Leftover Turkey to the Fridge, Stat | |||||
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Thursday, November 24, 2011
On Thanksgiving, let's be thankful.....and smart.
Tuesday, November 22, 2011
Finally, after all these years of water consumption, the European Union gives a reason to drink beer:
UK NEWS
EU SAYS WATER IS NOT HEALTHY
No water sold in the EU can now claim to protect against dehydration.
By Giles Sheldrick Exclusive
Friday November 18,2011
THE EU was ridiculed last night after it took three years to issue a new rule that water cannot be sold as healthy.
In a scarcely believable ruling, a panel of experts threw out a claim that regular water consumption is the best way to rehydrate the body. The bizarre diktat from Brussels has far-reaching implications for member states, including Britain, as no water sold in the EU can now claim to protect against dehydration.
European Commission President Jose Manuel Barroso has signed the order
Any producer breaching the order, signed by European Commission President Jose Manuel Barroso, faces being jailed for up to two years. It took the 21 scientists on the panel three years of analysis into the link between water and dehydration to come to their extraordinary conclusion.
“It is a perfect example of what the EU does best and makes the bendy banana law look positively sane.”
Conservative MEP Roger Helmer said: “The euro is burning, the EU is falling apart and yet here they are, highly paid, highly pensioned officials trying to deny us the right to say what is patently true.
“If ever there were an episode which demonstrates the folly of the great European project then this is it.”
A spokesman for the Department of Health said: “Of course water hydrates. While we support the EU in preventing false claims about commercial products, we need to exercise common sense as far as possible.”
Jose Manuel Barroso and David Cameron at a round table meeting earlier this year
German professors Dr Moritz Hagenmeyer and Dr Andreas Hahn, of the Institute for Food Science and Human Nutrition at Hanover Leibniz University, applied for approval for the seemingly uncontentious claim that “regular consumption of significant amounts of water can reduce the risk of development of dehydration”. However, bureaucrats refused to back them.
After a meeting in Italy a delegation of scientists concluded that reduced water content in the body was a symptom of dehydration rather than a risk factor that drinking water could control. Now their verdict has been turned into a regulation that will become UK law by December 6 and is bound to send shockwaves through the soft drinks industry.
Monday, November 21, 2011
Next time someone says you walk like a jackass, you'll be able to point to this study as the reason why:
Two feet or four, software is the same
All walking animals use the same basic nerve patterns to put one leg in front of the other(s)
Science News Web edition : Friday, November 18th, 2011
Although legged vertebrates come in many different shapes and sizes and exhibit a wide variety of walking styles, they may all employ a similar nerve system, located in the spine, to coordinate the muscle activity needed for locomotion, neurophysiologist Francesco Lacquaniti of the University of Rome Tor Vergata and colleagues report in the Nov. 18 Science.
Networks of spinal nerve cells, called central pattern generators, contain all the necessary information to time the muscles for the step cycle, says neuroscientist Sten Grillner of the Karolinska Institute in Stockholm, who was not involved in the study. The networks still need to be turned on by the brain, but once triggered, the spinal nerves handle locomotion all on their own. A message to start moving gets generated in the spinal cord and travels down the nerve pathway to specialized nerve cells that deliver the message directly to muscle fibers.
The central pattern generators are so autonomous that, in some cases, cats can still walk after having their spinal cords severely damaged. It doesn’t work the same in humans, who typically suffer permanent paralysis after significant spinal shock.
“CPGs are still a little bit mysterious,” says Lacquaniti. But he hopes that recognizing the similarities in nerve-muscle interactions between different species will help physicians design better approaches to rehabilitating damaged spinal cords and developing robotic prosthetics.
Many herd animals take their first steps a few minutes after being born, and several species of bird walk directly after hatching. But it takes a human baby a lot longer to learn how to walk unassisted, leading some scientists to believe that there must be something fundamentally different about the human gait. But even though the musculature and biomechanics in humans might be different, “the motor pathways are strikingly similar across species,” says Lacquaniti.
