Friday, January 8, 2009
Friday, January 8, 2009
ScienceDaily (Jan. 8, 2010) The music they listen to doesn't have any lyrics that tell them to grow, but new research from Tel Aviv University finds that premature babies who are exposed to music by 18th-century composer Wolfgang Amadeus Mozart gain weight faster -- and therefore become stronger -- than those who don't.
A new study carried out by Dr. Dror Mandel and Dr. Ronit Lubetzky of the Tel Aviv Medical Center affiliated with Tel Aviv University's Sackler School of Medicine has found that pre-term infants exposed to thirty minutes of Mozart's music in one session, once per day expend less energy -- and therefore need fewer calories to grow rapidly -- than when they are not "listening" to the music.
"It's not exactly clear how the music is affecting them, but it makes them calmer and less likely to be agitated," says Dr. Mendel, a lecturer at Tel Aviv University.
In the study, Dr. Mandel and Dr. Lubetzky and their team measured the physiological effects of music by Mozart played to pre-term newborns for 30 minutes. After the music was played, the researchers measured infants' energy expenditure again, and compared it to the amount of energy expended when the baby was at rest. After "hearing" the music, the infant expended less energy, a process that can lead to faster weight gain.
A "musical environment" for preemies
When it comes to preemies, one of the main priorities for doctors is to get the baby up to an acceptable body weight so he or she can be sent home. At the hospital, preterm babies may be exposed to infections and other illnesses, and a healthy body weight keeps them immune to other problems in the future.
While the scientists are not sure what occasioned the response, Dr. Mandel offers one hypothesis. "The repetitive melodies in Mozart's music may be affecting the organizational centers of the brain's cortex," he says. "Unlike Beethoven, Bach or Bartok, Mozart's music is composed with a melody that is highly repetitive. This might be the musical explanation. For the scientific one, more investigation is needed."
The study came about through an international project led by the U.S.-based consortium NIDCAP, whose goal is to create a set of standard practices to optimize the health and well-being of neonates. A number of environmental effects, such as tactile stimulation and room lighting, are already known to affect the survival and health of these very susceptible babies.
The TAU study is the first to quantify the effect of music, specifically Mozart, on newly born children. "Medical practitioners are aware that by changing the environment, we can create a whole new treatment paradigm for babies in neonatal care," says Dr. Mandel. "That's our main goal -- to improve their quality of life.
"The point of our research is to quantify these effects so that standards and care-guides can be developed. We still don't know the long-term effects of the music, or if other kinds of music will work just as well."
Is music "brain food" too?
The research is based on a controversial 1993 study showing that college students improved their IQs by listening to a Mozart sonata for 10 minutes. When the study was reported, parents in the U.S. started buying Mozart CDs, hoping to boost their children's brainpower.
Soon the Israeli researchers will start exploring different kinds of music to see if they can measure any similar effects on premature babies. One Israeli researcher suggested that rap music might evoke the same response as Mozart, since the pulsating and repetitive frequency in Mozart's music can be found in contemporary urban music as well.
The researchers will also survey mothers to discover what kind of music their babies were exposed to in the womb. They will then expose other neonates to the same music to scientifically verify any effect. The pieces to be played to the preterm babies will include ethnic music, rap music, pop music, and, of course, classical music like Bach, Beethoven and Mozart, says Dr. Mandel.
By Megan Brooks
Friday, January 8, 2009
NEW YORK (Reuters Health) Most Americans with major depression go untreated or under treated using a benchmark of American Psychiatric Association guidelines, according to a national study released this week.
Mexican Americans and African Americans are the least likely to receive treatment, especially treatment consistent with the guidelines, the study found. Those racial and ethnic disparities persisted regardless of health insurance coverage.
"Our findings support the conclusion that the U.S. mental health system is broken," Dr. Hector M. Gonzalez of Wayne State University, Detroit, and first author of the study, told Reuters Health by email.
The findings stem from interviews conducted between 2001 and 2003 with a diverse group of more than 15,000 Americans aged 18 and older.
A little more than 8 percent of the sample suffered from major depression, researchers found, including roughly 8 percent of Mexican Americans, Caribbean blacks, and non-Latino whites, and nearly 12 percent of Puerto Rican Americans.
Overall, only about half of those with depression received some type of treatment in the past year and less than a quarter had received "guideline-based" treatment, according to a report in the Archives of General Psychiatry.
(Earlier this week, a study suggested that mild to severe depression might be better treated with alternatives to antidepressant drugs, which do not help patients much more than an inactive placebo. See Reuters Health report, January 5, 2010.)
While 34 percent of those with depression received an antidepressant in the past year, only about 11 percent received guideline-based antidepressant therapy.
"Surprisingly," said Gonzalez, psychotherapy (talk therapy) was used more commonly by depressed Americans than antidepressant drugs; 44 percent said they had psychotherapy to combat their depression and for about 19 percent of these individuals, psychotherapy conformed to guidelines.
Depressed Mexican Americans and African Americans consistently had lower odds of receiving any type of treatment, let alone guideline-based treatment, in the past year. Depressed Puerto Rican and non-Latino whites were nearly twice as likely as Mexican Americans, Caribbean blacks, and African Americans to get recommended depression care, the authors report.
Having health insurance boosted the odds of depression care but not guideline-based care; this suggests, say the investigators, that while health insurance may equate to better access to depression treatment it does not ensure better care.
"Major depression is a leading cause of disability worldwide and in the US and thus is of high public health importance," Gonzalez told Reuters Health.
On January 1, the US Mental Health Parity Act, which promises to boost access to mental health care, took effect. But Gonzalez worries, "Even if patients are identified by clinicians as depressed, isolating or carving out mental health from the rest of medical services ensures that patients will fall between the institutional cracks and not get treatment."
"And that's for those who are 'better off' -- who have access to some mental health care. For ethnic and racial minorities, there are cultural, language and economic barriers to appropriate diagnosis on top of a fragmented mental health care system that leaves the vast majority of African and Mexicans untreated and under treated for depression," Gonzalez said.
Source: Archives of General Psychiatry, January 2010.
Friday, January 8, 2009
ScienceDaily (Jan. 8, 2010) University of Alberta medical researchers have made a major breakthrough in understanding a group of deadly disorders that includes the disease made famous in the movie Lorenzo's Oil.
Because this group of diseases is inherited, the discovery could help in screening carriers and lead to prevention or an effective treatment.
Richard Rachubinski, in the Faculty of Medicine & Dentistry, is an expert on structures in cells called peroxisomes which are involved in breaking down fatty acids. They are vital for humans. Babies born with a peroxizome disorder do not typically survive longer than a year because of impaired metabolism.
In his latest study, Rachubinski found another clue in the search to understand the peroxisome and the disorders caused by its malfunction. He and his team discovered that a protein family thought to be only involved in the early stages of making peroxisomes is actually crucial in ensuring peroxisomes transfer into other cells after they divide. All cells of the body must have peroxisomes to survive. These proteins are found in every living being, so they provide a universal mechanism not only for how peroxisomes are made but also for how peroxisomes are maintained in cells to keep them alive as they divide.
One peroxisome disorder is adrenoleukodystrophy, or ALD, the disease a boy named Lorenzo Odone suffered from. His parents' fight for a cure was made into the movie.
Rachubinski's findings have been published in the Journal of Cell Biology.
By Terri Coles
Friday, January 8, 2009
TORONTO (Reuters Health) Tea may protect against endometrial cancer, but more research is needed before it's clear if the antioxidant-rich beverage offers a real benefit, a recent analysis found.
Tea is the second most-consumed beverage in the world, after water, and multiple studies have looked into whether or not the drink brewed from the plant Camellia sinesis protects against various types of cancer. Animal studies have shown that the polyphenols found in tea may have a tumor-shrinking effect, but results focusing on endometrial cancer haven't shown a clear benefit.
Endometrial cancer - which forms in the lining of the uterus - is the fourth most common cancer in American women. The National Cancer Institute says there are 42,000 new cases in the United States each year, and nearly 7,800 deaths.
Researchers from the National Shanghai Center for New Drug Safety Evaluation and Research in China analyzed several published studies looking at the role of green and black tea in the prevention of endometrial cancer.
While the researchers found that existing research indicates that drinking tea - particularly green tea -- may offer some protection against endometrial cancer, they cautioned that the limited number of overall studies means that more investigation is needed.
The analysis of existing research, published in the American Journal of Obstetrics and Gynecology, included seven studies. The researchers first compared people who consumed tea regularly with those with the lowest or no tea consumption, and then compared low-consumption, moderate-consumption and high-consumption tea drinkers.
After accounting for the different ways the studies measured tea drinking, the researchers found that an increase in tea consumption of two cups daily was associated with a 25-percent reduced risk of developing endometrial cancer. The association was significant for green tea but not for black tea. There was also a protective effect shown in the Chinese and Japanese studies but not the American studies.
The researchers cautioned that the risk reduction seen in Asian studies but not the American studies may be the result of some other unexamined factor, such as diet, lifestyle or genetic differences. For example, American tea drinkers tend to drink black tea while most of tea drinkers in China and Japan drink green tea.
Finally, simply measuring tea exposure is difficult. Tea consumption in the different studies was measured by cups consumed daily, but cup size could vary among participants and across different countries.
If tea does offer a protective effect against endometrial cancer, it's likely due to a number of factors, the researchers suggested. Endometrial cancer is associated with late menopause or infertility, and the caffeine in tea can affect hormone levels.
Also, earlier research indicates that tea contains antioxidants that may affect cancer development. Tea also contains phytoestrogens, compounds that might protect against endometrial cancer because they could interfere with estrogen receptors.
It's difficult to apply the results of this analysis globally because the studies involved only looked at three countries, and because the researchers only found seven studies to review. However, the researchers said that because tea drinkers showed some evidence of a reduced risk of endometrial cancer, further investigation of the possible connection is worthwhile.
Source: American Journal of Obstetrics and Gynecology, December 2009.
Friday, January 8, 2009
ScienceDaily (Jan. 8, 2010) Abnormally high or low blood calcium levels are linked to an increased chance of premature death in non-dialysis kidney disease patients, according to a study appearing in an upcoming issue of the Clinical Journal of the American Society Nephrology (CJASN). The findings indicate the potential importance of finding drugs or other treatments that maintain normal blood calcium levels in non-dialysis patients.
Patients with chronic kidney disease (CKD) often have abnormally high or low blood calcium levels due to their compromised kidney function and the effects of commonly used medications. While abnormal calcium levels have been linked to higher premature death rates in dialysis patients, their effects in patients with earlier stages of CKD are less clear.
To investigate the issue, Csaba Kovesdy, MD (Salem VA Medical Center), and his colleagues examined the death rates associated with various blood calcium levels in 1,243 male US veterans with moderate-to-advanced CKD not requiring dialysis therapy. During the study, abnormally high calcium levels were linked to higher death rates among patients particularly when high calcium levels were present for a prolonged period of time. Specifically, compared with patients with normal blood calcium levels, patients with abnormally high levels had a 31% increased risk of dying during the study. Low calcium levels were also linked to higher death rates, but after much shorter periods of exposure to such levels. These patients had a 21% increased risk of dying.
The authors speculate that high calcium levels may be involved in processes that take a longer time to cause harm, such as the calcification of blood vessels or soft tissues, while low calcium levels may cause short-term deleterious effects such as heart rhythm abnormalities. The authors also noted that while their observations suggest that maintaining normal blood calcium levels is beneficial for non-dialysis CKD patients, prospective studies are needed to determine the target range for blood calcium and how such a target should be achieved.
Study co-authors include Olga Kuchmak, MD (Carilion Clinic), Jun Lu, MD (Salem Research Institute), and Kamyar Kalantar-Zadeh, MD PhD (Harbor-UCLA Medical Center and David Geffen School of Medicine at UCLA). Dr. Kovesdy and Dr. Kalantar-Zadeh have received grant support and/or honoraria from Fresenius, Genzyme and Shire. The other authors report no financial disclosures.
Csaba P. Kovesdy, Olga Kuchmak, Jun L. Lu, and Kamyar Kalantar-Zadeh. Outcomes Associated with Serum Calcium Level in Men with Non-Dialysis Dependent Chronic Kidney Disease. Clinical Journal of the American Society Nephrology, Jan. 7, 2010 DOI: 10.2215/CJN.06040809
Friday, January 8, 2009
FRIDAY, Jan. 8 (HealthDay News) -- Caffeine in coffee reduces the severity of liver fibrosis in patients with chronic hepatitis C virus, a new study has found.
Liver fibrosis (scarring of the liver) is the second stage of liver disease during which liver function declines because of accumulated connective tissue.
The new U.S. National Institutes of Health study included 177 patients, mean age 51, whose daily consumption of caffeine from food and beverages was tracked for two years.
Patients who consumed more than 308 milligrams of caffeine from coffee per day had milder liver fibrosis than other patients. The daily amount of caffeine intake found to be beneficial is equivalent to 2.25 cups of regular coffee. For each 67-milligram increase in caffeine consumption (about one half cup of coffee), there was a 14 percent decrease in the odds of advanced fibrosis for patients with hepatitis C virus.
Other sources of caffeine -- such as soft drinks, tea, caffeine-fortified drinks and caffeine pills -- didn't have the same helpful effect, according to the study published in the January issue of the journal Hepatology.
The researchers said further research is needed to determine whether the protective effects of coffee/caffeine increase at levels beyond normal daily intake.
The U.S. Centers for Disease Control and Prevention has more about hepatitis C.
Friday, January 8, 2009
ScienceDaily (Jan. 8, 2010) Despite a massive global research effort, many basics of Alzheimer's disease onset remain elusive. This has hampered development of treatments effective during the earliest stages of the disease, when prevention is most likely.
But a new discovery by University of Central Florida researchers has revealed a previously unknown mechanism that may drive the early brain function deterioration of Alzheimer's victims, thus opening a new exploratory path in the quest for an Alzheimer's cure.
The research, which will be published Jan. 8, 2010, in the peer-reviewed science and medicine journal PLoS ONE, also demonstrates how the unique application of an existing cell research technique could accelerate the discovery of treatments to exploit the new findings.
Researchers have known for years that a substance called amyloid-beta gums up brain cells when it becomes too concentrated, because it forms damaging deposits on the cells known as plaques. These prevent normal electrical signal generation in the cells, eventually killing them. That drives the memory loss and other problems that plague Alzheimer's sufferers.
Most Alzheimer's studies have focused on brain cells already damaged by amyloid-beta or the effects of high concentration of amyloid-beta. The University of Central Florida team, led by James Hickman, head of the UCF NanoScience Technology Center's Hybrid Systems Laboratory, instead explored impacts of very low amyloid-beta concentrations on healthy cells in an effort to mimic the earlier stages of Alzheimer's. The results were shocking.
Squelching the Signals
The UCF team found that over time, though there are no outward signs of damage, exposure to moderate amyloid-beta concentrations somehow prevents electrical signals from traveling normally through the cells. Because the effect is seen in otherwise healthy cells, Hickman believes the team may have uncovered a critical process in the progression of Alzheimer's that could occur before a person shows any known signs of brain impairment.
"What we're claiming is that before you have any behavioral clues, these electrical transmission problems may be occurring," he says.
If this proves true, then the team has opened a promising potential path to an Alzheimer's treatment that could block the onset of the mild cognitive impairment associated with early Alzheimer's. In contrast, all currently available treatments manage symptoms of Alzheimer's after they first appear -- when it is likely too late for prevention.
"I think it's a very important paper," says Dave Morgan, an Alzheimer's expert at the University of South Florida not involved in the research, "This opens up a whole series of important questions, and answering them may lead to alternative drugs or other agents to benefit Alzheimer's patients."
Accelerating Challenging Brain Studies
Kucku Varghese, a former graduate student in the Hickman lab now at the University of Florida, first demonstrated amyloid-beta's effects at low concentrations on healthy cells using a common cell research method that is laborious and unsuitable for long-term experiments. But the Hickman team quickly moved to more advanced experiments using microelectrode arrays (MEA) to study the new finding. MEA studies use cultures of neurons on plates embedded with tiny electrodes that can send and measure electrical signals through nearby cells without damaging them, allowing extended experimentation.
Hickman hopes to use MEAs and other tools to pinpoint the physiological and chemical changes within the brain cells that cause the loss of signal generation in healthy cells. Mechanisms responsible for the changes could offer potential targets for drugs, which pharmaceutical companies could search for using the MEA techniques demonstrated, and the mechanisms might provide a measurable target for early diagnosis of Alzheimer's.
"We're trying to find a marker that will lead to detection and treatment while slowing down Alzheimer's progression and can really make a difference by delaying or even preventing onset of the disease," says Hickman.
In addition to Hickman and Varghese, contributors to the paper include UCF NanoScience Technology Center researchers Peter Molnar, Mainak Das, Neelima Bhargava and Stephen Lambert. Lambert also is a UCF College of Medicine faculty member. Mark S. Kindy from the Medical University of South Carolina, where Hickman and Varghese have worked, also contributed to the study.
