NHS Choices

Smoking causes half of all deaths in 12 different cancers

NHS Choices - Behind the Headlines - Thu, 18/06/2015 - 13:00

"Roughly half of deaths from 12 smoking-related cancers may be linked directly to cigarette use, a US study estimates," the Mail Online reports. Due to similar smoking rates in the UK (19% of adults) and USA (17% of adults) there may be a similar pattern.

Researchers used data from previous studies to estimate the proportion of deaths from 12 cancers associated with smoking.

The researchers estimated that smoking may account for half of these cancer deaths overall.

Unsurprisingly, lung cancer was most strongly associated with smoking (accounting for 80% of deaths), followed by cancers of the mouth and throat.

It is important to note, however, that these are just estimates based on data taken from previous studies, which may have various limitations. Therefore, we cannot be certain that these figures on the proportion of cancers caused by smoking are 100% accurate – or directly applicable to the UK.

The results still make for sobering reading, with the World Health Organization (WHO) estimating that smoking kills nearly 6 million people a year worldwide, due to cancer and other diseases, such as heart disease.

If you are a smoker, the best thing you can do for your health is to stop smoking.

Where did the story come from?

This study was by researchers from the American Cancer Society in Atlanta; Harvard Medical School in Boston; National Cancer Institute in Bethesda, Maryland; and Fred Hutchison Cancer Research Center in Seattle. The analysis part of this work was funded by the American Cancer Society.

The study was published in the peer-reviewed medical journal JAMA Internal Medicine.

The Mail Online’s reporting of the study was accurate. However, one of the background quotes from the lead author – “e-cigarettes are now the most common form of tobacco use among high school students” – is open to criticism, as e-cigarettes do not contain any tobacco.

 

What kind of research was this?

This study was titled as a research letter, and the researchers used data from previous studies to estimate the proportion of deaths from 12 different cancers in the US in 2011 that could be attributed to smoking. 

The researchers say that the 2014 US Surgeon General’s Report estimated the number of cancer deaths overall and lung cancer deaths specifically that were caused by smoking. However, they missed out the other 11 that are reported to be caused by smoking. Previous data on smoking deaths due to these cancers is said to come from 10 or more years ago. Since then, smoking prevalence has decreased, but risk of cancer among smokers can increase over time. Because of this, the study aimed to look at more up-to-date information on specific cancer deaths in 2011.

The research used data from various previous studies and surveys. Specific methods on how these studies were identified and selected is not reported in this brief publication; therefore, it is not possible to comment on whether all relevant evidence will have been considered.

systematic review would probably have provided more detailed information. However, these types of reviews can be both expensive and time-consuming, and some research teams just don’t have the resources to carry them out.

 

What did the research involve?

The researchers obtained information on smoking prevalence from the 2011 National Health Interview Survey. This was based on interviews from a nationally representative sample.

Age- and sex-specific cancer risk for former and current smokers came from cohort studies that had assessed smoking in questionnaires, and then followed the people up looking for risk of cancer and cancer deaths. One data source was the Cancer Prevention Study II, which included people aged 35 to 54 years (covering the follow-up period 1982-88), and the source for other age groups was the Pooled Contemporary Cohort (follow-up period 2000-11) which has pooled data from five cohorts.

Using information from these data sources, the researchers calculated the population attributable fraction (PAF) of smoking for different cancer deaths. The PAF is the proportion of the number of deaths that are caused by smoking, or by what proportion the number of deaths would be reduced if there was no smoking. 

 

What were the basic results?

In 2011, there were 345,962 cancer deaths in adults aged 35 or over with the 12 different cancer sites examined. The researchers estimated that 167,805, or 48.5% (95% confidence interval (CI) 46.2 to 51.2%), of these overall cancer deaths were caused by cigarette smoking. Smoking accounted for 51.5% of cancer deaths in men and 44.5% of cancer deaths in women.

By far the largest proportions of smoking-attributable deaths were cancers of the lungs and airways. 80% of these cancer deaths – broken down as 83% for men and 76% for women – were estimated to be caused by smoking. The second highest proportion was for cancers of the larynx (vocal cords), where smoking accounted for 77% (72% in men and 93% in women).

Smoking accounted for around half of all deaths of the mouth, throat and oesophagus (food pipe), and just under half of bladder cancers.

Smoking was attributable to around a quarter of cervical and liver cancers.

The remaining cancers examined where the PAF of smoking was less than 20% were those of the kidney, pancreas, stomach, bowel, and a type of leukaemia.

 

How did the researchers interpret the results?

The researchers conclude, “Cigarette smoking continues to cause numerous deaths from multiple cancers, despite half a century of decreasing prevalence. The smoking downturn is likely reflected in the generally lower proportions of deaths caused by smoking in 2011 than in 2000 to 2004”.

 

Conclusion

This study has used data from previously published cohort studies and national surveys to estimate the proportion of cancer deaths that can be attributed to smoking in men and women. They examined 12 cancers that are already known to be associated with smoking and estimated that smoking may account for half of them overall. The vast majority of cancers of the lungs and airways were estimated to be caused by smoking.

It is important to note that these are only estimates. The study has used data from cohort studies to inform the risk of different cancers in former and current smokers, and those who have never smoked. However, these cohort studies may have various inherent limitations and potential biases in their designs, which cannot be analysed here. For example:

  • the populations studied may not be representative of everyone
  • the follow-up period may be too short to capture all newly developed cancers and cancer deaths caused by smoking
  • they may not have taken into account other confounders (e.g. alcohol intake, diet and physical activity)
  • there may be inaccuracies around assessments of lifetime smoking habits
  • they may not have been able to assess the effects of passive smoking from environmental exposure

Specific methods on how the cohorts and national survey were identified and selected are not reported in this brief publication. It is likely that the researchers will have selected the best available and most nationally representative evidence on which to form estimates. However, this cannot be assumed, and it is not possible to comment on whether all relevant evidence will have been considered.

Another point to bear in mind is that the cancers studied were selected as they are known to be linked to be smoking. It is possible that other cancers may be associated with smoking that are currently less well recognised. It is worth again highlighting that these are estimates for the US population – not the UK.

Despite limitations in terms of whether this study provides accurate estimates on the proportion of these cancer deaths that are caused by smoking, it nevertheless reinforces the health message. Smoking is known to have many detrimental effects on health, not only on risk of cancer, but for many other chronic diseases.

As the researchers conclude, “more comprehensive tobacco control, including targeted cessation support” seem to be an important way forward.

Even if you have been a smoker for many years, quitting will still provide a tremendous health benefit. For example, 10 years after you've stopped smoking, your lung cancer risk is half that of someone who has continued to smoke.

Read more methods you can use to quit smoking

Links To The Headlines

Half of all deaths from 12 different cancers are caused by smoking, study finds. Mail Online, June 17 2015

Links To Science

Siegel RL, Jacobs EJ, Newton CC, et al. Deaths Due to Cigarette Smoking for 12 Smoking-Related Cancers in the United States. JAMA Internal Medicine. Published online June 15 2015

Categories: NHS Choices

Knee surgery 'waste of time', researchers argue

NHS Choices - Behind the Headlines - Wed, 17/06/2015 - 12:50

"Knee surgery is 'pointless and potentially harmful' for thousands of patients," the Daily Mirror reports.

Researchers have looked at previous studies that had compared arthroscopic (keyhole) knee surgery with exercise or sham surgery (placebo) for middle-aged people with knee pain – specifically, knee pain caused by osteoarthritis or a tear in the cartilage, but not those with a ligament condition.

They found that both exercise and arthroscopy improved knee pain. Arthroscopy was slightly better, improving pain by a small amount, which was described as the equivalent to using a painkiller such as paracetamol or ibuprofen. There was no difference between the interventions for function of the knee.

Current UK guidelines recommend arthroscopy for people with knee osteoarthritis and a clear history of "mechanical locking", where a person is unable to bend or straighten the knee. People with this symptom were not analysed separately in this research, so it remains unclear whether this recommendation would change on the basis of this study.

Patient satisfaction reported after surgery appears to be positive.

Whether surgery is an option for you or not, UK guidelines recommend that all people with osteoarthritis should do exercise for local muscle strengthening and general aerobic fitness purposes.

 

Where did the story come from?

The study was carried out by researchers from the University of Southern Denmark, Copenhagen University Hospital, Odense University Hospital in Denmark and the University of Lund in Sweden. It was funded by the Swedish Research Council.

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

The UK media’s reporting of the story was possibly a little over-dramatic and gave the impression that these results would lead to a change in clinical guidelines. The Daily Telegraph said keyhole knee surgery "does little good and could kill patients". The Mail Online reported that experts were saying: "Surgeons should stop carrying out keyhole knee operations on middle-aged and elderly people."

The review concluded that the evidence did not support keyhole knee surgery for middle-aged or older patients with knee pain, with or without signs of arthritis, but this is not official advice.

This study is new, and while it may stimulate discussion about whether current advice is appropriate, it will not change it overnight. This research needs to be considered in light of all other evidence.

 

What kind of research was this?

This was a systematic review of randomised controlled trials (RCTs) on the benefits of arthroscopy for knee pain in middle-aged and older people. It included a meta-analysis, which pooled the results of the studies. This type of study can provide a clearer picture of clinical effectiveness than individual studies. It involves systematically identifying all the available evidence, assessing the quality and summarising the findings.

Arthroscopy is a type of keyhole surgery for the knee. It can be used to remove a damaged section of the cartilage (partial meniscectomy) or for removing any dead tissue that might be floating in the fluid of the knee joint and causing the knee to lock (debridement).

 

What did the research involve?

The researchers searched five medical databases, including Medline and Embase, for RCTs on the benefits of arthroscopy for people with or without osteoarthritis. The reference list of any relevant study was also reviewed, in an attempt to capture all available trials. They looked for any studies published up to 2014.

When looking at the potential harm of arthroscopy, they limited the time period to after the year 2000, due to surgical and anaesthetic advances in technique. They also opened up the search criteria to include adverse events reported in observational studies, as well as RCTs.

Two researchers independently sifted all of the results, which is important for reducing any potential bias.

Studies were excluded if the person had a ligament injury.

 

What were the basic results?

Nine trials were identified in which arthroscopy was compared to sham surgery or exercise. Sham surgery, sometimes called "placebo surgery", is the surgical equivalent of using a placebo pill to test a new drug. Sham surgery is thought to offer no benefit to the patient, but typically contains the same pre- and post-surgery elements of real surgery. These included a total of 1,270 people aged 49.7 to 62.8 years.

Both arthroscopy and exercise were shown to substantially improve symptoms. Arthroscopy was slightly better than control conditions for pain 3 to 24 months post-op. This difference was 2.4mm on a 0 to 100mm visual analogue scale for pain – essentially, a sliding scale of reported pain ranging from entirely pain-free to intolerable pain (95% confidence interval (CI) 0.4 to 4.3). There was no difference in physical function between arthroscopy or control conditions.

Arthroscopy was associated with side effects that included:

  • deep vein thrombosis (4.13 occurrences per 1,000 procedures) – a blood clot that usually develops in the blood vessels of the legs
  • pulmonary embolism (1.45 occurrences per 1,000 procedures) – a blood clot that develops inside the lungs
  • infection (2.11 occurrences per 1,000 procedures)
  • death (0.96 occurrences per 1,000 procedures)

 

How did the researchers interpret the results?

The researchers concluded that: "The small inconsequential benefit seen from interventions that include arthroscopy for the degenerative knee is limited in time and absent at one to two years after surgery. Knee arthroscopy is associated with harms. Taken together, these findings do not support the practise of arthroscopic surgery for middle-aged or older patients with knee pain with or without signs of osteoarthritis."

 

Conclusion

This systematic review has found there is little difference between arthroscopy and exercise in the treatment of knee pain, excluding people with damage to their ligaments. Both arthroscopy and exercise improved symptoms for people with and without osteoarthritis. However, there were rare but serious risks associated with the arthroscopy procedure.

In 2008, the National Institute for Health and Care Excellence (NICE) produced a guideline on the treatment of osteoarthritis and recommended that "referral for arthroscopic lavage and debridement should not be offered as part of treatment for osteoarthritis, unless the person has knee osteoarthritis with a clear history of mechanical locking". This systematic review did not separately analyse results for people with a history of mechanical locking – where a person is unable to bend or straighten the knee, which can occur when the cartilage is torn. Therefore, it is unclear whether this recommendation would change following this piece of research.

Before consenting to any type of surgery, it is recommended that you ask your surgeon or clinical in charge of your care for an explanation of both the potential benefits and risks of surgery, so you can make an informed decision.

The NHS Choices Health A-Z section contains details of the most widely used types of surgery. 

Links To The Headlines

Knee surgery is 'pointless and potentially harmful' for thousands of patients says study. Daily Mirror, June 16 2015

Common knee surgery only has 'inconsequential benefits', experts say. The Independent, June 17 2015

Is keyhole knee surgery HARMFUL? Negative consequences of operations in middle-aged or older patients said to outweigh long-term benefits. Mail Online, June 17 2015

Keyhole knee surgery 'does little good and could kill patients’. The Daily Telegraph, June 16 2015

Links To Science

Thorlund JB, Juhl CB, Roos EM, Lohmander LS. Arthroscopic surgery for degenerative knee: systematic review and meta-analysis of benefits and harms. BMJ. Published online June 16 2015

Categories: NHS Choices

Could avocados hold the key to treating leukaemia?

NHS Choices - Behind the Headlines - Wed, 17/06/2015 - 12:22

"Avocados could hold the key to helping beat rare form of leukaemia," The Independent reports; specifically acute myeloid leukaemia, which is an uncommon and aggressive cancer of the white blood cells.

The headline may give readers the impression that eating avocados may help fight leukaemia, which is not the case. Researchers were actually looking at a compound found in avocado seeds that is not eaten, called avocatin B, which appears to be effective against leukaemia cells in the laboratory.

The researchers tested 800 compounds against human leukaemia cells. Avocatin B was the most effective compound to cause the leukaemia cells to die. It did not have an effect on normal blood cells.

This is an exciting discovery and there are now plans to use this compound to begin development of a new drug, though of course this will be a long road.

Current treatments for leukaemias involve chemotherapy and, in some cases, stem cell transplants (previously, and somewhat inaccurately, known as bone marrow transplants). Stem cell transplants offer the chance of a cure. People aged between 16 and 30 can join the stem cell register, and if you are a match for a patient, you could save their life. The register is managed by the Anthony Nolan charity and you can find out how to register here.

 

Where did the story come from?

The study was carried out by researchers from the University of Waterloo and Mount Sinai Hospital in Canada and the University of Perugia in Italy. It was funded by the Leukemia & Lymphoma Society of Canada, the Natural Sciences and Engineering Research Council of Canada and the Canadian Institutes of Health Research.

The study was published in the peer-reviewed medical journal Cancer Research.

The media in general have reported on the study accurately though have not pointed out that the compound avocatin B was obtained from the seed of the avocado and not from the flesh that is eaten.

So headlines such as "An avocado a day keeps leukaemia away" are inaccurate and misleading.

 

What kind of research was this?

This was a laboratory study looking at the effect of an avocado extract on acute myeloid leukaemia.

Acute myeloid leukaemia is an aggressive cancer of the blood. Blood cells are made in the bone marrow from stem cells – the type of cells that are not specialised and can divide and produce a wide range of specialised cells. In acute myeloid leukaemia, there is an overproduction of myeloid white blood cells, which are usually involved in fighting infections.

When this system goes into overdrive, the bone marrow releases large numbers of immature myeloid blood cells into the circulation. They do not continue to develop into normal myeloid blood cells. The production of large numbers of these cells causes a reduction in the production of normal blood cells, which leads to the symptoms of leukaemia.

