Category: Health

{Zika also may have serious effects on the heart, new research shows in the first study to report cardiovascular complications related to this virus, according to data being presented at the American College of Cardiology’s 66th Annual Scientific Session.}

In a study at the Institute of Tropical Medicine in Caracas, Venezuela, of nine adult patients with Zika and no previous history of cardiovascular disease, all but one developed a heart rhythm problem and two-thirds had evidence of heart failure.

It is known that Zika can cause microcephaly, a severe birth defect in babies born to women infected with the virus, and Guillain-Barré syndrome, a neurological condition that can lead to muscle weakness and, in severe cases, paralysis.

“We know that other mosquito-borne diseases, such as dengue fever and chikungunya virus, can affect the heart, so we thought we might see the same with Zika. But we were surprised by the severity, even in this small number of patients,” says Karina Gonzalez Carta, M.D., cardiologist and research fellow at Mayo Clinic and the study’s lead author.

The patients (six were female, and mean age was 47) were seen at the Department of Tropical Medicine in Venezuela within two weeks of having Zika-type symptoms. They reported symptoms of heart problems, most commonly palpitations followed by shortness of breath and fatigue. Only one patient had any previous cardiovascular problems (high blood pressure), and tests confirmed that all of the patients had active Zika infection. Patients underwent an initial electrocardiogram (EKG), a test that shows the electrical activity of the heart, and in eight of the patients, the EKG suggested heartbeat rate or rhythm concerns. These findings prompted a full cardiovascular workup using an echocardiogram, (24-hour) Holter monitor and a cardiac MRI study.

Serious arrhythmias were detected in eight patients: three cases of atrial fibrillation, two cases of nonsustained atrial tachycardia and two cases of ventricular arrhythmias. Heart failure was present in six cases. Of these, five patients had heart failure with low ejection fraction, when the heart muscle doesn’t pump blood as well as it should, and one had heart failure with preserved ejection fraction, when the heart becomes stiff and cannot relax or fill properly.

The patients have been followed since July 2016, and none of their cardiac issues have resolved, but symptoms have improved following treatment for heart failure or atrial fibrillation, Dr. Carta says.

“Following this research, we want patients who are suffering from Zika symptoms also to be aware of the cardiac symptoms because they might not connect the two,” Dr. Carta says. “The same is true for physicians because they might be focused on the Zika symptoms but not thinking about cardiac concerns.”

Dr. Carta will present the study, “Myocarditis, Heart Failure and Arrhythmias in Patients With Zika,” on Saturday, March 18, at 3:45 p.m. ET.

This study will be published simultaneously online in the Journal of the American College of Cardiology at the time of presentation.

Co-authors are: Iván Mendoza, M.D.; Igor Morr, M.D.; Francesca Misticchio, M.D.; Yolimar Meza, M.D.; Vicente Finizola, M.D.; Gerardo Chazzin, M.D.; Juan Marques, M.D.; all of Institute of Tropical Medicine in Caracas, Venezuela; Iván Mendoza Britto, M.D., Jackson Medical Group, Miami; and Thomas Allison, Ph.D., Mayo Clinic.

Source:Science Daily

{There are more than 25 drugs to control HIV, yet the virus remains one of the world’s biggest health problems. One of the many challenges with existing therapies is that a dormant version of the virus is always lurking in the background, ready to attack the immune system as soon as treatment is interrupted.}

Now, new research from The Rockefeller University and the National Institutes of Health suggests that treatment with two anti-HIV antibodies immediately after infection enables the immune system to effectively control the virus, preventing its return for an extended period.

“This form of therapy can induce potent immunity to HIV, allowing the host to control the infection,” says Michel Nussenzweig, head of the Laboratory of Molecular Immunology and an Investigator with the Howard Hughes Medical Institute. “It works by taking advantage of the immune system’s natural defenses, similar to what happens in some forms of cancer immunotherapy.”

