Week Ending FRIDAY July 31, 2009---------------------------News Archive / Return to News Alerts
Pregnant Women Subject to Dehydration in the Summer
Pregnant women have a higher incidence of insufficient amniotic fluid levels (oligohydramnios) in the summer months due to dehydration, according to a study conducted by researchers at Ben-Gurion University of the Negev (BGU).
The retrospective population-based study was published in the July issue of Archives of Gynecology and Obstetrics. The main objective of the study was to determine whether the summer season is a risk factor for oligohydramnios, by comparing the frequency of amniotic fluid loss during the summer months versus its frequency during the rest of the year.
In the study at Soroka University Medical Center in Beer-Sheva, Israel, the researchers evaluated pregnancies of patients with oligohydramnios that delivered from May to August during the years 1988-2007.
After excluding other causes of fluid loss, such as premature rupture of membranes, intra-uterine growth restriction or malformations, the study determined that higher rates of oligohydramnios were found in the summer months as compared to the rest of the year.
During the study period, there were 191,558 deliveries of which 4,335 were diagnosed with idiopathic oligohydramnios. Of these, a proportionally higher number, 1,553 deliveries (36 percent), occurred during these four summer months, while 2,782 deliveries occurred during the other eight months of the year (64 percent).
"It is important for pregnant women to drink appropriate amounts of water specifically in the summer -- about 10 glasses per day -- and avoid direct sun, not only for the health of the mother, but also in order to avoid fetal dehydration," explains Prof. Eyal Sheiner of the Faculty of Health and Sciences at Ben-Gurion University of the Negev.
Amniotic fluid is the nourishing and protecting liquid contained by the amnion of a pregnant woman. It protects the developing baby by cushioning the mother's abdomen, promotes muscular and skeletal development, and helps to protect the fetus from heat loss.
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Impact of DNA Damage in the Developing Brain
St. Jude technique yields clues about brain cells targeted by faulty single-strand DNA repair and offers new hints about the roots of neurological disease
Switching off a key DNA repair system in the developing nervous system is linked to smaller brain size as well as problems in brain structures vital to movement, memory and emotion, according to new research led by St. Jude Children’s Research Hospital scientists.
The work, published in the August issue of the journal Nature Neuroscience, also provides the first evidence that cells known as cerebellar interneurons are targeted for DNA damage and are a likely source of neurological problems in humans. The cerebellum coordinates movement and balance. The cerebellar interneurons fine tune motor control.
“These data will be important for understanding the role the DNA damage response plays in preventing neurological disease,” the investigators wrote.
The study also marks the first time researchers have switched off a pathway for repairing damaged single DNA strands in an organ system, in this case the mouse brain and nervous system. While the results suggest certain brain cells are particularly vulnerable, investigators report that with time DNA damage accumulates throughout the nervous system. Some mice in the study eventually develop seizures and difficulty walking.
Peter J. McKinnon, Ph.D., a member of St. Jude Genetics and Tumor Cell Biology, said the work provides a new model for understanding how single-strand DNA damage affects the nervous system and offers a new focus for tracking the origins of neurological disease.
The research also reflects growing scientific interest in damage to single strands of DNA. “A variety of human disease syndromes result from problems in the DNA-repair system,” explained McKinnon, the paper’s senior author.
DNA is the double-stranded molecule found in nearly every cell. In organisms both simple and complex, it serves as the biochemical blueprint for assembling and sustaining life. Diseases like cancer have long been associated with unrepaired damage to both strands of DNA. Single-strand DNA damage is far more common, but was generally considered less catastrophic to the cell.
But the last decade brought evidence linking single-strand DNA damage with human diseases, including ataxia with oculomotor apraxia (AOA1) and spinocerebellar ataxia with axonal neuropathy (SCAN1). Both disorders are inherited and are characterized by progressive difficulty with walking and other movement. AOA1 is among the most common form of certain inherited movement disorders in Japan and Portugal. McKinnon said those reports sparked new interest in single-strand DNA repair.
This study focused on Xrcc1, a protein long recognized as the master regulator of a pathway essential for single-strand DNA repair in the nervous system. The brain is thought to be particularly susceptible to such damage because neurons consume large amounts of oxygen, which can result in excessive production of free radicals and leave them vulnerable to single-strand DNA damage. Because brain cells do not divide, they cannot use the backup repair systems found in other tissues.
Investigators developed a way to switch off Xrcc1 production in the mouse brain and nervous system as development began. The system meant Xrcc1 still worked normally in the rest of the body.
The strategy used mice developed to make a particular enzyme, known as cre recombinase, in just the nervous system. St. Jude researchers then developed a mouse that carried an Xrcc1 gene outfitted with biochemical tags targeting the gene for inactivation by the enzyme. The result was a mouse whose nervous system lacked Xrcc1 and so was unable to efficiently repair the single-strand DNA damage.
The shutdown triggered a dramatic decline of interneurons throughout the cerebellum. In a subgroup of those cells, the damage triggered apoptosis, or programmed cell death. But the findings suggested the greatest loss occurred as the immature cerebellar interneurons, or progenitor cells, were poised to complete differentiation. In those cells, McKinnon said, loss of Xrcc1 activated the p53 pathway and blocked the cells from completing the cell cycle. “The cells appear to undergo permanent arrest,” said McKinnon, noting it is one of the few in vivo examples of the p53 pathway leading to cell cycle arrest rather than apoptosis.
In the hippocampus, which plays a role in memory and emotion, investigators reported abnormal gene expression and neuronal function. Some neurons were eventually replaced by scar tissue in a process known as gliosis. Overall changes in the hippocampus mimicked those found in the brains of adults with the seizure disorder known as temporal lobe epilepsy. In this study, the loss of Xrcc1 also resulted in seizures in mice.
Anesthesia Not Harmful for Babies During Birth Process
Mayo Clinic researchers have found that children exposed to anesthesia during Cesarean section are not at any higher risk for learning disabilities later in life than children not delivered by C-section
These findings are reported in the current issue of the journal Anesthesiology.
VIDEO ALERT: Additional audio and video resources, including comments by Drs. Sprung and Flick describing the research, are available on the Mayo Clinic News Blog.
"We found that the incidence of learning disabilities was equal between children who were delivered vaginally and those who were delivered via C-section but with general anesthesia," says Juraj Sprung, M.D., Ph.D., a Mayo Clinic anesthesiologist who led the study. "It's reassuring that the anesthetics required for Cesarean delivery do not appear to cause long-term brain problems."
The study was conducted with data from the Rochester Epidemiology Project. Researchers analyzed the medical records of 5,320 children born between 1976 and 1982 to mothers living in Olmsted County. They compared birth records with scholastic achievement and IQ tests administered to the children later in life as part of their schooling.