Kucku Varghese, Peter Molnar, Mainak Das, Neelima Bhargava, Stephen Lambert, Mark S. Kindy, James J. Hickman. A New Target for Amyloid Beta Toxicity Validated by Standard and High-Throughput Electrophysiology. PLoS ONE, 2010; 5 (1): e8643 DOI: 10.1371/journal.pone.0008643
Thursday, January 7, 2010
By Julie Steenhuysen
Thursday, January 7, 2010
CHICAGO (Reuters) Prolonged exposure to cocaine can cause permanent changes in the way genes are switched on and off in the brain, a finding that may lead to more effective treatments for many kinds of addiction, U.S. researchers said on Thursday.
A study in mice by Ian Maze of Mount Sinai School of Medicine in New York and colleagues found that chronic cocaine addiction kept a specific enzyme from doing its job of shutting off other genes in the pleasure circuits of the brain, making the mice crave the drug even more.
The study helps explain how cocaine use changes the brain, said Dr. Nora Volkow, director of the National Institute on Drug Abuse, part of the National Institutes of Health, which funded the study published in the journal Science.
"This finding is opening up our understanding about how repeated drug use modifies in long-lasting ways the function of neurons," Volkow said in a telephone interview.
For the study, the team gave one group of young mice repeated doses of cocaine and another group repeated doses of saline, then a single dose of cocaine.
They found that one way cocaine alters the reward circuits in the brain is by repressing gene 9A, which makes an enzyme that plays a critical role in switching genes on and off.
Other studies have found that animals exposed to cocaine for a long period of time undergo dramatic changes in the way certain genes are turned on and off, and they develop a strong preference for cocaine.
This study helps explain how that occurs, Volkow said, and may even lead to new ways of overcoming addiction.
In the study, Maze and colleagues showed these effects could be reversed by increasing the activity of gene 9A.
"When they do that, they completely reverse the effects of chronic cocaine use," Volkow said.
She said this mechanism is likely not confined to cocaine addiction, and could lead to a new area of addiction research for other drugs, alcohol and even nicotine addition.
"One of the questions we've had all along is, after discontinuing a drug, why do you continue to be addicted?
"This is one of the mechanisms that probably is responsible for these long-lasting modifications to the way people who are addicted to drugs perceive the world and react to it," she said.
(Editing by Todd Eastham)
By Amy Norton
Thursday, January 7, 2010
NEW YORK (Reuters Health) A healthy weight and regular exercise may help protect men from one of the most common side effects of prostate cancer surgery, a new study suggests.
Researchers found that among 165 men who had their prostate glands removed due to cancer, those who were not obese and were getting regular exercise before surgery had the lowest prevalence of long-term urinary incontinence.
What's more, even among obese men, those who had been physically active before surgery were less likely to be incontinent one year after surgery.
All of the men in the study had undergone radical prostatectomy, where a surgeon removes the prostate gland and some of the surrounding tissue. Urinary incontinence and sexual dysfunction are common side effects, though both often improve over time.
So far, most efforts to prevent lasting side effects have focused on improving surgical techniques -- limiting damage to the nerves, muscles and blood vessels around the prostate gland.
But these latest findings suggest that there are also lifestyle measures men can take to cut their risk of lingering urinary incontinence, said lead researcher Dr. Kathleen Y. Wolin, an assistant professor of surgery at Washington University School of Medicine in St. Louis.
"This is another reason for men to get up and get active," she told Reuters Health in an interview.
In general, men with prostate cancer, like all other men, are encouraged to follow a healthy lifestyle, which includes regular exercise. A study published last month found that among men with prostate cancer, those who got as little as 15 minutes of exercise per day had lower death rates than inactive men during the two-decade study period.
"We strongly recommend that men with prostate cancer talk with their physicians about how to fit physical activity into their lives if they are currently sedentary," Wolin said.
For their study, published in the Journal of Urology, Wolin and her colleagues looked at urinary incontinence rates among 165 men roughly one year after radical prostatectomy. Before surgery, all of the men had reported on their exercise habits; those who said they exercised for at least one hour per week were considered active.
Overall, the researchers found that obese, sedentary men had the highest rate of long-term incontinence, at 41 percent. Active, non-obese men had the lowest rate, at 16 percent.
Among obese men who were physically active, one-quarter were incontinent, which was identical to the rate among non-obese, inactive men -- suggesting, the researchers say, that exercise can offset the negative effects of obesity.
Exactly why exercise might prevent incontinence is unclear. One possibility, Wolin said, is that exercisers have better overall muscle tone, which may help with bladder control.
Another potential reason is that long-time exercisers are more likely to follow their doctors' advice on performing post-surgery Kegel exercises, which strengthen the pelvic-floor muscles and may improve incontinence and sexual function.
According to Wolin, more studies are needed to see whether certain types and intensities of exercise are more effective than others -- and how exercise habits after prostate surgery may affect long-term incontinence risk.
Source: Journal of Urology, February 2010.
Thursday, January 7, 2010
ScienceDaily (Jan. 7, 2010) Many people have traded in their gas-guzzling old "clunkers" for newer and more efficient models or cut back on energy use at home by opting for Energy Star appliances and compact fluorescent light bulbs. But, when it comes to our muscles, a little less efficiency might be just what the doctor ordered, suggests a report in the January Cell Metabolism, a Cell Press publication.
The researchers from the Mayo Clinic and the University of Iowa have new insight into an important "fuel gauge" in muscle. They've also uncovered evidence in mice that treatments designed to disrupt those so-called sarcolemmal ATP-sensitive K+ (KATP) channels specifically in muscles might allow us to control our weight by increasing the number of calories our muscles will burn with regular activity or exercise.
"The channels sense even minor changes in nucleotide energy and respond by shortening the duration of action potentials and limiting energy-demanding muscle contractility and maintenance of ion composition," said Alexey Alekseev of the Mayo Clinic. "If you don't have the channel, you will consume more energy. The system normally has an energy-saving role, but with a sedentary lifestyle and excess of food, it favors obesity."
"In some ways it may seem paradoxical to fight against what is a very good system for fueling our muscles with energy efficiency," added Leonid Zingman of the University of Iowa. "On the other hand, it's also paradoxical that many of us today have an excessive food supply and we don't need to move."
Earlier work had shown that the KATP channels found at the surface of heart and skeletal muscle cells play a role under severely stressful conditions such as heart disease, acting as a kind of safety valve. But their everyday role remained unclear. After all, Alekseev said, ischemic heart disease really is a modern human problem, not one experienced by organisms living in their natural environments.
Now, they show that the KATP channels are responsible for keeping those muscle and heart cells pumping without expending any more energy than they have to. Animals with skeletal muscles that are deficient for the KATP channels store less glucose in the form of glycogen and less fat to become leaner. The animals' weight loss persists even when they eat diets that are high in fat. That reduction in stored muscle energy comes with a price of reduced physical endurance, however.
The researchers conclude that "sarcolemmal KATP channels govern muscle energy economy, and their downregulation in a tissue-specific manner could present an anti-obesity strategy by rendering muscle increasingly thermogenic at rest and less fuel efficient during exercise."
The findings also point Zingman to another general principle when it comes to our weight.
"For me, the most surprising thing was how small changes can translate to significant changes with time," he said, noting that mice with and without the channels start out the same in terms of body weight but start to diverge from one another by the time they reach four months in age. "Limiting energy consumption by a small fraction with every movement or beat of the heart can add up to a significant change in total energy consumption. Small actions may really make a huge difference."
The researchers include Alexey E. Alekseev, Mayo Clinic, Rochester, MN; Santiago Reyes, Mayo Clinic, Rochester, MN; Satsuki Yamada, Mayo Clinic, Rochester, MN; Denice M. Hodgson-Zingman, Mayo Clinic, Rochester, MN, University of Iowa, Iowa City, IA; Srinivasan Sattiraju, Mayo Clinic, Rochester, MN; Zhiyong Zhu, University of Iowa, Iowa City, IA; Ana Sierra, University of Iowa, Iowa City, IA; Marina Gerbin, Mayo Clinic, Rochester, MN; William A. Coetzee, New York University School of Medicine, New York, NY; David J. Goldhamer, University of Connecticut, Storrs, CT; Andre Terzic, Mayo Clinic, Rochester, MN; and Leonid V. Zingman, Mayo Clinic, Rochester, MN, University of Iowa, Iowa City, IA
By Alan Mozes
Thursday, January 7, 2010
THURSDAY, Jan. 7 (HealthDay News) -- The popular herbal supplement St. John's wort does not appear to relieve the pain and discomfort that accompanies irritable bowel syndrome (IBS), new research suggests.
The finding is the first to indicate that an herbal preparation long-touted as an effective alternative treatment for mild and moderate depression does not appear to treat IBS.
"People are definitely looking for alternative treatment options, and as a physician I have patients showing up all the time with supplements and asking me, 'Should I be taking this?'" said study author Dr. Yuri A. Saito, an assistant professor of medicine at the Miles and Shirley Fiterman Center for Digestive Diseases at the Mayo Clinic in Rochester, Minn. "But there is a global paucity of clinical trials with respect to natural alternative agents, so it's not always possible to give a good answer," Saito added.
"So we decided to see whether St. John's wort -- which is a bona fide, effective treatment for mild-to-moderate depression -- is effective as a treatment for irritable bowel syndrome, which no one had done before," Saito said. "And unfortunately, we found that at conventional doses of 900 milligrams a day, we did not see any clear benefit over placebo."
Saito and her colleagues report their findings in the January issue of the American Journal of Gastroenterology.
The authors point out that St. John's wort held promise as a potential IBS treatment, given that depression is often linked to the onset of IBS. In fact, prescription antidepressants are frequently used for the treatment of the syndrome, which affects between 10 percent and 22 percent of the U.S. population.
Therefore, to test St. John's wort as a treatment for IBS, the research team tracked 70 patients aged 18 to 70 between 2006 and 2008.
All the patients had a confirmed diagnosis of IBS, and over a 12-week period half were treated with two daily doses of St. John's wort (450 milligrams each), while the other half were given placebos.
Biweekly monitoring of symptom relief and a post-study follow-up revealed that both the St. John's wort group and the placebo group experienced a "pattern of improvement," with some dissipation of the bloating, constipation, diarrhea, pain and discomfort typically caused by IBS. No patient in either group experienced any serious side effects.
However, the placebo group actually fared better, ending up with a significantly greater reduction in IBS symptoms than the St. John's wort group, the study authors found.
What's more, by the study's conclusion, more patients in the placebo group said their IBS symptoms had improved moderately or a lot and more indicated a willingness to continue taking their treatment, compared to the St. John's wort group.
"Unfortunately, a lot of people out there are purchasing supplement products based on trial-and-error," Saito noted. "But even though I wouldn't have any hesitation about recommending St. John's wort for depression, based on this I think I'd feel reasonably comfortable telling my IBS patients to save their money because I don't think St. John's wort is going to help."
In reaction to the findings, Douglas MacKay, vice president of scientific and regulatory affairs for the Council for Responsible Nutrition, the leading trade organization for the dietary supplement industry -- suggested the current study was too small to be considered definitive or generalizable to all IBS patients.
"Additionally, it is important to point out that those treated with St. John's wort were not depressed," noted MacKay, "so this study does not answer the question of whether or not St. Johns wort may have benefit for depressed individuals who also suffer from IBS, which is a common subtype of individuals with IBS. We would like to see more research conducted with depressed individuals with IBS, where St. John's wort may be most effective."
On the other hand, he observed that the study does "reiterate the strong safety profile of St. John's wort," and stressed that the supplement continues, therefore, to be a safe choice for patients coping with mild-to-moderate depression.
For more on irritable bowel syndrome, visit the National Digestive Diseases Information Clearinghouse.
Thursday, January 7, 2010
ScienceDaily (Jan. 7, 2010) If you're an aging baby boomer hoping for a buffer physique, there's hope. A team of American scientists from Texas and Michigan have made a significant discovery about the cause of age-related muscle atrophy that could lead to new drugs to halt this natural process.
This research, available online the FASEB Journal, shows that free radicals, such as reactive oxygen species, damage mitochondria in muscle cells, leading to cell death and muscle atrophy. Now that scientists understand the cause of age-related muscle loss, they can begin to develop new drugs to halt the process.
"Age-related muscle atrophy in skeletal muscle is inevitable. However, we know it can be slowed down or delayed," said Holly Van Remmen, Ph.D., co-author of the study, from the Sam and Ann Barshop Institute for Longevity and Aging Studies at the University of Texas Health Science Center at San Antonio. "Our goal is to increase our understanding of the basic mechanisms underlying sarcopenia to gain insight that will help us to discover therapeutic interventions to slow or limit this process."
To make this discovery, Van Remmen and colleagues used mice that were genetically manipulated to prevent them from having a protective antioxidant (CuZnSOD). As a result of not being able to produce this antioxidant, the mice had very high levels of free radicals (reactive oxygen species) and lost muscle mass and function at a much faster rate than normal mice. Additionally, the muscles of the genetically modified mice were much smaller and weaker than those of normal mice. Scientists believe that these findings mimic effects of the normal aging process in humans, but at an accelerated rate.
"I don't expect to see baby boomers gracing the pages of body building magazines tomorrow. But this research is important because it identifies molecules responsible for the aging of our muscles: free radicals," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. "Stop these from acting and we'll all look younger, stronger and fit at any age.
Youngmok C. Jang, Michael S. Lustgarten, Yuhong Liu, Florian L. Muller, Arunabh Bhattacharya, Hanyu Liang, Adam B. Salmon, Susan V. Brooks, Lisa Larkin, Christopher R. Hayworth, Arlan Richardson, and Holly Van Remmen. Increased superoxide in vivo accelerates age-associated muscle atrophy through mitochondrial dysfunction and neuromuscular junction degeneration. The FASEB Journal, 2009; DOI: 10.1096/fj.09-146308
By Kate Kelland
Thursday, January 7, 2010
LONDON (Reuters) A global scarcity of scientific research on using nanotechnology in foods means food safety authorities are unable to properly regulate products that may be beneficial or harmful, a British science panel said on Friday.
The science and technology committee of Britain's upper house of parliament said in a report that use of nanoparticles in food and food packaging is likely to grow dramatically in the next decade, but too little is known about their safety.
"The technologies have the potential to deliver some significant benefits to consumers, but it is important that detailed and thorough research into potential health and safety implications ... is undertaken now to ensure that any possible risks are identified," said Lord Krebs, chair of the Science and Technology Committee which produced the report.
Nanotechnology is the design and manipulation of materials thousands of times smaller than the width of a human hair, called nanoparticles.
The technology has been hailed as a new way to make stronger and more lightweight materials, better cosmetics and tastier or healthier foods, but Friday's report said a paucity of scientific research across the world meant its potential benefits and risks in food were largely unknown.
According to Krebs whose committee heard evidence from food producer groups, regulators and scientific experts from across the world, the global market for nanotechnology in food was $410 million in 2006 and is set to grow to $5.6 billion in 2012.
"We are on the cusp of a potentially explosive growth in this novel approach to food manufacture and processing," he told a news briefing.
There are currently at least 600 products involving nanomaterials on the market but only around 80 of them are food or food-related and only two of those are available in the UK.
The report called for new rules to compel food companies to tell regulators about any work they are doing with nanoparticles in food, and also called for a voluntary public register of food products and packaging containing nanomaterials available.
Krebs said the food industry in Britain and worldwide was being "quite obscure" about any work they are doing on using nanotechnology for products or packaging -- an attitude he described as "exactly the wrong approach".
"The food industry must be much more open with the public about research it has undertaken in this area and where it sees nanomaterials being used in food production in future," he said.
Stephen Holgate, a clinical professor of immunopharmacology at the University of Southampton, who advised the committee on its report, said some studies suggest nanoparticles behave differently in the body than larger ones.
"Most of the research so far... has shown that these particles can penetrate barriers and get into the system -- and they can find their way into the liver, into the kidney and even into the brain," he told reporters. "Knowing that, we really need now to concentrate on finding out what their effects are."
The report's authors warned that the lessons of a public backlash against genetically modified food in Europe showed that "secrecy breeds mistrust, and that openness and transparency are crucial to maintain public confidence."
(Editing by Philippa Fletcher)
Thursday, January 7, 2010
THURSDAY, Jan. 7 (HealthDay News) -- An enzyme that normally helps break down stored fats becomes highly active in some cancer cells and makes them more likely to spread, researchers have found.
When the enzyme, called monoacylglycerol lipase (MAGL), goes into overdrive in cancer cells, it breaks down stored fats to produce large amounts of free fatty acids, which are the building blocks of cell membranes and of fatty molecules that serve as signals between cells. These free fatty acids then produce other smaller molecules that promote cancer growth and progression, the study authors noted.
The finding that stored fats in cancer cells can cause them to become more aggressive offers a possible explanation for the reported link between obesity and cancer, according to the researchers at the Scripps Research Institute in California. They also said MAGL may offer a new target for treating aggressive forms of cancer or for preventing cancer progression.
"Historically, research has focused on the mechanisms leading to cancer formation, and therapies have focused on taking out cancer cells. But here we were looking for pathways that lead to cancer aggressiveness," corresponding author Benjamin Cravatt, chair of the Scripps Research Department of Chemical Physiology, said in a news release.
He noted that people who eat high-fat foods are constantly introducing free fatty acids into their bodies.
