redOrbit Staff & Wire Reports – Your Universe Online
Leaving the car at home and walking, cycling or even taking the bus to work could improve your health, researchers from University College London (UCL) and the London School of Hygiene & Tropical Medicine claim in a new study.
In their British Medical Journal (BMJ) paper, Dr. Ellen Flint, a research fellow in social epidemiology at the London School, and her colleagues reported that people using active or public modes of transportation for their daily commute tended to have lower body weight and body fat composition than those who used private transportation to get to and from their place of employment.
Dr. Flint and her fellow researchers set out to examine the relationship between active commuting and two established markers for obesity: body mass index (BMI) and body fat percentage. They reviewed 7,534 BMI measurements and 7,424 percentage body fat measurements from men and women taking part in Understanding Society, a nationally representative UK study that collected the health information of 20,000 participants.
Of those individuals, 76 percent of men and 72 percent of women commuted to work through private motorized transportation, while 10 percent of men and 11 percent of women said they used public transportation such as buses or trains and 14 percent of men and 17 percent of women walked or biked to work.
The overall BMI score for male participants was 28, and the BMI score for women was 27, the authors said. Typically, a BMI of 18.5 to 24.9 indicates optimal weight. A BMI lower than 18.5 suggests the person is underweight, a BMI of more than 25 could indicate that a person is overweight and a number over 30 suggests the individual is obese.
“Compared with using private transport, commuting by public and active modes significantly and independently predicted lower BMI and healthier body composition, for both men and women,” the London School explained in a statement Wednesday.
“Men who commuted via public or active modes had BMI scores around 1 point lower than those who used private transport, equating to a difference in weight of 3kg (almost half a stone) for the average man,” it added. “Women who commuted via public or active transport had BMI scores around 0.7 points lower than their private transport using counterparts, equating to a difference in weight of 2.5kg (5.5lb) for the average woman.”
The findings for body fat percentage were similar in size and significance, and the researchers said the relationship remained even after they adjusted for potentially confounding factors such as age, disability, social class, monthly income, diet and workplace activity. They noted that the differences were larger than those observed in most individually-focused diet and exercise related interventions to encourage weight loss or prevent obesity.
Despite the size of the study, however, Dr. Flint and her colleagues said that they cannot declare a causal relationship between the use of private, non-active transportation and weight. However, while they report that additional research is required to confirm the cause-and-effect relationship, they do suggest considering the use of walking, cycling or public transport to travel to and from work as part of a broader health and anti-obesity strategy.
“Given that the majority of commuters in the UK use private transport as their main mode of travel, there are potentially large population-level health gains to be made by shifting to more active modes of commuting,” said Dr. Flint, who authored the study along with London School professor of population health Steven Cummins and UCL professor of lifecourse studies Amanda Sacker.
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Matt Swayne, Penn State

Love and commitment can make sex physically more satisfying for many women, according to a Penn State Abington sociologist.

In a series of interviews, heterosexual women between the ages of 20 and 68 and from a range of backgrounds said that they believed love was necessary for maximum satisfaction in both sexual relationships and marriage. The benefits of being in love with a sexual partner are more than just emotional. Most of the women in the study said that love made sex physically more pleasurable.

“Women said that they connected love with sex and that love actually enhanced the physical experience of sex,” said Beth Montemurro, associate professor of sociology.

Women who loved their sexual partners also said they felt less inhibited and more willing to explore their sexuality.

“When women feel love, they may feel greater sexual agency because they not only trust their partners but because they feel that it is OK to have sex when love is present,” Montemurro said.

While 50 women of the 95 that were interviewed said that love was not necessary for sex, only 18 of the women unequivocally believed that love was unnecessary in a sexual relationship.

Older women who were interviewed indicated that this connection between love, sex and marriage remained important throughout their lifetimes, not just in certain eras of their lives.

The connection between love and sex may show how women are socialized to see sex as an expression of love, Montemurro said. Despite decades of the women’s rights movement and an increased awareness of women’s sexual desire, the media continue to send a strong cultural message for women to connect sex and love and to look down on girls and women who have sex outside of committed relationships.

“On one hand, the media may seem to show that casual sex is OK, but at the same time, movies and television, especially, tend to portray women who are having sex outside of relationships negatively,” said Montemurro.

In a similar way, the media often portray marriage as largely sexless, even though the participants in the study said that sex was an important part of their marriage, according to Montemurro, who presented her findings on Aug. 19 at the annual meeting of the American Sociological Association.

“For the women I interviewed, they seemed to say you need love in sex and you need sex in marriage,” said Montemurro.

From September 2008 to July 2011, Montemurro conducted in-depth interviews with 95 women who lived in Pennsylvania, New Jersey and New York. The interviews generally lasted 90 minutes.

Although some of the women who were interviewed said they had sexual relationships with women, most of the women were heterosexual and all were involved in heterosexual relationships.

Funds from the Career Development Professorship and the Rubin Fund supported this work.

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Chris Bunting, University of Leeds

Stimulating nerves in your ear could improve the health of your heart, researchers have discovered.

A team at the University of Leeds used a standard TENS machine like those designed to relieve labor pains to apply electrical pulses to the tragus, the small raised flap at the front of the ear immediately in front of the ear canal.

The stimulation changed the influence of the nervous system on the heart by reducing the nervous signals that can drive failing hearts too hard.

Professor Jim Deuchars, Professor of Systems Neuroscience in the University of Leeds’ Faculty of Biological Sciences, said: “You feel a bit of a tickling sensation in your ear when the TENS machine is on, but it is painless. It is early days—so far we have been testing this on healthy subjects—but we think it does have potential to improve the health of the heart and might even become part of the treatment for heart failure.”

The researchers applied electrodes to the ears of 34 healthy people and switched on the TENS (Transcutaneous electrical nerve stimulation) machines for 15-minute sessions. They monitored the variability of subjects’ heartbeats and the activity of the part of the nervous system that drives the heart. Monitoring continued for 15 minutes after the TENS machine was switched off.

Lead researcher Dr Jennifer Clancy, of the University of Leeds’ School of Biomedical Sciences, said: “The first positive effect we observed was increased variability in subjects’ heartbeats. A healthy heart does not beat like a metronome. It is continually interacting with its environment—getting a little bit faster or a bit slower depending on the demands on it. An unhealthy heart is more like a machine constantly banging out the same beat. We found that when you stimulate this nerve you get about a 20% increase in heart rate variability.”

The second positive effect was in suppressing the sympathetic nervous system, which drives heart activity using adrenaline.

Dr Clancy said: “We measured the nerve activity directly and found that it reduced by about 50% when we stimulated the ear. This is important because if you have heart disease or heart failure, you tend to have increased sympathetic activity. This drives your heart to work hard, constricts your arteries and causes damage. A lot of treatments for heart failure try to stop that sympathetic activity—beta-blockers, for instance, block the action of the hormones that implement these signals. Using the TENS, we saw a reduction of the nervous activity itself.”

The researchers found significant residual effects, with neither heart rate variability or sympathetic nerve activity returning to the baseline 15 minutes after the TENS machine had been switched off.

The technique works by stimulating a major nerve called the vagus, which has an important role in regulating vital organs such as the heart. There is a sensory branch of the vagus in the outer ear and, by sending electrical current down the nerves and into the brain, researchers were able to influence outflows from the brain that regulate the heart. Vagal nerve stimulation has previously been used to treat conditions including epilepsy.

Professor Deuchars said: “We now need to understand how big and how lasting the residual effect on the heart is and whether this can help patients with heart problems, probably alongside their usual treatments. The next stage will be to conduct a pre-clinical study in heart failure patients.”

The research is published in the journal Brain Stimulation and was funded by the University of Leeds.

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redOrbit Staff & Wire Reports – Your Universe Online
One of the deadliest infectious diseases in the world may have been carried to the Americans by seals and sea lions, not European explorers as previously believed, claims a new study published online Wednesday in the journal Nature.
Tuberculosis is responsible for killing as many as two million people each year, and according to researchers from the Arizona State University and an international team of experts, scientists have long debated the origins of the disease. Their research indicates that its arrival in the New World likely predated that of other European diseases, including influenza and chicken pox.
ASU anthropological geneticist Anne Stone, Johannes Krause of the University of Tubingen in Germany and their colleagues analyzed pre-Columbian Mycobacterial tuberculosis genomes and concluded that the disease likely spread from humans in Africa to seals and sea lions. In turn, those marine animals were the one who brought the disease to South America, transmitting it to the natives living there before the first Europeans made landfall.
According to Ed Yong of National Geographic, the team of investigators analyzed three Peruvian skeletons that were approximately 1,000 years old and had the warped spines and ribs that were indicative of the disease.
They extracted DNA from the skeletons that included sequences belonging to Mycobacterium tuberculosis. The study authors calculated that these bacteria, which are the pathogens responsible for causing tuberculosis, last shared a common ancestor with modern M. tuberculosis strains approximately 6,000 years ago.
“That was the first big surprise,” Yong said, explaining that scientists had long believed tuberculosis was an ancient disease and that all of the strains affecting humans evolved from a common ancestor living over 70,000 years ago. The new research, however, reveals that this microbe was actually less than one-tenth that old.
“It’s not just the discrepancy that’s baffling,” the National Geographic reporter added. “By 6,000 years ago, humans had already spread around the world, including all over the Americas. The land bridge that connected Asia and North America had long since flooded. And it would be several millennia before any Europeans sailed across the Atlantic. So if tuberculosis originated in Africa, how did it get into South America?”
Yong went on to explain that the researchers considered many possibilities as to how the disease made the journey, originally suggesting seals facetiously. Even so, they compared the genomes of many specious of tuberculosis bacteria with seals and various other animals, including humans, cows, chimpanzees and goats. As it turns out, the closest relatives of the Peruvian strains were, in fact, the ones that came from seals.
Kirsten Bos from the University of Tubingen told him that the researchers “had a good laugh” over the suggestion that seals might have been responsible for bringing the disease to the New World. “It seemed so silly,” she added. “We couldn’t believe that was what the data was showing, but it was pretty clear.”
“The source of tuberculosis in the New World long has been a question for researchers,” added Elizabeth Tran, Biological Anthropology program director in the National Science Foundation’s (NSF) Division of Behavioral and Cognitive Sciences. “This paper provides strong evidence that marine mammals may have been the likely culprits, bringing tuberculosis to South America long before Europeans arrived there.”
However, Stone noted that European strains are not in the clear, as she and her colleagues hypothesize that once they did arrive in the Americas, they completely replaced the strains originally carried over by the aquatic animals. She said that it is not clear what the timeframe for this replacement was, or what role they played in the deaths of 95 percent of the 20 million natives living in the New World before the arrival of Europeans.
“This is one question that we hope to address in the future,” she said, adding that it was “likely that the new European strain, which is more virulent, was a culprit – particularly since tuberculosis is really good at spreading during times of social crowding and distress.”
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By Bruce Goldman, Stanford University Medical Center

When investigators at the Stanford University School of Medicine applied light-driven stimulation to nerve cells in the brains of mice that had suffered strokes several days earlier, the mice showed significantly greater recovery in motor ability than mice that had experienced strokes but whose brains weren’t stimulated.

These findings, which will be published online Aug. 18 in Proceedings of the National Academy of Sciences, could help identify important brain circuits involved in stroke recovery and usher in new clinical therapies for stroke, including the placement of electrical brain-stimulating devices similar to those used for treating Parkinson’s disease, chronic pain and epilepsy. The findings also highlight the neuroscientific strides made possible by a powerful research technique known as optogenetics.

Stroke, with 15 million new victims per year worldwide, is the planet’s second-largest cause of death, according to Gary Steinberg, MD, PhD, professor and chair of neurosurgery and the study’s senior author. In the United States, stroke is the largest single cause of neurologic disability, accounting for about 800,000 new cases each year — more than one per minute — and exacting an annual tab of about $75 billion in medical costs and lost productivity.

The only approved drug for stroke in the United States is an injectable medication called tissue plasminogen activator, or tPA. If infused within a few hours of the stroke, tPA can limit the extent of stroke damage. But no more than 5 percent of patients actually benefit from it, largely because by the time they arrive at a medical center the damage is already done. No pharmacological therapy has been shown to enhance recovery from stroke from that point on.

But in this study — the first to use a light-driven stimulation technology called optogenetics to enhance stroke recovery in mice — the stimulations promoted recovery even when initiated five days after stroke occurred.

“In this study, we found that direct stimulation of a particular set of nerve cells in the brain — nerve cells in the motor cortex — was able to substantially enhance recovery,” said Steinberg, the Bernard and Ronni Lacroute-William Randolph Hearst Professor in Neurosurgery and Neurosciences.

About seven of every eight strokes are ischemic: They occur when a blood clot cuts off oxygen flow to one or another part of the brain, destroying tissue and leaving weakness, paralysis and sensory, cognitive and speech deficits in its wake. While some degree of recovery is possible — this varies greatly among patients depending on many factors, notably age — it’s seldom complete, and typically grinds to a halt by three months after the stroke has occurred.

Animal studies have indicated that electrical stimulation of the brain can improve recovery from stroke. However, “existing brain-stimulation techniques activate all cell types in the stimulation area, which not only makes it difficult to study but can cause unwanted side effects,” said the study’s lead author, Michelle Cheng, PhD, a research associate in Steinberg’s lab.

For the new study, the Stanford investigators deployed optogenetics, a technology pioneered by co-author Karl Deisseroth, MD, PhD, professor of psychiatry and behavioral sciences and of bioengineering. Optogenetics involves expressing a light-sensitive protein in specifically targeted brain cells. Upon exposure to light of the right wavelength, this light-sensitive protein is activated and causes the cell to fire.

Steinberg’s team selectively expressed this protein in the brain’s primary motor cortex, which is involved in regulating motor functions. Nerve cells within this cortical layer send outputs to many other brain regions, including its counterpart in the brain’s opposite hemisphere. Using an optical fiber implanted in that region, the researchers were able to stimulate the primary motor cortex near where the stroke had occurred, and then monitor biochemical changes and blood flow there as well as in other brain areas with which this region was in communication. “We wanted to find out whether activating these nerve cells alone can contribute to recovery,” Steinberg said.

By several behavioral, blood flow and biochemical measures, the answer two weeks later was a strong yes. On one test of motor coordination, balance and muscular strength, the mice had to walk the length of a horizontal beam rotating on its axis, like a rotisserie spit. Stroke-impaired mice whose primary motor cortex was optogenetically stimulated did significantly better in how far they could walk along the beam without falling off and in the speed of their transit, compared with their unstimulated counterparts.

The same treatment, applied to mice that had not suffered a stroke but whose brains had been similarly genetically altered and then stimulated just as stroke-affected mice’s brains were, had no effect on either the distance they traveled along the rotating beam before falling off or how fast they walked. This suggests it was stimulation-induced repair of stroke damage, not the stimulation itself, yielding the improved motor ability.

Stroke-affected mice whose brains were optogenetically stimulated also regained substantially more of their lost weight than unstimulated, stroke-affected mice. Furthermore, stimulated post-stroke mice showed enhanced blood flow in their brain compared with unstimulated post-stroke mice.

In addition, substances called growth factors, produced naturally in the brain, were more abundant in key regions on both sides of the brain in optogenetically stimulated, stroke-affected mice than in their unstimulated counterparts. Likewise, certain brain regions of these optogenetically stimulated, post-stroke mice showed increased levels of proteins associated with heightened ability of nerve cells to alter their structural features in response to experience — for example, practice and learning. (Optogenetic stimulation of the brains of non-stroke mice produced no such effects.)

Steinberg said his lab is following up to determine whether the improvement is sustained in the long term. “We’re also looking to see if optogenetically stimulating other brain regions after a stroke might be equally or more effective,” he said. “The goal is to identify the precise circuits that would be most amenable to interventions in the human brain, post-stroke, so that we can take this approach into clinical trials.”

Scott LaFee and Christina Johnson, University of California, San Diego

Research suggests mental illness doesn’t preclude enjoying life

Schizophrenia is among the most severe forms of mental illness, yet some people with the disease are as happy as those in good physical and mental health according to a study led by researchers at the University of California, San Diego School of Medicine.

The study is published online this week in the journal Schizophrenia Research.

“People tend to think that happiness in schizophrenia is an oxymoron,” said senior author Dilip V. Jeste, MD, Distinguished Professor of Psychiatry and Neurosciences.

“Without discounting the suffering this disease inflicts on people, our study shows that happiness is an attainable goal for at least some schizophrenia patients,” said Jeste, who is also the Estelle and Edgar Levi Chair in Aging and director of the Sam and Rose Stein Institute for Research on Aging at UC San Diego. “This means we can help make these individuals’ lives happier.”

In a survey of people with the disease, researchers found that 37 percent of patients reported being happy all or most of the time.

Of clinical significance in terms of helping people with mental illness, the patients’ happiness was unrelated to the severity or duration of their illness, to cognitive or physical function or to socioeconomic factors such as age and education, which among healthy adults have been linked to a greater sense of well-being.

Instead, the study shows that happiness among those with chronic forms of schizophrenia is associated with positive psychological and social attributes such as resilience, optimism and lower perceived stress.

The researchers believe that these positive psychosocial attributes could be taught through behavioral modification and mindfulness training techniques.

The study is based on a survey of 72 English-speaking outpatients with schizophrenia in the San Diego area. At the time of the survey, all but nine of the patients were on at least one anti-psychotic medication and 59 percent were residents in assisted-living facilities.

The comparison group for the study included 64 healthy men and women who were part of an ongoing study on successful aging. These participants were not currently using alcohol or illicit substances and did not have diagnoses of dementia or other neurological problems. Participants ranged in age from 23 to 70 years old; the mean age for both groups was 50 years.

The survey probed respondents’ happiness during the previous week, asking them to rate statements such as “I was happy” and “I enjoyed life” on a scale from “never or rarely” to “all or most of the time.”

Responses suggest that about 37 percent of schizophrenia patients were happy most or all of the time, compared with about 83 percent for those in the comparison group.

Approximately 15 percent of schizophrenia patients reported being never or rarely happy. By contrast, none of in the comparison group reported such a low level of happiness for the week prior.

People’s self-reported happiness was then examined in relation to other factors, such as age, gender, education, living situation, medication status, anxiety levels and other mental health metrics, as well as physical health, cognitive function, and a list of “psychosocial factors” that included perceived stress, attitude toward aging, spirituality, optimism, resilience and personal mastery.

“People with schizophrenia are clearly less happy than those in the general population at large, but this is not surprising,” said lead author Barton W. Palmer, PhD, professor in the UC San Diego Department of Psychiatry. “What is impressive is that almost 40 percent of these patients are reporting happiness and that their happiness is associated with positive psychosocial attributes that can be potentially enhanced.”

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April Flowers for redOrbit.com – Your Universe Online

Baldness, or alopecia, affects millions of people around the world. It can range from male pattern baldness (where the hair thins out gradually) to alopecia universalis (which is a total loss of all body hair). Alopecia is an equal opportunity condition, affecting both men and women across races, socio-economic statuses and age. For example, UK actor Joseph Gatt (recently seen as a Thenn wildling on HBO’s Game of Thrones) developed alopecia universalis at the age of 14.  Different types of alopecia have different causes.

Alopecia areata (a common autoimmune disease) is characterized by patches of baldness, which BBC News health reporter Smitha Mundasad says affects roughly two in every 1,000 UK citizens. This is the type of alopecia that researchers at Columbia University Medical School (CUMC) have recently been studying. They have identified the immune cells responsible for destroying hair follicles and have developed and tested a new, FDA-approved drug that eliminated the immune cells and restored hair growth in a small number of patients. Their results are described in a recent issue of Nature Medicine.

The researchers, including Raphael Clynes, MD, PhD, and CUMC professor in the Departments of Dermatology and of Genetics and Development Angela M. Christiano, PhD, report early results from an ongoing clinical trial of the drug. These results include complete hair regrowth in several patients with moderate-to-severe alopecia areata. The report includes data from three participants, each of whom experienced total hair regrowth within five months of beginning treatment.

“We’ve only begun testing the drug in patients, but if the drug continues to be successful and safe, it will have a dramatic positive impact on the lives of people with this disease,” said Clynes.

The hair loss from alopecia areata can be disfiguring, as it is often lost in patches on the scalp, face and body. To date, there are no known treatments that can completely restore hair. People with this condition often suffer from significant psychological stress and emotional trauma.

The mechanism for hair loss — the hair follicle being surrounded and attacked by the immune system, causing the follicle to enter a dormant state — has been known for decades. Which particular immune cell was responsible, however, remained a mystery. Four years ago, Dr. Christiano’s genetic study of more than 1,000 patients with alopecia areata uncovered the first major clue — the hair follicles send a “danger” signal, not previously linked to alopecia areata, which attracts the immune cells to the follicle and provokes the attack.

The current study initially started by studying mice with alopecia areata, tracking back from the danger signal to identify the specific set of T cells that initiate the attack. Follow-up examinations of both mice and human cells revealed how the T cells attack, and suggested possible pathways to be targeted by a new class of drugs called JAK inhibitors.

The team tested two FDA-approved JAK inhibitors separately: ruxolitinib and tofacitinib. Both were able to block the immune pathways and stop the attack on hair follicles. Mice with extensive hair loss from the disease had full hair restoration within 12 weeks with both drugs. The hair persisted for several months after treatment was stopped with both drugs, as well.

The researchers collaborated with Julian Mackay-Wiggan, MD, MS, director of the Clinical Research Unit in the Department of Dermatology at CUMC and a practicing dermatologist at NewYork-Presbyterian/Columbia who treats patients with multiple types of hair loss to initiate a small open-label clinical trial of ruxolitinib, as it already had FDA approval for treatment of a blood disorder. The participants, seven women and two men, all had moderate-to-severe alopecia areata with more than a 30 percent hair loss. Within four to five months of beginning treatment, three of the participants saw complete hair restoration, along with the disappearance of the attacking T cells from the scalp.

“We still need to do more testing to establish that ruxolitinib should be used in alopecia areata, but this is exciting news for patients and their physicians,” Dr. Clynes said. “This disease has been completely understudied—until now, only two small clinical trials evaluating targeted therapies in alopecia areata have been performed, largely because of the lack of mechanistic insight into it.”

“The timeline of moving from genetic findings to positive results in a clinical trial in only four years is astoundingly fast and speaks to this team’s ability to perform translational science of the highest caliber,” said David Bickers, MD, the Carl Truman Nelson Professor of Dermatology and chair of the Department of Dermatology at CUMC and dermatologist-in-chief at NewYork-Presbyterian/Columbia. “There are few tools in the arsenal for the treatment of alopecia areata that have any demonstrated efficacy. This is a major step forward in improving the standard of care for patients suffering from this devastating disease.”

Dr. Christiano, who suffers from alopecia areata herself, says that it is all too often dismissed as simply an appearance altering condition. “Nothing could be further from the truth,” she said. “Patients with alopecia areata are suffering profoundly, and these findings mark a significant step forward for them. The team is fully committed to advancing new therapies for patients with a vast unmet need.”

The New York Times cautions, however, that the treatment will likely not work for everyone, and not enough is known yet of side effects or safety concerns. Dr. George Cotsarelis, a dermatologist at the University of Pennsylvania, agrees that people should approach this “cure” with caution. The study participants received the drug as a twice daily pill instead of a topical cream, meaning that they were “treated systemically with a very toxic drug” known to cause liver and blood problems, infections and other negative outcomes. Dr. Cotsarelis said that if the drug could be applied topically, it would “be an amazing breakthrough.”

The team plans to continue with larger clinical trials, which will include the other JAK inhibitor, tofacitinib — originally approved for rheumatoid arthritis.

redOrbit Staff & Wire Reports – Your Universe Online

Youngsters who are more physically fit have more fibrous and compact white-matter tracts in the brain than their less-fit counterparts, according to new research appearing in the August 19 edition of the journal Frontiers in Human Neuroscience.

Researchers from the University of Illinois at Urbana-Champaign, the University of Pittsburgh, the University of Iowa and Michigan State University recruited two dozen 9- and 10-year-old children, and then used a technique known as diffusion tensor imaging (DTI) to analyze water diffusion in tissues in five of their brains’ white-matter tracts.

After controlling for several variables, including each youngster’s IQ and whether or not they had been diagnosed with learning disabilities, the researchers determined significant fitness-related differences in the integrity of several white-matter tracts, including the corpus callosum (which connects the brain’s left and right hemispheres) and the superior longitudinal fasciculus (a pair of structures that connect the frontal and parietal lobes).

“Previous studies suggest that children with higher levels of aerobic fitness show greater brain volumes in gray-matter brain regions important for memory and learning,” study author Laura Chaddock-Heyman, a postdoctoral researcher at the University of Illinois’s department of psychology, said in a statement Tuesday. “Now for the first time we explored how aerobic fitness relates to white matter in children’s brains.”

While the study does not prove that physical fitness can actually make children smarter, it does provide evidence to support that notion, said HealthDay News reporter Randy Dotinga. While previous research had discovered an association between higher levels of fitness and improved attentiveness, memory and academic skills, Chaddock-Heyman and her colleagues set out to learn more about the impact of exercise in the brains of young children.

In addition to differences in the corpus callosum and the superior longitudinal fasciculus, the researchers also uncovered a link between fitness and the superior corona radiata, which connect the cerebral cortex to the brain stem. The researchers explained that all three of these tracts have been found to influence memory and attention.

“Previous studies in our lab have reported a relationship between fitness and white-matter integrity in older adults. Therefore, it appears that fitness may have beneficial effects on white matter throughout the lifespan,” said co-author psychology professor and Beckman Institute for Advanced Science and Technology director Arthur Kramer.

Chaddock-Heyman, Kramer and their colleagues are now looking to expand on their work, which is in the second year of a five-year randomized, controlled trial to determine whether or not white-matter tract integrity improves in youngsters who begin and maintain a new physical fitness routine. The researchers said that they are looking for changes in their subjects’ aerobic fitness levels, their brain structure and function, and their genetic regulation.

“Prior work from our laboratories has demonstrated both short- and long-term differences in the relation of aerobic fitness to brain health and cognition,” said University of Illinois kinesiology and community health professor Charles Hillman. “However, our current randomized, controlled trial should provide the most comprehensive assessment of this relationship to date.”

So what are the overall implications of this research? Megan Herting, a postdoctoral fellow with the division of research on Children, Youth, and Families at Children’s Hospital of Los Angeles, told Dotinga that it is hard to say at this point, as the research also revealed that kids with lower fitness levels also tended to weigh more.

“It is unclear if it is actually fitness or ‘fatness’ that may be affecting the brain. Studies show that individuals with obesity have different brains compared to their healthier-weight peers,” she said. “These findings do challenge that if you are aerobically fit, you are likely to be dumb. In fact, from an evolutionary perspective, we were made to move. So rather than fitness being ‘good’ for the brain and cognition, it is feasible that being sedentary may be ‘bad.’”

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Diana Yates, Life Sciences Editor, University of Illinois

Practicing hatha yoga three times a week for eight weeks improved sedentary older adults’ performance on cognitive tasks that are relevant to everyday life, researchers report.

The findings involved 108 adults between the ages of 55 and 79 years of age, 61 of whom attended hatha yoga classes. The others met for the same number and length of sessions and engaged in stretching and toning exercises instead of yoga.

At the end of the eight weeks, the yoga group was speedier and more accurate on tests of information recall, mental flexibility and task-switching than it had been before the intervention. The stretching-and-toning group saw no significant change in cognitive performance over time. The differences seen between the groups were not the result of differences in age, gender, social status or other demographic factors, the research team reported.

Hatha yoga is an ancient spiritual practice that involves meditation and focused breathing while an individual moves through a series of stylized postures, said Neha Gothe, who led the study with University of Illinois kinesiology and community health professor Edward McAuley. Beckman Institute director Arthur Kramer also contributed to the study. Gothe is now a professor at Wayne State University.

“Hatha yoga requires focused effort in moving through the poses, controlling the body and breathing at a steady rate,” Gothe said. “It is possible that this focus on one’s body, mind and breath during yoga practice may have generalized to situations outside of the yoga classes, resulting in an improved ability to sustain attention.”

“Participants in the yoga intervention group showed significant improvements in working memory capacity, which involves continually updating and manipulating information,” McAuley said. “They were also able to perform the task at hand quickly and accurately, without getting distracted. These mental functions are relevant to our everyday functioning, as we multitask and plan our day-to-day activities.”

Previous studies have found that yoga can have immediate positive psychological effects by decreasing anxiety, depression and stress, Gothe said.

“These studies suggest that yoga has an immediate quieting effect on the sympathetic nervous system and on the body’s response to stress,” she said. “Since we know that stress and anxiety can affect cognitive performance, the eight-week yoga intervention may have boosted participants’ performance by reducing their stress.”

The results of the study are only preliminary and involve a fairly short-term intervention, the researchers said. Further research is needed to confirm the results and reveal the underlying brain mechanisms at play.

The team reported its findings in The Journals of Gerontology Series A: Biological Sciences and Medical Sciences. The National Institute on Aging at the National Institutes of Health supported this research.

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Group Health Research Institute

Both mother and fetus are at increased risk for complications of flu infection during pregnancy. And prenatal care providers say they’re advising women to get the flu vaccine, in line with recommendations from various organizations. But many pregnant women don’t understand the importance of this advice—and don’t get the vaccine.

Robert Arao, MPH, a biostatistician at Group Health Research Institute, did a statewide survey—the first of its kind—to assess what doctors think and do about flu vaccines for pregnant women. Mr. Arao was at the Oregon Health & Science University (OHSU) and the Oregon Health Authority’s (OHA) Public Health Division when he did this work. He e-published “Influenza vaccination of pregnant women: attitudes and behaviors of Oregon physician prenatal care providers” with Kenneth D. Rosenberg, MD, MPH and Katrina Hedberg, MD, MPH, of OHA’s  Public Health Division, and Shannon McWeeney, PhD, of OHSU, in the Maternal and Child Health Journal.

They found that most doctors who provide prenatal care in Oregon understood the importance of flu vaccination during pregnancy and communicated it to their patients. The research team mailed a survey to a random sample of more than 1,000 obstetricians and family physicians in Oregon. Of the survey respondents who had provided prenatal care in the last year, nearly nine in 10 said they routinely recommended flu vaccine to their healthy pregnant patients. Doctors who were younger, saw more pregnant patients, or both were even more likely to do so.

“Women understand the importance of not putting potential toxins, like alcohol and tobacco, into their body during pregnancy,” Mr. Arao said, “But women need to understand that getting a flu vaccination during pregnancy protects both the mother and the baby.”

Nationwide, only half of American women get flu vaccine while pregnant, and three quarters of pregnant women who receive a recommendation from a clinician actually get the vaccine. And in the Pacific Northwest, rates for many vaccinations tend to be lower than those for the nation as a whole.

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Rayshell Clapper for redOrbit.com – Your Universe Online
On August 11, 2014, people were rocked by the news that Robin Williams had committed suicide by asphyxiation. He hung himself according to one CNN article. For many, the shock was too confusing. Williams helped the world through his stage performances, shows, and movies. He did charity work, entertained the troops, and spread laughter to many. His sudden suicide hurt many.
A Huffington Post report included a written statement from Susan Schneider, Williams’ wife, who shared with the public that Williams suffered from depression, anxiety, and had recently been diagnosed with the early stages of Parkinson’s Disease. Schneider explained that her husband was not yet ready to share his diagnosis with the world.
MedLine Plus, a service of the National Institutes of Health, defines Parkinson’s as a type of movement disorder which occurs when nerve cells in the brain do not produce enough dopamine. It can be genetic or environmental. Symptoms have gradual development and include the following:
• Trembling of hands, arms, legs, jaw, and face
• Stiffness of the arms, legs, and trunk
• Slowness of movement
• Poor balance and coordination
Parkinson’s not only affects the brain and motor skills, but it also most definitely has an impact on the patient’s mental and emotional health. In fact, a recent study conducted by Northwestern University investigators has found that depression is not only a common symptom of Parkinson’s Disease, but also often goes untreated in many patients. This, perhaps, could provide more insight into Robin Williams’ suicide as he suffered from depression and had recently been diagnosed with Parkinson’s.
The Northwestern investigators “looked at records of more than 7,000 people with Parkinson’s disease. Among those with high levels of depressive symptoms, only one-third had been prescribed antidepressants before the study began, and even fewer saw social workers or mental health professionals for counseling…The investigators then focused their analysis on the remaining two-thirds of patients with depressive symptoms who were not receiving treatment at the start of the study. Throughout a year of observation, less than 10 percent of them received prescriptions for antidepressants or referrals to counseling. Physicians were most likely to identify depression and advocate treatment for patients with the severest depression scores.”
Depression in itself has a great impact on one’s well-being and decision making; however, pair that with Parkinson’s and a lack of treatment for the depression, and the patient has a formula for tragedy. Symptoms of depression warrant attention, especially in those who suffer from other diagnoses. The National Institutes of Mental Health list the following as signs and symptoms of depression:
• Persistent sad, anxious, or “empty” mood
• Feelings of hopelessness, pessimism
• Feelings of guilt, worthlessness, helplessness
• Loss of interest or pleasure in hobbies and activities
• Decreased energy, fatigue, being “slowed down”
• Difficulty concentrating, remembering, making decisions
• Difficulty sleeping, early-morning awakening, or oversleeping
• Appetite and/or weight changes
• Thoughts of death or suicide
• Suicide attempts
• Restlessness, irritability
• Persistent physical symptoms
As anyone can see, depression is not just “feeling blue.” These symptoms are devastating for those who suffer. Furthermore, compound any one or any combination of the symptoms of depression with something like Parkinson’s and tragedy can strike, especially if the depression goes untreated. As Northwestern identified in its study, the majority of patients diagnosed with Parkinson’s had depression that went untreated.
As Dr. Danny Bega, the first author of the study put it, “Physicians must be more vigilant about screening patients for depression as part of a routine assessment of Parkinson’s disease, and the effectiveness of different treatments for depression in this population need to be assessed.” To save future people from the sad fate that Robin Williams chose, we must be more vigilant and aware of our loved ones with depression and Parkinson’s Disease.
The full study is published in the Journal of Parkinson’s Disease.
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Parkinson’s Disease: A Complete Guide for Patients and Families – A Johns Hopkins Press Health Book

Lee-Ann Donegan, Penn Medicine

Study Examined Patients Over First Two Years of Treatment

New Penn Medicine research shows that neuropsychiatric symptoms such as depression, anxiety and fatigue are more common in newly diagnosed Parkinson’s disease (PD) patients compared to the general population. The study also found that initiation of dopamine replacement therapy, the most common treatment for PD, was associated with increasing frequency of impulse control disorders and excessive daytime sleepiness. The new findings, the first longitudinal study to come out of the Parkinson’s Progression Markers Initiative (PPMI), were published in the August 15, 2014, issue of Neurology, the medical journal of the American Academy of Neurology.

The PPMI, a landmark, multicenter observational clinical study sponsored by The Michael J. Fox Foundation for Parkinson’s Research, uses a combination of advanced imaging, biologics sampling and behavioral assessments to identify biomarkers of Parkinson’s disease progression. The Penn study, which represents neuropsychiatric and cognitive data from baseline through the first 24 months of follow up, was conducted in collaboration with the Philadelphia VA Medical Center and the University Hospital Donostia in Spain.

The study examined 423 newly diagnosed, untreated Parkinson’s patients and 196 healthy controls at baseline and 281 people with PD at six months. Of these, 261 PD patients and 145 healthy controls were evaluated at 12 months, and 96 PD patients and 83 healthy controls evaluated at 24 months.

PD patients were permitted to begin dopamine therapy at any point after their baseline evaluation.

“We hypothesized that neuropsychiatric symptoms would be common and stable in severity soon after diagnosis and that the initiation of dopamine replacement therapy would modify their natural progression in some way,” says senior author, Daniel Weintraub, MD, associate professor of Psychiatry and Neurology at the Perelman School of Medicine at the University of Pennsylvania and a fellow in Penn’s Institute on Aging.

The Penn team showed that while there was no significant difference between PD patients and healthy controls in the frequency of impulse control disorders, a neuropsychiatric symptom that can lead to compulsive gambling, sexual behavior, eating or spending, 21 percent of newly diagnosed PD patients screened positive for such symptoms at baseline. That percentage did not increase significantly over the 24-month period.

However, six patients who had been on dopamine therapy for more than a year at the 24-month evaluation showed impulse control disorders or related behavior symptoms while no impulse control incident symptoms were reported in PD patients who had not commenced dopamine therapy. Dopamine therapy did help with fatigue, with 33 percent of patients improving their fatigue test score over 24 months compared with only 11 percent of patients not on dopamine therapy.

The investigators also found evidence that depression may be undertreated in early PD patients: Two-thirds of patients who screened positive for depression at any time point were not taking an antidepressant.

PPMI follows volunteers for five years, so investigators plan to expand upon these results, which Weintraub still considers preliminary. “We will more closely look at cognitive changes over time,” he says. “Two years is not a sufficient period of follow up to really look at meaningful cognitive decline.”

The perspective of time is what makes the PPMI such an important initiative, Weintraub points out, since many patients with the disease live for 10 to 20 years following their diagnosis. “It’s really a chance to assess the frequency and characteristics of psychiatric and cognitive symptoms in PD, compare it with healthy controls, and then also look at its evolution over time,” he says. “The hope is that we will be able to continue this work so that we can obtain long-term follow up data on these patients,” says Weintraub.

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Rayshell Clapper for redOrbit.com – Your Universe Online

Cancer is a diagnosis that everyone wants to avoid. In many cases, cancer happens as a result of our lifestyle choices, while some are unfortunately genetically predisposed.

Regardless of whether cancer occurs due to genetics or lifestyle habits, there are some things we can all do to help prevent cancer. The American Institute for Cancer Research (AICR) recommends certain foods to help protect against cancer. Primarily, plant foods like vegetables, fruits, whole grains, and beans are all helpful in protecting our bodies and lowering the risks of certain cancers.

This comes first from the fact that vegetables and fruits are low in calories, and the AICR further reports that excess body fat increases the risk of seven cancers: esophagus, pancreas, colon and rectum, endometrium, kidney, postmenopausal breast, and gallbladder. Moreover, whole grains and beans are rich in fiber and have moderate calories. Plus, vegetables, fruits, whole grains, and beans each are rich in minerals, vitamins, and phytochemicals that have demonstrated anti-cancer effects.

For all these reasons – from weight management to vitamins, minerals, and anti-cancer effects, the AICR recommends that people fill two-thirds of their plates with vegetables, fruit, whole grains, and beans. The United States Department of Agriculture and ChooseMyPlate.gov already recommend filling at least half your plate with fruits and veggies, so it should not be too difficult to make it two-thirds.

Those plant foods well researched and confirmed as good anti-cancer foods include the following:

• Berries
• Dark green leafy veggies
• Garlic
• Grapes
• Grape juice
• Green tea
• Tomatoes

In addition, those plant foods that have recently been updated and added to the list of foods that fight cancer include the following:

• Apples
• Blueberries
• Broccoli
• Cruciferous veggies
• Cherries
• Coffee
• Cranberries
• Flaxseed
• Grapefruit
• Legumes (including dry beans, peas, and lentils)
• Soy
• Walnuts
• Whole grains
• Winter squash

Furthermore, the AICR expects the following foods to be added soon:

• Acai berries
• Blackberries
• Raspberries
• Carrots
• Chili peppers
• Citrus fruits (including oranges and lemons)
• Kale and other greens
• Mushrooms
• Nuts
• Onion
• Papayas
• Pomegranates
• Spinach
• Strawberries
• Sweet potatoes
• Watermelons and other melons

The variety of these foods makes them easy to incorporate into any diet, but the tastiness of almost all of these will make our taste buds just as happy as our bodies. Simply adding a leafy green salad and berry medley to our meals will give us the minerals, vitamins, and phytonutrients our bodies need to fight cancer as well as keep us from gaining weight.

At each meal, if we just consciously incorporate more of these foods, especially those already committed to the list of foods that fight cancer (see the first two lists above), into our meals, then we will know that we are doing our level best to protect our bodies from cancer.

Although some genetically predisposed cancers are harder to protect against, the good news is that the AICR’s list of foods that fight cancer may also aid in cancer survival and treatment. In all cases, research continues actively on each of these foods.

As the AICR article states, “No single food or food component can protect you against cancer by itself. But strong evidence does show that a diet filled with a variety of plant foods such as vegetables, fruits, whole grains and beans helps lower risk for many cancers.”

Just knowing that research supports the importance of plant foods in our diets in order to protect from cancer should help us to eat more of them. Cancer is something that we should all work to avoid.

April Flowers for redOrbit.com – Your Universe Online

Our bodies play host to millions of bacteria. In fact, they outnumber our own cells by about 100-fold. And yet, we hold the notion that we are in charge of our own lives, not the bacteria that has just hitched a ride.

A new study, published in BioEssays, tells a different story. The findings reveal that the bacteria within our bodies may very well be affecting our cravings and our moods to ensure that we eat what they want. The research team — from UC San Francisco, Arizona State University and University of New Mexico — say these bacteria could be driving us to obesity.

The research team performed a review of recent scientific literature, finding that microbes influence human eating behavior and dietary choices, forcing the human host to consume the particular nutrients they grow best on. Different species of bacteria need different nutrients. For example, some prefer fat, while others prefer sugar.

Dr. Athena Aktipis, PhD and co-founder of the Center for Evolution and Cancer with the Helen Diller Family Comprehensive Cancer Center at UCSF, says that bacteria not only have to compete with each other for food and to retain a niche within their ecosystem — aka us — they also have different goals for our actions than we do.

The diverse ecosystem of bacteria within our digestive system is known collectively as the gut microbiome. Our decisions could be influenced by signaling molecules released into our gut by the microbiome. Our gut is linked closely to the immune system, the endocrine system and the nervous system, making our physiologic and behavioral responses susceptible to influence from these signaling molecules.

“Bacteria within the gut are manipulative,” said Carlo Maley, PhD, director of the UCSF Center for Evolution and Cancer. “There is a diversity of interests represented in the microbiome, some aligned with our own dietary goals, and others not.”

Maley suggests that we are not entirely without recourse. By deliberately choosing and altering what we consume, we can influence the compatibility of the gut microbiome, measurably changing it within 24 hours of diet change.

“Our diets have a huge impact on microbial populations in the gut,” Maley said. “It’s a whole ecosystem, and it’s evolving on the time scale of minutes.” An example would be the bacteria found in the human gut biomes in Japan, able to digest seaweed because it is a popular choice in the diet.

The researchers believe that the gut bacteria might be affecting our choices and behaviors by acting through the vagus nerve, which connects 100 million nerve cells from the digestive tract to the base of the brain.

“Microbes have the capacity to manipulate behavior and mood through altering the neural signals in the vagus nerve, changing taste receptors, producing toxins to make us feel bad, and releasing chemical rewards to make us feel good,” said Aktipis, who is currently in the Arizona State University Department of Psychology.

The research team, which included University of New Mexico’s Department of Emergency Medicine’s Joe Alcock, MD, emphasizes that further research is necessary to fully understand the level of influence our gut bacteria might hold over us. For example, if bacteria that digest seaweed were transplanted into the human gut, would it lead the host to eat more seaweed?

For those seeking to improve their health, the authors say there is encouraging news in how quickly the microbiome can be changed. This change can be affected by food and supplement choices, probiotics and antibiotics. Creating an optimized balance of power among bacterial species in our gut may allow us to lead less obese and healthier lives, overall.

“Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating,” the authors wrote.

Image 2 (below): This image illustrates the relationship between gut bacteria and unhealthy eating. Credit: Courtesy of UC San Francisco

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Constant Craving: What Your Food Cravings Mean and How to Overcome Them by Doreen Virtue

Caroline Arbanas, Washington University in St. Louis

Anyone who has suffered from kidney stones is keenly aware of the lack of drugs to treat the condition, which often causes excruciating pain.

A new mouse study, however, suggests that a class of drugs approved to treat leukemia and epilepsy also may be effective against kidney stones, researchers at Washington University School of Medicine in St. Louis report.

The drugs are histone deacetylase inhibitors, or HDAC inhibitors for short. The researchers found that two of them — Vorinostat and trichostatin A — lower levels of calcium and magnesium in the urine. Both calcium and magnesium are key components of kidney stones.

The research is available online in the Journal of the American Society of Nephrology.

“We’re hopeful this class of drugs can dissolve kidney stones because its effects on reducing calcium and magnesium are exclusive to kidney cells,” said senior author Jianghui Hou, PhD, assistant professor of medicine. “In the mice, we achieved dramatic effects at a fraction of the dosage used to treat leukemia and without significant side effects.”

Most kidney stones form when the urine becomes too concentrated, allowing calcium and magnesium to crystallize and stick together. Intense pain develops when stones get stuck in the urinary tract and block the flow of urine.

Diet can play a role in the condition. Not drinking enough water or eating a diet with too much salt, which promotes calcium to be released into the urine, increases the risk of stones. Some people also are genetically prone to developing kidney stones, and they naturally release too much calcium into the urine.

Typically, doctors recommend drinking lots of water to help pass kidney stones from the body. Thiazide, a type of drug used to treat high blood pressure, sometimes is prescribed to treat the stones because it reduces calcium in the urine. But the drug also increases magnesium in urine, countering its effectiveness against kidney stones.

In the new study, Hou and his colleagues showed that Vorinostat, approved to treat leukemia and epilepsy, and trichostatin A, an antifungal drug, mimic a natural process in the kidney that reabsorbs calcium and magnesium into the urine.

Kidneys, in addition to filtering waste from the blood into the urine, also play an essential role in reclaiming minerals that the body needs to carry out basic functions of life. Normally, some calcium and magnesium in the blood are filtered into the urine and then reabsorbed back into the blood, depending on the body’s need for these essential minerals.

Hou’s earlier work showed this process is heavily dependent on the activity of a gene called claudin-14. When the activity of claudin-14 is idled, the kidney’s filtering system works like it’s supposed to. But when the gene is activated, calcium and magnesium are blocked from re-entering the blood.

The gene’s expression is controlled by two snippets of RNA, a sister molecule of DNA, Hou’s previous research has shown.

As part of the new study, Hou and his colleagues found that Vorinostat and trichostatin A do not act directly on the claudin-14 but mimic these so-called micro-RNA molecules, keeping the activity of the gene in check. That the drugs can modify the activity of micro-RNAs make them attractive as potential treatments for kidney stones.

In the mice, small doses of Vorinostat, for example, reduced calcium levels in the urine by more than 50 percent and magnesium levels by more than 40 percent. Similar results were noted for trichostatin A.

“Kidney cells were very sensitive to the drug,” Hou explained. “We used one-twentieth of the dose typically used in humans and achieved significant results. We now want to test the drug in clinical trials for patients with kidney stones.”

Mice don’t develop kidney stones, so it will be important to test the drugs against kidney stones in patients, but the current study provides proof of principle that HDAC inhibitors regulate the same pathway that leads to kidney stones, he said.

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Rayshell Clapper for redOrbit.com – Your Universe Online

We love to ignore information on health and nutrition. We want to know the latest in nutrition, but we also want to do only what is convenient for us. And in a day and age when nutrition studies flip flop from one position to another, we can easily pick and choose what nutrition information we want to follow.

Tufts University recently released information about nutrition debunking the junk advice out there. The “10 Red Flags of Junk Science” is an initiative of the Food and Nutrition Science Alliance, which is a partnership of professional nutrition science associations including the Academy of Nutrition and Dietetics, the American College of Nutrition, and the American Society for Nutrition. Let’s see just what advice the 10 Red Flags of Junk Science has for those thirsty for nutrition information.

1. Recommendations that Promise a Quick Fix

The first bit of advice given is to ignore any product that promises to lose weight fast. If there are any scientific studies about the effectiveness of a product, they are usually done by the manufacturer, so there really is no unbiased proof. These quick-fix product claims are also peppered with medical jargon to further fool the consumer. The short of it is, we should not let these companies manipulate us.

2. Dire Warnings of Danger from a Single Product or Regimen

One year it is too much sugar while the next focuses on the dangers of too many carbs, but the truth is there is not one thing to blame for being overweight or unhealthy otherwise. Typically, it is a combination of products and lack of exercise. So the next time we hear about how all that fat is the culprit, we need to let that go in one ear and out the other for the most part. Yes, too much fat in our diet is unhealthy, but it will not be the sole reason for weight gain.

3. Claims that Sound too Good to Be True

If it sounds too good, then it probably is. Research and study just what the science is behind any too-good-to-be-true claims.

4. Simplistic Conclusions Drawn from a Complex Study

Though most people want the answers to be simple and black or white, the truth is that most science is very complicated and requires analytical thinking and digging in order to understand it. Anything that seems like it has the be-all-end-all answer that is so simple it seems silly probably is not trustworthy or may be flat out wrong.

5. Recommendations Based on a Single Study

We should also be wary of any recommendations that come from just a single study. Scientific method demands more than one study. As the Tufts piece points out, “The point, says [Assistant Professor Diane] McKay, is that with any nutrition study, you have to look at how it fits in with everything else that has been found to date.” We have to compare findings and understand the bigger picture, not just the fresh and new one.

6. Statements Refuted by Reputable Scientific Organizations

If a nutrition statement that seems too good to be true, too simplistic or claims to be a quick fix catches our eye, we should definitely check out what reputable scientific organizations have to say about things. Here is a list of quality government agencies and nutrition organizations:

• Centers for Disease Control and Prevention
• Food and Drug Administration
• United States Department of Agriculture
• National Institutes of Health
• Academy of Nutrition and Dietetics
• American Heart Association
• American Institute for Cancer Research

Any statements refuted by these organizations are suspect.

7. Lists of “Good” and “Bad” Foods

These lists are problematic because foods are not all good or all bad. Balance and moderation are necessary. A candy bar on rare occasion is not terrible just as a little ice cream will not kill a person. The key, though, is restraint, moderation, and balance. Indulge on occasion, but make sure to eat healthy, well-balanced meals regularly.

8. Recommendations Made to Help Sell a Product

Tufts puts it best here: “If the health article you are reading conveniently ends with a sales pitch for a supplement, or if all the studies referenced at the end of a diet book are by the person who wrote the book, your quackery alarm should go off.” This does not automatically mean the recommendations or studies are wrong, but it does mean that we should be cautious and research deeper.

9. Recommendations Based on Studies Not Peer Reviewed

In science, peer review is necessary for reliability and accuracy. Outside peer reviewers ensure that a study is honest, has well-conducted research and credible findings, and that the study and findings are significant.

10. Recommendations from Studies that Ignore Differences Among Individuals or Groups

Nutrition is not a “one size fit all” science. Nutrition is individual, so any study claiming all or nothing or making blanket statements is likely not reliable.

With all the nutrition studies, facts, and information, it is good to have some guidance on what to believe, what to research further, and what to be suspect of.

> Read the full report by Julie Flaherty of Tufts University.

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Shop Amazon – Hot New Releases – Updated Every Hour

Herb Booth, University of Texas, Arlington

A computer science and engineering associate professor and her doctoral student graduate are using a genetic computer network inference model that eventually could predict whether a person will suffer from bipolar disorder, schizophrenia or another mental illness.

The findings are detailed in the paper “Inference of SNP-Gene Regulatory Networks by Integrating Gene Expressions and Genetic Perturbations,” which was published in the June edition of Biomed Research International. The principal investigators were Jean Gao, an associate professor of computer science and engineering, and Dong-Chul Kim, who recently earned his doctorate in computer science and engineering from UT Arlington.

“We looked for the differences between our genetic computer network and the brain patterns of 130 patients from the University of Illinois,” Gao said. “This work could lead to earlier diagnosis in the future and treatment for those patients suffering from bipolar disorder or schizophrenia. Early diagnosis allows doctors to provide timely treatments that may speed up aid to help affected patients.”

The UT Arlington researchers teamed with Jiao Wang of the Beijing Genomics Institute at Wuhan, China; and Chunyu Liu, visiting associate professor at the University of Illinois Department of Psychiatry, on the project.

Gao said the findings also could lead to more individualized drug therapies for those patients in the early stages of mental illnesses.

“Our work will allow doctors to analyze a patient’s genetic pattern and apply the appropriate levels of personalized therapy based on patient-specific data,” Gao said.

One key to the research is designing single nucleotide polymorphism or SNP networks, researchers said.

“SNPs are regulators of genes,” said Kim, who joins the University of Texas-Pan American this fall as an assistant professor. “Those SNPs visualize how individual genes will act. It gives us more of a complete picture.”

The paper is a culmination of four years of work.

Khosrow Behbehani, dean of the College of Engineering, said the research merges the power of computer science and engineering, psychology and genetics.

“This research holds a lot of promise in the area of genetic expression,” Behbehani said. “If successful, it opens up the possibility of applying the method to other pathological conditions.”

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redOrbit Staff & Wire Reports – Your Universe Online

Adults can develop post-traumatic stress disorder (PTSD) in response to an early-childhood event, even if they have no explicit memory of that trauma, claim the authors of a study appearing in Friday’s edition of the journal Biological Psychiatry.

According to the University at Albany and the University of California, Los Angeles (UCLA) scientists behind the new research, there are many different types of memory, and that only some types are required for PTSD to develop. In fact, they said that there have even been case reports of individuals who have experienced events resulting in brain damage who went on to develop PTSD-like symptoms despite having no recollection of the incident itself.

Those case reports suggest that explicit memory may not be an absolute prerequisite for PTSD, the study authors explained. In order to test this hypothesis, Dr. Andrew Poulos of the UCLA Brain Research Institute and his colleagues devised a study to examine what parts of a traumatic early life experience remains if the memory is lost.

The experiment required exposing juvenile rodents to one session of unpredictable stress in the form of sudden, inescapable footshocks when they were just 19 days old. Later, when the creatures reached adulthood, the investigators tested them for memory of the incident and evaluated their fear response.

“Early trauma exposed rats displayed stereotypic footshock reactivity, yet by adulthood, hippocampus-dependent contextual fear-related memory was absent,” the authors wrote. “However, adult rats showed sensitized fear learning, aberrant basal circadian fluctuations of corticosterone, increased amygdalar glucocorticoid receptors, decreased time spent in the open arm of an elevated plus maze, and an odor aversion associated with early-life footshocks.”

In other words, as Poulos explained in a statement, his team found that the rodents “failed to remember the environment in which they were traumatized” but nonetheless continued to demonstrate “a persistent increase in anxiety related behavior and increased learning of new fear situations. These heightened levels of fear and anxiety corresponded with drastic changes in the daily rhythms of the circulating hormone corticosterone.”

Corticosterone is a hormone that is partially responsible for regulating the body’s response to stress, and the research also revealed that levels of a receptor for this hormone increased in the amygdala, a region of the brain essential to the learning of fear. Poulos said that future research on this subject will allow them to determine if the increase in both corticosterone and the receptors prepares the organism for increased anxiety levels.

The combination of the research team’s findings indicate that failure to remember a specific traumatic event does not necessarily preclude an organism from experiencing some of the negative consequences of such an occurrence, including elevated anxiety levels and a heightened sense of fear. They concluded that symptoms and neuropathology associated with human PTSD is possible, even when there is no explicit memory of the early trauma.

“These data highlight the importance of the many ways in which the brain processes traumatic experiences. Psychotherapy tends to focus heavily on the articulation of trauma memories,” said Dr. John Krystal, Editor of Biological Psychiatry. “However, the current study highlights that these explicit memories may not represent all brain processes that drive distress and disability.”

“In other words there may be a mismatch between what people think and how they feel about their traumatic experiences. Thus, there may be role in treatment for measuring other dimensions of response, such as physiologic arousal, through which some of these other forms of learning are expressed,” he added.

Rayshell Clapper for redOrbit.com – Your Universe Online

Schizophrenia affects about one percent of the world’s population and, if untreated, leaves sufferers struggling with their relationships, jobs, and lives as a whole.

According to the National Institute of Mental Illnesses, schizophrenia is a debilitating brain disorder whereby those diagnosed with this mental illness “may hear voices other people don’t hear. They may believe other people are reading their minds, controlling their thoughts, or plotting to harm them. This can terrify people with the illness and make them withdrawn or extremely agitated. People with schizophrenia may not make sense when they talk. They may sit for hours without moving or talking. Sometimes people with schizophrenia seem perfectly fine until they talk about what they are really thinking.”

Current explanations from the National Institute of Mental Illness show that schizophrenia is caused by two major factors: genes and environment and differing brain chemistry and structure. For the former, schizophrenia definitely runs in families with a 10 percent occurrence in those who have a first-degree relative with the disorder. First-degree relatives include parents and siblings. Those who have second-degree relatives – aunts, uncles, grandparents, or cousins — have a higher risk than others as well. And if one has an identical twin diagnosed with schizophrenia, that person has a 40 to 65 percent chance of developing the disorder.

But genes are not the only area of concern. “Scientists think interactions between genes and the environment are necessary for schizophrenia to develop. Many environmental factors may be involved, such as exposure to viruses or malnutrition before birth, problems during birth, and other not yet known psychosocial factors.”

As for brain structure and chemistry, current science believes than an imbalance in the chemical reactions of the brain further plays a role. Specifically, the chemical reactions involving the neurotransmitters dopamine and glutamate seem to contribute to schizophrenia. Moreover, the brains of those with schizophrenia look different than the brains of healthy people.

The existing treatment regimen relies heavily on antipsychotic drugs, but these come with a plethora of side effects including drowsiness, blurred vision, skin rashes, restlessness, and many more. These drugs can control the symptoms of schizophrenia but can also have a damaging effect on the quality of life through the side effects. These drugs work more like an “off button” to schizophrenia and many other daily actions and feelings.

Monash University researchers may have found an answer, however.

According to recent research led by Dr. Rob Lane of the Monash Institute for Pharmaceutical Studies and published in the journal Nature Chemical Biology, they have discovered a new class of drugs that work more like a “dimmer switch” to control schizophrenia instead of an off button that turns off much more than the symptoms of schizophrenia.

Co-author Professor Arthur Christopoulos explains the new class of drug: “The idea behind our research is to develop a drug that doesn’t completely block dopamine. We found a molecule that, rather than blocking the effect of dopamine at the D2 receptor, acts to subtly dial down dopamine’s effect, a bit like a dimmer switch…This means that if we can get just the right amount of dial-down, we could treat the symptoms of the disease and avoid some of these side-effects.”

The Monash team will continue their research by collaborating with chemists at MIPS to attempt developing a better version of the drug used in the study. With further development, this new class of drugs could help people diagnosed with schizophrenia control their illness while allowing them to avoid the negative side effects associated with schizophrenia.

If this new class of drugs can help those who suffer from schizophrenia at all, then it definitely needs development.