The study builds on a previous project, reported in March, which found that children exposed to a single dose of anesthesia during the first three years of life had no increased risk for learning disabilities, but those exposed multiple times had an almost doubled risk for later identification of learning disabilities.
Prolonged exposure to anesthetics has been shown to cause brain abnormalities in young animals, which was the impetus behind these two studies. Scientists think that the brains of young animals and humans are more vulnerable to a variety of problems because they are undergoing rapid growth. The brain is forming vital connections between cells during this time.
Not only did the researchers find that the use of anesthesia during delivery was not harmful to the baby, they found that babies delivered by Cesarean using an epidural anesthetic (which numbs only the lower region of the body and does not involve the mother going to sleep) had a substantially reduced risk for learning disabilities later in life. "The risk was reduced by about 40 percent compared to children delivered vaginally and those delivered via Cesarean section but with general anesthesia," says Dr. Sprung.
Study co-author and Mayo Clinic anesthesiologist Randall Flick, M.D., cautions that because this study is preliminary, changes to medical practice should not be considered at this point. "What we've found is an association between two things," says Dr. Flick. "One is the way a child was delivered, either vaginally or under regional or general anesthesia. The other is a difference in the incidence of learning disabilities as the child attended school. It's important to recognize there may be many other factors that impact learning disabilities."
The team is investigating whether use of an epidural on a mother during natural labor has similar effects on the incidence of learning disabilities in children as a C-section with an epidural.
Dr. Flick says the research team also is working with the U.S. Food and Drug Administration (FDA) on a related study that looks more closely at young children with specific medical conditions who have been exposed to anesthesia and compares them to children with similar medical conditions who were not exposed to anesthesia. The study is part of a national SAFEKIDS Initiative that the FDA is undertaking with several academic and clinical institutions to study the effects of anesthetics and sedatives on brain development in infants and young children.
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How Children Treat Their Peers With Undesirable Traits
A study by Kansas State University researchers is looking at how third and sixth-grade children perceive and interact with peers who have various undesirable characteristics, such as being overweight or aggressive
The researchers' study explored third-graders and sixth-graders's perceptions of the ability of the peer to control or change such traits. The K-State research team presented their results in May at the Association for Psychological Science annual convention in San Francisco, Calif.
"This study provides some evidence that if a child feels that an undesirable characteristic is under some sort of personal control, they are less likely to respond favorably to someone who displays that characteristic," Livengood said. "The study implies that if a child doesn't have experience with that particular undesirable characteristic, they are less likely to respond favorably to someone with that specific quality."
The researchers found that children who perceive themselves or a friend as similar to a peer with an undesirable characteristic might experience heightened empathy for that peer, and then might respond in a positive manner toward the peer. The findings also showed that boys, more than girls, tended to have negative attitudes toward peers with undesirable characteristics.
The study included third-graders and sixth-graders who completed questionnaires that had descriptions of hypothetical peers. The peers included a poor student, nonathletic student, obese student, aggressive student, shy student, asthmatic student and a student with attention deficit hyperactivity disorder.
When the children read a brief description of a hypothetical peer, they were asked to rate statements regarding the peer's personal control and change over the characteristic, and how they would respond to such a person. The children also were asked to indicate if they or a friend were similar to the peer.
The findings showed that the more the children agreed that the peers were at fault for their characteristic, the more they agreed that they would tease those peers, and the less they agreed that they would like or help those peers if they needed assistance.
According to the researchers, the sixth-grade boys displayed stronger agreement than the sixth-grade girls that the peers were at fault for the undesirable characteristic and that they would tease them. They also had less agreement that they would help such a peer if they needed assistance.
The study showed that the aggressive and asthmatic peers tended to receive the most extreme ratings. The aggressive peer was rated high on having fault for the characteristic and low on having a desire to change. The asthmatic peer was rated high on having the characteristic caused by something in the peer's body or brain and low on having fault for the characteristic.
The children's ratings showed that they consistently anticipated treating the asthmatic peer more favorably than the aggressive peer. The researchers said it appeared that the children perceived the highly aggressive peer's behavior as under personal control, and the asthmatic peer was perceived as suffering a medical condition that was largely out of personal control to cause or change. The obese peer also was rated high on having fault for the characteristic.
The children agreed more strongly that girls would improve more than boys with the help of adults to alter an undesirable characteristic. The researchers said since girls tend to seek assistance from adults and comply with directives from adults more frequently than boys, the children might have anticipated that girls would respond more favorably than boys.
THURSDAY July 30, 2009---------------------------News Archive / Return to News Alerts
Women Benefit From Physical Activity More Than Men
A long-term study of over 8,700 middle-aged men and women provides race and gender specific data on the cholesterol effects of physical activity, with the interesting result that women, particularly African-American women, experience greater benefits as a result of exercise than men
Many experimental studies have found that physical exercise can improve cholesterol levels and subsequently decrease the risks of cardiovascular disease; however, few of these studies have included enough participant diversity to provide ethnic breakdowns.
The analysis of this large Atherosclerosis Risk in Communities (ARIC) Study, which appears in the August issue of Journal of Lipid Research, was carried out by Keri Monda and colleagues at North Carolina and Baylor.
They found that over a 12 year period, all individuals who increased their exercise by about 180 metabolic units per week (equivalent to an additional hour of mild or 30 minutes of moderate activity per week) displayed decreased levels of triglycerides and increased levels of the "good" HDL cholesterol.
However, statistically significant decreases in the "bad" LDL cholesterol were only observed in women, with particularly strong effects in menopausal women and African-American women. And total cholesterol levels were only significantly decreased in African-American women.
The authors speculate that these novel differences may arise from hormonal differences between the sexes, especially considering the extra effects seen post-menopause. The racial differences observed may stem from genetic variations that require further exploration.
The authors also note that their exercise data was assessed by questionnaire and this was non-scientific, though the particular methodology used has been extremely reliable in other studies.
They also note that all evaluated participants were healthy, so these results cannot be generalized to individuals with diabetes or those on cholesterol-lowering medications.
Reprogramming Human Cells Without Inserting Genes
A research team has discovered a new avenue for reprogramming cells that could eventually lead to treatments for a range of human diseases and traumatic injuries by coaxing a patient's own cells to repair and regenerate the damaged tissues
The research team was made up of faculty at Worcester Polytechnic Institute's (WPI) Life Sciences and Bioengineering Center (LSBC) and investigators at CellThera, a private company also located at the LSBC. They have discovered a new way to turn on stem cell genes in human fibroblasts (skin cells) without the risks associated with inserting extra genes or using viruses.
The research team reported its findings in the paper "Induction of Stem Cell Gene Expression in Adult Human Fibroblasts without Transgenes," published online July 21, 2009 (in advance of September print publication) as a "fast track" paper from the journal Cloning and Stem Cells. (Cloning, Stem Cells. 2009 Jul 21.) "We show that by manipulating culture conditions alone, we can achieve changes in fibroblasts that would be beneficial in development of patient-specific cell therapy approaches," the authors wrote in the paper.
