“Work currently underway suggests that an interaction between genetic factors and the composition of the bacteria that inhabit the human gut may predispose certain individuals towards obesity. These results potentially provide insight into the mechanisms by which genetics may predispose some people to obesity. They could also help pave the way towards a future in which genetic screening in conjunction with individually tailored treatments could help people at risk for obesity to maintain a healthy weight,” says Margaret Zupancic, of the Institute for Genome Sciences at the University of Maryland School of Medicine, who presented one of the studies.

Zupancic and her colleagues analyzed the gut bacterial communities of lean and obese individuals belonging to the Old Order Amish of Lancaster County, Pennsylvania — a population relatively homogenous in regard to both genetics and lifestyle. Initially they found no correlation between the composition of the gut bacteria and obesity, but when they factored in the genetic makeup of the participants, certain patterns began to emerge.

One pattern was a statistically significant correlation between whether the participant carried a given variant of the FTO gene (a gene associated with obesity) and the presence of certain bacterial groups in the digestive tract.

The researchers also found that in people with certain genetic variations in taste receptor genes, a low level of bacterial diversity in the gut correlated with a higher likelihood of obesity, while a high level of diversity correlated with a lower likelihood of obesity.

“While this work is still at a relatively early stage, results such as these could lead to applications such as probiotic or antibiotic-based treatments for obesity that could be individualized based on a person’s unique genetic and gut microbial makeup,” says Zupancic.

Another study from the Fred Hutchinson Cancer Research Center analyzed the gut microbes of women between 40 and 45 years of age. The researchers found a positive correlation between the population of one specific type of bacteria, Bacteroidetes, and body fat percentage in the participants.

Not all research presented at the meeting found differences in bacterial populations in the gut and obesity. One study, focusing specifically on children and childhood obesity, failed to identify any significant differences in the gut microbial communities of obese and normal-weight children.

The researchers subsequently analyzed the ability of the microbes to extract and convert dietary energy. They found higher levels of short-chain fatty acids in the feces of obese children.

“This suggests that although obese and normal-weight children have similar gut microbial communities, the gut microbes in obese children are more efficient at converting dietary substrates into energy,” says Amanda Payne of the Institute of Food Health and Nutrition ETH, Zurich, Switzerland.

Short-chain fatty acids are converted into triglycerides and glucose by the liver, a process estimated to provide an additional 10% of dietary energy. The increased production of short-chain fatty acids by gut microbes in obese children could potentially supply more dietary energy, resulting in weight gain.

“While the importance of a balanced diet and regular exercise should not be discounted, our results may help contribute to the development of novel approaches in treating childhood obesity by modulating the composition and activity of the gut microbiota in order to reduce energy extraction from undigested food,” says Payne.

Story Source:
The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Society for Microbiology, via EurekAlert!, a service of AAAS.

The study, which included 5,500 obese pregnant women at Magee-Womens Hospital of UPMC, investigated levels of gestational weight gain related to three adverse outcomes: babies born too small, too large or too early. The women in the study were stratified by level of obesity, or body mass index (BMI), and defined as class 1 (BMI 30 to 34.9), class 2 (BMI 35 to 39.9) and class 3 (BMI 40 and over).

Nearly 10 percent of the study participants lost weight during pregnancy. Weight loss was generally associated with an increased risk of preterm births and infants with restricted growth. For severely obese women, however, very minimal weight gain (less than 5 pounds) or weight loss was not detrimental to newborn health.

The study also found that women who gained a large amount of weight were at increased risk of pre-term births and infants who were overgrown, suggesting that very high weight gain also is related to adverse birth outcomes.

“Some clinicians have been pushing weight restriction for all classes of obese women,” said Lisa M. Bodnar, Ph.D., M.P.H., R.D., lead author of the study and assistant professor of epidemiology, obstetrics and gynecology, University of Pittsburgh. “Our study indicates that a single standard for optimal weight gain for obese women may not fit the bill. Instead, we need to consider level of obesity and advise women accordingly.”

The authors suggest the following pregnancy weight gain ranges to optimize birth outcomes: 20 to 30 pounds for class 1 women; 5 to 20 pounds for class 2 women and less than 10 pounds for class 3 women. Women who gain less than the suggested amounts can still have healthy pregnancies provided their dietary intake is being monitored to ensure proper nutrition, say the authors.

