Placenta on toast? Could we derive benefits from ingesting afterbirth?

Almost all non-human mammals eat placenta for good reasons. Are we missing something? A paper by neuroscientists at the University at Buffalo and Buffalo State College suggests that ingestion of components of afterbirth or placenta -- placentophagia -- may offer benefits to human mothers and perhaps to non-mothers and males. 

They say this possibility does not warrant the wholesale ingestion of afterbirth, for some very good reasons, but that it deserves further study. 

Mark Kristal, PhD, professor of psychology and neuroscience at UB, directs the graduate program in behavioral neuroscience, and has studied placentophagia for more than 40 years. He is recognized as a principle expert in the field. 

Kristal's article "Placentophagia in Human and Nonhuman Mammals: Causes and Consequences," will be published in the March 30 issue of the journal Ecology of Food and Nutrition, which will be devoted to the subject of placentophagia. 

Kristal's co-authors are Jean M. DiPirro, PhD, associate professor, Department of Psychology, Buffalo State College, and Alexis C. Thompson, PhD, research associate professor, UB Department of Psychology and a research scientist in the UB Research Institute on Addictions. 

They point out that the benefits of placenta ingestion (as well as the ingestion of amniotic fluid) by non-human mammalian mothers are significant. It provokes an increase in mother-infant interaction, for instance, and increases the effects of pregnancy-mediated analgesia in the delivering mother. It also potentiates opioid circuits in the maternal brain that facilitate the onset of caretaking behavior, and suppresses postpartum pseudopregnancy, thereby increasing the possibilities for fertilization. 

"Human childbirth is fraught with additional problems for which there are no practical nonhuman animal models," says Kristal, citing postpartum depression, failure to bond and maternal hostility toward the infant. 

He says ingested afterbirth may contain components that ameliorate these problems, but although there have been many anecdotal claims made for human placentophagia, the issue has not been tested empirically. 

"If such studies are undertaken," he says, "the results, if positive, will be medically relevant. If the results are negative, speculations and recommendations will persist, as it is not possible to prove the negative." 

Kristal says there is a current fad of ingesting encapsulated placenta, which mirrors unverified reports in the 1960s and 1970s of people in back-to-nature communes cooking and eating human placentas. The upsurge in recent anecdotal reports of the benefits of taking placenta by new mothers, irrespective of dose, method of preparation, or time course, suggests more of a placebo effect than a medicinal effect. 

"People will do anything," Kristal says, "but we shouldn't read too much significance into reports of such exceptions, even if they are accurate, because they are neither reliable nor valid studies. My own studies found no evidence of the routine practice of placentophagia in other cultures, findings supported by a recent extensive study by anthropologists at the University of Nevada, Las Vegas. 

"The more challenging anthropological question is," he says, "'Why don't humans engage in placentophagia as a biological imperative as so many other mammals apparently do?' because we clearly do not do this as a matter of course today and apparently never have. Perhaps for humans, there is a greater adaptive advantage to not eating the placenta." The paper discusses some possibilities in this regard. 

"Whether or not we learn why humans do not do this, it is important for us to search for the medicinal or behavioral benefits of components of afterbirth for the same reasons that we search for plant-based medicinal substances," Kristal says. 

"The outcome of such a quest need not be an exhortation for women to eat afterbirth, but for scientists to isolate and identify the molecule or molecules that produce the beneficial effect and use it to design pharmacological tools," he says. 

He adds, "In the case of Placental Opioid-Enhancing Factor or POEF and enhanced opioid-mediated analgesia, for instance, we have determined through earlier studies that not only is the effect nonspecific in regard to species, but it is also nonspecific in regard to sex. 

"That means that although males, who in all probability do not make the molecule, have the ability to respond to it," Kristal says. 

Source: University at Buffalo [March 27, 2012]

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How the smell of food affects how much you eat

Bite size depends on the familiarly and texture of food. Smaller bite sizes are taken for foods which need more chewing and smaller bite sizes are often linked to a sensation of feeling fuller sooner. New research published in BioMed Central's open access journal Flavour, launched today, shows that strong aromas lead to smaller bite sizes and suggests that aroma may be used as a means to control portion size. 

The aroma experience of food is linked to its constituents and texture, but also to bite size. Smaller bites sizes are linked towards a lower flavour release which may explain why we take smaller bites of unfamiliar or disliked foods. In order to separate the effect of aroma on bite size from other food-related sensations researchers from the Netherlands developed a system where a custard-like dessert was eaten while different scents were simultaneously presented directly to the participants nose. 

The results showed that the stronger the smell the smaller the bite. Dr Rene A de Wijk, who led the study, explained, "Our human test subjects were able to control how much dessert was fed to them by pushing a button. Bite size was associated with the aroma presented for that bite and also for subsequent bites (especially for the second to last bite). Perhaps, in keeping with the idea that smaller bites are associated with lower flavour sensations from the food and that, there is an unconscious feedback loop using bite size to regulate the amount of flavour experienced." 

This study suggests that manipulating the odour of food could result in a 5-10% decrease in intake per bite. Combining aroma control with portion control could fool the body into thinking it was full with a smaller amount of food and aid weight loss. 

BioMed Central's open access journal Flavour, launched today is a peer-reviewed, open access, online journal that publishes interdisciplinary articles on flavour, its generation, perception, and influence on behaviour and nutrition. Flavour aims to understand the psychophysical, psychological and chemical aspects of flavour, which include not only taste and aroma, but also chemesthesis, texture, and all the senses. 

Source: BioMed Central [March 20, 2012]

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How a Single Gene Mutation Leads to Uncontrolled Obesity

Researchers at Georgetown University Medical Center have revealed how a mutation in a single gene is responsible for the inability of neurons to effectively pass along appetite suppressing signals from the body to the right place in the brain. What results is obesity caused by a voracious appetite. 

