Disturbed sleep associated with decline in cognition over time; no link with total hours of sleep per night
Women who experienced cognitive decline over a 13 to 15 year period after age 65 were more likely to sleep poorly than women whose cognition did not decline, according to a study led by researchers at the San Francisco VA Medical Center (SFVAMC).
The women’s cognitive decline was associated with interrupted or fitful sleep. Total sleep time per night made no difference, says lead author Kristine Yaffe, MD, chief of geriatric psychiatry at SFVAMC and professor of psychiatry, neurology, epidemiology, and biostatistics at the University of California, San Francisco (UCSF).
“This indicates that it’s not how long you sleep, but how well you sleep,” she says.
The study appears in the July 17, 2007 issue of Neurology.
Yaffe speculates that there are three possible explanations for the association between cognitive decline and disturbed sleep. She says the first and most likely reason is that whatever neurodegenerative condition is starting to cause cognitive decline, such as Alzheimer’s disease, is also affecting areas of the brain that govern sleep.
“Sleep is very complex,” notes Yaffe. “It involves a coordinated series of neurologic functions that we don’t entirely understand. It’s not unlikely that early neurodegenerative disease could start having an effect on sleep centers as well.”
Another possibility is that someone who is becoming cognitively impaired is sleeping poorly “because they’re aware of their condition and they’re worried about it.”
Finally, Yaffe says that other factors entirely, such as brain inflammation or genetic changes, might cause both cognitive decline and sleep disturbance at the same time.
The researchers studied 2,474 women who were part of a larger ongoing prospective study of risk factors for osteoporosis that began in 1986. The mean age of the women was 68.9 years at the beginning of the study. Their cognitive health was measured at regular intervals over the course of the study using two standard cognitive tests: the Mini-Mental State Examination and the Trail Making Test, Part B, known as Trails B.
After 13 to 15 years in the study, the women were fitted with an actigraph, a small device worn on the wrist that measures movement and is known from previous studies to be highly accurate in differentiating sleep from wakefulness. The women wore the device for at least three consecutive 24-hour periods.
Women who performed progressively worse on both cognitive tests over time were significantly more likely to have difficulty falling asleep and staying asleep than women whose performance did not decline. Women who performed progressively worse on the Trails B test also napped significantly more during the day.
The association between cognitive decline and poor sleep remained even after the researchers adjusted for a host of other demographic factors such as age, education, depression, exercise, and health status.
“It’s been known for some time that people with cognitive problems often have sleep problems, but those studies have mostly been done on severely demented people in nursing homes,” observes Yaffe. “Ours was the first study to look at the relationship between sleep and cognition in healthy women dwelling in the community who did not have dementia to begin with.”
Yaffe offers several cautions concerning the results of the study. First, men and African-American women were excluded from the original osteoporosis study because both of those groups have low incidence of osteoporotic fractures. Additionally, sleep patterns were measured only once, “so it’s more of a snapshot.”
However, Yaffe says that the research group has received a grant from the National Institutes of Health to continue tracking sleep patterns and cognitive health over time in the same study cohort. “Hopefully, we’ll be able to tell if cognitive changes lead to sleep disturbances, or if the reverse is true, or if they have a common independent cause.”
Co-authors of the paper were Terri Blackwell, MA, of the California Pacific Medical Center Research Institute (CPMCRI); Deborah E. Barnes, PhD, of SFVAMC and UCSF; Sonia Ancoli-Israel, PhD, of the University of California, San Diego and the VA San Diego Healthcare System; and Katie Stone, PhD, of CPMCRI, for the Study of Osteopororic Fractures Group.
The study was supported by grants from the National Institutes of Health and the National Institute on Aging.
SFVAMC has the largest medical research program in the national VA system, with more than 200 research scientists, all of whom are faculty members at UCSF.
UCSF is a leading university that advances health worldwide by conducting advanced biomedical research, educating graduate students in the life sciences and health professions, and providing complex patient care.