"We have shown that cancer cells have their own pathways to produce free fatty acids, which will enable them to become more aggressive. Less malignant cancer cells do not appear to have adopted an autonomous pathway to increase their own pools of free fatty acids. Thus, taking free fatty acids from the diet could assist these cells in developing a more malignant phenotype," Cravatt said.
The study was published in the Jan. 8 issue of the journal Cell.
The U.S. National Cancer Institute has more about obesity and cancer.
By Terri Coles
Thursday, January 7, 2010
TORONTO (Reuters Health) Less than a quarter of Americans eats the five daily servings of fruits and vegetables that the National Cancer Institute recommends, but online programs may help boost those numbers, a new study hints.
As part of the Making Effective Nutrition Choices study, some 2500 people logged on to a website providing information on the benefits of eating more fruits and vegetables and ways to incorporate these healthy foods into their diets.
Three months into the study about 70 percent of subjects were eating five or more servings of fruits and vegetables on an average day, up from 20 percent at the starting point. That increase held for the rest of the year-long study.
It was surprising to see such a large jump in the number of participants reaching the guidelines so early on, said study leader Dr. Christine Cole Johnson, and also to have those results hold for the next nine months. "In most nutritional studies, you're happy if you get a half-serving increase," Johnson said. But this study showed average increases of at least two servings daily.
Because the study included men and women aged 21 to 65 from around the country, the results indicate that a well-designed website could be used to educate more widely on the importance of fruit and vegetable consumption, Johnson said. "We think this could reach a large number of people and change habits on a national level," she said.
The results of the study are published in the latest issue of the American Journal of Public Health.
In the study, conducted at five U.S. sites, the researchers assessed change in fruit and vegetable intake associated with visiting a website that provided tailored nutritional information, with or without motivational emails, and an untailored "control" website.
The two websites had the same basic design, but the tailored website provided personalized nutritional information based on responses to a survey given at the outset, while the control site provided general information about nutrition related to fruits and vegetables. With the tailored website, "the messages they were given were based on concerns they had (about increasing consumption) and how to address those," Johnson said.
When the study began, the participants averaged 4.4 fruit and vegetable servings daily according to a 16-item "food frequency" questionnaire and 3.3 according to a 2-item questionnaire about average daily fruit and vegetable consumption.
By the end of the study, both questionnaires showed that daily fruit and vegetable consumption had increased by more than two servings, on average. Participants who accessed the tailored website showed comparable increases, whether or not they received email counseling, of about 2.7 servings daily, while those who used the generic website increased their daily servings by about 2.35.
The study participants reported an overall high level of satisfaction with the websites and the information they received on them, Johnson said. Statistically, it's hard to say what effect the motivational emails had on the results, she said, but study participants reported that they liked that feature and found it helpful.
Non-minority women over 50 with high levels of education were the most likely to stick with the program and increase their servings, the study found.
It was somewhat surprising, Johnson noted, that the web-based program was less popular with younger participants. Study co-author Dr. Gwen Alexander is currently working on a program aimed at younger participants. "It needs to be in front of them, accessible and easy," Alexander said.
Source: American Journal of Public Health, January 2010.
Wednesday, January 6, 2010
Wednesday, January 6, 2010
WEDNESDAY, Jan. 6 (HealthDay News) -- Fat mass plays an important role in building bone mass in teenage girls and having too little may increase their risk of osteoporosis later in life, new research has found.
In the study, researchers measured cortical bone mass (the hard outer layer of bone) in 4,005 girls and boys, mean age 15.5 years. The results showed that fat mass had a positive influence on bone mass, particularly in girls, where the effect was about 70 percent greater than in boys.
The study is scheduled for publication in the February issue of the Journal of Clinical Endocrinology & Metabolism.
"The effect of fat mass on bone mass appears to be strongest in girls," study lead author Jonathan Tobias, of the University of Bristol in England, said in an Endocrine Society news release. "Girls clearly have more fat mass than boys and our findings show that whereas the greater lean mass in boys contributes to their greater cortical bone mass, this effect is partly counteracted by the greater fat mass in girls," Tobias explained.
"Fat mass in girls during puberty may have a long-term impact on bone health as they grow into adulthood. Excessive reduction in fat mass could have adverse effects on the developing skeleton particularly in girls, leading to an increased risk of osteoporosis later in life," Tobias said.
The National Osteoporosis Foundation has more about osteoporosis prevention.
Wednesday, January 6, 2010
ScienceDaily (Jan. 6, 2010) Researchers from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) determined that patients with chronic hepatitis C virus (HCV) who consumed more than 308 mg of caffeine daily had milder liver fibrosis. The daily amount of caffeine intake found to be beneficial is equivalent to 2.25 cups of regular coffee. Other sources of caffeine beyond coffee did not have the same therapeutic effect.
Details of this study are available in the January 2010 issue of Hepatology, a journal published by Wiley-Blackwell on behalf of the American Association for the Study of Liver Diseases.
Liver fibrosis or scaring of the liver is the second stage of liver disease and characterized by a degradation of liver function due to accumulated connective tissue. Past studies have looked at modifiable behaviors, such as coffee consumption, that mitigate the progression of liver disease. A number of studies have looked at the benefits of higher coffee intake with results that include: lower prevalence of chronic liver disease, reduced risk of hepatocellular carcinoma (liver cancer), and lower risk of death from cirrhosis complications. "From data collected to date it remains unclear whether coffee itself, or caffeine provides the beneficial effect," said Apurva Modi, M.D. and lead author of the current study that focuses on caffeine intake and its impact on liver fibrosis.
From January 2006 to November 2008 all patients evaluated in the Liver Disease Branch of the National Institutes of Health were asked to complete a questionnaire to determine caffeine consumption. Questions were asked pertaining to all sources of caffeine including regular and diet soft drinks; regular and decaffeinated coffee; black, green, Chinese and herbal teas; cocoa and hot chocolate; caffeine-fortified drinks; chocolate candy; caffeine pills; and medications with caffeine. Participants were asked about their frequency of caffeine consumption, which was quantified as never; 1-3 times per month; 1, 2-4, or 5-6 times per week; 1, 2-3, 4-5, and 6 or more times per day.
The analysis included 177 participants who were undergoing liver biopsy with a mean age of 51 years and mean body mass index (BMI) of 27.5. Of those in the cohort 56% were male, 59% Caucasian, 19% Black, 19% Asian, 3% Hispanic, and 68% had chronic HCV. Daily consumption of caffeine from food and beverages raged from none to 1028 mg/day with an average of 195 mg/day, which is equivalent to 1.4 cups of coffee daily. Most caffeine consumed came from regular coffee (71%) followed by caffeinated soda (13%), and black tea (4%). Repeated administration of the questionnaire within a 6-month period displayed consistent responses suggesting caffeine intake does not significantly change over time.
Patients with an Ishak fibrosis score of less than 3 had a mean caffeine intake of 212 mg/day compared with 154 mg/day for those with more advanced fibrosis. The Ishak fibrosis score is the preferred system that measures degree of liver scarring with 0 representing no fibrosis through 6 indicating cirrhosis. For each 67 mg increase in caffeine consumption (about one half cup of coffee) there was a 14% decrease in the odds of advanced fibrosis for patients with HCV. "Our data suggest that a beneficial effect requires caffeine consumption above a threshold of approximately 2 coffee-cup equivalents daily," noted Dr. Modi. The protective effects of consuming more than 308 mg of caffeine daily persisted after controlling for age, sex, race, liver disease, BMI and alcohol intake for all study participants.
Researchers further evaluated caffeine and coffee separately to determine the individual effect of each on fibrosis. Results showed that consumption of caffeinated soda, green or black tea was not associated with reduced liver fibrosis. However, a significant protective effect could have been missed due to small numbers, as 71% of total caffeine consumed came from coffee.
Caffeinated coffee had the most pronounced effect on reduced liver fibrosis. The authors suggest that further research is needed to determine if the protective benefits of coffee/caffeine intake plateau at amounts beyond the daily consumption threshold.
Apurva A Modi, Jordan J Feld, Yoon Park, David E Kleiner, James E. Everhart, T. Jake Liang, and Jay H. Hoofnagle. Increased caffeine consumption is associated with reduced hepatic fibrosis. Hepatology, 2009; NA DOI: 10.1002/hep.23279
By Amy Norton
Wednesday, January 6, 2010
NEW YORK (Reuters Health) Young children whose mothers took folic acid supplements in late pregnancy may have an increased risk of developing asthma, a new study hints.
The findings, published in the American Journal of Epidemiology, appear to be the first to link mothers' use of folic acid in pregnancy to their children's later asthma risk.
Researchers emphasize that it is too early to give pregnant women any specific advice based on the results.
Moreover, the study does not implicate folic acid use in early pregnancy.
This is an important finding, note the researchers, because adequate folic acid around the time of conception helps lower the risk of certain birth defects of the brain and spine. Known as neural tube defects, these anomalies include spina bifida, a paralyzing defect of the spine, and anencephaly, a fatal defect where most or all of the brain fails to develop.
Experts advise women to take 400 micrograms of folic acid per day shortly before conceiving and in the first trimester of pregnancy, a critical window of time when neural tube defects take shape.
The current findings "don't contradict" that advice, lead researcher Dr. Michael Davies, of the University of Adelaide in Australia, told Reuters Health in an email.
However, he added, since folic acid is necessary only in the first trimester to prevent neural tube defects, further studies should look at whether more-specific guidelines on folic acid use during the remainder of pregnancy can and should be developed.
For their study, Davies and his colleagues looked at asthma rates among more than 400 children whose mothers had been followed since pregnancy. A little less than 12 percent of the children had developed asthma by age 3, and the same percentage had the lung disease at age 5.
Overall, the study found, children whose mothers took folic acid in late pregnancy -- from the 30th week on -- were one-quarter more likely to have asthma at age 3 compared with children whose mothers did not take folic acid at that point in pregnancy.
They were also more likely to have persistent asthma symptoms from the age of 3 through age 5.
Most mothers who took folic acid in late pregnancy did not take it as a stand-alone supplement, but as part of a multivitamin; they typically got 300 micrograms of folic acid per day from supplements.
There was no link between mothers' folate intake from food and their children's asthma risk; folate is the natural form of folic acid, found in foods such as beans and lentils, orange juice, peanuts and green vegetables like spinach and broccoli.
That latter finding, Davies noted, should encourage women to eat a healthy diet, including folate-rich foods, throughout pregnancy.
It is not entirely clear why folic acid supplements in late pregnancy would promote asthma in some children. However, Davies pointed to recent animal research suggesting that folate can alter the activity of immune-system-regulating genes in the lung tissue -- potentially making it more susceptible to allergic reactions.
Since the fetal immune system develops later in pregnancy, folic acid use at this point could theoretically affect a child's future risk of asthma.
Davies stressed, however, that a single study is rarely enough to change health policies and practices.
"We would like to see systematic replication of our findings and clinical trials in various populations," he said, "so that we can provide appropriate, refined and targeted advice."
Source: American Journal of Epidemiology, December 15, 2009.
Wednesday, January 6, 2010
ScienceDaily (Jan. 6, 2010) Researchers have identified two cellular proteins that are important factors in hepatitis C virus infection, a finding that may result in the approval of new and less toxic treatments for the disease, which can lead to liver cancer and cirrhosis.
An estimated 270 to 300 million people worldwide are infected with hepatitis C and the conventional treatments -- interferon and ribavirin -- can have significant side effects. A new drug targeting cellular proteins rather than viral proteins would be a valuable addition to the treatment arsenal, said Samuel French, an assistant professor of pathology and senior author of the study.
French and his team set out to identify the cellular factors involved in hepatitis C replication and, using mass spectrometry, found that heat shock proteins (HSPs) 40 and 70 were important for viral infection. HSP 70 was previously known to be involved, but HSP 40 was linked for the first time to hepatitis C infection, French said. They further showed that the natural compound Quercetin, which inhibits the synthesis of these proteins, significantly inhibits viral infection in tissue culture.
"This is an important finding because we can block these proteins with the idea of reducing the level of the virus in people and, ideally, completely eliminate it," said French, who also is a researcher at UCLA's Jonsson Comprehensive Cancer Center.
The study appeared in the most recent issue of the journal Hepatology.
Since Quercetin has been shown to inhibit hepatitis C infection, French said, a Phase I clinical trial will be launched at UCLA to determine if the compound is safe and effective.
Quercetin is a plant-derived bioflavonoid, and is used by some people as a nutritional supplement. Laboratory studies show it may have anti-inflammatory and antioxidant properties, and it is being investigated for a wide range of potential health benefits. Currently, there are early-stage clinical trials testing quercetin for safety and efficacy against sarcoidosis, asthma and glucose absorption in obesity and diabetes.
"Because Quercetin targets cellular proteins rather than viral proteins, there is less likelihood of developing viral resistance," French said. "Cellular proteins cannot change like viral proteins can."
Many patients in the United States have a type of hepatitis C virus that does not respond to the standard treatments. In these cases, if the virus can't be blocked, end-stage liver disease and, ultimately, death may occur. Once HSP 40 and 70 were identified, French and his team used Quercetin in an attempt to block the proteins and found that the compound "reduced infectious particle production at non-toxic concentrations," according to the study.
"Quercetin may allow for the dissection of the viral life cycle and has potential therapeutic use to reduce virus production with low associated toxicity," the study states.
The UCLA clinical trial will most likely target those with type 1 hepatitis C, which is the non-responsive type prevalent in this country. Only about 50 percent of those with type 1 hepatitis C respond to treatment, French said.
Volunteers with type 1 hepatitis C who opt not to undergo conventional therapies would be recruited for the study. In other studies in other diseases, Quercetin has resulted in no significant side effects, French said.
"A non-toxic treatment for chronic hepatitis C would be great because our current therapies have significant side effects and only a certain percentage of the patient population responds," French said.
The three-year study was funded by the National Institutes of Health, the Cure Digestive Diseases Research Center and the Stein Oppenheimer Endowment Award.
By Alicia Chang
AP Science Writer
The Associated Press
Wednesday, January 6, 2010
ALHAMBRA, Calif. The fight against fat is going high-tech. To get an inside look at eating and exercise habits, scientists are developing wearable wireless sensors to monitor overweight and obese people as they go about their daily lives.
The experimental devices are designed to keep track of how many minutes they work out, how much food they consume and even whether they are at a fast-food joint when they should be in the park. The goal is to cut down on self-reported answers that often cover up what's really happening.
In a lab in this Los Angeles suburb, two overweight teenagers help test the devices by taking turns sitting, standing, lying down, running on a treadmill and playing Wii. As music thumps in the background, wireless sensors on their chests record their heart rates, stress levels and amount of physical activity. The information is sent to a cell phone.
"I can't feel my legs," 15-year-old Amorette Castillo groans after her second treadmill run.
Traditional weight-loss interventions rely mainly on people's memory of what they ate for dinner and how many minutes they worked out. But researchers have long known that method can be unreliable since people often forget details or lie.
The new devices are being designed in labs or created with off-the-shelf parts. Some similar instruments are already on the market, including a model that tracks calories burned by measuring motion, sweat and heat with armbands.
But the devices in development aim to be more sophisticated by featuring more precise electronics and sometimes even video cameras. Many emerging systems also strive to provide instant feedback and personalized treatment for wearers.
At the University of Southern California lab, the teens alternated between being sedentary and active as researchers resolved the technical bugs. Later this year, some will wear the body sensors at home on weekends. If they get too lazy, they will get pinged with a text message.
"We'll be able to know real-time if they're inactive, if they're active," said Donna Spruijt-Metz, a USC child obesity expert in charge of the project.
The devices are made possible by advances in technology such as accelerometers that can measure the duration and intensity of a workout. They also use Bluetooth-enabled cell phones that can take pictures of meals and send information back.
Will all this wizardry lead to a slimmer society? Scientists say there's reason to hope. Getting an accurate picture of what people eat and how often they move around will help researchers develop personalized weight-loss advice.
Obesity is epidemic in the United States with two-thirds of adults either overweight or obese. It's a major health concern for children and adolescents, who are at higher risk for high blood pressure, high cholesterol and diabetes as they grow older.
A federally funded pilot project by the Pennington Biomedical Research Center in Louisiana is exploring whether people can lose more weight when tracked by technology.
Participants carry around Blackberry Curves to snap pictures of their meals and leftovers. They also wear a quarter-sized device on their shoe that counts the number of steps they take.
Counselors pore over the incoming data and give individually tailored health advice through e-mail or telephone. Every month, the participants get their weight checked, and their progress is compared against a separate group that receives only generic health tips.
The study involves just seven people, but researchers eventually hope to have 40.
"It's highly personalized. You get feedback very quickly," said Corby Martin, who heads Pennington's Ingestive Behavior Laboratory.
By using technology to capture eating and exercise details, researchers hope to bypass self-reporting that can sometimes give an incomplete picture.
But some medical experts are concerned about ethical questions. Even if people agree to be tracked, researchers worry about intruding into the rest of their lives and the lives of those around them.
"As a researcher, I'm a professional voyeur, and I like to find out whatever I can about human subjects," said William McCarthy, a professor of public health and psychology at the University of California, Los Angeles. "But if I were a subject, I'd be concerned about the level of detail that's being captured about my behavior from moment to moment."