Early on, the emerging field of regenerative medicine focused on embryonic stem cells, which are pluripotent, meaning they can grow into all the tissues of an adult organism. In the pluripotent state, several genes are known to be active, helping to control the stem cells. These genes, including OCT4, SOX2 and NANOG, are accepted as markers of pluripotency because they are active in stem cells, but become dormant once the stem cells begin to differentiate and head down the path to developing into a specific kind of cell type and tissue.
While the study of embryonic stem cells continues to yield important knowledge, research teams around the world are also working to change, or reprogram, fully-differentiated cells like skin cells, back to a more pluripotent state. Called induced pluripotent stem cells (iPS), these reprogrammed cells could be used to regenerate tissue without some of the problems associated with embryonic stem cells, including ethical questions and the potential for embryonic stem cells to be rejected by a patient's immune system or to grow out of control and cause tumors.
The first induced pluripotent stem cells were created in 2007 by Shinya Yamanaka's team at Kyoto University in Japan, which inserted extra copies of four known stem cell genes, including OCT4 and SOX2, into human skin cells. Those genes began expressing proteins that changed the skin cells back to a more pluripotent state. This technique, which has since been repeated by other labs and refined to the point were fewer additional genes are needed to achieve reprogramming, was a major scientific breakthrough. Its potential for use in human therapies is limited, however, because inserting new genes into adult cells, either directly or by using viruses to carry the genetic payload, can cause a host of problems.
In the current study, the team at WPI and CellThera turned on the existing, yet dormant, stem cell genes OCT4, SOX2 and NANOG already in the skin cells by lowering the amount of atmospheric oxygen the cells were exposed to, and by adding a protein called fibroblast growth factor 2 (FGF2) to the culture medium. (FGF2 is a naturally occurring protein that is known to be vital for maintaining the pluripotency of embryonic stem cells.)
Furthermore, once the stem cell genes were activated and began expressing proteins, the team found those proteins migrated back into the nucleus of the skin cells, precisely as would occur in induced pluripotent stem cells. "This was an exciting observation," said Raymond Page, PhD, research assistant professor of biology and biotechnology at WPI and lead author on the paper. "Having these proteins localize to the nucleus is the first step of reprogramming these cells."
Even more surprising, the team found that the stem cell genes OCT4, SOX2 and NANOG were not completely dormant in untreated skins cells, as was presumed. Those genes were, in fact, sending out messages, but those messages were not being translated into the proteins that do the work of making cells pluripotent. "This was quite unexpected," said Tanja Dominko, DVM, PhD, associate professor of biology and biotechnology at WPI and president of CellThera. "Not only does this data force us to rethink what the true markers of pluripotency may be, it suggests there is a natural mechanism at work in these cells regulating the stem cell gene expression. That opens a whole new line of inquiry."
Pregnant Women At Front of H1N1 Vaccine Line
Pregnant women should be the first to get vaccinated against the new pandemic H1N1 influenza virus, federal health experts told a U.S. advisory panel on Wednesday
Pregnant women are at special risk from the new strain, and vaccinating them protects their newborns, too, Dr. Anthony Fiore of the U.S. Centers for Disease Control and Prevention told a meeting of vaccine advisers to his agency.
He said a CDC working group has designated 42 million Americans who should be vaccinated first -- pregnant women, people with an infant too young to be vaccinated in the household, healthcare workers, children aged up to 4 years and children with chronic conditions making them at high risk of flu complications.
The committee was to issue its recommendations later on Wednesday.
Five companies are making H1N1 vaccine for the U.S. market -- AstraZeneca's MedImmune unit, Australia's CSL Ltd, GlaxoSmithKline Plc, Novartis AG and Sanofi-Aventis SA. It is not clear how many doses of vaccine will be available.
"Seasonal influenza vaccination should begin as soon as it is available for all groups currently recommended for seasonal vaccine," Fiore told the Advisory Committee on Immunization Practices.
He said seasonal and pandemic vaccines can be administered on the same visit but noted that trials in human volunteers are looking at the question and the advice may be changed later.
Fiore also released new CDC data showing that obese people do not have an especially high risk of death or complications from swine flu, as some earlier studies had suggested.
Fiore said the working group was assuming that people will need two doses of vaccine to be fully protected, but the clinical trials are also looking at this issue.
When giving vaccine, clinics should assume that more supply is coming, Fiore said. "If you vaccinate somebody in that initial target (group), don't go set aside in your mind or your refrigerator that second dose," he said. "You worry about that when the person comes back."
The U.S. government has taken delivery of 20 million doses of a vaccine against the new pandemic H1N1 swine flu, has ordered a total of 195 million doses and should be ready to start an immunization campaign in October, said Robin Robinson of the U.S. Department of Health and Human Services.
Data from human trials of the new vaccine, which have just begun, will not be available until late September, officials said.
H1N1 swine flu is now so widespread that the World Health Organization has stopped counting individual cases. Health experts are afraid it could worsen, especially when the Northern Hemisphere's influenza season starts in the autumn.
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New Male Chlamydia Test Is Fast and Pain-Free
A new urine test developed with funding from the Wellcome Trust, UK will allow doctors to diagnose Chlamydia infection in men within the hour, improving the ability to successfully treat the infection on the spot and prevent re-transmission
Chlamydia, caused by the bacterium Chlamydia trachomatis, is the most common sexually-transmitted bacterial infection in the United Kingdom (UK), particularly amongst sexually active men and women aged 16-24 years.
In the majority of cases, the disease is asymptomatic in both men and women. If symptoms show, they may include discharge or pain when passing urine for men. Recent research suggests that, if untreated even when no symptoms show it may be a cause of reduced fertility. In women, it can lead to even more serious complications, such as pelvic inflammatory disease, chronic pelvic pain and ectopic pregnancy.
In 2008, young people accounted for two thirds of all new episodes of uncomplicated Chlamydia infections diagnosed in genitourinary medicine clinics. In England, as many 68 young men in every 1,000 carry the infection; the figure is nearly 84 out of 1,000 for young women. Since the mid-1990s, the number of diagnosed infections has risen an average of 7,500 per year to over 123,000.
Once diagnosed, Chlamydia can be treated easily with a one-off antibiotic pill. However, until now, male rapid tests for Chlamydia have been relatively inaccurate and involved urethral swabs, which can cause discomfort.
"Horror stories about painful swabs have put men off getting tested for Chlamydia, and other non-invasive tests are expensive, technically complex and take days to obtain the result," explains Dr Helen Lee from the University of Cambridge. "This has led to many cases of infection in men going undiagnosed and being transmitted to their female partners, with potentially more serious complications."