Contact: Steve Tokar
University of California – San Francisco
Scientists have only recently begun to speculate that what’s referred to as “junk” DNA – the 96 percent of the human genome that doesn’t encode for proteins and previously seemed to have no useful purpose – is present in the genome for an important reason. But it wasn’t clear what the reason was. Now, researchers at the University of California, San Diego (UCSD) School of Medicine have discovered one important function of so-called junk DNA.
Genes, which make up about four percent of the genome, encode for proteins, “the building blocks of life.” An international collaboration of scientists led by Michael G. Rosenfeld, M.D., Howard Hughes Medical Investigator and UCSD professor of medicine, found that some of the remaining 96 percent of genomic material might be important in the formation of boundaries that help properly organize these building blocks. Their work will be published in the July 13 issue of the journal Science.
“Some of the ‘junk’ DNA might be considered ‘punctuation marks’ – commas and periods that help make sense of the coding portion of the genome,” said first author Victoria Lunyak, Ph.D., assistant research scientist at UCSD.
In mice, as in humans, only about 4 percent of the genome encodes for protein function; the remainder, or “junk” DNA, represents repetitive and non-coding sequences. The research team studied a repeated genomic sequence called SINE B2, which is located on the growth hormone gene locus, the gene related to the aging process and longevity. The scientists were surprised to find that SINE B2 sequence is critical to formation of the functional domain boundaries for this locus.
Functional domains are stretches of DNA within the genome that contain all the regulatory signals and other information necessary to activate or repress a particular gene. Each domain is an entity unto itself that is defined, or bracketed, by a boundary, much as words in a sentence are bracketed by punctuation marks. The researchers’ data suggest that repeated genomic sequences might be a widely used strategy used in mammals to organize functional domains.
“Without boundary elements, the coding portion of the genome is like a long, run-on sequence of words without punctuation,” said Rosenfeld.
Decoding the information written in “junk” DNA could open new areas of medical research, particularly in the area of gene therapy. Scientists may find that transferring encoding genes into a patient, without also transferring the surrounding genomic sequences which give structure or meaning to these genes, would render gene therapy ineffective.
Contributors to the paper include Lluis Montoliu, Rosa Roy and Angel Garcia-Díaz of the Department of Molecular and Cellular Biology, Centro Nacional de Biotecnología in Madrid, Spain; Christopher K. Glass, M.D., Ph.D., UCSD Department of Cellular and Molecular Medicine; Esperanza Núñez, Gratien G. Prefontaine, Bong-Gun Ju, Kenneth A. Ohgi, Kasey Hutt, Xiaoyan Zhu and Yun Yung, Howard Hughes Medical Institute, Department of Molecular Medicine, UCSD School of Medicine; and Thorsten Cramer, Division of Endocrinology, UCSD Department of Medicine.
The research was funded in part by the Howard Hughes Medical Institute and the National Institutes of Health.
Contact: Debra Kain
University of California – San Diego
This release is also available in French.
Quebec City, July 12, 2007 – Dr. Philippe De Wals of Université Laval’s Department of Social and Preventive Medicine today publishes a study clearly indicating that the addition of folic acid to flours has led to a 46% drop in the incidence of congenital neural tube deformation (mainly anencephaly and spina bifida) in Canada. Such deformations either result in the child’s death or in major health problems, including physical and learning disabilities. Dr. De Wals’s work as head of a team of a dozen Canadian researchers appears today in the New England Journal of Medicine.
The neural tube is the basis of the embryo’s nervous system. Poor development of the neural tube, which is sometimes due to a lack of folic acid, can result in major health problems. Folic acid is found in green vegetables, fruit, whole grains, and meat. However, even a balanced diet won’t supply enough folic acid for a pregnant mother and the child she is carrying. Before1998, Canadian medical authorities were already recommending that women in their child-bearing years consume vitamin supplements containing folic acid. “Canada decided to add folic acid to all flour produced in the country because formation of the neural tube in embryos is particularly intense during the first four weeks of pregnancy, which is before a lot of women even know they’re pregnant. Since half of Canadian pregnancies are unplanned and the human body can’t store folic acid, it is better to integrate folic acid into the food chain than to focus exclusively on taking vitamin supplements,” stated Dr. De Wals. Health Canada still recommends taking folic acid supplements to women in their child-bearing years.
