Over-the-counter mouthrinses really do put a stop to bad breath.  The first systematic review on the effectiveness of mouthrinses shows that they play an important role in reducing levels of bacteria and chemicals that cause mouth odours.  Pick which one you use though, because some can temporarily stain your tongue and teeth, warns this new review from The Cochrane Library.

Bad breath is a very common complaint affecting around half the population in developed countries.  The smell is generated by bacteria that accumulate on the tongue and produce sulphur compounds including hydrogen sulphide.  This is the same compound that makes rotten eggs smell bad.  To combat this, mouth rinses are classified in two categories, those that kill the bacteria producing the sulphur compounds and those that neutralise or mask the odour of these compounds.  Antibacterial mouthrinses are widely used to treat bad breath, despite some uncertainty about their effectiveness.

“We found that antibacterial mouthrinses, as well as those containing chemicals that neutralise odours, are actually very good at controlling bad breath,’ says lead researcher, Zbys Fedorowicz, who works at the Ministry of Health in Bahrain.

Although the different mouthrinses had similar effects on odours, the researchers point out that products containing chlorhexidine resulted in noticeable but temporary staining of the tongue and teeth, and also can temporarily alter taste sensations.

The review, carried out by a team of Cochrane Researchers, included the results of five separate trials involving 293 participants.  The team found that mouthrinses employing antibacterial agents such as chlorhexidine and cetylpyridinium were significantly more effective than placebos in reducing mouth odours, as judged by human noses.  Mouthrinses containing chlorine dioxide and zinc were more effective in neutralising odour compounds.

Researchers also noted that more studies are needed to compare the effectiveness of different mouthrinses in treating bad breath.  And they say that despite the growing trend for electronic assessment of mouth odours, the human nose should remain the gold standard.

“There’s no substitute for a human nose when it comes to sniffing out bad breath,” says Fedorowicz.

Moderate consumption of red wine may decrease the risk of lung cancer in men, according to a report in the October issue of Cancer Epidemiology, Biomarkers & Prevention¸ a journal of the American Association for Cancer Research.

“An antioxidant component in red wine may be protective of lung cancer, particularly among smokers,” said Chun Chao, Ph.D., a research scientist at Kaiser Permanente Department of Research and Evaluation in Pasadena, California.

Chao analyzed data collected through the California Men’s Health Study, which linked clinical data from California’s health system with self-reported data from 84,170 men aged 45 to 69 years. Researchers obtained demographics and lifestyle data from surveys computed between 2000 and 2003, and identified 210 cases of lung cancer.

Researchers measured the effect of beer, red wine, white wine and liquor consumption on the risk of lung cancer. Adjustments were made for age, race/ethnicity, education, income, body mass index, history of chronic obstructive pulmonary disease or emphysema, and smoking history.

Among the study participants, there was on average a two percent lower lung cancer risk associated with each glass of red wine consumed per month. The most substantial risk reduction was among smokers who drank one to two glasses of red wine per day. The researchers reported a 60 percent reduced lung cancer risk in these men. Researchers warned men to stop smoking as the best way to reduce lung cancer risk; noting that even men who drank one to two glasses of red wine per day still face higher lung cancer risk than do non-smokers.

No clear associations with lung cancer were noted for consumption of white wine, beer, or liquor. “Red wine is known to contain high levels of antioxidants. There is a compound called resveratrol that is very rich in red wine because it is derived from the grape skin. This compound has shown significant health benefits in preclinical studies,” Chao said.

Chao said their findings should not be construed to recommend heavy alcohol consumption.

A fatty acid found in abundance in olive oil and other “healthy” unsaturated fats has yet another benefit: it helps keep the body satisfied to prolong the time between meals.

A new study in the October Cell Metabolism, a publication of Cell Press, reveals that once this type of fat, known as oleic acid, reaches the intestine, it is converted into a lipid hormone (oleoylethanolamide, or OEA) that wards off the next round of hunger pangs.  The researchers said it may be the first description of an ingredient in food that directly provides the raw materials for a hormone’s production.

The findings in rats may yield insight into the precise dietary makeup of fat and protein for optimal hunger control, the researchers said.  (Protein plays in important role in limiting hunger as well, but by different means.)  The newly discovered signaling pathway might also be tapped into with drugs designed to control appetite by supplementing OEA levels or blocking its breakdown.  Similarly, in conditions where people don’t eat enough, the researchers speculate that treatments targeting this system might improve the appetite.

