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Applied Biotechnology, Cancer, Genetics, Pediatrics, Research

Gene-sequencing rare tumors – and what it means for cancer research and treatment

Gene-sequencing rare tumors - and what it means for cancer research and treatment

Sequencing the genes of cancer patients’ tumors has the potential to surmount frustrating problems for those who work with rare cancers. Doctors who see patients with rare tumors are often unsure of which treatments will work. And, with few patients available, researchers are unable to assemble enough subjects to compare different therapies in gold-standard randomized clinical trials. But thanks to gene sequencing, that is about to change.

Though this specific research was not intended to shape the child’s treatment, similar sequencing could soon help doctors decide how to treat rare cancers in real time

That’s the take-away from a fascinating conversation about the implications of personalized tumor-gene sequencing that I had recently with two Stanford cancer experts. Cancer researcher Julien Sage, PhD, is the senior author of a recent scientific paper describing sequencing of a pediatric tumor that affects only one in every 5 million people. Alejandro Sweet-Cordero, MD, an oncologist who treats children with cancer at Lucile Packard Children’s Hospital Stanford, is leading one of Stanford’s several efforts to develop an efficient system for sequencing individual patients’ tumors.

In their paper, Sage’s team (led by medical student Lei Xu) analyzed the DNA and RNA of one child’s unusual liver tumor, a fibrolamellar hepatocellular carcinoma. The cause of this form of cancer has never been found. Curious about what genes drove the tumor’s proliferation, the scientists identified two genes that were likely culprits, both of which promoted cancer in petri dishes of cultured cells. One of the genes, encoding the enzyme protein kinase A, is a possible target for future cancer therapies.

Though this specific research was not intended to shape the child’s treatment, similar sequencing could soon help doctors decide how to treat rare cancers in real time. Sweet-Cordero is working to develop an efficient system for getting both the mechanics of sequencing and the labor-intensive analysis of the resulting genetic data completed in a few weeks, instead of the two to three months now required. “We’re trying to use this kind of technology  to really help patients,” Sage said. “If you’re dealing with a disease that may kill the patient very fast, you want to act on it as soon as possible.”

In addition to giving doctors clues about which chemotherapy drugs to try, gene sequencing gives them a new way to study tumors.

“What’s really important is that, instead of categorizing tumors based on how they look under a microscope, we’ll be able to categorize them based on their gene-mutation profile,” Sweet-Cordero said. Rather than setting up clinical trials based on a tumor’s histology, as doctors have done in the past, scientists will group patients for treatment trials on the basis of similar mutations in their tumors. “In my mind, as a clinical oncologist, this is the most transformative aspect of this technology,” he said. This is especially true for patients with rare tumors who might not otherwise benefit from clinical trials at all.

And for childhood cancers, knowing a tumor’s gene mutations could also help doctors avoid giving higher doses of toxic chemotherapy drugs than are truly needed.

“The way we’ve been successful in pediatric oncology is by being extremely aggressive,” Sweet-Cordero said. Oncologists take advantage of children’s natural resilience by giving extremely strong chemotherapy regimens, which beat back cancer but can also have damaging long-term side effects. “We end up over-treating significant groups of patients who could survive with less aggressive therapy,” Sweet-Cordero said. “If we can use genetic information to back off on really toxic therapies, we’ll have fewer pediatric cancer survivors with significant impairments.”

Meanwhile, Stanford cancer researchers are also tackling a related problem: the fact that not all malignant cells within a tumor may have the same genetic mutations, and they may not all be vulnerable to the same cancer drugs. Next month, the Stanford Cancer Institute is sponsoring a scientific symposium on the concept, known as tumor heterogeneity, and how it will affect the future of personalized cancer treatments.

Sage’s research was supported by the Lucile Packard Foundation for Children’s Health, Stanford NIH-NCATS-CTSA UL1 TR001085 and Child Health Research Institute of Stanford University. Sage and Sweet-Cordero are both members of the Stanford Cancer Institute, and the National Cancer Institute-designated Cancer Center.