In fact, newborn rats and newborn humans had nearly identical neurological stepping profiles, the researchers found. And adult rats, cats, macaques and guinea fowl demonstrated motor nerve patterns that very closely resembled those of stepping human toddlers. “Our findings suggest that all types of vertebrate locomotion may derive from an ancestral neural network,” Lacquaniti says.
To compare the nerve activity of human locomotion to that of felines, rodents, birds and other primates, the researchers used strategically placed electrodes to measure the electrical activity in 24 walking muscles in newborns (who were held up and allowed to make the walking motion), toddlers, preschoolers and adults.
The motor nerves of newborns exhibited two patterns of electrical activity that appeared as long waves on a monitoring device called an electromyograph. These same two electrical patterns were present in older participants, but so were two new patterns — not waves, but flat lines with sharp peaks.
“In adults, we saw much shorter pulses of neural activity because they time muscle contraction at precise phases of the gait cycle,” says Lacquaniti. Adults get the most out of each stride, minimizing muscle use to save energy, something human newborns haven’t yet learned how to do. The longer waves of nerve activity seen in babies are evidence of prolonged muscle contractions, “a very uneconomical way to move,” says Lacquaniti.
Adults don’t totally abandon the less efficient nerve patterns that first get them stepping, but refine such patterns and overlay new ones to improve the timing of the step cycle and maximize energy use while walking around. Newborns can only partially support their body weight and swing their limbs, but adults use additional nerve pathways to roll the foot heel-to-toe on the ground, seamlessly decelerating and accelerating once again.
Once perfected, the human gait is a marvel of physics, Lacquaniti says. Standing straight aligns all the leg and hip joints, reducing the torque around each hinge, which basically means less force is required to move human legs. The human walking motion isn’t a completely ideal pendulum (some energy is wasted), but adults have learned how best to exploit their alternately swinging legs, using the inertia of body motion to take the burden off leg and hip muscles.
There are disadvantages to walking on two legs — primarily a lack of balance — but the ability to amble and keep hands free for other tasks trumps instability issues. It’s possible that human locomotion evolved primarily to free hands for carrying tools, food and children, Lacquaniti says. As a result of such multitasking, humans now depend more on commands from the brain to coordinate locomotion.
Being more reliant on the brain’s commands may be a major reason why humans don’t regain motor function after a spinal injury the same way cats can — an unfortunate by-product of human locomotive evolution, suggests Lacquaniti. But the most important thing this study reveals is that the human walking style is simply an elaboration on a common plan of vertebrate locomotion, with central pattern generators as the shared foundation.
Continuing to study the nerve patterns that drive locomotion in other animals could be the key to getting patients with spinal cord damage or conditions like cerebral palsy walking again.
Thursday, November 17, 2011
Drinking more coffee may not help, but there is a relation between heavy coffee consumption and a reduced risk of Parkinson's Disease.
Medscape Medical News from the:
This coverage is not sanctioned by, nor a part of, the American Society of Human Genetics.
Haydeh Payami, PhD, professor of genetics and neurology, State University of New York, and senior research scientist, New York State Department of Health Wadsworth Center in Albany, New York, and colleagues conducted a multicenter genome-wide association and interaction study in an attempt to identify genes that enhance or diminish the protective effects of caffeinated coffee; the ultimate goal would be to use these genes as biomarkers for pharmacogenetic prevention and treatment of PD.
"We and others have previously identified susceptibility genes for PD," Dr. Payami told Medscape Medical News. "The novelty of what we did in this study is that we introduced an environmental factor into the model and when we put coffee in the model, we were extremely lucky in that we pulled out one of the most important genes in the nervous system called GRIN2A, which encodes for glutamate, and glutamate has been implicated in PD for a long time."
