Medical News

Social care reforms announced

Medical News - Tue, 01/19/2038 - 06:14

Most of the UK media is covering the announcement made in Parliament by Jeremy Hunt, Secretary of State for Health, about proposed changes to social care.

The two confirmed points to have garnered the most media attention in the run-up to the announcement are:

  • a ‘cost cap’ of £75,000 worth of care costs – after this point the state would step in to meet these care costs
  • raising the current means-testing threshold for people to be eligible for state-funded social care from £23,520 to £123,000

The government expects these changes will lead to fewer people having to sell their homes in order to pay for their long-term care needs.

Speaking in Parliament, Mr Hunt said that the current system was ‘desperately unfair’ as many older people face ‘limitless, often ruinous’ costs. The minister stated that he wants the country to be ‘one of the best places in the world to grow old’.

 

What is social care?

The term social care covers a range of services provided to help vulnerable people improve their quality of life and assist them with their day-to-day living.

People often requiring social care include:

  • people with chronic (long-term) diseases
  • people with disability
  • the elderly – particularly those with age-related conditions, such as dementia

Social care services can include:

  • healthcare
  • equipment
  • help in your home or in a care home
  • community support and activities
  • day centres

 

How does the current adult social care system work?

Currently, state funding for social care is based on two criteria:

  • means – people with assets of more than £23,520 do not qualify for funding
  • needs – most local authorities will only fund care for people assessed to have substantial or critical needs

The majority of people currently requiring social care pay for it privately. These are known as ‘self-funders’.

 

What prompted these reforms to adult social care?

Put simply, on average, the UK population is getting older.

When the welfare state was created in the early 20th century, it was not expected that people would someday routinely live into their 70s, 80s, and even 90s.

The increase in life expectancy is a good thing, however, it brings a new set of challenges.

While people are living longer, they are also spending more of their lives in ill health. Older people are more likely to have potentially complex care needs that can be expensive to manage.

Many people are currently ineligible for state-funded social care under the existing laws. To meet the costs of these care needs, these ‘self-funders’ have, in many cases, had to sell or remortgage their home, or sell other assets to pay for the costs of their care.

Without reforms, experts agree that the cost of social care for both the state (through taxes) and to ‘self-funders’ is likely to become increasingly problematic.

To try and find the best way to resolve some of the difficulties of fairly funding adult social care, the Department of Health set up a commission. This independent commission reported its findings to ministers in July 2011. The government considered these findings in its white paper on care and support published in July 2012, and in the drafting of the proposed new legislation.

 

What happens next?

The government has introduced a Social Care Bill which will need to be passed by the Houses of Parliament.

If the bill is successfully passed it is expected the amendments will come into force by 2017.

 

Edited by NHS Choices. Follow Behind the Headlines on twitter.

Links To The Headlines

Social care: Jeremy Hunt hails 'fully-funded solution'. BBC News, February 11 2013

Social care reforms: Almost 2 million pensioners will be denied state help. The Daily Telegraph, February 11 2013

Social care reform: how your family may be affected. The Daily Telegraph, February 11 2013

Dilnot 'regrets' decision to set social care cap at £75,000. The Guardian, February 11 2013

Hunt statement on adult social care cap: Politics live blog. The Guardian, February 11 2013

Categories: Medical News

Immune changes found in people with CFS/ME

Medical News - Mon, 03/02/2015 - 14:39

"Distinct stages to chronic fatigue syndrome identified," reports BBC News online.

People with chronic fatigue syndrome (CFS), sometimes called myalgic encephalopathy (ME), can have debilitating exhaustion affecting their everyday life that does not go away with sleep or rest.

The authors of this study say there are no laboratory tests to diagnose or manage the condition, despite efforts to find biological markers of the disease.

They aimed to address this by looking for differences in immune system signalling chemicals (cytokines) between people with CFS/ME and healthy controls.

Comparing all CFS/ME participants with controls found few differences. However, differences were found when the CFS/ME group was divided into those with short- (three years or less) and long-term (more than three years) disease.

These results suggest that people with CFS/ME may have higher levels of some cytokines until around the three-year mark, at which point the differences disappear. 

The study is not reliable enough on its own to prove that the disease has distinct stages, and it doesn't give us any more clues as to how or why these particular cytokines might be involved in the condition.

Other studies, and study types, are needed to build on these initial findings.

Find out more about CFS/ME.

 

Where did the story come from?

The study was led by researchers from Columbia University Mailman School of Public Health in New York, and was funded by the CFI/Hutchins Family Foundation and the US National Institutes of Health.

It was published in the peer-reviewed journal Science Advances.

The BBC reported the story accurately, and included useful quotes from independent experts who commented on this research.

 

What kind of research was this?

This case-control study used data from two cohort studies to investigate biological makers of CFS/ME.
 
This type of study is an effective way of finding out the ways in which people with a disease – in this case, CFS/ME – differ from those without.

However, the links established usually mean that the two things are found together, not that one causes the other.

 

What did the research involve?

The study used disease diagnostic information and blood samples taken from two recent large multicentre US cohort studies of people with CFS/ME.

The researchers analysed the relationship of 51 immune system chemical messengers called cytokines with diagnosis of CFS/ME and other clinical variables, such as the duration and severity of the disease.

People without CFS/ME (the controls) were matched with people with CFS/ME based on key variables known to affect immune status, including the season of sampling, geographic site, age and sex.

The main analysis looked for statistically significant differences in the 51 immune system markers in people with and without CFS/ME.

 

What were the basic results? All CFS/ME versus all controls

Comparing all 298 people with CFS/ME with all 348 controls led to few statistically significant results. In rare instances where there were differences, levels of cytokines were lower in people with CFS/ME.

Short- and long-duration CFS/ME versus controls

In a sub-analysis, the researchers looked at the effect of grouping CFS/ME into short-duration (having the condition for three years or less) and long-duration (more than three years) disease.

They found significant differences in more than half the 51 immune system markers tested in the group of 52 people early on in the course of the disease, relative to the healthy controls. These differences were not present in the 246 people with longer-duration illness.

Cytokine levels, which differed between short- and long-duration groups, were correlated with duration of illness.

The two most prominent cytokines associated with short-duration CFS/ME were interferon-gamma and interleukin-12p40, both known to be important for an effective immune system.

 

How did the researchers interpret the results?

On the BBC website, lead author Dr Mady Hornig said: "It appears that ME/CFS patients are flush with cytokines until around the three-year mark, at which point the immune system shows evidence of exhaustion and cytokine levels drop … this shows there are distinct stages to the disease."

In their research paper, the researchers suggested that their findings "have critical implications for the discovery of interventional strategies and early diagnosis of ME/CFS".

 

Conclusion

This case-control study found cytokine differences in people diagnosed with CFS/ME for three years or less, compared with healthy controls. The same was not found for people with CFS/ME of more than three years' duration.

The study authors interpreted this as a sign that CFS/ME might have two stages. The implications are that this may one day help researchers better understand the disease, and potentially develop new ways of testing and diagnosing the condition.

Optimism notwithstanding, there are significant limitations to this study design, meaning it cannot say anything reliable or solid on its own. Further research needs to repeat, confirm and build on its findings.

Professor Michael Sharpe, professor of psychological medicine at the University of Oxford, said: "Whilst this finding that some patients with CFS/ME have an immune abnormality is potentially interesting, we should treat it with great caution … This type of study [a case-control study] is notorious for producing findings that other researchers subsequently fail to replicate."

He added: "Everyone who has worked clinically with patients with CFS/ME knows this is a real illness; this study neither proves nor disproves that observation."

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

Links To The Headlines

First biological proof that ME is real found by scientists. The Daily Telegraph, February 27 2015

Chronic fatigue syndrome: Scientists now have 'robust' evidence that points to biological cause. The Independent, February 27 2015

Distinct stages to chronic fatigue syndrome identified. BBC News, February 28 2015

Links To Science

Hornig M, et al. Distinct plasma immune signatures in ME/CFS are present early in the course of illness. Science Advances, Published February 27 2015

Categories: Medical News

MS stem cell treatment only a 'miracle' for some

Medical News - Mon, 03/02/2015 - 13:28

The Daily Telegraph reports a “miracle” stem cell therapy that reverses multiple sclerosis and which, according to The Sunday Times, gets “wheelchair-bound” people dancing.

Multiple sclerosis (MS) affects nerves in the brain and spinal cord, causing problems with muscle movement, balance and vision. It’s an autoimmune disease, where the body’s immune system attacks its own nerve cells. There is currently no cure, but many different treatments are available to help with symptoms.

This study was mainly about relapsing remitting MS, the most common type, where people have distinct attacks of symptoms, which then fade away either partially or completely.

The new treatment was very aggressive. It used high doses of chemotherapy to “knock out” the existing faulty cells of the immune system, before rebuilding it using stem cells taken from the patient’s own blood. This, in effect, gave the immune system a chance to reboot from scratch.

The therapy was tested in 145 patients and led to significant reductions in their levels of disability in almost 64% of people up to four years after treatment. Improvements were seen in quality of life and other ratings of symptoms and disability. Because of the difficulty in treating MS effectively, any improvements are good news.

The downside is that there was no control group. We don’t know if some people would have improved on their own, or whether the improvements are any better than best available care. It’s also worth noting that not everyone will be able to tolerate the aggressive chemotherapy used, and that the technique did not work for people with more severe or longstanding MS (over 10 years).

Find out more about multiple sclerosis.

 

Where did the story come from?

The study was led by researchers from Northwestern University Feinberg School of Medicine, Chicago, US, and was funded by the Danhakl family, the Cumming Foundation, the Zakat Foundation, the McNamara Purcell Foundation, and Morgan Stanley and Company.

Two study authors declared financial conflicts of interest by serving as consultants to pharmaceutical companies including Biogen Idec, which makes treatments for patients with “neurological, autoimmune and hematological disorders”.

The study was published in the peer-reviewed Journal of the American Medical Association.

Generally, the papers reported the story accurately. It is always difficult to justify the use of a “miracle” cure, because it means different things to different people – and the improvements cited for some people do seem worthy of the tag. However, while the treatment looks promising, it’s at an early stage of development. The treatment is very aggressive, and also tested in specific types of MS, so may not be suitable for all people with MS. Similarly, the treatment has not yet been proven effective or safe in large enough groups for the results to be reliable.

We have not been able to independently assess if the truth of the claims that “wheelchair-bound” MS patients who were treated in this way are now able to dance.

 

What kind of research was this?

This was a case-series testing a new stem cell treatment in people with relapsing remitting MS or secondary progressive MS.

Most people in the study had relapsing-remitting MS, which tends to have distinct attacks of symptoms, which then fade away either partially or completely. This is the most common type of MS, affecting around 85% of people with the condition, according to the MS Society.

The research also included a smaller group of people with secondary progressive MS. Many people with relapsing remitting MS progress to this form, where there is a sustained build-up of disability that no longer fades away. There is no cure for MS, but many different treatments are available to help with symptoms.

Case series are useful to test new treatments, but they have several limitations, meaning they can’t prove the treatments are effective very accurately or reliably. The big downside is a lack of a comparison group, called a control group. This means that you never know how much better or worse the new treatment is compared with an existing treatment, or doing nothing. This limitation applies to this study.

 

What did the research involve?

The study gave 123 patients with relapsing remitting MS and 28 with secondary progressive MS a stem cell transplant. The transplants were carried out at a single US institution between 2003 and 2014, and researchers followed the patients for up to five years to see how they did.

The average age of participants was 36 (ranging from 18 to 60) and most were women (85%). The average follow-up after treatment was 2.5 years.

The new treatment used chemotherapy drugs cyclophosphamide and alemtuzumab or cyclophosphamide and thymoglobulin, followed by infusion of stem cells isolated from the patients’ blood.

Before treatment, participants were subjected to a range of questionnaires and assessments to rate their symptoms, level of disability and quality of life. These were repeated at regular intervals after to measure any changes.

The main measure of interest was an improvement in score of 1.0 or more on the Expanded Disability Status Scale (EDSS). The EDSS is a way of quantifying disability in MS and monitoring changes over time. It is widely used in clinical trials and in the assessment of people with MS.

The main analysis compared EDSS ratings before and after treatment, looking for statistically significant improvements. Similar comparisons were done for other measures of MS-related disability and quality of life.

 

What were the basic results? Change in disability scores

There was significant improvement in disability up to four years after treatment. Reductions in the EDSS (disability) score of 1.0 or more were seen in half of patients at two years (50%, 95% confidence interval (CI) 39% to 61%) and almost two out of every three people at four years (64%, 95% CI 46% to 79%).

Scores from the EDSS improved significantly. Before treatment, the average (median) EDSS score was 4.0, which improved to 3.0 at two years and to 2.5 at four years. Both were statistically significant reductions.

Taking the reduction of 4.0 to 2.5, this means the person went from having “Significant disability, but self-sufficient and up and about some 12 hours a day. Able to walk without aid or rest for 500m” to “Mild disability in one functional system or minimal disability in two functional systems”.

However, some people did not improve. The EDSS score did not improve in people with secondary progressive MS or in those with disease duration longer than 10 years.

Ratings of disability and quality of life

Many other measures also improved, including neurological function, walking function, hand function and self-reported quality of life. The tests also involved a brain scan assessing the size of inflammation at a specific part of the spinal cord in the upper back (the T2 vertebra), which is said to correlate with disease severity. After treatment, the size of the damage reduced, and stayed lower up to two years longer.

Improvements quoted in the news

Some of the more miraculous findings were reported in the news, but not in the study publication itself. The Telegraph, for example, reported: “Patients who have been wheelchair-bound for 10 years have regained the use of their legs … while others who were blind can now see again.”

We couldn’t confirm these biblical results, based on the publication alone. They may have come from interviews with the study team or case studies provided by the research institutions.

 

How did the researchers interpret the results?

The researchers summed up that, “Among patients with relapsing remitting MS, nonmyeloablative hematopoietic stem cell transplantation was associated with improvement in neurological disability and other clinical outcomes.”

To their knowledge: “this [was] the first report of significant and sustained improvement in the EDSS score following any treatment for MS”.

 

Conclusion

This case-series showed that a new stem cell treatment reduced the disability in people with relapsing remitting MS up to four years after treatment. It worked in more than half of those given treatment. The authors claim that this was the first time this had been achieved, and is important because there is currently no cure for MS.

Given the relative lack of alternative treatments for MS, these results are encouraging. However, there are issues to bear in mind.

The average EDSS score before treatment in the group was 4.0. The scale goes from 10 (death due to MS), to 1.0 (no disability). Ratings above 5.0 involve impairment with walking. An average of 4.0 suggests most people didn’t have the more severe forms of MS. A small number of people with more severe MS were included in the study, but too few to reach any reliable conclusions about this subgroup. Therefore, the results are most applicable to those with non-severe relapsing remitting MS.

The treatment only improved the main outcome (EDSS improvement of 1.0 or more) in 50% of people after two years, meaning it didn’t work in the other half. It worked for slightly more people after four years. It also didn’t work in people with MS over 10 years or those with secondary progressive MS. This suggests that selecting the most appropriate patient group for this treatment will be important. It doesn’t look like it would work for everyone.

These preliminary findings are from an uncontrolled study. This means we don’t know if, or how much, the new treatment is better than any existing treatment, or doing nothing. The treatment was described by a study author in the Telegraph as being very aggressive, and only suitable for people who were fit enough to withstand the effects of chemotherapy. Chemotherapy is not without risk. Further studies will need to pay careful attention to weighing up the benefits and risks of this therapy.

