2012年6月27日 星期三

Viewing Images of High-Calorie Foods Brings On High-Calorie Cravings, Research Finds


Viewing Images of High-Calorie Foods Brings On High-Calorie Cravings, Research Finds

ScienceDaily (June 25, 2012) — You're minding your own business when a food craving suddenly hits, and if you just saw an image of a cupcake, or consumed a sugary soda, that may be no accident.
Researchers at the University of Southern California (USC) will present preliminary findings June 26 at the Endocrine Society's annual meeting demonstrating that viewing pictures of high-fat foods and drinking sweetened beverages while viewing the pictures stimulate appetite and reward centers in the brain.
"Studies have shown that advertisements featuring food make us think of eating, but our research looked at how the brain responds to food cues and how that increases hunger and desire for certain foods," said Kathleen Page, principal investigator and assistant professor of clinical medicine at the Keck School of Medicine of USC. "This stimulation of the brain's reward areas may contribute to overeating and obesity, and has important public health implications."
Page's presentation, "Fructose Compared to Glucose Ingestion Preferentially Activates Brain Reward Regions in Response to High-Calorie Food Cues in Young, Obese Hispanic Females," will be made on June 26, during the Endocrine Society meeting, which takes place from July 23 to 26 in Houston, Texas.
Page and colleagues used functional magnetic resonance imaging (fMRI) to measure the brain responses of 13 obese, Hispanic adolescent women ranging in age from 15 to 25. Women were chosen because prior research indicates they are more responsive to food cues; the study group was narrowed to Hispanic women because of the high risk of obesity and type 2 diabetes in the Hispanic community.
The women's brain responses were scanned twice as they looked at pictures of high-calorie foods, such as hamburgers, cookies, and cakes, and low-calorie foods such as fruits and vegetables. After seeing the high-calorie and low-calorie groupings, the participants rated their hunger and desire for sweet or savory foods on a scale from one to 10.
Halfway through the scans, the women drank 50 grams of glucose -- equivalent to a can of soda -- and another time, they drank 50 grams of fructose. Glucose and fructose are the main components of table sugar and high-fructose corn syrup.
"We hypothesized that the reward areas in the women's brains would be activated when they were looking at high-calorie foods, and that did happen," said Page. "What we didn't expect was that consuming the glucose and fructose would increase their hunger and desire for savory foods."
The researchers also noted that fructose stimulated more hunger and desire in the participants' brains than glucose did.
"Our bodies are made to eat food and store energy, and in prehistoric days, it behooved us to eat a lot of high-calorie foods because we didn't know when the next meal was coming," Page said. "But now we have much more access to food, and this research indicates added sweeteners might be affecting our desire for it."
With many questions unanswered about whether these cravings are environmental (caused by obesity) or genetic, Page plans to study what happens to the brains of obese individuals while they are dieting.
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Hormone, Oxytocin, Shows Potential as Weight-Loss Treatment


Hormone, Oxytocin, Shows Potential as Weight-Loss Treatment

ScienceDaily (June 25, 2012) — A reproductive hormone helps regulate food intake and energy metabolism without causing adverse effects, a new animal study finds. The results were presented June 25 at The Endocrine Society's 94th Annual Meeting in Houston.
Secreted by the brain, the neural hormone, oxytocin, helps initiate contractions of the uterus and breast-milk-producing glands during childbirth and nursing. Prior research by lead author Yuko Maejima, Ph.D., and her co-investigators also linked oxytocin to the process of controlling energy intake and use.
"These findings reveal novel anti-obese and anti-metabolic-syndrome effects of oxytocin," said Maejima, who also is an assistant professor in the physiology department at Jichi Medical University in Shimotsuke, Tochigi, Japan. "Thus, our results provide an avenue for developing an oxytocin-based effective and safe treatment of obesity."
Excess weight is a risk factor for numerous diseases, including diabetes, heart and blood-vessel disease, and cancer, and is a major problem throughout the world. Obesity rates have more than doubled since 1980, according to statistics from the World Health Organization, which indicate that more than 1.4 billion adults are overweight and upwards of 500 million are obese.
In an obese animal model, the investigators found that daily injections of oxytocin reduced the amount of food the animals consumed, as well as decreased their body weight during, and for nine days after, treatment.
Similar results were observed with oxytocin administered by implanted mini pumps. This drug-delivery method also reduced fat in the liver, improved glucose tolerance, and decreased abdominal fat, which is a major risk factor for heart and blood-vessel, or cardiovascular disease. Additionally, the mini pumps decreased the size of fat-storage cells, or adipocytes, but did not adversely affect blood pressure or activity levels.
"The finding that peripheral oxytocin treatment has no effect on the normal blood-pressure levels or the locomotor activity of this mouse model suggests that oxytocin may not influence the cardiovascular system or emotions," Maejima said.
To induce obesity, investigators first fed the animal model a high-fat diet. They then administered oxytocin via injection for 17 days, and through the implantable mini pumps for 13 days.
Funding for this study came from: The Ministry of Education, Culture, Sports, Science and Technology of Japan; The Ichiro Kanehara Foundation; Suzuken Memorial Foundation; Itoe Okamoto scientific award SHISEIKAI; Mochida Memorial Foundation for Medical and Pharmaceutical Research; Japan Society for the Promotion of Science; and Takeda Science Foundation.
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Low Vitamin D Levels Linked to Weight Gain in Some Older Women