The study was reported here during the 12th International Congress of Human Genetics (ICHG)/61st American Society of Human Genetics (ASHG) Annual Meeting and was published in the August 2011 issue of PLoS Genetics.
Epidemiologic Studies
As Dr. Payami explained, experimental studies have long implicated caffeine as being neuroprotective, and epidemiologic studies have shown that caffeinated coffee is protective: people who drink a lot of it seem to have a lower risk for PD. However, reasoning that not everybody stands to benefit equally from coffee's neuroprotective benefit, "we thought we should go after the genes that interact with coffee," she said. The most significant result was the novel appearance of a block of linked single-nucleotide polymorphisms that map to the GRIN2A gene on chromosome 6, Dr. Payami and colleagues report.
This locus had not before been detected in PD genome-wide association studies (GWASs) because its effect was modest. Considered in the context of its interaction with coffee, however, GRIN2A surpassed all PD-associated genes in significance, including the SNCA gene, which until now had had the strongest association with the disease in GWASs.
Dr. Payami and colleagues stratified the cohort into heavy or light coffee drinkers (light included non-coffee drinkers) and carried out another GWAS in each group.
Results showed that heavy coffee drinkers carrying 1 variant of the GRIN2A gene had an 18% lower risk for PD compared with light coffee drinkers, whereas heavy coffee drinkers with another variant of the same gene had a 59% lower risk compared with light coffee drinkers.
Thus, as the investigators point out, PD risk reduction by heavy coffee use — estimated to be 27% on average — was genotype-specific and varied according to GRIN2A genotype.
"Just drinking a lot of coffee doesn't reduce your risk of PD. It depends on the GRIN2A genotype you are carrying," reaffirmed Dr. Payami. What makes this gene-environment interaction study novel — the first of its kind to show a robust interaction between a gene and an environmental factors through a hypothesis-free genome-wide study — is the implication it may have for the treatment of PD.
Currently, 2 different classes of medications have been tested for possible use in PD: adenosine antagonists, which are caffeine-like, and glutamate antagonists, which are GRIN2A related. Both drug classes were found to be safe but not effective enough to achieve regulatory approval.
"Our study proposes a new hypothesis, which is, not everybody in these clinical trials [is] responding equally to these drugs, and if these drugs are anything like coffee, maybe the GRIN2A genotype would be a marker [for treatment response]," Dr. Payami said.
Dr. Payami reported preliminary results from the study at the World Parkinson Congress in Glasgow, Scotland, in September 2010. However, results reported at this year's ICHG/ASHG meeting not only had been replicated in 3 separate data sets but have achieved genome-wide significance since the preliminary report. Results have also been published.
Dr. Payami has disclosed no relevant financial relationships.
PLoS Genet. 2011;7:e1002237. Full text
12th International Congress of Human Genetics (ICHG)/61st American Society of Human Genetics (ASHG) Annual Meeting. Abstract #287. Presented October 15, 2011.
Tuesday, November 15, 2011
Something else to consider while you're considering things to prevent SIDs:
SIDS prevention can flatten baby's head
Posted: 10/25/2011 12:33:03 PM PDT
New parents are somewhat prepared for the challenges they face with baby, at least when it comes to sleep issues and breast-feeding. Everyone talks about those.
By the time Muller's daughter, Layla, was three months old, there was a flat spot on the right side of the back of her head. And, when she looked at Layla's face, she noticed that her ears were not aligned.
"We were told it would go away on its own," Muller says. "But it didn't."
Whether in a crib or car seat, infants spend the majority of their time on their backs. And, since 1992, when the American Academy of Pediatrics advised parents to stop putting their babies on their bellies in order to prevent Sudden Infant Death Syndrome, plagiocephaly has increased fourfold. While the condition is cosmetic and can be corrected or improved with a helmet or physical therapy, treatment can be long and carry a hefty price tag. But, with awareness and positional changes, experts say plagiocephaly is preventable.