 

What did the research involve?

The researchers tested 800 natural health products against human acute myeloid leukaemia cells in the laboratory.

Human acute myeloid leukaemia cells were obtained and grown in dishes. They were then exposed to each of the products.

The most effective compound at causing leukaemia cell death was then tested on normal blood stem cells. These samples of peripheral blood stem cells were collected from healthy volunteers. They had been given a drug called G-CSF, which stimulates the body to produce increased numbers of these stem cells from the bone marrow and release them into the circulation.

The researchers then injected acute myeloid cells exposed to avocatin B into mice. They compared their ability to grow and develop in the bone marrow with acute myeloid cells that had not been exposed.

 

What were the basic results?

The compound avocatin B was effective in causing leukaemia cells to die. It was particularly effective against immature myeloid blood cells. It did not affect normal peripheral blood stem cells. When the researchers treated immature myeloid cells with avocatin B, their ability to develop in the bone marrow of mice was reduced.

The study authors say that previous research has found that the immature myeloid blood cells found in leukaemia contain more mitochondria than normal blood cells. Mitochondria are the specialised compartments in cells that generate energy. The experiments seemed to indicate that it was this difference that caused avocatin B to be effective against the leukaemia cells rather than normal blood cells.

Avocatin B is a compound made of two 17-carbon lipids that was extracted from avocado pear seeds.

How did the researchers interpret the results?

The researchers concluded that their laboratory studies demonstrated that avocation B "induced selective toxicity toward leukaemia and LSCs [leukaemia stem cells] with no toxicity toward normal cells".

 

Conclusion

This study has identified a compound that may lead to a new drug for treating acute myeloid leukaemia. As the research has only so far been conducted in a laboratory setting, it should be stressed that this is the beginning of a long road in drug development and may not necessarily lead to a successful treatment.

It is also important to note that the compound was extracted from the seed of the avocado and not from the flesh.

Current treatments for leukaemias involve chemotherapy and in some cases stem cell transplants.

Stem cell transplants offer the chance of a cure. People aged between 16 and 30 can join the stem cell register, managed by the Anthony Nolan charity, and if you are a match for a patient, you could save their life. Most people can donate stem cells via their blood, a process similar to donating blood itself. This is known as peripheral blood stem cell collection and is both painless and extremely safe.  

Links To The Headlines

Avocados could hold the key to helping beat rare form of leukaemia. The Independent, June 16 2015

How avocado could help fight CANCER: Fat from the fruit 'targets leukaemia cells and stops them growing' - raising hopes for a new drug. Mail Online, June 16 2015

Links To Science

Lee EA, Angka L, Rota SG, et al. Targeting Mitochondria with Avocatin B Induces Selective Leukemia Cell Death. Cancer Research. Published online June 15 2015

Categories: NHS Choices

Four out of ten Brits may naturally show fewer flu symptoms

NHS Choices - Behind the Headlines - Tue, 16/06/2015 - 14:00

Thinking of throwing a sicky? Your usual alibi might be a little less convincing after today’s report by The Independent that "Four in 10 Britons immune to flu symptoms, leading to hopes of a new vaccine".

A survey of 1,414 people found that 43% of them had a type of immune cell – T cells – that partially protects against the symptoms of a flu infection.

Researchers found that T cells target specific parts of the flu virus machinery, called nucleoprotein. So the lucky 43% had less flu symptoms after becoming infected.

The logic is that if people have fewer symptoms, they are less likely to spread the virus through coughs and sneezes, and this may slow the spread of both seasonal and pandemic flu strains, such as swine flu. The logic is plausible, but was not directly tested in this study.

The research team suggested vaccines that boost T cell numbers might be worth exploring as an alternative to those that try to stop flu virus infection altogether.

An added potential benefit of their finding was that protection from symptoms of one virus strain showed similar signs in another. That said, only two virus types were tested, so we don’t know whether this "cross-reactivity" is widespread.

We know coughs and sneezes spread diseases, but do you know what to do about it? Read how to prevent flu

 

Where did the story come from?

The study was led by researchers from University College London and was funded by a large range of charity, government and university sources, including the Medical Research Council, the British Heart Foundation and Cancer Research UK. 

The study was published in the peer-reviewed American Journal of Respiratory and Critical Care Medicine.

Generally, the UK media reported the story accurately. Hope of a new vaccine was widely discussed by the media. This was not investigated in the study, so remains speculative at this stage.

 

What kind of research was this?

This was a cohort study looking to understand naturally existing resistance to the symptoms of flu in the hope the knowledge might one day be useful in lessening the spread of seasonal and pandemic flu.

The study authors say that a high proportion of flu (influenza) infections do not cause flu symptoms like coughing and sneezing – which is the main way the virus spreads from person to person.

Animal, human and observational studies suggest T cells, part of the immune system, are involved in lessening flu symptoms in some people, but the impact of this at a population level is not known.

The T cells are thought to target an important part of the flu virus machinery called nucleoprotein. Nucleoprotein exists across many strains of flu virus, so T cell-linked immunity against this key part of the virus may help to confer protection from symptoms for a wide range of different strains. If true, the hope is this might be harnessed to form a more effective vaccine and limit the spread of both seasonal and pandemic flu through coughs and sneezes.

 

What did the research involve?

The researchers measured flu-specific T-cells in an English population cohort during seasonal and pandemic periods between 2006 and 2010.

A total of 1,414 unvaccinated individuals had T cell measurements. They were part of a "Flu Watch Study". The study recruited successive groups each year via random selection of households from general practice registers across England.

Blood samples were taken prior to the natural circulation of flu virus to measure baseline antibody and T cell responses. Participants were then followed up intensively over the flu season to determine who got ill with flu. This involved weekly follow-up from late autumn to late spring, using automated telephone calls or emails.

Nasal swabs were also taken and analysed in the laboratory to confirm flu infection.

 

What were the basic results?

The study found people with T cells targeting flu virus nucleoprotein before exposure to the virus generally had less symptomatic disease (odds ratio, 0.27; 95% confidence interval, 0.11 to 0.68) during pandemic and seasonal periods.

They found T cells reacting to a specific flu virus (H3N2) also reacted to a different one (H1N1).

Influenza-specific T cell responses were detected in 43% of people, indicating a lot of people carried some level of immunity that showed lesser symptoms.

This link was independent of baseline antibodies. The antibodies actually help prevent flu infection, whereas the T cells are involved in lessening symptoms. So this confirmed people were still getting infected, but symptoms were varying in line with T cell characteristics.

 

How did the researchers interpret the results?

"Naturally occurring cross-protective T cell immunity protects against symptomatic PCR-confirmed disease in those with evidence of infection and helps to explain why many infections do not cause symptoms. Vaccines stimulating T cells may provide important cross-protective immunity."

 

Conclusion

A study of 1,414 unvaccinated people showed those with T cells targeting virus nucleoprotein still got infected by flu, but had fewer symptoms. The logic is that people with fewer symptoms are less likely to spread the virus through coughs and sneezes, which may slow the spread of both seasonal and pandemic flu strains.

This is plausible, but was not directly tested in this study, so we don't know if it's true in real life. The research team suggested vaccines that boost T cell numbers might be worth exploring, as an alternative to those that try to stop virus infection altogether. An added potential benefit of their finding was that lessened symptoms in one virus strain showed similar signs in another.

That said, only two virus types were tested, so we don't know whether this "cross-reactivity" is more widespread.

The findings suggest around 43% of people had some form of this natural immunity, but it's not clear if this is across a broad range of flu viruses or just a couple.

The study is encouraging, but is in its early stages of understanding, raising as many questions as it answers. For example:

  • Is it possible to boost this natural symptom immunity in those that have it?
  • How common is this natural immunity in the public?
  • Is it possible to transfer this symptom immunity to those that don’t have it?
  • How useful is this at preventing new cases of flu or deaths from flu?

If you are particularly vulnerable to the effects of a flu infection due to factors such as having a chronic disease or being aged 65 or over, then you should take advantage of the seasonal flu vaccine. Read more about who should get the “flu jab”

Links To The Headlines

Four in 10 Britons immune to flu symptoms, leading to hopes of a new vaccine. The Independent, June 16 2015

Half 'have natural flu protection'. BBC News, June 15 2015

Never had flu? That's because half of us are immune to its symptoms: Findings raise prospect of jab to reduce severity of all types of the illness. Mail Online, June 16 2015

New flu jab could prevent future pandemics. The Times, June 16 2015

Four in 10 Brits immune to flu symptoms raising hopes of new vaccine. The Daily Telegraph, June 15 2015

Links To Science

Hayward AC, Wang L, Goonetilleke N, et al. Natural T Cell-mediated Protection against Seasonal and Pandemic Influenza. Results of the Flu Watch Cohort Study. American Journal of Respiratory and Critical Care Medicine. Published online June 15 2015

Categories: NHS Choices

Eating chocolate may slightly lower your risk of stroke

NHS Choices - Behind the Headlines - Tue, 16/06/2015 - 12:00

“Two chocolate bars a day can SLASH the risk of heart disease and stroke,” the Daily Mirror reports.

The headline is prompted by the results from a large study involving Norfolk residents, investigating how chocolate is linked to cardiovascular diseases. These are diseases that affect the heart and blood vessels, such as coronary heart disease and stroke.

By comparing the highest chocolate consumers with complete chocolate abstainers, they found that chocolate was linked to a lower risk of stroke and cardiovascular disease. However, the risk for coronary heart disease was not statistically significant, so the aforementioned results could have been down to chance.

The biggest caution in taking these results at face value is the possibility that some of the benefits linked to chocolate are actually linked to the person being generally healthier overall.

There were signs of this in the study. For example, the researchers found that higher chocolate consumption was linked to some healthy qualities and behaviours, such as being more physically active.

It is also important not to overlook the large amounts of fat and sugar in chocolate that can contribute to weight gain. If you are overweight or obese, by definition, your weight is probably damaging your health and eating lots of chocolate will make the problem worse.

Read more about how to maintain a healthy weight

 

Where did the story come from?

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

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

The story was very widely reported by the UK media. Generally, the study facts were reported accurately, but the wider implications and inherent limitations of the study were not fully explained. For example, most coverage correctly said that study participants reporting higher chocolate consumption were generally healthier in many other ways, but did not explain how this makes it particularly hard to attribute any health benefits to chocolate on its own.

BBC News provided a useful quote from an independent expert, Dr Tim Chico: "The message I take from this study is that if you are a healthy weight, then eating chocolate (in moderation) does not detectably increase risk of heart disease and may even have some benefit. I would not advise my patients to increase their chocolate intake based on this research, particularly if they are overweight."

 

What kind of research was this?

This was a prospective cohort study looking at the effect of eating chocolate on cardiovascular disease.

Cardiovascular disease is a general term that describes a disease of the heart or blood vessels, and is one of the UK's largest causes of death.

There are four main types of cardiovascular disease. They are:

  • coronary heart disease – when the flow of oxygen-rich blood to the heart is blocked
  • stroke – when blood supply to the brain is blocked
  • peripheral arterial disease – when bloodflow to your limbs, usually your legs, are blocked
  • aortic disease – problems with the aorta, the largest blood vessel in the body, which takes blood from your heart to the rest of your body, which may need to be treated with an aortic valve replacement

Chocolate, more so the dark variety, contains flavonoids. These are plant chemicals that have antioxidant properties, that many speculate give it health-promoting properties, including keeping hearts and blood vessels healthy.

Small experimental and observational studies, the Aberdeen researchers report, indicate that chocolate might be good for heart and blood vessel health, but the picture is not clear, as these studies have design limitations. This research group wanted to use a large group of people, tracked over a long period of time, to improve the evidence base and better understand if chocolate might be affecting cardiovascular disease risk in real life.

 

What did the research involve?

The researchers analysed data from a cohort study, which assessed chocolate consumption at baseline and then followed people over an average of 11 years to see who developed cardiovascular disease. They then supplemented this research with a systematic review and meta-analysis of literature.

Researchers analysed data from 20,951 adult men and women taking part in the EPIC-Norfolk study, a large UK-based cohort study started in the 1990s to look at the connection between diet, lifestyle factors and disease. Average chocolate intake was measured once at the start of the study, before people were tracked over decades, to see if they developed or died from cardiovascular disease. The main analysis looked at how chocolate consumption affected the risk of developing or dying from cardiovascular disease, taking into account a range of other known risk factors, like smoking and alcohol consumption.

EPIC-Norfolk cohort participants are men and women who were aged between 40 and 79 when they joined the study, and who lived in Norwich and the surrounding towns and rural areas. They have been contributing information about their diet, lifestyle and health through questionnaires and health checks over two decades.

Chocolate consumption was measured at a single point in time at the start of the study (1993 to 1997). They were asked to indicate which foods they ate from a large list and how often.

Three questions from the food questionnaire related to chocolate consumption:

  • “Chocolates singles or squares” (average portion size of 8g)
  • “Chocolate snack bars – for example, Mars, Crunchie” (average portion size of 50g)
  • “Cocoa, hot chocolate (cup)” (average portion size of 12g powder weight; the liquid to make up the beverage was not included)

Frequency categories were multiplied by the portion size to get the amount of chocolate eaten daily (g/day). The sum of the weights of these food items consumed, rather than their flavonoid or cocoa content, were the important measure in this study. 

This average daily chocolate consumption was divided into five equal groups, from highest consumption to lowest. The lowest group didn’t eat or drink any chocolate at all and acted as the comparison group.

After the food questionnaire, participants were tracked for a mean average of 11.3 years to see if they developed or died from cardiovascular disease, coronary heart disease or stroke.

Both admission to hospital and deaths due to these conditions were included in the analysis.

After some people were excluded because of missing data, extreme chocolate intake (thought to be an error), or pre-existing cardiovascular disease, it left 20,951 people for the analysis.

The analysis adjusted for a range of common confounders associated with cardiovascular disease, including:

  • gender
  • age
  • smoking
  • physical activity
  • energy intake
  • alcohol
  • body mass index (BMI)
  • systolic blood pressure
  • LDL cholesterol (bad cholesterol)
  • HDL cholesterol (good cholesterol)
  • having diabetes
  • C-reactive protein – a protein associated with inflammation inside the body

To supplement the EPIC-Norfolk-derived results, the researchers also carried out a systematic review and meta-analysis of research related to chocolate and cardiovascular disease.

 

What were the basic results?EPIC

Higher chocolate consumption was associated with lower age, more physical activity and lower prevalence of diabetes mellitus.

Higher chocolate consumption was more common in men and among smokers. Higher chocolate intake was associated with a higher energy intake, with lower contributions from protein and alcohol sources, and higher contribution from fat and carbohydrates.

The percentage of participants with coronary heart disease in the highest and lowest fifth of chocolate consumption was 9.7% and 13.8%, and the respective rates for stroke were 3.1% and 5.4%.

The confounder-adjusted risk of coronary heart disease was 9% less for those in the top quintile of chocolate consumption (16 to 99g/ day) compared with those not consuming chocolate (hazard ratio (HR) 0.91, 95% confidence interval (CI) 0.80 to 1.04). The confidence interval spans 1, meaning this result could be due to chance alone.

By contrast, chocolate consumption in the highest consuming group was associated with significantly less risk for stroke (HR 0.78, 95% CI 0.63 to 0.98) and cardiovascular disease (defined as the sum of coronary heart disease and stroke, HR 0.89, 95% CI 0.79 to 1.00) compared with chocolate abstainers.

Systematic review

The systematic review and meta-analysis included eight studies (seven cohort studies, one randomised control trial). These were combined with results from the EPIC-Norfolk study to get pooled results (total 157,809 participants).