The research was conducted in macaque monkeys, using a model of HIV infection called simian-human immunodeficiency virus (SHIV). Although this model does not precisely mimic human HIV infection, the findings suggest that immunotherapy should be explored as a way of controlling the virus and boosting an immune response that might be capable of controlling the infection in people. The study publishes on March 13 in Nature.

{{Long-term control}}

The two drugs used in the study, 3BNC117 and 10-1074, belong to a class of molecules called broadly neutralizing antibodies. They were discovered by the Nussenzweig laboratory in studies of “elite controllers,” people whose immune systems have a rare ability to fight off the virus. Each antibody binds to a different site of the virus, preventing its damaging effects from different angles.

13 monkeys were inoculated with the SHIV virus, and then given three intravenous infusions of the two antibodies over a two-week period. The treatment suppressed the virus to levels near or below the limit of detection, and its effect lasted for as long as six months. After the antibodies had cleared out of the monkeys’ bodies, the virus rebounded in all but one animal.

But then, 5 to 22 months later, something remarkable happened: six of the monkeys spontaneously regained control of the virus. Their virus levels once again plummeted to undetectable levels and remained suppressed for another 5 to 13 months.

These six monkeys were also able to maintain healthy levels of key immune cells after receiving the antibody infusions.

In addition, four other monkeys that did not regain complete control of the virus nevertheless showed promising responses to the treatment: they maintained extremely low viral loads and healthy levels of key immune cells for two to three years after infection. In total, 10 of the 13 monkeys benefitted from antibody immunotherapy.

{{Feasibility in humans}}

Nussenzweig and colleagues also investigated what aspect of the immune system was helping the monkeys ward off the virus’s return. They gave the six controller monkeys an antibody that targets and depletes a type of immune cell called cytotoxic T cells. Infusion of this antibody immediately increased the amount of SHIV in the monkeys’ blood and decreased cytotoxic T cell levels, indicating that these cells play a key role in preventing SHIV replication after therapeutic antibody infusion.

The researchers are now repeating this experiment after a longer exposure to the virus, waiting two to six weeks after SHIV infection before administering the therapeutic antibody infusions. This is how long it usually takes for an HIV-infected person to be diagnosed and able to receive treatment.

Clinical trials testing the antibody combination in humans are also underway at The Rockefeller University Hospital.

Source:Science Daily

{Lactobacillus affects mood, anxiety in mice; researchers optimistic findings should hold true in humans}

Researchers at the University of Virginia School of Medicine have reversed depression symptoms in mice by feeding them Lactobacillus, a probiotic bacteria found in live-cultures yogurt. Further, they have discovered a specific mechanism for how the bacteria affect mood, providing a direct link between the health of the gut microbiome and mental health.

Based on their findings, the researchers are optimistic that their discovery will hold true in people and are planning to confirm their findings in patients with depression.

“The big hope for this kind of research is that we won’t need to bother with complex drugs and side effects when we can just play with the microbiome,” explained lead researcher Alban Gaultier, PhD. “It would be magical just to change your diet, to change the bacteria you take, and fix your health — and your mood.”

Treating Depression

Depression is one of the most common mental health conditions in the United States, with up to 7 percent of people experiencing a major depressive episode, Gaultier noted. “It’s a huge problem and the treatments are not very good, because they come with huge side effects,” he said.

The role of the gut microbiome — the bacteria that live inside us — has been of tremendous interest to researchers studying depression and other health conditions, both mental and physical. Gaultier, of the UVA Department of Neuroscience and its Center for Brain Immunology and Glia, set out to see if he could find a concrete link between depression and gut health. “When you’re stressed, you increase your chance of being depressed, and that’s been known for a long, long time,” he said. “So the question that we wanted to ask is, does the microbiome participate in depression?”

The answer appears to be yes. Looking at the composition of the gut microbiome before and after mice were subjected to stress, Gaultier’s team found that the major change was the loss of Lactobacillus. With the loss of Lactobacillus came the onset of depression symptoms. Feeding the mice Lactobacillus with their food returned them to almost normal. “A single strain of Lactobacillus,” Gaultier observed, “is able to influence mood.”