Dr Sorrel Bickley, from the MS Society, cautiously welcomed the results in the Telegraph, saying: "Momentum in this area of research is building rapidly and we're eagerly awaiting the results of larger, randomised trials and longer-term follow-up data.

“New treatments for MS are urgently needed, but as yet there are no stem cell therapies licensed for MS anywhere in the world. This means they aren't yet established as being both safe and effective. This type of stem cell therapy is very aggressive and does carry significant risks, so we would strongly urge caution in seeking this treatment outside of a properly regulated clinical trial."

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

Links To The Headlines

Dancing, walking and running again, the wheelchair-bound MS patients after they were given 'miraculous' stem cell treatment. Mail Online, March 1 2015

‘Miraculous’ stem cell treatment may reverse symptoms of multiple sclerosis. The Daily Telegraph, March 1 2015

Stem cell reboot has MS patients dancing. The Times, March 1 2015

Links To Science

Burt KB, et al. Association of Nonmyeloablative Hematopoietic Stem Cell Transplantation With Neurological Disability in Patients With Relapsing-Remitting Multiple Sclerosis. JAMA, Published January 20 2015

Categories: Medical News

Healthy older adults carry leukaemia mutations

Medical News - Fri, 02/27/2015 - 16:00

BBC News reports that, according to researchers, “It is ‘almost inevitable’ that your blood will take the first steps towards leukaemia as you age”.

Researchers analysed the blood of 4,219 people, looking for DNA errors (mutations) linked to blood cancers (leukaemia).

The number of mutations in healthy older people without the disease was higher than expected. The research focused on 15 genetic hotspots of leukaemia-linked mutations and found them in 0.8% of individuals aged under 60, and 19.5% of those aged 90 or older. 

The media quoted figures suggesting that more than 70% of people in their 90s would have some form of leukaemia-associated mutation. This was based on predictions of the prevalence of other mutations outside of the 15 tested. 

The good news is that this form of age-related leukaemia is highly unlikely to kill you. The bad news is you are far more likely to die of something else before the mutations trigger the onset of leukaemia.

Still, as some are predicting that average lifespans will rise dramatically in the decades ahead, the results of this study could become more of an issue for future generations, and might also apply to other cancer types.

 

Where did the story come from?

The study was carried out by researchers from Wellcome Trust Sanger Institute, Cambridge (UK), and was funded by the Wellcome Trust, Leukaemia Lymphoma Research, the Kay Kendal Leukaemia Fund and the Spanish Ministerio de Economía y Competitividad  Subprograma Ramón y Cajal.

The study was published in the peer-reviewed medical journal Cell Reports. It is open-access, so is free to read and download online.

Generally, the media reported the story accurately. The Independent quoted Dr Vassiliou, senior author of the study, reassuring readers that: “These mutations will be harmless for the majority of people, but for a few unlucky carriers, they will take the body on a journey towards leukaemia. We are now beginning to understand the major landmarks on that journey”.

One small gripe is with the choice of figures used. The main study result was that leukaemia-linked mutations were found in 0.8% of under-60s and 19.5% of over 90s. This was based on studying 15 leukaemia-linked hotspots. 

Both the Independent and the BBC quoted figures suggesting that 20% of 50 to 60 year olds, and over 70% of over 90s, had dormant leukaemia-linked mutations. These much higher figures come from the study discussion and were not directly tested in the current research. They were figures based on assumptions about combining results from the 15 hotspots with other non-hotspot mutations from previous studies. We are not able to appraise the non-hotspot mutations studies, so we don’t know how accurate these figures are.

 

What kind of research was this?

This was a genetic study investigating how common small, leukaemia-linked DNA changes were in cancer-free adults.

Cancers, including leukaemia, develop through the combined action of mutations that are acquired over time. The researchers say that leukaemia-associated DNA mutations can occur without evidence of the disease. They wanted to find out how common these were in healthy people, and how common they were as people got older.

 

What did the research involve?

The researchers analysed DNA samples at 15 pre-defined leukaemia-associated mutation hotspots, using highly sensitive tests. They analysed the DNA of 4,219 people aged 17 and over.

The majority of DNA tests were on healthy people, but for comparison, they analysed the genes of a number of blood cells from people with myeloid leukaemia.

The production of the range of different types of mature white blood cells starts with a small number of stem cells. More specialised cells develop from these, like tree branches. The stem cells replicate themselves, producing clones. Some of these clones receive signals from the body, causing them to replicate and develop (differentiate) into more specialised white blood cells. Different signals produce different types of cells. The researchers were looking at what stage in the production process the mutations were occurring. If the mutations happened early in the differentiation process, they would be found in many downstream white cell types. If they occurred later, then they would be found in fewer cell types.

 

What were the basic results?

The main results were that age-related leukaemia-linked mutations were much more common than previously predicted.

Using only the 15 hotspots studied, they identified leukaemia-linked mutations in 0.8% of individuals under 60, rising to 19.5% of those aged 90 years and over. Coupling these estimates with other mutation rates from previous studies (outside of the 15 hotspots tested) they came up with much higher estimates. They predicted that more than 70% of people aged 90 or older would have some form of leukaemia-associated mutation. The 70% figure made it into the media coverage; the 19.5% was not mentioned.

On closer inspection, they found that mutations DNMT3A-R882 were most common and, although their prevalence increased with age, were found in individuals as young as 25. By contrast, mutations affecting spliceosome genes SF3B1 and SRSF2, closely associated with the myelodysplastic syndromes, were identified only in those aged over 70 years, with several individuals harbouring more than one mutation.

Myelodysplastic syndrome is an uncommon condition of unknown cause, that can lead to a drop in the number of healthy blood cells being produced. In some cases, it can progress into acute myeloid leukaemia.

Mutations in gene NPM1 were not seen in the group. This gene is thought to act as a “gatekeeper” to leukaemia. If it goes wrong, your risk of leukaemia rises considerably. As the group were symptom-free, it is not surprising that this gene was not affected in most people.

 

How did the researchers interpret the results?

The study group said: “individuals without overt features of a haematological [blood] disorder may harbor hemopoietic cell clones [blood stem cells] carrying leukemia-associated mutations” and that accumulating these mutations “is an almost inevitable consequence of aging in humans”

 

Conclusion

This study estimated that 0.8% of individuals under 60, and 19.5% of those aged 90 years and over, had leukaemia-linked mutations. These mutations caused no immediate harm and the people didn’t have leukaemia. The mutations were lurking in the background, but could have the potential to contribute to leukaemia in the future.

The research primarily focused on 15 genetic hotspots of leukaemia-linked mutations.

However, in their discussion, they predicted that more than 70% of people aged 90 or older would have some form of leukaemia-associated mutation. This formed the basis of their comment that these mutations seem an inevitable part of ageing. It is important to realise that this much higher estimate was not directly tested in the study. That is not to say it is not true, but we can’t confirm or refute it either way. Further research could confirm this prediction.

Scientists know that cancer is caused by the accumulation of genetic mutations over many years. This is why most cancers occur in older people, and the risk of cancer increases with age. What is surprising about this study is the relatively high prevalence of leukaemia-linked background mutations in healthy adults. The implication is that if people were to live a lot longer, say 150 years, they might expect to get leukaemia. In theory, this could also apply to some other types of cancer.

This is all largely theoretical. The impact on the average person is minimal, though if lifespans continue to increase, it could be a potential problem for your grandchildren.

It’s important to remember that we can all reduce our risk of cancer by making some simple changes to our lifestyle.

For example, healthy eating, taking regular exercise and stopping smoking will help to lower your risk.

Read more about how a healthy lifestyle can help to reduce your chances of developing cancer

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

Links To The Headlines

DNA develops to acquire genetic mutations linked with cancer as you get older, says study. The Independent, February 26 2015

Leukaemia mutations 'almost inevitable', researchers say. BBC News, February 27 2015

Links To Science

McKerrell T, Park N, Moreno T, et al. Leukemia-Associated Somatic Mutations Drive Distinct Patterns of Age-Related Clonal Hemopoiesis. Cell Reports. February 26 2014

Categories: Medical News

Does deadly diet drug DNP defeat diabetes?

Medical News - Fri, 02/27/2015 - 14:30

"A chemical [DNP] which caused munitions factory workers to lose weight inexplicably in the First World War could cure diabetes," The Daily Telegraph reports. The banned weight loss drug looked effective and safe when given in a modified form to rats bred to have diabetes.

The potential benefits of DNP surfaced in WW1 munitions workers who lost a lot of weight after being exposed to it. DNP sped up their metabolism, leading to rapid weight loss. After being made into a weight loss drug in the 1930s, it was quickly withdrawn, as it was proven highly toxic.

The problem was that it sped up the metabolism to a dangerously high rate, causing a range of serious side effects, and some deaths. Illegal sales of the drug have caused a number of deaths in the UK in recent years.

Researchers at Yale University wanted to see if it was possible to harness DNP’s metabolic properties, while removing the toxic effects.

They created a slow-release version of DNP, called CRMP, which improved the way the liver processed fat and improved other measures linked to type 2 diabetes risk in rats. As it delivered DNP at a much lower dose over time, there were no toxic effects.

This is encouraging research that should lead to further studies.

The version of DNP that is available through illegal sales, typically via the internet, is toxic, even in tiny amounts. Do not take it under any circumstances.

 

Where did the story come from?

The study was carried out by researchers from Yale University and was funded by United States National Institutes of Health and Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Denmark.

Yale University has applied for a patent-related to the use of CRMP and things working in a similar way for the treatment of metabolic diseases, including non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes.

The study was published in the peer-reviewed journal Science Express.

The Daily Telegraph’s coverage was factually accurate. They made it clear the research was in rats, but also explained how: "the [research] team is confident that the research would translate to humans and are keen to start trials".

 

What kind of research was this?

This was an animal study investigating potential new uses for the banned chemical DNP for non-alcoholic fatty liver disease, which in turn, is a major risk factor for type 2 diabetes. Alternatively, both conditions can develop in tandem.

DNP has a murky past. Starting life as an ingredient of explosives in WW1, its potential use as a weight loss drug was recognised in workers handling the agent. They sweated profusely, had sky-high temperatures and lost a lot of weight. In the 1930s, it was sold as a wonder weight loss drug. However, it was quickly withdrawn, because it was highly toxic, causing side effects and, in some cases, death. 

DNP was also linked to deaths in 2013, after a resurgence among bodybuilders. This lead to the Food Standards Agency issuing a public warning about the risks of DNP, saying that: “DNP is an industrial chemical that is extremely dangerous to human health.” 
 
NAFLD is the term used when there is a build-up of fat within the liver cells that is not caused by alcohol intake. It is usually seen in people who are overweight or obese, and is associated with metabolic syndrome. A healthy liver should contain little or no fat. Most people with NAFLD do not develop serious liver problems and just have stage 1 of the disease (simple fatty liver). The most important thing that people with NAFLD can do is to go on a gradual weight loss programme and exercise regularly.

It is known that DNP has benefits on NAFLD, obesity and regulating blood glucose, but is usually too toxic to be used as a treatment. The chemical targets the mitochondria in cells. These are the little "batteries" responsible for making energy in cells, which is essential for life.

DNP speeds up the metabolism; however, our metabolic system operates at the rate it does for a reason – it is safe. Speeding up the metabolism may help burn off fat, but it can also trigger a number of dangerous side effects and potentially cause death.

This research team tried to devise a way to harness the benefits of DNP, while minimising its toxic side effects. All their experiments were in rats. This is the usual approach when testing chemicals to treat diseases, particularly dangerous ones. People and rats, both mammals, share lots of common biology, but there are differences.

 

What did the research involve?

The researchers gave groups of rats low levels of DNP and monitored its effect on fat content in the liver and other measures linked to a higher risk of type 2 diabetes. They were looking to confirm the benefits reported in previous studies.

After encouraging results, they modified DNP to create CRMP (controlled-release mitochondrial protonophore). They fed this to rats in small amounts of peanut butter to see whether it had the same benefits, with fewer side effects.

The benefits and side effects of DNP were compared with CRMP in a range of experiments lasting up to six weeks. During the experiments, rats were fed a high-fat diet and the researchers paid particular attention to changes in the function of the liver in dealing with this fat.

 

What were the basic results?

The main result was that CRMP caused fewer side effects than raw DNP, while maintaining similar benefits, including burning lots of fat, improved glucose tolerance and lower insulin levels.

When testing for specific effects, CRMP prevented the development of the rat version of NAFLD in rats fed a high-fat diet for two weeks. Similarly, it seemed to improve blood glucose regulation when given to rats with diabetes for two weeks, also improving their blood fat levels.

CRMP released the DNP-active chemical at a more gradual rate, and over a longer period, than giving straight DNP. This meant the levels in the blood did not spike as much and were lower overall. This seems to be the key to avoiding some of the worst side effects.

One of the biggest side effects of DNP was that it caused a potentially fatal very high temperature. The researchers were able to find a dose of CRMP that was beneficial to the liver, without causing a huge rise in temperature.

 

How did the researchers interpret the results?

The researchers said: "we have shown that altering the pharmacokinetics of DNP to promote a low sustained systemic release can increase the therapeutic window of this agent by more than 500-fold. Daily CRMP administration reversed NAFLD, insulin resistance, T2D [type 2 diabetes], and liver fibrosis in rats without detectable toxicity".

They added: "These data support the potential utility of mitochondrial protonophores and other mitochondrial uncoupling agents for the treatment of the related epidemics of NASH, metabolic syndrome and T2D."

 

Conclusion

This study created a slow release version of DNP, called CRMP, that improved the way the liver processed fat and improved other measures linked to type 2 diabetes risk in rats. It did this when given for up to six weeks without the toxic side effects known to be associated with unmodified DNP.

This is encouraging research, which appears to have partially tamed some of the toxic effects of DNP, while protecting its benefits. Researchers will build on this in further studies in rats and possibly people, if these results are confirmed in more studies.

However, the current version of DNP that is available for sale illegally online is toxic to humans, even in tiny amounts, and has been linked to a number of deaths. Do not take it under any circumstances.

The study used a chemically-modified version of DNP, called CRMP, in rats. DNP on its own remains as dangerous as ever to people. CRMP’s safety in humans has not yet been tested.

This study showed proof of the concept that DNP can be modified to make it safer in rats, while maintaining its benefits. This has not yet been proven in humans.

The authors are planning further safety studies, reporting in the Telegraph that: "Given these promising results in animal models of fatty liver disease and type 2 diabetes, we are pursuing additional preclinical safety studies to take this approach to the clinic."

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

Links To The Headlines

First World War explosive could reverse diabetes, says Yale University. The Daily Telegraph, February 26 2015

Links To Science

Perry RJ, Zhang D, Zhang X, et al. Controlled-release mitochondrial protonophore reverses diabetes and steatohepatitis in rats. Science. Published online February 26 2015

Categories: Medical News

Over two hours screen time a day may raise a child's blood pressure

Medical News - Thu, 02/26/2015 - 14:50

"Watching TV for more than two hours a day increases the risk of raised blood pressure in children," The Daily Telegraph reports.

A large study, involving more than 5,000 children who were followed up over two years, found a link between time sitting in front of a screen and an increase in blood pressure rates.

It found that a worryingly high number of children – more than one in 10 – developed high blood pressure, a major risk factor for cardiovascular diseases (CVDs) in later life. CVDs are conditions that can damage the heart and blood vessels, such as a stroke.

Children who spent more than two hours a day on “screen time” over the two years were at increased risk, as were those with low levels of physical activity.

This study supports previous evidence that a sedentary lifestyle and low levels of physical activity are associated with high blood pressure, although it does not prove that the former causes the latter.

