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“Sugar is so harmful that it should be controlled and taxed in the same way as tobacco and alcohol,” according to health experts quoted in today’s Daily Express. The researchers say that sugar indirectly contributes to 35 million deaths a year worldwide.

The news is based on a comment article by US health scientists, who argue that there has been a massive rise in diseases such as heart disease, cancer and diabetes since we began eating more sugar contained in processed food. The researchers argue that many of the health effects of excess sugar consumption are similar to those of alcohol, and that sugar should, therefore, be controlled and taxed in a similar way. They advocate introducing a tax on processed foods with added sugar, limiting sales during school hours and placing age limits on purchase. Interestingly, the authors rate sugar as more dangerous to health than saturated fat and salt, which they call dietary “bogeymen”.

It is important to highlight that the researchers’ article is a comment piece and, therefore, primarily reflects their views and opinions, rather than presenting direct research on the issue. While it is certainly an interesting concept, there is still a lack of evidence supporting the effectiveness of such measures and, crucially, whether the public would actually accept them.

 

Where did the story come from?

The article was written by researchers from the University of California. There is no information about any external funding. It was published in the comment section of the peer-reviewed scientific journal Nature.

The article was covered fairly by the papers, many of which included comments from UK experts including the UK Food and Drink Federation, which represents food manufacturers. The BBC also quoted an expert from the British Heart Foundation, who reportedly said that taxing salt and fat alongside sugar should also be considered.

 

What kind of article was this?

This was a comment piece in which experts discuss the global burden of general chronic disease related to sugar consumption and the need to regulate certain dietary items. In particular, the authors draw parallels between the health effects of sugar and the use of alcohol and tobacco, arguing that sugar should be regulated in a similar manner.

It is important to highlight that this was a comment piece only and, as such, it primarily reflects the views and opinions of the authors. A formal systematic review of the literature does not appear to have been conducted and, as such, it is not certain whether all relevant evidence and resources related to sugar consumption and its health effects will have been consulted.

Also, the short piece looks at the issue from a global perspective and, therefore, is not a direct commentary on sugar consumption in the UK. In fact, a map showing average added sugar consumption per day across different nations shows that people in the UK consume a relatively low amount of sugar, at least compared with the rest of the world. Much of the article’s content may be focused on policies suited to the US, which has by far the greatest per-head sugar consumption, at more than 600 calories worth of sugar per day.

 

What does the article say?

The article points out that, for the first time in human history, non-communicable diseases such as heart disease, cancer and diabetes, pose a greater health burden worldwide than infectious disease. While alcohol, tobacco and diet are all targeted as risk factors for these diseases by policymakers, only the first two – alcohol and cigarettes – are regulated by governments to protect public health. (Although, as it points out, Denmark taxes food high in saturated fats and is now considering taxing added sugar.) The authors argue that fat and salt have become the current “dietary bogeymen” in the US and Europe, but that most doctors no longer believe that fat is the “primary culprit” of such disease. Doctors are apparently calling for attention to be turned towards the dangers of excess sugar consumption.

The authors estimate that over the past 50 years sugar consumption has tripled worldwide, mainly as a result of it being added to cheap processed foods. While excess sugar is thought to be a key cause of the obesity epidemic, they argue that obesity itself is not the root cause of disease but that its presence is a marker for metabolic damage. This, they say, could explain why 40% of those with metabolic syndrome (a collection of the key metabolic changes that lead to heart disease and diabetes) are not obese.

 

Why do they think sugar is dangerous?

The authors say that although sugar is described as “empty calories”, a growing body of evidence suggests that fructose (one component of table sugar) can trigger processes that lead to liver toxicity and a host of other chronic diseases. “A little is not a problem but a lot kills – slowly,” they say.

The authors argue that sugar meets all the four criteria used by health policy makers to justify the regulation of alcohol. These are:

• Unavoidability. While sugar was only available as fruit and honey at certain times of the year to our ancestors, it is now present in nearly all processed foods. In some parts of the world people are consuming more than 500 calories worth of sugar per day.
• Toxicity. There is growing evidence that excess sugar has an effect on human health beyond simply adding calories and can cause many of the same problems as alcohol, including high blood pressure, high blood fats, insulin resistance and diabetes.
• Potential for abuse. The authors argue that, like tobacco and alcohol, sugar acts on the brain to encourage dependence. Specifically, it interferes with the workings of a hormone called ghrelin (which signals hunger to the brain) and it also affects the action of other important compounds.
• Negative impact on society. The economic and human costs of these diseases place excess consumption of sugar in the same category as smoking and drinking.

 

What do they think should be done?

While the authors accept that sugar is “natural” and a “pleasure”, they argue that, like alcohol, too much of a good thing is toxic. Strategies to reduce consumption of alcohol and tobacco show that government controls, such as taxation and imposing age limits, work better than educating people. They make several proposals for controlling sugar, including:

• taxing any processed foods with added sugar, including drinks
• reducing the hours during which retailers can sell food containing added sugar
• tightening the licensing requirements on vending machines and snack bars selling sugary products
• controlling the numbers of fast food outlets and convenience stores
• limiting sales during school hours or imposing an age limit for drinks with added sugar

Finally, they argue that regulating sugar will not be easy, but it can be done with enough pressure for change, citing bans on smoking in public places as an example of what can be achieved.

 

What does this mean for me?

This article will be of interest to food scientists, health policy makers and the public alike, but the use of strategies to restrict the consumption of added sugar is complicated and, indeed controversial. The implications of such moves would need to be considered in both medical and societal terms. They would need both medical evidence to support their effectiveness and assurance that the public would accept drastic changes, such as age limits on buying sweets. For example, in recent years, Denmark has imposed taxes on fatty foods, a move that has divided opinions greatly.

It is generally accepted that added sugar or excessive sugar consumption is bad for health and dietitians advise restricting sugar intake to the occasional “treat”. However, to what extent sugar is directly to blame for the rise in chronic disease and how much is due to other dietary components, such as saturated fat and salt, is open to debate. The current article does not appear to be a formal systematic review of the literature, and it is not certain whether all relevant evidence and resources related to sugar consumption and its health effects have been consulted. As such, it should be considered primarily to reflect the views and opinions of the authors.

In the UK at present, policymakers generally favour encouraging healthier eating through education and the provision of healthier options. This is carried out through public health campaigns such as 5 A DAY or by introducing new food ranges to schools. Whether this approach alone is adequate and whether healthier eating patterns should be encouraged by government regulation, is a crucial area of debate.