Previously: Smoking gun or hit-and-run? How oncogenes make good cells go bad, Stanford researchers identify genes that cause disfiguring jaw tumor and Blood will tell: In Stanford study, tiny bits of circulating tumor DNA betray hidden cancers

Neuroscience, Pediatrics, Research, Stanford News

Kids’ brains reorganize as they learn new things, study shows

Kids' brains reorganize as they learn new things, study shows

arithmeticWhy do some children pick up on arithmetic much more easily than others? New Stanford findings from the first longitudinal brain-scanning study of kids solving math problems are shedding light on this question. The work gives interesting insight into how a child’s brain builds itself while also absorbing, storing and using new information. It turns out that the hippocampus, already known as a memory center, plays a key role in this construction project.

Published this week in Nature Neuroscience, the research focuses on what’s happening in the brain as children shift from counting on their fingers to the more efficient strategy of pulling math facts directly from memory. To conduct the study, the research team collected two sets of magnetic resonance imaging scans, about a year apart, on a group of grade-schoolers. From our press release:

“We wanted to understand how children acquire new knowledge, and determine why some children learn to retrieve facts from memory better than others,” said Vinod Menon, PhD, the Rachel L. and Walter F. Nichols, MD, professor of psychiatry and behavioral sciences at Stanford and the senior author of the study. “This work provides insight into the dynamic changes that occur over the course of cognitive development in each child.”

The study also adds to prior research into the differences between how children’s and adults’ brains solve math problems. Children use certain brain regions, including the hippocampus and the prefrontal cortex, very differently from adults when the two groups are solving the same types of math problems, the study showed.

“It was surprising to us that the hippocampal and prefrontal contributions to memory-based problem-solving during childhood don’t look anything like what we would have expected for the adult brain,” said postdoctoral scholar Shaozheng Qin, PhD, who is the paper’s lead author.

The study found that as children aged from an average of 8.2 to 9.4 years, they counted less and pulled facts from memory more when solving math problems. Over the same period, the hippocampus became more active and forged new connections with other parts of the brain, particularly several regions of the neocortex. But comparison groups of adolescents and adults were found on brain scans not to be making much use of the hippocampus when solving math problems. In other words, Menon told me, “The hippocampus is providing a scaffold for learning and consolidating facts into long-term memory in children.” And the stronger the scaffold of connections in an individual child, the more readily he or she pulled math facts from memory.

Now that the scientists have a baseline understanding of how this brain-building process normally works, they hope to run similar brain-scanning tests on children with math learning disabilities, with the aim of understanding what goes awry in the brains of children who really struggle with math.

Previously: Unusual brain organization found in autistic kids who best peers at math, Peering into the brain to predict kids’ responses to math tutoring and New research tracks “math anxiety” in the brain
Photo by Yannis

From August 11-25, Scope will be on a limited publishing schedule. During that time, you may also notice a delay in comment moderation. We’ll return to our regular schedule on August 25.

Autism, Pediatrics, Research, Stanford News

Stanford research clarifies biology of oxytocin in autism

Stanford research clarifies biology of oxytocin in autism

For years, scientists have been trying to sort out the role oxytocin plays in autism. The developmental disorder affects one in 68 U.S. children, causing social and communication deficits, repetitive behaviors and sensory problems. Oxytocin, which functions in the blood as a hormone and in the brain as a neurotransmitter, has long been known to have roles in enhancing social ability. Based on research in animal models, some people have speculated that oxytocin deficiency might contribute to autism. But prior human studies of the purported connection have produced a confusing picture.

The previous hypotheses saying that low oxytocin was linked to autism were maybe a little bit simplistic. It’s much more complex…

Now, a new Stanford paper publishing online this week in Proceedings of the National Academy of Sciences adds interesting details to our understanding. The study is the largest ever to examine blood oxytocin levels in children with autism and two comparison groups without autism: kids who have autistic siblings and children who do not have siblings with autism.

