Tag: Nutrition

Study shows broad health benefits from periodic use of diet that mimics fasting in mice and yeast — which appear to translate to humans, also. A diagram of the fasting mimicking diet (FMD) protocol developed by the scientists, which retains the health benefits of prolonged fasting. In mice, FMD improved metabolism and cognitive function, decreased bone loss and cancer incidence, and extended longevity. In humans, three monthly cycles of a 5-day FMD reduced multiple risk factors of aging.

Want to lose abdominal fat, get smarter and live longer? New research led by USC’s Valter Longo shows that periodically adopting a diet that mimics the effects of fasting may yield a wide range of health benefits. In a new study, Longo and his colleagues show that cycles of a four-day low-calorie diet that mimics fasting (FMD) cut visceral belly fat and elevated the number of progenitor and stem cells in several organs of old mice — including the brain, where it boosted neural regeneration and improved learning and memory.

The mouse tests were part of a three-tiered study on periodic fasting’s effects — testing yeast, mice and humans — set to be published by Cell Metabolism on June 18. Mice, which have relatively short life spans, provided details about fasting’s lifelong effects. Yeast, which are simpler organisms, allowed Longo to uncover the biological mechanisms that fasting triggers at a cellular level. And a pilot study in humans found evidence that the mouse and yeast studies were applicable to humans.

Bimonthly cycles that lasted four days of an FMD which started at middle age extended life span, reduced the incidence of cancer, boosted the immune system, reduced inflammatory diseases, slowed bone mineral density loss and improved the cognitive abilities of older mice tracked in the study. The total monthly calorie intake was the same for the FMD and control diet groups, indicating that the effects were not the result of an overall dietary restriction.

In a pilot human trial, three cycles of a similar diet given to 19 subjects once a month for five days decreased risk factors and biomarkers for aging, diabetes, cardiovascular disease and cancer with no major adverse side effects, according to Longo. ‘Strict fasting is hard for people to stick to, and it can also be dangerous, so we developed a complex diet that triggers the same effects in the body,’ said Longo, Edna M. Jones professor of biogerontology at the USC Davis School of Gerontology and director of the USC Longevity Institute. Longo has a joint appointment at the USC Dornsife College of Letters, Arts and Sciences. ‘I’ve personally tried both, and the fasting mimicking diet is a lot easier and also a lot safer.’

The diet slashed the individual’s caloric intake down to 34 to 54 percent of normal, with a specific composition of proteins, carbohydrates, fats and micronutrients. It decreased amounts of the hormone IGF-I, which is required during development to grow, but it is a promoter of aging and has been linked to cancer susceptibility. It also increased the amount of the hormone IGFBP-, and reduced biomarkers/risk factors linked to diabetes and cardiovascular disease, including glucose, trunk fat and C-reactive protein without negatively affecting muscle and bone mass.

Longo has previously shown how fasting can help starve out cancer cells while protecting immune and other cells from chemotherapy toxicity. ‘It’s about reprogramming the body so it enters a slower aging mode, but also rejuvenating it through stem cell-based regeneration,’ Longo said. ‘It’s not a typical diet because it isn’t something you need to stay on.’ For 25 days a month, study participants went back to their regular eating habits — good or bad — once they finished the treatment. They were not asked to change their diet and still saw positive changes.

Longo believes that for most normal people, the FMD can be done every three to six months, depending on the abdominal circumference and health status. For obese subjects or those with elevated disease risk factors, the FMD could be recommended by the physician as often as once every two weeks. His group is testing its effect in a randomized clinical trial, which will be completed soon, with more than 70 subjects. ‘If the results remain as positive as the current ones, I believe this FMD will represent the first safe and effective intervention to promote positive changes associated with longevity and health span, which can be recommended by a physician,’ Longo said. ‘We will soon meet with FDA officers to pursue several FDA claims for disease prevention and treatment.

Despite its positive effects, Longo cautioned against water-only fasting and warned even about attempting the fasting mimicking diet without first consulting a doctor and seeking their supervision throughout the process.’Not everyone is healthy enough to fast for five days, and the health consequences can be severe for a few who do it improperly,’ he said. ‘Water-only fasting should only be done in a specialized clinic. Also, certain types of very low calorie diets, and particularly those with high protein content, can increase the incidence of gallstones in women at risk’.

‘In contrast,’ he added, ‘the fasting mimicking diet tested in the trial can be done anywhere under the supervision of a physician and carefully following the guidelines established in the clinical trials.’ Longo also cautioned that diabetic subjects should not undergo either fasting or fasting mimicking diets while receiving insulin, metformin or similar drugs. He also said that subjects with body mass index less than 18 should not undergo the FMD diet. For the study, Longo collaborated with researchers and clinicians from USC as well as from Texas, Italy and England. The study was funded by the National Institute on Aging

http://www.sciencedaily.com/   Science Dail

http://www.sciencedaily.com/releases/2015/06/150618134408.htm  Original web page at Science Daily

Mouse study suggests that emulsifiers alter gut bacteria, leading to the inflammatory bowel condition colitis. Chemicals known as emulsifiers are often added to processed foods such as ice cream. Artificial preservatives used in many processed foods could increase the risk of inflammatory bowel diseases and metabolic disorders, according to research published on 25 February in Nature.

