Newswise — Westminster, Colo. — The popular Paleo diet is based on eating foods thought to be available to our ancestors during the Paleolithic era, before the advent of dairy or processed grains. Findings from a small study suggest that people who followed the Paleo diet for only eight weeks experienced positive effects on heart health. Preliminary findings from this research will be presented at the American Physiological Society’s Inflammation, Immunity and Cardiovascular Disease conference. “Very few studies have examined the Paleo diet in seemingly healthy participants, despite the prevalence of this dietary practice in health and fitness enthusiasts,” said study author Chad Dolan, a graduate student researcher at University of Houston Laboratory of Integrative Physiology. The researchers asked eight healthy people who normally consumed a traditional Western diet high in processed foods to switch to the Paleo diet—which consists of minimally processed foods—for eight weeks. The participants received a sample Paleo diet menu and recipe guide, as well as initial counseling on how to incorporate the Paleo diet into their everyday lives. They were told to eat as much food as they wanted while following the diet. The researchers found that the study participants experienced a 35 percent increase in levels of interlukin-10 (IL-10), a signaling molecule secreted by immune cells. A low IL-10 value can predict increased heart attack risk in people who also have high levels of inflammation. Scientist think that high IL-10 levels may counteract inflammation, providing a protective effect for blood vessels. Although the researchers have not yet analyzed inflammation levels in the study participants, the increase in IL-10 could suggest a lower risk for cardiovascular disease after following the Paleo diet. The researchers also observed changes in other biomarkers of inflammation, but further investigation is needed to understand whether these changes indicate increased inflammation or a protective mechanism at work. Even though the study was not designed to promote weight loss, the participants did drop some pounds during the eight-week trial. Compared with what they regularly ate before the study, participants reported consuming around 22 percent fewer calories and 44 percent fewer grams of carbohydrates on the Paleo diet. This preliminary feasibility study did not include a control group of people not following the diet, making it difficult to determine if the changes observed in inflammation biomarkers resulted from specific food choices, reduced calories, fewer carbohydrates or weight loss. “This study’s findings add to the possibility that short-term dietary changes from a traditional Western pattern of eating to foods promoted in the Paleo diet may improve health—or, at the very least, the diet does not have negative health implications in terms of the parameters we studied,” Dolan said. “If our research continues to show that the Paleo diet produces detectable changes in healthy individuals, it will substantiate claims made by those supporting this diet for the past few decades and provide preliminary evidence for another therapeutic strategy for cardiovascular disease and coronary artery disease prevention.” The researchers caution that the current findings are both preliminary and incomplete in this group of participants. They plan to conduct a study with a greater number of people who follow the diet for a longer period of time to analyze how it affects various risk factors for cardiovascular and coronary artery disease, cellular immune function and metabolic health. The study was a collaborative effort between the Human Performance Laboratory at Chatham University in Pittsburgh and the University of Houston Laboratory of Integrative Physiology. Dolan will present “Effects of an 8-week Paleo dietary intervention on inflammatory cytokines” at a poster session on Friday, Aug. 26, from 12:45 to 2:45 p.m. in the Westminster IV room of the Westin Westminster Hotel.
Newswise — Researchers know that youth with a family history of alcoholism have a greater risk of developing an alcohol use disorder; this heightened vulnerability may be due to impulsive behavior. For this study, researchers examined “waiting” impulsivity – a tendency toward prematurely responding to a reward, and previously associated with a predisposition to drinking. The study sample comprised young, moderate-to-heavy social drinkers who were either positive (FHP) or negative (FHN) for a family history of alcoholism. Impulsivity was assessed after an alcoholic or non-alcoholic drink. Two groups of young male and female social drinkers (34 women, 30 men; 18-33 years old) were given alcohol (0.8g/kg) or a placebo. The FHP group (n= 24) had first-degree relatives with problems of alcohol misuse; the FHN group (n=40) did not. Participants completed four variants of the Five-Choice Serial Reaction Time task, which measures waiting impulsivity. Other types of impulsive behavior were also tested, using the Stop Signal Reaction Time, Information Sampling Task, Delay Discounting Questionnaire, Two-Choice Impulsivity Paradigm, and Time Estimation. The FHP drinkers showed higher waiting impulsivity levels than FHN drinkers when tested for attentional load. However, the FHP group showed less impulsive behavior on the Information Sampling Task. All participants showed alcohol-impaired inhibitory control on the Stop Signal Reaction Time test. In summary, assessing exaggerated waiting impulsivity may help identify those offspring of alcoholics who are at risk for developing alcohol addiction.