There are many factors that can affect blood pressure, including genetics, development in the womb, socioeconomic status and weight.

That said, the more time your child spends watching TV or playing on their PlayStation 4, the less time they are physically active.

In the UK, children aged five to 18 are advised to do at least 60 minutes of physical activity a day.

 

Where did the story come from?

The study was carried out by researchers from several academic centres worldwide, including the University of Glasgow in the UK. It was funded by the European Community Sixth Research, Technological Development and Demonstration Framework Programme.

The study was published in the peer-reviewed medical journal International Journal of Cardiology.

Both The Daily Telegraph’s and the Daily Mail’s reporting was fair, although neither paper included comment from independent experts, and they failed to explain the fact that this kind of study cannot prove cause and effect.

 

What kind of research was this?

This was an observational cohort study looking at the incidence of pre-high blood pressure and high blood pressure in children in Europe and any association between blood pressure, levels of physical activity and sedentary behaviour.

The study’s authors say high blood pressure is one of the most important factors for cardiovascular disease, and studies have shown that blood pressure levels in children and adolescents are linked to high blood pressure in adulthood. However, little is known about the risk factors for high blood pressure in childhood. Their hypothesis is that low levels of physical activity (and high levels of sedentary behaviour may contribute to the development of high blood pressure.

Sedentary behaviour was classified as the amount of time parents reported their children spending in front of a screen – whether watching TV, videos or playing computer games. It did not include other kinds of sedentary activity – such as reading.

Blood pressure is measured in millimetres of mercury (mmHg) and is recorded as two figures:

  • systolic pressure – the pressure of the blood when your heart beats to pump blood out
  • diastolic pressure – the pressure of the blood when your heart rests in between beats, which reflects how strongly your arteries are resisting blood flow

In children, high blood pressure is defined as blood pressure greater than the 95th percentile for their age, height and gender.

 

What did the research involve?

The researchers used data from a study of 16,224 children from eight European countries (Spain, Germany, Hungary, Italy, Cyprus, Estonia, Sweden and Belgium) looking at the effects of diet and lifestyle on health. The current analysis was based on 5,221 children who were between two and 10 years old at the start of the study, for whom all data was available. Of these, 5,061 children were re-examined two years later.

The children had their systolic and diastolic blood pressure measured at the start of the study and at two years follow-up. Pre-high blood pressure was defined as systolic or diastolic blood pressure from the 90th to 95th percentile for their age and height; and high blood pressure was defined as systolic or diastolic blood pressure above the 95th percentile for age and height.

Physical activity in the children was measured using an accelerometer – an electronic device which measures the intensity of exercise. The unit had to be worn for at least six hours a day, for at least three days during one week (two weekdays and one weekend day).

From this, the researchers calculated the time children spent in moderate physical activity and in vigorous physical activity. Moderate activity includes activities such as cycling, while vigorous activity includes running, football and energetic dancing.

The children were classified into two groups – those who met current physical activity guidelines – doing at least 60 minutes of physical activity daily – and those who did not meet the guidelines. They were further classified as to whether changes in physical activity levels had taken place over the two years.

The children’s parents were asked to fill in a questionnaire on their children’s sedentary behaviour, as measured by hours of TV/DVD/video viewing and computer/games-console use for both typical weekdays and weekend days. Researchers used this information to calculate the children’s “total screen time” per day. Participants were classified into two groups – those who met (US) guidelines on total screen time (two hours or less a day) and those who did not. Researchers also calculated changes in sedentary behaviour at two years.

They also included a range of potential confounders, including season, sex, age, parental education and waist circumference.

Researchers estimated the relationship between physical activity levels, reported screen time and the risk of developing high blood pressure or pre-high blood pressure. 

 

What were the basic results?
  • Researchers found that the yearly incidence of pre-high blood pressure was 121 per 1,000 children, and high blood pressure was 110 per 1,000 children.
  • Children who maintained sedentary behaviour of more than two hours a day during the two year follow-up had a 28% higher risk of having  high blood pressure (relative risk (RR) 1.28, 95% confidence interval (CI) 1.03 to 1.60).
  • Children not performing the recommended amount of physical activity (60 minutes a day) at the start of the study had a 53% higher risk of high blood pressure (RR 1.53, 95% CI 1.12 to 2.09).
  • There was no association between pre- high blood pressure and children’s behaviours.

 

How did the researchers interpret the results?

The researchers say that the incidence of pre-high blood pressure and  high blood pressure is high in European children, with those doing less than 60 minutes of physical activity daily or spending two hours or more per day in front of a screen at higher risk. They say that the results suggest regular physical activity should be promoted and sedentary behaviour discouraged in children to prevent high blood pressure and its consequences in adulthood.

 

Conclusion

The study found a worryingly high incidence of high blood pressure in children of just over 10%, instead of the expected 5%. It also found that low levels of physical activity and high levels of “screen time” raised the risk.

Although researchers adjusted their analysis for a range of other factors which might affect blood pressure (called confounders), it is always possible that other unmeasured factors could have affected the results. In addition, the study was reliant on parental estimates of the amount of sedentary behaviour their children had per day, which may be an over- or underestimate. Wearing the accelerometer may also have influenced the amount of physical activity that was performed on those days, which could also affect the results.

It’s generally agreed that many of today’s children spend too much time in front of a screen – and too little on physical activity. The real question is – what can we do about it?  

Children are more likely to accept changes to their lifestyle if they involve the whole family.  Read more about getting healthy as a family.

Also, evidence has shown that placing limits on the use of any type of screen equipment in the hours before bedtime can improve the quality of their sleep. This could then help them improve their energy and activity levels during the day.

Read more about how TVs, phones and screens impair kids' sleep.

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

Links To The Headlines

Too much TV could raise a child’s blood pressure: Watching more than two hours a day ‘makes them 30% more likely to have condition’. Mail Online, February 26 2015

Children who watch TV for more than two hours a day 'at greater risk of high blood pressure'. The Daily Telegraph, February 26 2015

Links To Science

de Moraes ACF, Carvalho HB, Siani A, et al. Incidence of high blood pressure in children — Effects of physical activity and sedentary behaviors: The IDEFICS study: High blood pressure, lifestyle and children. International Journal of Cardiology. Published online November 26 2014

Categories: Medical News

Longer sleep linked to stroke

Medical News - Thu, 02/26/2015 - 14:00

“Too much sleep could kill you,” is the baseless and needlessly alarmist headline on the front cover of today’s Daily Express.

The study it is reporting on actually showed that people who sleep for more than eight hours a night had a 46% increased risk of stroke over the following 10 years, compared with people sleeping six to eight hours.

While these results certainly warrant further investigation, it does not show that the increased sleep caused strokes, let alone death.

The researchers assessed the usual sleep patterns of nearly 10,000 adults in 1998 and again in 2002, looking for associations between the amount of sleep and the number of people having a stroke over the next 10 years.

They also pooled the results from similar studies. These also showed a 45% increased risk for people who sleep more than eight hours.

When the results were analysed by sex, the link was statistically significant for women, but not men. This wasn’t made clear in the UK media coverage. Women’s risk was 80% higher, which is almost double the 46% risk when the sexes were combined.

The study took into account cardiovascular risk factors such as high blood pressure and cholesterol, but not other illnesses. Without accounting for other illnesses, it is not clear what association the length of sleep has with risk of stroke from these studies. As that widely used, though valid, scientific cliché goes: “further research is needed”.

 

Where did the story come from?

The study was carried out by researchers from the University of Cambridge and the University of Warwick. It was funded by the Medical Research Council and Cancer Research UK.

The study was published in the peer-reviewed medical journal Neurology. The study was published on an open-access basis, meaning that anyone can read and download it for free online. There is also a related editorial.

The quality of the UK media's reporting of the study was mixed. The Independent and The Daily Telegraph took a measured approach, making clear the uncertainties of the study.

The Daily Mirror somewhat contradicted itself, saying first that: “Shock study reveals sleeping for longer than eight hours 'could cause a stroke'.” Whereas later on, it correctly says: “Importantly, the study only found an association between sleep length and risk of stroke. It did not find that sleeping for too long actually causes stroke.”

The Daily Express and the Metro said that increased sleep causes strokes, when this is not actually what the study found.

At most, the study found that increased sleep is associated with an increased risk of stroke in women, but it did not take illnesses other than diabetes, high blood pressure and previous stroke into account, which could have affected the results.

A lot of the media carried a useful quote from Yue Leng, from the University of Cambridge, saying: “It’s apparent both from our own participants and the wealth of international data that there’s a link between sleeping longer than average and a greater risk of stroke. What is far less clear, however, is the direction of this link. Whether longer sleep is a symptom, an early marker or a cause of cardiovascular problems.”

 

What kind of research was this?

This was a cohort study, which aimed to see if there was an association between sleep duration and risk of stroke. The researchers also performed a systematic review to find other relevant research, and pooled all the results in a meta-analysis.

A cohort study is the most appropriate type of study when looking at the long-term effect of sleep patterns, as it would not be feasible or ethical to conduct a randomised controlled trial over a long time period. Combining the results with other similar studies in a meta-analysis increases the strength of the evidence. However, due to the nature of the study types, they can only show an association between sleep duration and risk of stroke – they cannot prove that sleep duration causes a stroke.

 

What did the research involve?

The researchers assessed the regular sleep patterns of nearly 10,000 adults, looking for links between the amount of sleep they got and the number of people who had a stroke over the next 10 years. They systematically searched for similar studies and pooled their own results with these others in a meta-analysis.

The researchers recruited 9,692 participants from a larger longstanding study called the European Prospective Investigation of Cancer-Norfolk cohort, EPIC-Norfolk. They were given a questionnaire in 1998-2000, and again in 2002 to 2004, asking how much sleep they usually have over a 24-hour period, with the following options:

  • less than four hours
  • four to six hours
  • six to eight hours
  • eight to 10 hours
  • 10 to 12 hours
  • more than 12 hours

They were also asked if they sleep well, to which they could respond “yes” or “no”.

Participants were excluded from the study if they had already had a stroke. The researchers then obtained all cases of stroke from the National Health Services district database and the UK Office of National Statistics up until March 2009.

They analysed the results according to the average sleep duration, or the change in sleep duration between the two questionnaires. They also took into account all of the following potential confounding factors:

  • age
  • sex
  • social class
  • education
  • marital status
  • smoking
  • alcohol intake
  • hypnotic drug use (sedatives and “sleeping tablets”)
  • family history of stroke
  • physical activity
  • major depressive disorder in the previous year
  • previous heart attack
  • diabetes
  • use of blood pressure medication
  • body mass index (BMI)
  • blood pressure
  • cholesterol

Finally, they performed the systematic review and meta-analysis using all available trials up until May 2014.

 

What were the basic results?

The average age of the participants at the start of the study was 62, and ranged from 42 to 81 years. Most of them slept between six and eight hours per day (69%), with 10% sleeping for more than eight hours. In total, 346 people had a stroke during the 9.5-year follow-up period.

After adjusting for all of the confounding factors listed above, sleep of more than eight hours:

  • increased the risk of stroke by 46% (hazard ratio (HR) 1.46, 95% confidence interval (CI) 1.08 to 1.98)
  • increased the risk of stroke in women by 80% (HR 1.80, 95% CI 1.13 to 2.85)
  • was not associated with stroke in men

There was no statistically significant association between sleep of less than six hours and stroke.

The systematic review identified 11 relevant studies, including 559,252 participants from seven countries. They were followed up for between 7.5 and 35 years. The pooled relative risks for sleep duration and stroke were:

  • increased risk of 15% for sleep of less than six hours (relative risk (RR) 1.15, 95% CI 1.07 to 1.24)
  • increased risk of 45% for sleep of more than eight hours (RR 1.45, 95% CI 1.30 to 1.62)

 

How did the researchers interpret the results?

The researchers concluded that this study, “suggested a significant increase in stroke risk among long sleepers and a modest increase among short sleepers”. They say that, “the underlying mechanism needs further investigation”.

 

Conclusion

This cohort study found that, overall, people who sleep for more than eight hours have a 46% increased risk of stroke. When analysed separately, there was no statistically significant association for men, but a much higher increased risk for women, of 80%.

A major strength of the study is the number of potential confounding factors that the researchers tried to account for, including many cardiovascular risk factors. However, it did not account for other illnesses such as sleep apnoea or cancer, which may have had an effect on the amount of sleep and risk of stroke.

In addition, the study is reliant on the information provided in the questionnaires, which may not be entirely accurate:

  • alcohol intake is famously under-reported
  • perception of sleep duration and actual duration may be different and could be affected by illness and memory problems

The results of the meta-analysis were in line with the results of this study, though they also found an increased risk for people who have less than six hours sleep.

Professor Kay-Tee Khaw, senior author on the study, said in the Mirror that: “We need to understand the reasons behind the link between sleep and stroke risk”. She added that, “With further research, we may find that excessive sleep proves to be an early indicator of increased stroke risk, particularly among older people.”

In conclusion, without accounting for other illnesses, it is not clear what association the length of sleep has with risk of stroke from these studies. Known modifiable risk factors that can reduce your risk of stroke are to stop smoking, eat healthily, do physical exercise, and keep blood pressure and cholesterol within normal limits through lifestyle and use of medication where required.

If you are concerned that your normal sleep patterns have changed for no apparent reason, visit your GP.

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

Links To The Headlines

Weekend lie-in danger: Sleeping for eight hours can increase the risk of a stroke - especially for women over 63. Mail Online, February 26 2015

People who sleep more than eight hours are more likely to have a stroke, research shows. The Independent, February 25 2015

Sleeping more than eight hours raises stroke risk, Cambridge University warns. The Daily Telegraph, February 25 2015

Shock study reveals sleeping for longer than eight hours 'could cause a stroke'. Daily Mirror, February 25 2015

Sleeping too much ‘increases your risk of having a stroke’, study reveals. Metro, February 25 2015

Too MUCH sleep could KILL YOU: More than eight hours a night can double risk of stroke. Daily Express, February 26 2015

Links To Science

Leng Y, Cappuccio FP, Wainwright NWJ, et al. Sleep duration and risk of fatal and nonfatal stroke. Neurology. Published online February 25 2015

Categories: Medical News

'Game changer' HIV drug cuts infection risk by 86%

Medical News - Wed, 02/25/2015 - 16:00

"Scientists hail discovery of 'game-changer' that cuts the risk of infection among gay men by 86%," The Independent reports. The drug, Truvada, has proved very successful in a "real-world" trial involving 545 participants.

Truvada is currently used as part of a treatment plan for people with HIV. It stops the virus from replicating, which helps protect the immune system.

Researchers wanted to see if it could also prevent the infection taking hold in the first place and have now presented initial results at a conference.

They recruited gay men, other men who have sex with men (MSM) and transgender women who were HIV negative and at high risk of HIV infection from 13 sexual health clinics in England. They randomly assigned them to either immediately start taking Truvada each day, or to wait and start taking it 12 months later.

The researchers also wanted to see if taking the medication made people more likely to increase their sexual risk-taking behaviour because they thought they were protected.

It is reported that both groups had the same rate of other sexually transmitted infections (STIs), an indication that sexual risk-taking did not change. The incidence of HIV infection in their first year of the study was much smaller in the Truvada group, at three people compared to 19 in the group who had to wait for a year before starting taking Truvada.

The researchers plan to submit the study to a peer-reviewed journal in April and are working with a range of stakeholders to determine whether a Truvada service could be commissioned across the NHS for high-risk individuals.

 

Where did the story come from?