The Chlamydia Rapid Test, a urine test developed by Dr Lee and colleagues at Diagnostics for the Real World (DRW) and the University of Cambridge, can be used with minimal training. It is designed to be used in conjunction with FirstBurst, a device for collecting the first voided urine from men. FirstBurst collects six times the amount of Chlamydia bacteria compared to a standard urine sample. The test then uses a unique signal amplification system developed by DRW to boost the test's sensitivity and gives the results in less than an hour.
Today, the British Medical Journal publishes an evaluation† of the test, which shows that it is significantly more accurate than existing urine-based rapid tests. The researchers took samples from over 1,200 men at two clinical sites. They found that the test correctly identified Chlamydia infection in 84.1% of samples, more accurate than the nearest competitor rapid tests for men.
"Without an effective and rapid testing programme for men, we are unlikely to succeed in efforts to control Chlamydia infection," says Dr Lee. "This new test is both accurate and swift, allowing men attending the clinics to be tested and treated on site in one visit."
The researchers also questioned participants about their willingness to wait for the test result. The vast majority 96% - said they were willing to wait an hour or more.
The Chlamydia Rapid Test has received regulatory approval and is on the market in France, where it is used in clinics, and will shortly come onto the market in Spain, Portugal, Italy and a number of other European countries.
"If we are to stem the tide in the spread of Chlamydia, we have to step up a gear in our ability to diagnose and treat this infection," says Dr Ted Bianco, Director of the Wellcome Trust's Technology Transfer Division, which funded the development of the test. "Right now, our tests are too slow to permit on the spot treatment or too insensitive to detect an adequate proportion of cases. The new assay offers a way forward. Health authorities everywhere that are serious about tackling Chlamydia need to put this 'test to the test' in the context of their national programmes of control."
It is hoped that the new test will also be of particular use in the developing world, where management of Chlamydia in men is often based on self-diagnosis and specific diagnostic tests are rarely available. A high prevalence of Chlamydia infection amongst sex workers in these countries means that male customers are likely to transmit infection to other sexual partners. The Chlamydia Rapid Test requires minimum instrumentation and does not need to be carried out by a medically-trained professional.
WEDNESDAY July 29, 2009---------------------------News Archive / Return to News Alerts
Being An Active Preschooler Pays Off Throughout Childhood
Being active at age 5 helps kids stay lean as they age even if they don't remain as active later in childhood, a new University of Iowa study shows
"We call this effect 'banking' because the kids benefit later on, similar to having a savings account at a bank. The protective effect is independent of what happens in between," said lead author Kathleen Janz, professor of health and sport studies in the UI College of Liberal Arts and Sciences. "The implication is that even 5-year-olds should be encouraged to be as active as possible because it pays off as they grow older."
The UI team tested the body fat and activity level of 333 kids at ages 5, 8 and 11 using gold-standard technology: a special scanner that accurately measures bone, fat and muscle tissue, and an accelerometer that measures movement every minute. The kids wore accelerometers to record their activity level for up to five days, providing much more reliable data than relying on kids or parents to track minutes of exercise.
The study, published this month in the American Journal of Preventive Medicine, indicates that kids who are active at age 5 end up with less fat at age 8 and 11, even when controlling for their accumulated level of activity.
The average 5-year-old in the study got 30 minutes of moderate to vigorous exercise per day. For every 10 minutes on top of that, kids had one-third of a pound less fat tissue at ages 8 and 11.
Janz said further investigation is needed to learn what happens to the active kids' bodies that keeps them in better shape down the road. It may be possible that the active 5-year-olds didn't develop as many fat cells, improved their insulin response, or that something happened metabolically that provided some protection even as they became less active.
The study also indicated that boys are more likely to experience the sustained benefit from being active as preschoolers, possibly because they are more active at age 5 than girls, highlighting a need to especially encourage young girls to exercise.
"The CDC recommends that kids get at least 60 minutes of age-appropriate physical activity every day, and an activity like coloring madly won't cut it," Janz said.
The challenge is that it can be difficult to measure minutes of activity, since kids exert themselves in short bursts -- think sprinting after a ball -- rather than continuous activities, like jogging. So what can parents do?
"Avoid long periods -- more than 60 minutes -- of sedentary activity, insist that schools provide morning and afternoon recesses and whenever possible get kids outside. Kids who meet the CDC activity recommendations tend to be kids who spend a fair amount of time outdoors enjoying unstructured play," Janz said. "In the end, it doesn't take that much extra physical activity to see a measurable outcome. Even 10 extra minutes a day makes a difference in protecting against excessive fat gains."
Common Household Pesticides Linked To Childhood Cancer
A new study by researchers at the Lombardi Comprehensive Cancer Center at Georgetown finds a higher level of common household pesticides in the urine of children with acute lymphoblastic leukemia (ALL), a cancer that develops most commonly between three and seven years of age
The findings are published in the August issue of the journal Therapeutic Drug Monitoring. Researchers caution that these findings should not be seen as cause-and-effect, only that the study suggests an association between pesticide exposure and development of childhood ALL.
“In our study, we compared urine samples from children with ALL and their mothers with healthy children and their moms. We found elevated levels of common household pesticides more often in the mother-child pairs affected by cancer,” says the study’s lead investigator, Offie Soldin, PhD, an epidemiologist at Lombardi. Soldin cautions, “We shouldn’t assume that pesticides caused these cancers, but our findings certainly support the need for more robust research in this area.”
The study was conducted between January 2005 and January 2008 with volunteer participants from Lombardi and Children’s National Medical Center who live in the Washington metropolitan area. It included 41 pairs of children with ALL and their mothers (referred to as "cases"), and 41 pairs of healthy children and their mothers (referred to as "controls"). For comparison purposes, the case pairs were matched with control pairs by age, sex and county of residence.
Previous studies in agricultural areas of the country have suggested a relationship between pesticides and childhood cancers, but researchers say this is the first study conducted in a large, metropolitan area.
Urine samples were collected from all child-mother pairs and analyzed by the Centers for Disease Control and Prevention to look for evidence of organophosphates (OP), the chemical name of some household pesticides.
The body breaks down OP into metabolites which can be tracked in urine samples. The researchers say pesticides were detected in the urine of more than half of the participants, but levels of two common OP metobolites, diethylthiophosphate (DETP) and diethyldithiophosphate (DEDTP), were higher in the children with ALL compared to the control children.
Also for the study, the mothers completed a questionnaire to collect information about the family’s exposure to pesticides, their medical history, home and neighborhood characteristics, diet, and history of smoke exposure.
More case mothers (33 percent) than controls (14 percent) reported using insecticides in the home (p<0.02), however there was no correlation found between high levels of the OP metabolites in urine and reported use of pesticides.
“We know pesticides sprays, strips, or ‘bombs,’ are found in at least 85 percent of households, but obviously not all the children in these homes develop cancer. What this study suggests is an association between pesticide exposure and the development of childhood ALL, but this isn’t a cause-and-effect finding,” Soldin explains.