Importantly, diets high in processed foods that are riddled with saturated fats might throw a wrench into this system of metabolic control, the researchers said.

” Eating is one of the most important things animals do,” said Daniele Piomelli of the University of California, Irvine.  “This is just one of many things that control it.  That said, a system like this could be forced to inactivation by inappropriate feeding,” he said, noting that saturated fats generally lack in oleic acid.

While such diets may lead people to overeat, Piomelli said it will also be of interest to see if this mechanism may be defective in some who tend to eat in excess.

Previous studies had shown that feeding stimulates cells in the intestinal lining to produce OEA, which, when administered as a drug, decreases meal frequency by engaging receptors called peroxisome proliferator-activated receptors a (PPARa).

Piomelli’s team now reports that infusion of fat into the small intestine stimulates the release of OEA, whereas infusion of protein or carbohydrate does not.  They also demonstrate that OEA production uses dietary oleic acid and is disrupted in mutant mice lacking the membrane fatty-acid transporter CD36.  Treatments that disrupt CD36 or PPARa undermine the hunger control otherwise driven by fat.

Overall, the results suggest that activation of small-intestinal OEA release, enabled by CD36-mediated uptake of oleic acid from the diet, serves as a molecular sensor linking fat consumption to satiety.  (Piomelli said satiety is perhaps best described as the opposite of hunger.)

” In conclusion,” the researchers wrote, “our studies identify OEA as a key physiological signal that specifically links dietary fat ingestion to across-meal satiety.  Nutritional and pharmacological strategies aimed at magnifying this lipid-sensing mechanism, such as inhibitors of OEA degradation, might be useful in the treatment of obesity and other eating disorders.”

A Brazilian palm berry sweeping the globe as a popular health food though little research has been done on it – now may have its purported benefits better understood.

In the first research involving people, the acai (ah-sigh-EE) berry has proven its ability to be absorbed in the human body when consumed both as juice and pulp.  That finding, by a team of Texas AgriLife Research scientists, was published in a recent issue of the Journal of Agricultural and Food Chemistry.

Showing the berry’s absorption in humans is important because it is known to contain numerous antioxidants.  The berry is heavily marketed in the U.S. as a health food.

The study involved 12 healthy volunteers who consumed a single serving of acai juice or pulp.  Researchers believe the results point to the need for continued research on the berry which is commonly used in juices, beverages, smoothies, frozen treats and dietary supplements.

“Acai is naturally low in sugar, and the flavor is described as a mixture of red wine and chocolate,” said lead investigator Dr. Susanne Talcott, “so what more would you want from a fruit?”

Talcott, who also is assistant professor with the Texas A&M University’s nutrition and food science department, said that previous studies have shown the ability of the human body to absorb target antioxidants (from other produce), but “no one had really tested to see if acai antioxidants are absorbed in humans.”

Sales of acai products have increased dramatically in the U.S. where it has been touted as a metabolism booster, weight reducer and athletic enhancer.  Advertisements use buzzwords such as health, wellness, energy, taste and organic.

About the only buzzword not used with acai is “local.”  The berries are harvested in the Brazilian rainforest from acai palms that may reach heights in excess of 60 feet one of the same palms used to harvest edible hearts of palm.

The fruit is about the size of a large blueberry yet only the outermost layers of the fruit, the pulp surrounding a large internal seed, are edible, Talcott noted.

Talcott and her co-researcher and husband Dr. Steve Talcott began studying the palmberry in 2001.  His first scientific report on acai, apparently the first such study in English, was published in 2004.

Initially, their studies on the berry examined antioxidant and nutritional components in pulp and juice.  Later studies showed the berry’s activity against cancer cells, Talcott noted.

With that background, the researchers then decided to find out whether those elements were actually being absorbed into the human body or being eliminated unused as waste.

“Like vitamin C, the body can only absorb so much at a time,” Steve Talcott explained.

He said the researchers now “need to determine potential disease-fighting health benefits, so we can make intelligent recommendations on how much acai should be consumed.

For the clinical trial, people were given acai pulp and acai juice containing half the concentration of anthocyanins as the pulp and each compared to the control foods: applesauce and a non-antioxidant beverage.