Newswise — Westminster, Colo.— A new therapy that involves engineered gut bacteria may one day help reduce the health problems that come with obesity. Incorporating the engineered bacteria into the guts of mice both kept them from gaining weight and protected them against some of the negative health effects of obesity. Researchers will present their findings today at the American Physiological Society’s Inflammation, Immunity and Cardiovascular Disease conference. More than one-third of adults in the U.S. are obese, putting them at greater risk for conditions such as fatty liver disease—caused by fatty deposits building up in the liver—and atherosclerosis, the hardening and narrowing of the arteries. Scientists have recently discovered that the microorganisms living in our gut, known as the gut microbiota, play an important role in obesity and may offer a new therapeutic target. Researchers led by Sean Davies, PhD, associate professor of pharmacology at Vanderbilt University, are studying whether obesity-related diseases might be treated or even prevented by altering the gut microbiota. To find out, they engineered gut bacteria that produce a small lipid that helps suppress appetite and reduce inflammation. People who are obese typically produce less of this lipid, which is made by the small intestine. “We have previously shown that this approach with engineered bacteria could inhibit obesity when standard mice were fed a high-fat diet,” Davies said. “Our new studies focused on mice highly prone to develop atherosclerosis and fatty liver disease, and we showed that the engineered bacteria were beneficial not only in inhibiting obesity, but also in protecting against fatty liver disease and somewhat against atherosclerosis.” The researchers found that standard mice fed a high-fat diet while also receiving the engineered bacteria via drinking water gained less body weight and body fat than mice given standard drinking water or control bacteria. They also gave the engineered bacteria to mice with increased susceptibility to atherosclerosis and fatty liver disease. These mice accumulated less fat in the liver and showed reduced expression of markers of liver fibrosis, compared to mice that did not receive the treatment. The treated mice also exhibited a modest trend toward reduced atherosclerotic plaques. “Some day in the future, it might be possible to treat the worst effects of obesity simply by administering these bacteria,” Davies said. “Because of the sustainability of gut bacteria, this treatment would not need to be every day.” Davies will present “Altering the microbiota for weight control” at the Inflammation and Hypertension during Pregnancy and Gender Differences symposium on Friday, Aug. 26, from 8:30 to 9 p.m. in the Westminster III room of the Westin Westminster Hotel.
Newswise — Texas A&M researchers have shown, for the first time, evidence that standing desks in classrooms can slow the increase in elementary school children’s body mass index (BMI)—a key indicator of obesity—by an average of 5.24 percentile points. The research was published today in the American Journal of Public Health. “Research around the world has shown that standing desks are positive for the teachers in terms of classroom management and student engagement, as well as positive for the children for their health, cognitive functioning and academic achievement,” said Mark Benden, PhD, CPE, an associate professor in the Department of Environmental and Occupational Health at the Texas A&M School of Public Health and an author of the study. “It’s literally a win-win, and now we have hard data that shows it is beneficial for weight control.” Twenty-four classrooms at three elementary schools (eight in each of the three schools) in College Station, Texas, participated in the study. At each school, four classrooms were outfitted with stand-biased desks (which allow students to sit on a stool or stand at will) and four classrooms in each school acted as a control and utilized standard classroom desks. The researchers followed the same students—193 in all—from the beginning of third grade to the end of fourth grade. The researchers found that the students who had the stand-biased desks for both years averaged a three percent drop in BMI while those in traditional desks showed the two percent increase typically associated with getting older. However, even those who spent just one year in classrooms with stand-biased desks had lower mean BMIs than those students in traditional seated classrooms for their third and fourth grade years. In addition, there weren’t major differences between boys and girls, or between students of different races, suggesting that this intervention works across demographic groups. “Classrooms with stand-biased desks are part of what we call an Activity Permissive Learning Environment (APLE), which means that teachers don’t tell children to ‘sit down,’ or ‘sit still’ during class,” Benden said. “Instead, these types of desks encourage the students to move instead of being forced to sit in poorly fitting, hard plastic chairs for six or seven hours of their day.” Many school-based initiatives for weight loss focus on better, more nutritious cafeteria lunches, and although these programs are important, they don’t focus on the other side of weight control: calories expended. Previous studies from Benden’s lab have shown that children who stand burn 15 percent more calories, on average, than those who sit in class, but this is the first study showing, over two years, that BMI decreases over time (versus controls) when using a stand-biased desk. “It is challenging to just measure weight loss with children,” Benden said, “because children are supposed to be gaining weight as they get older and taller.” At the beginning of this study, which was funded by the National Institutes of Health (NIH), roughly 79 percent of the students were of normal weight category, 12 percent were overweight and nine percent were obese, according to height and weight measurements made by the researchers. These are better numbers