Low Vitamin D Levels Linked to Weight Gain in Some Older Women

ScienceDaily (June 25, 2012) — Older women with insufficient levels of vitamin D gained more weight than those with sufficient levels of the vitamin, according to a new study funded by the National Institutes of Health and published online June 25 in the Journal of Women's Health. The study of more than 4,600 women ages 65 and older found that over nearly five years, those with insufficient levels of vitamin D in their blood gained about two pounds more than those with adequate levels of the vitamin.
"This is one of the first studies to show that women with low levels of vitamin D gain more weight, and although it was only two pounds, over time that can add up," said study author Erin LeBlanc, MD, an endocrinologist and researcher at the Kaiser Permanente Center for Health Research in Portland, Ore. "Nearly 80 percent of women in our study had insufficient levels of vitamin D. A primary source of this important vitamin is sunlight, and as modern societies move indoors, continuous vitamin D insufficiency may be contributing to chronic weight gain."
Vitamin D was in the news recently when a panel of primary care experts -- the US Preventive Services Task Force -- said healthy postmenopausal women may need higher doses of the vitamin to prevent fractures, and that there isn't enough evidence to recommend the supplements for younger people. Other expert groups, including the Endocrine Society, have a different take, saying many adults do need vitamin D supplements to keep their bones healthy. 1
"Our study only shows an association between insufficient levels of vitamin D and weight gain, we would need to do more studies before recommending the supplements to keep people from gaining weight," Dr. LeBlanc said. "Since there are so many conflicting recommendations about taking vitamin D for any reason, it's best if patients get advice from their own health care provider."
She points out that this study was conducted among older women who, for the most part, were not trying to lose weight -- though some of them did so as a natural result of aging. About 60 percent of the 4,659 women in the study remained at a stable weight (within 5 percent of their starting weight) over the 4.5-year study period, 27 percent lost more than 5 percent of their body weight, and 12 percent gained more than 5 percent of their body weight.
Most women in the study (78 percent) had less than 30 nanograms per millimeter (ng/ml) of vitamin D in their blood -- the level defined as sufficient by the Endocrine Society panel of experts who set clinical guidelines on vitamin D deficiency (pdf). These women had higher baseline weight to begin with: 148.6 pounds, compared with 141.6 pounds for women whose vitamin D levels were 30 ng/ml or above. Insufficient levels had no association with weight changes in the entire group of women, or in the group that lost weight. But in the group of 571 women who gained weight, those with insufficient vitamin D levels gained more -- 18.5 pounds over five years -- than women who had sufficient vitamin D. The latter group gained 16.4 pounds over the same period.
This study is part of a larger project called the Study of Osteoporotic Fractures that has been ongoing for more than two decades. During 1986-88, SOF enrolled nearly 10,000 women ages 65 and older and tracked their medical history through office and home visits, mailed surveys and telephone calls. The women are from Baltimore, Minneapolis, Portland, Ore. and the Monongahela Valley near Pittsburgh. The SOF study is supported by grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases and the National Institute on Aging.
Authors include Erin S. LeBlanc, MD, MPH, Joanne H. Rizzo, MPA, Kathryn L. Pedula and Teresa A. Hillier, MD, from the Kaiser Permanente Center for Health Research in Portland, Ore.; Kristine E. Ensrud, MD, from the Veterans Affairs Medical Center and Department of Medicine and Division of Epidemiology & Community Health, University of Minnesota in St. Paul; Jane Cauley, MD, Department of Epidemiology, University of Pittsburgh; and Marc Hochberg, MD, from the Department of Medicine, University of Maryland in Baltimore.
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Experimental Drug Helps Diabetes Patients Lose Weight


Experimental Drug Helps Diabetes Patients Lose Weight

ScienceDaily (June 25, 2012) — An experimental drug helped significantly more overweight patients with diabetes shed pounds, compared with placebo, a new study finds. The results were presented June 23 at The Endocrine Society's 94th Annual Meeting in Houston.
"This new medication is promising because of the amount of weight loss it produces, the resultant improvement in important risk factors for diabetes, and, particularly in the lower dose studied, in its tolerability," said study lead author Donna H. Ryan, M.D., professor emeritus at Pennington Biomedical Research Center (LSU System) in Baton Rouge, LA.
Diabetes treatment involves weight management and medications to control blood-sugar levels and risk factors. If left untreated, diabetes can increase the danger of developing heart and blood-vessel diseases. Since one of the main risk factors for all of these diseases is obesity, weight loss is important to both prevention and treatment.
Focusing on type 2 diabetes, investigators found that patients who took the experimental weight-loss drug phentermine/topiramate, combined with diet and exercise modifications, were more likely to lose moderate amounts of weight than those who received a sugar-pill placebo and the diet and exercise intervention.
The percentage of study participants losing more than 10 percent of their initial weight while decreasing their blood pressure and hemoglobin A1c, was:
• 14 percent on low-dose phentermine/topiramate
• 31 percent on high-dose phentermine/topiramate
• 4 percent on placebo
Phentermine/topiramate is a combined medication that works by decreasing appetite. The main side effects associated with the drug were constipation and tingling sensations in the fingers. Patients who took phentermine/topiramate were also more likely to develop low blood sugar than those who received placebo.
This study was an analysis of diabetic patients who enrolled in weight-loss studies testing medications given with lifestyle intervention. Investigators randomly assigned 357 patients with type 2 diabetes to receive either low-dose phentermine/topiramate (7.5 milligrams), high-dose phentermine/topiramate (15 milligrams), or placebo. Neither investigators nor patients knew who was receiving the drug versus placebo in the double-blinded study. Participants' average age was 53 years, 66 percent were female, most were white, and their average weight was 222 pounds. Follow-up was one year.
VIVUS, the company that developed phentermine/topiramate, funded the study.
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'Dessert With Breakfast Diet' Helps Avoid Weight Regain by Reducing Cravings


