January 4, 2010

Job stress may raise diabetes risk in women
Last Updated: 2010-01-01 13:00:33 -0400 (Reuters Health)
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
http://www.reutershealth.com/archive/2010/01/01/eline/links/20100101elin001.html

Earlier bedtimes may help protect adolescents against depression and suicidal thoughts
American Academy of Sleep Medicine, January 1, 2010
WESTCHESTER, Ill. — A study in the Jan. 1 issue of the journal Sleep found that adolescents with bedtimes that were set earlier by parents were significantly less likely to suffer from depression and to think about committing suicide, suggesting that earlier bedtimes could have a protective effect by lengthening sleep duration and increasing the likelihood of getting enough sleep.
Results show that adolescents with parental set bedtimes of midnight or later were 24 percent more likely to suffer from depression (odds ratio = 1.24) and 20 percent more likely to have suicidal ideation (OR=1.20) than adolescents with parental set bedtimes of 10 p.m. or earlier. This association was appreciably attenuated by self-reported sleep duration and the perception of getting enough sleep. Adolescents who reported that they usually sleep for five or fewer hours per night were 71 percent more likely to suffer from depression (OR=1.71) and 48 percent more likely to think about committing suicide (OR=1.48) than those who reported getting eight hours of nightly sleep. Participants who reported that they "usually get enough sleep" were significantly less likely to suffer from depression (OR=0.35) and suicidal ideation (OR=0.71).
Lead author James E. Gangwisch, PhD, assistant professor at Columbia University Medical Center in New York, N.Y., said that the results strengthen the argument that short sleep duration could play a role in the etiology of depression.
"Our results are consistent with the theory that inadequate sleep is a risk factor for depression, working with other risk and protective factors through multiple possible causal pathways to the development of this mood disorder," said Gangwisch. "Adequate quality sleep could therefore be a preventative measure against depression and a treatment for depression."
Data were collected from 15,659 adolescents and their parents who had participated in the National Longitudinal Study of Adolescent Health (Add Health), a school-based, nationally representative, probability-based sample of U.S. students in grades seven to 12 in 1994 to 1996. Seven percent of participants (1,050) were found to have depression using the Centers for Epidemiologic Study-Depression Scale, and 13 percent (2,038) reported that they seriously thought about committing suicide during the past 12 months. Depression and suicidal ideation were associated with later parental set bedtime, shorter sleep duration, self-perception of not getting enough sleep, female sex, older age and lower self-perception of how much parents care.
Fifty-four percent of parents reported that their adolescent had to go to bed by 10 p.m. or earlier on weeknights, 21 percent reported setting a bedtime of 11 p.m., and 25 percent reported setting a bedtime of midnight or later. Caucasians were more likely than adolescents of other racial/ethnic groups to have a parental set bedtime of 11 p.m. Nearly 70 percent of adolescents reported going to bed at a time that complied with the weeknight bedtime that was set by their parents. Adolescents reported going to bed only about five minutes later on average than their parental set bedtime.
The average adolescent-reported sleep duration was seven hours and 53 minutes, which contrasted sharply with the nine or more hours of nightly sleep that the AASM recommends for adolescents. Participants with a parental set bedtime of 10 p.m. or earlier reported that they usually slept for an average of eight hours and 10 minutes, which was 33 minutes more than adolescents with a bedtime of 11 p.m. (seven hours, 37 minutes) and 40 minutes more than those with a bedtime of midnight or later (seven hours, 30 minutes). With the exception of sleep durations of 10 hours or more per night, higher average self-reported sleep durations were associated with progressively earlier average bedtimes.
The authors reported that there are a number of potential mechanisms by which chronic partial sleep deprivation could contribute to depression and suicidal ideation. A lack of sleep may affect the modulation of emotional brain responses to aversive stimuli; produce moodiness that hinders the ability to cope with daily stresses and impairs relationships with peers and adults; and affect judgment, concentration and impulse control.
They also suggested that behavioral interventions that involve educating adolescents and their parents about healthier sleep hygiene practices and helping them modify maladaptive sleep habits could sever as primary preventative measures against depression and suicidal ideation.
An abstract of this study (#1064) was presented in Seattle, Wash., on June 9, 2009, at SLEEP 2009, the 23rd Annual Meeting of the Associated Professional Sleep Societies LLC (APSS).
http://www.eurekalert.org/pub_releases/2010-01/aaos-ebm122809.php