than nationally, where 14.9 percent of children were overweight and 16.9 percent were obese in 2012. The fact that the students who started at a healthy weight benefited from stand-biased desks as much as they did might indicate that these desks help students who aren’t overweight maintain their BMI, while at the same time help those who start out overweight or obese get to a healthier weight. These desks, designed by Benden and his team, are called stand-biased, not “standing” because they do include a tall stool the students can perch on if they so choose. They also include a footrest, a vital feature because it allows children to get their lower backs out of tension and reduce leg fatigue to stand more comfortably over time. These United States-patented desk designs are now licensed to Stand2Learn, which has commercialized the products through translational research focused on moving university studies to publicly available solutions. “Sit less, move more,” Benden said. “That’s our message.” ###
Newswise — Neurons in the brain interact by sending each other chemical messages, so-called neurotransmitters. Gamma-aminobutyric acid (GABA) is the most common inhibitory neurotransmitter, which is important to restrain neural activity, preventing neurons from getting too trigger-happy and from firing too much or responding to irrelevant stimuli. Researchers led by Dr Tobias Bast in the School of Psychology at The University of Nottingham have found that faulty inhibitory neurotransmission and abnormally increased activity in the hippocampus impairs our memory and attention. Their latest research -- "Hippocampal neural disinhibition causes attentional and memory deficits" -- published in the academic journal Cerebral Cortex, has implications for understanding cognitive deficits in a variety of brain disorders, including schizophrenia, age-related cognitive decline and Alzheimer's, and for the treatment of cognitive deficits. The hippocampus -- a part of the brain that sits within our temporal lobes -- plays a major role in our everyday memory of events and of where and when they happen -- for example remembering where we parked our car before going shopping. This research has shown that a lack of restraint in the neural firing within the hippocampus disrupts hippocampus-dependent memory; in addition, such aberrant neuron firing within the hippocampus also disrupted attention -- a cognitive function that does not normally require the hippocampus. Increased activity can be more detrimental than reduced activity Dr Bast, said: "Our research carried out in rats highlights the importance of GABAergic inhibition within the hippocampus for memory performance and for attention. The finding that faulty inhibition disrupts memory suggests that memory depends on well-balanced neural activity within the hippocampus, with both too much and too little causing impairments. This is an important finding because traditionally, memory impairments have mainly been associated with reduced activity or lesions of the hippocampus. "Our second important finding is that faulty inhibition leading to increased neural activity within the hippocampus disrupts attention, a cognitive function that does not normally require the hippocampus, but depends on the prefrontal cortex. This probably reflects that there are very strong neuronal connections between hippocampus and prefrontal cortex. Our finding suggests that aberrant hippocampal activity has a knock-on effect on the prefrontal cortex, thereby disrupting attention." "Overall, our new findings show that increased activity of a brain region, due to faulty inhibitory neurotransmission, can be more detrimental to cognitive function than reduced activity or a lesion. Increased activity within a brain region can disrupt not only the function of the region itself -- in this case hippocampus-dependent memory -- but also the function of other regions to which it is connected -- in this case prefrontal cortex-dependent attention." Adding to existing research findingsDr Bast's research is motivated by recent clinical findings that patients in early stages of schizophrenia, age-related cognitive decline and Alzheimer's show faulty inhibition and increased activity within the hippocampus. The new study, where inhibition in the hippocampus of rats was disrupted before the animals took part in tests of attention and memory, revealed that such faulty inhibition and aberrant activity within the hippocampus causes the type of memory and attentional impairments seen in patients. This research adds to the team's recent findings, where they found that attention was disrupted by faulty inhibition and increased activity within the prefrontal cortex, a brain region important for attention. Dr Bast, said: "Overall, these findings highlight that higher brain functions, such as attention and memory, depend on well-balanced neural activity within the underlying brain regions." Potential target for new treatments This research has important implications for treating cognitive impairments. The findings show that simply 'boosting' the activity of the key memory and attention centres in the brain (the hippocampus and prefrontal cortex), which has been a long-standing strategy for cognitive enhancement, will not necessarily improve memory and attention, but can actually impair these functions. What's important is to re-balance activity within these regions. Dr Bast, said: "One emerging idea is that early stages of cognitive disorders, such as schizophrenia and age-related cognitive decline and Alzheimer's, are characterised by faulty inhibition and too much activity; this excess neural activity leads then to neuronal damage and the reduced brain activity characterizing later stages of these disorders. So, rebalancing aberrant activity early on may not only restore attention and memory, but also prevent further decline. "We have new studies on the way where we aim to identify medicines that might be able to re-balance neural activity within hippocampus and prefrontal cortex and to restore memory and attention."
