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Health News from NHS Choices

Constantly updated health news across a range of subjects.

NHS Choices News

  • Study offers insight into genetics of schizophrenia

    "More than 100 schizophrenia genes have been pinpointed," reports the Daily Mail. In one of the largest studies of its kind, researchers have gained further insights into the genetics of the condition, which it is hoped could lead to new treatments.

    Researchers have identified genetic differences at 108 positions in the genome (the complete set of DNA that "defines" an individual organism) that are more likely to be present in people with schizophrenia.

    The study compared the genetic make-up of more than 36,000 people with schizophrenia with that of more than 110,000 controls. They found differences in 108 positions in the genome, 83 of which had not previously been reported.

    A particularly interesting finding was evidence of genetic differences in genes active in the immune system. Whether or not the immune system plays a role in the development of schizophrenia is a possibility not previously considered by most experts.

    This study provides further evidence of a genetic element to the condition, but it does not prove that the genetic differences actually cause schizophrenia.

    However, it is hoped these results will lead to new avenues of research that can be explored, and may eventually lead to better treatments for the condition.

     

    Where did the story come from?

    The study was led by researchers from Cardiff University and involved hundreds of researchers from around the world as part of the Schizophrenia Working Group of the Psychiatric Genomics Consortium.

    It was funded by the US National Institute of Mental Health and grants from governmental bodies and charities.

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

    The UK media reported the study accurately. The Independent's coverage was particularly informative, providing independent expert opinions on the findings.

    It also included a balanced viewpoint from charities highlighting the need for holistic care regardless of whether new drug treatments are developed.

    People living with schizophrenia usually require a combination of medication and talking treatments, such as cognitive behavioural therapy (CBT), to better control their symptoms.

     

    What kind of research was this?

    This was a genome-wide association study that aimed to combine all of the data from published and unpublished studies that had analysed the genetic make-up of people with schizophrenia, comparing this data with the genetics of people who do not have the condition.

    This type of study is able to identify small variations in genes present more frequently in people with a particular disease, compared with people without the disease.

    But it is only able to show an association and cannot prove that the genetic variations found cause the disease.

    This type of study is useful, however, as it can point to new areas that may be involved in the disease process. These can then be investigated further in other types of studies and could eventually lead to new treatments.

     

    What did the research involve?

    The researchers obtained data from all the available genome-wide association studies of people with schizophrenia from around the world. This included 46 European case-control samples, three east Asian case-control samples, three European family-based studies, and results from Icelandic population studies.

    Overall, the genetic make-up of 36,989 people with schizophrenia was compared with that of 113,075 healthy controls. This involved sophisticated analysis looking at 9.5 million genetic variants.

     

    What were the basic results?

    The researchers found variations in 108 loci (positions in the genome) that met genome-wide significance, 83 of which had not been previously implicated in schizophrenia. Genome-wide significance means there is a statistically significant possibility a variation is associated with a condition.

    Of these 108 loci, 75% coded for proteins. Several of the proteins are thought to have a role in schizophrenia. Variations were found in a gene that codes for the dopamine receptor, the main target of medication to treat schizophrenia, and other genes involved in neurotransmission and synaptic plasticity.

    The researchers also found variations occurred in genes expressed in the brain, as well as in genes expressed in the immune system.

     

    How did the researchers interpret the results?

    The researchers concluded that they have identified variations in genes expressed in the brain. More specifically, they found variations in the gene that encodes a protein that has been a target for drug therapies for schizophrenia for years, as well as in other genes involved in neurotransmission.

    They have also found variations in genes expressed in the immune system, which they say provides "support for the speculated link between the immune system and schizophrenia".

    However, they are also excited about the fact there are variations in a number of other genes and how this creates "the potential to provide entirely new insights into aetiology [the cause of the disease]".

     

    Conclusion

    This large genome-wide association study has found genetic variations in 108 loci more likely to be found in people with schizophrenia than in healthy controls.

    While some of these variations fell in genes that code for proteins that are already targets for drug treatments for schizophrenia, variations at 83 of the loci had not previously been implicated as being involved in schizophrenia. This provides new insights for further research.