He and his team then went on to determine the mechanism by which Lactobacillus influences depression. They found that the amount of Lactobacillus in the gut affects the level of a metabolite in the blood called kynurenine, which has been shown to drive depression. When Lactobacillus was diminished in the gut, the levels of kynurenine went up — and depression symptoms set in.

“This is the most consistent change we’ve seen across different experiments and different settings we call microbiome profiles,” explained researcher Ioana Marin, a graduate student who is finishing up her PhD. work. “This is a consistent change. We see Lactobacillus levels correlate directly with the behavior of these mice.”

Testing in Humans

Gaultier was careful to call the symptoms seen in mice as “depressive-like behavior” or “despair behavior,” as mice have no way to communicate that they are feeling depressed. But those symptoms are widely accepted as the best available model for looking at depression in creatures other than humans.

Based on the new findings, Gaultier plans to begin studying the effect in people as soon as possible. He intends to examine the effects of Lactobacillus on depression in patients with multiple sclerosis, a group in which the disorder is common. Promisingly, the same biological substances and mechanisms Lactobacillus uses to affect mood in mice are also seen in humans, suggesting the effect may be the same.

In addition to looking at the effects in people, the researchers are continuing to explore the important role of kynurenine. “There has been some work in humans and quite a bit in animal models talking about how this metabolite, kynurenine, can influence behavior,” Marin said. “It’s something produced with inflammation that we know is connected with depression. But the question still remains: How? How does this molecule affect the brain? What are the processes? This is the road we want to take.”

While there is no harm in people with depression eating yogurt, people receiving treatment for depression should not stop taking their medications without consulting their physicians. More studies, the researchers noted, are needed.

Source:Science Daily

{Just as a sprinter’s body and muscles are ready for action as they wait for the starting gun to fire, brain networks at rest appear to be waiting in a state of potentiation to execute even the simplest of behaviors.}

This evidence comes from a new paper published this week in the journal PLoS One, reporting on a study led by professors Vaibhav Diwadkar, Ph.D., at Wayne State University’s School of Medicine and Steven L. Bressler, Ph.D., interim director of Florida Atlantic University’s Center for Complex Systems and Brain Sciences.

In the study, “Potentiation of motor sub-networks for motor control but not working memory: Interaction of dACC and SMA revealed by resting-state directed functional connectivity,” the researchers used a simple experimental task, having each participant perform a simple motor control behavior (tapping their forefinger to a visual cue) that alternated between behavior and rest. Brain activity was acquired using functional MRI (fMRI), a technique that allows collection of dynamic signals from within the brain when the subject is doing a task as well as when they are at rest.

Using relatively complex modeling of fMRI signals, the team studied brain network interactions between two important brain regions: the dorsal anterior cingulate cortex (dACC), used for control, and the supplementary motor area (SMA), used for motor movements. In their previous studies, the team highlighted the importance of directional network interactions from the dACC to the SMA during simple motor behavior. In the PLoS One paper, they showed a compelling and opposite effect: during the rest periods that alternated between the motor behavior task, network interactions from the SMA to the dACC were now increased.

According to Diwadkar, who co-directs the Brain Imaging Research Division in the Department of Psychiatry & Behavioral Neurosciences, “These results suggest that directional interactions from the SMA to the dACC during the rest period may in fact potentiate task-related interactions in the opposite direction.” He further noted that the studies confirm what has been long suggested and independently demonstrated: that the brain’s networks are always in a state of potentiation for action, precisely because it is impossible to predict what they will be required to do at any given time. Therefore, it is unlikely that the brain can ever be at true rest.

This paper is one of the few attempts to systematically investigate directional interactions between brain networks in the resting state and show how this state might potentiate the opposite direction of the same network task-related processing.

