“Disabled people could soon re-grow damaged or diseased limb joints,” said the Daily Mirror. The newspaper said that the prospect of a new technique, using people’s own stem cells rather than transplanted ones “offers hope to millions suffering crippling pain”.

The study behind this news attempted to grow new cartilage in rabbits by drawing the rabbits’ own circulating stem cells to a scaffolding of bone-like substances implanted into their shoulder joints. To assess the technique the researchers then observed the rabbits’ movement and took samples from the joint to see if new cartilage had formed. The rabbits regenerated cartilage and were soon able to bear weight.

The real test of this technology will come if it is eventually applied to humans. While the researchers have tried growing cartilage to attach to artificial joints they say that regeneration of other tissues may also be possible with their technique. However, this type of research proceeds in small steps and so it is too soon to say if this could ever be a reliable alternative to a simple artificial hip replacement in humans.

 

Where did the story come from?

The study was carried out by researchers from Columbia University Medical Center, the University of Missouri and Clemson University in the US. It was funded by the New York State Stem Cell Science programme and the US National Institutes of Health. The study was published in the peer-reviewed medical journal The Lancet.

Several newspapers have accurately reported this research, with some pointing out that experts have said that even if the technique is successful in eventual human trials, a conventional hip replacement might still be the best option. The Daily Mirror goes further, claiming that this early animal research offers “new hope for millions”.

 

What kind of research was this?

The researchers explain that they wanted to test a new approach to generating new tissues. In this case, they wanted to test whether they could grow new sections of the cartilage naturally found on the surface of joints. Rather than directly transplanting stem cells from an external source, which some experiments have attempted, they instead wanted to provide an artificial surface that could attract the body’s own circulating stem cells and encourage them to deposit and grow on this artificial scaffolding.

The study was well conducted, and the research paper features cautious reminders that this is very preliminary work that still needs much more research to assess the feasibility of applying this technology to humans.

 

What did the research involve?

The researchers designed a ‘proof of concept’ study to see if it was technically possible to grow new cartilage in rabbits by attracting their circulating stem cells to a new form of scaffolding.

They compared two ‘bioscaffolds’ in an experiment on 23 rabbits. Ten scaffolds were covered in a growth factor called TGFβ3 and implanted into the rabbits, while ten rabbits were implanted with scaffolds lacking the growth factor chemical. Three rabbits also had operations to remove the joint without a bioscaffold replacement (the ‘defect only’ rabbits).

To produce these bioscaffolds, the researchers first used a computer to trace the surface shape and size of a rabbit shoulder joint. They then made a bioscaffold out of a composite of a biodegradable polymer, a polyester and a substance called hydroxyapatite, a mineral that forms a large part of normal bone.

The whole joint surface of the shoulder in the rabbits was then surgically removed and replaced with these bioscaffolds that either lacked or contained the transforming growth factor. The researchers then assessed the movement of the joints and ability of the rabbits’ shoulders to bear weight at 1–2, 3–4 and 5–8 weeks after surgery. At four months they took a sample of bone and cartilage from the live rabbits and checked them for things such as cracks, thickness, density, cell numbers and mechanical properties.

 

What were the basic results?

All the animals in the group given the scaffolds infused with growth factor fully resumed weight bearing and movement 3–4 weeks after surgery. The rabbits that had received the bioscaffolds infused with growth factor showed more consistent improvement than the rabbits that had received the bioscaffolds lacking the growth factor. Defect-only rabbits limped at all times.

When the sample of scaffolding and cartilage was removed at four months after surgery, joint-facing surfaces of the TGFβ3-infused bioscaffolds were fully covered with hyaline cartilage, a pad of tough but flexible cartilage that naturally lines joints. There was only isolated cartilage formation in the other implant group and no cartilage formation in the defect-only rabbits.

 

How did the researchers interpret the results?

The researchers say that their findings suggest that the cartilage layer across the entire surface of synovial joints (lubricated, freely moving joints) “can regenerate without cell transplantation”.

They go on to call for further investigation into the technique, saying that the regeneration of complex tissues seems probable when using ‘homing’ (having a surface or environment that attracts the body’s circulating cells) in tissues that need repair.

 

Conclusion

This interesting study has demonstrated the potential of a new technique. The researchers point out the areas that need further investigation:

• They do not yet know where the stem cells (or progenitor early cartilage cells) came from. Although they think that some of these cells are derived from stem or progenitor cells of synovium, bone marrow, fat cells and perhaps blood vessels, more research will be needed to find out exactly where they came from.
• They suspect that if TGFβ3 can attract multiple cell types then more research will be needed to find out how to target the specific cell populations needed for the regeneration of more complex tissues.
• They say that it is good news that the regenerated cartilage is strong enough for weight bearing in rabbits.

The real test of this technology will come if it is eventually applied to humans. The researchers were not just thinking of growing cartilage to attach to artificial joints, and explain that regeneration of other tissues may also be possible with their technique. However, this type of research proceeds in small steps and so it is too soon to say if this could ever be a reliable alternative to a simple artificial hip replacement in humans.

Links To The Headlines

Hip hope from stem cell technique. BBC News, July 29 2010

The 'grow your own' hip and knee replacements with full range of movement. Daily Mail, July 29 2010

Regrowing limb joints. Daily Mirror, July 29 2010

Links To Science

Lee CH, Cook JL, Mendelson A et al. Regeneration of the articular surface of the rabbit synovial joint by cell homing: a proof of concept study. The Lancet, Early Online Publication, July 29 2010

“Kicking and lashing out while asleep could mean you’re more likely to develop dementia or Parkinson’s disease,” reported the Daily Mail. It said a study has found a link between a sleep disorder and a higher risk of certain types of dementia up to 50 years later.

The study looked at people diagnosed with one of several related neurological conditions and analysed their history of a severe form of REM sleep behaviour disorder (RBD), a condition in which people can act out recurrent dreams and move excessively while asleep.

The study was not designed to look at the strength of the link between RBD and dementias, as patients in the study were selected because they were known to have had both of these conditions. Therefore, it is not possible to say from this study whether restless sleep is a predictor of future dementia as is implied in the newspaper headline. More research into whether RBD could be an early sign of the brain changes that lead to dementia later on would be useful.

 

Where did the story come from?

The study was carried out by researchers from the Department of Neurology at the Mayo Clinic in the US. The researchers received several individual grants and awards. The study was published in the peer-reviewed medical journal Neurology.

The Daily Mail has concentrated on the theoretical link between a group of neurological conditions and this sleep disorder. Previous research has indicated that there is some association between the two, but the strength of this relationship is unclear and, at this stage, RBD cannot be used to predict later disease.

 

What kind of research was this?

The stage of sleep in which your brain activity increases and when dreaming may occur is known as rapid eye movement (REM) sleep because, during this phase, your eyes start to move quickly and flicker.

This research looked at the association between a sleep disorder called REM sleep behaviour disorder (RBD) and a group of neurological conditions including Parkinson’s disease, multiple system atrophy (MSA) and dementia with Lewy bodies (DLB). RBD is a sleep disorder where people act out recurrent dreams and move excessively while asleep, and in this study injured themselves or their partners as a result.

To investigate this, the researchers used the records from a specialist neurological clinic of 27 patients who had been diagnosed with RBD and then went on to develop degenerative neurological symptoms at least 15 years later.

The researchers confirmed the diagnoses of RBD and analysed the records to define the types and timing of diseases and symptoms the patient developed. They used these data to calculate the length of time between the first sign of restless sleep and the diagnosis of a range of dementias.

This was a case series analysis in which all the participants were selected because they had both conditions. As such, it cannot demonstrate a link between the conditions as there was no comparison group. However, the researchers refer to previous research that they say has demonstrated this link. They say that the first study to document this relationship reported that nearly 40% of patients with isolated, idiopathic RBD developed a parkinsonian disorder an average of 12.7 years later. This current study was mainly interested in the question of whether the length of time between RBD and dementia could be even longer than 12.7 years.

 

What did the research involve?