The study was carried out by researchers from the Medical Research Council Clinical Trials Unit at University College London, Public Health England and 12 NHS trusts across England. It was co-funded by the Medical Research Council and Public Health England.

The results of the study were presented at the Conference on Retroviruses and Opportunistic Infections in Seattle, Washington. The study has not yet been published, so has not gone through external peer review to ensure the methodology and findings are reliable. The Medical Research Council reports that the study will be submitted to a peer-reviewed journal in April.

As the study has not yet been published, this article is based on the information so far released from the Medical Research Council and Public Health England.

Most of the UK media’s reporting of the study is accurate. An exception to this is the headline from The Daily Telegraph – "HIV drug taken before and after sex cuts risk by 86pc", which is misleading as it implies that Truvada could be taken like a morning after pill, but this has not been tested.

It is highly likely that taking it in this manner would not be effective.

 

What kind of research was this?

This was a randomised controlled trial that aimed to see if Truvada was effective in reducing the incidence of HIV infection in gay and other MSM, and trans-women.

The use of drugs such as Truvada to prevent infection, rather than treat infection, is known as Pre-Exposure Prophylaxes (PrEP). Truvada is an anti-retroviral (anti-HIV) drug, which is usually used to treat HIV. It contains two antiviral compounds called emtricitabine and tenofovir disoproxil fumarate. The drug is taken once a day. Anti-retrovirals work by stopping the virus replicating in the body, allowing the immune system to repair itself and preventing further damage. They have proved very successful, though resistance can be a problem, so people with HIV are usually required to take a combination of drugs.

Truvada has already been shown to be effective in reducing the incidence of HIV infection compared to placebo (dummy pill). The purpose of this study was to see if taking Truvada changed sexual risk-taking behaviour, by making people feel that they were less likely to be infected and thus increasing their exposure to HIV.

This kind of research is important because among gay men, MSM, and trans-women in the UK the rate of HIV infection remains high at 2,800 in 2013.

 

What did the research involve?

The researchers recruited 545 gay men, MSM, and trans-women who were HIV negative into the PROUD study (Pre-exposure Option for reducing HIV in the UK: immediate or Deferred). The participants were randomly assigned to have Truvada immediately (N=276) or to wait and have it after 12 months (N=269).

The participants were recruited from 13 sexual health clinics in England between November 2012 and April 2014. People were eligible to be included in the study if they had reported having anal sex without a condom in the previous three months and planned to do so again in the near future. This put them in the very high risk category.

Participants in both groups were advised to continue other risk prevention strategies such as condom use. They were also asked to keep a short diary, fill out a monthly questionnaire and attend a clinic appointment every three months.

 

What were the basic results?

Those taking Truvada were 86% less likely to be infected with HIV:

  • HIV infection occurred in three people taking Truvada compared to 19 in the group who had to wait for a year.
  • The infection rate in the Truvada group was 1.3 people infected per 100 people followed up for one year (100 person-years).
  • The infection rate in the waiting group was 8.9 per 100 person-years.

Sexual risk-taking behaviour was judged not to have increased in the Truvada group as there was no difference between the groups in terms of the number of participants who had a sexually transmitted infection (STI).

No results were provided from the diaries or questionnaires.

 

How did the researchers interpret the results?

The chief investigator of the study, Sheena McCormack, is reported to have said: "These results are extremely exciting and show PrEP is highly effective at preventing HIV infection in the real world." They are now working with a range of stakeholders to determine whether a PrEP service could be commissioned across the NHS.

 

Conclusion

The results of this unpublished study were presented at a conference in Seattle and have been reported by the Medical Research Council, who helped fund it. As it has not been published, some important details are not yet known, such as:

  • The researchers report that there was "high adherence" to taking the medication, but it is not known how regularly it was taken, or how many people stopped taking it and why.
  • No details have been provided about any side effects experienced on the medication.
  • The incidence of STIs was used to determine whether taking Truvada changed sexual risk-taking behaviour. It is currently unclear which STIs were compared between the two groups. Three common STIs are viral (genital herpes, genital warts and human papilloma virus), so it is possible that the Truvada reduced their incidence in addition to HIV. This could be an added bonus, but we will need to await publication of the study to look at this.

A limitation of the study is the amount of contact the participants had with the sexual health clinics. They were asked to fill out monthly questionnaires and attend a clinic every three months. It is possible this frequent contact with services caused this particular group to be more aware of the risks of HIV infection.

The researchers plan to submit the study to a peer-reviewed journal in April. In the meantime, they are working with a range of stakeholders to determine whether a PrEP service could be commissioned across the NHS. It has been suggested that men may wish to take PrEP during periods in their life when their sexual risk is highest, rather than continuously. This will no doubt be among the many considerations that will be taken into account.

In conclusion, the researchers report that PrEP reduced HIV infection by 86% in this very high risk group when it was taken on a daily basis. Full publication of this study, and any further developments, are awaited.

The most effective method of reducing your risk of HIV if you are sexually active – and whether you are gay, bisexual, trans or straight, is to always use a condom.

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

Links To The Headlines

HIV pill: Scientists hail discovery of 'game-changer' that cuts the risk of infection among gay men by 86%. The Independent, February 24 2015

Daily pill Truvada cuts spread of HIV by 86%, study shows. The Guardian, February 24 2015

'Give HIV drugs to healthy gay men'. BBC News, February 24 2015

HIV Drug: 'Game Changer' Hopes For Gay Men. Sky News, February 25 2015

Healthy gay men should be given HIV treatment to PREVENT infection, 'game-changing' trial suggests. Mail Online, February 24 2015

Healthy gay men 'should be offered HIV drugs'. ITV News, February 25 2015

HIV drug taken before and after sex cuts risk by 86pc. The Daily Telegraph, February 25 2015

Categories: Medical News

Depression linked to violent crime

Medical News - Wed, 02/25/2015 - 13:30

"Depressed people are three times more likely to commit a violent crime," the Daily Mirror reports. Research into Swedish crime and medical data found that depression was linked with an increased risk of a person committing a violent crime.

It is important to stress from the outset that while the number of depressed people involved in a violent crime was above average, it was still small.

3.7% of men and 0.5% of women were convicted of committing a violent crime after being identified as clinically depressed, compared to 1.2% of men and 0.2% of women in the general population.

This was a well-designed study, but it’s important that the findings are not misinterpreted or used to add to the stigma of depression.

Also, the study does not show that depression causes crime. It only found an association between depression and a criminal conviction. It is possible that a third factor – such as poverty, unemployment or early trauma – can explain this link.

The study only included patients diagnosed and treated for depression by outpatient psychiatric services. People who required inpatient admissions and those treated by their GPs were excluded, so it may not be representative of people with different severities of depression.

If you are suffering from symptoms of depression, it is important to talk to your GP, especially if you find yourself lashing out at people. It’s important to remember that depression is treatable.

 

Where did the story come from?

The study was carried out by researchers from the University of Oxford and funded by the Wellcome Trust and the Swedish Research Council. Two authors declare financial ties with pharmaceutical companies, including Shire, Eli Lilly, Servier, Cephalon/Teva, Merck and GlaxoSmithKline. 

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

Most of the UK media’s coverage was fair and included comments from independent experts. 

The exception was The Daily Telegraph, as its headline, "Depression to blame for 46,000 violent crimes a year", was dangerously misleading. This headline does not relate to the results of the study, which was conducted in Sweden. In addition, the study found an association between depression and convictions for crime, but it did not show that depression was "to blame".

 

What kind of research was this?

This was an observational study that looked at the risk of violent crime in people with depression. In a second study, the authors investigated the association between depressive symptoms and violent crime in a cohort of twins, to assess the potential role of genetic and environmental factors.

The authors say that depression is associated with a wide range of adverse outcomes, including suicide, self-harm and early death, but any association with violent crime is uncertain.

 

What did the research involve?

The authors conducted two studies on people from Sweden. The first compared the rates of violent crime in people with depression and their siblings, compared to the general population. The second study followed a cohort of twins, assessed any symptoms of depression in 2005, and followed them up to see if any committed a violent offence.

The first was a population study in Sweden of 47,158 people diagnosed with at least two episodes of depressive disorders between 2001 and 2009. Those requiring inpatient admission were excluded, as were those with other psychiatric diagnoses. They were age- and sex-matched to 898,454 people in the general population, to compare the odds of their being convicted of violent crime. They analysed the results, taking account of various factors – low income, immigrant status, history of self-harm, previous criminality, and drug and alcohol abuse.

Data on convictions for violent crimes was obtained from the country’s national Crime Register and defined as:

  • homicide
  • attempted homicide
  • aggravated assault
  • common assault
  • robbery
  • arson
  • any sexual offence
  • illegal threats or intimidation

Researchers also compared the odds of violent crime conviction among 15,534 half-siblings and 33,516 full siblings of depressed people, compared to the general population.

In the second study, they looked at a sample of 23,020 adult twins born between 1959 and 1986, who had participated in an adult or child and adolescent Swedish Twin study. They were asked to fill in a questionnaire in 2005 to measure depressive symptoms using a recognised depression scale, and they were then followed for any violent outcome through linkage to the Crime Register. The aim of this second study was to assess whether any association between depression and violent crime could be due to common genetic or environmental factors.

 

What were the basic results?

In the first study, researchers identified 47,158 individuals (17,249 men and 29,909 women) with outpatient diagnoses of depression between 2001 and 2009. The average age of diagnosis was 32 years for men and 31 for women. They were followed for an average of three years.

During the follow-up period, 641 men (3.7%) and 152 (0.5%) women with depression were convicted of committing a violent crime, compared with 1.2% of men and 0.2% of women in the general population.

After adjusting for various sociodemographic factors, they calculated that individuals with depression were three times more likely to be convicted of a violent crime compared to people in the general population (odds ratio (OR) 3.0, 95% confidence interval (CI) 2.8 to 3.3). 

In people with either a previous criminal history, or a history of substance abuse or self-harm, the risk of being convicted for a violent crime was highest.

The odds of violent crime in brothers and sisters of people with depression were also significantly higher than in the general population, after adjusting the results to take into account age, sex, low family income and being born abroad:

  • half-siblings (adjusted OR 1.2, 95% CI 1.1-1.4)
  • full siblings (adjusted OR 1.5, 95% CI 1.3-1.6)

This, say the researchers, suggests that family background may be a confounding factor (confounder) in association between depression and a criminal conviction.

In the twin study, 88 violent crimes were recorded in the 5.4 years of follow-up.

Depressive symptoms were associated with a slightly increased risk of violent crime (hazard ratio (HR) 1.09, 95% CI 1.06 to 1.13).

 

How did the researchers interpret the results?

The researchers say that even after adjusting their findings for possible confounders, such as genetics and early family background, a diagnosis of depression modestly increased the risk of violent crime.

They argue that clinical guidelines should consider recommending violence risk assessment in certain subgroups with depression.

 

Conclusion

This was a large, well-conducted study that found an association between depression and violent crime. However, there were several limitations. As the authors point out, it did not include people who only go to their GPs – rather than psychiatric services – with depressive symptoms, or people who required inpatient admission for depression, so the results may not represent all people with depression.

Also, it was only conducted in one country, so the findings may not be generalisable to others.

As the authors say, they had no information about the treatment their patients had or were undergoing, so we cannot know how much treatment for depression was a factor in the findings.

The study did its best to take account of confounders that might influence the risk of violent crime, or explain both a diagnosis of depression and the likelihood of committing a crime, including family background. It is always possible that both measured and unmeasured confounders, such as early trauma or poor care as a child, can influence the results.

It’s also worth noting that depressed people were found to be more likely to be convicted of crimes – not that they actually committed more crimes. Given the nature of depression, which is associated with feelings of guilt and hopelessness, it is possible that depressed people are less likely to try to avoid being caught and less likely to try to avoid a conviction – for example, by seeking legal advice.

The results of this study would appear to suggest that current UK clinical guidelines on depression may benefit from being amended, by including advice on the small risk of violence in depressed people. They certainly shouldn’t be taken as "proof" that all depressed people are dangerous.

If you or someone you know is suffering from symptoms of depression, it is important to talk to a healthcare professional. 

Find information on mental health services in your local area.

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

Links To The Headlines

Depressed people are three times more likely to commit a violent crime, research shows. Daily Mirror, February 25 2015

Depression linked to violent crime, study finds. BBC News, February 25 2015

Depression to blame for 46,000 violent crimes a year, says Oxford University. The Daily Telegraph, February 25 2015

Links To Science

Fazel S, Wolf A, Chang Z, et al. Depression and violence: a Swedish population study. The Lancet – Psychiatry. Published online February 25 2015

Categories: Medical News

Peanut butter for non-allergic babies may reduce later allergies

Medical News - Tue, 02/24/2015 - 10:32

"The cure for peanut allergy – peanuts, from the age of four months," says The Guardian.

This is dangerous headline advice, potentially leading parents to think they can simply give peanuts to an allergic child and cure them. This is irresponsible. Parents are also advised not to give peanuts – or any whole nuts – to children under the age of five, because of the risk of choking.

There are ongoing trials to assess whether medically supervised gradual introduction to peanut protein can help children with a peanut allergy – but the study on which the headline is based did not do this. It looked at whether foods containing peanuts, such as peanut butter, may play a role in helping to reduce the risk of children developing a peanut allergy.

The news is based on a well-designed trial in 640 infants aged between four and 11 months, who were not already allergic to peanuts, but were at increased risk of developing allergies due to having other food allergies or eczema. It compared the effects of giving the infants regular small amounts of peanut protein (in the form of smooth peanut butter or snacks containing peanut butter) or avoiding peanuts altogether up to the age of five.

It found that early introduction of peanut products (not whole nuts) reduced the proportion that developed a peanut allergy by age five, compared to those avoiding peanuts completely.

It is important to know that this study was not about treating infants or children who already have a peanut allergy. All children had a skin prick test before starting the trial, and those who showed an allergic reaction to peanut protein were excluded. Those who developed an allergic reaction stopped eating the products.

If your child shows signs of a peanut allergy, you should not try to feed them peanuts, and should instead consult your GP.

 

Where did the story come from?

The study was carried out by researchers from King’s College London, Guy’s and St Thomas' National Health Service Foundation Trust, and other research centres in the UK and US. It was funded by the US National Institute of Allergy and Infectious Diseases, Food Allergy Research and Education, the UK Medical Research Council, Asthma UK, the UK National Institute for Health Research, the US National Peanut Board and the UK Food Standards Agency.

The study was published in the peer-reviewed New England Journal of Medicine, and has been made open access, so is available for free online.

Other than the Guardian’s print and The Daily Telegraph's headlines (both referring to "peanuts" rather than peanut products), the media generally reported on this study well. It’s worth noting that the headline slips might be due to a King's College London press release entitled "Eating peanut at an early age prevents peanut allergy in high-risk infants", which is not as clear as it could be.

Other sources avoided saying that the infants were fed "peanuts" in their headlines. For example, the Mail Online avoided a sensationalist headline and gave sensible warnings to parents not to try this at home.

 

What kind of research was this?

This was a randomised controlled trial (called the Learning Early about Peanut Allergy (LEAP) trial) looking at whether introducing children to peanuts at an early age could reduce the risk of them developing a peanut allergy.

Peanut allergy in children is reported to have doubled in westernised countries in the past decade, with between one in 100 and three in 100 children being affected. Peanut allergy is the most common cause of anaphylactic shock and death due to food allergy.

UK and US guidelines have in the past recommended pregnant and breastfeeding women and infants at high risk of allergy to avoid "allergenic" foods such as peanuts. However, this was not shown to reduce the likelihood of developing food allergies, so this recommendation was withdrawn.

