Medical News

High-factor sunscreen doesn’t cut melanoma risk

Medical News - Thu, 06/12/2014 - 14:00

“High-factor sun cream cannot…protect against the deadliest form of skin cancer,” The Guardian reports. Research involving mice with a predisposition to develop melanoma found that sunscreen only delayed, rather than prevented, the onset of melanoma.

Malignant melanoma occurs when cells that produce melanin – pigment that darkens the skin – rapidly divide and grow uncontrollably.

A mutation in a gene crucial for cell growth, BRAF, has been found in several cancers, including around half of melanoma cases. Mice in this study were given this mutation, and all of them developed melanoma when exposed to UV light.

Sunscreen factor 50 delayed the onset and reduced the number of tumours, but did not prevent melanoma.

The study also found that in the mice with the BRAF mutation, UV light damaged another part of the DNA that stops cells dividing too rapidly – tumour suppressor genes called TP53. Sunscreen did not prevent this damage, which means that the cells could grow unchecked.

Mutations in the BRAF gene found in melanomas are not the inherited type, and in humans may be caused by UV exposure and other environmental factors.

It should not be interpreted from this study that sunscreen is useless, but you cannot rely on it solely, especially if you have risk factors for melanoma, such as pale skin and having lots of moles.

Sunscreen should be used in combination with other preventative methods, such as wearing appropriate clothing when the sun is at its hottest.

 

Where did the story come from?

The study was carried out by researchers from the University of Manchester, the Institute of Cancer Research and the Royal Surrey County Hospital. It was funded by Cancer Research UK, the Wenner-Gren Foundations and a FEBS Long-Term Fellowship.

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

It was accurately covered in the UK media, with many news sources including useful quotes from independent experts about the research's implications. 

 

What kind of research was this?

This was a laboratory study that used mice to look at how effective sunscreen is at reducing the risk of developing melanoma, following exposure to UV light.

Melanoma is the most malignant form of skin cancer. It is the fifth most common cancer in the UK, with 13,348 new cases occurring each year, according to figures from 2011.

Melanoma occurs when melanocytes grow uncontrollably. These are the cells that produce the protective pigment melanin, which gives skin its colour. People with darker skin have more active melanocytes, which transfer more melanin to other cells to protect them from UV light.

A mutation in the BRAF gene that regulates growth and division of cells has been found in melanoma. It is known as an “oncogene”, as it can cause normal cells to become cancerous if it has a mutation. Several different BRAF gene mutations have been found in melanoma and some cancers of the colon, rectal, ovary and thyroid.

It is not known how UV light causes melanoma, but an abnormal BRAF gene has commonly been found at an early stage in the development of melanoma. The researchers wanted to study the process, so used mice that had this particular BRAF gene mutation (called BRAF [V600E]).

Another gene, tumour protein 53 (TP53), makes a protein called tumour suppressor 53 (Trp53) that stops cells dividing too rapidly or uncontrollably. If there is a mutation in this gene, there is no safety check and the cells can grow and multiply unchecked, causing a tumour. Trp53 has been implicated in non-melanoma skin cancer, but was not thought to be involved in melanoma.

 

What did the research involve?

Mice with the BRAF gene mutation in their melanocytes were used in a variety of experiments and compared to mice without the BRAF mutation.

The backs of the mice were shaved and one half was protected with a cloth.

Newborn mice were given a single exposure to UV light at a dose that would mimic mild sunburn in humans. Those also given the BRAF mutation were compared to those without.

Adolescent mice were given the BRAF mutation and then either:

  • not exposed to UV light
  • given weekly exposure to UV light for up to six months
  • repeated exposure to UV light 30 minutes after sunscreen factor 50 had been applied

 

What were the basic results?

The newborn mice given the BRAF mutation developed melanoma. This was found to be due to the inflammatory response of the skin.

In the adolescent mice given the BRAF mutation:

  • melanoma occurred in 70% of the mice with no UV exposure after about 12.6 months. They had, on average, 0.9 tumours (this somewhat unusual average is due to the fact that some mice had no tumours – much like the famous example of 2.4 children)
  • all mice developed melanoma after repeated UV exposure within 7 months. They had, on average, 3.5 tumours each; 98% of them were on the skin exposed to the UV light
  • all mice given sunscreen developed melanoma within 15 months. They had, on average, 1.5 tumours each, and were more common on the sunscreen-protected skin than the cloth-protected skin

Mice without the BRAF gene mutation did not develop melanoma after exposure to UV rays.

UV light caused damage to the DNA. This was evidenced by finding mutations in the Trp53 tumour suppressor protein in 40% of cases. These mutant Trp53 proteins increased the BRAF-driven growth of the melanoma.

 

How did the researchers interpret the results?

The researchers conclude that this study reveals “two UVR melanoma pathways: one driven by inflammation in neonates and one driven by UVR-induced mutations in adults”. They also found that “sunscreen (UVA superior, UVB sun protective factor [SPF] 50) delayed the onset of UVR-driven melanoma, but only provided partial protection”. They “advocate combining it with other sun avoidance strategies, particularly in at-risk individuals with BRAF-mutant naevi [moles]”.

 

Conclusion

This study found that in mice given the BRAF mutation, sunscreen did not prevent them from developing melanoma, although it did delay it and reduce the number of tumours. The mechanism for this appears to include damage to a tumour suppressor gene, TP53, which has previously been implicated in other skin cancers. Sunscreen did not prevent mutations occurring in this gene, but did reduce the number of mutations.

The study's authors accepte that sunscreen protects against squamous cell carcinoma – a type of skin cancer – but that there was uncertainty around its ability to protect against malignant melanoma – a second type of skin cancer. This study indicated that sunscreen did reduce the risk of developing melanoma in the mice, but that protection was not 100%. These preliminary findings in mice will need to be confirmed in humans for the results to be more credible and reliable.

These results were applicable only to those with an existing mutation in the BRAF gene. Mutations in the BRAF gene can be inherited, but these are not thought to be linked to skin cancers. Acquired mutations in the BRAF gene do increase the risk of melanoma, and can be present in moles. These people have a heightened risk of skin cancer. The complication that arises from this is that UV light might cause this mutation, setting off a cycle of cell and DNA damage, leading to cancer. This means that overexposure to the sun still increases your risk of skin cancer risk factors, whether you have the mutation or not.

People with known risk factors for melanoma should use high-factor sunscreen in combination with other preventative methods, such as wearing appropriate clothing and staying in the shade when the sun is at its hottest (between 11am and 3pm). If you are desperate for a tan, fake is the best way to go.

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

Links To The Headlines

High-factor sunscreen cannot give complete protection against skin cancer. The Guardian, June 12 2014

Skin cancer: Sunscreen 'not complete protection'. BBC News, June 11 2014

Wearing sunscreen may NOT prevent skin cancer, study claims. Mail Online, June 12 2014

Sunscreen does not protect against deadliest skin cancer. The Daily Telegraph, June 12 2014

Links To Science

Viros A, Sanchez-Laorden B, Pedersen M, et al. Ultraviolet radiation accelerates BRAF-driven melanomagenesis by targeting TP53. Nature. Published online June 11 2014

Categories: Medical News

Making mosquitoes male may manage malaria

Medical News - Wed, 06/11/2014 - 18:19

"Mosquitoes modified to only give birth to males in bid to wipe out malaria," The Daily Telegraph reports after new research has found an innovative way of tackling the global problem of malaria.

The technique used in this latest research is both brutal and elegant. Female mosquitoes, which spread malaria to humans through their bite, were genetically modified so that their offspring were overwhelmingly (95%) male. This male-only trait was inherited and repeated with future generations, and has the potential to wipe the species out.

It is not yet known if the genetically modified mosquitoes are able to compete with wild mosquitoes in their natural environment, as the studies have so far only been conducted in cages in a laboratory.

If the mosquitoes can have an effect in the wild, in the short-term this could reduce the spread of malaria by cutting the number of female mosquitoes. In the long-term, the species could potentially be completely eliminated.

Future studies would have to ensure that wiping out the type of mosquito that carries malaria does not upset the ecosystem and cause more problems.

A famous example of this type of ecological upset is the introduction of cane toads in Australia to manage the beetle population. The toads proved highly adaptive to the environment and are now a major pest.

 

Where did the story come from?

The study was carried out by researchers from Imperial College London, the University of Perugia in Italy, and the Fred Hutchinson Cancer Research Center in the US.

It was funded by the US National Institutes for Health and the European Research Council.

The study was published in the peer-reviewed medical journal, Nature Communications. It is open access, so it is free to read online.

The UK media's coverage was good, with The Guardian providing expert comments on the study balanced by a quote from Dr Helen Williams, director of GeneWatch UK, regarding the potential risks of interrupting the ecosystem.

 

What kind of research was this?

This was a laboratory study of mosquitoes that aimed to find a way of reducing their numbers, as female mosquitoes – which bite humans – spread malaria.

The number of female mosquitoes in the mosquito population and their speed of reproduction are both believed to be ways of controlling their population size. If there was a way to increase the proportion of male offspring, this could therefore reduce the population size.

Previous attempts in caged experiments using naturally occurring mutations – which gave a higher number of male offspring in two types of mosquito called Aedes and Culex – were unsuccessful because the females had a natural resistance to them.

The researchers aimed to genetically modify mosquitoes using a synthetic enzyme, based on the naturally occurring mutations, to damage the X chromosome in males. This would mean that they are potentially only able to pass on the Y chromosome during reproduction, thereby only producing male offspring.

 

What did the research involve?

The researchers investigated the effect of different enzymes on damaging the X chromosome of male mosquitoes in the laboratory and then performed various experiments using live mosquitoes.

They created an enzyme that targets and damages the X chromosome in the male mosquito species Anopheles gambiae, which carries malaria.

The researchers ensured that the process only damaged the X chromosome in the male mosquito and did not affect the Y chromosome so that the offspring were not sterile.

If they were sterile, they would not be able to reproduce and the effects of the genetically modified mosquitoes would be limited to one generation.

This would then require an unimaginable number of mosquitoes to be injected for there to be any impact on numbers.

The researchers performed various experiments to see if the genetic mutation would be passed on to future generations.

They tested the level of damage to the X chromosome caused by various enzymes and at different temperatures until they found the optimal genetic modification that was able to produce mostly males without affecting the fertility rate.

 

What were the basic results?

The offspring of genetically modified male mosquitoes were more than 95% male. The enzyme that damages the X chromosome was inherited by these males, causing them to have male offspring.

In five independent cage experiments, putting in three times the number of genetically modified males to normal males caused the suppression of the wild-type mosquito. All mosquitoes were eventually eliminated in four of the cages within six generations.

In the small fraction of female offspring produced by the genetically modified males, their offspring were mostly female when they were fertilised by wild male mosquitoes.

The male offspring had a 50% chance of having the genetic modification. When they were crossed with wild female mosquitoes, however, they were still more likely to have males.

 

How did the researchers interpret the results?

The researchers concluded that, "Distorter male mosquitoes can efficiently suppress caged wild-type mosquito populations, providing the foundation for a new class of genetic vector control strategies."

However, they acknowledge that, "The robustness of these traits under variable natural conditions remains to be studied."

 

Conclusion

This study found that genetically modifying the X chromosome in male mosquitoes can cause more than 95% of their offspring to be male in caged experiments. This genetic modification is inherited by these offspring, who then have similar high numbers of male offspring.

While these results are promising, it is not clear whether the small fraction of female offspring would be enough to eventually reverse the process and create mosquitoes resistant to the effects of the enzyme.

These studies were just performed on the species Anopheles gambiae, which carries malaria. It is not yet known what effect reducing or eliminating the species would have on the population size of other mosquitoes or the ecological system.

This would need to be considered carefully before any genetically modified species was released into the environment. Our ecosystem is incredibly complex, so tinkering with it could lead to a range of unexpected and unwanted consequences.

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

Links To The Headlines

Mosquitoes modified to only give birth to males in bid to wipe out malaria. The Daily Telegraph, June 10 2014

GM mosquito designed to kill off females may limit spread of malaria. The Times, June 11 2014

GM mosquitoes a 'quantum leap' towards tackling malaria. The Guardian, June 10 2014

GM lab mosquitoes may aid malaria fight. BBC News, June 10 2014

Could malaria be wiped out by GM mosquitoes? Scientists find a way to kill off disease-carrying female of the species. Daily Mail, June 10 2014

New GM Mosquito 'Could Help Defeat Malaria'. Sky News, June 10 2014

Links To Science

Galizi R, Doyle LA, Menichelli M, et al. A synthetic sex ratio distortion system for the control of the human malaria mosquito. Nature Communications. Published online June 10 2014

Categories: Medical News

Red meat consumption linked to breast cancer

Medical News - Wed, 06/11/2014 - 14:26

“Eating a lot of red meat in early adult life may slightly increase the risk of breast cancer,” BBC News reports.

The news is based on a large US study that looked at the protein dietary intake of almost 90,000 female nurses and their risk of breast cancer over a 20-year period.

Previous studies have focused on the dietary intake of those in their "midlife" and older populations. In this particular study, however, researchers were interested in finding the potential link between diet and breast cancer risk in early adulthood.

The main finding was that a higher intake of red meat (which included both processed and unprocessed meat) was associated with a 22% increased risk of breast cancer.

The results suggest that women who chose healthier sources of protein – such as chicken, nuts and lentils – had a decreased risk of breast cancer.

The study is certainly not without its limitations, particularly because it relied on participants’ recall of dietary intake.

However, there is evidence that reducing your consumption of red meat to 70g a week or less could also reduce your risk of bowel cancer.

 

Where did the story come from?

The study was carried out by researchers from Harvard School of Public Health in the US, Shahid Beheshti University of Medical Sciences in Tehran, Iran, and other US institutions.

It was funded by the National Institutes of Health and was published in the peer-reviewed journal BMJ. The article has been published on an open-access basis, meaning it is freely available to read online.

The researchers previously carried out an early analysis of this study with a 12-year follow up period and published their findings. Their current publication has a longer follow-up period, of 20 years. 

The story was covered extensively in the UK media, and most of the coverage accurately reflects the study’s findings.

However, the Mail Online reported that “three bacon rashers a day raises breast cancer risk for young women”, but it is unclear where the figure of three rashers came from.

The study only reports data for total red meat consumption, including both processed and unprocessed, with precise quantities (in either grams or number of items) not provided.

 

What kind of research was this?

This was a prospective cohort study investigating the link between dietary protein in early adulthood and the risk of breast cancer.

A cohort study looks at how particular exposures affect groups of people over time. This type of research is normally used to look at the effect of suspected risk factors that cannot be controlled experimentally – for example, the effect dietary protein plays on the risk of breast cancer. Results from prospective studies are usually considered as more robust then retrospective studies, which either use data that was collected in the past for another purpose, or ask participants to remember what happened to them in the past.

 

What did the research involve?

The study included 88,803 female nurses aged between 24 and 43, all from the US. These women had all participated in a wider study (Nurses Health Study II) and had completed a questionnaire about usual dietary intake in the past year, in 1991.

The researchers considered the findings from the 1991 questionnaire to represent dietary intake in early adulthood. 

The nurses then completed the same, or a similar, questionnaire in 1995, 1999, 2003 and 2007. In the questionnaires, responses were given for commonly used portion sizes, with nine categories of intake frequency that ranged from “never or less than once per month” to “six or more per day”.

For analysis purposes, women were categorised into one of five categories, according to food group or nutrient intake.

The researchers were interested in investigating the potential link between total intake of unprocessed red meat (e.g. beef, pork, lamb) and processed red meat (e.g. hot dogs, bacon, salami) before menopause and the subsequent risk of breast cancer up to 2011 (in the 20-year follow-up period).

