Health Intelligence Report 28 Nov 2007
19th Edition Compiled by Ralph Turchiano
EDITOR’S TOP 5 (For Most Interesting)
1. Sweet magnolia: Tree bark extract fights bad breath and tooth decay
2. Fear is stronger motivator to get fit than hope for those worrying about their bodies, says study
3. MU study finds that sitting may increase risk of disease
4. New research helps explain how tumors go undetected by the body
5. Omega-3 fatty acids protect against Parkinson’s, study says (DHA)
In this Issue:1. 63 percent of diabetics risk serious foot problems by wearing the wrong-sized shoes 2. Immune system can drive cancers into dormant state 3. Sweet magnolia: Tree bark extract fights bad breath and tooth decay 4. New research helps explain how tumors go undetected by the body 5. Tonsillectomy may increase costs without benefits in some children 6. Sinus problems are treated well with safe, inexpensive treatment 7. MU study finds that sitting may increase risk of disease 8. Progress in coronary disease death rates grinds to near halt in young adults 9. Rogue bacteria involved in both heart disease and infertility 10. New study finds blood-spinal cord barrier compromised in mice with ALS 11. CU study: Lead levels even well below U.S. standard may affect brain function in children 12. Regular Exercise Reduces Risk of Blood Clots 13. Not enough ‘good’ cholesterol makes it harder to recover from stroke 14. High-glycemic index carbohydrates associated with risk for developing type 2 diabetes in women 15. Omega-3 fatty acids protect against Parkinson’s, study says 16. Ozone can affect heavier people more 17. Fear is stronger motivator to get fit than hope for those worrying about their bodies, says study Scientists identify gene responsible for statin-induced muscle pain
Public release date: 13-Nov-2007
63 percent of diabetics risk serious foot problems by wearing the wrong-sized shoes
More than six out of ten people with diabetes are walking around in the wrong-sized shoes, exposing themselves to serious foot problems that could lead to amputation, according to research in the November issue of IJCP, the International Journal of Clinical Practice.
And the World Health Organization has said that the number of people suffering from diabetes could double to 366 million by 2030 and that 80 per cent of diabetic foot amputations could be prevented.
The team found that 63 per cent of the patients were wearing the wrong-sized shoes. For example, 45 per cent were wearing the wrong width fitting, with the majority being too narrow.
“When people stand up their feet change shape as the arch of the foot flattens and the foot becomes wider and longer” explains Dr Leese. “Taking both these sets of measurements into account, only 37 per cent of the patients were actually wearing the right-sized shoes.
Public release date: 18-Nov-2007
Immune system can drive cancers into dormant state
St. Louis, Nov. 18, 2007 — A multinational team of researchers has shown for the first time that the immune system can stop the growth of a cancerous tumor without actually killing it.
Scientists have been working for years to use the immune system to eradicate cancers, a technique known as immunotherapy. The new findings prove an alternate to this approach exists: When the cancer can’t be killed with immune attacks, it may be possible to find ways to use the immune system to contain it. The results also may help explain why some tumors seem to suddenly stop growing and go into a lasting period of dormancy.
The study’s authors call the cancer-immune system stalemate equilibrium. During equilibrium, the immune system both decreases the cancer’s drive to replicate and kills some of the cancerous cells, but not quickly enough to eliminate or shrink the tumor.
Scientists first proposed that the immune system might be able to recognize cancer cells as potentially harmful more than a century ago. Under a theory that came to be called cancer immunosurveillance, researchers suggested that if this recognition took place, the immune system would attack tumors with the same weapons it uses to eliminate invading microorganisms. Current immunotherapy efforts use therapeutic agents to increase the chances that the immune system will recognize and attack tumors.
But cancer immunosurveillance has been controversial. The theory had begun to fall out of favor over the years, and in 2001, Schreiber, graduate students Vijay Shankaran and Gavin Dunn, and Lloyd Old, M.D., director of the New York branch of the Ludwig Institute for Cancer Research, proposed a major revision. They called their new model cancer immunoediting.
“We don’t think the immune system has evolved to handle cancers,” Schreiber notes. “Cancer is typically a disease of the elderly, who have moved beyond their reproductive years, so there probably was no evolutionary pressure for the immune system to find a way to fight cancer.”
