Neuroscience

Articles and news from the latest research reports.

Posts tagged alcohol consumption

184 notes

Researchers Identify Key Factor in Transition from Moderate to Problem Drinking A team of UC San Francisco researchers has found that a tiny segment of genetic material known as a microRNA plays a central role in the transition from moderate drinking to binge drinking and other alcohol use disorders. Previous research in the UCSF laboratory of Dorit Ron, PhD, Endowed Chair of Cell Biology of Addiction in Neurology, has demonstrated that the level of a protein known as brain-derived neurotrophic factor, or BDNF, is increased in the brain when alcohol consumed in moderation. In turn, experiments in Ron’s lab have shown, BDNF prevents the development of alcohol use disorders. In the new study, Ron and first author Emmanuel Darcq, PhD, a former postdoctoral fellow now at McGill University in Canada, found that when mice consumed excessive amounts of alcohol for a prolonged period, there was a marked decrease in the amount of BDNF in the medial prefrontal cortex (mPFC), a brain region important for decision making. As reported in the October 21, 2014 online edition of Molecular Psychiatry, this decline was associated with a corresponding increase in the level of a microRNA called miR-30a-5p. MicroRNAs lower the levels of proteins such as BDNF by binding to messenger RNA, the molecular middleman that carries instructions from genes to the protein-making machinery of the cell, and tagging it for destruction. Ron and colleagues then showed that if they increased the levels of miR-30a-5p in the mPFC, BDNF was reduced, and the mice consumed large amounts of alcohol. When mice were treated with an inhibitor of miR-30a-5p, however, the level of BDNF in the mPFC was restored to normal and alcohol consumption was restored to normal, moderate levels. “Our results suggest BDNF protects against the transition from moderate to uncontrolled drinking and alcohol use disorders,” said Ron, senior author of the study and a professor in UCSF’s Department of Neurology. “When there is a breakdown in this protective pathway, however, uncontrolled excessive drinking develops, and microRNAs are a possible mechanism in this breakdown. This mechanism may be one possible explanation as to why 10 percent of the population develop alcohol use disorders and this study may be helpful for the development of future medications to treat this devastating disease.” One reason many potential therapies for alcohol abuse have been unsuccessful is because they inhibit the brain’s reward pathways, causing an overall decline in the experience of pleasure. But in the new study, these pathways continued to function in mice in which the actions of miR-30a-5p had been tamped down—the mice retained the preference for a sweetened solution over plain water that is seen in normal mice. This result has significant implications for future treatments, Ron said. “In searching for potential therapies for alcohol abuse, it is important that we look for future medications that target drinking without affecting the reward system in general. One problem with current alcohol abuse medications is that patients tend to stop taking them because they interfere with the sense of pleasure.”

Researchers Identify Key Factor in Transition from Moderate to Problem Drinking

A team of UC San Francisco researchers has found that a tiny segment of genetic material known as a microRNA plays a central role in the transition from moderate drinking to binge drinking and other alcohol use disorders.

Previous research in the UCSF laboratory of Dorit Ron, PhD, Endowed Chair of Cell Biology of Addiction in Neurology, has demonstrated that the level of a protein known as brain-derived neurotrophic factor, or BDNF, is increased in the brain when alcohol consumed in moderation. In turn, experiments in Ron’s lab have shown, BDNF prevents the development of alcohol use disorders.

In the new study, Ron and first author Emmanuel Darcq, PhD, a former postdoctoral fellow now at McGill University in Canada, found that when mice consumed excessive amounts of alcohol for a prolonged period, there was a marked decrease in the amount of BDNF in the medial prefrontal cortex (mPFC), a brain region important for decision making. As reported in the October 21, 2014 online edition of Molecular Psychiatry, this decline was associated with a corresponding increase in the level of a microRNA called miR-30a-5p.

MicroRNAs lower the levels of proteins such as BDNF by binding to messenger RNA, the molecular middleman that carries instructions from genes to the protein-making machinery of the cell, and tagging it for destruction.

Ron and colleagues then showed that if they increased the levels of miR-30a-5p in the mPFC, BDNF was reduced, and the mice consumed large amounts of alcohol. When mice were treated with an inhibitor of miR-30a-5p, however, the level of BDNF in the mPFC was restored to normal and alcohol consumption was restored to normal, moderate levels.