Their study, published March 18th on Nature Medicine's website, suggests there might be a way to stimulate expression of that gene to treat obesity caused by uncontrolled eating. 

The research team specifically found that a mutation in the brain-derived neurotrophic factor (Bdnf) gene in mice does not allow brain neurons to effectively pass leptin and insulin chemical signals through the brain. In humans, these hormones, which are released in the body after a person eats, are designed to "tell" the body to stop eating. But if the signals fail to reach correct locations in the hypothalamus, the area in the brain that signals satiety, eating continues. 

"This is the first time protein synthesis in dendrites, tree-like extensions of neurons, has been found to be critical for control of weight," says the study's senior investigator, Baoji Xu, Ph.D., an associate professor of pharmacology and physiology at Georgetown. 

"This discovery may open up novel strategies to help the brain control body weight," he says. 

Xu has long investigated the Bdnf gene. He has found that the gene produces a growth factor that controls communication between neurons. 

For example, he has shown that during development, BDNF is important to the formation and maturation of synapses, the structures that permit neurons to send chemical signals between them. The Bdnf gene generates one short transcript and one long transcript. He discovered that when the long-form Bdnf transcript is absent, the growth factor BDNF is only synthesized in the cell body of a neuron but not in its dendrites. The neuron then produces too many immature synapses, resulting in deficits in learning and memory in mice. 

Xu also found that the mice with the same Bdnf mutation grew to be severely obese. 

Other researchers began to look at the Bdnf gene in humans, and large-scale genome-wide association studies showed Bdnf gene variants are, in fact, linked to obesity. 

But, until this study, no one has been able to describe exactly how BDNF controls body weight. 

Xu's data shows that both leptin and insulin stimulate synthesis of BDNF in neuronal dendrites in order to move their chemical message from one neuron to another through synapses. The intent is to keep the leptin and insulin chemical signals moving along the neuronal highway to the correct brain locations, where the hormones will turn on a program that suppresses appetite. 

"If there is a problem with the Bdnf gene, neurons can't talk to each other, and the leptin and insulin signals are ineffective, and appetite is not modified," Xu says. 

Now that scientists know that BDNF regulates the movement of leptin and insulin signals through brain neurons, the question is whether a faulty transmission line can be repaired. 

One possible strategy would be to produce additional long-form Bdnf transcript using adeno-associated virus-based gene therapy, Xu says. But although this kind of gene therapy has proven to be safe, it is difficult to deliver across the brain blood barrier, he adds. 

"The better approach might be to find a drug that can stimulate Bdnf expression in the hypothalamus," Xu says. "We have opened the door to both new avenues in basic research and clinical therapies, which is very exciting." 

Source: Georgetown University Medical Center [March 18, 2012]

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Nanoparticles in Food, Vitamins Could Harm Human Health, Researchers Warn

Billions of engineered nanoparticles in foods and pharmaceuticals are ingested by humans daily, and new Cornell research warns they may be more harmful to health than previously thought. 

An intestinal cell monolayer after exposure to nanoparticles, shown in green [Credit: Cornell University]

A research collaboration led by Michael Shuler, the Samuel B. Eckert Professor of Chemical Engineering and the James and Marsha McCormick Chair of Biomedical Engineering, studied how large doses of polystyrene nanoparticles -- a common, FDA-approved material found in substances from food additives to vitamins -- affected how well chickens absorbed iron, an essential nutrient, into their cells. 

The results were reported online Feb. 12 in the journal Nature Nanotechnology. 

According to the study, high-intensity, short-term exposure to the particles initially blocked iron absorption, whereas longer-term exposure caused intestinal cell structures to change, allowing for a compensating uptick in iron absorption. 

The researchers tested both acute and chronic nanoparticle exposure using human gut cells in petri dishes as well as live chickens and reported matching results. They chose chickens because these animals absorb iron into their bodies similarly to humans, and they are also similarly sensitive to micronutrient deficiencies, explained Gretchen Mahler, Ph.D. '08, the paper's first author and former Cornell graduate student and postdoctoral associate. 

The researchers used commercially available, 50-nanometer polystyrene carboxylated particles that are generally considered safe for human consumption. They found that following acute exposure, a few minutes to a few hours after consumption, both the absorption of iron in the in vitro cells and the chickens decreased. 

But following exposure of 2 milligrams per kilogram for two weeks -- a slower, more chronic intake -- the structure of the intestinal villi began to change and increase in surface area. This was an effective physiological remodeling that led to increased iron absorption. 

"This was a physiological response that was unexpected," Mahler said. 

Shuler noted that in some sense this intestinal villi remodeling was positive because it shows the body adapts to challenges. But it serves to underscore how such particles, which have been widely studied and considered safe, cause barely detectable changes that could lead to, for example, over-absorption of other, harmful compounds. 

Human exposure to nanoparticles is only increasing, Shuler continued. 

"Nanoparticles are entering our environment in many different ways," Shuler said. "We have some assurance that at a gross level they are not harmful, but there may be more subtle effects that we need to worry about." 

The paper included Cornell co-authors Mandy Esch, a research associate in biomedical engineering; Elad Tako, a research associate at the Robert W. Holley Center for Agriculture and Health; Teresa Southard, assistant professor of biomedical sciences; Shivaun Archer, senior lecturer in biomedical engineering; and Raymond Glahn, senior scientist with the USDA Agricultural Research Service and courtesy associate professor in the Department of Food Science. The work was supported by the National Science Foundation; New York State Office of Science, Technology and Academic Research; Army Corp of Engineers; and U.S. Department of Agriculture. 

Author: Anne Ju | Source: Cornell University [February 16, 2012]

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Stressed kids more likely to become obese

The more ongoing stress children are exposed to, the greater the odds they will become obese by adolescence, reports Cornell environmental psychologist Gary Evans in the journal Pediatrics (129:1). 