In a study done in mice, chemicals known as emulsifiers were found to alter the make-up of bacteria in the colon — the first time that these additives have been shown to affect health directly. About 15 different emulsifiers are commonly used in processed Western foods for purposes such as smoothing the texture of ice cream and preventing mayonnaise from separating. Regulatory agencies such as the US Food and Drug Administration (FDA) rule that emulsifiers are “generally regarded as safe”, because there is no evidence that they increase the risk of cancer or have toxic effects in mammals. But when immunologist Andrew Gewirtz at Georgia State University in Atlanta and his colleagues fed common emulsifiers carboxymethylcellulose and polysorbate-80 to mice, they found evidence that the chemicals affected the animals’ health. Although their diet was not otherwise changed, healthy mice whose water contained the chemicals became obese and developed metabolic problems such as glucose intolerance. In mice genetically engineered to be prone to inflammatory gut diseases, emulsifiers also seemed to increase the severity and frequency with which the animals developed inflammatory bowel disease.

The most severe health effects were seen in mice that consumed the chemicals at a level similar to a person whose diet consists of only ice cream, says Gewirtz. But the researchers saw effects even at one-tenth of the concentration of emulsifiers that the FDA allows in a food product. To understand why emulsifiers affected the health of mice, researchers analysed bacteria from the animals’ colons. They found less diversity in the microbial species than in healthy mice, and found evidence that the microbes had migrated closer the cells lining the gut. Gewirtz and his colleagues suspect that the emulsifiers can break down the heavy mucus that lines the mammalian gut and prevents bacteria from coming into contact with gut cells. If this happens, the bacteria cause inflammation in the gut, which can also lead to changes in metabolism. Gewirtz says that previous studies may have missed these links because newly developed food additives are tested in large swathes of the population, masking any subtle effects in people whose genetics or gut-microbe composition predispose them to these diseases. For regulators, he says, “the idea that a subset of the population may be sensitive isn’t on the radar.”

This lack of specificity could explain why nutritionists and public-health agencies are constantly revising their dietary guidelines — just this month, for example, an advisory council to the US government recommended eliminating guidelines on cholesterol consumption. “If you look over a 50-year perspective, you would see that the recommendations go back and forth, back and forth,” says immunologist Eran Elinav of the Weizmann Institute of Science in Rehovot, Israel. “No one is lying or cheating, many of these studies are well-designed studies, but they all look at large populations.” Last year, Elinav and computational biologist Eran Segal, a colleague at the Weizmann Institute, found that artificial sweeteners such as saccharin can cause metabolic diseases such as obesity and diabetes by changing the make-up of bacteria in the gut in both mice and humans. They are now compiling a database of genetic and microbiome data from about 1,000 volunteers, measuring their metabolic response to different test foods. They hope that this will eventually allow nutritionists to make specific dietary recommendations for individuals based on these parameters. Elinav and Segal hope to incorporate consumption of emulsifiers, sweeteners and other artificial additives into their study, but caution that there are many components to inflammatory and metabolic diseases. “This is for sure not the only driving factor” for inflammatory bowel disease, Elinav says.

Gewirtz says that many more human and animal studies need to be completed before regulatory agencies would consider changing how additives are approved — after all, removing preservatives from foods would cause them to rot sooner, posing a different health risk. He hopes to do a study in humans soon and is already collecting biopsies from surgery patients to study where different bacteria live in the colon. But the findings have been enough to convince Gewirtz and co-author Benoit Chassaing, a microbiologist at Georgia State, to start checking the labels of the foods they buy, although both say they are not trying to eliminate emulsifiers entirely. It is not easy to find emulsifier-free food, Gewirtz says, and products marketed as ‘organic’ are just as likely to contain these agents. “When it comes to people making their own decisions, between our studies and others out there, it’s better to eat less processed food,” he says.

Nature doi:10.1038/nature.2015.16984

http://www.nature.com/news/index.html Nature

http://www.nature.com/news/food-preservatives-linked-to-obesity-and-gut-disease-1.16984 Original web page at Nature

Neuroscientists at NYU Langone Medical Center have shown that calorie-reduced diets stop the normal rise and fall in activity levels of close to 900 different genes linked to aging and memory formation in the brain. In a presentation prepared for the Society for Neuroscience annual meeting in Washington, D.C., on Nov. 17, researchers say their experimental results, conducted in female mice, suggest how diets with fewer calories derived from carbohydrates likely deter some aspects of aging and chronic diseases in mammals, including humans. “Our study shows how calorie restriction practically arrests gene expression levels involved in the aging phenotype — how some genes determine the behavior of mice, people, and other mammals as they get old,” says senior study investigator and NYU Langone neuroscientist, Stephen D. Ginsberg, PhD. Ginsberg cautions that the study does not mean calorie restriction is the “fountain of youth,” but that it does “add evidence for the role of diet in delaying the effects of aging and age-related disease.” While restrictive dietary regimens have been well-known for decades to prolong the lives of rodents and other mammals, their effects in humans have not been well understood. Benefits of these diets have been touted to include reduced risk of human heart disease, hypertension, and stroke, Ginsberg notes, but the widespread genetic impact on the memory and learning regions of aging brains has not before been shown. Previous studies, he notes, have only assessed the dietary impact on one or two genes at a time, but his analysis encompassed more than 10,000 genes. Ginsberg, an associate professor at NYU Langone and its affiliated Nathan S. Kline Institute for Psychiatric Research, says the research “widens the door to further study into calorie restriction and anti-aging genetics.” For the study, female mice, which like people are more prone to dementia than males, were fed food pellets that had 30 percent fewer calories than those fed to other mice. Tissue analyses of the hippocampal region, an area of the brain affected earliest in Alzheimer’s disease, were performed on mice in middle and late adulthood to assess any difference in gene expression over time.