In addition to this, they looked at links between breast cancer and other protein-rich foods, including:

  • poultry (e.g. chicken, turkey)
  • fish
  • eggs
  • legumes (e.g. tofu, lentils, soybeans)
  • nuts

The main outcome the researchers were interested in was the number of breast cancer cases identified through self-reporting and confirmed with pathology. New cases of breast cancer were identified every two years, through questionnaires.

The researchers used statistical techniques to analyse their results and adjusted the results for multiple factors, including family history of breast cancer, energy intake and smoking.

They analysed their results for all women, as well as by menopausal status.

Women were considered premenopausal if they still had menstrual periods or had a hysterectomy with at least one ovary remaining, and were younger than 46 (for smokers) or 48 years (for non-smokers).

Women were considered postmenopausal if they reported no longer having menstrual periods or had undergone surgery to remove both their ovaries.

They also estimated the effect of substituting one serving per day of poultry, fish, legumes, eggs or nuts for one serving of red meat.

 

What were the basic results?

The average age of women in 1991 was 36.4 years. Over the 20-year follow-up period, there were 2,830 cases of breast cancer recorded. The main findings of the study were that:

  • higher intake of total red meat was associated with an increased risk of overall breast cancer (relative risk [RR] 1.22, 95% confidence interval [CI] 1.06 to 1.40 for highest fifth of red meat consumption, compared to the lowest fifth of consumption)
  • higher intakes of poultry, fish, eggs, legumes and nuts were not associated with overall risk of breast cancer
  • higher intake of poultry was associated with a lower risk of breast cancer among postmenopausal women (RR 0.73, 95% CI 0.58 to 0.91) for highest fifth of consumption compared to lowest fifth), but not in premenopausal women (RR 0.93, 95% CI 0.78 to 1.11 for highest fifth compared to lowest fifth of consumption)

Findings were not presented for processed vs. unprocessed meats and risk of breast cancer.

When estimating the effects of exchanging different protein sources:

  • substituting one serving of legumes (such as nuts, peas and lentils) a day for one serving of red meat a day was associated with a 15% lower risk of breast cancer among all women (RR 0.85, 95% CI 0.73 to 0.98) and a 19% lower risk among premenopausal women (RR 0.81, 95% CI 0.66 to 0.99)
  • substituting one serving of poultry a day for one serving of red meat a day was associated with a 17% lower risk of overall breast cancer (RR 0.83, 95% CI 0.72 to 0.96) and a 24% lower risk of postmenopausal breast cancer (RR 0.76, 95% CI 0.59 to 0.99)
  • substituting one serving a day of combined legumes, nuts, poultry and fish for one serving a day of red meat was associated with a 14% lower risk of overall breast cancer (RR 0.86, 95% CI 0.78 to 0.94) and premenopausal women (RR 0.86, 95% CI 0.76 to 0.98)

 

How did the researchers interpret the results?

The researchers concluded that a higher intake of red meat in early adulthood may be a risk factor for breast cancer, and that replacing red meat with a combination of legumes, poultry, nuts and fish may reduce this risk.

 

Conclusion

Overall, this cohort study found that a higher intake of red meat was associated with higher risk of breast cancer among a large group of US female nurses. The studies strengths include the large population size, the study’s prospective nature and the fact there was a relatively long follow-up period (20 years).

The researchers note limitations to their study, which should be considered when interpreting the findings. These include the fact that:

  • the participants were predominantly white, educated US females, so caution should be taken when generalising the findings to other races or ethnic groups
  • dietary intake was assessed using a food frequency questionnaire, which relied on participants recalling their dietary intake over the previous year. It is likely that participants did not accurately report their dietary intake, which introduces some measurement bias
  • the researchers adjusted their results for multiple confounders (e.g. family history of breast cancer and smoking); however, it is possible that other factors, which the researchers did not take into account, could have affected results
  • the findings related to substituting foods are estimates only and may not reflect actual effects of protein substitution

It is important to note that this is only one study and needs to be interpreted alongside the wider body of current evidence related to dietary factors and cancer risk.

It is not yet clear whether this study, alongside other potential future evidence, will lead to a different set of conclusions about dietary links with breast cancer.

However, it should not be concluded from this particular study alone that red meat and processed meat increase the risk of breast cancer.

To try and reduce your risk of cancer overall, you should follow a healthy, balanced diet high in fruit and vegetables, and low in saturated fats and sugars, as well as limiting your alcohol intake and exercising in line with recommendations.     

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

Links To The Headlines

Red meat 'linked to breast cancer'. BBC News, June 11 2014

Replace red meat with chicken to cut breast cancer risk. The Daily Telegraph, June  11 2014

Three bacon rashers a day 'raises breast cancer risk for young women': Frequently eating red meat can raise chance of developing disease by more than 20%. Mail Online, June 10 2014

Women who eat lots or red meat 'at increased risk' of breast cancer. Daily Mirror, June 10 2014

Breast cancer link to higher red meat consumption greeted with scepticism. The Guardian, June 10 2014

Links To Science

Farvid MS, Cho E, Chen WY, et al. Dietary protein sources in early adulthood and breast cancer incidence: prospective cohort study. BMJ. Published online June 10 2014

Categories: Medical News

Tomato extract's heart effects exaggerated

Medical News - Tue, 06/10/2014 - 16:17

“Ketchup with everything: tomato sauce helps fight heart disease,” is the misleading headline in The Daily Telegraph.

The headline follows a small study conducted into lycopene tablets, which involved 36 people with cardiovascular disease and 36 healthy volunteers. Lycopene is the pigment that gives tomatoes (and some other fruit and veg) their distinctive colour. It has been the subject of numerous research projects in recent years, as it is thought to have antioxidant properties that may help protect against diseases that affect the heart and blood vessels (cardiovascular diseases).

This latest study found that people with cardiovascular disease who took statins saw their blood vessels dilate (widen) to a greater extent after they were treated with a chemical called acetylcholine if they had been taking lycopene every day for two months, rather than a placebo.

The lycopene tablet had no significant effect on any of the other outcomes the researchers looked at, and no effect on healthy volunteers (apart from increasing lycopene levels in the blood).

While improving the dilation of blood vessels may hypothetically reduce the risk of cardiovascular disease, this remains unproven in a real life setting.

Larger, longer-term studies are required to determine whether taking lycopene actually cuts the risk of heart attack and stroke.

 

Where did the story come from?

The study was carried out by researchers from the University of Cambridge and Cambridge University Hospitals NHS Foundation trust in the UK, and the University of Tartu, in Estonia. Funding was provided by Cambridge University Hospitals NHS Foundation Trust. The individual researchers were funded by the Wellcome Trust, the British Heart Foundation, the Estonian Science Foundation, the European Union Social Fund and the National Institute of Health Research Cambridge Comprehensive Biomedical Research Centre.

The study was published in the peer-reviewedopen-access journal PLOS One and can be read for free online.

Misleading headlines aside, the media have reported the story accurately and highlighted that larger studies are required to determine whether the effects shown here will have real health benefits.

 

What kind of research was this?

This was a randomised controlled trial (RCT) that aimed to investigate the effects of lycopene, the red pigment found in tomatoes (and certain other fruits and vegetables), on the blood vessels of patients with cardiovascular disease who were taking statins, as well as on healthy volunteers.

Previous research has found a link between reduced cardiovascular disease and the “Mediterranean diet”; the researchers wanted to see if this could be, at least partially, due to lycopene.

RCTs are the best way of demonstrating a cause-and-effect relationship. However, this was a small-scale trial, and the findings need to be replicated in a larger group of people.

 

What did the research involve?

The researchers randomised 36 patients with cardiovascular disease who were taking statins to either 7mg lycopene or a placebo daily for a two-month period.

The researchers then looked at the responses of blood vessels in the arm to acetylcholine – a chemical that causes them to dilate.

They also looked at the responses of blood vessels to other chemicals that cause them to dilate or contract, arterial stiffness, blood pressure, levels of different markers in the blood, as well as safety and tolerability.

The researchers then repeated these tests with 36 healthy volunteers.

 

What were the basic results?

Among the patients with cardiovascular disease who were randomised to take lycopene, dilation after acetylcholine improved by 53% and was significantly different to dilation in patients with cardiovascular disease who were randomised to take placebo.

There were no differences in the response of blood vessels to other chemicals, in arterial stiffness, blood pressure or the levels of different markers in the blood, apart from lypocene levels.

Lycopene had no effect in healthy volunteers on any of the outcomes investigated, apart from levels of lycopene in the blood. 

 

How did the researchers interpret the results?

The researchers concluded that “despite optimal secondary prevention medication, endothelial function [the function of the cells that line blood vessels] is impaired in patients with cardiovascular disease, and this is improved by oral supplementation with 7 mg lycopene, without any concomitant changes in traditional risk factors such as [blood pressure] or lipid profiles, or measures of inflammation. In contrast, we were unable to demonstrate any changes in endothelial function or other parameters after lycopene treatment in [healthy volunteers].”

 

Conclusion

This study found that the blood vessels in people with cardiovascular disease who were taking statins dilated more after they were treated with a chemical called acetylcholine if they had been taking lycopene every day for two months, compared to those taking placebo pills.

The lycopene tablet had no significant effect on any of the other outcomes the researchers looked at, and no effect in healthy volunteers, although it did increase lycopene levels in the blood. 

Although impaired endothelial function is a known predictor of future heart disease, this is, at best, a surrogate outcome. It is no substitute for following up people over time to see if improvement in endothelial function actually does translate into reduced deaths from heart attacks and stroke. 

Due to this limitation, much larger RCTs, with a follow-up period measured in years rather than months, are required to determine whether taking lycopene actually cuts the risk of cardiovascular disease.

Many unanswered questions remain about why eating a Mediterranean diet seems to reduce the risk of heart attack and stroke, but the benefits of the diet seem to be real.

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

Links To The Headlines

Ketchup with everything: tomato sauce helps fight heart disease. The Daily Telegraph, June 10 2014

'Tomato pill' hope for stopping heart disease. BBC News, June 9 2014

Tomato extract relieves damaged arteries, finds Cambridge study. The Guardian, June 9 2014

£1-a-day tomato pill that helps your heart: Treatment can increase blood vessel flow by 50% in patients with cardiac problems. Mail Online, June 10 2014

Tomato pill could prevent heart attacks say experts. Daily Express, June 10 2014

Links To Science

Gajendragadkar PR, Hubsch A, Mäki-Petäjä KM, et al. Effects of Oral Lycopene Supplementation on Vascular Function in Patients with Cardiovascular Disease and Healthy Volunteers: A Randomised Controlled Trial. PLOS One. Published online June 9 2014

Categories: Medical News

One in three adults in England 'has prediabetes'

Medical News - Tue, 06/10/2014 - 14:00

"One in three adults in England 'on cusp' of diabetes," BBC News and others report. The media reports are based on a study that estimated that 35.3% of adults in the UK now have prediabetes (also known as borderline diabetes).

Prediabetes is where blood sugar levels are abnormally high, but lower than the threshold for diagnosing diabetes. It is estimated that around 5-10% of people with prediabetes will go on to progress to "full-blown" type 2 diabetes in any given years.

Researchers analysed information from the Health Survey for England (HSE). This is a survey that combines questionnaire-based answers with physical measurements and the analysis of blood samples from a representative sample of the English population.

This study found that there has been a significant increase between 2003 and 2011 in the proportion of people aged 16 or older with prediabetes, from 11.6% in 2003 to 35.3% in 2013.

Known risk factors, confirmed in this study, include age (40 and above), body mass index (25 and above), being of south Asian ethnicity, and having high blood pressure.

If you think you may be at high risk of prediabetes, you can ask your GP for a blood test. It is often possible to prevent the condition progressing into diabetes proper through lifestyle changes, such as improving your diet and exercising more.

 

Where did the story come from?

The study was carried out by researchers from the University of Florida and the University of Leicester, and was somewhat surprisingly funded by the US Department of Defense.

It was published in the peer-reviewed BMJ Open, an open access medical journal, so the study is free to read online.

This study was accurately reported in the UK media, with many articles also helpfully outlining the complications of diabetes, its impact on public health, and some relevant contextual information.

For example, this included information about the NHS Health Check programme, which invites people between the ages of 40 and 74 to have a check to assess their risk of heart disease, stroke, kidney disease and diabetes, and to give support and advice to help people reduce or manage their risk.

But as the NHS Health Check programme is in its infancy, it is hard to estimate what the likely take-up will be in the future and what impact it will have on public health.

 

What kind of research was this?

This was a cross-sectional study that aimed to report trends in the prevalence of prediabetes among people aged 16 or older in England.

Cross-sectional studies are the ideal way of determining how many people have a condition.

 

What did the research involve?

The research used information collected by the Health Survey for England (HSE) in the years 2003, 2006, 2009 and 2011.

The HSE is an annual population-based survey that combines questionnaire-based answers with physical measurements and the analysis of blood samples from a random sample of participants.

People were classified as having prediabetes if they had glycated haemoglobin (an indicator of blood sugar levels) between 5.7% and 6.4% and had not previously been diagnosed with diabetes.

Glycated haemoglobin is formed when haemoglobin is exposed to glucose in the blood. As the amount of glucose in the blood increases, the fraction of haemoglobin that is glycated increases.

Diabetes is diagnosed when the level is 6.5% or above. However, there is no internationally agreed lower level for prediabetes.

The American Diabetes Association uses 5.7% as the lower cut-off level, but a UK expert group for the National Institute for Health and Care Excellence (NICE) recommend 6.0-6.4%.

 

What were the basic results?

The prevalence of prediabetes increased over the study period. It was:

  • 11.6% in 2003
  • 20.4% in 2006
  • 32.6% in 2009
  • 35.3% in 2011

Age, being overweight, obesity, blood pressure level and cholesterol level exhibited significant relationships with prediabetes in all years that these were measured.

People with greater socioeconomic deprivation were more likely to have prediabetes in 2003 and 2006, but the relationship was no longer significant in 2009 and 2011.

The researchers found that predictors of prediabetes in 2003 and 2011 included:

  • being 40 years or older
  • being of south Asian ethnicity
  • having a high body mass index (BMI) of 25 or over
  • having been diagnosed with high blood pressure
  • being socioeconomically deprived (being in the second most deprived quintile)

 

How did the researchers interpret the results?

The researchers concluded that, "There has been a marked increase in the proportion of adults in England with prediabetes. The socioeconomically deprived are at substantial risk.

"In the absence of concerted and effective efforts to reduce risk, the number of people with diabetes is likely to increase steeply in coming years."

 

Conclusion

This study indicates that there had been an increase between 2003 and 2011 in the proportion of people aged 16 or older with prediabetes, with more than a third of adults in 2011 having prediabetes.

The study is useful because it is based on information from the Health Survey for England (HSE), which sampled a representative sample of the English population.

However, the researchers defined prediabetes using cut-offs used by the American Diabetes Association (5.7-6.4%), but in the UK NICE recommends higher cut-offs to identify people at high risk of diabetes (6.0-6.4%).

There are several ways you can reduce your risk of developing type 2 diabetes:

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

Links To The Headlines

One in three adults in England 'on cusp' of diabetes. BBC News, June 10 2014

One in three adults have borderline diabetes, study finds. The Daily Telegraph, June 10 2014

Study reveals sharp rise in English people at risk of getting type 2 diabetes. The Guardian, June 9 2014

One in three adults 'on cusp of diabetes' in England. The Independent, June 10 2014

A third of adults have 'borderline' diabetes - but most don't know: Rising tide of obesity means number who have 'prediabetes' has trebled since 2006. Daily Mail, June 10 2014

Obesity levels mean number of adults with diabetes has tripled in just eight years. Daily Mirror, June 9 2014

One In Three Adults Have Borderline Diabetes. Sky News, June 10 2014

Over a third of adults have 'borderline diabetes'. ITV News, June 10 2014

Links To Science

Mainous III AG, Tanner RJ, Baker R, et al. Prevalence of prediabetes in England from 2003 to 2011: population-based, cross-sectional study. BMJ Open. Published online June 9 2014

Categories: Medical News

Is obesity jab 'two years away'?

