Health impacts of mobile phone use to be explored in long-term study

A new decades-long study launched 22 April to investigate whether there is a link between the use of mobile phones and long-term health problems such as cancer.

The international study will run for 20- 30 years and will follow the health of at least 250,000 participants aged 18-69 in five European countries – UK, Denmark, Sweden, Finland and the Netherlands.

There are currently over six billion mobile phone devices in use worldwide. Studies of short term use of mobile phones and health have been reassuring, other than well known associations with risk of motor accidents. However, there are still some uncertainties about the health effects of mobile phone use, since some diseases take many years to develop and so far few people have been using mobile phones for that period of time.

Dr Mireille Toledano, co-Principal Investigator of the study from the School of Public Health at Imperial College London, said: “For the benefit of current users and for future generations, it is important for us to carry out long term health monitoring of a large group of mobile phone users so that we can identify if there are any possible health effects from this new and widespread technology that has become so central to our everyday lives.”

Professor Paul Elliott, Principal Investigator of the study from the School of Public Health at Imperial College London, said: “Scientists have been looking at the effects of mobile phones on health for several years and so far, reviews of the research have been reassuring with respect to mobile phone use and health problems in the short term. However, as mobile phones have only been in widespread use for a relatively short time, we haven’t been able to carry out long-term studies until now.

“COSMOS aims to fill in important gaps in our knowledge of mobile phones and health. By looking at large numbers of people across Europe over a long period of time, we should be able to build up a valuable picture of whether or not there is any link between mobile phone use and health problems over the long term.”

Experts call for more research into insulin-cancer connection

The benefits of using insulin to treat diabetes far outweigh the risks, but a review published online by the International Journal of Clinical Practice, suggests that commonly used diabetes therapies may differ from each other when it comes to their influence on cancer risk.

Cancer expert Professor Michael Pollak from McGill University, Montreal, Canada, teamed up with diabetes expert Professor David Russell-Jones from The Royal Surrey County Hospital, Guildford, UK, to review more than three decades of laboratory and population studies.

At the outset the authors are keen to point out that the current evidence is far from clear-cut and further research is needed to examine the risks and mechanisms that appear to link insulin with tumour growth.

Nonetheless, they believe that their findings will be of special interest to clinicians advising diabetic patients who have also been diagnosed with cancer or have a strong family history of cancer.

“The inter-relationships between cancer and diabetes deserve more attention as both of these diseases are becoming more prevalent globally and it is increasingly more common to see patients with both conditions” says Professor Pollak.

The paper also reflects the views expressed by experts at scientific meetings held in 2009 to assess the relative risk of malignancy associated with diabetes itself and with the use of different insulin products and other diabetes treatments. These meetings followed the publication of a series of epidemiological studies in 2009 that raised questions concerning the relative risk of cancer incidence associated with the basal insulin analogue, insulin glargine.

“Recent publications have resurrected awareness and focused attention on an issue that first emerged more than a decade ago, when it was shown that artificial modification of the molecular structure of insulin could result in increased cell division” says Professor Pollak.

“Our review showed that people with diabetes, particularly those with type 2 diabetes, may face an increased risk of cancer and that their cancer may be modified by treatment choices.

“Research suggests that metformin, which is used to treat some patients with diabetes, may provide a protective effect, while insulin and/or certain insulin analogues may promote tumour growth.”

The review found that diabetes appears to be associated with an intrinsic increase in cancer incidence. A number of metaanalyses have been carried out, showing that:

● Diabetic patients were 30% more likely to develop colorectal cancer (15 studies covering 2.5 million patients).

● Women with diabetes had a 20% greater risk of developing breast cancer, according to 20 studies.

● People with diabetes had an 82% higher risk of developing pancreatic cancer (36 studies covering more than 9,000 patients).

Professor Pollak points out that in the meantime “we agree with statements issued by the major diabetes organisations that there is no need to panic. Insulin has an excellent risk benefit ratio and any absolute risks between the different treatments are likely to be small”.