“Our results suggest BDNF protects against the transition from moderate to uncontrolled drinking and alcohol use disorders,” said Ron, senior author of the study and a professor in UCSF’s Department of Neurology. “When there is a breakdown in this protective pathway, however, uncontrolled excessive drinking develops, and microRNAs are a possible mechanism in this breakdown. This mechanism may be one possible explanation as to why 10 percent of the population develop alcohol use disorders and this study may be helpful for the development of future medications to treat this devastating disease.”

One reason many potential therapies for alcohol abuse have been unsuccessful is because they inhibit the brain’s reward pathways, causing an overall decline in the experience of pleasure. But in the new study, these pathways continued to function in mice in which the actions of miR-30a-5p had been tamped down—the mice retained the preference for a sweetened solution over plain water that is seen in normal mice.

This result has significant implications for future treatments, Ron said. “In searching for potential therapies for alcohol abuse, it is important that we look for future medications that target drinking without affecting the reward system in general. One problem with current alcohol abuse medications is that patients tend to stop taking them because they interfere with the sense of pleasure.”

Filed under alcohol alcohol consumption microRNA prefrontal cortex miR-30a-5p neuroscience science

106 notes

Study debunks alcohol consumption assertions ALCOHOL consumption is not a direct cause of cognitive impairment in older men later in life, a study conducted by the University of Western Australia has found.  The study, published in the Journal of Neurology, used Mendelian randomisation to analyse the genetic data from 3,542 men between the ages of 65 and 83 years.  The scientists measured the participants’ cognitive function three to eight years after recording their alcohol consumption.  Lead author, Western Australian Centre for Health and Ageing Director and UWA Professor Osvaldo Almeida says the team investigated the triangular association between alcohol consumption, cognitive impairment and a genetic polymorphism that modulates the efficiency of a critical enzyme of alcohol metabolism.  “We found a genetic variation that increases absenteeism and decreases the total amount of alcohol consumed,” Prof Almeida says. “If alcohol were a cause of cognitive impairment, one would expect that this genetic variation would be associated with lower risk of cognitive impairment in later life [because people with this genetic variation drink less or not at all].  “That was not the case. Hence, we concluded that the association between alcohol use and cognitive impairment is not due to a direct effect of alcohol.” The study also presented results that are consistent with the possibility, but do not necessarily prove, that regular moderate drinking decreases the risk of cognitive impairment in older men. Prof Almeida says the reasons for these results were unclear. “But evidence from a randomised trial looking at the effect of the Mediterranean diet [which includes nuts, olive oil, vegetables and wine] on health outcomes is supportive of this hypothesis,” he says.  “One may argue that people who drink in moderation have a lifestyle where, in general, things are done in moderation.  “This approach to life may decrease health hazards in general.” Prof Almeida says that although the results didn’t show alcohol affecting cognitive impairment, other studies have found excessive alcohol use to be associated with worse physical health, widowhood and poor social support.  “[These studies] led to the assumption that alcohol must directly damage the brain and cause cognitive impairment,” he says.  “This study shows that such an assumption is wrong.  “It also suggests that alcohol may have a small protective effect that we need to understand better in order to develop new interventions that might contribute to prevent dementia without all the bad outcomes associated with alcohol.”

Study debunks alcohol consumption assertions

ALCOHOL consumption is not a direct cause of cognitive impairment in older men later in life, a study conducted by the University of Western Australia has found. 

The study, published in the Journal of Neurology, used Mendelian randomisation to analyse the genetic data from 3,542 men between the ages of 65 and 83 years. 

The scientists measured the participants’ cognitive function three to eight years after recording their alcohol consumption. 

Lead author, Western Australian Centre for Health and Ageing Director and UWA Professor Osvaldo Almeida says the team investigated the triangular association between alcohol consumption, cognitive impairment and a genetic polymorphism that modulates the efficiency of a critical enzyme of alcohol metabolism. 

“We found a genetic variation that increases absenteeism and decreases the total amount of alcohol consumed,” Prof Almeida says.

“If alcohol were a cause of cognitive impairment, one would expect that this genetic variation would be associated with lower risk of cognitive impairment in later life [because people with this genetic variation drink less or not at all]. 

“That was not the case. Hence, we concluded that the association between alcohol use and cognitive impairment is not due to a direct effect of alcohol.”

The study also presented results that are consistent with the possibility, but do not necessarily prove, that regular moderate drinking decreases the risk of cognitive impairment in older men.

