Medical News

Impact of daytime naps on children's sleep quality uncertain

Medical News - Wed, 02/18/2015 - 14:30

“Daytime naps ‘should stop at the age of two’: Children have poorer quality sleep if they rest during the afternoon,” is the inaccurate headline on the Mail Online.

Researchers have pooled all of the available evidence on the effects of napping in childhood.

As they acknowledge, many of the studies were of a poor quality due to lack of reliable evidence.

Out of the 26 studies, just one looked at the effect of napping on sleep in children under the age of three. It found that napping was associated with a shorter night’s sleep in children over the age of two. This study did not assess the quality of sleep.

The quality of sleep was assessed in three studies of children over the age of three. The quality of sleep was found to be reduced in those that napped.

Across the other studies, there were no clear findings on the effects of napping in terms of behaviour, cognitive function or physical health, regardless of age.

The review does not support the notion that parents should automatically stop their children from napping after their second birthday. It actually calls for more rigorous research in this area, so firmer conclusions can be drawn.

We would tentatively suggest that, based on the lack of evidence, the best people to decide whether an individual child benefits from an afternoon nap are the parents.

 

Where did the story come from?

The study was carried out by researchers from Queensland University of Technology and James Cook University in Queensland. No external funding was reported.

The study was published in the peer-reviewed medical journal Archives of Disease in Childhood.

Mail Online’s reporting of the study is poor and may cause unnecessary alarm among parents.

The paper took the findings from just one of the studies and produced a dramatic headline that naps should stop at the age of two.

This is not a recommendation from the review, which actually found that an association between daytime napping and later onset of sleep, shorter duration and poorer quality sleep was found in children over the age of three.

The review is clear that these findings were based on poor-quality studies, so are not reliable.

There is huge variation in children’s sleeping patterns and requirements, with children naturally growing out of the need for naps at different rates. This review highlights the need for better studies in this area, rather than a blanket cut-off age for all.

 

What kind of research was this?

This was a systematic review of all studies that have assessed the effect of napping on child health and development.

The authors highlight the ongoing debate on the optimal amount of sleep recommended in early childhood. Previous research had looked at the overall amount of sleep in a 24-hour period and the effect this had on children’s health. The authors say this influenced the promotion of napping, to make up the optimal number of hours. However, this does not take into account the effect napping may have on the quality and length of night-time sleep. The aim of this study was to see what effect napping had on a child’s night-time sleep, behaviour, cognitive functioning (ability to think and reason), and physical health.

 

What did the research involve?

The researchers searched six databases for any type of study that has looked at the effects of napping in children from birth up to the age of five. They then examined the reference lists of any relevant studies, to ensure they had not missed any.

The quality of each study was assessed using the internationally recognised GRADE system. This is an ongoing attempt to achieve a consensus on what represents high-, medium- or low-quality evidence.

In general, randomised controlled trials (RCTs) are rated as high-quality and observational studies as low-quality, though this also depends on the methodology. It takes into account the number of participants and the risk of the studies being biased.

Due to the fact that young children lack the capacity to consent to take part in studies involving specific interventions (such as making them stay awake during the day), there were no RCTs on napping available for analysis.

 

What were the basic results?

There were 26 studies that met the inclusion criteria. All were low-quality and none were RCTs, for the reasons discussed above.

With regards to night-time sleep:

  • one Japanese study of 967 children found there was no difference in night-time sleep when associated with the duration of napping in children younger than two; children older than two had later onset of sleep and less night-time sleep after napping
  • two additional studies of children aged between three-and-a-half and seven found napping was associated with later onset of night-time sleep
  • four studies of children aged three or more found reduced night-time sleep duration after napping
  • three studies of children aged three or more found poorer quality of sleep after napping

Behaviour and cognitive outcomes in children who nap compared to those who don’t were mixed across the studies, which were carried out on children from birth to age seven.

Similarly, there was very poor evidence available of the effect of naps or no naps on physical health at any age. 

 

How did the researchers interpret the results?

The authors say “the evidence indicates that beyond the age of two years, napping is associated with later night sleep onset and both reduced sleep quality and duration”. They say that “the evidence regarding behaviour, health and cognition is less certain”. They suggest that “in preschool children presenting with sleep problems, clinicians should investigate napping patterns”.

 

Conclusion

This systematic review has found that the available evidence on the effect of napping on young children is poor. One study found that in children aged over two years, naps were associated with later sleep onset and shorter duration. The rest of the studies assessing night-time sleep were in children over the age of three. In these children, naps were associated with later onset of night-time sleep, with shorter duration and poorer quality.

There was no clear evidence of the effect of having naps or not having naps on behaviour, cognitive function or physical health.

While systematic reviews cover all of the evidence available for a particular question, they are limited by the quality of the available studies. This analysis is restricted to the facts reported by the systematic review and does not independently assess the quality of the included studies.

With this in mind, none of the studies were RCTs. The findings of this review need to be taken within the context of their poor quality, which limits the reliability of the findings. Five of the nine studies looking at the effect of naps on sleep were scored the lowest possible score for quality. The main issues reported were that the studies:

  • analysed less than seven days of sleep data
  • relied on parental report, rather than direct observation
  • had a small sample size

There is huge variation in children’s sleeping patterns and requirements, with children naturally growing out of the need for naps at different rates. This review highlights the need for better studies in this area, rather than a blanket cut-off age for all.

Due to the paucity of high-quality evidence, we would certainly not recommend changing your child’s sleeping patterns if it seems to suit them.

Read about common sleep problems in children

Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Daytime naps 'should stop at the age of two': Children have poorer quality sleep if they rest during the afternoon. Mail Online, February 18 2015

Links To Science

Thorpe K, Staton S, Sawyer E, et al. Napping, development and health from 0 to 5 years: a systematic review. Archives of Disease in Childhood. Published online February 17 2015

Categories: Medical News

Plain packaging 'may help smokers to cut down'

Medical News - Tue, 02/17/2015 - 19:05

"Plain packaging reduced unconscious triggers to smoke," BBC News reports.

This claim is based on two related experiments where smokers were either exposed to a picture of a branded pack of cigarettes, a picture of a plain pack (containing a graphic health warning), or nothing at all, and were asked to choose a reward of either chocolate or a cigarette.

Researchers found people exposed to the plain pack were, over time, 9% more likely to choose a chocolate reward compared with people exposed to the branded pack, so their consumption of cigarettes was reduced.

This study has inherent limitations, meaning we shouldn't really count on seeing a similar reduction in smoking through the use of plain packaging in the real world, as the study's authors acknowledge themselves.

Professor Marcus Munafò, a co-author of the study, explained: "In the natural environment, smoking may be governed by a whole range of factors … It is not clear to what extent plain packaging will reduce smoking when these other factors are at play."

The biggest real-world experiment is already underway in Australia, where plain packaging was introduced by law in 2012. Recent information released by the Australian government does show a subsequent modest reduction in smoking rates.

 

Where did the story come from?

The study was carried out by researchers from the universities of Exeter and Bristol in the UK, and the University of New South Wales, Australia.

It was funded by the British Heart Foundation, Cancer Research UK, the Economic and Social Research Council, the Medical Research Council, and the National Institute for Health Research.

The study was published in the peer-reviewed science journal Addiction on an open-access basis, so it is free to read online.

BBC News summarised the results of several related studies on plain cigarette packaging.

The Guardian reported on a study in the same journal looking at whether plain packaging would help reduce the number of people taking up the habit. This study is also available online to read for free.

 

What kind of research was this?

This was an experimental study investigating how cigarette packaging influences smokers' desire to smoke.

The research team says that in current smokers, plain cigarette packs are less appealing, provoke less craving and motivation to purchase, reduce short-term self-reported smoking rates, and increase attention to health warnings when compared with branded packs.

Although these studies suggest plain packs may reduce smoking motivation, the research team thought further direct evidence of whether plain packs reduce the amount people smoke was needed to gain insight into the potential effectiveness of a plain packaging policy.

Experimental studies like this are useful in isolating single elements of a decision-making process in artificial laboratory conditions. But they don't reflect the more complex decision-making environment of normal life. A judgement call needs to be made about how relevant the experimental condition is to normal life, and this isn't an exact science.

 

What did the research involve?

The team reported two similar experiments: one small (n=23), the other larger (n=121).

Smokers had to choose between pressing a key that might earn cigarettes, or a key that might earn chocolate. They were uncertain about which key was most likely to pay off in each test.

Just before participants made each choice, they were presented with either a picture of a branded cigarette pack, a picture of a plain cigarette pack, or nothing (as a control). This aimed to show whether the pictures influenced choice preference.

Participants were eligible for the study if they smoked between 5 and 20 cigarettes a day every day of the week and smoked within one hour of waking. The average age in the larger group was 21, and they smoked an average of 10 cigarettes a day.

 

What were the basic results?

The combined results showed branded packs increased the probability of smokers choosing a cigarette by 10% compared to when nothing was presented. The plain packs did not. The implication is that plain packs are less effective at prompting smokers to purchase cigarettes compared with branded packs.

Branded pack pictures prompted a tobacco choice in 62% of decisions, compared with 53% using plain packaging. The difference – 9% – was rounded up to a cleaner-sounding 10% for the press release.

 

How did the researchers interpret the results?

The team concluded that, "Plain packaging may reduce smoking in current smokers by degrading cue-elicited tobacco-seeking."

In the press release, co-author Lee Hogarth said that, "Our study demonstrated that, under some circumstances, plain packaging can reduce cigarette-seeking behaviour. Policymakers must consider how much weight to place on this observation when considering the potential pros and cons of introducing plain packing as a national policy."

 

Conclusion

This small study showed that priming adult smokers with a picture of a branded cigarette packet causes more of them to seek cigarettes compared with unbranded cigarettes – around 10% more.

But this study has problems, meaning we can't really rely on its findings. The biggest of these was fully acknowledged by the study authors themselves.

Professor Marcus Munafò, a co-author of the study, explained: "The experimental procedure only modelled the ability of pack stimuli to promote a cigarette-seeking choice.

In the natural environment, smoking may be governed by a whole range of factors, including tobacco withdrawal, the presence of other people smoking, time of day, and so on. It is not clear to what extent plain packaging will reduce smoking when these other factors are at play.”

The biggest real-world experiment is already happening in Australia, where plain packaging was introduced by law in 2012. The wider evidence showing whether plain packaging reduces smoking-related death and disease in adults or children was not discussed in this study, so we cannot comment. Taken on its own, this specific study adds weak evidence to the debate. There may be stronger evidence elsewhere.

On this point, the Addiction journal's editor-in-chief, Professor Robert West, said in the BBC article: "All the pieces are building the same picture, which is that it is going to have a reduction; none of the studies are pointing in the other direction." But he admitted it was not possible to know if plain packaging had reduced the number of young smokers in Australia.

He said the data was "suggestive, but not conclusive", as "the effect would have to be enormous for it to be picked up in the overall prevalence data".

The current UK government has pledged to introduce plain packaging legislation in this country in 2016. But there is a general election between now and then, so any government formed after that may have different plans and priorities.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Cigarette packet law 'would save lives'. BBC News, February 17 2015

Plain cigarette packaging can deter the take-up of smoking, studies suggest. The Guardian, February 17 2015

Links To Science

Hogarth L, Maynard OM, Munafò MR. Plain cigarette packs do not exert Pavlovian to instrumental transfer of control over tobacco-seeking. Addiction. Published online November 13 2015

Categories: Medical News

Molecule could protect against Alzheimer's disease

Medical News - Tue, 02/17/2015 - 13:30

"Alzheimer's breakthrough: scientists home in on molecule which halts development of disease," The Daily Telegraph reports. The so-called "chaperone molecule", known as "Brichos", helps prevent the clumping of proteins, which can lead to the death of brain cells.

Scientists don't know what causes Alzheimer's disease, but people who have the condition tend to have abnormally high amounts of stringy proteins called amyloid plaques in their brains. The plaques interfere with brain cells, damaging brain function.

News of a molecule that could stop some of this damage is encouraging, but declaring a "breakthough" is premature. We don't know if this molecule has an effect on humans, because the experiments were all carried out on mice.

Although Brichos stopped damage occurring in a specific amyloid-related biological pathway, some of the damage associated with Alzheimer's disease could occur via other routes.

As the researchers point out, Brichos would probably not be a suitable candidate for a drug treatment. Because of its composition, it could be absorbed by the body before it reached the brain.

The hope is that there may be more "chaperone molecules" out there that do have the ability to cross the blood-brain barrier and help prevent brain cell damage.

 

Where did the story come from?

The study was carried out by researchers from the University of Cambridge, a trio of Swedish institutions – Karolinska Institutet, Lund University, and the Swedish University of Agricultural Sciences – and Tallinn University in Estonia.

It was funded by several health foundations, charities and research grants from national and international non-commercial organisations. No conflicts of interest were declared.

The study was published in the peer-reviewed science journal, Nature Structural and Molecular Biology.

The UK media's reporting was somewhat overexcited, with most framing the study as a breakthrough, implying that a treatment was inevitable.

Many showed no restraint by failing to talk about the drawbacks of the research, which were outlined by the researchers themselves in their conclusion.

Headlines from The Independent and The Guardian reporting a "possible breakthrough" were the most balanced. The Mirror went bigger, reporting a "Major Alzheimer's breakthrough".

The Mail Online and Daily Telegraph also towed the "breakthrough" line. Arguably, these are all overstatements as there is no guarantee that any of this works when used on humans. At the moment, we only know it works in mice.

Some sources, such as The Times, talked about the possibility of this research leading to a statin-type drug, taken as a preventative measure by people who were free of any dementia-like symptoms. This development is, currently, just speculation.

We also suspect that many people would be reluctant to take such a drug if they were free of any symptoms – a suspicion prompted by the ongoing controversy about statins, and whether the potential benefits outweigh any risk of side effects.

 

What kind of research was this?

This was mainly laboratory research, looking into the complex biological processes involved in Alzheimer's disease.

Alzheimer's disease is the most common type of dementia, affecting almost 500,000 people in the UK. Symptoms of Alzheimer's include progressive loss of mental ability, associated with the gradual death of brain cells.

While the cause is unknown, Alzheimer's disease has been associated with the build-up of proteins called amyloid plaques in the brain.

The researchers say fine fibres (fibrils) that make up the amyloid plaques kick-start toxic reactions around them, which ultimately cause further damage to the surrounding brain cells. The researchers wanted to see if they could stop or lessen this secondary damage.

 

What did the research involve?

The research studied purified amyloid protein fibrils under a variety of controlled conditions in the laboratory. They used these experiments to better understand how the fibrils formed, and how they catalysed other toxic reactions that could be causing damage to brain cells.

They also tested a short protein section (a molecule of amino acids) called Brichos to see if it could interfere with the processes they were seeing, and lessen the damage.

Experiments used lab-grown human cells, as well as mouse brain tissue.

None of the experiments investigated whether Brichos could prevent symptoms of dementia or Alzheimer's in mice or people. It was looking at chemical reactions, not symptoms.

 

What were the basic results?

The Brichos protein stopped reactions caused by the amyloid fibrils, reducing their toxicity in mice brain cells.

The experiments showed that Brichos did this by binding to the surfaces of amyloid fibrils. This specific binding stopped the toxic chain reactions that usually lead to damaging aggregation of other proteins. In essence, some of the disease process had been stopped.

 

How did the researchers interpret the results?

The authors summarised: "These results reveal that molecular chaperones [like Brichos] can help maintain protein homeostasis by selectively suppressing critical microscopic steps within the complex reaction pathways responsible for the toxic effects of protein misfolding and aggregation."

They said Brichos was just the first protein they had investigated, and there may be other molecules that work in a similar way.

 

Conclusion

This study showed that a molecule called Brichos can selectively block some of the toxic effects linked to the accumulation of amyloid protein in the brains of mice. The research on Brichos is at a very early stage, having only been tested in mice.

Dr Laura Phipps of Alzheimer's Research UK says: "This study has revealed clues on how to block one important chain of events in the disease." Dr Doug Brown of the Alzheimer's Society added: "This revelation is exciting, as it gives scientists a whole new way of looking at the problem, opening the doors to possible new treatments."

Contrast this with the Mail Online outlining that this discovery "raises the prospect of a treatment which could be routinely taken in middle age to stop dementia. It could even result in a pill that could be used to treat dementia in the same way that statins are used to prevent heart disease today".