Blood and urine samples at 12 and 24 hours after consumption showed significant increases in antioxidant activity in the blood after both the acai pulp and applesauce consumption, she said.  Both acai pulp and acai juice showed significant absorption of antioxidant anthocyanins into the blood and antioxidant effects.  The research couple said future studies hopefully will help determine whether the consumption of acai will result in any disease-preventing health benefit and the proper serving sizes for a beneficial dose for people.

“Our concern has been that it is sold as a super food – and it definitely has some good attributes – but it is not a solution to all diseases,” she said.  “There are a great number of foods on the market, and this could just be part of a well-balanced diet.”

Chemicals used in the environment to kill bacteria could be making them stronger, according to a paper published in the October issue of the journal Microbiology.  Low levels of these chemicals, called biocides, can make the potentially lethal bacterium Staphylococcus aureus remove toxic chemicals from the cell even more efficiently, potentially making it resistant to being killed by some antibiotics.

Biocides are used in disinfectants and antiseptics to kill microbes.  They are commonly used in cleaning hospitals and home environments, sterilizing medical equipment and decontaminating skin before surgery.  At the correct strength, biocides kill bacteria and other microbes.  However, if lower levels are used the bacteria can survive and become resistant to treatment.

“Bacteria like Staphylococcus aureus make proteins that pump many different toxic chemicals out of the cell to interfere with their antibacterial effects,” said Dr Glenn Kaatz from the Department of Veterans Affairs Medical Center in Detroit, USA.  “These efflux pumps can remove antibiotics from the cell and have been shown to make bacteria resistant to those drugs.  We wanted to find out if exposure to biocides could also make bacteria resistant to being killed by the action of efflux pumps.”

The researchers exposed S. aureus taken from the blood of patients to low concentrations of several biocides and dyes, which are also used frequently in hospitals.  They looked at the effect of exposure on the bacteria and found that mutants that make more efflux pumps than normal were produced.

“We found that exposure to low concentrations of a variety of biocides and dyes resulted in the appearance of resistant mutants,” said Dr Kaatz.  “The number of efflux pumps in the bacteria increased.  Because the efflux pumps can also rid the cell of some antibiotics, pathogenic bacteria with more pumps are a threat to patients as they could be more resistant to treatment.”

If bacteria that live in protected environments are exposed to biocides repeatedly, for example during cleaning, they can build up resistance to disinfectants and antibiotics.  Such bacteria have been shown to contribute to hospital-acquired infections.

“Scientists are trying to develop inhibitors of efflux pumps.  Effective inhibitors would reduce the likelihood of additional resistance mechanisms emerging in bacteria,” said Dr Kaatz.  “Unfortunately, inhibitors evaluated to date do not work on a wide range of pathogens so they are not ideal to prevent resistance.”

“Careful use of antibiotics and the use of biocides that are not known to be recognised by efflux pumps may reduce the frequency at which resistant strains are found,” said Dr Kaatz.  “Alternatively, the combination of a pump inhibitor with an antimicrobial agent or biocide will reduce the emergence of such strains and their clinical impact.”

If the current financial climate has taught us anything, it’s that a system where over-borrowing goes unchecked eventually ends in disaster.  It turns out this rule applies as much to our bodies as it does to economics.  Instead of cash, our body deals in energy borrowed from muscle and given to the brain.

Unlike freewheeling financial markets, the lending process in the body is under strict regulation to ensure that more isn’t lent than can be afforded.  New research by scientists at the Salk Institute for Biological Studies reveals just how this process is implemented.

“We have all seen the sub-prime mortgage crisis,” says Marc Montminy, M.D., Ph.D., a professor in the Clayton Foundation Laboratories for Peptide Biology who led the current study.  “If you take out a loan, sooner or later you’ve got to pay your debt, and the same is true in fasting metabolism.”

The Salk researchers’ findings, which are published ahead of print in the Oct. 5 edition of the journal Nature, may pave the way for novel therapies for sufferers of metabolic diseases in whom such regulation can spiral out of control.

Most tissues in our bodies respond to fasting by switching from their usual high-octane energy source—glucose—to burning a low-octane, cheaper alternative-fat.  For our brains, however, only the high-performance fuel will do.  If no food-derived glucose is available, the body must manufacture its own supply to maintain the brain in the manner to which it is accustomed.  It does so by taking energy from muscle in the form of protein and converting it to glucose in the liver, a process known as gluconeogenesis.  The sugar is then shipped via the bloodstream to the brain to keep it running smoothly.