Positional plagiocephaly develops during the first eight to 12 weeks of life and progresses until the baby can roll over and spend more time off his back, says Mark Dias, a Pennsylvania pediatric neurosurgeon and plagiocephaly spokesman for the American Academy of Pediatrics.
"There's no convincing medical evidence that plagiocephaly does anything rather than make a child's head look odd," Dias says. "Some people have talked about an increased risk of ear infections, eye problems, scoliosis, and hip dysplasia associated with it, but that hasn't been proven."
Boys are particularly vulnerable. They account for two-thirds of all cases because they have increased fluid around the outside of the brain that makes their heads more susceptible to being molded, Dias says. With that in mind, the best weapon against plagiocephaly is awareness.
"Parents should always be looking at their baby's head," he says. "Give them supervised tummy time when they're awake. Carry them upright. And alternate which side they turn their heads while sleeping." Dias says positional changes can improve head flatness by 50 percent.
They're certainly working for Jennifer Telford's 7-month-old son, Trent. He began sucking his right thumb at age 10 weeks. According to his mom, that's when he developed a preference for and flatness on his right side.
In addition to plagiocephaly, their pediatrician diagnosed Trent with torticollis, a condition where the neck muscle is short or tight on one side and makes it difficult for baby to turn the other way. It is present in 15 percent of plagiocephaly cases.
Physical therapy
Trent is a good candidate for physical therapy. In mild to moderate cases, pediatricians recommend (and insurance companies often cover) regular visits to a physical therapist who works with the child on stretching and strengthening exercises to build the weaker neck muscles, Dias says.
"This gives us peace of mind, so we know we're doing everything so he develops correctly," says Telford, of Pleasant Hill. "It's reassuring to go to the therapist, although I think it would have gotten better on its own. Once he started spending more time on his tummy, it got a lot better."
It's difficult to say when a flat head will round out. Dias says improvement is based on the degree of deformity and how the child's head grows and develops. But with positional changes and physical therapy, you should generally notice a difference by nine months of age, when the child is rolling over and spending less time on his back.
Help from helmet
When positional changes are not enough or the deformity is moderate to severe, experts recommend helmet therapy. Using three-dimensional digital scans, providers create a customized mold of the baby's head and design a lightweight helmet out of foam, says Trish Collins, a certified orthotist with Centers for Independent Rehabilitative Services in Oakland.
"I like to see them by four months of age," says Toth, who sees about 80 babies a month with positional plagiocephaly. "What is nice about the helmet is it takes the guilt and pressure off the family to get up in the middle of the night and change the baby's position."
Dias is less fond of helmet therapy. He recommends helmets about 20 percent of the time because long term studies show that infants who have been treated with helmets are no better off than those who did nothing, he says. In other words, no matter what they do, their heads always will be a little flat.
It took a week for little Christopher Henry to adapt to his helmet. According to his mother, Holly, of San Jose, Christopher wore it for four months. She found it made nursing difficult, she says.
"It seemed uncomfortable for sleep, too, but he got used to it, and it worked," Holly says.
Obvious improvement
Not completely. Christopher, now 19 months old, has been out of his helmet for almost a year. Holly says her son's ears and eyes are symmetrical, but his head is still a bit flat. "I can tell when I look down at the top of his head," she says.
But, in case her son, Ian, ever went bald or wanted to shave his head, she didn't want him to feel self-conscious, she says. Ian is 9 months old and has been wearing a helmet decorated with bright cars and trucks for two months.
Her baby is perfectly happy in it. If anything, Kimball says the helmet is hard on her.
"I can't quite get close enough to kiss him," she says. "I'll aim for his cheek and then he turns his head and whacks me in the face with his helmet."
Preventing plagiocephaly
Friday, November 11, 2011
FIBER - Healthy food that helps lower weight, improves cholesterol levels, and now study shows may well reduce your risk for colon cancer. What's not to like?