The studies measured chocolate consumption in different ways, adjusted for different confounders, and measured different health outcomes related to cardiovascular disease. Consequently, only similar studies were combined in meta-analyses.

Overall, the different meta-analysis showed that:

  • chocolate consumption was linked with significantly lower risk of coronary heart disease across five studies (pooled relative risk (RR) 0.71, 95% CI 0.56 to 0.92)
  • the risk of coronary heart disease mortality from one study showed no significant difference with and without chocolate consumption (RR 0.98, 95% CI 0.88 to 1.10).
  • for risk of stroke with chocolate consumption, there was significantly lower risk of both stroke incidence (pooled RR 0.79, 95% CI 0.70 to 0.87; five studies) and mortality (RR 0.85, 95% CI 0.74 to 0.98; one study)
  • there was a lower risk of any cardiovascular event (pooled RR 0.75, 95% CI 0.54 to 1.05, two studies, not statistically significant) and cardiovascular mortality (pooled RR 0.55, 95% CI 0.36 to 0.83; three studies, statistically significant)

 

How did the researchers interpret the results?

The research authors said: “Cumulative evidence suggests that higher chocolate intake is associated with a lower risk of future cardiovascular events, although residual confounding cannot be excluded. There does not appear to be any evidence to say that chocolate should be avoided in those who are concerned about cardiovascular risk”.

 

Conclusion

This study used a large prospective cohort of English residents to estimate the risk chocolate poses to cardiovascular death and disease. In addition, they systematically combed the research literature for other similar studies, combining their results with that of other researchers.

By comparing the highest chocolate consumers with chocolate abstainers, they found that chocolate was linked to a lower risk of stroke and cardiovascular disease. The risk for coronary heart disease was not statistically significant.

Results from the meta-analysis of eight additional studies showed higher chocolate consumption was linked with lower risk of cardiovascular disease, stroke and death from cardiovascular disease. Two studies showed cardiovascular events were not statistically linked with chocolate consumption.

The biggest reservation for believing these results is the possible role of residual confounding, rightly highlighted by the study authors themselves. In the cohort study part, chocolate consumption was linked to a range of healthy qualities and behaviours, such as lower blood pressure and more physical activity. There is a real possibility that some of the benefits linked to chocolate are actually linked to the person being generally healthier in other ways.

The researchers did their best to account for this using standard statistical techniques, but the possibility remains.

This is just one explanation. Another is that the flavonoids in chocolate do benefit heart and blood vessel health. Although plausible, this study cannot prove this. There are far too many other elements in the mix to pinpoint the risk reduction observed for chocolate.

The study has a number of other smaller limitations that make its results a little less reliable. Chocolate consumption was measured at a single point in time at the start of the study. This does not take account of changes in chocolate consumption over the following decades. Chocolate consumption was measured without consideration of the flavonoid content. Not all chocolate contains the same amount of flavonoids – thought to be the potential disease-preventing ingredient – so lumping them together could have clouded the picture.

Overall, though the message seems to be that if you are generally healthy, eating a little chocolate probably won’t do any harm, and may in fact do some good, this is not actually proven in this study.

The issue arises when chocolate affects your weight. We know that chocolate is high in sugar and fat, both of which can contribute to weight gain. Being overweight or obese is bad for your health, including your heart and blood vessels. 

Links To The Headlines

Two chocolate bars a day can SLASH the risk of heart disease and stroke. Daily Mirror, June 16 2015

More evidence that chocolate may be good for the heart, say researchers. The Guardian, June 16 2015

Eating two chocolate bars A DAY 'cuts your risk of heart attack and stroke by up to 25%' - and milk is just as good as dark. Mail Online, June 16 2015

Study Links Chocolate To Lower Risk Of Stroke. Sky News, June 16 2015

Two bars of chocolate a day 'lowers risk of stroke and heart disease'. The Daily Telegraph, June 16 2015

Link between eating chocolate and lowered stroke risk. ITV News, June 16 2015

Links To Science

Kwok CS, Boekholdt SM, Lentjes MAH, et al. Habitual chocolate consumption and risk of cardiovascular disease among healthy men and women. Heart. Published online June 15 2015

Categories: NHS Choices

Potential breakthrough for osteoporosis announced

NHS Choices - Behind the Headlines - Mon, 15/06/2015 - 15:25

"Bone could be regrown to treat osteoporosis after breakthrough," The Daily Telegraph reports. This headline follows the development of a new drug that may increase bone formation, which could potentially combat osteoporosis. But this has only been tested in the lab so far and has not yet been proven to work in humans.

The researchers took inspiration from a class of drugs called thiazolidinediones, which are used to treat type 2 diabetes by improving sensitivity to the hormone insulin.

A side effect of these types of drugs is they reduce the number of stem cells that turn into bone-producing cells. The researchers turned this side effect on its head by developing a drug that appears to have the opposite effect, increasing the number of stem cells that develop into bone-producing cells. Another potential positive is that these early results in mice suggest the drug does not appear to have a negative effect on insulin sensitivity.

The drug has so far been tested on human stem cells in the laboratory and in mice over 21 days to look for side effects. While it could potentially regrow bone lost through conditions such as osteoporosis, this has not yet been demonstrated. The drug increased the number of human cells that turned into bone-forming cells, but bone production was not assessed in the mice.

The researchers say their results are promising enough to commence further animal studies. This process takes time, and not all drugs get through these tests. If the drug does prove to be successful and safe enough in animal studies, it would then progress to human trials.  

Where did the story come from?

The study was carried out by researchers from the Scripps Research Institute in Florida and the University of Adelaide. It was funded by the US National Institutes of Health, the Abrams Charitable Trust, and the Klorfine Family Fellowship. The study was published in the peer-reviewed medical journal, Nature Communications.

The Daily Telegraph incorrectly reported that the drug "already exists, because it [is] used in the treatment of diabetes to regulate insulin production". This is not the case – the drug used to treat diabetes causes a reduction in bone formation. The drug in development has been designed to have the opposite effect.

The Telegraph also said the drug "increased the rate of bone grown in mice". While the researchers may now have progressed to testing this, it was not reported to be the case in this study. Even if these tests have now been done, they would not have undergone peer review and publication yet, so we can't judge how robust they are. 

What kind of research was this?

This was a combination of laboratory experiments on human stem cells in the laboratory and in mice.

Peroxisome proliferator-activated receptor gamma (PPARγ) is a receptor present on stem cells, the immature cells from bone marrow that can become different types of cells.

Receptors are protein molecules that react to specific chemical signals, much in the way a lock can be opened by a key.

Stimulation of PPARγ causes the stem cells to turn into adipocytes (fat cells) rather than osteoblasts (the cells involved in bone formation).

A class of drugs called thiazolidinediones, or glitazones, target PPARγ to improve insulin sensitivity for people with type 2 diabetes. A side effect of this drug is that fewer osteoblasts are formed.

A chemical compound called SR1664 develops, which partially blocks the receptor, still improving the insulin sensitivity but without reducing the number of stem cells that turn into osteoblasts.

From this, the researchers have developed another chemical compound called SR2595, which stimulates the PPARγ receptor to have the opposite effect, causing the stem cells to turn into osteoblasts.  

What did the research involve?

The researchers carried out various experiments to look at the structure of PPARγ and how it interacts with SR1664. They used this information to help them design SR2595.

Human stem cells grown in the laboratory were exposed to SR2595, and researchers looked at whether this made the cells become bone-forming osteoblasts.

Mice were given the drug for 21 days to find out whether the SR2595 would worsen insulin sensitivity. The researchers assessed the level the drug reached in the mice's bodies and looked at their insulin sensitivity, as well as food consumption and body weight.  

What were the basic results?

The number of human stem cells that became osteoblasts increased when they were treated with SR2595 in the lab.

Mice given SR2595 did not have any change in insulin sensitivity, fasting insulin levels, food consumption or body weight. 

How did the researchers interpret the results?

The researchers concluded that the results on SR2595 were sufficient to now conduct further animal experiments. 

Conclusion

This research has shown that a new chemical compound called SR2595 appears to stimulate human stem cells in the laboratory to develop into bone-forming cells rather than fat cells.

It is not yet known whether this would occur in humans or other mice. Even if this is the case, it is also not known whether the increased numbers of bone-forming cells would have the desired effect of increasing bone growth for people with osteoporosis.

Early results from mice indicate the compound may not have a negative effect on insulin sensitivity, but this was only assessed over a period of 21 days in seven-week-old mice. Further animal studies of longer duration will be required to evaluate whether the drug works, and then whether it is safe.

While weakening of the bones is often an inevitable part of ageing, there are still steps you can take to improve your bone health. The recipe for strong bones is a healthy balanced diet that includes calcium, exposure to summer sunlight for most of our vitamin D, and regular exercise, as well as avoiding certain risk factors, such as smoking and too much alcohol.

Read more about bone health.

Links To The Headlines

Bone could be regrown to treat osteoporosis after breakthrough. The Daily Telegraph, June 12 2015

New drug could help scientists to regrow bones meaning conditions such as osteoporosis could be treatable. Mail Online, June 13 2015

Links To Science

Marciano DP, Kuruvilla DS, Boregowda SV, et al. Pharmacological repression of PPARγ promotes osteogenesis. Nature Communications. Published online June 12 2015

Categories: NHS Choices

Does owning a cat put your family at risk of schizophrenia?

NHS Choices - Behind the Headlines - Mon, 15/06/2015 - 14:00

“Scientists have discovered a link between people who own cats and the development of mental illnesses, including schizophrenia, and believe a parasite may be to blame,” The Independent reports.

The researchers suggest that toxoplasma gondii (T. gondii), a type of parasite found on infected cats, may be a cause of developing mental illness in later life. T. gondii was blamed for children’s poor reading skills in a study we analysed earlier this month.

The parasite has also been linked to an increased risk of suicide, as we discussed back in 2012.

This latest study used data from over 2,000 families in the United States to look at the number of people who were living with schizophrenia or schizoaffective disorder and owned a cat in childhood. This data was compared to findings of previous studies, conducted by the same study group, with the aim of confirming a link.

A large proportion of study participants were in contact with a household cat as a child, similar to the results found previously.

This study was unable to prove the link between cats and mental illness, and does not give any definite reasons for their observed links. Therefore, we should not be too concerned about the findings.  

 

Where did the story come from?

The study was carried out by researchers from the Stanley Medical Research Institute and Johns Hopkins University, in the United States. Funding was provided by the Stanley Medical Research Institute. No conflicts of interest were declared by the authors. The study was published in the peer-reviewed medical journal Schizophrenia Research.

This story has been reported by a number of UK media sources; however, describing cat ownership as having a “strong link” to schizophrenia is misleading. In fact, there are reports that owning a pet can be of value for some people, in terms of mental health and quality of life, such as older people and patients recovering from major illness.

 

What kind of research was this?

This study used data from a cross-sectional study conducted at the National Alliance for the Mentally Ill (NAMI) annual convention in 1982. Analysis of the responses was carried out to assess whether there was a link between cat ownership and schizophrenia. This type of study is unable to prove cause and effect, but it can show possible associations, which can provide a route for further research.

 

What did the research involve?

The researchers used data from a questionnaire conducted at the NAMI in 1982; participants had a family member with schizophrenia or schizoaffective disorder.

The study included 2,125 questionnaires of families who lived in 46 states and the District of Columbia, and attempted to replicate the findings of their previous research linking cat ownership and mental illness. As no control group was used in the 1982 questionnaire, the researchers used the “middle parents” group from the American Veterinary Medical Association (AMVA), as this population was the most similar to their study group.

Questions included details of pregnancy, childhood and family medical history, and cat and dog ownership up to age 17, including ages of pet exposure.

 

What were the basic results?

The number who owned a cat when the affected person was between birth and age 13 was 50.6%. This result is similar to those found in previous studies in 1992 (50.9%) and 1997 (51.9%). 

Among the “middle parents” control group from the 1992 AMVA, 42.6% owned a cat, which was virtually identical to the controls in the 1997 survey. The difference between the rate of cat ownership in the NAMI families and those in the AVMA control group was significant.

 

How did the researchers interpret the results?

The researchers suggest that cat ownership in childhood is significantly more common in families where the child later develops a chronic mental condition such as schizophrenia. They suggest this link may be due to the parasite T. gondii found on cats. They go on to say, “It is important to ascertain whether or not cat ownership in childhood is a risk factor for later schizophrenia, since it is a risk factor which could be minimised. We therefore urge our colleagues in other countries to collect data on cat and other pet ownership, and a major goal of this paper is to encourage such research”.

 

Conclusion

This study aimed to replicate the researchers' previous findings, which suggest that cat ownership in childhood is a possible risk factor for developing schizophrenia in later life. This study is able to draw a link, but cannot prove cause and effect. There is a suggestion that this link may be due to the parasite T. gondii, which is transferred from cats to humans if they come into contact with the faeces of infected cats, or eating or drinking contaminated food or water.

Even if this link between cats and mental illness was proven to be true, contact is unavoidable; children could become infected by playing in a public play area, even if their family did not own a cat.

This is because the T. gondii parasite can survive in soil for several months.

Is has also been suggested that exposure to cats provides risk in terms of other infectious agents shed by cats or by allergic exposures, since increased levels of childhood allergic reactions have been associated with increased risk of schizophrenia in later life.

The sample in the survey was also not representative of the whole population. NAMI members tended to be middle and upper class socioeconomically and their affected family member tended to be more severely affected than average.

To ascertain whether or not cat ownership in childhood is a risk factor for later-life schizophrenia, further research must be conducted that is able to prove cause and effect. Though the gold standard for evidence-based medicine, a randomised controlled trial would not be possible (we hope) for ethical reasons.

It is thought that schizophrenia is a very complex condition that can arise due to a combination of environmental and genetic factors, so simply owning a cat is unlikely to be a major risk factor for the condition.

Links To The Headlines

Could owning a CAT give you schizophrenia? Study finds strong link. Mail Online, June 12 2015

Scientists find link between cat ownership and schizophrenia. The Independent, June 12 2015

There's A Link Between Cat Ownership And Schizophrenia. The Huffington Post, June 11 2015

Links To Science

Torrey EF, Simmons W, Yolken RH. Is childhood cat ownership a risk factor for schizophrenia later in life? Schizophrenia Research. Published online April 18 2015

Categories: NHS Choices

Marriage health claims are inconclusive

NHS Choices - Behind the Headlines - Fri, 12/06/2015 - 15:00

“Marriage is more beneficial for men than women,” says The Daily Telegraph, while The Guardian reports: “Divorce not bad for your long-term health”. Both headlines are prompted by a new study looking at the long-term effects of relationships on health.

The study used a UK cohort of people born in 1958, who had their relationship status assessed at various younger ages. At age 44-46, they had examinations, where various health markers where measured, including blood inflammatory and clotting factors, lung function and metabolic syndrome (a collection of risk factors that increases risk of cardiovascular disease). 

Generally, men who never married or cohabited seemed to have the poorest health markers in midlife, compared to men who married and stayed married. Meanwhile, women who married in their late 20s to early 30s tended to have the best health markers in midlife. Strangely, there seemed to be the suggestion that divorcing was “good” for men and women by being associated with reduced risk of metabolic syndrome, compared with staying married.

If you are enjoying (or thought you were enjoying) the single life, then you should take these findings lightly. There is likely to be a complex interaction between personal relationships, health and lifestyle factors, and other life events and influences.

It should also be noted that researchers looked at various health indicators, not actual diseases. Therefore, the study does not provide conclusive answers about how marital status may influence health or the mechanisms behind it.

 

Where did the story come from?