Gluconeogenesis needs to be turned on rapidly in response to fasting, but shutting it off again is just as crucial.  “You don’t want gluconeogenesis to be prolonged,” says postdoctoral researcher and co-first author Yi Liu, Ph.D. “Because it uses muscle as a protein source, it will eventually lead to muscle wastage.”  Adds Montminy, “The question has always been how is the production of glucose turned on, and how is shut off again?”

Previous work by the Montminy lab and others has shown that two key proteins, CRTC2 and FOXO1, are needed to turn on glucose-making genes during fasting.  CRTC2 is activated by glucagon, a hormone whose levels go up when we stop eating.  FOXO1, on the other hand, is activated when levels of the food-stimulated hormone insulin drop below a certain threshold.  CRTC2’s and FOXO1’s activity needs to be tightly regulated, since producing too much glucose would result in over-borrowing of energy from muscle tissue.

To uncover the mechanism that ensures that this doesn’t happen, the Salk researchers created mice containing the gene for luciferase, a light-emitting enzyme usually found in fireflies, engineered in such a way that it was only turned on when CRTC2 was active.  Using imaging equipment, they could then detect CRTC2 activity in the livers of live mice simply by measuring how much they glowed.

When the mice were fasted, CRTC2 was rapidly activated, and the livers lit up, but to the scientists’ surprise, after six hours the light went out.  Experimentally decreasing the levels of CRTC2 or FOXO1 confirmed there was a two-stage fasting-response.  Lowering CRTC2 reduced gluconeogenesis only early on, while less FOXO1 only affected late glucose production.  As in a relay race, during fasting the baton for glucose production appeared to be passed from CRTC2 in stage one to FOXO1 in stage two.

The crucial switch from CRTC2 to FOXO1 comes in the form of SIRT1, a nutrient sensor that accumulates in the late fasting stage.  Yi discovered that SIRT1 has opposite effects on CRTC2 and FOXO1: it sends the former to the recycling bin, while it activates the latter, and thus the baton is safely transferred from CRTC2 to the FOXO1.

Why does the body want to change between these two regulators of glucose production?  Again, it comes down to body economics.  CRTC2 acts as a rapid response unit to quickly produce high levels of glucose when it detects glucagon.  Switching to FOXO1 later on slows down this production to more sustainable levels, while at the same time helping to produce ketone bodies, an alternative fuel the brain can use that does not require taking protein from muscle.  “It is just like paying your loan back,” says Montminy.  “Later on you produce blood sugar at a different rate than you did at the beginning.”

Knowledge of how this nutrient switch is working may help design new drugs to regulate sugar levels in diabetes patients.  In, particular, chemical activators of the SIRT1 switch may be key.  “This way we could provide control for patients with insulin resistance,” says Montminy, “as typically their blood sugars are elevated after overnight fasting because the switches that regulate the glucose-producing enzymes are too active.”  Perhaps, then, a pharmacological rescue package for patients whose lending systems have been left unregulated may be on the horizon.

Exposure to Bisphenol A (BPA), phthalates and flame retardants (PBDEs) are strongly associated with adverse health effects on humans and laboratory animals.  A special section in the October 2008 issue of Environmental Research, “A Plastic World” provides critical new research on environmental contaminants and adverse reproductive and behavioral effects.

Plastic products contain “endocrine disrupting chemicals” that can block the production of the male sex hormone testosterone (phthalates used in PVC plastic), mimic the action of the sex hormone estrogen (bisphenol A or BPA used in polycarbonate plastic), and interfere with thyroid hormone (brominated flame retardants or PBDEs used in many types of plastic).

Two articles report very similar changes in male reproductive organs in rats and humans related to fetal exposure to phthalates.  Two articles show that fetal exposure to BPA or PBDEs disrupts normal development of the brain and behavior in rats and mice.  Two other articles provide data that these chemicals are massively contaminating the oceans and causing harm to aquatic wildlife.

The other studies integrate new laboratory research with a broader view reflecting exposures to a variety of chemicals in plastic.  These ubiquitous chemicals found in many plastics act independently and together to adversely affect human, animal and environmental health.

The articles show amongst others the massive contamination of the Pacific Ocean with plastic, and the amount of contamination has increased dramatically in recent years; animal brain structure, brain chemistry and behavioral effects from exposure to BPA and “phthalate syndrome” in rats’ male offspring.