Newswise — New Brunswick, N.J., – Thanks to a two-year, $70,000 commitment from Embrace Kids Foundation, the Rutgers Robert Wood Johnson Medical School Comprehensive Sickle Cell Center housed at Rutgers Cancer Institute of New Jersey is expanding to include a Pediatric Sickle Cell and Hemoglobinopathies Nurse Navigator position. The Center receives referrals from the state’s newborn screening program and from pediatricians in the central New Jersey region. Sickle cell disease, an inherited disorder in which the red blood cells become hard and sticky, clogging the blood flow, affects approximately 100,000 Americans, according to the Centers for Disease Control and Prevention. The disease, which can result in repeated episodes of severe pain, infections and anemia, occurs in one in every 365 African-American births and in one out of every 16,300 Hispanic-American births. Other affected populations include those whose ancestors are from Latin America, the Caribbean, Saudi Arabia, India, and Mediterranean countries. The primary focus of the Pediatric Sickle Cell and Hemoglobinopathies Nurse Navigator is to enhance patient services, remove barriers to care, and improve care coordination. The nurse navigator supports the families of infants identified by newborn screening, beginning at the first point of contact, and facilitates communication between the family and care team. This includes collaborating with psychosocial counselors and service organizations to direct families to various resources. The navigator also educates families about their disease and treatment process including identifying clinical trials for which the patient may be eligible. And as adolescent patients begin to transition into an adult hematology care setting, the navigator plays a vital role in making sure the teenager is informed and connected to treatment and other resources. Sickle cell disease is a lifelong condition that is marked by episodic medical setbacks. “The impact of this disease is disruptive to the family unit on many levels,” notes Embrace Kids Foundation Executive Director Glenn Jenkins. “The role of the Pediatric Sickle Cell and Hemoglobinopathies Nurse Navigator is integral in getting families back on track and returning a youngster to a normal childhood. Embrace Kids Foundation is pleased to be able to support this critical work in partnership with Jason and Devin McCourty through their Tackle Sickle Cell campaign.” “Due to research and clinical advancements, the average life expectancy of babies born today with sickle cell disease has greatly improved, and many likely will live late into adulthood. However, this goal cannot be achieved unless medical care takes a comprehensive, multidisciplinary approach with emphasis placed on prevention of long-term complications and timely treatment,” notes Richard Drachtman, MD, section chief, pediatric hematology/oncology at Rutgers Cancer Institute and professor of pediatrics at Rutgers Robert Wood Johnson Medical School. “With this commitment from Embrace Kids Foundation, we will be able to further empower patients and families with the knowledge and resources necessary to assume self-care to maximize longevity and quality of life. We thank Embrace Kids Foundation for its dedication to this population.” About Rutgers Cancer Institute of New JerseyRutgers Cancer Institute of New Jersey (www.cinj.org) is the state’s only National Cancer Institute-designated Comprehensive Cancer Center. As part of Rutgers, The State University of New Jersey, the Cancer Institute of New Jersey is dedicated to improving the detection, treatment and care of patients with cancer, and to serving as an education resource for cancer prevention. Physician-scientists at Rutgers Cancer Institute engage in translational research, transforming their laboratory discoveries into clinical practice. To make a tax-deductible gift to support the Cancer Institute of New Jersey, call 848-932-8013 or visitwww.cinj.org/giving. Follow us on Facebook at www.facebook.com/TheCINJ. The Cancer Institute of New Jersey Network is comprised of hospitals throughout the state and provides the highest quality cancer care and rapid dissemination of important discoveries into the community. Flagship Hospital: Robert Wood Johnson University Hospital. System Partner: Meridian Health (Jersey Shore University Medical Center, Ocean Medical Center, Riverview Medical Center, Southern Ocean Medical Center, and Bayshore Community Hospital). Affiliate Hospitals: JFK Medical Center, Robert Wood Johnson University Hospital Hamilton (CINJ Hamilton), and Robert Wood Johnson University Hospital Somerset. ###