“Future research would help us understand the exact role of pesticides in the development of cancer. We hypothesize that pre-natal exposure coupled with genetic susceptibility or an additional environmental insult after birth could be to blame.” .
Mom & Dad's Genes' Play Tug-of-War Well Into Childhood
An analysis of rare genetic disorders in which children lack some genes from one parent suggests that maternal and paternal genes engage in a subtle tug-of-war well into childhood, and possibly as late as the onset of puberty
This striking new variety of intra-family conflict, described this week in the Proceedings of the National Academy of Sciences, is the latest wrinkle in the two-decades-old theory known as genomic imprinting, which holds that each parent contributes genes that seek to nudge his or her children's development in a direction most favorable, and least costly, to that parent.
"Compared to other primates, human babies are weaned quite early, yet take a very long time to reach full nutritional independence and sexual maturity," says author David Haig, George Putnam Professor of Organismic and Evolutionary Biology in Harvard University's Faculty of Arts and Sciences. "Human mothers are also unusual among primates in that they often care for more than one child at a time. Evidence from disorders of genomic imprinting suggests that maternal and paternal genes may skirmish over the pace of human development."
Previous research has offered evidence of a genetic struggle for supremacy only during fetal development: In the womb, some genes of paternal origin have been shown to promote increased demands on mothers, leading to fetal overgrowth, while genes of maternal origin tend to have the opposite effect. This new work suggests maternal and paternal genes continue to engage in internal genetic conflict past childbirth.
"This analysis suggests that human life history, and especially humans' unusual extended childhood, may reflect a compromise between what's best for mothers, fathers, and the offspring themselves," Haig says.
Haig delved into clinical case reports on patients with four rare genetic disorders. He found evidence that children with disorders characterized by dominance of some maternal genes -- Silver-Russell syndrome, Prader-Willi syndrome, and Temple syndrome -- place fewer demands on their mothers' resources.
For example, newborns with all three disorders display a weak desire to nurse, and slower childhood growth in general. Many also show early onset of puberty, which often marks a point at which children become less dependent on their mothers' sustenance.
Conversely, babies with Beckwith-Wiedemann syndrome, in which some maternally derived genes are suppressed and paternal genes dominate, are born heavy with particularly large tongues. These individuals usually end up being tall, owing to their rapid growth both in the womb and as young children. They have a high frequency of childhood cancers.
"Clinical data from imprinting disorders suggest paternally-expressed genes promote, and maternally-expressed genes inhibit, childhood growth," Haig writes.
Haig adds that further longitudinal study of feeding and development in individuals with Silver-Russell syndrome, Prader-Willi syndrome, Temple syndrome, and Beckwith-Wiedemann syndrome is needed to more fully understand the role of genomic imprinting in such disorders.
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Precursor Sperm Cells Can Be Converted Into Other Cell Types
Researchers have found a way to directly convert spermatogonial stem cells, the precursors of sperm cells, into tissues of the prostate, skin and uterus
Their approach, described this month in the journal Stem Cells, may prove to be an effective alternative to the medical use of embryonic stem cells.
The hunt for alternatives to embryonic stem cells has led to some promising yet problematic approaches, some of which involve spermatagonial stem cells (SSCs). Researchers recently observed, for example, that SSCs grown in the laboratory will eventually give rise to a few cells that look and act like embryonic stem cells. This process can take months, however, and only a small percentage of the SSCs are converted into "embryonic stem-like" cells.
Other researchers have used viruses to insert genes into SSCs that will spur them to turn into ES-like cells. But this approach is difficult and the use of viruses to ferry in the needed genes has caused concern.
The new method, recently developed at the University of Illinois, takes advantage of the unusual interaction of two tissue types: the epithelium and the mesenchyme. The epithelium lines the cavities and surfaces of glands and many organs and secretes enzymes and other factors that are essential to the function of these tissues. The mesenchyme is the connective tissue in embryos. (In adults, the connective tissue is called stroma.)
In the 1950s, scientists discovered that the epithelium takes its developmental instructions from the mesenchyme. For example, when researchers put bladder epithelial cells on the mesenchyme of a prostate gland, the bladder cells were changed into prostate epithelium. The prostatic mesenchyme had altered the fate of the bladder epithelium.
"The mesenchyme it's the director; it's controlling the show," said University of Illinois veterinary biosciences professor Paul Cooke, who led the new study with postdoctoral researcher Liz Simon.
Cooke began the effort with what even he considered an unlikely proposition. "Could we take spermatagonial stem cells and cause them to directly change into other cell types by putting them with various mesenchymes and growing them in the body?" he said. "I thought it was possible, but I didn't think it would work."
The experiment did work, however. When Simon placed SSCs from inbred mice on prostate mesenchyme and grafted the combination into living mice, the SSCs became prostatic epithelium. When combined with skin mesenchyme and grown in vivo, the SSCs became skin epithelum. The researchers were even able to convert SSCs into uterine epithelium by using uterine mesenchyme. The newly formed tissues had all the physical characteristics of prostate, skin or uterus, and produced the telltale markers of those tissue types, Cooke said. They also stopped looking and behaving like SSCs.
To assure that their tests were not contaminated with epithelial cells from the source of the mesenchyme cells, the researchers repeated the experiments using a mouse whose cells contained a gene that fluoresces green under ultraviolet light. The SSCs were obtained from a green-fluorescing mouse, but the mesenchyme came from a non-fluorescing mouse. This enabled the researchers to trace the fate of the SSCs. If the newly formed prostatic epithelium glowed green even though the mesenchyme did not, for example, the researchers knew that the SSCs had been converted into prostatic epithelium.
Cooke hopes that a more streamlined approach can be developed that makes use of a man's own SSCs and stroma (the adult equivalent of the mesenchyme) to produce new skin cells or other tissues when needed for example, to replace skin damaged in a burn. And his team is investigating the use of ovarian stem cells instead of SSCs to see if the same results can be obtained with ovarian tissue.
TUESDAY July 28, 2009---------------------------News Archive / Return to News Alerts
How The body's Immune Cells Decide What To Destroy
The mechanism used by 'Natural Killer' immune cells in the human body to distinguish between diseased cells, which they are meant to destroy, and normal cells, which they are meant to leave alone, is revealed in new detail in research published today (Tuesday 28 July) in PLoS Biology.
Understanding how this aspect of the body's natural defences works could help medical researchers develop new ways of boosting these defences to treat disease.
Natural Killer (NK) cells - a type of white blood cell - are a major component of the human body's innate immune system. Over 1,000 NK cells are found in every drop of blood. They provide a fast frontline defence against tumours, viruses and bacterial infections, by latching onto and killing cells in the human body that are cancerous or are infected with a virus or a bacterial pathogen.
On their journey round the human body NK cells regularly latch onto normal non-diseased cells too, before moving off, leaving them unharmed. Previously, the process by which NK cells made the right decision to kill or not kill another cell was unclear.