Links To The Headlines

Sugar ‘is toxic and must be regulated just like cigarettes’, claim scientists. Daily Mail, February 2 2012

Sugar tax needed, say US experts. BBC News, February 2 2012

Tax harmful sugar. Daily Express, February 2 2012

Links To Science

Lustig RH, Schmidt LA, Brindis LD. Public health: The toxic truth about sugar. Nature, February 2 2012

Britain is in the grip of a new “flesh-eating bug spread by sneezes and coughs”, according to the front page of today’s Metro. The newspaper says that the bacteria are spreading across Britain, as they can be caught through people coughing and sneezing on crowded trains and buses.

This unsettling news put some of the Behind the Headlines team off grabbing their free copy of the Metro at the station this morning, not because of the fear of catching deadly germs from the paper, but because its report was alarmist and overblown. The basis of this news is a laboratory study that investigated why healthcare-acquired meticillin-resistant staphylococcus aureus (MRSA) bacteria rarely cause infections in healthy individuals. The study found that healthcare-acquired MRSA has a high level of antibiotic resistance, but that this property comes at a cost of reduced virulence (being less able to cause infection). Conversely, the study found that the type of MRSA that is usually caught in a community setting is more virulent, but weaker against treatment with antibiotics.

This study has not investigated the transmission, effects or number of cases of community-acquired MRSA in the UK, which formed the basis of many news reports on the research. The researchers state that MRSA outside the healthcare system and in the community is a growing concern, but cases are still very rare. This interesting research contributes to our knowledge of MRSA, rather than warning us of a germ-based Armageddon.

 

Where did the story come from?

The study was carried out by researchers from the University of Bath and the University of Nottingham in the UK; University College Dublin in Ireland; and Texas A&M Health Science Centre and the University of Texas in the US. It was funded by the UK Medical Research Council and a Biotechnology and Biological Sciences Research Council Studentship. The study was published in the peer-reviewed Journal of Infectious Diseases.

This story was widely covered. Most reports were alarmist, concentrating on the supposed emergence of a dangerous, highly infectious new form of community-acquired MRSA. Many newspapers suggested that transmission is easy, that it can lead to a “flesh-eating form of pneumonia”, and that cases are on the increase. These claims seem to be based on the press release for the research rather than the research paper itself. The study was actually laboratory-based research that had investigated why healthcare-acquired MRSA bacteria rarely cause infections in healthy individuals. Although there was some investigation of community-acquired MRSA, the results do not justify the news coverage.

 

What kind of research was this?

This was a laboratory-based study. It aimed to examine why healthcare-acquired MRSA bacteria rarely cause infections in healthy individuals. Healthcare-acquired, or hospital-acquired, means that the bacteria cause infections that mostly occur in healthcare environments.

The researchers initially covered the nature of MRSA and how it resists certain types of antibiotics. It is already known that MRSA is resistant to the antibiotics meticillin and oxacillin because it has acquired a piece of DNA called a ‘mobile genetic element’. Meticillin is an old antibiotic that is now no longer used and has been replaced by flucloxacillin.

Many staphylococcus aureus bacteria have now also developed resistance to the penicillin group of antibiotics (because they produce enzymes that can make penicillin inactive), but are usually still susceptible to the antibiotic flucloxacillin. MRSA, however, does not have this susceptibility to flucloxacillin, and is, therefore, harder to treat than most staphylococci bacteria, needing stronger antibiotics still.

One particular genetic element that is key for deciding the properties of MRSA is called the ‘staphylococcal cassette chromosome mec’ (SCCmec). There are several different versions of this cassette, which each provide bacteria with slightly different properties. The researchers state that healthcare-acquired MRSA have type I, II or III SCCmec elements, whereas community-acquired MRSA have type IV and V elements. These different cassettes all contain a gene (mecA) that codes for a protein called PBP2a, located in the cell wall of the bacteria. PBPs (penicillin binding proteins) are a normal part of the cell wall of many bacteria. Many antibiotics work by inactivating PBPs, which cause the bacteria to die. However, the version of PBP encoded by mecA, PBP2a, is less sensitive to antibiotics, allowing the bacteria to survive.

 

What did the research involve?

The researchers initially determined whether deleting the mecA gene, which encodes the PBP2a cell wall protein, affects the toxicity of MRSA. They then took a healthcare-acquired MRSA strain and a version of this strain that they genetically modified to delete the mecA gene, and performed tests to see how each was able to break up a type of immune cell called a T cell in the laboratory.

The researchers then investigated the ability of the different strains to respond to ‘signalling molecules’, which normally cause the bacteria to activate their production of toxins. The virulence of these strains was confirmed using mouse experiments.

The researchers then compared the production of the PBP2a cell wall protein, T-cell toxicity and the resistance of healthcare-acquired MRSA to antibiotics, compared with community-acquired MRSA.

 

What were the basic results?

The researchers found that deleting the mecA gene caused the MRSA to become more toxic. This was because the expression of mecA results in cell wall changes that interfere with MRSA’s ability to detect or respond to signals to switch on toxin expression. MRSA with mecA deleted was also more virulent in a mouse model, causing mice to lose weight or die.

The researchers then compared MRSA strains with different SCCmec elements: those with type II elements (typical of healthcare-acquired MRSA) and those with type IV elements (typical of community-acquired MRSA). They found that typical community-acquired MRSAs had lower resistance to the antibiotic oxacillin, were more toxic to the immune system’s T-cells and expressed less PBP2a.

 

How did the researchers interpret the results?

“As a direct result of its high level of antibiotic resistance, healthcare-acquired MRSA is impaired in its ability to cause infection, which can explain its inability to cause infection in community settings, where antibiotic usage and the prevalence of susceptible patients are low.” In other words, healthcare-acquired MRSA makes a trade-off, sacrificing its ability to spread to healthy individuals in order to fight off a greater range of antibiotics.

 

Conclusion

This interesting study helps explain why healthcare-acquired MRSA infections are rarely found in healthy individuals. It found that expression of a gene that produces one of the proteins responsible for MRSA’s antibiotic resistance caused it to be less toxic. It also showed that typical community-acquired MRSA strains express less of this antibiotic-resistance protein, but are more toxic.

However, this intriguing lab study did not investigate the transmission, effects or number of cases of community-acquired MRSA in the UK, discussion of which formed the majority of the news reports. On this basis, the research itself does not support the claims that we are under siege from an ‘airborne, bacteria-resistant, flesh-eating superbug’, as newspapers have today suggested.

