Scientists have shown in the laboratory that metal nanoparticles damaged the DNA in cells on the other side of a cellular barrier. The nanoparticles did not cause the damage by passing through the barrier, but generated signalling molecules within the barrier cells that were then transmitted to cause damage in cells the other side of the barrier.

The research was carried out by a team at the University of Bristol and colleagues, and is published online this week in Nature Nanotechnology.

The team grew a layer of human cells (about 3 cells in thickness) in the lab. They then used this barrier to examine the indirect effects of cobalt-chromium nanoparticles on cells that were lying behind this barrier.

The amount of DNA damage seen in the cells behind the protective barrier was similar to the DNA damage caused by direct exposure of the cells to the nanoparticles.

Dr Patrick Case, senior author on the study, said: “We need to be clear that our experimental set up is not a model of the human body. The cells receiving the exposure were bathed in culture media, whilst in the body they might be separated from the barrier by connective tissue and blood vessels. The barrier cells were malignant cell line and 3 cells in thickness whilst all barriers in the body are less thick and of non malignant cells.”

Gevdeep Bhabra, lead author on the paper, said: “Even though this work was done in the laboratory, our results suggest the existence of a mechanism by which biological effects can be signalled through a cellular barrier, thus it gives us insights into how barriers in the body such as the skin, the placenta and the blood-brain barrier might work.”

Professor Ashley Blom, Head of Orthopaedic Surgery at the University of Bristol, added: “If barriers in the body do act in this way, then it gives us insight into how small particles such as metal debris or viruses may exert an influence in the body. It also highlights a potential mechanism whereby we might be able to deliver novel drug therapies in the future.”

These findings suggest that the indirect, as well as the direct, effects of nanoparticles on cells might be important when evaluating their safety.

A major report on managing the health effects of climate change, launched jointly by ‘The Lancet’ and UCL today, says that climate change is the biggest global-health threat of the 21st century.

Lead author Professor Anthony Costello (UCL Institute for Global Health) says that failure to act will result in an intergenerational injustice, with our children and grandchildren scorning our generation for ignoring the climate change threat – with moral outrage similar to how we today look back on those who brought in and did nothing to stop slavery.

‘Managing the Health Effects of Climate Change’ is the work of UCL academics from many disciplines across the university – including health, anthropology, geography, engineering, economics, law and philosophy. Professor Costello says that this climate-change project brought down the traditional interdisciplinary barriers common at all universities, and hopes it could act as a model for global governance bodies to work together.

The UCL team focused on key areas: patterns of disease and mortality, food security, water and sanitation, shelter and human settlements, extreme events, and population migration.

Professor Costello says: “The big message of this report is that climate change is a health issue affecting billions of people, not just an environmental issue about polar bears and deforestation. The impacts will be felt not just in the UK, but all around the world – and not just in some distant future but in our lifetimes and those of our children.”

Disease and mortality

The UCL–Lancet Commission discusses the global health implications of the Intergovernmental Panel on Climate Change (IPCC) projections – from the optimistic average global temperature rise of 2 degrees C to the catastrophic 6 degrees C. The authors consider a wide range of pathways through which climate change could exert its effects on health, some of which may happen before others. Changing patterns of disease and mortality would emerge in a greater rate of transmission and geographic spread of traditionally tropical endemic diseases such as malaria and dengue fever. Heat – the ‘silent’ killer – has a major effect on mortality, with the 2003 heatwave causing up to 70,000 excess deaths in Europe. While some people believe populations in India and Africa may be more resistant to heatwaves, there is little evidence of this and major heatwaves could increase death rates in these populations more than in high-income countries.