'Dessert With Breakfast Diet' Helps Avoid Weight Regain by Reducing Cravings

ScienceDaily (June 25, 2012) — Dieters have less hunger and cravings throughout the day and are better able to keep off lost weight if they eat a carbohydrate-rich, protein-packed breakfast that includes dessert. These findings come from a new study that was presented June 25 at The Endocrine Society's 94th Annual Meeting in Houston.
"The goal of a weight loss diet should be not only weight reduction but also reduction of hunger and cravings, thus helping prevent weight regain," said Daniela Jakubowicz, MD, the study's principal investigator.
Jakubowicz, a senior physician at Tel Aviv University's Wolfson Medical Center in Holon, Israel, and her co-authors studied nearly 200 nondiabetic obese adults who were randomly assigned to eat one of two low-calorie diets. Both diets had the same number of daily calories -- about 1,600 for men and 1,400 for women -- but differed mainly in the composition of breakfast.
One group received a low-carbohydrate diet, featuring a 304-calorie breakfast with only 10 grams of carbohydrates, or "carbs." The other group ate a 600-calorie breakfast with 60 grams of carbs, which included a small sweet, such as chocolate, a doughnut, a cookie or cake. Both diets contained protein (such as tuna, egg whites, cheese and low-fat milk) at breakfast, but the "dessert with breakfast diet" had 45 grams of protein, 15 grams more than in the low-carb diet.
Halfway through the eight-month study, participants in both groups lost an average of 33 pounds (15.1 kilograms, or kg) per person, which Jakubowicz said shows that "both diets work the same." However, in the last four months of the study, the low-carb group regained an average of 22 pounds (11.6 kg) per person, while participants who ate the dessert with breakfast diet lost another 15 pounds (6.9 kg) each, the authors reported.
In addition, the study subjects who ate the dessert with breakfast diet reported feeling less hunger and fewer cravings compared with the other group. Subjects' food diaries showed that the dessert with breakfast group had better compliance in sticking to their calorie requirements. Women who ate the dessert with breakfast diet were allowed 500 calories for lunch and about 300 calories for dinner. Men in that group could eat a 600-calorie lunch and up to 464 calories at dinner.
As further evidence supporting the dessert with breakfast diet, the levels of ghrelin, the so-called "hunger hormone," dropped much more after breakfast than in the low-carb group: 45.2 percent versus 29.5 percent, respectively, according to the abstract.
Jakubowicz attributed the better results from the dessert with breakfast diet to meal timing and composition. She said the diet's high protein content reduced hunger; the combination of protein and carbs increased satiety, or feeling full; and the dessert decreased cravings for sweet, starchy and fatty foods. Such cravings often occur when a diet restricts sweets and can result in eating many fattening foods that are not allowed on the diet, she said.
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Ratio of Appetite-Regulating Hormones Marker of Successful Dieters


Ratio of Appetite-Regulating Hormones Marker of Successful Dieters

ScienceDaily (June 25, 2012) — A pre-diet measurement of two hormones related to weight regulation can help predict which dieters will be more likely to maintain their weight loss and who will not, according to a new study. The results were presented June 24 at The Endocrine Society's 94th Annual Meeting in Houston.
With obesity rates in many countries steadily climbing, more people are turning to diets to lose weight. But, for many people, maintaining the weight loss can be extremely difficult, leading to a frustrating cycle of weight loss and gain.
"The current study shows for the first time a clinically useful marker to identify, at an early time, patients who have difficulties in maintaining their body weight," said study author Ana B. Crujeiras , Ph.D., doctor at University Hospital of Santiago de Compostela (CHUS) and Biomedical Network Research Center in Physiopathology of obesity and Nutrition (CIBERobn) in Santiago de Compestela, Spain. "This difficulty is one of the most significant obstacles for obesity therapy, and currently there are no biological markers that effectively demonstrate clinical usefulness in predicting weight-loss regain."
To address this problem, investigators analyzed the role of two hormones related to appetite regulation. Leptin is made by the cells found in fat tissue, and ghrelin is mainly manufactured by cells in the stomach. Previous research by Crujeiras and co-investigators showed that patients who later regained weight had higher leptin and lower ghrelin levels before starting a restricted-calorie diet.
In the current study, investigators found the pre-diet leptin/ghrelin ratio to be two times higher among study participants who later regained weight than among those who did not. Additionally, they identified cut-off points, which predicted more than 60 percent of patients who would later regain 10 percent or more of the weight they initially lost.
"Calculating the leptin/ghrelin ratio prior to the participation in a weight-reduction program might provide the opportunity to individualize weight-loss therapeutic programs according to patients' needs, counteracting the weight-regain rate, and, as a consequence, achieving successful management of obesity," Crujeiras said.
Among women, the leptin/ghrelin ratio identified 70 percent of participants who later regained weight. Among men, the rate was even higher at 95 percent. Women, however, were less likely than men to be incorrectly identified as future weight gainers.
Eighty-eight overweight or obese patients, with a body mass index greater than 25, enrolled in the eight-week study. They were 44 percent female, their average age was 35 years, and all were white.
After an initial fast, participants' blood levels of leptin and ghrelin were measured. They then followed a reduced calorie diet for eight weeks. At the six-month follow-up, 40 dieters had regained the weight they had lost, while the remaining 48 had not. The Biomedical Network Research Centre in Physiopathology of obesity and Nutrition (CIBERobn), Institute of Health Carlos III (ISCIII), Spanish Ministry of Economy and Competitiveness; Galician Research, Development and Technological Innovation plan (INCITE), Galician Ministry for Innovation and Industry; and Special Research about Nutrition, Obesity and Health, University of Navarra funded the study.
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Secondhand Smoke Is Linked to Type 2 Diabetes and Obesity