The researchers found the same range of blood oxytocin levels across all three groups, with similar numbers of children with low, medium and high oxytocin levels in each category. Although, as expected, the kids with autism had social deficits, blood oxytocin level was clearly linked to social ability within each group. Children with autism who had low blood oxytocin had poorer social ability than autistic children with high blood oxytocin, for example, and typically developing kids with low blood oxytocin also had poor social ability compared to other typically developing children.

From our press release on the research:

“It didn’t matter if you were a typically developing child, a sibling or an individual with autism: Your social ability was related to a certain extent to your oxytocin levels, which is very different from what people have speculated,” said Antonio Hardan, MD, professor of psychiatry and behavioral sciences and the study’s senior author. Hardan is a child and adolescent psychiatrist who treats children with autism at [Lucile Packard Children's Hospital Stanford].

“The previous hypotheses saying that low oxytocin was linked to autism were maybe a little bit simplistic,” he said. “It’s much more complex: Oxytocin is a vulnerability factor that has to be accounted for, but it’s not the only thing leading to the development of autism.”

The findings suggest that, although oxytocin deficiency may not explain all cases of autism, some kids with autism may still benefit from oxytocin-like medications. The researchers caution that their study needs to be repeated with measures of oxytocin in cerebrospinal fluid, since this liquid that bathes the brain may give better information about the nuances of oxytocin biology.

A Duke University scientist commented for a story on NPR’s health blog, Shots, about what the findings imply for the potential value of oxytocin therapy:

“It could be that if a kid has low oxytocin levels then they might benefit,” says Simon Gregory, a genomics researcher at Duke University who was not involved in the study. He is part of another group investigating the use of oxytocin to treat people with autism.

Gregory says it’s not surprising that children with autism have widely varying levels of oxytocin. “Autism isn’t a disease, it’s a spectrum” that can’t be linked to any one cause, he told Shots.

Stanford’s research team is also doing more work to clarify further details of the biology of oxytocin in autism.

Previously: Volunteers sought for autism drug study, Using Google Glass to help individuals with autism better understand social cues and “No, I’m not ready yet”: A sister’s translation for her brother with autis

Autism, Neuroscience, Pediatrics, Research, Stanford News

Finding of reduced brain flexibility adds to Stanford research on how the autistic brain is organized

Finding of reduced brain flexibility adds to Stanford research on how the autistic brain is organized

A Stanford brain-imaging study has just shown that the brains of children with autism are less able to switch from rest to taking on a new task than the brains of typically developing children.

According to the study, which appears this week in the scientific journal Cerebral Cortex, instead of changing to accommodate a job, connectivity in key brain networks of autistic children looks similar to connectivity in the resting brain. The degree of inflexibility was linked to the intensity of children’s autism symptoms: those with less flexibility had more severe restrictive and repetitive behaviors, one of the hallmarks of the developmental disorder.

From our press release on the research:

“We wanted to test the idea that a flexible brain is necessary for flexible behaviors,” said Lucina Uddin, PhD, a lead author of the study. “What we found was that across a set of brain connections known to be important for switching between different tasks, children with autism showed reduced ‘brain flexibility’ compared with typically developing peers.” Uddin, who is now an assistant professor of psychology at the University of Miami, was a postdoctoral scholar at Stanford when the research was conducted.

“The fact that we can tie this neurophysiological brain-state inflexibility to behavioral inflexibility is an important finding because it gives us clues about what kinds of processes go awry in autism,” said Vinod Menon, PhD, the Rachel L. and Walter F. Nichols, MD, professor of psychiatry and behavioral sciences at Stanford and the senior author of the study.

The study is the first to examine unusual patterns of connectivity in the brains of children with autism while they are performing tasks; Menon’s team has previously published research on connectivity between different regions of the autistic brain at rest. Some regions of the autistic brain are over-connected to each other, that work has shown, and the degree of over-connection is linked to children’s social deficits, perhaps in part because it interferes with their ability to derive pleasure from human voices. Menon’s lab has also explored how differences in the organization of the autistic brain may contribute to better math performance in some people with autism.