Food security, water and sanitation

Food and water security will be a major issue as climate change progresses. Scientists believe that crops are much more sensitive to temperature changes than first thought – a 1 degree C change can make a difference of 17% in yields. Professor Costello says: “If we are going to get early changes in the next 20 or 30 years, falling crop yields could trigger more of an effect through rising food prices. Look at what happened last year when food prices rose globally. And one billion people currently have calorie-deficient diets – this situation will get worse as demand increases from India, China and other nations with a population boom.” Up to 250 million people in Africa will face water shortages by 2020 if no action is taken on adaptation. Water and sanitation are crucial to prevent gastroenteritis and malnutrition. Melting glaciers, and changing river flows and rainfall patterns, are already causing flooding and droughts.

Urbanisation and extreme events

Rapid urbanisation, particularly in developing nations, leads to inadequate housing, particularly slums, which are the most exposed during extreme climatic events. Extreme events, including cyclones and hurricanes, have doubled over the past 20 years, according to the insurance companies who insure against them. But in an event such as a cyclone, a rich nation would normally have relatively few casualties compared to poorer countries. Consider Hurricane Katrina with a loss of 1,850 lives compared with the recent cyclone in Burma which is thought to have claimed 150,000 lives. Of the 20 largest cities in the world, 13 are on a coast. While sea levels have been predicted to rise, from anywhere between 0.5m and 1.2m over the 21st century, some predictions as high as 5m are beginning to emerge. This would be catastrophic.

A tipping point

Professor Costello says: “We might be reaching a tipping point in public opinion. I think the health lobby has come late to this debate and should have been saying more. Young people realise this is the great issue of our age.”

He proposes three action points leading from this report: “First, we have to add the health lobby to the mitigation debate – they must emphasise the threat to our children and grandchildren from greenhouse-gas emissions and deforestation. Second, there must be a focus on health systems – there is massive inequality in health systems throughout the world. Because of this, the loss of healthy life years as a result of global environmental change is predicted to be 500 times higher in Africa than in European nations, despite Africa making a minimal contribution to the causes of climate change. Third, we must develop win–win situations whereby we mitigate and adapt to climate change and at the same time significantly improve human health and wellbeing. There are major health benefits from low-carbon lifestyles, which can reduce obesity, heart and lung disease, diabetes and stress.”

He concludes: “We believe that all the main players – in health, politics, science, technology and civil society – must come together. The UCL–Lancet Commission laid out a framework for action, and we have called for a collation of information on the health effects of climate change leading up to a major international conference in the next two years. We especially want representation from poorer nations. This conference would set out some clear indicators, targets and accountability mechanisms. We need a new 21st-century public-health movement to deal with climate change.”

‘Lancet’ editorial

An accompanying editorial in ‘The Lancet’ states: “UCL is a university that has combined a distinguished history of moral engagement with a more recent revitalised global purpose, expressed through its strengthened commitment to global health in teaching, research and institution building. In preparing to undertake its work for this first Lancet Commission, the UCL team, led by Anthony Costello, reached out beyond health to engineers, political scientists, lawyers, geographers, anthropologists, economists, philosophers, and students, among others. They discovered new ways to review evidence and integrate ideas collaboratively.

“And through these efforts, they identified five critical challenges that scientists, clinicians, and policymakers will have to address if climate change is not to become the biggest catastrophe threatening human survival. First, there is a massive gap in information, an astonishing lack of knowledge about how we should respond to the negative health effects of climate change. Second, since the effects of climate change will hit the poor hardest, we have an immense task before us to address the inadequacies of health systems to protect people in countries most at risk. Third, there is a technology challenge. Technologies do have the potential to help us adapt to changes in climate. But these technologies have to be developed out of greater research investments into climate change science, better understanding about how to deliver those technologies in the field, and a more complete appreciation of the social and cultural dimensions into which those technologies might be implanted. A fourth challenge is political: creating the conditions for low-carbon living. And finally there is the question of how we adapt our institutions to make climate change the priority it needs to be. …

“Our commitment is long term. With UCL and other partners, we plan to convene an international summit in two years’ time to review progress and priorities in our collective responses to the urgent and alarming health effects of climate change.”