Now, a team of researchers from Imperial College London have used high speed microscopy imaging techniques to observe the NK cell decision making process in action. This has revealed striking differences in the behaviour of NK cells when interacting with healthy or diseased cells.
The outcome of the decision making process is determined by how receptors on the surface of the NK cell interact with proteins on the surface of the captured cell. Every NK cell has two types of surface receptors - activators, which turn the killing mechanism 'on' and inhibitors which turn the killing mechanism 'off'.
Professor Davis and his colleagues discovered that if a captured cell is diseased or cancerous, it interacts with a large number of the NK cell's activating receptors, which makes the NK cell stop dead in its tracks and spread out over the captured cell. During this spreading process the NK cell continuously reads the 'on' and 'off' signals from its surface contact with the captured cell. If the 'on' signals dominate, the NK cell prolongs contact with the captured cell and eventually kills it.
Conversely if the captured cell is healthy, it interacts with more of the NK cell's inhibiting receptors - and fewer of its activating receptors - meaning that the 'off' signals dominate and the 'stopping and spreading' process does not occur, allowing the NK cell to quickly move off in search of a new target.
Principal investigator of the new study, Professor Dan Davis from Imperial College London's Department of Life Sciences, explains:
"Scientists have known for a long time that the proteins on the surface on Natural Killer cells are involved in answering the 'to kill or not to kill?' question, but we've not known exactly how these molecular cues are translated into the correct response. Our research has shown that information gleaned from its surface receptors tells the Natural Killer cell whether to stop patrolling and commence killing, or to move off quickly, and harmlessly, in search of another target."
Dr Fiona Culley, lead author of the study from the National Heart and Lung Institute at Imperial, says that finding out how NK cells use this process to sift out diseased cells from normal ones paints a very clear picture of how these cells do their vital work:
"Considering that NK cells play such an important part in our immune response to cancer and disease, relatively little is known about their functionality - how exactly they work and how they interact with the cells they encounter inside us. This study adds significantly to our understanding of how Natural Killer cells distinguish between healthy and diseased cells."
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The Metabolic Effects of Assisted Reproduction on Offspring
Research to be presented at the Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB), the foremost society for research into all aspects of eating and drinking behavior, finds that assisted reproductive techniques alter the expression of genes that are important for metabolism and the transport of nutrients in the placenta of mice
The results underscore the need for greater understanding of the long-term effects of new assisted reproductive techniques in humans.
Millions of children, roughly 1-2% of all births in the U.S. and Europe, have been born to couples experiencing fertility problems through the use of assisted reproductive techniques (ART) such as in vitro fertilization (IVF). However, relatively little research has been conducted to evaluate the long term effects of ART.
It is suggested that children born following some assisted reproductive techniques have increased incidence of metabolic problems, such as higher blood pressure, higher fasting glucose levels and more body fat.
Mice generated through IVF show similar problems, and new research suggests that this may be linked to altered expression of genes in the placenta that are important for fetal growth and development before birth. “Our preliminary data suggest that transfer of nutrients or growth factors from mother to fetus may be changed by assisted reproductive techniques, and this change may contribute to increased body weight and decreased glucose tolerance in the adult offspring”, said the lead author of the study, Kellie Tamashiro.
The researchers are interested in examining the effect of assisted reproductive techniques on the metabolic status of offspring using a mouse model. In the current study, they measured the expression of genes important for transporting nutrients and growth factors from the mother to the fetus during pregnancy.
They measured insulin-like growth factor 2 (Igf2) and glucose transporters 1 and 3 (Glut1 and Glut3) in placentas from female mice impregnated either by natural mating or by one of two different assisted reproductive techniques: in vitro fertilization (IVF) and intracytoplasmic sperm injection (ICSI). IVF involves incubating egg and sperm together, and is the most common form of assisted reproduction in humans. ICSI is increasingly used in the clinical setting to address male infertility. The ICSI technique involves injecting the sperm’s head directly into the egg since the sperm is unable to fertilize the egg on its own.
Mouse embryos derived from IVF and ICSI were transferred to a surrogate mother mouse, and the pups were delivered by caesarean-section. IVF and ICSI increased Glut1 and Glut3 expression in the placenta compared with natural mating. These results suggest that artificial manipulations used in assisted reproductive techniques may increase offspring susceptibility to metabolic consequences through alterations in placental nutrient transfer from mother to the fetus.
“It is important to point out that it is premature to extrapolate these preliminary results in mice directly to humans. Further evaluation of assisted reproductive techniques and their long term effects are required. Rigorous testing of new assisted reproductive techniques prior to their use in clinical settings is needed to determine their safety for both mother and child”, said Tamashirol.
Overhauling The Old Immune System Model of Operation
Research at the Walter and Eliza Hall Institute into the mechanics of how two types of white blood cells grow and die is fundamentally changing the development of computer models used to predict how immune system cells respond to pathogens
A team led by Professor Phil Hodgkin, head of the institute’s Immunology Division, is investigating the proliferation and survival of T and B lymphocytes white blood cells that are crucial to the body’s ability to generate immunity.
When lymphocytes are exposed to pathogens they are stimulated to undergo a series of cell divisions, which increases their number of lymphocytes many hundredfold. After a period of time, the cells stop dividing and 95 per cent of the newly-generated cells die.
Although there is considerable variation in the number of divisions cells go through before they die, existing computer models assume all cells are mechanically identical. However, biologists have long been aware that cells never behave identically. But variation is usually dismissed as ‘noise’ or irrelevant biologically.
“About 10 years ago I was struck by the thought that by ignoring the immense amount of variation in cells we might be missing something important,” said Professor Hodgkin. “What if the variation is a design feature of the cells? What if they’re doing it deliberately? My lab has been pursuing the implications of this idea ever since.”
In order to revamp existing computer models of the immune response and capture individual cellular response, Drs Edwin Hawkins, John Markham and Mr Liam McGuinness at the Walter and Eliza Hall Institute, for the first time followed hundreds of lymphocytes and their offspring through all their cell divisions until their deaths. They also recorded how this variation in lymphocyte behaviour was transmitted through each cell generation. The research has been published today in the Proceedings of the National Academy of Sciences USA.
“We found that all the offspring of a single cell died at the same cell division; their lifespan is programmed from that very first cell,” says Hodgkin. “We also observed that cell ‘siblings’ took a similar amount of time to die. This tells us that a very large part of the fate of individual cells is locked in and programmed early.”
To Hodgkin, it appeared that when a lymphocyte first divided - chemicals produced were progressively diluted as the cell went through each division. When these chemicals fell below a certain threshold, the cells stopped dividing and died.
“With accurate information on the time it takes for a lymphocyte to divide, the time taken to die and the number of cell divisions an individual cell goes through, we can develop new mathematical models that are correct not only at a single-cell level but that also hold true for a whole population of cells.”