While the Mail's vision – among other news sources – is certainly possible, it is premature. There is no guarantee this research will lead to effective treatments for Alzheimer's disease.

And it should also be noted this study has limitations, which should be considered.

Brichos stopped secondary damage occurring in a specific amyloid-related disease pathway. But damage could occur by other means. And it doesn't appear to reverse existing damage.

Most people with Alzheimer's disease are diagnosed when they already have significant damage to their brain that has caused symptoms severe enough to affect their daily lives. So any "treatment" would need to be taken before symptoms appear, thereby acting as more of a prevention.

Similarly, as Brichos doesn't stop the amyloid plaques forming, it is unlikely to be fully preventative. There may also be side effects when using Brichos on people. It is also likely that Brichos will be absorbed by the body before it reaches the brain.

All these issues and many more will need to be ironed out by further research.

This study is certainly a step in the right direction, because it improves our understanding of the biology of Alzheimer's disease. But it is too early to say whether Brichos will lead to useful treatments or preventative medicines in the future.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Alzheimer's breakthrough: scientists home in on molecule which halts development of disease. The Daily Telegraph, February 17 2015

Alzheimer's researchers find molecule that delays onset of disease. The Guardian, February 16 2015

Alzheimer's breakthrough as scientists discover how to stop disease in its tracks, paving the way for 'statin-like' drug. Mail Online, February 17 2015

Major Alzheimer's breakthrough as scientists close to blocking spread of disease. Daily Mirror, February 16 2015

Possible breakthrough in search for Alzheimer's drugs. The Independent, February 16 2015

Scientists could be closer to curing Alzheimer's. ITV News, February 16 2015

Links To Science

Cohen SIA, Arosia P, Presto J, et al. A molecular chaperone breaks the catalytic cycle that generates toxic Aβ oligomers. Nature Structural and Molecular Biology. Published online February 16 2015

Categories: Medical News

Media heralds the discovery of 'infidelity gene'

Medical News - Mon, 02/16/2015 - 15:00

“Women are more likely to cheat on their partner if they carry the ‘infidelity gene’,” reports the Mail Online. They say that this gene “only has an impact on women”.

The headline is based on a study by Finnish researchers who were interested in a long-standing evolutionary puzzle: why do some women cheat on their partners? From an evolutionary perspective, the more partners a man has the more chances to pass on their genes. But as women can only have one pregnancy at a time, the benefit of having multiple partners is less clear (in strictly evolutionary terms).

The researchers looked at more than 7,000 twins and siblings who had been in relationships for over a year. Analyses comparing identical twins with non-identical twins or siblings suggested that some of the variation in infidelity behaviour seen could be accounted for by genetics.

The researchers also found that certain variations in the gene encoding a receptor for the hormone vasopressin were more common in women who reported having sex with more than one person in the past year, than in women who had sex with just one person. This association was not found in men.

This study only found an association between variations in one gene and infidelity.

Infidelity is likely to have complex influences, and while this might include a genetic component, this is unlikely to boil down to a single “infidelity gene”.

 

Where did the story come from?

The study was carried out by researchers from the University of Queensland in Australia and other research centres in Australia, Sweden and Finland. Study authors were funded by the Australian Research Council and the Academy of Finland.

The study was published in the peer-reviewed journal Evolution and Human Behavior (sic).

The Mail Online’s headline oversimplifies what is likely to be an issue with complex causes.

The study does not suggest that there is a single “infidelity gene”, and the authors themselves note that their findings are tentative.

 

What kind of research was this?

This was a cross-sectional study looking at possible genetic reasons for infidelity.

In evolutionary terms, having sex with people who are not your partner if you are a man increases your chances of fathering more children and passing on your genes. As women can only carry one baby at a time, the evolutionary reasons why infidelity might be advantageous are less clear.

One theory is that women could increase the “genetic benefits” for their children if they become pregnant by having sex with a man who has “higher-quality genes” than their partner. However, evidence gathered from socially monogamous birds suggests this may not be the case.

Another theory is that any genetic variations which predispose men to infidelity could also predispose women to infidelity. Therefore, if these genetic variations give rise to a better chance of a man’s genes being passed on, they will also exist in women, even though there is no advantage. The researchers wanted to assess if this could be the case in humans.

The methods used in this study are commonly used to look at how much variation in a particular trait might be explained by genes in a given population, and also to look for associations with particular genetic variations. However, the results may not be representative of other populations. It is also not possible to say with certainty whether any associations identified directly cause or contribute to the outcome – particularly when talking about a complex behaviour such as infidelity.

 

What did the research involve?

The researchers first looked at how much of infidelity might be accounted for by genetic factors. They then looked at whether variations in two genes (oxytocin and vasopressin receptor genes) were associated with infidelity.

In their first analysis, the researchers assessed infidelity in 7,378 twins and their siblings who were in long-term relationships (married or with a steady sexual partner for at least a year). The participants were asked how many different sexual partners they had had in the past year, and those who reported having more than one partner were counted as having been unfaithful (“extrapair mating”, to use the study’s terminology).

They analysed whether infidelity behaviour was more likely to be shared by identical twins (who have the same genes) than non-identical twins or siblings (who only share half of their genes, on average). If identical twins share a behaviour more than non-identical twins or siblings, this indicates that genetics could be playing a role. Twins and siblings are considered to share their environment to a similar extent.

The researchers also looked at whether brother-sister sibling pairs tended to show the same infidelity behaviour. If they did, this might suggest that the theory that the genes affecting fidelity in men might also affect fidelity in women might be responsible for this similarity.

In the second part of their study, they looked at whether variations in the genes encoding receptors for the hormones vasopressin and oxytocin were associated with infidelity. These hormones and their receptors have been found to affect pair-bonding behaviour in voles, and to be associated with social behaviour in humans.

The researchers looked at 19 single “letter” variations and two other variations in and around the two main genes of interest: AVPR1A and OXTR. The researchers also looked at 120 variations in and around other genes.

 

What were the basic results?

The researchers calculated that genetics may account for around 62% of the variation in infidelity behaviour in men in the population, and 40% in women. They found that brother-sister sibling pairs were not particularly similar in their likelihood of being unfaithful to their partner. This suggested that the genes which might be affecting infidelity in men were not likely to be affecting infidelity in women.

They found that variations in the gene for the vasopressin receptor AVPR1A were associated with infidelity behaviour in women, but not men. Variations in the oxytocin receptor gene (OXTR) were not associated with infidelity behaviour in either sex.

 

How did the researchers interpret the results?

The researchers conclude that they “found significant genetic influences accounting for around half the variation in extrapair mating in both sexes, confirming biological underpinnings to the behaviour”. They note that the AVPR1A association they found “should be regarded as tentative until subjected to rigorous replication”.

 

Conclusion

This study has suggested that there may be some genetic influence on variations in infidelity behaviour. It also identified variations in a gene for AVPR1A that were linked to infidelity in women, but not men.

The limitations to this study include the following:

  • The researchers note that some of their results are not very precise (have wide confidence intervals) as infidelity was relatively uncommon.
  • Some of the findings relating to the two genes (AVPR1A and OXTR) differed from what might be expected, based on the findings of some other studies of related behaviours, such as social pair bonding.
  • Many studies have found associations between genetic variations and complex behaviours that have not been confirmed in later studies.
  • An association does not necessarily mean that one factor causes the other.

Infidelity is likely to have complex influences, and while this might include a genetic component, it is unlikely to boil down to a single “infidelity gene”, as suggested by the media.

As the authors themselves note, the findings should be considered tentative until they are confirmed.

The study may be of interest to evolutionary biologists, but it doesn’t mean that your genes are an excuse for infidelity (especially in the week after Valentine’s Day).

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Women are more likely to cheat on their partner if they carry the ‘infidelity gene’, scientists discover. Mail Online, February 15 2015

Links To Science

Zietsch BP, Westberg L, Santtila P, Jem P. Genetic analysis of human extrapair mating: heritability, between-sex correlation, and receptor genes for vasopressin and oxytocin. Evolution and Human Behavior. Published online October 17 2015

Categories: Medical News

Super-strength 'skunk' cannabis linked to psychosis

Medical News - Mon, 02/16/2015 - 13:00

" 'Skunk-like cannabis' increases risk of psychosis, study suggests," BBC News reports after a new study found high-potency strains of "skunk" cannabis – infamous for both its strength and its pungent smell – could be linked to one in four cases of new-onset psychosis. Psychosis is a mental health condition characterised by symptoms such as hallucinations and delusions.

The study compared cannabis use patterns among 410 people from south London who attended hospital with a first episode of psychosis, and 370 people from the general population without the condition.

It found the daily use of cannabis was associated with an increased risk of psychosis, and use of high-potency cannabis was associated with a greater increase in risk.

The researchers used their figures to estimate that 24% of new psychosis cases in the study population could be attributed to the use of skunk. But it's important to note this figure would not apply to populations where skunk use is less common than in the south London population the study looked at.

The figure also assumes that skunk definitely directly causes psychosis, which this study cannot prove by itself. However, there is growing concern that this could be the case, and other studies also support an association between cannabis use and psychosis.

If you are troubled by symptoms such as paranoia, depression and anxiety, and are concerned about your cannabis use, ask your GP for advice.

 

Where did the story come from?

The study was carried out by researchers from King's College London and Mount Sinai School of Medicine in the US.

It was funded by the UK National Institute of Health Research, the South London and Maudsley NHS Foundation Trust, the Institute of Psychiatry at King's College London, the Psychiatry Research Trust, the Maudsley Charity Research Fund, and the European Community's Seventh Framework Programme.

The study was published in the peer-reviewed medical journal, Lancet Psychiatry. It has been published on an open-access basis, so it is available online to download (PDF, 439kb) for free.

The Daily Telegraph is just of one of many media sources to make the mistake of extrapolating the "24% of first-episode psychosis caused by high potency cannabis" figure to the whole of Britain.

In fact, this figure is based on the high levels seen in south London in this study. It is also an estimate based on the assumption that skunk definitely causes psychosis, and that no other confounding factors are having an effect.

Links To The Headlines

'Skunk-like cannabis' increases risk of psychosis, study suggests. BBC News, February 16 2015

Super strong cannabis responsible for quarter of new psychosis cases. The Daily Telegraph, February 15 2015

Smoking skunk cannabis triples risk of a serious psychotic episode, says research. The Guardian, February 16 2015

Almost a quarter of new psychosis cases linked to strong 'skunk like' cannabis. The Independent, February 15 2015

Strong cannabis causes one in four cases of psychosis: Users three times more likely to have an episode than those who have never tried it. Daily Mail, February 16 2015

Cannabis responsible for quarter of new psychosis cases, scientists warn. Daily Mirror, February 16 2015

Potent Cannabis Linked To Psychosis Cases. Sky News, February 16 2015

Peril of 'skunk' cannabis: Drug could be responsible for paranoia and schizophrenia. Daily Express, February 16 2015

Links To Science

Di Forti M, Marconi A, Carra E, et al. Proportion of patients in south London with first-episode psychosis attributable to use of high-potency cannabis: a case-control study (PDF, 439kb). Lancet Psychiatry. Published online February 16 2015

Categories: Medical News

When Minnie met Mickey: is rodent romance all in the mind?

Medical News - Fri, 02/13/2015 - 19:00

With Valentine’s Day fast approaching, the Mail Online thoughtfully cushions its readers against possible rejection ahead of time: “You may have lit the candles, opened the wine and dimmed the lights. But, inexplicably, your partner still doesn't want to have sex ... Don't worry, it's not you – it’s your partner's hormones”.

Unless Mail Online readers are amorous hairy-backed rodents with groundbreaking wine opening and fire making skills, these statements are wide of the mark. The study it is reporting on didn’t involve people at all, only mice. 

The study found a link between activity in a specific area of the brain, sexually receptive state and social behaviour in female mice. The brain region involved was the ventrolateral region of the ventromedial hypothalamus (VMHvl), an area implicated in rodent sociosexual behaviour, aggression and mating. A plausible biological mechanism for the finding was that hormones stimulate the VMHvl. This was put forward by the researchers, but is unproven.

While mice and people have similar biology, studying sexual behaviour in female mice can only give you limited insight into sexual behaviour in humans.

Ultimately, this information is mainly useful for other research scientists. The average person on the street should take this research with a pinch of salt, or perhaps a slice of cheese.

 

Where did the story come from?

The study was carried out by researchers from the mysteriously named Champalimaud Centre for the Unknown in Portugal, and was funded by a Marie Curie Reintegration grant, Fundação para a Ciência e a Tecnologia postdoctoral fellowship, Uehara postdoctoral fellowship, and a Fundação Bial research grant.

The study was published in the peer-reviewed science journal Current Biology.

The Mail Online's report read as if the research was carried out with people and was directly applicable to human-to-human sexual interactions. This is a mistake, given the likely differences between the sexual behaviour and decision-making processes in female mice, compared with women. While similarities may exist, there are likely to be crucial differences.

 

What kind of research was this?

This was an animal study looking at how social behaviour, brain activity and reproductive state were linked and related to the sexual behaviour of mice.

The researchers explained that: “Social encounters often start with routine investigatory behaviors [sic] before developing into distinct outcomes, such as affiliative or aggressive actions. For example, a female mouse will initially engage in investigatory behavior with a male, but will then show copulation or rejection, depending on her reproductive state. To promote adaptive social behavior, her brain must combine internal ovarian signals and external social stimuli, but little is known about how socially evoked neural activity is modulated across the reproductive cycle.”

Their research investigated a specific region of the mice's brains called the ventrolateral region of the ventromedial hypothalamus (VMHvl). The VMHvl has been implicated in rodent sociosexual behaviour, it has access to social sensory stimuli, and is involved in aggression and mating. Furthermore, many VMHvl neurons express ovarian hormone receptors (they respond to the effects of hormones), which play a central role in female sociosexual behaviour.

 

What did the research involve?

The research involved recording activity in the VMHvl brain region of freely behaving, naturally cycling, female mice while they were interacting with potential mates of both genders.

Subject animals had regular estrous cycles (reproductive cycles), and were categorised into two different reproductive states:

  • sexually receptive (estrous)
  • not receptive (non-estrous)

Because the team were interested in the investigatory phase of social behaviour, copulation was not allowed during the chronic single-unit recording experiments to avoid pregnancy or pseudo-pregnancy. (Pseudo-pregnancy in mice is when a female experiences the hormonal changes associated with pregnancy, but does not actually conceive any offspring).

They said both events would lead to profound neuro-endocrine changes and cause the female to be in a different physiological state.

 

What were the basic results?

They found that a large fraction of VMHvl neurons were activated in female mice in the presence of other mice, with a clear increase in activity specifically in the presence of males. The activity of most VMHvl neurons was modulated throughout social interactions, rather than in response to specific social events.

Furthermore, VMHvl neuronal responses to male, but not female, mice were greater during the sexually receptive state. Thus, male-evoked VMHvl responses are modulated by the reproductive state.

 

How did the researchers interpret the results?

The results, they say: “suggest the existence of gender-specific inputs to VMHvl neurons and the ability of these inputs to be differentially modulated by ovarian hormones”.

They added that they were the first group to their knowledge to show: “electrophysiological evidence that the activity of hypothalamic neurons is modulated during social encounters, in a gender-specific and reproductive state-dependent manner”.

 

Conclusion

This research suggests a link between activity in a specific area of the brain, sexually receptive state, and social behaviour in female mice. The brain region involved was the ventrolateral region of the ventromedial hypothalamus (VMHvl). The VMHvl has been implicated in rodent sociosexual behaviour, aggression and mating, and has ovarian hormone receptors. This implies a plausible biological mechanism by which hormonal state influences brain activity, which influences sexual behaviour.

However, these links weren’t proven by this study. They did not, for example, look at the effect of blocking specific hormone receptors in the VMHvl to pinpoint which ones were important and behind the behaviour. This would have confirmed the likely role of hormones more directly and more precisely.

As interesting as this is research is, it has limited applicability to people at the moment. This is because we can’t be sure that similar processes are happening in women. Similarly, there are a myriad of other cultural, social and individual personality factors at play in person-to-person sexual behaviour interactions that differ from those in mice.