“Obese women may face increased complications of pregnancy,” said Barbara Abrams, Dr.P.H., R.D., senior author of the study and professor of epidemiology, maternal and child health and public health nutrition, University of California, Berkeley. “Appropriate weight gain may lessen these risks for the baby, so we strongly encourage all obese women to receive nutrition and lifestyle counseling throughout their pregnancies.”

In addition to Drs. Bodnar and Abrams, authors of the study include Anna Maria Siega-Riz, Ph.D., R.D., Gillings School of Global Public Health, University of North Carolina, Chapel Hill; Hyagriv N. Simhan, M.D., and Katherine P. Himes, M.D., University of Pittsburgh School of Medicine and Magee-Womens Research Institute.

The research was supported by the National Institutes of Health.

Now, UCLA researchers have found that the same gene allele, which is also carried by roughly one-quarter of U.S. Hispanics, 15 percent of African Americans and 15 percent of Asian Americans, may have another deleterious effect.

Reporting in the early online edition of the journal Proceedings of the National Academy of Sciences, senior study author Paul Thompson, a UCLA professor of neurology; lead authors April Ho and Jason Stein, graduate students in Thompson’s lab; and colleagues found that the FTO variant is also associated with a loss of brain tissue. This puts more than a third of the U.S. population at risk for a variety of diseases, such as Alzheimer’s.

Using magnetic resonance imaging, the researchers generated three-dimensional “maps” of brain volume differences in 206 healthy elderly subjects drawn from 58 sites in the U.S. as part of the Alzheimer’s Disease Neuroimaging Initiative, a large, five-year study aimed at better understanding factors that help the brain resist disease as it ages.

They found that there was consistently less tissue in the brains of those who carry the FTO allele, compared with non-carriers. Individuals with the “bad” version of the FTO gene had an average of 8 percent less tissue in the frontal lobes, the “command center” of the brain, and 12 percent less in the occipital lobes, areas in the back of the brain responsible for vision and perception. Further, the brain differences could not be directly attributed to other obesity-related factors such as cholesterol levels, diabetes or high blood pressure.

Thompson called the findings worrying and mysterious.

“The results are curious. If you have the bad FTO gene, your weight affects your brain adversely in terms of tissue loss,” he said. “If you don’t carry FTO, higher body weight doesn’t translate into brain deficits; in fact, it has nothing to do with it. This is a very mysterious, widespread gene.”

People who carry this specific DNA sequence are heavier on average, and their waist circumference is half an inch bigger.

This is a large percentage of the population, said Thompson, who is also a member of UCLA’s Brain Research Institute and the UCLA Laboratory of Neuro Imaging.

“This is a shocking finding. Any loss of brain tissue puts you at greater risk for functional decline,” he said. “The risk gene divides the world into two camps ― those who have the FTO allele and those who don’t.”

But the news is not necessarily completely negative, Thompson said, because “carriers of the risk gene can exercise and eat healthily to resist both obesity and brain decline.”

Thompson sees both a public health message and a science message in this finding.

“Half of the world carries this dangerous gene. But a healthy lifestyle will counteract the risk of brain loss, whether you carry the gene or not. So it’s vital to boost your brain health by being physically active and eating a balanced diet,” he said.

And from a scientific standpoint, he said, “the gene discovery will help to develop and fine tune the anti-dementia drugs being developed to combat brain aging.”

Funding for the study came from the National Institutes of Health and from private industry.

Hypnosis has long been promoted as a means of helping dieters to avoid feeling hungry or being overwhelmed with cravings. Unfortunately, the basic, “You will no longer desire such-and-such food items” post-hypnotic instruction has produced less than stellar results.

But a new twist on the hypnosis theme has been markedly successful in at least one reported case, in which a British woman was placed in a hypnotic state and taken step-by-step through an imagined surgery in a make-believe OR to fit her with a gastric band, and then told that her stomach was now the size of a golf ball and could only accommodate small portions of food.

Within five months, the woman had lost over 80 pounds, was five dress sizes smaller and most dramatically, completely free of the type two diabetes that had afflicted her. Whether this was a fluke or hypnosis can help people lose weight if the suggestions presented are elaborate and convincing enough, isn’t yet clear, but either way, this underscores the growing sense that the key to a slimmer body is most often the mind.
Could a Photo of Louie Anderson on Your Refrigerator Door be the Answer?