Some patients with these neurological disorders have reported that their first experience of restless sleep happened many years previously. The aim of this study was to explore a theory based on this anecdotal evidence that RBD symptoms can predate Parkinson’s disease by several decades.

The researchers were interested in a range of conditions thought to be caused by abnormal deposition of a protein called alpha-synuclein in the brain. These diseases included Parkinson's disease, dementia with Lewy bodies and multiple system atrophy, which are all neurodegenerative diseases that appear later in life.

The researchers used the Mayo Clinic’s records to identify all patients who had been evaluated for these diseases between 2002 and 2006. They then selected all those who had a history of RBD and for whom there was at least 15 years between onset of RBD and their neurodegenerative symptoms. To be eligible, patients also had to have been assessed by a specialist in a sleep lab and by at least one other neurological specialist in the Mayo Clinic’s behavioural neurology or movement disorders sections.

RBD was diagnosed if abnormal flailing movements occurred during sleep, with sleep-related injuries or movements that were potentially injurious or disruptive. Symptoms of physical activity during sleep were provided by the patient and bed partner. Patients were then divided into probable and definite RBD. The numbers of patients with the different disorders were counted, and the interval between RBD and symptom onset for the neurological disorder recorded.

 

What were the basic results?

The researchers identified 550 patients with RBD and one of the three neurodegenerative disorders of interest.

Of the 550 patients, 27 (4.9%) had first started experiencing RBD more than 15 years before the onset of neurodegenerative disease symptoms. Of these, 13 had developed Parkinson’s disease, Parkinson’s with mild cognitive impairment or Parkinson disease dementia. Another 13 had developed probable dementia with Lewy bodies and one had developed parkinsonism-predominant MSA.

Most of the patients were male (24 [89%]). The average (median) interval between RBD symptoms and neurodegenerative syndrome symptom onset was 25 years (range 15–50 years), and the median age at onset of restless sleep was 49 years.

 

How did the researchers interpret the results?

The researchers say that their cases add a new time dimension to theories on the evolution of neurodegenerative syndromes characterised by alpha-synuclein deposition. They say that, until now, the estimated interval between changes in the brain and disease onset had been about 5-6 years, but this study suggests that it may be longer.

 

Conclusion

These findings suggest that the brain changes associated with certain neurodegenerative diseases could begin many years before the symptoms start to show.

There are a few points to note about this study:

• This study was not set up to evaluate the strength of the association between RBD and neurodegenerative disease, and it does not shed any light on how many people with restless sleep go on to develop neurological conditions.
• The study only looked at a few specific types of dementia and not the more common Alzheimer’s or vascular type of dementia. As such, these findings are even less applicable to people concerned about the more common dementias.
• These participants had a very specific form of severe sleep disturbance, involving lashing out and characteristic brain wave patterns during their sleep. Many people will have the occasional restless night of sleep, but most are unlikely to have RBD. The results of this study are unlikely to apply to them.

In general, this study provides some insight into these rare conditions and will be of interest to doctors, scientists and the public. The results should not be interpreted to mean that restless sleep can be used to predict future dementias or neurological diseases.

Links To The Headlines

Kicking and lashing during sleep 'could signal dementia or Parkinson's disease'. Daily Mail, July 29 2010

Links To Science

Claassen DO, Josephs KA, Ahlskog JE, et al. REM sleep behavior disorder preceding other aspects of synucleinopathies by up to half a century. Neurology 2010, [Published online before print] July 28, 2010

“Loneliness is a killer” and is “as bad for your health as alcoholism, smoking and overeating”, reported the Daily Mail.

The research behind this story looked at studies on the effects of social relationships on health and disease. It found that having stronger social relationships generally increased a person’s likelihood of survival over an eight-year period by 50% compared to people with fewer social relationships.

The researchers point out that the 148 studies they included in their analysis measured the strength of social relationships in very different ways, and that they did not all take into account other factors that could influence the risk of death.

Although this study found that people generally lived longer if they had larger networks of family and friends, it does not spell doom for those with smaller or less intimate social networks. The study could not show why there was a relationship between social networks and health. The researchers put forward two theories: that social networks may provide a cushion against stress or that they may encourage healthier lifestyles.

 

Where did the story come from?

The study was carried out by researchers from Brigham Young University, which also funded the research along with TP Industrial Inc. The study was published in the open access peer-reviewed journal PLoS Medicine.

The newspapers reflected the content of the research accurately.

 

What kind of research was this?

This was a systematic review and meta-analysis that investigated the extent to which social relationships influence the risk of death and which aspects of these relationships contributed to the risk.

The researchers said that there are two possible ways that social relationships may influence health. The first is that friends and family may help people deal with stress and prevent it from building up. The second reason is that they encourage people to have healthy behaviours, as people with these social networks are more likely to conform to social norms of health and self-care.

A systematic review is the best way to find all the information available in a research area. However, the researchers reported that there was a large variation in how social relationships were measured, making it more difficult to directly compare different studies. The researchers focussed on three major components of social relationships that were consistently evaluated to see how each of these components contributed to health:

• the degree of integration in social networks
• the social interactions that are intended to be supportive (received social support)
• the beliefs and perceptions of support availability held by the individual (perceived support)

 

What did the research involve?

The researchers searched for studies published between 1990 and 2007 using medical and scientific journal databases. They used the search terms “mortality”, “death”, “decease(d)”, “died”, “dead” and “remain(ed) alive” in addition to search words linked to social isolation, including “social”, “interpersonal”, “support”, “network”, “integration”, “participation”, “cohesion”, “relationship”, “capital” and “isolation”. If they found a review article using this search strategy, they looked at the references included in its reference list to make sure they had not omitted any relevant studies.

The researchers included studies that provided quantitative data on the association between death and an individual’s social relationships. As they were interested in the effect of social relationships on disease, they excluded studies where people had died as a result of suicide or injury. They also excluded studies where the measurement of social support was a treatment (for example, a support group for bereavement counselling) and studies that looked at the effects of having a pet or having faith in a god. Studies where individuals gave support (such as caregivers) rather than received support were also excluded.

Each paper was assessed and rated by four researchers. Data within the studies were often reported as odds ratios or hazard ratios, which show the risk of an outcome in people with a particular risk factor relative to those without the risk factor. The researchers used various statistical techniques to combine results between studies to give overall odds ratios for the risk of disease or death.

 

What were the basic results?

The researchers identified 148 studies that met their inclusion criteria and had data that could be pooled. The studies included data from over 300,000 individuals from North America (51%), Europe (37%), Asia (11%) and Australia (1%). The average age of the participants was 64 years. The participants were followed for an average of seven-and-a-half-years, and an average of 29% died during follow-up.

The researchers found that when they combined data from studies that had taken any type of measure of social interaction (for example, the number of people in a social network, amount of received support and amount of perceived support), the odds of survival was increased by 50% in those with stronger social interactions compared to weaker social interactions (odds ratio [OR] 1.50, 95% confidence interval [CI] 1.42 to 1.59).

In the 63 studies that only looked at the structural measures of social relationships (for example, how many people are in a social network), the odds of survival increased by 57% for individuals with stronger social networks compared to weaker ones (OR 1.57, 95% CI 1.46 to 1.70).

Twenty-four studies looked at functional measures of social relationships only, such as received or perceived social support. They found that stronger functional social relationships were associated with a 46% increase in odds of survival (OR 1.46, 95% CI 1.28 to 1.66).

 

How did the researchers interpret the results?

The researchers say that individuals with adequate social relationships have a 50% greater likelihood of survival (over 7.5 years) than those with poor or insufficient social relationships. They report that the size of this effect is similar to or larger than that seen with smoking, obesity and physical activity.

They suggest that their meta-analysis should promote further research into treatments that explicitly account for social relationship factors across levels of healthcare such as prevention, evaluation, treatment, compliance and rehabilitation. They also suggest that hospitals and clinics could involve patient support networks in implementing and monitoring treatment regimes.