Links To The Headlines

Flesh-eating bug spread by sneezes and coughs. Metro, February 2 2012

Deadly new superbug is heading for Britain. Daily Express, February 2 2012

New deadly MRSA strain on its way to the UK from USA. Daily Mirror, February 2 2012

Super-strong MRSA bug heading to UK. The Sun, February 2 2012

Flesh-eating bug spread by coughs and sneezes spreading across the UK. Daily Mail, February 2 2012

Links To Science

Rudkin JR, Edwards AM, Bowden MG et al.Methicillin Resistance Reduces the Virulence of Healthcare-Associated Methicillin-Resistant Staphylococcus aureus by Interfering With the agr Quorum Sensing System. Journal of Infectious Diseases, February 1 2012

“Signs of autism can be detected in six-month-old babies by measuring brain activity,” the Daily Mail has reported. While the Mail was correct, the research has not yet proved to be a perfect diagnostic test.

This and other related headlines are based on a study that assessed the brain activity of 104 infants aged 6-10 months as they watched an image of an adult’s face whose eyes moved from looking away from them, to directly at the infant, then away again. Researchers called these eye movements ‘dynamic eye-gaze shifts’. They then assessed whether differences in brain activity in response to the eye-gaze shifts were related to autism developing in the same children at three years.

Children who did not develop autism showed large spikes in brain activity when they saw the ‘gaze shifts’. Much smaller spikes in brain activity were detected in the infants who went on to develop autism, raising the prospect that autism could be identified earlier than is currently clinically possible.

However, this test was not 100% accurate. Some babies showing low brain activity spikes did not go on to develop autism and vice versa. As the groups overlap, there cannot be a simple and useful cut-off value to predict autism.

Developing and refining this type of test into something that can be routinely used to detect autism in infants is likely to take some time and will certainly require more research on larger groups of infants with autism and unselected healthy infants too.

 

Where did the story come from?

The study was carried out by a collaboration of researchers from English, Canadian and Australian universities and was funded by the UK Medical Research Council. It was published in the peer-reviewed science journal Current Biology.

The media reporting of this story was generally well balanced. Many stories included quotes from the study authors that a definitive test would take time to develop and that the current assessment is not 100% effective.

 

What kind of research was this?

This study was a prospective longitudinal study investigating whether the brain function of infants aged 6-10 months differed in response to viewing faces that changed the direction of their gaze. The researchers then looked at whether these brain function differences could predict a diagnosis of autism at three years of age.

The authors report that there are currently no reliable methods of predicting autism in infants younger than about two years of age. Current diagnosis relies on the detection of behavioural symptoms of autism that typically develop in a child’s second or third year. Behaviours associated with autism include impairments in social skills and communication, and the presence of rigid, stereotyped and repetitive behaviours.

The authors say previous research shows typical infants’ sensitivity to eye gaze in the first year of life predicts a range of social and communication skills that emerge later. Detecting autism at an early age could potentially lead to ways of better supporting the child during early development, improving their wellbeing and life chances.

 

What did the research involve?

The researcher recruited a group of 104 infants – 54 at risk of autism because of a family history of the condition and 50 controls, with no family history of autism. The infants were followed from 6-10 months through to three years of age.

The researchers measured the 6 to 10-month-old infants’ response to changing images of faces. They did this by recording event-related potentials (ERPs), which are a measure of brain electrical activity in response to a thought or perception. In this study, ERPs were used to measure the perception of a face changing between looking directly at the infant and then away from them. The researchers called this ‘dynamic gaze-shift stimuli’.

The researchers also tracked the eyes of the infants to examine the amount of time they spent looking at the eye region of the faces they were shown. This allowed the researchers to assess whether different responses to the eye gaze were due to differences in attention to the eye region or whether brain functions were more important.

The researchers reported that dynamic gaze-shift stimuli are more likely to engage wider social brain mechanisms than static images as they mimic a real social interaction more closely. However, researchers compared their dynamic gaze results with that from ‘static gaze’, (images of a face whose eyes were looking at, or away from, the infant) to see how they compared to each other.

The brain activity levels of infants at risk of autism were contrasted with the controls. The researchers then looked at how the brain function differences at 6-10 months related to a later diagnosis of autism. An independent team assessed whether the infants had autism at two and three years old.

 

What were the basic results?

The brain activity of the control group showed large spikes of activity in response to eye gaze changes when the face image held a gaze toward, compared to away from, the infant. The brain activity spikes of infants at risk of autism were significantly smaller in response to the same stimulus.

The differences in brain activity of the control group verse at risk group were not restricted to the dynamic gaze results. Similar results were seen when static images were used.

The researchers found that those who did not go on to develop autism at three years of age showed large spikes in brain activity relating to the changes in eye gaze at 6-10 months. Crucially, those that did develop autism showed significantly smaller spikes in brain activity. The static image test did not predict a later diagnosis of autism.

Eye tracking information was available for 93 of the 104 infants. There was no difference in the time at-risk infants and control infants spent looking at the faces’ eyes relative to other areas of the face.

 

How did the researchers interpret the results?

The authors conclude that ‘brain function measures can successfully differentiate groups of infants at risk [of autism] from low-risk control within the ?rst year of life’. They go on to say that ‘response to dynamic gaze shifts during the first year of life distinguished the group of infants who later develop autism’.

 

Conclusion

This small study highlights a potential method of identifying children who are likely to develop autism at 6-11 months, much earlier than the current method of diagnosis. The authors suggest this could potentially pave the way for more selective targeting of early intervention efforts and procedures to these children, increasing their life chances.

While this study provides intriguing results it is important to bear in mind some practical limitations. For instance, while the average differences between the brain function of the infants that went on to develop autism compared to those that did not were significantly different, individual values from the two groups did overlap. This means that there is probably no useful clinical cut-off value to predict autism. Similarly, the researchers do not describe how the controls were selected or report how good the test was at diagnosing autism, known as the ‘test sensitivity’. Reporting these key results would have helped us better assess the accuracy and importance of these findings.

Much larger studies would be needed to establish a suitable brain activity level to use to identify as child as ‘likely to develop autism’. These studies could better assess the natural variation in brain activity from a large group of infants. Similarly, it is unlikely a future autism assessment would rely on a single test, such as dynamic eye gaze, but would instead use a combination of tests.

The uncertainty about what cut-off values to use, and the drawbacks of using a single predictive test, makes the development of an early identification test more complex. It may be some time before a predictive test is routinely available to identify infants likely to develop autism earlier than is currently possible.

Links To The Headlines

Autism: Brainwaves ’show risk from age of six months’. BBC News, January 27 2012

Signs of autism ‘can be detected in six-month-old babies’ by measuring brain activity. Daily Mail, January 27 2012

Signs of autism at six months. The Daily Telegraph, January 27 2012

Early test to detect autism. The Independent, January 27 2012

Links To Science

Elsabbagh M, Mercure E, Hudry K, et al. Infant neural sensitivity to dynamic eye gaze is associated with later emerging autism. Current Biology. 2012;22:1-5

“Sugar is so harmful that it should be controlled and taxed in the same way as tobacco and alcohol,” according to health experts quoted in today’s Daily Express. The researchers say that sugar indirectly contributes to 35 million deaths a year worldwide.