Public release date: 18-Nov-2007
Sweet magnolia: Tree bark extract fights bad breath and tooth decay
Journal of Agricultural and Food Chemistry
“Sweet magnolia” does more than describe the fragrant blossoms of a popular evergreen tree. It also applies to magnolia bark’s effects on human breath. Scientists in Illinois are reporting that breath mints made with magnolia bark extract kill most oral bacteria that cause bad breath and tooth decay within 30 minutes. The extract could be a boon for oral health when added to chewing gum and mints, they report in a study scheduled for the Nov. 14 issue of the ACS’ Journal of Agricultural and Food Chemistry, a bi-weekly publication.
The extract also showed strong antibacterial activity against a group of bacteria known to cause cavities. Mints and chewing gum containing the extract may also provide a “portable oral care supplement to dentifrice (toothpaste), where brushing is not possible,” the study states.
Public release date: 19-Nov-2007
New research helps explain how tumors go undetected by the body
Scientists studying how immune cells are regulated in healthy individuals, have made a key discovery in understanding why tumours may go undetected by the immune system and remain untreated by the body’s own natural defences. The findings, published online this week (between 19 – 23 November) by the Proceedings of the National Academy of Sciences, could lead to new treatments for tumours.
Under normal circumstances, the immune system creates sustained inflammation around a dangerous pathogen or injury which tells the body that there is a problem. However, in the case of tumours, certain cellular mechanisms counteract inflammation which can cause the tumour to go undetected, making it even harder for the body to expel.
The researchers at King’s College London, funded by the Biotechnology and Biological Sciences Research Council (BBSRC), discovered that regulatory T cells can reverse the role of a key immune cell called a macrophage which is normally involved in causing inflammation. Regulatory T cells are cells that regulate the immune system to stop it over-responding to every external stimulus and only deal with genuinely harmful pathogens or injuries. The research shows that they can achieve this by encouraging macrophages to instead dampen down the inflammatory response that is automatically induced by all possible threats to the body, even those that turn out to be harmless.
Dr Leonie Taams, research leader explains: “A relatively harmless stimulus, such as a small cut, will automatically be treated by the body as something dangerous and will cause macrophages to promote inflammation. We discovered that it is then the regulatory T cells’ responsibility to make the macrophages promote anti-inflammation to counteract the initial response, as it is not a real danger. This helps keep the immune system stable and prevents the body over-reacting to everything in its environment.
“However problems can occur with tumours, where many regulatory T cells promoting a strong anti-inflammatory response are present. Neutralising an inflammatory response in this scenario can cause the tumour to fall under the radar of the body’s immune system and ‘trick’ it into believing that there is no problem.
“We hope to be able to use this new knowledge about the relationship between regulatory T cells and macrophages to find more effective treatments for tumours. Interestingly, we also hope to use the same knowledge to achieve the opposite result and block chronic inflammation such as that which occurs in rheumatoid arthritis.”
Ralph’s Note – This brings an interesting question to whether long term inflammation suppression through NSAID’s or the like. Can Indirectly be carcinogenic.
Public release date: 19-Nov-2007
Tonsillectomy may increase costs without benefits in some children
Dutch study suggests that among children with mild or moderate symptoms of throat infections, surgery to remove the tonsils may be more expensive but not necessarily more beneficial than watchful waiting, according to a report in the November issue of Archives of Otolaryngology–Head & Neck Surgery, one of the JAMA/Archives journals.
Tonsillectomy—removal of the tonsils—with or without removal of the adenoids (tissue at the back of the throat) is one of the most frequently performed surgical procedures on children, according to background information in the article. However, the number of procedures performed varies widely by country. In 1998, adenotonsillectomies were performed on 115 per 10,000 children in the Netherlands, 65 per 10,000 British children and 50 per 10,000 American children. This suggests that different indications for surgery are used in each country.
Erik Buskens, M.D., Ph.D., of University Medical Center Utrecht, Utrecht, the Netherlands, and colleagues conducted a clinical trial involving 300 children age 2 to 8 who were recommended for adenotonsillectomy between 2000 and 2003. A group of 151 children were randomly assigned to have surgery within six weeks, while 149 were assigned to watchful waiting, which involved close monitoring and additional interventions as necessary. Parents kept diaries of all the children’s upper respiratory tract symptoms, measured their temperature daily and recorded any costs associated with their care. Follow-up visits occurred after three, six, 12, 18 and 24 months.
Public release date: 19-Nov-2007
Sinus problems are treated well with safe, inexpensive treatment
ANN ARBOR, Mich. — An inexpensive, safe and easy treatment is an effective method for treating chronic nasal and sinus symptoms – more effective, in fact, than commonly used saline sprays, according to a new study from University of Michigan Health System researchers.