The Grand Challenge of Global Health

The cross-fertilisation and application of our expertise is being coordinated through the UCL Institute for Global Health. It is developing an institution-wide agenda leading to strategies, programmes, research and teaching to bring our combined expertise to bear on the Grand Challenge of Global Health.

A daily dose of aspirin can prevent the occurrence of cancer in people with a genetic predisposition towards Lynch syndrome, a Newcastle University scientist has told Europe’s largest cancer congress.

Lynch syndrome is a condition which accounts for around 5 per cent of all colon cancers.

John Burn: We believe that aspirin may have an effect on the survival of aberrant stem cells in the colon.

Professor John Burn, from the Institute of Human Genetics at Newcastle University told the congress ECCO 15 – ESMO 34 held in Berlin on September 21 2009, that he believed that he and his colleagues may have uncovered a simple way of controlling cancer stem cells, which are essential to the formation of malignant tumours.

The clinical trial, which involved 1071 carriers of the Lynch syndrome mutation in 42 centres worldwide, randomised participants to a daily dose of 600mg aspirin and/or 30g Novelose, a resistant starch that escapes digestion in the small intestine.

“Although there were many reports that aspirin might have a beneficial effect in a range of cancers”, said Professor Burn, “they were from case control and epidemiological studies. We decided that the only way to achieve conclusive proof was to undertake a randomised trial in a high risk population.”

Lynch syndrome, often called hereditary nonpolyposis colorectal cancer (HNPCC), is a type of inherited cancer of the digestive tract, particularly the colon and rectum. People with Lynch syndrome have an increased risk of cancers of the stomach, small intestine, liver, gallbladder ducts, upper urinary tract, brain, skin, and prostate. Women carriers also have a high risk of developing endometrial and ovarian cancers.

These patients tend to develop cancer quickly, so the scientists expected to see answers at an early stage. The first results were disappointing, however; at an average of 29 months after randomisation the scientists saw no evidence of the benefits of aspirin in the high risk population studied.

“Our original design allowed for long term post trial follow-up,” said Professor Burn. “We’ve managed to track down most of those who completed the trial – around 75 per cent of the original consent cohort – with information extending up to 10 years from randomisation. We have found that, around four years after randomisation, there was a divergence in the incidence of cancers between the aspirin and placebo groups. To date, there have been only six colon cancers in the aspirin group as opposed to 16 who took placebo. There is also a reduction in endometrial cancer. This is a statistically significant result and we are delighted – all the more so because we stopped giving the aspirin after 4 years, yet the effect is continuing, and is directly correlated with the duration of aspirin use on the trial.”

Although scientists believe that diet is a major factor in the prevention of colorectal cancers, there are no randomised trial data which can prove it, since running proper, controlled trials of diet is extremely difficult. However, there is a strong inverse relationship between colon cancer and how much starch people eat. Resistant starch, after escaping digestion in the upper gut, is fermented in the colon and forms short chain fatty acids which are powerful anti-cancer agents.

“Our very large colon probably evolved to capture such nutrients from our forefathers’ diets”, explained Professor Burn, “because we were giving starch as well as aspirin we would also have expected to see a decrease in cancers in the placebo group. However, there could be a number of reasons for this result – perhaps patients didn’t take the starch every day, or that it simply wasn’t resistant enough.”

There were minor problems due to aspirin side effects; out of over 1000 people 11 in the aspirin group had notable gastro-intestinal bleeds or ulcers as opposed to 9 in the placebo group. But this was counter-balanced by fewer strokes and heart attacks in the aspirin group. The mechanism by which aspirin protects against cancer has yet to be elucidated, but the scientists believe that cancer stem cells are involved.