Medical News - Mon, 06/09/2014 - 14:26

“New obesity jab could be available within two years,” the Mail Online reports. The headline comes following news that scientists have identified a protein that may help stimulate the production of brown fat.

Brown fat helps keep mammals warm. In humans, it is mostly found in newborn babies, who are particularly vulnerable to cold. As we age, we do not need brown fat as much, and in adulthood we have mostly white fat. Excess white fat (obesity) can damage your health, whereas brown fat has been linked to protection against obesity and type II diabetes; as such, it has attracted increasing interest and research.

Brown fat also helps to burn calories when the body is exercising (or, less pleasantly, when you are cold enough to shiver). Unlike white fat, it acts like muscle, keeping the body firm and toned.

The study, which involved mice rather than people, found that the new protein helped stimulate the production of brown fat. 

The optimism surrounding these findings is based on the hope that researchers could potentially harness the effects of this molecule to develop an obesity treatment in the future.

However, claims that an “obesity jab could be available within two years” seem overly optimistic.

Studies on people are needed before any claims of this kind can be made.

 

Where did the story come from?

The study was carried out by researchers from Harvard Medical School and the Dana-Farber Cancer Institute, in the U.S., and was funded by grants from the US National Institutes of Health and JPB Foundation.

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

The Mail Online’s headline that “a new obesity job could be available within two years” is not supported by the publication, although the authors did state that the “therapeutic potential in metabolic diseases is obvious”. 

There was a related study, performed by the same research team, in which the effects of the hormone irisin were studied, also in mice. Evidence suggests that irisin can also help stimulate production, by turning white fat into brown fat.

Somewhat confusingly, the Mail Online and the Daily Express seem to have reported on the findings of both studies as if they were a single piece of research.

 

What kind of research was this?

This was a laboratory study that used mice to identify and investigate the function of hormones released in muscles in response to exercise and cold.

Obesity levels in middle- and high-income countries is high and continuing to rise, with associated diseases including type 2 diabetes, cardiovascular disease and cancer.

As a result, the authors state there is increasing interest in brown fat – which uses energy to create heat and stops mammals becoming overly cold. In humans, brown fat is mostly found in newborn babies, who are particularly vulnerable to cold (as they have a large surface area to body volume ratio and are unable to shiver). As we age, we do not need as much brown fat to keep us warm, and have mostly white fat. However, brown fat has also been linked to protection against obesity and type II diabetes. Some hope that finding a way to make the body produce more brown fat, or convert white fat into brown fat, may help prevent obesity.

Exercising is a simple way to increase energy expenditure, and helps prevent obesity and associated metabolic disorders. It also increases the circulating levels of certain hormones released from muscle, which are known to mediate some of the beneficial effects of exercise.

The researchers wanted to see if there was the potential to harness some of these hormones to artificially mimic the beneficial effects of exercise, and investigated the role of brown fat in this process.

 

What did the research involve?

The research involved numerous genetic and protein studies involving mice. They were looking for molecules that were released during exercise and in response to cold, which would give them clues as to how exercise and brown fat activity were generating health benefits. By screening numerous molecules, they sought to identify those that were having the most important effects. 

What were the basic results?
  • The experiments identified a molecule called meteorin-like (Metrnl), which was present in muscle and fat.
  • Circulating levels of Metrnl rose after mice exercised and when they were exposed to the cold. 
  • Metrnl was found to stimulate energy expenditure and converted regular fat into heat-producing brown fat. Metrnl also improved glucose tolerance – a sign of metabolic health – in mice fed a high-fat diet. It was doing this by interacting with many aspects of the body’s immune system and its temperature regulation systems.
  • Blocking Metrnl action stopped these beneficial effects – confirmation that it was heavily involved in this process.  
  • Metrnl levels increased as a result of repeated bouts of prolonged exercise, but not during short-term muscle activity.

 

How did the researchers interpret the results?

The researchers concluded that Metrnl’s “therapeutic potential in metabolic diseases is obvious. The recombinant Metrnl protein used here hints at that potential, but other proteins with better pharmacological properties will be required”.

 

Conclusion

This study identified a molecule that is induced by exercise and exposure to cold. It has been implicated in stimulating brown fat development and improving glucose tolerance – both of which have been linked to a lower risk of obesity and type II diabetes, giving hope that harnessing the effects of this molecule could create obesity treatments.

However, this optimism appears premature, as the research was conducted solely in mice. It will need to be reproduced and validated in humans to see if it is safe and effective at stimulating weight loss or other benefits. These remain unproven at this stage.

Other promised potential “anti-obesity jabs” include leptin and irisin, neither of which have delivered convincing results in human trials. This serves to highlight that when a new compound shows promise in mice, these don’t necessarily translate into effective medicines for humans.

On this basis, the Mail’s headline that a “new obesity jab could be available within two years” appears unjustified.

Rather than holding out hope of some magic medical bullet to beat or treat obesity, it’s best to try and lose weight through healthy eating and exercise. Our free 12-week NHS Weight Loss plan can help you achieve sustainable weight loss.

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

Links To The Headlines

New obesity jab could be available within two years after scientists discover hormone that helps the body burn fat. Mail Online, June 6 2014

New drug boosting immune system could beat obesity and diabetes. Daily Express, June 6 2014

Links To Science

Rao RR, Long JZ, White JP, et al. Meteorin-like Is a Hormone that Regulates Immune-Adipose Interactions to Increase Beige Fat Thermogenesis. Cell. Published online June 5 2014

Categories: Medical News

Cannabis can damage lives, researchers argue

Medical News - Mon, 06/09/2014 - 14:00

“Smoking marijuana as a teenager lowers IQ for life, scientists warn,” the Mail Online reports. The headline is prompted by a critical review looking at the evidence about the potential harms associated with cannabis use.

This latest review was written by researchers from the US National Institute on Drug Abuse and provides an overview of the potential harms associated with cannabis use, ranging from increased risk of car accidents to an adverse effect on “life achievement”.

The Mail’s coverage of the story was an accurate representation of the research, although it took the review findings at face value and did not mention any of its limitations. The most important of which is that it does not appear to be a systematic review, where all available evidence on a particular topic is assessed.

It is unclear whether this study was prone to “cherry picking” – where evidence that supports the researchers’ arguments is included while evidence that opposes it is ignored. This has the potential to bias the findings and conclusions.

The timing of the study is also interesting. After the quasi-legalisation of cannabis in the states of Colorado and Washington there have been increasing calls to roll-out similar laws across America.

Many of the review's conclusions were tentative or indicated more research was needed. Based on this review alone, research into the effects of cannabis use in humans has not yet yielded any firm conclusions and often paints an unclear or inconsistent picture.

 

What is the basis for these current news reports about cannabis?

The authors state cannabis (marijuana) is the most commonly used illicit drug in the US with around 12% of people over the age of 12 reporting use in the past year, with particularly high rates among young people.

The regular use of cannabis in adolescence was of particular concern to the review group because of a higher chance of potential harm in younger groups.

The review highlighted a popular belief of cannabis as a harmless vice. Given the loosening of laws and regulation on recreational use in in some US states (Colorado and Washington), some may see this as giving legitimacy to this idea. And in response to the increase in the legalisation of cannabis for medical and recreational use in the US, patients may be more likely to ask their doctors about its potential benefits and risks to health.

The authors indicated many scientific studies report harmful effects associated with cannabis but others do not, which has led to heated debate about whether cannabis is harmful.

The review aimed to assess the current state of the science on the adverse health effects of recreational cannabis use, focusing on those areas for which the evidence is strongest.

 

What did the report find?

The review was broad, covering addiction, neurodevelopment, mental illness, risk of cancer and life chances.

Risk of addiction

The authors indicated that, “despite some contentious discussions regarding the addictiveness of marijuana, the evidence clearly indicates that long-term marijuana use can lead to addiction”. Around 9% of those who experiment with cannabis become addicted, and this figure rises to 50% of those who smoke it every day, the review said.

Effect on brain development and IQ

The negative effects of cannabis use on the brain were said to be particularly prominent if use starts in adolescence or young adulthood. The review flagged up one study that found an association between frequent use of cannabis from adolescence into adulthood with significant declines in IQ.

Role as a gateway drug

There is a theory that using cannabis in early adulthood could encourage the use of other addictive drugs such as nicotine or alcohol. The review found animal studies that were consistent with this theory. However, they also acknowledged they didn’t know whether people with more addictive tendencies are more likely to try cannabis, alcohol and nicotine, or whether cannabis use itself directly increased the chances of them trying these things.

Mental illness

Regular cannabis use was reported to be associated with an increased risk of anxiety and depression, but causality has not been established.

It has also been linked to psychosis (including those associated with schizophrenia), especially among people with a pre-existing genetic vulnerability, and worsens illness in people with schizophrenia.

The authors say it is difficult to establish causality in these types of studies, because factors other than cannabis use may be directly associated with the risk of mental illness. Other factors could also predispose a person to both cannabis use and mental illness. This makes it difficult to confidently attribute the increased risk of mental illness to cannabis use.

Effect on school performance and lifetime achievement

The review indicated that cannabis use impairs critical cognitive functions, both during acute intoxication and for days after use. For this reason, students who smoke cannabis could be functioning at a cognitive level that is below their natural capability for considerable periods of time. However, the results from studies included in the review were inconsistent.

Some studies suggested the long term negative effects of cannabis use on learning may be reversible, whereas others indicated memory and attention got significantly worse the more years someone had been using cannabis regularly.

Some studies suggested early cannabis use is associated with impaired school performance and an increased risk of dropping out of school, but there were other factors that could explain this link. For example, shared environmental factors like growing up in a neighbourhood where drug use is high and academic achievement low.

Risk of motor-vehicle accidents

There were studies indicating that both immediate exposure and long-term exposure to cannabis impair driving ability. According to a meta-analysis, the overall risk of involvement in an accident increases by a factor of about two when a person drives soon after using cannabis. The risk associated with the use of alcohol in combination with cannabis was reported to be greater than that associated with the use of either drug alone.

Risk of lung cancer

The effects of long-term cannabis smoking on the risk of lung cancer are unclear and often complicated by the fact many cannabis smokers also smoke tobacco – which is known to cause cancer. Separating the health effects of the two types of smoking remains a challenge. The researchers warned that the strength of cannabis in circulation is increasing and so any potential risks may also be increasing.

 

Can we believe the review’s findings?

The review’s main weakness is that it didn’t describe how it searched and reviewed the evidence on this subject and whether this was systematic. This means that key evidence may have been missed, leading the authors to potentially draw biased conclusions. It is not possible to say that the results were biased; only that without the methods, there remains a risk that they are.

A second limitation is that the evidence behind the review’s conclusions was drawn largely from early animal studies, or from observational studies that couldn’t establish cause and effect. This means we can’t really make clear cut, definitive statements about the health effects of cannabis use as the evidence, at least the evidence identified in this review, was not strong in most areas. The long term effects of cannabis use, for example, remain in the authors’ words “poorly understood”.

The review generally highlighted a scarcity or lack of knowledge on the beneficial or harmful effects of cannabis. This may be a true reflection of the evidence base, or may be in part because the review has not included all the relevant evidence.

One of the biggest challenges in studying the effects of cannabis is that due to its legal status in much of the world, researchers could not legally use cannabis in the “gold standard” of studies – a randomised controlled trial. There could also be ethical problems in randomly assigning people to use cannabis who don’t already, given its potentially damaging effects.

As more and more parts of the world are now legalising (or at least partially decriminalising) cannabis, research of this type could potentially be carried out and may allow us to learn more about the benefits and risks of this widely used drug.

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

Links To The Headlines

Smoking marijuana as a teenager lowers IQ for LIFE, scientists warn. Mail Online, June 6 2014

Links To Science

Volkow ND, Baler RD, Compton WM, Weiss SRB. Adverse Health Effects of Marijuana Use. The New England Journal of Medicine. Published online June 5 2014

Categories: Medical News

Sleep 'promotes memory-related brain changes'

Medical News - Fri, 06/06/2014 - 18:19

"The mechanism by which a good night's sleep improves learning and memory has been discovered by scientists," is the somewhat overeager reporting on the BBC News website. While the study had intriguing results, it only involved mice.

This study in mice looked at if and how sleep helps memory and learning. The researchers got mice to perform a running task, running both forwards and backwards on a rotating rod.

Some of the mice were allowed to sleep afterwards and some were sleep deprived. The mice were then microscopically examined to see how sleep, or the lack of it, influenced the connections between the nerve cells in the brain.

Mice who were allowed to sleep experienced the formation of new dendrites (spinous projections at the end of nerve cells), which pass electrical signals from one nerve cell to another.

The formation of new dendrites may be linked to changes in the brain that are associated with learning and experience (changes to the brain's plasticity). But if the mice were deprived of sleep, these new connections did not develop.

The study may not have a direct application to humans, however, and much of the mystery of sleep remains to be discovered. But this research could be another small piece of the puzzle that suggests that sleep is one of the ways we may help consolidate our learning.

 

Where did the story come from?

The study was carried out by researchers from the New York University School of Medicine in the US and Peking University Shenzhen Graduate School in China, and was funded by the US National Institutes of Health, a Whitehall Foundation research grant, and a grant from the American Federation for Aging Research.

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

The main body of the BBC News reporting is accurate, though the headline "Sleep's memory role discovered" is probably far too definitive for the limited, if interesting, research outlined in the study.

 

What kind of research was this?

This study in mice aimed to see how sleep helps memory and learning. The researchers did this by getting mice to perform a running task. 

Some of the mice were allowed to sleep afterwards, while some were sleep deprived. The mice's brains were then microscopically examined to see how sleep influenced the connections between the nerve cells in the brain.

The researchers say that it is believed that sleep has an effect on the connections (synapses) between nerve cells, which are important for the formation of memories. But the role that sleep plays in learning and experience-dependent changes to the synapses is said to be unclear.

 

What did the research involve?

This study aimed to see how performing a running task remodels the spinous projections (dendrites) that form the connections between nerve cells, and then see how this was influenced by sleep.

A group of mice were trained to run forwards on an accelerated rotating rod. The spinous projections connecting the nerve cells in the brain were microscopically examined before and after the task.

These mice were compared to a group of mice who had not received the rotating rod training. The researchers then looked at the effect of training the mice to run either forwards or backwards on the rod.

After these tests, the researchers examined the potential role of sleep in the process. They compared mice who were allowed to sleep in the seven hours after a period of forward running on the rod with mice who were sleep deprived by continuous gentle handling for seven hours after the task.

They then tested whether the effect of sleep deprivation could be "rescued" by allowing the mice to sleep in the 16 hours after the initial seven hours of sleep deprivation.

 

What were the basic results?

The mice had an increased development of new spinous projections between nerve cells in the brain in the 24 hours after the rotating rod task when compared with mice who had not done the task. 

When they repeated the running task, this time allowing the mice to run forwards or backwards, the researchers found that backwards running led to the formation of a different set of spinous projections.

The researchers then compared mice who were allowed to sleep after the rotating rod task with mice who were sleep deprived. They found that the sleep-deprived mice showed a significantly reduced formation of new spinous projections between nerve cells.

Even if the sleep-deprived mice were allowed to train on the rotating rod for double the amount of time beforehand, it made no difference – they still demonstrated fewer nerve cell connections than the mice who were allowed to sleep.

The 16-hour recovery sleep after the initial deprivation had no effect – they had fewer projections, suggesting the effects of sleep deprivation could not be "rescued".

For mice who had been allowed to sleep, the projections between the nerve cells were demonstrated to persist in the following days, supporting the common understanding that a skill is learned and persists for long periods of time with minimum interference from other learning.

When looking at specific sleep stages, the researchers found that deprivation of REM sleep (the deepest period of sleep in which dreams are thought to occur) in particular did not diminish the synapses. This suggests that non-REM sleep may be involved in forming new nerve connections after learning.