The news is based on a comment article by US health scientists, who argue that there has been a massive rise in diseases such as heart disease, cancer and diabetes since we began eating more sugar contained in processed food. The researchers argue that many of the health effects of excess sugar consumption are similar to those of alcohol, and that sugar should, therefore, be controlled and taxed in a similar way. They advocate introducing a tax on processed foods with added sugar, limiting sales during school hours and placing age limits on purchase. Interestingly, the authors rate sugar as more dangerous to health than saturated fat and salt, which they call dietary “bogeymen”.

It is important to highlight that the researchers’ article is a comment piece and, therefore, primarily reflects their views and opinions, rather than presenting direct research on the issue. While it is certainly an interesting concept, there is still a lack of evidence supporting the effectiveness of such measures and, crucially, whether the public would actually accept them.

 

Where did the story come from?

The article was written by researchers from the University of California. There is no information about any external funding. It was published in the comment section of the peer-reviewed scientific journal Nature.

The article was covered fairly by the papers, many of which included comments from UK experts including the UK Food and Drink Federation, which represents food manufacturers. The BBC also quoted an expert from the British Heart Foundation, who reportedly said that taxing salt and fat alongside sugar should also be considered.

 

What kind of article was this?

This was a comment piece in which experts discuss the global burden of general chronic disease related to sugar consumption and the need to regulate certain dietary items. In particular, the authors draw parallels between the health effects of sugar and the use of alcohol and tobacco, arguing that sugar should be regulated in a similar manner.

It is important to highlight that this was a comment piece only and, as such, it primarily reflects the views and opinions of the authors. A formal systematic review of the literature does not appear to have been conducted and, as such, it is not certain whether all relevant evidence and resources related to sugar consumption and its health effects will have been consulted.

Also, the short piece looks at the issue from a global perspective and, therefore, is not a direct commentary on sugar consumption in the UK. In fact, a map showing average added sugar consumption per day across different nations shows that people in the UK consume a relatively low amount of sugar, at least compared with the rest of the world. Much of the article’s content may be focused on policies suited to the US, which has by far the greatest per-head sugar consumption, at more than 600 calories worth of sugar per day.

 

What does the article say?

The article points out that, for the first time in human history, non-communicable diseases such as heart disease, cancer and diabetes, pose a greater health burden worldwide than infectious disease. While alcohol, tobacco and diet are all targeted as risk factors for these diseases by policymakers, only the first two – alcohol and cigarettes – are regulated by governments to protect public health. (Although, as it points out, Denmark taxes food high in saturated fats and is now considering taxing added sugar.) The authors argue that fat and salt have become the current “dietary bogeymen” in the US and Europe, but that most doctors no longer believe that fat is the “primary culprit” of such disease. Doctors are apparently calling for attention to be turned towards the dangers of excess sugar consumption.

The authors estimate that over the past 50 years sugar consumption has tripled worldwide, mainly as a result of it being added to cheap processed foods. While excess sugar is thought to be a key cause of the obesity epidemic, they argue that obesity itself is not the root cause of disease but that its presence is a marker for metabolic damage. This, they say, could explain why 40% of those with metabolic syndrome (a collection of the key metabolic changes that lead to heart disease and diabetes) are not obese.

 

Why do they think sugar is dangerous?

The authors say that although sugar is described as “empty calories”, a growing body of evidence suggests that fructose (one component of table sugar) can trigger processes that lead to liver toxicity and a host of other chronic diseases. “A little is not a problem but a lot kills – slowly,” they say.

The authors argue that sugar meets all the four criteria used by health policy makers to justify the regulation of alcohol. These are:

• Unavoidability. While sugar was only available as fruit and honey at certain times of the year to our ancestors, it is now present in nearly all processed foods. In some parts of the world people are consuming more than 500 calories worth of sugar per day.
• Toxicity. There is growing evidence that excess sugar has an effect on human health beyond simply adding calories and can cause many of the same problems as alcohol, including high blood pressure, high blood fats, insulin resistance and diabetes.
• Potential for abuse. The authors argue that, like tobacco and alcohol, sugar acts on the brain to encourage dependence. Specifically, it interferes with the workings of a hormone called ghrelin (which signals hunger to the brain) and it also affects the action of other important compounds.
• Negative impact on society. The economic and human costs of these diseases place excess consumption of sugar in the same category as smoking and drinking.

 

What do they think should be done?

While the authors accept that sugar is “natural” and a “pleasure”, they argue that, like alcohol, too much of a good thing is toxic. Strategies to reduce consumption of alcohol and tobacco show that government controls, such as taxation and imposing age limits, work better than educating people. They make several proposals for controlling sugar, including:

• taxing any processed foods with added sugar, including drinks
• reducing the hours during which retailers can sell food containing added sugar
• tightening the licensing requirements on vending machines and snack bars selling sugary products
• controlling the numbers of fast food outlets and convenience stores
• limiting sales during school hours or imposing an age limit for drinks with added sugar

Finally, they argue that regulating sugar will not be easy, but it can be done with enough pressure for change, citing bans on smoking in public places as an example of what can be achieved.

 

What does this mean for me?

This article will be of interest to food scientists, health policy makers and the public alike, but the use of strategies to restrict the consumption of added sugar is complicated and, indeed controversial. The implications of such moves would need to be considered in both medical and societal terms. They would need both medical evidence to support their effectiveness and assurance that the public would accept drastic changes, such as age limits on buying sweets. For example, in recent years, Denmark has imposed taxes on fatty foods, a move that has divided opinions greatly.

It is generally accepted that added sugar or excessive sugar consumption is bad for health and dietitians advise restricting sugar intake to the occasional “treat”. However, to what extent sugar is directly to blame for the rise in chronic disease and how much is due to other dietary components, such as saturated fat and salt, is open to debate. The current article does not appear to be a formal systematic review of the literature, and it is not certain whether all relevant evidence and resources related to sugar consumption and its health effects have been consulted. As such, it should be considered primarily to reflect the views and opinions of the authors.

In the UK at present, policymakers generally favour encouraging healthier eating through education and the provision of healthier options. This is carried out through public health campaigns such as 5 A DAY or by introducing new food ranges to schools. Whether this approach alone is adequate and whether healthier eating patterns should be encouraged by government regulation, is a crucial area of debate.