Researchers Dr. Philippe De Wals and Fassiatou Tairou of Université Laval’s Faculty of Medicine compared the incidence of neural tube deformations before and after the introduction of folic acid–enriched flours for over 2 million births in Canada. Between 1993 and 1997, the incidence was 1.58 per 1,000 births. Between 2000 and 2002, the rate dropped 46% to 0.86. The biggest improvement occurred in the parts of Canada that had the highest rates of neural tube deformation before 1998—Newfoundland, Prince Edward Island, and Nova Scotia. In Québec, the drop was also pronounced, but closer to the Canadian average.
Currently, only Canada, the United States, and Chile require that folic acid be added to flour. The effectiveness of this practice, as demonstrated by Dr. De Wals’s team, could encourage other countries to follow suit. Every year, approximately 200,000 cases of spina bifida and anencephaly occur worldwide. Adding folic acid to food could reduce that number by half.
Contact: Martin Guay
CHICAGO (July 12, 2007) — A new study to be published in the July issue of the Journal of the American College of Surgeons shows that one academic medical center recouped its investment in electronic health records within 16 months. The new analysis counters concerns of health care providers reluctant to invest in electronic medical records systems.
The widespread loss of paper medical records in New Orleans after Hurricane Katrina is one of several factors behind the recent push to get surgeons and other health care providers to go electronic, according to David A. Krusch, MD, FACS, of the University of Rochester Department of Surgery and co-author of the study.
“Health care providers most frequently cite cost as primary obstacle to adopting an electronic medical records system. And, until this point, evidence supporting a positive return on investment for electronic health records technologies has been largely anecdotal,” said Dr. Krusch.
The study measured the return on investment of installing electronic health records at five ambulatory offices representing 28 providers within the University of Rochester (NY) Medical Center. Starting in November 2003, the offices implemented a Touchworks EHR system from Chicago-based Allscripts over the next five months. The study compared the cost of activities such as pulling charts, creating new charts, filing time, support staff salary, and transcription when done electronically in the third quarter of 2005, versus the cost of those same activities performed manually in the third quarter of 2003.
The University of Rochester Medical Center estimated that the new electronic medical records system reduced costs by $393,662 per year, nearly two-thirds of that coming from a sharp reduction in the time required to manually pull charts. Given that its electronic system cost $484,577 to install and operate, it took the University of Rochester Medical Center 16 months to recoup its investment. After the first year, it cost about $114,016 annually to operate the new system, which translates to a savings of $279,546 a year for the medical center, or $9,983 per provider.
The complete study, “A Pilot Study to Document the Return on Investment for Implementing an Ambulatory Electronic Health Record at an Academic Medical Center”, will appear in the July issue of the Journal of the American College of Surgeons. In addition to Krusch, Dara L. Grieger, MD, of the University of Rochester Department of Surgery and Stephen H. Cohen, MN, CPE, also co-authored the article.
The American College of Surgeons is a scientific and educational organization of surgeons that was founded in 1913 to raise the standards of surgical practice and to improve the care of the surgical patient. The College is dedicated to the ethical and competent practice of surgery. Its achievements have significantly influenced the course of scientific surgery in America and have established it as an important advocate for all surgical patients. The College has more than 71,000 members and it is the largest organization of surgeons in the world. For more information, visit http://www.facs.org.
Contact: Sally Garneski
Weber Shandwick Worldwide
July 10, 2007
ANN ARBOR, Mich.—Organic farming can yield up to three times as much food as conventional farming on the same amount of land—according to new findings which refute the long-standing assumption that organic farming methods cannot produce enough food to feed the global population.