Researchers at the University of British Columbia took some young adults and had them each view a series of slides of stress-inducing visuals. Some of the viewers saw slides of people who were obviously sick — blowing their nose, looking miserable, laid up in bed, etc. — while others did not. Then they all had their blood analyzed.

It turns out that those who saw the sick-person slides had elevated levels of interleukin-6, which the immune system cranks out when it prepares to fight an infection. Their immune systems had geared up to fight illness just from being shown examples thereof.

This is fairly striking, the notion that the body responds defensively to images that it perceives as unhealthy. It raises the question, “Could people trying or hoping to lose weight stimulate their bodies to burn more calories and/or be less hungry just by looking at photos of overweight people?”

Alas, logic leads to the answer, “Probably not.” After all, if that were the case, the overweight wouldn’t need exercise, diet programs or will power, just full-length mirrors.

(By Robert S. Wieder for CalorieLab Calorie Counter News)

Janet Wojcicki, PhD, MPH, UCSF assistant professor of pediatrics, and Melvin Heyman, MD, MPH, professor of pediatrics and chief of pediatric gastroenterology, hepatology and nutrition at UCSF Children’s Hospital, discuss how “Let’s Move” might have the greatest impact on reversing the childhood obesity epidemic in the New England Journal of Medicine. Their perspective piece is available online and will appear in the April 21, 2010, issue of the journal.

When the First Lady introduced “Let’s Move” in February 2010, she outlined the campaign’s central anti-obesity strategies. These include revamping the nutritional labeling of products by the U.S. Department of Agriculture, improving the nutritional standards of school lunches, increasing opportunities for children to engage in physical activity, and improving access to high-quality foods throughout the country.

According to Wojcicki and Heyman, these intervention strategies do have the potential to alter the course of the childhood obesity epidemic to some extent. However, because “Let’s Move” focuses primarily on school-age children — many of whom already are overweight or obese — the program in its current form does not constitute a truly comprehensive obesity intervention plan.

“These types of behavioral and nutrition interventions in schools or within the home have only limited success in preventing weight gain in children,” the authors say. “Obesity prevention must start as early as possible, since school-age children already have an unacceptably high prevalence of obesity and associated medical conditions.”

The authors cite the 2007-2008 National Health and Nutrition Examination Survey, which found that nearly one-third of American children two years and older are overweight or obese, and even higher proportions among low-income children and ethnic minorities.

With those numbers in mind, Wojcicki and Heyman assert that in order to have the greatest impact, “Let’s Move” must include prevention efforts that directly target pregnant women, infants and pre-school-age children.

“Including prevention efforts for these groups will have the longest-term effect on the obesity epidemic in the United States,” they say.

For example, Wojcicki and Heyman recommend that “Let’s Move” incorporate interventions that aim to reduce weight gain and cigarette smoking in mothers-to-be. Studies have shown that excessive weight gain and smoking during pregnancy each are associated with an increased risk for obesity later in life.

The authors also advocate for interventions designed to increase the amount of time infants are breastfed and the amount of sleep babies get, as shorter-than-recommended durations of breastfeeding and suboptimal amounts of sleep also put a child at greater risk for becoming obese. According to Wojcicki and Heyman, these types of interventions are crucial to include in a comprehensive obesity prevention effort, because they affect a child’s lifetime risk of obesity.

“By directly emphasizing the potential risks for lifetime obesity that present in infancy and early childhood and providing the structure and direction for interventions in these areas, the campaign could increase its overall impact on reversing the childhood obesity epidemic,” they conclude.

Wojcicki currently is investigating pre- and post-natal factors that might shape future dietary habits and the development of obesity in a group of Latino families. The children are entering their third year of life, and already Wojcicki and her team of researchers at UCSF have found patterns of eating behavior that may lead to future weight problems. Wojcicki’s research is supported by funding in part from the NIH and from philanthropic support.

Adapted from materials provided by University of California – San Francisco.

“Japanese people need more dietary intake of folate and vitamin B-6, which may lead to the prevention of heart disease,” said Hiroyasu Iso, M.D., professor of public health at Osaka University.

The findings on the value of B vitamins were consistent with studies in Europe and North America, although the dietary consumption of vitamin B-6 is generally lower in Japan than in the United States.