 

Conclusion

The study showed an association between the strength of social relationships and lower mortality rates. However, as the researchers highlighted, many different measures of the strength of social interactions are used, and this study does not classify what constitutes a healthy social life. Owing to the high variability of the studies included in this meta-analysis, the researchers looked at social relationships in very broad terms. There are some limitations to this research, some of which the authors highlight:

• Behavioural risk factors for disease, such as smoking and drinking alcohol, were adjusted for in some but not all of the studies included in this meta-analysis. Some of the effect on mortality may, therefore, be due to these and other factors that were not adjusted for in the analyses, rather than social factors.
• The participants included in the individual studies varied greatly. For example, some studies included people who had diseases at the start of the study and looked at how their social relationships affected the outcome of their disease, while other studies looked at people who were healthy at the start of their follow-up.
• Most measures of social relationships did not take into account the quality of the relationship and assumed that all relationships were positive.
• The researchers used various standard methods to try to assess whether publication bias could have contributed to their results. Publication bias means that scientific research that has negative results (finds no association) is less likely to be published than studies that have positive results. Although the researchers say that, based on their calculations, this is unlikely to have had an effect, publication bias is an important factor in this type of meta-analysis and may still have affected the results.
• It is difficult to directly compare the effects of loneliness seen in this meta-analysis with results seen in other studies of smoking, physical inactivity or other unhealthy behaviours, as the people participating in the studies may not be comparable.

The link between social relationships and disease is likely to be complex, as people who are seriously ill may have reduced capacity for social interaction and this could affect their social networks. It may also represent something that happens naturally with aging: that as people get older, their social networks get smaller. This study highlights that social relationships may play a role in health and disease, but further work is needed to assess what type of social interactions are helpful and the biology underlying this.

Links To The Headlines

Can your friendships save your life? The Guardian, July 28 2010

Popular people live longer. The Daily Telegraph, July 28 2010

Having pals 'helps you live longer'. Daily Mirror, July 28 2010

Loneliness is a killer: It's as bad for your health as alcoholism, smoking and over-eating, say scientists. Daily Mail, July 28 2010

Links To Science

Holt-Lunstad J, Smith TB, Bradley Layton J. Social Relationships and Mortality Risk: A Meta-analytic Review. PLoS Medicine 7(7)

“Maternal love helps you deal better with stress and anxiety later in life,” according to the Daily Mail. The newspaper said that a study has found that children whose mothers showed them high levels of affection at eight months of age experienced lower levels of distress as adults.

The study followed 482 individuals from birth until their mid thirties, and this unusually long follow-up time is one of the study’s strengths. The main limitation of this study is that many unmeasured factors may influence a person’s adult wellbeing, for example paternal affection as a child, or health or work status as an adult. It is also important to note that the adults in this study were, on average, in the normal range of emotional functioning.

It is likely that a complex mix of factors influences our adult wellbeing, and it seems plausible that our childhood experiences could be among them. However, the interactions between these numerous factors mean that teasing out the effects of individual factors is likely to be difficult and that maternal affection may not necessarily be the principal factor behind mental resilience.

 

Where did the story come from?

The study was carried out by researchers from Duke University, Harvard School of Public Health and Brown University in the US. One of its authors received partial funding from the US National Institutes of Mental Health. The study was published in the peer-reviewed Journal of Epidemiology and Community Health.

The Daily Mail and BBC News have reported on this research. The Daily Mail points out a strength of the study, saying that “most previous studies have relied on people's recollections - whereas this research tracked participants from early childhood to adult life”. The BBC also makes the important point that “the influence of other factors, such as personality, upbringing and schooling, could not be ruled out”.

 

What kind of research was this?

This was a prospective cohort study that looked at the association between maternal affection early in a child’s life and their emotional functioning as an adult.

The researchers looked at children who had originally been part of the National Collaborative Perinatal Project (NCPP), which had enrolled their mothers during pregnancy from 1959 to 1966. At the age of eight months, the interaction of mothers with their children was observed and rated according to how affectionate it was. The emotional functioning of the offspring was assessed when they became adults. The researchers then looked to see whether there were relationships between a mother’s level of affection at eight months and adult emotional functioning.

 

What did the research involve?

An evaluation of maternal affection was made by a psychologist while the mother and baby attended cognitive and developmental testing as part of the NCPP study. Levels of affection were rated as: “negative” or “occasionally negative” (both indicating a low level of affection), “warm” (indicating normal affection), and “caressing” or “extravagant” (both indicating a high level of affection). For the current analyses the “negative”, “occasionally negative” and “warm” groups were pooled, while “caressing” and “extravagant” were pooled into a high affection group.

A sample of 1,062 NCPP offspring were contacted in 1996, when they were on average 34 years old. Of these individuals, 482 agreed to participate and had complete data available for analyses. Emotional functioning was assessed using a standard symptom checklist (Symptom Checklist-90, SCL-90). This checklist includes an assessment of four common types of distress, including distress due to:

• somatisation: psychological distress manifesting itself through physical symptoms
• interpersonal sensitivity: the extent to which an individual can recognise or understand another’s emotions or feelings
• anxiety
• hostility/anger

An overall distress score was calculated based on these four types of distress. These scores were calculated in such a way that they ranged from 0 to 100, where the average score in a normal population would be 50, and a normal range considered to be 40 to 60.

The researchers took into account factors that could influence the analysis, including parental socio-economic status and maternal history of mental illness (based on self-report), which were assessed as part of the NCPP. They also took into account age, race, high-school completion and marital status of the adult offspring.

 

What were the basic results?

Approximately 10% of mothers displayed a low level of affection for their child at the age of eight months, 85% showed a normal level of affection and 6% showed a high level of affection.

Participants whose mothers showed a high level of affection to them at the age of eight months showed lower levels of overall distress as adults than those whose mothers showed normal or low levels of affection. The high-affection group had an overall average distress score of 50.39 and the low/normal affection group an overall average distress score of 55.38. When looking at the specific areas of distress, the relationship was strongest in the area of anxiety, where the high and low/normal groups differed by 7.15 points, and least strong in the area of hostility, where the high and low/normal groups differed by 3.29 points.

 

How did the researchers interpret the results?

The researchers concluded that “early nurturing and warmth have long-lasting positive effects on mental health well into adulthood”.

 

Conclusion

This study’s findings suggest that maternal affection early in life may influence adult distress levels. Strengths of this research include assessment of maternal affection by an independent observer and the following-up of participants from childhood into adulthood. However, there are some limitations:

• Only a subset of children from the original study was followed up. Inclusion of all of the children might have influenced the results if the children who did not participate differed from those who did.
• There may be factors other than maternal affection that are influencing results. Although the researchers took some of these into account, there are many others that may be having an effect, including paternal affection or general family affection as a child, or health and work conditions as an adult.
• Although maternal affection was rated by independent observers, the ratings of affection are likely still to be subjective to some extent (for example, what one observer considered negative might be normal to another observer). The researchers attempted to counteract this by providing extensive training for the assessors and carrying out quality control across the study sites.
• Maternal affection was only assessed on one occasion (at the age of eight months), and may not be representative of overall maternal affection throughout childhood.
• It is also important to note that both groups of adults (those receiving low/normal and those receiving high levels of affection as babies) had distress scores within the normal range.

There are likely to be many factors influencing our adult wellbeing, and it seems plausible that this could include our childhood experiences. However, the number of factors and the possible interactions between these factors means that teasing out the effects of individual factors is likely to be difficult.

Links To The Headlines

Maternal love helps you deal better with stress and anxiety later in life. Daily Mail, July 27 2010

Motherly love 'does breed confidence'. BBC News, July 27 2010

Links To Science

Maselko J, Kubzansky L, Lipsitt L,  Buka SL. Mother's affection at 8 months predicts emotional distress in adulthood. Journal of Epidemiology and Community Health 2010; Published Online First July 26 2010

Many newspapers have reported on new official guidelines for how women can manage their weight before, during and after pregnancy. The advice comes from the National Institute for Health and Clinical Excellence (NICE).