 

How did the researchers interpret the results?

The researchers conclude that their findings indicate that sleep has a key role in promoting learning-dependent connections between nerve cells, which contribute to memory storage.

 

Conclusion

This research in mice furthers our understanding of the important role that sleep plays in consolidating our learning and memory.

When mice learned to run on a rotating rod, the task led to the formation of new spinous projections (dendrites) at the end of nerve cells, which pass electrical signals from one nerve cell to another.

However, if the mice were deprived of sleep, these new connections did not develop.

This effect could not be "rescued", regardless of whether they were allowed to train for a much longer period before being sleep deprived, or if they were allowed to sleep for a long period after their initial sleep deprivation.

The researchers also found that most of the changes to the nerve cell connections seemed to be occurring during non-REM sleep, rather than REM sleep.

The results of this study may not have a direct application to humans. But if further evidence proves that it does, it suggests that attempting to compensate for the adverse effects of missing sleep, such as sleeping for 16 hours after pulling an all-nighter, may be futile: The mice were unable to "rescue" the beneficial effects to the brain if they were sleep deprived for a significant amount of time.

Known harmful effects of not getting enough sleep include:

  • detrimental effects on mood, such as irritability
  • impaired cognitive function
  • increased vulnerability to infection

Read more about Why a lack of sleep can be bad for your health.

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

Links To The Headlines

Sleep's memory role discovered. BBC News, June 6 2014

Sleep may help memories form by promoting new synapses. New Scientist, June 5 2014

We May Finally Know Why Sleep Improves Memory. Io9.com, June 5 2014

Links To Science

Yang G, Lai CSW, Cichon J, et al. Sleep promotes branch-specific formation of dendritic spines after learning. Science. Published online June 6 2014

Categories: Medical News

5:2 diet style an 'immune booster,' study finds

Medical News - Fri, 06/06/2014 - 14:00

“Fasting for at least two days regenerates immune systems damaged by ageing or cancer treatment, research has shown,” the Daily Express reports. However, the study that is being reported on only involved mice, not humans.

Prolonged or intermittent fasting has become an increasingly popular strategy to achieve weight loss. This has been demonstrated through the incredibly popular 5:2 diet, where participants eat normally for five days a week and then fast for the remaining two.

There have been reports that the 5:2 diet can lead to weight loss for some people, with others claiming that fasting can boost immune function and prevent chronic diseases.

In this study, which used only mice, the researchers aimed to see whether prolonged fasting could reverse the toxic effects of chemotherapy – specifically, damage to white blood cells and bone marrow activity, which leaves the body weakened and vulnerable to infection.

Researchers found that mice fasting for two to five days before being given chemotherapy showed a faster recovery in terms of their white blood cell count. A later-stage clinical trial in humans is reported to be underway.

It is extremely important to stress that if you are undergoing chemotherapy treatment, you should not make any kind of radical changes to your diet unless advised to by your doctor. Doing so could make you vulnerable to complications.

 

Where did the story come from?

The study was carried out by researchers from the University of Southern California, Ohio University and the University of Palermo, in Italy. The study was supported by the National Institutes of Health and Aging and was published in the peer-reviewed science journal Cell. It has been published on an open-access basis, so it is free to read online.

The Daily Telegraph’s reporting of the study was accurate and included discussion from experts, who said that while the findings may have relevance for people receiving cancer treatment, further study is needed, and prolonged fasting should only be considered under the guidance of a doctor. As the Professor of Regenerative Medicine at UCL, Chris Mason, suggests: “The most sensible way forward would be to synthesise this effect with drugs. I am not sure fasting is the best idea. People are better eating on a regular basis.”

The Daily Express’s coverage, while not inaccurate, was not as clear as it should be. It is not until the last part of the article that you realise the study involved mice, not humans.

 

What kind of research was this?

This was a scientific study using mice, which aimed to look at the effect prolonged fasting might have on reversing the toxic effects of chemotherapy.

This included how it affected bone marrow regeneration and circulating white blood cells – key components of the body’s immune system.

The researchers explain how immune system defects are central to the ageing process and are associated with a range of diseases. One of the effects of chemotherapy is DNA damage and cell death, to both circulating blood cells and to stem cells of the bone marrow, which are responsible for producing new blood cells.

This leads to reduced numbers of red blood cells (which carry oxygen), platelets (which help blood to clot) and white blood cells (which make up the body’s immune system), leaving the body weakened and vulnerable to infection.

All of this can result in a wide range of side effects for people undergoing chemotherapy.

The authors state that prolonged fasting for two to five days activates cellular pathways in mice and humans, which enhance the resistance of cells to toxins, such as chemotherapy. Previous studies in mice have found that prolonged fasting leads to this protective effect, by reducing levels of insulin-like growth factor-1 (IGF-1) – a protein involved in growth and development, with a similar function to insulin.

The theory is that the reduction of IGF-1 resulting from prolonged fasting may allow regeneration of stem cells in the bone marrow, and so help to reverse the toxic effects of chemotherapy.

 

What did the research involve?

Mice were divided into two groups who were either fed or fasted prior to being injected with chemotherapy drugs for two weeks. The researchers looked at white blood cell counts during and after chemotherapy treatment, and also assessed DNA damage in circulating blood cells and bone marrow cells.

As their previous study had shown that prolonged fasting leads to a reduction in IGF-1 levels, and they believed that this was responsible for the protection against chemotherapy, they also looked at what would happen when mice genetically engineered to have IGF-1 deficiency were given chemotherapy without having fasted.

 

What were the basic results?

The researchers found that multiple cycles of prolonged fasting protected mice from some of the toxic effects of chemotherapy, reducing DNA damage to both circulating white blood cells and bone marrow stem cells. It also led to the regeneration of bone marrow stem cells. Mice who were given chemotherapy but fed as normal showed prolonged white blood cell depletion, while mice who had fasted beforehand saw their white blood cell count return to normal levels at a faster rate.

As expected, they found that using mice genetically engineered to have IGF-1 deficiency – replicating the effects of prolonged fasting – also showed faster recovery of their bone marrow stem cells. This confirmed that the effect on bone marrow stem cells was probably being mediated by a reduction in IGF-1 levels. Reduction of IGF-1 signalling seemed to promote the renewal of bone marrow stem cells.

 

How did the researchers interpret the results?

The study authors concluded that their results “indicate that cycles of an extreme dietary intervention represent a powerful mean[s] to modulate key regulators of cellular protection and tissue regeneration, but also provide a potential therapy to reverse or alleviate the immunosuppression caused by chemotherapy treatment and ageing”.

 

Conclusion

This scientific study suggests that multiple cycles of prolonged fasting may be able to reverse some of the toxic effects of chemotherapy in mice, by causing the regeneration of stem cells in bone marrow.

This allowed white blood cell counts to return to normal much faster after chemotherapy, compared to mice that were allowed to eat normally.

The study researchers indicated very early-stage study in humans (not appraised here), which found that fasting for 72 hours, rather than 24 hours, in combination with chemotherapy reduced some of the toxic effects of chemotherapy, in line with the findings in mice.

However, the study’s authors acknowledge that these results are very tentative and will need to be confirmed in larger, more robust, human studies.

phase 2 randomised control trial is said to be underway. 

Based on this study alone, it can be stated that people receiving cancer treatment, including chemotherapy, should not fast for extended periods of time without fully consulting a health professional, as this could be damaging to their health in other ways. Appropriate nutrition is very important for people with cancer, during treatment and when recovering from treatment. You should not make any significant changes to your diet without first seeking the advice and guidance of the health professionals treating you.

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

Links To The Headlines

Going without food for TWO DAYS can regenerate the body. Daily Express, June 6 2014

Fasting for three days can regenerate entire immune system, study finds. The Daily Telegraph, June 6 2014

Fasting 'revives immune system'. MSN News, June 6 2014

Links To Science

Cheng C, Adams GB, Perin L, et al. Prolonged Fasting Reduces IGF-1/PKA to Promote Hematopoietic-Stem-Cell-Based Regeneration and Reverse Immunosuppression. Cell Stem Cell. Published online June 5 2014

Categories: Medical News

Three-person IVF in 'two years'

Medical News - Thu, 06/05/2014 - 16:45

"Scientists will be ready to create babies from three people in around two years, if it is made legal," BBC News reports. The UK fertility regulator, the 

The main conclusion of the review is that the proposed techniques appear to be safe, but there are still a number of experiments that should be performed before treatments are offered to suitable patients.

There would also need to be a change to the law, ratified by parliament, before treatments could be legally offered.

 

What are mitochondrial diseases?

Almost all of the genetic material in our bodies is inside the cell nucleus that contains 23 chromosomes inherited from our mother and 23 inherited from our father. However, there is also a small amount of genetic material contained in cellular structures called mitochondria, which produce the cell’s energy. Unlike the rest of our DNA, this small amount of genetic material is passed to the child only from the mother. There are a number of rare diseases caused by gene mutations in the mitochondria. Women carrying these mutations will pass them directly to their child, with no influence from the father.

The IVF technique being considered aims to prevent these “mitochondrial diseases” by replacing the mother’s mitochondria with healthy mitochondria from a donor, thereby creating a healthy embryo. The child would then have the genetic material of three people – the majority still from the mother and father, but with around 1% of mitochondrial DNA coming  from a donor. 

 

What is mitochondria replacement?

There are two IVF mitochondria replacement techniques currently at the research stage, called pronuclear transfer and spindle transfer. These are the techniques under debate.

Pronuclear transfer involves an egg during the process of fertilisation. In the laboratory, the nucleus of the egg and the nucleus of the sperm, which have not yet fused together (the pronuclei), are taken from the fertilised egg cell containing the “unhealthy” mitochondria and placed into the donor-fertilised egg cell that has had its own pronuclei removed. This early stage embryo would then be placed into the mother’s body. The new embryo would contain the transplanted chromosomal DNA from both of its parents, but would have “donor” mitochondria from the other egg cell.

The alternative mitochondria replacement technique of spindle transfer involves egg cells prior to fertilisation. The nuclear DNA from an egg cell with “unhealthy” mitochondria is removed and placed into a donor egg cell that contains healthy mitochondria and has had its own nucleus removed. This “healthy” egg cell can then be fertilised.

Pronuclear transfer and spindle transfer are said to be potentially useful for the few couples whose child may have severe or lethal mitochondrial disease, and who would have no other option for having their own genetic child. It is estimated that in the UK, around 10-20 couples a year could benefit from these treatments. 

 

How many children does mitochondrial disease affect?

It is estimated that around 1 in 200 children are born each year with some form of mitochondrial disease. Some of these children will have mild or no symptoms, but others can be severely affected – with symptoms including muscle weakness, intestinal disorders and heart disease – and have reduced life expectancy.

 

What ethical concerns have been raised about the techniques?

There are obvious ethical implications from creating an embryo with genetic material from three parents.

Among the questions raised are:

  • Should the details of the donor remain anonymous or does the child have the right to know who their “third parent” is?
  • What would be the long-term psychological effects on the child knowing it was born using donated genetic tissue?

Opponents of these types of treatments cite what can be broadly summarised as the “slippery slope” argument; this suggests that once a precedent has been set for altering the genetic material of an embryo prior to implantation in the womb, it is impossible to predict how these types of techniques might be used in the future.

Similar concerns were raised, however, when IVF treatments were first used during the 1970s; today, IVF is generally accepted.  

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

Links To The Headlines

Three-person babies 'in two years' - says science review. BBC News, June 3 2014

Three-parent babies 'could be a reality within two years' after report finds controversial IVF techniques are 'not unsafe’. Mail Online, June 3 2014

Three-parent babies ‘safe’ to be born. Metro, June 3 2014

Three-parent babies are 'not unsafe' as human trials planned. The Daily Telegraph, June 3 2014

 

Categories: Medical News

Air pollution linked to irregular heartbeat and lung blood clots

Medical News - Thu, 06/05/2014 - 15:00

"Air pollution is linked to increased risk of developing an irregular heartbeat and blood clots in the lung," BBC News reports.

A large study found that short-term exposure to small particulate matter – a form of air pollution linked to cars and other sources – was linked to a raised risk of death from these conditions.

Small particulate matter is known to potentially be dangerous – because of its size (which can be 100 times thinner than a human hair), it can bypass the body's defences against foreign objects and affect the heart and the lungs.

Reassuringly, though, the study found no clear evidence of a link between air pollution and the risk of having a heart attack or stroke.

But the link found between irregular heartbeats (atrial fibrillation) and blood clots in the lungs (pulmonary embolism) is still a matter of concern. Both conditions can cause serious complications, especially in vulnerable people with a pre-existing health condition.

The study reinforces the fact that we should not become complacent about the health dangers posed by all forms of pollution.

 

Where did the story come from?

The study was carried out by researchers from the London School of Hygiene and Tropical Medicine and was funded by the Department of Health.

It was published in the peer-reviewed medical journal Heart and has been made available on an open access basis, so it is free to read online.

BBC News' and The Guardian's coverage was fair and the BBC included useful comments from independent experts.

 

What kind of research was this?

This study set out to explore the short-term impact of air pollution on cardiovascular disease. Using a case-crossover design, it analysed links between the information taken from three national databases on cardiovascular disease and short-term exposure to various types of air pollution.

The researchers say that high levels of some air pollutants are associated with an increased risk of cardiovascular outcomes, although the mechanism involved is uncertain. 

The study aimed to further our understanding of these mechanisms by examining the relationship between air pollution and a range of cardiovascular events.

 

What did the research involve?

Over the period 2003-09, the researchers used data from three national databases on cardiovascular disease in England and Wales. These included:

  • the Myocardial Ischaemia National Audit Project (MINAP), which tracks hospital admissions for acute coronary syndrome and heart attack (from 2003-09)
  • Hospital Episode Statistics (HES) on emergency admissions (from 2003-08)
  • figures from the Office for National Statistics (ONS) on recorded deaths (from 2003-06)

Using the last two databases, researchers looked at a range of cardiovascular disease events, including heart attacks, all strokes, ischaemic heart disease, chronic ischaemic heart disease, pulmonary embolism, atrioventricular conduction disorders, arrhythmias, atrial fibrillation and heart failure.

Arrhythmia is an abnormality of the heart rhythm and can be dangerous. Atrial fibrillation is a type of arrhythmia where the heart beats very fast and irregularly. A pulmonary embolism is a blockage in the pulmonary artery, which is the blood vessel that carries blood from the heart to the lungs.

The researchers looked at some 400,000 heart attacks, more than 2 million emergency admissions for cardiovascular problems, and 600,000 deaths from cardiovascular disease.

Using data from the monitoring station nearest to where patients lived, they looked at the average levels of air pollutants over a period of five days. Pollutant effects were adjusted for the ambient air temperature – recorded by the UK Meteorological Office – and the day of the week.

The air pollutants included carbon monoxide, nitrogen dioxide, particulate matter (PM10 and PM2.5), sulphur dioxide and ozone. Particulate matter refers to usually invisible particles floating in the air. They can be large (up to 10 micrometers, or PM10) or small (up to 2.5 micrometers, or PM2.5).

In their analysis, the researchers used a case-crossover approach, where the day of each health event was the case and all other days within the same month were controls.

 

What were the basic results?

The researchers found that:

  • The only clear link between deaths from cardiovascular disease and pollution was between PM2.5 particles and deaths from arrhythmias, atrial fibrillation and pulmonary embolism.
  • The pollutant nitrogen dioxide was associated with a raised risk of hospital admission for a variety of cardiovascular events, including cardiovascular disease overall (increased risk from 10th to 90th percentile of 1.7%, 95% confidence interval [CI] I 0.9 to 2.6), non-myocardial infarction cardiovascular disease (2.0%, 95% CI 1.1 to 2.9), arrhythmias (2.9%, 95% CI 0.6 to 5.2), atrial fibrillation (2.8%, 95% CI 0.3 to 5.4) and heart failure (4.4%, 95% CI 2.0 to 6.8).
  • Only nitrogen dioxide was associated with an increased risk of hospital admission for heart attack, of a type called non-ST elevation myocardial infarction (non-STEMI) (3.6% 95% CI 0.4 to 6.9). A non-STEMI heart attack is where the supply of blood to the heart is only partially blocked, rather than completely blocked.  As a result, a smaller section of the heart is damaged and there is a lower risk of fatality.