    The study's strengths include the large number of cases and controls involved.

    But this study cannot prove that these genetic variants cause schizophrenia. It remains likely that a combination of environmental factors and genetic susceptibility increases the risk of the condition.

    A further consideration is the huge variability in the level of severity and the type of symptoms that can be present within the "umbrella" diagnosis of schizophrenia.

    It is hoped the identification of these genes will pave the way towards a greater understanding of this complex condition.

    Read more about schizophrenia, the current treatments for the condition and the available support.

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

    Links To The Headlines

    New DNA hope on schizophrenia: Discovery of 100 genes could help to transform treatment for the condition. Daily Mail, July 22 2014

    DNA hope on schizophrenia: Research breakthrough points at over 100 genes. The Independent, July 22 2014

    'Eighty new genes linked to schizophrenia'. BBC News, July 22 2014

    Schizophrenia gene study: what we've learned is how little we know. The Daily Telegraph, July 22 2014

    Links To Science

    Schizophrenia Working Group of the Psychiatric Genomics Consortium. Biological insights from 108 schizophrenia-associated genetic loci. Nature. Published online July 22 2014



  • Probiotics 'may improve blood pressure'

    “Eating probiotics may lower blood pressure,” The Daily Telegraph reports.

    Probiotics, so-called “friendly bacteria”, have been found to moderately reduce blood pressure in a new study.

    The study is what is known as a systematic review, which is essentially a study of studies. Researchers combined the results of nine randomised controlled trials (regarded as the “gold standard” in evidence-based medicine).

    The results suggest that probiotics led to a modest but significant reduction in blood pressure.

    The reliability of any systematic review depends on the included studies, and the researchers point out that there were some weaknesses in the studies they included. For example, six of the trials were only conducted on 20 to 40 people. With such a small sample size, any effect on blood pressure could have been the result of chance.

    As the lead researcher is quoted as saying in the media, more research is required before doctors can confidently recommend probiotics for high blood pressure control and prevention.

    Proven methods to improve blood pressure levels include quitting smoking, sticking to the recommended levels of alcohol consumption, eating a healthy diet (in particular, reducing salt consumption) and taking regular exercise.

     

    Where did the story come from?

    The study was carried out by researchers from Griffith University and Gold Coast Health, Australia. No source of funding was reported.

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

    The story was accurately reported in the media, though the Daily Express’s claims that eating “a pot a day [could] … help save your life” is probably overstating the findings of the study.

     

    What kind of research was this?

    This was a systematic review and meta-analysis that aimed to determine the effect of probiotic consumption on blood pressure. Systematic reviews aim to identify all the evidence related to a specific research question and synthesise the findings from individual studies or reports in an unbiased way. Meta-analysis is a mathematical technique for combining the results of individual studies to arrive at one overall measure of the effect of a treatment.

    The researchers also aimed to use their results to provide information on the most effective probiotic and dose, and how long probiotics need to be taken.

    A systematic review, when performed well, should give the best possible estimate of the true effect of probiotics on blood pressure.

     

    What did the research involve?

    The researchers searched databases of published literature and trials to identify randomised controlled trials (RCTs) that had given people probiotics and had assessed the effect on blood pressure.

    Once they had identified relevant trials, the researchers assessed them to see if they were well-performed and extracted data.

    The results of all the trials were then combined to produce a "bottom line" on the effectiveness of probiotics on blood pressure.

     

    What were the basic results?

    The researchers included nine RCTs with 543 participants in total. Six of the trials had between 20 and 40 participants.

    Some trials involved healthy people, others included patients with hypertension (high blood pressure), hypercholesterolemia (high levels of cholesterol in the blood), metabolic syndrome (a combination of diabetes, high blood pressure and obesity) or who were overweight or obese. The species and dose of probiotics used, and how they were given, also varied across the trials.

    Trials used either yoghurt, fermented and sour milk, probiotic cheese, encapsulated supplements or rose-hip drinks.