University of Pittsburgh engineer Mingui Sun has developed a necklace equipped with a video camera that records where a person goes and what he or she eats. Before a researcher sees the data, it's filtered by a computer that blurs out other people's faces.
The device is not smart enough to know whether the wearer ate a Big Mac or tofu. So a researcher inputs the food, and the computer calculates the portion size, calories and nutrients.
Sun's lab workers are wearing the prototype, and he hopes to test it on real people by the middle of the year.
Another concern is whether people, particularly youngsters, will stick with it.
Fellow Pittsburgh researcher Dana Rofey recently completed a study of 20 overweight female preteens and teens who wore armbands tracking the number of steps taken and calories burned daily.
Researchers found the armbands were worn 75 percent of the time. Though the study did not include a comparison group, researchers were pleased with the high compliance rate.
On a recent weekday, Castillo and another study volunteer, 13-year-old Eric Carles, headed straight from school to the USC lab, where they strapped the sensors on and went through a sort of circuit training. The project manager timed them as a postdoctoral student recorded the session through a one-way mirror.
Through periods of sitting, standing and exercising, they chatted about scary movies and upcoming exams. Wearing the devices felt "weird" to Castillo initially, but she has since grown used to it.
Castillo admits she doesn't exercise as she often as she would like and has a sweet tooth for chocolate. Carles, who plays after-school sports, confesses he eats a lot. The teens were willing to try anything to help them lose weight.
After enduring more than two hours of required physical activity, the two were allowed to do whatever they want. Researchers called it "free living," and it offered a glimpse into the activities teens would choose when they test the sensors at home.
The two chose to play a music video game. With Castillo on drums and Carles on the guitar, they rocked out to Duran Duran and Bon Jovi as researchers looked on.
By JoAnne Allen
Wednesday, January 6, 2010
WASHINGTON (Reuters) A study in mice suggests using cellphones may help prevent some of the brain-wasting effects of Alzheimer's disease, U.S. researchers said on Wednesday.
After long-term exposure to electromagnetic waves such as those used in cell phones, mice genetically altered to develop Alzheimer's performed as well on memory and thinking skill tests as healthy mice, the researchers wrote in the Journal of Alzheimer's Disease.
The results were a major surprise and open the possibility of developing a noninvasive, drug-free treatment for Alzheimer's, said lead author Gary Arendash of the University of South Florida.
He said he had expected cell phone exposure to increase the effects of dementia.
"Quite to the contrary, those mice were protected if the cell phone exposure was stared in early adulthood. Or if the cellphone exposure was started after they were already memory- impaired, it reversed that impairment," Arendash said in a telephone interview.
Arendash's team exposed the mice to electromagnetic waves equivalent to those emitted by a cellphone pressed against a human head for two hours daily over seven to nine months.
At the end of that time, they found cellphone exposure erased a build-up of beta amyloid, a protein that serves as a hallmark of Alzheimer's disease.
The Alzheimer's mice showed improvement and had reversal of their brain pathology, he said.
"It (the electromagnetic wave) prevents the aggregation of that bad protein of the brain," Arendash said. "The findings are intriguing to us because they open up a whole new field in neuroscience, we believe, which is the long-term effects of electromagnetic fields on memory."
Arendash said his team was modifying the experiment to see if they could produce faster results and begin testing humans.
Despite decades of research, there are few effective treatments and no cure for Alzheimer's, the most common form of dementia. Many treatments that have shown promise in mice have had little effect on humans.
More than 35 million people globally will suffer from Alzheimer's disease or other forms of dementia in 2010, according to the Alzheimer's Association.
There has been recent controversy about whether electromagnetic waves from cellphones cause brain cancer.
Co-author Chuanhai Cao said the mice study is more evidence that long-term cellphone use is not harmful to the brain.
Groups such as the World Health Organization, the American Cancer Society, and the National Institutes of Health, have all concluded that scientific evidence to date does not support any adverse health effects associated with the use of cellphones.
(Editing by Alan Elsner)
By Stephanie Nano
Associated Press Writer
The Associated Press
Wednesday, January 6, 2010
NEW YORK Looks like doctors aren't the only ones who should scrub before surgery. Bathing patients with an antiseptic and squirting medicated ointment up their noses dramatically cut the rate of dangerous staph infections afterward, researchers found.
A second study found the antiseptic did a better job of preventing infections than the reddish-brown iodine solution that's been used for decades to swab the skin before an operation.
Infections are a vexing problem for hospitals. Some 30 million surgical procedures are done each year, and up to a half million Americans develop surgical-site infections, mostly from staph bacteria.
While attention has been focused on ways to stop health care workers from spreading bugs, patients can also contaminate themselves with the germs they harbor in their noses or on their skin.
"A lot of people think it's all from the outside world, but these are your own germs," said Dr. Robert Weinstein, an infectious disease expert at Cook County's Stroger Hospital in Chicago.
Two new studies, published in Thursday's New England Journal of Medicine, tried different approaches to killing those bacteria to see if that reduced the number of post-surgery infections.
U.S. researchers tested a newer antiseptic against the iodine solution commonly used to prep surgery patients and found it cut all surgical-site infections by 40 percent. The study's leader, Dr. Rabih Darouiche, of the Michael DeBakey VA Medical Center in Houston, and other experts expect the newer antiseptic to replace iodine.
In the Netherlands, where the newer antiseptic prep is already used, researchers screened patients and treated those who had staph bacteria to see if there was any additional benefit. Treatments with nasal ointment and antiseptic baths reduced staph infections by nearly 60 percent compared to dummy treatments.
"This is the single most effective way of preventing surgical-site infections," said researcher Dr. Henri Verbrugh of the Erasmus University Medical Center in Rotterdam.
The Dutch researchers and others had tested the staph-killing ointment before with mixed results. They attribute the positive outcome to the development of a rapid screening test, the addition of the antiseptic bath and continuing the treatment for five days.
The study was done at five hospitals in the Netherlands and involved 917 mostly surgical patients who tested positive for staph bacteria when they were admitted. They were treated with either mupirocin ointment twice daily and daily baths with antiseptic chlorhexidine soap or dummy ointment and soap.
Over the next six weeks, about 3 percent of the treated group had staph infections compared to about 8 percent in the dummy treatment group. The treatment also cut average hospital stays by two days.
The U.S. study at six hospitals included 849 patients who were having surgeries with a moderate risk for infection. The incision area was cleaned with either the iodine scrub or a mixture of chlorhexidine and alcohol. A month later, the overall infection rate in the chlorhexidine group was about 10 percent compared to 16 percent for iodine.
Darouiche said the two preps both work against a variety of germs but the newer blue-tinted antiseptic works quicker and longer. It costs more on average $12 vs. $3 for the iodine prep but Darouiche said the expense is outweighed by the thousands saved by preventing costly infections.
Dr. Richard Wenzel, who wrote an editorial on the studies, said the U.S. research supports switching antiseptics. But he said the pre-surgery screening should be for those at higher risk of infection, including patients having heart surgery or getting an implant.
Wenzel, of Virginia Commonwealth University in Richmond, Va., said patients can play a role by asking about infection rates connected with their hospital and doctor. Prevention guidelines call for patients to get antibiotics right before surgery and for hair to be clipped, not shaved.
The two studies "offer remarkably safer strategies for all patients who require surgery," he wrote.
The U.S. study was funded by CareFusion Corp., formerly part of Cardinal Health Inc., which makes the antiseptics tested. The researchers report getting grants and consulting fees from the company, and one is a company employee. The Dutch study was funded by a number of drugmakers; some of the researchers receive advisory board and lecture fees from them.
On the Net:
New England Journal: http://www.nejm.org
Wednesday, January 6, 2010
NEW YORK (Reuters Health) Getting enough selenium in your diet could help protect you from cancer of the esophagus, a large new study suggests.
People with the highest levels of this antioxidant mineral were at the lowest risk of developing squamous cell carcinoma of the esophagus, Dr. Jessie Steevens of Maastricht University Medical Center in The Netherlands and her colleagues found.
The amount of selenium in the soil where food is grown determines its selenium content. There's some evidence for a link between selenium levels and stomach and esophageal cancer, and Steevens and colleagues say it's important to look at subtypes of these cancers separately because they are likely to have different causes.
The researchers looked at the relationship between selenium levels and three different types of cancer: esophageal squamous cell carcinoma (ESCC), which arises from the cells lining the upper esophagus; esophageal adenocarcinoma (EAC), which begins in gland cells located where the esophagus joins the stomach; and gastric cardia adenocarcinoma (GCA), which involves the upper part of the stomach.
"EAC and GCA are specifically of interest," the investigators wrote in the journal Gastroenterology, because the incidences of these cancers have risen in the US and Europe during the past decades.
The researchers looked at data from the Netherlands Cohort Study, which followed 120,852 men and women 55 to 69 years old for 16 years. They compared selenium levels in 64 patients who developed ESCC during follow-up; 112 EAC patients; 114 GCA patients; and 2,072 cancer-free controls. All had provided toenail clippings at the study's outset; the selenium content of a person's nails is considered to be an accurate measurement of their levels of the mineral over the previous year.
The higher a person's selenium levels, the researchers found, the lower their likelihood of developing ESCC. GCA also was associated with selenium levels, but the relationship was "borderline significant"; it was stronger for women than for men. Overall there was no relationship between selenium levels and EAC, but when the researchers looked separately at women and people who had never smoked, they did find an association between higher selenium levels and EAC risk. There was also a relationship between selenium intake and EAC risk in people with lower intakes of several antioxidant nutrients.
The findings, conclude the researchers, suggest that low selenium levels may increase risk of ESCC and GCA, as well as EAC in women, never-smokers, and people with low antioxidant intakes. They caution, however, that the findings need to be confirmed by other researchers.
Source: Gastroenterology, online December 14, 2009.
By Ed Edelson
Wednesday, January 6, 2010
WEDNESDAY, Jan. 6 (HealthDay News) -- New research indicates that the darker skin of blacks may increase their risk of heart disease and stroke because it reduces production of vitamin D, which is made during exposure to sunlight.
Several studies have associated low levels of vitamin D with an increased risk of cardiovascular disease and "the biggest source of vitamin D levels is sunlight," said Dr. Kevin Fiscella, a professor of family medicine and community and preventive medicine at the University of Rochester, and co-author of a paper in the January/February issue of the Annals of Family Medicine. "People with dark skin who live at higher latitudes, where the intensity of sunlight is less, may be at greater risk."
But the issue abounds with unanswered questions, starting with whether there is a real cause-and-effect relationship of vitamin D levels and cardiovascular risk, and ending with whether supplements that increase blood levels of the vitamin lower that risk, Fiscella said.
"We don't truly know the answer," Fiscella said. "That is the really pivotal question, what happens to cardiovascular risk if you correct blood levels of vitamin D. We do know that small supplements for middle-aged people don't seem to have any effect."
In the study, Fiscella and Dr. Peter Franks of the University of California, Davis, looked at data on more than 15,000 U.S. adults in a national nutritional study. They found that overall, the 25 percent of adults with the lowest levels of vitamin D had a 40 percent higher risk of cardiovascular death. When they singled out blacks, the report found a 38 percent higher incidence of such deaths than among whites. Most of that difference was related to lower levels of vitamin D.
"The first issue is clarifying whether vitamin D is truly an independent risk factor for cardiovascular disease," Fiscella said. There are reasons to believe that it is, since too-low levels of the vitamin are associated with development of high blood pressure, kidney disease and diabetes, he said, but the case is not proven.
A second issue concerns the proper level of intake of the vitamin. "A consensus is evolving that the current levels recommended are too low, and those with darker skin need higher levels," Fiscella said.
The current recommendation is a daily intake of 400 International Units (IUs) for most adults, and 600 IU for those over 70. Fiscella declined to make a recommendation.
There was no such hesitation on the part of Dr. James O'Keefe Jr., director of preventive cardiology at the Mid America Heart Institute in Kansas City, who has done his own studies of vitamin D and the heart.
"I recommend for most people 2,000 IU a day," O'Keefe said. "African-Americans probably need closer to 4,000 or 5,000."
Too few Americans have their vitamin D levels checked regularly, "so I tell people to get their vitamin D levels checked," O'Keefe said. "Three out of four Americans will need a vitamin D supplement."
While it hasn't been proven that raising vitamin D levels reduces cardiovascular risk, studies now underway will answer that question, O'Keefe said. Meanwhile, he said, "vitamin D supplements are very cheap" and it is difficult to overdose on the vitamin, although bone problems can develop with a daily intake of 10,000 or more IU, he said.
Fiscella is much more cautious. "I don't think we have great data on what happens at very high levels," he said. "If you recommend very high doses, some people will develop very high blood levels, and we don't have good enough data to say on the population level what the impact of very high levels would be."
A fact sheet on vitamin D is provided by the U.S. Office of Dietary Supplements.
By Ben Hirschler
Wednesday, January 6, 2010
LONDON (Reuters) The more scientists look, the more complex cancer seems to become.
British scientists said on Wednesday they had found a batch of new gene mutations linked to kidney cancer, suggesting even this apparently "straightforward" cancer type can be divided into subtypes requiring tailored treatment.
Clear cell renal cell carcinoma (ccRCC), the most common type of kidney cancer, stands out from other cancers because it is remarkably consistent and the majority of cases are known to be driven by mutations in a single gene, called VHL.
Yet when researchers conducted a large DNA sequencing study of more than 3,500 genes from around 100 tumor samples, they found evidence that additional mutations in other genes were also driving cells to become cancerous.
Three of the genes were involved in modifying proteins called histones, which help package DNA into chromosomes and are critical to the functioning of cells, they reported in the journal Nature.
"Even in this clearest of cases, we see evidence for substantial genetic heterogeneity," said Andy Futreal, co-leader of the Cancer Genome Project at the Wellcome Trust Sanger Institute in Cambridge.
While none of the new mutations accounted for more than 5 percent of cancer cases, the discovery should ultimately help in diagnosis and better selection of treatments for patients.
The latest findings underline the case for personalized medicine, or tailoring drugs to the genetic make-up of individual patients.
Scientists at the Sanger Institute last month also produced genetic "maps" identifying thousands of genetic mutations behind melanoma skin cancer and lung cancer.
Several personalized drugs are already used in cancer, including Roche's Herceptin for breast cancer and AstraZeneca's Iressa for lung cancer.
For drugmakers, tailored medicine is both an opportunity and a challenge as sub-dividing tumors by their molecular type shrinks the market for individual therapies.
Kidney cancer kills more than 100,000 people worldwide each year. Recent new drugs against the disease include Pfizer's Sutent and Bayer's Nexavar, which block cell proliferation and starve tumors of blood supply.
(Editing by Elizabeth Fullerton)
January 6, 2010
WEDNESDAY, Jan. 6 (HealthDay News) -- Targeting two different enzymes simultaneously may hold promise for treating people with Alzheimer's disease, researchers report.
This "cocktail" strategy, described in the Jan. 6 issue of Science Translational Medicine, outperformed a one-enzyme-at-a-time treatment and also avoided the troublesome side effects seen with that strategy, Johns Hopkins scientists say.
"This does give an idea that moderate reduction of both of these [enzymes] in combination could have an effective response and get rid of all the side effects," said Ian Murray, an assistant professor of neuroscience and experimental therapeutics at Texas A&M Health Science Center College of Medicine in College Station.
So far the results have only been seen in mice, although clinical trials could be on the horizon.
Most experts believe that Alzheimer's is caused by the overproduction of amyloid beta protein or amyloid plaque in the brain.
Two enzymes, beta-secretase and gamma-secretase, produce amyloid plaque by cleaving or breaking down the parent protein, known as amyloid precursor protein (APP).
"They work hand in hand, one after the other and act like scissors, cutting up this [APP] protein into smaller bits and smaller bits called amyloid peptide, which we think is the cause of Alzheimer's disease when it's abnormally accumulated in the brain," explained study senior author Philip C. Wong, a professor of pathology and of neuroscience at Johns Hopkins University School of Medicine in Baltimore.
"They both are required for generation of amyloid beta peptide," he added.
Researchers and pharmaceutical companies hope to figure out how to inhibit these enzymes as a way to treat Alzheimer's.
But beta secretase and gamma secretase have other jobs, too, which likely would be affected by any attempt to reduce their activity.
"Initially we knocked out each one individually and showed that if you reduce the activity you do have good efficacy in terms of reducing amyloid burden, but it also led to other problems," Wong said.
In this trial, the researchers tried a new approach: reducing levels of both enzymes at the same time in genetically altered mice. That worked.
"The combination of reducing both enzymes simultaneously will give you a better outcome in terms of reducing the amyloid and attenuating the learning and memory behavior you see in these animal models," Wong said. "Moreover, we did not see any evidence of side effects."
Compounds to inhibit these genes are nearing possible use in clinical trials, the authors stated.
"It does hold promise for future studies in human subjects," Murray said. But, no actual drugs were used in the study, only genetic alterations to mimic the desired effect of a future drug, he added.
Another potential obstacle is amyloid beta's recently discovered role in synaptic function, or connections and communication between neurons.
"Too much or too little amyloid beta is detrimental, so it seems that you have to have a balance," Murray pointed out.