Researchers from the University of Michigan found that in developed countries, yields were almost equal on organic and conventional farms. In developing countries, food production could double or triple using organic methods, said Ivette Perfecto, professor at U-M’s School of Natural Resources and Environment, and one the study’s principal investigators. Catherine Badgley, research scientist in the Museum of Paleontology, is a co-author of the paper along with several current and former graduate and undergraduate students from U-M.
“My hope is that we can finally put a nail in the coffin of the idea that you can’t produce enough food through organic agriculture,” Perfecto said.
In addition to equal or greater yields, the authors found that those yields could be accomplished using existing quantities of organic fertilizers, and without putting more farmland into production.
The idea to undertake an exhaustive review of existing data about yields and nitrogen availability was fueled in a roundabout way, when Perfecto and Badgley were teaching a class about the global food system and visiting farms in Southern Michigan.
“We were struck by how much food the organic farmers would produce,” Perfecto said. The researchers set about compiling data from published literature to investigate the two chief objections to organic farming: low yields and lack of organically acceptable nitrogen sources.
Their findings refute those key arguments, Perfecto said, and confirm that organic farming is less environmentally harmful yet can potentially produce more than enough food. This is especially good news for developing countries, where it’s sometimes impossible to deliver food from outside, so farmers must supply their own. Yields in developing countries could increase dramatically by switching to organic farming, Perfecto said.
While that seems counterintuitive, it makes sense because in developing countries, many farmers still do not have the access to the expensive fertilizers and pesticides that farmers use in developed countries to produce those high yields, she said.
After comparing yields of organic and convention farms, the researchers looked at nitrogen availability. To do so, they multiplied the current farm land area by the average amount of nitrogen available for production crops if so-called “green manures” were planted between growing seasons. Green manures are cover crops which are plowed into the soil to provide natural soil amendments instead of synthetic fertilizers. They found that planting green manures between growing seasons provided enough nitrogen to farm organically without synthetic fertilizers.
Organic farming is important because conventional agriculture—which involves high-yielding plants, mechanized tillage, synthetic fertilizers and biocides—is so detrimental to the environment, Perfecto said. For instance, fertilizer runoff from conventional agriculture is the chief culprit in creating dead zones—low oxygen areas where marine life cannot survive. Proponents of organic farming argue that conventional farming also causes soil erosion, greenhouse gas emission, increased pest resistance and loss of biodiversity.
For their analysis, researchers defined the term organic as: practices referred to as sustainable or ecological; that utilize non-synthetic nutrient cycling processes; that exclude or rarely use synthetic pesticides; and sustain or regenerate the soil quality.
Perfecto said the idea that people would go hungry if farming went organic is “ridiculous.”
“Corporate interest in agriculture and the way agriculture research has been conducted in land grant institutions, with a lot of influence by the chemical companies and pesticide companies as well as fertilizer companies—all have been playing an important role in convincing the public that you need to have these inputs to produce food,” she said.
Contact: Laura Bailey
Phone: (734) 647-1848
Pittsburgh, Pa. – July 06, 2007 – A recent study in Journal of Neuroimaging suggests that cognitively normal adults exhibiting atrophy of their temporal lobe or damage to blood vessels in the brain are more likely to develop Alzheimer’s disease. Older adults showing signs of both conditions were seven-times more likely to develop Alzheimer’s than their peers.
“Alzheimer’s disease, a highly debilitating and ultimately fatal neurological disease, is already associated with other risk factors such as poor cognitive scores, education or health conditions,” says study author Caterina Rosano. “This study, because it focused on healthy, cognitively normal adults, shows that there other risk factors we need to consider.”
MRI images of participants’ brains were examined to identify poor brain circulation, damaged blood vessels and/or atrophy of the medial temporal lobe. Subjects showing any one or a combination of these symptoms were more likely to develop Alzheimer’s in the following years.