The importance of the guidelines is borne out by figures suggesting that more pregnant women than ever are overweight or obese. The Guardian suggests that, “15-20% of women getting pregnant are overweight or obese”. The Daily Mail puts the number higher, saying that “almost half of expectant mothers are overweight or obese”. It goes on to spell out the dangers of being obese or overweight during pregnancy, which include “fatal health conditions such as blood clots, pre-eclampsia, miscarriages and stillbirths”.

The newspapers also dispel the myth that women should eat for two during pregnancy. Further advice reported in the press includes taking at least 30 minutes of moderate exercise per day during pregnancy, and that pregnant women should avoid dieting and only need to have an extra 200 calories a day in the last three months of their pregnancy.

These guidelines are published by NICE, and are evidence-based. They are designed so that doctors can give women up-to-date reliable advice to follow to maintain a healthy weight before, during and after their pregnancy.

 

Where did the advice come from?

The advice has just been published by the National Institute for Health and Clinical Excellence (NICE) as part of its public health programme. NICE produces guidance on the promotion of good health and the prevention of ill health for those working in the NHS, local authorities and the wider public and voluntary sector.

 

What are the health risks of being obese during pregnancy?

Women who are obese (with a BMI over 30) when they become pregnant face an increased risk of complications such as diabetes, miscarriage, pre-eclampsia, blood clots and death. Obese women are also more likely to have an induced or longer labour, post-delivery bleeding and slower wound healing after delivery. They also tend to be less mobile, which can result in a need for more pain-relieving drugs during labour. These can be difficult to administer in obese women, resulting in a greater need for general anaesthesia with its associated risks.

For women who have gained weight between pregnancies, even a relatively small gain of 1-2 BMI units can increase the risk of high blood pressure or diabetes during their next pregnancy and may also increase the chance of giving birth to a large baby.

 

What sort of diet does NICE recommend?

NICE offers the following dietary advice to help women to achieve and maintain a healthy weight:

• Base meals on starchy foods (such as potatoes, bread, rice and pasta), choosing wholegrain where possible.
• Eat foods rich in fibre.
• Eat at least five portions of fruit and vegetables per day in place of foods higher in fat or calories.
• Eat as little as possible of fried foods, and drinks and confectionery high in sugars and fats.
• Eat breakfast.
• Watch portion size of meals and how often they are eaten.

 

What should women aim to weigh before getting pregnant?

Women with a BMI of 30 or more can achieve significant health benefits if they lose between 5-10% of their weight. Further weight loss to achieve a BMI within the healthy range of 18.5 and 24.9 is encouraged.

 

What about weight during pregnancy?

The amount of weight a woman may gain in pregnancy varies a great deal, and only some of it is due to increased body fat. The unborn child, placenta, amniotic fluid and increases in maternal blood and fluid volume all contribute to weight gain during pregnancy.

• Dieting during pregnancy is not recommended as it may harm the health of the child.
• There is no need to ‘eat for two’ or drink full-fat milk (as opposed to lower-fat milk). Energy needs do not change in the first six months of pregnancy. Only in the last three months do a woman’s energy needs increase by around 200 calories per day.
• Moderate-intensity physical activity will not harm the mother or baby. At least 30 minutes per day of moderate intensity activity is recommended. This can include activities such as swimming or brisk walking. If women have not exercised routinely up to that point, they should begin with no more than three 15-minute sessions a week, increasing gradually to daily 30-minute sessions.
• There are no formal evidence-based guidelines from the UK Government or professional bodies on what constitutes appropriate weight gain during pregnancy.

 

How do I safely lose weight after giving birth?

Women are encouraged to breastfeed, but are advised against dieting while breastfeeding. Women who feed their babies with breastmilk only for the first six months may require an additional 330 calories a day, but this may differ between individuals, and some of these additional calories will be derived from fat stores built up during pregnancy.

If the pregnancy and delivery are uncomplicated, mothers may start a mild exercise programme consisting of walking, pelvic floor exercises and stretching immediately after giving birth, but women should not resume high-impact activity too soon. Women who have had complicated deliveries or caesareans should not resume pre-pregnancy levels of physical activity before consulting their medical caregiver.

Health professionals should be able to provide details of appropriate community-based services for women who want support to lose weight.

 

Where can I get more information?

Women should consult their GP or midwife about maintaining a healthy lifestyle before, after and during their pregnancy.

Links To The Headlines

Mothers must lose baby weight before getting pregnant again, NICE says. The Daily Telegraph, July 28 2010

Weight, exercise and pregnancy confusion. BBC News, July 28 2010

Mothers who lose weight before further pregnancy 'reduce risks'. The Guardian, July 28 2010

Don't eat for two, pregnant mothers are told amid obesity fears. Daily Mail, July 28 2010

“Drinking alcohol can reduce the severity of the symptoms of rheumatoid arthritis,” according to the Daily Mail. The newspaper said that non-drinkers “are four times more likely to develop rheumatoid arthritis than those who drink alcohol on more than ten days a month”.

The research behind this news used a questionnaire to ask people with rheumatoid arthritis and a group of healthy volunteers about how often they drank alcoholic drinks. The results showed that frequency of alcohol consumption was associated with both the risk of developing rheumatoid arthritis and the severity of the disease.

However, this research has many limitations, including the fact that it did not examine the quantities of alcohol actually consumed or follow drinking habits over time. The research may initiate another line of investigation but, on its own, the evidence is not strong enough to inform us whether or not alcohol helps rheumatoid arthritis. Combining certain arthritis medications with alcohol may be dangerous. People with rheumatoid arthritis should speak to a doctor or pharmacist for specific advice on this matter.

 

Where did the story come from?

The study was carried out by researchers from the University of Sheffield and the Sheffield Teaching Hospitals NHS Foundation Trust. It was funded by the Arthritis Research Campaign and published in the peer-reviewed medical journal Rheumatology.

The Daily Telegraph pointed out that the study had not looked at the amount of alcohol the participants drank and the Daily Mail said that no details of the type of alcohol were given, which were both good points to make.

The Sun said that “the only treatment is a course of painkillers”. This is not true. Patients can be given a variety of other treatments that reduce the inflammation associated with this disease.

 

What kind of research was this?

This was a case control study comparing a group of people with rheumatoid arthritis with a control group of healthy people. It looked at whether the frequency of alcohol consumption had any effect on the likelihood of developing rheumatoid arthritis or the severity of the disease. The researchers also looked at the association between drinking alcohol and the severity of disease in a separate cross-sectional analysis.

The researchers were interested in this potential relationship as they say that there is evidence from a Scandinavian case control study that suggests that there was a ‘dose-dependent effect’ of alcohol on the risk of developing rheumatoid arthritis (meaning that the more alcohol a person drank, the lower their risk of arthritis). They wanted to follow up this potential association using a UK cohort. They additionally wanted to look at whether alcohol affects disease severity, as they say there have been no investigations into this.

As this was a case control study it cannot determine whether alcohol causes a particular effect. Studies of this type can only find associations between factors, which then would require further follow up.

 

What did the research involve?

The study recruited 873 white Caucasian patients with rheumatoid arthritis and 1,004 healthy controls from the Royal Hallamshire Hospital in Sheffield between 1999 and 2006.

The patients had experienced rheumatoid arthritis for at least three years. The patients and controls were asked about their smoking and alcohol exposure in a self-completed questionnaire that was given to patients at the start of the study. Participants were asked to define their previous drinking behaviour as ‘never’ or ‘ever to regular’ and record the number of days on which they had consumed at least one alcoholic drink over the previous month. They were categorised according to the number of recent days on which they drank. The categories were: ‘no alcohol’, ‘1-5 days’, ‘6-10 days’ and ‘more than 10 days’. Smoking status was also recorded, with patients categorised either as ‘current smoker’, ‘previous smoker’ or ‘never smoker’.