“For the first time a series of articles will appear together that identify that billions of kilograms of a number of chemicals used in the manufacture of different types of plastic can leach out of plastic products and cause harm to the brain and reproductive system when exposure occurs during fetal life or prior to weaning,” emphasized Dr. Frederick vom Saal, Guest Editor of the “Plastic World”.

“Not only are these studies of scientific importance, they also contribute to the ongoing US congressional hearings involving the Food and Drug Administration,” remarked Gert-Jan Geraeds, Publisher of Environmental Research, “As such, “The Plastic World” has a broader societal impact and raises awareness of increasingly important environmental issues”.

America does a mediocre job caring for its sickest people.  The nation, says a new report, gets a C.

Palliative care programs make patients facing serious and chronic illness more comfortable by alleviating their pain and symptoms and counseling patients and their families.

Only Vermont, Montana and New Hampshire earned an A, according to America’s Care of Serious Illness: A State-by-State Report Card on Access to Palliative Care in Our Nation’s Hospitals, a report based on a study in the October 2008 issue of the Journal of Palliative Medicine.  Three states – Oklahoma, Alabama and Mississippi – got an F.

“The good news is that hospitals nationwide have implemented palliative care programs quickly over the last six years,” said R. Sean Morrison, MD, director of the non-profit National Palliative Care Research Center and senior author of the study.  “The bad news is that if you live in the South or you have to rely on public or small community hospitals, you’re in trouble.”

Ninety million Americans are living with serious illnesses such as cancer, heart disease, diabetes, Parkinson’s, stroke and Alzheimer’s.  As the baby boomers age, this number will more than double over the next 25 years.

“Americans are living longer – but with serious illnesses,” said Dr. Diane E. Meier, director of the Center to Advance Palliative Care and co-author of the study.  “Without palliative care, people with serious illnesses like cancer often suffer unnecessarily from severe fatigue, pain, shortness of breath, nausea and other symptoms from their disease and treatments.”

The study suggests that in states with more palliative care programs, patients are less likely to die in the hospital; don’t have to go to the intensive care unit as much in the last six months of life; and spend fewer days in intensive care or the coronary unit in the last six months.

That also saves hospitals money, which could help lower health care costs.

When dining at Chinese Buffets, overweight individuals serve themselves and eat differently than normal weight individuals.  This may lead them to overeat, according to a recent study by Cornell University’s Food and Brand Lab.  Compared to normal weight diners, overweight individuals sat 16 feet closer to the buffet, faced the food, used larger plates, ate with forks instead of chopsticks, and served themselves immediately instead of browsing the buffet.

“What’s crazy is that these people are generally unaware of what they’re doing – they’re unaware of sitting closer, facing the food, chewing less, and so on,” say Brian Wanink, lead author of this study and of the book “Mindless Eating: Why We Eat More Than We Think.”

The study was published in the journal Obesity and includes observations of 213 diners at 11 all-you-can-eat Chinese restaurant buffets across the country.  Study participants included a range of normal weight to obese diners, none of whom were Asian.  Major study findings include:

* 27% of normal-weight patrons faced the buffet compared to 42% of obese diners.

* Overweight diners sat an average of 16 feet closer than normal-weight diners.

* 16% of obese diners sat at a booth rather than a table compared to 38% of normal weight diners

* 71% of normal-weight diners browsed the buffet before serving themselves compared to 33% of obese diners

* 24% of normal-weight people used chopsticks compared with 9% of overweight people

“When food is more convenient people tend to eat more,” say coauthor Collin R. Payne, New Mexico State University.

“These seemingly subtle differences in behavior and environment may cause people to overeat without even realizing it.”

An overload of calories throws critical portions of the brain out of whack, reveals a study in the October 3rd issue of the journal Cell, a Cell Press publication.  That response in the brain’s hypothalamus—the “headquarters” for maintaining energy balance—can happen even in the absence of any weight gain, according to the new studies in mice.

The brain response involves a molecular player, called IKKß/NF-?B, which is known to drive metabolic inflammation in other body tissues.  The discovery suggests that treatments designed to block this pathway in the brain might fight the ever-increasing spread of obesity and related diseases, including diabetes and heart disease.

“This pathway is usually present but inactive in the brain,” said Dongsheng Cai of the University of Wisconsin-Madison.  Cai said he isn’t sure exactly why IKKß/NF-?B is there and ready to spring into action in the brain.  He speculates it may have been an important element for innate immunity, the body’s first line of defense against pathogenic invaders, at some time in the distant past.