    The trials gave people between a single species and three species of probiotic at the same time, and the daily dose of probiotics varied between 109 colony-forming units and 1012 colony-forming units. A colony-forming unit is an estimate of the amount of micro-organisms, usually bacteria or fungi, in a given sample.

    The duration of the trials varied from three weeks to nine weeks.  

    After combining the results of the trials the researchers found that:

    • Probiotic consumption significantly reduced systolic blood pressure by 3.56 mm Hg compared to control (systolic blood pressure is the "top" number and is the blood pressure in the arteries when the heart beats).
    • Probiotic consumption significantly reduced diastolic blood pressure by 2.38 mm Hg compared to control (diastolic blood pressure is the "bottom" number and is the blood pressure in the arteries between heart beats).

    By combining the results of different sub-groups of studies they found that:

    • Using dairy products as the source of probiotics resulted in significant reductions in systolic and diastolic blood pressure, whereas using other sources of probiotics did not.
    • Using multiple species of probiotics resulted in significant reductions in systolic and diastolic blood pressure, whereas using a single species did not.
    • Using a dose of at least 1011 colony-forming units per day resulted in significant reductions in systolic and diastolic blood pressure, whereas using lower doses did not.
    • Taking probiotics for at least eight weeks resulted in significant reductions in systolic and diastolic blood pressure, whereas taking probiotics for shorter periods did not.
    • People who had blood pressure of 130/85 mm Hg (higher than ideal but still normal) or higher had significant improvements in diastolic blood pressure but people with blood pressure less than 130/85 mm Hg did not.

     

    How did the researchers interpret the results?

    The researchers concluded that their results suggest consuming probiotics may improve blood pressure by a modest degree, and that this effect may be greater if blood pressure is high to begin with, multiple species of probiotics are consumed, probiotics are taken for eight weeks or longer, and if each dose contains at least 1011 colony-forming units.

    They go on to say that “the reduction [in blood pressure] reported in this meta-analysis is modest; however, even a small reduction of [blood pressure] may have important public health benefits and cardiovascular consequences.”

     

    Conclusion

    This systematic review and meta-analysis has found that probiotic consumption results in moderate reductions in blood pressure.

    The results of a systematic review depend on the included studies, and the researchers point out that there were some weaknesses in the studies they included. They say that “more randomised, controlled studies with larger sample groups, longer durations and adequate blinding of conditions trials are needed to confirm the effect of different probiotic species and products on BP [blood pressure] and hypertension.”

    Analysis of subgroups of studies led the researchers to conclude that blood pressure improvements may be greater among those with elevated blood pressure, when the daily dose of probiotics is at least 1011 colony-forming units, when more than one species of probiotic is taken and when probiotics are taken for at least eight weeks.

    However, they also point out that these conclusions are based on the results of only a few studies, and the majority of them were very small – six of the trials were only conducted on between 20 and 40 people.

    As the lead researcher is quoted as saying in the media, more research is required before doctors can confidently recommend probiotics for high blood pressure control and prevention.

    Proven methods to improve blood pressure levels include quitting smoking, sticking to the recommended levels of alcohol consumption, eating a healthy diet (in particular, eating a low salt diet) and taking regular exercise.

    Read more about how to improve your blood pressure.

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

    Links To The Headlines

    Eating probiotics may lower blood pressure. The Daily Telegraph, July 22 2014

    Eating probiotic yoghurt could lower blood pressure and protect against heart disease. Mail Online, July 21 2014

    Yoghurt can beat high blood pressure, claims new study. Daily Express, July 22 2014

    Links To Science

    Khalesi S, Sun J, Buys N, Jayasinghe R. Effect of Probiotics on Blood Pressure - A Systematic Review and Meta-Analysis of Randomized, Controlled Trials. Hypertension. Published online July 21 2014



  • HIV 'reservoirs' may form earlier than expected

    "Early HIV drugs 'may not stop virus'," BBC News reports. The report is based on a study of HIV treatments in monkeys, and has been linked by the BBC to the emergence of HIV in a four-year-old girl thought to have been cured of the virus as the result of treatment from birth – the so-called "Mississippi girl".