How Ubiquitin Chains Are Added to Cell-Cycle Proteins: May Lead to Targeted Cancer Therapies
ScienceDaily (Jan. 4, 2010) — Researchers from the California Institute of Technology (Caltech) have been able to view in detail, and for the first time, the previously mysterious process by which long chains of a protein called ubiquitin are added by enzymes called ubiquitin ligases to proteins that control the cell cycle. Ubiquitin chains tag target proteins for destruction by protein-degrading complexes in the cell.
"We found that ubiquitin ligases build ubiquitin chains very rapidly by transferring ubiquitins one at a time," says Raymond Deshaies, professor of biology at Caltech and Howard Hughes Medical Institute investigator.
Their findings, and the innovative process by which they were obtained, are described in this week's issue of the journal Nature.
Ubiquitin is one of nature's most unusual proteins. Unlike most of its protein brethren, ubiquitin has to be physically attached to other proteins to do its job.
"As its name implies, ubiquitin is found in essentially every kind of eukaryotic cell," says Caltech graduate student Nathan Pierce, the Nature paper's lead author.
In their Nature paper, the Caltech team looked at the process of ubiquitylation, the method by which ubiquitin and ubiquitin chains are added to target proteins. The target proteins used in the study, cyclin E and β-Catenin, are both involved in controlling the cell cycle.
It was already known, Pierce explains, that the addition of a chain of four or more ubiquitins to a target protein marks that protein for annihilation. The destruction of cyclin E is critical for the accurate replication of DNA, while the degradation of β-Catenin keeps cells from dividing during development at the wrong time. If β-Catenin is not degraded, cells proliferate excessively and become predisposed to tumorigenesis. Meanwhile, cells that don't degrade cyclin E accumulate DNA damage and mutations, which can help fuel the unchecked growth of a tumor.
It was also already known that ubiquitin chains are added to the protein using three different enzymes, dubbed E1, E2, and E3. Simply put, E1 activates ubiquitin for transfer, then passes it over to E2. E3 then gets into the act. A form of E3 called a RING ligase (RING stands for "really interesting new gene") plays a key role in the tagging of cyclin E and β-Catenin; according to Pierce, the RING ligase "simultaneously binds to E2 and the target protein (like cyclin E), and then causes E2 to transfer the ubiquitin to the target protein."
Despite all of this knowledge, one question has remained: is the chain transferred to the protein in an already assembled form, or are the ubiquitins moved over one at a time?
"The process is so complicated and so fast," Pierce notes, "that we weren't able to see how the chain is actually built."
To address that issue, Pierce created a sort of biological stop-motion animation that allowed the Caltech team to watch every step in the transfer of ubiquitin from E2 onto the cyclin E protein substrate.
"We devised methods to take snapshots of ubiquitin ligase reactions at a rate of up to 100 'pictures' every second," says Deshaies. "This enables us to see things that would normally evade detection. "
Previous studies had looked at the reaction on the scale of seconds or minutes, Pierce adds. But through an innovative use of a laboratory tool called a quench-flow machine -- a machine that allows for extreme precision in the stopping, or "quenching," of a reaction -- the team was able to look at what was going on over intervals of just 10 milliseconds in both yeast and human proteins.
"Prior methods did not have sufficient time resolution to see what was going on," says Deshaies. "It's as if you gave an ice-cream cone to a kid and took pictures every minute. You would see the ice cream disappear from the first photo to the next, but since the pictures are too far apart in time, you would have no idea whether the child ate the ice cream one bite at a time, or swallowed the entire scoop in one gulp."
The new method revealed the biological equivalent of small, single bites of ice cream. "Using our approach," Deshaies says, "we could see that our ubiquitin ligase builds ubiquitin chains one ubiquitin at a time."
"Once we knew what the steps were, we calculated the rates at which they occur," adds Pierce. "And from those rates, we were able to really describe the biology of how this system works."
The quest doesn't stop there, of course. "One thing we have to understand now is, how do ubiquitin ligases achieve the speeds that they do?" asks Deshaies. "What special mechanisms do they have to enable them to build chains rapidly? And the flip side of the coin: What sets the speed limit? Why can't our ubiquitin ligase work even faster?"
A recent paper published in the journal Cell by Gary Kleiger, a postdoctoral scholar in the Deshaies lab, answered some of these speed-related questions. By measuring the rates at which E2 and E3 interacted with one another, Kleiger was able to demonstrate their unusually fast association -- faster than predicted for normal proteins. E2 and E3 use oppositely-charged surfaces to attract each other, thereby speeding up the formation of a functional complex of the two proteins. This helps explain how the rapid sequential additions of ubiquitin described in the Nature paper are possible.
Gaining these kinds of insights into the ubiquitin system is important, Deshaies says, because ubiquitin ligases play a critical role in a number of human diseases, including cancer, due to their role in the regulation of the cell cycle.
"Once we understand these aspects of how ubiquitin ligases work, and what limits their speed, we will be in an excellent position to think about how we might develop drugs that attack the ligase's Achilles' heel, to make its slowest step even slower," he says. "If we can slow down ubiquitin ligases enough, they may become too slow to get their job done -- to build chains -- in the time available to them to do so. Being able to develop drugs to block their function would open up a new frontier in medicine."
"We were able to invent HIV therapeutics because we understand how reverse transcriptase works," adds Pierce. "The same applies here. We need to understand how these enzymes work if we're ever going to be able to target them with therapeutics."
In addition to Pierce and Deshaies, other researchers involved in the study included Kleiger and Shu-ou Shan, assistant professor of chemistry at Caltech.
The work described in the Nature paper was funded by a Gordon Ross Fellowship, National Institutes of Health training and research grants, and the Howard Hughes Medical Institute.
Nathan W. Pierce, Gary Kleiger, Shu-ou Shan, Raymond J. Deshaies. Detection of Sequential Polyubiquitylation on a Millisecond Time-Scale. Nature, 2009; DOI: 10.1038/nature08595
http://www.sciencedaily.com/releases/2009/12/091214162311.htm