Prof Almeida says the reasons for these results were unclear.

“But evidence from a randomised trial looking at the effect of the Mediterranean diet [which includes nuts, olive oil, vegetables and wine] on health outcomes is supportive of this hypothesis,” he says. 

“One may argue that people who drink in moderation have a lifestyle where, in general, things are done in moderation. 

“This approach to life may decrease health hazards in general.”

Prof Almeida says that although the results didn’t show alcohol affecting cognitive impairment, other studies have found excessive alcohol use to be associated with worse physical health, widowhood and poor social support. 

“[These studies] led to the assumption that alcohol must directly damage the brain and cause cognitive impairment,” he says. 

“This study shows that such an assumption is wrong. 

“It also suggests that alcohol may have a small protective effect that we need to understand better in order to develop new interventions that might contribute to prevent dementia without all the bad outcomes associated with alcohol.”

Filed under alcohol consumption alcohol cognitive impairment genetic polymorphism neuroscience science

326 notes

A gene mutation for excessive alcohol drinking found Researchers have discovered a gene that regulates alcohol consumption and when faulty can cause excessive drinking. They have also identified the mechanism underlying this phenomenon. The study showed that normal mice show no interest in alcohol and drink little or no alcohol when offered a free choice between a bottle of water and a bottle of diluted alcohol. However, mice with a genetic mutation to the gene Gabrb1 overwhelmingly preferred drinking alcohol over water, choosing to consume almost 85% of their daily fluid as drinks containing alcohol - about the strength of wine. The consortium of researchers from five UK universities – Newcastle University, Imperial College London,  Sussex University, University College London and University of Dundee – and the MRC Mammalian Genetics Unit at Harwell, funded by the Medical Research Council (MRC), Wellcome Trust and ERAB, publish their findings today in Nature Communications. Dr Quentin Anstee, Consultant Hepatologist at Newcastle University, joint lead author said: “It’s amazing to think that a small change in the code for just one gene can have such profound effects on complex behaviours like alcohol consumption. “We are continuing our work to establish whether the gene has a similar influence in humans, though we know that in people alcoholism is much more complicated as environmental factors come into play. But there is the real potential for this to guide development of better treatments for alcoholism in the future.” Identifying the gene for alcohol preference Working at the MRC Mammalian Genetics Unit, a team led by Professor Howard Thomas from Imperial College London introduced subtle mutations into the genetic code at random throughout the genome and tested mice for alcohol preference. This led the researchers to identify the gene Gabrb1 which changes alcohol preference so strongly that mice carrying either of two single base-pair point mutations in this gene preferred drinking alcohol (10% ethanol v/v - about the strength of wine), over water. The group showed that mice carrying this mutation were willing to work to obtain the alcohol-containing drink by pushing a lever and, unlike normal mice, continued to do so even over long periods. They would voluntarily consume sufficient alcohol in an hour to become intoxicated and even have difficulty in coordinating their movements. The cause of the excessive drinking was tracked down to single base-pair point mutations in the gene Gabrb1, which codes for the beta 1 subunit, an important component of the GABAA receptor in the brain. This receptor responds to the brain’s most important inhibitory chemical messenger (GABA) to regulate brain activity. The researchers found that the gene mutation caused the receptor to activate spontaneously even when the usual GABA trigger was not present. These changes were particularly strong in the region of the brain that controls pleasurable emotions and reward, the nucleus accumbens, as Dr Anstee explains: “The mutation of the beta1 containing receptor is altering its structure and creating spontaneous electrical activity in the brain in this pleasure zone, the nucleus accumbens. As the electrical signal from these receptors increases, so does the desire to drink to such an extent that mice will actually work to get the alcohol, for much longer than we would have expected.” Professor Howard Thomas said: “We know from previous human studies that the GABA system is involved in controlling alcohol intake. Our studies in mice show that a particular subunit of GABAA receptor has a significant effect and most importantly the existence of these mice has allowed our collaborative group to investigate the mechanism involved. This is important when we come to try to modify this process first in mice and then in man.” Leading to a treatment for alcohol addiction Initially funded by the MRC, the 10-year project aimed to find genes affecting alcohol consumption. Professor Hugh Perry, Chair of the MRC’s Neurosciences and Mental Health Board, said: “Alcohol addiction places a huge burden on the individual, their family and wider society. There’s still a great deal we don’t understand about how and why consumption progresses into addiction, but the results of this long-running project suggest that, in some individuals, there may be a genetic component. If further research confirms that a similar mechanism is present in humans, it could help us to identify those most at risk of developing an addiction and ensure they receive the most effective treatment.”