“Our findings are compelling because brain networks are in patterns of incessantly complex directional interactions,” said Diwadkar. “Directionality is difficult to measure, and our complex analyses show that it is possible to estimate this from fMRI data.”

According to Diwadkar, the team’s findings reveal aspects not only of normative brain function but may also provide new directions for characterizing disordered network interactions in neuropsychiatric syndromes. They will be investigating these questions in obsessive-compulsive disorder with David Rosenberg, M.D., the Miriam L. Hamburger Endowed Chair of Child Psychiatry and chair of the Department of Psychiatry and Behavioral Neurosciences at Wayne State University; and in schizophrenia with Dr. Jeffrey Stanley, Ph.D., associate professor of psychiatry. Diwadkar and Bressler are continuing to collaborate on several directions of research focusing on brain network function and dysfunction.

Source:Science Daily

{Eating healthier food could reduce greenhouse gas emissions, says a new study.}

You are what you eat, as the saying goes, and while good dietary choices boost your own health, they also could improve the health care system and even benefit the planet. Healthier people mean not only less disease but also reduced greenhouse gas emissions from health care.

As it turns out, some relatively small diet tweaks could add up to significant inroads in addressing climate change.

That’s the finding of a new study led by UC Santa Barbara researchers, who analyzed the potential effects of healthier model diets for the United States. The results appear in the journal Climatic Change.

“To my knowledge, this is the first time anyone has done this,” said study director David Cleveland, a research professor in UCSB’s environmental studies program and geography department. “People have looked at what effect diets have both on climate and on health, but they’ve never examined the potential to mitigate climate change through the food system and the health care system together.”

The food system contributes about 30 percent of total U.S. greenhouse gas emissions, with the largest proportion coming from animal-based food. In addition, the poor quality of the standard U.S. diet — including high levels of red and processed meat and low levels of fruits and vegetables — is a major factor in a number of preventable diseases. The U.S. spends $3 trillion on health care every year — 18 percent of the gross domestic product — much of it allocated to diseases associated with poor diets.

Cleveland and colleagues first used data from published meta-analyses that examined the effect of foods on diseases. Then, using life-cycle assessment data for the foods that changed in the healthier model diets, they analyzed the effects of the diets on greenhouse gas emissions for the food system. For the health care system, the researchers estimated the change in risk of diabetes, colorectal cancer and coronary heart disease due to the healthier diets and the subsequent effect on both health care costs and greenhouse gas emissions.

To create healthier model diets, the researchers altered the standard 2,000-calorie-a-day U.S. diet, changing the sources of about half of those calories. The different model diets progressively reduced the amount of red and processed meats, with the most stringent diet eliminating them completely. Fruit and vegetable intake was doubled, and peas and beans increased to replace the meat protein removed. Refined grains were partially replaced with whole grains. Added sugar, which Cleveland noted is a known health risk, was not reduced. Neither was dairy, eggs, fish or non-red meat.

“This means our estimates are probably very conservative, both in terms of health and climate change implications,” Cleveland said. “Just changing half of the diet and including only some of the diseases associated with diets, we found a huge effect.

“Food has a tremendous impact on the environment,” he added. “That means that there is enormous potential for our food choices to have positive effects on our environment as well on our health and our health care costs.”

That is exactly what the scientists found. The adoption of healthier model diets reduced the relative risk of coronary heart disease, colorectal cancer and Type 2 diabetes by 20 to 40 percent. Health care costs went down by $77 billion to $93 billion annually and direct greenhouse gas emissions dropped by 222 kilograms to 826 kilograms per person per year.

“In the third diet — which contained no red or processed meats — there was a savings of $95 billion out of the total annual cost of $230 billion for those three diseases,” Cleveland explained. “That’s not huge compared to the $3 trillion total in health care costs, but it’s a start. Results like these can also help motivate individual and policy changes.”

In terms of climate policy, the healthier diets could contribute up to 23 percent of the U.S. Climate Action Plan goal to reduce net greenhouse gas emissions 17 percent below 2005 levels by 2020, Cleveland said. Further, the diets could generate up to 134 percent of California’s goal of reaching 1990 emission levels by 2020.