“Similarly to heart disease, brain blood vessel damage is more likely to occur in patients with high blood pressure, high cholesterol or diabetes,” says Rosano. “Since we know that prevention of these conditions can lower risk of heart attack and stroke, it is likely that it would also lower the risk of developing Alzheimer’s.”
This study is published in Journal of Neuroimaging. Media wishing to receive a PDF of this article may contact firstname.lastname@example.org.
Dr. Caterina Rosano is a physician neuroepidemiologist and assistant professor of epidemiology with the Center for Aging and Population Health at the University of Pittsburgh. She is currently developing a model to predict the incidence of cognitive and physical functional limitations in older adults. She can be reached for questions at email@example.com .
Journal of Neuroimaging addresses the full spectrum of human nervous system disease including stroke, neoplasia, degenerative and demyelinating disease, epilepsy, infectious disease, toxic-metabolic disease, psychoses, dementias, heredo-familial disease and trauma. Each issue offers original clinical articles, case reports, articles on advances in experimental research, technology updates, and neuroimaging CPCs. For more information, please visit http://www.blackwellpublishing.com/jon.
Wiley-Blackwell was formed in February 2007 as a result of the merger between Blackwell Publishing Ltd. and John Wiley & Sons, Inc.’s Scientific, Technical, and Medical business. Together, the companies have created a global publishing business with deep strength in every major academic and professional field. Wiley-Blackwell publishes approximately 1,250 scholarly peer-reviewed journals and an extensive collection of books with global appeal. For more information on Wiley-Blackwell, please visit http://www.blackwellpublishing.com or http://interscience.wiley.com.
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Kennedy Krieger Institute
Researchers at the Kennedy Krieger Institute recognize children with autism earlier than ever before, paving the way for earlier intervention and improved outcomes
(Baltimore, MD) — In a study published today in the Archives of General Psychiatry, researchers from the Kennedy Krieger Institute in Baltimore, Maryland found that autism can be diagnosed at close to one year of age, which is the earliest the disorder has ever been diagnosed. The study, which evaluated social and communication development in autism spectrum disorders (ASD) from 14 to 36 months of age, revealed that approximately half of all children with autism can be diagnosed around the first birthday. The remaining half will be diagnosed later, and their development may unfold very differently than children whose ASD is diagnosable around the first birthday. Early diagnosis of the disorder allows for early intervention, which can make a major difference in helping children with autism reach their full potential.
Researchers examined social and communication development in infants at high and low risk for ASD starting at 14 months of age and ending at 30 or 36 months (a small minority of the children exited the study at 30 months). Half of the children with a final diagnosis of ASD made at 30 or 36 months of age had been diagnosed with the disorder at 14 months, and the other half were diagnosed after 14 months. Through repeated observation and the use of standardized tests of development, researchers identified, for the first time, disruptions in social, communication and play development that were indicative of ASD in 14-month olds. Multiple signs indicating these developmental disruptions appear simultaneously in children with the disorder.
Dr. Rebecca Landa, lead study author and director of Kennedy Krieger’s Center for Autism and Related Disorders, and her colleagues identified the following signs of developmental disruptions for which parents and pediatricians should be watching:
Abnormalities in initiating communication with others: Rather than requesting help to open a jar of bubbles through gestures and vocalizations paired with eye contact, a child with ASD may struggle to open it themselves or fuss, often without looking at the nearby person.
Compromised ability to initiate and respond to opportunities to share experiences with others: Children with ASD infrequently monitor other people’s focus of attention. Therefore, a child with ASD will miss cues that are important for shared engagement with others, and miss opportunities for learning as well as for initiating communication about a shared topic of interest. For example, if a parent looks at a stuffed animal across the room, the child with ASD often does not follow the gaze and also look at the stuffed animal. Nor does this child often initiate communication with others. In contrast, children with typical development would observe the parent’s shift in gaze, look at the same object, and share in an exchange with the parent about the object of mutual focus. During engagement, children have many prolonged opportunities to learn new words and new ways to play with toys while having an emotionally satisfying experience with their parent.