“We do not think that the mechanisms discussed to date are likely to provide an explanation”, said Professor Burn. “For example, the inflammatory enzyme COX2 is over-expressed in early cancer, but our results suggest an effect that predates the cancer, and may even predate the adenoma which precedes it. We believe that aspirin may have an effect on the survival of aberrant stem cells in the colon. These cancer stem cells are normally resistant to chemotherapy, but if a stem cell mutates but does not reveal its potential until an adenoma is formed, and if aspirin reduced the chances of such cells surviving, this would explain our results.”

The team intends to undertake a further study to see whether a smaller dose of aspirin would have the same beneficial effect or not.

“We are planning to ask all people with Lynch syndrome to agree to “toss a coin” and take, say, either one or two aspirin tablets per day. Then we can see whether the people on the lower dose have the same protection, with fewer side effects. The problem is that, to have a significant result, this will need about 10 times as many people, but the good news is that everyone gets treated,” said Professor Burn.

The University of California is launching an unprecedented statewide collaboration for breast cancer patients with the goal of revolutionizing the course of their care by designing and testing new approaches to research, technology and health care delivery.

Laura J. Esserman MD

Named the ATHENA Breast Health Network, the groundbreaking project will initially involve 150,000 women throughout California who will be screened for breast cancer and followed for decades through the five UC medical centers. ATHENA is a University of California system-wide project supported by a $5.3 million University of California grant and a $4.8 million grant from the Safeway Foundation.

The project is expected to generate a rich collection of data and knowledge that will shape breast cancer care in the way the renowned Framingham heart study changed the care of patients with heart disease.

“ATHENA is a model of multi-institutional collaboration and demonstrates the enormous potential in shared systems,” said John D. Stobo, MD, UC senior vice president for health sciences and services. “This is a great example of the power of our statewide university network of academic medical centers; this initiative will demonstrate that the total of what can be accomplished by UC functioning as an integrated system can far exceed the sum of contributions by the individual campuses. ATHENA represents an unprecedented opportunity to play a leadership role in driving critical changes in health care. The public nature of the UC institutions make them uniquely positioned to study the appropriateness and effectiveness of treatment. It also allows for the applied use of new scientific evidence, much of which has been developed in the UC medical centers, to truly change the delivery of care.”

The medical centers involved in the large-scale demonstration project are UC San Francisco as the host campus, UC Davis, UC Los Angeles, UC San Diego, and UC Irvine. Also participating in the collaboration are the UC Berkeley School of Public Health, the Northern California Cancer Center, Quantum Leap Healthcare Collaborative, the National Cancer Institute’s BIG Health Consortium, and the Center for Medical Technology Policy.

“We are excited to be supporting this innovative collaboration that, to date, has the clearest potential to produce ground breaking research that will bring us closer to a cure,” said Larree Renda, Safeway Inc. executive vice president, chief strategist and administrative officer and chair of the Safeway Foundation.

Breast cancer, the most common cancer in women, is a devastating and costly disease, striking more than 200,000 women annually and killing more than 40,000 women each year, according to the American Cancer Society. In the United States, more than $20 billion is spent annually screening and treating the disease.

ATHENA is designed to more efficiently integrate financing, technology, research and clinical care, creating an infrastructure model that could be utilized for many medical conditions.

“Our goal is to improve survival and reduce suffering from breast cancer, to accelerate research and compress the time to implement innovations in clinical practice,” said ATHENA principal investigator Laura Esserman, MD, MBA, professor of surgery and radiology, director of the UCSF Carol Franc Buck Breast Care Center and co-leader of the breast oncology program at the UCSF Helen Diller Family Comprehensive Cancer Center.

“By working together as a community, the University of California medical centers, their affiliates, primary care and specialty physicians and patient advocates will work to change the options for patients today and create a better future for all women at risk for developing breast cancer,” she added.

The goals of the ATHENA initiative are:

To create common systems to integrate clinical research and care across the UC campuses to advance the science of prevention, screening, diagnosis, and treatment of breast cancer.

To drive innovation across the UC system to deliver and finance more effective and efficient systems for personalized and biologically targeted care, using breast cancer as a prototype.