Nine-year-old children who were chronically exposed to such stressors as poverty, crowded housing and family turmoil gain more weight and were significantly heavier by age 13 than they would have been otherwise, the study found. The reason, Evans and his co-authors suggest, is that ongoing stress makes it tougher for children to control their behavior and emotions -- or self-regulate. That, in turn, can lead to obesity by their teen years. 

"These children are heavier, and they gain weight faster as they grow up. A very good predictor of adults' ability to follow healthy habits is their ability to self-regulate. It seems reasonable that the origins of that are probably in childhood. This [research] is starting to lay that out," said Evans, the Elizabeth Lee Vincent Professor of Human Ecology in the Departments of Design and Environmental Analysis and of Human Development in Cornell's College of Human Ecology. 

Evans conducted the study with former students Thomas Fuller-Rowell, Ph.D. '10, now a Robert Wood Johnson postdoctoral fellow at the University of Wisconsin-Madison, and Stacey Doan, Ph.D. '10, an assistant professor of psychology at Boston University. 

The researchers measured the height and weight of 244 9-year-olds in rural New York state and calculated their various physical and psycho-social stressors -- for example, exposure to violence, living in a substandard house or having no access to such resources as books. They also measured the children's ability to delay gratification by offering them a choice between waiting for a large plate of candy versus having a medium plate immediately. The researchers measured the children's height and weight again four years later. 

While the study doesn't prove that a child's inability to delay gratification causes her to gain weight, there's strong evidence to suggest that it does, Evans said. First, previous studies have shown that chronic stress is linked to weight gain in children and teenagers, and that children eat more sugary, fatty foods when stressed. 

Second, there's a plausible neurocognitive mechanism that may help better understand this behavior, Evans said. "There's some evidence that parts of the brain that are vulnerable and sensitive to stress, particularly early in life, are some of the same parts involved in this self-regulatory behavior." 

The study has implications for education policies such as No Child Left Behind that emphasize testing cognitive abilities but ignore children's ability to control their behavior and emotions, Evans said. 

"A child's ability to self-regulate is not just predictive of things like whether you're going to have trouble with weight -- it predicts grades, graduating from high school. A 4-year-old's ability to self-regulate even predicts SAT scores. This is a very powerful phenomenon," he said. 

The findings also have implications for interventions and policies aimed at reducing individual stressors. "If it's the cumulative impact of stress on these families that is important, that means an intervention that only looks at one stressor -- say, just drug abuse, which is how most interventions are designed -- is doomed to fail," Evans concluded. 

Author: Susan Kelley | Source: Cornell University [January 21, 2012]

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Understanding how bacteria come back from the dead

Salmonella remains a serious cause of food poisoning in the UK and throughout the EU, in part due to its ability to thrive and quickly adapt to the different environments in which it can grow. New research involving a team of IFR scientists, funded by BBSRC, has taken the first detailed look at what Salmonella does when it enters a new environment, which could provide clues to finding new ways of reducing transmission through the food chain and preventing human illness. 

Bacteria can multiply rapidly, potentially doubling every 20 minutes in ideal conditions. However, this exponential growth phase is preceded by a period known as lag phase, where no increase in cell number is seen. Lag phase was first described in the 19th Century, and was assumed to be needed by bacteria to prepare to exploit new environmental conditions. Beyond this, surprisingly little was known about lag phase, other than bacteria are metabolically active in this period. But exactly what are bacteria doing physiologically during this period? 

To fill in this knowledge gap researchers at IFR, along with colleagues at Campden BRI, a membership-based organisation carrying out research and development for the food and drinks industry, have developed a simple and robust system for studying the biology of Salmonella during lag phase. In this system, lag phase lasts about two hours, but the cells sense their new environment remarkably quickly, and within four minutes switch on a specific set of genes, including some that control the uptake of specific nutrients. 

For example, one nutrient accumulated is phosphate which is needed for many cellular processes, and a gene encoding a phosphate transporter was the most upregulated gene during the first four minutes of lag phase. The cellular uptake mechanisms for iron were also activated during lag phase, and are needed for key aspects of bacterial metabolism. This increase in iron leads to a short term sensitivity to oxidative damage. Manganese and calcium are also accumulated in lag phase, but are lost from the cell during exponential growth. 

This new understanding of Salmonella metabolism during lag phase show how rapidly Salmonella senses favourable conditions and builds up the materials needed for growth. This study was carried out by two BBSRC-CASE studentships, which were partially funded by Campden BRI. 

Future research to work out the regulatory mechanisms behind these processes and the switch from lag phase to exponential growth will tell us more about how Salmonella can flourish in different environments, and could point to new ways of controlling its transmission in the food chain.  

Source: Norwich BioScience Institutes [February 02, 2012]

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'Genetic programming': The mathematics of taste

The design of aromas — the flavors of packaged food and drink and the scents of cleaning products, toiletries and other household items — is a multibillion-dollar business. The big flavor companies spend tens of millions of dollars every year on research and development, including a lot of consumer testing. 

[Graphic: Christine Daniloff]

But making sense of taste-test results is difficult. Subjects’ preferences can vary so widely that no clear consensus may emerge. Collecting enough data about each subject would allow flavor companies to filter out some of the inconsistencies, but after about 40 flavor samples, subjects tend to suffer “smell fatigue,” and their discriminations become unreliable. So companies are stuck making decisions on the basis of too little data, much of it contradictory. 

One of the biggest flavor companies in the world has turned to researchers in MIT’s Computer Science and Artificial Intelligence Laboratory (CSAIL) for help. To analyze taste-test results, the CSAIL researchers are using genetic programming, in which mathematical models compete with each other to fit the available data and then cross-pollinate to produce models that are more accurate still. 

The Swiss flavor company Givaudan asked CSAIL principal research scientist Una-May O’Reilly, postdoc Kalyan Veeramachaneni and the University of Antwerp’s Ekaterina Vladislavleva to help interpret the results of tests in which 69 subjects evaluated 36 different combinations of seven basic flavors, assigning each a score according to its olfactory appeal. 