A gene mutation for excessive alcohol drinking found

Researchers have discovered a gene that regulates alcohol consumption and when faulty can cause excessive drinking. They have also identified the mechanism underlying this phenomenon.

The study showed that normal mice show no interest in alcohol and drink little or no alcohol when offered a free choice between a bottle of water and a bottle of diluted alcohol.

However, mice with a genetic mutation to the gene Gabrb1 overwhelmingly preferred drinking alcohol over water, choosing to consume almost 85% of their daily fluid as drinks containing alcohol - about the strength of wine.

The consortium of researchers from five UK universities – Newcastle University, Imperial College London,  Sussex University, University College London and University of Dundee – and the MRC Mammalian Genetics Unit at Harwell, funded by the Medical Research Council (MRC), Wellcome Trust and ERAB, publish their findings today in Nature Communications.

Dr Quentin Anstee, Consultant Hepatologist at Newcastle University, joint lead author said: “It’s amazing to think that a small change in the code for just one gene can have such profound effects on complex behaviours like alcohol consumption.

“We are continuing our work to establish whether the gene has a similar influence in humans, though we know that in people alcoholism is much more complicated as environmental factors come into play. But there is the real potential for this to guide development of better treatments for alcoholism in the future.”

Identifying the gene for alcohol preference

Working at the MRC Mammalian Genetics Unit, a team led by Professor Howard Thomas from Imperial College London introduced subtle mutations into the genetic code at random throughout the genome and tested mice for alcohol preference. This led the researchers to identify the gene Gabrb1 which changes alcohol preference so strongly that mice carrying either of two single base-pair point mutations in this gene preferred drinking alcohol (10% ethanol v/v - about the strength of wine), over water.

The group showed that mice carrying this mutation were willing to work to obtain the alcohol-containing drink by pushing a lever and, unlike normal mice, continued to do so even over long periods. They would voluntarily consume sufficient alcohol in an hour to become intoxicated and even have difficulty in coordinating their movements.

The cause of the excessive drinking was tracked down to single base-pair point mutations in the gene Gabrb1, which codes for the beta 1 subunit, an important component of the GABAA receptor in the brain. This receptor responds to the brain’s most important inhibitory chemical messenger (GABA) to regulate brain activity. The researchers found that the gene mutation caused the receptor to activate spontaneously even when the usual GABA trigger was not present.

These changes were particularly strong in the region of the brain that controls pleasurable emotions and reward, the nucleus accumbens, as Dr Anstee explains: “The mutation of the beta1 containing receptor is altering its structure and creating spontaneous electrical activity in the brain in this pleasure zone, the nucleus accumbens. As the electrical signal from these receptors increases, so does the desire to drink to such an extent that mice will actually work to get the alcohol, for much longer than we would have expected.”

Professor Howard Thomas said: “We know from previous human studies that the GABA system is involved in controlling alcohol intake. Our studies in mice show that a particular subunit of GABAA receptor has a significant effect and most importantly the existence of these mice has allowed our collaborative group to investigate the mechanism involved. This is important when we come to try to modify this process first in mice and then in man.”

Leading to a treatment for alcohol addiction

Initially funded by the MRC, the 10-year project aimed to find genes affecting alcohol consumption. Professor Hugh Perry, Chair of the MRC’s Neurosciences and Mental Health Board, said: “Alcohol addiction places a huge burden on the individual, their family and wider society. There’s still a great deal we don’t understand about how and why consumption progresses into addiction, but the results of this long-running project suggest that, in some individuals, there may be a genetic component. If further research confirms that a similar mechanism is present in humans, it could help us to identify those most at risk of developing an addiction and ensure they receive the most effective treatment.”