And, "it has been suggested that reduction of amyloid beta at late stages in the disease may not have any benefit, as the neurological damage has already occurred," he added. "However, clinical trials with amyloid beta vaccination suggest that reduction of amyloid beta halts cognitive decline in this disease [so] there is promise for such therapy."
Visit the Alzheimer's Association for more on this condition.
Wednesday, January 6, 2010
ScienceDaily (Jan. 6, 2010) New UK research, published in PLoS ONE, has not reproduced previous findings that suggested Chronic Fatigue Syndrome may be linked to a recently discovered virus. The authors of the study, from Imperial College London and King's College London, say this means that anti-retroviral drugs may not be an effective treatment for people with the illness.
An estimated three in 1000 people have Chronic Fatigue Syndrome (CFS), or myalgic encephalomyelitis (ME), experiencing severe physical and mental fatigue that is not alleviated by rest, together with other symptoms such as muscle pain, headache, joint pain and depression. Diagnosing CFS is difficult, as symptoms vary and there is no standard test. The fundamental cause of CFS is unknown and it is usually treated using rehabilitation techniques such as cognitive behavioural therapy or graded exercise therapy.
In October 2009, a group of US scientists published research in the journal Science that suggested that a recently discovered virus called XMRV could be linked to CFS. In their study, 68 out of 101 patients with the illness and 8 out of 218 healthy controls appeared to be infected with the virus.
However, in the study, researchers found no evidence that patients with CFS had the XMRV virus, after analysing tissue samples from 186 patients with CFS using sensitive molecular testing techniques.
This more recent analysis showed no molecular evidence for XMRV in any of the samples from CFS patients. The researchers say this means that anti-retrovirals should not be used to treat CFS, as they would be unlikely to have an effect on the symptoms. However, several labs in the US now offer CFS patients treatments based on the earlier findings that linked the condition with XMRV.
Professor Myra McClure, one of the authors of the study from the Division of Medicine at Imperial College London, said: "Our research was carried out under rigorous conditions -- we looked at samples from well-studied patients, and we used very sensitive testing methods to look for the virus. If it had been there, we would have found it. The lab in which we carried out the analysis had never housed any of the murine leukaemia viruses related to XMRV, and we took great care to ensure there was no contamination.
"We are confident that our results show there is no link between XMRV and Chronic Fatigue Syndrome, at least in the UK. The US study had some dramatic results that implied people with the illness could be treated with anti-retrovirals. Our recommendation to people with Chronic Fatigue Syndrome would be not to change their treatment regime, because our results suggest that anti-retrovirals would not be an effective treatment for the condition," added Professor McClure.
After reading the US study, clinical researchers from King's College London sent blood samples from 186 CFS patients to the Imperial Retrovirology Laboratory team. King's has been running an NHS service for CFS patients for nearly twenty years, and the previously stored samples came from patients had been fully investigated and examined, meaning that CFS was the correct diagnosis.
The Imperial scientists extracted the DNA from the samples and analysed it using a sensitive technique, called Polymerase Chain Reaction (PCR), which can locate tiny fragments of virus DNA. The scientists analysed control samples of water at the same time to ensure there was no contamination. They also looked for a specific marker fragment of human DNA in the sample to make sure the technique was working.
The water controls contained no DNA, showing that the samples were not contaminated. All the test samples, from patients and healthy controls, contained the human DNA they looked for, suggesting the technique was working well.
Dr Anthony Cleare, Reader in Psychiatric Neuroendocrinology, one of the authors of the study from the Chronic Fatigue Syndrome Clinic at King's College London, said: "Chronic Fatigue Syndrome is a serious and debilitating condition. It can also be extremely frustrating for people with the illness, as we have yet to identify its fundamental cause, or come up with any definitive treatments. The recent US study generated real excitement among doctors and patients alike as it seemed to open up a new line of research. Unfortunately, we have not been able to replicate those findings."
"It is important to emphasise that [these] findings do not invalidate all previous research, some of which has shown that CFS can be triggered by other infective agents, such as Epstein Barr Virus or Giardia parasites. As ever in science, no single study is conclusive and there are lots of other research groups working on this at the moment. We await their results with interest," added Professor Simon Wessely, another author of the study from the Chronic Fatigue Syndrome Clinic at King's College London.
Erlwein et al. Failure to Detect the Novel Retrovirus XMRV in Chronic Fatigue Syndrome. PLoS ONE, 2010; 5 (1): e8519 DOI: 10.1371/journal.pone.0008519
Tuesday, January 5, 2009
Tuesday, January 5, 2009
ScienceDaily (Jan. 5, 2010) In theory, Vitamins C and E and magnesium could help prevent or limit diabetic retinopathy (DR), a potentially blinding disease, since each nutrient causes the body to respond in ways that alter retinopathy mechanisms. For example, in animal models Vitamins C and E suppress production of a growth factor, VEG-F, which can promote abnormal blood vessels in the retina. And high dietary levels of magnesium are associated with lower blood pressure and blood sugar, both of which correlate with a lower risk of retinopathy.
A research team led by Amanda Adler, MD, PhD, Institute of Metabolic Science, Cambridge, United Kingdom, surveyed studies published from 1988 through 2008 on the impact of these micronutrients on DR. Based on 15 selected studies comprising 4,094 individuals, Dr. Adler says to the evidence is not strong enough yet to recommend Vitamins C or E or magnesium supplements for patients with diabetes. She thinks the research should continue, though, and recommends specific parameters.
"It is a very attractive proposition that what one eats, rather than a medication, might reduce the risk of diabetic complications. Ideally, future studies would include frequent measurement of intake of these three nutrients through diet and supplements, standardized exams to identify DR, and agreed-upon biomarkers to assess DR progression," Dr. Adler said. "If such studies showed apparent protection against DR, then a randomized clinical trial could determine more precisely how a person with diabetes might, or might not, alter his intake of any of these nutrients," she said.
The Adler survey found that in hospital-based studies, participants with higher levels of Vitamin C in their blood were less likely to have DR, but in population-based studies there was no association between dietary intake of Vitamin C and DR. For Vitamin E, no studies showed an association between blood levels or dietary intake and DR risk. For magnesium, one study showed an association between low blood levels of magnesium and DR progression, but other studies were inconclusive.
This research was published in the January 2010 issue of Ophthalmology, the journal of the American Academy of Ophthalmology.
Tuesday, January 5, 2009
NEW YORK (Reuters Health) Despite some hopeful hints from earlier research, a new study finds that older women on hormone replacement therapy may not gain any protection from disability as they age.
Researchers have speculated that waning estrogen levels may contribute to muscle loss and other declines in physical function as women age. Muscle cells have receptors for estrogen, and recent research has linked higher blood levels of the hormone to greater muscle strength in elderly women.
The findings raise the question of whether women on hormone replacement therapy (HRT) tend to have better physical functioning as they age compared with women who never took hormones.
The current study, reported in the journal Menopause, suggests this is not the case.
Researchers found that among nearly 2,400 older women who had been randomly assigned to take HRT or a placebo, both groups showed similar dips in muscle strength and walking speed over six years.
The women in the study were all age 65 or older when they started taking HRT, so it is not clear whether hormone replacement at younger ages might help preserve a woman's physical functioning, note the researchers, led by Dr. Yvonne L. Michael of Drexel University School of Public Health in Philadelphia.
But for now, they conclude, the findings suggest that HRT does not stave off physical decline and disability in older women.
The findings are based on a subgroup of women who had taken part in the Women's Health Initiative (WHI), a large U.S. clinical trial begun in 1993 in which postmenopausal women were randomly assigned to take either HRT or placebo pills.
The WHI was halted in 2002, when researchers found that women on HRT had higher risks of heart attack, stroke, breast cancer and blood clots than placebo users. As a result, experts now advise that while HRT is effective at relieving menopausal symptoms -- like hot flashes and vaginal dryness -- women should take it at the lowest dose and for the shortest time possible.
In their study, Michael and her colleagues focused on a subgroup of WHI participants who were age 65 or older and disability-free when they entered the study. Over six years, the women periodically took tests of physical function -- including measures of grip strength, walking speed and their ability to sit down and get up from a chair.
On average, the researchers found, the women's grip strength declined over time by 12 percent, while their walking pace slowed by 11 percent and their performance on the timed "chair-stand" test dipped by 3.5 percent. There were no significant differences between the HRT and placebo groups.
There was evidence that minority women improved their grip strength on HRT. However, Michael's team writes, that finding should be "interpreted cautiously," in part because there is no known reason for such an effect.
They say that future studies should look at whether there are, in fact, racial differences in any effects of HRT on women's physical functioning.
Source: Menopause, February 2010.
Tuesday, January 5, 2009
ScienceDaily (Jan. 5, 2010) Inheritance of an extra copy of the gene- β -amyloid precursor protein, APP, in individuals with Down syndrome leads to the inevitable development of early onset Alzheimer's disease, known to be linked to the deposition of Amyloid β peptide or Aβ in the brain. However, a new study published online by Proceedings of the National Academy of Sciences identifies βCTF, a small protein found in APP, as a novel factor for the development of Alzheimer's disease related endosome abnormalities, which have also been tied previously to the loss of brain cells in Alzheimer's disease.
"In the study, using the cells from individuals with Down syndrome that are genetically predisposed to developing Alzheimer's disease, we showed that elevated levels of βCTF, independent of Aβ, cause a specific pattern of endosome defects with similar pathology of brain cells in Alzheimer's disease," said Ying Jiang, PhD, lead author and clinical instructor in the Department of Psychiatry at NYU Langone Medical Center. "Our research was successfully able to pinpoint that βCTF causes Alzheimer's disease -related endosome defects and that we could successfully reverse these endosome defects by lowering βCTF levels in the cells."
Endosomes are membrane compartments in cells that support cell survival by absorbing outside nutrients and are crucial in neuronal functions. In Alzheimer's disease, endosome abnormalities are the earliest neuropathologic features to develop, appearing even earlier in cases where one of several major genetic risk factors for the disease in inherited. Endosomes are also suspected sites of Aβ production in the cells.
"In the field of Alzheimer's research, we have been questioning whether Aβ is the only target to better understand the progression of Alzheimer's disease and if lowering Aβ is the only hoped-for therapy," said Ralph Nixon, MD, PhD, professor, psychiatry and cell biology, director, NYU Center of Excellence on Brain Aging and the Silberstein Alzheimer's Institute at NYU Langone Medical Center. "This study demonstrates that an alternative protein factor, βCTF, derived from the gene APP, is also unequivocally involved in Alzheimer's disease and may be of additional importance for the development of future effective therapies."
Funding for this study was made possible through the National Institute on Aging (NIA) of the National Institutes of Health (NIH) The study was done in collaboration with NYU Langone Medical Center (NY, New York), the Center for Dementia Research at the Nathan Kline Institute (Orangeburg, NY); Mailman Research Center at McLean Hospital (Belmont, MA); Departments of Psychiatry and Neuropathology at Harvard Medical School (Boston, MA).
Tuesday, January 5, 2009
TUESDAY, Jan. 5 (HealthDay News) -- Obesity now poses as great a threat to Americans' quality of life as smoking, a new study shows.
Researchers at Columbia University and The City College of New York analyzed 1993-2008 data from the Behavioral Risk Factor Surveillance System that included interviews with more than 3.5 million adults. The results showed that the quality-adjusted life years (QALYs) lost to obesity are equal to, or greater than, those lost because of smoking.
From 1993 to 2008, the number of adult smokers decreased 18.5 percent and smoking-related QALYs lost remained relatively stable at 0.0438 QALYs lost per population. Over that same time, the proportion of obese Americans increased 85 percent, resulting in 0.0464 QALYs lost. Obesity had a larger effect on disease, while smoking had a greater impact on deaths, the researchers found.
"Although life expectancy and quality-adjusted life expectancy have increased over time, the increase in the contribution of mortality to QALYs lost from obesity may result in a decline in future life expectancy. Such data are essential in setting targets for reducing modifiable health risks and eliminating health disparities," the researchers wrote.
The study is published in the February issue of the American Journal of Preventive Medicine.
Another recent study concluded that if both smoking and obesity rates in the United States remain unchanged, life expectancy in the nation will be reduced by almost nine months. That study was published in the Dec. 3 issue of the New England Journal of Medicine.
The U.S. National Institute of Diabetes and Digestive and Kidney Diseases outlines the health effects of being overweight.
Tuesday, January 5, 2009
ScienceDaily (Jan. 5, 2010) Peripheral artery disease (PAD) affects 5 million individuals in the U.S. and is the leading cause of limb amputations. Doctors have long considered exercise to be the single best therapy for PAD, and now a new study helps explain why. Led by researchers at Beth Israel Deaconess Medical Center and published in the Online Early Edition of the Proceedings of the National Academy of Sciences (PNAS), the findings demonstrate that a protein called PGC-1alpha plays a key role in the process.
"Exercise is a staple of healthy living," notes senior author Zoltan Arany, MD, PhD, an investigator in BIDMC's Cardiovascular Institute and Assistant Professor of Medicine at Harvard Medical School. "One of the many benefits of exercise, endurance exercise in particular, is the generation of new blood vessels in leg muscles." Known as angiogenesis, this naturally occurring process comes to the rescue when an injury or artery blockage leaves normal tissue starved for blood.
PAD is a common circulatory problem in which narrowed arteries reduce blood flow to the limbs. The end result is leg pain primarily encountered while walking. More seriously, PAD is also likely to be a sign of widespread accumulation of fatty deposits in the arteries, which may be reducing blood flow to the heart and brain as well as to the legs.
The PGC-1alpha molecule was first identified more than 10 years ago. Last year, Arany was part of a research team that discovered that when body parts are jeopardized by poor circulation, PCG-1alpha senses dangerously low levels of oxygen and nutrients and, in response, spurs the growth of new blood vessels. Knowing that muscle adapts to endurance-type exercise by triggering angiogenesis, Arany and his coauthors set out to better understand the mechanisms behind this orchestrated process, and to determine if PGC-1alpha had a hand in the outcome.
The researchers studied mice in cages equipped with electronically monitored running wheels. As predicted, voluntary exercise was found to lead to robust angiogenesis in mouse skeletal muscle. The investigators also found that the mice that were lacking PGC-1alpha failed to grow new blood vessels in response to exercise. Ultimately, their experiments demonstrated that exercise activates beta-adrenergic signaling, which leads to a robust induction of PGC-1alpha.
"Our data strongly suggest a new paradigm for the process of angiogenesis in response to exercise, demonstrating that upstream beta-adrenergic signaling, likely stemming from increased nerve activity, triggers angiogenesis," the authors write. (Interestingly, they add, this suggests that the use of beta blockers in patients with PAD might block some of the benefits of exercise. These medications are widely used to treat patients with coronary artery disease, and patients with PAD often have concurrent CAD.)
"With this study, we have found that the protein PGC-1 alpha can single-handedly transform muscle to be capable of greater endurance and increase the blood content of that muscle. Being able to increase blood vessel density could help wound healing and even prevent amputations in millions of patients with diabetes and vascular disease of the limbs," notes Arany. "Exercise remains one of the most effective interventions for a number of chronic diseases, including obesity, diabetes, atherosclerosis and neurodegenerative diseases. PAD is a leading cause of morbidity and the most common cause of limb amputation in the U.S. and yet even the best medical therapy available is less effective than simply walking daily."
This study was supported by funding from the National Heart, Lung, and Blood Institute and by the Smith Family Foundation.
Study coauthors include BIDMC investigators Jessica Chinsomboon (first author), Robyn Thom, Jonathan Shoag, Glenn Rowe, Naoki Sawada and Srilatha Raghuram; and Dana-Farber Cancer Institute investigators Jorge Ruas and Rana Gupta.
By Joanne Allen
Tuesday, January 5, 2009
WASHINGTON (Reuters) Enzyme-blocking chemicals in pomegranates may reduce the risk of estrogen-fueled breast cancers, U.S. researchers said on Tuesday.
An acid found in pomegranates appears to block aromatase, an enzyme that converts androgen to estrogen, a hormone that plays a role in the development of breast cancer, the researchers wrote in the journal Cancer Prevention Research.
"We identified some of these chemicals in pomegranates that actually have properties that can suppress aromatase," researcher Shiuan Chen, of the City of Hope cancer research and treatment center in Duarte, California, said in a telephone interview.
Many women who have had breast cancer take medicines called aromatase inhibitors -- such as Pfizer's Aromasin, Novartis' Femara and AstraZeneca Plc's Arimidex -- to keep estrogen from feeding tumors.
Chen and colleagues studied whether compounds, or phytochemicals, in pomegranates can suppress aromatase and ultimately block cancer growth. They found that 10 natural compounds in the fruit may potentially prevent estrogen-related breast cancer.
Chen said the compounds would not be a replacement for aromatase inhibitors.
"We do not recommend people start taking this as a replacement for the AI's," Chen said. "They (pomegranate compounds) are not as potent as the real drugs so we think that the interest probably is more on the prevention end rather than in a therapeutic purpose."
Other researchers not associated with the study told the journal that the results are promising, and suggested more studies involving animals and humans were needed to confirm the findings.
"It's not clear that these levels could be achieved in animals or in humans because the (compounds) are not well absorbed into blood when provided in the diet," said Gary Stoner of Ohio State University.