” In today’s society, this pathway is mobilized by a different environmental challenge—overnutrition,” he said.  Once activated, “the pathway leads to a number of dysfunctions, including resistance to insulin and leptin,” both important metabolic hormones.

Earlier studies showed that overnutrition can spark inflammatory responses in the peripheral metabolic tissues, including the muscles and liver, and therefore cause various metabolic defects in those tissues that underlie type 2 diabetes.  As a result, scientists identified IKKß as a target for an anti-inflammatory therapy that was effective against obesity-associated diabetes.

Yet whether metabolic inflammation and its mediators played a role in the central nervous system remained uncertain.  Now, the researchers show that a chronic high-fat diet doubles the activity of this inflammatory pathway in the brains of mice.  Its activity is also much higher in the brains of mice who are genetically predisposed to obesity, they found.

The researchers report that that increased activity of the IKKß/NF-?B pathway can be divorced from obesity itself -infusions of either glucose or fat into the brains of mice alone led to this inflammatory brain reaction.

Further studies revealed that this activity in the brain leads to insulin and leptin resistance.  Insulin lowers blood sugar by causing cells of the body to take it up from the bloodstream.  Leptin is a fat hormone important for appetite control.

Moreover, the researchers found that treatments preventing the activity of IKKß/NF-?B in the animals’ brains protected them from obesity.

While chronic inflammation is generally considered a consequence of obesity, the new results suggest the inflammatory reaction might also be a cause of the imbalance that leads to obesity and associated diseases, including diabetes.  As Cai says, it appears that inflammation and obesity are “quite intertwined.”  An abundance of calories itself promotes inflammation, while obesity also feeds back to the neurons to further promote inflammation in a kind of vicious cycle.

The findings could lead to treatments that might stop this cycle before it gets started.

“Our work marks an initial attempt to study whether inhibiting an innate immune pathway in the hypothalamus could help to calibrate the set point of nutritional balance and therefore aid in counteracting energy imbalance and diseases induced by overnutrition,” the researchers said.  “We recognize that the significance of this strategy has yet to be realized in clinical practice; currently, most anti-inflammatory therapies have limited direct effects on IKKß/NF-?B and limited capacity to be concentrated in the central nervous system.  Nonetheless, our discoveries offer potential for treating these serious diseases.”

If realized, such a strategy would likely offer a safe approach given that the critical pathway appears to be unnecessary in the hypothalamus under normal circumstances, they noted.

A carefully framed combination of moderate exercise and nutritional supplements could help older people maintain an active lifestyle for longer.

A Manchester Metropolitan University study has found that taking carbohydrate and protein supplements just before and just after low-resistance exercise could boost muscle performance and slow muscle wastage in people over retirement age.

Moreover, this combination appears to deliver greater fitness benefits than undertaking heavy-resistance training with or without changing one’s nutritional habits.

This was the first-ever study of the combination of structured exercise and nutritional supplements to focus wholly on older people.  Undertaken as part of the SPARC (Strategic Promotion of Ageing Research Capacity) initiative, the findings will be discussed at this year’s BA Festival of Science in Liverpool on Thursday 11th September.  SPARC is supported by the Engineering and Physical Sciences Research Council (EPSRC) and the Biotechnology and Biological Sciences Research Council (BBSRC).

This groundbreaking study involved a carefully selected sample of around 60 healthy, independent-living adults aged 65 and over.

The volunteers were randomly divided into groups who underwent different 12 week programmes of physical exercise and nutritional supplementation.  Everyone was then re-assessed at the end of the programme.

Some groups undertook low-resistance exercise once a week; others undertook high-resistance exercise twice a week.  Within each group, some of the volunteers took protein and carbohydrate supplements while others did not.

When all the participants were re-assessed at the end of the 12 week programme, it was observed that muscle size and strength had increased in all groups.

However, the results suggested that older people would derive the most benefits if they took appropriate supplements coupled with low-intensity exercise.

“Maintaining muscle performance and arresting muscle wastage can offer older people real improvements in their quality of life,” says Dr Gladys Pearson, who led the research.  “Though we still need to assess precisely what level of exercise gives the best results, we believe we’ve shown that regular low-resistance exercise complemented by the right nutritional supplements could boost the well-being of the UK’s ageing population.”