Researchers analyzed data from 23,119 men and 35,611 women (ages 40-79) who completed food frequency questionnaires as part of the large Japan Collaborative Cohort (JACC) Study. During a median 14 years of follow-up, 986 died from stroke, 424 from heart disease and 2,087 from all diseases related to the cardiovascular system.

Investigators divided participants into five groups based on their intake of folate, vitamin B-6 and vitamin B-12. Comparing those with the diets lowest and highest for each nutrient, they found that higher consumption of folate and vitamin B-6 was associated with significantly fewer deaths from heart failure in men, and significantly fewer deaths from stroke, heart disease and total cardiovascular diseases in women. Vitamin B-12 intake was not associated with reduced mortality risk.

The protective effects of folate and vitamin B-6 didn’t change when researchers adjusted for the presence of cardiovascular risk factors, nor when they eliminated supplement users from the analysis. Folate and vitamin B-6 may help guard against cardiovascular disease by lowering homocysteine levels, the investigators said. Homocysteine is an amino acid in the blood that’s affected by diet and heredity. Folic acid and other B vitamins help break down homocysteine in the body.

A direct causal link hasn’t been established, but evidence has shown that too much homocysteine may damage the inner lining of arteries and promote the formation of blood clots.

Sources of folate include vegetables and fruits, whole or enriched grains, fortified cereals, beans and legumes. Sources of vitamin B-6 include vegetables, fish, liver, meats, whole grains and fortified cereals.

Co-authors include: Renzhe Cui, M.D.; Chigusa Date, M.D.; Shogo Kikuchi, M.D.; Akiko Tamakoshi, M.D.; and the JACC study group. Author disclosures and funding sources are on the manuscript.

Source: medicalnewstoday.com

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In a review article in the April 16 edition of Science, nutrition and longevity researchers at Washington University School of Medicine in St. Louis, University College in London and the Andrus Gerontology Center at the University of Southern California, report that calorie restriction influences the same handful of molecular pathways related to aging in all the animals that have been studied.

Aware of the profound influence of calorie restriction on animals, some people have cut their calorie intake by 25 percent or more in hopes of lengthening lifespan. But first author Luigi Fontana, MD, PhD, is less interested in calorie restriction for longer life than in its ability to promote good health throughout life.

“The focus of my research is not really to extend lifespan to 120 or 130 years,” says Fontana, research associate professor of medicine at Washington University and an investigator at the Istituto Superiore di Sanità in Rome, Italy. “Right now, the average lifespan in Western countries is about 80, but there are too many people who are only healthy until about age 50. We want to use the discoveries about calorie restriction and other related genetic or pharmacological interventions to close that 30-year gap between lifespan and ‘healthspan.’ However, by extending healthy lifespan, average lifespan also could increase up to 100 years of age.”

Fontana and his co-authors write about how cutting calorie intake between 10 percent and 50 percent decreases the activity of pathways involving insulin-like growth factor (IGF-1), glucose and TOR (target of rapamycin), and considerably increases lifespan in animals.Genetic mutations involved in those pathways have the same effect. Those animals have far fewer problems with diseases related to aging, such as cancer, cardiovascular disease and cognitive problems.

“About 30 percent of the animals on calorie restriction die at an advanced age without any diseases normally related to aging,” Fontana says. “In contrast, among animals on a standard diet, the great majority (94 percent) develop and die of one or more chronic diseases such as cancer or heart disease. In 30 percent to 50 percent of the animals on calorie restriction, or with genetic mutations in these aging-related pathways, healthspan is equal to lifespan. They eventually die, but they don’t get sick.”

Unfortunately, many humans are moving in the opposite direction. As obesity reaches epidemic rates in Western countries, Fontana says rather than closing the 30-year gap between healthspan and lifespan, the gap is likely to grow. It’s even possible lifespan may decrease as people develop preventable diseases such as atherosclerosis, type 2 diabetes and certain forms of cancer.

Those growing rates of obesity are a reason some scientists think calorie restriction will never catch on, regardless of its potential benefits. But, Fontana says, if researchers who study nutrition and aging can understand how calorie restriction lengthens life and makes people healthier, it may be possible to develop less drastic interventions or medicines that influence pathways affected by calorie restriction and help keep people healthy as they get older.