 

How did the researchers interpret the results?

The researchers say their study found no clear evidence for the effects of pollution on STEMI heart attacks (the most serious type) and stroke, but it did for pulmonary embolism and irregular heartbeat. Lead researcher Dr Ai Milojevic told BBC News that the strongest link was in the over-75s and in women.

They concluded that although it is likely that air pollutants affect cardiovascular health in several different ways, the lack of effects on STEMI heart attacks and stroke suggests it may partly act through "non-thrombotic" pathways – in other words, not through blood clotting.

 

Conclusion

This was a large national study that looked in detail at links between people's short-term exposure to air pollutants and national records on hospital admissions for heart attack, emergency admissions for all cardiovascular problems, and deaths from cardiovascular disease.

The study had some limitations – for example, as the authors say, it did not include heart attacks that took place before hospital admission. It also used fixed monitoring sites, which may not accurately reflect personal exposure to air pollution. 

For the public, the results of this study are probably confusing. That's because the researchers were interested in finding out which particular cardiovascular events are linked to pollution so that they could further understand the ways in which pollutants act on the cardiovascular system.

They found links between pollution and irregular heartbeat and blood clots in the lung – both of which can be dangerous – but not between pollution and heart attacks or strokes.

Most experts believe that pollution – especially small particulate matter – can have an effect on health. It is sensible to avoid areas with severe pollution, especially for those with chronic disease.

You can find updates on air pollution at Defra's UK air information resource pages and from Defra's freephone helpline on 0800 55 66 77. The helpline also offers health advice.

Read more advice about air pollution.


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

Links To The Headlines

Pollution link to irregular heartbeat and lung clotting. BBC News, June 5 2014

Air pollution linked to irregular heart beat, study finds. The Guardian, June 5 2014

Links To Science

Milojevic A, Wilkinson P, Armstrong B, et al. Short-term effects of air pollution on a range of cardiovascular events in England and Wales: case-crossover analysis of the MINAP database, hospital admissions and mortality. Heart. Published online June 5 2014

Categories: Medical News

Cannabis and sunshine may damage sperm quality

Medical News - Thu, 06/05/2014 - 14:25

''Cannabis doubles younger men's risk of infertility, study finds,'' reports The Independent. The same study also found a drop in sperm quality during the summer months.

The paper reported on the results of a study that saw men attending fertility clinics, looking at the effects of lifestyle on one element of male fertility – known as sperm morphology, which refers to the size and shape of sperm.

Sperm with abnormal sperm morphology are less likely to lead to a successful conception.

Researchers found that cannabis use was associated with a higher rate of abnormal morphology – the same trait seen in sperm samples produced during the summertime.

No other lifestyle factors, such as alcohol and smoking, were seen to have an effect.

It is important to point out that only one aspect of sperm quality was analysed. Other aspects, such as sperm motility (how good a “swimmer” each individual sperm is) or sperm count, were not studied.

The study was also reliant on the self-reporting of alcohol, smoking and cannabis use, which is likely to have been underestimated.

Until a more comprehensive look at lifestyle effects on fertility is provided, it is safe to say that choosing a healthy lifestyle is not going to reduce the chances of conceiving and will provide a healthier environment in which to bring up a child.

 

Where did the story come from?

The study was carried out by researchers from The University of Sheffield, the University of Manchester and the University of Alberta, Canada. It was funded by the UK Health and Safety Executive, the UK Department of Environment, Transport and the Regions, the UK Department of Health and the European Chemical Industry Council.

The study was published in the peer-reviewed medical journal Human Reproduction. The article is open access, meaning it is free to view and download online.

The media has largely ignored the fact that this study only looked at the shape of the sperm and not the sperm count, sperm motility or, indeed, fertility itself.

This may give readers the misleading impression that it has been proven that lifestyle factors such as obesity, smoking and excessive alcohol consumption do not have any negative influence on fertility rates. This is definitely not the case.

Read more about the risk factors for infertility.

 

What kind of research was this?

This was a cross-sectional study of men attending fertility clinics to see if there was a link between the shape of sperm (sperm morphology) and lifestyle.

The data came from a large study, which has also looked for links between lifestyle and other measures of sperm quality.

Semen analysis looks at numerous factors such as the acidity, quantity and thickness of the semen, as well as sperm quality.

This is assessed by the morphology, concentration (sperm count) and motility (ability to swim). Previous analysis using the same data set looked at concentration and motility, and did not find any conclusive lifestyle risk factors. This analysis only took the shape into account.

 

What did the research involve?

The researchers recruited 2249 men out of 4257 who had attended fertility clinics in the UK and were eligible for the study. They completed a questionnaire, had an interview on their lifestyle and also undertook a semen analysis. Statistical analysis then looked for links between the lifestyle of those men who had normal-shaped sperm and those who did not.

Men aged 18 and over were recruited to the study from 14 fertility centres in the UK between 1999 and 2002. They were eligible if they had been trying to conceive without success for at least 12 months and had not previously had semen analysis, or did not know the results of any analysis. They also had to understand English.

Exclusion criteria included:

  • having a known medical condition that could cause fertility, such as cystic fibrosis
  • previous treatment than can cause infertility, such as radiotherapy and chemotherapy
  • previous sterilisation of either couple, such as vasectomy or tubal ligation

The men who agreed to take part were given a brief questionnaire to complete at home, which asked about their job, lifestyle and health. They were asked to abstain (from ejaculation) for three to five days and then returned to the clinic. A research nurse then asked further questions about the type of underwear and clothing the person wore, any recreational drug use and fertility history. During the latter part of the study, their body mass index (BMI) was calculated and ethnic group recorded. They were excluded if they did not answer all of the questions.

Semen samples were then analysed. Cases with reduced fertility were defined as having a normal shape in less than 4% of the 200 sperm that were assessed. If there were less than 200 sperm on the slide, they were excluded from the analysis.

They then compared the lifestyle factors of men who had normal shaped sperm in less than 4% of the 200 sperm that were assessed, compared to those who had more than 4% normal-shaped sperm.

 

What were the basic results?

The study recruited 2249 men, representing just over half (53%) of those who were eligible.

Of those recruited, 173 were excluded because:

  • 81 had no sperm on the slide
  • 47 had fewer than 200 sperm on the slide
  • 43 were contaminated
  • 2 were lost

They further excluded all men who were recruited in the first six months of the study, because during this time there was a very high proportion of men with less than 4% of normal-shaped sperm (54.7%) compared to during the rest of the study (16.1%). The researchers did not know why, so excluded them in case they biased the results.

The analysis included 318 men who had less than 4% normal-shaped sperm out of 200, compared to 1970 who did.

Men who used cannabis in the previous three months were more likely to have poor shape than those who didn’t (Odds Ratio [OR] 1.55, 95% Confidence Interval [CI] 1.04-2.30). The effect was greater in men aged 30 or less (OR 1.94, 95% CI 1.05 to 3.60).

Samples collected in the summer were more likely to be reduced shape compared to those collected in the winter (OR 1.99, 95% CI 1.43 to 2.72)

Samples collected after abstinence of more than six days were less likely to be of abnormal shape (OR 0.64, 95% CI 0.43 to 0.95).

No other risk factors had a significant link to sperm shape.

 

How did the researchers interpret the results?

The authors conclude that the study “has identified few modifiable factors associated with poor sperm morphology, with the only practical advice to men attempting conception being to limit exposure to cannabis if they are regular users. We would argue that the results of this study, in combination with our papers that investigated the effect of lifestyle and occupation on poor motile sperm concentrations, suggest that men can make relatively few lifestyle changes to improve semen quality, either to enhance natural conception or improve their chances in assisted conception”.

 

Conclusion

This study has found that the shape of sperm is less likely to be normal when samples are provided in summer and if cannabis has been consumed in the previous three months. It has also found that normal-shaped sperm are more likely to be produced after six days of abstinence. It did not find any other links between lifestyle factors and sperm shape.

The results of this study alone do not show that lifestyle factors other than cannabis are harmless. Male fertility is not just determined by the shape of the sperm; it is also dependent on the concentration, motility and viability of the sperm, as well as the quality of semen. Lifestyle factors could potentially have an effect if they were all combined.

A further limitation of this study, acknowledged by the authors, is that less than half the men attending the fertility clinics met the study's inclusion criteria, and of those who did, only two out of five agreed to participate. The reasons for this are unclear, but could theoretically be because they did not want to disclose their lifestyle.

The men with less than 4% normal sperm shape per 200 were not matched to the “controls” for social and health background data. This is usually conducted so that other confounding factors can be taken into account.

In addition, the study relied on self-reporting in the form of a questionnaire and an interview; it is likely that levels of smoking, alcohol and cannabis use were underestimated.

Whether or not it can be proved that smoking has an effect on fertility, there are many reasons why a potential parent should not smoke. These include the risk of exposure to secondhand smoke for the mother and the risks of a child growing up in a smoking household, such as asthma or even cot death (sudden infant dead syndrome).

Current recommendations on protecting your fertility, such as quitting smoking and moderating your consumption of alcohol, are unchanged.

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

Links To The Headlines

Cannabis doubles younger men's risk of infertility, study finds. The Independent, June 5 2014

Cannabis cuts men's fertility - but smoking, drinking and wearing tight underwear don't, say scientists'. Daily Mail, June 5 2014

Summer loving may not be recipe for getting pregnant, study finds. The Daily Telegraph, June 5 2014

Links To Science

Pacey AA, Povey AC, Clyma JA, et al. Modifiable and non-modifiable risk factors for poor sperm morphology. Human Reproduction. Published online June 4 2014

Categories: Medical News

'Male hormones' in womb linked to autism

Medical News - Wed, 06/04/2014 - 14:30

“Boys who develop autism may be exposed to higher levels of hormones…in the womb,” The Daily Telegraph reports.

Autistic spectrum disorder (ASD), commonly known as autism, is more common in males, but the reason why is still unknown. One hypothesis is that there may be factors in the development of male infants that increase their risk of ASD, such as exposure to certain hormones.

This study measured sex hormone levels in the amniotic fluid (which surrounds and supports the baby) of over 300 boys. Hormone levels were found to be higher in boys who developed ASD. 

However, this does not necessarily mean this is the cause of ASD. The average levels were higher, but many of the boys who developed ASD had normal and low levels, meaning there has to be other factors that play a role in the development of these conditions.

These findings have no immediate implications.

The researchers argue that even if a higher level is proven in larger studies, and is found to be a causative factor, any attempt to block the effects of hormones using drugs would be unwise, due to the risk of side effects.

This research did not show that the higher levels of the hormones caused ASD, which is still believed to be due to a combination of genetic and environmental factors.

 

Where did the story come from?

The study was carried out by researchers from the University of Cambridge and the Statens Serum Institute Copenhagen. It was funded by the Medical Research Council UK, alongside project grants from Nancy Lurie Marks Family Foundation, Wellcome Trust and the Autism Research Trust. The study was published in the peer-reviewed medical journal Molecular Psychiatry. It has been published on an open-access basis, meaning is free to read online.

The UK media reported the story accurately, apart from the headlines describing the hormones as “male”. All five hormones studied are present in both sexes, and it is only the level of testosterone that is higher in men.

The media acted responsibly by including important commentary from the lead author of the study, Professor Baron-Cohen, clarifying that the study’s results do not mean it would be possible to carry out prenatal tests for ASD or treat the condition in the womb using hormonal treatments.

 

What kind of research was this?

This was a retrospective cohort study, using data from the Danish Historic Birth Cohort.

It aimed to see if there was a link between the sex hormone levels in the amniotic fluid (which surrounds the baby in the womb) and the development of autistic spectrum disorders (ASDs).

This is because ASD is diagnosed much more frequently in males, and previous research has suggested that sex hormones and cortisol affect the developing brain. 

A retrospective cohort study is useful when a randomised controlled trial (RCT) is not possible.

Attempts can be made to account for confounders (other factors that may be causing any effects seen), but there could still be other explanations for the results, so it is difficult to imply direct causation.

 

What did the research involve?

Researchers measured hormone levels in the amniotic fluid samples of boys born between 1993 and 1999. They then compared the levels of hormones in 128 that later developed an autistic spectrum disorder (ASD) with 217 that didn’t (the controls).

The researchers used amniotic fluid samples that had been frozen and stored at -20°C. They used mass spectrometry techniques (where devices are used to analysis the molecular composition of a substance) to measure the level of hormones.

Specifically, cortisol (the stress hormone that is essential for life) and four sex hormones – progesterone, 17α-hydroxy-progesterone, androstenedione and testosterone – were analysed.

The researchers recorded the following potential confounding factors:

  • maternal age
  • paternal age
  • birth weight
  • gestational age (weeks of pregnancy) when the amniotic fluid sample was taken
  • apgar score (indicating the physical health of the newborn immediately after birth)
  • sample storage time

The Danish Psychiatric Register was searched over 2009 and 2010 to identify all diagnosed cases of ASD, according to the WHO-recognised International Classification of Diseases (ICD-10), which were linked with the amniotic samples.

They decided to limit the study to males for two reasons. The first was that when they looked at all samples, there were only 24 girls who developed an ASD, which was deemed to be too small a sample to produce meaningful results. Secondly, there was significant variation in two of the confounding factors between girls who developed ASD and those that didn’t – fathers were significantly older and birth weight was lower, compared to the controls.

Statistical analysis was performed to measure any difference between the two groups and also to account for the confounding factors listed above.

 

What were the basic results?

The average level of each hormone was higher in boys who developed ASD, but the exact measurements were not provided in the study.

All five hormones were of a similar level across the control group. They were also of a similar level in the ASD group, but the mean average was higher than in the control group. The researchers say that this indicates a similar mechanism for the production of these hormones, as there wasn’t one that was substantially higher or lower than any other.

They interpreted that one overall “steroidogenic factor” (a protein that stimulates sex hormone and cortisol production) was significantly higher in the ASD group compared to the control group, and was causing the difference.

There was no statistically significant difference between the groups for any of the confounding factors, and no change to the results when their analysis was adjusted for these factors.

 

How did the researchers interpret the results?

The researchers say this is “the first direct evidence that steroidogenic activity is elevated in fetal development of those who later receive diagnoses on the autism spectrum”.

The researchers are quick to point out that the “source of elevated steroidogenic activity in the fetal development of autism was not tested in the current study, and more research will be needed to understand how different sources – such as the foetus, mother, placenta or other environmental factors – might contribute to such elevations”.

They are also tentative about the elevated level of cortisol seen, stating that: “the current results may suggest a link between [pre-birth] stress and autism via heightened fetal cortisol; however, it is unclear if the association here is due to heightened [pre-birth] stress or is driven by a more primary fetal sex steroid influence that has a side effect of boosting fetal cortisol levels”.

 

Conclusion

This study found that the levels of four sex hormones and cortisol were slightly higher in the amniotic fluid of boys who developed ASD, compared to those who didn’t.

However, this does not necessarily mean it is the cause of ASD. The study accounted for some confounding factors, and the average levels were higher, but many of the boys who developed ASD had normal or low levels. This means that other factors must play a role in the development of the condition.

Although it was a well-designed study, limitations reported by its authors include analysing samples that were over 10 years old, which may have changed over time, despite being frozen at -20°C.

There are no immediate implications for these findings; this is just one part in the long process of figuring out the cause of ASD. It is still believed to be due to a combination of genetic and environmental factors.