The study was carried out by researchers from University College London, London School of Hygiene and Tropical Medicine, and London School of Economics and Political Science. The study received funding from the Economic and Social Research Council, and the National Centre for Research Methods node “Pathways, Biosocial Influences to Health”.

The study was published in the peer-reviewed medical journal American Journal for Public Health.

The study was reported widely in the UK media, with some sources focusing on the apparent difference in health outcomes between married men and women, while others discussed the findings relating to divorce and separation.

The reporting was broadly accurate, though the limitations of the study were not discussed. 

What kind of research was this?

This study used data collected from a large ongoing prospective cohort to look at relationship patterns over the course of a lifetime, and how they were associated with health in midlife.

As the researchers say, various studies from different countries have suggested that married people have better overall health than unmarried people. It has also been suggested that somehow changing any health inequalities relating to marital status could improve population health. However, to do this, the mechanisms linking marital status need to be better understood. That is what this study aimed to look into, by examining changes in partnership status over a 21-year period and its association with health indicators in midlife.

The main limitation of this study is that it cannot prove direct cause and effect, or explain the influence that any relationship changes may have been having. There is likely to be a complex interaction between personal relationships and other health, lifestyle and life events and influences.

 

What did the research involve?

This study used data collected from the British National Child Development Study. This is an ongoing cohort study that included all people born in one week in 1958, and periodically followed them up to adulthood. This study used data collected in four assessments – in 1981 (age 23), 1991 (age 33), 2000 (age 42) and 2002-04 (44-46 years).

Relationship status was recorded at each assessment, and health outcomes measured at the final assessment in 2002-04, when the person had a clinical examination. The markers of health outcomes included looking at inflammatory markers in the blood, measuring lung function, and looking for metabolic syndrome (a collection of risk factors that increases risk of cardiovascular disease). 

In their statistical models looking at how change in relationship status was associated with these various disease markers, they took into account various early life and early adulthood characteristics. This included things such as socioeconomic status and parental occupation, education, health, disability and cognitive status in childhood years.

The overall analysis, including those with complete data, was based on 10,226 people (5,256 women and 4,970 men).

 

What were the basic results?

The researchers split men and women into six groups, according to their partnership status. The most common group of men (62%) were those who married in their 20s or early 30s and had remained married. For women, 42% married in their early 20s and remained married; the next most common group (23%) married later, in their late 20s or early 30s, but remained married. 

Findings in men

Men who never married or cohabited (accounting for 11% of those studied) had generally poorer health markers compared with the most common group of men who married or stayed married. This included poorer lung function and higher levels of certain inflammatory markers and blood clotting factors. Men who had cohabited but not married (8%) also had poorer lung function than those who stayed married. Meanwhile, the 8% of men who married and then divorced and didn’t remarry were less likely to have metabolic syndrome compared with men who remained married. 

Findings in women

In women, the second most common group, who married in their late 20s or early 30s, had the best health. They had lower levels of a blood clotting factor and better lung function than those who married earlier. Meanwhile, women who married but later divorced (9%) were less likely to have metabolic syndrome than the most common group, who married young and stayed married.

 

How did the researchers interpret the results?

The researchers conclude: “Partnership status over the life course has a cumulative effect on a wide range of objectively measured health indicators in midlife.”

 

Conclusion

These findings should be taken quite lightly and should not give cause for concern, regardless of marital status. It is very difficult to draw meaningful interpretations from these findings, with the analyses showing mixed results.

Generally, they found that men who never married or cohabited seemed to have the poorest health markers in midlife, compared to men who married and stayed married. Meanwhile, women who married in their late 20s to early 30s tended to have the best health markers in midlife.

Strangely, there seemed to be the unusual suggestion that divorcing was “good” for men and women by being associated with reduced risk of metabolic syndrome, compared with staying married.

However, this study does not prove cause and effect. There are complex interactions between personal relationships, health and lifestyle factors, and other life events and influences. This study is not able to pull this apart and explain the possible underlying reasons for any links between relationship status and the measured health markers.

Importantly, the outcomes measured are only that – a varied collection of blood inflammatory and clotting factors, lung function and metabolic syndrome. These may increase the risk of, or be associated with, actual diseases, but these indicators are not diseases in themselves. For example, the fact that women who married later had lower levels of a particular blood clotting factor and better lung function than those who married earlier on a single assessment day, does not necessarily mean they are all healthier. These midlife health markers may not be good indicators of this cohort’s future health and disease outlook.

Also, this is a specific cohort of people born in 1958. Their marital status and relationship patterns may not be a good parallel for those from other generations, or from other cultures or countries. For example, people in successively younger generations tend to marry later, or may be less likely to marry than those of older generations.

The findings will be of interest in the fields of human sociology and psychology, and will add to the bulk of existing research looking at how marital status may influence health. However, this study alone does not provide conclusive answers about the nature of any relationship or the mechanisms behind it.

Connecting with other people can improve your mental wellbeing, which could also improve physical health, but we wouldn’t recommend rushing down the aisle based on the results of this study. 

Links To The Headlines

Marriage is more beneficial for men than women, study shows. The Daily Telegraph, June 11 2015

Divorce not bad for your long-term health, study suggests. The Guardian, June 12 2015

Marriage is more beneficial to men than women, study finds. The Independent, June 12 2015

Divorce is no health risk — as long as you find someone else. The Times, June 12 2015

Links To Science

Ploubidis GB, Silverwood RJ, DeStavola B, Grundy E. Life-Course Partnership Status and Biomarkers in Midlife: Evidence From the 1958 British Birth Cohort. American Journal of Public Health. American Journal of Public Health. Published online June 11 2015

Categories: NHS Choices

Half a handful of nuts a day 'reduces early death risk'

NHS Choices - Behind the Headlines - Fri, 12/06/2015 - 13:15

"A handful of nuts can save your life, says new study," The Daily Telegraph reports after a Dutch study found a link between daily nut consumption and a reduced chance of dying from a number of chronic diseases, including cancer and heart disease.

The study assessed the dietary and lifestyle habits of middle-aged to elderly adults from the Netherlands and followed them up over the next 10 years.

Overall, researchers found people who ate nuts had a decreased risk of death from any cause as well as various specific causes, such as cardiovascular diseases and cancer, compared with those who didn't eat any nuts. The most reduced risk was found with the consumption of 5-10g of nuts a day.

However, not all risk reductions were significant and some of the researchers' analyses were based on very small numbers, which means some of the results may not be that reliable.

Also, it is possible nut consumption is just one factor that's part of an overall healthier diet and lifestyle, and people who regularly eat nuts may be healthy in other ways.

Nuts are a good source of healthy unsaturated fats, protein, and a range of vitamins and minerals, so having them as a daily snack isn't a bad idea (provided you're not allergic). Unsalted nuts are the healthiest option. 

Where did the story come from?

The study was carried out by researchers from Maastricht University Medical Centre in the Netherlands, and was funded by the study authors, who report no conflicts of interest. 

It was published in the peer-reviewed journal, the International Journal of Epidemiology.

The UK media's reporting of the study was accurate, though the inherent limitations of the study were not made clear to readers.  

What kind of research was this?

This cohort study aimed to look at how the consumption of peanuts, tree nuts (such as Brazil nuts and almonds) and peanut butter was associated with mortality.

The researchers say nut intake has often been associated with lower mortality, but often studies have focused on cardiovascular outcomes and have not looked at death from other causes. Dose-response relationships are said to remain unclear.

This study looked into this using a large cohort of middle-aged to elderly people, who provided dietary and lifestyle information and were then followed up for 10 years.

The researchers looked at deaths and causes of death. They supplemented this by a search for the results of other similar published cohorts.

But the main limitation with this study is it cannot prove direct cause and effect, and any associations seen could be influenced by other factors. 

What did the research involve?

Data was taken from the Netherlands Cohort Study, which recruited 120,852 middle-aged to elderly men and women (age 55 to 69 years) in 1986.

At enrolment, participants completed questionnaires on dietary intake, medical conditions, smoking and other lifestyle factors. The food frequency questionnaire covered food and drink consumed over the past year.

Nut and peanut butter consumption was assessed by questioning the frequency and portion size of peanuts, other nuts, mixed nuts and peanut butter, and summed to give total nut intake.

The cohort was followed for 10 years until 1996. Information on deaths and causes of death was obtained from Statistics Netherlands and the Central Bureau for Genealogy, which use valid medical codes (the International Classification of Diseases, ICD).

There were 18,091 deaths during the 10-year period. The researchers decided to compare the questionnaires of the people who died (cases) with a random sample of 5,000 people from the cohort who had not died (controls). 

They excluded cases and controls who reported cancer or cardiovascular disease at study enrolment or those with incomplete questionnaire data, leaving a final sample of 10,382 people who died and a comparison group of 3,693 surviving members of the cohort.

They also conducted a supplementary literature search of one medical database to identify other published cohorts looking at links between nut consumption and cause of death. 

What were the basic results?

Overall, the study found the average total nut intake in the cohort was 8.1g a day for men and 4.4g a day for women, with peanut butter 1.4g and 1.2g, respectively.

They found higher nut intake was associated with various other factors, including higher fruit, vegetable and alcohol intake, higher educational level, and, in women, not smoking and a lower body mass index (BMI).

In analyses adjusted for age and various other health and lifestyle factors, the researchers found there was a significant trend for people consuming more nuts to have reduced risk of death compared with those not eating nuts:

  • people eating 0.1-5g daily had a 12% reduced risk (hazard ratio [HR] 0.88, 95% confidence interval [CI] 0.78 to 0.99)
  • people eating 5-10g daily had a 26% decreased risk (HR 0.74, 95% CI 0.63 to 0.88)
  • people eating at least 10g a day had a 23% reduced risk (HR 0.77, 95% CI 0.66 to 0.89)

Looking at specific cause of death, they found trends for the risk of death from the following diseases to be reduced by nut consumption compared with no consumption:

  • cancer
  • cardiovascular diseases overall (and heart disease and stroke specifically)
  • respiratory disease
  • diabetes
  • neurodegenerative diseases (not specified, but includes Alzheimer's disease, for example)
  • other causes of death

However, within the individual disease categories, as with overall deaths, there wasn't a consistent linear pattern where increasing nut consumption was associated with lower risk.

For overall deaths and various diseases, the risk decrease seemed to be lowest for the middle consumption category (5-10g a day).

In some cases, the risk decrease for a particular consumption category just fell short of being statistically significant (one of the confidence intervals touching 1.0 or 1.1), meaning we can't be sure this is a real decreased risk compared with non-consumption.

The researchers found peanut and tree nut consumption were linked with a decreased cause of death, but peanut butter alone was not. Possible reasons given for the differences between nuts and peanut butter were the addition of salt and trans fats in peanut butter.

Combining the results of other studies identified through their literature search found a 15% decreased mortality risk for the highest compared with lowest nut consumption (HR 0.85, 95% CI 0.77 to 0.93).

How did the researchers interpret the results?

The researchers concluded that, "Nut intake was related to lower overall and cause-specific mortality, with evidence for non-linear dose-response relationships. Peanut butter was not related to mortality." 

Conclusion

This Dutch cohort of middle-aged to elderly adults generally found people were less likely to die in the following 10 years if they ate a small number of nuts a day compared with none.

The study has strengths in its large sample size and that cause of death was followed up for the full cohort using valid medical codes.

However, there are various points to bear in mind before we jump to the conclusion that nuts are the magic ingredient that will slash our risk of death.

No clear trends

It is difficult to draw any clear interpretations about how nut consumption may be associated with risk of death overall or from specific causes.

There weren't clear linear trends where increasing consumption was associated with increasingly decreased risk, and often the middle consumption category (5-10g per day) had the lowest risk.

This is roughly a small handful of nuts, depending on the type of nut. Not all of the risk decreases for different consumption categories or diseases were significant, meaning we can't be sure there is any real decreased risk compared with non-consumption.

Small sub-group size

When looking at specific cause of death, some of the analysis was based on very small numbers of people.

The analysis for diabetes came from the comparison of 85 diabetes deaths in the non-consumption group, 46 in the 0.1-5g category, only eight deaths in the 5-10g category, and 19 in the more than 10g category.

Analyses based on such small numbers of people may be less reliable and are more likely to give significant findings by chance.

Use of food frequency questionnaires

Nut consumption was assessed through food frequency questionnaire. Though this is a valid method, it may introduce inaccuracies.

For example, many people may find it difficult to estimate roughly how many nuts, or grams of nuts, they eat a day on average over the course of a year. It is also not clear whether this takes nuts in cooked or baked items into account.

Potential confounders

Although the researchers have adjusted for various medical and lifestyle factors in their analyses, it is still possible that these effects, and other unmeasured factors, have not been fully accounted for.

That is, it is difficult to pin the direct cause of any decreased risk on nuts specifically. If nuts are associated, it is possible they are just one factor in an overall healthier diet and lifestyle.

Lack of information on cause of death

The study has looked at cause of death, but has not explored within these categories. For example, neurodegenerative disease or cardiovascular disease encompasses various diseases and health problems.

Specific population

Though this study involved a large cohort, these people are all a specific population of middle-aged to elderly adults from the Netherlands. The results may not be applicable to younger populations or those from other countries.

This study will add to the wide body of literature looking into the health benefits of different diet and lifestyle patterns.

But nuts aren't for everyone: some people can have severe life-threatening allergic reactions to them. And it doesn't provide proof that nuts alone are the magic health ingredient for a longer life.

Despite constant media reporting, there is no such thing as a single superfood that will prevent ill health and premature death. Eating a daily portion of nuts will do you little good if you smoke, don't take any exercise, drink alcohol to excess, and are overweight or obese.

The best way to stay healthy is to take regular exercise and aim for a healthy and balanced diet that includes plenty of fruit, vegetables and fibre, limited saturated fat, salt and sugar, watch how much alcohol you drink, and avoid smoking.

Links To The Headlines

A handful of nuts can save your life, says new study. The Daily Telegraph, June 11 2015

Snacking On Nuts 'Could Cut Risk Of Early Death'. Sky News, June 11 2015

Snacking on nuts could prevent early death from cancer and heart disease. ITV News, June 11 2015

Half a handful of NUTS a day can prevent early death: Peanuts 'slash risk of cancer, dementia, heart attacks and diabetes'. Daily Mail, June 11 2015

Nuts 'protect against early death'. BBC News, June 11 2015

Eat a few peanuts a day to slash risk of early death. The Times, June 11 2015

Links To Science

van den Bradnt PA, Schouten LJ. Relationship of tree nut, peanut and peanut butter intake with total and cause-specific mortality: a cohort study and meta-analysis. The International Journal of Epidemiology. Published online June 11 2015

Categories: NHS Choices

Could brain-eating cannibals provide the key to treating CJD?

NHS Choices - Behind the Headlines - Thu, 11/06/2015 - 14:00

“Eating brains helped Papua New Guinea tribe become disease resistant,” The Daily Telegraph reports.

Some of the Fore people, who used to eat the brains of dead relatives as a mark of respect, may have developed resistance to prion diseases such as Creutzfeldt Jacob disease (CJD).

Prion diseases occur in humans and animals, and are caused by a build-up of abnormally folded proteins in the brain. Prion diseases can be passed on by eating infected tissue, such as beef that has been exposed to prions. This is known as bovine spongiform encephalopathy (BSE, or “mad cow disease”). There is currently no cure for prion diseases.

A tribe in Papua New Guinea were nearly wiped out by a prion disease called kuru. The infection was spread as a result of their tradition of eating the brains of deceased relatives at their mortuary feasts. Some people were resistant to the infection, and this was thought to be due to a mutation called V127 in the gene encoding the prion protein.

This study used genetically modified mice to test whether this genetic mutation was protective against kuru and CJD. The tests showed that mice with this genetic mutation were indeed resistant to these prion diseases.