If you are having trouble wooing the woman of your dreams, we suspect offering to expose her hypothalamus to hormones isn’t going to do you any favours.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Turned down in the bedroom? Don't worry, it's not you - it's your partner's hormones that are to blame. Mail Online, February 13 2015

Links To Science

Nomoto K, Lima SQ. Enhanced Male-Evoked Responses in the Ventromedial Hypothalamus of Sexually Receptive Female Mice. Current Biology. Published online February 12 2015

Categories: Medical News

HRT increases ovarian cancer risk by small amount

Medical News - Fri, 02/13/2015 - 15:30

“HRT nearly doubles the risk of ovarian cancer,” The Daily Telegraph reports. While this may sound alarming, the actual increase in risk for individual women is small, because ovarian cancer is rare.

Hormone replacement therapy (HRT) uses synthetic versions of hormones to relieve symptoms of the menopause, such as hot flushes. Concerns have been raised that HRT could also increase the risk of cancers associated with hormones, such as breast cancer and ovarian cancer.

A new detailed review looking at the result of 52 previous studies did find a statistically significant higher risk (43%) in current HRT users compared with HRT non-users, even in those with less than five years of HRT use.

It is important to put the risk in context; in real terms, for every 1,000 women using HRT for five years, there will be just one additional ovarian cancer diagnosis. And if prognosis is typical, there will be one additional ovarian cancer death for every 1,700 users.

In ex-HRT users, risks decreased the longer ago HRT use had stopped, but risks during the first few years after stopping remained significant.

Women should not suddenly stop taking HRT without consulting their doctor. The risks and benefits associated with HRT need to be weighed up on an individual basis and in agreement between you and your doctor.

 

Where did the story come from?

The study was carried out by researchers from a Collaborative Group on Epidemiological Studies of Ovarian Cancer based in Oxford and funded by the Medical Research Council and Cancer Research UK.

The study was published in the peer-reviewed medical journal The Lancet on an open-access basis, so is free to read online or download as a PDF.

Refreshingly, most of the UK media resisted running the study as a scare story by just talking about the relative risk increase of 43%, and also included information on absolute risk increase at an individual level.

Including this information is a marked improvement on the usual reporting style used by the UK press, especially when it comes to “HRT and cancer” stories.

An unfortunate reminder of the poorer standard of coverage was shown in the Daily Express. It seemed to pump up the scare factor of the story, leading with: “Alert” as HRT “doubles risk of ovarian cancer”. It didn’t mention that this doubling of risk (actually around a 43% increase) was a relative risk. The absolute risk increase was smaller, as ovarian cancer is quite rare.
 

What kind of research was this?

This was a systematic review and meta-analysis looking at the effect of HRT on ovarian cancer risk.

HRT is a treatment used to relieve symptoms of the menopause. It uses either oestrogen only, or a combination of oestrogen and progestogen, known as combination therapy. Symptoms of the menopause include hot flushes, night sweats, mood swings and trouble concentrating. Long-term effects of reduced levels of oestrogen include bone thinning, which increases the risk of fractures, and cardiovascular disease.

HRT is known to be an effective method of controlling menopausal symptoms, and it can make a significant difference to a woman’s quality of life and wellbeing. HRT can also reduce a woman’s risk of developing osteoporosis and cancer of the colon and rectum. Long-term use is rarely recommended, and bone density will decrease rapidly after HRT is stopped.

However, there are risks alongside these benefits. There is evidence that combined HRT slightly increases the risk of developing breast cancer, womb cancer, ovarian cancer and having a stroke. Systemic HRT also increases your risks of deep vein thrombosis (DVT) and pulmonary embolism (blockage in the pulmonary artery). Other medicines are available to treat osteoporosis that do not carry the same level of associated risk.

This study sought to take a closer look at the link between HRT and ovarian cancer.

 

What did the research involve?

The study team identified all relevant research (published and unpublished) assessing hormone therapy use and ovarian cancer risk since 1998. They found 52 relevant studies containing individual participant information and combined the results – called a meta-analysis.

The meta-analysis looked at how different durations of HRT use (more or less than five years) affected ovarian cancer risk, and whether this risk reduced back to normal levels after HRT was stopped. Other information collected included: ever-use, current use, age at first and last use, and constituents of each preparation.

The main analysis compared ovarian cancer risk in women using HRT (current users, ex-users, short-term, long-term users etc.) with those that had never used HRT. The main analysis focused on data from prospective studies only, to avoid possible biases of participation and recall. Sensitivity analysis used both retrospective and prospective studies to check the robustness of the main results. 

 

What were the basic results?

Overall, information was available on 21,488 postmenopausal women with ovarian cancer (cases) from 52 studies (17 prospective and 35 retrospective). The prospective studies contributed more than half of the cases (12,110), with an average (mean) diagnosis year of 2001, 55% (6,601) of whom had used HRT for an average (median) of six years.

Women currently using HRT

Ovarian cancer risk was strongly related to how long ago women used HRT. In prospective studies, risk was greatest in women who, when last asked, had been current HRT users (relative risk (RR) 1.41, 95% confidence interval (CI) 1.32-1.50). Among them, risk was significantly increased even in those who, at diagnosis, had less than five years (median duration three years) of hormone therapy use (RR 1.43, 95% CI 1.31-1.56). This means that women currently using HRT when last asked were 43% more likely to develop ovarian cancer than women who had never used HRT, even if they’d been using HRT for less than five years – the previously generally accepted safe time period. This is the figure that made the news, and was described in some places as almost doubling the risk. This increases the previously known risk from less than one per 1,000 women to one per 1,000 women.

Women who’d used HRT in the past, but had now stopped

Ovarian cancer risk was significantly higher in women who had been recent ex-users and would, at the time of cancer diagnosis, have still been within five years of last use (RR 1.23, 95% CI 1.09-1.37). Risk decreased the longer ago hormone therapy had last been used.

However, women who had used hormone therapy for at least five years (median duration nine years) and then stopped were still at significantly increased risk more than five years later (RR 1.10, 95% CI 1.01-1.20). The median time since last use was 10 years. This suggested that long-term use might have a small but significant lingering effect on increasing ovarian cancer risk.

Type of ovarian tumour

In prospective studies, risks in current or recent users were increased only for the two most common ovarian tumour types: serous (RR 1.53, 95% CI 1.40-1.66) and endometrioid (1.42, 95% CI 1.201.67).

Type of HRT

In current or recent users, ovarian cancer risk was significantly increased with use of both oestrogen-only and oestrogen-progestogen types, with little variation between the risks. Both preparations raised the risk by 37% relative to non-HRT users in the prospective studies (RR 1.37, 95% CI 1.29 to 1.46).

Sensitivity analysis

For prospective and retrospective studies combined, the risks were similar to those in prospective studies alone, except that the risks in current users seemed to be somewhat smaller. Other sensitivity analyses left the main findings in prospective studies largely unchanged. This took account of any changes due to variation in year of birth, ethnic origin, education, age at menarche, height, alcohol consumption, smoking, and family history of ovarian or breast cancer.

 

How did the researchers interpret the results?

The researchers concluded that: “The increased risk may well be largely or wholly causal; if it is, women who use hormone therapy for five years from around the age of 50 have about one extra ovarian cancer per 1,000 users and, if its prognosis is typical, about one extra ovarian cancer death per 1,700 users.”

They say: “At present, the World Health Organization, European and US guidelines about hormone therapy do not mention ovarian cancer, and the UK guidelines (which are due to be revised) state only that risk may be increased with long-term use. The definite risk of ovarian cancer that is observed, even with less than five years of use, starting at around the age of 50, is directly relevant to current patterns of hormone therapy use, and hence directly relevant to medical advice, personal choices, and the current efforts to revise UK and worldwide guidelines.”

 

Conclusion

This systematic review and meta-analysis showed that ovarian cancer risk was significantly increased in current HRT users, even in those with less than five years of HRT use (the average was three years). In ex-users, risks decreased the longer ago HRT use had stopped, but risks during the first few years after stopping remained significant. Furthermore, about a decade after stopping, long-duration hormone therapy use (average nine years of HRT use), there still seemed to be a small excess risk.

The review has a few limitations, however. The main one is that the review was heavily influenced by just two of the 52 included studies. These represented about 75% of the people studied, and neither corrected for use of oral contraceptives.

However, overall this review is robust enough for us to be relatively confident that these findings are generally applicable to women in the UK and are broadly reliable, given the available evidence.

The risk of HRT raising ovarian risk is not new, but this study seems to firm up the knowledge base and suggests the risk may come into play with shorter HRT use than previously thought. For example, current UK guidelines state that ovarian cancer risk may be increased with long-term use. These guidelines are regularly updated and this evidence will be considered when their recommendations are reviewed.

Prof Rod Baber, President of the International Menopause Society, said via the Science Media Centre that: “… this risk in absolute terms then comes down to one excess case of ovarian cancer per 2,000 users after five years of use means that for women using HRT this risk is very very low in absolute terms.”

As much of the UK media pointed out, while the risk increase found here is worth noting and investigating further, women should not stop taking HRT without consulting their doctor. What often gets lost in the mix when the media discuss HRT is that it brings very real benefits to the quality of life, which should not be discounted. Most experts agree that if HRT is used on a short-term basis (no more than five years), the benefits usually outweigh the risks.

The benefits and risks associated with HRT need to be weighed up on an individual basis and in agreement between you and your doctor.

You can read more about the benefits and risks of using HRT.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

HRT increases ovarian cancer risk. BBC News, February 13 2015

HRT nearly doubles the risk of ovarian cancer, experts warn. The Daily Telegraph, February 13 2015

HRT can increase a woman's chances of developing ovarian cancer, research shows. The Independent, February 13 2015

'Long-term HRT use raises risk of ovarian cancer': Chance increases by 40% after using treatment for five years. Mail Online, February 13 2015

HRT treatment raises risk of ovarian cancer, says study. The Guardian, February 13 2015

Alert as hormone replacement therapy ‘doubles risk’ of ovarian cancer. Daily Express, February 13 2015

Links To Science

Collaborative Group on Epidemiological Studies of Ovarian Cancer. Menopausal hormone use and ovarian cancer risk: individual participant meta-analysis of 52 epidemiological studies. The Lancet. Published online February 12 2015

Categories: Medical News

Could a 30-minute 'power nap' make up for a bad night's sleep?

Medical News - Thu, 02/12/2015 - 18:05

"Indulging in a power nap can repair the damage caused by a lack of sleep," the Daily Mail reports. But the study that prompted the headline is very small – involving just 11 healthy young men.

It has long been known that a lack of sleep at night can have a negative impact on the immune system and stress levels.

Researchers wanted to see if two short naps during the day, each lasting 30 minutes, could repair some of the damage caused by a poor night's sleep of just two hours.

They measured biological indicators (biomarkers) such as stress hormones, and then compared them to controls in an attempt to gauge the effects of the short nap.

One of the three stress hormones measured was increased the day after the men were sleep-deprived, but not if they were allowed to take naps. The level of a protein involved in immune responses (Interleukin-6, or IL-6) was reduced after little sleep, but not if the men had naps.

The implications of these findings are unclear. Measuring one immune biomarker, such as IL-6, does not provide any insight into whether the immune system has "recovered", as it is involved in both activating and dampening the immune system.

Nor does this study show that naps relieve stress. The level of one stress-related hormone, noradrenaline, was increased after sleep deprivation, but this may have been affected by other factors.

So the results of this small study do not show whether naps improve the immune system or the body's response to stress.

If you are struggling with daytime sleepiness, you may need to improve the quality and duration of your sleep during the night.

 

Where did the story come from?

The study was carried out by researchers from the University of Paris Descartes and the Institut de recherche biomédicale des armées.

It was funded by the insurance company RÉUNICA and the Societé Française de Recherche et Médecine du Sommeil.

The study was published in the peer-reviewed Journal of Clinical Endocrinology and Metabolism on an open access basis, so it is free to read online.

The Daily Express informed readers that, "Even if you only get two hours of proper sleep, a half-hour snooze will relieve stress and bolster the immune system by restoring hormones and proteins."

But we can't say conclusively that a nap can do either of these things based on the results of this small, short-term study.

Only one of the three stress-related hormones tested was raised if the men did not take a nap. There are other reasons this could occur, and it was not clear if the study ruled these out.

The Express also failed to point out that this study was conducted on just 11 healthy young men over three days.

The Mail Online reported the study more accurately, but did not point out any of the limitations of this kind of research.

 

What kind of research was this?

This was a randomised cross-over study that aimed to look at whether naps could counteract the effect of restricted sleep on specific markers of stress and immune system response.

A group of healthy male volunteers were studied after their sleep was restricted to two hours. In one session they were allowed naps afterwards, but naps were not allowed in the other session.

The researchers measured various stress hormone levels and one immune system protein called IL-6, looking at whether the restricted sleep and naps had any effect on these levels.

The study design allows comparison of the same group of people under different conditions. This type of study needs to be careful to make sure the effects of one set of conditions do not carry over on to the other period, which is why the researchers need to allow a period of "washout" time between the two sessions.

A study of this nature does not have a separate control group – participants are compared to themselves under different conditions; in a sense they serve as their own controls. This can make it easier to detect differences that result from the conditions, as the groups being compared are essentially the same.

 

What did the research involve?

Eleven young men were recruited to the study through advertisements in the hospital and university campus. They were aged between 25 and 32, had a body mass index (BMI) within the healthy range of 19 to 25, and were non-smokers.

All were considered to be healthy and none had depression, anxiety or emotional distress according to a commonly used measurement tool (the Hospital Anxiety and Depression Scale). The men normally slept seven to nine hours a night on average and did not report any sleeping problems.

The men had two admissions to the sleep laboratory in random order. In the "sleep-restricted" admission, the volunteers slept from midnight to 8am on the first night, were restricted to sleeping from 2am to 4am on the second night, and were then allowed to sleep from 8pm until they woke up on the final night.

They were not allowed to sleep at any other time and were kept awake by staff with films and games.

The same night-time sleep protocol was used for the "sleep restriction plus nap" admission, but the volunteers were allowed to have a 30-minute nap at 9.30am after the restricted night's sleep, and again at 3.30pm.

The men were asked to try to be asleep from midnight to 8am for a week before the admissions, and to record their sleep in a daily diary.

During each three-day stay, their activity levels were monitored and they were provided with meals up to a maximum of 2,500 calories a day. They were not allowed to have any:

  • medication
  • alcohol
  • coffee
  • tea
  • cola
  • chocolate

A monitor that records brain electrical activity (an EEG) was attached to each participant for the duration of each admission to record whether they were awake or asleep.

Urine samples were taken every three hours between 10am and 7pm to test for three hormones that help regulate the body's response to stress: noradrenaline, adrenaline and dopamine.

Salivary samples were taken every two hours while the men were awake, and tested for Interleukin-6 (IL-6) levels. IL-6 is a protein that is part of the immune system. It plays a complex role – it stimulates the body's immune system to react, but also reduces inflammation, depending on the circumstances.

 

What were the basic results?

After the sleep-restricted night, the level of noradrenaline in the men's urine was 2.5 times higher in the afternoon than at the same time of day after a night of eight hours' sleep. There was no increase in noradrenaline if they had been allowed the naps.

There was no significant difference between the sleep-restricted and non-restricted days, or with and without naps, in terms of the levels of adrenaline, dopamine or testosterone in the men's urine samples.

Levels of IL-6 were significantly lower at 10am and 7pm after the restricted sleep night compared with after eight hours' sleep. The levels were not lower if the men had napped.

After the recovery night's sleep, adrenaline and dopamine levels were increased in the afternoon in the "sleep-restricted" session, but not in the "sleep-restricted plus nap" session. IL-6 salivary levels were the same as after the eight hours' sleep in both sessions.

 

How did the researchers interpret the results?

The researchers concluded that: "Napping as a countermeasure to sleep restriction could, in addition to benefits on alertness, improve neuroendocrine stress and immune recovery with a potential prophylactic long-term effect on cardiovascular health."

They acknowledge that interpretation of the varying levels of the immune system marker IL-6 is complex as it can be a sign of inflammation, but it may also be involved in preventing inflammation.

 

Conclusion

This was a small study that is interesting on an intellectual level, but has little real-world practical applications or implications.

This study found the levels of one stress-related hormone (noradrenaline) increased after restricted sleep, but not if the men had naps. However, this does not prove that naps "relieve stress", as the media has indicated.

Noradrenaline is just one of several hormones that fluctuate during the day in response to a variety of bodily functions. Although it is known as one of the stress hormones, this refers to stress on the body, which can include exercise and excitement.