The study’s authors were at great pains to stress that using drugs to target sex hormones would be unjustified. Aside from related ethical issues, it is unclear whether such an approach would be safe or effective.

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

Links To The Headlines

Boys who develop autism 'exposed to higher levels of hormone in the womb'. The Daily Telegraph, June 3 2014

Autism linked to 'male hormones'. BBC News, June 3 2014

Autistic boys exposed to higher levels of hormones in womb, study finds. The Guardian, June 3 2014

Autism linked to higher levels of 'male hormones' in the womb. The Independent, June 3 2014

Links To Science

Baron-Cohen S, Auyeung B,  Nørgaard-Pedersen B, et al. Elevated fetal steroidogenic activity in autism. Molecular Psychiatry. Published online June 3 2014

Categories: Medical News

Centenarians are outliving 'lifestyle' diseases

Medical News - Wed, 06/04/2014 - 14:26

"Centenarians have found a way to beat the common diseases of old age," BBC News reports. A UK study found that the over-100s are less likely to die of diseases associated with lifestyle and more likely to die from infections such as pneumonia.

Over a 10-year period, researchers examined trends in outcomes for centenarians in England, comparing them with younger elderly people who died in their 80s.

They had a particular interest in place of death because this can have an impact on health budgets, as dying in a hospital is often associated with higher costs.

This was intended to inform service provision for centenarians because of the increasing number of people worldwide who are now living beyond the age of 100, which could be as high as around 3 million by 2050.

The study found that centenarians were less likely to die of what are known as non-communicable diseases. These are diseases such as cancer or heart disease that can be caused by unhealthy lifestyle choices, including smoking, obesity and lack of exercise.

But centenarians were found to be more likely to die of diseases that many of us assume are a thing of the past, such as pneumonia.

Ultimately, these findings will be a useful tool for planning future services for people in this age group.

 

Where did the story come from?

The study was carried out by researchers from Kings College London and Sussex Community NHS Trust, and was funded by the National Institute for Health Research.

It was published in the peer-reviewed open access journal, PLOS Medicine, so it is freely available to read online.

The story was covered appropriately by both BBC News and the Daily Mail.

The Daily Express claims that the findings of the study amount to a "scandal". It is hard to see how the newspaper can justify such emotive language.

If anything, the fact that more people are living over 100 is testament to the success of the NHS in improving public health.

 

What kind of research was this?

This was a population-based retrospective observational study comparing place of death and other characteristics.

These characteristics included cause of death for people aged 100 years or older in comparison to a group of younger elderly people over a 10-year period in England.

In an observational study, researchers simply observe groups of people without changing their exposures or circumstances.

A retrospective study relies on data collected in the past, such as from national databases, as was the case in this study. Data collected retrospectively may not be as reliable as data collected prospectively.

However, as the data collected in this study came from national databases, the information is likely to be fairly accurate.

 

What did the research involve?

The researchers included individuals aged 100 years or older at the time of their death who died in England between 2001 and 2010. The only causes of death excluded were accident or violence.

This group was compared with individuals aged 80 to 99 years in the same time period.

The main outcome the researchers were interested in was place of death, which was grouped into five categories:

  • hospital
  • nursing home (defined as providing 24-hour long-term care with nursing)
  • residential care home (defined as providing 24-hour long-term care without nursing)
  • home
  • elsewhere

The researchers used death registration data from England's Office for National Statistics (ONS) from 2001 to 2010 to obtain information about each individual's place of death.

The database was also used to gather information on each person's:

  • age
  • gender
  • marital status
  • usual residence
  • year of death
  • underlying cause of death
  • contributing cause(s) of death

They linked this data with local data on deprivation, settlement type (for instance, urban, town or village), and care home bed capacity. Statistical methods were used to analyse the data.

 

What were the basic results?

There were 35,867 individuals included in this study who were aged 100 years or older (range 100 to 115 years). Most were women (86.75) and most were widowed (85.0%).

The number of centenarian deaths per year in England increased by 56% in 10 years from 2,823 in 2001 to 4,393 in 2010.

The main findings of the study were:

  • most centenarians died in a care home, with 26.7% dying in a nursing home (95% confidence interval [CI] 26.3% to 27.2%) and 34.5% dying in a residential care home (95% CI 34.0% to 35.0%)
  • dying in a hospital was the next most common place of death (27.2%, 95% CI 26.7% to 27.6%)
  • the proportion of deaths in nursing homes (-0.36% annually) decreased over 10 years, while there was little change in hospital deaths (0.25% annually)

Centenarians were more likely to die of:

  • pneumonia (17.7%, 95% CI 17.3% to 18.1%) compared with people aged 80 to 84 years (6.0%, 95% CI 5.9% to 6.0%)
  • old age/frailty (28.1%, 95% CI 27.6% to 28.5%) compared with people aged 80 to 84 years (0.9%, 95% CI 0.9% to 0.9%)

Centenarians were less likely to die from:

  • cancer (4.4%, 95% CI 4.2% to 4.6%) compared with people aged 80 to 84 years (24.5%, 95% CI 24.6% to 25.4%)
  • heart disease (8.6%, 95% CI 8.3% to 8.9%) compared with people aged 80 to 84 years (19.0%, 95% CI 18.9% to 19.0%)

More care home beds being available per 1,000 people was associated with fewer deaths in hospital.

 

How did the researchers interpret the results?

The researchers concluded that centenarians are more likely to have their cause of death certified as pneumonia and frailty, and were less likely to die from cancer or heart disease, compared with younger elderly patients.

They said that reducing reliance on hospital care at the end of life requires recognition of centenarians' increased likelihood to "acute" decline, notably from pneumonia.

They recommend that wider provision of anticipatory care is introduced to enable people to remain in their usual residence, as well as increasing care home bed capacity.

 

Conclusion

This study provides useful information on the place and cause of death of people who live to be 100 years or older compared with a younger elderly population in England. It also provides useful information on trends that have occurred over a 10-year period.

The study's strengths include the large sample of centenarians involved in the research based on data from national registries, which is likely to be reliable.

However, death certificates do not contain information on people's preferences for care in the period before death, so we cannot use the results of this study to draw conclusions about what kind of care this group prefers at the end of life.

Other limitations of this study include that many deaths are classified as being the result of "old age", which may reflect diagnostic uncertainty or limited medical investigations.

The researchers say that certifying death as old age limits the interpretation of the cause of death and therefore the guidance of health services.

But the fact that people who died over the age of 100 were less likely to die from cancer and heart disease than people who died in their 80s is perhaps not so surprising.

Given that these people have lived to such an age suggests that they have not developed these conditions, or if they did they were not associated with mortality.

This may be the result of a wide variety of genetic, socioeconomic, health and lifestyle factors, so this study cannot provide us with any answers about the secret to living beyond the age of 100.

But adopting well-established lifestyle habits such as having a healthy diet, avoiding smoking, taking regular exercise and trying to achieve or maintain a healthy weight certainly won't hurt.

Primarily, these findings will be a useful tool in planning future services for these older populations.

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

Links To The Headlines

Centenarians 'outliving diseases of old age'. BBC News, June 4 2014

Rise of the 100-year-old puts NHS under strain: Centenarian population expected to hit half a million in 30 years. Daily Mail, June 4 2014

Centenarian death toll is a hospital scandal. Daily Express, June 4 2014

Links To Science

Evans CJ, Ho Y, Daveson BA, et al. Place and Cause of Death in Centenarians: A Population-Based Observational Study in England, 2001 to 2010. PLOS Medicine. Published online June 3 2014

Categories: Medical News

Just five sunburns increase your cancer risk

Medical News - Tue, 06/03/2014 - 18:19

“Five serious sunburns increase the risk of deadly skin cancer by 80%,” The Daily Telegraph reports. A US study has found that sun overexposure during the teenage years significantly increases the risk of developing skin cancer in later life.

The study followed over 110,000 nurses over 20 years, using questionnaires.

It found that women who had five or more blistering sunburns between the ages of 15 and 20, compared to those that had none, were 80% more likely to develop melanoma (the most aggressive form of skin cancer).

Other risk factors included red hair colour, high sunburn reaction as a child/adolescent and sun bed use – all of which were found to be associated with an increased risk of all three types of skin cancer.

An unexpected result was that increased exposure to ultraviolet rays (radiation produced by the sun, as well as sunbeds and lamps) in adulthood was associated with an increased risk of non-melanoma forms of skin cancer (squamous cell carcinoma and basal cell carcinoma), but not melanoma.

However, this does not mean it is relatively safe to have high levels of UV exposure as an adult, as the UV exposure was not accurately measured in this study. Additional factors, such as how much time the women actually spent outside and if they exposed their skin to the sun, were not taken into account.

Skin cancer is one of the most common cancers in the UK, and this study confirms the necessity for taking precautionary measures to stay safe in the sun. 

 

Where did the story come from?

The study was carried out by researchers from Brigham and Women’s Hospital and Harvard Medical School, and was funded by the Brigham and Women’s Hospital and grants from the National Institutes of Health.

The study was published in the peer-reviewed medical journal Cancer Epidemiology, Biomarkers and Prevention.

In general, the Mail Online covered the story accurately, but one of their headlines was misleading and potentially dangerous. They reported that “UV radiation exposure in later life does not affect melanoma risk”. Although the estimated UV exposure as an adult was not associated with melanoma in this study, there were major limitations in how the estimate was made, which was not addressed in the coverage.

Prolonged exposure to UV radiation, at any age, is not recommended. At best, it can cause premature ageing of the skin. At worst, it can increase the risk of developing skin cancer. Though this study only found an association with other non-melanoma types of skin cancer, UV exposure is also a well-established risk factor for melanoma. 

 

What kind of research was this?

This was a cohort study of US nurses over 20 years. The researchers wanted to investigate the relationship between a number of potential risk factors and the likelihood of developing skin cancer.

An observational cohort study is appropriate for looking at the strength of a relationship between exposure and risk of developing a disease, but it cannot prove that the exposure causes the disease. 

However, there is a wide body of evidence that suggests prolonged exposure to sunlight increases the risk of skin cancer.

 

What did the research involve?

The study followed 116,430 US nurses from 1989 to 2009. The researchers used health-related questionnaires every two years to look for associations between factors such as sun exposure, hair colour, lifestyle and development of skin cancer.

The nurses were aged between 25 and 42 at the beginning of the study. The amount of sun exposure they had over the course of the study was measured by “UV [ultraviolet] flux”.

There are two main types of UV: ultraviolet A (UVA) and ultraviolet B (UVB).

UV flux is an estimate of the amount of UVB and part of UVA waves that hit the earth’s surface, which takes cloud cover into account.

It is calculated for each state in the US using Robertson-Berger meters, which are electronic devices that measure UV radiation. The researchers estimated the amount of UV flux acquired by each woman over the length of the study using their address and accounting for changes of address. At the beginning of the study, the nurses lived in 14 different states; the researchers hoped this would capture different levels of exposure. They were then categorised into low, medium and high exposure.

The questionnaires included other potential risk factors, such as:

  • number of moles on the legs
  • sunburn reaction as a child/adolescent
  • number of blistering sunburns between the ages of 15 and 20
  • natural hair colour
  • use of sunbeds
  • family history of melanoma
  • smoking and alcohol intake
  • body mass index (BMI) and physical activity levels
  • amount of night shifts
  • menopausal status

If the women reported that they had squamous cell carcinoma (SCC) or melanoma, their medical records were reviewed to confirm the diagnosis. It was not deemed necessary to validate any report of basal cell carcinoma.

Women were excluded from the statistical analysis if they:

  • were not Caucasian 
  • had any cancer at the beginning of the study
  • had missing residence information
  • did not report the type of skin cancer

 

What were the basic results?

Out of the 108,916 women:

  • 6,955 developed basal cell carcinoma (BCC)
  • 880 developed squamous cell carcinoma (SCC)
  • 779 developed melanoma (445 had invasive melanoma, where the cancer has spread below the top outer layer of skin [epidermis]).

Women with a history of five or more blistering sunburns between the ages of 15 and 20, compared to those who had none, had:

  • an 80% increased risk of melanoma (Relative Risk [RR] 1.80, 95% Confidence Interval [CI] 1.42 to 2.28)
  • a 68% increased risk of SCC (RR 1.68, 95% CI 1.34 to 2.11)
  • a 68% increased risk of BCC (RR 1.68, 95% CI 1.55 to 1.82)

Cumulative exposure to UV rays, adjusting for all of the other factors, found:

  • no association with exposure to and risk of melanoma
  • women in the highest fifth of exposure were more than twice as likely to develop SCC than those in the lowest fifth (RR 2.53, 95% CI 1.11 to 5.77)
  • women in the highest fifth of exposure were more than twice as likely to develop BCC than those in the lowest fifth (RR 2.35, 95% CI 1.79 to 3.07)

Other factors that increased the risk of all types of skin cancer were red hair colour and high sunburn reaction as a child/adolescent, as well as sunbed usage. The risk of two or more types of skin cancer was increased by a family history of melanoma, the number of moles on a person's legs and greater alcohol intake.

 

How did the researchers interpret the results?

They conclude that the “risks of BCC and SCC were associated with sun exposures in both adulthood and early life, whereas melanoma risk was predominantly associated [with] sun exposure in early life. Host factors, including red hair, sun reaction as a child/adolescent and number of blistering sunburns between ages 15 and 20 years of age, were strong predictors of all 3 types of skin cancer”.

 

Conclusion

This study has provided further evidence of the link between skin damage from sun exposure and the increased risk of all types of skin cancer.

Strengths of the study include the large size of the cohort and the fact that over 90% of the women were followed up for the whole 20-year duration of the research.

However, there were several limitations. The accuracy of using UV flux to determine exposure is debatable, as it only captures the level of UV rays that a woman living in that state could be exposed to. It does not measure how much skin exposure a woman has actually had. For example, it did not assess basic factors, such as the amount of time spent outdoors, whether the woman wears clothing or a hat to cover the skin while in the sun, the use of sun cream or the type and frequency of holidays in the sun.

The study only included Caucasian women, so it is unclear how applicable the results are to men and people of other ethnicities.

It was also reliant on accurate self-reporting and recall. Some of the women were 42 when the study started, and they may not have remembered how many times they had blistering of the skin from sunburn 27 years earlier.

Overall, the risk factors that are already known were associated with an increased risk of all three types of skin cancer.

The study also highlights the importance of young people being careful to avoid sunburn as, aside from being highly unpleasant, it could increase the risk of developing skin cancer, both in the short term and in later life.

It should be noted that this study does not change the existing advice for reducing the risk of skin cancer.

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

Links To The Headlines

Suffering sunburn five times increase skin cancer risk. The Daily Telegraph, June 2 2014

Getting badly sunburnt just FIVE times as teenager makes you 80% more likely to develop the most deadly type of skin cancer. Mail Online, June 2 2014

Links To Science

Wu S, Han J, Laden F, et al. Long-term Ultraviolet Flux, Other Potential Risk Factors, and Skin Cancer Risk: A Cohort Study. Cancer Epidemiology, Biomarkers & Prevention. Published online May 2014

Categories: Medical News

Learning second language 'slows brain ageing'

Medical News - Tue, 06/03/2014 - 14:26

"Learning a second language can have a positive effect on the brain," BBC News reports after a Scottish study found that participants who spoke two or more languages tended to perform better in intelligence tests than people who only spoke English.

The researchers looked at a group of 853 people who had been given intelligence tests in 1947 at the age of 11 and were then retested when they were in their 70s. They were asked if they had learned any additional languages and, if so, when they had acquired the language and how often they used it. 

Almost a third of people spoke a second language. The researchers found that people speaking two languages (bilingual) performed significantly better than predicted from their baseline cognitive abilities at the age of 11. The strongest associations were seen in tests of general intelligence and reading.

A significant strength of the study is its timescale – tracking people over the course of seven decades is no mean feat, although this was done retrospectively. However, the study did not assess whether participants had cognitive impairment or dementia, so it cannot tell us whether being bilingual is protective against the development of these conditions.