It is still not clear whether avoiding or introducing allergenic foods early on is a better way to avoid food allergies later in life. Researchers in the current study wanted to compare these strategies to find out which might be better for reducing the chance of developing a peanut allergy.

A randomised controlled trial is the best way of comparing different interventions or approaches. Assigning people randomly should ensure that the groups are well balanced, and therefore any differences between the groups should be due to the different interventions.

 

What did the research involve?

The researchers enrolled infants aged between four and 11 months of age with severe eczema, egg allergy, or both, and randomly assigned them to either peanut exposure or peanut avoidance.

Infants in the exposure group who did not show signs of a peanut allergy were given at least six grams (g) of peanut protein a week up to the age of 60 months. Infants in the avoidance group were not given any peanut products. The researchers tested the children during the trial to see if any of them developed a peanut allergy.

Crucially, before starting the trial, they tested the infants using a skin prick test, using peanut protein to identify those who showed signs of an allergic reaction with a wheal (a small raised area of the skin). Those who developed a large wheal (area of raised or reddened skin) at the site of exposure (more than 4mm in diameter), as this is a strong sign of an allergic reaction, were excluded from the study. Those showing a slight reaction (wheals of up to 4mm) were included, but analysed separately to those showing no skin reaction.

Those who had been allocated to the peanut exposure group then had a further "food challenge" test to see if they reacted to eating a small amount of peanut protein (2 to 3.9g). Those who showed a slight reaction to peanuts in the skin prick test were instructed to avoid them, but still analysed as part of the "peanut exposed" group. This was to make sure the groups stayed balanced.

The peanut protein used in the study was a commercially available snack made from peanut butter and puffed maize, called Bamba, or smooth peanut butter (Duerr’s or Sunpat brands) if the infant did not like the snack. The researchers assessed how well the families stuck to the assigned diet for the infants with a standard food questionnaire.

The researchers had telephone calls with the parents every week until the infants were 12 months old, then every fortnight up to the age of 30 months, then monthly. They assessed the infants face-to-face at ages 12, 30 and 60 months, and in any cases where the infant showed signs of a possible peanut allergy. At these visits, they again assessed whether the child showed signs of being allergic to peanuts. This started with a skin prick test with peanut protein.

Those who reacted to the skin prick test, had shown any signs of allergic reaction to peanut protein, sesame or tree nuts, or had an anaphylactic reaction to any food during the study, were given gradually increasing amounts of peanut protein, while being closely observed for any reaction. If they showed a reaction, the test was stopped.

The researchers doing this test did not know which group each infant had been part of. All other children were given 5g of peanut protein and also observed for any reaction. Eleven children who had inconclusive results on the food challenge tests, or who missed the test, were assessed based on their medical history, skin prick test and level of peanut allergy-related antibodies in their blood.

The researchers then compared what proportion of children in each group had developed a peanut allergy, to see if it differed. They looked at children who showed a positive skin prick test at the start of the study and those who showed a negative skin prick test separately.

 

What were the basic results?

Overall, 628 out of the 640 infants recruited (98%) provided enough information for their data to be analysed.

Among the 530 children who were negative on the first skin prick test, 13.7% of those who avoided peanuts had developed a peanut allergy by 60 months, compared to only 1.9% of the peanut exposed group.

Among the 98 children who were positive on the first skin prick test, 35.3% of those who avoided peanuts had developed a peanut allergy by 60 months, compared to 10.6% of the peanut exposed group.

These results were statistically significant, meaning that they were unlikely to have occurred by chance. Similar results were obtained even in a "worst case scenario", where all participants in the peanut exposure group with missing data were assumed to be allergic, and the opposite assumed for the peanut avoidance group.

There were no deaths among the infants in the study, and there was no difference between the groups in serious adverse events or need for hospitalisation. There were more adverse events overall in the peanut exposed group. The events that were more common in the peanut exposed groups included upper respiratory tract infection, viral skin infection, gastroenteritis, urticaria (hives – a raised, itchy rash), and conjunctivitis. These events were generally mild to moderate in severity for both groups.

 

How did the researchers interpret the results?

The researchers concluded that, "the early introduction of peanuts significantly decreased the frequency of the development of peanut allergy among children at high risk for this allergy".

They say that this, “raises questions about the usefulness of deliberate avoidance of peanuts as a strategy to prevent allergy”.

 

Conclusion

This well-designed randomised controlled trial has found that the early introduction of regular small amounts of peanut protein to infants at high risk of having allergies reduced the proportion who developed a peanut allergy by age five, compared to avoiding peanuts completely.

The study looked at a group of infants who were at a particularly high risk of going on to develop food allergies, because they already had severe eczema or an allergy to eggs, or both.

It is important to know that this study was not about treating infants or children who already had a peanut allergy. Those who showed a strong reaction on a skin prick test were excluded from the study, and those who showed an allergic reaction to eating peanut protein during the study were advised not to eat them. The results of this study do not apply to this group, and the researchers say they don’t know if their approach would work and be safe in this group.

The main limitation to the study was that parents and children could not be blinded to which group they were part of. However, the use of objective tests for allergic reactions should mean that their views cannot influence this outcome. There appeared to be a high level of compliance with the group allocations, but this was largely based on reports from the parents, so may not be fully accurate.

Overall, this study suggests that eating peanut products early in life may reduce the risk of children with a tendency towards allergies developing a peanut allergy up to age five. The researchers now plan to follow the participants for longer to see if the effects are maintained over time, even if they stop eating peanut products. As a number of experts point out in the media, this is not yet at a stage where it could be recommended to families to try at home.

If your child shows signs of a peanut allergy, do not try to feed them peanuts, and instead consult your GP. 

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

Links To The Headlines

Feed babies peanut products to reverse rise in allergy, say scientists. The Guardian, February 23 2015

What to know about new research on babies, peanut allergies. Mail Online, February 23 2015

Feeding peanuts to babies protects from peanut allergies, scientists find. The Daily Telegraph, February 23 2015

Peanut allergy 'cut by early exposure'. BBC News, February 23 2015

Links To Science

Du Toit G, et al. Randomized Trial of Peanut Consumption in Infants at Risk for Peanut Allergy. New England Journal of Medicine. Published online February 23 2015

Categories: Medical News

Anger possibly linked with non-fatal heart attacks

Medical News - Tue, 02/24/2015 - 10:32

"'Plate-throwing rage' raises heart attack risk nearly 10 fold," The Daily Telegraph reports, slightly inaccurately.

This headline reports on a study that found that just seven out of 313 people had felt "very angry" in the two hours before a heart attack – compared to their normal levels of anger. Despite the headline, none of the participants had felt furious or angry to the point of throwing plates or any other objects.

The participants in the study had all been admitted to a cardiac unit following a heart attack. They completed questionnaires to estimate their levels of anger in the 48 hours before the heart attack and their usual levels in the preceding year.

Anger was assessed on a seven-point scale, and seven people reported being "very angry, body tense, maybe fists clenched, ready to burst" (a score of five) in the two hours before the heart attack. This level of anger was associated with 8.5 times the risk of a heart attack in the next two hours than other times.

This type of study alone cannot prove that anger caused the heart attack. And as so few people reported feeling angry before the heart attack, the results are not precise.

The study also relies on accurate recall not only of the period before the heart attack, but also of the usual levels of anger that were reached during the preceding year. People may be more likely to remember anger associated with a dramatic event like a heart attack than anger at other times, and this would affect results.

 

Where did the story come from?

The study was carried out by researchers from the Royal North Shore Hospital in Sydney and the University of Sydney. There was no external funding.

The study was published in the peer-reviewed medical journal Acute Cardiovascular Care on an open-access basis.

The media headlines exaggerated the findings of this study, with the Mail Online inaccurately reporting that anger "can cause" a heart attack.

This type of study cannot prove cause and effect. The Daily Mirror failed to explain that the results were only based on seven people.

 

What kind of research was this?

This was a case crossover study looking at whether episodes of anger are associated with an increased likelihood of heart attack shortly after they occur.

This type of study is uncommon, and aims to assess whether a brief condition or set of circumstances has a temporary impact on risk of an outcome shortly after they occur. It is similar to a case control study, but each case acts as its own control. Case crossover studies then look at how likely the outcome was to occur just after the circumstances occur, compared with any other time.

 

What did the research involve?

The researchers recruited people admitted to a cardiac unit with suspected heart attack. The participants reported on how angry they were over the previous 48 hours, and also their usual levels of anger. The researchers then looked at whether people were more likely to have had their heart attack in the four hours after an angry episode than at other times in the year.

They also looked at the likelihood of having high levels of anger or anxiety just before the heart attack compared to at other points in the year.

All people admitted to a single cardiac unit (in Sydney, Australia) with suspected heart attack between 2006 and 2012 were eligible for the study. The final 313 participants were those who had evidence of a blockage in an artery supplying the heart (coronary artery) found during angiography (a procedure that looks at the blood flow to the heart).

These participants completed a detailed questionnaire within four days of admission, which included questions about their activities in the 48 hours before the heart attack. They were also asked to rate their level of anger in this period, describe any events that caused it, and estimate how frequently they experienced each level of anger per year, using the following seven-point scale:

  1. calm
  2. busy, but not hassled
  3. mildly angry, irritated and hassled, but it does not show
  4. moderately angry, so hassled it shows in your voice
  5. very angry, body tense, maybe fists clenched, ready to burst
  6. furious, forced to show it physically, almost out of control
  7. enraged, out of control, throwing objects, hurting yourself or others

They also filled out another standard questionnaire about their level of anger and anxiety. They analysed the results comparing the likelihood and level of anger two hours before the heart attack and two to four hours before with their usual yearly estimated likelihood and levels of anger. They also compared the likelihood and level of anger and anxiety in the preceding two hours with the level 24 to 26 hours before.

 

What were the basic results?

The average age of the participants was 58 and most of them were male (85%). No one reported anger levels of above five (“very angry, body tense, maybe fists clenched, ready to burst”) – so despite the headlines, no-one threw anything.

In the two hours before heart attack:

  • seven people reported an anger level of five 
  • the risk of experiencing a heart attack within two hours of an anger level of five or more was raised by 8.5 times compared with other times (relative risk (RR) 8.5, 95% confidence interval (CI) 4.1 to 176)
  • two people had an anger level of four, and this was not associated with a significant increase in risk of heart attack in the next two hours (RR 1.3, 95% CI 0.3 to 5.1)

In the two to four hours before the heart attack:

  • one person reported an anger level of five or more, but this was not significantly associated with risk of heart attack
  • three people had an anger level of four, which was also not associated with an increased risk

When looking at the levels of anxiety in the two hours before heart attack compared to the level at the same time the previous day, people whose anxiety was in the top 75% of levels (75th percentile) had an increased relative risk of heart attack (RR 2.0, 95% CI 1.1 to 3.8) and this increased for those in the top 90% of levels (RR 9.5, 95% CI 2.2 to 40.8).

 

How did the researchers interpret the results?

The researchers concluded that episodes of intense anger, defined as being "very angry, body tense, clenching fists or teeth", are associated with increased risk of a heart attack within two hours. Anxiety was also associated with increased risk of heart attack in the next four hours.

 

Conclusion

This study found that an anger level of five of more (according to their scale) was associated with 8.5 times the risk of a heart attack than at other times. However, there are a number of limitations when considering this result.

Firstly, very few people reported feeling angry shortly before the heart attack – just seven people out of the 313 participants. Therefore the confidence interval for the main result is wide, meaning the results are not particularly precise, and we can’t be certain of the size of the association with risk.

Secondly, the study relies on accurate recall, not only of the period before the heart attack, but also of the usual levels of anger that were reached during the preceding year. As well as the potential for misremembering, it is open to what is called "recall bias". This is where someone is more likely to remember the anger they experienced just before their heart attack if they think it may have contributed to it, than anger at other times in the year.

In conclusion, the study by itself does not prove that increased levels of anger or anxiety directly cause heart attacks. However, a recent systematic review (that we have not assessed) suggests that similar studies also support an increase in risk shortly after outbursts of anger.

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

Links To The Headlines

'Plate-throwing rage' raises heart attack risk nearly 10 fold. The Daily Telegraph, February 24 2015

Malcolm Tucker style rants can increase risk of a heart attack. Daily Mirror, February 24 2015

Losing your temper CAN cause a heart attack: Being angry increases the risk eightfold. Daily Mail, February 24 2015

How anger raises heart attack risks. Daily Express, February 24 2015

Links To Science

Buckley T, et al. Triggering of acute coronary occlusion by episodes of anger. Acute Cardiovascular Care. Published February 23 2015

Categories: Medical News

Many deaths of mentally ill in custody 'avoidable'

Medical News - Mon, 02/23/2015 - 19:00

“Hundreds of deaths in mental health units ‘were avoidable’,” says a report on the front page of today’s Independent. The Guardian highlights 662 mentally ill detainee deaths from 2010 to 2013.

Both stories follow an inquiry by the Equality and Human Rights Commission (EHRC) into the deaths of people with mental health conditions while detained in police custody, prisons or psychiatric hospitals.

The inquiry looked at whether people who were detained had been treated correctly according to EHRC guidelines. The inquiry focused on two basic rights: the right to life and the right to non-discrimination.

Over the period 2010 to 2013, there were 367 deaths from non-natural causes of adults with mental health conditions while detained in psychiatric wards and police custody. A further 295 adults died in prison, many of whom had mental health conditions.

The inquiry identified many areas of concern, including a lack of information sharing between professionals, insufficient involvement of family members, inappropriate use of restraint, and failure to learn from past incidents.

The Commission recommends that rigorous systems are put in place to ensure that any incidents are thoroughly and transparently investigated, and acted upon.

 

What did the EHRC investigate?

The Commission’s report looked into deaths in detention for those with mental health conditions. The inquiry looked at the period 2010 to 2013 in three detention areas:

  • Psychiatric hospitals. Detention in hospital means being held under the Mental Health Act, which is sometimes referred to as being “sectioned”. In 2012/13, there were said to be over 50,000 such detentions and the number has since been increasing.
  • Police custody. The Mental Health Act allows for a person “in crisis in a public space” to be held in police custody as a “place of safety” when there is insufficient other health-based support available. In 2012/13, there were reported to be 7,761 occasions when the Act was used to hold an individual in police cells.
  • Prisons. The prison service does not record the number of imprisoned people who have mental health conditions; however, they are likely to affect a large proportion of inmates. The most recent data – from 1997 – reported that 92% of male prisoners were suffering from psychosis, neurosis, personality disorder, alcohol misuse or drug dependence.

The Commission wanted to establish the extent to which there has been compliance with Article 2 (the right to life) and Article 14 (the right to non-discrimination) of the European Convention on Human Rights. It wanted to see whether improved compliance with these civil rights rules could reduce deaths in psychiatric hospitals, prisons and police custody.

 

What did the inquiry find about deaths in detention?

From 2010 to 2013, there were 367 deaths from non-natural causes of adults with mental health conditions while detained in psychiatric wards and police custody. A further 295 adults died in prison, many of whom had mental health conditions.

The inquiry found that the same mistakes are being repeated across prisons, police cells and psychiatric hospitals. This includes, for example, the failure to appropriately monitor patients and prisoners at serious risk of suicide, even in cases where their records recommend constant or frequent observation. It also includes failure to remove “ligature points” in psychiatric hospitals, which are known to be often used in suicide attempts.