“However, careful consideration of the choices available might be wise for patients who face a high biological risk of cancer, for example those with a family or personal history of cancer. Clinicians need to be prepared to provide up-to-date advice to these people, as ongoing research continues.

“It is important to recognise that the initially surprising observation that diabetics receiving metformin treatment are substantially less likely to have cancer than expected have now been reproduced in several studies.

The possibility that this off-patent drug may have uses in cancer prevention or treatment, as well as in the treatment of type 2 diabetes, is receiving serious attention from research teams of endocrinologists and oncologists.”

● Citation: M. Pollak, D Russel-Jones. Insulin analogues and cancer risk: cause for concern or cause célèbre? International Journal of Clinical Practice, Volume 64, Issue 5 DOI: 10.1111/j.1742-1241.2010.02354.

Researchers a step closer to new drug delivery technique

Scientists at the University of Greenwich in the United Kingdom have got a step closer to a sought after drug deliver technique – that is to find a vehicle that can carry drugs not just to a specific cell, but a specific organelle inside the cell and accurately measure how it behaves when it gets there.

This has proved elusive despite two decades of research, according to the Journal of Controlled Release. The researchers led by Dr Simon Richardson, for the first time provide direct evidence that nanomedicines can be delivered to select organelles and manipulated to carry beneficial agents like genes.

“Drug delivery is important for everyone because it has the potential to deliver new treatments for diseases which are currently incurable; and to deliver existing drugs more effectively,” Dr Richardson.

“We are trying to smuggle healthy genes inside cells. Genes are large molecules which have up till now proved too big to get in without serious risk to the patient. Our research is at the cutting edge of efforts to turn gene therapy, and new molecular medicines, from risky and scifiesque to safe and routine.”

As well as proving that material like genes can be delivered to the target organelle, the team was also able to show how the delivery vehicle behaves once inside.

Professor Kinam Park, Editor of the Journal of Controlled Release, where this research was published said the study was “distinguished from others by its thoroughness and unequivocal data” and concludes: “…the approach used by Richardson’s team can be useful in developing more efficient delivery vehicles for drug targeting in general.”

● Citation: S.C.W. Richardson et al. Intracellular fate of bioresponsive poly (amidoamine)s in vitro and in vivo. Journal of Controlled Release, issue 142. doi:10.1016/j.jconrel.2009.09.025.

Family history is strong predictor of obstructive CAD

In the largest study of its kind to date using cardiac computed tomography angiography, people with a family history of early signs of coronary artery disease are at higher risk of developing obstructive coronary artery disease and plaque in their arteries, Henry Ford Hospital researchers say.

Researchers analyzed the data from more than 8,200 patients who underwent cardiac computed tomography angiography and found that those with a family history of coronary artery disease, or CAD, have a 28% chance of developing the disease themselves than those with no family history. Family history of CAD also was independently associated with an increased prevalence of plaque in the arteries.

The study was presented at the 59th annual American College of Cardiology Scientific Sessions in Atlanta in March.

“This is the first study to show that family history of premature coronary artery disease is a significant predictor of obstructive coronary artery disease using coronary computed tomography," said Mouaz Al-Mallah, MD, director of Cardiac Imaging Research at Henry Ford and lead author of the study.

While family history is a well-known risk factor for premature coronary artery disease, the researchers examined whether family history was linked to obstructive coronary artery disease in patients who underwent cardiac computed tomography angiography, a diagnostic imaging tool that looks at the coronary arteries and evaluates the amount of blockage from plaque.

For the study researchers analysed data of patients using the Advanced Cardiovascular Imaging Consortium.

“Based on past research and our findings, we believe cardiac computed tomography angiography would likely identify a high risk group of patients with advanced plaque buildup,” said Dr Al-Mallah.

Risk of newborn heart defects increases with maternal obesity

The more obese a woman is when she becomes pregnant, the greater the likelihood that she will give birth to an infant with a congenital heart defect, according to a study conducted by researchers at the US National Institutes of Health (NIH) and the New York state Department of Health.