Newswise — A study by Johns Hopkins researchers of more than 13,000 people has found that even after accounting for such risk factors as high blood pressure, high cholesterol and diabetes, so-called morbid obesity appears to stand alone as a standout risk for heart failure, but not for other major types of heart disease. In a report on the research, published online on July 28 in theJournal of the American Heart Association, the Johns Hopkins team says morbidly obese individuals were more than two times more likely to have heart failure than comparable people with a healthy body mass index, after accounting for high blood pressure, cholesterol and blood sugar levels. And yet, after accounting for these factors, people with morbid obesity weren't any more likely to have a stroke or coronary heart disease -- basically disease of the heart's arteries," due in part to inflammation and an accumulation of plaque in the heart and surrounding blood vessels. The researchers caution that their study suggests a strong, independent link between severe obesity and heart failure but does not definitively determine cause and effect. Nevertheless, they say, their findings suggest that while treating hypertension, diabetes and other conditions associated with obesity may be sufficient to prevent coronary heart disease and stroke, this approach may not be enough to prevent an increased risk of heart failure, for which weight loss may be the only foolproof, currently available preventive measure. The federal government estimates that one in three Americans is obese and more than 5 percent are morbidly obese -- defined as a body mass index of greater than 35. According to the U.S. Centers for Disease Control and Prevention, almost 6 million people in the United States are living with heart failure, a condition of aging marked by enlarged and/or weakened heart muscle and diminished blood-pumping efficiency, resulting in shortness of breath, fatigue, weakness, trouble breathing when lying down, and swelling in the ankles and feet. Overall, there is a 50 percent mortality rate for people with heart failure five years after diagnosis. "Obesity in our study has emerged as one of the least explained and likely most challenging risk factors for heart failure because there is no magic pill to treat it, no drugs that can easily address the problem like there are for high cholesterol and high blood pressure," says Chiadi Ndumele, M.D., M.H.S., assistant professor of medicine and member of the Ciccarone Center for the Prevention of Heart Disease at the Johns Hopkins University School of Medicine. "Even with diet and exercise, people struggle to lose weight and keep it off, and for the morbidly obese, the struggle is often insurmountable." Although it isn't completely clear why obesity alone is linked to heart failure independent of risk factors and not to stroke or coronary heart disease, Ndumele says that there is evidence to suggest that extra body weight exerts a higher metabolic demand on the heart and that fat cells in the abdomen may even release molecules toxic to heart cells. Obesity has long been known to increase the likelihood of high blood pressure, elevated blood cholesterol and diabetes -- all established risk factors for heart and blood vessel diseases. Treating and controlling these conditions have formed the bedrock strategies for reducing the risk of cardiovascular disease, Ndumele says. To learn if this was truly the case for all types of cardiovascular disease, Ndumele and his colleagues looked at the medical records of 13,730 participants in the Atherosclerosis Risk in Communities Study who had body mass indexes in healthy ranges or higher at the start of the study and no initial heart disease. The group was composed of 63.8 percent women and 16.9 percent African-Americans. The average age was 54, and body mass index ranged from 18 to 50. All were followed for approximately 23 years to assess links between body mass index and heart failure, coronary heart disease or stroke. The records also included data for participants' height, weight, and levels of blood sugar, cholesterol and triglycerides, along with smoking status, alcohol use, professions and exercise levels. After the final participant follow-up in 2012, there were 2,235 recorded cases of heart failure, 1,653 cases of coronary heart disease and 986 strokes. In their initial assessment, the Johns Hopkins researchers controlled for differences that might be due to age, sex, race, education level, career, smoking history, exercise and alcohol consumption. Severe obesity was associated with a nearly fourfold higher risk of heart failure and about a twofold higher risk for both coronary heart disease and stroke compared with rates for those with a normal body mass index. Next, the researchers controlled for other heart disease risk factors, such as diabetes, high blood pressure, or high levels of cholesterol and triglycerides. After this adjustment, Ndumele's team no longer saw an increase in risk for coronary heart disease or stroke in people with obesity. However, the increased risk for heart failure remained. For every five-unit higher body mass index, there was an almost 30 percent higher risk of developing heart failure across all participants. "Even if my patients have normal blood sugar, cholesterol and blood pressure levels, I believe I still have to worry that they may develop heart failure if they are severely obese," says Ndumele. "If our data are confirmed, we need to improve our strategies for heart failure prevention in this population."