    HIV infection levels in the blood can be managed through antiretroviral therapy (ART), allowing most people to live a normal life. But if the therapy is stopped, the virus re-emerges from "viral reservoirs" in the body that are immune to ART.

    It was thought these reservoirs are formed during the initial infection, when the virus spreads to the bloodstream. But this study has shown the monkey version of HIV can form reservoirs within three days of infection. This occurs before the virus is detectable in the bloodstream.

    It is likely such rapid development of reservoirs also occurs in humans and gives very limited chances of success for current ART to prevent their formation.

    This is likely to have happened to the "Mississippi girl", who is reported to have been given ART within hours of birth and for 18 months afterwards, until she stopped attending appointments. The virus was not detectable and she was believed to have been cured, but it has now resurfaced.

    Read the latest BBC report on the "Mississippi girl" for more information.

    Drug development for treating the HIV virus will therefore continue to focus on new techniques to target the cells in these reservoirs.

     

    Where did the story come from?

    The study was carried out by researchers from Harvard and universities and institutes in Massachusetts, Bioqual in Maryland, Gilead Sciences in California, and the US Military HIV Research Program in Maryland.

    It was funded by the National Institutes of Health, the US Army Medical Research and Material Command, the US Military HIV Research Program, and the Ragon Institute of MGH, MIT and Harvard.

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

    The BBC reported the story accurately and informatively.

     

    What kind of research was this?

    This was an animal study using rhesus monkeys to investigate simian immunodeficiency virus (SIV), a monkey virus similar to HIV. The researchers wanted to investigate the speed of infection – in particular, how quickly "viral reservoirs" are formed.

    HIV infection is known to create what are known as viral reservoirs. These are pockets of infected memory CD4+ cells that are the source of reactivation of the virus when antiretroviral therapy (ART) is stopped.

    It was believed these reservoirs are formed during the initial stages of infection, when the virus is present in the bloodstream (viraemia), but it was not known how quickly they form.

    As ART is largely ineffective against the cells located in the reservoirs, the researchers wanted to know if there is a window of opportunity after infection to prevent the reservoirs forming in the first place.

     

    What did the research involve?

    Twenty rhesus monkeys were given an injection of SIV into the lining of the rectum. At this point, the virus was not detectable in the bloodstream.

    Some of the monkeys then received antiretroviral therapy (ART), starting on either day 3, 7, 10 or 14 after infection and continued for 24 weeks. Control monkeys did not receive ART.

    The monkeys were monitored during the six months to see if and when the virus was detectable in the bloodstream, lymph nodes and rectal lining. They were also monitored for 24 weeks after the ART was stopped to see if or how quickly the SIV came back.

     

    What were the basic results?

    After stopping treatment, SIV infection became detectable in the bloodstream of all of the monkeys. This took a little longer to occur in the monkeys that started treatment on day 3 (mean 21 days) compared with days 7, 10 or 14, (mean 7 days), but it still occurred.

    This indicated the viral reservoirs, where cells are able to effectively hide from ART, are formed within the first three days of infection with SIV.

    The virus was not detectable in the blood of monkeys given ART on day 3, either before the injections started or during the next 24 weeks. The researchers did find the virus in lymph nodes and the rectal lining, but both reduced during ART treatment.

    All other monkeys had detectable, rapidly increasing levels of the virus in the blood, lymph nodes and rectal lining. The ART reduced the levels compared with the control monkeys.

    The levels of the treated monkeys became undetectable within three to four weeks, and this continued for the treatment period. The control monkeys had sustained, high levels of virus in the bloodstream throughout the length of the study.

    Monkeys given ART on days 10 and 14 had viral infection in the lymph nodes, which initially reduced a little but then remained constant from week 12.

     

    How did the researchers interpret the results?

    The researchers conclude that: "These data demonstrate that the viral reservoir is seeded rapidly after intrarectal SIV infection of rhesus monkeys, during the 'eclipse' phase, and before detectable viraemia. This strikingly early seeding of the refractory viral reservoir raises important new challenges for HIV-1 eradication strategies."

     

    Conclusion

    This study has shown SIV infection spreads to locations in the bodies of monkeys, forming "viral reservoirs" during the first three days of infection, before the virus is detectable in the bloodstream.