The researchers say that there are different subsets of rheumatoid arthritis. Patients with the ‘CCP-positive’ form of the disease have CCP antibodies in their blood. The researchers measured the amounts of CCP antibodies in the patients and in 100 of the controls. The researchers also accessed the medical records of the patients to examine information about how many joints were affected, how much pain the patients were in and the level of disability the patients experienced due to their condition.

In rheumatoid arthritis the patient may experience damage to the bone and cartilage. A radiologist assessed radiographs of the hands and feet of the patients to give a score of joint damage. A sample of 10% of the radiographs was checked by another assessor to verify that the scoring was consistent.

The researchers used an established statistical method called ‘logistic regression’ to assess the effect of alcohol on rheumatoid arthritis. In their calculations they adjusted their model to account for age, gender and smoking status. They used this model to assess whether the severity of rheumatoid arthritis was different depending on how much alcohol a person drank.

 

What were the basic results?

They found that the patients in the rheumatoid arthritis group were older on average and more likely to smoke than the controls. There was also a higher proportion of females in the arthritis group than in the control group. The controls were also more likely to drink, with only 10.9% of controls reporting no regular alcohol consumption compared with 36.7% of the arthritis patients. Likewise, a greater number of controls reported that they drank on more than 10 days per month (30%) compared with 16% of the patients.

The researchers found that there was no difference in the alcohol consumption in patients with the CCP-positive form of the disease compared with other rheumatoid arthritis patients. However, they did find that there was a difference in the alcohol consumption of the patients depending on the medication they were taking. For example, patients taking the anti-rheumatoid drug methotrexate (alone or with other anti-rheumatoid arthritis drugs called DMARDs) were less likely to consume alcohol frequently than patients taking other drugs for the condition.

When they compared the risk of developing rheumatoid arthritis by looking at the alcohol consumption in the control group and rheumatoid arthritis group, non-regular drinkers had a higher risk of developing rheumatoid arthritis compared with regular drinkers (Odds ratio [OR] 2.31, 95% confidence interval CI, 1.73 to 3.07). They also found that, compared with the most frequent drinkers, never-drinkers had an increased risk of developing rheumatoid arthritis (OR 4.17, 95% CI 3.01 to 5.77).

Increasing frequency of alcohol consumption was associated with decreased rheumatoid arthritis severity. This was the case for all of the measures of rheumatoid arthritis, and the association still existed after the researchers had taken into account the gender of the patients and whether the patients were CCP-positive or not.

The researchers had found that how regularly people on certain types of anti-rheumatoid arthritis drugs drank alcohol differed depending on the type of medication they took. People taking methotrexate (with or without DMARDs) drank less frequently. They looked at people’s history of alcohol consumption (never-drinkers or ever to regular drinkers) in groups of patients taking methotrexate and found that ever-drinkers had lower rheumatoid arthritis severity scores on average than never-drinkers.

 

How did the researchers interpret the results?

The researchers suggest that increased consumption of alcohol is associated with a significant dose-dependent reduction in susceptibility to rheumatoid arthritis and that there is a further association between higher frequencies of alcohol consumption and reduced severity of rheumatoid arthritis.

 

Conclusion

This study appears to show an association between a higher frequency of alcohol consumption and both reduced risk of developing rheumatoid arthritis and decreased severity of the disease. However, there are limitations to this study (many of which the researchers highlight), which mean that the conclusions should be interpreted cautiously:

• This study required the patients to recall their own alcohol consumption, meaning the patients and controls may have over- or under-estimated the amount of alcohol they had consumed.
• The study asked the participants about the frequency of their drinking rather than about how much they typically drank. As we cannot tell what quantities of alcohol were consumed, it is therefore possible that some individuals who drank less frequently might actually have consumed equal or greater amounts of total alcohol than those who drank more regularly.
• The study relied on one questionnaire and may not give an indication of people’s changing drinking patterns over time or long-term drinking habits.
• The questionnaire did not ask about the type of alcoholic drink the participants drank. Different drinks may have different effects owing to the other chemicals besides alcohol found in them.
• The questionnaire did not ask whether patients’ drinking habits had changed since their diagnosis. The study did find that the type of drug a patient was taking influenced how much they drank. Patients with rheumatoid arthritis may also drink less frequently because their disease may cause changes in their lifestyle, for example, people with a more severe disabling condition may drink socially less frequently.
• The patient group was older and had a higher proportion of women than the control group. Although the researchers attempted to account for this in their analysis, the differences in the two groups may have influenced the likelihood that people would be regular drinkers. Women and older individuals may be less frequent drinkers than younger men.
• This study only included white Caucasian people. It is not clear whether this research would be applicable to the UK population as a whole.

This study has a number of limitations, and because of these it is not possible at this time to say whether alcohol has a beneficial effect on rheumatoid arthritis. Follow-up research, such as a randomised controlled trial, is necessary to assess whether alcohol can have any effect on the severity of rheumatoid arthritis. As drugs taken for rheumatoid arthritis can have toxic effects on the liver, it is advised that patients avoid alcohol. People with rheumatoid arthritis should follow medical advice on drinking and speak to their doctor or pharmacist if they have any concerns.

Links To The Headlines

Alcohol linked to lower risk of arthritis. The Daily Telegraph, July 28 2010

Good news, booze cuts risk of getting arthritis. Metro, July 28 2010

How having a drink can reduce severity of arthritis symptoms. Daily Mail, July 28 2010

How tippling beats crippling arthritis. The Sun, July 28 2010

 

Links To Science

Maxwell JR, Gowers IR, Moore DJ and Wilson AG. Alcohol consumption is inversely associated with risk and severity of rheumatoid arthritis. Rheumatology, July 28 2010

“A weekly dose of oily fish may help prevent the most common cause of blindness in old age,” said the Daily Express. The newspaper said that a US study found that people who ate at least one portion of oily fish a week cut their risk of advanced age-related macular degeneration (AMD) by 60% compared with people who ate fewer portions.

This study compared the diet of more than 2,000 older adults and recorded whether or not they had AMD. As the study assessed both of these factors at only a single point in time it is not possible to say whether people’s diets directly affected their development of AMD. The small number of people with advanced AMD also reduces confidence in the results from this study.

Previous studies, including more reliable cohort studies, have already suggested a link between consuming higher levels of omega-3 fatty acids and reduced AMD risk. As such, this new study does not add much to our knowledge. The best way to determine whether omega-3 supplementation can reduce the risk of AMD would be to conduct a randomised controlled trial directly testing omega-3 against a placebo.

 

Where did the story come from?

The study was carried out by researchers from Johns Hopkins University in Chicago and was funded by the US National Institute on Aging. It was published in the peer-reviewed medical journal Opthalmology.

The Daily Express has reported this research accurately, but did not mention any of its limitations.

 

What kind of research was this?

This was a cross-sectional study called the Salisbury Eye Evaluation (SEE) study. It looked at the relationship between consumption of oily fish and age-related macular degeneration (AMD), a progressive eye condition in which either breakdown of a layer covering the retina or abnormal blood vessels on the back of the eye causes vision to deteriorate. AMD (also known as ARMD) is a common cause of blindness that becomes more common as people get older. It has been suggested that eating a diet high in omega-3 fatty acids (found in oily fish and some other foods) may reduce the risk of developing the condition.

Cross-sectional studies look at different factors (in this case diet and sight) at only a single point in time. This means that it is not possible to say for sure which factor came first and, therefore, whether one factor could be causing the other.

A better design for looking at the relationship between dietary intake of oily fish and risk of AMD in the population would be a prospective cohort study. which takes a sample of people without AMD, assesses their diets and follows them over time to see who develops AMD.

However, the results of both cross-sectional and cohort studies are susceptible to being influenced by factors other than the one of interest. Therefore, to answer the question of whether taking omega-3 supplements reduces risk of AMD the best design would be a randomised controlled trial.

 

What did the research involve?

The researchers enrolled a random sample of people aged 65 to 84 living in Salisbury, Maryland, in the US. The participants filled in detailed questionnaires about their normal eating habits and also had an eye examination to determine whether they had AMD. The researchers then looked at whether there was a higher proportion of people with AMD among the group who ate more fish (both fish in general and fish high in omega-3 fatty acids) or among the group who ate less of these foods.