Whole Grain Fiber, Colorectal Cancer Risk Linked
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Individuals eating three daily servings of whole grains had a significantly, though modestly, lower risk of colorectal cancer, according to pooled data from nearly 800,000 individuals -- perhaps the largest and strongest analysis ever conducted. A 90-gram per day increase in dietary fiber from whole grains -- the amount a person would consume from three servings -- was associated with a risk reduction of 17% (95% CI 11% to 22%) for colorectal cancer, Teresa Norat, PhD, of Imperial College London, and colleagues reported online in BMJ. The finding emerged from a meta-analysis of 25 case-control or prospective cohort studies of diet and colorectal cancer risk, with millions of participants in total. The researchers also found that "high" versus "low" intake of total dietary fiber was associated with a significant reduction in risk (12%, 95% CI 6% to 18%). For each 10-gram increase in total daily fiber intake among two million participants in 16 studies, the risk was lowered by 10% (95% CI 6% to 14%), with the benefit more apparent for colon versus rectal cancer. But fiber sources other than cereals and whole grains appeared to have less impact on risk. Norat and colleagues reported the following relative risks associated with fiber intake from fruits, vegetables, and legumes:
They added that, on the basis of other past studies, public adoption of such recommendations would also have a range of other health benefits, including lower rates of cardiovascular disease, type 2 diabetes, obesity, "and possibly overall mortality." In an accompanying editorial, two Danish researchers concurred, and argued as well that the associations probably do represent causality. "Many of the specific mechanisms involved in the health benefits of whole grains still need to be explored and explained in detail," wrote Anne Tjonneland, PhD, and Anja Olsen, PhD, of the Danish Cancer Society. "But factors such as increased satiety, stabilized glucose homoeostasis and insulin response, and the fermentation of fiber and resistant starch in the colon to produce short chain fatty acids are probably important." They added that additional research could shed light on whether specific types of grains vary in their effects on reducing cancer risk, noting that some studies had pointed to whole grain rye as possibly better than others. Perhaps more important, the editorialists also recommended more investigation of the barriers to consumption of whole grains, which largely have to do with consumer preference. In conducting the meta-analysis, Norat and colleagues searched for studies with prospective cohort, case-cohort, or nested case-control designs that specifically examined associations between dietary fiber and colorectal cancer. Cross-sectional or retrospective case-control studies were not considered. The 25 they came up with had enrollments ranging from 8,000 to 520,000. All the individual study results were adjusted for age, with most also accounting for other major risk factors such as sex, smoking status, education level, and physical activity. Follow-up continued for 3.5 to 17 years. The two largest studies included in the analysis -- the NIH-AARP Diet and Health Study, with 292,000 participants, and the European Prospective Investigation into Cancer and Nutrition, with 520,000 -- had medians of 4.5 and 6.2 years of follow-up, respectively. These and five other of the larger studies quantified intake of different sources of dietary fiber, which Tjonneland and Olsen indicated was especially important. However, a major limitation to the meta-analysis was that many of the studies examined diet composition only at enrollment, and the definition of fiber may have varied considerably among the studies. In most cases, the individual study investigators relied on participants to report their dietary composition. Also, not all studies adjusted for every major confounder, Norat and colleagues noted. The meta-analysis was supported by the World Cancer Research Fund. All study authors and the editorialists declared they had no conflicts of interest. | ||
| Primary source: BMJ Source reference: Aune D, et al "Dietary fibre, whole grains, and risk of colorectal cancer: systematic review and dose-response meta-analysis of prospective studies" BMJ 2011; DOI: 10.1136/bmj.d6617. Additional source: BMJ Source reference: Tjønneland A, et al "Fibre and prevention of chronic diseases" BMJ 2011; DOI: 10.1136/bmj.d6938. |
Wednesday, November 9, 2011
A breakthrough in understanding autism hopefully leads to new directions for future studies.