According to the inquiry report, psychiatric hospitals are an “opaque system”. The Commission found it difficult to access information about non-natural deaths in psychiatric hospitals, such as individual investigation reports. This contrasts with prisons and police settings, where there is an independent body in charge of investigating deaths and ensuring that lessons are learnt.

The Commission also found misplaced concerns about data protection, leading to failures to share important information, such as concerns of other professionals about mental health, or suicidal tendencies not being passed on to prison staff. Similarly, failure to involve families to support the person being detained make it difficult for the family to pass on information that might have prevented deaths. Poor communication between staff, including lack of updates on risk assessments after self-harm or suicide attempts, was also highlighted.

Other significant findings included:

  • The availability of drugs, including “legal highs”, in prison.
  • Evidence of bullying and intimidation in prisons in the lead-up to someone talking their own life. This can result in a person being locked up alone in a cell for their own safety, because there is nowhere else for them to go. This can lead to deterioration of the person’s mental state.
  • Inappropriate use of restraint in people with mental health conditions, including “face-down” restraint. There were also increasing reports of police officers being called out to restrain people on psychiatric wards.
  • A high number of deaths occurred shortly after a person ended a period of detention, suggesting insufficient mental health support and follow-up.

 

What does the EHRC recommend?

The EHRC recommends:

  • Structured ways of learning from deaths and near misses in all settings where people with mental illness are detained, to ensure that improvements are made.
  • Individual prisons, hospitals and police settings should focus more strongly on meeting the basic responsibilities of keeping detainees safe. It recommends better staff training, and for the inspection regimes to explicitly monitor this. 
  • The Commission wants more “transparency”, to allow services to be scrutinised and held to account. The Commission suggests that the “statutory duty of candour”, which is being introduced in April 2015 and applies to all NHS bodies in England, could help to achieve this.

 

What happens next?

Mark Hammond, the EHRC’s chief executive says: “This Inquiry reveals serious cracks in our systems of care for those with serious mental health conditions. We need urgent action and a fundamental culture shift to tackle the unacceptable and inadequate support for vulnerable detainees.

“The improvements we recommend aren't necessarily complicated or costly: openness and transparency, and learning from mistakes are just about getting the basics right. In particular, by listening and responding to individuals and their families, organisations can improve the care and protection they provide.”

The Commission says it is now going to follow up its recommendations with the relevant organisations.

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

Links To The Headlines

Mental health deaths in detention 'avoidable'. BBC News, February 23 2015

Hospital psychiatric detainees more at risk of preventable death. The Guardian, February 23 2015

Too many deaths in custody are preventable but staff lack mental health expertise, says human rights body. The Independent, February 23 2015

Categories: Medical News

Media overstates dementia benefits of Mediterranean diet

Medical News - Mon, 02/23/2015 - 18:55

“New diet to fight dementia,” claims the Sunday Express, while The Independent reports: “Mediterranean diet could help beat dementia”.

Despite the media focus on the Mediterranean diet, this was only a small part of a review which aimed to discover whether some modifiable risk factors (such as high cholesterol or high blood pressure) were linked to the risk of developing dementia in people with existing mild cognitive problems.

The review found collated relevant studies, covering a wide variety of potential risk factors, finding the most evidence around diabetes, high blood pressure and mental health.

Researchers found that the evidence suggested diabetes increased the risk of “conversion” from mild cognitive impairment to dementia. However, this increased risk was not adjusted for other potential confounding factors such as physical activity or smoking – which could influence the results.

The researchers found a single study assessing the Mediterranean diet in people with one type of mild cognitive impairment (particular problems remembering specific events). It found that the Mediterranean diet was associated with a reduced risk of developing Alzheimer’s among people with this type of mild cognitive impairment. However, it does not provide strong enough evidence to suggest that following the Mediterranean diet will definitely reduce the risk of a person with mild cognitive impairment developing dementia.

While this review is helpful, there is still a lot to be learned about risk factors for dementia and how to reduce risk.

 

Where did the story come from?

The study was carried out by researchers from University College London and Johns Hopkins Bayview Medical Center, Baltimore, US. One of the authors reported receiving financial support from various sources including the National Institute on Aging and National Institute of Mental Health, as well as various pharmaceutical companies. The other authors reported no financial relationships with commercial bodies.

The study was published in the peer-reviewed medical journal the American Journal of Psychiatry.

The main body of The Independent’s article is quite representative of this study, focusing on links with diabetes and mental health symptoms and risk of dementia. However, the choice to focus the headline on the Mediterranean diet is quite confusing and misleading. The Mediterranean diet was not the main focus of the review or its findings, and the evidence on it in the review comes from only one study. The Express' coverage was similarly skewed in focusing on diet.

 

What kind of research was this?

This was a systematic review that looked at which modifiable behaviours are associated with the development of dementia in people who have mild cognitive impairment (MCI).

The researchers say that recent public health campaigns have increased the recognition and diagnosis of MCI – described as a state between normal ageing and dementia. MCI is where someone (or a relative or doctor) has concerns about their cognitive symptoms, but they have normal functional activities and do not meet a diagnosis of dementia.

Almost half of people with MCI are reported to develop dementia within the following three years. However, ways to prevent the onset of dementia are unclear. The researchers had conducted a previous review of randomised controlled trials investigating treatments for MCI, but they found no consistent evidence that any of the treatments reduced the person’s cognitive decline, or the risk of the person developing dementia.

In the absence of trial evidence, they aimed next to look at observational studies to get an idea of which modifiable risk factors (such as different lifestyle choices) are associated with an increased or reduced risk of dementia. This may help to identify ways people might be able to reduce the risk of dementia developing. 

A systematic review is the best way of gathering all the available evidence on a particular question. However, such reviews are always going to be inherently limited by the quality of the underlying studies identified.

 

What did the research involve?

The researchers searched two literature databases (PubMed and Web of Knowledge) using relevant search terms to identify published longitudinal studies of “potentially modifiable risk factors” in people with MCI that looked at dementia outcomes.

The researchers defined MCI as cognitive impairment identified from objective neuropsychological tests, in the absence of dementia or significant functional impairment. Dementia outcomes were dementia of any cause, or Alzheimer’s dementia specifically.

They assessed the quality of identified studies, specifically looking for studies which recruited a representative sample of the general older population, had followed at least 70% of the included participants for at least one year, and used objective assessment methods for diagnosing MCI and dementia.

They also graded the quality of evidence supporting each of their conclusions as follows:

  • grade 1 evidence: consistent evidence from higher-quality studies
  • grade 2 evidence: evidence from a single higher-quality study or consistent evidence from other studies
  • inconsistent evidence: described as “troublingly inconsistent”

 

What were the basic results?

The search identified 62 relevant studies, nine of which were considered high-quality. 30 of these studies were pooled in meta-analysis. The studies looked at the following risk factors in people with MCI, as follows:

Diabetes

The pooled results of seven of 10 studies (grade 2 evidence) found people with MCI who had diabetes were at increased risk of developing dementia during follow-up compared to those without diabetes (unadjusted odds ratio (OR) 1.65, with a 95% confidence interval (CI) of 1.12 to 2.43).  

High blood pressure

The pooled results of seven of 11 studies (grade 2 evidence) did not find that this was associated with significantly increased odds of dementia (OR 1.19, 95% CI 0.81 to 1.73).

High cholesterol

Two studies (grade 2 evidence) found high cholesterol did not predict development of dementia (OR 0.92, 95% CI 0.50 to 1.68).

Smoking

Three studies (grade 1 evidence) found that smoking seemed to be associated with a decreased risk of dementia, but the relationship was no longer significant in the individual studies after adjusting for age. This suggested that the reason for the association could be due to smokers being more likely to die before they developed dementia.

Alcohol

Three higher-quality studies did not find any clear association between moderate alcohol consumption and development of dementia (grade 2 evidence).

Metabolic syndrome

One identified study (grade 2 evidence) found that metabolic syndrome predicted any-cause dementia in a specific type of MCI, termed "amnestic MCI". This was defined to be, “MCI with progressive symptoms and particular impairment of episodic memory”.

Mental health factors

The pooled results of four studies (grade 2 evidence) found an association between neuropsychiatric symptoms and dementia (OR 3.11, 95% CI 1.38 to 7.02). Pooled results of 13 studies did not find a significant association between depression symptoms and dementia (OR 1.35, 95% CI 0.89 to 2.06).

However, there was variability across studies. The studies following samples from the population that reported conversion from any type of MCI consistently found depressive symptoms were associated with increased risk of development of all-cause dementia (grade 1 evidence). However, the findings of studies in people with amnestic MCI and in groups of people with MCI identified through medical clinics were less consistent.

There was inconsistent evidence on any association with anxiety or apathy.

Dietary factors

The Mediterranean diet was the media focus, but only one study was identified, including 482 people with MCI. It was of high quality, and reported that a Mediterranean diet (low in meat and dairy products; high in fruits, vegetables, legumes, cereals and fish) was associated with a lower risk of conversion from amnestic MCI to Alzheimer’s dementia (grade 2 evidence). Of other dietary factors, three studies found suggestions that lower folate level is associated with an increased risk of conversion to dementia (grade 2 evidence).

Education

Seven studies (grade 1 evidence) found that number of years in education for people with amnestic dementia did not predict dementia.

 

How did the researchers interpret the results?

The researchers conclude that diabetes increases the risk of conversion from mild cognitive impairment to dementia.

They report that other potentially modifiable risk factors include the metabolic syndrome, neuropsychiatric symptoms, and low dietary folate. They suggest that dietary interventions and interventions to reduce neuropsychiatric symptoms may decrease risk of onset of new cases of dementia.

 

Conclusion

This was a systematic review that identified longitudinal studies that have looked at the association between modifiable risk factors in people with mild cognitive impairment and the development of dementia.

Despite the media headlines highlighting the Mediterranean diet, this was only a small part of this review – just one study of around 400 people that found the Mediterranean diet reduced risk of conversion from one type of MCI (amnestic MCI) to Alzheimer’s dementia.

So, despite the often-studied potential health benefits of the Mediterranean diet, this single study does not provide firm and conclusive evidence that following the Mediterranean diet will reduce the risk of a person with MCI developing dementia. Ideally, these findings need to be confirmed in other studies.

Such a systematic review is always going to be inherently limited by the underlying quality and methods of the included studies. This research found the largest body of evidence for diabetes, high blood pressure and mental health factors.

The largest body of evidence in this review suggested that diabetes increases the risk of conversion from MCI to dementia. However, even then this increased risk was in analysis that was not adjusted for other potential confounders. For example, with a condition such as diabetes, it’s possible that other cardiovascular risk factors may be involved in any association with the development of dementia, particularly vascular dementia.

It is also important to recognise that while this review did not find association with other factors such as high cholesterol, smoking or alcohol and dementia development, this is not to say these modifiable risk factors are definitely “safe”. The review only found few and variable quality studies addressing these factors.

It is important to note that the researchers’ previous systematic review of randomised controlled trials did not find that any interventions reduced the risk of conversion from MCI to dementia. In the absence of such evidence, observational studies can provide an idea of which factors look like they could be increasing risk. However, we can’t say for sure that changing them will definitely reduce risk.

Overall, this systemic review provides a summary of the currently available evidence on MCI and the risk factors for dementia in people with MCI. However, there is still much to be learned about risk factors for dementia and how to reduce risk.

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

Links To The Headlines

New diet to fight dementia: Best evidence yet that diet of fish & veg can beat the disease. Daily Express, February 21 2015

Mediterranean diet could help beat dementia finds UCL study. The Independent, February 22 2015

Links To Science

Cooper C, et al. Modifiable Predictors of Dementia in Mild Cognitive Impairment: A Systematic Review and Meta-Analysis. American Journal of Psychiatry. Published online February 22 2014

Categories: Medical News

New HPV vaccine may protect against 90% of cervical cancers

Medical News - Fri, 02/20/2015 - 16:30

"New HPV vaccine stops 90% of cervical cancers," the Mail Online reports. The vaccine, which protects against nine common strains of the cancer-causing human papilloma virus (HPV), has proved both safe and effective in a study involving 14,000 women. HPV is one of the major causes of cervical cancer, as well as genital warts.

The current HPV vaccine, Gardasil, which the NHS offers to all girls aged 12 to 13, protects against the two most common strains associated with cervical cancer, as well as an additional two strains known to cause genital warts. Research suggests Gardasil can prevent around 70% of potential cervical cancers.

The new vaccine covers these four strains and five additional ones. This latest study indicates this may provide protection against 90% of cases. And researchers found the new vaccine reduced the incidence of cancer from these extra five strains to 0.1 cases per 1,000 person-years, compared with 1.6 cases per 1,000 person-years.

It is important to note that the study was conducted in women aged 16 to 26, which is much older than the 12 to 13 age group currently offered vaccination, and may affect the results. In addition, the participants were only followed up for 4.5 years. Longer studies including other age groups are now required.

 

Where did the story come from?

The study was carried out by researchers from universities and institutes in Austria, Norway, Denmark, Germany, the UK, the US, Canada, Brazil, Hong Kong, Mexico, Thailand, Columbia, Taiwan, and Australia.

It was funded by the pharmaceutical company Merck. There are potential conflicts of interest, as many of the authors have affiliations with Merck.

The study was published in the peer-reviewed journal, the New England Journal of Medicine.

The Mail's reporting was confusing as it opened with the incorrect information that the "current vaccine used in the UK, Gardasil, protects against nine HPV strains". If this were the case, there would be no reason to assess the effectiveness of a new vaccine.

The current vaccine actually only protects against two strains that cause 70% of cervical cancers, and two strains that cause genital warts.

And despite the irresponsible suggestion to the contrary, we wouldn't recommend that you decline the offer of a smear test – cervical cancer screening – if recommended.

 

What kind of research was this?

This was a randomised, double-blind clinical trial comparing the effectiveness of a new vaccine against HPV with the current vaccine.

In the UK, around 3,100 women are diagnosed with cervical cancer each year. A major cause of cervical cancer is infection from the human papilloma virus (HPV). There are more than 100 types of HPV, and at least 15 of them are considered to be high risk.

In the UK, the HPV vaccine, which is offered to all girls aged 12 to 13, gives protection against four types of HPV: 6, 11, 16 and 18. Two of these types – HPV 16 and 18 – are believed to cause more than 70% of cases of cervical cancer.

The vaccine also protects against strains HPV 6 and 11, which are responsible for 90% of genital wart cases.

The new 9vHPV vaccine covers these four strains as well as five others (31, 33, 45, 52 and 58). This has the potential to increase the protection against cervical cancer from 70% to 90%, according to the prevalence of these strains in a global study of 10,575 cases of cervical cancer.

 

What did the research involve?

Women aged 16 to 26 were given either the current Gardasil vaccine or the new 9vHPV vaccine, and the rates of HPV infection were then compared.

The study recruited 14,215 women from Asia Pacific, Europe, Latin America and North America, and randomly assigned them to receive three doses of the 9vHPV vaccine or three doses of the current HPV vaccine over the course of six months. Their average age was 22 and the age when they first had sexual intercourse was 17.

Women were eligible for the study if they had:

  • no history of an abnormal smear test result
  • no more than four sexual partners in their lifetime
  • no previous abnormality on cervical biopsy

The women had swabs taken for 14 types of HPV on the day they first received the vaccine and then every six months for 4.5 years. They also had a smear at each visit and, if this was abnormal, they had a colposcopy (a more detailed examination of the cervix).

Statistical analyses were performed comparing the outcomes for women who had no evidence of HPV infection when they were first vaccinated or the subsequent seven months. Additional analyses were performed for those who did have HPV infection during this time.