The food frequency questionnaire asked about how often participants ate certain foods over the previous year, and how large the serving sizes were. There were six fish and shellfish categories that were adapted to suit commonly eaten local dishes:

• fried fish: fried fish or fish sandwich
• oysters: oyster fritters or fried oysters
• tuna: tuna fish, tuna salad or tuna casserole
• shellfish: shrimp or lobster
• crab: crab, crab cakes or crab salad
• other fish: other fish baked or fried

The researchers calculated the amount of omega-3 fatty acids in each type of fish and shellfish using nationally accepted reference figures. Crab, other fish, oysters and fried fish were considered to have high omega-3 fatty acid content (more than 0.4g per 100g serving). The researchers calculated how much of each food category was eaten each week on average by each participant. Those eating one or more servings of fish and shellfish overall per week or eating more fish and shellfish high in omega-3 were compared with those eating less than one serving of these foods per week.

A standard test was used to test the participants for AMD, which involved having a photograph taken of the back of the eye. Two independent assessors, who did not know anything about the participants’ diets, examined the photographs for the characteristic signs of AMD. Based on their findings, people with AMD were grouped by how advanced their condition was:

• AMD 3: eyes with new blood vessels (neovascular or geographic atrophy) on the photo
• AMD 2: eyes with pigment abnormalities, but not classified as AMD 3
• AMD 1: eyes with the large yellow or white accumulations (drusen) that are diagnostic of AMD, but not classified as AMD 3 or AMD 2

The diets of those in each group were compared to the diets of those in a control group without AMD.

Participants also provided information on their other characteristics, including their gender, age, race, smoking status and education. Their body mass index was also calculated. The researchers then took these characteristics, as well as overall calorie consumption, into account in their analyses. A total of 2,391 participants (94.9% of those enrolled) provided sufficient data to be included in the final set of analyses.

 

What were the basic results?

Eye tests showed that:

• about three-quarters of the participants (77.1%, 1,943 people) did not have AMD
• 9.0% (227 people) had the earliest stages of AMD (AMD 1)
• 6.1% (153 people) were in the intermediate stages (AMD 2)
• 2.7% (68 people) had advanced AMD (AMD 3)

The researchers found that people who had any of the three stages of AMD did not differ from those who did not have AMD in the amount of fish and shellfish they ate each week. All participants ate about 1.1 servings of fish and shellfish a week on average.

However, people who had advanced AMD (AMD 3) were 60% less likely to eat one or more servings of fish or shellfish high in omega-3 fatty acids than people without AMD (odds ratio 0.4, 95% confidence interval 0.2 to 0.8).

There was no difference between those with early or intermediate AMD (AMD 1 or 2) and those without AMD in terms of consumption of fish or shellfish high in omega-3 fatty acids.

 

How did the researchers interpret the results?

The researchers conclude that their findings “support a protective effect of fish/shellfish intake against advanced AMD”. They say that future studies are needed to clarify further “the association between the consumption of fish, shellfish, zinc, and omega-3 fatty acids and the risk of AMD”.

 

Conclusion

This study showed an association between level of consumption of fish and shellfish high in omega-3 fatty acids and advanced AMD. However, it has a number of limitations that need to be taken into account:

• This study assessed diet and the presence of AMD at the same point in time, and cannot show what the participants’ fish eating habits were before the development of AMD. Therefore, it is not possible to say whether these eating habits may have directly influenced risk of developing AMD.
• The only significant association found was between advanced AMD 3 and lower consumption of fish and shellfish high in omega-3 fatty acids. However, the number of participants who had advanced AMD was small (only 68 people). Therefore, the results of this analysis may not be very robust. It is not clear why the researchers chose to divide AMD into three types, as previous studies have relied on simpler early- and late-AMD categories.
• The researchers carried out multiple statistical analyses. This increases the likelihood that some significant differences may be found by chance.
• As with all studies of this type, other factors that differ between groups with higher and lower fish consumption may be influencing the results. The researchers did take some of these into account, but there may be unknown or unmeasured factors still having an effect.
• People may find it difficult to recall their food intake accurately over an extended period, and therefore there may be inaccuracies.
• A number of previous studies have suggested that oily fish may slow or prevent AMD. It may be the case that these preliminary findings, which have received a great deal of media and internet attention, could influence the fish consumption of people with AMD and distort any potential relationships that may or may not exist between diet and AMD. However, the researchers thought this was unlikely to affect the current study, as it was carried out between 1993 and 1995, which they say was before published associations between fish consumption and AMD were first made.

Studies have already suggested a link between eating higher levels of omega-3 fatty acids and reduced risk of AMD, and the current study does not add much to our knowledge. The best way to determine whether omega-3 supplementation could be used to reduce risk of AMD would be to carry out a randomised controlled trial.

Links To The Headlines

How oily fish diet can cut risk of blindness. Daily Express, July 27 2010

Links To Science

Swenor BK, Bressler S, Caulfield L, West SK. The Impact of Fish and Shellfish Consumption on Age-Related Macular Degeneration. Opthalmology, July 13 2010 [Online publication]

“Homeopathy will continue to be available on the NHS despite an influential health committee condemning it as medically unproven,” reported The Daily Telegraph.

The newspaper, together with several other media outlets, was reporting the Department of Health’s response to a report by the House of Commons cross-party Select Committee on Science and Technology, published in February.

That committee had said homeopathic medicine should no longer be funded on the NHS and called for a ban on the medicines carrying medical claims on their labels.

It found no evidence the medicines are any more effective than a placebo (the same as taking a sugar pill and believing it works). The British Medical Association agreed, with a leading member recently describing homeopathy as “witchcraft”.

The Department of Health based its decision to continue funding homeopathy on “choice”, not efficacy, reported the newspapers.

“We believe in patients being able to make informed choices about their treatments, and in a clinician being able to prescribe the treatment they feel most appropriate in particular circumstances,” said a spokesman.

“Our continued position on the use of homeopathy within the NHS is that the local NHS and clinicians, rather than Whitehall, are best placed to make decisions on what treatment is appropriate for their patients.”

 

What is homeopathy?

Homeopathy is a type of complementary and alternative medicine (CAM). CAMs are treatments that are not part of conventional Western medicine. Like most CAMs, homeopathy's use and efficacy (how well it works in placebo controlled trials) are controversial, and most mainstream scientists reject it as a concept and consider that it only works because of the placebo effect.

 

What’s the idea behind it?

Homeopaths believe that homeopathy can help with any condition that the body has the potential to repair itself. The practice has two essential principles:

• That a substance that can cause symptoms of illness will cure those same symptoms if given in extremely small doses. For example, a very small amount of caffeine might be used to treat insomnia.
• The more you dilute a substance, the more you increase its power to treat symptoms that it would otherwise cause. The dilution of the substance must be performed in a very specific way, with an increasing number of dilutions resulting in the solution becoming more potent.

 

To what extent are the substances diluted?

Ben Goldacre, the author of Bad Science, has described the process:

“The typical dilution is called ‘30C’: this means that the original substance has been diluted by 1 drop in 100, 30 times. On the Society of Homeopaths site, in their ‘What is homeopathy?’ section, they say that ‘30C contains less than 1 part per million of the original substance.’

“This is an understatement: a 30C homeopathic preparation is a dilution of 1 in 100^30, or rather 1 in 10^60, which means a 1 followed by 60 zeroes, or – let’s be absolutely clear – a dilution of 1 in 1,000,000,000,000,000,000,000,000,000,000,000,000, 000,000,000,000,000,000,000,000.

“To phrase that in the Society of Homeopaths’ terms, we should say: “30C contains less than one part per million million million million million million million million million million of the original substance.”

“At a homeopathic dilution of 100C, which they sell routinely, and which homeopaths claim is even more powerful than 30C, the treating substance is diluted by more than the total number of atoms in the universe. Homeopathy was invented before we knew what atoms were, or how many there are, or how big they are. It has not changed its belief system in light of this information.”