In this study, we do not know what the men were doing when these higher levels were recorded and whether this differed from the time when the lower levels were recorded. They could have been exercising, watching films, or playing games, therefore affecting their results.

Although activity was reported to be "controlled" by monitoring, it was not clear whether this meant that activity was restricted in all periods, and the results were not adjusted to take activity into account.

Also, the other two stress-related hormones measured were not affected by sleep restriction or naps.

This study has not proven that naps improve the immune system, which has been reported in the media. IL-6 has a complex role in both stimulating and dampening the immune response in different circumstances.

Therefore, a one-off reading of IL-6 like this, without any other markers of the immune system, is difficult to interpret accurately.

What may have been a more relevant outcome is what effect a nap might have on concentration and the ability to think clearly and reason after a night of poor sleep.

This could have been achieved through psychometric testing, although the numbers would still have been small, limiting the power of the study to detect an effect.

Further limitations include the fact the study conditions did not mimic normal life – the participants had to stay in the sleep laboratory for three days at a time and were not allowed to drink tea, coffee or alcohol. They were also only sleep-deprived on one night. This means the results may not reflect what would happen in normal circumstances.

It is not clear what the men's normal daily schedules were like and whether having a break for three days from hectic life would have been less stressful, or conversely if being cooped up in a laboratory would have felt claustrophobic.

In conclusion, this study of just 11 men does not prove that naps successfully counteract the negative effects of losing a night's sleep on the immune system or symptoms of stress.

Many adults fall into bad habits when it comes to sleep, such as drinking alcohol before bedtime or overstimulating the mind late in the evening. You may need to improve your sleep hygiene – adopting better habits that will help promote better sleep. Read more about sleep hygiene

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Power napping really IS good for you: A 30-minute snooze can repair the damage caused by a lack of sleep. Daily Mail, February 10 2015

Power naps can counter lost sleep, new study reveals. Daily Express, February 11 2015

Links To Science

Faraut B, Nakib S, Drogou C, et al. Napping Reverses the Salivary Interleukin-6 and Urinary Norepinephrine Changes Induced by Sleep Restriction. The Journal of Clinical Endocrinology & Metabolism. Published online February 10 2015

Categories: Medical News

Long-term smoking 'may cause' brain shrinkage

Medical News - Thu, 02/12/2015 - 14:00

“Smokers have thinner brain cortex and could have impaired thinking,” The Independent reports. MRI scans of long-term smokers show signs that the cerebral cortex – the grey matter of the brain – which plays a key role in thinking and memory, was thinner than expected.

The study looked at brain scans of more than 500 people aged 73 to see if there were any noticeable differences between smokers, ex-smokers and people who never smoked.

Smokers had the thinnest cortex on the MRI scans. However, despite some media reports, none of the participants had dementia or memory loss, and the researchers did not reveal any differences between the groups in terms of cognitive ability. The smoking group was limited in size to 36 participants (possibly because smokers are less likely to live until they are 73).

Thinning was also seen in ex-smokers compared to never smokers (these groups both had more than 200 participants). However as the study only took one measurement at one point in time, it cannot tell us either if this thinning in ex-smokers is due to smoking or if it partially recovers once a person quits smoking.

The authors acknowledge that this study doesn’t prove that smoking caused the cortex to thin as the measurement was only taken once. However, we already know that smoking is unhealthy and it is always a good idea to quit however long you have been smoking.

 

Where did the story come from?

The study was carried out by researchers from Edinburgh University, McGill University in Montreal, and Harvard Medical Schools in Massachusetts. It was funded by a Research Ageing Program grant, the Age UK-funded Disconnected Mind project, the UK Medical Research Council, the Scottish Funding Council, the UK Biotechnology and the Biological Sciences Research Council.

The study was published in the peer-reviewed medical journal Molecular Psychiatry on an open-access basis so it is free to read online.

The media has implied that there are direct links between having a thinner cortex and experiencing memory and cognitive problems, but this was not a result presented by this research.

 

What kind of research was this?

This was a cross sectional study comparing the thickness of the cortex of the brain between people who currently smoked, ex-smokers and non-smokers. The people are part of an ongoing, longstanding cohort study of people born in 1936.

This type of study can show associations, but it is not able to prove that one factor (smoking in this case) causes the other (thinning cortex). Ideally the study would assess people’s brain and smoking habits over time to see whether the changes come after a person takes up smoking and not before.

However, such a study is likely to be expensive to do and take a long time, so often researchers start with a cross sectional study. (And for this cohort, such a study would have been impossible, as MRI scanners weren’t invented until the 1970s).

randomised controlled trial would not be ethical for this type of research, so an observational study like this is appropriate.

 

What did the research involve?

The researchers compared the thickness of the cortex of people aged 73 who were current smokers, ex-smokers and non-smokers. The cortex thins naturally as we age, but researchers wanted to see if this process was accelerated in smokers.

A group of 504 people from a longstanding study called the Lothian Birth Cohort 1936 (LBC 1936) was recruited into the study. This original study had started collecting data on people born in the Lothian region of Scotland in 1936 including mental ability and intelligence, which was tested when they were 11 years old.

The 504 participants (260 women and 244 men) were invited to have a brain MRI scan to measure the thickness of their cerebral cortex – the grey matter of the brain. None of them had any evidence of dementia, according to self-report and scoring more than 24 out of 30 on Mini Mental State Examination (MMSE) – a test commonly used to look for cognitive problems.

The participants were assessed on a range of factors, including:

  • smoking status, including age starting, age stopping (if they stopped) and average number smoked per day
  • recent alcohol consumption
  • socioeconomic status
  • cognitive testing and other psychological assessments
  • history of any medical conditions
  • physical examination, including blood pressure and lung function
  • blood tests

The researchers then analysed the results to look for any association between the thickness of the cortex and smoking history. They adjusted their results for gender and exact age.

 

What were the basic results?

There were 36 current smokers, 223 ex-smokers and 245 non-smokers. There was no significant difference between the groups in terms of gender, intelligence or socioeconomic status aged 11. However, those who never smoked were less likely to have a history of cardiovascular disease, had better lung function and drank fewer units of alcohol per week.

Current smokers had a significantly:

  • thinner cortex over most of the brain than people who had never smoked
  • thinner cortex than ex-smokers, but the difference was less than compared to never smokers

Ex-smokers had a significantly thinner cortex than non-smokers, but the difference was not as large as for current smokers compared to non-smokers. Those ex-smokers who had stopped smoking a longer time ago tended to have less difference in cortex thickness than those who stopped more recently.

 

How did the researchers interpret the results?

The researchers concluded that “smokers need to be informed that cigarettes are associated with accelerated cortical thinning, a biomarker of cognitive aging”. They also say that “the potential to at least partially recover from smoking-related thinning might serve as a strong motivational argument to encourage smoking cessation”.

 

Conclusion

This study has shown an association between smoking and a thinner cortex, though it cannot prove that smoking caused the cortex to thin. The study was cross sectional, so cannot say which came first – the smoking or the cortex differences. Also, confounding factors other than smoking may be contributing.

Strengths of the study include:

  • Having access to measurements of cognitive ability when the participants were 11 years old, before most of them would have started smoking, as a potential indicator of cortex thickness.
  • The radiologists were blinded to which MRIs came from each group, reducing the risk of them introducing bias based on interpreting scans differently for people they knew to be smokers.
  • All participants were the same age when they had the MRI scan, so age did not need to be adjusted for in the results. This is important because the cortical thickness naturally decreases with age.
  • The fact that those who gave up smoking seemed to have less difference to the non-smokers than those who continued to smoke fits with the idea that the two factors might be related to each other rather than arising just by chance.

Limitations acknowledged by the authors include:

  • The number of current smokers was small, only 36.
  • It is possible there were differences in cortex thickness before a person started smoking. They say that structural changes in the frontal part of the brain related to impulse control may have made it more likely for people to start smoking in the first place.

All this considered, it has long been known that smoking is bad for you.

Aside from the risk of cancerheart disease and stroke, smoking may also increase the risk of dementia type conditions, such as vascular dementia and Alzheimer’s disease.

So, if smoking by itself does not directly cause cortical thinning, it is a good idea to quit if you smoke, whatever your age. Quitting, however long you have smoked, should lead to an increase in life expectancy and quality of life. Help and advice on quitting can be found here.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Smokers have thinner brain cortex and could have impaired thinking. The Independent, February 11 2015

Smoking shrinks your brain and may damage your memory, study finds. Metro, February 11 2015

Smoking shrinks critical part of the brain – leading to memory loss. Daily Mirror, February 10 2015

Links To Science

Karama S, Ducharme S, Corely J, et al. Cigarette smoking and thinning of the brain’s cortex. Molecular Psychiatry. Published online February 10 2015

Categories: Medical News

Obesity damage to eggs may be reversible

Medical News - Wed, 02/11/2015 - 15:00

“Damaging effect of obesity on a woman’s eggs can now be reversed,” is the potentially misleading headline from the Mail Online today.

The over-egged headline refers to a mouse study showing that signs of lower fertility due to obesity could be reversed using experimental drugs. This was not tested in humans, however.

Maternal obesity is known to lower the chance of successful conception, as well as increasing the risk of miscarriage.

The study compared the fertility of mice before and after they became obese due to a genetic condition that makes them overeat. When given IVF drugs, their fertility at the start was similar to mice of a healthy weight, but as the mice became obese, their fertility reduced. They became less able to develop eggs, and any eggs produced were less likely to be fertilised. The researchers also found that once obese, there was reduced activity of mitochondria (the part of the cell that converts food to energy) in the eggs.

All of these effects were reversed if the obese mice were given either a drug called Salubrinal or BGP-15. BGP-15 is an experimental, unlicensed drug that is being trialled for use in people with type 2 diabetes.

The study does not prove that the reduced mitochondrial activity causes obesity in the offspring, but it is a plausible explanation that will require further research.

The immediate impact of this research to women is minimal, as this is very early stage research. However, the study does reinforce the message that women should maintain a healthy weight before pregnancy.

Where did the story come from?

The study was carried out by researchers from the University of Adelaide, Monash University, and the Baker IDI Heart and Diabetes Institute in Melbourne. It was funded by the National Health and Medical Research Council of Australia, the Operational Infrastructure Support Program of the Government of Victoria, and the Women’s and Children’s Hospital Foundation. 

The study was published in the peer-reviewed journal Development.

In general, the media headlines implied that these drugs have been tested on women, when this is not the case. For example, the Mail Online’s article did not mention that the research was carried out on mice, and had not actually been tested for this use in humans. This means we don’t know if the drug would have the same effect in people as it does in mice.

The Independent’s coverage was more balanced. It acknowledged the mouse origins of the research, but could have done more to spell out why this was a limitation. The article usefully included a quote from Professor Adam Balen, “a leading expert in reproductive medicine at the University of Leeds, and chair of the British Fertility Society” who said: “while any drug treatment was a long way off, the findings were ‘very interesting’”. He added that the important message to take away from this study is that: “women [need] to be nutritionally healthy before they get pregnant”.

 

What kind of research was this?

This was an animal study looking at the effect of obesity on fertility in mice.

Previous animal studies have indicated that obesity affects the metabolism and growth of offspring, and rat studies have shown that obesity alters the egg before fertilisation. The authors also highlight that overweight women are more likely to require assisted reproduction, and the success rates are lower.

The researchers had already done studies using obese female mice to investigate what biological changes obesity might be causing. They found that mice fed high-fat diets had eggs with signs of intracellular stress. This included higher fat content, increased reactive oxygen species and altered mitochondria. Mitochondria are the parts of the cell that convert food to energy and feature heavily in the debate on whether three-parent fertility technology can or should be used in the UK.

In this study, they wanted to see whether this alteration in mitochondria was associated with reduced fertility, whether it is passed on to the offspring, and whether it affected the weight of the growing foetus. They also wanted to find out if the use of two experimental drugs that reduce intracellular stress could reverse these changes.

 

What did the research involve?

The researchers compared the fertility of obese mice with healthy-weight mice in a variety of experiments.

Mice with a genetic disorder similar to Alstrom syndrome in humans were used, and compared to mice of a healthy weight. This syndrome causes overeating that leads to severe obesity, increased insulin and diabetes, despite eating a low-fat diet.

The mice were given IVF drugs to stimulate their eggs to become ready for fertilisation. The following aspects were measured, comparing mice before and after they had become obese with healthy-weight mice:

  • the number of eggs stimulated by IVF drugs
  • the level of mitochondria activity in the eggs
  • the number of eggs able to be fertilised
  • weight of the growing foetus when implanted into mice of a healthy weight

The researchers then repeated the experiments after giving obese mice an experimental drug once per day for four days, to see if this could reverse the effects of obesity on the eggs and their development. The drug was either:

  • Salubrinal – an experimental drug that reduces cell stress responses
  • BGP-15 – an experimental drug that has been shown to protect against obesity-induced insulin resistance in mice. It is currently undergoing human trials for type 2 diabetes

 

What were the basic results?

Before the mice were obese, the same number of eggs developed after stimulation with IVF drugs as in healthy-weight mice. After they were obese, a reduced number of eggs were produced. This indicated that the fertility of the mice was affected by obesity, rather than the syndrome.

When obese mice were given either Salubrinal or BGP-15 for four days before the IVF drugs, the number of eggs developed more than doubled and was almost the same as for the healthy-weight mice. The number of eggs also increased when these drugs were given to healthy-weight mice.

The eggs of obese mice had indications of higher levels of intracellular stress and decreased mitochondrial activity. Obese mice given either drug did not have reduced mitochondrial activity.

Fewer fertilised eggs from obese mice survived compared to healthy-weight mice by four hours after fertilisation, or two days later. The same numbers survived if they were given IVF before they had become obese, or if obese mice had been given either Salubrinal or BGP-15.

When they implanted the fertilised eggs into normal-weight mice, compared to foetuses from healthy-weight mice:

  • foetuses from obese mice were significantly heavier
  • foetuses from obese mice given Salubrinal or BGP-15 were the same weight

 

How did the researchers interpret the results?

The researchers concluded that eggs from obese mice give rise to foetuses that are heavier and have reduced mitochondrial activity. They say that obesity causes intracellular stress in the eggs. They found that if either of two experimental drugs were given before fertilisation, this could reverse the following effects of obesity:

  • reduced response to IVF drugs
  • reduced mitochondrial activity
  • reduced fertilisation rate
  • developing foetus of increased weight

 

Conclusion

This mouse study has shown that obesity reduces fertility, but the exact mechanism remains unclear. It found that eggs from obese mice had reduced mitochondrial activity compared to when the mice were of a healthy weight, and this reduced mitochondrial activity is evident in the growing foetus. The researchers give a plausible explanation that it is the damaged mitochondria that causes the reduced fertility and increased weight; however, this is just a theory. The study does not prove that obesity causes reduced mitochondrial activity or that this would cause the offspring to be obese. The weight of the growing foetuses of obese mice was greater, but none were born.

Strengths of the study include the type of obese mice used (which are known as “Blobby mice” in Australia). Mice with this syndrome become obese regardless of the type of food they eat, because of the volume they consume. In this experiment, the researchers did not want to compare healthy-weight mice with obese mice that had become so because of just eating a high-fat diet, as this could confound the results.

While studies of other mammals such as mice are useful, they cannot tell us exactly what happens in humans. It is known that fertility rates improve when women who are overweight or obese lose weight, and this can be achieved through small changes such as increasing your activity levels and reducing your intake of calories.

The drugs in this trial are not yet available for humans, other than BGP-15 in a trial for type 2 diabetes. Neither of them have been tested in any fertility trials on humans. For further tips on improving your fertility, see our fertility pages.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Damaging effect of obesity on a woman's eggs can now be reversed: Drug can 'restore egg quality to original level'. Mail Online, February 10 2015

Health risks for obese mothers and their babies can be reversed. The Independent, February 10 2015

Links To Science

Wu LL, Russell DL, Wong SL, et al. Mitochondrial dysfunction in oocytes of obese mothers: transmission to offspring and reversal by pharmacological endoplasmic reticulum stress inhibitors. Development. Published online February 2015

Categories: Medical News

Unemployment and job insecurity linked to increased risk of suicide

Medical News - Wed, 02/11/2015 - 14:00

“Unemployment causes 45,000 suicides a year worldwide,” The Guardian reports. The story comes from a study that looked at the association between suicide rates and unemployment in 63 countries across the world.