Filed under alcohol consumption genes genetic mutation Gabrb1 GABA neuroscience science

70 notes

Drinking alcohol during pregnancy affects learning and memory function in offspring? Maternal alcohol consumption during pregnancy has detrimental effects on fetal central nervous system development. Maternal alcohol consumption prior to and during pregnancy significantly affects cognitive functions in offspring, which may be related to changes in cyclin-dependent kinase 5 because it is associated with modulation of synaptic plasticity and impaired learning and memory. Prof. Ruiling Zhang and team from Xinxiang Medical University explored the correlation between cyclin-dependent kinase 5 expression in the hippocampus and neurological impairments following prenatal ethanol exposure, and found that prenatal ethanol exposure could affect cyclin-dependent kinase 5 and its activator p35 in the hippocampus of offspring rats. These findings, which reported in the Neural Regeneration Research (Vol. 8, No. 18, 2013), propose new insights into the mechanisms underlying the role of ethanol exposure in central nervous system injuries, and provide a new strategy for treating the consequences of prenatal ethanol exposure.

Drinking alcohol during pregnancy affects learning and memory function in offspring?

Maternal alcohol consumption during pregnancy has detrimental effects on fetal central nervous system development. Maternal alcohol consumption prior to and during pregnancy significantly affects cognitive functions in offspring, which may be related to changes in cyclin-dependent kinase 5 because it is associated with modulation of synaptic plasticity and impaired learning and memory. Prof. Ruiling Zhang and team from Xinxiang Medical University explored the correlation between cyclin-dependent kinase 5 expression in the hippocampus and neurological impairments following prenatal ethanol exposure, and found that prenatal ethanol exposure could affect cyclin-dependent kinase 5 and its activator p35 in the hippocampus of offspring rats. These findings, which reported in the Neural Regeneration Research (Vol. 8, No. 18, 2013), propose new insights into the mechanisms underlying the role of ethanol exposure in central nervous system injuries, and provide a new strategy for treating the consequences of prenatal ethanol exposure.

Filed under pregnancy alcohol alcohol consumption fetal development cognitive function neuroscience science

215 notes

Researchers find that alcohol consumption damages brain’s support cells Alcohol consumption affects the brain in multiple ways, ranging from acute changes in behavior to permanent molecular and functional alterations. The general consensus is that in the brain, alcohol targets mainly neurons. However, recent research suggests that other cells of the brain known as astrocytic glial cells or astrocytes are necessary for the rewarding effects of alcohol and the development of alcohol tolerance. The study, first-authored by Dr. Leonardo Pignataro, was published in the February 6th issue of the scientific journal Brain and Behavior. "This is a fascinating result that we could have never anticipated. We know that astrocytes are the most abundant cell type in the central nervous system and that they are crucial for neuronal growth and survival, but so far, these cells had been thought to be involved only in brain’s support functions. Our results, however, show that astrocytes have an active role in alcohol tolerance and dependence," explains Dr. Pignataro. The team of researchers from Columbia and Yale Universities analyzed how alcohol exposure changes gene expression in astrocyte cells and identified gene sets associated with stress, immune response, cell death, and lipid metabolism, which may have profound implications for normal neuronal activity in the brain. “Our findings may explain many of the long-term inflammatory and degenerative effects observed in the brain of alcoholics,” says Dr. Pignataro. “The change in gene expression observed in alcohol-exposed astrocytes supports the idea that some of the alcohol consumed reaches the brain and that ethanol (the active component of alcoholic beverages) is locally metabolized, increasing the production free radicals that react with cell components to affect the normal function of cells. This activates a cellular stress response in the cells in an attempt to defend from this chemical damage. On the other hand, the body recognizes these oxidized molecules as “foreign objects” generating an immune response against them that leads to the death of damage cells. This mechanism can explain the inflammatory degenerative process observed in the brain of chronic alcoholics, allowing for the development of different and novel therapeutically approaches to treat this disease” added Dr. Pignataro. The consequences of alcohol on astrocytes revealed in this study go far beyond what happens to this particular cell type. Astrocytes play a crucial role in the CNS, supporting normal neuronal activity by maintaining homeostasis. Therefore, alcohol changes in gene expression in astrocytes may have profound implications for neuronal activity in the brain. These findings will help scientists better understand alcohol-associated disorders, such as the brain neurodegenerative damage associated with chronic alcoholism and alcohol tolerance and dependence. “We hope that this newly discovered role of astrocytes will give scientists new targets other than neurons to develop novel therapies to treat alcoholism,” Leonardo Pignataro concluded.

Researchers find that alcohol consumption damages brain’s support cells

Alcohol consumption affects the brain in multiple ways, ranging from acute changes in behavior to permanent molecular and functional alterations. The general consensus is that in the brain, alcohol targets mainly neurons. However, recent research suggests that other cells of the brain known as astrocytic glial cells or astrocytes are necessary for the rewarding effects of alcohol and the development of alcohol tolerance. The study, first-authored by Dr. Leonardo Pignataro, was published in the February 6th issue of the scientific journal Brain and Behavior.