    Cells in the reservoirs are resistant to treatment with ART and are the source of rebound infection when treatment is stopped. Because of the similarities between SIV and HIV, it is likely an equivalent chain of events occurs when humans are infected with the HIV virus.

    This appears to have been the case for the "Mississippi girl", a four-year-old girl who was treated with ART for the first 18 months of her life and was presumed to be cured, but has now shown evidence of the infection.

    This research indicates drug-resistant HIV reservoirs are likely to occur rapidly during infection in humans, and remain a challenging target for drug development.

    Although it is not yet possible to eradicate HIV infection, long-term treatment with ART can help most people live full and normal lives. 

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

    Links To The Headlines

    Early HIV drugs 'may not stop virus'. BBC News, July 21 2014

    A proof of concept for an HIV cure exists. Now even our setbacks are useful. The Guardian, July 21 2014

    Links To Science

    Whitney JB, et al. Rapid seeding of the viral reservoir prior to SIV viraemia in rhesus monkeys. Nature. Published online July 20 2014



  • Could new potential treatment mean safer IVF?

    “Dozen babies born using 'safer' IVF treatment,” reads today’s headline in The Independent.

    This headline was based on a new study providing proof of concept that the natural hormone kisspeptin-54 could be used to stimulate egg maturation in women requiring in vitro fertilisation (IVF).

    The modified IVF treatment on trial, which is hoped to be safer than standard IVF, led to 12 healthy babies being born from 53 women undergoing a single IVF treatment.

    One of the main hopes is that using kisspeptin-54 could lead to a safer version of IVF by reducing the need to use human chorionic gonadotropin (hCG), which has a small risk of causing ovarian hyperstimulation syndrome (OHSS). This can be potentially fatal. However, this study was much too small to prove kisspeptin-54 was safer. Much larger trials are required to prove this, and are the logical next step for this early stage research.

    The study looked mainly at different doses of kisspeptin-54, but did not compare it with current IVF treatment. It will be vital for future clinical trials to include a control group, so that the effectiveness and safety of the new IVF treatment can be directly compared to the existing treatment, to see which is better overall.

     

    Where did the story come from?

    The study was carried out by researchers from Imperial College London and Hammersmith Hospital, and was funded by the Medical Research Council, Wellcome Trust and National Institute for Health Research.

    The study was published in The Journal of Clinical Investigation, a peer-reviewed medical journal.

    The media’s reporting of this story has been generally accurate, with the BBC including important quotes at the end of their piece, illustrating some of the research's key limitations. The Independent’s coverage did not highlight the limitations inherent in the study, and instead focused on the potential positives of the finding, leaving readers with a less balanced account.

     

    What kind of research was this?

    This was a randomised clinical trial (RCT) investigating whether a new hormone could be used in the early stages of IVF to potentially improve its safety.

    IVF is one of several techniques available to help couples with fertility problems have a baby. During IVF, eggs are surgically removed from the woman's ovaries and fertilised with sperm in a laboratory. The fertilised egg is grown for a few days in the lab, and the best one or two embryos are then returned to the woman's womb to implant, grow and develop.

    IVF starts with women being given hormones to suppress their natural monthly cycle. They are then given fertility-stimulating hormones to increase the number of immature eggs produced in the ovaries. These are too immature to be collected, so a second hormone is injected, typically human chorionic gonadotropin (hCG), to stimulate these eggs to mature. These matured eggs can then be collected for fertilisation in the laboratory.

    However, hCG tends to linger in the body and is associated with a small risk of the ovaries being stimulated too much, causing the condition OHSS. The researchers wanted to see if there was a safer way of stimulating women’s ovaries to produce mature eggs for the IVF process, but without the increased risk of OHSS.

    In previous research, the group had come across a naturally occurring hormone called kisspeptin-54, which when faulty makes a person infertile, as they cannot go through puberty. They thought there was a chance it might stimulate egg maturation over a shorter period of time, lessening the chance of the ovaries being overstimulated, theoretically reducing the risk of OHSS. They designed a clinical trial to investigate whether it was possible to use kisspeptin-54 instead of hCG in the IVF process, specifically to stimulate egg maturation.