According to Cleveland, the findings add weight to the conclusion of several other recent studies: Diet change must be part of successful climate change mitigation policies, and climate change mitigation must be included in policies to improve the food system.

This creates an important opportunity for the University of California, Cleveland noted. “The UC Carbon Neutrality Initiative should have a major focus on climate change mitigation via the food system,” he said. “And the UC Global Food Initiative should have a major focus on the relationships among food, climate and health.”

Source:Science Daily

{Using marijuana raises the risk of stroke and heart failure even after accounting for demographic factors, other health conditions and lifestyle risk factors such as smoking and alcohol use, according to research scheduled for presentation at the American College of Cardiology’s 66th Annual Scientific Session.}

Coming at a time when marijuana, medically known as cannabis, is on track to become legal for medical or recreational use in more than half of U.S. states, this study sheds new light on how the drug affects cardiovascular health. While previous marijuana research has focused mostly on pulmonary and psychiatric complications, the new study is one of only a handful to investigate cardiovascular outcomes.

“Like all other drugs, whether they’re prescribed or not prescribed, we want to know the effects and side effects of this drug,” said Aditi Kalla, MD, Cardiology Fellow at the Einstein Medical Center in Philadelphia and the study’s lead author. “It’s important for physicians to know these effects so we can better educate patients, such as those who are inquiring about the safety of cannabis or even asking for a prescription for cannabis.”

The study drew data from the Nationwide Inpatient Sample, which includes the health records of patients admitted at more than 1,000 hospitals comprising about 20 percent of U.S. medical centers. Researchers extracted records from young and middle-aged patients — age 18-55 years — who were discharged from hospitals in 2009 and 2010, when marijuana use was illegal in most states.

Marijuana use was diagnosed in about 1.5 percent (316,000) of more than 20 million health records included in the analysis. Comparing cardiovascular disease rates in these patients to disease rates in patients not reporting marijuana use, researchers found marijuana use was associated with a significantly increased risk for stroke, heart failure, coronary artery disease and sudden cardiac death.

Marijuana use was also linked with a variety of factors known to increase cardiovascular risk, such as obesity, high blood pressure, smoking and alcohol use. After researchers adjusted the analysis to account for these factors, marijuana use was independently associated with a 26 percent increase in the risk of stroke and a 10 percent increase in the risk of developing heart failure.

“Even when we corrected for known risk factors, we still found a higher rate of both stroke and heart failure in these patients, so that leads us to believe that there is something else going on besides just obesity or diet-related cardiovascular side effects,” Kalla said. “More research will be needed to understand the pathophysiology behind this effect.”

Research in cell cultures shows that heart muscle cells have cannabis receptors relevant to contractility, or squeezing ability, suggesting that those receptors might be one mechanism through which marijuana use could affect the cardiovascular system. It is possible that other compounds could be developed to counteract that mechanism and reduce cardiovascular risk, Kalla said.

Because the study was based on hospital discharge records, the findings may not be reflective of the general population. The study was also limited by the researchers’ inability to account for quantity or frequency of marijuana use, purpose of use (recreational or medical), or delivery mechanism (smoking or ingestion).

Kalla suggested that the growing trend toward legalization of marijuana could mean that patients and doctors will become more comfortable speaking openly about marijuana use, which could allow for better data collection and further insights into the drug’s effects and side effects.

Source:Science Daily

{Researchers from Canada, South Africa and Italy have identified a new gene that can lead to sudden death among young people and athletes.}

The gene, called CDH2, causes arrhythmogenic right ventricle cardiomyopathy (ARVC), which is a genetic disorder that predisposes patients to cardiac arrest and is a major cause of unexpected death in seemingly healthy young people.