The study is the first of its kind to show greater efficacy of saline irrigation treatments versus saline spray for providing short-term relief of chronic nasal symptoms, the authors report. Participants in the study who were treated with irrigation experienced a much greater benefit than those who were treated with saline spray, in terms of both the severity and frequency of their symptoms.
“The irrigation group achieved a clinically significant improvement in quality of life in terms of the severity of their symptoms, whereas the spray group did not,” says lead author Melissa A. Pynnonen, M.D., clinical assistant professor in the U-M Department of Otolaryngology. “Strikingly, they also experienced 50 percent lower odds of frequent nasal symptoms compared with the spray group.”
The findings, which appear in the new issue of the Archives of Otolaryngology – Head & Neck Surgery, could be significant for the multitudes of people who suffer from chronic nasal and sinus conditions. In the United States, 36 million people are affected by chronic rhinosinusitis each year, and millions more are affected by other types of allergic and non-allergic rhinitis.
Public release date: 19-Nov-2007
MU study finds that sitting may increase risk of disease
COLUMBIA, Mo. – Most people spend most of their day sitting with relatively idle muscles. Health professionals advise that at least 30 minutes of activity at least 5 days a week will counteract health concerns, such as cardiovascular disease, diabetes and obesity that may result from inactivity. Now, researchers at the University of Missouri-Columbia say a new model regarding physical activity recommendations is emerging. New research shows that what people do in the other 15 and a half hours of their waking day is just as important, or more so, than the time they spend actively exercising.
In a series of studies that will be presented at the Second International Congress on Physical Activity and Public Health in Amsterdam, Hamilton, Theodore Zderic, a post-doctoral researcher, and their research team studied the impact of inactivity among rats, pigs and humans. In humans, they studied the effects of sitting in office chairs, using computers, reading, talking on the phone and watching TV. They found evidence that sitting had negative effects on fat and cholesterol metabolism. The researchers also found that physical inactivity throughout the day stimulated disease-promoting processes, and that exercising, even for an hour a day, was not sufficient to reverse the effect.
“The enzymes in blood vessels of muscles responsible for ‘fat burning’ are shut off within hours of not standing,” Hamilton said. “Standing and moving lightly will re-engage the enzymes, but since people are awake 16 hours a day, it stands to reason that when people sit much of that time they are losing the opportunity for optimal metabolism throughout the day.”
Only 28 percent of Americans are getting the minimal amount of recommended exercise. Hamilton predicts that eventually there will be health campaigns with doctors advocating limiting sitting time, just like they ask people to limit sun and second hand smoke exposure.
“The purpose of medical research is to offer effective new strategies for people whom the existing therapies are not working,” Hamilton said. “Because our research reveals that too little exercise and excessive sitting do not change health by the same genes and biological mechanisms, it offers hope for people who either are not seeing results from exercise or can not exercise regularly. The lifestyle change we are studying is also unlike exercise because it does not require that people squeeze an extra hour into their days and/or get sweaty at the gym, but instead improving the quality of what they already are doing. One misrepresentation is that people tend to say ‘I sit all the time, so your studies suggest that I can’t even work,’ but Ben Franklin and Thomas Jefferson showed us that you can be very productive and still do great work in an office with a ‘standing’ desk.”
Public release date: 19-Nov-2007
Progress in coronary disease death rates grinds to near halt in young adults
Before you plop in front of the television for a day of football, pizza and beer, you might consider this: New research shows that in young adults, decades of hard-won progress in reducing the risk of heart disease appears to be stalling, as recent death rates from coronary disease remain almost unchanged in young men and may even be increasing in women.
The research, conducted at the Centers for Disease Control and Prevention in Atlanta, appears in the November 27, 2007, issue of the Journal of the American College of Cardiology (JACC).
For the study, Dr. Ford and his colleague, Simon Capewell, M.D., of the University of Liverpool, U.K., analyzed United States vital statistics data between 1980 and 2002 for people aged 35 and older. Overall, the news was good: The death rate from coronary disease fell by 52 percent in men and 49 percent in women. When considered from a different perspective, the death rate from coronary disease among men declined, on average, by 2.9 percent per year during the 1980s, 2.6 percent per year during the 1990s, and 4.4 percent per year from 2000 to 2002. Among women, the average annual death rate declined by 2.6 percent, 2.4 percent, and 4.4 percent, respectively.
The numbers told a strikingly different story when the researchers reviewed the data by age. Among men aged 35 to 54, the average annual rate of death from coronary disease fell by 6.2 percent in the 1980s, slowed to 2.3 percent in the 1990s, and leveled off with an annual decline of just 0.5 percent between 2000 and 2002.