 

Why do people accuse homeopaths of witchcraft?

The phrase is pejorative. Some people use it because the process of creating homeopathic medicines involves unusual traditions, such as knocking the solution against a leather and horsehair surface during the dilution process.

 

What’s the major criticism of homeopathy?

The key criticism is that there is no reliable scientific evidence to suggest it is any more effective than a placebo. Normally, drugs that are no more effective than a placebo are judged ineffective and not given a licence or funded by the NHS. Prescribing placebo treatments, critics say, damages the trust that exists between doctors and their patients.

Critics of homeopathy say the reason the medicines are ineffective is because in homeopathic remedies the original substance is diluted to such an extent that no molecules of the substance remain in the remedy.

Homeopaths have argued that the critics are missing the point of the dilution process. The homeopaths claim it is not necessary for any of the original substance to remain as the dilution process somehow imprints a ‘memory’ of the substance into the water.

 

What did the Select Committee on Science and Technology conclude?

The Select Committee on Science and Technology concluded that:

• There is no evidence that homeopathy works beyond the placebo effect, which is a position that the Government agrees with.
• By providing homeopathy on the NHS, the Government runs the risk of appearing to endorse it as a working system of medicine. There is also the danger that when doctors prescribe placebos, they risk damaging the trust that exists between them and their patients.
• Given that the existing scientific literature shows no good evidence of efficacy, further clinical trials of homeopathy are not justified.

 

What was the Government’s response?

The Government has decided to continue to allow homeopathic hospitals and treatments to be received on the NHS, where local doctors recommend them.

It agrees that the efficacy of a treatment is important, but said there are many considerations when making policy decisions, and that patient choice is an important factor to consider.

“We believe that providing appropriate information for commissioners, clinicians and the public, and ensuring a strong ethical code for clinicians, remain the most effective ways to ensure quality outcomes, patient satisfaction and the appropriate use of NHS funding.

The Government also said that it noted the Committee’s view that allowing for the provision of homeopathy may risk seeming to endorse it, and that it would keep the position under review.

 

What does the Government Chief Scientific Adviser say?

The Government Chief Scientific Adviser has expressed his concern that the public may assume that NHS homeopathic treatments are ‘efficacious’, whereas the principal reason for their availability is to provide patient choice.

To enable the public to make informed choices, he will work with the Department of Health to ensure that the public has access to clear information on the evidence for homeopathy.

His position, as stated in the Government response, remains that “the evidence of efficacy and the scientific basis of homeopathy is highly questionable”.

 

How much does homeopathy cost the NHS each year?

Exact figures for the cost of homeopathy are not collected. However, there are currently four homeopathic hospitals in England, and in the region of 25,000 homeopathic items are prescribed each year. Total costs are thought to be in the region of 3-4 million a year.

Links To The Headlines

Homeopathy will not be banned by NHS despite critical report. The Daily Telegraph, July 27 2010

More homeopathy on NHS as health cash is squeezed. The Daily Mail, July 27 2010

“Education ‘helps brain compensate for dementia changes,’” BBC News reported today, saying that people who stay in education longer appear to be less affected by the brain changes that occur during dementia. According to the newstory, European researchers have found that those with more education were as likely to show biological dementia signs in their brains at death but less likely to have displayed symptoms of the disease while alive.

The underlying study compared education, symptoms of dementia and post-mortem brain samples in about 900 people who donated their brains for research after death. It demonstrated that greater education was linked to reduced clinical dementia but did not have any bearing on changes in brain biology. It seems the brain will change with age regardless of education but that people with more education are more likely to compensate and therefore stave off the symptoms of dementia.

This study has some shortcomings, including how representative the small sample of people who agreed to post-mortem brain examination were to the general population.  However, it will be of interest to neurologists, who must now unpick why more education can reduce clinical symptoms of dementia, but not the brain signs of dementia.

 

Where did the story come from?

The study was carried out by researchers from Gothenburg University in Sweden and the SUNY Downstate Medical Centre in Brooklyn, US. It was funded by the Swedish Research Council, the Swedish Council for Working Life and Social Research, the Alzheimer’s Association, the US National Institutes of Health, and a number of other Swedish organisations. It was published in the peer-reviewed medical journal Brain.

BBC News has covered this research in a balanced way and has sought feedback from the researchers and other experts in this field, who say this is an important study and that further research is needed to find out why an education can protect the brain from dementia.

 

What kind of research was this?

This cohort study was set up to determine whether more time in education reduces dementia risk by examining any potential link between time in education during earlier life, symptoms of dementia while alive and brain pathology at death.

Some studies have shown that people with higher levels of education in earlier life are at lower risk of clinical dementia during ageing. There are two theories for this observation: either that education protects against dementia-related pathology (changes in the brain), or that more-educated people may have the same brain pathology but may somehow compensate for it.

The researchers used a large sample of individuals followed over time to investigate these theories.

 

What did the research involve?

The data for the study is from a source called EClipSE (Epidemiological Clinicopathological Studies in Europe) that brings together data from three observational studies that started between 1985 and 1991. Upon entry to the study, the researchers recorded the participants’ number of years of education earlier in life, with some participants also providing consent for post-mortem brain donation. The total combined sample in the three studies was 20,944 people, but the EClipSE study includes only those 970 people who agreed to donate their brains after death.

As part of their original studies all participants in the final EClipSE sample were given further interviews at intervals of one to seven years to collect demographic and cognitive information and to establish the presence of dementia and other health-related conditions. Some patients were not included in the final analyses because the data about education, dementia diagnosis or age was missing.

Different aspects of brain pathology were assessed through autopsy after death and were generally scored in each study as none, mild, moderate or severe. The length of education was classed as either 0-3 years, 4-7 years, 8-11 years or 12 years and above. A statistical technique called logistic regression analysis was then used to assess whether there was a link between dementia and years in education.

As all of the people in one of the studies were over 85 years, and therefore had less education on average than those in the others studies, the researchers excluded this group from some of their analyses to see whether this made a difference to their results.

 

What were the basic results?

The study found that greater time in education was associated with a reduced risk of clinical dementia (that is, dementia symptoms) at death (odds ratio [OR] 0.89, 95% confidence interval [CI] 0.83 to 0.94). Brain pathology was not dependent on the amount of education received. The brains of people who had more education seemed in general to weigh more than those from people who had less education, even after adjusting for the influence of age, sex and the original study of participation.

When the researchers analysed by subgroups of different brain weights they found that, compared to those with less education, education was protective for brains of low to medium weight. This protective effect was not seen in high-weight brains.

 

How did the researchers interpret the results?

The researchers conclude that greater time in education did not protect individuals from developing neural degeneration or vascular neuropathology by the time they died, but that it did seem to prevent or mitigate the effect of that these biological changes had on the clinical symptoms of dementia before death.

They say the findings suggest that an understanding of the mechanisms that protect brain function in the presence of biological changes to the brain “may be of considerable value to society”.

 

Conclusion

This cohort study has assessed how time spent in education was linked to both brain pathology (that is, biological changes) and symptoms of dementia before death. These are some of the points to consider when interpreting these results:

• The three studies that combined data for the EClipSE sample had different methodologies, including different ways of determining status of clinical dementia at death. For example, one relied on interviews in the last years of life, informant interviews after death and death certificates, while another study relied on assessments by neurologists.
• Brain samples were also analysed in different ways, and in two of the three studies, those who agreed to donate their brains were older and more cognitively impaired than those who did not consent. It is difficult to anticipate how these differences may affect the overall results, but it may have introduced bias in the analysis of results.
• Education was only assessed at entry into the studies while follow up occurred many years into the future. This study is making a comment on education in early life and may not account for further or tertiary education that the participants received during the course of follow up.
• The researchers highlight some other shortcomings with their research including the fact that they did a number of subgroup analyses and did not adjust for these multiple comparisons. This may increase the likelihood of finding false positive associations.