Increased Risk of Death, Stroke in Postmenopausal Women Taking Antidepressants, Study Finds
ScienceDaily (Jan. 4, 2010) — Women participating in the Women's Health Initiative study who reported taking an antidepressant drug had a small but statistically significant increase in the risk of stroke and of death compared with participants not taking antidepressants. The authors of a report in the December 14 Archives of Internal Medicine note that their findings are not conclusive but may signify a need for additional attention to patients' cardiovascular risk factors.
"Depression is a serious illness with its own health risks, and we know that antidepressants can be life-saving for some patients. No one should stop taking their prescribed medication based on this one study, but women who have concerns should discuss them with their physicians," says Jordan W. Smoller, MD, ScD, of the Massachusetts General Hospital (MGH) Department of Psychiatry, the study's lead author. "Older women taking antidepressants can talk with their physicians about their cardiovascular risk, work on modifying other risk factors, and discuss the risks and benefits of various treatment options. We need to study this association more to determine exactly what it signifies."
Depression is a known risk factor for cardiovascular disease and premature death, and one of the reasons that tricyclic antidepressants are used less frequently is their potential for negative effects on heart function. Selective serotonin reuptake inhibitor (SSRI) antidepressants have fewer side effects in general and are known to have aspirin-like effects on bleeding, which could protect against clot-related cardiovascular disorders. Since the use of antidepressants has increased greatly in recent years and since older women are also at risk for cardiovascular disease, a team of researchers from several academic medical centers examined the link between antidepressant use and cardiovascular disease in such patients.
The Women's Health Initiative (WHI) of the National Institutes of Health followed more than 160,000 postmenopausal U.S. women for up to 15 years, examining risk factors for and potential preventive measures against cardiovascular disease, cancer and osteoporosis. For the current study, the research team began with data from more than 136,000 WHI participants who were not taking antidepressant drugs when they entered the study. At their first follow-up visit, either one or three years after study entry, about 5,500 of those women reported currently taking an antidepressant. The research team compared that group's subsequent history of cardiovascular disease with that of participants who had not started taking antidepressants.
While the study did not find any relationship between antidepressant use and heart disease, during a follow-up period averaging nearly six years, participants taking antidepressants did have an increased risk of death from any cause and of hemorrhagic stroke among those taking SSRIs. The overall risks were small -- remaining less than 2 percent annually for all groups -- but the increase was statistically significant. "There are a lot of things this study couldn't tell us, such as whether this risk truly is attributable to the drugs and not to depression itself and whether participants were being treated for depression or for anxiety, which also has cardiovascular risks," Smoller says. "We also don't know whether there is any similar association in younger women or in men, since they were not part of this study."
"Previous studies have shown that depression itself has risks as high as those seen with medication in this study," he adds. "There are other effective forms of therapy for patients at high cardiovascular risk who also have depression, so concerned women can explore these options with their physicians. But for most patients with significant depression, the benefits of antidepressants will outweigh the risks." Smoller is an associate professor of Psychiatry at Harvard Medical School.
Senior author Sylvia Wassertheil-Smoller, PhD, of Albert Einstein College of Medicine is also a principal investigator in the Women's Health Initiative. Additional co-authors are Matthew Allison, MD, MPH, University of California, San Diego; Barbara Cochrane, PhD, RN, University of Washington; David Curb, MD, MPH, University of Hawaii; Roy Perlis, MD, MSc, MGH; Jennifer Robinson, MD, MPH, University of Iowa; Milagros Rosal, PhD, University of Massachusetts Medical Center; and Nanette Wenger, MD, Emory University. Both the Women's Health Initiative and the current study were supported by grants from the National Institutes of Health.
Jordan W. Smoller; Matthew Allison; Barbara B. Cochrane; J. David Curb; Roy H. Perlis; Jennifer G. Robinson; Milagros C. Rosal; Nanette K. Wenger; Sylvia Wassertheil-Smoller. Antidepressant Use and Risk of Incident Cardiovascular Morbidity and Mortality Among Postmenopausal Women in the Women's Health Initiative Study. Arch Intern Med, 2009; 169 (22): 2128-2139
http://www.sciencedaily.com/releases/2009/12/091214162311.htm