     

    What did the research involve?

    The researchers randomly allocated 53 women who had opted for IVF to different doses of kisspeptin-54 treatment. They wanted to see whether it could partially replace the hormone normally used to stimulate the maturation of eggs during IVF.

    All of the women were given follicle-stimulating hormone (FSH) to stimulate the ovaries to produce lots of immature eggs. They were also given gonadotropin releasing hormone (GnRH) antagonist injections to prevent the eggs from leaving the ovaries too early. They were then given different doses of kisspeptin-54 to trigger egg maturation. When at least three ovarian follicles (immature eggs) of 18 mm or greater diameter were visible on an ultrasound scan, the women were given an injection of kisspeptin-54 to trigger egg maturation.

    The women were recruited from a list of women requiring IVF treatment at Hammersmith Hospital, London. The inclusion criteria were specific and included:

    • age 18-34 years
    • early follicular phase level of serum FSH ≤12 mIU/ml
    • serum anti-Mullerian hormone of 10-40 pmol/l (1.4-5.6 ng/ml)
    • both ovaries intact, regular menstrual cycles of 24-35 days duration
    • body mass index (BMI)18-29 kg/m2 (this includes women of a healthy weight and overweight, but not those who are obese or underweight)

    Women were excluded if they:

    • had moderate or severe endometriosis
    • had poor response to, or more than one previous cycle of, IVF treatment
    • had clinical or biochemical hyperandrogenemia (an excess of androgens)
    • had polycystic ovarian syndrome

    The researchers primarily wanted to know whether a single treatment of kisspeptin produced egg maturation. They assessed this by looking at the number of mature eggs, and the percentage of all eggs collected that were mature. Secondary outcomes included the later stages of IVF, such as fertilisation rates, successful implantation rates, pregnancy rates and healthy births.

    Importantly, there was no control group of women who received normal IVF with gonadotropins to act as a comparison, so only the relative effects of the different doses of kisspeptin were under investigation. The study did not compare the effect of the experimental kisspeptin IVF treatment with regular IVF treatment.

     

    What were the basic results?

    Egg maturation was observed in response to each tested dose of kisspeptin-54, and the average (mean) number of mature eggs per woman broadly increased in a dose-dependent manner.

    Fertilisation of eggs and transfer of embryos to the uterus occurred in 92% (49/53) of patients treated with kisspeptin-54.

    Clinical pregnancy rates using the technique were 23% (12/53) overall. 10 of the 53 women gave birth to healthy babies (12 babies in total, as two women had twins) following the kisspeptin IVF. Two women who initially became pregnant had a miscarriage.

    In terms of safety and side effects, kisspeptin was reported to be well tolerated by all of the women. Five negative events were recorded in the group, but these were related to established complications of IVF, rather than the new hormone treatment. Two patients experienced an ectopic pregnancy, one had a heterotopic pregnancy (where an ectopic pregnancy and a viable intrauterine pregnancy occur at the same time) and two had miscarriages.

     

    How did the researchers interpret the results?

    They said the study "demonstrates that a single injection of kisspeptin-54 can induce egg maturation in women with subfertility undergoing IVF therapy. Subsequent fertilisation of eggs matured following kisspeptin-54 administration and transfer of resulting embryos can lead to successful human pregnancy.”

     

    Conclusion

    This study provided a “proof of concept” that the naturally occurring hormone kisspeptin-54 can be used to stimulate egg maturation in women requiring IVF. The modified IVF – which is hoped to be safer than standard IVF – led to 12 healthy babies being born from 10 mums. Out of the 53 women undergoing a single IVF treatment, this gave a 19% success rate.

    Researchers hoped that using kisspeptin-54 could lead to a safer version of IVF by reducing the risk of OHSS. Although theoretically plausible, this study was much too small to prove that the new technique was safer; much larger trials will be required to prove this. What this study does prove is that it is possible to achieve IVF success to stimulate egg maturation by using kisspeptin-54.