It found that between 2000 and 2011, one in five of an estimated 233,000 annual suicides were linked to unemployment.

The study cannot prove that unemployment causes suicide, although it certainly suggests a strong association.

The research is useful because it looks at the possible link between suicide and unemployment in the long term and not just during times of economic crisis. It estimates that unemployment between 2000 and 2011 was associated with nine times as many suicides annually as those that were attributable to the 2008 economic recession.

Interestingly, it also found that in countries where being out of work is uncommon the link between suicide risk and a rise in unemployment is stronger.

This could be due to a sense of being stigmatised. In the UK, there are regular media stories about people perceived as abusing the benefit system, but these are likely to be the exception, not the rule. Such distorted coverage may increase the sense of stigmatisation.

The researchers make the suggestion that professionals such as social workers and human resource officers who deal with people who are unemployed or at risk of redundancy, should be given advice to spot possible warning signs, as this may help prevent potential suicides.

 

Where did the story come from?

The study was carried out by researchers from the University of Zurich in Switzerland. There is no information about external funding.

The study was published in the peer-reviewed medical journal The Lancet Psychiatry.

While The Guardian and the Mail Online’s coverage was generally accurate, they both fell into the trap of assuming correlation equals causation – wrongly stating that a direct cause and effect relationship has been proven between unemployment and suicide rates.

Unemployment may have an influence on suicide rates, though other factors such as depression and poor health could also play a part.

So a headline such as The Guardian’s “Unemployment causes 45,000 suicides a year worldwide, finds study” is incorrect.

 

What kind of research was this?

This was an observational study that looked at the association between suicide and unemployment in 63 countries between 2000 and 2011. Importantly this was a period that included times of economic stability as well as the 2008 global economic recession and its aftermath.

The researchers say that previous research suggests an association between the 2008 economic crisis, rising unemployment and increased suicide rates, with men and those of working age particularly affected.

Unemployment may increase the risk of suicide through mechanisms such as an increased risk of depression, financial strain and reduced affordability of mental health care.

However, they say a specific effect of unemployment on suicide rates has not been clearly shown.

 

What did the research involve?

The researchers extracted data on suicide rates from 2000 to 2011 by age and sex, from the mortality database of the World Health Organization. They looked at the number of suicides per 100,000 population for the following four age categories, by sex: 15-24 years, 25-44 years, 45-64 years and 65 years and older.

They extracted four economic indicators from 2000 to 2011 from the world economic database of the International Monetary Fund. These were the unemployment rate, Gross Domestic Product (GDP), growth rate and inflation.

For their analysis they selected 63 countries drawn from the four world geographic regions – the Americas, northern and western Europe, southern and eastern Europe, and non-Americas and non-Europe. The countries were chosen based on completeness of data available and sample size.

Using statistical methods they analysed the link between unemployment rates, suicide and other economic factors.

 

What were the basic results?

The study found that the link between unemployment and suicide was similar in all four world regions. It estimates that in the 63 countries studied between 2000 and 2011:

  • there were about 233,000 suicides annually
  • suicides associated with unemployment totalled about 45,000 annually, making up about 20% of all suicides
  • suicide associated with unemployment rose by 4,983 from 2007 to 2009 (the period of the recent economic downturn)
  • men and women of all ages were equally vulnerable to suicide associated with unemployment
  • overall, the relative risk of suicide decreased by 1.1% (95% confidence interval (CI) 0.8-1.4%) annually, during this period

Researchers also found a six-month time lag between higher suicide rate and a rise in unemployment, There was also a stronger association between suicide and unemployment in countries where baseline unemployment was low.

 

How did the researchers interpret the results?

The researchers say that in countries where unemployment is uncommon, a rise in job losses might trigger greater fears and insecurity than in countries with higher previous unemployment rates. They also comment on the time lag between suicide and the rise in unemployment, suggesting that downsizing and labour market restructuring may create additional stress and a sense of job insecurity.

Suicide associated with unemployment might be severely underestimated if studies focus only on times of economic crisis they argue. “There is a continuous need to focus on preventing suicides, even more so in economically prosperous, stable time periods than in times of lower prosperity, when resources are scarcer,” they say, with prevention efforts needed in countries with both low and high unemployment rates.

 

Conclusion

This large study suggests there is a strong association between suicide and unemployment in times of economic stability as well as in times of economic recession. 

However, analysis at world regional level is unable to take account of clinical and psychosocial factors associated with suicide and further research into individuals at risk in times of high unemployment would be useful. In addition, there is missing information from large countries such as China, India and most of Africa, which may affect the reliability of their estimates.

As an accompanying paper in The Lancet Psychiatry notes, fluctuating unemployment is only one effect of economic recession that may affect mental health. Other economic strains include falling income, zero hour contracts, job insecurity and debt.

Read more advice about coping in times of job and economic uncertainty.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Unemployment causes 45,000 suicides a year worldwide, finds study. The Guardian, February 11 2015

Unemployment is linked to 45,000 suicides a year. Mail Online, February 11 2015

Links To Science

Nordt C, Warnke I, Kawohl W. Modelling suicide and unemployment: a longitudinal analysis covering 63 countries, 2000–11. The Lancet Psychiatry. Published online February 11 2015

Categories: Medical News

'Smart insulin' could be used to treat type 1 diabetes

Medical News - Tue, 02/10/2015 - 15:30

The Guardian today reports that “smart insulin” may ease the burden on type 1 diabetes – a condition that means the body cannot produce insulin.

This means that those with the condition require frequent insulin shots to stabilise their blood glucose levels. However, this can be a difficult balancing act, as glucose levels can fluctuate throughout the day. Fluctuations can also be potentially dangerous, as they can lead to complications such as hypoglycaemia (low blood glucose).

This was an animal study looking into the development of a new type of “smart insulin” that contains a “molecular switch”, allowing it to directly respond to blood glucose levels, to bring them under control.

When injected into diabetic mice, it was able to normalise their blood glucose levels when they were given glucose challenges (where mice are given a sugary drink) even as long as 13 hours after the initial injection. This suggested that the modified insulin could help with blood glucose control and have a long duration.

Though promising, this research is in the very early stages. This modified insulin has so far only been tested in mice. It is far too early to know whether there could be a new insulin treatment available for type 1 diabetes.   

 

Where did the story come from?

The study was carried out by researchers from Massachusetts Institute of Technology in the US, and was funded by donations from the Leona M. and Harry B. Helmsley Charitable trust and the Tayebati Family Foundation. The study was published in the peer-reviewed journal PNAS.

The Guardian put a generally positive spin on the results, outlining the potential benefits the new insulin might bring to people with diabetes. It did well in mentioning that the research was done on mice. However, it didn’t really say or discuss why this was an important limitation of the research. While mice share many of our biological traits, we can never be sure that a drug that works in mice will work in humans (or be safe).

Only at the end of the piece was a note of caution introduced. This came from Dr Richard Elliott, of Diabetes UK, who said: “Years of further research and clinical trials will be needed to find out if a similar drug could be used safely and effectively by people with diabetes”.

BBC News’ reporting of the study was less optimistic, as they were quick to mention that “it will take years of testing before treatments could become a reality for patients”.

 

What kind of research was this?

This was an animal study that looked at developing a type of insulin that is tailored to the individual.

Type 1 diabetes is a condition where the body’s immune system destroys the insulin-producing cells of the pancreas, making the person reliant on life-long insulin injections. There are currently various types of insulin, ranging from some that act quickly and have a short-lasting effect, to those that have a much slower onset and last for longer periods. The type or combination of insulin preparations used will vary considerably from one individual with type 1 diabetes to another.

However, most people will experience difficulty at some point in their insulin treatment, such as problems controlling their blood glucose levels. This means they are potentially at risk of complications such as glucose becoming dangerously low (hypoglycaemia) or high (hyperglycaemia).

In this study, the researchers aimed to prepare a type of insulin that has a “molecular switch” that switches it on or off, depending on glucose levels. They tested it in mice. It is hoped that this treatment could one day give more targeted insulin therapy with better glucose control.

 

What did the research involve?

The research team prepared their modified insulin, which contains two small chemical molecules bound to insulin. One of the molecules (phenylboronic acid, PBA) is a “glucose sensor”, while the other molecule (an aliphatic domain) helps to give it a long “half-life” so it has similar duration in terms of action to long-acting insulin.

The researchers then tested this new insulin treatment in a mouse model of type 1 diabetes (mice that had been given a treatment to destroy their insulin-producing cells). The mice fasted overnight and were then given injections of the modified insulin at different doses, combined with glucose challenges (given a sugary solution to simulate eating a meal). Blood glucose levels were continuously monitored throughout the tests.

The main analysis compared the glucose control achieved with the new insulin to that achieved using standard insulin injections, all using diabetic mice. They also compared the effects of their insulin with glucose challenges given to healthy, non-diabetic mice.

 

What were the basic results?

Briefly, the researchers found that their treatment was successful when given to mice with type 1 diabetes. It rapidly normalised their blood glucose levels following the glucose challenge and also demonstrated longer-term effects. In some tests, the modified insulin was able to normalise blood glucose levels in glucose challenges given up to 13 hours after the initial injection.

Their “best-performing” insulin was also demonstrated to give better blood glucose control than standard long-acting insulins. When given a glucose challenge, the diabetic mice given the modified insulin were also able to normalise their blood glucose levels in a similar way to healthy non-diabetic mice.

 

How did the researchers interpret the results?

The researchers say their study is the first of their knowledge to have demonstrated the effects of a modified insulin molecule in a live animal model. They say that this approach to insulin modification “could afford both long-term and glucose-mediated insulin activity, thereby reducing the number of administrations and improving the fidelity of [blood glucose] control”.

 

Conclusion

This animal study has demonstrated promise for a modified insulin molecule that contains a “molecular switch”, allowing it to respond to blood glucose levels. When injected into diabetic mice, it was able to normalise their blood glucose levels in response to glucose challenges, sometimes many hours after the initial injection.

This suggested, as the researchers hoped, that the modified insulin could give targeted blood glucose control, and also have a long duration of action, similar to current long-acting insulins.

The researchers hope that this could one day lead to the development of an insulin treatment for people with type 1 diabetes that would give better blood glucose and reduce the risk of complications such as hypoglycaemia.

Though promising, this research is in the very early stages, having only been tested in mice. There are many more developmental hurdles to pass before this innovation could be a new treatment for people. The first stage would be seeing whether the treatment could be developed for testing in humans, then seeing whether it is safe, then gradually conducting trials in successively larger numbers of people. This will determine whether it is safe and effective compared with other insulins used by people with type 1 diabetes.

While it is perfectly fine to be optimistic, there are no guarantees. Promising research in mice does not necessarily lead to effective treatments for humans.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

'Smart' insulin may ease burden of type 1 diabetes patients, research suggests. The Guardian, February 9 2015

'Smart' insulin hope for diabetes. BBC News, February 10 2015

Links To Science

Chou D, Webber MJ, Tang DC, et al. Glucose-responsive insulin activity by covalent modification with aliphatic phenylboronic acid conjugates. PNAS. Published online February 9 2015

Categories: Medical News

1980s fat guidelines 'lacked evidence,' study argues

Medical News - Tue, 02/10/2015 - 15:00

"Butter isn't bad for you after all: Major study says 80s advice on dairy fats was flawed," is the headline on the front of the Daily Mail as a new study argues dietary fat guidelines introduced in the 1980s lacked a rigorous evidence base.

The study in question looked at guideline advice on saturated fat published in 1983 in the UK and in 1977 in the US. The researchers wanted to see if the evidence available at the time – specifically, the results of randomised controlled trials (RCTs) – supported the recommendations made.

The researchers identified six RCTs available at the time. The pooled results showed that specific advice to control saturated fat intake did not have a significant effect on deaths from heart disease or other causes.

But it is very important that these findings are interpreted in the correct context – this means we cannot conclude the recommendations were "incorrect".

We do not know what evidence was used to back up the official guidelines in the late 70s and early 80s. They could have looked at studies other than RCTs, such as observational studies (where health outcomes are studied over time).

This new review considered just six RCTs published before 1983, and all of them were conducted in men, most of whom already had heart disease.

Current dietary advice is not stuck in the 1980s, wearing shoulder pads and sporting a bubble perm. It has evolved as new evidence has emerged. In fact, a small amount of saturated fat is recommended as part of a balanced, Mediterranean-style diet.

But it would be a mistake to conclude from this evidence that you can eat as much saturated fat as you like without damaging your health.

 

Where did the story come from?

The study was carried out by researchers from the University of the West of Scotland, Cardiff Metropolitan University, and the University of South Wales in the UK, and Saint Luke's Mid America Heart Institute in the US.

No sources of funding are reported and the authors declare no conflicts of interest. But the lead author of the study, Zoë Harcombe, does run a commercial diet plan called The Harcombe Diet®, which promotes "eating real food", including dairy products.

The study was published in the peer-reviewed medical journal, Open Heart. This is an open-access journal, so the study can be read online for free or downloaded as a PDF.

Overall, the media reporting was poor and potentially quite dangerous for several reasons. Much of the reporting gives the impression that the claim "saturated fats are not bad for you" represents a change in official dietary advice. This is not the case. The claim is the opinion of a small group of researchers.

The headline writing was particularly sensationalist. Journalists took the findings at face value, writing potentially scaremongering headlines, and may leave their readers questioning the evidence base for the current guidelines. Debate on national guidelines is always welcome, but much of the debate in the media was ill-informed.

Even if you did accept the claim that saturated fat is not especially harmful, it certainly does not follow that eating more of it would be good for you, as the Daily Express bizarrely claimed: "Fat is key to living longer". A diet high in saturated fat could in fact lead to obesity.

A more balanced account of the relevance of this study was given in the accompanying Open Heart editorial, which is also open access.

Various dietary experts have considered this research in a broader context. The consensus from the experts is that only focusing on evidence from RCTs for dietary guidelines is somewhat unrealistic and narrow, and missed useful evidence of other types.

Some went a lot further. Professor Christine Williams, professor of human nutrition at the University of Reading, said: "The claim that guidelines on dietary fat introduced in the 1970s and 80s were not based on good scientific evidence is misguided and potentially dangerous."

 

What kind of research was this?

This was a systematic review and meta-analysis of research published 30 or more years ago.

It aimed to investigate whether national dietary advice introduced in the 1970s and 80s in the US and the UK to reduce coronary heart disease (CHD) by reducing saturated fat intake was backed up by contemporaneous evidence from randomised controlled trials (RCT), which are seen as the "gold standard" in evidence-based medicine.

In the US, public health dietary advice was issued by the Select Committee on Nutrition and Human Needs in 1977. This was followed in 1983 by UK public health dietary advice from the National Advisory Committee on Nutritional Education.

The authors state these recommendations advised that people reduce their overall fat consumption to 30% of their total energy intake, and reduce their saturated fat consumption to 10% of their total energy intake.

The researchers discuss several possible limitations of these publications, saying they included wording that was far from conclusive, such as "tended to be related", and how neither publication made reference to any RCTs available at the time.

The authors of this review therefore aimed to look for RCTs available when the dietary guidance was published to see whether the available evidence supported the recommendations.

 

What did the research involve?

The authors searched the literature databases Medline and the Cochrane Library to identify studies published up to 1983. They restricted their search to these two databases because others did not provide adequate coverage of the early publications this review was interested in.

They looked for RCTs in adults of at least one year's duration where:

  • people were randomised to a dietary intervention (a programme that attempted to control or modify specific elements of their diet)
  • the aim of the study was to look at whether a reduction or modification in dietary fat or cholesterol had an effect
  • health outcome data on all-cause mortality, CHD mortality and cholesterol measurements was available

Six RCTs met their inclusion criteria:

  1. Rose Corn Oil Trial
  2. Research Committee Low-fat Diet
  3. MRC Soya-bean Oil
  4. LA Veterans Study
  5. Oslo Diet Heart Study
  6. The Sydney Diet Heart Study

The researchers extracted data from these studies and considered their quality and risk of bias. They pooled the results of these trials in a meta-analysis.

 

What were the basic results?

The six RCTs included a total of 2,467 men, and all but one of the studies looked at secondary prevention. This means the participants already had cardiovascular disease.

The researchers involved in these RCTs looked at whether dietary intervention could reduce the risk of further disease events, such as a heart attack. The average study duration was five to six years.