Newswise — New research led by scientists from King's College London and the University of Bristol has found that a high-fat, high-sugar diet during pregnancy may be linked to symptoms of ADHD in children who show conduct problems early in life. Published today in the Journal of Child Psychology and Psychiatry, this study is the first to indicate that epigenetic changes evident at birth may explain the link between unhealthy diet, conduct problems and ADHD. Early onset conduct problems (e.g. lying, fighting) and attention-deficit/hyperactivity disorder (ADHD) are the leading causes of child mental health referral in the UK. These two disorders tend to occur in tandem (more than 40 per cent of children with a diagnosis of conduct disorder also have a diagnosis of ADHD) and can also be traced back to very similar prenatal experiences such as maternal distress or poor nutrition. In this new study of participants from the Bristol-based 'Children of the 90s' cohort, 83 children with early-onset conduct problems were compared with 81 children who had low levels of conduct problems. The researchers assessed how the mothers' nutrition affected epigenetic changes (or DNA methylation) of IGF2, a gene involved in fetal development and the brain development of areas implicated in ADHD - the cerebellum and hippocampus. Notably, DNA methylation of IGF2 had previously been found in children of mothers who were exposed to famine in the Netherlands during World War II. The researchers from King's and Bristol found that poor prenatal nutrition, comprising high fat and sugar diets of processed food and confectionary, was associated with higher IGF2 methylation in children with early onset conduct problems and those with low conduct problems. Higher IGF2 methylation was also associated with higher ADHD symptoms between the ages of 7 and 13, but only for children who showed an early onset of conduct problems. Dr Edward Barker from King's College London said: 'Our finding that poor prenatal nutrition was associated with higher IGF2 methylation highlights the critical importance of a healthy diet during pregnancy. 'These results suggest that promoting a healthy prenatal diet may ultimately lower ADHD symptoms and conduct problems in children. This is encouraging given that nutritional and epigenetic risk factors can be altered.' Dr Barker added: 'We now need to examine more specific types of nutrition. For example, the types of fats such as omega 3 fatty acids, from fish, walnuts and chicken are extremely important for neural development. 'We already know that nutritional supplements for children can lead to lower ADHD and conduct problems, so it will be important for future research to examine the role of epigenetic changes in this process.' ###
Newswise — The majority of smokers who successfully switch to vaping say they have fewer respiratory infections, according to a study led by Queen Mary University of London (QMUL). The on-line survey of 941 respondents assessed subjective changes in respiratory symptoms in smokers who switched to vaping for at least two months. The results, published in theJournal of Addiction Research & Therapy, show that 66 per cent of respondents reported an improvement in respiratory symptoms, 29 per cent reported no change and 5 per cent reported worsening. Senior author Professor Peter Hajek from QMUL said: "There is no doubt that e-cigarettes are much safer than conventional cigarettes, but smokers are still led to believe that they're dangerous. This misinformation includes a misreported study on rats that claimed that vaping may increase vulnerability to infections. These new findings from human vapers show that this is not the case. "The study needs to be interpreted with caution because it is based on self-reported data, and further studies using objective measures are needed. However, the present results provide sufficient information to suggest that vaping does not increase infection rates and may in fact lead to a decrease in infections." Some previous cell and animal studies have been interpreted as suggesting that vaping may increase vulnerability to infection, but these studies did not use realistic exposure levels. Human trials have reported no significant adverse respiratory effects associated with e-cigarette use for up to 1.5 years and a follow-up study of smokers with asthma who switched to vaping found significant improvements. The researchers say that it is not surprising that the survey respondents noticed improvements in their respiratory health. This is because smoking increases susceptibility to respiratory infections and stopping smoking can be expected to have a positive effect. In addition to this, vaping may also provide some antimicrobial protection through the e-liquid ingredient propylene glycol, though further evidence is needed to confirm this. The main limitation of the study is that the reports are subjective. Future studies should assess respiratory symptoms objectively and on unselected samples of vapers. Despite the limitations, the researchers say that the study provides a reasonable reassurance that vaping does not promote respiratory infections and may in fact reduce them. ###