Dr. Powel Brown, an oncologist at the University of Texas, said in a statement that future studies should focus on testing pomegranate juice for its effect on estrogen levels, menopausal symptoms, breast density or even as a cancer preventive agent.
More than 400,000 women die from breast cancer globally every year. About 75 percent of breast cancers are estrogen-receptor positive, meaning they are fed by estrogen.
Previous research has shown that pomegranate juice is rich in antioxidants -- vitamins and other substances -- that may help prevent diseases such as cancer, heart disease and Alzheimer's disease. (Editing by Xavier Briand)
Tuesday, January 5, 2009
TUESDAY, Jan. 5 (HealthDay News) -- Concentrations of several biomarkers begin to grow three years before women are diagnosed with ovarian cancer, but only reach substantial elevation levels over the 12 months before diagnosis, new research finds.
The findings, published online in the Journal of the National Cancer Institute, expand on previous research into biomarkers known as CA125, HE4, mesothelin, B7-H4, decoy receptor 3 and spondin-2.
Researchers from Fred Hutchinson Cancer Research Center in Seattle examined blood serum samples from a lung cancer study. They compared samples from 34 women who were diagnosed with ovarian cancer to samples from 70 healthy patients.
The concentrations of CA125, HE4 and mesothelin increased slightly in the ovarian cancer patients about three years before they were diagnosed with the disease.
"Serum markers likely will form a key element in any screening regimen, with the lead time and other parameters of each marker or combination of markers being taken into account. The careful evaluation technique applied in the current study fits into a staged approach necessary for testing performance of early markers of disease," Patricia Hartge, of the U.S. National Cancer Institute, wrote in a commentary accompanying the study.
For more on ovarian cancer, see the U.S. National Cancer Institute.
Tuesday, January 5, 2009
ScienceDaily (Jan. 5, 2010) A child's blood pressure, body mass index, blood glucose level and other laboratory tests and simple office measures may predict the risk of developing type 2 diabetes nine and 26 years later, according to a report in the January issue of Archives of Pediatrics & Adolescent Medicine, one of the JAMA/Archives journals.
"In the past 25 years, the prevalences of obesity and type 2 diabetes mellitus have increased concomitantly, and the age at onset of type 2 diabetes mellitus has dropped precipitously, especially in black females," the authors write as background information in the article. Models to identify children at high and low risk of type 2 diabetes could provide diagnostic and therapeutic insights and help clinicians target prevention efforts.
John A. Morrison, Ph.D., of Cincinnati Children's Hospital Medical Center, and colleagues analyzed data from two studies. The National Growth and Health Study followed 1,067 black and white girls enrolled at ages 9 and 10 for nine years, and the Princeton Follow-up Study tracked 822 black and white schoolchildren for 22 to 30 years beginning in 1973 to 1976.
In the Princeton Follow-up Study, individuals were more likely to have diabetes at age 39 years if they had high systolic (top number) blood pressure, a high body mass index, glucose levels of at least 100 milligrams per deciliter, low high-density lipoprotein (HDL, or "good" cholesterol) levels and high triglyceride levels in childhood. "When body mass index, systolic blood pressure and diastolic [bottom number] blood pressure were all lower than the 75th percentile and there was no parental diabetes mellitus, the likelihood of children developing type 2 diabetes mellitus 22 to 30 years later was only 1 percent," the authors write.
In the National Growth and Health Study, childhood high systolic blood pressure, insulin concentration and having a parent with diabetes increased the risk of having diabetes at age 19. "If childhood body mass index, systolic blood pressure and diastolic blood pressure were all lower than the 75th percentile, the likelihood of type 2 diabetes mellitus at age 19 years was 0.2 percent, 0.2 percent if the parents were also free of diabetes mellitus and 0.3 percent if childhood insulin was also less than the 75th percentile," the authors write.
"Our data have practical clinical value in assessment of pre-teenaged and teenaged children, since children with systolic blood pressure, triglyceride, body mass index and insulin in the top fifth percentile, a glucose concentration of at least 100 milligrams per deciliter and a parent with diabetes could be targeted for primary prevention of type 2 diabetes mellitus through diet, exercise and possibly insulin-sensitizing drug intervention, with special focus on overweight children with positive family history of diabetes mellitus," they conclude.
This research was supported in part by grants from the National Institutes of Health, the American Heart Association, by the Taft Research Fund and by the Lipoprotein Research Fund of the Jewish Hospital of Cincinnati.
John A. Morrison; Charles J. Glueck; Paul S. Horn; Ping Wang. Childhood Predictors of Adult Type 2 Diabetes at 9- and 26-Year Follow-ups. Arch Pediatr Adolesc Med, 2010; 164 (1): 53-60 [link]
By Amy Norton
Tuesday, January 5, 2009
NEW YORK (Reuters Health) While some research has suggested that moderate drinking may lower a person's odds of suffering a stroke, a new study finds that it may have little long-term impact on stroke risk or stroke severity.
The findings, reported in the journal Stroke, come from a more than two-decade follow-up of nearly 22,000 U.S. male doctors. Researchers found that overall, there was no strong association between the men's drinking habits and their odds of suffering a stroke.
Nor was there a clear connection between alcohol intake and the severity of disability following a stroke.
Some past studies, though not all, have suggested that light-to-moderate drinking may be protective against stroke -- as it appears to be against heart disease. But the current study, which followed participants for an average of 22 years, was longer term than those earlier studies, the researchers point out.
In addition, a number of other studies have found that the protective effect of moderate drinking is generally weak and fades with longer-term follow-up, noted senior researcher Dr. Tobias Kurth, of the French national health institute INSERM, in Paris, and Brigham and Women's Hospital in Boston.
As for the potential effects of drinking habits on stroke outcomes, few studies have looked at that question, Kurth told Reuters Health in an email.
The current findings, he said, suggest that moderate drinking before a stroke has no "great benefit" on a man's ability to function after a stroke.
The findings are based on data from the Physicians' Health Study, which included roughly 22,000 U.S. male doctors between the ages of 40 and 84 at its start in 1982. At the outset and each year afterward, the men reported on their lifestyle habits, including alcohol intake, and any new medical diagnoses.
Over an average of 22 years, the men suffered a total of 1,393 strokes and 766 transient ischemic attacks, or "mini-strokes."
There was evidence that very light drinking -- one drink per week -- lowered the risk of stroke slightly, compared with no drinking at all. Men who drank at that level also had a lower risk of having a severely disabling stroke.
However, more-moderate levels of drinking showed no effect on stroke risk or disability after a stroke.
The findings, Kurth's team writes, "do not support a strong association" between alcohol intake and the risk of stroke or stroke outcomes.
There is good evidence, however, that heavier drinking -- several drinks per day or more -- may raise stroke risk. Few men in the current study said they had more than one drink per day.
"This is quite important," Kurth said, "since our study should not be taken as evidence that heavy drinking has no consequences on stroke risk."
He noted that future studies should look at whether similar findings are seen among women.
Source: Stroke, January 2010.
Tuesday, January 5, 2009
ScienceDaily (Jan. 5, 2010) Researchers have found that even a very little bit of the fat hormone leptin goes a long way when it comes to correcting diabetes. The hormone controls the activity of a gene known as IGFBP2 in the liver, which has antidiabetic effects in animals and could have similar therapeutic effect in humans, according to a report published by Cell Press in the January issue of Cell Metabolism.
The new findings confirm what some at least had already suspected: that leptin's antidiabetic effects are independent of the hormone's well-known ability to reduce body weight.
"It was surprising to me how potent leptin was in treating diabetes," said Jeffrey Friedman of Rockefeller University. "It had a highly significant impact at plasma levels that were undetectable."
Earlier studies had shown that leptin treatment effectively corrects high blood sugar and insulin levels in leptin-deficient mice and humans. Leptin's usefulness as a therapy has also been shown in some clinical settings, in people with rare metabolic disorders. But it wasn't clear exactly how the hormone produced in fat tissue acts to improve diabetes.
Studies to address that question had been complicated by the fact that leptin also causes marked weight loss, which by itself can improve diabetes, the researchers explained. To get around that issue in the new study, Friedman and his colleagues first identified the lowest dose of leptin that could correct insulin resistance and diabetes without leading animals to eat less or lose weight.
They then looked to see how that very low-level infusion of leptin changes the activity of genes in the animals' livers. That survey led them to IGFBP2.
Treatments designed to increase IGFBP2 expression in obese and diabetic mice reversed their diabetes. Further study showed that animals treated with the protein responded to insulin three times better than untreated ones.
They also found that leptin-deficient patients do indeed have lower blood levels of IGFBP2 at baseline and that those levels can be raised with low-dose leptin treatment.
Friedman said that future experiments in mice lacking IGFBP2 altogether are needed to confirm that the protein is required for leptin's antidiabetic influence. Now that they know that very high levels of IGFBP2 can act to improve diabetes, they'll also need to explore the effects of normal physiologic levels.
"In summary," the researchers concluded, "we have developed a set of conditions in which leptin treatment potently improves diabetes independent of its ability to correct weight and food intake. This protocol was used to identify IGFBP2 as a leptin-regulated gene whose expression is correlated with leptin's antidiabetic effect Further studies will reveal whether IGFBP2 shows similar antidiabetic effects in clinical settings."
The researchers include Kristina Hedbacker, Rockefeller University, New York, NY; Kivanc¸ Birsoy, Rockefeller University, New York, NY; Robert W. Wysocki, Rockefeller University, New York, NY, Howard Hughes Medical Institute, New York, NY; Esra Asilmaz, Rockefeller University, New York, NY; Rexford S. Ahima, University of Pennsylvania School of Medicine, Philadelphia, PA; I. Sadaf Farooqi, University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, UK; and Jeffrey M. Friedman, Rockefeller University, New York, NY, Howard Hughes Medical Institute, New York, NY.
By Andrew Stern
Tuesday, January 5, 2009
CHICAGO (Reuters) Mild to severe depression might be better treated with alternatives to antidepressant drugs, which do not help patients much more than an inactive placebo, researchers said Tuesday.
Combining data from six studies that examined the effectiveness of two commonly prescribed antidepressants -- paroxetine and imipramine -- found the drugs produced benefits only slightly greater than a placebo in patients with mild to severe depression.
"They would have done just as well or just about as well with a placebo," said Robert DeRubeis, a psychologist at the University of Pennsylvania, Philadelphia, who with colleagues performed the meta-analysis.
Paroxetine is one of a popular class of drugs, selective serotonin reuptake inhibitors, and is sold under the brand name Paxil by GlaxoSmithKline. Imipramine is an older tricyclic antidepressant drug developed in the 1950s.
The so-called placebo effect is powerful in treating depression, where people believe they are helped even though they are taking an inactive sugar pill, DeRubeis said.
In the report published in the Journal of the American Medical Association involving nearly 800 patients, the drugs' impact was noticeably stronger than a placebo in people diagnosed with very severe cases of depression.
Using a scoring system for depression where a diagnosis of 24 or above indicates a very severe case, the researchers said patients treated with drugs saw their scores drop by 13 points, compared to a drop of 9 points for those given a placebo.
But for those with initial depression scores of 23 or below the drop averaged 8 points for those given antidepressants and 7 points for those given a placebo. Roughly half of those prescribed antidepressants fit into the mild to severe categories.
"Our data should give some pause" to doctors and patients weighing antidepressants, DeRubeis said in a telephone interview. "They should give some consideration to other alternatives."
Exercise has been shown to be helpful to stem depression, as does psychotherapy, and even "self-treatment" with the aid of the plethora of self-help literature, he said.
A spokeswoman for GlaxoSmithKline said the report "contributes to the extensive research" into antidepressants, noting that Paxil received U.S. government approval in 1992 and has helped "millions of people battling mental illness.
"The studies used for the analysis in the JAMA paper differ methodologically from studies used to support the approval of paroxetine for major depressive disorder, so it is difficult to make direct comparisons between the results," spokeswoman Sarah Alspach said.
At least 27 million Americans take antidepressants, nearly double the number that did in the mid-1990s, according to a study by Columbia University and University of Pennsylvania researchers reported in the Archives of General Psychiatry.
More than 164 million prescriptions for antidepressants were written in 2008, totaling nearly $10 billion in U.S. sales, according to IMS Health. Global sales were twice that.
(Editing by Eric Walsh)
Tuesday, January 5, 2009
ScienceDaily (Jan. 5, 2010) A team of researchers in California and Massachusetts has developed a "cocktail" of different nanometer-sized particles that work in concert within the bloodstream to locate, adhere to and kill cancerous tumors.
"This study represents the first example of the benefits of employing a cooperative nanosystem to fight cancer," said Michael Sailor, a professor of chemistry and biochemistry at the University of California, San Diego and the primary author of a paper describing the results, which is being published in a forthcoming issue of the Proceedings of the National Academy of Sciences.
In their study, the UC San Diego chemists, bioengineers at MIT and cell biologists at UC Santa Barbara developed a system containing two different nanomaterials the size of only a few nanometers, or a thousand times smaller than the diameter of a human hair, that can be injected into the bloodstream. One nanomaterial was designed to find and adhere to tumors in mice, while the second nanomaterial was fabricated to kill those tumors.
These scientists and others had previously designed nanometer-sized devices to attach to diseased cells or deliver drugs specifically to the diseased cells while ignoring healthy cells. But the functions of those devices, the researchers discovered, often conflicted with one another.
"For example, a nanoparticle that is engineered to circulate through a cancer patient's body for a long period of time is more likely to encounter a tumor," said Sangeeta Bhatia, a physician, bioengineer and a professor of Health Sciences and Technology at the Koch Institute for Integrative Cancer Research at MIT and a coauthor of the study. "However, that nanoparticle may not be able to stick to tumor cells once it finds them. Likewise, a particle that is engineered to adhere tightly to tumors may not be able to circulate in the body long enough to encounter one in the first place."
When a single drug does not work in a patient, a doctor will commonly administer a cocktail containing several drug molecules. That strategy can be very effective in the treatment of cancer, where the rationale is to attack the disease on as many fronts as possible. Drugs may sometimes work together on a single aspect of the disease, or they may attack separate functions. In either case, drug combinations can provide a greater effect than either drug alone.
Treating tumors with nanoparticles has been challenging because immune cells called mononuclear phagocytes identify them and yank them from circulation, preventing the nanomaterials from reaching their target.
Ji-Ho Park, a graduate student in Sailor's UC San Diego laboratory, and Geoffrey von Maltzahn, a graduate student in Bhatia's MIT laboratory, headed the effort to develop two distinct nanomaterials that would work in concert to overcome that obstacle and others. The first particle is a gold nanorod "activator' that accumulates in tumors by seeping through its leaky blood vessels. The gold particles cover the whole tumor and behave like an antenna by absorbing otherwise benign infrared laser irradiation, which then heats up the tumor.
After the nanorods had circulated in the bloodstream of mice that had epithelial tumors for three days, the researchers used a weak laser beam to heat the rods that attached to the tumors. This sensitized the tumors, and the researchers then sent in a second nanoparticle type, composed of either iron oxide nanoworms or doxorubicin-loaded liposomes. This "responder" nanoparticle was coated with a special targeting molecule specific for the heat-treated tumor. Much of that work was done in the laboratory of Erkki Ruoslahti, a cell biologist and professor at the Burnham Institute for Medical Research at UC Santa Barbara, and another co-author of the study.
"Think of them like soldiers attacking an enemy base," said Sailor. "The gold nanorods are the Special Forces, who come in first to mark the target. Then the Air Force flies in to deliver the laser-guided bomb. The devices are designed to minimize collateral damage to the rest of the body."
While one type of nanoparticle improves detection of the tumor, he said, the other is designed to kill the tumor. The researchers designed one type of responder particle with strings of iron oxide, which they called "nanoworms," that show up brightly in a medical magnetic resonance imaging, or MRI, system. The second type is a hollow nanoparticle loaded with the anti-cancer drug doxorubicin. With the drug-loaded responder, the scientists demonstrated in their experiments that a tumor growing in a mouse can be arrested and then shrunk.
"The nanoworms would be useful to help the medical team identify the size and shape of a tumor in a patient before surgery, while the hollow nanoparticles might be used to kill the tumor without the need for surgery," said Sailor.
"This study is important because it is the first example of a combined, two-part nanosystem that can produce sustained reduction in tumor volume in live animals," said Sailor.
The project was funded by grants from the National Cancer Institute of the National Institutes of Health. Bhatia is a Howard Hughes Medical Institute Investigator.
Tuesday, January 5, 2009
TUESDAY, Jan. 5 (HealthDay News) -- A fat hormone known as leptin controls a gene in the liver that's linked to the dampening of diabetes in animals, researchers have found.
The finding suggests that the hormone could potentially have the same effect in people.
Earlier research had found that leptin treatment helps regulate blood sugar and insulin levels in mice and humans that don't have enough leptin in their bodies. The new study, published in the January issue of Cell Metabolism, shows that leptin works at low levels by affecting the gene, known as IGFBP2.
"It was surprising to me how potent leptin was in treating diabetes," lead investigator Jeffrey Friedman, of Rockefeller University, said in a news release from the journal. "It had a highly significant impact at plasma levels that were undetectable."