Secondhand Smoke Is Linked to Type 2 Diabetes and Obesity

ScienceDaily (June 25, 2012) — Adults who are exposed to secondhand smoke have higher rates of obesity and Type 2 diabetes than do nonsmokers without environmental exposure to tobacco smoke, a new study shows. The results were presented June 24 at The Endocrine Society's 94th Annual Meeting in Houston.
"More effort needs to be made to reduce exposure of individuals to secondhand smoke," said study co-author Theodore C. Friedman, MD, PhD, chairman of the Department of Internal Medicine at Charles R. Drew University, Los Angeles.
Studies have shown an association between cigarette smoking and an increased rate of Type 2 diabetes despite the fact that most smokers are leaner than nonsmokers and obesity is a risk factor for Type 2 diabetes. Although some studies have suggested a relationship between Type 2 diabetes and passive, or secondhand, smoking, Friedman said these studies have not verified exposure to secondhand smoke through serum (blood) levels of cotinine. Cotinine is a metabolite of nicotine, and serum cotinine measures a person's exposure to tobacco smoke.
In their current study, Friedman and his fellow researchers used serum cotinine levels to verify passive smoking. They examined data from more than 6,300 adults who participated from 2001 to 2006 in the National Health and Nutrition Examination Survey (NHANES), a nationally representative sample of the U.S. population.
The investigators defined current smokers, which made up 25 percent of the sample, as survey participants who reported that they smoke cigarettes and who had a measured serum cotinine level greater than 3 nanograms per milliliter (ng/mL). Nonsmokers (41 percent of the sample) were those who answered "no" to the question "Do you smoke cigarettes?" and who had a cotinine level below 0.05 ng/mL. Participants who answered "no" to this question but whose cotinine level was above 0.05 ng/mL were defined as secondhand "smokers" (34 percent).
In analyzing these groups, the researchers controlled for age, sex, race, alcohol consumption and physical activity. They found that, compared with nonsmokers, secondhand smokers had a higher measure of insulin resistance, a condition that can lead to Type 2 diabetes; higher levels of fasting blood glucose, or blood sugar; and a higher hemoglobin A1c, a measure of blood sugar control over the past three months.
Secondhand smokers also had a higher rate of Type 2 diabetes, as defined by a hemoglobin A1c greater than 6.5 percent. Secondhand smokers had a similar rate of diabetes to that of current smokers, according to Friedman.
Secondhand smokers also had a higher body mass index (BMI), a measure of body fat, compared with nonsmokers, Friedman reported. Current smokers had a lower BMI than nonsmokers but a higher hemoglobin A1c. When the researchers controlled for BMI, they found that secondhand smokers and current smokers still had a higher hemoglobin A1c than did nonsmokers.
"This finding shows that the association between secondhand smoke and Type 2 diabetes was not due to obesity," Friedman said. "More studies are needed to show whether secondhand smoke is a cause of diabetes."
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Why Do Fat Cells Get Fat? New Suspect Identified