In women aged 35 to 54, the average annual rate of death from coronary disease fell by 5.4 percent in the 1980s and slowed to 1.2 percent in the 1990s. Between 2000 and 2002, the death rate actually increased by an average of 1.5 percent per year. This increase was not statistically significant. However, in even younger women—those aged 35 to 44—the rate of death from coronary disease increased by an average of 1.3 percent annually between 1997 and 2002, a finding that was statistically significant.
Public release date: 19-Nov-2007
Rogue bacteria involved in both heart disease and infertility
Researcher uncovers how chlamydia sabotages human immunity
Chlamydia pneumoniae is a microbe that normally causes pneumonia and bronchitis, but it has long been associated with atherosclerosis, a cardiovascular disease also called “hardening of the arteries.”
“It was a frightening prospect,” says Azenabor, “that atherosclerosis could come from a bacterial infection.” He decided to look for an explanation.
Chlamydiae are unusual, says the Nigerian-born scientist, because, unlike most other bacteria, they use the same form of cholesterol for metabolism that human cells use. Chlamydiae also are intracellular pathogens, meaning that they can only grow and reproduce inside of another cell.
But these bacteria have another peculiar ability.
Normally, when a pathogen invades human tissue, the immune response unleashes “killer cells” called macrophages, which stretch to engulf the attacker and destroy it with toxin-producing enzymes.
Chlamydiae fight back, says Azenabor, His work shows that, as they are ingested, these two species of Chlamydia can manipulate the functions of protective cells like macrophages in creative ways.
One of the keys lies in the macrophages’ cell walls, which store cholesterol and usually tightly control it.
But when it’s infected with C. pneumoniae, the microbe traffics cholesterol from the macrophage cell membrane to its own, causing a change in the macrophage that makes it rigid and unable to move.
The bacterium also disturbs the macrophage’s production of toxins in a process that transforms them into “signaling molecules,” which support functions that keep the bacterium alive.
“C. pneumoniae really wants to hijack the cell functions for its own use, like a parasite would,” he says. “The macrophage, though, wants to kill Chlamydia, but its killing ability has been converted to signaling.”
This is the reason the infection becomes chronic, Azenabor says. “Because of signaling, everything else in the human cell is still fine except for the altered toxins, so the bacteria can reproduce in a short time.”
As the macrophages become immobile, they accumulate in the blood vessel walls, setting the stage for atherosclerosis.
Infection and pregnancy
Armed with new information about how C. pneumoniae sabotages the immune response, Azenabor, who had also been studying the effects of estrogen on macrophages, turned his attention to another Chlamydia-related puzzle.
How is Chlamydia trachomatis, the species that causes a sexually transmitted disease, involved in the occurrence of spontaneous abortions or miscarriages?
He was immediately drawn to the protective cells in the placenta during early pregnancy – the trophoblasts.
“It’s not for nothing that trophoblasts are the early cells,” says Azenabor. “They prevent any kind of infection that could threaten the fertilized egg. They produce toxic chemicals similar to those of macrophages.”
Trophoblasts act like macrophages in many ways, and their functions are mediated by the hormones estrogen and progesterone. And cholesterol is the molecule used to produce those hormones.
Azenabor’s research shows that, like its cousin, C. trachomatis does take cholesterol from the trophoblast, and it also reproduces once inside the cell.
“It’s the same old story,” says Azenabor. “Only this time the attacked cell is a trophoblast instead of a macrophage, and the depleted cholesterol hinders production of estrogen and progesterone instead of altering toxin production.”
Azenabor’s lab members are continuing their inquiry, and they then will need to test the theories with live animals.
But the scientist is optimistic. Already he has a patented process for blocking the effects of calcium signaling for C. pneumoniae.
“If we can prevent C. trachomatis from becoming chronic, we could apply this remedy to pregnancy,” he says.
While conducting postdoctoral work at McMaster University in Ontario, he won the Canadian Distinguished Scientist Award in 1998, and moved to the University of Waterloo.
Azenabor joined the UWM faculty in 2001, after working as a scientist in a Chlamydia lab at UW–Madison. He jumped at the chance to start his own lab at UWM. Since arriving here he has won several honors, including the Shaw Distinguished Scientist Award from the James D. and Dorothy Shaw Fund in the Greater Milwaukee Foundation.
Although he didn’t plan on working with Chlamydia for this long, he is now a leading researcher in the field. One attraction, he says, is the work is unpredictable.
“When you begin,” he says, “you never know where you are going to go.”