Vitamin C 'Cures' Mice With Accelerated Aging Disease
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."
Laurent Massip, Chantal Garand, Eric R. Paquet, Victoria C. Cogger, Jennifer N. O'Reilly, Leslee Tworek, Avril Hatherell, Carla G. Taylor, Eric Thorin, Peter Zahradka, David G. Le Couteur, and Michel Lebel. Vitamin C restores healthy aging in a mouse model for Werner syndrome. The FASEB Journal, 2010; 24 (1): 158
http://www.sciencedaily.com/releases/2010/01/100104101210.htm

Licorice Root: Trip to the Candy Store Might Help Ward Off Rare, but Deadly Infections
ScienceDaily (Jan. 4, 2010) — As it turns out, children were not the only ones with visions of sugar plums dancing in their heads over this past holiday season. In a new research report published in the January 2010 issue of theJournal of Leukocyte Biology, a team of scientists from the University of Texas Medical Branch and Shriners Hospitals for Children shows how a compound from licorice root (glycyrrhizin from Glycyrrhiza glabra) might be an effective tool in battling life-threatening, antibiotic-resistant infections resulting from severe burns.
Specifically, they found that in burned mice, glycyrrhizin improved the ability of damaged skin to create small proteins that serve as the first line of defense against infection. These proteins, called antimicrobial peptides, work by puncturing the cell membranes of bacteria similar to how pins pop balloons.
"It is our hope that the medicinal uses of glycyrrhizin will lead to lower death rates associated with infection in burn patients," said Fujio Suzuki, Ph.D., one of the researchers involved in the work. Suzuki also said that more research is necessary to determine if this finding would have any implications for people with cystic fibrosis, who can develop Pseudomonas aeruginosa infections in their lungs.
To make this discovery, Suzuki and colleagues used three groups of mice. The first group was normal, the second group was burned and untreated, and the third group was burned and treated with glycyrrhizin. The skin of the untreated burned mice did not have any detectable antimicrobial peptides that prevent bacteria from growing and spreading, but the normal mice did. The skin of the untreated burned mice also had immature myeloid cells, which indicate an inability of the skin to produce antimicrobial peptides needed to prevent infection. The mice treated with glycyrrhizin, however, were more like the normal mice as they had the antimicrobial peptides and no immature myeloid cells.
"Burns are the most painful of all injuries," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology, "and the deadly Pseudomonas infections that can result from severe burns do more than add insult to those injuries. This research should serve as an important stepping stone toward helping develop new drugs that help prevent or treat Pseudomonas."
http://www.sciencedaily.com/releases/2010/01/100104101215.htm