Autism Linked to Excess Neurons
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| Children with autism appear to have bigger brains with more neurons than normal for their age, a small preliminary study affirmed. Postmortem examinations of seven boys with autism showed 67% more neurons in the prefrontal cortex (1.94 billion), which controls social and emotional development as well as communication, compared with six controls (1.16 billion, P=0.002), Eric Courchesne, PhD, of the University of California San Diego, and colleagues found. Autistic brains also weighed 17.6% above normal for age (P=0.001), the group reported in the Nov. 9 issue of the Journal of the American Medical Association. Neuron counts in the autistic children should have been accompanied by brain weights of 29.4% versus the observed 17.6% enlargement, they said. "Thus, the size of the autistic brain, overlarge though it is, might actually underestimate the pathology of excess neuron numbers," the group explained. Researchers have long documented abnormal enlargement of the brain during childhood that persists for about 20% of individuals with autism. These new findings are the first direct evidence that neurons, and not glial or other cell types, appear to be responsible, the researchers pointed out. Neurons in nearly all regions of the brain are generated before birth and the excessive head and brain growth also occur before clinical manifestations of the disorder, an accompanying editorial noted. Thus, the results "add significantly to mounting biological evidence that the developmental neuropathology of idiopathic autism begins before birth in some, possibly all, cases," Janet E. Lainhart, MD, of the University of Utah in Salt Lake City, and Nicholas Lange, ScD, of Harvard University Schools of Medicine and Public Health in Belmont, Mass., wrote in the editorial. What may be happening is unchecked proliferation of neurons, or a failure of the normal process of neuronal pruning through apoptosis in the third trimester and early postnatal period, Courchesne's group suggested. They obtained brains from several tissue banks and had expert anatomists, blinded to diagnosis, conducted unbiased stereotactic cell counts for the entire dorsolateral and mesial portions of the prefrontal cortex, rather than just estimating counts from density in small blocks. The donors were all boys, ages 2 to 16 years, who had died in 2000 to 2006, largely due to hypoxia (drowning, hanging, or electrocution). There also was one death from a car crash, one from rhabdomyosarcoma, and one from possible cardiac arrest. The seven autism cases fell across the spectrum of disability, with some having had normal language and daily functional abilities and others being highly impaired on both counts. None had Asperger's syndrome or pervasive development disorder-not otherwise specified. Neuron counts in the children with autism were:
Whereas brain weight in controls correlated strongly with their number of prefrontal neurons (P=0.004), the same wasn't true for the children with autism. Glia counts overall and in the prefrontal cortex regions came out similar between groups. The researchers cautioned that their sample of autism cases wasn't big enough to determine any links with behavior, nor could the small sample of controls be taken as representative of all healthy young children. Importantly, girls with autism may differ, so further studies may be needed to test whether that is the case, they noted. This study was supported by Autism Speaks, Cure Autism Now, The Peter Emch Family Foundation, the Simons Foundation, The Thursday Club Juniors, and the University of California San Diego-National Institutes of Health Autism Center of Excellence, and by a grant from the National Institute of Mental Health. Tissue was provided by the National Institute of Child Health and Development Brain and Tissue Bank for Developmental Disorders, the Brain and Tissue Bank for Developmental Disorders, Autism Tissue Program, and direct donations to the Courchesne laboratory. One of the researchers reported being owner and employee of Sinq Systems, a contract research organization that performed data collection and analysis for the study, and also being an applicant on a pending patent for analysis of microscopic structure. Lainhart and Lange reported having no conflicts of interest to disclose. | ||
| Primary source: Journal of the American Medical Association Source reference: Courchesne E, et al "Neuron number and size in prefrontal cortex of children with autism" JAMA 2011; 306(18): 2001-2010. Additional source: Journal of the American Medical Association Source reference: Lainhart JE, Lange N "Increased neuron number and head size in autism" JAMA 2011; 306(18): 2031-2032. |
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