“We’re making progress in identifying a brain basis of autism, and we’re starting to get traction in pinpointing systems and signaling mechanisms that are not functioning properly,” Menon told me. “This is giving us a better handle both in thinking about treatment and in looking at change or plasticity in the brain.”

Previously: Greater hyperconnectivity in the autistic brain contributes to greater social deficits, Unusual brain organization found in autistic kids who best peers at math and Stanford study reveals why human voices are less rewarding for kids with autism

Genetics, In the News, Pediatrics, Research

New Yorker story highlights NGLY1 research

New Yorker story highlights NGLY1 research

PackardGirl260x190The new issue of the New Yorker, out today, includes a fascinating medical story with a notable Stanford connection. As we’ve described before, a team of scientists from institutions around the world reported earlier this year on their discovery of a new genetic disease, NGLY1 deficiency. Stanford’s Gregory Enns, MB, ChB, was co-lead author of the paper describing the new finding, and one of his patients, Grace Wilsey, was among the small group of children in whom the disease first was identified. Grace’s inability to make tears when she cries was a key clue in unlocking the mystery of the disease.

But, as the New Yorker piece (subscription required) explains in detail, there’s much more to the story than that. In particular, it tells how the families of patients – especially Grace’s parents, Matt and Kristen Wilsey, and Matt and Cristina Might, who are the parents of index patient Bertrand Might – successfully encouraged researchers at different institutions to collaborate with each other in a way that advanced the discovery with exceptional speed. This was counter to the usual practice in science, the story explains. Typically, scientists avoid sharing data with competitors, even if doing so would advance the research:

If a team hunting for a new disease were to find a second case with the help of researchers from a competing lab, it could claim to have “solved” a new disease. But it would also have to share credit with competitors who may have done nothing more than grant access to existing data. When I asked [Duke University geneticist and NGLY1 deficiency co-discoverer Vandana] Shashi if she could imagine a scenario that would result in one research team’s publishing a paper with data from a different research group working on a similar project, she said, “Not that I can think of.”

David Goldstein [another Duke geneticist who collaborated with Shashi] added, “It’s not an overstatement to say that there are inherent conflicts of interest at work.” Daniel MacArthur, a genetics researcher at Massachusetts General Hospital, is even more blunt. “It’s an enormous deal,” he told me. “And it’s a big criticism of all of us, but it’s a criticism we all need to hear. The current academic publication system does patients an enormous disservice.”

Fortunately for patients like Grace and Bertrand, and for the doctors who want to help them, the culture is shifting. One marker of the shift is the NIH’s announcement earlier this month that it will be expanding its Undiagnosed Diseases Program to a network of seven sites across the country (including Stanford) and building in a requirement that all seven centers share data with each other.

Another is that researchers are realizing that families like the Wilseys and Mights will continue to make an impact. In fact, the Wilsey family has recently launched the Grace Wilsey Foundation to raise awareness about NGLY1 deficiency and promote investigation of possible treatments for the disease.

As Shashi puts it at the conclusion of the New Yorker story:

“Gone are the days when we could just say, ‘We’re a cloistered community of researchers, and we alone know how to do this.’”

Previously: NIH network designed to diagnose, develop possible treatments for rare, unidentified diseases and Crying without tears unlocks the mystery of a new genetic disease
Photo of Grace Wilsey courtesy of Lucile Packard Children’s Hospital Stanford

Chronic Disease, Research, Science, Stanford News, Technology

Stanford team develops nanotech-based microchip to diagnose Type 1 diabetes

Stanford team develops nanotech-based microchip to diagnose Type 1 diabetes

Dr. Brian Feldman?s M.D. hold a computer chip that he develop that will benefit diabetic patients at the Stanford School of Medicine,  on Thursday, July 4, 2014.  ( Norbert von der Groeben/ Stanford School of Medicine )

Years ago, when patients showed up at the doctor with excessive thirst, frequent urination and unexplained weight loss – in other words, the classic symptoms of diabetes mellitus – diagnosing them was usually just a matter of checking for high blood sugar. Yes, they needed to be treated for the correct form of the disease, but the two main types were found in different populations. So, in most cases, no lab test was needed to figure out whether someone had Type 1 or Type 2 diabetes; demographic factors were enough to make the distinction.