Links To The Headlines

Sugar ‘is toxic and must be regulated just like cigarettes’, claim scientists. Daily Mail, February 2 2012

Sugar tax needed, say US experts. BBC News, February 2 2012

Tax harmful sugar. Daily Express, February 2 2012

Links To Science

Lustig RH, Schmidt LA, Brindis LD. Public health: The toxic truth about sugar. Nature, February 2 2012

Britain is in the grip of a new “flesh-eating bug spread by sneezes and coughs”, according to the front page of today’s Metro. The newspaper says that the bacteria are spreading across Britain, as they can be caught through people coughing and sneezing on crowded trains and buses.

This unsettling news put some of the Behind the Headlines team off grabbing their free copy of the Metro at the station this morning, not because of the fear of catching deadly germs from the paper, but because its report was alarmist and overblown. The basis of this news is a laboratory study that investigated why healthcare-acquired meticillin-resistant staphylococcus aureus (MRSA) bacteria rarely cause infections in healthy individuals. The study found that healthcare-acquired MRSA has a high level of antibiotic resistance, but that this property comes at a cost of reduced virulence (being less able to cause infection). Conversely, the study found that the type of MRSA that is usually caught in a community setting is more virulent, but weaker against treatment with antibiotics.

This study has not investigated the transmission, effects or number of cases of community-acquired MRSA in the UK, which formed the basis of many news reports on the research. The researchers state that MRSA outside the healthcare system and in the community is a growing concern, but cases are still very rare. This interesting research contributes to our knowledge of MRSA, rather than warning us of a germ-based Armageddon.

 

Where did the story come from?

The study was carried out by researchers from the University of Bath and the University of Nottingham in the UK; University College Dublin in Ireland; and Texas A&M Health Science Centre and the University of Texas in the US. It was funded by the UK Medical Research Council and a Biotechnology and Biological Sciences Research Council Studentship. The study was published in the peer-reviewed Journal of Infectious Diseases.

This story was widely covered. Most reports were alarmist, concentrating on the supposed emergence of a dangerous, highly infectious new form of community-acquired MRSA. Many newspapers suggested that transmission is easy, that it can lead to a “flesh-eating form of pneumonia”, and that cases are on the increase. These claims seem to be based on the press release for the research rather than the research paper itself. The study was actually laboratory-based research that had investigated why healthcare-acquired MRSA bacteria rarely cause infections in healthy individuals. Although there was some investigation of community-acquired MRSA, the results do not justify the news coverage.

 

What kind of research was this?

This was a laboratory-based study. It aimed to examine why healthcare-acquired MRSA bacteria rarely cause infections in healthy individuals. Healthcare-acquired, or hospital-acquired, means that the bacteria cause infections that mostly occur in healthcare environments.

The researchers initially covered the nature of MRSA and how it resists certain types of antibiotics. It is already known that MRSA is resistant to the antibiotics meticillin and oxacillin because it has acquired a piece of DNA called a ‘mobile genetic element’. Meticillin is an old antibiotic that is now no longer used and has been replaced by flucloxacillin.

Many staphylococcus aureus bacteria have now also developed resistance to the penicillin group of antibiotics (because they produce enzymes that can make penicillin inactive), but are usually still susceptible to the antibiotic flucloxacillin. MRSA, however, does not have this susceptibility to flucloxacillin, and is, therefore, harder to treat than most staphylococci bacteria, needing stronger antibiotics still.

One particular genetic element that is key for deciding the properties of MRSA is called the ‘staphylococcal cassette chromosome mec’ (SCCmec). There are several different versions of this cassette, which each provide bacteria with slightly different properties. The researchers state that healthcare-acquired MRSA have type I, II or III SCCmec elements, whereas community-acquired MRSA have type IV and V elements. These different cassettes all contain a gene (mecA) that codes for a protein called PBP2a, located in the cell wall of the bacteria. PBPs (penicillin binding proteins) are a normal part of the cell wall of many bacteria. Many antibiotics work by inactivating PBPs, which cause the bacteria to die. However, the version of PBP encoded by mecA, PBP2a, is less sensitive to antibiotics, allowing the bacteria to survive.

 

What did the research involve?

The researchers initially determined whether deleting the mecA gene, which encodes the PBP2a cell wall protein, affects the toxicity of MRSA. They then took a healthcare-acquired MRSA strain and a version of this strain that they genetically modified to delete the mecA gene, and performed tests to see how each was able to break up a type of immune cell called a T cell in the laboratory.

The researchers then investigated the ability of the different strains to respond to ‘signalling molecules’, which normally cause the bacteria to activate their production of toxins. The virulence of these strains was confirmed using mouse experiments.

The researchers then compared the production of the PBP2a cell wall protein, T-cell toxicity and the resistance of healthcare-acquired MRSA to antibiotics, compared with community-acquired MRSA.

 

What were the basic results?

The researchers found that deleting the mecA gene caused the MRSA to become more toxic. This was because the expression of mecA results in cell wall changes that interfere with MRSA’s ability to detect or respond to signals to switch on toxin expression. MRSA with mecA deleted was also more virulent in a mouse model, causing mice to lose weight or die.

The researchers then compared MRSA strains with different SCCmec elements: those with type II elements (typical of healthcare-acquired MRSA) and those with type IV elements (typical of community-acquired MRSA). They found that typical community-acquired MRSAs had lower resistance to the antibiotic oxacillin, were more toxic to the immune system’s T-cells and expressed less PBP2a.

 

How did the researchers interpret the results?

“As a direct result of its high level of antibiotic resistance, healthcare-acquired MRSA is impaired in its ability to cause infection, which can explain its inability to cause infection in community settings, where antibiotic usage and the prevalence of susceptible patients are low.” In other words, healthcare-acquired MRSA makes a trade-off, sacrificing its ability to spread to healthy individuals in order to fight off a greater range of antibiotics.

 

Conclusion

This interesting study helps explain why healthcare-acquired MRSA infections are rarely found in healthy individuals. It found that expression of a gene that produces one of the proteins responsible for MRSA’s antibiotic resistance caused it to be less toxic. It also showed that typical community-acquired MRSA strains express less of this antibiotic-resistance protein, but are more toxic.

However, this intriguing lab study did not investigate the transmission, effects or number of cases of community-acquired MRSA in the UK, discussion of which formed the majority of the news reports. On this basis, the research itself does not support the claims that we are under siege from an ‘airborne, bacteria-resistant, flesh-eating superbug’, as newspapers have today suggested.

Links To The Headlines

Flesh-eating bug spread by sneezes and coughs. Metro, February 2 2012

Deadly new superbug is heading for Britain. Daily Express, February 2 2012

New deadly MRSA strain on its way to the UK from USA. Daily Mirror, February 2 2012

Super-strong MRSA bug heading to UK. The Sun, February 2 2012

Flesh-eating bug spread by coughs and sneezes spreading across the UK. Daily Mail, February 2 2012

Links To Science

Rudkin JR, Edwards AM, Bowden MG et al.Methicillin Resistance Reduces the Virulence of Healthcare-Associated Methicillin-Resistant Staphylococcus aureus by Interfering With the agr Quorum Sensing System. Journal of Infectious Diseases, February 1 2012

“Mind-boggling! Science creates computer that can decode your thoughts and put them into words,” the Daily Mail’s headline exclaimed today, while The Daily Telegraph heralded an era in which a “mind-reading device could become a reality”.