For each subject, O’Reilly and her colleagues randomly generate mathematical functions that predict scores according to the concentrations of different flavors. Each function is assessed according to two criteria: accuracy and simplicity. A function that, for example, predicts a subject’s preferences fairly accurately using a single factor — say, concentration of butter — could prove more useful than one that yields a slightly more accurate prediction but requires a complicated mathematical manipulation of all seven variables. 

After all the functions have been assessed, those that provide poor predictions are winnowed out. Elements of the survivors are randomly recombined to produce a new generation of functions; those are then evaluated for accuracy and simplicity. The whole process is repeated about 30 times, until it converges on a set of functions that accord well with the preferences of a single subject.  

Because O’Reilly and her colleagues’ method produces profiles of individual test subjects’ tastes, it can sort them into distinct groups. It could be, for instance, that test subjects tend to have strong preferences for either cinnamon or nutmeg but not both. By marketing one product to cinnamon lovers and another to nutmeg lovers, a company could do much better than by marketing one product to both. “For every one of these 36 flavors, someone hated it and someone liked it,” O’Reilly says. “If you try to identify a flavor that the whole panel likes, you end up settling for a little bit less.” 

O’Reilly and her colleagues haven’t had an opportunity to empirically determine whether their models correctly predict subjects’ responses to new flavors. So to try to establish their model’s accuracy, they instead built another model. First, they developed a set of mathematical functions that represent subjects’ true taste preferences. Then they showed that, given the limitations of particular test designs, their algorithms could still divine those preferences. Although they developed the model purely to validate their approach, O’Reilly says, flavor researchers were intrigued by the possibility of using it to develop more accurate and efficient test protocols. 

“People have been playing with these [evolutionary] techniques for decades,” says Lee Spector, a professor of computer science at Hampshire College and editor-in-chief of the journal Genetic Programming and Evolvable Machines, where the MIT researchers’ latest paper appears. “One of the reasons that they haven’t made a big splash until recently is that people haven’t really figured out, I think, where they can pay off big.” Taste preference, Spector says, “is a pretty brilliant area in which to apply the evolutionary methods — and it looks as though they’re working, also, so that’s exciting.” 

Author: Larry Hardesty | Source: Massachusetts Institute of Technology [January 24, 2012]

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Dried Licorice Root Fights the Bacteria That Cause Tooth Decay and Gum Disease

Scientists are reporting identification of two substances in licorice -- used extensively in Chinese traditional medicine -- that kill the major bacteria responsible for tooth decay and gum disease, the leading causes of tooth loss in children and adults. In a study in ACS' Journal of Natural Products, they say that these substances could have a role in treating and preventing tooth decay and gum disease. 

Stefan Gafner and colleagues explain that the dried root of the licorice plant is a common treatment in Chinese traditional medicine, especially as a way to enhance the activity of other herbal ingredients or as a flavoring. Despite the popularity of licorice candy in the U.S., licorice root has been replaced in domestic candy with anise oil, which has a similar flavor. 

Traditional medical practitioners use dried licorice root to treat various ailments, such as respiratory and digestive problems, but few modern scientific studies address whether licorice really works. (Consumers should check with their health care provider before taking licorice root because it can have undesirable effects and interactions with prescription drugs.) To test whether the sweet root could combat the bacteria that cause gum disease and cavities, the researchers took a closer look at various substances in licorice. 

They found that two of the licorice compounds, licoricidin and licorisoflavan A, were the most effective antibacterial substances. These substances killed two of the major bacteria responsible for dental cavities and two of the bacteria that promote gum disease. One of the compounds -- licoricidin -- also killed a third gum disease bacterium. The researchers say that these substances could treat or even prevent oral infections. 

Source: American Chemical Society [January 04, 2012]

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New Gene That Regulates Body Weight Discovered

Abraham Kovoor was studying a brain protein, called RGS9-2, that he had previously related to the involuntary, random and repetitive body movements that are side effects of drugs used to treat Parkinson's disease and schizophrenia. 

While studying these side effects, which are called dyskinesia, Kovoor, an assistant professor in the University of Rhode Island's College of Pharmacy, discovered that RGS9-2 also plays a role in regulating body weight. 

Results of his study were published in the November issue of PLoS One, an open-access, peer-reviewed scientific and medical research journal. 

Kovoor and his collaborators found that humans with a gene variation that could reduce RGS9-2 levels had a significantly higher body mass index. 

Similarly, when they examined a strain of mice in which the RGS9-2 gene was deleted, so that these mice do not make RGS9-2 protein, they found that these weighed more than the wild-type strain and the percentage of body fat was much greater. Conversely, when RGS9-2 protein is over-expressed in rats, they found that the rats lost weight. 

Because RGS9-2 is normally expressed in the brain's striatum, a section of the brain involved in both motor control and reward responses, Kovoor and his fellow researchers thought that the weight gain could be a result of an increased reward response triggered during eating. 

"You would expect more eating from the mice without RGS9-2 (because they were the ones that gained weight), but that was not the case," Kovoor said. "Studies with humans, rats and mice implicate RGS9-2 as a factor in regulating body weight. But we had to look at another factor other than feeding behavior." 

"Our research shows that the striatum, through RGS9-2, has a role in regulating body weight that is independent of the motivation, movement and reward responses," Kovoor said. "We have identified a new gene that likely regulates weight gain through metabolism." 

Surprised by the discovery, Kovoor said he and his team have been studying RGS9-2 and its role in the movement side effects of drug therapy for Parkinson's disease and schizophrenia for almost a decade. 

In fact, a company he established, Kovogen LLC, now based in Mystic, Conn., is developing methods for predicting which individuals are more likely to get these irreversible and debilitating side effects so that drug treatment can be optimized and tailored for individual patients. 