    Another factor limiting the interpretation of the results is the fact that there was no control group. The study did not compare the effect of the experimental kisspeptin-54 treatment with regular IVF treatment. Therefore, the study told us about the relative effects of the different doses of kisspeptin, rather than how they stacked up against the current IVF treatment. This is something fully acknowledged by the research authors, but much less clear in the media's reporting.

    Future studies will need to examine not only whether the new treatment is safe, but also whether it leads to the similar success rates in terms of fertilisation and healthy births as the current technique.

    The BBC carries a quote indicating that the next clinical trials will take place in women with polycystic ovary syndrome (PCOS), who are more vulnerable to overstimulation. This will be a useful way to investigate the potential safety benefits of this technique in this higher risk group.

     

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

    Links To The Headlines

    Dozen babies born using 'safer' IVF treatment. The Independent, July 20 2014

    'Safer IVF' with kisspeptin hormone shows promise. BBC News, July 19 2014

    Natural 'chocolate hormone' that makes IVF safer: Women desperate to become mothers could soon benefit from treatment named after Hershey's sweet. Daily Mail, July 19 2014

    First babies born from safe new IVF technique. The Daily Telegraph, July 19 2014

    Links To Science

    Jayasena CN, et al. Kisspeptin-54 triggers egg maturation in women undergoing in vitro fertilization. The Journal of Clinical Investigation. Published online July 18 2014



  • Obese women may have 'food learning impairment'

    "Obese women show signs of food learning impairment," is the headline on the BBC News website.

    It reports on a behavioural study involving 67 individuals of normal weight and 68 obese individuals.

    Each participant was shown a series of either blue or purple squares, and then asked to predict whether the square would yield a reward. Depending on the phase of the experiment, this would be a picture of either food or money, followed by actual food or money at the end of the experiment.

    The pattern of rewards was not random – one colour square was more weighted to provide a reward than another. Crucially, halfway through the experiment the reward pattern was reversed.

    Researchers were interested in seeing how long it took for participants to recognise and adapt to the shift.

    They found obese women were less able to recognise and adapt to the shift compared with other groups (non-obese women and men of any weight) when the rewards were food based. However, their performance was the same as other groups when the rewards involved money.

    According to the researchers, the implication is that an image of food somehow skews the rational predictive and decision making part of the brain in obese women (but, strangely, not obese men).

    Overall, this study will add to research in the field of behavioural learning related to food, but on its own it provides a very limited explanation or new therapeutic angles for tackling the obesity epidemic.

     

    Where did the story come from?

    The study was carried out by researchers from Yale University and School of Medicine, and Icahn School of Medicine at Mount Sinai, New York. No sources of financial support are reported.

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

    BBC News' reporting of the research is broadly accurate. However, the limitations of this piece of experimental research were not acknowledged – deficits in learning were seen in a very specific test scenario in a small group of people. 

    The LA Times provides a more informative summary of how the experiment was carried out and the alleged implications of the results.

     

    What kind of research was this?

    This was an experimental study that aimed to see if there is a difference in learning when responding to food cues, comparing obese people with those of a normal weight.

    One of the main drivers of the global obesity epidemic is known to be the consumption of foods high in fat and sugar. The "rewarding" properties of these types of foods are thought to be what causes us to keep on eating them.

    However, it is thought these reward circuits in the brain may differ between people, causing some to have a propensity for overeating and obesity. This is what this study aimed to investigate.

     

    What did the research involve?

    The study included 67 individuals of a normal weight (35 of these were women) and 68 obese individuals (of which 34 were women) who were recruited from the community.

    They took part in a behavioural learning test assessing their reward association. The participants had to try to work out the relationship between two different coloured squares (blue and purple), and images of either food or monetary rewards. 

    Half the participants took part in a money task where the reward was either $5 or $10, and half took part in a food task where the reward was either 10 or 15 peanut M&Ms, or 6 or 12 pretzels (depending on the person's preference).

    In the first part of the test, a picture of a reward appeared after the colour A one-third of the time, and never after colour B (total: 14 presentations of each colour, intermixed with 7 presentations where colour A was associated with the reward).