High Fat Diet Increases Inflammation in the Mouse Colon
ScienceDaily (Jan. 2, 2010) — Colorectal cancer, the third most common type of cancer worldwide, has been linked to an increased prevalence of the Western diet: one high in fat and low in fiber, vitamin D and calcium. Now, a team of scientists led by researchers at Rockefeller University have shown what happens to colon tissue when mice are fed such a diet: an inflammatory response that could be the trigger for carcinogenic processes. Their results are published in the November 2009 issue ofThe Journal of Nutrition.
"There is convincing evidence that increased intake of red meat, processed meat and alcohol can increase risk of colorectal cancer, whereas greater consumption of dietary fiber, milk and calcium might decrease risk," says Peter Holt, a senior research associate in the Laboratory of Biochemical Genetics and Metabolism at Rockefeller. "Our findings show that a Western diet induces oxidative stress and alters immune responses in the colon of mice long before tumors occur."
The researchers fed experimental mice either a standard diet containing five percent fat and ample amounts of calcium and vitamin D or a Western diet containing 20 percent fat and adequate but marginal levels of calcium and vitamin D for three or six months.
As expected, animals consuming the Western diet were heavier and had more fat tissue than those on the control diet. Microarray analysis identified 41 genes that were being expressed at significantly different levels between the Western diet and control animals. Most of these genes were related to metabolic processes such as lipid metabolism and glutathione metabolism, which is important for preventing damage caused by oxidation. In addition, expression of a series of genes collectively associated with immune and inflammatory responses was altered. The Western diet also increased the number of macrophages, cells associated with inflammation in the colon, as well as several proteins such as myeloperoxidase and MCP-1 and colonic oxidative stress genes associated with inflammation.
Taken together, Holt says, these data suggest that macrophage recruitment and oxidative stress is a potential early mechanism underlying the carcinogenic effect of the Western diet.
Erdelyi et al. Western-Style Diets Induce Oxidative Stress and Dysregulate Immune Responses in the Colon in a Mouse Model of Sporadic Colon Cancer. Journal of Nutrition, 2009; 139 (11): 2072
http://www.sciencedaily.com/releases/2009/12/091231163503.htm

Will Higher Global Temperatures Make It Easier for Viruses to Jump Species?

ScienceDaily (Jan. 2, 2010) — An interdisciplinary team of researchers at the University of Idaho soon will begin investigating whether viruses that have adapted to higher temperatures -- similar to increases due to global warming -- can jump species more easily.
Thanks to a $911,000 grant from the National Institutes of Health, a group that includes a computational biophysicist, an evolutionary biologist and a mathematician will conduct the study. Their results could shed light on the characteristics of host-switching viruses -- such as the avian flu or H1N1 -- in a world of increasing temperatures.
"It's a pretty simple experiment, but it's a wild ... idea," said Holly Wichman, professor of biology and the evolutionary biologist of the group.
"But, if it turns out that our idea is right, it could have enormous implications," added Marty Ytreberg, professor of physics and the computational biophysicist of the group.
The virus being studied is known as bacteriophage ψX174. It was the first genome ever sequenced and often is used by scientists who study evolution because it has a small genome and multiplies quickly. This allows mutations and evolution to occur rapidly.
Through previous experiments together, the team observed mutations that allow the virus to survive in higher temperatures might also increase the stability of the capsid -- the protein shell that encloses the genetic material of a virus. If true, this increased stability may make the virus more mutable, more likely to mutate and thus have an increased ability to jump hosts.
To test the theory, the virus will be subjected to mutations that are known to enable it to survive at higher temperatures. Then, the team will investigate if this ability results in more stabilizing mutations than the original strain that lives at lower temperatures. The team also will investigate whether or not the stabilizing mutations allow the virus to switch hosts more easily.
For this project, Ytreberg will use computational modeling to analyze if the mutations stabilize the capsid. And Paul Joyce, professor of mathematics and statistics, will use statistical and spatial modeling to explore how these beneficial mutations spread through a structured environment.
"It's a really fun project because you work with people that are in different areas," said Wichman. "You get to learn how people in other parts of science think. And since none of us are afraid to ask dumb questions, we just keep making each other explain things until we understand. Having to explain yourself really solidifies your ideas, I think."
Funding comes from federal stimulus money made available through a competitive application process to institutions that receive a Centers of Biomedical Research Excellence (COBRE) grant. The program is designed to build capacity and increase competitiveness at institutions located in states that have historically received a small proportion of NIH funds.
http://www.sciencedaily.com/releases/2009/12/091231114110.htm

New Study Confirms: Organic Food is Far Healthier Than Conventional
David Gutierrez, NaturalNews.com  January 3, 2010 

(NaturalNews) Organic produce is nutritionally superior to so-called "conventional" produce, according to a comprehensive review conducted by researchers from the University of Aix-Marseille for the French food agency (AFSSA) and published in the journal Agronomy for Sustainable Development.

"This critical literature review indicates that organic agriculture, as developed until now, has the potential to produce high-quality products with some relevant improvements in terms of anti-oxidant phytomicronutrients, nitrate accumulation in vegetables and toxic residue levels," the researchers wrote.