Of late, there’s been much more cross-over between the two groups. To treat patients correctly, it’s important to diagnose the right form of diabetes, but there’s a problem: The only test that does so is expensive, cumbersome and available only in hospitals.

So it’s great news that Stanford scientists are developing a new Type 1 diabetes test, described in a paper published online this week in Nature Medicine. The new nanotechnology-based microchip, which researcher Brian Feldman, MD, PhD, holds in the photo above, tests patients’ blood for the auto-antibodies that cause Type 1 diabetes. The new test is cheap, portable, and uses much less blood than the older diagnostic test. Unlike the old test, it requires no radioactive reagents and is simple enough to use in low-tech settings.

The test uses a nanotech enhancement (specifically, nano-sized islands of gold; hence the golden glow of the chip that Feldman is holding) to help detect auto-antibodies. In addition to diagnosing new patients, this technology will also enable better research into how Type 1 diabetes develops, as our press release explains:

…[P]eople who are at risk of developing Type 1 diabetes, such patients’ close relatives, also may benefit from the test because it will allow doctors to quickly and cheaply track their auto-antibody levels before they show symptoms. Because it is so inexpensive, the test may also allow the first broad screening for diabetes auto-antibodies in the population at large.

“The auto-antibodies truly are a crystal ball,” Feldman said. “Even if you don’t have [Type 1] diabetes yet, if you have one auto-antibody linked to diabetes in your blood, you are at significant risk; with multiple auto-antibodies, it’s more than 90 percent risk.”

Feldman’s team has started a biotech company to further develop the test and is seeking FDA approval for the new method. In addition, Stanford University and the researchers have filed a patent for the new technique.

Previously: A simple blood test may unearth the earliest signs of heart transplant rejection, Stanford microbiologist’s secret sauce for disease detection and One family’s story on caring for their children with type 1 diabetes
Photo by Norbert von der Groeben

Patient Care, Research, Stanford News

New study shows standardization makes hospital hand-offs safer

New study shows standardization makes hospital hand-offs safer

A study published online this week in Pediatrics offers encouraging results from a large-scale effort to tackle a persistent safety problem in hospitals. The study is the first scientific investigation of a multi-hospital project to improve patient hand-offs, the times when a patient’s care is being transferred from one person to another.

When hand-offs go wrong, the doctors and nurses taking over a patient’s care may not understand the individual’s diagnosis or current problems. They might not know which tests have been completed or which medication doses have already been given. These types of errors can, at best, waste everyone’s time, and, at worst, harm patients.

Fortunately, these latest findings demonstrate how hospitals can cut back dramatically on such problems. The one-year study of 23 pediatric hospitals across the country found a significant drop in hand-off related care failures when the process was standardized. Researchers examined both shift changes and patient transfers from one hospital department to another. The rate of hand-off related care failures went from slightly over 25 percent at baseline to about 8 percent by the end of the study. (Researchers didn’t measure actual harm to patients, but rather communication failures that could have resulted in harm had they gone unnoticed.)

“Surprisingly, this manuscript was amongst the first of its kind to actually show a decrease hand-off-related care failures,” senior author Paul Sharek, MD, medical director of quality management and chief clinical patient safety officer at Lucile Packard Children’s Hospital Stanford, said in an e-mail.

How did they improve so dramatically? By defining every element of the hand-off, including the interactions’ intent, content, process and team leadership. At the end of the study, the researchers identified several elements of good hand-offs, including the need for active participation by both sending and receiving teams; a defined opportunity for the receiving team to ask questions; a script of all the important hand-off elements; and a summary of basic issues and next steps for each patient. Overall, caregivers were satisfied with the new process, suggesting they’d buy into it for the long run.