"When you see Michael J. Fox continuously weaving and shaking, his movements are actually dyskinesia, a reaction to the medication used to treat his Parkinson's. Many people mistakenly assume that the shaking is a result of his Parkinson's disease, but the disease itself causes rigidity. Anti-psychotic drugs, which are used to treat schizophrenia, also cause similar involuntary movements that are irreversible. 

"When we began looking at RGS9-2, nobody had an inkling as to why these drugs cause dyskinesias. We showed very early on that RGS9-2 modulates the function of the dopamine receptors, and dopamine receptors are the major targets of Parkinson's and anti-psychotic drugs," Kovoor said. 

"We treated RGS9-2 knockout mice (those without the RGS9-2 gene) with anti-psychotic drugs or with L-DOPA, a drug used to treat Parkinson's disease, and the mice all rapidly developed dyskinetic movement disorders when being treated. 

"RSG9-2 provided a springboard for investigating how drugs produce these disorders," Kovoor said. 

In fact, prompted by Kovoor's discovery, one of his collaborators, Stephen Gold, and his colleagues at the University of Texas, were able to show that gene therapy with RGS9-2 could suppress drug-induced dyskinesias in monkeys. 

"Separately, we were looking to see if we could predict the risk susceptibility for these (movement) disorders by searching for variations in the RGS9-2 gene in humans." 

Kovoor and his fellow researchers at the University of California in San Francisco also monitored the body mass index of patients in their study. "We noticed that study subjects with a variation in the RGS9-2 gene, which could weaken expression of the gene, had a higher body mass index." 

Parallel experiments in mice and rats confirmed these findings implicating RGS9-2 in weight regulation. 

Source: University of Rhode Island [January 04, 2012]

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When overeating, calories, not protein, contribute to increase in body fat

In a study conducted among 25 healthy individuals living in a controlled setting who were randomized to overconsumption of different levels of protein diets, those consuming the low-protein diet had less weight gain compared to those consuming normal and high protein diets, and calories alone, and not protein appeared to contribute to an increase in body fat, according to a study in the January 4 issue of JAMA. The researchers also found that protein did contribute to changes in energy expenditure and lean body mass. 

"Obesity has become a major public health concern with more than 60 percent of adults in the United States categorized as overweight and more than 30 percent as obese," according to background information in the article. The role of diet composition in response to overeating and energy dissipation is unclear. 

George A. Bray, M.D., of the Pennington Biomedical Research Center, Baton Rouge, La., and colleagues conducted a study to determine whether the level of dietary protein differentially affected body composition, weight gain, or energy expenditure under tightly controlled conditions. The randomized controlled trial included 25 U.S. healthy, weight-stable male and female volunteers, ages 18 to 35 years, with a body mass index between 19 and 30. The first participant was admitted to the inpatient metabolic unit in June 2005 and the last in October 2007. After consuming a weight-stabilizing diet for 13 to 25 days, participants were randomized to receive diets containing 5 percent of energy from protein (low protein), 15 percent (normal protein), or 25 percent (high protein), which they were overfed during the last 8 weeks of their 10- to 12-week stay in the inpatient metabolic unit. Compared with energy intake during the weight stabilization period, the protein diets provided approximately 40 percent more energy intake, which corresponds to 954 calories a day. 

All participants in the study gained weight and there were no differences by sex. The rate of weight gain in the low protein diet group was significantly less than in the other 2 groups (6.97 lbs. [3.16 kg] vs. 13.3 lbs [6.05 kg] for the normal protein diet group and 14.4 lbs [6.51 kg] in the high protein diet group). 

"Body fat increased similarly in all 3 protein diet groups and represented 50 percent to more than 90 percent of the excess stored calories. Resting energy expenditure, total energy expenditure, and body protein did not increase during overfeeding with the low protein diet," the authors write. 

Lean body mass (body protein) decreased during the overeating period by 1.5 lbs. (0.70 kg) in the low protein diet group compared with a gain of 6.3 lbs. (2.87 kg) in the normal protein diet group and 7 lbs. (3.18 kg) in the high protein diet group. Resting energy expenditure (normal protein diet: 160 calories/day; high protein diet: 227 calories/day) increased significantly with the normal and high protein diets. 

"In summary, weight gain when eating a low protein diet (5 percent of energy from protein) was blunted compared with weight gain when eating a normal protein diet (15 percent of energy from protein) with the same number of extra calories. Calories alone, however, contributed to the increase in body fat. In contrast, protein contributed to the changes in energy expenditure and lean body mass, but not to the increase in body fat," the researchers write. 

"The key finding of this study is that calories are more important than protein while consuming excess amounts of energy with respect to increases in body fat." 

Source: JAMA and Archives Journals [January 03, 2012]

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Exercise cuts bowel cancer risk

Researchers at the University of Western Australia (UWA) and the Western Australian Institute for Medical Research (WAIMR) have found people who engage in vigorous physical activity may be protected against types of colorectal cancer. 

The study, published in the Cancer Causes Control journal, used a Western Australian cohort.  

Researchers examined 870 participants who had bowel cancer and a control group of 996 who did not have the disease. 

Study participants were asked to answer questions about their recreational physical activity, lifestyle, diet, medication and occupation. 

UWA PhD student Terry Boyle, also supported by the Lions Cancer Institute, says the study confirms previous research that shows the most physically active have a lower risk of bowel cancer than the least active.  

“It also gives us some clues as to what types of activity are the most effective at reducing bowel cancer risk,” Mr Boyle says.  

The study found people who performed regular vigorous physical activity over their lifetime had a 40 per cent reduced risk of cancer of the distal (lower) colon and rectum. 

“These results suggest that vigorous activity like jogging, cycling, swimming, tennis, hockey, netball and football may be the most effective physical activities to lower the risk of bowel cancer,” Mr Boyle says. 