"This is a fascinating result that we could have never anticipated. We know that astrocytes are the most abundant cell type in the central nervous system and that they are crucial for neuronal growth and survival, but so far, these cells had been thought to be involved only in brain’s support functions. Our results, however, show that astrocytes have an active role in alcohol tolerance and dependence," explains Dr. Pignataro.

The team of researchers from Columbia and Yale Universities analyzed how alcohol exposure changes gene expression in astrocyte cells and identified gene sets associated with stress, immune response, cell death, and lipid metabolism, which may have profound implications for normal neuronal activity in the brain. “Our findings may explain many of the long-term inflammatory and degenerative effects observed in the brain of alcoholics,” says Dr. Pignataro. “The change in gene expression observed in alcohol-exposed astrocytes supports the idea that some of the alcohol consumed reaches the brain and that ethanol (the active component of alcoholic beverages) is locally metabolized, increasing the production free radicals that react with cell components to affect the normal function of cells. This activates a cellular stress response in the cells in an attempt to defend from this chemical damage. On the other hand, the body recognizes these oxidized molecules as “foreign objects” generating an immune response against them that leads to the death of damage cells. This mechanism can explain the inflammatory degenerative process observed in the brain of chronic alcoholics, allowing for the development of different and novel therapeutically approaches to treat this disease” added Dr. Pignataro.

The consequences of alcohol on astrocytes revealed in this study go far beyond what happens to this particular cell type. Astrocytes play a crucial role in the CNS, supporting normal neuronal activity by maintaining homeostasis. Therefore, alcohol changes in gene expression in astrocytes may have profound implications for neuronal activity in the brain.

These findings will help scientists better understand alcohol-associated disorders, such as the brain neurodegenerative damage associated with chronic alcoholism and alcohol tolerance and dependence. “We hope that this newly discovered role of astrocytes will give scientists new targets other than neurons to develop novel therapies to treat alcoholism,” Leonardo Pignataro concluded.

Filed under alcohol alcohol consumption glial cells astrocytes gene expression neuronal activity neuroscience science

165 notes

Monday’s medical myth: alcohol kills brain cells Do you ever wake up with a raging hangover and picture the row of brain cells that you suspect have have started to decay? Or wonder whether that final glass of wine was too much for those tiny cells, and pushed you over the line? Well, it’s true that alcohol can indeed harm the brain in many ways. But directly killing off brain cells isn’t one of them. The brain is made up of nerve cells (neurons) and glial cells. These cells communicate with each other, sending signals from one part of the brain to the other, telling your body what to do. Brain cells enable us to learn, imagine, experience sensation, feel emotion and control our body’s movement. Alcohol’s effects can be seen on our brain even after a few drinks, causing us to feel tipsy. But these symptoms are temporary and reversible. The available evidence suggests alcohol doesn’t kill brain cells directly. There is some evidence that moderate drinking is linked to improved mental function. A 2005 Australian study of 7,500 people in three age cohorts (early 20s, early 40s and early 60s) found moderate drinkers (up to 14 drinks for men and seven drinks for women per week) had better cognitive functioning than non-drinkers, occasional drinkers and heavy drinkers. But there is also evidence that even moderate drinking may impair brain plasticity and cell production. Researchers in the United States gave rats alcohol over a two-week period, to raise their alcohol blood concentration to about 0.08. While this level did not impair the rats’ motor skills or short-term learning, it impacted the brain’s ability to produce and retain new cells, reducing new brain cell production by almost 40%. Therefore, we need to protect our brains as best we can. Excessive alcohol undoubtedly damages brain cells and brain function. Heavy consumption over long periods can damage the connections between brain cells, even if the cells are not killed. It can also affect the way your body functions. Long-term drinking can cause brain atrophy or shrinkage, as seen in brain diseases such as stroke and Alzheimer’s disease. There is debate about whether permanent brain damage is caused directly or indirectly. We know, for example, that severe alcoholic liver disease has an indirect effect on the brain. When the liver is damaged, it’s no longer effective at processing toxins to make them harmless. As a result, poisonous toxins reach the brain, and may cause hepatic encephalopathy (decline in brain function). This can result in changes to cognition and personality, sleep disruption and even coma and death. Alcoholism is also associated with nutritional and absorptive deficiencies. A lack of Vitamin B1 (thiamine) causes brain disorders called Wernicke’s ncephalopathy (which manifests in confusion, unsteadiness, paralysis of eye movements) and Korsakoff’s syndrome (where patients lose their short-term memory and coordination). So, how much alcohol is okay? To reduce the lifetime risk of harm from alcohol-related disease or injury, the National Health and Medical Research Council recommends healthy adults drink no more than two standard drinks on any day. Drinking less frequently (such as weekly rather than daily) and drinking less on each occasion will reduce your lifetime risk. To avoid alcohol-related injuries, adults shouldn’t drink more than four standard drinks on a single occasion. This applies to both sexes because while women become intoxicated with less alcohol, men tend to take more risks and experience more harmful effects. For pregnant women and young people under the age of 18, the guidelines say not drinking is the safest option. So while alcohol may not kill brain cells, if this myth encourages us to rethink that third beer or glass of wine, I won’t mind if it hangs around.