The results suggest that this mutation could be responsible for the kuru resistance seen in the survivors. It is hoped this finding may eventually help to develop effective treatments for prion diseases, but much more research will be needed to get to that point.

Links To The Headlines

Eating brains helped Papua New Guinea tribe become disease resistant, claims research. The Daily Telegraph, June 10 2015

Eating human brains helped Papua New Guinea tribe resist disease, research shows. The Guardian, June 10 2015

Scientists find CJD resistance gene. BBC News, June 10 2015

Links To Science

Asante EA, Smidak M, Grimshaw A, et al. A naturally occurring variant of the human prion protein completely prevents prion disease. Nature. Published online June 10 2015

Categories: NHS Choices

Facebook and Twitter could be used to help people quit smoking

NHS Choices - Behind the Headlines - Thu, 11/06/2015 - 13:00

"Using social media to kick the [smoking] habit means you're 'TWICE as likely to succeed'," the Mail Online reports. A study of a Canadian social media campaign aimed at helping young people quit smoking found it was twice as successful as telephone helplines.

The Break It Off (BIO) campaign compared stopping smoking to getting out of a toxic relationship with a terrible boyfriend or girlfriend, and allowed participants to share their progress on Facebook.

Researchers compared the effectiveness of the BIO campaign with anti-smoking telephone helplines. They conducted a trial involving 238 participants aged 19 to 29 who used one of the two methods to stop smoking. After three months, 32% of BIO participants and 14% of the Smokers' Helpline users had quit the habit for 30 days.

But the analysis was only performed on people who completed a survey and not on all of the participants in the study. This and numerous other biases make the results less reliable.

Still, the arguments made by the researchers are persuasive. Many young people do not have access to a landline, so may be unlikely to use telephone helplines, but most young people in developed nations have a smartphone.

This means anti-smoking campaigns aimed at young people may be more effective if they're delivered via social media rather than traditional media formats, such as print and television.  

Where did the story come from?

The study was carried out by researchers from the University of Waterloo, the University of Toronto, and the Canadian Cancer Society, and was funded by research grants from the Canadian Cancer Society Research Institute.

It was published in the peer-reviewed medical journal, Nicotine and Tobacco Research.

The Mail Online reported this story accurately, outlining the worldwide smoking problem and the potential strength of social media in reaching this target audience. But the story did not explain that the results were biased or point out any of the study's limitations.  

What kind of research was this?

This quasi-experimental study aimed to examine the effect of the Break It Off (BIO) social media campaign to help young adults stop smoking, comparing it with the Canadian Smokers' Helpline.

While this study design is appropriate, a randomised control trial would be better as participants would randomly be assigned to groups, reducing the chance of any possible bias.

Any internet-based research is prone to confounding factors, and in this case there were issues with low study recruitment and high loss to follow-up.

What did the research involve?

The study included young adult smokers aged 19 to 29 years from a number of Canadian provinces. Participants took part in one of two interventions aimed at smoking cessation: the Break It Off (BIO) campaign and the Canadian Smokers' Helpline.

The BIO campaign was run by the Canadian Cancer Society, and aimed to provide support and encourage young adults to "break up" with their smoking addiction. Participants were recruited to use the campaign's website between February and September 2012.

The site guided users through the challenging stages of ending an unhealthy relationship with smoking and provided information on quit methods. Visitors could upload a video of their "break-up with smoking" experience, as well as announce their "break-up status" to friends via Facebook. Three months after registration, participants were emailed a link to an online follow-up survey.

BIO participants received a $10 iTunes redemption code as an incentive for registering and another $15 iTunes redemption code when they completed the follow-up survey.

The researchers compared the campaign to the use of the Canadian Smokers' Helpline before September 2011. This is a telephone-based smoking cessation service. It is an established intervention, and provides smokers who want to quit with information, self-help materials, referrals to other resources, tailored motivational counselling, and proactive follow-up counselling.

The helpline was promoted in the media and through referrals from health organisations and professionals. The follow-up survey was conducted via telephone interview between October 2010 and September 2011.

At follow-up, participants were questioned on the following:

  • smoking status
  • cigarette consumption
  • heaviness of smoking (number of cigarettes smoked per day and time of first cigarette in the morning)
  • intention to quit
  • use of any cessation aid
  • whether they had taken at least one action towards quitting

Seven and 30-day abstinence rates were measured at three-month follow-up for both groups. The helpline participants provided the date of the last cigarette they smoked to determine abstinence at three months based on a seven-month follow-up.

Quit rates were based on those participants who completed the follow-up surveys. For both treatment groups, respondents who completed the follow-up survey but did not provide answers to the prevalence questions were considered to be smokers.

Participants were analysed on an intention-to-treat principle. This means participants were analysed in the groups they had been allocated to, regardless of whether they received or adhered to this intervention. 

What were the basic results?

A total of 238 participants completed the study and were included in the analysis. Follow-up rates were low – 34% for the BIO group and 52% for the helpline.

Differences were found between the groups at the start of the study: users of the helpline were more likely to be female, white and have received a high school education or less.

More participants in the helpline group intended to quit in the next 30 days (81% versus 70%) and were much more likely to be daily smokers (82% versus 59%). BIO users had significantly higher seven-day and 30-day quit rates compared with users of the helpline.

The seven-day quit rate for BIO (47%) was more than double that of the helpline (15%) after controlling for confounding factors such as education, ethnicity, and daily or occasional cigarette use. Quit rates at 30 days were 32% for BIO and 14% for the helpline.

BIO participants were more likely to make a quit attempt during the three-month intervention period (91%) compared with helpline participants (79%). Participants in both groups cut down the number of cigarettes smoked – 89% of BIO participants versus 79% in the helpline group.

Having a post-secondary education or higher and only smoking occasionally was found to be associated with an increased odds of quitting smoking.  

How did the researchers interpret the results?

The researchers concluded that, "A large number of young adults prefer a forum such as BIO for help to quit smoking in comparison to traditional quitline services.

"The reach of the campaign and findings on quitting success indicate that a multi-component digital and social media campaign offers a promising opportunity to promote smoking cessation." 

Conclusion

This quasi-experimental study compared the effects of two smoking cessation interventions. The study reported that the use of social media and multi-component digital interventions is more effective in promoting smoking cessation than traditional quitline services.

However, the researchers based their findings solely on the people who completed the final surveys, which will bias the results. This study has a number of other limitations, including the non-random assignment to study group, small sample size, and large loss to follow-up.

The studies were also performed at different time points, which may have affected the results, and some of the BIO participants may also have used the Smokers' Helpline and vice versa. The BIO participants also received incentives for participation, adding more potential for bias.

A very specific target group was included in the study. While this does reduce generalisability, young adults in Canada have the highest rate of smoking, but their use of cessation services is low.

The results of this study are promising and address a major public health issue. A much larger-scale trial needs to be carried out with a longer follow-up period, random allocation, and sub-group analysis for all possible social media and digital platforms to assess which are the most effective in aiding smoking cessation.

As the researchers discuss, smartphone ownership is expected to reach five billion people by 2025. Campaigns based on smartphone use, including social media, are likely to reach a wide audience, as well as being more cost-effective than other methods.

Links To The Headlines

Could Facebook or Twitter help you quit smoking? Using social media to kick the habit means you're 'TWICE as likely to succeed'. Mail Online, June 10 2015

Links To Science

Baskerville NB, Azagba S, Norman C, et al. Effect of a Digital Social Media Campaign on Young Adult Smoking Cessation. Nicotine and Tobacco Research. Published online June 4 2015

Categories: NHS Choices

Does your birthday affect your disease risk?

NHS Choices - Behind the Headlines - Wed, 10/06/2015 - 14:35

"Scientists Find Surprising Link Between Birth Month And Disease Risk," the Huffington Post reports. Using data mining techniques on 1.7 million electronic medical records, US researchers found an association between birth month and certain chronic diseases, as well as less serious conditions such as insect bites.

Fifty-five diseases were found to be associated with birth month – 19 were previously reported in the literature, 20 were for conditions with close relationships to those previously reported, and 16 were new associations.

The newly found associations were a mixed bag, ranging from various cardiovascular diseases (such as high blood pressure and heart failure) and prostate cancer, to incidents such as bruising and insect bites.

The researchers speculate, based on the findings of other studies, why seasonal factors may contribute to specific disease risk, suggesting it could be the result of exposure to antigens such as pollen, varying vitamin D levels, and possibly how old a child is when they first start school. Many unmeasured factors may also be involved in any links.

Overall, this study is not proof that being born in a particular month means you are more or less likely to develop any particular disease. 

But there are effective ways you can reduce your risk of developing chronic diseases in later life. These include stopping smoking, drinking alcohol in moderation, and maintaining a healthy weight through diet and exercise. These steps should help keep your cholesterol and blood pressure at a healthy level. 

Where did the story come from?

The study was carried out by researchers from Colombia University and was funded by National Library of Medicine training grants.

It was published in the peer-reviewed Journal of the American Medical Informatics Association. The study has been published on an open access basis, so it is free to read online or download as a PDF.

This story was covered widely by the press. Most sources took a light-hearted, tongue-in cheek approach, with the Metro saying: "It's still not fully understood why this should be – but just to cheer you up, here's a calendar of the diseases you're at increased risk of, depending on when you're born." 

What kind of research was this?

This modelling study aimed to explore the relationship between season or birth month and lifetime disease risk.

The researchers carried out their study using health record data collected from a large US medical centre database. They say similar studies have focused on looking at associations with specific diseases, so sometimes do not look at rarer diseases.

For this reason, they didn't carry out this research with any particular theory in mind, but just aimed to look at any associations found when looking at millions of records.

This large-scale analysis of massive chunks of data is often referred to as data mining. Data mining is now widely used thanks to improvements in the speed and capabilities of modern computers.

Such a study is good for looking at associations on a large scale, as it can encompass a large number of diseases.

But without testing any particular theory – such as exposure X increases your risk of disease Y – the study can only give us observations and associations. These may not be causative links, and many other unmeasured factors may be involved in any of the links found.  

What did the research involve?

The researchers called their approach the Season-Wide Association Study (SeaWAS), an algorithm looking for diseases with seasonal associations.

They used health record data from the Colombia University Medical Center, where diseases were recorded using standard disease codes (International Classification of Diseases version 9, ICD-9) that were then mapped to specific codes developed for this database (Systemized Nomenclature for Medicine-Clinical Terms, SNOMED-CT).

This coding method is said to capture more medical information than ICD-9 codes and is designed to be transferable across institutions, which will enhance data sharing.

All data was extracted for individuals born between 1900 and 2000 – 1,749,400 people – who were treated at the Colombia University Medical Center between 1985 and 2013. The average age (median) was 38 years.

Analyses were performed to check whether yearly and sex-based variation in the birth month distribution would affect the results. This was found to be minimal.

Associations were investigated between birth month and all recorded conditions. A control group of randomly sampled individuals from the same population without any disease was used to compare monthly birth rate between the case and control populations for each condition.

The study was supplemented by a search of the literature to identify other studies that also looked at links between birth month and disease to see how the SeaWAS findings compared. 

What were the basic results?

The researchers found 55 diseases that were significantly dependent on birth month. Nineteen diseases had been reported in the literature – 20 were for conditions with close relationships to those reported, and 16 were previously unreported.

The 16 previously unreported associations included nine with cardiovascular conditions, such as atrial fibrillation, high blood pressure and heart failure. The remainder included a mixed bag of other conditions, ranging from prostate cancer to coughs, colds and sexually transmitted infections, and bruising and non-venomous insect bites.

Overall, most disease associations were found with October births and the fewest were with May births. Asthma was most associated with July and October babies, and attention deficit hyperactivity disorder (ADHD) with November. March births had most associations with heart problems and winter births with neurological problems. 

How did the researchers interpret the results?

The researchers concluded that, "SeaWAS confirms many known connections between birth month and disease, including: reproductive performance, ADHD, asthma, colitis [bowel inflammation], eye conditions, otitis media (ear infection), and respiratory syncytial virus [a common cause of chest infection in young babies]."

They went on to state they discovered 16 associations with birth month that had never been explicitly studied previously, nine of which were related to cardiovascular conditions. 

Conclusion

This modelling study used a large US medical centre database to explore the relationship between month of birth and lifetime disease risk. The study found a number of associations between birth month and risk of disease, some of which had been previously reported in the literature, as well as other new associations.

While these findings are of interest, this study can only demonstrate observations and associations. The study does not provide proof that being born in any particular month is the direct cause of any future disease development.

There may be many unmeasured factors behind any associations between disease risk and birth month. The study has not been able to look into interactions or explore the lifetime genetic, medical, lifestyle or environmental influences on any individual.

Though the study had strengths in that it used a large medical database where conditions were coded according to a valid system, this is data from just one source. The findings are representative of people from only one region in the US, and they may not be generalisable to other regions or countries.

The researchers addressed this issue and state that the effects observed are likely the result of the climate effects of the region, saying their findings would be most comparable to northern European climates. The researchers hope that lifestyle and diet recommendations can be made once associations are drawn.

But the media reporting of this study, which suggests the month you're born in is a way to predict how you will become ill or die, should be taken very cautiously at this stage. Future research will be needed to see if the same links are observed in studies conducted in different regions, and then explore possible reasons behind these associations.

For now, this study does not provide proof that being born in a particular month means you are more or less likely to develop any particular disease.

There is nothing you can do about the month you were born in, but you can take steps to reduce your risk of disease in later life: have a healthy diet, take regular exercise, avoid smokingmoderate your alcohol intake and maintain a healthy weight.

Links To The Headlines

Scientists Find Surprising Link Between Birth Month And Disease Risk. The Huffington Post, June 10 2015

How your birth month determines if you will get sick: Researchers reveal the ailments you are most at risk from. Mail Online, June 10 2015

Your birth month dictates how you will die – so here's a calendar! Metro, June 9 2015

Links To Science

Boland MR, Shahn Z, Madigan D, et al. Birth Month Affects Lifetime Disease Risk: A Phenome-Wide Method. Journal of American Medical Informatics Association. Published online June 3 2015

Categories: NHS Choices

Woman gives birth using ovaries she had frozen as a child

NHS Choices - Behind the Headlines - Wed, 10/06/2015 - 13:00

The UK papers today welcome news of a world first in fertility treatment. As The Guardian concisely summarises: "A young woman in Belgium has become the first to give birth to a healthy baby after having her fertility restored by a transplant of ovarian tissue that was removed and frozen when she was a child".

The woman was born with sickle cell anaemia, a serious inherited blood disorder where the red blood cells, which carry oxygen around the body, develop abnormally. This can cause severe pain and organ damage.

Due to the severity of her condition, a decision was taken to perform a stem cell transplant.

This involves taking blood stems cells from a healthy donor and transplanting them into the recipient's bone marrow. The donor blood stem cells allow the recipient to make healthy red blood cells, white immune cells and platelets. While this offers hope of a cure, it requires the immune system to be suppressed, which usually destroys the functioning of ovaries, leaving patients infertile.

A decision was made to take a sample of ovarian tissue and freeze it, to see if could be used at a later date.

The hope now is that a similar technique could be used for other teenagers who require potentially fertility-threatening treatment, such as those with acute lymphoblastic leukaemia (cancer of the white blood cells).

Using frozen ovarian tissue to restore fertility has happened before; however, this is the first time a live birth has followed the use of tissue frozen at such a young age.

 

What is the basis for these current reports?

News of the success was published as a case report in Human Reproduction, a peer-reviewed medical journal.

They case study was produced by the Université libre de Bruxelles (Belgium) and funded by the Fondation Belge contre le Cancer and the Fonds de la Recherche Scientifique (FNRS).