The researchers found that, on average, obesity increases a woman's chance of having a baby with a heart defect by around 15%. The risk increases with rising obesity. Moderately obese women are 11% more likely to have a child with a heart defect, and morbidly obese women are 33% more likely.

"The current findings strongly suggest that by losing weight before they become pregnant, obese women may reduce the chances that their infants will be born with heart defects," said Alan E. Guttmacher, MD, acting director of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), the NIH Institute that conducted the study.

Congenital heart defects are the most common type of birth defect in the US, affecting 8 in every 1,000 newborns.

These defects consist of a number of problems in the structure of the heart and range from minor to life threatening. In the United States, 1 in 5 women are obese at the beginning of pregnancy. Previous studies have shown that maternal obesity during pregnancy is associated with complications for mothers and infants.

Obesity increases the risk for pregnancy-induced hypertension, preeclampsia (a serious form of hypertension during pregnancy), gestational diabetes, and cesarean delivery. Infants born to women who were obese during pregnancy are themselves at increased risk for overweight and type II diabetes later in life.

Previous research by NICHD scientists and others has also shown an association between maternal obesity and birth defects, such as neural tube defects – serious malformations of the spinal column. In the United States, 1 in 5 women are obese at the beginning of pregnancy. The findings were published online in the American Journal of Clinical Nutrition.

“The trend is unmistakable: the more obese a woman is, the more likely she is to have had a child with a heart defect,” James L. Mills, MD, MS, NICHD's Division of Epidemiology, Statistics and Prevention Research, lead author of the study, said. “If a woman is obese, it makes sense for her to try to lose weight before becoming pregnant,”

Dr Mills said. “Not only will weight loss improve her own health and that of her infant, it is likely to have the added benefit of reducing the infant's risk for heart defects.”

● Citation: James L Mills et al. Maternal obesity and congenital heart defects: a population-based study. Am J Clin Nutr (7 April 2010). doi:10.3945/ajcn.2009.28865

Researchers develop bone-hard biomaterial

Screws used in surgical operations are often made of titanium. They usually have to be removed after a while or replaced by new ones. A new biomaterial makes this unnecessary. It promotes bone growth and is biodegradable. Football players, skiers, tennis players – they all fear a crucial ligament rupture. If the knee ligaments are damaged the patient usually has to undergo a surgery to restore the stability of the joint.

In the surgical procedure the torn ligament is replaced by a piece of tendon from the leg, which is fixed to the bone by means of an interferential screw. The problem is that the screws are made of titanium. After a certain time the patient has to undergo a further surgery so that the material can be removed.

Researchers at the Fraunhofer Institute for Manufacturing Engineering and Applied Materials Research (IFAM) in Bremen want to spare cruciate ligament victims and other bone patients this additional procedure.

They have therefore developed a screw which is biocompatible and also biodegradable over time. “We have modified biomaterials in such a way that they can be formed into robust bioactive and resorbable screws by means of a special injection molding process,” explains Dr Philipp Imgrund, head of the biomaterial technology department at IFAM.

“Depending on the composition they biodegrade in 24 months.” Biodegradable screws made of polylactic acid are already used in the medical field, but they have the disadvantage that when they degrade they can leave holes in the bone.

The IFAM researchers have therefore improved the material and developed a moldable composite made of polylactic acid and hydroxylapatite, a ceramic which is the main constituent of the bone mineral.

“This composite possesses a higher proportion of hydroxylapatite and promotes the growth of bone into the implant,” says Imgrund.

The engineers at IFAM have developed a granulate from the biomaterials which can be precision-processed using conventional injection molding methods, obviating the need for any post-processing such as milling. The complex geometry is achieved in a net-shape process, producing a robust screw.

The properties of this prototype come very close to those of real bone. Its compressive strength is more than 130 newtons per square millimeter, whereas real bone can withstand between 130 and 180. What’s more, the injection molding process has a positive side effect.