    The colours were reversed in the second part of the test, so a picture of a reward appeared after the colour B one-third of the time, and never after colour A was paired with the reward in one-third of the trials, and the colour B was never paired with the rewards (total: 18 presentations of each colour, intermixed with 9 presentations, where colour B was associated with the reward).

    When the participants were shown a colour, they had to indicate on a scale of one to nine the degree to which they expected to get a reward.

    The researchers asked all participants to fast for four hours before taking part in the trials to try to increase the salience (importance) of the food rewards.

    The participants were told at the end of the tasks that they would received the accumulated amount of all the money or food they saw during the experiment. This resulted in $100 in the money condition and a bag of peanut M&Ms or pretzels in the food condition. 

    The researchers examined the differences between obese people and people with normal body mass indexes (BMIs), and looked to see if there were differences between men and women.

     

    What were the basic results?

    The researchers found a significant association between test performance and BMI. The magnitude of the difference between obese and normal-weight participants was further influenced by the test modality (food or money) and whether the participant was male or female. 

    When looking at all participants who took part in the food tests, they found that compared to normal weight people, obese people had a food-specific learning deficit. However, when they split the group by gender, they found the association was significant only in obese women, but not in obese men.

    Obese women were less able to tell which of the two colours was associated with the food on the first part of the test, or then able to switch this association on the second part of the test.

    Meanwhile, on the monetary test, there was no significant learning deficit between obese and normal-weight men or women.

     

    How did the researchers interpret the results?

    The researchers say their analyses demonstrated a "robust negative association between BMI and learning performance in the food domain in female participants" – that is, as BMI goes up, learning performance goes down when food is part of the equation. The same impairment was not observed in obese men.

    They say: "These findings suggest that obesity may be linked to impaired reward-based associative learning and that this impairment may be specific to the food domain."

     

    Conclusion

    This experimental study included fairly small groups of obese and normal-weight men and women.

    It found that, overall, obese women demonstrated a learning deficit when food was used as a reward compared with normal-weight women.

    On the food tasks, obese women were generally less able to discriminate between which of the two colours was associated with the food, and then to respond when the association was switched.

    The difference was not significant between obese men and normal-weight men. There was also no difference among participants when money was used as a reward.

    While this may possibly demonstrate some difference in food-related learning and reward associations between obese and normal-weight people – and specifically obese and normal-weight women – the applications of this single small piece of research seem to be quite limited.

    The study only included a small number of people in the US: 67 normal-weight individuals and 68 obese individuals. These people where then divided between the two monetary and food tasks.

    This meant all of the results related to the "food-related learning deficit in obese women" were obtained from tests in only 18 obese and 18 normal-weight women.

    This is a very small group, and it is possible the results could be down to chance. Other groups of people, including those of different countries and cultures, could have given different results.

    This was also only a single very specific test, seeing if people could spot which of two colours was associated with the food reward of either some M&Ms or pretzels. Interpreting the meaning from this single test is very difficult. It tells us very little about how people become obese.

    For example, someone being unable to link which particular colour is associated with a food item doesn't tell us about the various drivers that have led to that individual becoming obese.

    Even if we do take the findings of the study at face value, it leaves several important questions unanswered.

    For example, does "food-related learning deficit" lead to obesity, or does being obese make it more likely you will go on to develop a food-related learning deficit?

    And why were these deficits only seen in obese women and not obese men?

    One possible answer to the second question is this could be because of the very small samples of men and women tested. The findings of no difference in men but a difference in women could be purely down to chance, and there may not be a difference between the genders at all. 

    While the psychology of obesity is certainly an avenue worth investigating further, it is difficult to see what insights or opportunities for new treatments this study could offer.

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

    Links To The Headlines

    Obese women 'show signs of food learning impairment'. BBC News, July 18 2014

    When food's the reward, obese women's judgment fails them. LA Times, July 17 2014

    Links To Science

    Zhang Z, Manson KF, Schiller D, Levy I. Impaired Associative Learning with Food Rewards in Obese Women. Current Biology. Published online July 17 2014