Public release date: 20-Nov-2007
New study finds blood-spinal cord barrier compromised in mice with ALS
Tampa, FL — The blood-spinal cord barrier is functionally impaired in areas of motor neuron damage in mice modeling amyotrophic lateral sclerosis (ALS), report researchers at the University of South Florida Center for Aging and Brain Repair. The barrier disruption was found in mice at both early and late stages of ALS, a progressive neurodegenerative disease affecting nerve cells in the brain and the spinal cord.
The study, “Evidence of Compromised Blood-Spinal Cord Barrier in Early and Late Symptomatic SOD1 Mice Modeling ALS,” appears online in PLoS ONE, an international, peer-reviewed journal published by the Public Library of Science.
The blood-brain barrier (BBB) and blood-spinal cord barrier (BSCB) control the exchange of substances between the blood and the central nervous system. These barriers, formed by cells lining the blood vessels in the brain and the spinal cord, protect nerve cells by restricting entry of potentially harmful substances and cells of the immune system. Impairment in cellular machinery of the BBB and BSCB may lead to a barrier breakdown in many brain and spinal cord diseases or injuries.
“We detected vascular leakage in the cervical and lumbar spinal cord microvessels of ALS mice not only at the end-stage of disease but also in those with early disease symptoms,” said lead author Svitlana Garbuzova-Davis, PhD, DSc, assistant professor in the USF Center for Aging and Brain Repair. “This may suggest that large molecules such as the antibody IgG and other blood proteins appear in the spinal cord due to vascular leakage, one possible mechanism accelerating motor neuron damage.”
Public Release: 20-Nov-2007
CU study: Lead levels even well below U.S. standard may affect brain function in children
Even very small amounts of lead in children’s blood — amounts well below the current federal standard — are associated with reduced IQ scores, finds a new, six-year Cornell study.
The study examined the effect of lead exposure on cognitive function in children whose blood-lead levels (BLLs) were below the Centers for Disease Control and Prevention (CDC) standard of 10 micrograms per deciliter (mcg/dl) — about 100 parts per billion. The researchers compared children whose BLLs were between 0 and 5 mcg/dl with children in the 5-10 mcg/dl range.
“Even after taking into consideration family and environmental factors known to affect a child’s cognitive performance, blood lead played a significant role in predicting nonverbal IQ scores,” said Richard Canfield, a senior researcher in Cornell’s Division of Nutritional Sciences and senior author of the study in the journal Environmental Health Perspectives. “We found that the average IQ scores of children with BLLs of only 5 to 10 mcg/dl were about 5 points lower than the IQ scores of children with BLLs less than 5 mcg/dl. This indicates an adverse effect on children who have a BLL substantially below the CDC standard, suggesting the need for more stringent regulations,” he said.
In the United States over the last several months, nearly 50 specific products, including millions of toys for young children, have been recalled due to excessive lead in the paint, plastics and metal. “Our findings emphasize the very real dangers associated with low-level exposures, to which lead in toys can contribute,” Canfield said.
“The bottom line,” according to Canfield, “is that lead is a persistent neurotoxin that causes brain damage. The fact that lead has been found in millions of toys, even toys specifically designed for children to put into their mouths, presents an unacceptable risk. Our findings suggest the need to re-evaluate the current federal standards for lead in consumer products and the current definition of an elevated BLL in children.”
Public Release: 20-Nov-2007
Regular Exercise Reduces Risk of Blood Clots
Leiden, The Netherlands – November 20, 2007 – According to a new study published in Journal of Thrombosis and Haemostasis, regular participation in sports reduces the risk of developing blood clots by 39 percent in women and 22 percent in men.
“Women were shown to be even more likely to reap the benefits of regular sporting activities than men,” says F.R. Rosendaal, co-author of the study. “When we excluded women who were pregnant or receiving oral contraceptive or hormone replacement therapy – all possible causes of blood clots – the risk for women was reduced by 55 percent.”
The findings also show that people who did not participate in sports were more than four-times as likely to develop a blood clot if they were obese (with a body mass index of 30 or greater) than lean (with a body mass index of less than 25).
“When we looked at the results, we found that, overall, the mere fact that people took part in a sporting activity at least once a week was enough to lower their risk of blood clots,” say the authors.
Public release date: 26-Nov-2007
Not enough ‘good’ cholesterol makes it harder to recover from stroke
ST. PAUL, Minn. – People are at an increased risk of memory problems and greater disability after stroke if they have low levels of “good” cholesterol and high levels of homocysteine, an amino acid acquired mostly from eating meat. The findings are published in the November 27, 2007, issue of Neurology®, the medical journal of the American Academy of Neurology.