 

The authors report no conflicts of interest

The UK media reported the story accurately, though the Mail Online seems to have caused confusion among its readers (as can been seen by the comments), by using the headline "World first gives fertility hope to millions of cancer patients". It should have made clear that while the treatment described in the study may be of potential use to teenagers and women with cancer, the case report actually involved sickle cell anaemia, which is a genetic, not a cancerous, disorder.

 

What was her medical background?

The case report described an unnamed 27-year-old woman born in the Republic of Congo and diagnosed with sickle cell anaemia at the age of five.

Sickle cell anaemia is a serious inherited blood disorder, where the red blood cells, which carry oxygen around the body, develop abnormally. Mild to moderate cases can usually be controlled with medication. More serious cases require surgery to prevent organ damage.

By 13, and following a move to Belgium, her condition became so severe that doctors in Brussels decided she needed a stem cell transplant. This is a transplant of very early stage blood cells that can then divide and develop into the different types of blood cell.

The transplant is intense and requires the patient's existing immune system to, effectively, be wiped out using chemotherapy or radiotherapy to prevent rejection of the new tissue. The faulty blood and immune cells are then replaced with new, healthy ones from the stem cell transplant. When stem cell transplants are given, the cells can either come from the patient themselves (taken prior to treatment), or from a donor. In this case the person had sickle cell anaemia, so produced abnormal red blood cells. Healthy stem cells were donor cells taken from her sibling.

The strong treatment regimen to suppress the immune system often results in infertility.

Aware of this, the doctors surgically removed and froze 62 fragments of the girl’s right ovary before she started the bone marrow transplant. She was 13 years and 11 months old at the time and had not yet started her periods. However, at around 10 years of age, she had breast development and hormone levels showing signs that she had started puberty.

During treatment, which involved a combination of chemotherapy and other immunosuppressant drugs, her remaining left ovary was damaged and she was infertile. Her periods were artificially induced using drugs at 15 years of age.

The good news was that the stem cell transplant worked, as she was largely cured of sickle cell anaemia.

 

What happened in the transplant?

Ten years after the stem cell transplant, she wanted to start a family.

She had robot-assisted surgery to put back the ovarian tissue fragments. Four thawed fragments were attached to her existing left ovary and 11 were grafted on the right-hand side. 

Four months later, her hormone levels reached a fertile level, she began having natural periods at five months, and maintained regular periods thereafter.

She was not able to conceive during the first two years after transplant, but this was because of male infertility with her partner. 

However, this relationship ended and she was able to conceive naturally with a new partner and delivered a healthy boy in November 2014.

 

What do the authors conclude?

The transplant team says: "This case reports the first live birth after transplantation of ovarian tissue harvested before menarche [the first period]."

They add that: "These data highlight the need to further investigate the viability of ovarian tissue transplantation for restoring fertility when the cryopreservation [freezing] procedure occurs before the patient starts puberty."

 

What are the implications of this?

The findings are promising for girls who have had ovarian tissue frozen before receiving intensive chemotherapy, radiotherapy or other immunosuppressant treatments, providing hope that they may be able to have a healthy pregnancy and baby in the future. Such intensive treatment may be given not only for blood diseases such as sickle cell anaemia, but more commonly for blood or tissue cancers.

It is, however, important to note that this is a single case study. The study authors say there have been at least 35 live births that have followed women who have had ovarian tissue frozen. This is said to be the first case where a live birth has resulted from tissue obtained at a pre-pubertal or pubertal age. However, it is unclear how consistent the method would be in other girls and women, and it may not work for everyone. 

In this case, the girl had breast development and hormone levels suggesting early signs of puberty at the time the ovarian tissue was originally frozen, but had not yet had a period. It seems crucial to establish how early the tissue can be harvested, and whether the stage of puberty influences the chance of success.

 

Is this available in the UK?

The Human Fertilisation & Embryology Authority (HFEA), which regulates fertility clinics and related research in the UK, states the following about fertility preservation for young cancer patients:

"Pre-pubertal patients who undergo medical treatment which may affect their future fertility may have the option of tissue freezing. This may be an option for young patients who are unable to produce mature sperm and eggs to preserve their future fertility.

"Where treatment involves patients of 16 years and younger, the decision of whether to store a child’s reproductive material may rest with the parents. A practitioner must decide whether a child is able to consent to his or her own medical treatment without the need for parental permission or knowledge."

For further help and advice about fertility preservation, speak with the health professional in charge of your or your child's care.   

Links To The Headlines

Woman gives birth after pioneering ovarian tissue transplant. The Guardian, June 10 2015

Woman who had ovary tissue removed and frozen makes history by becoming a mum. Daily Mirror, June 10 2015

Baby Born After Frozen Ovarian Tissue Transplant. Sky News, June 10 2015

Baby born from ovary frozen in mother's childhood. BBC News, June 10 2015

World's first birth from frozen ovary. The Daily Telegraph, June 10 2015

Woman gives birth using ovary tissue frozen when she was a CHILD: World first gives fertility hope to millions of cancer patients as mother welcomes baby boy after undergoing chemotherapy at 13. Mail Online, June 10 2015

Links To Science

Demeestere I, Simon P, Dedeken L, et al. Live birth after autograft of ovarian tissue cryopreserved during childhood. Human Reproduction. Published online June 9 2015

Categories: NHS Choices

Breast cancer 'tumour trigger' that spreads disease discovered

NHS Choices - Behind the Headlines - Tue, 09/06/2015 - 15:00

"Experts have identified a 'trigger' which enables breast cancer cells to spread,” the Daily Mirror reports. The trigger – a protein called CCL3 – appears to help cancerous cells spread into the lungs. The hope is that targeting the protein could help prevent any spread and reduce the number of deaths from breast cancer.

Scottish-based researchers found specific chemical signals and receptors on immune cells called macrophages that were orchestrating some of the spread of cancer. By genetically tampering with a protein involved in the process, they were able to reduce some of the spread and growth of cancer, raising hopes that this might be a future treatment avenue.

Tampering with the genetics in the same way as the mice would not be a viable human treatment. The protein is common, so disrupting it may cause side effects. However, there are potentially other ways of blocking it more specifically, such as new targeted drugs, so this research could lead to new treatment options.

The study didn’t tell us whether the mice lived longer, experienced less pain or responded better to other treatments. It should also be noted that cancer spread was not completely halted, just reduced. Therefore, we don’t know whether this approach would benefit humans.

This is a positive development in the understanding of how cancer spreads and becomes more life-threatening, but there are no immediate treatment implications.

 

Where did the story come from?

The study was carried out by researchers from the University of Edinburgh and Albert Einstein College of Medicine, New York. It was funded by the United States Department of Defence, US National Institutes of Health grants, and the Wellcome Trust (UK).

The study was published in the Journal of Experimental Medicine, a peer-reviewed medical journal.

Generally, the UK media reported the story accurately, suggesting that the new discovery offered hope, rather than anything more concrete or immediate. Most said the research was carried out on mice, but few explained how this might limit the relevance of the results on humans.

 

What kind of research was this?

This was a laboratory study looking to better understand how breast cancer spreads to the lungs in mice.

Breast cancer is the most common cancer in the UK. The lifetime risk of being diagnosed with breast cancer is 1 in 8 for women in the UK. While survival rates are generally high compared to other cancers – almost 8 out of 10 women diagnosed will survive for at least 10 years after a diagnosis – there are still many deaths. This, the research tells us, is mainly due to the breast cancer cells spreading to other parts of the body – called metastatic cancer.

Macrophages are cells of the immune system that seek and destroy things like cell debris and bacteria. They recognise proteins on the surface of cells. If recognised as safe, they leave them alone, but if recognised as a threat, they attempt to engulf and digest the foreign body.

There are a large number of clinical studies, the researchers’ say, that indicate a strong correlation between poor prognosis of breast cancer and high infiltration of macrophages in the tumour. They thought the macrophages were helping the tumour spread from the breast to other parts of the body, particularly the lungs.

To investigate the role of macrophages, the researchers used mice genetically engineered to develop breast cancer. Using mice versions of human diseases is a useful way to better understand the disease processes and look for cures without putting humans at risk. Any positive findings will eventually be tested in humans, as the results in mice are not always the same. This is because the disease and underlying biology of the mammals can differ in important ways.

 

What did the research involve?

The researchers used mice specially bred to develop breast cancer, to mimic the human disease. The research team studied the genetic and chemical signals involved in breast tumour development and its spread to the lungs. They also documented the behaviour and biochemistry of immune cells involved in the processes, such as macrophages.

Macrophages, like many other immune cells, respond to a range of external chemical signals that bind to receptors on their surface. This can stimulate them into developing in different ways, and tell them where to go and what to do. Some chemical signals cause the release of more signalling molecules, resulting in a cascade of chemical commands. The result could be to signal more macrophages to the area, or command them to grow and divide. These complex webs of chemical communication are often referred to as signalling pathways.

Using standard genetic manipulation techniques, they were able to delete key parts of the cancer signalling pathway to see what would happen. By switching on and off different signalling pathways, and points in the pathways, they slowly built up a better understanding about what was going on.

 

What were the basic results?

They found that macrophages were attracted to the breast cancer tumour and some were involved in helping the tumour spread to the lungs. These macrophages were changed by the tumour and were called “metastasis-associated macrophages (MAMs)".

The researchers discovered that these MAMs then responded to chemical signals linked to the tumour, called cytokines, receiving these signals through receptors in their cell membranes. Stimulation from cytokine CCL2 increased the number of MAMs. These MAMs then secreted cytokine CCL3, which further increased the number of MAMs at the site of the metastases – in this case, the lungs.

Using genetic manipulation, the scientists deleted various receptors in this chain, so the MAMs could no longer respond to these particular signals. This reduced the number of tumour cells spreading to the lungs and reduced the growth of metastases, suggesting that this particular signalling pathway was important in the process.

 

How did the researchers interpret the results?

They concluded that drugs targeted at inhibiting the CCR1 receptor that is stimulated by the CCL3 at the site of metastases could reduce the impact of the macrophages and “may have a therapeutic impact” in metastatic breast cancer, with less side effects. This is because the drugs would target MAMs rather than normal macrophages. They say that attempts to block earlier stages of this complex pathway have been shown to impair the immune system, reducing the ability to fight infection.

 

Conclusion

An Edinburgh-based team used mice engineered to develop breast cancer to better understand how it spreads from breast tissue to the lung, where it can be fatal. They identified specific chemical signals and receptors on immune cells called macrophages that were involved in the spread. By genetically tampering with one of the signalling pathways, they were able to reduce some of the cancer spread, raising hopes that this might be a future treatment avenue.

Fiddling with the genetics in the same way as was done for the mice would probably not be a viable treatment for humans. Aside from ethical and technical issues, genetic manipulation of this nature could lead to a range of side effects.

However, there are potentially other ways of blocking the same signalling pathway.

The results were encouraging, but they are at a very early research stage. Right now, we don’t know if this would work in humans, because it has only been tested in mice. While biologically similar, mice and humans do differ in potentially important ways. The only way to know if disrupting this signalling pathway might be useful in minimising breast cancer spread to the lungs would be to do experiments on humans.

We also don’t know if this treatment helped the mice live longer, experience less pain or respond better to other treatments. Similarly, the genetic manipulation didn’t stop the cancer spreading completely to the lungs, it just reduced it. Hence, we are a long way off stopping the spread totally, but it is a step in the right direction.  

Links To The Headlines

Breast cancer 'stopped from spreading in body' as new study gives hope to patients. Daily Mirror, June 9 2015

Breast cancer breakthrough after scientists find trigger that causes disease to spread to the lungs: Discovery will pave way for life-saving new drugs. Mail Online, June 9 2015

Breast cancer spread ‘trigger’ discovered. The Guardian, June 8 2015

Scientists discover 'trigger' which could stop breast cancer spreading. The Daily Telegraph, June 9 2015

New hope on breast cancer therapy. Scottish Express, June 9 2015

Links To Science

Kitamura T, Qian B, Soong D, et al.CCL2-induced chemokine cascade promotes breast cancer metastasis by enhancing retention of metastasis-associated macrophages. The Journal of Experimental Medicine. Published online June 8 2015

Categories: NHS Choices

Wet wipes may help spread hospital bugs

NHS Choices - Behind the Headlines - Tue, 09/06/2015 - 13:00

"A new study finds that detergent wipes are spreading bugs in hospitals," The Daily Telegraph reports. This isn't strictly true, as the study didn't do any tests in hospitals. But through laboratory experiments, researchers found seven commonly used brands of wet wipe could transfer bacteria from one surface to another.

Researchers tested seven detergent cleaning wipes they say are used in UK hospitals. They looked at three common causes of hospital-acquired infection: Staphylococcus aureus, a common cause of skin infections; Clostridium difficile, which can upset the digestive system; and Acinetobacter baumannii, which is usually harmless for most people, but can be very dangerous for people with a weakened immune system.

They found using the same wipe on different surfaces seemed to help these three germs spread. The study also found large variation in the ability of the different types of wipes to kill these three germs.

The authors mention a "one wipe, one surface, one direction approach," but they suspect people use the wipes on multiple surfaces in reality. As this was an experimental study, we do not know whether the use of wipes in this way would have a real-world impact and, if so, what that impact would be. We also don't know how wipes compare with other cleaning methods.

Still, this study does reinforce the importance of infection control in hospital, something that staff, visitors and patients can help to maintain by taking simple steps such as washing their hands frequently. 

Where did the story come from?

The study was carried out by researchers from Cardiff University and was funded by the university. It was published in the American Journal of Infection Control, a peer-reviewed journal.

Generally, the UK media reported the story accurately given the information they were presented with. However, an inconsistency did creep in at the research reporting stage and was replicated in most of the subsequent press coverage.

The researchers made the statement: "All the wipes repeatedly transferred large number of S. aureus on to three consecutive surfaces except wipe G, for which transfer of bacteria was below the limit of detection for this test."

But in the conclusion, this was summarised to: "All of the wipes repeatedly transferred bacteria and spores on to multiple surfaces". This shortened version in the conclusion made it into most of the media coverage. 

What kind of research was this?

This study looked at the effectiveness of detergent cleaning wipes for cleaning germs.

The researchers say the majority of current UK infection control policies advocate the use of detergent and water, or microfibre and water, for cleaning soiled or contaminated surfaces, adding that detergent wipes (wet wipes) are increasingly being used.

However, the team claim there is no good information about the ability of wet wipes to remove disease-causing microbes, or whether they could subsequently transfer microbes from one surface to another. 

What did the research involve?

The study picked seven detergent wipes currently used in healthcare facilities in the UK, and tested how good they were at killing three microbes from a stainless steel surface.

The microbes of choice were Staphylococcus aureus, Acinetobacter baumannii, and Clostridium difficile, representing common – and sometimes lethal – sources of hospital-acquired infections.

The wipes were tested to see how good they were at:

  • removing micro-organisms from the surfaces
  • preventing bacteria transfer when the same wipe was used to clean three consecutive surfaces

After using a 10-second "standard wiping protocol", the researchers measured the ability of the wipes to kill bacteria and spores using a standardised European method of assessment for chemical disinfectants.

Wiping experiments were independently repeated three times to get an average, and were analysed using appropriate methods. 

What were the basic results?

The detergent wipes tested in this study showed big differences in their ability to remove the three germs from surfaces after a 10-second wipe.

They performed quite differently depending on the germs tested. Broadly speaking, the wipes were able to remove a lot of Acinetobacter baumannii, but performed worse for Staphylococcus aureus and Clostridium difficile spores.

Almost all wipes also repeatedly transferred significant amounts of bacteria or spores over three consecutive surfaces, except for one, which registered no transfer.