Still, learning another language is a good way of keeping the mind active, learning about different cultures and meeting new people, all of which can improve quality of life. Read more about how learning new skills can improve wellbeing.

 

Where did the story come from?

The study was carried out by researchers from the University of Edinburgh and was funded by Age UK.

It was published in the peer-reviewed journal, Annals of Neurology.

The story was covered appropriately by BBC News and the Daily Express.

The Mail Online, however, had a headline that was not representative of the study's findings, reporting that "extra languages can help prevent dementia", which is not what the study looked at.

The current study looked at the association of languages with cognitive functioning later in life.

To establish whether or not bilingualism prevents dementia, participants would have to be monitored for the rest of their lives.

However, an earlier study has suggested that being bilingual could delay the onset of dementia by several years.

 

What kind of research was this?

This was a retrospective cohort study looking at whether learning a second language other than English had an association with cognitive functioning at around the age of 70. It involved a relatively small group of people based in Edinburgh.

A retrospective study relies on data on exposures and outcomes that have been collected in the past (through medical records or as part of another study, for example) or through people remembering what happened to them in the past.

Data used in this way may not be as reliable as data collected prospectively (when the data is collected specifically for the study as events happen). This is because it relies on the accuracy of records made at the time, which can be inaccurate.

This study relies on information provided by older adults, who may already have some degree of cognitive impairment, which could introduce further inaccuracies.

 

What did the research involve?

The research was carried out on participants from the Lothian Birth Cohort 1936 (1,091 people) who took an intelligence test in 1947 at the age of 11, and were retested between 2008 and 2010 when they were in their 70s (853 people).

This cohort was unique in that they were native English speakers of European origin who were born, raised and living in and around Edinburgh. No immigrants were included.

The researchers say that by using this birth cohort, they were able to question whether learning a second language influences later cognitive performance after adjusting for childhood intelligence.

Intelligence testing consisted of a series of assessments, including:

  • a range of fluid-type general intelligence tests, including letter-number sequencing
  • a range of memory tests
  • speed of information testing
  • reading tests that examined the pronunciation of 50 irregular English words as part of the National Adult Reading Test (NART)
  • verbal fluency testing, where participants were asked to say as many words as possible beginning with the letters C, F and L, with a one-minute timeframe for each letter
  • the Moray House Test, which mainly tests verbal reasoning skills

It is unclear if the intelligence tests performed were the same as those carried out on participants when they were 11.

Bilingualism was assessed using a questionnaire where participants were asked whether they had learned any languages other than English, how many, and at what age.

They were also asked how often they used the languages (daily/weekly/monthly/less than monthly/never) across three areas: conversation, reading and media.

The researchers were interested in:

  • the age of additional language acquisition (never/early/late)
  • the number of languages (monolingual/bilingual/multilingual)
  • the frequency the additional language(s) were used (no second language/no active use/active use)

In their analysis, the researchers adjusted the results for childhood intelligence, age at time of testing, sex and social class.

 

What were the basic results?

Of the 853 participants who completed the intelligence retesting between 2008 and 2010, 262 people (30%) reported having learned at least one other language to a level that allowed them to communicate.

Of these, 195 learned the second language before the age of 18 (though only 19 [2%] before the age of 11) and 65 learned it after this age.

The researchers report that 160 people knew two languages (bilingual) and 85 people knew three or more languages (multilingual).

The researchers found that people who spoke two languages (bilingual) performed significantly better than predicted from their baseline cognitive abilities. The strongest associations were seen in tests of general intelligence and reading.

The cognitive effects of bilingualism showed a consistent pattern, affecting reading, verbal fluency and general intelligence to a higher degree than memory, reasoning and processing speed.

Other results of note are described below.

Age of language acquisition

For early language acquisition, significant positive associations were found in the tests for general intelligence and reading. For late language acquisition, significant positive associations were found in the tests of general intelligence, processing speed and reading. 

Number of languages

Bilingualism showed a significant positive association with tests of reading, while multilingualism showed significant positive associations with general intelligence, reading and verbal fluency.

Frequency of use

For passive bilingualism (no active use of the language for the past five years), the main associations were seen in the tests of general intelligence, reading and verbal fluency. For active bilingualism (use of the language in the past five years), the main associations were seen in the tests of general intelligence and reading.

However, there was a significant association between childhood intelligence and performance at the age of 73 for the active group on the Moray House Test – a significant effect of active bilingualism was only found for lower childhood intelligence.

In terms of the type of bilingualism, different effects were seen for early versus late acquisition depending on childhood intelligence. Overall, people with high intelligence appeared to benefit more from early acquisition, and those with low intelligence from late acquisition, but neither group showed negative effects.

Knowing three or more languages produced stronger associations than knowing two languages. There was little difference seen in the comparison between active and passive bilinguals, which the researchers say might be a result of the low frequency of use of the second language, even in active language users. 

 

How did the researchers interpret the results?

The researchers concluded that their results suggest a protective effect of bilingualism against age-related cognitive decline independent of childhood intelligence, including in those who acquired their second language in adulthood.

In discussing the findings, lead researcher Dr Thomas Bak is reported in the media as saying: "These findings are of considerable practical relevance. Millions of people around the world acquire their second language later in life. Our study shows that bilingualism, even when acquired in adulthood, may benefit the ageing brain."

 

Conclusion

Overall, this study suggests an association between cognitive functioning later in life and having learned another language or languages.

A strength of the research is that it took into account childhood intelligence, which previous studies are not reported to have accounted for.

There remain some important limitations, however:

  • Bilingualism was assessed using a questionnaire and not by proficiency testing, which may have biased the results. It is possible that some participants may have overestimated their ability to speak languages other than English.
  • The researchers adjusted the results for childhood intelligence at age 11, but this may not have fully accounted for the person's overall cognitive ability and educational level in later childhood and adulthood. Also, despite adjusting for age at testing, sex and social status, there may be other hereditary, health and lifestyle factors at play that, taken overall, make it difficult to know whether acquiring and using a second language in itself has a direct and independent effect on cognitive ability.
  • The researchers report that the birth cohort was homogenous, so findings from this study may not be generalisable to a different group of people (people who have migrated to another country, for example). Also, the study was carried out among a relatively small group of people based in Edinburgh, so the results should be interpreted with caution when generalising to other populations.
  • The study did not assess whether participants had cognitive impairment or dementia, so it cannot tell us whether being bilingual is protective against the development of these conditions.

While it may seem a commonsense proposition that keeping the brain active will protect against dementia, the evidence is inconsistent. Various brain training exercises have been studied with varying degrees of success.

However, there is evidence that keeping the mind active at any age does improve mental wellbeing, whether it's learning a new language, teaching yourself to cook, or going to a museum. Read more about learning for mental wellbeing.

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

Links To The Headlines

Learning second language 'slows brain ageing'. BBC News, June 2 2014

Being bilingual may keep brain sharp in old age: Learning extra languages can help prevent onset of dementia, study claims. Mail Online, June 2 2014

Being bilingual boosts brain power. Daily Express, June 2 2014

Links To Science

Bak TH, Nissan JJ, Allerhand MM, et al. Does bilingualism influence cognitive aging? Annals of Neurology. Published online May 2014

Categories: Medical News

Breast cancer gene and smoking is a 'lethal mix'

Medical News - Mon, 06/02/2014 - 14:17

"Smoking and the breast cancer risk gene BRCA2 combine to 'enormously' increase the chance of developing lung cancer," BBC News reports.

The BRCA2 gene, which is known to increase breast cancer risk, appears to also up the risk of lung cancer in smokers.

A new study analysed the genetic make-up of more than 10,000 people with lung cancer to identify genetic and lifestyle risk factors for the disease.

One of the genetic variants they identified was linked to the BRCA2 gene and increased a person's risk of having lung cancer – specifically, squamous cell carcinoma – by 2.47 times.

This may have important implications for identifying who should undergo lung cancer screening, especially those considered to be high risk.

But cancer involves the accumulation of genetic damage in many gene regions rather than just one, so identifying these single genetic risks is not the full picture.

In addition to genetic risks, which you can't change, there are lifestyle risk factors, the biggest of which is smoking.

If you smoke, you are significantly increasing your risk of developing lung cancer later in life. And it seems that if you also have the BRCA2 gene variant, the risks may be even greater.

The results of this study reinforce the dangers of smoking and how stopping smoking is probably the best way to improve your health.

 

Where did the story come from?

The study was carried out by a large collaboration of researchers from around the world, and was funded by the US National Institutes of Health and numerous other cancer research-funding bodies and institutions.

It was published in the peer-reviewed science journal, Nature Genetics.

BBC News reported the story accurately, emphasising that not smoking is the best way to reduce your risk of developing lung cancer (as well as many other cancers).

 

What kind of research was this?

This was a cross-sectional study looking for genetic traits that may raise the risk of developing lung cancer.

Lung cancer, the researchers state, causes more than one million deaths worldwide each year and is mainly caused by tobacco smoking.

But some studies have indicated there is an underlying genetic component to the risk of developing the life-threatening condition.

This study sought to better understand this link by comparing the genetics of people with and without the disease.

This type of study is a useful first step in identifying potential links between genes and disease, but it cannot prove that a certain gene causes a disease. More biological studies are needed to prove the underlying mechanism by which a gene causes or contributes to disease. 

 

What did the research involve?

The research compared large groups of people with lung cancer and those without the disease to see how their underlying genetic variation differed. They also wanted to see whether these differences might be related to the risk of getting the disease.

The main analysis compared the genetics of 11,348 people with lung cancer with 15,861 people without. Any differences identified in this group were then validated in a comparison of a further 10,246 people with lung cancer and 38,295 without. In total, 75,750 people fed into the analysis.

Participants were of European ancestry. The two main types of lung cancer (adenocarcinoma and squamous cell carcinoma) were included.

 

What were the basic results?

The comparisons identified three gene variants associated with lung cancer.

These were:

  • BRCA2 – this leads to a more than doubling of the relative risk for squamous cell carcinoma (odds ratio [OR] 2.47, 95% confidence interval [CI] not reported) and a 47% increase for adenocarcinoma (OR 1.47, 95% CI not reported). This gene is involved in repairing DNA and is known to significantly increase the risk of breast cancer when it does not function correctly.
  • CHEK2 – leading to around a 62% reduction in relative risk (OR 0.38, 95% CI not reported). The CHEK2 gene controls elements of how a cell self-destructs or stops growing when DNA gets damaged.
  • 3q28 – leading to a 13% higher risk of adenocarcinoma only (OR 1.13, 95% CI not reported)

The researchers indicated that the risk of developing lung cancer is approximately doubled for a smoker carrying the BRCA2 variant, which is 2% of the population. This may have implications for identifying high-risk smokers for lung cancer screening.

 

How did the researchers interpret the results?

The study authors stated that, "These findings provide further evidence for inherited genetic susceptibility to lung cancer and its biological basis.

"Additionally, our analysis demonstrates that imputation can identify rare disease-causing variants with substantive effects on cancer risk from pre-existing genome-wide association study data."

 

Conclusion

This study identified new genetic variants linked to the risk of lung cancer in European adults. One of the variations was linked to the BRCA2 gene, which is already known to be associated with a higher risk of developing breast cancer.

The study provided some new evidence of the potential genetic origin of lung cancer, but provided no proof that the genetic variants caused the cancer. However, each of the genetic variants had a plausible biological link to the way in which it might cause cancer.

But cancer often involves the accumulation of genetic damage in many gene regions rather than just one, so identifying these single genetic risks is not the full picture.

In addition to genetic risks, which you can't change, there are lifestyle risk factors that influence risk, the biggest of which is smoking. If you smoke, you are significantly increasing your risk of developing lung cancer later in life.

It appears that if you also have the BRCA2 gene variant, the risks may be even higher. The study estimated that around 2% of the population are smokers who also carry the BRCA2 variation, but it was unclear how the researchers arrived at this estimate or if this would be similar in the UK population.

The study's results would be improved by analysing genetic variation in more diverse populations, as the people in this study were described as mainly of European descent.

Professor Peter Johnson, Cancer Research UK's chief clinician, explained to the BBC that, "We've known for two decades that inherited mutations in BRCA2 made people more likely to develop breast and ovarian cancer, but these new findings show a greater risk of lung cancer too, especially for people who smoke."

As Professor Johnson rightly concludes, "The single most effective way to reduce the risk of lung cancer is to be a non-smoker."

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

Links To The Headlines

Smoking and breast cancer gene combine 'to raise risk'. BBC News, June 1 2014

Links To Science

Wang Y, McKay JD, Rafnar T, et al. Rare variants of large effect in BRCA2 and CHEK2 affect risk of lung cancer. Nature Genetics. Published online June 1 2014

Categories: Medical News

You can train a toddler to eat veggies, study claims

Medical News - Mon, 06/02/2014 - 14:00

“Children can learn to eat new vegetables if they are introduced regularly before the age of two,” BBC News reports. A new study suggests that the key is to introduce them 'early and often'.

The challenge of introducing vegetables into a child’s diet is that some toddlers, as their parents will testify, are notoriously fussy eaters.

This new study, involving 403 English, French and Danish toddlers, suggests that the best way to get toddlers to eat vegetables (in this case artichoke puree) was repeatedly offering them the food at an early stage.

This potentially provides hope for parents to persist with new foods if they receive a tepid response from their child the first time round.

The results are consistent with current guidelines suggesting children should start solid foods from six months of age.

 

Where did the story come from?

The study was led by researchers from the University of Leeds and involved Universities in Denmark and France. It was funded by the European Community’s Seventh Framework Programme and the Regional Council of Burgundy.

The study was published in the peer-reviewed medical journal PLOS One. The article is open access, meaning it is free to view and download online.

BBC News reported the study accurately.

 

What kind of research was this?

This was a cross-sectional study assessing young children’s eating habits and preferences toward vegetables.

The researchers remind us that vegetable intake is generally low among children, who can appear fussy about food in the pre-school years. This is a battle for parents and some strategies include masking the taste of vegetables with other foods or adding sugar. There is some evidence, they say, that repeatedly offering a child a food makes them more likely to try it and get used to it, but the results in studies of this have varied in effectiveness.

This study sought to better understand the factors that can influence young children’s response to new vegetables in early years.

 

What did the research involve?

The research involved UK, French and Danish children aged four months to three years old and fed them artichoke puree on five to 10 different occasions to gauge their acceptance of the new vegetable.

They also tested whether adding sweeteners or added energy to the puree made the toddlers eat more of it.

In total, 403 preschool children from the UK (108, aged 6–36 m), France (123, aged 4–8 m) and Denmark (172, aged 6–36 m) took part in the study.

Children were given up to 200g (2x100g pots) of basic artichoke puree, and the amount they ate was weighed. Children were randomly assigned into one of three groups:

  • repeated exposure (basic artichoke puree, 112)
  • flavour-flavour learning (basic artichoke puree with added sweetness, 112)
  • flavour-nutrient learning (basic artichoke puree with added energy, 108)

The added sweetener was sugar (sucrose) and the added energy was sun flour oil, an energy dense fat.

Each child received five to 10 exposures to one of the purees (variation due to unplanned absences from nursery) during a state of hunger, either before a main meal or as an afternoon snack (UK and Denmark) or at the beginning of a meal (France). The UK children were offered 100g per exposure and in Denmark and France children were offered up to 200g.

The main analysis looked at whether repeatedly offering the child the food was linked to how much they ate. It also looked at whether the addition of sweeteners or added energy influenced how much the children ate.

 

What were the basic results?

The researchers combined the results from the different countries and identified four main food pattern groups:

  • Most children (40%) were “learners”. This group increased intake of puree over time as they seemingly got used to it.
  • 21% consumed more than 75% of what was offered each time and were labelled “plate-clearers” by the researchers.
  • 16% were considered “non-eaters” eating less than 10g by the fifth attempt at giving them the puree.
  • The remainder were classified as “others” (23%) since their pattern was highly variable.