Accurate computer-based models of the immune response are a holy grail for scientists as they promise to unlock new therapies for infectious diseases, and allow careful investigation of autoimmune conditions.
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Making Implantable Bone Material, Thanks to Stem Cells
Scientists are closer to understanding how to grow replacement bones with stem cell technology, thanks to research published today in the journal Nature Materials
Many scientists are currently trying to create bone-like materials, derived from stem cells, to implant into patients who have damaged or fractured bones, or who have had parts of diseased bones removed. The idea is that, ultimately, these bone-like materials could be inserted into cavities so that real bone could meld with it and repair the bone.
So far, scientists have found they can grow small ‘nodules’ of what appears to be bone-like material in the laboratory from different types of bone cells and stem cells. All of these cell types are attracting considerable interest as promising candidates for future implants in people with clinical trials already underway. However, scientists still need to thoroughly explore and understand the in-depth chemical properties and structure of the bone-like materials they are growing.
Now, scientists from Imperial College London have compared the ‘bone-like’ material grown from three different commonly used clinically relevant cell types and have discovered significant differences between the quality of bone-like material that these can form.
For example, the researchers have discovered that the ‘bone-like’ materials that were grown from bone cells from mouse skull and mouse bone marrow stem cells successfully mimicked many of the hallmarks of real bone, which include stiffness. However, they found that the ‘bone-like’ material grown from mouse embryonic stem cells was much less stiff and less complex in its mineral composition when compared to the other materials. The researchers suggest that further research is now needed to explore the implications of these results for different stem cell therapies.
MONDAY July 27, 2009---------------------------News Archive / Return to News Alerts
Pinpointing The Cause Of Colic
Researchers at The University of Texas Health Science Center at Houston say one organism discovered during their study may unlock the key to what causes colic, inconsolable crying in an otherwise healthy baby
“Right now, pediatric gastroenterologists can treat just about anything that comes through the door,” said J. Marc Rhoads, M.D., professor of pediatrics at The University of Texas Medical School at Houston, which is part of the UT Health Science Center at Houston. “With colic, there is no evidence-based treatment we can offer. Colic can be a dangerous situation for a baby. The parent’s frustration over the crying can lead to maternal frustration, post-partum depression and even thoughts of harming the baby.”
Published in today’s online edition of the Journal of Pediatrics, the study pointed to an organism called Klebsiella, a normally occurring bacterium that can be found in the mouth, skin and intestines. In the study of 36 babies, half of which had colic, researchers found the bacterium and gut inflammation in the intestines of the babies with colic.
“We believe that the bacterium may be sparking an inflammatory reaction, causing the gut inflammation,” said Rhoads, the lead investigator for the study. “Inflammation in the gut of colicky infants closely compared to levels in patients with inflammatory bowel disease. Colic could prove to be a precursor to other gastrointestinal conditions such as irritable bowel syndrome, celiac disease and allergic gastroenteropathies.”
Babies in the study were fed breast milk and/or formula. Previous research articles have not shown significant data supporting the theory that breastfeeding protects infants against colic. The babies in the study were recruited from UT Physicians’ pediatric clinics and Kelsey-Seybold clinics.
Colic is defined as unexplained and severe crying in an otherwise healthy newborn. It usually occurs in infants three months old or younger and lasts for more than three hours daily for at least three days a week.“Colic is a very common condition. It affects about 15 percent of normal, healthy infants. More than half of infanticides fall into the age category of colic. We may be able to prevent deaths if we can find a treatment,” Rhoads said.
Right now, pediatricians prescribe special hypoallergenic infant formula to try and treat colic, but none of it has been proven in studies to be effective in treating the condition.
“During our study, we also found that the babies that didn’t have colic had more types of bacteria in their intestines. The presence of more bacteria may indicate that specific bacterial species (phylotypes) are beneficial to humans,” Rhoads said.
The study was funded by the Gerber Foundation.
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Research Links Type 2 Diabetes To Faulty Immune System
Crack open the latest medical textbook to the chapter on type 2, or adult-onset, diabetes, and you'll be hard pressed to find the term "immunology" anywhere - because metabolic conditions and immunologic conditions are, with a few exceptions, distant cousins
However, a group of papers appearing in Nature Medicine, two of which are from Harvard Medical School researchers, have linked type 2 diabetes with immunology in a way that might persuade leading researchers to start viewing them as siblings.
In the first study, researchers used two common over-the-counter allergy medications to reduce both obesity and type 2 diabetes in mice. The medications, called Zaditor and cromolyn, stabilize a population of inflammatory immune cells called mast cells. In the second study, researchers found that a kind of white blood cell called a regulatory T cell, once thought to manage only other white blood cells, also acts as a liaison between the metabolic and immune systemsin this case, controlling inflammation in fat tissue. Fat tissue from obese and insulin-resistant mice and people is marked by a dramatic absence of this cell type, in dramatic contrast to an already reported overabundance in fat tissue of inflammatory immune cells called macrophages.
"It seems that we're seeing the emergence of a new biomedical discipline: immunometabolism," says HMS professor of pathology Diane Mathis, senior author on one of the papers. Both papers will appear online July 26 in Nature Medicine.
Type 1 and type 2 diabetes both involve abnormalities in the insulin-producing beta cells of the pancreas, but their root causes are completely different. Type 1 diabetes is an autoimmune disease in which the immune system attacks the pancreas, destroying its ability to produce insulin. In contrast, type 2 diabetes is a strictly metabolic condition in which cells grow increasingly deaf to insulin signals and thus lose their ability to metabolize glucose. In both cases, glucose mounts in the blood, at times to fatal levels.
But it is becoming increasingly clear that we should also think of type 2 diabetes in the context of immune function, Harvard scientists assert.
Guo-Ping Shi, Biochemist from the Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, began to suspect such a connection when, in a previous study, he found mast cells present in a variety of inflammatory vascular diseases. Mast cells are immune cells that facilitate healing in wounded tissue, primarily by increasing blood flow to the site. However, in certain conditions mast cells build up to levels far beyond what the body needs. As a result these cells become unstable and eventually, like punctured trash bags, leak molecular "garbage" into the tissue. This can result in chronic inflammation that causes asthma and certain allergies.
As Shi and postdoctoral research fellow Jian Liu discovered, mast cells were far more abundant in fat tissue from obese and diabetic humans and mice than they were in normal weight fat tissue. This led to an obvious question: by regulating mast cells, could we then control the symptoms?
To find out, Shi and colleagues took a group of obese and diabetic mice and, for a period of two months, treated them with either ketotifen fumarate (also called Zaditor) or cromolyn, both over-the-counter allergy drugs. "We knew from published research that both cromolyn and Zaditor help stabilize mast cells in people suffering from allergy or asthma," said Shi. "It's almost as if the drugs place an extra layer of plastic on the ripped trash bag. So it seemed like a logical place to begin."