To be recognized as "organic," a food product must be produced without the use of genetic modification or chemical fertilizers or pesticides, and must promote sustainable cropping methods. In the United States, organically produced meat and dairy must be raised without the use of synthetic growth hormones or antibiotics. Hormones and antibiotics are banned in animal production across the board in the European Union.

Recently the United Kingdom's Food Standards Agency (FSA) reviewed existing research on the nutritional content of organic produce concluded that there was no difference, nutritionally, between organic and non-organic produce. The FSA study did not examine the reasons most often given by consumers of organic produce, namely benefits to the environment, farm workers, and consumer health due to lower chemical use.

Yet the AFSSA review calls the FSA's conclusions into question. After conducting an "up-to-date exhaustive and critical evaluation of the nutritional and sanitary quality of organic food," French researchers concluded that organic produce is clearly nutritionally superior.

Organic produce contains more minerals, such as iron and magnesium, than non-organic produce, and higher levels of antioxidants such as phenols and salicylic acid.

"Organic plant food overall contain double the amount of phenolic compounds," the researchers wrote.

Animal foods produced organically contained significantly more polyunsaturated fat than non-organic animal products. In addition, organic vegetables contained 50 percent less nitrates than non-organic produce. No more than 6 percent of organic produce tested contained pesticide residue.
http://www.naturalnews.com/027854_organic_food_nutrition.html

New study: amino acids could heal brain damage
S. L. Baker, NaturalNews.com  January 3, 2010 

(NaturalNews) A head-on car collision, a stumble that slams your head to the ground, a wound from a military battle in Afghanistan, a violent criminal assault -- these and other causes of sudden blows to the head can result in traumatic brain injury (TBI). According to the National Institutes of Health (NIH), TBI can be mild, moderate, or severe, depending on the extent of the damage to the brain. And symptoms can range from dizziness, headaches and memory problems to difficulty thinking, coma or even a vegetative state.

Unfortunately, there is no effective medical treatment for TBI. Although doctors can relieve the dangerous swelling that occurs after a traumatic braininjury, there is currently no way to reverse the underlying brain damage that can lead to cognitive losses in memory, learning and other functions. But neuroscientists think that could change, thanks to a natural treatment. A new study recently published in the online issue of the Proceedings of the National Academy of Sciences suggests natural amino acids hold the key to healing brain injuries. 

For the National Institutes of Health (NIH) funded research, neuroscientists fed amino acids to brain-injured mice. The results? The animals' cognitive abilities were restored. That, the researchers stated in a media release, may set the stage for the first effective treatment for cognitive impairments suffered by people with TBI. If these results from animal studies can be translated to human medicine, the impact will be huge, they added -- because every 23 seconds, a man, woman or child in the United States suffers a TBI.

"We have shown in an animal model that dietary intervention can restore a proper balance of neurochemicals in the injured part of the brain, and simultaneously improves cognitive performance," said study leader Akiva S. Cohen, Ph.D., a neuroscientist at The Children's Hospital of Philadelphia, in a statement to the press.

For their study, the researchers used a mix of three branched chain amino acids (BCAAs), specifically leucine, isoleucine and valine. BCAAs are crucial to brain health because they are precursors of two neurotransmitters -- glutamate and gamma-aminobutyric acid, or GABA. These neurotransmitters work together to balance brain activity. Specifically, glutamate excites neurons, stimulating them to fire, while GABA dampens down the firing of brain cells. A TBI can upset this balance and keep the brain from functioning normally. 

Frequently, a TBI damages the structure deep in the brain involved in higher learning and memory known as the hippocampus. In their new study, the scientists discovered that an injury to the hippocampus reduces levels of BCAAs. That throws the critical balance of neurotransmitters in the hippocampus into disarray, causing some localized regions of the brain to be more excitable and others less excitable.

To test the idea that dietary BCAAs would restore the normal balance of neural responses to brain-injured animals, the scientists worked with mice that had been conditioned to fear a mild electric shock in their cage. The animals had developed a "freezing" response when placed in the cage because they anticipated a shock. Then the research team created brain injuries in one group of mice with this conditioned fear response and, a week later, compared this group to animals conditioned to the fear response that had no TBI. The injured mice had partially lost their memory of past shocks and so had fewer "freezing" responses. 

However, when the brain-injured mice were given water to drink that contained BCAAs, the amino acid cocktail restored their learning ability and they regained the same normal responses as the uninjured animals. Moreover, additional experiments showed that BCAAs had restored the animals' normal balance of neural activity. 