The research was conducted on mice and designed to study the effects of leptin on diabetes without the corresponding weight loss that the hormone can cause. The study authors found that treated animals responded better to insulin -- three times better, in fact.
New research will focus on mice that don't have the IGFBP2 gene, to see if it's responsible for leptin's ability to fight diabetes.
The U.S. National Diabetes Information Clearinghouse has more on diabetes.
Tuesday, January 5, 2009
ScienceDaily (Jan. 5, 2010) A Mayo Clinic research study published in the January issue of the American Journal of Gastroenterology finds that St. John's wort is not an effective treatment for irritable bowel syndrome (IBS). While antidepressants are frequently used to treat IBS, to date, no study has examined the success of using the herbal supplement St. John's wort in treating IBS.
"Our study investigated if herbal antidepressants such as St. John's wort could benefit irritable bowel disease patients," says Yuri Saito, M.D., M.P.H., gastroenterologist and lead physician scientist on the study. "Several of the chemical neurotransmitters that are in the brain are also in the colon. Therefore, it's been thought that antidepressants may affect sensation in the colon in a similar way to how they affect sensation in the brain. Our goal was to evaluate the usefulness of St John's wort in treating IBS."
In this placebo-controlled trial, 70 participants with IBS were randomized where half the patients received St. John's wort and the other half received a placebo for three months. In all, 86 percent of the participants were women, and the median age was 42 years. After three months of observing symptoms such as stomach pain, diarrhea, constipation and bloating, Mayo researchers found that the placebo group had a better response than the group taking the herbal supplement, St. John's wort.
"Because people tend to struggle with IBS for several years, patients are really looking for inexpensive, over-the-counter treatments such as St. John's wort," says Dr. Saito. "Unfortunately, our study showed that St. John's wort was not successful in helping IBS patients."
St. John's wort is an herbal supplement derived from the St. John's wort plant. It has been shown to be helpful in several medical conditions such as depression as well as other pain syndromes. Research has shown it to be as effective as conventional, prescription anti-depressants in treating mild to moderate depression.
"The challenge with IBS is that there is no cure, no one treatment tends to be wholly effective and some treatments come with significant side effects," explains Dr. Saito. "However, well-designed studies of herbal supplements are important so that physicians and patients can make informed decisions about which supplements to recommend or try. Studies of alternative treatments are generally lacking and patients are forced to use a "trial and error" approach to over-the-counter treatments for their IBS."
IBS is a common disorder that affects the colon and commonly causes cramping, abdominal pain, bloating, gas, diarrhea and constipation. Approximately 58 million people struggle with IBS, mostly women.
Other members of the Mayo Clinic research team included Enrique Rey, M.D.; Ann Almazar-Elder; W. Scott Harmsen; Alan Zinsmeister, Ph.D.; G. Richard Locke , M.D.; and Nicholas Talley, M.D., Ph.D.
Monday, January 4, 2010
By Amy Norton
Monday, January 4, 2010
NEW YORK (Reuters Health) Overweight middle-aged men may have a higher risk of heart problems and strokes and die earlier than their thinner peers -- even in the absence of some traditional risk factors, a new study suggests.
Some past research has suggested that when obese and overweight adults do not have the so-called metabolic syndrome, their risks of diabetes, heart disease and stroke are no higher than those of normal-weight people.
Metabolic syndrome refers to a collection of risk factors for diabetes and heart problems -- including abdominal obesity, high blood pressure, elevated blood sugar, low levels of "good" HDL cholesterol and high triglycerides (another type of blood fat). It is typically diagnosed when a person has three or more of those conditions.
In the current study, which followed more than 1,700 Swedish men for 30 years, overweight and obese men had increased risks of conditions including heart attack and stroke, even when in the absence of metabolic syndrome.
Among all men without metabolic syndrome, those who were overweight were 52 percent more likely to have heart attacks, strokes, and other complications than normal-weight men were, while obese men had nearly double the risk.
The findings are published in the American Heart Association journal Circulation.
"Our study shows that overweight (and) obese men without the metabolic syndrome are at higher risk" for heart disease, stroke, and other related conditions, study leader Dr. Johan Arnlov, of Uppsala University in Sweden, told Reuters Health by email. "This is in contrast to some previous studies that have suggested that obesity in the absence of the metabolic syndrome is a 'healthy' condition."
The study does, however, point up the added threat of having metabolic syndrome.
Obese men with metabolic syndrome had the highest risks -- showing 2.5 times the risk of heart disease and stroke, and related conditions, and of death, during the study period as men who were normal-weight and free of metabolic syndrome at the outset.
In addition, metabolic syndrome was harmful for normal-weight men as well; those with the condition were 63 percent more likely to develop heart disease, stroke, and related conditions than their counterparts who were free of metabolic syndrome.
According to Arnlov, the findings suggest that weight loss should be a goal for heavy men, regardless of whether they have metabolic syndrome. At the same time, being thin does not mean equate to a healthy heart -- though, Arnlov pointed out, metabolic syndrome is much more common among overweight people.
The findings are based on 1,758 men who, at the outset, were 50 years old and free of diabetes and previous hospitalizations for heart disease, stroke, and related conditions. Of the 955 normal-weight men, 64 had metabolic syndrome, as did 125 of 707 overweight men, and 66 of 96 obese men.
Over the next 30 years, 681 men suffered a heart attack, stroke or other major related complication. A total of 845 died.
Heavy men without metabolic syndrome had increased risks of such complications and death even with age, smoking and levels of "bad" LDL cholesterol taken into account.
It is not entirely clear why overweight men were at increased risk, but one issue the study did not address was physical fitness, AHA spokesman Dr. Barry Franklin noted in the news release from the heart association.
He suggested that as a "New Year's resolution," overweight adults recognize that there are health benefits to be gained from shedding even a few pounds through diet changes and exercise.
Arnlov said that future studies should look at whether similar findings are seen in women. However, he added, "I don't think we should consider obesity without the metabolic syndrome to be benign in women just because we don't have the data yet."
Source: Circulation, online December 28, 2009.
Monday, January 4, 2010
MONDAY, Jan. 4 (HealthDay News) -- Researchers report they stopped the growth of blood vessels that are crucial to tumor survival by lowering the level of a protein found in brain cells.
The protein, known as delta-catenin, is known for its effects on the growth of the brain cells called neurons, but is also produced by cells in human blood vessels. Researchers found that they could disrupt the development of blood vessels that are connected to tumors and wounds by diminishing levels of the protein.
The researchers, from Vanderbilt University Medical Center in Tennessee, noted that the process did not disrupt the normal development of blood vessels. Because of this, manipulation of the protein could help fight cancer, they believe.
The study findings were published online Jan. 4 in the Journal of Experimental Medicine.
For more on cancer, head to the U.S. National Library of Medicine.
By Kate Kelland
Monday, January 4, 2010
LONDON (Reuters) Smoking is well known as a risk factor for type 2 diabetes, but scientists said on Monday that quitting the habit can raise the risk even more in the short term.
A study by U.S. researchers found that people who stop smoking have a 70 percent increased risk of developing type 2 diabetes in the first six years without cigarettes as compared to people who never smoked.
The researchers said they suspected the increased diabetes risk comes from extra weight gain common in people who quit.
But they said no one should use their findings as an excuse to continue smoking -- a habit which can also cause lung disease, heart disease, strokes and many types of cancer.
"The message is: Don't even start to smoke," said Hsin-Chieh Yeh of the Johns Hopkins University School of Medicine in the United States, who led the study.
"If you smoke, give it up. That's the right thing to do. But people have to also watch their weight," she added.
Type 2 diabetes -- often called adult-onset diabetes -- is a common disease that interferes with the body's ability to properly use sugar and insulin, a substance produced by the pancreas which normally lowers blood sugar after eating.
Overweight people and those with a family history of the disease have an increased risk of developing it, as do smokers.
Diabetes is reaching epidemic levels, with an estimated 180 million people suffering from it around the world.
Diabetes cases are forecast to triple in the United States in the next 25 years to 44 million with the costs of caring for them rising to $336 billion a year.
Yeh's study, published in the Annals of Internal Medicine journal, looked at almost 11,000 middle-aged adults who did not yet have diabetes from 1987 to 1989. The patients were
followed for up to 17 years and data about diabetes status, glucose levels, weight and more were collected at regular intervals.
The researchers found that people who quit smoking had a 70 percent increased risk of developing type 2 diabetes in the first six years after stopping compared to people who never smoked. The risks were highest in the first three years, and returned to normal after 10 years.
Among those who did not stop smoking the risk was lower, but the chance of developing diabetes was still 30 percent higher compared with those who never smoked.
Tobacco is the leading preventable cause of death in the world, killing more than 5 million people a year. A report by the World Lung Foundation last August said smoking could kill a billion people this century if trends hold.
(Editing by Charles Dick)
By Jennifer Thomas
Monday, January 4, 2010
MONDAY, Jan. 4 (HealthDay News) -- The rate of children aged 2 to 5 who are given antipsychotic medications has doubled in recent years, a new study has found.
Yet little is known about either the effectiveness or the safety of these powerful psychiatric medications in children this age, said researchers from Columbia University and Rutgers University, who looked at data on more than 1 million children with private health insurance.
"It is a worrisome trend, partly because very little is known about the short-term, let alone the long-term, safety of these drugs in this age group," said study author Dr. Mark Olfson, a professor of clinical psychiatry at Columbia University in New York City.
Prescribing antipsychotics to children in the upper range of that age span -- ages 4 and 5 -- is justifiable only in rare, intractable situations in which all other treatments, including family and psychological therapy, have been tried and are not working, Olfson said.
And it's questionable whether 2- and 3-year-olds should ever be prescribed antipsychotics, Olfson said.
The study is published in the January issue of the Journal of the American Academy of Child & Adolescent Psychiatry.
Presumably, only children with the most severe mental problems would be given the potent drugs. Yet, less than half of children on antipsychotics had received any mental health services, including a mental health assessment or treatment from a psychotherapist or psychiatrist, the study authors noted.
"You don't see the kinds of mental health services you would expect to see if we were dealing with the most profoundly disturbed toddlers," Olfson said, raising the question of whether doctors had done everything they could to help the child before turning to medications.
The overall numbers of children prescribed antipsychotics remains small, at less than one half of one percent of the national sample. But the numbers are rising. In 1999-2001, about one in 1,300 were being treated with antipsychotics. By 2007, that had risen to one in 630, according to Olfson.
For 5-year-olds, about one in 650 were being treated in 1999-2001. That doubled, to one in 329, in 1997, he noted.
Research published online in December in the journal Health Affairs by the same research team suggested children on Medicaid are even more likely than children with private insurance to be prescribed antipsychotics.
The most common antipsychotic drug prescribed to children was risperidone (Risperdal), which accounted for nearly three-quarters of antipsychotic prescriptions. In adults and teens, risperidone is used to treat schizophrenia and bipolar disorder. Risperidone is also approved by the U.S. Food and Drug Administration to treat unstable mood or irritability in children with autism aged 5 and up.
Children who were most likely to receive risperidone were male and aged 4 or 5, according to the report. The most common diagnosis was pervasive developmental disorder or mental retardation, attention deficit/hyperactivity disorder or disruptive behavior disorder.
Previous research has shown children on the drugs may experience metabolic and endocrine abnormalities. Little is known about their impact on the developing brain, Olfson added.
"I don't want to minimize the problems children can have at this age, but there are psychological treatments that have been proven to help parents and the kids that emphasize the quality of the parent-child relationship," Olfson said.
One reason for the uptick may be increasing numbers of children diagnosed with autism and some research showing risperidone may help with autism-related irritability, the researchers noted.
Dr. Peter Jensen, co-director of the division of child psychiatry and psychology at the Mayo Clinic, agreed that the trend is concerning. "We have no doubt there are prescribing practices out there that are very, very worrisome," Jensen said.
It's imperative that children receive a full mental health assessment before getting these drugs, to understand the family situation and school environment and if there is a family history of psychiatric problems, as well as undergoing a physical exam to rule out other medical problems.
"These agents should not be used as an adjunct to a family stressed to the max," Jensen said. "With kids who are 2 to 5, most can be managed without these medicines. Rarely a 5-year-old goes on them. But a child of 2 or 3, in my experience, I have never had to put them on [an antipsychotic]. There is so much else that can be done."
The stress and difficulty of coping with a child who has significant mental health issues, the need to have a child behave well enough to be permitted to attend school, as well as lack of adequate coverage for family therapy and mental health services, may push doctors and parents into believing they have little choice other than medicating the child, Jensen said.
The U.S. National Mental Health Information Center has more on children and mental health issues.
By Amy Norton
Monday, January 4, 2010
NEW YORK (Reuters Health) A new study provides further evidence that the measles-mumps-rubella vaccine is not associated with an increased risk of autism.
Concerns that the MMR shot could cause autism were first raised a decade ago by British physician Andrew Wakefield, who, based on a study of 12 children, proposed that there was a link between the vaccine and bowel disease and autism.
That research has since been widely discredited, and numerous international studies have failed to find a connection between MMR vaccination and autism.
This latest study included 96 Polish children ages 2 to 15 who had been diagnosed with autism. Researchers compared each child with two healthy children the same age and sex who had been treated by the same doctor.
Some of the children had received the MMR vaccine, while others had not been vaccinated at all or had received a vaccine against measles only.
Poland has been slower to introduce the MMR than other European countries, but over the past decade, the vaccine has slowly been replacing the measles-only shot.
Overall, the study found, children who had received the MMR vaccine actually had a lower risk of autism than their unvaccinated peers. Nor was there any evidence of an increased autism risk with the measles-only vaccine.
"Parents should be convinced about the safety of MMR vaccine," lead researcher Dr. Dorota Mrozek-Budzyn, of Jagiellonian University in Krakow, wrote in an email to Reuters Health.
She noted that the infectious diseases the MMR shot prevents can sometimes have serious complications.
Measles, for instance, can lead to pneumonia or brain inflammation, and one or two children die out of every 1,000 who contract the virus, according to the U.S. Centers for Disease Control and Prevention. Mumps can cause painful testicular swelling, brain inflammation and, in rare cases, hearing loss.
Most of the children in the current study had received either the MMR or measles vaccine, according to a report in the Pediatric Infectious Disease Journal.
Of the 96 children with autism, 8 had received no vaccine against measles, while about 41 percent had received the MMR shot and half had received the measles-only vaccine.
Among the healthy children, 55 percent had gotten the MMR shot, while 45 percent had received the measles vaccine; only one child remained unvaccinated.
When the researchers looked only at children who had been vaccinated before their autism diagnosis, they found that children who had received the MMR vaccine had an 83 percent lower risk of autism than unvaccinated children. Similarly, the measles-only vaccine was associated with a 56 percent lower risk.
When the researchers looked at children who had been vaccinated before showing any symptoms of autism, MMR vaccination was again linked to a lower risk of the disorder. The measles-only vaccine showed no effect on autism risk.
The study does not answer the question of why vaccinated children had a lower autism risk. But one possibility, according to Mrozek-Budzyn, is that some children started showing potential signs of autism, or possibly other health problems, before receiving the MMR or measles vaccine. Doctors or parents may then have avoided vaccination.
Source: Pediatric Infectious Disease Journal, May 2010.
Monday, January 4, 2010
MONDAY, Jan. 4 (HealthDay News) -- New research suggests that body measurements and laboratory tests may predict the likelihood that a child will develop type 2 diabetes later in life.
Researchers analyzed long-term studies of 1,067 black and white girls followed for nine years after the age of 9 or 10, and of 822 black and white children followed for 22 to 30 years beginning in the mid-1970s.
The findings appear in the January issue of the Archives of Pediatrics & Adolescent Medicine.
The authors found that participants in the second study were more likely to have diabetes at the age of 39 if they had high childhood levels of blood pressure, body-mass index, glucose and triglycerides. Low levels of "good" cholesterol also spelled trouble.
"When body-mass index, systolic blood pressure and diastolic [bottom number] blood pressure were all lower than the 75th percentile and there was no parental diabetes mellitus, the likelihood of children developing type 2 diabetes mellitus 22 to 30 years later was only 1 percent," the authors wrote.
Those in the first study had a higher risk of diabetes at age 19 if they had parents with diabetes and higher levels of systolic blood pressure and insulin concentration.
The findings could help encourage prevention efforts in children who appear likely to develop diabetes, the researchers suggested.
The U.S. Centers for Disease Control and Prevention has more on diabetes.
By Carla K. Johnson
AP Medical Writer
The Associated Press
Monday, January 4, 2010
CHICAGO An expert panel says there's no rigorous evidence that digestive problems are more common in children with autism compared to other children, or that special diets work, contrary to claims by celebrities and vaccine naysayers.
Painful digestive problems can trigger problem behavior in children with autism and should be treated medically, according to the panel's report published in the January issue of Pediatrics and released Monday.
"There are a lot of barriers to medical care to children with autism," said the report's lead author, Dr. Timothy Buie of Harvard Medical School. "They can be destructive and unruly in the office, or they can't sit still. The nature of their condition often prevents them from getting standard medical care."