“Given the increasing recognition of the risk of hand-offs in health care, these findings reassure us that large-scale improvements in hand-0ff safety can be achieved rapidly,” the researchers write.

Previously: Less burnout, better safety culture in hospitals with hands-on executives, new study shows, How efforts to mine electronic health records influence clinical care and Automated safety checklists prevent hospital-acquired infections, Stanford team finds

Immunology, In the News, Infectious Disease, Parenting, Pediatrics, Public Health

Side effects of childhood vaccines are extremely rare, new study finds

Side effects of childhood vaccines are extremely rare, new study finds

Pneumococcus-vaccineAs you may have heard about elsewhere, a new paper published today on the safety of childhood vaccines provides reassurance for parents and pediatricians that side effects from vaccination are rare and mostly transient. The paper, a meta-analysis appearing in Pediatrics, updates a 2011 Institute of Medicine report on childhood vaccine safety. It analyzed the results of 67 safety studies of vaccines used in the United States for children aged 6 and younger.

“There are no surprises here; vaccines are being shown over and over again to be quite safe,” said Cornelia Dekker, MD, medical director of the vaccine program at Lucile Packard Children’s Hospital Stanford, who chatted with me about the study earlier today. “The safety record for our U.S.-licensed vaccines is excellent. There are a few vaccines for which they document that there are indeed adverse events, but the frequency is quite rare, and in almost all cases they are very easy to manage and self-limited.”

A Pediatrics commentary (.pdf) accompanying the new study puts the value of immunization in context:

Modeling of vaccine impact demonstrates that routine childhood immunizations in the 2009 US birth cohort would prevent ~42,000 deaths and 20 million cases of disease and save $13.5 billion in direct health care costs and $68.8 billion in societal costs.

The commentary goes on to contrast the risks of vaccines with the potential complications of vaccine-preventable diseases:

The adverse events identified by the authors were rare and in most cases would be expected to resolve completely after the adverse event. This contrasts starkly with the natural infections that vaccines are designed to prevent, which may reduce the quality of life through permanent morbidities, such as blindness, deafness, developmental delay, epilepsy, or paralysis and may also result in death.

The study found evidence against suspected links between vaccines and several acute and chronic diseases. For instance, the researchers found high-quality evidence that several different vaccines are not linked to childhood leukemia and that the measles, mumps and rubella (MMR) vaccine is not linked to autism. The DTaP vaccine is not linked to diabetes mellitus, and the Hepatitis B vaccine is not connected to multiple sclerosis, according to moderate-quality evidence.

The evidence does connect a few vaccines to side effects. For instance, the MMR, pneumococcal conjugate 13 and influenza vaccines are linked to small risks of febrile seizures, with the risk of such seizures increasing slightly if the PCV-13 and flu vaccines are given together.

“A febrile seizure can be quite alarming, but fortunately it does not have long-lasting consequences for child,” Dekker said, noting that the risk of such seizures from vaccines is around a dozen per 100,000 doses of vaccine administered.

The rotavirus vaccine is linked to risk of intussusception, an intestinal problem that can also occur with rotavirus infection itself. But the benefits of rotavirus vaccination “clearly outweigh the small additional risk,” Dekker said.

The study confirmed earlier research showing that some vaccines, including MMR and varicella, cause problems for immunocompromised children, such as kids who have HIV or who have received organ transplants. Since they can’t safely receive vaccines, this group of children relies on the herd immunity of their community to protect them.

“It’s not as if the parents of immunocompromised kids have a choice about whether to vaccinate,” Dekker told me. “They have to depend on others to keep immunization levels high, and that starts breaking down when more people hold back from having their healthy kids fully immunized.”

Dekker hopes the new findings will encourage more parents to have their healthy kids fully vaccinated.