Of the possible mechanisms linking physical activity and colon cancer, there is evidence to suggest that obesity and vitamin D may have a great effect on distal colon cancer than proximal colon cancer. 

While the link between physical activity and colon cancers remains opaque, this study supports the suggestion that lifestyle factors are more strongly tied to distal colon cancer than proximal colon cancer.  

Another finding showed physical activity performed after the age of 51 years, may be more beneficial in reducing the risk of distal colon cancer than physical activity performed earlier in life. 

“This shows that it really is never too late to start being physically active,” Mr Boyle says. 

Author: Gina Ravenscroft | Source: Science Network/Western Australia [December 20, 2011]

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Diet, nutrient levels linked to cognitive ability, brain shrinkage

New research has found that elderly people with higher levels of several vitamins and omega 3 fatty acids in their blood had better performance on mental acuity tests and less of the brain shrinkage typical of Alzheimer's disease – while "junk food" diets produced just the opposite result. 

The study was among the first of its type to specifically measure a wide range of blood nutrient levels instead of basing findings on less precise data such as food questionnaires, and found positive effects of high levels of vitamins B, C, D, E and the healthy oils most commonly found in fish. 

The research was done by scientists from the Oregon Health and Science University in Portland, Ore., and the Linus Pauling Institute at Oregon State University. It was published today in Neurology, the medical journal of the American Academy of Neurology. 

"This approach clearly shows the biological and neurological activity that's associated with actual nutrient levels, both good and bad," said Maret Traber, a principal investigator with the Linus Pauling Institute and co-author on the study. 

"The vitamins and nutrients you get from eating a wide range of fruits, vegetables and fish can be measured in blood biomarkers," Traber said. "I'm a firm believer these nutrients have strong potential to protect your brain and make it work better." 

The study was done with 104 people, at an average age of 87, with no special risk factors for memory or mental acuity. It tested 30 different nutrient biomarkers in their blood, and 42 participants also had MRI scans to measure their brain volume. 

"These findings are based on average people eating average American diets," Traber said. "If anyone right now is considering a New Year's resolution to improve their diet, this would certainly give them another reason to eat more fruits and vegetables." 

Among the findings and observations: 

• The most favorable cognitive outcomes and brain size measurements were associated with two dietary patterns – high levels of marine fatty acids, and high levels of vitamins B, C, D and E. 

• Consistently worse cognitive performance was associated with a higher intake of the type of trans-fats found in baked and fried foods, margarine, fast food and other less-healthy dietary choices. 

• The range of demographic and lifestyle habits examined included age, gender, education, smoking, drinking, blood pressure, body mass index and many others. 

• The use of blood analysis helped to eliminate issues such as people's flawed recollection of what they ate, and personal variability in nutrients absorbed. 

• Much of the variation in mental performance depended on factors such as age or education, but nutrient status accounted for 17 percent of thinking and memory scores and 37 percent of the variation in brain size. 

• Cognitive changes related to different diets may be due both to impacts on brain size and cardiovascular function. 

The epidemiology of Alzheimer's disease has suggested a role for nutrition, the researchers said in their study, but previous research using conventional analysis, and looking in isolation at single nutrients or small groups, have been disappointing. The study of 30 different blood nutrient levels done in this research reflects a wider range of nutrients and adds specificity to the findings. 

The study needs to be confirmed with further research and other variables tested, the scientists said. 

Source: Oregon State University [December 28, 2011]

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New Crop Growth with Ancient Seeds

An increasing number of Americans are paying closer attention to the source of the food they eat, and experts say it's a trend that's growing globally. 

Deputy Director Belle Starr and Executive Director Bill McDorman both from the Native Seeds/SEARCH organization show us various seeds collected from tribes and tell us about their developments such as their Native Seed Library that will launch January 15th, 2012.

Native Seeds/SEARCH, a non-profit in Southern Arizona that encourages the use and protection of local, organic seeds versus industrially produced hybrid seeds and genetically modified seeds. 

Native Seeds Executive Director Bill McDorman says he's noticing a growing interest from consumers who are taking the time to connect the dots between food, health and environment. 

"I think they say overall since 1903 we've lost maybe up to 96 percent of the genetic diversity that forms the foundation for our agriculture," McDorman says. "That means 96 percent of the varieties that were around for farmers to grow aren't around any more." 

Native Seeds, founded nearly 30 years ago, is inaugurating a new program in January, launching the first seed library in Arizona. Deputy Director Belle Starr says it's an opportunity for people to learn more about growing local food, its history and nature. 

Participants are encouraged to write and share information about which plants do best in their areas and bring seeds to the library so that others can try them out. It's a way of propagating knowledge and harvesting the benefits. 

"And this really, really supports and enhances the local genetic diversity, especially neighbourhood by neighbourhood," Starr says. 

The seed library will be at the Native Seeds retail story at 3061 N. Campbell Ave. in Tucson. Native Seeds/SEARCH's offices are at 3584 E. River Road in Tucson and its farm is in Patagonia. 

Author: Tony Paniagua | Source: Arizoa Public Media [December 19, 2011]

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Starving orangutans might help to better understand obesity and eating disorders in humans

Rutgers Evolutionary Anthropologist Erin Vogel thinks new research published today in Biology Letters, a Journal of the Royal Society, examining how endangered Indonesian orangutans – considered a close relative to humans -- survive during times of extreme food scarcity might help scientists better understand eating disorders and obesity in humans. 

Endangered Indonesian orangutans survive during times of extreme food scarcity and starvation [Credit: Erin Vogel]

"There is such a large obesity epidemic today and yet we don't really understand the basis of the obesity condition or how these high-protein or low-protein diets work," said Vogel, whose research, Bornean orangutans on the brink of protein bankruptcy, represents the first time scientists have looked at how these long-haired, orange-colored apes -- that depend on low-protein fruit to survive -- endure protein cycling, or period bouts of protein deprivation. "I think studying the diets of some of our closest living relatives, the great apes; may help us understand issues with our own modern day diets," she said. 