Irregularities when playing with toys: Instead of using a toy as it is meant to be used, such as picking up a toy fork and pretending to eat with it, children with ASD may repeatedly pick the fork up and drop it down, tap it on the table, or perform another unusual act with the toy.
Significantly reduced variety of sounds, words and gestures used to communicate: Compared to typically developing children, children with ASD have a much smaller inventory of sounds, words and gestures that they use to communicate with others.
“For a toddler with autism, only a limited set of circumstances – like when they see a favorite toy, or when they are tossed in the air – will lead to fleeting social engagement,” said Landa. “The fact that we can identify this at such a young age is extremely exciting, because it gives us an opportunity to diagnose children with ASD very early on when intervention may have a great impact on development.”
The current study reveals that autism often involves a progression, with the disorder claiming or presenting itself between 14 and 24 months of age. Some children with only mild delays at 14 months of age could go on to be diagnosed with ASD. Landa and her colleagues observed distinct differences in the developmental paths, or trajectories, of children with early versus later diagnosis of ASD. While some children developed very slowly and displayed social and communication abnormalities associated with ASD at 14 months of age, others showed only mild delays with a gradual onset of autism symptoms, culminating in the diagnosis of ASD by 36 months.
If parents suspect something is wrong with their child’s development, or that their child is losing skills during their first few years of life, they should talk to their pediatrician or another developmental expert. This and other autism studies suggest that the “wait and see” method, which is often recommended to concerned parents, could lead to missed opportunities for early intervention during this time period.
“What’s most exciting about these important advancements in autism diagnosis is that ongoing intervention research leads us to believe it is most effective and least costly when provided to younger children,” said Dr. Gary Goldstein, President and CEO of the Kennedy Krieger Institute. “When a child goes undiagnosed until five or six years old, there is a tremendous loss of potential for intervention that can make a marked difference in that child’s outcome.”
While there are currently no standardized, published criteria for diagnosing children with autism at or around one year of age, Landa’s goal is to develop these criteria based on this and other autism studies currently underway at the Kennedy Krieger Institute. Landa and her colleagues at the Institute plan on releasing preliminary diagnostic criteria for very young children with autism in an upcoming report.
Participants in the current study included infants at high risk for ASD (siblings of children with autism, n=107) and low risk for ASD (no family history of autism, n=18). Standardized tests of development and play-based assessment tools were used to evaluate social interaction, communication and play behaviors in both groups at 14, 18 and 24 months of age. Researchers assigned diagnostic impressions at every age, indicating whether there were clinically significant signs of delay or impairment. After their last evaluation at 30 or 36 months, each participant was then given a final diagnostic classification of ASD, non-ASD impairment, or no impairment. The ASD group was further divided into an Early ASD diagnosis group and a Later ASD diagnosis group based on whether they were given a diagnosis of ASD at 14 or 24 months.
Autism spectrum disorders (ASD) is the nation’s fastest growing developmental disorder, with current incidence rates estimated at 1 in 150 children. This year more children will be diagnosed with autism than AIDS, diabetes and cancer combined, yet profound gaps remain in our understanding of both the causes and cures of the disorder. Continued research and education about developmental disruptions in individuals with ASD is crucial, as early detection and intervention can lead to improved outcomes in individuals with ASD.
About the Kennedy Krieger Institute
Internationally recognized for improving the lives of children and adolescents with disorders and injuries of the brain and spinal cord, the Kennedy Krieger Institute in Baltimore, MD serves more than 13,000 individuals each year through inpatient and outpatient clinics, home and community services and school-based programs. Kennedy Krieger provides a wide range of services for children with developmental concerns mild to severe, and is home to a team of investigators who are contributing to the understanding of how disorders develop while pioneering new interventions and earlier diagnosis. For more information on Kennedy Krieger Institute, visit http://www.kennedykrieger.org.