To create a biospecimen repository that has broad racial and ethnic representation.

To reduce morbidity and mortality by gaining a molecular understanding of breast cancer and factors that fuel breast cancer risk.

To improve understanding of who is at risk for what kind of cancer, and whether the risk of that cancer is significant or minimal.

To generate the evidence for developing more effective and less toxic treatments and to drive innovation in prevention, diagnosis and treatment.

To provide tools to change the way patients and providers interact to prevent and manage the disease.

The science fueling personalized medicine is experiencing explosive growth. Molecular tests are now available that can analyze a breast cancer tumor and categorize the risk of breast cancer recurrence with and without treatments, according to Esserman.

“Giving doctors sophisticated tools to tailor treatments to the individual tumor will revolutionize care, potentially enabling thousands of women to safely forgo toxic treatments and providing those at high risk of dying from their cancer with more targeted and effective treatments,” said Esserman. “Equally, if not more exciting, is the promise of molecular tools to more accurately predict the risk of getting breast cancer, which may ultimately lead to better ways to prevent the disease.”

Women who present for breast cancer screening at the five UC medical centers and their affiliates will be enrolled into the ATHENA Breast Health Network and followed for decades. All women undergoing screening and treatment will be offered the opportunity to collaborate by contributing information about themselves, any risk factors they have, including health status, and other related lifestyle behaviors, such as diet, tobacco and drug use, environmental factors, gynecological history and family risk. This information will be used to help target prevention services now and in the future. Women diagnosed with breast cancer will additionally join a “survivorship cohort” comprised of women who have been diagnosed with breast cancer.

“We will be able to create a state-wide cohort of women at risk of breast cancer and develop the optimal methods for the early detection of all types of breast cancer,” said Robert Hiatt, MD, PhD, professor and co-chair of the Department of Epidemiology and Biostatistics at UCSF. He is also director of population sciences and deputy director of the UCSF Helen Diller Family Comprehensive Cancer Center, and his research focuses on breast cancer and the environment. “The size and diversity of the survivorship cohort and the depth and quality of the information we’ll have will be unprecedented and will enable the development and testing of robust new models of cancer outcomes and prognosis.”

The UC system is particularly well-positioned for a project of ATHENA’s magnitude because the medical centers annually screen as many as 80,000 women, and diagnose 2,500 patients with breast cancer. Still, said Esserman, the new project calls for “a re-imagining and then a re-engineering so that we can continually improve what we do—to improve our current processes, to streamline communication and access to information among care providers and patients, and to improve the efficiency of services.”

The potential rewards are significant, she stressed. “This project will standardize the collection of structured data from both patients and physicians so that it is computable, interoperable, and reusable, and it will integrate molecular profiling at the time of diagnosis, and create an unparalleled biospecimen repository. The result will be a network that enables personalized care informed by science and that fuels the accelerated and continuous improvement in treatment options and outcomes,” said Esserman. “With ATHENA, wisdom will be waging war against breast cancer and the learning system will continue to evolve until we have cured this disease.”

While the ATHENA Breast Health Network focuses on breast cancer, the tools and infrastructure developed for this project are readily transferable to other cancers and conditions. ATHENA has the potential to serve as a transformative model to drive innovation, alter the culture of research and clinical practice and ultimately change health care delivery, according to the project team.

For further information, visit http://www.AthenaCareNetwork.org.

The Great North Run

Scientists at Newcastle University are launching a ground-breaking study tying into the Great North Run to find out why some of us can run faster than others – despite doing the same amount of training.

The research team, led by Professor Patrick Chinnery, is asking the 54,000 people taking part in next month’s Bupa Great North Run to provide a saliva sample in a bid to find out whether our DNA is linked to race performance.

DNA – the genetic code we inherit from our parents – is important for our physical ability and previous work has shown that variations in the protein-building blocks of muscle can influence performance.