Monday’s medical myth: alcohol kills brain cells

Do you ever wake up with a raging hangover and picture the row of brain cells that you suspect have have started to decay? Or wonder whether that final glass of wine was too much for those tiny cells, and pushed you over the line?

Well, it’s true that alcohol can indeed harm the brain in many ways. But directly killing off brain cells isn’t one of them.

The brain is made up of nerve cells (neurons) and glial cells. These cells communicate with each other, sending signals from one part of the brain to the other, telling your body what to do. Brain cells enable us to learn, imagine, experience sensation, feel emotion and control our body’s movement.

Alcohol’s effects can be seen on our brain even after a few drinks, causing us to feel tipsy. But these symptoms are temporary and reversible. The available evidence suggests alcohol doesn’t kill brain cells directly.

There is some evidence that moderate drinking is linked to improved mental function. A 2005 Australian study of 7,500 people in three age cohorts (early 20s, early 40s and early 60s) found moderate drinkers (up to 14 drinks for men and seven drinks for women per week) had better cognitive functioning than non-drinkers, occasional drinkers and heavy drinkers.

But there is also evidence that even moderate drinking may impair brain plasticity and cell production. Researchers in the United States gave rats alcohol over a two-week period, to raise their alcohol blood concentration to about 0.08. While this level did not impair the rats’ motor skills or short-term learning, it impacted the brain’s ability to produce and retain new cells, reducing new brain cell production by almost 40%. Therefore, we need to protect our brains as best we can.

Excessive alcohol undoubtedly damages brain cells and brain function. Heavy consumption over long periods can damage the connections between brain cells, even if the cells are not killed. It can also affect the way your body functions. Long-term drinking can cause brain atrophy or shrinkage, as seen in brain diseases such as stroke and Alzheimer’s disease.

There is debate about whether permanent brain damage is caused directly or indirectly.

We know, for example, that severe alcoholic liver disease has an indirect effect on the brain. When the liver is damaged, it’s no longer effective at processing toxins to make them harmless. As a result, poisonous toxins reach the brain, and may cause hepatic encephalopathy (decline in brain function). This can result in changes to cognition and personality, sleep disruption and even coma and death.

Alcoholism is also associated with nutritional and absorptive deficiencies. A lack of Vitamin B1 (thiamine) causes brain disorders called Wernicke’s ncephalopathy (which manifests in confusion, unsteadiness, paralysis of eye movements) and Korsakoff’s syndrome (where patients lose their short-term memory and coordination).

So, how much alcohol is okay?

To reduce the lifetime risk of harm from alcohol-related disease or injury, the National Health and Medical Research Council recommends healthy adults drink no more than two standard drinks on any day. Drinking less frequently (such as weekly rather than daily) and drinking less on each occasion will reduce your lifetime risk.

To avoid alcohol-related injuries, adults shouldn’t drink more than four standard drinks on a single occasion. This applies to both sexes because while women become intoxicated with less alcohol, men tend to take more risks and experience more harmful effects.

For pregnant women and young people under the age of 18, the guidelines say not drinking is the safest option.

So while alcohol may not kill brain cells, if this myth encourages us to rethink that third beer or glass of wine, I won’t mind if it hangs around.

Filed under brain nerve cells glial cells alcohol alcohol consumption cognitive function brain damage science

free counters