalance has been observed in several genetic disorders including Fragile X and Rett syndromes, both of these, like AS, can be associated with autism.

Angelman syndrome occurs in one in 15,000 live births. The syndrome often is misdiagnosed as cerebral palsy or autism. Its characteristics, along with seizures, include cognitive delay, severe intellectual disability, lack of speech (minimal or no use of words), sleep disturbance, hand flapping and motor and balance disorders.

The most common genetic defect of the syndrome is the lack of expression of the maternally inherited allele of gene UBE3A on chromosome 15.

This loss of gene function in AS animal models has been linked to decreased release of an excitatory neurotransmitter which increases the activity of other neurons. But that seems at odds with the high seizure activity observed in AS patients. The new study may clarify this issue.

In his lab in UNC’s Neuroscience Research Center, Philpot and graduate student Michael L. Wallace, the study’s first author, explored the neurocircuitry of an Angelman syndrome mouse model. These mice show behavioral features similar to humans with AS, including seizures.

The researchers used electrophysiological methods to record excitatory and inhibitory activity from individual neurons. These involved highly precise recording electrodes, microscopic tips attached to individual neurons. “In this way you can record from precise neuron types and tell which neuron you’re recording from and what its activity is,” explained Philpot.

"You can stimulate it to drive other neurons and also record the activity on other neurons onto it."

The researchers found that neurotransmitters sent from inhibitory neurons and carrying chemical messages meant to stop excitatory neurons from increasing their activity were defective.

In addition, they found that AS model mice have a defect in their inhibitory neurons which decreases their ability to recover from high levels of activity. “One of the reasons why inhibition is so important is that it’s needed to ensure that brain activity is regulated,” Philpot said. “Inhibition plays an important role in timing of information transfer between neurons, and if the timing is messed up, as you might observe if you had a decrease in inhibition, then a lot of information is lost in that transfer.”

"We found a disproportionately large decrease in inhibition to excitation," Wallace said. "We think that the circuit we investigated is in a hyperexcitable state and may be underlying some of the epileptic problems observed in the AS animal model. This improperly regulated brain activity might also underlie cognitive impairments in AS.”

Philpot says one of their goals is to understand exactly how these changes in the connections between neurons underlie seizures in AS. “A very long term goal is to try to get better treatments for these individuals because their epilepsy is very hard to treat.”

Provided by University of North Carolina Health Care

Source: medicalxpress.com

ScienceDaily (June 6, 2012) — 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: Science Daily