Even then, the research team say the percentage of total micro-organisms transferred from the wipes after wiping was low for a number of wipes. 

How did the researchers interpret the results?

The team said: "Because detergent cleaning is advocated in many national guidance documents, it is imperative that such recommendations and guidance take into account the wipe limitations found in this study.

"The issue of potential transfer on to multiple surfaces needs to be addressed to avoid the potential spread of microbial pathogens." 

Conclusion

This research suggests detergent cleaning wipes used in UK hospitals and the home show large variability in their ability to kill three selected microbes, including Staphylococcus aureus and Clostridium difficile.

Researchers tested seven commonly used wipes and found they varied a lot in their ability to kill the bugs. More worryingly, it looked like the wipes were picking up the germs rather than killing them – in almost all the wipes tested, the bugs were spread if they were used on a different surface.

The implication of this is that wipes shouldn't be used on consecutive surfaces. The authors mention that "a one wipe, one surface, one direction approach" is recommended, but they suspect people use them on multiple surfaces in reality.

This is a single study, so we don't know for sure that its results are reliable. There were some inaccuracies – for example, in how the study estimated the starting level of contamination in the tests.

The best way to find out would be to repeat the experiments, ideally using wiping protocols used in hospitals, and on the most common surfaces. Only stainless steel surfaces were tested here. Extending the number of bugs tested would also improve the study, as only three specific types were tested.

It also wasn't clear whether the amount of contamination after wiping was enough to cause or significantly raise the risk of infection. We don't know how often the wipes are used in hospital, or whether they are used alongside other more effective cleaning methods.

Hospital infection can be life threatening, so ensuring cleaning practices are evidence-based and effective is likely to be a priority. This research highlights how some wipes may not be as effective for specific germs on specific surfaces as we might assume.

Hospital cleaning protocols are continuously being assessed and refined, so this study will undoubtedly add to this process. 

Links To The Headlines

Wet wipes could be spreading bacteria in homes and hospitals. The Daily Telegraph, June 9 2015

Superbugs 'spread by hospital wet wipes'. BBC News, June 8 2015

Hospital bugs 'spread by use of wet wipes to clean wards' according to first study of its kind. Daily Mail, June 8 2015

Links To Science

Ramm L, Siani H, Wesgate R, Maillard J. Pathogen transfer and high variability in pathogen removal by detergent wipes. American Journal of Infection Control. Published online May 18 2015

Categories: NHS Choices

New blood test for viral infections shows promise

NHS Choices - Behind the Headlines - Mon, 08/06/2015 - 14:00

"New test uses a single drop of blood to reveal entire history of viral infections," The Guardian reports.

Every time you are infected by a virus, your immune system produces specific types of antibodies in response. These antibodies remain in your body long after the infection has gone. The new test, called VirScan, is able to assess all these antibodies, building up a detailed immune "history" of viral infections.

Researchers looked at how well the test performed on blood samples from more than 500 people from North and South America, Africa and Asia.

The test correctly identified most of the people with known infections – though there were cases of both false negatives (saying an infection was not present even though it was) and false positives (wrongly diagnosing infection when there was none).

The test could theoretically be expanded to cover other types of organisms that cause human disease, such as bacteria, but this has not been tested yet. The test will also need to be updated as new viruses are discovered or as they change.

This test should be thought of as being at an early stage, likely to undergo further development and testing before it is ready for wider use.  

Where did the story come from?

The study was carried out by researchers from Harvard University and other research centres in the US, Europe, Peru, Thailand and South Africa.

It was funded by the US National Institutes of Health, the International AIDS Vaccine Initiative, the South African Research Chairs Initiative, the Victor Daitz Foundation, the Howard Hughes Medical Institute, the HIVACAT program and CUTHIVAC, the Thailand Research Fund, and the Chulalongkorn University Research Professor Program, NSF.

Some of the authors of the study are listed as inventors on a patent application related to the techniques used in the study (the use of bacteriophage phage display libraries to detect antiviral antibodies).

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

BBC News covered this story well and did not overstate the potential uses of the technique. Experts quoted in the story caution that while this technology may prove very useful in research, it may not be appropriate for diagnosing individual patients with diseases such as HIV.

The Mail Online suggested the test could be used to "help doctors diagnose patients with 'mystery illnesses'." But we do not yet know how this test performs compared with existing diagnostic methods for viral diseases.

Doctors and diagnostic laboratories would need to know that the new test performs as well as existing methods before they consider using it for diagnostic purposes or how well it identifies "mystery illnesses". 

What kind of research was this?

This laboratory study aimed to develop a new blood test that could detect all of a person's previous viral infections at once.

Existing tests for viruses tend to look for a specific single virus and do not detect other viral infections. These tests tend to be based on detecting a virus' genetic material in our blood or how our immune system responds.

Once a viral infection has been successfully fought off by the body, its genetic material may not be detected, but an immune "memory" of the virus can last for decades. This research looked at developing a test for any virus based on looking at our immune memory of previous viral infections.

The researchers hoped this would help them better study the interaction between our immune system and these viruses. It is thought this interaction may influence the development of diseases involving the immune system, such as type 1 diabetes, and potentially even help the immune system fight other infections.  

What did the research involve?

Our immune system makes special proteins called antibodies to fight viruses and other infections. These antibodies work by "recognising" and binding to specific proteins and other molecules on the cell that are produced by the virus.

The immune system remembers the viruses it has been exposed to and continues to produce antibodies against them at a low level, even after the virus has been removed from the body. The researchers took advantage of this in developing their new test.

The researchers started by generating almost 100,000 bits of protein from more than 1,000 strains of all 206 different viral species identified as infecting humans. They were able to do this using genetic information from these viruses, as these sequences carry instructions for making all of the viruses' proteins.

The proteins were made in viruses that typically infect bacteria, called bacteriophages or just phages. These bacteriophages were genetically engineered to each produce one small bit of protein from a human virus, and thousands were then placed on a tiny microchip.

The researchers then took blood samples from 569 participants from four countries (the US, Peru, Thailand and South Africa) on four different continents. They extracted the part of the blood that contains antibodies (the serum) and washed a small amount (less than a microlitre) of this over the microchip.

When antibodies recognise a viral protein they have been exposed to before, they bind to it. This response allowed the researchers to identify which of the bacteriophages had antibodies bound to them, and how much.

They then assessed what viral protein each of those bacteriophages were producing and which viruses they came from. These were the viruses the person would have been exposed to in the past.

The researchers particularly looked for cases where the person's antibodies recognised more than one piece of protein from a given virus, as this would give greater confidence that the person really had been exposed to this virus. They also developed ways to help tell antibody reactions apart from related viruses that produce similar proteins.

They then compared which viruses people in different countries had been exposed to. Some of the participants had known viral infections, such as HIV or hepatitis, so the researchers checked how well this test picked these up.  

What were the basic results?

The researchers found the VirScan test was able to detect 95% or more of known infections with HIV or hepatitis C that had already been diagnosed with existing single virus tests.

VirScan was also able to correctly differentiate between different forms of the hepatitis C virus in 69% of people with known infections. Similar results were found for its ability to detect and differentiate between similar herpes simplex viruses (HSV1 and HSV2).

The researchers found the participants had antibodies against an average of 10 viral species. Younger participants tended to have had fewer viral exposures than older participants from the same country.

This is what would be expected, as they have had less time to be exposed. The pattern of different infections seen in participants from different countries was also similar to what was expected.

The researchers found there were some bits of viral protein that people who had been exposed to that virus almost always produced antibodies against. This suggests that these bits of protein are particularly good at causing a similar immune response in different people and therefore might be useful in making vaccines.

The researchers also found some "false positives" where their test appeared to be detecting pieces of viral protein because of their similarity to proteins from bacteria. 

How did the researchers interpret the results?

The researchers concluded that the VirScan test provides a way to study all current and past viral infections in people using a small sample of blood. The method can be performed in samples from large numbers of people at the same time and is able to distinguish between related viruses.

They said: "VirScan may prove to be an important tool for uncovering the effect of host-virome interactions on human health and disease, and could easily be expanded to include new viruses as they are discovered, as well as other human pathogens, such as bacteria, fungi, and protozoa [single celled micro-organisms that cause diseases such as malaria]." 

Conclusion

This research has developed a test that is able to identify past viral infections using a small sample of blood, giving an insight into a person's history of viral infections. The test could theoretically be expanded to cover other types of organisms that cause human disease, such as bacteria.

No test is perfect, however, and there were some cases where a known infection was not identified (false negative) and where an infection was picked up that was not thought to have really occurred (false positive). The test detects antibodies generated in response to viruses as the result of vaccination.

Antibody response also reduces over time, so the test may not be able to identify all previous infections. The researchers thought this was why they detected less exposure to some common viral infections, such as flu, than they expected.

The use of shorter bits of protein may also mean that some antibodies that recognise larger sections of the protein, or only recognise the protein after it has other molecules added to it, may not be identified.

While the test showed promise for telling different related viral strains apart, the researchers note it won't be as good at this as some genetic tests.

The test is reported to potentially cost only $25 per sample, but it is unclear whether this included the cost of all the machines needed to carry out the testing. Not all diagnostic labs may have access to these machines.

This test should be thought of as being at an early stage. While it might be able to cover other organisms, this has not been tested yet. The researchers suggest it could eventually be used as a first-stage rapid screen for viral infections, which could be followed up by more specific diagnostic tests. Again, more research will be needed to test this.

VirScan will also need to be updated as new viruses are discovered or as viruses change. For now, it is likely to have further development and largely be used as a research tool, rather than for diagnosing disease.

Links To The Headlines

New test uses a single drop of blood to reveal entire history of viral infections. The Guardian, June 4 2015

This blood test can tell you every virus you’ve ever had. The Independent, June 7 2015

The simple blood test that reveals EVERY virus you've ever had - and could help doctors diagnose patients with 'mystery illnesses'. Mail Online, June 5 2015

Revolutionary £16 blood test reveals every virus you've ever had - breakthrough could help GPs fight future diseases. Daily Mirror, June 5 2015

Test unravels history of infection. BBC News, June 4 2015

Meet The Blood Test VirScan That Can Reveal Every Virus You've Ever Been Infected With. The Huffington Post, June 5 2015

Links To Science

Xu G, Kula T, Xu Q, et al. Comprehensive serological profiling of human populations using a synthetic human virome. Science. Published online June 5 2015

Categories: NHS Choices

'Missing link' between brain and immune system discovered

NHS Choices - Behind the Headlines - Mon, 08/06/2015 - 12:00

“Newly discovered vessels beneath skull could link brain and immune system,” The Guardian reports. It is has been suggested that the discovery, which has been described as textbook-changing, could lead to new treatments for a range of neurological conditions.

Until now, it was thought that the brain was not connected to the lymphatic system. This is an essential part of the immune system that helps fight infection, while draining excess fluid from tissue.

In this study, scientists discovered previously unknown lymphatic vessels in the outer layers of the brain. These vessels appeared to link the brain and spinal cord with the rest of the body’s immune system. This study used mice and human samples, vessel structure was investigated in the mice, and the observations followed up in the human samples.

Further study will be needed to confirm that the system works the same in humans, but the discovery may require a reassessment of our assumptions about lymph drainage in the brain and its role in diseases involving brain inflammation or degeneration, such as Alzheimer’s disease and multiple sclerosis.

It is too early to say whether the findings could one day have any implications for the treatment of these types of conditions.

 

Where did the story come from?

The study was carried out by researchers from The University of Virginia and was funded by Fondation pour la Recherche Médicale and by The National Institutes of Health. The study was published in the peer-reviewed scientific journal Nature.

The study has generated a great deal of media excitement, both in the UK and internationally.

This excitement seems largely driven by quotes released by the researchers themselves, such as Professor Kevin Lee, who was widely quoted as saying: “The first time these guys showed me the basic result, I just said one sentence: ‘They’ll have to change the textbooks’.”

However, media reports, such as the Mail Online stating that “[the discovery] could help treat conditions such as autism and Alzheimer’s” is premature, and cannot be concluded from this stage of the research.

 

What kind of research was this?

This was an animal study using mice to investigate the structure and function of lymphatic vessels in the brain.

It is said to have been previously understood that the central nervous system (brain and spinal cord) did not have a typical lymphatic drainage system. Lymph is the immune fluid that circulates round the body, containing white blood cells to fight infection and destroy abnormal cells.

This study aimed to look at the circulation of lymph in the mouse brain, potentially creating a greater understanding of the workings of the brain and disease processes. However, mice and humans do not have identical biology, so the findings may not be directly applicable. 

 

What did the research involve?

The scientists used adult mice to look at brain structure and the circulation of lymph.

The study involved complex laboratory techniques. This included the use of a fluorescent antibody to assess the alignment of cells within the brain, examination for markers associated with a lymphatic drainage system and looking at the functional capacity of identified vessels to carry lymphatic fluid to and from the brain. 

Human samples taken from the brain at autopsy were used to investigate any structures found in mice.

 

What were the basic results?

The scientists found that the outer protective layers of the mouse brain (the meninges) showed cells that were clearly lined up, which suggested that these were vessels with a unique function. These cells showed the characteristic features of functional lymphatic vessels. These vessels appeared able to carry both fluid and immune cells from the fluid surrounding the brain and spinal cord (the cerebrospinal fluid), and were connected to the lymph nodes in the neck.

The location of these vessels may have been the reason they have not been discovered to-date, thereby causing the belief that there is no lymphatic drainage system in the brain.

 

How did the researchers interpret the results?

The researchers state: “The presence of a functional and classical lymphatic system in the central nervous system [brain and spinal cord] suggests that current dogmas regarding brain tolerance and the immune privilege of the brain should be revisited”. This new understanding may mean current thinking about how the brain works needs to be reassessed. The researchers go on to say it could be the malfunction of these vessels that could be the cause of a variety of brain disorders, such as multiple sclerosis and Alzheimer’s disease.

 

Conclusion

This mouse study has examined the circulation of lymph in the brain. It discovered previously unknown lymphatic vessels in the outer layers of the mouse brain. If accurate, the findings may call for a review of how the immune system in the brain functions, and shed new light on its role in brain diseases involving brain inflammation or degeneration.

Though animal research can give a good insight into biological and disease processes, and how they may work in humans, the processes in humans and mice are not identical. Further studies are needed to confirm these findings and to assess whether this knowledge is transferable to humans.

As such, it is too early to say whether the findings could one day have any implications for the treatment of degenerative brain conditions such as multiple sclerosis or Alzheimer’s.  

Links To The Headlines

Newly discovered vessels beneath skull could link brain and immune system. The Guardian, June 5 2015

Landmark discovery about the brain 'will have scientists rewriting textbooks' - and could help treat conditions such as autism and Alzheimer's. Mail Online, June 5 2015

Links To Science

Louveau A, Smirnov I, Keyes TJ, et al. Structural and functional features of central nervous system lymphatic vessels. Nature. Published online June 1 2015

Categories: NHS Choices

Depression 'starts in the womb' claim is unproven

NHS Choices - Behind the Headlines - Fri, 05/06/2015 - 14:30

“The seeds of depression can be sown in the womb,” is the claim in the Mail Online.

While a new study did find that depression during pregnancy was linked to an increased risk of depression in adult offspring, a range of factors could be contributing.

The study analysed data collected from 103 pregnant mothers whose mental health was assessed though interviews during pregnancy and up to the time the time their child was 16. The children also answered questions of a similar nature about their mental health once they reached the age of 25. The researchers also assessed whether they had experienced maltreatment.