Of the six studies, four looked at giving vegetable oil (three of which assessed it as a replacement for saturated fat), one looked at a roughly 20% fat diet, and one looked at a 10% saturated fat diet.

As this new study points out, five of the six RCTs did not look at either a total fat consumption of 30% or saturated fat as 10% of energy intake, as given in the offical recommendations made in the 70s and 80s.

Across the studies, 30.2% of the intervention groups and 29.8% of the control groups died. The pooled results of all the studies found no statistically significant effect of the dietary interventions on deaths from all causes (relative risk [RR] 0.996, 95% confidence interval [CI] 0.865 to 1.147).

The pooled results did not find that the dietary interventions had any significant effect on coronary heart disease mortality specifically (RR 0.989, 95% CI 0.784 to 1.247).

Cholesterol levels fell in both intervention and control groups, though there was a greater reduction in the intervention groups. The pooled reduction in the intervention groups was a reduction of 12.6% (give or take 6.7%), while the reduction in the control groups was 6.5% (give or take 5.1%).

 

How did the researchers interpret the results?

The researchers say that: "No randomised controlled trial had tested government dietary fat recommendations before their introduction.

"Dietary recommendations were introduced for US and UK citizens by 1983, in the absence of supporting evidence from RCTs."

They state that: "The present review concludes that dietary advice not merely needs review; it should not have been introduced."

 

Conclusion

This research found the pooled results of six RCTs available prior to 1983, which all looked at interventions to moderate saturated fat intake, did not find this had an effect on deaths from heart disease or any other cause.

But it is very important that the specific purpose of this review is considered, and the findings are interpreted in the right context.

This review specifically looked at nutrition guidance given in the US in 1977 and in 1983 in the UK. In particular, the researchers looked at two recommendations:

  • reduce overall fat consumption to 30% of total energy intake
  • reduce saturated fat consumption to 10% of total energy intake

The researchers specifically wanted to see whether RCTs available at that time supported those recommendations. But there are some specific points to consider from the results of this analysis.

Evidence considered by the 1977 and 1983 guidelines

We are not able to review the methods used by the US and UK government bodies in forming their nutrition recommendations. We also do not know what evidence they considered.

The authors of the current review state that: "Both documents acknowledged that the evidence was not conclusive ... the Dietary Goals for the US noted 'there will undoubtedly be many people who will say we have not proven our point.' The UK publication referred to 'a strong consensus of opinion'."

We cannot comment further on how this nutrition guidance may have been produced, or how they may have considered their evidence and formed their recommendations.

It is possible the methods used by these organisations more than 30 years ago may have differed from those used in producing the most robust evidence-based guidelines today.

But we cannot conclude that the recommendations were unreasonable, or not backed by any supporting evidence, just by looking at the information included in this systematic review.

It is likely the guidance from more than 30 years ago may have considered observational evidence looking at how saturated fat intake was related to mortality and heart disease.

While the lack of RCTs at the time may potentially be of concern, it is also not particularly surprising. RCTs involving diet are notoriously difficult to run because of compliance issues: researchers can never be sure that participants are sticking to their recommended diet plans. Also, exposing participants to an intervention you think may be harmful is unethical.

It is also not fair to say observational study designs are of no value. In fact, when looking at issues such as dietary patterns, there is often more information available from observational studies. These types of studies can review a person's longer-term lifetime dietary patterns and see how this is related to health outcomes.

We therefore cannot conclude that the recommendations made over 30 years ago were "incorrect". This review has kept a narrow focus, only looking at RCTs available at the time.

Other types of study, such as long-term population-based studies, can provide rich and useful information, and may have been considered when the guideline recommendations were being formed.

Issues with the RCTs included in the review

The finding there is no link between saturated fat intake and deaths from heart disease and other causes is based on six very specific RCTs. These studies are all likely to have differences in terms of their design, the methods used, their duration, and their quality.

The studies only included men, so the results may not be applicable to women, for a start. And five out of six included men who already had heart disease.

The studies also looked at the relatively short-term effects of specific interventions (such as substituting vegetable oil) and whether this influenced outcomes. They did not look at lifetime dietary patterns. Overall, they found the interventions did not affect outcomes.

This review's findings do not mean that current government nutritional advice and recommendations (the eatwell plate) are wrong.

National dietary guidance is based on all the relevant evidence that has accumulated to date, and is updated regularly to consider important new evidence. Current guidance will have considered a much larger body of research than the guidance issued in 1983. 

There's nothing wrong with the occasional buttered scone. But, based on the current body of evidence, it would be potentially dangerous to think you can eat as much saturated fat as you want without it having an effect on your health.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Butter ISN'T bad for you after all: Major study says 80s advice on dairy fats was flawed. Daily Mail, February 9 2015

Fat guidelines lacked any solid scientific evidence, study concludes. The Guardian, February 10 2015

Dietary advice from the 1970s found to be a big fat mistake. The Independent, February 10 2015

Food fat warnings 'should not have been introduced'. The Daily Telegraph, February 9 2015

Fat Guidelines 'Shouldn't Have Been Introduced'. Sky News, February 10 2015

FAT is the key to living longer: Previous diet advice was WRONG, say experts. Daily Express, February 10 2015

Links To Science

Harcombe Z, Baker JS, Cooper SM, et al. Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart. Published online February 9 2015

Categories: Medical News

Do men have greater chewing power than women?

Medical News - Mon, 02/09/2015 - 18:55

"Why men wolf down their meals while women take their time: The sexes have different chewing patterns," the Mail Online reports, after a Korean study found men had "greater eating power" than women.

This small study compared the chewing behaviours of 48 young Korean men and women in controlled laboratory conditions.

It found men took bigger bites, had greater chewing power, and ate faster than women. Women chewed more and took longer to finish their food.

But this study has considerable limitations – mainly, that its results may not apply to wider populations, such as people of different ages or from different countries.

This highly controlled experiment, where participants ate plain boiled rice while monitors were attached to their jaws, may not even be representative of how the volunteers would chew in a real-life situation.

Overall, this research is not sufficient to conclusively say that men and women have different chewing patterns, or what the implications of this might be.

It is probably better to concern yourself with what and how much you are eating rather than how long you take to chew and swallow your food.

 

Where did the story come from?

The study was carried out by researchers from Semyung and Hanyang Universities in the Republic of Korea. It was funded by the Korean Ministry of Food, Agriculture, Forestry and Fisheries.

The study was published in the peer-reviewed journal Physiology and Behavior, and is available to read online or download as a PDF on an open-access basis.

The Mail Online's reporting was generally accurate, but did not point out the relatively limited applicability and implications of this study.

 

What kind of research was this?

This was an experiment comparing eating behaviours and chewing in men and women. It also looked at whether obesity influenced these behaviours.

The researchers say some previous studies found that obese individuals chew faster and take bigger bites than those who are not obese, while other studies have reached different conclusions.

They say there have been similar findings looking at the different ways men and women eat.

This study design is reasonable for assessing eating behaviours, but the highly controlled setting of the experiment may not be representative of people's behaviours in everyday life.

 

What did the research involve?

The researchers recruited 24 male and 24 female volunteers to eat portions of rice. They compared the volunteers' reported eating behaviours, and also measured their chewing under controlled conditions in the lab.

They then looked at whether there were differences between men and women, or between those who were heading towards being obese (pre-obese) and those who were not.

To be eligible to take part, the volunteers had to be aged 20 to 29 years, have a full set of healthy teeth, and no eating disorders. The researchers recruited people who were:

  • non-obese – body mass index (BMI) between 18.5 and 23, and a waist circumference less than 80cm for women and 90cm for men
  • pre-obese – BMI 25 or over, and a waist circumference of 80cm or more for women, and 90cm or more for men

The volunteers filled out a standard questionnaire assessing their subjective views about their control of three dietary behaviours:

  • restraint – ability to cognitively control eating behaviour
  • disinhibition – susceptibility to eating in response to emotional factors and sensory cues, such as smells
  • hunger – susceptibility to eating in response to hunger

They then took part in the eating experiment in the lab. They fasted for 12 hours overnight and had not exercised for 24 hours. They were then all given 152g of boiled rice to eat served with 200ml of water.

The researchers asked the volunteers to rate their hunger and fullness before and after eating the rice. While the volunteers were eating the rice, the researchers measured their chewing using sensors attached to the jaw.

 

What were the basic results?

The researchers found that:

  • pre-obese volunteers reported greater susceptibility to eating in response to emotional factors and sensory cues than non-obese volunteers
  • women and men differed in their chewing, but pre-obese and non-obese individuals did not
  • men took bigger bites than women
  • men's chewing power (the muscle pressure exerted by their jaws) was greater than women's
  • men ate faster than women
  • women chewed more than men
  • women took longer to finish their rice than men

The researchers found men who reported greater susceptibility to eating in response to emotional factors and sensory cues tended to eat faster.

Both men and women who reported greater susceptibility to eating in response to emotional factors and sensory cues tended to have a smaller bite size and less chewing power.

 

How did the researchers interpret the results?

The researchers concluded that, "The results suggest that the effects of gender, and, in part, obesity, on eating responses may be explained as chewing performance."

They say this means that, "Gender-specific interventions and counselling aimed at slowing the rate of ingestion could be promising behavioural treatments for obese persons."

 

Conclusion

This small study suggests that chewing behaviours in controlled laboratory conditions differ between young Korean men and women.

But this study of just 48 people has considerable limitations. Its results may not apply to wider populations, such as people of different ages or from different countries.

This highly controlled experiment, where participants ate plain boiled rice while monitors were attached to their jaws, may not even be representative of how the volunteers would chew in a real-life situation.

The many statistical tests carried out also mean that some may be statistically significant by chance.

Although the researchers found some differences between men and women in chewing, they did not find any between those who were considered pre-obese and those who were not obese.

It is not possible to say from this study whether the "gender-specific interventions and counselling aimed at slowing the rate of ingestion" would indeed "be promising behavioural treatments for obese persons", as suggested by the authors.

This study does not provide compelling evidence of differences between men and women in "masticatory performance", or whether these can lead to increased fitness, better health, or weight loss.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Why men wolf down their meals while women take their time: The sexes have different chewing patterns. Mail Online, February 9 2015

Links To Science

Park S, Weon-Sun S. Differences in eating behaviors and masticatory performances by gender and obesity status. Physiology & Behavior. Published online October 18 2014

Categories: Medical News

Type 1 diabetes 'more dangerous' in women

Medical News - Mon, 02/09/2015 - 14:00

"Type 1 diabetes is more dangerous for women than men, study finds,” The Daily Telegraph reports. A large review found gender inequality in overall deaths among people with type 1 diabetes, and also deaths due to heart disease.

These results come from a systematic review of studies looking at how risk of death in men and women with type 1 diabetes differs from their counterparts without the disease. It pooled results from 26 studies, and found that type 1 diabetes was associated with a greater increase in risk of death from any cause, or death from heart disease, over a given period in women than it is in men.

The researchers suggest it may be because diabetes is less well controlled among girls and women than among boys and men. If this proves to be the case, then greater efforts may be targeted towards to improving diabetes management in women.

Type 1 diabetes is, at the moment, an incurable condition, so it is important to stay informed about the best way to live with diabetes, whatever your gender.

 

Where did the story come from?

The study was carried out by researchers from the Universities of Queensland and other universities in Australia, the Netherlands, UK and US. The researchers were funded by a Niels Stensen Fellowship, an Australian National Health and Medical Research Council Fellowship, and an Australian Research Council Future Fellowship. The study was published in the peer-reviewed medical journal The Lancet.

The Daily Telegraph covers this study reasonably well; however, the results are expressed in a way that could be misleading. It says, for example, that “female patients are twice as likely to die from heart disease than men with [type 1 diabetes]”. It is not quite as simple as this. As men do not generally live as long as women, researchers needed to take this into account in their analyses – otherwise, the figures would not be showing them the potential impact of diabetes, but the effect of gender.

So, to get a fair idea of the potential impact of diabetes, the researchers did not directly compare rates of death in men and women. Instead, they first compared the risk of death over a given period in women with type 1 diabetes to that of women in the general population, to see what effect diabetes had in women. The equivalent comparison was then made for men.

These figures were then compared to see whether type 1 diabetes had a greater or lesser effect on risk of death in women than in men.

 

What kind of research was this?

This was a systematic review that aimed to determine whether there was any difference between men and women with type 1 diabetes and their likelihood of dying within any given period.

The researchers say that although management of type 1 diabetes has improved, the condition is still associated with an increased risk of death over a given period, compared to the general population. They say that some studies have suggested that men and women may differ in how much type 1 diabetes affects their risk of death, but no review has ever pooled the results of these studies.

A systematic review is the best way to identify and summarise the best-quality studies available to answer a given question. This review statistically pooled (meta-analysed) the results of the studies it identified. The meta-analysis includes more people than each individual study alone, and this means it is better able to detect differences between groups, if they exist.

 

What did the research involve?

The researchers systematically searched one major research literature database (PubMed) to identify studies that identified risk of death in men and women with diabetes over time. They selected those studies which had data that would allow them to compare the effect of type 1 diabetes in terms of risk in men and women. They then extracted and pooled the results of these studies to see if there was a difference overall.

The researchers only included studies that provided information on deaths in a form that they could use. This meant either hazard ratios (HR), comparing deaths among people with and without type 1 diabetes, or standardised mortality ratios (SMR), comparing deaths among people with type 1 diabetes against what would be expected among people with similar characteristics in the general population.

As men and women have different expected lifespans, researchers were looking for studies which compared deaths among women with type 1 diabetes versus women without the disease, and did the same for men. This meant they could compare the likelihood of a person of each gender dying to someone of the same gender without the disease. They then compared these figures.

The researchers were mainly interested in deaths from any cause, but also looked at deaths from specific causes separately. They also looked at new diagnoses of various conditions, including coronary heart disease (where a build-up of fatty substances causes blockage in the arteries providing blood to the heart muscle) and cardiovascular disease (coronary heart disease, stroke, or other cardiovascular disease). They also looked at various factors which might affect the outcome, such as how long the studies followed people for, or the quality of the study.

The researchers complied with accepted standards for pooling of this study type and for reporting their systematic review.

 

What were the basic results?

The researchers identified 26 studies that provided the data they wanted. These studies included 214,114 people, although not all of them were included in all of the analyses.

It found that during follow up, women with type 1 diabetes were 5.8 times more likely to die than women in the general population, and men with type 1 diabetes were 3.8 times more likely to die than men in the general population. Overall this equated to a 37% greater relative increase in likelihood of death than men with the condition (ratio of SMRs for women versus men: 1.37, 95% confidence interval [CI] 1.21 to 1.56). There was statistical evidence that different studies in this analysis had varying results. Some of this variability seemed to be due to differences between the studies in exactly how likely men and women were to die.

Women with type 1 diabetes also had a greater relative increase than men with the condition in terms of risk of:

  • a new diagnosis of coronary heart disease (ratio 2.54, 95% confidence interval (CI) 1.80 to 3.60)
  • a new diagnosis of stroke (ratio 1.37, 95% CI 1.03 to 1.81)
  • dying from kidney disease (ratio 1.44, 95% CI 1.02 to 2.05)
  • dying from cardiovascular disease (ratio 1.86, 95% CI 1.62 to 2.15)

There was no difference between men and women in how type 1 diabetes affected their risk of cancer or accident and suicide.

 

How did the researchers interpret the results?

Researchers concluded that “women with type 1 diabetes have a roughly 40% greater excess risk of all-cause mortality, and twice the excess risk of fatal and nonfatal vascular events, compared with men with type 1 diabetes”. They say that greater understanding of this issue “is likely to have profound clinical implications for how women with type 1 diabetes are treated and managed throughout their life course”.

 

Conclusion

This systematic review suggests that type 1 diabetes is associated with a greater increase in risk of death in women than men.

A systematic review is the best way to identify and summarise the best-quality studies available to answer a given question. The pooling (meta-analysis) of the studies' results means the review includes more people than the individual studies, and is therefore better able to detect differences between groups.

The figures presented are comparisons of the relative increases in risk of death associated with type 1 diabetes within each gender. As women generally live longer than men, even though the relative increase in risk in women with type 1 diabetes may be greater than in men, the women’s actual (absolute) risks of death in a given period may not differ as much, and could still be less than men’s risks.