Some pediatricians' offices "can't handle those kids," Buie said, especially if children are in pain or discomfort because of bloating or stomach cramps. Pain can set off problem behavior, further complicating diagnosis, especially if the child has trouble communicating as is the case for children with autism.
Autism is a spectrum of disorders affecting a person's ability to communicate and interact with others. Children with autism may make poor eye contact or exhibit repetitive movements such as rocking or hand-flapping. About 1 in 110 U.S. children have autism, according to a recent government estimate.
More than 25 experts met in Boston in 2008 to write the consensus report after reviewing medical research. The Autism Society and other autism groups funded the effort, but gave no input.
The report refutes the controversial idea that there's a digestive problem specific to autism called "leaky gut" or "autistic enterocolitis." The hypothesis was first floated in 1998 in a now-discredited study by British physician Dr. Andrew Wakefield. His paper tied a particular type of autism and bowel disease to the measles vaccine.
The new report says the existence of autistic enterocolitis "has not been established." Buie said researchers and doctors have avoided digestive issues in autism because of their connection with Wakefield's disputed research, which set off a backlash against vaccines that continues to this day.
The new report calls for more rigorous research into the prevalence of digestive problems and whether special diets might help some children.
For now, the report states, available information doesn't support special diets for autism.
Diets have been promoted by actress Jenny McCarthy, whose best-seller "Louder Than Words" detailed her search for treatments for her autistic son.
Nearly 1 in 5 of children with autism are on a special diet, according to a project that tracks what treatments parents are trying. Most of them were on diets that eliminate gluten, found in many grains, or casein, a protein in milk, or both, according to the Interactive Autism Network at the Kennedy Krieger Institute in Baltimore, Md.
The new report advises doctors to watch for nutritional deficiencies in patients with autism. It recommends a nutritionist get involved if a patient is on a special diet or only eats certain foods.
The report drew praise from Rebecca Estepp of Poway, Calif., who believes a special diet is helping her autistic son. She said the paper gives pediatricians credible recommendations they've needed.
"I'm filled with hope after reading this report," said Estepp of the support group Talk About Curing Autism. "I wish this report would have come out 10 years ago when my son was diagnosed."
Lee Grossman, president of the Autism Society, a funder, said many doctors have written off autistic children's digestive problems as untreatable.
"I think we still have a lot to learn about the gut and how it contributes to behavioral symptoms," Grossman said. "We have a lot to learn about how to treat this."
Buie said his clinic has various techniques for treating children with problem behavior. They schedule early morning appointments so children aren't delayed in the waiting room or blow bubbles during a blood draw as a distraction. As a last resort, they use anesthesia.
"If a child is going to be asleep because of a dental evaluation or an MRI study, we will do our endoscopy, our blood work, spinal tap, haircuts or teeth cleaning at the same time," Buie said. "Our nurses do beautiful haircuts."
Monday, January 4, 2010
ScienceDaily (Jan. 4, 2010) A new research discovery published in the January 2010 print issue of the FASEB Journal suggests that treatments for disorders that cause accelerated aging, particularly Werner's syndrome, might come straight from the family medicine chest. In the research report, a team of Canadian scientists shows that vitamin C stops and even reverses accelerated aging in a mouse model of Werner's syndrome, but the discovery may also be applicable to other progeroid syndromes.
People with Werner's syndrome begin to show signs of accelerated aging in their 20s and develop age-related diseases and generally die before the age of 50.
"Our study clearly indicates that a healthy organism or individuals with no health problems do not require a large amount of vitamin C in order to increase their lifespan, especially if they have a balanced diet and they exercise," said Michel Lebel, Ph.D., co-author of the study from the Centre de Recherche en Cancerologie in Quebec, Canada. "An organism or individual with a mutation in the WRN gene or any gene affected by the WRN protein, and thus predisposes them to several age-related diseases, may benefit from a diet with the appropriate amount of vitamin C."
Scientists treated both normal mice and mice with a mutation in the gene responsible for Werner's syndrome (WRN gene) with vitamin C in drinking water. Before treatment, the mice with a mutated WRN gene were fat, diabetic, and developing heart disease and cancer. After treatment, the mutant mice were as healthy as the normal mice and lived a normal lifespan. Vitamin C also improved how the mice stored and burned fat, decreased tissue inflammation and decreased oxidative stress in the WRN mice. The healthy mice did not appear to benefit from vitamin C.
"Vitamin C has become one of the most misunderstood substances in our medicine cabinets and food," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. "This study and others like it help explain how and why this chemical can help to defend some, but certainly not all, people from premature senescence."
By Julie Steenhuysen
Monday, January 4, 2010
CHICAGO (Reuters) Mammograms should begin at 40 for women with an average risk of breast cancer and by 30 for high-risk women, according to guidelines released on Monday by two groups that specialize in breast imaging, contradicting controversial guidelines from a U.S. advisory panel last year.
The joint recommendations from the American College of the Radiology and the Society of Breast Imaging take into account the success of annual mammography screening starting at 40, said Dr. Carol Lee of Memorial Sloan-Kettering Cancer Center in New York, whose study appears in the Journal of the American College of Radiology.
"The significant decrease in breast cancer mortality, which amounts to nearly 30 percent since 1990, is a major medical success and is due largely to earlier detection of breast cancer through mammography screening," Lee said in a statement.
The recommendations have been in the works for about two years, but they serve in part as a rebuttal to guidelines issued in November by the U.S. Preventive Services Task Force, which recommended against routine breast mammograms for women in their 40s to spare them some of the worry and expense of extra tests to distinguish between cancer and harmless lumps.
Those recommendations contradicted years of messages about the need for routine breast cancer screening starting at age 40, sparking a rebellion from breast cancer specialists who argued the guidelines would confuse women and result in more deaths from breast cancer.
"Amidst all the furor, the ACR and the SBI stand firmly behind their recommendation that screening mammography should be performed annually beginning at age 40 for women at average risk for breast cancer," Lee and colleagues wrote.
The recommendations also cover the use of magnetic resonance imaging or MRI and breast ultrasound in women who are at high risk of breast cancer because they have mutations in the BRCA1 or BRCA2 genes or a family history of breast cancer.
In these women, breast mammograms should begin by age 30, but not before age 25, when the risk of radiation exposure from the mammograms begins to outweigh the benefits of screening.
Dr. Phil Evans of the University of Texas Southwestern Medical Center in Dallas and president of the Society for Breast Imaging, said the guidelines are based on the latest clinical trial data.
"Where the data was not present, we looked at recommendations that reflect expert consensus opinion," he said in a telephone interview.
He said they also help fill in some gaps in terms of how to screen high-risk women. In women who have BRCA mutations, the group recommends annual MRI screening, a more sensitive test, in addition to mammograms starting by age 30.
Women who have a greater than 20 percent lifetime risk of breast cancer based on family history should also have annual MRI scans starting at 30.
For high-risk women who cannot get an MRI, often because of claustrophobia, a breast ultrasound should be used instead, Evans said.
The two groups did not consider the harms associated with routine screening at an earlier age, such as false positive results, which the task force was trying to balance.
"The reason for that is there have been studies that have shown women would rather have their cancer found, even if it means having to have a biopsy. The harms, from most studies we've seen, did not seem to be all that real," Evans said.
(Editing by Philip Barbara)
Monday, January 4, 2010
ScienceDaily (Jan. 4, 2010) If you're pregnant and looking for an excuse to eat bacon and eggs, now you've got one: a new research study published in the January 2010 print issue of the FASEB Journal by a team of University of North Carolina researchers shows that choline plays a critical role in helping fetal brains develop regions associated with memory. Choline is found in meats, including pork, as well as chicken eggs.
"Our study in mice indicates that the diet of a pregnant mother, especially choline in that diet, can change the epigenetic switches that control brain development in the fetus," said Steven Zeisel, the senior scientist involved in the work and a senior member of the FASEB Journal's editorial board. "Understanding more about how diet modifies our genes could be very important for assuring optimal development."
Zeisel and colleagues made this discovery by feeding two groups of pregnant mice different diets during the window of time when a fetus develops its hippocampus, that part of the brain responsible for memory. The first group received no choline while the other received choline (1.1g/Kg). The group that received no choline had changes in epigenetic marks on the proteins (histones) that wrap genes in cells responsible for the creation of new brain cells (neural progenitor cells). Then, by isolating these cells from the developing brains and growing them in cell culture, the scientists determined the expression of genes for two proteins that regulate neuronal cell creation and maturation. These two proteins (G9a and Calb1) were changed in the brains of fetuses whose mothers were fed low choline diets.
"We may never be able to call bacon a health food with a straight face, but the emerging field of epigenetics is already making us rethink those things that we consider healthful and unhealthful," said Gerald Weissmann, MD, Editor-in-Chief of the FASEB Journal. "This is yet another example showing that good prenatal nutrition is vitally important throughout a child's entire lifetime."
The Agricultural Research Service's Nutrient Data Laboratory makes a database available to the public in an effort to help them get healthful amounts of choline in their diets. The database provides researchers and consumers with the means to estimate daily choline intake from consumption of more than 400 different foods and can be accessed at http://www.ars.usda.gov/main/site_main.htm?modecode=12-35-45-00. The Agricultural Research Service says that "experts suggest that an adequate choline intake is 425 milligrams a day for women and 550 milligrams a day for men. Top sources of choline include meat, nuts, and eggs."
By Joene Hendry
Monday, January 4, 2010
NEW YORK (Reuters Health) White, middle-aged women working in British civil service jobs may want to keep an eye on their blood sugar. Those reporting high levels of job strain and little work-related social support appear to be at increased risk for developing type 2 diabetes, according to a new study.
Such clerical and support jobs usually involve high demands but limited control over job tasks and schedules, study investigator Alex Heraclides, a PhD student at University College London noted in an email to Reuters Health.
Heraclides and colleagues assessed job related stressors over an average of nearly 12 years in 5,895 British civil servants who were initially free of diabetes. During this time 308 workers, 92 of whom were women, developed type 2 diabetes - the kind closely linked to obesity.
The investigators failed to see an association between job stressors in male workers and diabetes risk. The story was markedly different, however, among female workers.
Among the women, about "10 percent of all type 2 diabetes cases would have been prevented," Heraclides told Reuters Health, had the job-related stressors of little control, high demands, and little social support been eliminated.
In the study population as a whole, workers who developed diabetes were older, more likely to be employed in low-level jobs, expressed greater stress from life events, weighed more, and had other biological characteristics that put them at heightened risk for diabetes.
Among the female workers, biological factors tied to diabetes risk as well as lower versus higher employment "only explained a third of the effect," Heraclides said.
People need to recognize the importance stress plays in their overall physical health, the researcher added, by looking at stress exposures as another unhealthy factor similar to obesity, low physical activity, and poor diet.
Source: Diabetes Care, December 2009
Monday, January 4, 2010
ScienceDaily (Jan. 4, 2010) Prostate cancer patients who have a prostate-specific antigen (PSA) value of less than or equal to 1.5 at two years after external beam radiation therapy (EBRT) are less likely to have a cancer recurrence and cancer-related death, according to a study in the December 1 issue of the International Journal of Radiation Oncology*Biology*Physics, the official journal of the American Society for Radiation Oncology (ASTRO).
PSA levels in a prostate cancer patient are monitored after a patient's treatments, and after a successful course of EBRT the levels should decline gradually over the following 18 to 24 months. A continued rise in PSA can indicate relapsing disease.
Prior studies have attempted to categorize PSA response patterns after treatment in an effort to identify patients with an increased chance of a relapse earlier; however, most did not use a fixed point after treatment to predict outcomes.
Researchers at the Memorial Sloan-Kettering Cancer Center department of Radiation Oncology and Epidemiology and Biostatistics in New York, sought to determine the significance of a patient's reaching a certain PSA level at a specific point in time after EBRT.
The study authors found that patients with a PSA value of less than or equal to 1.5 at two years had a 2.4 percent incidence of distant metastases at five years after treatment and a 7.9 percent incidence at 10 years after treatment. Patients with a PSA value higher than 1.5 experienced a significantly higher rate of metastases at five and 10 years after treatment (10 percent and 17.5 percent, respectively).
"In the past, patients with a relapsing cancer after receiving radiation were not identified until several years after treatment and at that point it may be too late to effectively salvage their recurrence," Michael Zelefsky, M.D., lead author of the study and a radiation oncologist at Memorial Sloan-Kettering Cancer Center, said. "If we can catch these future instances of cancer recurrence earlier in prostate cancer patients, then we have a much higher chance of reducing the mortality associated with the cancer."
By Amy Norton
Monday, January 4, 2010
NEW YORK (Reuters Health) A number of studies have linked chronic sleep deprivation to a heightened risk of obesity, diabetes and heart disease. Now, a small study suggests that low levels of physical activity during the day may partly account for the connection.
In a study of 15 healthy men, researchers found that a couple nights of grabbing only four hours of sleep caused the men to curtail their physical activity compared with days where they had gotten the standard eight hours the night before.
In contrast, there was no evidence that sleep loss altered blood levels of appetite-regulating hormones or caused the men to eat more the next day -- effects that have been seen in a number of previous studies.
The implication is that there may be a broader range of reasons for the link between sleep loss and weight and health, the researchers report in the American Journal of Clinical Nutrition.
Practically speaking, the findings offer adults another reason to get enough sleep.
For healthy adults, that means regularly getting seven to eight hours per night, lead researcher Dr. Sebastian M. Schmid, of the University of Luebeck in Germany, told Reuters Health in an email.
A number of large epidemiological studies have found associations between poor sleep and higher risks of obesity and other health problems. Since then, a few small studies done in the sleep lab have attempted to find the possible reasons for the connection.
In some, researchers have found evidence that sleep loss alters the regulation of the hunger hormones leptin and ghrelin, and may boost daytime appetite. Leptin, which helps regulate body weight, is secreted by fat cells; low blood levels of the hormone promote hunger, while increases tell the brain that the body is full and encourage calorie burning. Ghrelin is secreted by the stomach to boost appetite.
But another possibility is that sleep-deprived people are just too tired to be physically active during the day.
While that seems logical, apparently no human studies had examined the question before.
For the new study, Schmid and his colleagues had 15 healthy, normal-weight men go through two consecutive nights with four hours of sleep and two nights with eight hours of sleep.
After the first night, the men spent the day doing their normal activities, while wearing a wrist device that recorded their movements. After the second night, they came to the sleep lab, where they again wore the wrist devices and also had their levels of leptin and ghrelin measured and their calorie intake monitored.
The researchers found that, unexpectedly, the men showed no differences in their hormone levels, hunger or food intake after the four-hour night compared with the eight-hour night.
They were, however, less active after sleep-deprived nights -- devoting both fewer minutes to physical activity and a smaller proportion of that time to more-intense exercise.
When the men got eight hours of sleep, they spent an average of 25 percent of their active time performing higher-intensity exercise; that declined to about 22 percent with four hours of sleep.
Over time, such differences could affect a person's weight and general health, according to Schmid's team.
The findings do not mean that sleep loss has no effects on hunger hormones and appetite, as earlier studies have suggested that it does. However, Schmid said, the results do suggest that even modest sleep restriction -- so common in today's society -- reduces physical activity, while hormones and appetite are "less affected."
Source: American Journal of Clinical Nutrition, December 2009.
Monday, January 4, 2010
ScienceDaily (Jan. 4, 2010) The roe of hake, lumpsucker and salmon is the best dietary source of Omega 3, according to a study carried out by researchers at the University of Almería (UAL). The scientists analysed the eggs, or roe, of 15 marine animals, and found all of these contained high levels of these fatty acids, which are essential to the human body.
Until now there had been no precise understanding of the nutritional potential of the roe of marine animals, but a team of researchers from the UAL has now shown that this is one of the best natural sources of Omega 3 fatty acids, which are essential for ensuring the correct development of a wide variety of metabolic functions in the human body.
"We have classified these eggs as unequivocal sources of Omega 3, and have proven that this appears at high concentrations in all the species studies," José Luis Guil Guerrero, director of this study and a researcher in the Food Technology Department of the UAL, said.
The results, published in the European Journal of Lipid Science and Technology, show that Omega 3 fatty acids are present in all fish roe, but especially in the eggs of Atlantic bonito (Sarda sarda), mackerel (Scomber scombrus), squid (Loligo vulgaris), cuttlefish (Sepia sp.), lumpsucker (Cyclopterus lumpus), hake (Merluccius merluccius) and salmon (Salmo salar).
The team studied the fatty acid content in the eggs of 15 marine animals, focusing their research on two types of Omega 3 -- eicosapentaenoic acids (EPA) and docosahexaenoic acids (DHA). More than 30% of the fatty acids found in these eggs were EPA and DHA.
The conclusions of the study also show that minimal consumption of lumpsucker, hake or salmon roe satisfies the human body's Omega 3 essential fatty acid requirements, because of its levels of EPA y DHA. A lack of these compounds is associated with cardiovascular disease, hypertension, depression, diabetes, poor development of the nervous and reproductive systems, and inflammatory diseases, such as Crohn's disease.
"Aside from their nutritional importance, we could also make use of roe to extract its oil, which is rich in PUFAs (polyunsaturated fatty acids) and can be used as a dietary supplement, since it has a higher Omega 3 content than regular oils, for example salmon and tuna oil," explains Guil Guerrero.