Why Do Fat Cells Get Fat? New Suspect Identified

ScienceDaily (June 25, 2012) — As the world fights obesity at the human level, scientists at the University of Michigan and their colleagues have made a surprising finding at the microscopic level that could help fuel that fight.
Their work helps explain why fat-storing cells get fatter, and burn fat slower, as obesity sets in. If their findings from mice can be shown to apply to humans, they may provide a new target for obesity-fighting drugs.
By studying the tiny signals that fat-storing cells send to one another, the team has shown a crucial and previously unknown role for a molecule called Sfrp5.
The results, which appear online June 25 and will be in the July issue of the Journal of Clinical Investigation, surprised them.
In a series of experiments, the team showed that Sfrp5 influences a signaling pathway known as WNT to stimulate fat cells -- called adipocytes -- to grow larger and to suppress the rate at which fat is burned in the mitochondria inside them.
By stopping cells from making Sfrp5, they were able to make mice that didn't get as fat as quickly because their adipocytes didn't grow large -- even when the mice were fed a high-fat diet. They even showed the impact when transplanting fat from Sfrp5 -- deficient mice into other mice.
The research was performed with National Institutes of Health funding in the U-M Medical School laboratory of Ormond MacDougald, Ph.D., the Faulkner Professor in the Department of Molecular & Integrative Physiology, a professor of internal medicine and a member of U-M's Brehm Center for Diabetes Research.
Working with postdoctoral fellow and first author Hiroyuki Mori, Ph.D., and colleagues, MacDougald says the team built on its previous findings about the importance of WNT signaling in fat cell development.
"WNT signaling plays a crucial role in regulating, and inhibiting, white fat cell growth and the recruitment of new cells to store fat," he explains. "But it appears that in obesity, Sfrp5 can interfere with that signaling, and may create a feedback loop that keeps stimulating production of more of itself."
He notes that the new results contradict previous work published by another group, which found essentially the opposite role for Sfrp5. A commentary accompanying the new U-M paper, by scientists from Denmark, notes the strong evidence behind the new findings and emphasizes the importance of further research on the topic.
MacDougald and his team zeroed in on Sfrp5 after years of studying WNT signaling between adipocytes. They and other teams had already seen that the amounts of Sfrp5 produced within fat tissue were higher in obese animals.
They were able to breed mice that could not make the molecule, and expected to see that these mice resisted obesity because they couldn't convert more cells into adipocytes to store excess fat from their high-fat diet.
But instead, they found that the mice without Sfrp5 did have just as many fat cells as other mice -- but that these cells didn't accumulate fat and grow bigger. As a result, the mice didn't get fat, no matter how rich their diet.
Looking more closely at Sfrp5-deficient mice, they saw a surge of activity in expression of genes related to mitochondria -- the furnaces inside cells that burn fat or other fuel to power cell activity. It was as if the furnaces had been stoked when Sfrp5 wasn't present, so fat could be burned at a higher rate than normal.
"From our results, we believe that Sfrp5 is an important moderator of mitochondrial activity, the first time this has been seen for the WNT signaling pathway in adipocytes," says Mori. "This underscores the complexity of WNT signaling."
In essence, MacDougald says, Sfrp5 poses as a decoy receptor for WNT signals to bind to, keeping them from binding to the receptors on the cell surface that they otherwise would bind to. With WNT signaling reduced, cells store fat and grow larger, and don't burn it as quickly. Then, the cells produce even more Sfrp5, creating the feedback loop that perpetuates the tendency for adipocytes to accumulate lipid.
While pharmaceutical companies are already looking at WNT signaling as a possible target for drugs related to bone formation, the new findings suggest that perhaps the same signaling pathway could be a target for anti-obesity drugs.
But, MacDougald cautions, the findings need to be explored further in both mice and humans. With the obesity epidemic putting hundreds of millions of people at risk of all types of diseases, that research has a special urgency behind it.
In addition to MacDougald and Mori, the research team included Tyler C. Prestwich, who received a Ph.D. from U-M's Cell and Molecular Biology program and is a co-first author, Michael A. Reid, former U-M postdoctoral fellow and Proteostasis Therapeutics employee Kenneth Longo, former postdoctoral fellow Isabelle Gerin, current fellow William Cawthorn, Vedrana S. Susulic, Venkatesh Krishnan, and Andy Greenfield.
The work was supported by grants DK51563 and DK62876 from the NIH's National Institute for Diabetes and Digestive and Kidney Diseases, and by Mori's mentor-based postdoctoral fellowship from the American Diabetes Association. The team used two core research facilities at the U-M Medical School: the Animal Phenotyping Core of the Nutrition Obesity Research Center, supported by NIH grant DK089503, and the Morphology Core of the Michigan Diabetes Research and Training Center, supported by NIH grant P60DK020572.
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Effect of Three Common Diets On Energy Expenditure Following Weight Loss Detailed


Effect of Three Common Diets On Energy Expenditure Following Weight Loss Detailed