The outcomes measured were incidences of cervical, vaginal and vulval cancers. They did not directly compare the two vaccines for infection with the four types of HPV.

 

What were the basic results?

For all women who entered the study:

  • The incidence of high-grade cervical, vulval and vaginal disease was 14.0 per 1,000 person-years in women given either vaccine. High-grade disease included invasive cancers and abnormal changes that have a high likelihood of developing into invasive cancer.
  • In women not initially infected with HPV, the incidence was 2.4 per 1,000 person-years in those given the new 9vHPV vaccine compared with 4.2 per 1,000 person-years for those given the current vaccine. This means the new vaccine was 42.5% more effective (95% confidence interval [CI] 7.9 to 65.9) in women who were not infected with HPV at the time they had the vaccination. In women who were already infected with HPV when they had their first vaccine, there was no difference in incidence.

For women who did not have HPV infection for the first seven months of the study who completed the vaccination course and had no study violations, called the per-protocol efficacy population:

  • The incidence of disease from the extra five types of HPV was 0.1 per 1,000 person-years in the 9vHPV group compared with 1.6 per 1,000 person-years in the current vaccine group (1 case versus 30), meaning the vaccine was more effective for these women.

The new 9vHPV caused slightly more pain, swelling and redness than the current vaccine. There were two serious events related to the vaccine in either group.

 

How did the researchers interpret the results?

The authors concluded that the 9vHPV vaccine provided the same amount of protection as the qHPV vaccine for the four vaccines that they both cover.

It also prevented infection and disease related to the five extra strains in susceptible women when compared with the normal qHPV vaccine. The 9vHPV vaccine did not protect against other strains of the virus.

 

Conclusion

This double-blind randomised trial has shown that the new HPV vaccine provides increased protection from additional strains of HPV that cause cervical, vulval and vaginal cancers.

Strengths of the study include:

  • Blinding of the pathologists to the vaccine type, and blinding of the participants (they didn't know which vaccine they had been given), which reduces any bias – a double-blind randomised controlled trial is considered the gold standard of how best to assess a treatment or intervention.
  • The large number of women included in the study, with diverse ethnic backgrounds, makes it likely that the results would be applicable to most women in this age group.

However, there are some limitations:

  • It is widely reported in the media that the two vaccines offer the same protection for the original four HPV strains, but there was no direct comparison between the vaccines for their ability to protect against the four types of HPV virus. The comparison was restricted to incidence of invasive cancers and high-grade abnormalities, which may take longer to occur than the 4.5 years of the study's duration. The researchers acknowledge that longer studies are required, however.
  • The study group were much older than the age of girls who are currently vaccinated, presumably so that they could provide their own consent to participate. This may have a bearing on the results.

Further studies will be required to address these issues before it is known whether there will be a change in the type of vaccine offered in the UK.

While vaccination is an important component in reducing the risk of these types of cancer, it is important to reduce the risk in other ways, too.

This includes not smoking, as this increases the risk of cervical cancer – chemicals from cigarettes have been found in cervical mucus, and it is thought this damages the cervix. Safe sex, such as using condoms, is also important.

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

Links To The Headlines

New HPV vaccine stops 90% of cervical cancers and could mean fewer women need smear tests in future. Mail Online, February 19 2015

Links To Science

Joura EA, Giullano AR, Iversen O, et al. A 9-Valent HPV Vaccine against Infection and Intraepithelial Neoplasia in Women. The New England Journal of Medicine. Published online February 19 2015

Categories: Medical News

Sunlight UV damage to skin persists even after dark

Medical News - Fri, 02/20/2015 - 15:00

“Moving immediately into the shade does not stop sun damage, as UV rays can continue damaging skin cells hours after exposure,” The Guardian reports. Ultraviolet (UV) light is known to cause damage to DNA in skin cells, which increases the risk of the most serious type of skin cancer: melanoma.

This study aimed to examine the biological mechanisms that may be involved in this process.

Researchers used pigment-producing skin cells from mice (melanocytes) and found that it is the pigment melanin that plays a role in the damage process.

Exposure to UV light causes melanin to produce small molecules, called cyclobutane pyrimidine dimers (CPDs). The CPDs form abnormal bonds between the “building blocks” in the DNA helix. These CPDs are formed at the time of UV exposure, but the research showed that the formation of CPDs also continues for three or more hours after UV exposure has stopped (“after dark”). After this, DNA repair mechanisms step in.

Some tests using human melanocytes were also performed. This was said to similarly demonstrate the continued formation of CPDs after dark, but the effects were much more variable. It is unclear whether the situation in humans is completely identical.

Overall, the findings reinforce the risks of over-exposure to sunlight. It is easy to forget that the sun is a giant nuclear fusion reactor that emits radiation. Therefore, it is important to be sun-smart to reduce your risk of skin cancer.

You don’t need to get a suntan, let alone sunburn, to harvest the vitamin D-boosting effect of sunlight.

 

Where did the story come from?

The study was carried out by researchers from Yale University School of Medicine in the US and other institutions in Brazil, Japan and France. The study was supported by various grants, including those from the Department of Defence and National Institutes of Health. 

The study was published in the peer-reviewed scientific journal Science Magazine.

The UK media’s reporting of the study was accurate, though some of the headlines were potentially confusing. For example, headlines such as The Daily Telegraph’s “Sunlight damages DNA even in the dark” and The Guardian’s “Exposure to sun poses risk of skin cancer even in the dark” could be taken the wrong way. People may be concerned that when they go out at night, the sun is damaging their skin and they need to cover up. The results of the study actually suggest that the damage caused by UV exposure to the skin continues for some hours after the exposure has stopped (e.g. after you have come in for the evening, after a day at the beach). 

 

What kind of research was this?

This was a laboratory study aiming to see by what processes UV light causes damage to the DNA in skin cells.

Melanin is the pigment in skin and hair cells, which is present in variable amounts across individuals. The amount and type of pigment in your skin, such as pheomelanin and eumelanin, are associated with the risk of developing melanoma – the most serious type of skin cancer.

People with blonde and red hair have higher amounts of yellow pheomelanin relative to brown eumelanin in their skin and hair, which puts them at higher risk than people with darker skin and hair.

Previous research has demonstrated that when melanin, particularly yellow pheomelanin, is exposed to UV light, this produces reactive oxygen species (ROS) – molecules that can cause cell damage and "breaks" in the DNA. Looking at the DNA abnormalities present in melanoma, it seems that in most cases there are distortions to the DNA helix. This is due to the presence of molecules called cyclobutane pyrimidine dimers (CPDs), which cause abnormal bonds between the “building blocks” in the DNA.

Ultraviolet A type radiation (UVA) makes up around 95% of the UV entering the atmosphere. However, the researchers say that although UVA is clearly linked to melanoma, UVA is not very good at making these CPDs directly. The researchers therefore aimed to look at the biochemical pathways that cause the pigment-producing skin cells (melanocytes) to produce CPDs.

 

What did the research involve?

The researchers carried out a variety of laboratory experiments, where melanocytes from mouse and human skin were exposed to UVA and UVB light. They used special laboratory techniques to examine the DNA in the cells, looking for the generation of CPDs at the time of UV exposure and for some time after UV exposure had been discontinued (“after dark”).   

The researchers then carried out further studies to see what biochemical processes may be causing the melanocytes to produce CPDs.

 

What were the basic results?

The researchers showed that exposure to UVA light causes the immediate production of CPDs. Unexpectedly, CPD generation continued for three or more hours after UVA exposure was stopped. After this, the formation of CPDs was offset by DNA repair mechanisms.

Experiments using melanocytes from albino mice suggested that it was the melanin pigment that was involved in the continued production of CPDs after dark, as pigment-free melanocytes did not continue to produce CPDs after UVA had been stopped.

Half of all CPDs produced after UVA exposure to mouse melanocytes were found to be formed in this “after dark” period, when exposure had stopped. Further tests with UVB light showed that most of the CPDs produced occurred after dark. Further tests in the mice suggested that the red-yellow pigment pheomelanin is both a “poorer shield” against the generation of CPDs at the time of UV exposure, and a stronger generator of CPDs after dark.

Tests with the human melanocytes similarly demonstrated the production of CPDs after dark, but in human cells the response was said to be much more variable. The researchers considered that this could be due to genetic differences, though they could not look into this further due to privacy restrictions on the donated skin.

When looking into the underlying biochemical pathways involved in the production of CPDs after dark, they found that this was due to UV-induced reactive oxygen and nitrogen species combining and causing excitation (the application of energy) of an electron in the melanin pigment. The energy produced during this process is transferred to the DNA and causes the formation of CPDs.

 

How did the researchers interpret the results?

The researchers conclude that pigment-producing skin cells (melanocytes) cause the production of “dark CPDs”, even after UV exposure ends. They say that melanin, while it may protect against cancer in one respect (e.g. people with darker skin having lower risk), it may also be cancer-causing (carcinogenic).

They also say that their findings “validate the long-standing suggestion that chemically generated excited electronic states are relevant to mammalian biology”.

 

Conclusion

This laboratory research examined the biochemical processes by which UV exposure causes damage to the DNA in skin cells, and so increases the risk of melanoma.

The research which used mouse pigment cells in the laboratory, confirmed that the melanin pigment plays a role. Exposure to UV light causes melanin to produce CPD molecules, which cause abnormal bonds to form between the “building blocks” in the DNA helix. The research showed that the formation of CPDs continues for three or more hours after UV exposure has stopped (“after dark”) before DNA repair mechanisms step in. The melanin pigment is necessary for the continued formation of CPDs after dark (pigment-free cells did not do this), and there was also the suggestion that different types of melanin could have differing effects. For example, the red-yellow pigment pheomelanin seemed to be a stronger generator of CPDs after dark. 

However, it should be noted that most of these results came from experiments using mouse pigment cells. Although UV exposure to human melanocytes was said to similarly cause the continued formation of CPDs after dark, the effects were reported to be much more variable. The researchers considered that this could be due to genetic differences, but they were not able to explore this further, due to privacy restrictions.

Therefore, these results must be predominantly considered to be applicable to mice. Although this is likely to be a good indication of the biochemical pathways that may occur in human skin cells after UV exposure, it is not know if the results would be completely identical.

Overall, the findings show that at whatever time UV exposure causes most damage to the skin – either at the time of exposure, or in the continuing hours afterwards – it does cause DNA damage to the skin, which is linked to the risk of skin cancer. The study again highlights the importance of safety in the sun, including the use of sunscreen, sunglasses and skin coverage.

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

Links To The Headlines

Exposure to sun poses risk of skin cancer even in the dark, study finds. The Guardian, February 19 2015

Could using sunscreen at NIGHT prevent skin cancer? Damage caused by UV light continues for hours after dark, finds study. Mail Online, February 19 2015

Sunlight damages DNA even in the dark, Yale scientists find. The Daily Telegraph, February 19 2015

A day on the beach can lead to cancer-causing damage AFTER the sun has set. Daily Mirror, February 19 2015

Links To Science

Premi S, Wallisch S, Mano CM, et al. Chemiexcitation of melanin derivatives induces DNA photoproducts long after UV exposure. Science. Published online February 20 2015

Categories: Medical News

Nanoparticles used to treat damaged arteries

Medical News - Thu, 02/19/2015 - 16:00

“New trials suggest microscopic stealth drones could be used to seek and repair damaged arteries," The Daily Telegraph, somewhat overexcitedly, reports.

A study in mice has found promising results for a targeted treatment where nanoparticles are used to deliver a "repair protein" to sections of arteries affected by atherosclerosis.

Atherosclerosis occurs when fatty material collects in the lining of arteries, causing inflammation. The body tries to repair this, covering the areas with fibrous tissue, creating "plaques". Continued fatty build-ups collect on these plaques and eventually the repair system fails, and the plaques rupture. This may cause a blood clot to enter the circulation and cause a heart attack or stroke.

In this study, researchers have identified a protein called annexin A1, which is usually part of the repair process. They took a section of this protein and covered it in a nanoparticle (a microscopic particle). They then attached proteins to the surface that would "stick" to the plaques.

The nanoparticles targeted the plaques in mice with advanced atherosclerosis, where they slowly released the section of annexin A1, which helped to improve the repair system. 

Further studies in pigs and then primates are now planned. If successful, human trials may then be conducted.

 

Where did the story come from?

The study was carried out by researchers from Colombia University in New York, Brigham and Women’s Hospital in Boston, and Barts and the London School of Medicine. It was funded by the US National Institutes for Health, the Wellcome Trust and the David Koch Prostate Cancer Foundation. The authors have disclosed a competing interest, in that an international patent has been filed for the inflammatory resolving nanoparticles.

The study was published in the peer-reviewed journal Science Translation Medicine.

We suspect that somebody at The Daily Telegraph has been reading too much science fiction, which led to their description of "microscopic stealth drones". Microscopic? Yes. Stealth drones? No.

That aside, the media reported this study accurately, though descriptions of nanoparticles "mending" or "repairing" damaged arteries, are not exactly what occurred. The new technique helped to stabilise plaques and reduce the damaging inflammation, but did not remove them.

 

What kind of research was this?

This was an animal experiment, which aimed to test a new technique to resolve atherosclerotic plaques.

Atherosclerosis (hardening and thinning of the arteries) occurs when fatty material collects in the lining of arteries, causing inflammation. This in turn causes the body to try to repair the area by forming a protective fibrous tissue over the top. These areas, called plaques, continue to build up and restrict blood flow. Eventually, the inflammation continues, but the repair process stops working. The plaques then have a thin layer of this fibrous tissue and so are more likely to rupture, causing a blood clot to break off, which can lead to a stroke or heart attack.

Prevention of atherosclerosis involves a healthy diet, not smoking, and doing exercise, though plaques may still develop. Current treatments aim to reduce the amount of cholesterol in the blood using statins, treating high blood pressure to reduce the likelihood of a plaque rupturing, and drugs such as aspirin to thin the blood and prevent it sticking to the plaques and causing a clot.

The researchers' main aim was to find a way to reduce the inflammation that is occurring within the plaques as an additional treatment strategy. Other novel attempts, such as with genetic manipulation or immunosuppressant drugs, dampen down the whole immune system, leaving it vulnerable to infection. This new technique, using targeted nanoparticles, means that a limited amount can be circulated in the bloodstream, without affecting the normal immune response.

 

What did the research involve?

The researchers isolated a human protein called annexin A1, which normally helps to resolve inflammation. They took a component of this, called Ac2-26, and covered it in a nanoparticle, which is a microscopic particle with a diameter of 100 nanometers or less. They attached peptides to the surface of these nanoparticles that would effectively "stick" to the plaques.

They injected mice with advanced atherosclerosis once per week for five weeks with either these nanoparticles, a scrambled version of the nanoparticles, Ac2-26, or a control of normal saline (salty water). The researchers then looked at the first part of the aorta (the main artery taking oxygenated blood from the heart to the body) and the main artery that supplies the brain.

 

What were the basic results?

The nanoparticles stuck to the plaques and released the Ac2-26 proteins. Compared to the other mice, those given the nanoparticles had:

  • increased collagen (the protective fibrous layer covering the plaques)
  • reduced reactive oxygen species (these accumulate during acute inflammation, but an excess amount can damage tissues)
  • increased anti-inflammatory cytokines (communication cells of the immune system)
  • 80% reduced area of plaque necrosis (breakdown)

In short, this acted to resolve the inflammation and stabilise the plaques. These changes were not present in the spleen or liver, indicating that the nanoparticles were likely to have just targeted the plaques.

 

How did the researchers interpret the results?