The mice were divided into four groups. The first was the control group; the second group was simply switched to a healthy diet; the third was given cromolyn or ketotifen fumarate; and the fourth was both given the drug and switched to a healthy diet. While symptoms of the second group improved moderately, the third group demonstrated dramatic improvements in both body weight and diabetes. The fourth group exhibited nearly 100 percent recovery in all areas.
To bolster these findings, Shi and colleagues then took a group of mice whose ability to produce mast cells was genetically impaired. Despite three months of a diet rich in sugar and fat, these mice neither became obese nor developed diabetes. "The best thing about these drugs is that we know it's safe for people," says Shi. "The remaining question now is: Will this also work for people?" Shi now intends to test both cromolyn and ketotifen fumarate on obese and diabetic non-human primates.
Beyond friendly fire
In findings independent of Shi, researchers at Harvard Medical School and Joslin Diabetes Center discovered that a class of immune system cells called regulatory T cells, or Tregs, were abundant in the abdominal fat tissue of normal-weight humans and mice, but were virtually absent in the same tissue from obese and diabetic humans and mice.
Their numbers were inversely correlated with the numbers of a class of inflammatory immune cells, macrophages, in a sense creating parallel universes of fat. While obese and diabetic fat tissue was full of inflammatory macrophages and nearly absent of Tregs, normal-weight fat tissue was the diametric opposite.
"For immunologists this is very important, because Tregs had always been thought to control other T cells and that's it," says Markus Feuerer, a postdoctoral researcher in the lab of HMS professors of pathology Diane Mathis and Christophe Benoist. "But this is an entirely new concept." Mathis and Benoist collaborated on the study with Steven Shoelson, HMS professor of medicine at the Joslin Diabetes Center.
"I come at this studying the effects of obesity and why it can spread systemically to cause chronic health problems," says Shoelson, an endocrinologist. "It's possible that the inflammation caused by macrophages results in insulin resistance. And it's more likely, from what we've just seen, that Tregs are keeping the macrophages in check in normal fat tissue, thus preventing inflammation."
For over a decade, Tregs have been known as guardians for the immune system, ensuring that when white blood cells attack a foreign pathogen they don't become overzealous and harm healthy host tissue in a kind of friendly fire. Malfunctioning Tregs, however, have recently been implicated in diseases as diverse as multiple sclerosis and certain cancers.
"Now we're seeing that Tregs may be needed to prevent metabolic abnormalities as well," says Mathis. She adds, half joking, "As an immunologist, I always thought that type 2 diabetes was a pretty boring condition. After these findings, I'm starting to change my mind."
The Risk of Gaining Weight With Injectable Birth Control
Researchers at the University of Texas Medical Branch at Galveston have identified women who are likely to gain weight while using depot medroxyprogesterone acetate, more commonly known as Depo-Provera or the birth control shot. These findings dispel the myth that all women who use DMPA will gain weight and will help physicians to counsel patients appropriately.
“DMPA-related weight gain is linked to increased abdominal fat, a known component of metabolic syndrome, which raises the risk of obesity-related conditions such as cardiovascular disease, stroke and diabetes,” said corresponding author Dr. Abbey Berenson, professor in UTMB’s department of obstetrics and gynecology.
The researchers recommend that physicians tailor counseling based on women’s risk factors, closely monitor weight at each three-month follow-up visit and suggest a different contraception method to patients who gain significant weight within the first six months of use.
Researchers found that early gainers exhibited three major risk factors: A body mass index under 30, having children before starting DMPA and a self-reported increase in appetite after six months of DMPA use.
The study, which appears in the August issue of Obstetrics and Gynecology, followed 240 women ages 16-33 who used DMPA for up to three years. Researchers looked at several potential predictors of weight gain, including age, race, baseline obesity prior to DMPA use, lifestyle variables such as smoking and exercise level, and weight gain at six months. They found that those who had gained more than 5 percent of their body weight within six months, or after just two injections of DMPA, continued to gain significant weight during the next 30 months.
While previous studies have associated birth control-related weight gain with a higher BMI, Berenson’s study suggests that a lower BMI - under 30 - is more predictive. “The amount of DMPA administered to a woman does not change based on weight, as occurs with some medications,” Berenson said. “The drug may be more concentrated in the tissue of a woman with a BMI under 30 and may contribute to excessive weight gain, but more research is needed.”
The biological mechanism of DMPA-related weight gain is still unknown, but researchers note that possible mechanisms include glucocorticoid-like activity, how the body breaks down simple carbohydrates such as glucose, and DMPA-associated interference with insulin action. Previous findings seem to argue against the theory that weight gain could be due to the drug’s perceived effects on increased caloric intake and decreased energy expenditure, but ongoing research is needed to confirm or discount varying possible explanations.
DMPA is an injected contraceptive administered to patients every three months. According to the American College of Obstetricians and Gynecologists, more than 2 million American women use DMPA, including approximately 400,000 teens. DMPA is relatively inexpensive compared with some other forms of birth control, has a low failure rate and doesn’t need to be administered daily, which contributes to the contraceptive’s popularity.
This study builds upon UTMB research released earlier this year that found DMPA users gain significant weight not seen among women using oral or nonhormonal contraception. The study was supported by the National Institute of Child Health and Human Development. Yen-Chi L. Le, of UTMB’s department of obstetrics and gynecology, and Mahbubur Rahman, of UTMB’s Center for Interdisciplinary Research in Women’s Health, contributed to this research.
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Early Periods May Reduce Ovarian Cancer Survival
Women whose menstrual periods start at a young age are less likely to survive ovarian cancer than their peers whose periods start later, new research shows
Similarly, women who have more menstrual cycles over their lifetime also have worse survival.
"Although we have relatively good knowledge about the influence of reproductive factors on the risk of developing ovarian cancer, knowledge is rather limited regarding the reproductive factors that may influence survival after diagnosis with this serious disease," Dr. Cheryl L. Robbins said in a statement.
As reported in the journal Cancer Epidemiology, Biomarkers, and Prevention, Robbins' group analyzed data from 410 women with ovarian cancer who were enrolled in the Cancer and Steroid Hormone study (1980 to 1982). During 9 years of follow-up, 212 women died.
Menstrual period onset before 12 years of age increased the risk of death by 51 percent relative to periods beginning at age 14 or older.
The results also indicate that patients with the highest number of lifetime menstrual cycles were 67 percent more likely to die during follow-up than were those with the lowest number of cycles.
The 15-year survival rates for women with the most lifetime menstrual cycles and those with the fewest were 33.3 and 56.7 percent, respectively.
"The significance of this paper is in suggesting new research directions, not in any immediate treatment changes," Dr. Mary B. Daly, an editorial board member of Cancer Epidemiology, Biomarkers, and Prevention, said in a statement.