ScienceDaily (June 26, 2012) — In an examination of the effect on energy expenditure and components of the metabolic syndrome of 3 types of commonly consumed diets following weight loss, decreases in resting energy expenditure and total energy expenditure were greatest with a low-fat diet, intermediate with a low-glycemic index diet, and least with a very low-carbohydrate diet, suggesting that a low-fat diet may increase the risk for weight regain compared to the other diets, according to preliminary research published in the June 27 issue of JAMA.
"Many people can lose weight for a few months, but most have difficulty maintaining clinically significant weight loss over the long term. According to data from the National Health and Nutrition Examination Survey (1999-2006), only 1 in 6 overweight and obese adults report ever having maintained weight loss of at least 10 percent for 1 year," according to background information in the article. One explanation for the poor long-term outcome is that weight loss elicits biological adaptations -- specifically a decline in energy expenditure and an increase in hunger -- that promote weight. According to the authors, the effect of dietary composition on energy expenditure during weight-loss maintenance has not been studied.
Cara B. Ebbeling, Ph.D., of Children's Hospital Boston, and colleagues conducted a study to evaluate the effects of 3 weight-loss maintenance diets on energy expenditure, hormones, and components of the metabolic syndrome. The study, conducted between June 2006 and June 2010, included 21 overweight and obese young adults. After achieving 10 percent to 15 percent weight loss while consuming a run-in diet, participants consumed an isocaloric low-fat diet (60 percent of energy from carbohydrate, 20 percent from fat, 20 percent from protein; high glycemic load), low-glycemic index diet (40 percent from carbohydrate, 40 percent from fat, and 20 percent from protein; moderate glycemic load), and very low-carbohydrate diet (10 percent from carbohydrate, 60 percent from fat, and 30 percent from protein; low glycemic load) in random order, each for 4 weeks. The primary outcome measured was resting energy expenditure (REE), with secondary outcomes of total energy expenditure (TEE), hormone levels, and metabolic syndrome components.
The researchers found that energy expenditure during weight-loss maintenance differed significantly among the 3 diets. The decrease in REE from pre-weight-loss levels, measured by indirect calorimetry in the fasting state, was greatest for the low-fat diet (average relative to baseline, -205 kcal/d), intermediate with the low-glycemic index diet (-166 kcal/d), and least for the very low-carbohydrate diet (-138 kcal/d). The decrease in TEE also differed significantly by diet (average -423 kcal/d for low fat; -297 kcal/d for low glycemic index; and -97 kcal/d for very low carbohydrate).
"Hormone levels and metabolic syndrome components also varied during weight maintenance by diet (leptin; 24-hour urinary cortisol; indexes of peripheral and hepatic insulin sensitivity; high-density lipoprotein [HDL] cholesterol; non-HDL cholesterol; triglycerides; plasminogen activator inhibitor 1; and C-reactive protein), but no consistent favorable pattern emerged," the authors write.
"The results of our study challenge the notion that a calorie is a calorie from a metabolic perspective," the researchers write. "TEE differed by approximately 300 kcal/d between these 2 diets [very low-carbohydrate vs. low-fat], an effect corresponding with the amount of energy typically expended in 1 hour of moderate-intensity physical activity."
"These findings suggest that a strategy to reduce glycemic load rather than dietary fat may be advantageous for weight-loss maintenance and cardiovascular disease prevention. Ultimately, successful weight-loss maintenance will require behavioral and environmental interventions to facilitate long-term dietary adherence. But such interventions will be most effective if they promote a dietary pattern that ameliorates the adverse biological changes accompanying weight loss," the researchers conclude.
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Dieting? Study Challenges Notion That a Calorie Is Just a Calorie


Dieting? Study Challenges Notion That a Calorie Is Just a Calorie

ScienceDaily (June 26, 2012) — A new study published June 26 in the Journal of American Medical Association challenges the notion that "a calorie is a calorie." The study, led by Cara Ebbeling, PhD, associate director and David Ludwig, MD, director of the New Balance Foundation Obesity Prevention Center Boston Children's Hospital, finds diets that reduce the surge in blood sugar after a meal--either low-glycemic index or very-low carbohydrate-may be preferable to a low-fat diet for those trying to achieve lasting weight loss. Furthermore, the study finds that the low-glycemic index diet had similar metabolic benefits to the very low-carb diet without negative effects of stress and inflammation as seen by participants consuming the very low-carb diet.
Weight re-gain is often attributed to a decline in motivation or adherence to diet and exercise, but biology also plays an important role. After weight loss, the rate at which people burn calories (known as energy expenditure) decreases, reflecting slower metabolism. Lower energy expenditure adds to the difficulty of weight maintenance and helps explain why people tend to re-gain lost weight.
Prior research by Ebbeling and Ludwig has shown the advantages of a low glycemic load diet for weight loss and diabetes prevention, but the effects of these diets during weight loss maintenance has not been well studied. Research shows that only one in six overweight people will maintain even 10 percent of their weight loss long-term.
The study suggests that a low-glycemic load diet is more effective than conventional approaches at burning calories (and keeping energy expenditure) at a higher rate after weight loss. "We've found that, contrary to nutritional dogma, all calories are not created equal," says Ludwig, also director of the Optimal Weight for Life Clinic at Boston Children's Hospital. "Total calories burned plummeted by 300 calories on the low fat diet compared to the low carbohydrate diet, which would equal the number of calories typically burned in an hour of moderate-intensity physical activity," he says.
Each of the study's 21 adult participants (ages 18-40) first had to lose 10 to 15 percent of their body weight, and after weight stabilization, completed all three of the following diets in random order, each for four weeks at a time. The randomized crossover design allowed for rigorous observation of how each diet affected all participants, regardless of the order in which they were consumed:
  • A low-fat diet,which reduces dietary fat and emphasizes whole grain products and a variety of fruits and vegetables, composed of 60 percent of daily calories from carbohydrates, 20 percent from fat and 20 percent from protein.
  • A low-glycemic index diet made up of minimally processed grains, vegetables, healthy fats, legumes and fruits, with 40 percent of daily calories from carbohydrates, 40 percent from fat and 20 percent from protein. Low glycemic index carbohydrates digest slowly, helping to keep blood sugar and hormones stable after the meal.
  • A low-carbohydrate diet, modeled after the Atkins diet, composed of 10 percent of daily calories from carbohydrates, 60 percent from fat and 30 percent from protein.
The study used state-of-the-art methods, such as stable isotopes to measure participants' total energy expenditure, as they followed each diet.
Each of the three diets fell within the normal healthy range of 10 to 35 percent of daily calories from protein. The very low-carbohydrate diet produced the greatest improvements in metabolism, but with an important caveat: This diet increased participants' cortisol levels, which can lead to insulin resistance and cardiovascular disease. The very low carbohydrate diet also raised C-reactive protein levels, which may also increase risk of cardiovascular disease.
Though a low-fat diet is traditionally recommended by the U.S. Government and Heart Association, it caused the greatest decrease in energy expenditure, an unhealthy lipid pattern and insulin resistance.
"In addition to the benefits noted in this study, we believe that low-glycemic-index diets are easier to stick to on a day-to-day basis, compared to low-carb and low-fat diets, which many people find limiting," says Ebbeling. "Unlike low-fat and very- low carbohydrate diets, a low-glycemic-index diet doesn't eliminate entire classes of food, likely making it easier to follow and more sustainable.
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Genetic Variant Is Linked to Obesity and Insulin Resistance