“These findings show metabolic stress plays a significant role in stroke recovery,” said study author George C. Newman, MD, PhD, with Albert Einstein Healthcare Network in Philadelphia, PA, and member of the American Academy of Neurology.
“People with low levels of HDL, high levels of homocysteine, and diabetes are twice as likely as those without such problems to have poorer cognitive function and greater disability after stroke,” said Newman. “The study also found stroke recovery was the most difficult for people over the age of 57 with high levels of homocysteine, which is a risk factor for heart problems and associated with low levels of vitamin B6, B12, folic acid and kidney disease.”
Public release date: 26-Nov-2007
High-glycemic index carbohydrates associated with risk for developing type 2 diabetes in women
Eating foods high on the glycemic index, which measures the effect of carbohydrates on blood glucose levels, may be associated with the risk for developing type 2 diabetes in Chinese women and in African-American women, according to two studies in the November 26 issue of Archives of Internal Medicine, one of the JAMA/Archives journals. However, eating more cereal fiber may be associated with a reduced risk for type 2 diabetes in African-American women
Researchers remain uncertain regarding exactly how diet, including carbohydrate intake, affects the development of type 2 diabetes, according to background information in the articles. Studies have revealed that the body absorbs carbohydrates from different foods at different rates. This leads to varying effects on levels of blood glucose and the hormone insulin, which converts glucose into energy. Foods high on the glycemic index, such as rice and other simple carbohydrates, cause a rapid spike and then a drop in blood glucose, whereas high-fiber foods tend to be lower on the glycemic index and have a more gradual effect. Some evidence has linked high–glycemic index foods with the risk of developing type 2 diabetes.
Ralph’s Note- As long as schools of nutrition teach that a calorie is no more than just a unit of energy. Than how calories from certain foods effect the body will never be properly addressed. There is obvious differences of how a 100 calories from broccoli effect the body as opposed to 100 calories from table sugar.
Public release date: 26-Nov-2007
Omega-3 fatty acids protect against Parkinson’s, study says
Quebec City, November 26, 2007—Omega-3 fatty acids protect the brain against Parkinson’s disease, according to a study by Université Laval researchers published in the online edition of the FASEB Journal, the journal of the Federation of American Societies for Experimental Biology. This study, supervised by Frederic Calon and Francesca Cicchetti, is the first to demonstrate the protective effect of a diet rich in omega-3 fatty acids against Parkinson’s.
The researchers observed that when mice were fed an omega-3 rich diet, they seemed immune to the effect of MPTP, a toxic compound that causes the same damage to the brain as Parkinson’s. “This compound, which has been used for more than 20 years in Parkinson’s research, works faster than the disease itself and is just as effective in targeting and destroying the dopamine-producing neurons in the brain,” points out Calon
By contrast, another group of mice that were fed an ordinary diet developed the characteristic symptoms of the disease when injected with MPTP, including a 31% drop in dopamine-producing neurons and a 50% decrease in dopamine levels.
Analyses revealed that omega-3 fatty acids—in particular DHA (docosahexaenoic acid), a specific type of omega-3—had replaced the omega-6 fatty acids already present in the brains of the mice that had been given omega-3 supplementation.
“This demonstrates both the importance of diet on the brain’s fatty acid composition and the brain’s natural inclination for omega-3 fatty acids,” observes Calon. Since concentrations of other types of omega-3’s had remained similar in both groups of mice, researchers suggest that the protective effect against Parkinson’s comes essentially from DHA.
Another conclusion to be drawn from this finding is that a brain containing a lot of omega-6 fatty acids may be a fertile ground for Parkinson’s disease. These fatty acids, abundant in foods rich in either vegetable oil or animal fat, are already under suspicion for their role in the body’s inflammatory response, cardiac disease, arthritis, and Alzheimer’s. In a balanced diet, the ratio between omega-6 and omega-3 fatty acids should be 4 to 1. However, the average Western diet contains 10 to 20 times more omega-6’s than omega-3’s.
“In North America, the average intake of DHA is between 60 to 80 mg a day, while experts recommend a daily minimum of 250 mg,” explains Calon. “Our results suggest that this DHA deficiency is a risk factor for developing Parkinson’s disease, and that we would benefit from evaluating omega-3’s potential for preventing and treating this disease in humans,” concludes the researcher.