Age was a significant predictor of eating pattern, with older pre-school children more likely to be non-eaters. Plate-clearers had higher enjoyment of food and experienced less fullness than non-eaters who scored highest on food fussiness.

Children in the added energy group consumed less artichoke over the intervention period suggesting adding energy to increase intake is not effective in promoting intake of vegetables in young children.

 

How did the researchers interpret the results?

The study’s main conclusion was that their “results demonstrated that the younger children were less fussy, enjoyed food more and had lower satiety responsiveness, representing a profile of characteristics that together contributed to increased acceptance of a novel food”.

The study authors said to the BBC that, "if you want to encourage your children to eat vegetables, make sure you start early and often” and, “even if your child is fussy or does not like veggies, our study shows that five to 10 exposures will do the trick".

 

Conclusion

This small study indicates that repeatedly offering young children a new food (artichoke puree) early in life may increase the chance they eat it and this may become harder later on.

The study results should be interpreted in light of the study limitations, which include:

  • Potential errors in the measurement of some variables. For example, the age at which the children were first fed solid food and duration of breastfeeding were self-reported and may contain error, especially in the older children.
  • The purees were served cold to the children in the UK and Denmark and warm to the French children and this might have influenced intake. The French group tended to be younger so if warming the puree increased the children’s appetite for it, this could show up as younger children liking it, a bogus result.
  • The study only tested one vegetable, artichoke puree. Different results may have been found with other vegetables.
  • Whilst repeatedly offering children the puree (on five to 10 occasions) helped them eat more, especially in younger pre-school children, it is not clear how long this effect would last, or whether it could potentially reverse later in life. The authors say durable effects were observed at three and six months after the study but it was not clear if the effects would continue after this time.

The implications of the study findings are that new vegetables are best introduced to children at a young age. This is consistent with current guidelines suggesting children should start solid foods from six months of age

If your child is a particularly fussy eater, there are a number of tips that may help.

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

Links To The Headlines

Offer vegetables early and often to fussy toddlers, study says. BBC News, May 31 2014

Links To Science

Caton SJ, Blundell P, Ahem SM, et al. Learning to Eat Vegetables in Early Life: The Role of Timing, Age and Individual Eating Traits. PLOS One. Published online May 30 2014

Categories: Medical News

Is sleeping in a light room linked to obesity?

Medical News - Fri, 05/30/2014 - 15:00

"Sleeping in a room with too much light has been linked to an increased risk of piling on the pounds," BBC News reports. The news comes from a study that assessed self-reported sleeping habits and body weight measurements in a group of women at a single point in time.

The researchers did find a significant link between light levels in women's rooms at night and their risk of being overweight and obese. However, the study could not provide evidence that light was causing the difference in obesity risk. The authors were aware of this limitation and cautiously described their results as "intriguing".

The researchers speculated that melatonin may play a role in underpinning this link. Melatonin is a hormone whose production is inhibited by exposure to light and is thought to play a role in metabolism.

Sleeping in a darkened room is recommended as it helps promote better and more refreshing sleep patterns.

But this study doesn't provide evidence that simply darkening your room at night will help you lose weight or stop weight gain if you regularly eat more and exercise less than you should.

If you want to lose weight, try the NHS Choices weight loss guide to get started.

 

Where did the story come from?

The study was carried out by researchers from the University of Oxford and was funded by Breakthrough Breast Cancer and the Institute of Cancer Research.

It was published in the peer-reviewed American Journal of Epidemiology.

The UK media's reporting was accurate and explained plainly that the researchers were not sure if light levels at night were causing obesity or, if so, how this might occur.

 

What kind of research was this?

This was a cross-sectional analysis of women taking part in the Breakthrough Generations study. This is a long-term ongoing cohort study of women aged 16 years or older living in the UK which aims to identify the causes of breast cancer.

Carrying too much fat (obesity) can damage your health and is known to influence the risk of developing breast cancer, so it was one of the factors assessed in the study.

The researchers also reported that animal studies have shown light exposure causes weight gain, even when energy intake and physical activity (the main influencers on body weight) are kept the same.

They wanted to investigate whether disruption in sleep caused by too much light at night might be contributing to obesity. They say this theory has not yet been investigated adequately in humans.

As this was a cross-sectional analysis, it assessed both the exposure (light at night) and outcome (weight or body fat) at one single point of time. This means that it cannot prove cause and effect as it cannot tell us what came first: whether obesity causes women to sleep in lighter rooms, or if lighter rooms cause women to become obese.

The alternative explanations are that it is simply a spurious link caused by an additional factor (confounder) or that the link is a statistical anomaly that may later be disproved.

 

What did the research involve?

The research used questionnaire data from 113,000 women in the Breakthrough Generations study. The women were aged 16 years or older, lived in the United Kingdom and recruited between 2003 and 2012.

The participants were asked about light levels in their room at night. The researchers then looked for links between this and different measures of their weight.

The women were asked to rate the amount of light in their bedrooms at night as:

  • light enough to read (lightest level)
  • light enough to see across the room but not read (lightest level)
  • light enough to see your hand in front of you but not across the room (middle level)
  • too dark to see your hand, or you wear a mask (darkest level)

The two lightest levels were combined into one category because of low numbers in each group.

Their answers were compared with different measures of body weight (BMI) and body fatness (waist to hip ratio, waist circumference, and waist to height ratio).

The group were mainly Caucasian (98.8%). The participants' ages ranged from 16 to 103, with an average age of 47.

The main analysis took into account factors other than light levels that might influence women's obesity risk (confounders).

The fully adjusted analysis took into account:

  • age
  • having a child under the age of five
  • socioeconomic status
  • night shift work in the previous 10 years
  • strenuous physical activity
  • alcohol consumption
  • sleep duration
  • current smoking status

 

What were the basic results?

In the group, 1.3% were underweight, 52.3% were a healthy weight, 28.9% were overweight and 13.7% were obese. A further 3.8% had missing information.

The probability (odds) of women being overweight or obese was progressively lower among those who slept in darker rooms. This link was seen for the middle and darkest levels, as well as BMI and waist to hip ratio.

For example, women sleeping in the darkest rooms were 21% less likely to be obese than those sleeping in the lightest rooms, as measured by BMI (odds ratio [OR] 0.83, 95% confidence interval [CI] 0.79 to 0.88).

No links were found between women being underweight and light levels at night.

 

How did the researchers interpret the results?

The researchers state that, "In this analysis of over 113,000 United Kingdom women, [different measures of weight and body fatness] increased with increasing lightness of the room slept in at night.

"These associations were still present after adjustment for age, socioeconomic status, alcohol consumption, strenuous physical activity, night shift work, having a young child, sleep duration, and current smoking."

However, the study authors are appropriately cautious and distance themselves from saying that light exposure at night could cause obesity, instead describing their results as "intriguing".

Professor Anthony Swerdlow from the Institute of Cancer Research told the BBC that, "There might be other explanations for the association, but the findings are intriguing enough to warrant further scientific investigation."

In terms of the impact on people today, he said: "There is not sufficient evidence to know if making your room darker would make any difference to your weight."

 

Conclusion

This cross-sectional study found a link between light levels in women's rooms at night and their risk of being overweight and obese. However, it is not able to prove that light caused the difference in obesity risk.

The authors fully acknowledge this and cautiously described their results as "intriguing" and warranting "further scientific investigation".

The main drawback of this study was that it was cross-sectional. This means it cannot prove cause and effect; it can only highlight potential associations.

The study raises the question of how differences in light levels at night might affect obesity levels. When considering whether these results might be showing a real effect, the scientific community will need to think of plausible explanations for the results and carry out further studies to test these.

One theory is that too much light while you are trying to sleep disrupts people's natural biological clock, which has developed over millions of years in response to natural light cycles of dawn and dusk.

However, the association could also run in the other direction. Obese people may be heavier sleepers, so they are more likely to sleep in lighter environments. 

There has been increasing interest in potential negative biological reactions to artificial light and disrupted sleep and their impact on biological and mental functioning. No doubt research in this area will continue.

The results may be "intriguing" from a research perspective, but for the average person this study does not provide any convincing evidence that darkening your room at night will help you lose weight or stop weight gain, or, conversely, that sleeping in a lighter room will cause you to gain weight.

For now, the message about how to maintain a healthy weight is simple and unchanged: eat a healthy balanced diet and get plenty of exercise.

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

Links To The Headlines

Light bedrooms 'link to obesity'. BBC News, May 30 2014

Sleeping with light on increases risk of obesity. The Daily Telegraph, May 30 2014

Light at night linked to obesity. MSN News, May 30 2014

Links To Science

McFadden E, Jones ME, Schoemaker MJ, et al. The Relationship Between Obesity and Exposure to Light at Night: Cross-Sectional Analyses of Over 100,000 Women in the Breakthrough Generations Study. American Journal of Epidemiology. Published online May 29 2014

Categories: Medical News

Watching porn associated with male brain shrinkage

Medical News - Fri, 05/30/2014 - 14:30

“Viewing porn shrinks the brain,” reports the Daily Mail.

In a small study, MRI scans found that men who watched the most pornography had less grey matter – complex brain tissue – compared to men who watched the least.

It found a weak to moderate correlation between the number of hours of porn viewed a week and smaller and less active areas of the brain associated with reward and sexual stimulation in men.

The higher the number of hours of porn watched, the smaller the volume of grey matter and brain signalling.

In essence, the researchers thought this might be a sign “porn users” may be dampening down the sexual stimulation and reward centres in their brain through over stimulation.

However, one of the big issues with studies like this is that you can’t tell cause and effect. This could point to a somewhat unusual ‘chicken and egg situation’. It could be the case that men with weaker, smaller and less active areas of the brain crave greater stimulation so they are more likely to watch more porn.

In conclusion, this study does not provide any convincing evidence that viewing porn shrinks the brain, but tentatively highlights a possibility that it might.

 

Where did the story come from?

The study was carried out by researchers from the Center for Lifespan Psychology in Berlin, Germany and was funded by the German Federal Ministry of Education and Research (BMBF). The study was published in the peer-reviewed medical journal JAMA Psychiatry.

Generally, the media reported the story accurately, although the Mail’s actual reporting of the study was accurate, its headline that “viewing porn shrinks the brain” was overly certain as no cause and effect relationship was proven.

 

What kind of research was this?

This was a cross sectional study to determine whether frequent pornography viewing was associated with the frontostriatal network – an area of the brain associated with reward seeking, novelty seeking and addictive behaviour.

The researchers say that since pornography appeared on the Internet, the accessibility, affordability, and anonymity of consuming visual sexual stimuli have increased and attracted millions of users.

Incredibly, one study estimated that around 50% of all internet traffic is pornography-related.

They indicated that pornography consumption has elements of reward-seeking, novelty-seeking and addictive behaviour. They hypothesized that people watching a lot of porn may overstimulate these areas. So, as a natural counterbalance, this might lead to the dampening down of these brain responses. Similar to the way a drug addict might need higher doses to get the same effect as the body adapts.

The research looked to see whether the size and function of specific parts of the brain related to these behaviours were different across different levels of porn viewing.

One of the big issues with studies like this is that you can’t tell cause and effect or which came first. For example, the study can’t tell us whether watching porn leads to brain changes or whether people born with certain brain types watch more porn.

A longitudinal study, where participants are tracked over time, would be needed to investigate this fully.

 

What did the research involve?

The study recruited 64 healthy men between the ages of 21 and 45 years and asked them questions about their porn viewing habits.

They also took images of the men’s brains to determine the size of different areas and investigated how their brain signalling reacted to pornographic pictures using brain scans. 

Two questions were used to estimate and categorise porn consumption across a full week:

  • “How many hours on average do you spend watching pornographic material during a weekday?”
  • “How many hours on average do you spend watching pornographic material during a day of the weekend?”

Additional questionnaires assessed other factors the researches thought might influence the results, including:

  • sexual use of the internet
  • sexual addiction
  • internet addiction
  • signs of psychiatric disease
  • substance use
  • depression

The study only recruited men, the rationale given by the researchers was that men are exposed to pornography at a younger age, consume more pornography, and are more likely to encounter problems related to it compared with women. This seems like a reasonable assumption based on what we know about pornography consumption.

Those with abnormal brain scans were also excluded from the study, as were those with medical or neurological disorders.

The main statistical analysis looked for links between weekly measure of porn consumption (pornography hours) and the volume and function of specific areas of the brain.

 

What were the basic results?

The average porn viewing estimate was four hours a week, ranging from 0 to 19.5 hours. The findings grouped into those assessing the structure of the brain and those assessing the signalling and function of the brain.

Structural brain volume

They found that higher number of hours viewing porn correlated with a reduction in grey matter in an area of the brain called the right caudate nucleus. This association remained after eliminating a second correlation with internet addiction and sexual addiction. An association was also found between higher porn consumption over many years and less grey matter in this brain area. The researchers interpreted this as a sign of the effects of longer-term porn exposure.

Functional brain signalling in reaction to pornographic images

From this set of experiments the researchers found the men reporting more porn consumption had less brain signalling within the left dorsolateral prefrontal cortex (DLPFC) of the brain implicating, the researchers say, that participants who consumed more pornographic material had less connectivity between the right caudate and left DLPFC.

They also implicated an area of the brain called the left putamen as involved in processing sexual content.

 

How did the researchers interpret the results?

The researchers concluded the grey matter volume in the right caudate of the striatum “is smaller with higher pornography use”. They said that there is a lot of research suggesting the striatum is important in reward processing. So taken together they believed this supported their theory that “that intense exposure to pornographic stimuli results in a down regulation of the natural neural response to sexual stimuli.”

 

Conclusion

This small structural and functional brain study indicates there might be a correlation between more hours of porn viewed a week and smaller and less active areas of the brain associated with reward and sexual stimulation in men.

In essence, this suggests porn users might be dampening down the sexual stimulation and reward centres in their brain through over stimulation.

One of the big issues with studies like this is that you can’t tell cause and effect or which came first, an issue the study authors recognised. For example, the study can’t tell us whether watching more porn leads to changes in reward and sexual stimulation centres in the brain, or whether people born with brains wired for high reward and sexual stimulation will watch more porn. A longitudinal study would be needed to untangle cause and effect.

In addition, although a correlation existed it was not particularly strong, on a scale of 1 (perfect correlation) to 0 (no correlation) the correlation (strength of the link) between porn hours and grey matter volume was 0.432.

This estimate may also be subject to error from confounding, error in categorising porn use from self-reports, and bias from other sources. 

Related to this is the fact the study recruited relatively few men (64). A study with many more people would give evidence that is much more reliable and would be able to validate whether this correlation is real and what its true size might be.

The authors put forward a clear and intriguing rationale for their research and findings “pornography exposure might lead to wearing and down regulation of the underlying brain structure, as well as function, and a higher need for external stimulation of the reward system and a tendency to search for novel and more extreme sexual material”.

However, this research study alone does not prove this is the case, and warrants further study; especially due to the massive increase in pornography consumption that has accompanied the growth of the internet.

There is scant evidence on the pros and cons of pornography to physical or mental health, a research void that will hopefully be filled in the future. However, there is some evidence that porn can be addictive and evidence withstanding, is unlikely to be a substitute for a loving relationship.

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

Links To The Headlines

Porn viewing linked to less grey matter in brain. The Guardian, May 29 2014

Viewing porn shrinks the brain: Researchers find first possible link between viewing pornography and physical harm. Daily Mail, May 30 2014

Is porn literally shrinking men's brains? The Daily Telegraph, May 29 2014

Watching too much porn shrinks men’s brains and makes them stupid – apparently. Metro, May 29 2014

Links To Science

Kühn S, Gallinat J. Brain Structure and Functional Connectivity Associated With Pornography Consumption. JAMA Psychiatry. Published online May 29 2014

Categories: Medical News