You’d be forgiven for thinking famous mind readers such as Derren Brown had just produced a telepathy implant. Instead, these reports are from a small study of 15 people that culminated in researchers being able to reconstruct the sound patterns of words using brain activity alone.

This research involved attaching electrical sensors directly to brains of people undergoing brain surgery to understand how they processed individual words that were played to them. The researchers demonstrated that the brain breaks words down into complex patterns of electrical activity. They were then able to create a mathematical algorithm that decoded and translated the brain activity back into a rough version of the original sound.

But the reconstructed words were not of good enough quality to be recognised by a human listener when played. The words were only recognised when the original and reconstructed sound patterns were compared visually.

This exciting and new research does raise the prospect of brain activity one day being translated into words using an implant. Such technology could help the vast numbers of people suffering from problems affecting speech. But it is important to recognise that this research is in its very early stages and a clinically effective implant is likely to be a long way off.

 

Where did the story come from?

The study was carried out by a collaboration of North American universities led by researchers from the University of California, Berkeley. It was funded by several academic grants and was published in the peer-reviewed science journal Public Library of Science (PLoS) Biology.

The researchers report that the human brain has evolved complex mechanisms to decode highly variable sounds into meaningful elements of language, such as words. Understanding this complex decoding in humans has proved difficult, as it requires recording brain activity on the exposed brain (with the skull removed).

This study took advantage of cases of rare brain surgery for epilepsy and brain tumours that allowed researchers to measure brain activity by attaching sensors directly to the brain surface. This provided a unique opportunity to understand how the human brain recognises speech.

This study received wide media coverage due to its futuristic appeal and was often given a sci-fi angle, with some suggesting a “mind-reading device could become reality”. This research does raise the possibility of developing a device that could interpret thoughts into speech in the future. However, it is important to note the authors’ own caution – that the technology of translating thoughts into words needs to be vastly improved before such a device could become a reality.

 

What kind of research was this?

This was a small study of 15 people undergoing brain surgery for epilepsy or brain tumour. It looked at whether the complex brain activity involved in processing spoken words, such as the sound wave form and syllable rate, could be reconstructed using a computer program.

The researchers believe that the brain processes internal thoughts in a similar way to hearing sounds, and hope that this type of technology could eventually be used to help those who cannot talk, such as those in a coma or in the much-feared “locked-in syndrome”.

 

What did the research involve?

Fifteen patients undergoing brain surgery for epilepsy or brain tumour were asked to listen to 47 real or invented words and sentences from different English speakers. All patients had normal language capabilities when they were enrolled in the study.

During this process electrical signals from the brain were recorded using multiple sensors attached directly to the part of the brain called the lateral temporal cortex, which includes the superior temporal gyrus (STG), thought to be very important in the processing of speech.

To understand and mimic the brain activity involved in processing heard words, the researchers used an approach referred to as “stimulus reconstruction”. In this case, the stimulus was hearing a spoken word.

Hearing words causes a large amount of brain activity involved in recognising and processing the different aspects of the sounds of the words, for example the different sound frequencies and timing of syllables. The word reconstruction involved creating a mathematical program (like that used in computer software) capable of decoding the vast amount of brain activity in such a way that it was possible to identify the original words heard by the participant.

The reconstructed signals from different mathematical models (linear and non-linear) were compared to those detected directly from the brain surface to see how good they were at mimicking the brain’s activity when hearing spoken words. The researchers also used the models to identify the most important areas of the brain involved in processing this information and what other factors influenced the accuracy of the sound reconstructions.

 

What were the basic results?

When constructing the mathematical models they found that the STG region of the brain was important in creating an accurate prediction of the sound pattern of the original word.

The sound patterns generated by the mathematical model allowed the identification of specific words to be generated directly from the brain activity of patients listening to the words. These took the form of visual representations of the word sound pattern. A total of 47 words were presented in pairs and, on average, the model correctly identified the word in approximately nine out of every ten instances (89%). This was significantly better than 50% correct identification, which would be seen simply by guessing.

Importantly, however, the quality produced from reconstructing the words was not good enough for them to be recognised by a human listener when played. The words were only recognised when the original and reconstructed sound patterns were compared visually.

The researchers found that different types of mathematical models performed better at reconstructing the sounds of words with particular characteristics.

 

How did the researchers interpret the results?

The authors concluded that their results demonstrated that key aspects of speech signals can be reconstructed from STG activity.

 

Conclusion

This study of 15 people undergoing brain surgery has demonstrated a method of reconstructing the sound of a heard word using only the signals obtained from the brain. This study represents an important progression in the field of speech reconstruction, which has the potential to improve the lives of many who suffer from speech difficulties in the future.

But the words, when reconstructed, were not of good enough quality to be recognised by a human listener when played. The words could only be identified when the original and reconstructed sound patterns were compared visually. The researchers suggest that improving the brain sensors detecting the STG brain activity may, in the future, improve the reconstructed sound to a level that could be understood by a person listening.

The mathematical formula used to reconstruct the words is at a very early stage and would need a significant amount of improvement and development before it could be considered for use in an implant or similar device in the future. Similarly, future speech reconstruction research would need to demonstrate it was effective in a large range of words, sentence patterns and languages. Currently, the mathematical program has only been tested on a limited vocabulary of 47 English words.

This research represents an intriguing first demonstration of the potential of speech reconstruction technology to transform the lives of people with communication problems in the future.

Links To The Headlines

Science decodes ‘internal voices’. BBC News, February 1 2012

Mind-reading device could become reality. The Daily Telegraph, February 1 2012

Mind-boggling! Science creates computer that can decode your thoughts and put them into words. Daily Mail, February 1 2012

Mind-reading program translates brain activity into words, The Guardian, February 1 2012

Links To Science

Pasley BN, David SV, Mesgarani N, et al. Reconstructing Speech from Human Auditory Cortex. PloS Biology. Published online January 31 2012

“Heartburn pills taken by thousands of women ‘raise risk of hip fractures by up to 50 per cent’,” the Daily Mail reported today. The headline is based on a large new study of drugs called proton pump inhibitors (PPIs), which are commonly used to treat heartburn, acid reflux and ulcers.

The study found that post-menopausal women who regularly took PPIs for at least two years were 35% more likely to suffer hip fracture than non-users, a figure that increases to 50% for women who were current or former smokers. However, although this increase in risk is large, the overall risk of fractures remains small.