According to Vogel, an assistant professor of anthropology in Department of Anthropology and Center for Human Evolutionary Studies, in the School of Arts and Sciences, the research shows that it is only during high periods of high caloric and protein intake that orangutans put on fat, a scientific fact that is sometimes ignored by those who believe that high protein, low carbohydrate diets are the best way to lose weight. She said it is only when caloric intake is restricted that orangutans use these fat reserves for energy and eventually dip into their protein (muscle) reserves – a condition that is seen with eating disorders like anorexia. 

Orangutans in particular are interesting to study, Vogel said, because they are the only documented species of non-human ape to store fat when food is abundant in the wild and use these fat reserves when preferred fruits become scarce, presumably something done by our early hominin ancestors. 

Vogel and her research team, analyzed samples collected over a five-year period to study the effects of protein recycling, which included examining urinary metabolites and nitrogen stable isotopes – compounds and byproducts in Orangutan urine. What they determined is that these primates are able to endure prolonged protein deficits without starving to death by consuming higher protein leaves and inner bark and obtaining energy from their stored body fat and even muscles for an extended period of time when low-protein fruit is unavailable. 

"We discovered through this research that the daily amount of protein the orangutans take in when fruit is not available is inadequate for humans and one-tenth of the intake of mountain gorillas. But it is sufficient to avert a severe protein deficit," said Vogel. The Bornean orangutan population has fallen drastically in the last 50 years in Indonesia to less than 55,000 and on the island of Sumatra to less than 5,000 due to a massive amount of illegal logging and further clearing of the land to develop palm oil plantations in their now impoverished rainforest habitat. Vogel says that although some palm oil companies argue that clearing partially logged areas of the rainforest for palm oil plantations is not detrimental to the existence of the orangutan because their natural habitat has already been taken away, this research on protein cycling indicates that even areas that have been partially stripped of trees are better for orangutan survival than no forest area at all. 

Source: Rutgers University [December 13, 2011]

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New study puts eco-labels to the test

A new report released today by the University of Victoria ranks eco-labels intended to distinguish seafood produced with less damage to the environment. It is the first study to evaluate how eco-labels for farmed marine fish compare to unlabeled options in the marketplace.

"How Green is Your Eco-label?" is designed to help seafood buyers sort through competing sustainability claims and better identify those labels that result in farming methods with less damage to the ocean. Key findings include:

• "Organic" labels lead the pack, although a few fall noticeably short;

• Many eco-labels are not much better than conventional farmed seafood options when it comes to protecting the ocean environment;

• Scale is a big challenge for eco-labels: For the most part, eco-labels are awarded based on an individual farm's environmental footprint. However, the cumulative environmental effects of many farms can quickly overwhelm the benefits of reductions in impacts by a single farm or small group of certified farms. 

"Our research shows that most eco-labels for farmed marine fish offer no more than a 10 percent improvement over the status quo," said John Volpe, Ph.D., a marine ecologist at the University of Victoria and lead author of the report. "With the exception of a few outstanding examples, one-third of the eco-labels evaluated for these fish utilize standards at the same level or below what we consider to be conventional or average practice in the industry."

Supported by the Pew Environment Group, the study, which was reviewed by several independent experts, uses a well-established quantitative methodology derived from the 2010 Global Aquaculture Performance Index  to determine numerical scores of environmental performance for 20 different eco-labels for farmed marine finfish, such as salmon, cod, turbot, and grouper. These scores were used to rank performance among the various eco-labels. The assessment did not look at eco-labels for freshwater farmed fish, such as tilapia or catfish.

The authors used 10 environmental factors to assess the eco-labels, including antibiotic use, the ecological effect of farmed fish that escape from pens, sustainability of the fish that serve as feed, parasiticide use, and industrial energy needed in aquaculture production.

"Eco-labels can help fish farmers produce and consumers select environmentally preferable seafood, but only if the labels are based on meaningful standards that are enforced," said Chris Mann, director of Pew's Aquaculture Standards Project. "Seafood buyers at the retail or wholesale level should demand that evidence of sustainability be demonstrated, not merely asserted."

The report concludes that government policies and regulations, as well as effective eco-labels, are necessary to limit the environmental impacts of production.

Source: Pew Environment Group [December 07, 2011]

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Vegetables, fruits, grains reduce stroke risk in women

Swedish women who ate an antioxidant-rich diet had fewer strokes regardless of whether they had a previous history of cardiovascular disease, in a study reported in Stroke: Journal of the American Heart Association. 

"Eating antioxidant-rich foods may reduce your risk of stroke by inhibiting oxidative stress and inflammation," said Susanne Rautiainen, M.Sc., the study's first author and Ph.D. student at the Karolinska Institutet in Sweden. "This means people should eat more foods such as fruits and vegetables that contribute to total antioxidant capacity." 

Oxidative stress is an imbalance between the production of cell-damaging free radicals and the body's ability to neutralize them. It leads to inflammation, blood vessel damage and stiffening. 

Antioxidants such as vitamins C and E, carotenoids and flavonoids can inhibit oxidative stress and inflammation by scavenging the free radicals. Antioxidants, especially flavonoids, may also help improve endothelial function and reduce blood clotting, blood pressure and inflammation. 

"In this study, we took into account all the antioxidants present in the diet, including thousands of compounds, in doses obtained from a usual diet," Rautiainen said. Researchers collected dietary data through a food-frequency questionnaire. They used a standard database to determine participants' total antioxidant capacity (TAC), which measures the free radical reducing capacity of all antioxidants in the diet and considers synergistic effects between substances. 

Researchers categorized the women according to their TAC levels — five groups without a history of cardiovascular disease and four with previous cardiovascular disease. 