Previous studies have revealed that people with brain injuries show mild functional improvements after receiving BCAAs through an intravenous line (IV). Dr. Cohen stated the new study suggests that BCAAs used as a dietary supplement could offer more sustained benefits than amino acids given through IVs. Early-phase clinical trials of dietary BCAAs in patients with mild to moderate traumatic brain injuries are expected to begin over the next year.
http://www.naturalnews.com/027849_amino_acids_brain_damage.html

Warning: Pet Food Contaminated With High Levels of Fluoride
David Gutierrez, NaturalNews.com  January 2, 2010 

(NaturalNews) A study conducted by the Environmental Working Group (EWG) found high levels of fluoride contamination in eight major national brands of dog food, raising concerns that pets may be at risk of bone cancers and other consequences of fluoride exposure.

Fluoride is a naturally occurring element that may help prevent tooth decay when applied to the exterior of teeth. When ingested, whether via drinking water or food, fluoride builds up in teeth and bones and can lead to health conditions including tooth mottling (dental fluorosis), neurotoxicity, hormonal disruption, and damage to the reproductive and developmental systems. A number of studies have shown that boys who drink fluoridated tap water between the ages of six and eight are significantly more likely to develop a rare and fatal bone cancer known as osteosarcoma.

The rate of osteosarcoma in dogs is almost 10 times that in humans. It is unknown whether this is caused by a greater vulnerability or increasedfluoride exposure.

Researchers tested 10 brands of dog food marketed for both adults and puppies, finding that eight of them -- all major national brands -- contained fluoride levels between 1.6 and 2.5 times as high as the Environmental Protection Agency's (EPA's) maximum allowed level in drinking water. A dog also consuming fluoridated water would be exposed to levels 3.5 times the EPA's limit, the researchers concluded.

The primary source of the fluoride contamination seemed to be bone meal and other animal byproducts (including chicken or beef meal and chicken or poultry by-product meal) used as filler. The one vegetarian brand tested had no fluoride contamination, and neither did the brand produced by a small manufacturer.

Fluoridated tap water probably also contributed a small but significant amount of fluoride to the dog food, the researchers said.

EWG recommends that consumers seeking to protect their dogs from fluoride purchase only dog foods that do not contain bone meal or other animal byproducts.
http://www.naturalnews.com/027846_fluoride_pet_food.html

Mushroom drug cancer secret probe
Scientists have discovered how a promising cancer drug, first discovered in a wild mushroom, works.
BBC News (Health), December 29, 2009
The University of Nottingham team believe their work could help make the drug more effective, and useful for treating a wider range of cancers.
Cordycepin, commonly used in Chinese medicine, was originally extracted from a rare kind of parasitic mushroom that grows on caterpillars.
The study will appear in the Journal of Biological Chemistry.
The cordyceps mushroom has been studied by medical researchers for some time - the first scientific publication on cordycepin was in 1950.
However, although the drug showed great promise, it was quickly degraded in the body.
It can be given with another drug to combat this - but the second drug can produce side effects that limit its potential use.
As a result, researchers turned their interest to other potential candidate drugs, and exactly how cordycepin worked on the body's cells remained unclear.
“ It could lay the groundwork for the design of new cancer drugs that work on the same principle ” 
Dr Cornelia de Moor University of Nottingham
Researcher Dr Cornelia de Moor said: "Our discovery will open up the possibility of investigating the range of different cancers that could be treated with cordycepin.
"It will be possible to predict what types of cancers might be sensitive and what other cancer drugs it may effectively combine with.
"It could also lay the groundwork for the design of new cancer drugs that work on the same principle."
The researchers have also developed a method to test how effective the drug is in new preparations, and combinations with other drugs, which might solve the problem of degradation more satisfactorily.
Dr De Moor said: "This is a great advantage as it will allow us to rule out any non-runners before anyone considers testing them in animals."
The Nottingham team observed two effects on the cells - at a low dose cordycepin inhibits the uncontrolled growth and division of the cells, and at high doses it stops cells from sticking together, which also inhibits growth.
“ The knowledge generated by this research demonstrates the mechanisms of drug action and could have an impact on one of the most important challenges to health ” 
Professor Janet Allen Biotechnology and Biological Sciences Research Council
Both of these effects probably have the same underlying mechanism - that cordycepin interferes with how cells make proteins.
At low doses cordycepin interferes with the production of mRNA, the molecule that gives instructions on how to assemble a protein.
And at higher doses it has a direct impact on the making of proteins.
Professor Janet Allen is director of research at the Biotechnology and Biological Sciences Research Council, which funded the study.
She said: "This project shows that we can always return to asking questions about the fundamental biology of something in order to refine the solution or resolve unanswered questions.
"The knowledge generated by this research demonstrates the mechanisms of drug action and could have an impact on one of the most important challenges to health."
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/8428340.stm