Dr Pearson and her team now aim to look at the effectiveness of novel combinations of strength training and nutritional supplementation as a way of speeding recovery and improving mobility for old and young orthopaedic surgery patients.

Individuals who have a genetic mutation associated with high body mass index (BMI) may be able to offset their increased risk for obesity through physical activity, according to a report in the September 8 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.

There is a widely acknowledged genetic component to BMI and obesity, according to background information in the article.  Recently, a strong association has been shown between BMI and variants of one gene, known as the fat mass and obesity associated (FTO) gene.  The mutations associated with obesity are present in about 30 percent of European populations and are associated with a 1.75-kilogram (about 3.9 pounds) increase in body weight.  Lifestyle factors such as diet and physical activity are also important contributors to weight gain, but it is unknown exactly how they interact with genetics.

Evadnie Rampersaud, M.S.P.H., Ph.D., then of the University of Maryland School of Medicine in Baltimore and now of the University of Miami, and colleagues analyzed DNA samples of 704 healthy Amish adults (average age 43.6, 53 percent men and 47 percent women) recruited from 2003 to 2007.  Participants also underwent a series of physiological tests, including a seven-day measurement of physical activity using an instrument known as an accelerometer.

A total of 54 percent of the men and 63.7 percent of the women were overweight, and 10.1 percent of the men and 30.5 percent of the women were obese.  In the genetic analysis, 26 single-nucleotide polymorphisms (SNPs, or changes in a single base letter of DNA) in the FTO gene were associated with BMI.

The researchers then divided participants into two groups based on their physical activity levels and assessed the relationship between BMI and the two strongest SNPs.  Both SNPs were associated with BMI only in individuals who had low physical activity scores for their age and sex; they had no effect on those with above-average physical activity scores.

“Activity levels in the ‘high-activity’ stratum were approximately 900 calories [860 calories for women and 980 calories for men] higher than in the ‘low-activity’ stratum, which, depending on body size, corresponds to about three to four hours of moderately intensive physical activity, such as brisk walking, house cleaning or gardening,” the authors write.

“In conclusion, we have replicated the associations of common SNPs in the FTO gene with increased BMI and risk to obesity in the Old Order Amish,” they conclude.  “Furthermore, we provide quantitative data to show that the weight increase resulting from the presence of these SNPs is much smaller and not statistically significant in subjects who are very physically active.  This finding offers some clues to the mechanism by which FTO influences changes in BMI and may have important implications in targeting personalized lifestyle recommendations to prevent obesity in genetically susceptible individuals.”

Common genetic variations affecting nicotine receptors in the nervous system can significantly increase the chance that European Americans who begin smoking by age 17 will struggle with life-long nicotine addiction.  Published July 11 in the open-access journal PloS Genetics, this research – led by scientists at the University of Utah together with colleagues from the University of Wisconsin – highlights the importance of preventing early exposure to tobacco through public health policies.

These common genetic variations, or single nucleotide polymorphisms (SNPs), are changes in a single unit of DNA.  A haplotype is a set of SNPs that are statistically linked.  The researchers found that one haplotype for the nicotine receptor put European American smokers at a greater risk of heavy nicotine dependence as adults, but only if they began daily smoking before the age of 17.  A second haplotype actually reduced the risk of adult heavy nicotine dependence for people who began smoking in their youth.

The researchers studied 2,827 long-term European American smokers, recruited in Utah and Wisconsin, and to the National Heart, Lung, and Blood Institute’s Lung Health Study.  They assessed the level of nicotine dependence for all smokers, recording the age they began smoking daily, the number of years they smoked, and the average number of cigarettes smoked per day.  DNA samples were taken from all smokers, and the researchers recorded the occurrence of common SNPs, grouped into four haplotypes, which had been identified earlier in a subset of participants.

They found that people who began smoking before the age of 17 and possessed two copies of the high-risk haplotype had from a 1.6-fold to almost 5-fold increase in risk of heavy smoking as an adult.  For people who began smoking at age 17 or older, presence of the high-risk haplotype did not significantly influence their risk of later addiction.

Although the authors caution that different haplotype frequencies would likely be observed in different ethnic populations, Robert Weiss, Ph.D., professor of human genetics at the University of Utah and lead author of the study, explains: “We know that people who begin smoking at a young age are more likely to face severe nicotine dependence later in life.  This finding suggests that genetic influences expressed during adolescence contribute to the risk of lifetime addiction severity produced from the early onset of tobacco use.”