For women with no history of cardiovascular disease who had the highest TAC, fruits and vegetables contributed about 50 percent of TAC. Other contributors were whole grains (18 percent), tea (16 percent) and chocolate (5 percent). 

The study found: 

• Higher TAC was related to lower stroke rates in women without cardiovascular disease. 

• Women without cardiovascular disease with the highest levels of dietary TAC had a statistically significant 17 percent lower risk of total stroke compared to those in the lowest quintile. 

• Women with history of cardiovascular disease in the highest three quartiles of dietary TAC had a statistically significant 46 percent to 57 percent lower risk of hemorrhagic stroke compared with those in the lowest quartile. 

"Women with a high antioxidant intake may be more health conscious and have the sort of healthy behaviors that may have influenced our results," Rautiainen said. "However, the observed inverse association between dietary TAC and stroke persisted after adjustments for potential confounders related to healthy behavior such as smoking, physical activity and education." 

For the study, researchers used the Swedish Mammography Cohort to identify 31,035 heart disease-free women and 5,680 women with a history of heart disease in two counties. The women were 49-83 years old. 

Researchers tracked the cardiovascular disease-free women an average 11.5 years and the women with cardiovascular disease 9.6 years, from September 1997 through the date of first stroke, death or Dec. 31, 2009, whichever came first. 

Researchers identified 1,322 strokes among cardiovascular disease-free women and 1,007 strokes among women with a history of cardiovascular disease from the Swedish Hospital Discharge Registry. 

"To the best of our knowledge, no study has assessed the relation between dietary TAC and stroke risk in participants with a previous history of cardiovascular disease," Rautiainen said. "Further studies are needed to assess the link between dietary TAC and stroke risk in men and in people in other countries, but we think our results are applicable." 

Source: American Heart Association [December 01, 2011]

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"Just Chill?" Relaxing Can Make You Fatter

Conventional wisdom says that exercise is a key to weight loss — a no-brainer. But now, Tel Aviv University researchers are revealing that life as a couch potato, stretched out in front of the TV, can actually be "active inactivity" — and cause you to pack on the pounds. 

Such inactivity actually encourages the body to create new fat in fat cells, says Prof. Amit Gefen of TAU's Department of Biomedical Engineering. Along with his Ph.D. student Naama Shoham, Prof. Gefen has shown that preadipocyte cells — the precursors to fat cells — turn into fat cells faster and produce even more fat when subject to prolonged periods of "mechanical stretching loads" — the kind of weight we put on our body tissues when we sit or lie down. 

The research, which has been published in the American Journal of Physiology — Cell Physiology, demonstrates another damaging effect of a modern, sedentary lifestyle, Prof. Gefen notes. "Obesity is more than just an imbalance of calories. Cells themselves are also responsive to their mechanical environment. Fat cells produce more triglycerides, and at a faster rate, when exposed to static stretching." 

Stretching the fat 

Prof. Gefen, who investigates chronic wounds that plague bed-ridden or wheelchair-bound patients, notes that muscle atrophy is a common side effect of prolonged inactivity. Studying MRI images of the muscle tissue of patients paralyzed by spinal cord injuries, he noticed that, over time, lines of fat cells were invading major muscles in the body. This spurred an investigation into how mechanical load — the amount of force placed on a particular area occupied by cells — could be encouraging fat tissue to expand. 

In the lab, Prof. Gefen and his fellow researchers stimulated preadipocytes with glucose or insulin to differentiate them into fat cells. Then they placed individual cells in a cell-stretching device, attaching them to a flexible, elastic substrate. The test group of cells were stretched consistently for long periods of time, representing extended periods of sitting or lying down, while a control group of cells was not. 

Tracking the cultures over time, the researchers noted the development of lipid droplets in both the test and control groups of cells. However, after just two weeks of consistent stretching, the test group developed significantly more — and larger — lipid droplets. By the time the cells reached maturity, the cultures that received mechanical stretching had developed fifty percent more fat than the control culture. 

They were, in effect, half-again fatter. 

According to Prof. Gefen, this is the first study that looks at fat cells as they develop, taking into account the impact of sustained mechanical loading on cell differentiation. "There are various ways that cells can sense mechanical loading," he explains, which helps them to measure their environment and triggers various chemical processes. "It appears that long periods of static mechanical loading and stretching, due to the weight of the body when sitting or lying, has an impact on increasing lipid production." 

Counting more than calories 

These findings indicate that we need to take our cells' mechanical environment into account as well as pay attention to calories consumed and burned, believes Prof. Gefen. Although there are extreme cases, such as people confined to wheelchairs or beds due to medical conditions, many of us live a too sedentary lifestyle, spending most of the day behind a desk. Even somebody with healthy diet and exercise habits will be negatively impacted by long periods of inactivity. 

Next, Prof. Gefen and his fellow researchers will be investigating how long a period of time a person can sit or lie down without the mechanical load becoming a factor in fat production. But in the meantime, it certainly can't hurt to get up and take an occasional stroll, he suggests. 

Source: American Friends of Tel Aviv University [December 01, 2011]

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Study shows Mediterranean diet improves sexual health in men

The Mediterranean diet has been in the headlines recently because a new study published on ‘Journal of Sexual Medicine’ shows that the diet is beneficial to help avoid strokes. 

Recognized for its ability to help improve heart health, the Mediterranean Diet also can help kick-start a flagging libido in men with metabolic syndrome. 

While studies show that the Mediterranean Diet can help overcome erectile dysfunction (ED), or impotence in men with metabolic syndrome, the Mediterranean Diet is a healthful diet for men with and without metabolic syndrome, and with or without sexual dysfunction. 

For men with metabolic syndrome, about 400,000 Greek men, the diet helps to overcome erectile dysfunction (ED), or impotence. 

In fact, studies show that many of these men with ED cure their problem after following a Mediterranean-style diet, combined with exercise. 

Source: Greek Reporter [December 01, 2011]

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