Genetic Variant Is Linked to Obesity and Insulin Resistance

ScienceDaily (June 26, 2012) — A large study in people at risk of diabetes has found a direct association between the presence of a small genetic alteration in a hormone receptor and increased body fat and insulin resistance. The results, presented June 26 at The Endocrine Society's 94th Annual Meeting in Houston, suggest an adverse role for a previously described genetic variant, the BclI polymorphism.
"Our findings support the idea that even small variations in hormone receptor sensitivity can have metabolic implications, such as obesity or diabetes," said co-author Bastiaan Havekes, MD, PhD, of Maastricht University Medical Center, Maastricht, the Netherlands.
"Endocrinologists should not just focus on hormone levels themselves. Taking into account hormone receptor sensitivity could help in better understanding hormone-mediated effects on metabolism," he said.
The inherited BclI polymorphism occurs in the gene encoding for the glucocorticoid receptor, which controls the actions of glucocorticoids, steroid hormones that affect every system in the body. This small variant makes the receptor more sensitive to glucocorticoids, resulting in greater effects with similar hormone levels, Havekes said.
The effects of this change appear to be similar to, although much smaller than, the excessive glucocorticoid exposure that can occur from certain medications or diseases, Havekes said. Such excess exposure can result in weight gain, especially around the abdomen, as well as in disturbed blood sugar metabolism. This exposure most often occurs from long-term use of prednisone or other glucocorticoid medications, which are widely used to treat inflammatory diseases or to suppress the immune system. It also can result from endocrine diseases such as Cushing's syndrome. Cushing's causes overproduction in the body of the glucocorticoid cortisol, often called the "stress hormone."
Patients in this study, however, did not have known excess exposure to glucocorticoids, according to Havekes. He and his co-investigators studied 1,228 adults who participated in one of two Dutch studies focusing on diabetes in the general population. More than half of the study participants had either prediabetes (23 percent) or Type 2 diabetes (33 percent). All subjects underwent genetic testing for the BclI polymorphism.
The researchers found that 519 subjects did not carry the alternative form of the gene, or G-allele, for the BclI polymorphism on either chromosome. Another 540 subjects were heterozygous carriers, meaning the G-allele was present on one of the two chromosomes. The remaining 169 subjects were homozygous carriers and therefore carried the G-allele on both chromosomes.
Those who had the BclI polymorphism on each chromosome had a significantly higher body mass index and larger waist and hip circumferences than did noncarriers or heterozygous carriers, the authors reported. This was reflected by greater insulin resistance, meaning that insulin is less effective at lowering blood glucose (blood sugar).
"Determining an individual's genetic risk profile for metabolic disease is of paramount importance to prevent development of cardiovascular diseases," he said. "Future studies concerning cardiovascular risk profiling should perhaps consider the BclI polymorphism."
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2012年6月9日 星期六

Alcohol consumption and obesity higher in rural Australia, report finds


Alcohol consumption and obesity higher in rural Australia, report finds

  • May 24, 2012
  • Matt Paish
A nationwide study, published today by Roy Morgan Research, has found that people living in rural Australia are more likely to consume alcohol and be overweight and obese.
The Roy Morgan State of the Nation Report 11, which includes a focus on rural Australia, surveyed 10,987 Australians living in cities and 8,049 living in country areas during the 12 months to March 2012.
The survey found that 72.2 per cent of those living in country areas drunk alcohol in an average four week period, compared with 68 per cent of city residents.
Beer, spirits and ready-to-drink products were all more popular in the country, whereas wine and cider were consumed by a higher proportion of city dwellers, according to the survey’s findings.
The survey also found that 31.3 per cent of country residents are deemed an acceptable weight, compared with 37.8 per cent of those in the city. As well as this difference, 35.3 per cent of country residents were found to be overweight compared with 34.8 per cent of those in the city.
Commenting on the findings, Roy Morgan Research’s Norman Morris said, “The State of the Nation report also identified reduced participation in sport and exercise for country residents compared to those in the city, as well as less agreement with healthy eating attitudes, such as thinking about calorie consumption and concern for cholesterol levels.
“The increased prevalence of drinking, and a larger body mass among country residents is concerning given the reduced medical services available in rural areas. Although, as  part of the focus on rural Australia, a Roy Morgan Poll telephone survey on country residents found that only 5 per cent considered health to be the most important issue facing Australia today,” Mr Morris added
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2012年6月8日 星期五