This study will be of interest to neurologists as it supports what other studies have found, a link between education and reduced risk of clinical dementia. It furthers the understanding of how this protection may be occurring by also finding no association between education and brain pathology.

Links To The Headlines

Education 'helps brain compensate for dementia changes'. BBC News, July 26 2010

Getting a university degree 'can slow down dementia'. Daily Mail, July 26 2010

Links To Science

Brayne C, Ince P, McKeith I, et al. Education, the brain and dementia: neuroprotection or compensation? Brain 2010; 133: 2210-16 [Awaiting publication]

A study has found that "the risk of women dying during pregnancy increases more than threefold after IVF," The Daily Telegraph reported. It said researchers believe the increased risk may come from the body rejecting donated eggs or from underlying health problems that "may come to the fore during artificial conception".

This study from the Netherlands looked at all deaths potentially related to IVF, since the procedure was first used in the country in 1984. It found six out of 100,000 deaths were related to IVF treatment itself. However, no IVF treatment-related deaths have occurred there since 1997 when practices changed, so these deaths rates do not apply to IVF today. For IVF pregnancies, there were a relatively low 42.5 estimated deaths out of 100,000 women.

The estimated rate of IVF pregnancy-related deaths may have been higher when compared with women conceiving naturally, but this is not unexpected given that women receiving IVF tend to be older and therefore at greater risk of adverse pregnancy outcomes. The main value in this study is in highlighting how difficult it is to collect data on negative outcomes of IVF pregnancies. The researchers' suggestion to collect more information on IVF pregnancies seems sensible.

 

Where did the story come from?

The study was carried out by researchers from Radboud University Nijmegen Medical Centre and other academic and medical institutions in Holland. It is not clear how the study was funded. The work was published in the (peer-reviewed) medical journal Human Reproduction.

The Telegraph had written a short article about this research that failed to highlight the rarity of death during pregnancy and the failure of this research to adjust for age (which is likely to confound the relationship between IVF treatment and pregnancy complications).

 

What kind of research was this?

This was a cross-sectional study assessing all deaths ‘that may have been related to IVF in the Netherlands’. The first IVF treatment in the Netherlands was performed in 1984 and the researchers collected data on all maternal deaths between then and 2008 (the time of the study) from a variety of different sources.

 

What did the research involve?

The researchers explain there is no single reliable source for data relating to IVF complications in the Netherlands. As a solution, they used several sources with an aim of collecting all data on deaths that were possibly related to IVF treatment between 1984 and 2008. This included information collected by the national IVF Working Committee and involved contacting all gynaecologists in all the hospitals in the Netherlands for any mortality data relating to IVF treatment or in the pregnancy after IVF treatment. They also used data from a large cohort study called OMEGA and from the Netherlands Society of Obstetrics and Gynaecology. There was some overlap between these data sources.

Maternal deaths were defined as the death of a woman during delivery, or their death within 42 days of a termination from any cause related to (direct death) or aggravated by (indirect death) the pregnancy, but not from accidental or incidental causes.

From these data, the researchers calculated the maternal mortality rate, which was the number of direct and indirect maternal deaths for every 100,000 live births up to 42 days after termination of pregnancy. These were separated into three categories: directly related to IVF treatment, directly related to IVF pregnancy and, not known to be related to either.

In their discussion, the researchers make comparisons between the mortality rates from their study and equivalent rates in women who conceive naturally, and also the general population for women whose deaths were not related to treatment or pregnancy. These comparisons were non-statistical.

 

What were the basic results?

Between 1984 and 2008, there were six deaths related directly to IVF treatment and 17 related to IVF pregnancies. From these figures, and by assuming that over the study period, approximately 100,000 women would have received IVF and that about 40% of them would have got pregnant, the researchers estimate the following:

• The IVF treatment-related mortality was six for every 100,000 live births.
• The IVF pregnancy-related mortality was 42.5 for every 100,000 (compared with 12.1 for every 100,000 live children born between 1993 and 2005). Causes of death included pre-eclampsia with cerebral haemorrhage, sepsis, vascular dissection, pulmonary embolism, liver failure, portal hypertension, small vessel disease, suicide, meningitis and amniotic fluid embolism.

In total, the mortality rate (death from causes not related to IVF treatment or pregnancy) in the study population was 31 for every 100,000 women. This was less than half that of overall mortality for women aged 20–50 years in the general population (71.3 for every 100,000 women a year).

 

How did the researchers interpret the results?

The researchers conclude that the better overall mortality in women receiving IVF is probably due to the ‘healthy woman effect’. This means that women receiving IVF are likely to be healthier and have a higher socio-economic status than the general population.

The increase in deaths related to IVF pregnancies is likely to be due to the high number of multiple pregnancies and the use of donor egg IVF in older women.

They say that, “the fact that only a few deaths directly related to IVF are reported in the literature whereas we observed six in the Netherlands indicates worldwide under-reporting of IVF-related mortality”. They highlight the importance of reporting all deaths related to IVF to the appropriate organisations.

 

Conclusion

This cross-sectional study determined the rate of deaths due to IVF treatment or pregnancies in the Netherlands between 1984 and 2008. The Daily Telegraph’s headline and report are potentially misleading. The news article focuses primarily on the increased risk of women’s bodies rejecting donated eggs or underlying health problems coming to the fore. However, it is a fact that women who have IVF tend to be older and are therefore at greater risk of having adverse outcomes.

Also, the report that risk of death is three times higher than natural conceptions fails to mention that the actual number of women who died of potential IVF related problems in this study remained relatively low, at only 43 for every 100,000 women who had IVF.

There are a number of important points to consider when interpreting this study and the reporting of it in the media:

• The deaths the researchers classified as being related to IVF treatment all occurred before 1997. The researchers themselves say that since then, 'no more deaths directly related to IVF occurred in the Netherlands'. This may greatly reassure women receiving IVF treatment or who are considering it. The major causes of death directly related to IVF were due to the conditions ovarian hyperstimulation syndrome and sepsis. The researchers say there is now a better awareness of the possible adverse effects of IVF and that techniques have changed accordingly (in the Netherlands).
• The researchers note that the ‘higher maternal mortality in IVF pregnancies’ can be attributed to women being older and so they are at greater risk of poorer pregnancy outcomes (for example, multiple gestation). Their comparisons with the death rates in natural births did not statistically account for the likely effects of age. However, they do highlight this as the likely reason for the differences.
• Importantly, the researchers say they did not have 'the exact figures for the number of women being treated with IVF in the Netherlands'. This is an essential figure for them to calculate the rates of adverse events, but the researchers estimated that 'about 100,000 women had an IVF treatment in the period 1984-2008'. They also estimated that of these, 40% became pregnant. These are estimations that cannot be validated in the absence of data. There are likely to be age-specific IVF treatment rates and indeed success rates that could have been used here to make these comparisons more accurate.
• Another point not highlighted by the researchers is the apparently better overall survival of women receiving IVF (that is, deaths not related to pregnancy or treatment). In this population of all women who had IVF over 24 years, only 31 for every 100,000 were estimated to have died (from causes not known to be related to IVF treatment or IVF pregnancy) compared with 71.3 for every 100,000 a year for women aged between 20 and 50 years in the general population.
• The results must be interpreted in the context of a small number of deaths overall. This was estimated as being only 42.5 deaths in the 100,000 women who were estimated to have had IVF over 24 years of treatment.

The researchers clearly state that their study illustrates how difficult it is to collect data about deaths that may be related to IVF and therefore it is difficult to draw valid conclusions from it. The study's main value is that it highlights this difficulty, and the researchers’ call for better recording of this information seems sensible and would enable better monitoring of the safety of IVF.

Links To The Headlines

Pregnant IVF women more at risk of death. The Daily Telegraph, July 28 2010

Links To Science

Braat DDM, Schutte JM, Bernardus RE, et al. Maternal death related to IVF in the Netherlands 1984–2008. Human Reproduction 2010, originally published online on May 19