Now Newcastle University researchers want to examine energy production over a long distance.

They think that subtle differences in the DNA that is the blueprint for the energy-producing parts of the muscle – called mitochondria – influence physical fitness. They are now asking for the help of the thousands of Great North runners who will be tackling the 13.1 mile course.

With the help of race organisers, Nova International, an email has been sent to every runner asking if they would be willing to provide a saliva sample and their race number. The scientists will then find out the race time and see whether the DNA variants are linked to performance.

Professor Patrick Chinnery says, “The aim of this study is to find out whether our physical fitness is influenced by DNA – the genetic code that we have inherited from our parents.

“By comparing how many hours of training people have done against the genetic make-up of the energy-burning parts of their cells we hope to work out if there’s a link.

“We’re keen for as many as possible of the 54,000 runners to help us in this ground-breaking research – and the results could revolutionise the way people train in the future.”

The findings will develop understanding of the biology that underpins physical fitness and stamina – and could provide benefits for long-distance runners who wish to improve their performance and yet avoid dangerous complications.

Aspirin: wonder drug... again

A daily dose of aspirin can prevent the occurrence of cancer in people with a genetic predisposition towards Lynch syndrome, a Newcastle University scientist has told Europe’s largest cancer congress.

Lynch syndrome is a condition which accounts for around 5 per cent of all colon cancers.

Professor John Burn, from the Institute of Human Genetics at Newcastle University told the congress ECCO 15 – ESMO 34 held in Berlin on September 21 2009, that he believed that he and his colleagues may have uncovered a simple way of controlling cancer stem cells, which are essential to the formation of malignant tumours.

The clinical trial, which involved 1071 carriers of the Lynch syndrome mutation in 42 centres worldwide, randomised participants to a daily dose of 600mg aspirin and/or 30g Novelose, a resistant starch that escapes digestion in the small intestine.

“Although there were many reports that aspirin might have a beneficial effect in a range of cancers”, said Professor Burn, “they were from case control and epidemiological studies. We decided that the only way to achieve conclusive proof was to undertake a randomised trial in a high risk population.”

Lynch syndrome, often called hereditary nonpolyposis colorectal cancer (HNPCC), is a type of inherited cancer of the digestive tract, particularly the colon and rectum. People with Lynch syndrome have an increased risk of cancers of the stomach, small intestine, liver, gallbladder ducts, upper urinary tract, brain, skin, and prostate. Women carriers also have a high risk of developing endometrial and ovarian cancers.

These patients tend to develop cancer quickly, so the scientists expected to see answers at an early stage. The first results were disappointing, however; at an average of 29 months after randomisation the scientists saw no evidence of the benefits of aspirin in the high risk population studied.

Lynch syndrome is a condition which accounts for around 5 per cent of all colon cancers.

“Our original design allowed for long term post trial follow-up,” said Professor Burn. “We’ve managed to track down most of those who completed the trial – around 75 per cent of the original consent cohort – with information extending up to 10 years from randomisation. We have found that, around four years after randomisation, there was a divergence in the incidence of cancers between the aspirin and placebo groups. To date, there have been only six colon cancers in the aspirin group as opposed to 16 who took placebo. There is also a reduction in endometrial cancer. This is a statistically significant result and we are delighted – all the more so because we stopped giving the aspirin after 4 years, yet the effect is continuing, and is directly correlated with the duration of aspirin use on the trial.”

Although scientists believe that diet is a major factor in the prevention of colorectal cancers, there are no randomised trial data which can prove it, since running proper, controlled trials of diet is extremely difficult. However, there is a strong inverse relationship between colon cancer and how much starch people eat. Resistant starch, after escaping digestion in the upper gut, is fermented in the colon and forms short chain fatty acids which are powerful anti-cancer agents.