The discovery, published in Circulation: Cardiovascular Genetics, is the result of international collaboration that began 15 years ago. It is led by a South African team headed by Bongani Mayosi, a professor of cardiology at the University of Cape Town and Groote Schuur Hospital, along with researchers of the Italian Auxologico Institute of Milan and the University of Pavia. A team of investigators from the Population Health Research Institute of McMaster University and Hamilton Health Sciences, led by Dr. Guillaume Paré, performed the genetic sequencing, as well as the bioinformatics analysis for the study.

“This is important news for families who have had a young family member suffer a sudden cardiac death, for them to know a genetic cause has been identified,” said Paré, who is an associate professor of pathology and molecular medicine with the Michael G. DeGroote School of Medicine.

“Our team was happy to contribute to the finding that a mutation in CDH2 is the underlying culprit in a portion of these patients. This will pave the way for preventative interventions and genetic counselling.”

According to the Heart and Stroke Foundation of Canada, there are about 40,000 cardiac arrests in Canada each year, and less than one in 10 people are estimated to survive a cardiac arrest that happens outside of a hospital.

Inherited forms of cardiomyopathy often cause sudden cardiac arrest death in young people under the age of 35. In ARVC, the heart tissue is replaced by fatty and fibrous tissue. This process encourages the development of cardiac arrhythmias such as tachycardia and ventricular fibrillation, which cause loss of consciousness and cardiac arrest. In the case of ventricular fibrillation, without a ready electrical defibrillation, it causes sudden death in a few minutes.

For 20 years, Mayosi followed a South African family affected by ARVC that had experienced several cases of juvenile sudden death. Excluding all genetic causes known at the time, the Italian researchers sequenced all the coding regions of the genome in two ill members of the family. The genetic mutation responsible for the disease in the family, CDH2, was narrowed down from more than 13,000 common genetic variants present in the two ill patients.

CDH2 is responsible for the production of Cadherin 2 or N-Cadherin, a key protein for normal adhesion between the cardiac cells. The gene’s discovery was validated by finding a second mutation on the same gene in another patient with ARVC from a different family. It was known from previous studies that genetically modified mice without this protein tend to have malignant ventricular arrhythmias and sudden death.

The researchers said identifying the gene is important because it helps to clarify the genetic mechanisms underlying ARVC, and it also makes the early detection of ARVC possible in otherwise unsuspecting people.

Often, the diagnostic clinical signs of the disease only become clear after many years. However, if a subject with ARVC is a carrier of a mutation on the gene CDH2, other members of his family who are genetically affected can be identified within a few weeks and preventive strategies could be started immediately. This may lead to a reduction of cases of sudden death in patients with the mutation, the researchers concluded.

Source:Science Daily

{Gentle sound stimulation — such as the rush of a waterfall — synchronized to the rhythm of brain waves significantly enhanced deep sleep in older adults and improved their ability to recall words, reports a new Northwestern Medicine study.}

Deep sleep is critical for memory consolidation. But beginning in middle age, deep sleep decreases substantially, which scientists believe contributes to memory loss in aging.

The sound stimulation significantly enhanced deep sleep in participants and their scores on a memory test.

“This is an innovative, simple and safe non-medication approach that may help improve brain health,” said senior author Dr. Phyllis Zee, professor of neurology at Northwestern University Feinberg School of Medicine and a Northwestern Medicine sleep specialist. “This is a potential tool for enhancing memory in older populations and attenuating normal age-related memory decline.”

The study will be published March 8 in Frontiers in Human Neuroscience.

In the study, 13 participants 60 and older received one night of acoustic stimulation and one night of sham stimulation. The sham stimulation procedure was identical to the acoustic one, but participants did not hear any noise during sleep. For both the sham and acoustic stimulation sessions, the individuals took a memory test at night and again the next morning. Recall ability after the sham stimulation generally improved on the morning test by a few percent. However, the average improvement was three times larger after pink-noise stimulation.

The older adults were recruited from the Cognitive Neurology and Alzheimer’s Disease Center at Northwestern.