'Lifeless' prions can 'evolve'
Scientists have shown for the first time that "lifeless" prion proteins, devoid of all genetic material, can evolve just like higher forms of life.
BBC News Science, January 1, 2010
The Scripps Research Institute in the US says the prions can change to suit their environment and go on to develop drug resistance.
Prions are associated with 20 different brain diseases in humans and animals.
The scientists say their work suggests new approaches might be necessary to develop therapies for these diseases.
In the study, published in the journal Science, the scientists transferred prion populations from brain cells to other cells in culture and observed the prions that adapted to the new cellular environment out-competed their brain-adapted counterparts.
When returned to the brain cells, the brain-adapted prions again took over the population.
Charles Weissmann, head of Scripps Florida's department of infectology who led the study, said: "On the face of it, you have exactly the same process of mutation and adaptive change in prions as you see in viruses.
“ This is a timely reminder that prion concerns are not going away and that controls to stop abnormal prions being transmitted to humans through the food system or through blood transfusions must be vigorously maintained ” 
Professor John Collinge, Medical Research Council Prion Unit
"This means that this pattern of Darwinian evolution appears to be universally active.
"In viruses, mutation is linked to changes in nucleic acid sequence that leads to resistance.
"Now, this adaptability has moved one level down- to prions and protein folding - and it's clear that you do not need nucleic acid (DNA or RNA) for the process of evolution."
Mammalian cells normally produce cellular prion protein or PrPC.
During infections, such as the human form of mad cow disease known as vCJD, abnormal or misfolded proteins convert the normal host prion protein into its toxic form by changing its conformation or shape.
"It was generally thought that once cellular prion protein was converted into the abnormal form, there was no further change", Mr Weissmann said.
"But there have been hints that something was happening.
"When you transmit prions from sheep to mice, they become more virulent over time.
PRION DISEASES 
   Human prion diseases such as Creutzfeldt Jakob disease (CJD) can arise sporadically, be acquired by infection or be inherited because of a mutant gene coding for the prion protein
   They are relatively rare but have occurred in epidemic form in Papua New Guinea as a result of brain cannibalism
   Animal prion diseases include scrapie in sheep and goats, chronic wasting disease in deer and elk and transmissible mink encephalopathy
   Bovine spongiform encephalopathy (BSE) first appeared in UK in mid-1980s
   It is estimated that more than two million UK cattle were infected
   Variant CJD (vCJD) caused by the same prion strain as BSE was first recognised in the mid-1990s
"Now we know that the abnormal prions replicate, and create variants, perhaps at a low level initially.
"But once they are transferred to a new host, natural selection will eventually choose the more virulent and aggressive variants."
Professor John Collinge, of the Medical Research Council's (MRC) Prion Unit, described the research as exciting confirmation of a hypothesis that he had proposed two years ago, that there could be a "cloud" or whole array of prion proteins in the body.
He called it the cloud hypothesis.
He said: "The prion protein is not a clone, it is a quasi-species that can create different protein strains even in the same animal.
"The abnormal prion proteins multiply by converting normal prion proteins.
"The implication of Charles Weissmann's work is that it would be better to cut off that supply of normal prion proteins rather than risk the abnormal prion adapting to a drug and evolving into a new more virulent form.
"You would do this by trying to block the sites on the normal prion protein that the abnormal form locks on to to do its conversion.
"We know there is an antibody that can do this in mice and the Medical Research Council's Prion Unit have managed to engineer a human antibody to do this.
Chemical libraries
"It is currently undergoing safety tests and we hope to move to clinical trials by the end of 2011"
Professor Collinge said the MRC was also trying to find more conventional chemical compounds to do this and has been collaborating with the chemical company GlaxoSmithKline (GSK).
He said: "They have given us access to their chemical libraries, which contain millions of compounds, and we have already identified some that may work well.
"This is a timely reminder that prion concerns are not going away and that controls to stop abnormal prions being transmitted to humans through the food system or through blood transfusions must be vigorously maintained."
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/8435320.stm