Newswise — Obstructive sleep apnea – a disorder that affects nearly one out of four people between the ages of 30 and 70 – is a common cause of high blood pressure. In the Aug. 17, 2016, issue of the journal Science Signaling, researchers based primarily at the University of Chicago describe the signaling cascade that leads to this form of hypertension and suggest ways to disrupt those signals and prevent elevated blood pressures. “Our results, using a rodent model, establish a mechanism that is the cause of apnea-associated hypertension,” said study leader Nanduri Prabhakar, PhD, director of the Institute for Integrative Physiology and Center for Systems Biology of Oxygen Sensing at the University of Chicago. “They also offer a novel way to block the process, preventing this form of hypertension and restoring normal blood pressures.” The connection between sleep apnea and high blood pressure begins in the carotid body, a small cluster of cells located in the carotid arteries, which pass through the right and left sides of the neck. Chemosensory cells in the carotid bodies constantly measure oxygen levels in the blood and use that information to regulate breathing. When people with sleep apnea periodically slow or stop their breathing during sleep, their blood-oxygen levels plummet. The carotid bodies recognize this deficit and quickly release signals to increase breathing and bring oxygen levels back to normal. These signals, however, can also increase blood pressure, which can lead to strokes during sleep. “In both central and obstructive sleep apnea, the acute elevations in blood pressure associated with apneic episodes may predispose patients to hemorrhagic stroke, while chronic hypertension increases the risk of heart failure,” the authors wrote. “Thus, controlling hypertension in sleep apnea patients is a major clinical problem.” So the researchers carefully mapped out the chain of signaling events that began with sleep-disordered breathing and led to the onset of hypertension. When an episode of apnea causes low blood oxygen levels, the carotid bodies quickly detect the decrease and begin to generate reactive oxygen species (a natural byproduct of the normal metabolism of oxygen). These inactivate heme oxygenase-2, an enzyme that generates carbon monoxide (CO). This leads to an increase in hydrogen sulfide, which stimulates the carotid bodies to send out chemical signals to take in more oxygen. Unfortunately, those signals also stimulate the sympathetic nervous system and cause blood vessels to constrict, boosting blood pressure. The standard therapies for hypertension caused by constricted vessels “do not work in this form of hypertension,” Prabhakar said. In the 1960s, when the relationship between the carotid bodies and asthma was being first investigated, researchers tried to treat the disease by surgical removal of the carotid bodies. However, some of those patients developed sleep apnea. Although carotid body resection prevented hypertension, that approach came with serious side effects. Because they lacked the urge to breathe more during exertion, patients were unable to exercise safely, Prabhakar said, adding that “some died in their sleep from extended apneic episodes.” The authors suggest instead that drugs designed to inhibit the enzyme cystathionine-y-lyase – required for the production of hydrogen sulfide, the signal to increase oxygen intake – could be used to disrupt the cascade of signals leading to apnea-related hypertension. “A major finding of the present study is that blockade of hydrogen sulfide synthesis is sufficient to prevent carotid body activation and hypertension in intermittent hypoxia-exposed rodents,” the authors note. Treating rats with a cystathionine-y-lyase inhibitor L-propargylglycine (L-PAG) “restored normal carotid body function, sympathetic nerve activity and blood pressure, and blocked hypertensive responses to simulated apneas.” “Our results,” they conclude, “suggest that inhibiting cystathionine-y-lyase to reduce hydrogen sulfide signaling in the carotid body with more potent inhibitors than L-PAG may be a novel approach to treat hypertension in patients with sleep apnea.” The National Institutes of Health supported this effort. Additional authors were Guoxiang Yuan, Ying-Jie Peng, Shakil Khan, Jayasri Nanduri, Amritha Singh and Ganesh Kumar from the University of Chicago, and Chirag Vasavda, Gregg Semenza and Solomon Snyder of Johns Hopkins University School of Medicine.