The degree of slow wave sleep enhancement was related to the degree of memory improvement, suggesting slow wave sleep remains important for memory, even in old age.

Although the Northwestern scientists have not yet studied the effect of repeated nights of stimulation, this method could be a viable intervention for longer-term use in the home, Zee said.

Previous research showed acoustic simulation played during deep sleep could improve memory consolidation in young people. But it has not been tested in older adults.

The new study targeted older individuals — who have much more to gain memory-wise from enhanced deep sleep — and used a novel sound system that increased the effectiveness of the sound stimulation in older populations.

The study used a new approach, which reads an individual’s brain waves in real time and locks in the gentle sound stimulation during a precise moment of neuron communication during deep sleep, which varies for each person.

During deep sleep, each brain wave or oscillation slows to about one per second compared to 10 oscillations per second during wakefulness.

Giovanni Santostasi, a study coauthor, developed an algorithm that delivers the sound during the rising portion of slow wave oscillations. This stimulation enhances synchronization of the neurons’ activity.

After the sound stimulation, the older participants’ slow waves increased during sleep.

Larger studies are needed to confirm the efficacy of this method and then “the idea is to be able to offer this for people to use at home,” said first author Nelly Papalambros, a Ph.D. student in neuroscience working in Zee’s lab. “We want to move this to long-term, at-home studies.”

Northwestern scientists, under the direction of Dr. Roneil Malkani, assistant professor of neurology at Feinberg and a Northwestern Medicine sleep specialist, are currently testing the acoustic stimulation in overnight sleep studies in patients with memory complaints. The goal is to determine whether acoustic stimulation can enhance memory in adults with mild cognitive impairment.

Previous studies conducted in individuals with mild cognitive impairment in collaboration with Ken Paller, professor of psychology at the Weinberg College of Arts and Sciences at Northwestern, have demonstrated a possible link between their sleep and their memory impairments.

Source:Science Daily

{Among Swedish women, being overweight or obese early in pregnancy was associated with increased rates of cerebral palsy in children, according to a study appearing in the March 7 issue of JAMA.}

Despite advances in obstetric and neonatal care, the prevalence of cerebral palsy has increased from 1998 through 2006 in children born at full term. Few preventable factors are known to affect the risk of cerebral palsy. Maternal overweight and obesity are associated with increased risks of preterm delivery, asphyxia-related neonatal complications, and congenital malformations, which in turn are associated with increased risks of cerebral palsy. It is uncertain whether risk of cerebral palsy in offspring increases with maternal overweight and obesity severity and what could be possible mechanisms.

Eduardo Villamor, M.D., Dr.P.H., of the University of Michigan, Ann Arbor, and colleagues conducted a study that included women with children born in Sweden from 1997 through 2011. Using national registries, children were followed for a cerebral palsy diagnosis through 2012.

Of 1,423,929 children included (average gestational age, 39.8 weeks), 3,029 were diagnosed with cerebral palsy over a median 7.8 years of follow-up. Analysis of the data indicated that maternal overweight (body mass index [BMI] of 25 to 29.9) and increasing grades of obesity (BMI 30 or greater) were associated with increasing rates of cerebral palsy. Results were statistically significant for children born at full term, who comprised 71 percent of all children with cerebral palsy, but not for preterm infants.

An estimated 45 percent of the association between maternal BMI and rates of cerebral palsy in full-term children was mediated through asphyxia-related neonatal complications.

The authors note that although the effect of maternal obesity on cerebral palsy may seem small compared with other risk factors, the association is of public health relevance due to the large proportion of women who are overweight or obese. “The number of women with a BMI of 35 or more globally doubled from approximately 50 to 100 million from 2000 through 2010. In the United States, approximately half of all pregnant women have overweight or obesity at the first prenatal visit. Considering the high prevalence of obesity and the continued rise of its most severe forms, the finding that maternal overweight and obesity are related to rates of cerebral palsy in a dose-response manner may have serious public health implications.”

Source:Science Daily