This was a large, well conducted study that suggests that long-term use of PPIs is associated with a small increase in risk of hip fracture, although the researchers point out that the risk seems to be confined to women with a history of smoking. Unlike previous research, this study took careful account of other factors that might affect risk such as body weight and calcium intake.

Women who are concerned about their use of PPIs are advised to consult their GP.

 

Where did the story come from?

The study was carried out by researchers from Massachusetts General Hospital, Boston University and Harvard Medical School and was funded by the US National Institutes of Health. The study was published in the peer-reviewed British Medical Journal.

Although the Mail’s headline is technically correct, it gives the impression that these drugs carry a very large increase in the risk of hip fracture. In fact, the study found that, in absolute terms, the increase in risk for regular users was small. Researchers found that among the women in the study who regularly used PPIs, about two in every 1,000 fractured a hip each year. In non-users, this figure was about 1.5 in every 1,000. This is a increase of about five fractures a year in every 10,000 women taking PPIs.

The Mail did point out this “absolute difference” towards the end of its story. Both the Mail and the BBC included comments from independent experts.

 

What kind of research was this?

The researchers point out that PPIs are among the most commonly used drugs worldwide. In the US they are available over the counter, but in the UK are available only on prescription. They are used for symptoms of heartburn, gastro-oesophageal reflux disease (GORD) and stomach ulcers. PPIs are thought to work by reducing acid production in the stomach. Concern has grown over a potential association between long-term use of these drugs and bone fractures, although the researchers say that previous studies have had conflicting results and many did not take other factors (called confounders) that might affect the risk of fracture into account.

In their cohort study of nearly 80,000 post-menopausal women, the researchers set out to examine the association between long-term use of PPIs and the risk of hip fracture. Unlike a randomised controlled trial, a cohort study cannot prove cause and effect. However, cohort studies enable researchers to follow large groups of people for long periods and they are useful for looking at potential long-term risks and benefits of treatments. The study was prospective, which means it followed participants in time, rather than collecting information retrospectively. This makes it more reliable.

 

What did the research involve?

This study took its data from a large ongoing US study called the Nurses Health Study, which began in 1976 and which sent health questionnaires every two years to 121,700 female nurses aged 30-55.

From 1982 participants were asked to report all previous hip fractures and in each biennial questionnaire, women were asked if they had sustained a hip fracture over the previous two years. Those who reported a hip fracture were sent a follow-up questionnaire asking for more details. Fractures from bad accidents, such as falling down a flight of stairs, were excluded from the study. A review of medical records for 30 of the women validated all self-reported fractures.

From 2000 to 2006 the women were asked if they had regularly used a PPI in the previous two years. In earlier questionnaires (1994, 1996, 1998 and 2000), the women were also asked if they had regularly used other drugs for acid reflux, called H2 blockers.

The biennial questionnaires also included questions on other factors including menopausal status, body weight, leisure activities, smoking and alcohol use, use of hormone replacement therapy (HRT) and other medicines. Researchers used a validated food frequency questionnaire to calculate the women’s total intake of calcium and vitamin D.

They then analysed the data for any association between regular use of PPIs and hip fracture, adjusting their findings for key confounders such as body weight, physical activity, smoking and alcohol and calcium intake. They also took into account whether the reasons for using a PPI might have affected the results.

Finally, they carried out a systematic review combining their results with 10 previous studies on the risk of hip fracture and the long-term use of PPIs.

 

What were the basic results?

The researchers documented 893 hip fractures during the period of the study. They also found that, in 2000, 6.7% of women regularly used a PPI – a figure that had risen to 18.9% by 2008.

• Amongst women who had regularly taken a PPI at any time, there were 2.02 hip fractures per 1,000 person years, compared with 1.51 fractures per 1,000 person years among non-users.
• Women who regularly used PPIs for at least two years had a 35% higher risk of hip fracture than non-users (age adjusted hazard ratio (HR) 1.35; 95% confidence interval (CI) 1.13 to 1.62), with longer use associated with increasing risk. Adjustment for risk factors, including body mass index, physical activity and intake of calcium did not alter this association (HR 1.36; CI 1.13 to 1.63).

The increased risk did not change when researchers also took into account the reasons for PPI use:

• Current and former smokers who regularly used PPIs were 51% more likely to have a hip fracture than non-users (HR 1.51; (CI) 1.20 to 1.91).
• Among women who never smoked there was no association between PPI use and hip fracture (HR 1.06; (CI) 0.77 to 1.46).
• In a meta-analysis of these results with 10 previous studies, the risk of hip fracture in users of PPI was higher compared to non–users of PPIs (pooled odds ratio 1.30; CI 1.25 to 1.36).

The researchers also found that two years after women stopped taking PPIs, their risk of hip fracture returned to a similar level to that in women who had never taken them. Also, women taking H2 blockers had a “modest” increased risk of hip fracture but the risk was higher in women who took PPIs.

 

How did the researchers interpret the results?

The researchers conclude that their results provide “compelling evidence” of a risk between PPI use and hip fracture. They say the findings suggest that the need for long-term, continuous use of PPIs should be carefully evaluated, particularly among people who have smoked or are still smokers.

They suggest that PPIs may increase the risk of fracture by impairing the absorption of calcium, although in this study the risk of fracture was not affected by dietary calcium intake. The finding that the risk was confined to women with a history of smoking (an established risk factor for fracture) indicates that smoking and PPIs may act together (have a “synergistic effect”) on fracture risk.

 

Conclusion

This large study had several strengths. Unlike some previous studies, it collected information on and took into account other key risk factors for fracture, including body weight, smoking, alcohol use and physical activity. It also looked at the women’s use of PPIs every two years (rather than just asking them once) and took into account variations in use during this time in their analysis.

 

However, as the authors note, it also had some limitations:

• It did not ask about the brands of PPI used, nor the doses of PPI the women took, both of which could affect risk of fracture.
• The information about hip fracture was self-reported and not confirmed by medical records (although a smaller study has found self-reporting of hip fracture to be reliable).
• Also, the study did not record the women’s bone mineral density (BMD). Low[?] BMD is an important risk factor for fracture and adding a measure of this could have strengthened the study.

Finally, because this was a cohort study, other factors both measured and unmeasured may have affected the results, even though researchers took many of these into account in their analysis. Socio-economic status and education, for example, were not established. Because this was a study of registered nurses, the applicability of the results to other socio-economic groups might be limited.

This study found that the long-term, regular use of these drugs is associated with a small increased risk in hip fracture among older women, a risk that seems to be confined to past or current smokers. Women who regularly take PPIs and who are concerned about these findings are advised to talk to their GP. Whether any change in use of this commonly prescribed drug is needed requires further study. 

Links To The Headlines

Indigestion drugs taken by millions linked to hip fractures. The Daily Telegraph, February 1 2012

Heartburn pills taken by thousands of women ‘raise risk of hip fractures by up to 50 per cent’. Daily Mail, February 1 2012

Ulcer drugs ‘link to fractures’. BBC News, February 1 2012

Links To Science

Khalili H, Huang ES, Jacobsen BC, et al. Use of proton pump inhibitors and risk of hip fracture in relation to dietary and lifestyle factors: a prospective cohort study. British Medical Journal. Published online January 31 2012

 

“Mind-boggling! Science creates computer that can decode your thoughts and put them into words,” The Daily Mail’s headline exclaimed today, while the Daily Telegraph heralded an era in which a “mind-reading device could become a reality”.

You’d be forgiven for thinking famous mind readers such as Derren Brown had just produced a telepathy implant. Instead, these reports are from a small study of 15 people that culminated in researchers being able to reconstruct the sound patterns of words using brain activity alone.

This research involved attaching electrical sensors directly to brains of people undergoing brain surgery to understand how they processed individual words that were played to them. The researchers demonstrated that the brain breaks words down into complex patterns of electrical activity. They were then able to create a mathematical algorithm that decoded and translated the brain activity back into a rough version of the original sound.

But the reconstructed words were not of good enough quality to be recognised by a human listener when played. The words were only recognised when the original and reconstructed sound patterns were compared visually.

This exciting and new research does raise the prospect of brain activity one day being translated into words using an implant. Such technology could help the vast numbers of people suffering from problems affecting speech. But it is important to recognise that this research is in its very early stages and a clinically effective implant is likely to be a long way off.

 

Where did the story come from?

The study was carried out by a collaboration of North American universities led by researchers from the University of California Berkeley. It was funded by several academic grants and was published in the peer-reviewed science journal Public Library of Science Biology.

The researchers report that the human brain has evolved complex mechanisms to decode highly variable sounds into meaningful elements of language, such as words. Understanding this complex decoding in humans has proved difficult, as it requires recording brain activity on the exposed brain (with the skull removed).

This study took advantage of cases of rare brain surgery for epilepsy and brain tumours that allowed researchers to measure brain activity by attaching sensors directly to the brain surface. This provided a unique opportunity to understand how the human brain recognises speech.

This study received wide media coverage due to its futuristic appeal and was often given a sci-fi angle, with some suggesting a “mind-reading device could become reality”. This research does raise the possibility of developing a device that could interpret thoughts into speech in the future. However, it is important to note the authors’ own caution – that the technology of translating thoughts into words needs to be vastly improved before such a device could become a reality.

 

What kind of research was this?

This was a small study of 15 people undergoing brain surgery for epilepsy or brain tumour. It looked at whether the complex brain activity involved in processing spoken words, such as the sound wave form and syllable rate, could be reconstructed using a computer program.

The researchers believe that the brain processes internal thoughts in a similar way to hearing sounds, and hope that this type of technology could eventually be used to help those who cannot talk, such as those in a coma or in the much-feared “locked-in syndrome”.

 

What did the research involve?

Fifteen patients undergoing brain surgery for epilepsy or brain tumour were asked to listen to 47 real or invented words and sentences from different English speakers. All patients had normal language capabilities when they were enrolled in the study.

During this process electrical signals from the brain were recorded using multiple sensors attached directly to the part of the brain called the lateral temporal cortex, which includes the superior temporal gyrus (STG), thought to be very important in the processing of speech.

To understand and mimic the brain activity involved in processing heard words, the researchers used an approach referred to as “stimulus reconstruction”. In this case, the stimulus was hearing a spoken word.

Hearing words causes a large amount of brain activity involved in recognising and processing the different aspects of the sounds of the words, for example the different sound frequencies and timing of syllables. The word reconstruction involved creating a mathematical program (like that used in computer software) capable of decoding the vast amount of brain activity in such a way that it was possible to identify the original words heard by the participant.

The reconstructed signals from different mathematical models (linear and non-linear) were compared to those detected directly from the brain surface to see how good they were at mimicking the brain’s activity when hearing spoken words. The researchers also used the models to identify the most important areas of the brain involved in processing this information and what other factors influenced the accuracy of the sound reconstructions.

 

What were the basic results?

When constructing the mathematical models they found that the STG region of the brain was important in creating an accurate prediction of the sound pattern of the original word.

The sound patterns generated by the mathematical model allowed the identification of specific words to be generated directly from the brain activity of patients listening to the words. These took the form of visual representations of the word sound pattern. A total of 47 words were presented in pairs and, on average, the model correctly identified the word in approximately nine out of every ten instances (89%). This was significantly better than 50% correct identification, which would be seen simply by guessing.

Importantly, however, the quality produced from reconstructing the words was not good enough for them to be recognised by a human listener when played. The words were only recognised when the original and reconstructed sound patterns were compared visually.

The researchers found that different types of mathematical models performed better at reconstructing the sounds of words with particular characteristics.

 

How did the researchers interpret the results?

The authors concluded that their results demonstrated that key aspects of speech signals can be reconstructed from STG activity.

 

Conclusion

This study of 15 people undergoing brain surgery has demonstrated a method of reconstructing the sound of a heard word using only the signals obtained from the brain. This study represents an important progression in the field of speech reconstruction, which has the potential to improve the lives of many who suffer from speech difficulties in the future.

But the words, when reconstructed, were not of good enough quality to be recognised by a human listener when played. The words could only be identified when the original and reconstructed sound patterns were compared visually. The researchers suggest that improving the brain sensors detecting the STG brain activity may, in the future, improve the reconstructed sound to a level that could be understood by a person listening.

The mathematical formula used to reconstruct the words is at a very early stage and would need a significant amount of improvement and development before it could be considered for use in an implant or similar device in the future. Similarly, future speech reconstruction research would need to demonstrate it was effective in a large range of words, sentence patterns and languages. Currently, the mathematical program has only been tested on a limited vocabulary of 47 English words.

This research represents an intriguing first demonstration of the potential of speech reconstruction technology to transform the lives of people with communication problems in the future.

Links To The Headlines

Science decodes ‘internal voices’. BBC News, February 1 2012

Mind-reading device could become reality. The Daily Telegraph, February 1 2012

Mind-boggling! Science creates computer that can decode your thoughts and put them into words. Daily Mail, February 1 2012

Mind-reading program translates brain activity into words, The Guardian, February 1 2012

Links To Science

Pasley BN, David SV, Mesgarani N, et al. Reconstructing Speech from Human Auditory Cortex. PloS Biology. Published online January 31 2012