Normally, the powder injection molded part has to be compressed at very high temperatures of up to 1,400° Celsius. “We only need 140 degrees for our composite materials,” says Imgrund. In future the engineers intend to develop other bioimplants using their energysaving process.

Scientists gain new insight into process of cell immortalisation

Researchers at Umeå University have shown that cells that grow forever – that are immortalised – get this capacity through gradual changes in the expression of genes that govern the repair of DNA damage and regulate growth and cell death.

The research also shows that activation of the enzyme complex telomerase, which is necessary for unlimited growth, occurs late in this process.

This discovery provides new insights into the series of events that needs to occur for cells to become immortalised, and it will have an impact on future studies of leukemia, for example. The study, published in the April issue of the journal Aging Cell, was performed by a research team directed by Professor Göran Roos at the Department of Medical Bioscience, Pathology.

It is about how cells’ telomers (repetitive DNA sequences on the ends of chromosomes) are regulated during the process that leads to eternal life of cells. One type of blood cells, lymphocytes, were analysed on repeated occasions during their cultivation in an incubator until they achieved the ability to grow an unlimited number of cell divisions, a process that is termed immortalisation.

In experiments, immortalisation can be achieved following genetic manipulation of cells in various ways, but in the lymphocytes under study this occurred spontaneously. This is an unusual phenomenon that can be likened to the development of leukemia in humans, for example.

The ends of chromosomes, the telomers, are important for the genetic stability of cells. In normal cells telomers are shortened with every cell division, and at a certain short telomer length they stop dividing.

With the occurrence of genetic mutations the cells can continue to grow even though their telomers continue to be shortened. At a crticially short telomer length, however, a so-called crisis occurs, with imbalance in the genes and massive cell death.

In rare cases the cells survive this crisis and become immortalised. In previous studies this transition from crisis to eternal life has been associated with the activation of telomerase, an enzyme complex that can lengthen cells’ telomers and help stabilise the genes. A typical finding is also that cancer cells have active telomerase.

The study shows that cells initially lose telomer length with each cell division, as expected, and after a while enter a crisis stage with massive cell death. Those cells that survive the crisis and become immortalised evince no activation of telomerase; instead, this happens later in the process.

The Umeå researchers found that the expression of genes that inhibit telomerase is reduced in cells that get through the crisis, but telomerase was not activated until positively regulating factors were activated, thus allowing the telomers to become stabilised through lengthening.

By analysing the genetic expressions the scientists were able to show that the cells that survived the crisis stage had mutations in genes that are key to the repair of DNA damage and the regulation of growth and cell death.

The studies were carried out in collaboration with the Centre for Oncology and Applied Pharmacology, University of Glasgow and the Maria Skodowska-Curie Memorial Cancer Centre and Institute of Oncology, Warsaw.

● Citation: Degerman S, et al: Telomerase upregulation is a postcrisis event during senescence bypass and immortalization of two Nijmegen breakage syndrome T cell cultures. Aging Cell. 2010; 9 (2): 220-2358. DOI: 10.1111/j.1474-9726.2010.00550.

New marker for CAD risk

In an article published in March 2010 in the Journal of the American College of Cardiology, Canadian researchers from The Providence Heart + Lung Institute and the University of British Columbia detail their finding that high levels of an enzyme, myeloperoxidase, in the blood of Coronary Artery Disease (CAD) patients more than doubles the risk for death over a 13-year period.

Myeloperoxidase is an enzyme associated with oxidative stress, which damages arterial tissue. The research team looked at blood samples and records from a group of patients admitted to hospital in the early 1990s with symptoms of heart disease.

Over a 13-year period, mortality was more than double for patients with high blood levels of myeloperoxidase than for those with lower levels.

Based on this work, the researchers were able to develop a new classification of risk for CAD patients based on their levels of myeloperoxidase. Measurement of the enzyme provides added predictive value for cardiovascular death when compared to traditional risk factors such as smoking and diabetes.

“We hope that the discovery of new markers of cardiovascular risk will help identify specific patients who could benefit from more aggressive treatment strategies,” said lead investigator, Dr John Hill.

                                  
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