There are some other limitations and points to note:

  • This study is only about type 1 diabetes, so results may not apply to those with type 2 diabetes.
  • The review only searched one literature database, and also looked for relevant studies mentioned in the studies they identified. Ideally, systematic reviews search more than one literature database to increase their chances of finding all relevant studies.
  • The pooled studies did have differences in their designs and methods, and this may influence the results. There was statistical evidence that there were differences in the results of the individual studies, which the researchers were not entirely able to explain. In part, it related to different risks of death in the populations being studied. This may mean that the pooled results are not representative of each different study population. The researchers also say it means their results “remain speculative until confirmed by future studies”.
  • The review pooled observational studies. Factors other than type 1 diabetes (confounders) could be influencing the results seen. The individual studies differed in the extent to which they took these factors into account, so they could still be having an effect. The researchers think that this is unlikely to be a big issue, as the same confounders should be affecting men and women, and therefore effectively cancelling each other out.

It is likely that more research will go into exploring why this difference might exist. The researchers suggest it may be because girls’ and women’s diabetes is less well controlled, or due to hormonal differences. The researchers were not able to look at diabetes control in men and women in the included studies to see if there was a difference. If the difference does prove to be due to poorer diabetes control, then greater efforts could be targeted towards improving diabetes management in women.

Whatever the reason for these findings, they do not take away from the fact that good diabetes control is important for both genders, to maintain a person’s health and reduce the risk of complications from the disease.

The NHS offers information and support services for people living with all forms of diabetes.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Type 1 diabetes is more dangerous for women than men, study finds. The Daily Telegraph, February 7 2015

Links To Science

Huxley RR, Peters SAE, Mishra GD, Woodward M. Risk of all-cause mortality and vascular events in women versus men with type 1 diabetes: a systematic review and meta-analysis. The Lancet – Diabetes and Endocrinology. Published online February 5 2015

Categories: Medical News

Finger length 'not a pointer' for future sexual behaviour

Medical News - Fri, 02/06/2015 - 19:00

"How to work out if your partner is cheating on you? Check their fingers," the Daily Mirror advises. The news comes from research founded on the theory that humans are believed to display two types of mating pattern – one more promiscuous, and the other more monogamous.

Previous animal and human studies have already suggested higher testosterone exposure is associated with longer ring to index finger ratios. And high testosterone has been linked to sexual promiscuity.

To look into this further, the researchers studied two separate samples. One sample of just over 500 people completed an online survey of their sexual behaviour. A completely separate sample had their finger lengths measured.

The results from the first sample found more men tended towards the promiscuous side, and more women towards the monogamous.

The second sample's results found more men have longer ring fingers than index fingers, while roughly equal proportions of women have either similar length fingers or longer ring fingers.

From this, the researchers inferred that – contrary to the findings of the survey – a more promiscuous pattern seems to be found in both sexes. Had women been more monogamous, as the survey suggested, they apparently should have had longer index fingers.

Whatever interpretation you could reasonably take, the study proves nothing about any association between sexual behaviour and the ratio of finger length.

Comparing two entirely different data sets takes you into "oranges and apples" territory – trying to find connections between two entirely different objects.

You also have to consider how representative people who chose to complete an online survey of sexual behaviour are of the general population.

 

Where did the story come from?

The study was carried out by psychology researchers at the University of Oxford and Northumbria University, and received funding from the European Research Council.

It was published in the peer-reviewed journal, Biology Letters, which is a publication of The Royal Society.

The article is open access, so it can be read online for free.

The UK media appear to have taken the study at face value, choosing not to report its important limitations. Namely, this study separately analysed sexual behaviour in one group and finger length in another group, and then drew links between the two.

But from the tone of the reporting, we suspect the journalists themselves were taking the findings of the study with a pinch of salt and with their tongues firmly in their cheeks.

If the suggestion that finger length can be used as a reliable predictive method for something as complex as human sexual behaviour sounds ridiculous, then it probably is ridiculous.

 

What kind of research was this?

This was a study looking at sexual behaviour patterns in one study sample, and the ratio of index and ring finger length in another study sample.

It aimed to look at the patterns of distribution of the two separate factors in these two separate samples, and from this see whether there may be an association between sexual behaviour and finger length.

The researchers say, in animal terms, humans are believed to fall midway between a monogamous and polygamous species, respectively a mix of longer-term and short-term mating patterns.

They say the extent to which any individual primarily pursues a "restricted" mating strategy, favouring exclusive pair-bonds, or an "unrestricted" strategy of promiscuity, is called "sociosexual orientation".

As a broad generalisation, males are usually considered more likely to favour promiscuous patterns than females as a way of getting more mating opportunities. 

The researchers say previous studies have shown that index to ring finger ratio is influenced by the amount of testosterone the growing foetus is exposed to in the womb, as well as the density of testosterone receptors.

Other studies in primates are also said to have shown finger length is associated with mating patterns.

This research tested the theory that there are two restricted and unrestricted types of people by looking at two large data sets – one sample completed a sociosexual orientation survey, and one sample had their index to ring finger ratio measured.

 

What did the research involve?

A total of 595 North American and British men and women (average age 25 years) completed the online sociosexual orientation survey (SOI-R).

Preferred mating strategy was said to be assessed using the "attitude" and "desire" subscales of the SOI-R, but this was not explained further.

A separate study collected data on index to ring finger ratios on the right hand of 1,314 British men and women.

The researchers then carried out analyses looking at the modelled distribution of sexual behaviours in the North American and British sample, and the distribution of finger length ratios in the other British sample.

 

What were the basic results? Sociosexual orientation survey

The researchers plotted distribution curves, where SOI-R score is plotted against density (the number of people who had that score). They did this for four separate groups: British men and women, and North American men and women.

All the groups of men and women showed what is called a "bimodal" distribution – two normal patterns of distribution. For all four groups, there was one pattern with a peak of normality at a lower SOI score (a more monogamous pattern), and a second pattern with a peak of normality at a higher SOI score (a more promiscuous pattern).   

There was a slight difference for men and women, though. For both North American and British men, the higher peak was at the higher SOI score, corresponding with slightly more men with a more promiscuous pattern.

Meanwhile, for both North American and British women, the opposite was seen – the higher peak was at a lower SOI score and corresponded with slightly more women following the monogamous pattern.

Finger length ratios

When similarly looking at the distribution of index to ring finger ratios for the other British sample, the researchers also found two normal distributions, but this time there was more of an overlap between the two curves.

For the sample of British men, the much higher peak was at a ratio of around 0.94 (ring finger slightly longer than index). There was a second much lower peak at a ratio of around 1 (similar length fingers).

For women, there was one common peak at around 0.94 and another equally common peak at a ratio of around 1.

Interpreted crudely, this means in men it is more common to have a longer ring finger than index finger, while in women equal numbers have fingers of the same length, or a ring finger longer than an index finger.

 

How did the researchers interpret the results?

The researchers concluded that: "This study is the first, to the best of our knowledge, to show statistically that both men and women exhibit two reproductive phenotypes of varying proportions."

But they go on to say that: "The proportional split in males slightly favours an unrestricted (short-term) mating strategy, with a 57:43 split on average, whereas females have a reversed split (47:53)."

The researchers then said that: "However, the mixing proportions in the [index to ring finger] ratio data set suggest that a slightly higher proportion of the unrestricted phenotype is present in both sexes (males approx. 62%, females approx. 50%)."

Presumably, this is based on previous research, which suggested testosterone levels are associated with finger ratios.

 

Conclusion

This research was founded on the theory that, as a species, humans are believed to display two types of mating pattern – one more promiscuous pattern made up of shorter-term attachments, and the other more monogamous pattern favouring longer term pair-bonds.

Traditionally, the male of a species is considered to favour the more promiscuous pattern to create more mating opportunities.

The research also centres on the other observation from previous human and animal studies, which found finger length is associated with mating patterns, and that index to ring finger ratio is influenced by testosterone levels.

The researchers used two separate samples for their study:

  • The first sample suggested there does seem to be two normal mating patterns for both men and women – one more promiscuous, and the other more monogamous. However, a higher proportion of men tend towards the more promiscuous side, while a higher proportion of women tend towards the more monogamous side.
  • The second sample, which assessed index to ring finger ratio, suggested more men have longer ring fingers than index fingers, while roughly equal proportions of women have either similar length fingers or their ring fingers are longer.

The researchers seem to imply from this that finger ratios actually show a more promiscuous pattern seems to be found in both sexes. This is because men tend to have longer ring fingers, which presumably ties up with higher testosterone levels and more promiscuous patterns.

However, women were found to have two equal distributions of finger length ratios. But if women were indeed more monogamous, as the other survey suggested, the researchers should have expected them to have longer index fingers.

Overall, this paints a rather unclear picture and it is hard to draw any reliable conclusions from this study.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

How to work out if your partner is cheating on you? Check their fingers. Daily Mirror, January 4 2015

Are you faithful or promiscuous? The answer could lie in your index finger. The Independent, January 5 2015

Are you promiscuous or faithful? Measure your index finger to find out. The Daily Telegraph, January 4 2015

Links To Science

Wlodarski R, Manning J, Dunbar RIM. Stay or stray? Evidence for alternative mating strategy phenotypes in both men and women. Biology Letters. Published online February 4 2015

Categories: Medical News

Flu jab is not a 'waste of time'

Medical News - Fri, 02/06/2015 - 13:10

“Flu jab given to millions is 'useless',” and "Flu jab is a waste of time," are the irresponsible headlines in The Daily Telegraph and the Daily Mail.

While recent research shows that the current seasonal flu vaccine only has 3% protection against the main circulating strain – A(H3N2) – in adults, it can still protect against other strains.

Both papers also ignore the fact that another version of the flu vaccine, in the form of a nasal spray designed for vulnerable children, is also available.

Discouraging parents of vulnerable children from getting vaccinated could increase the risk of serious childhood illnesses and possible hospitalisation.

 

Why is the flu vaccine not working?

There are many strains of the influenza virus and each one can mutate. It takes time to develop and produce vaccines against them. Global surveillance is used to predict which strains are likely to be circulating the following winter, and in February the World Health Organization (WHO) announces which strains the flu vaccine should cover. Last year, it decided to cover three flu varieties:

  • Influenza A (H1N1), also known as “swine flu"
  • Influenza A (H3N2)
  • Influenza B

In March, the WHO Global Influenza Surveillance and Response System detected a new strain of influenza A (H3N2), but this was too late to change the production of the vaccine.

It was also not known whether this particular strain would be the predominant strain this winter, which it has been, and so the vaccine is not effective against it.

How effective is it?

The vaccine is effective against the other strains of influenza, but not the new strain of influenza A (H3N2). The mid-season vaccine effectiveness rate is just 3.4%. Vaccination against this new strain and other possible mutations will be considered at the WHO meeting this February for next winter.

 

Reactions to the news

Dr Michael Skinner, Reader in Virology, Imperial College London said: “The current type of seasonal influenza vaccine is, at the moment, the best we have. Annually it saves tens of thousands of lives. Unusually, but not uniquely, this year one (H3N2) of the four targeted viruses ‘drifted’ (mutated) in an unanticipated direction after the vaccine was formulated for production, so that the vaccine offers little protection against the drifted H3N2.

"Even so, the vaccine still protects against the other three components (pre- and post-2009 H1N1 and B). And it does at least stop the virus drifting back along the path that had been predicted. To describe it as ‘useless’ would be misguided.”

 

Should you still get the jab?

The other strains can still cause infection so the vaccine is still recommended for pregnant women, people aged over 65 and those with any of the following conditions:

 

When to visit your GP

If you are otherwise fit and healthy, there is usually no need to visit your GP if you have flu-like symptoms.

The best remedy is to rest at home, keep warm and drink plenty of water to avoid dehydration.

You can take paracetamol or ibuprofen to lower a high temperature and relieve aches.

If you are in any of the high risk groups listed above then you should visit your GP.

Depending on your circumstances, your GP may recommend a short course of antiviral medication, such as Tamiflu (oseltamivir). 

Antivirals are not used for everyone with flu because this would lead to further mutations in the viruses and drug resistance, making them ineffective.

If you suspect you have the flu it is important to take steps to prevent it spreading; especially to one or more of the vulnerable groups listed above.

Always:

  • make sure you wash your hands regularly with soap and water
  • clean surfaces such as your keyboard, telephone and door handles regularly to get rid of germs
  • use tissues to cover your mouth and nose when you cough or sneeze
  • put used tissues in a bin as soon as possible

 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Flu jab given to millions is 'useless'. The Daily Telegraph, February 6 2015

Flu jab is a waste of time for 97% of patients: Vaccine developed only a year ago no longer 'matches' because the virus has mutated so much. Daily Mail, February 6 2015

Flu vaccine 'barely effective' against main viral strain. BBC News, February 5 2015

Useless flu jab blamed for surge in death toll. Daily Express, February 6 2015

Current winter flu jab works in only 3% of cases. ITV News, February 6 2015

Flu vaccine gives only ‘low protection’ in UK this winter, experts warn. The Guardian, February 5 2015

Flu jab given to millions offers almost no protection. The Times, February 6 2015

Flu Jab Found To Work In Just 3% Of Cases. Sky News, February 6 2015

Links To Science

Pebody RG, Warburton F, Ellis J, et al. Low effectiveness of seasonal influenza vaccine in preventing laboratory-confirmed influenza in primary care in the United Kingdom: 2014/15 mid-season results. Eurosurveillance. Published online February 5 2014

Categories: Medical News

'Facebook envy' associated with symptoms of depression

Medical News - Thu, 02/05/2015 - 15:00

"Facebook can cause depression in people who compare themselves with others," The Independent reports. A new study has examined the relationships between Facebook use, feelings of envy, and feelings of depression.

Researchers surveyed more than 700 US university students, aiming to look at the relationships between the extent of Facebook use and feelings of envy and depression.

Importantly, it found the extent of Facebook use in itself was not associated with depression symptoms.

However, increased Facebook use was associated with feelings of "Facebook envy", such as feeling envious when seeing photos of old friends on luxury holidays.

Increased feelings of envy were then associated with increased symptoms of depression.

The relationship between feelings of envy, Facebook usage, and symptoms of depression is likely to be a complex one, and overall the study does not prove a cause and effect relationship.

The idea that spending increased time looking at the posts of Facebook friends could contribute to feelings of envy, which could in turn lead to feelings of low mood, seems plausible.

But there are likely to be many other unmeasured factors that are also having an influence. These could include personal characteristics, lifestyle and physical and mental health.

If you are prone to envy, Facebook may not be the social network for you. Why not try Twitter, where, as we discussed last month, people often post "angry tweets" unlikely to provoke any feelings of envy.

Where did the story come from?

The study was carried out by researchers from Nanyang Technological University in Singapore, and Bradley University and the University of Missouri in the United States. No sources of financial support were reported.

It was published in the peer-reviewed journal, Computers in Human Behavior.

Overall, the UK media's reporting was generally accurate, though many of the headlines failed to make it clear that Facebook itself did not cause depression.

In fact, "Facebook envy" was the main mediator of any link – but many other unmeasured factors are likely to be having an influence.

What kind of research was this?

This was a cross-sectional study based on a survey of US college students, which aimed to investigate the association between Facebook use, envy and depression.

In it, the researchers discuss the various traumas surrounding the transition to college life for young adults, including moving away from home, gaining new freedom and forming new relationships.

They report how a previous study found US adults aged 18 to 24 are likely to suffer from symptoms of depression and anxiety, particularly college students.

As the researchers say, multiple factors are likely to contribute to this, but they state that, "policy makers and scholars have hypothesized that heavy use of online social networks such as Facebook and mobile technologies may contribute to the phenomenon".

The researchers aimed to look at whether or not heavy Facebook use among college students could lead to depression, and the factors that may influence this relationship.

What did the research involve?

In the background to their survey, the researchers first of all present a literature review, where they discuss studies that have examined various theories.

This review does not appear to be systematic in that no methodology is provided, so we can't be sure that all relevant research into these issues has been considered.

The researchers first of all discuss various studies that have examined what is called "social rank theory" – a theory that depression is a result of competition, where humans, like other animals, compete for food, mates, and resources.

They also discuss research covering the evolution of Facebook, "the most popular social networking site". 

They then discuss studies that have looked at the mental health of college students, and introduce the theory of "Facebook envy" as a lead-up to their questions:

  • What is the relationship between frequency of Facebook use and depression among college students?
  • What specific uses of Facebook predict Facebook envy?
  • Does Facebook envy mediate the relationship between Facebook use and depression among college students?