Previously: Measles is disappearing from the Western hemisphere, Measles are on the rise; now’s the time to vaccinate, says infectious-disease expert and Tips for parents on back-to-school vaccinations
Photo by Gates Foundation

Global Health, In the News, Pediatrics, Public Safety, Sexual Health, Women's Health

Stanford research shows rape prevention program helps Kenyan girls “find the power to say no”

Stanford research shows rape prevention program helps Kenyan girls "find the power to say no"

The San Francisco Chronicle has a great story today about a collaborative project that is reducing rape and sexual assault of impoverished girls in Kenya.

The story highlights the combined efforts of activists Jake Sinclair, MD, and his wife, Lee Paiva Sinclair, who founded nonprofit No Means No Worldwide to provide empowerment training to Kenayn girls, and the Stanford team that has been analyzing the results of their efforts. As we’ve described before, this work is a great example of the academic chops of Stanford experts’ being combined with on-the-ground activism to make a difference for an urgent real-world problem.

As the article explains:

The girls and hundreds of others like them have participated in a rape-prevention workshop created by Jake Sinclair and Lee Paiva, a San Francisco doctor and his artist wife who have been working in Kenya for 14 years.

Their program is working, and that’s not just according to the dozen or so testimonials online, the couple said. Two studies out of Stanford – one published in April this year, one the year before – have found that girls who have gone through the couples’ classes experience fewer sexual assaults after the workshops.

More telling, perhaps: More than half of the girls report using some tool they learned from the classes to protect themselves, from kicking a man in the groin to yelling at someone to stop.

“It’s great to see the girls just find their voice, to find the power to say ‘no,’ ” Sinclair said. “It’s so enlightening. You can see it in their eyes, that something’s changed.”

Stanford research scholar Clea Sarnquist, DrPH, who has played an important role in the project, adds:

“A lot of these girls are using voice and verbal skills first,” Sarnquist said. “That’s one of the key things, is teaching the girls that they have the right to protect themselves – that they have domain over their own bodies, and they have the right to speak up for their own self interest.”

The whole story is definitely worth a read.

Previously: Empowerment training prevents rape of Kenyan girls and Self-defense training reduces rapes in Kenya

Big data, Obesity, Pregnancy, Public Health, Women's Health

Maternal obesity linked to earliest premature births, says Stanford study

Maternal obesity linked to earliest premature births, says Stanford study

preemiefeetExpectant mothers who are obese before they become pregnant are at increased risk of delivering a very premature baby, according to a new study of nearly 1,000,000 California births.

The study, which appears in the July issue of Paediatric and Perinatal Epidemiology, is part of a major research effort by the March of Dimes Prematurity Research Center at Stanford University School of Medicine to understand why 450,000 U.S. babies are being born too early each year. Figuring out what causes preterm birth is the first step in understanding how to prevent it, but in many cases, physicians have no idea why a pregnant woman went into labor early.

The new study focused on preterm deliveries of unknown cause, starting from a database of nearly every California birth between January 2007 and December 2009 to examine singleton pregnancies where the mother did not have any illnesses known to be associated with prematurity.

The researchers found a link between mom’s obesity and the earliest premature births, those that happen before 28 weeks, or about six months, of pregnancy. The obesity-prematurity connection was  stronger for first-time moms than for women having their second or later child. Maternal obesity was not linked with preterm deliveries that happen between 28 and 37 weeks of the 40-week gestation period.

From our press release about the research:

“Until now, people have been thinking about preterm birth as one condition, simply by defining it as any birth that happens at least three weeks early,” said Gary Shaw, DrPH, professor of pediatrics and the lead author of the new research. “But it’s not as simple as that. Preterm birth is not one construct; gestational age matters.”

The researchers plan to investigate which aspects of obesity might trigger very early labor. For example, Shaw said, the inflammatory state seen in the body in obesity might be a factor, though more work is needed to confirm this.

Previously: How Stanford researchers are working to understand the complexities of preterm birth, A look at the world’s smallest preterm babies and New research center aims to understand premature birth
Photo by Evelyn

Stanford Medicine Resources: