More than one-third of Division I college athletes may have low vitamin D levels

A new study presented today at the 2015 Annual Meeting of the American Academy of Orthopaedic Surgeons (AAOS) found that more than one-third of elite, Division I college athletes may have low levels of vitamin D, which is critical in helping the body to absorb calcium needed to maintain bone mass, and to minimize musculoskeletal pain and injury risk.

Up to 1 billion people globally have insufficient or deficient vitamin D levels. Vitamin D is found in fish, regularly added to milk and dairy products in the U.S., and available as a supplement. Vitamin D also is produced in the body through sun exposure.

"Although multiple studies have demonstrated a high prevalence of vitamin D insufficiency across various populations, there is a paucity of data regarding elite level athletes," said orthopaedic surgeon and lead study author Diego Villacis, MD, administrative chief resident physician at the University of Southern California. "Recent studies also have demonstrated that vitamin D levels have a direct relationship with muscle power, force, velocity and optimal bone mass."

In this study, which appeared in the February 2014 online issue of Sports Health, researchers measured the serum 25-hydroxyvitamin D (serum 25) levels of 223 National Collegiate Athletic Association (NCAA) athletes (121 men and 102 women) between June 2012 and August 2012. The mean serum 25 level for the athletes, enrolled in a broad range of indoor and outdoor sports, was 40.1 ±14.9 ng/mL (?32 ng/mL is considered normal; 20 to <32 ng/mL, insufficient; and <20 ng/mL, deficient). Overall, 66.4 percent of participants had sufficient vitamin D levels and 33.6 percent, insufficient or deficient levels.

Men were 2.8 times more likely to have an abnormal vitamin D level, according to the results, and athletes with darker skin tones also faced a "much higher risk" for insufficient vitamin D. Black athletes were 19.1 times more likely to have abnormal vitamin D levels compared to white athletes, and Hispanics, 6.1 times more likely.

"Our study demonstrated abnormal vitamin D levels in nearly one out of three elite NCAA Division I athletes tested," said Dr. Villacis. "Although there is much more work to be done, our results open the possibility for improved performance and most importantly decreased risk of injury with correction of vitamin D levels. This may potentially be achieved simply and safely through modification of diet, sunlight exposure, and vitamin D supplementation."

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Low Vaccination Rates Fuel the 2015 Measles Outbreak

Inadequate vaccine coverage is likely a driving force behind the ongoing Disneyland measles outbreak, according to calculations by a research team at Boston Children's Hospital. Their report, based on epidemiological data and published online by JAMA Pediatrics, indicates that vaccine coverage among the exposed populations is far below that necessary to keep the virus in check, and is the first to positively link measles vaccination rates and the ongoing outbreak.

By examining case numbers reported by the California Department of Public Health and current and historical case data captured by the HealthMap disease surveillance system, the researchers--led by Maimuna Majumder, MPH, and John Brownstein, PhD, of Boston Children's Informatics Program--estimate that the measles vaccination rate among the case clusters in California, Arizona and Illinois is between 50 and 86 percent, far below the 96 to 99 percent necessary to create a herd immunity effect.

Measles is highly contagious. It's estimated that an infected individual in a population fully susceptible to measles will spread the virus to between 11 and 18 additional people. This number is called the virus's basic reproduction rate, or R0. In a population where at least some individuals are immune to measles, the virus spreads from person to person more slowly. The rate of spread in an immune population is called the virus's effective reproduction rate, or RE.

Using case data, R0 and measles' serial interval (the length of time for each successive wave of transmission to follow the one before), Majumder and Brownstein calculated that the virus's RE in the Disneyland outbreak is between 3.2 and 5.8. From there, the pair calculated their vaccination estimate.

The researchers are quick to note that their estimate does not reflect vaccination across the United States, the state of California or even among the population of Disneyland visitors at the outbreak's start. Rather, it reflects the vaccination rate among the exposed populations in each cluster of cases linked to the outbreak so far.

"It's as though you took everyone exposed to measles in the areas with case clusters, put them in a room and measured the level of vaccine coverage in that aggregate population," says Majumder.

Using the same data sources, the HealthMap team has separately released an interactive model illustrating how differing rates of vaccine coverage could affect the growth of a measles outbreak over time. The model, available at healthmap.org/measlesoutbreak, puts the effects of vaccination into stark relief. If a population is fully vaccinated against the virus, the model predicts that one case of measles will give rise to only two additional cases over 70 days. By contrast, if only 60 percent of a population is vaccinated, more than 2,800 cases will occur over the same time period.

"Our data tell us a very straightforward story--that the way to stop this and future measles outbreaks is through vaccination," says Brownstein, a digital epidemiologist and co-founder of HealthMap and VaccineFinder, an online service that allows users to search for locations offering a variety of vaccinations, including the MMR vaccine that protects against measles. "The fundamental reason why we're seeing the number of cases we are is inadequate vaccine coverage among the exposed.

"We hope these data encourage families to ensure they and their loved ones are vaccinated," he continues, "and help local public health officials in their efforts to control this outbreak."

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Folic Acid Supplementation Among Adults with Hypertension Reduces Risk of Stroke

In a study that included more than 20,000 adults in China with high blood pressure but without a history of stroke or heart attack, the combined use of the hypertension medication enalapril and folic acid, compared with enalapril alone, significantly reduced the risk of first stroke, according to a study appearing in JAMA. The study is being released to coincide with its presentation at the American College of Cardiology Annual Scientific Session.

Stroke is the leading cause of death in China and second leading cause of death in the world. Primary prevention (prevention prior to a first episode) is particularly important because about 77 percent of strokes are first events. Uncertainty remains regarding the efficacy of folic acid therapy for primary prevention of stroke because of limited and inconsistent data, according to background information in the article.

Yong Huo, M.D., of Peking University First Hospital, Beijing, China, and colleagues had 20,702 adults with hypertension without history of stroke or heart attack randomly assigned to receive daily treatment with a single-pill combination containing enalapril (10 mg) and folic acid (0.8 mg; n = 10,348), or a tablet containing enalapril alone (10 mg; n = 10,354). The trial was conducted from May 2008 to August 2013 in 32 communities in Jiangsu and Anhui provinces in China. Participants were tested for variations in the MTHFR C677T gene (CC, CT, and TT genotypes) that may affect folate levels.

During a median treatment duration of 4.5 years, first stroke occurred in 282 participants (2.7 percent) in the enalapril-folic acid group compared with 355 participants (3.4 percent) in the enalapril group, representing an absolute risk reduction of 0.7 percent and a relative risk reduction of 21 percent. Analyses also showed significant reductions among participants in the enalapril-folic acid group in the risk of ischemic stroke (2.2 percent vs 2.8 percent) and composite cardiovascular events (cardiovascular death, heart attack and stroke) (3.1 percent vs 3.9 percent).

There was no significant difference between groups in the risk of hemorrhagic stroke, heart attack, or all-cause death, or in the frequencies of adverse events.

The authors write that this trial (China Stroke Primary Prevention Trial; CSPPT), with data on individual baseline folate levels and MTHFR genotypes, has provided convincing evidence that baseline folate level is an important determinant of efficacy of folic acid therapy in stroke prevention. "The CSPPT is the first large-scale randomized trial to test the hypothesis using individual measures of baseline folate levels. In this population without folic acid fortification, we observed considerable individual variation in plasma folate levels and clearly showed that the beneficial effect appeared to be more pronounced in participants with lower folate levels."

"We speculate that even in countries with folic acid fortification and widespread use of folic acid supplements such as in the United States and Canada, there may still be room to further reduce stroke incidence using more targeted folic acid therapy -- in particular, among those with the TT genotype and low or moderate folate levels."

Editorial: Folate Supplements for Stroke Prevention

"The trial by Huo et al has important implications for stroke prevention worldwide," write Meir Stampfer, M.D., Dr.P.H., and Walter Willett, M.D., Dr.P.H., of the Harvard T. H. Chan School of Public Health and Channing Division of Network Medicine, Boston, in an accompanying editorial.

"Although the trial participants all had hypertension, there is little reason to doubt that the results would apply to normotensive persons, although the absolute effect would be smaller. It is possible to debate the ethics of whether a replication trial should be performed, especially because folic acid supplementation (or fortification) is safe and inexpensive, and carries other benefits. Large segments of the world's population, potentially billions of people, including those living in northern China, Bangladesh, and Scandinavia, have low levels of folate."

"Individuals with the TT genotype might particularly benefit, although it seems unlikely that genotyping for that purpose would be cost-effective. Also, some persons in the United States on the low end of the distribution of folate intake may benefit; effects in this subgroup would not have been detected in previous trials. Ideally, adequate folate levels would be achieved from food sources such as vegetables (especially dark green leafy vegetables), fruits and fruit juices, nuts, beans, and peas. However, for many populations, achieving adequate levels from diet alone is difficult because of expense or availability. This study seems to support fortification programs where feasible, and supplementation should be considered where fortification will take more time to implement."



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A breakfast of champions for diabetics

A breakfast of champions for diabetics

Our modern epidemic of obesity has led to an alarming rise in the incidence of diabetes. More than 382 million people on the planet suffer from diabetes, predominantly type-2 diabetes. For these people, blood sugar surges -- glucose spikes after meals -- can be life threatening, leading to cardiovascular complications.

A new Tel Aviv University study published in Diabetologia proposes a new way to suppress deadly glucose surges throughout the day -- eating a high-caloric breakfast and a more modest dinner. According to TAU's Prof. Daniela Jakubowicz and Dr. Julio Wainstein of the Wolfson Medical Center's Diabetes Unit, Prof. Oren Froy of the Hebrew University of Jerusalem, and Prof. Bo Ahrén of Lund University in Sweden, the combined consumption of a high-energy breakfast and a low-energy dinner decreases overall daily hyperglycaemia in type-2 diabetics.

"We found that by eating more calories at breakfast, when the glucose response to food is lowest, and consuming fewer calories at dinner, glucose peaks after meals and glucose levels throughout the day were significantly reduced," said Prof. Jakubowicz.

All in the timing

The new study was conducted on eight men and 10 women aged 30-70 with type-2 diabetes. Patients were randomized and assigned either a "B diet" or "D diet" for one week. The B diet featured a 2946 kilojoule (kj) breakfast, 2523 kj lunch, and 858kj dinner, and the D diet featured a 858 kj breakfast, 2523 kj lunch, and 2946 kj dinner. Both diets contained the same total energy measured in kilojoules, a food energy measurement similar to a calorie, but were consumed at different times through the day, with the larger meal taking place during breakfast in the B diet. The larger meal included two slices of bread, milk, tuna, a granola bar, scrambled egg, yoghurt and cereal; the smaller meal contained sliced turkey breast, mozzarella, salad and coffee.

Patients consumed their diets at home for six days before the day of testing. On the seventh day, each group consumed their assigned meal plan at the clinic, and blood samples were collected just before breakfast and at regular intervals after the meal. Blood sampling was repeated at the same intervals after lunch and dinner. Post-meal glucose levels were measured in each participant, as well as levels of insulin, c-peptide (a component of insulin), and glucagon-like-peptide 1 hormone (GLP-1, also known as incretin: an indicator of glucose metabolism that stimulates insulin release). Two weeks later, patients switched to the alternate diet plan, and the tests were repeated.

The results of the study showed that post-meal glucose elevations were 20% lower and levels of insulin, C-peptide, and GLP-1 were 20% higher in participants on the B diet compared with those on the D diet.

What -- and when -- to eat

Despite the fact that both diets contained the same calories, blood glucose levels rose 23 percent less after the lunch preceded by a large breakfast.

"By demonstrating that a diet of high-energy breakfasts and more modest dinners is more effective in lowering overall daily post-meal glucose surges, we suggest that such a regimen is a powerful therapeutic approach for improving glycemic control and may potentially reduce cardiovascular complications in type- 2 diabetics," said Prof. Jakubowicz. "It is not enough to tell the diabetic patient what he or she should or should not eat. It is more important to emphasize that a more advantageous meal schedule should be followed."

The researchers are currently engaged in an extended study of the benefits of high-energy breakfast and reduced-calorie dinners over time.


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The above story is based on materials provided by American Friends of Tel Aviv University. Note: Materials may be edited for content and length.



Journal Reference:

Daniela Jakubowicz, Julio Wainstein, Bo Ahrén, Yosefa Bar-Dayan, Zohar Landau, Hadas R. Rabinovitz, Oren Froy. High-energy breakfast with low-energy dinner decreases overall daily hyperglycaemia in type 2 diabetic patients: a randomised clinical trial. Diabetologia, 2015; DOI: 10.1007/s00125-015-3524-9
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American Friends of Tel Aviv University. "A breakfast of champions for diabetics." ScienceDaily. ScienceDaily, 16 March 2015. <www.sciencedaily.com/releases/2015/03/150316122723.htm>.

ACL injuries in female athletes traced to genes

Dr. William Landis, G. Stafford Whitby Chair in Polymer Science at The University of Akron, and his UA research associate Robin Jacquet discovered, with fellow collaborators, that a high occurrence in ACL injuries among female athletes may be traced to genes.
Credit: Lauren Collins

[Click to enlarge image]

Female athletes endure two to eight times more anterior cruciate ligament, or ACL, injuries than their male counterparts. Genes are likely a major factor, according to Dr. William Landis, G. Stafford Whitby Chair in Polymer Science at The University of Akron, and Dr. Kerwyn Jones, Chair of Pediatric Orthopedics for Akron Children's Hospital. The findings could change the way women athletes receive sports training and treatment for their injuries and could possibly lead to genetic counseling regarding athletic participation.

Jones and Landis have been probing the significant gap in ACL injury occurrence among young women and men athletes for years, exploring other potential attributes such as hormones and the gait or stance of women as compared to men.

"We wondered about the influence of genes and how they might affect the structure or integrity of these ligaments," Landis says, explaining that he and Jones examined 14 fresh surgical samples of ruptured ligament tissue taken from both female and male athletes who suffered non-contact injuries of the tissues. "After some very detailed and extensive analysis through gene microarray techniques, we discovered 32 genes that were expressed to much different degrees in the female injured ligaments compared with those of males."

Of the 32 expressed genes, the researchers closely examined three that gave rise to specific proteins related to ligament structure and integrity. They discovered that all three genes regulated ligament tissue in a much different manner in female compared to male tissue.

"The differences clearly may account for weaker anterior cruciate ligaments in the females compared to the males," Landis says.

Published in the Journal of Bone & Joint Surgery , the finding has significant implications in sports medicine and training, orthopedics and clinical practice. The discovery could open discussions about recommended genetic counseling for young women interested in participating in sports, with results either clearing them for participation or signaling a need for specialized training.

"We can't change genes," Jones says, "but we can help girls strengthen their core and improve their technique. Several exercises and prevention programs have been proven to reduce the number of ACL injuries and we can and should introduce them to all girl athletes starting in middle school."

Clinical treatment and training in sports for females and males would now likely need to be modified so that the anterior cruciate ligaments could be strengthened appropriately in order to reduce or avoid injuries to this tissue most common in females, Landis adds.

"It's also possible that genetic counseling may be used to guide personal decisions about taking part in athletics. The study presents an entirely new, unanticipated and extremely important perspective about anterior cruciate ligament injuries observed so often in female athletes compared to males," Landis says.

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Journal Reference:
J. S. Johnson, M. A. Morscher, K. C. Jones, S. M. Moen, C. J. Klonk, R. Jacquet, W. J. Landis. Gene Expression Differences Between Ruptured Anterior Cruciate Ligaments in Young Male and Female Subjects. The Journal of Bone & Joint Surgery, 2015; 97 (1): 71 DOI: 10.2106/JBJS.N.00246


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Infant gut bacteria and food sensitization: Associations in the first year of life

<<Being too clean is not healthy.  Perhaps we are caught in a negative feedback loop.>>

A new study from Canadian researchers at the University of Alberta and University of Manitoba is shedding new light on changes in intestinal bacteria of infants that can predict future development of food allergies or asthma.

The research, published in the February edition of the journal Clinical & Experimental Allergy and highlighted as the publication's "Editor's Choice," reveals that infants with a fewer number of different bacteria in their gut at three months of age are more likely to become sensitized to foods such as milk, egg or peanut by the time they are one year old. Infants who developed food sensitization also had altered levels of two specific types of bacteria, Enterobacteriaceae and Bacteroidaceae, compared to infants who didn't.

"Using DNA techniques to classify bacteria in the Scott and Guttman laboratories at the University of Toronto, we obtained information on the different types of 'good' bacteria present in infant stool collected at three months of age and then at one year of age," says Anita Kozyrskyj, professor in the Department of Pediatrics at the University of Alberta and senior author of the study. "We were able to then see which bacteria present at three months predicted the development of food sensitization at one year, as measured by a skin reaction test to the food."

"We are continuing to study this process," says Meghan Azad, assistant professor in the Department of Pediatrics & Child Health at the University of Manitoba and lead author of the study. "Ultimately, we hope to develop new ways of preventing or treating allergies, possibly by modifying the gut microbiota."

The study, funded by the Canadian Institutes of Health Research and AllerGen NCE, looked at data from 166 infants enrolled in the Canadian Healthy Infant Longitudinal Development (CHILD) Study. This landmark study involves more than 3,500 families and their newborn infants across Canada, including 1,000 in Manitoba and 750 in Edmonton, who are being closely monitored to determine the genetic and home environment factors that contribute to future allergies and asthma.

Researchers say the data on gut bacterial patterns during infancy can serve as a biomarker for future disease.

"It is something that one can measure that indicates increased risk of food sensitization by one year of age," says Kozyrskyj.

Both Kozyrskyj and Azad, who is also a research scientist at the Children's Hospital Research Institute of Manitoba, caution that the results don't necessarily mean the children will progress to full-blown food allergies in later life. The researchers will soon be expanding their sample size as data comes in from other children at CHILD Study sites in Edmonton, Winnipeg, Vancouver and Toronto. The hope is to eventually have data from as many as 2,500 children from across Canada. The researchers plan to follow them as they grow, examining results again at the ages of three and five.

"At the end of the day, we want to know if infants who show changes to normal gut bacteria composition will go on to develop food or other allergies, or even asthma," says Kozyrskyj.

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Scientists override body's inflammatory response

Scientists who have discovered the mechanism of a protein that suppresses inflammation in the body, say the information could potentially be used to develop new drugs to control inflammation.

The international study, led by a husband-and-wife team, Associate Professor Marcel Nold and Dr Claudia Nold from The Ritchie Centre at MIMR-PHI Institute of Medical Research and Monash University, focused on interleukin 37 (IL-37), a powerful inhibitor of inflammation that is generated by the body.

Previous research by the same team identified that IL-37, one of the rare anti-inflammatory mediators, acts much more broadly than others to regulate the immune response and protect the body from damage.

The new study, published in Nature Immunology, deciphers the mechanisms of how the body uses IL-37 as a molecular signal to regulate and control inflammation.

The team found that to achieve its protective effects, IL-37 utilises a set of very specific receptors on target cells. By binding to these receptors, IL-37 instructs those target cells to execute a cascade of events, which temper several of the molecular pathways by which the body mounts inflammatory responses.

Associate Professor Marcel Nold said inflammation is a double-edged sword.

"We all need inflammation to protect us from the harmful effects of bacteria, viruses or cancer. But in many diseases, there is too much inflammation; good examples are stroke, heart attack and auto immune diseases such as Crohn's Disease or lupus," he said.

"Rampant inflammation is harmful and leads to tissue damage, resulting in all kinds of side effects like pain, fatigue and regrettably also organ failure and death" Associate Professor Nold said.

Dr Claudia Nold said the study is universally applicable to all types of inflammation in patients of all ages, in conditions ranging from the common cold to serious life-threatening illnesses.

"IL-37 is able to override the body's own destructive responses to injury and disease, harnessing its fundamental mechanisms of action," she said.

To unravel the mechanistic details of IL-37's powerful effects, the research team used the Nobel Prize winning technique, Super Resolution Microscopy at Monash Micro Imaging and the Monash Institute of Pharmaceutical Sciences.

The advanced instruments allowed the scientists to see single molecules of IL-37 and its receptors, showing how IL-37 positions itself on the surface of target cells -- something that had never been done before in previous studies in this field.

Dr Claudia Nold said the new findings make the vast potential of IL-37 accessible to drug development.

"IL-37 is extremely potent and effective in controlling inflammation, but to make it medically useful we needed to know how it works and what it does to cells," she said.

"Now we have deciphered these mechanisms we can pursue the medical potential of IL-37. This can be done by mimicking its effects when there is too much inflammation, or by blocking it when there is too little, like in cancer," Dr Nold said.

"It's important to note that this research is very early stage, but if we build on our discoveries and develop them further, it will be possible to deliver substantial and meaningful benefits to patients suffering from lots of diseases, be they acute or chronic, in a newborn baby or a centenarian" added Associate Professor Nold.

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The above story is based on materials provided by Monash University. Note: Materials may be edited for content and length.

Journal Reference:
Claudia A Nold-Petry, Camden Y Lo, Ina Rudloff, Kirstin D Elgass, Suzhao Li, Michael P Gantier, Amelie S Lotz-Havla, Søren W Gersting, Steven X Cho, Jason C Lao, Andrew M Ellisdon, Björn Rotter, Tania Azam, Niamh E Mangan, Fernando J Rossello, James C Whisstock, Philip Bufler, Cecilia Garlanda, Alberto Mantovani, Charles A Dinarello, Marcel F Nold. IL-37 requires the receptors IL-18Rα and IL-1R8 (SIGIRR) to carry out its multifaceted anti-inflammatory program upon innate signal transduction. Nature Immunology, 2015; DOI: 10.1038/ni.3103


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Feast-and-famine diet could help extend life, study suggests

Think of it as interval training for the dinner table.

University of Florida Health researchers have found that putting people on a feast-or-famine diet may mimic some of the benefits of fasting, and that adding antioxidant supplements may counteract those benefits.

Fasting has been shown in mice to extend lifespan and to improve age-related diseases. But fasting every day, which could entail skipping meals or simply reducing overall caloric intake, can be hard to maintain.

“People don’t want to just under-eat for their whole lives,” said Martin Wegman, an M.D.-Ph.D. student at the UF College of Medicine and co-author of the paper recently published in the journal Rejuvenation Research. “We started thinking about the concept of intermittent fasting.”

Michael Guo, a UF M.D.-Ph.D. student who is pursuing the Ph.D. portion of the program in genetics at Harvard Medical School, said the group measured the participants’ changes in weight, blood pressure, heart rate, glucose levels, cholesterol, markers of inflammation and genes involved in protective cell responses over 10 weeks.

“We found that intermittent fasting caused a slight increase to SIRT 3, a well-known gene that promotes longevity and is involved in protective cell responses,” Guo said.

The SIRT3 gene encodes a protein also called SIRT3. The protein SIRT3 belongs to a class of proteins called sirtuins. Sirtuins, if increased in mice, can extend their lifespans, Guo said. Researchers think proteins such as SIRT3 are activated by oxidative stress, which is triggered when there are more free radicals produced in the body than the body can neutralize with antioxidants. However, small levels of free radicals can be beneficial: When the body undergoes stress -- which happens during fasting -- small levels of oxidative stress can trigger protective pathways, Guo said.

“The hypothesis is that if the body is intermittently exposed to low levels of oxidative stress, it can build a better response to it,” Wegman said.

The researchers found that the intermittent fasting decreased insulin levels in the participants, which means the diet could have an anti-diabetic effect as well.

The group recruited 24 study participants in the double-blinded, randomized clinical trial. During a three-week period, the participants alternated one day of eating 25 percent of their daily caloric intake with one day of eating 175 percent of their daily caloric intake. For the average man’s diet, a male participant would have eaten 650 calories on the fasting days and 4,550 calories on the feasting days. To test antioxidant supplements, the participants repeated the diet but also included vitamin C and vitamin E.

At the end of the three weeks, the researchers tested the same health parameters. They found that the beneficial sirtuin proteins such as SIRT 3 and another, SIRT1, tended to increase as a result of the diet. However, when antioxidants were supplemented on top of the diet, some of these increases disappeared. This is in line with some research that indicates flooding the system with supplemental antioxidants may counteract the effects of fasting or exercise, said Christiaan Leeuwenburgh, Ph.D., co-author of the paper and chief of the division of biology of aging in the department of aging and geriatric research.

“You need some pain, some inflammation, some oxidative stress for some regeneration or repair,” Leeuwenburgh said. “These young investigators were intrigued by the question of whether some antioxidants could blunt the healthy effects of normal fasting.”

On the study participants’ fasting days, they ate foods such as roast beef and gravy, mashed potatoes, Oreo cookies and orange sherbet -- but they ate only one meal. On the feasting days, the participants ate bagels with cream cheese, oatmeal sweetened with honey and raisins, turkey sandwiches, apple sauce, spaghetti with chicken, yogurt and soda -- and lemon pound cake, Snickers bars and vanilla ice cream.

“Most of the participants found that fasting was easier than the feasting day, which was a little bit surprising to me,” Guo said. “On the feasting days, we had some trouble giving them enough calories.”

Leeuwenburgh said future studies should examine a larger cohort of participants and should include studying a larger number of genes in the participants as well as examining muscle and fat tissue.



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The above story is based on materials provided by University of Florida. Note: Materials may be edited for content and length.


Journal Reference:
Martin P Wegman, Michael Guo, Douglas M Bennion, Meena N Shankar, Stephen M Chrzanowski, Leslie A Goldberg, Jinze Xu, Tiffany A Williams, Xiaomin Lu, Stephen I Hsu, Stephen D Anton, Christiaan Leeuwenburgh, Mark L Brantly.Practicality of Intermittent Fasting in Humans and its Effect on Oxidative Stress and Genes Related to Aging and Metabolism. Rejuvenation Research, 2014; 141229080855001 DOI: 10.1089/rej.2014.1624

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Interventional radiology treatment relieves chronic plantar fasciitis

Interventional radiology treatment relieves chronic plantar fasciitis

Patients suffering from chronic plantar fasciitis now have a new weapon against this debilitating foot ailment, according to research presented at the Society of Interventional Radiology's Annual Scientific Meeting. Researchers utilized ultrasound imaging and specific ultrasonic energy to penetrate, emulsify and remove diseased fasciitis tissue. Permanently removing damaged, pain-generating tissue allowed room for healthy tissue to regrow in its place, restoring normal function.

"Plantar fasciitis is so ubiquitous and such a difficult condition to live with, and yet patients have been limited in their treatment options," said Rahul Razdan, M.D., one of the study's researchers and an interventional radiologist at Advanced Medical Imaging in Lincoln, Neb. "While standard treatments, such as pain medication and physical therapy, can offer some relief, there have been no permanent answers. Consequently, safe and effective definitive treatments are highly desirable," he noted.

In the study, 100 patients were treated, beginning in August 2013. The patients presented with chronic, refractory plantar fasciopathy, and all patients had previously failed to respond to medications, activity modification and arch supports. Before treatment, patients reported how their foot pain affected their ability to manage everyday life through the Foot and Ankle Disability Index (FADI). FADI scores were collected from the patients at two weeks, six weeks and six months post treatment.

Two weeks after treatment, greater than 90 percent of patients reported improvement in symptoms, and these improvements were maintained at six months. Patients also reported being highly satisfied with the treatment and had no treatment-related complications.

"It is important for patients suffering from chronic plantar fasciitis to know that they have treatment options," added Razdan. "We have patients who are in so much pain they can't even play with their kids or take their dog for a walk. This ultrasonic treatment can give patients their lives back and let them enjoy their lives. We are excited to see significant results from this treatment," he said.

Chronic plantar fasciitis is the most common debilitating foot complaint, affecting approximately 10 percent of the population and accounting for more than 1 million office visits annually, said Razdan.

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Robust evidence that chronic fatigue syndrome is a biological illness

Researchers at the Center for Infection and Immunity at Columbia University's Mailman School of Public Health identified distinct immune changes in patients diagnosed with chronic fatigue syndrome, known medically as myalgic encephalomyelitis (ME/CFS) or systemic exertion intolerance disease. The findings could help improve diagnosis and identify treatment options for the disabling disorder, in which symptoms range from extreme fatigue and difficulty concentrating to headaches and muscle pain.

These immune signatures represent the first robust physical evidence that ME/CFS is a biological illness as opposed to a psychological disorder, and the first evidence that the disease has distinct stages. Results appear online in the new American Association for the Advancement of Science journal, Science Advances.

With funding to support studies of immune and infectious mechanisms of disease from the Chronic Fatigue Initiative of the Hutchins Family Foundation, the researchers used immunoassay testing methods to determine the levels of 51 immune biomarkers in blood plasma samples collected through two multicenter studies that represented a total of 298 ME/CFS patients and 348 healthy controls. They found specific patterns in patients who had the disease three years or less that were not present in controls or in patients who had the disease for more than three years. Short duration patients had increased amounts of many different types of immune molecules called cytokines. The association was unusually strong with a cytokine called interferon gamma that has been linked to the fatigue that follows many viral infections, including Epstein-Barr virus (the cause of infectious mononucleosis). Cytokine levels were not explained by symptom severity.

"We now have evidence confirming what millions of people with this disease already know, that ME/CFS isn't psychological," states lead author Mady Hornig, MD, director of translational research at the Center for Infection and Immunity and associate professor of Epidemiology at Columbia's Mailman School. "Our results should accelerate the process of establishing the diagnosis after individuals first fall ill as well as discovery of new treatment strategies focusing on these early blood markers."

There are already human monoclonal antibodies on the market that can dampen levels of a cytokine called interleukin-17A that is among those the study shows were elevated in early-stage patients. Before any drugs can be tested in a clinical trial, Dr. Hornig and colleagues hope to replicate the current, cross-sectional results in a longitudinal study that follows patients for a year to see how cytokine levels, including interleukin-17A, differ within individual patients over time, depending on how long they have had the disease.

Stuck in High Gear

The study supports the idea that ME/CFS may reflect an infectious "hit-and-run" event. Patients often report getting sick, sometimes from something as common as infectious mononucleosis (Epstein-Barr virus), and never fully recover. The new research suggests that these infections throw a wrench in the immune system's ability to quiet itself after the acute infection, to return to a homeostatic balance; the immune response becomes like a car stuck in high gear. "It appears that ME/CFS patients are flush with cytokines until around the three-year mark, at which point the immune system shows evidence of exhaustion and cytokine levels drop," says Dr. Hornig. "Early diagnosis may provide unique opportunities for treatment that likely differ from those that would be appropriate in later phases of the illness."

The investigators went to great lengths to carefully screen participants to make sure they had the disease. The researchers also recruited greater numbers of patients whose diagnosis was of relatively recent onset. Patients' stress levels were standardized; before each blood draw, patients were asked to complete standardized paperwork, in part to engender fatigue. The scientists also controlled for factors known to affect the immune system, including the time of day, season and geographic location where the samples were taken, as well as age, sex and ethnicity/race.

In 2012, W. Ian Lipkin, MD, director of the Center for Infection and Immunity, and colleagues reported the results of a multicenter study that definitively ruled out two viruses thought to be implicated in ME/CFS: XMRV (xenotropic murine leukemia virus [MLV]-related virus) and murine retrovirus-like sequences (designated pMLV: polytropic MLV). In the coming weeks, Drs. Hornig and Lipkin expect to report the results of a second study of cerebrospinal fluid from ME/CFS patients. In separate ongoing studies, they are looking for "molecular footprints" of the specific agents behind the disease -- be they viral, bacterial, or fungal -- as well as the longitudinal look at how plasma cytokine patterns change within ME/CFS patients and controls across a one-year period, as noted above.

"This study delivers what has eluded us for so long: unequivocal evidence of immunological dysfunction in ME/CFS and diagnostic biomarkers for disease," says Dr. Lipkin, senior author of the current study and the John Snow Professor of Epidemiology at Columbia's Mailman School. "The question we are trying to address in a parallel microbiome project is what triggers this dysfunction."

Co-authors include Andrew F. Schultz, Xiaoyu Che, and Meredith L. Eddy at the Center for Infection and Immunity; Jose G. Montoya at Stanford University; Anthony L. Komaroff at Harvard Medical School; Nancy G. Klimas at Nova Southeastern University; Susan Levine at Levine Clinic; Donna Felsenstein at Massachusetts General Hospital; Lucinda Bateman at Fatigue Consultation Clinic; and Daniel L. Peterson and Gunnar Gottschalk at Sierra Internal Medicine. The authors report no competing interests.

Support for the study was provided by the Chronic Fatigue Initiative of the Hutchins Family Foundation and the National Institutes of Health (AI057158; Northeast Biodefense Center-Lipkin).

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The above story is based on materials provided by Columbia University's Mailman School of Public Health. Note: Materials may be edited for content and length.


Journal Reference:
Mady Hornig, José G. Montoya, Nancy G. Klimas, Susan Levine, Donna Felsenstein, Lucinda Bateman, Daniel L. Peterson, C. Gunnar Gottschalk, Andrew F. Schultz, Xiaoyu Che, Meredith L. Eddy, Anthony L. Komaroff, W. Ian Lipkin.Distinct plasma immune signatures in ME/CFS are present early in the course of illness. Science Advances, 2015 DOI: 10.1126/sciadv.1400121

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