The odds of children whose mothers were depressed during pregnancy developing depression themselves in adulthood were about three times that of children whose mothers were not depressed during pregnancy. They also had about twice the odds of experiencing maltreatment as a child (not necessarily by the mother). 

Analyses suggested that the increased maltreatment might explain the link seen between maternal depression in pregnancy and depression in offspring as adults.

The researchers also make various suggestions as to why the links seen might exist. This included the possibility that maternal depression could impact on the child’s development by increasing levels of stress hormones in the womb; speculation that the Mail seems to have taken as proven fact.

In conclusion, it is not possible to say with certainty that maternal depression during pregnancy was directly causing the increase in depression risk seen.

Irrespective of this, it is important that women who experience depression during pregnancy get appropriate treatment and support. 

 

Where did the story come from?

The study was carried out by researchers from King’s College London and was funded by the Psychiatry Research Trust; the National Institute for Health Research (NIHR)/Wellcome Trust King’s Clinical Research Facility; the NIHR Biomedical Research Centre at South London and Maudsley National Health Service Foundation Trust; the Institute of Psychiatry, Psychology & Neuroscience, King’s College London; and the Medical Research Council United Kingdom.

The study was published in the peer-reviewed medical journal The British Journal of Psychiatry. It has been made available on an open-access basis, so it is free to read online or download as a PDF.

The Mail's reporting of the study is likely to add unnecessarily to expectant mothers’ concerns, as it does not highlight the limitations to the research, and the fact the research doesn't show cause and effect, or whether other factors are playing a role.

Also, the suggestion that “Screening pregnant women for [sic] condition [depression] could stop it being passed on” have not been tested in this study.

 

What kind of research was this?

This was a prospective cohort study called the South London Child Development Study (SLCDS), which started 1986. It aimed to assess whether a child’s exposure to a mother’s depression during and after pregnancy was linked to their risk of depression in adulthood, and also their risk of maltreatment as a child.

Previous research has shown a link between postnatal depression in the mother and later depression in the child, but no prospective studies have attempted to assess the link between a mother’s depression while pregnant and depression of the child when they reach adulthood.

A prospective cohort study is the best way of conducting such a study, but it still has limitations. Most important of these is the possibility that factors other than the one of interest (maternal depression) are contributing to links seen. When such studies follow up people over a long time period, as this study did, they are also prone to participants being lost to follow-up, which can bias results.

 

What did the research involve?

The researchers recruited expectant mothers in 1986 at 20 weeks into their pregnancy. They assessed their mental health during and after the pregnancy, up until the child was 16 years old. They also assessed whether the child was maltreated, and the child’s mental health when they reached 25. The researchers then analysed whether maternal depression at any stage was associated with the child’s depression or maltreatment.

Standardised one-to-one interviews were carried out with expectant mothers alone at 20 and 36 weeks, and together with their children at 4, 11, 16 and 25 years. The following were being assessed in these interviews:

  • maternal depression during pregnancy (at 20 and 36 weeks)
  • maternal postnatal depression (3, 12 and 48 months after birth)
  • maternal depression during offspring’s childhood (4, 11 and 16 years)
  • offspring maltreatment (up to age 17)
  • offspring depression in adulthood (18 to 25 years of age)

The researchers also collected information on other factors that may have contributed to or altered findings (potential confounders) so they could take these into account in their analyses.

Of the 153 women who completed the first interview, 103 (67%) completed the study and had their data analysed.

 

What were the basic results?

Of the mothers in the sample, 34% experienced depression during pregnancy and 35% suffered postnatal depression. Maltreatment was reported in 35% of offspring and about 38% met the criteria for depression in adulthood.

Before taking into account any potential confounders, children exposed to maternal depression in pregnancy had 3.4 times the odds of developing depression as adults compared to children who had not been exposed (odds ratio (OR) 3.4, 95% confidence interval (CI) 1.5 to 8.1). When taking into account child maltreatment and exposure to maternal depression when aged 1 to 16 years old, this association did not remain.

Children exposed to maternal depression in pregnancy were more likely to experience maltreatment as a child (OR 2.4, 95% CI 1.0 to 5.7). Analyses suggested that the maltreatment might be the “link” between maternal depression in pregnancy and offspring depression in adulthood.

 

How did the researchers interpret the results?

The researchers conclude that the study “shows that exposure to maternal depression during pregnancy increases offspring vulnerability for developing depression in adulthood”. The authors also state: “By intervening during pregnancy, rates of both child maltreatment and depressive disorders in the young adults could potentially be reduced. All expectant women could be screened for depression and those identified offered prioritised access to psychological therapies – as is currently recommended by the UK guidelines on perinatal mental health.”

 

Conclusion

This prospective cohort study found a link between depression in the mother during pregnancy and child maltreatment and depression in adulthood. The results suggested that the child maltreatment might be the intermediate “step” or “link” between maternal and offspring depression.

The study has strengths and limitations. The strengths are that it prospectively followed women and their children up over a long time period. The prospective nature of the study is the best way to collect such information. This allowed the study to used standardised diagnostic interviews to collect consistent information from participants.

The main limitation to the study is that we cannot be certain that the links seen are due to a direct effect of maternal depression during pregnancy. While the researchers did explore and take into account some potential confounders, other factors could be contributing. It is likely that a range of environmental and potentially genetic factors may be playing a role, especially for a condition as complex as depression, so it is difficult to disentangle their effects.

Another limitation is the study’s small sample size, and the fact that about a third of participants did not complete it. Also, the rates of depression in the study were relatively high, which the authors suggest might reflect the urban population studied. This means that the results may not be representative of the whole population and therefore may not be generalisable to other groups.

As data was collected by interview, and in some cases was regarding a past period of time, it is possible that participants would not have been truthful or may not accurately recall the information that could affect the results.

It seems that this study has found some association, but we should be cautious about what we conclude. However, it does highlight that many women do experience depression in pregnancy, and ensuring that this is treated appropriately is important to the mother’s health and wellbeing, as well as her child and family.

As the authors mention in their article, the use of antidepressants in expectant mothers is an area of debate, due to the potential for effects on the developing baby. Doctors may decide to prescribe them in situations where the benefits are considered to outweigh the potential risks.

It is also important to note that there are other forms of treatment available, such as talking therapies, including cognitive behavioural therapy. Pregnant women who are concerned that they may be depressed should not be afraid to talk to their healthcare professional about this, to ensure they get appropriate care.

Links To The Headlines

Could depression start in the WOMB? Children of mothers suffering mental illness in pregnancy are 'three times more likely to develop the condition'. Mail Online, June 5 2015

Links To Science

Plant DT, Pariante CM, Sharp D, Pawlby S. Maternal depression during pregnancy and offspring depression in adulthood: role of child maltreatment. British Journal of Psychiatry. Published online June 4 2015

Categories: NHS Choices

Children with autism may be supersensitive to change

NHS Choices - Behind the Headlines - Fri, 05/06/2015 - 14:00

"People with autism … are over-sensitive to the world," the Mail Online reports. It reports on an animal study involving a rat model of autism, where a chemical is used to mimic the development of autism in rats. The study found the "autistic" rats showed signs of anxiety and withdrawal when placed in unpredictable environments.

Researchers compared the rats when they were reared in one of three environments: a standard cage, or two types of enriched environment with toys and treats – one where these "enrichments" stayed the same and another where they changed unpredictably.

Overall, they found rats tended to do better in the predictable enriched environment than the standard or unpredictable enriched ones on various tests of sociability, behaviour and emotional response.

This study lends support to what is already generally understood about autism and autism spectrum disorder (ASD) – many people on the spectrum prefer stability and consistency in their environment and activities, and can often find changes to previously set routines upsetting.

However, it is too early to draw further conclusions from the results of this study. The causes of these developmental conditions are not clearly understood, and this rat model is unlikely to be entirely representative of humans with autism. This means we don't know how applicable the findings are or whether they could lead to new treatments. 

Where did the story come from?

The study was carried out by researchers from Yale University, the University of Michigan and the University of Louisiana at Lafayette in the US. It was supported by the Swiss National Science Foundation.

The study was published in the peer-reviewed scientific journal, Frontiers in Neuroscience. This is an open access journal, so the study is free to read online or download as a PDF.

The Mail Online reporting on this study is reasonable, and indicates at the start of the article that this research involved research in rats, not humans.  

What kind of research was this?

This was an animal study using a rat model of autism. It aimed to investigate environmental effects on behaviour and protein expression in the brain.

Autism spectrum disorder (ASD) is a lifelong developmental condition where those affected typically have difficulties with social interaction and communication, and often have quite rigid routines and activities.

People with autism often have some degree of intellectual impairment, while people with Asperger's syndrome usually have normal intelligence or heightened intelligence in some areas. There is no current agreement about whether there are particular underlying disease changes in the brains of people with ASD.

Because people with ASD usually have a preference for a consistent environment and activities, behavioural therapies often focus on these areas. This research aimed to focus on the environment that the child – or, in this case, the rat – grows up in.

The researchers investigated the theory that predictable environments would prevent distressed reactions, while unpredictable enriched environments would lead to abnormal behaviours.     

What did the research involve?

The study used a rat model of autism. When unborn rats are exposed to an antiepileptic drug called valproic acid (VPA), it has been shown to create behaviour similar to that seen in people with autism.

In this study, one group of unborn rats were exposed to VPA (given to the mother), while another group of control rats were exposed to inactive saline (salt water) injections.

When the rats were born, the researchers then tested the effect of housing the two groups of rats in one of three different environments:

  • standard laboratory conditions – standard bedding, housed in groups of three rats per cage, with the cages kept in a shared room
  • predictably enriching conditions – a constant setting of extra toys, treats, smells, running wheel, with six rats per cage (larger than the standard cage); the cages were also kept in an isolated room
  • unpredictably enriching conditions – same as for the predictably enriching conditions, but the stimuli were regularly changed during the week

The researchers then looked at the effect that the pre-birth exposure and the subsequent environment after birth had on behavioural outcomes such as sociability, pain perception, fear response and general anxiety. They also looked at the effect on an overall measure of "emotionality", which incorporated five of the other behavioural scores.   

What were the basic results?

The researchers found pre-birth exposure and the subsequent environment had an effect on the rats' social behaviour.

In the standard environment, the VPA rats showed a reduced preference for being social (assessed by how much they sniffed another rat) compared with the control rats, but the two rat groups did not differ in the unpredictable enriched environment.

In the predictable enriched environment, the sociability and exploration of the VPA rats was increased relative to the control rats, in whom it was reduced.

Pre-birth exposure and the subsequent environment had no effect on the rats' pain perception.

When looking at fear response (as indicated by the rats "freezing" in response to the expectation of a shock), VPA rats showed more fear than controls in the standard environment, but did not differ in the predictable enriched environment.

In the unpredictable enriched environment, the VPA rats showed a similar or heightened fear response compared with VPA rats in the standard environment. 

Looking at general anxiety (measured by exploring new environments), VPA rats generally explored less than control rats in the standard environments, though they tended towards higher exploration in the predictable enriched environments. 

In both rat groups, overall "emotionality" was increased by enrichment, but it increased to a greater extent in the VPA compared with control rats. In the VPA rats, "emotionality" scores were reduced in the predictable enriched environments. 

How did the researchers interpret the results?

The researchers concluded that, "Rearing in a predictable environment prevents the development of hyper-emotional features in an autism risk factor, and demonstrates that unpredictable environments can lead to negative outcomes, even in the presence of environmental enrichment." 

Conclusion

Overall, this study in a rat model of autism seems to support what is generally already understood about ASD: affected individuals often feel more comfortable with set patterns, routines and environments, and may find unpredictability more challenging.

However, it is hard to draw many solid conclusions from this study, particularly because it is difficult to know exactly how representative this rat model of autism is of humans with autism.

Animal research can often give a good insight into biological and disease processes and how they may work in humans, but we are not identical. With a complex condition such as autism, which does not have a clearly established cause or causes, it is difficult to fully replicate the condition in animals.

The researchers report the VPA model is a well-validated model of autism in rats and has some of the characteristics seen in people with autism. But it is likely differences still exist, so we can't be certain how applicable the findings are.

The study generally supports what is already understood about ASD, and may lend support to environmental and behavioural therapeutic approaches. However, we certainly can't say at this stage whether environmental manipulation in humans would have the ability to prevent or cure ASD.

Links To The Headlines

People with autism have 'supercharged' brains: Those with the condition are 'over-sensitive to the world - and not impaired'. Mail Online, June 4 2015

Links To Science

Favre MR, La Mendola D, Meystre J, et al. Predictable enriched environment prevents development of hyper-emotionality in the VPA rat model of autism. Frontiers in Neuroscience. Published online June 2 2015

Categories: NHS Choices

Breast changes in older women

NHS Choices - Live Well - Fri, 05/06/2015 - 01:00
Breast changes in older women

As you get older, it’s natural for your breasts to lose their firmness, change shape, shrink in size and become more prone to certain abnormal lumps.

In most cases, breast lumps are harmless but, whatever your age, it’s important that you report any new lumps to your doctor.

From around the age of 40, you can expect your breasts to change in size and shape. It’s normal for breast tissue to become less glandular and more fatty as you get older, which makes them feel less firm and full.

With age, there’s also an increasing risk of abnormal growths in the breast. These are often harmless breast lumps, like cysts, but they can also be a sign of serious conditions like breast cancer.

As the years go by, you might also notice a wider space between your breasts and that your breasts shrink in size, sometimes by a cup size or more (unless you put on weight, in which case your breasts may get bigger). The area around the nipple (the areola) tends to become smaller and may nearly disappear, and the nipple may turn in slightly.

Many of the breast changes that happen as you get older are caused by hormonal changes.

Declining oestrogen levels at the menopause make breast tissue dehydrated and less elastic, so that your breasts lose their once rounded shape and begin to sag.

On the plus side, you may stop having any of the premenstrual lumps, pain or nipple discharge that you used to have.

Breast cancer screening

Screening for breast cancer is currently offered on the NHS to women aged 50-70 in England. However, it’s in the process of being extended as a trial to some women aged 47-73.

Breast screening uses an X-ray test called a mammogram that can spot cancers when they are too small to see or feel.

This short video explains what happens when you have a mammogram.

It’s your choice whether to have breast screening, but bear in mind that most experts believe it’s beneficial in picking up breast cancer early.

If you’re over 70, you’ll stop receiving screening invitations through the post, but you can still carry on with screening if you want to. To arrange an appointment, contact your local breast screening unit.

Find breast screening units in your area.

Read more about breast cancer screening.

Dense breasts

Young women who have not yet gone through the menopause often have what’s known as dense breasts.

Dense breasts contain more glandular and less fat tissue than usual. It’s not the same as having firm breasts and it has nothing to do with how big or what shape your breasts are.

Having dense breasts isn’t abnormal and it’s not something that you can change, but a potential drawback is that dense breasts can make breast cancer screening more difficult, because the dense tissue can mask potential tumours on a mammogram.

Breast tissue tends to become less dense as you get older, especially after the menopause, so it becomes easier to detect breast cancers on a mammogram.

Breast lumps

Breast lumps are common around the menopause. They’re usually cysts, which are harmless lumps filled with fluid. But if you notice a lump, don’t wait to be offered screening – see your GP, to rule out breast cancer.

Breast cancer is most common in women over 50. Other warning signs of breast cancer include:

  • puckering of the skin
  • nipple changes (like scaling or discharge)
  • a swollen, red or "inflamed" breast

Read more about breast lumps.

Women over 70

Women over 70 are particularly at risk of breast cancer, because a woman’s risk of getting breast cancer increases with age. Don’t assume that because you’re in your 70s or older that you’re in the clear. Always report any unusual breast symptoms to your doctor.

Find out how to spot breast lumps.

Categories: NHS Choices

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