“Our very large colon probably evolved to capture such nutrients from our forefathers’ diets”, explained Professor Burn, “because we were giving starch as well as aspirin we would also have expected to see a decrease in cancers in the placebo group. However, there could be a number of reasons for this result – perhaps patients didn’t take the starch every day, or that it simply wasn’t resistant enough.”

There were minor problems due to aspirin side effects; out of over 1000 people 11 in the aspirin group had notable gastro-intestinal bleeds or ulcers as opposed to 9 in the placebo group. But this was counter-balanced by fewer strokes and heart attacks in the aspirin group. The mechanism by which aspirin protects against cancer has yet to be elucidated, but the scientists believe that cancer stem cells are involved.

“We do not think that the mechanisms discussed to date are likely to provide an explanation”, said Professor Burn. “For example, the inflammatory enzyme COX2 is over-expressed in early cancer, but our results suggest an effect that predates the cancer, and may even predate the adenoma which precedes it. We believe that aspirin may have an effect on the survival of aberrant stem cells in the colon. These cancer stem cells are normally resistant to chemotherapy, but if a stem cell mutates but does not reveal its potential until an adenoma is formed, and if aspirin reduced the chances of such cells surviving, this would explain our results.”

The team intends to undertake a further study to see whether a smaller dose of aspirin would have the same beneficial effect or not.

“We are planning to ask all people with Lynch syndrome to agree to “toss a coin” and take, say, either one or two aspirin tablets per day. Then we can see whether the people on the lower dose have the same protection, with fewer side effects. The problem is that, to have a significant result, this will need about 10 times as many people, but the good news is that everyone gets treated,” said Professor Burn.

Pregnant women are not getting enough Vitamin D

Many pregnant women are not getting enough Vitamin D even when they take supplements. The finding has been made as a result of research carried out by the Northern Ireland Centre for Food and Health (NICHE), which involves researchers from Queen’s University Belfast.

Dr Valerie Holmes from Queen’s School of Nursing and Midwifery co-authored the study which was published in the latest edition of the British Journal of Nutrition. The study was the first of its kind measuring the vitamin D status of pregnant women in Northern Ireland.

The Food Standards Agency recommends that all pregnant women take a daily dose of 10 micrograms of the vitamin. Deficiencies have been linked to rickets and lower bone density in children.

Although the main source of Vitamin D is synthesis following exposure to sunlight, it is also found in oily fish, eggs and in fortified foods including margarine and breakfast cereals and can also be taken as a food supplement.

The group studied 99 expectant mothers living in Northern Ireland and tested them at three separate times during their pregnancy.

Testing at 12 and 20 weeks of pregnancy revealed that as many as 96 per cent of the women had insufficient levels of vitamin D in their blood. Examination also revealed that at these test points, 35 per cent could be classified as vitamin D deficient at 12 weeks and 44 per cent at 20 weeks.

During the third trimester, at 35 weeks, 75 per cent had insufficient levels of the vitamin and 16 per cent of women were deficient.

Dr Holmes, from the Nursing and Midwifery Research Unit, said: “While studies in other countries have reported low levels of vitamin D in pregnancy, the high percentage of women in this study who had insufficient levels is remarkable.

“Northern Ireland’s northern latitude means that we are ‘in the dark’ in terms of sunshine, and makes the issue of adequate vitamin D dietary intake even more important.

“While vitamin D status was improved in women who reported taking multivitamin supplements, many still had insufficient levels, suggesting that the amount present in multivitamins formulated for pregnancy may be too low to maintain adequate levels.

“Stores of vitamin D in the newborn baby depend on the mother’s levels during pregnancy and where deficiency is severe there is an increased risk of rickets. Previous studies have reported a link between low levels of vitamin D in pregnancy and lower bone density in children.”

Dr Holmes said further research was needed to determine exactly how much vitamin D women need to take to maintain adequate levels during pregnancy. She added that if pregnant women have any concerns about their nutrition they should consult their midwife or GP.

The research was carried out in collaboration with the University of Ulster and Belfast City Hospital.