Public release date: 26-Nov-2007
Ozone can affect heavier people more
A new study provides the first evidence that people with higher body mass index (BMI) may have a greater response to ozone than leaner people. Short-term exposure to atmospheric ozone has long been known to cause a temporary drop in lung function in many people. This is the first study in humans to look at whether body weight influenced how much lung function falls after acute ozone exposure. Ozone is formed in the atmosphere in the presence of sunlight from other pollutants emitted from vehicles and other sources.
To examine the question of whether higher body mass index influences ozone responses in humans, the investigators took advantage of an earlier study led by Milan J. Hazucha and colleagues at the Center for Environmental Medicine, Asthma and Lung Biology /UNC and the USEPA Human Studies Facility in Chapel Hill, N.C. From this study, BMI was determined in 197 subjects who had been exposed to ozone for 90 minutes, during which they alternated 20 minutes of exercise with 10 minutes of rest. The subjects’ lung capacity and function were tested immediately before and after the exposure period using spirometry, a basic lung function test that measures the speed and volume of how fast and how much air is breathed out of the lungs.
“It has been known for a long time that in response to short-term exposure to ozone lung function tends to temporarily drop in many people. There has recently been interest in why some people’s lung function drops more than others – – age and perhaps genetics, as well as diet may play a role, ” said NIEHS researcher and co-author Stephanie London, M.D. “We were intrigued by recent mouse studies that showed that obesity increases lung responses to ozone and wanted to see whether this applied in humans.”
The physiologic mechanisms responsible for the decline in lung function after ozone exposure with increasing BMI are not clear, although the authors suggest that perhaps circulatory hormones and other inflammatory factors may play a role. These factors have been shown to affect airway hyper-responsiveness and inflammation in animal models.
Ralph’s note- Can partially explain the increase in asthma rates.
Public release date: 27-Nov-2007
Radiation exposure of pregnant women more than doubles in 10 years
CHICAGO – The past decade has seen an unprecedented increase in the use of radiologic exams on pregnant women, according to a study presented today at the annual meeting of the Radiological Society of North America (RSNA).
Through medical imaging examinations, we are exposing pregnant women to twice the amount of radiation as we did 10 years ago,” said Elizabeth Lazarus, M.D., assistant professor of diagnostic imaging at the Warren Alpert School of Medicine at Brown University in Providence, R.I. “Overall, the levels of radiation to which we are exposing pregnant women are low, but they do carry a slight risk of harm to the developing fetus.”
The investigators found that from 1997 to 2006, the number of imaging studies performed on pregnant women increased by 121 percent. The greatest increases were in the number of CT exams, which deliver more radiation than many other radiologic procedures. An abdominal CT exposes the patient to a radiation amount more than twice that of an x-ray of the lower gastrointestinal tract. An abdominal ultrasound exposes the patient to no ionizing radiation.
Other studies have shown that use of high-tech modalities, such as CT and magnetic resonance imaging (MRI), has increased in all patient populations throughout the United States. According to Dr. Lazarus, some of this increase is due to the development of new imaging techniques to better diagnose abnormalities, and some is due to motivation by hospitals and insurers to make fast diagnoses to shorten hospital stays and improve patient care.
Public Release: 27-Nov-2007
Fear is stronger motivator to get fit than hope for those worrying about their bodies, says study
Fear of looking unattractive can be a stronger motivation for keeping people going to the gym than the hope of looking good, a study says.
Researchers at the University of Bath, UK, interviewed 281 male and female undergraduates and got half to imagine a physically unattractive version of themselves they feared they might turn into.
They then asked this group to either imagine a scenario in which they dramatically failed to keep to a fitness programme or one in which they dramatically succeeded.
The researchers found that those who had been asked to think about a dramatic failure to keep to the programme were motivated to keep on training because they were fearful of not looking good.
Those who were asked to imagine they were succeeding in getting fit became less motivated to continue at the gym because they no longer had this fear of not looking good.
“How consumers see themselves in the future has a strong effect on how motivated they are to keep using a product or service,” said Professor Brett Martin, of the University of Bath’s School of Management, who carried out the study with Dr Rana Sobh of Qatar University.
“When people dwell on a negative future, fear motivates them, yet as they move away from their feared state – a flabby body, or a wrinkled skin – they become less motivated.
“However marketers should also be aware that those who are thinking positively will become discouraged if they don’t see success.”
Professor Martin and Dr Sobh have devised performance measures to ensure marketers achieve the optimal balance in their communications with consumers and keep them motivated.
The 281 undergraduates were in surveyed in Bath and 62 per cent were gym users.
Professor Martin and Dr Sobh found that 85 per cent of those who wanted to avoid a feared unattractive self responded to a scenario where they were failing in the gym by wanting to press on, compared with 65 per cent who were succeeding in the gym who were motivated to continue.