The authors concluded that their animal experiments "tested a proof-of-concept targeted NP [nanoparticles] with one type of proresolving mediator. To bring targeted resolution mediator nanotherapeutics to the clinic for patients at high risk for atherothrombotic vascular events, additional confirmatory studies will be needed, including evaluation in more predictive models, such as fat-fed pigs and non-human primates". They also acknowledge that "detailed toxicity studies will be needed to show the safety of both the NP material and the resolution mediator cargo".

 

Conclusion

This exciting study in mice has shown that nanoparticles can be manufactured to target the plaques that form in atherosclerosis, and help stabilise them. It appears that the nanoparticles honed in on the plaques, rather than affecting other organs such as the spleen or liver, which gives an early indication that there may not be substantial side effects. However, it will be necessary to see if the same holds true for other organs.

As with all mice studies, they give an indication of the likely biological effects of a new technique, but they do not provide the full picture of what may happen in humans, especially with regards to more subtle side effects.

The media have rather exaggerated the results of this study by claiming the technique repaired arterial damage. This is not the case; the nanoparticles were able to help stabilise the plaques and reduce the inflammation that is part of the process of plaque formation. However, the study did not show that the arteries went back to normal. The plaques were still present. This technique, if possible in humans, would be an additional strategy for "damage limitation" of atherosclerosis.

Researchers now plan to see if the techniques work in animals with more complicated bodies and biological systems, such as pigs and primates. If these hurdles are successfully passed, human trials may then begin.

Currently, the best way to slow down or try to prevent atherosclerosis is to lead a healthy lifestyle and reduce known risk factors.

This includes stopping smokingweight management and regular exercise. In some cases, cholesterol-lowering medications, such as statins, and blood-thinning medications, such as low-dose aspirin, may also be recommended.

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

Links To The Headlines

Drones could be used to seek out arteries to prevent heart attacks. The Daily Telegraph, February 18 2015

Nano drones mend arteries: Microscopic particles that seek out and repair damage could be future of treatment for heart disease and strokes. Mail Online, February 19 2015

Microscopic DRONES could be used to treat heart and stroke patients in the future. Daily Mirror, February 18 2015

Links To Science

Fredman G, Kamaly N, Spolitu S, et al. Targeted nanoparticles containing the proresolving peptide Ac2-26 protect against advanced atherosclerosis in hypercholesterolemic mice. Science Translational Medicine. Published online February 18 2015

Categories: Medical News

Researchers may have unmasked mystery of cannabis 'munchies'

Medical News - Thu, 02/19/2015 - 14:30

"Cannabis 'munchies' explained by new study," The Guardian reports. "Munchies" is widely used slang for a common effect of cannabis: sudden hunger pangs, even if a user has just eaten. A new study set out to find why cannabis causes increased appetite.

Previous studies have shown certain pathways of nerve cells in the hypothalamus of the brain (called pro-opiomelanocortin, or POMC) have a role in regulating our appetite.

This latest study found that when mice were given a chemical to stimulate cannabinoid receptors (the parts of the brain that respond to cannabis), this caused increased feeding.

A series of subsequent tests confirmed this feeding response was being driven by the activation of POMC nerve cells. This caused a release of beta-endorphins (opioid-like proteins that can have various feel-good effects).

The findings further our understanding of why cannabis may cause the "munchies".

The hope is that this effect could be harnessed for a more serious use, such as stimulating the appetite of people who have a reduced appetite due to illness.

Whether this could be possible is too early to say, based on this animal research.

While similar biological pathways may be involved, the processes may not be identical in humans, so it is currently uncertain whether a "munchie drug" could be created.

 

Where did the story come from?

The study was carried out by researchers from the Yale University School of Medicine and other institutions in the US, Germany and Australia.

It was funded by the US National Institutes of Health, the American Diabetes Association, The Klarmann Family Foundation, the Helmholtz Society (ICEMED), and the Deutsche Forschungsgemeinschaft (a German research institute).

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

The UK media accurately presents the general findings of this research, but none of the sources make it immediately apparent that this research was in mice.

Extrapolations of the findings, such as claiming this could help people who lose their appetite as the result of illness, while interesting, are not supported by this early-stage research.

 

What kind of research was this?

This was research in mice that aimed to see how cannabis affects our appetite.

The hypothalamus is a region of the brain that plays a role in regulating many of our bodily processes, such as hunger, sleep and body temperature. Hypothalamic POMC nerve cells are reported to be responsible for causing a feeling of fullness.

However, substances that we take into our body can disrupt our normal body rhythms.

One such substance is cannabinoids, which are chemicals that act on cannabinoid receptors in the body, the most notable being the compound found in cannabis. This often triggers hunger, even though a person is full.

Previous research has shown that activation of the cannabinoid receptor 1 (CB1R) can cause animals to eat excessively, despite being full.

This study aimed to see whether the reason for this could be because activation of CB1R is associated with decreased activity of POMC nerve cells, thereby turning off the signals that tell us we are full.

 

What did the research involve?

The researchers carried out a range of feeding experiments in mice to see how the stimulation of the cannabinoid receptor influenced feeding responses, and how this was being driven by the activation of POMC nerve cells.

They first carried out experiments to see what happened when they injected mice with a chemical that stimulates the cannabinoid receptor.

In the next experiment, they injected the mice with a different chemical that blocks the cannabinoid receptor.

They then demonstrated how the subsequent activation of POMC nerve cells drove feeding response, by injecting the mice with chemicals that either stimulate or block POMC cells. 

 

What were the basic results?

The researchers found that stimulation of the cannabinoid receptor increases feeding in mice. When mice were injected with a chemical to stimulate the cannabinoid receptor (ACEA), this increased feeding response. Subsequent injection of a chemical to block the cannabinoid receptor (RIMO) reduced food intake. 

The researchers then showed that the increased feeding associated with stimulation of the cannabinoid receptor was being driven by the activation of POMC nerve cells.

When mice who had been given ACEA where given a chemical that blocks POMC cells, this gradually diminished feeding over the course of a few hours. But when they were given a chemical to activate the POMC cells, this caused increased feeding.

The POMC gene is reported to code for two chemicals: alpha-melanocyte-stimulating hormone and beta-endorphin.

The researchers' subsequent experiments showed that the activation of the cannabinoid receptor selectively causes the release of beta-endorphin from the hypothalamus, and this causes increased feeding.

When mice were given a chemical to block the receptors for beta-endorphins, this blocked the cannabinoid receptor-induced feeding response. 

 

How did the researchers interpret the results?

The researchers concluded that, "These results uncover a previously unsuspected role of POMC [nerve cells] in the promotion of feeding by cannabinoids."

 

Conclusion

This research in mice demonstrates how cannabis may cause increased appetite. The findings show that when mice were given a chemical to stimulate cannabinoid receptors, this caused increased feeding.

A series of subsequent tests showed how this feeding response was being driven by the activation of POMC nerve cells in the hypothalamus.

Giving chemicals to block POMC activation led to gradual suppression of feeding, while giving a chemical to increase POMC activation caused enhanced feeding. This increased feeding response seemed to be because POMC activation was causing the release of beta-endorphin from the hypothalamus.

The findings further our understanding of why cannabis may cause the "munchies", but the results are only from experiments on mice.

Studies such as this can give a good indication of the effect that different chemicals can have upon animals and the biological pathways that may be involved.

However, the nerve cell stimulation and feeding response when humans take cannabis may not be identical to these tests, where mice were injected with chemicals to stimulate the cannabinoid receptors.

These findings currently have limited implications. Though the media suggests that the findings could be used to help people who have lost their appetite as the result of illness – presumably through using drugs to stimulate the cannabinoid receptors, rather than suggesting people smoke cannabis – this is pure speculation.

Regardless of how cannabis may trigger increased appetite, cannabis is a class B drug that is illegal to possess or supply to others, and can have very uncertain effects on our brain function.

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

Links To The Headlines

Reefer research: cannabis 'munchies' explained by new study. The Guardian, February 18 2015

Why cannabis triggers the munchies: Drug flicks a switch in the brain that turns on hunger, scientists discover. Mail Online, February 18 2015

Cannabis 'munchies' explained: scientists discover why weed makes stoners greedy. Daily Mirror, February 18 2015

This is why you get the munchies when you're stoned. Metro, February 18 2015

Links To Science

Koch M, Varela L, Kim JG, et al. Hypothalamic POMC neurons promote cannabinoid-induced feeding. Nature. Published online February 18 2015

Categories: Medical News

Menopausal symptoms 'last longer' than previously thought

Medical News - Wed, 02/18/2015 - 19:00

"Menopause lasts 'up to 14 years'," the Daily Mail reports, with The Daily Telegraph reporting a similar figure – but according to The Guardian, it's "12 years".

All three headlines are prompted by a new US study, which does suggest that, at least in some women, symptoms such as hot flushes can persist for more than a decade.

Menopausal symptoms such as hot flushes and night sweats are collectively known as vasomotor symptoms (VMS), as they are all caused by constrictions and dilations to blood vessels. These can lead to a sudden increase in blood flow, which can then cause hot flushes and excessive sweating.

The study found that on average, women who had frequent VMS did so for more than seven years, with symptoms continuing for over four years after their last menstrual period.

It should be noted that the study focused on a specific group of menopausal women who reported frequent VMS (for six days or more in the previous two weeks). It is not clear if this group is representative of all women going through the menopause.

VMS can usually be successfully controlled using hormone replacement therapy (HRT). HRT does carry a very small risk of triggering hormonal cancers such as breast cancer, and, as we discussed earlier this month, ovarian cancer.

But these risks should be balanced against the benefits HRT can bring to quality of life. There are also self-help techniques you can use to cope better with VMS. Your GP can provide more information about treatment options.

 

Where did the story come from?

The study was carried out by researchers from several academic centres in the US, and was funded by the US National Institutes of Health, the Department of Health and Human Services, the National Institute on Aging, the National Institute of Nursing Research, and the Office of Research on Women's Health.

One of the authors has financial ties with, and has acted in an advisory capacity to, a number of pharmaceutical companies.

The study was published in the peer-reviewed Journal of the American Medical Association (JAMA) Internal Medicine.

It is unclear why The Daily Telegraph and the Daily Mail reported that the menopause "lasts up to 14 years" and The Guardian decided "symptoms lasted up to 12 years", but all three headlines are potentially misleading.

The study found the average time frequent menopausal symptoms lasted was 7.4 years. Only a very small number of women had symptoms lasting more than a decade.

 

What kind of research was this?

This was an observational study looking at how long women going through the menopause experience hot flushes and night sweats. These are called vasomotor symptoms, and are caused by the decline in production of the female hormone oestrogen, which in turn can affect blood flow.

The authors also wanted to find out how long frequent symptoms persist after the final menstrual period and identify the risk factors for longer duration of symptoms.

They say vasomotor symptoms (VMS) can significantly affect quality of life and are experienced by up to 80% of menopausal women. These symptoms are also one of the chief menopause-related problems US women seek medical treatment for. Yet there are few robust estimates as to how long VMS lasts.

 

What did the research involve?

Between 1995 and 1997, researchers recruited 3,302 women for a large multi-ethnic, multiracial US study of the menopause.

The women had to be aged between 42 and 52 years, have an intact uterus and at least one ovary, report a menstrual cycle in the three months before they were screened, and not be pregnant or breastfeeding, or using oral contraceptives or HRT.

Of the initial 3,302 participants, 1,853 were excluded: 330 because they had surgery to remove their womb and ovaries, 583 because they began HRT, and 940 who did not report frequent VMS. The researchers analysed 1,449 women to find out how long they had menopausal symptoms overall.

Women were assessed at the start and followed up with annual visits for between 12.7 and 17.2 years. They were asked at each visit about their lifestyle, psychosocial factors, physical and psychological symptoms, and their medical, reproductive and menstrual history.

The women filled in a questionnaire at each visit about the frequency of hot flushes and night sweats in the previous two weeks.

These were recorded as occurring:

  • not at all
  • 1-5 days
  • 6-8 days
  • 9-13 days
  • every day

Frequent VMS was defined as occurring at least six days in the previous two weeks.

From the women's self-report of their bleeding patterns during each preceding year, the researchers also assessed whether women were premenopausal, peri-menopausal (near the menopause), or postmenopausal.

Of the 1,449 women, 881 were assessed for how long VMS symptoms lasted after the final menstrual period. Researchers excluded 406 because their final menstrual period could not be dated, 132 who had no frequent symptoms after their final menstrual period, and 30 who began HRT before the first post-final menstrual period report of VMS.

The researchers looked at the total duration of frequent VMS, and the duration of frequent VMS after the final menstrual period. They also assessed the influence of potential confounders, such as:

  • sociodemographic factors such as age, race, marital status and education
  • lifestyle
  • psychosocial factors such as attitude towards menopause, anxiety and stress

They analysed the duration of VMS using standard statistical methods.

 

What were the basic results?

The researchers found that in women with frequent hot flushes and night sweats:

  • the average duration of symptoms was 7.4 years
  • among 881 women who experienced an observable final menstrual period, the average duration of symptoms afterwards was 4.5 years
  • women who were premenopausal or early peri-menopausal when they first reported frequent VMS experienced these symptoms for the longest time overall (on average, for more than 11.8 years) and after the final menstrual period (on average for 9.4 years)
  • women who were postmenopausal at the onset of symptoms had the shortest total duration of symptoms (on average, 3.4 years)
  • compared with women of other racial or ethnic groups, African-American women reported the longest total duration of symptoms (on average, 10.1 years)
  • women of a younger age, lower educational level, greater perceived stress and symptom sensitivity, and higher depressive symptoms and anxiety when they first reported symptoms were more likely to experience symptoms for a longer time period

 

How did the researchers interpret the results?

The researchers say frequent vasomotor symptoms (VMS) lasted more than seven years during the menopausal transition for more than half of the women, and persisted for 4.5 years after the final menstrual period.

Longer-lasting VMS was associated with being premenopausal and having greater "negative affective factors" in women when they first experienced symptoms.

Healthcare professionals should advise women to expect that frequent symptoms of hot flushes and night sweats could last more than seven years, and they may last longer for African-American women.

 

Conclusion

This is an interesting study with a long follow-up period. It suggests the length of time women have hot flushes for may be underestimated.

However, it was carried out on US women and the results may not be generalisable to other populations.

That aside, unlike many other studies of its type, it did make an effort to include a range of ethnicities, including Chinese, Hispanic and African-American women.

The study relied on women self-reporting their symptoms only once each year, which may affect its reliability.

It also only looked at women who reported getting frequent vasomotor symptoms (at least six days in the previous two weeks). As a group, this sample may not be representative of menopausal women overall and may be more vulnerable to a longer duration of symptoms.

It is interesting that women who reported more anxiety about menopause also reported a greater duration of VMS.

The menopause is a perfectly natural event, and there are many ways women can learn to cope with its effects.

If symptoms are making you miserable, it’s worth talking to your GP. HRT is often effective, but if you are unable or unwilling to take it, alternatives to HRT are available.

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

Links To The Headlines

Menopause lasts 'up to 14 years': Study says doctors should advise women that symptoms may occur for longer than they previously thought. Daily Mail, February 17 2015

Menopause symptoms can last up to 12 years, study reveals. The Guardian, February 18 2015

Menopause symptoms like hot flushes can last 14 years. The Daily Telegraph, February 17 2015

Links To Science

Avis NE, Crawford SL, Greendale G, et al. Duration of Menopausal Vasomotor Symptoms Over the Menopause Transition. JAMA Internal Medicine. Published online February 16 2015

Categories: 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