Contact: Dr. Branwen Morgan
Professor Herbert Herzog, Director of the Neuroscience Research Program at the Garvan Institute of Medical Research, together with scientists from the US and Slovakia, have shown that neuropeptide Y (NPY), a molecule the body releases when stressed, can ‘unlock’ Y2 receptors in the body’s fat cells, stimulating the cells to grow in size and number. By blocking those receptors, it may be possible to prevent fat growth, or make fat cells die.
“We have known for over a decade that there is a connection between chronic stress and obesity,” said Professor Herzog. “We also know that NPY plays a major role in other chronic stress-induced conditions, such as susceptibility to infection. Now we have identified the exact pathway, or chain of molecular events, that links chronic stress with obesity.”
“There is not much we can do about the increased levels of NPY caused by stress, but we can do something about the damage it causes. If we can interfere before it causes fat to amass, it could have a major impact on cardiovascular disease, diabetes, and cancer (which all have links with obesity).”
“Basically, when we have a stress reaction, NPY levels rise in our bodies, causing our heart rate and blood pressure to go up, among other things. Stress reactions are normal, unavoidable, and generally serve a useful purpose in life. It’s when stress is chronic that its effects become damaging.”
Scientists at Georgetown University (Washington D.C), part of this collaborative study, have found a direct connection between stress, a high calorie diet and unexpectedly high weight gain. Stressed and unstressed mice were fed normal diets and high calorie (high fat and high sugar, or so called ‘comfort food’) diets. The mice on normal diets did not become obese. However, stressed mice on high calorie diets gained twice as much fat as unstressed mice on the same diet. The novel and unexpected finding was that when stressed and non-stressed animals ate the same high calorie foods, the stressed animals utilised and stored fat differently.
“Our findings suggest that we may be able to reverse or prevent obesity caused by stress and diet, including the worst kind of obesity; the apple-shaped type, which makes people more susceptible to heart disease and diabetes,” says senior author of the Nature Medicine paper, Professor Zofia Zukowska of Georgetown University. “Using animal models, in which we have either blocked the Y2 receptor, or selectively removed the gene from the abdominal fat cells, we have shown that stressed mice on high calorie diets do not become obese. “Even more surprisingly, in addition to having flatter bellies, adverse metabolic changes linked to stress and diet, which include glucose intolerance and fatty liver, became markedly reduced. We do not know yet exactly how that happens, but the effect was remarkable,” she said.
Professor Herzog believes that these research findings will have a profound effect on the way society will deal with the obesity epidemic. “There are millions of people around the world who have lived with high levels of stress for so long their bodies think it’s ‘normal’. If these people also eat a high fat and high sugar diet, which is what many do as a way to reduce their stress, they will become obese.”
“Until now, the pharmaceutical industry has focused on appetite suppressants with only moderate success. Our hope is that in the near future pharmaceutical companies, using the results of our research, will develop antagonists against the Y2 receptor that will bring about a reduction in fat cells.”
Notes to editors:
Stress-activated adipogenic pathway in fat tissue exaggerates diet-induced obesity and metabolic syndrome.
Kuo, L.E., Kitlinska, J.B., Tilan, J.U., Li, L., Baker, S.B., Johnson, M.D., Lee, E.W., Burnett, M.S., Fricke, S.T., Kvetnansky, R.K., Herzog, H. & Zukowska, Z.
Nature Medicine advance online publication, 1 July 2007
The study was co-funded by the National Institutes of Health, the American Heart Association, and the Slovak Research and Development Agency.
The Garvan Institute of Medical Research was founded in 1963. Initially a research department of St Vincent’s Hospital in Sydney, it is now one of Australia’s largest medical research institutions with approximately 400 scientists, students and support staff. Garvan’s main research programs are: Cancer, Diabetes & Obesity, Arthritis & Immunology, Osteoporosis, and Neuroscience. The Garvan’s mission is to make significant contributions to medical science that will change the directions of science and medicine and have major impacts on human health. The outcome of Garvan’s discoveries is the development of better methods of diagnosis, treatment, and ultimately, prevention of disease.
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