The study is based on an online survey of 736 college students from a large mid-western university. All participants were taking journalism courses. The majority (68%) were female, identified themselves as White American (78%), and the average age was 19 years.

The researchers asked participants to report the average number of hours a day they spend using Facebook. They also asked them to rate how often they did the following, using a five-point scale from (5) very frequently, to (1) never:

  • write a status update
  • post photos
  • comment on a friend's post
  • read the newsfeed
  • read a friend's status update
  • view a friend's photo
  • browse a friend's timeline

They then assessed envy by asking people to rate on a similar five-point scale how much they agreed with the following statements:

  • "I generally feel inferior to others."
  • "It is so frustrating to see some people always having a good time."
  • "It somehow doesn't seem fair that some people seem to have all the fun."
  • "I wish I could travel as much as some of my friends do."
  • "Many of my friends have a better life than me."
  • "Many of my friends are happier than me."
  • "My life is more fun than those of my friends."

The researchers assessed depression symptoms using the Center for Epidemiologic Studies Depression (CES-D) scale, reported to be one of the most commonly used measures of depression. The responses were analysed using statistical software.

What were the basic results?

The researchers found the following:

  • There was no significant direct relationship between Facebook use and depression symptoms.
  • There was a significant relationship between Facebook use and feelings of envy – those reporting heavier use reported stronger feelings of envy than those with lighter use.
  • Relationships between Facebook use and feelings of envy were not influenced by the number of Facebook friends a person had.
  • There was a significant relationship between Facebook envy and depression symptoms. In analyses adjusted for age, gender, time spent on Facebook, and number of friends, increased feelings of envy were significantly associated with increased depression symptoms. Envy was said to account for around a quarter of the variance in depression symptoms.
How did the researchers interpret the results?

Addressing their question of whether Facebook use is depressing, the researchers say: "It is not – unless it triggers feelings of envy."

The effect of depression when using Facebook is mediated by feelings of envy. When envy is controlled for, Facebook use actually lessens depression.

Conclusion

Overall, the results of this survey of US college students show Facebook use in itself is not associated with depression. However, increased Facebook use was found to be associated with "Facebook envy", and envy was then associated with depression symptoms.

The study does have various strengths. The researchers carried out statistical tests to ensure their sample size was adequate to address their questions, and also assessed depression symptoms using a validated scale.

With regard to the study design, they researchers say that,: "Since this study explores relationships among Facebook use, envy and depression, the survey method is appropriate."

While it is true the survey design can explore relationships between these factors, this is all it can do. The study still cannot prove direct cause and effect relationships.

There are likely to be many other unmeasured factors also having an influence on the extent of Facebook use and feelings of envy and depression, including personal characteristics, lifestyle, and physical and mental health.

There are also some further limitations to the strength of the findings. For example, questions on frequency of Facebook use and feelings of envy were all rated on five-point scales.

Though this is likely to be the only available (and most appropriate) method to assess these factors, it can still introduce error, as frequency can mean different things to different people.

For example, one person could reply they use Facebook "very frequently" when they look at it every 10 minutes, while another person could consider very frequent use to be looking once a day. Similarly, the questions about envy will also lead to a highly subjective response.

It is also worth noting that although the researchers used a validated depression scale in their study, they have only carried out statistical analyses looking at relationships between frequency of symptoms, frequency of Facebook use, and frequency of envy. They have not looked at actual diagnoses of depression.

The study also includes a selective sample of young university students from the US, all of whom were taking the same courses. They may not be representative of other population groups.

Overall, the general theory that spending increased time looking at the posts of Facebook friends could contribute to feelings of envy, which could in turn lead to feelings of low mood, seems plausible.

However, many other factors are still likely to be mediating this relationship in different individuals.

This study will contribute to the growing body of literature assessing the possible health effects of social media use. 

If you find yourself troubled by envious thoughts that lead to symptoms of depression, you may benefit from cognitive behavioural therapy. Arguably, envy is an unhelpful pattern of thinking that brings you no benefits, but plenty of grief.

Our Moodzone area of the site contains podcasts and resources that may help you tackle patterns of unhelpful thinking.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Facebook can cause depression in people who compare themselves with others. The Independent, February 4 2015

Facebook can lead to depression, researchers find. The Daily Telegraph, February 4 2015

Being jealous of Facebook friends 'leads to depression': Users who constantly compare their lives to others could be damaging their mental health. Daily Mail, February 4 2015

Facebook Could Make You Depressed – Study. Sky News, February 4 2015

Facebook makes you depressed: New research explains WHY social media leaves you feeling down. Daily Mirror, February 4 2015

Links To Science

Tandoc EC, Ferrucci P, Duffy M. Facebook use, envy, and depression among college students: Is facebooking depressing? Computers in Human Behavior. Published online February 2015

Categories: Medical News

E-cigarettes may make lungs vulnerable to infection

Medical News - Thu, 02/05/2015 - 13:50

“Vaping may not be as safe as smokers think, research suggests,” The Guardian reports. New research found that mice exposed to e-cigarette vapours comparable to a typical human level experienced mild lung damage and a reduced immune response to infection.

This may be due to the fact that the vapour produced by e-cigarettes contains free radicals (atoms and molecules that are toxic to cells).

Mice exposed to e-cigarettes daily for two weeks had increased levels of macrophages in their lungs. Macrophages are a type of white blood cell that remove damaged and dead cells, and are evidence of cell damage. These mice also had a worse response when infected with either a bacteria that causes pneumonia or the flu virus.

E-cigarettes vapour contains 1% of the amount of free radicals that are produced from normal cigarettes, so it is not clear from this study what effect this would have for humans.

Are e-cigarettes safer than normal cigarettes? Almost certainly. Are they 100% safe? Probably not.

If you are planning to quit smoking, especially if you have a lung condition such as chronic obstructive pulmonary disease, other types of nicotine replacement therapies (NRTs), such as patches, may be a safer option.

 

Where did the story come from?

The study was carried out by researchers from John Hopkins University in Maryland, the University of Tennessee Health Science Center and Louisiana State University. It was funded by the Flight Attendant Medical Research Institute and the US National Institutes of Health.

The study was published in the peer-reviewed medical journal PLOS ONE on an open-access basis, so the article is free to read online here.

The study was accurately reported in the UK media.

 

What kind of research was this?

This was an animal study looking at the effects of e-cigarettes on the immune system. The authors say that many people perceive e-cigarettes to be a healthy alternative to cigarettes. However, there have only been limited studies in humans and animals on their safety.

They report that on current evidence, the US Food and Drug Administration (FDA), the World Health Organization (WHO) and the European Respiratory Society do not consider them a safe alternative. This study in mice was designed to look specifically at the effect of e-cigarettes on the immune system and their ability to fight a bacterial and viral infection of the lungs after exposure to e-cigarette vapour.

 

What did the research involve?

Eight-week-old mice were randomly assigned to be either exposed to e-cigarettes or normal air, and then their response to viral and bacterial infections was compared.

The mice in the e-cigarette group were put in a chamber in which a smoke machine delivered the equivalent of a two-second puff of menthol e-cigarettes (1.8% nicotine) every 10 seconds for one-and-a-half hours. This occurred twice per day for two weeks. The researchers stated that this level of exposure was comparable to the exposure you would expect to see in an “average” e-cig user.

The vapour was analysed to see if it contained free radicals, which are toxic to cells. A subset group were exposed in the same way to traditional flavoured e-cigarettes, also containing 1.8% nicotine. This level of vapour exposure gave them an average blood level of cotinine, a breakdown product of nicotine, of 267ng/ml. In humans who smoke cigarettes and e-cigarettes, the level is usually between 200ng/ml and 800ng/ml, so this was fairly low exposure.

At the end of the last exposure, both groups of mice were infected via the nose with either a bacterial infection of Streptococcal pneumonia or the viral infection influenza. Macrophages from the lungs of some mice from each group were grown in dishes and also exposed to these infections, to study their response.

The researchers then compared the level of infection and the immune response in mice exposed and not exposed to e-cigarettes.

 

What were the basic results?

The e-cigarette vapour contained free radicals. The level was just less than 1% of that found in cigarette smoke.

Compared to the mice exposed to air, lungs from mice exposed to e-cigarettes had:

  • increased levels of oxidative stress (evidence of damage from free radicals)
  • a 58% increase in the number of macrophages, indicating that they needed to remove damaged cells

After infection with Streptococcal pneumonia:

  • mice exposed to e-cigarettes had higher levels of the bacteria in their lungs
  • the macrophages from mice exposed to both types of e-cigarettes were less able to deal with the infection when grown in dishes, which may be why there was a higher level of bacteria in the lungs

After infection with influenza, mice exposed to e-cigarettes:

  • had higher levels of the virus four days after the infection
  • lost more weight 10 to 12 days after infection, which was taken as an indicator of more severe illness
  • two out of the 10 mice died, compared to none in the air-exposed group

After infection with a higher dose of influenza, 60% of mice exposed to e-cigarettes died, compared to 30% in the air-exposed group.

 

How did the researchers interpret the results?

The researchers concluded that, “E-cig exposure is not a safe alternative to cigarette smoking”. They say that the exposure caused “airway inflammation, oxidative stress, and impaired anti-bacterial and anti-viral responses that include increased bacterial burden and viral titers in the lungs, impaired bacterial phagocytosis [removal of bacteria by immune cells], and increased virus-induced morbidity and mortality”.

 

Conclusion

This animal study has shown that the vapour from e-cigarettes contains free radicals, which are toxic to cells and are linked to cancer. Exposure to e-cigarettes caused inflammation in the lungs of mice, with increased numbers of macrophages, which mop up damaged and dead cells. Mice exposed to e-cigarette vapour also had a reduced ability to fight both bacterial and viral infections.

Taken together, this is convincing evidence suggesting that e-cigarettes are not harmless. However, the effect of e-cigarettes was not compared to normal cigarettes in this study, so it is not clear how much safer they might be. The study was also not conducted in humans. An animal study such as this can give us a good idea of the effects that a chemical could have in humans. However, mice and humans do not have identical biology, so we cannot be certain that the effects would be identical.   

The authors worryingly report that in the US, despite e-cigarettes being marketed as an aid to help people stop smoking, they are gaining popularity among people who have never smoked. This could soon be the case in the UK. Studies such as this show that they could still be bad for your health, and contribute to the growing body of research investigating e-cigarettes, both in terms of their effectiveness as aids to stop smoking, and their possible health effects.

There are many other ways to help you stop smoking that do not potentially expose the lungs to harm (though they may still have side effects). These include nicotine patches, gum and inhalers, as well as medication designed to reduce cravings for cigarettes, such as Zyban (bupropion). Read more about stop smoking treatments, as well as the NHS Stop Smoking Services that are available.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Vaping may not be as safe as smokers think, research suggests. The Guardian, February 4 2015

E-cigarettes 'increase the risk of flu and pneumonia'. The Independent, February 4 2015

E-cigarettes are 'NOT a safe alternative to smoking': Toxic chemicals harm the lungs and weaken the immune system, study claims. Mail Online, February 4 2015

E-Cigarettes Are Harmful To Lungs – Study. Sky News, February 5 2015

E-cigarettes are 'not a safe alternative'. ITV News, February 5 2015

Links To Science

Sussan TE, Gajghate S, Thimmulappa RK, et al. Exposure to Electronic Cigarettes Impairs Pulmonary Anti-Bacterial and Anti-Viral Defenses in a Mouse Model. PLOS One. Published online February 4 2015

Categories: Medical News

Flu and freezing weather may be driving up winter death rates

Medical News - Wed, 02/04/2015 - 16:00

"The current death rate in England and Wales is running about one-third higher than its normal rate for this time of year," BBC News reports. A combination of flu and very cold weather may be responsible.

The BBC's story comes from the latest official statistics on deaths in England and Wales. They show that in the last three weeks of January, death rates were significantly higher than predicted for the time of year.

In addition, over the last six weeks a significantly higher than predicted death rate was reported in people aged 65 and above living in England. 

Although the cause of these spikes is uncertain, experts point out they coincide with both seasonal increases in respiratory problems – in particular the flu – and the recent cold snap.

The number of deaths always rises in winter, especially among elderly people. This is because of the colder weather and increases in respiratory problems.

While flu is a viral infection, it can make the lungs vulnerable to bacterial infections, such as pneumonia, which can be fatal in the elderly.

Who should have the seasonal flu jab?

Flu is not a serious threat for most fit and healthy adults, but the elderly and those with other illnesses, such as diabetes and asthma, are at risk of developing serious complications, including pneumonia.

See your GP about the flu jab if you're 65 or over, or if you have any of the following problems (however old you are):

Your GP may advise you to have a flu jab if you have serious liver disease, multiple sclerosis (MS), or other diseases of the nervous system.

Read more about who should have the flu jab.

Pregnancy

If you're pregnant, you should have the flu jab, regardless of the stage of pregnancy you've reached.

Pregnant women are more prone to complications from flu that can cause serious illness for both mother and baby.

If you are pregnant and catch flu, talk to your GP urgently as you may need treatment with antiviral medicine.

Read more about the flu jab in pregnancy.

Children

The flu vaccine is recommended for:

  • children over the age of six months with a long-term health condition
  • healthy children aged two, three and four

Children aged between six months and two years of age who are eligible for the flu vaccine should have the flu jab.

Children eligible for the flu vaccine aged between two and 18 will usually have the flu vaccine nasal spray.

Read about who should have the children's flu vaccine.

Where did the story come from?

The figures used in the BBC story come from the Office for National Statistics (ONS), which produces figures on issues of public importance.

It is also based on an analysis of mortality figures from Public Health England (PHE), the body responsible for maintaining the nation's health. These are both government bodies.

The BBC also included an interview with Professor John Newton, chief knowledge officer at PHE. One explanation for the higher than usual death rates is the prevalence of the H3N2 sub-type, a flu virus.

Professor Newton reportedly said that while PHE tries to anticipate which subtypes of the virus may be circulating in any year so the virus can be vaccinated against, the type this year may have mutated and might not be as well matched to vaccines at the end of the flu season as at the beginning.

What were the figures?

The ONS has published weekly figures on deaths registered in England and Wales from December 5 2014.

This shows that in the week beginning January 9 2015, there was a total of 16,237 deaths, followed by a total of 14,866 deaths in the week beginning January 16 2015, and 13,934 deaths in the week beginning January 23 2015. 

This rate is about one-third higher in the last two weeks compared with deaths over the same period in the previous five years.

The majority of these deaths were in those aged 65 or over. For example, in the week starting January 16 2015, 13,083 of the deaths were in those aged 65 and over.

According to the ONS, in the week beginning January 9 2015 and January 23 2015, 3,515 and 3,215 of all deaths were registered as caused by respiratory disease. 

The PHE surveillance report points out the estimated 16,237 deaths in week two and the 14,866 deaths in week three of January was above the upper limit predicted for the time of year.

In England, PHE says there have been excess deaths from week 50 in 2014 up to week four in 2015 among those over the age of 65 in England. They point out the excess deaths coincide with circulating influenza and recent cold snaps.

Significant excess deaths were also seen in children under five and in 15- to 64-year-olds in the first week of this year.

Similar excess deaths were seen in Scotland and Wales during this period, but not in Northern Ireland.

How did the researchers interpret the results?

PHE says there are always a higher number of deaths in winter months compared with the summer, and that some peaks in mortality above the expected level typically occur in winter.

This is most commonly the result of factors such as cold snaps and the increase in respiratory viruses, particularly the flu.

However, PHE also says "acute" weekly excess mortality rates "triggers further investigations of spikes and informs any public health responses".

Conclusion

There are always more deaths in winter than other seasons, particularly among elderly people. But why these fairly dramatic spikes in the death rate have occurred is still not understood.

It should be noted these figures are provisional, as there can be a delay in the ONS receiving the data.

Although the media has focused on the likely cause being flu, the numbers provided are for all respiratory conditions. Cold weather can exacerbate many of these conditions, such as asthma and chronic obstructive pulmonary disease.

For most fit and healthy people, flu is not a serious threat, but the elderly and those with other illnesses, such as diabetes and asthma, are at risk of developing serious complications, including pneumonia.

It's important to stay healthy in winter and protect yourself against illness.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Death rate up by a third in January. BBC News, February 4 2015

Death rate rises as cold snap grips UK. The Guardian, February 4 2015

Categories: Medical News