Among people now practicing calorie restriction, he says side effects include reduced libido because calorie restriction reduces testosterone levels. They also tend to become cold more quickly because their thermal regulation changes as their metabolism slows and their core body temperature drops.

Fontana says as calorie restriction research advances on many fronts, it’s becoming clear that dietary advice once based on epidemiological data now makes sense from a molecular point of view. In the past, dietitians might recommend more fruits and vegetables or less meat and more whole grains. They based that advice on studies showing people who ate more vegetables or fewer animal products tended to have less cardiovascular disease.

“Now we have moved from epidemiology to molecular biology,” he says. “We know that certain nutrients, as well as lower calorie intake, can influence IGF-1 and other pathways. Soon we hope to be able to use that knowledge to help people live longer and healthier lives.

The five-year study in Queensland, which is likely to reflect national trends, found that while snacks and confectionery increased in price by about 31 percent, the price of fruit soared by more than 112 per cent.

Overall, fresh produce and other healthy foods increased in price by 50 per cent between 2000 and 2006, well above the 32.5 per cent inflation rate for food in general.

The research follows a report in the Herald last week, on obesity overtaking tobacco as the leading cause of illness and premature death for the first time, and Australia was unprepared for the huge number of health problems, this will cause.

The head of the school of exercise and nutrition sciences at Deakin University, David Crawford, said there was an urgent need for healthy food to be more available and for the issue to be put on the political agenda.

Professor Crawford said the recommendations of the National Preventative Health Task Force, released last year, were the best effort in 20 years to promote healthy eating and prevent disease.

The taskforce recommended the government consider extra taxation of unhealthy food in Australia, and introduce formal strategies to address price, choice and access to healthy food.

It is reported that individuals who ate a healthy, balanced diet of foods included nuts, fish, poultry, vegetables and were light on red meat, high fat foods, organ meat and butter were the least likely to develop Alzheimer’s disease. Individuals who engaged in a healthy lifestyle were said to have a 38 percent lower risk of developing Alzheimer’s that individuals who ate the foods that were previously mentioned.

“Following this dietary pattern seems to protect from Alzheimer’s disease,” said Dr. Nikolaos Scarmeas, associate professor of neurology at Columbia University Medical Center. “this is an observational study, not a clinical trial.”

Researches were able to control a list of different demographic factors for the study including age, education and ethnicity.
“Everything that increases the risk for heart disease – high cholesterol, obesity, high blood pressure, uncontrolled diabetes – all of these tings also increase the risk for Alzheimer’s,” said Dr. Samuel Gandy, a neurologist and cell bioligist at Mount Sinai School of Medicine.
The reasons for the connections that have been found are not completely clear at this time. Some have speculated that the foods mentioned earlier could impact the health of blood vessels throughout the body, which could in turn improve the health of blood vessels in the brain.

1. Persons who are obese in their youth are subject to a number of long-term health problems later in life, and are more than twice as likely to die before they reach the age of 55. Health experts have felt this to be true based on experience for years, but now a long-term study of 5,000 kids from age 11 onward has nailed it down: the higher your BMI, especially when young, the more probable it is that you will cash in prematurely. In some cases, several decades prematurely.

2. Persons who don’t become overweight until later in life still shorten their healthy lifespan compared to the more thin. A study of 17,000 American adults beginning at around age 50 found that every BMI point they gained thereafter reduced their chance of surviving to age 70 by 12 percent. Other findings: every 2.2 pounds a woman gains after age 18 lowers her chances of living past 70 by 5 percent; women who are already overweight at age 18 and go on to pack on another 22 pounds have just one chance in five of reaching age 70 without serious health problems, the most common being cancer, diabetes and heart disease.

Meanwhile, a recently published British study found that if you have a BMI of 30 to 35, expect to live three years less than the normal weighted, and if it’s over 40, a good 10 years less.

3. An eight-year Wake Forest University study of people over 60 found that those who followed a weight loss program and dropped around 10 pounds were only half as likely to die in that time as those who did not.

4. In a brief update to a recent CalorieLab post noting that obese drivers are statistically less likely to use their seat belts, thus raising their risk of injury from accidents, data analysis of 11,000 front-end crashes by the Medical College of Wisconsin reveals that obese men are much more likely to suffer serious injury to the upper body, especially to the head, spine and thorax.

(By Robert S. Wieder for CalorieLab Calorie Counter News)