Milk Ingredient Does a Waistline Good


Milk Ingredient Does a Waistline Good

ScienceDaily (June 5, 2012) — A natural ingredient found in milk can protect against obesity even as mice continue to enjoy diets that are high in fat. The researchers who report their findings in the June Cell Metabolism, a Cell Press publication, liken this milk ingredient to a new kind of vitamin.
"This is present in what we've all been eating since day one," says Johan Auwerx of École Polytechnique Fédérale de Lausanne.
The researchers identified this ingredient, known as nicotinamide riboside, as they were searching for alternative ways to boost the well-known gene SIRT1, which comes with benefits for both metabolism and longevity. One way to do that is to target SIRT1 directly, as the red wine ingredient resveratrol appears to do, at least at some doses.
Auwerx's team suspected there might be a simpler way to go about it, by boosting levels of one of SIRT1's molecular sidekicks, the cofactor NAD+.
This milk ingredient does just that in a rather appealing way. Not only is it a natural product, but it also gets trapped within cells, where it can do its magic.
Mice that take nicotinamide riboside in fairly high doses along with their high-fat meals burn more fat and are protected from obesity. They also become better runners thanks to muscles that have greater endurance.
The benefits they observe in mice wouldn't be easy to get from drinking milk alone, Auwerx says. It may be more likely that the compound would serve as a new kind of metabolism-boosting supplement. Tests done in people are now needed to help sort out those details.
On the other hand, he says, this milk substance ultimately offers the same benefits attributed to resveratrol, but in a different way. It's possible that many small effects of ingredients found in our diets could add up to slimmer waistlines -- perhaps longer lives, too.
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Is There a 'Healthy' Obesity Gene?


Is There a 'Healthy' Obesity Gene?

ScienceDaily (May 31, 2012) — Why is it that some obese people are healthier than others? This was one of the main questions Dr. Chaodong Wu of the College of Agriculture and Life Sciences -- Texas A&M University System -- and a group of researchers tried to answer in a recent study.
The study, which will appear in a July issue of the Journal of Biological Chemistry, used genetically modified mice to investigate the genetic aspects of why some obese people do not develop certain medical problems typically associated with obesity, especially Type 2 diabetes.
Wu noted that Xin Guo, a Ph.D. candidate in the college's department of nutrition and food sciences, contributed significantly to the study.
"Previous research had indicated that a regulatory enzyme which is encoded by the gene PFKFB3 protects against diet-induced fat tissue inflammation and systemic insulin resistance," said Wu, who also has a Texas AgriLife Research appointment. "Increasing evidence shows that fat deposition, or amount, is not directly associated with the inflammation or insulin resistance in the development of obesity-related metabolic diseases."
Wu said the inducible 6-phosphorofructo-2-kinase (iPFK2) enzyme links metabolic and inflammatory responses and may underlie what he refers to as "healthy" obesity.
"While many obese people develop Type 2 diabetes, heart conditions and other chronic health problems associated with being significantly overweight, other obese people do not," he said. "And while obesity in general is not healthy, some obese people do not develop the diseases more commonly associated with a less-than-healthy diet. Furthermore, a number of thinner people may have the sort of health problems more typically associated with obesity."
Wu said he and the other researchers theorized that these diseases are associated with the cellular inflammatory response brought on by obesity.
"We also thought this gene could conceivably be targeted for use in the treatment of diabetes, especially Type 2, commonly associated with obesity," he said. "We wanted to find out what might happen to a subject if that particular gene was activated."
Wu and his fellow researchers used laboratory mice to explore the effect of a targeted adipocyte overexpression of the gene/enzyme combination on diet-induced inflammatory responses and insulin sensitivity.
"We were trying to find out what it is in adipose, or fat, tissue that may trigger a negative response that leads to disease -- and how to modulate that response," he said. "In our study, we learned overexpression of the iPFK2 enzyme increases fat deposition, suppresses inflammatory responses and improves insulin sensitivity in both adipose and live tissues."
As an extension of this research, Wu said, it may be possible to identify a pharmacological agent or bioactive agent which may have the desired effect on this gene toward reducing obesity-related cellular inflammatory response.
"We're hoping that, as one of its outcomes, this research will help lead to finding bioactive compounds or some type of supplement that might be taken to help activate this gene toward the promotion of health," he said. "It would also be a good idea to compare and contrast this research with studies done on what constitutes a healthy diet and the effect of such a diet at a cellular level. "
Wu said that would allow for screening bioactive compounds in a healthy diet to determine to what degree these might be applicable for the treatment of disease brought on by unhealthy obesity in an animal model.
"As a further extension, one might study different types of obese people and try to isolate additional specific genes that determine a healthy versus an unhealthy obesity and find a way to modulate the expression of those genes toward disease prevention and health promotion," he said. "Once you find the link between the gene and the obese status of the individual, then you could work with experts in chemical research to produce or replicate whatever pharmacological or bioactive compound is needed to treat unhealthy obesity."
Wu said it is important to determine positively to what degree obesity as a health problem is due to a person's genetic makeup as it relates to their ability to store fat, as well as what type of fat -- saturated or non-saturated -- the individual may store.
"Fat composition is more important than fat deposition, or content," he said. "We know fat cells secrete some of their own bioactive compounds that we may be able to isolate and identify for use in promoting health."
Wu said it will be necessary to discover the role of certain genes in the composition and deposition of fats beyond what has already been identified as being stored in the adipose tissue of mice.
"Then we may be able to produce a dietary supplement or other bioactive compound that would have a positive health effect," he said. "This could be used as a targeted treatment for obesity-related diseases such as Type 2 diabetes in a way that would have limited or minimal side effects."
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