“This study adds to recent advances in understanding how genetic variation can affect susceptibility to nicotine addiction, success or failure of smoking cessation treatments, and the risk of disease associated with tobacco use,” says National Institute on Drug Abuse (NIDA) Director Dr. Nora Volkow.  “As we learn more about how both genes and environment play a role in smoking, we will be able to better tailor both prevention and cessation programs to individuals.”  The study was funded in part by NIDA and the National Heart, Lung, and Blood Institute (NHLBI), parts of the National Institutes of Health (NIH).

Fluoride toothpaste is prohibitively expensive for the world’s poorest people, according to a study published in BioMed Central’s open access journal Globalization and Health. Researchers revealed that the poorest populations of developing countries have the least access to affordable toothpaste.

The team, which includes Ann Goldman of the School of Public Health and Health Services at the George Washington University in Washington D.C., Robert Yee and Christopher Holmgren of the World Health Organization Collaborating Centre at Radboud University Medical Centre in Nijmegen, The Netherlands, and Habib Benzian of the FDI World Dental Federation compared the relative affordability of fluoride toothpaste in 48 countries.

Globalization has led to a worldwide tendency to eat a more westernized diet, which is higher in carbohydrates and refined sugars. This has resulted in an increasing prevalence of tooth decay in developing countries, which can lead to malnutrition and a reduced quality of life. The cost and relative unavailability of dental care in poorer countries means that tooth decay usually remains untreated.

Fluoride toothpaste is the most widely used method of preventing dental decay, but currently only 12.5% of the world benefits from it. The researchers believe that the low-use of fluoride toothpaste is due to its cost, which is too high in some parts of the world. This study is the first to attempt to quantify the affordability of toothpaste across the globe.

Questionnaires regarding the cost of fluoride toothpaste were completed by dental associations, non-government oral health organisations and individuals around the world. The cost of a year’s worth of toothpaste for one person was calculated as both a proportion of household expenditure and in terms of the number of days of work needed to cover the cost.

The results showed that in different income groups in various countries, as the per capita income decreased, the proportion of income needed to purchase a year’s supply of toothpaste increased; the poorest in each country being the hardest hit.

“Because of the importance of fluoride toothpaste in preventing tooth decay, it must be made more available to the world’s poorest populations,” commented Goldman, “steps should be taken to make fluoride toothpaste more affordable and more accessible.” The authors suggest that this can be done by exempting fluoride toothpaste from taxation, encouraging the local manufacture of fluoride toothpaste and persuading multinational manufacturers to implement different pricing policies for poorer countries.

Oral ingestion of pomegranate extract reduces the production of chemicals that cause inflammation suggests a study published in BioMed Central’s open access Journal of Inflammation. The findings indicate that pomegranate extract may provide humans with relief of chronic inflammatory conditions.

The group from the Department of Medicine of Case Western Reserve University, Cleveland Ohio, led by Tariq Haqqi, showed that blood samples collected from rabbits fed pomegranate extract inhibited inflammation.

Pomegranate extract is already used as a treatment in alternative medicine for inflammatory conditions, such as arthritis. Although pomegranate extract has antioxidant and anti-inflammatory actions in experiments on isolated tissues, it is not known whether ingestion of it can produce the same anti-inflammatory effects in living systems, either because the active compounds are not absorbed from the gut or because the levels of these compounds in the blood are not high enough.

Pomegranate extract, the equivalent of 175mls of pomegranate juice, was given to rabbits orally. The levels of antioxidants were measured in blood samples obtained after drinking the pomegranate extract and compared to blood samples collected before ingestion of pomegranate extract.

Plasma collected from rabbits following ingestion of pomegranate extract contained significantly higher levels of antioxidants than samples collected before ingestion of pomegranate extract; the extract also significantly reduced the activity of proteins that cause inflammation, specifically cyclooxygenase-2. It also reduced the production of pro-inflammatory compounds produced by cells isolated from cartilage.

The results of this study indicate the beneficial effects of pomegranate extract when ingested. According to Haqqi “the use of dietary nutrients or drugs based on them as an adjunct in the treatment of chronic inflammatory conditions may benefit patients”. He adds that, “Current treatment with anti-inflammatory drugs can have serious side effects following long-term use. Further research is needed, however, especially on the absorption of orally ingested substances into the blood.”