They found that 91 per cent of those thinking positively about their bodies responded to a scenario where they were succeeding in the gym by wanting to press on, compared with just 57 per cent of people who were failing in the gym and wanted to go on.
Public release date: 27-Nov-2007
Scientists identify gene responsible for statin-induced muscle pain
Atrogin-1 gene mediates muscle toxicity of popular cholesterol-lowering drugs
BOSTON – Statins, the popular class of drugs used to lower cholesterol, are among the most commonly prescribed medications in developed countries. But for some patients, accompanying side effects of muscle weakness and pain become chronic problems and, in rare cases, can escalate to debilitating and even life-threatening damage.
Now a study led by investigators at Beth Israel Deaconess Medical Center (BIDMC), helps explain the source of these problems. Published in the December 2007 issue of The Journal of Clinical Investigation, the findings offer the first evidence that a gene known as atrogin-1 plays a key role in statin-related muscle toxicity.
“Although it is not known exactly how many of the 500 million individuals who take statins experience muscle pain and weakness, muscle symptoms are generally considered the most common side effects of these medications,” explains co-senior author Vikas P. Sukhatme, MD, PhD, Vice Chair of Medicine for Interdepartmental and Translational Programs, Chief of the Division of Nephrology, and Chief of the Division of Interdisciplinary Medicine and Biotechnology at BIDMC.
“Statin users describe a wide spectrum of symptoms – at the most extreme end is a severe breakdown of skeletal muscle known as rhabdomyolysis,” says Sukhatme, who is also the Victor J. Aresty Professor of Medicine at Harvard Medical School (HMS). “At the other end is ‘grumbling muscles,’ milder, more diffuse muscle soreness and cramps. This kind of symptomatic muscle weakness and pain is quite frequent, but often difficult to quantitate.”
Known by such trade names as Lipitor, Zocor, Pavacol and Mevacor, statins lower cholesterol by inhibiting HMG-CoA reductase, a key enzyme in cholesterol synthesis.
Approximately five years ago, the study’s co-senior author Stewart Lecker, MD, PhD, and colleagues in the HMS laboratory of Alfred Goldberg, MD, first discovered the atrogin-1 gene, so named for its role in muscle atrophy.
“We learned that atrogin-1 is rapidly turned on in wasting muscle,” explains Lecker, who is an investigator in the Division of Nephrology at BIDMC and Assistant Professor of Medicine at HMS. Muscle wasting occurs in a large number of disease states, including cancer, AIDS, and kidney disease and can also occur when muscles are underused due to injury or lack of exercise. “In the absence of atrogin-1 activation,” he adds, “muscle atrophy is diminished.”
Since this initial discovery, atrogin-1 has been found in every existing model of muscle wasting, prompting Lecker and Sukhatme to investigate whether cholesterol-lowering statins might also be “turning on” this gene.
“We reasoned that since atrogin-1 plays a key role in the development of wasting in skeletal muscle, it might also mediate part of [patients’] sensitivity to statins,” the authors write.
They proceeded to conduct three separate experiments to test this hypothesis. They first examined the expression of the atrogin-1 gene in biopsies of 19 human quadricep muscles from five control patients, six patients with muscle pain who were not being treated with statins and eight patients with muscle pain/damage who were using statins. Their results showed that atrogin-1 expression was significantly higher among the statin users.
Next, the scientists studied statins’ effects on cultured muscle cells treated with various concentrations of lovastatin. Compared with control samples, the lovastatin-treated cells became progressively thinner and more damaged. But remarkably, say the authors, the cells lacking the atrogin-1 gene were resistant to statins’ deleterious effects.
Finally, the authors tested the drug in zebrafish. And, they showed that just as in mammalian muscle cell culture, lovastatin led to muscle damage, even at low concentrations; as the concentration was increased, so too was the damage. And, once again, they observed that fish lacking the atrogin-1 gene were resistant to statin-induced damage.
“These three complementary experiments demonstrate that atrogin-1 has a fundamental role in statin-induced toxicity,” notes Lecker. “Future experiments will be aimed at understanding how statins turn on the atrogin-1 response in muscle, and in ascertaining what transpires in muscle following atrogin-1 activation that leads to muscle damage and atrophy. The hope is that eventually patients will be able to glean statins’ positive benefits to cholesterol metabolism and reduction of cardiovascular events while being spared accompanying muscle toxicities.”
Ralph’s Note – So who does not have atrogin-1 ?
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