http://www.sciencedaily.com/  Science Daily

http://www.sciencedaily.com/releases/2014/11/141117110650.htm  Original web page at Science Daily

A diet of junk food not only makes rats fat, but also reduces their appetite for novel foods, a preference that normally drives them to seek a balanced diet, reports a study published in the open-access journal Frontiers in Psychology. The study helps to explain how excessive consumption of junk food can change behavior, weaken self-control and lead to overeating and obesity. The team of researchers, led by Professor Margaret Morris, Head of Pharmacology from the School of Medical Sciences, UNSW Australia, taught young male rats to associate each of two different sound cues with a particular flavor of sugar water — cherry and grape. Healthy rats, raised on a healthy diet, stopped responding to cues linked to a flavor in which they have recently overindulged. This inborn mechanism, widespread in animals, protects against overeating and promotes a healthy, balanced diet. But after 2 weeks on a diet that included daily access to cafeteria foods, including pie, dumplings, cookies, and cake — with 150% more calories — the rats’ weight increased by 10% and their behavior changed dramatically. They became indifferent in their food choices and no longer avoided the sound advertising the overfamiliar taste. This indicated that they had lost their natural preference for novelty. The change even lasted for some time after the rats returned to a healthy diet. The researchers think that a junk diet causes lasting changes in the reward circuit parts of the rats’ brain, for example, the orbitofrontal cortex, an area of the brain responsible for decision-making. They say these results may have implications for people’s ability to limit their intake of certain kinds of foods, because the brain’s reward circuitry is similar in all mammals. “The interesting thing about this finding is that if the same thing happens in humans, eating junk food may change our responses to signals associated with food rewards,” says UNSW Professor Morris. “It’s like you’ve just had ice cream for lunch, yet you still go and eat more when you hear the ice cream van come by.”

http://www.sciencedaily.com/  Science Daily

http://www.sciencedaily.com/releases/2014/08/140827151744.htm  Original web page at Science Daily

A new UCLA psychology study provides evidence that being overweight makes people tired and sedentary — not the other way around. Life scientists led by UCLA’s Aaron Blaisdell placed 32 female rats on one of two diets for six months. The first, a standard rat’s diet, consisted of relatively unprocessed foods like ground corn and fish meal. The ingredients in the second were highly processed, of lower quality and included substantially more sugar — a proxy for a junk food diet. After just three months, the researchers observed a significant difference in the amount of weight the rats had gained, with the 16 on the junk food diet having become noticeably fatter. “One diet led to obesity, the other didn’t,” said Blaisdell, a professor of psychology in the UCLA College of Letters and Science and a member of UCLA’s Brain Research Institute. The experiments the researchers performed, Blaisdell said, also suggest that fatigue may result from a junk food diet. As part of the study, the rats were given a task in which they were required to press a lever to receive a food or water reward. The rats on the junk food diet demonstrated impaired performance, taking substantially longer breaks than the lean rats before returning to the task. In a 30-minute session, the overweight rats took breaks that were nearly twice as long as the lean ones. The research is currently online and is scheduled for publication in the April 10 print edition of the journal Physiology and Behavior. After six months, the rats’ diets were switched, and the overweight rats were given the more nutritious diet for nine days. This change, however, didn’t help reduce their weight or improve their lever responses.

The reverse was also true: Placing the lean rats on the junk food diet for nine days didn’t increase their weight noticeably or result in any reduction in their motivation on the lever task. These findings suggest that a pattern of consuming junk food, not just the occasional binge, is responsible for obesity and cognitive impairments, Blaisdell said. “There’s no quick fix,” he noted. What are the implications for humans? Do people who are overweight become less healthy or do less healthy people become overweight? “Overweight people often get stigmatized as lazy and lacking discipline,” Blaisdell said. “We interpret our results as suggesting that the idea commonly portrayed in the media that people become fat because they are lazy is wrong. Our data suggest that diet-induced obesity is a cause, rather than an effect, of laziness. Either the highly processed diet causes fatigue or the diet causes obesity, which causes fatigue.” Blaisdell believes the findings are very likely to apply to humans, whose physiological systems are similar to rats’. Junk food diets make humans — and rats — hungrier, he said. In addition, the researchers found that the rats on the junk food diet grew large numbers of tumors throughout their bodies by the end of the study. Those on the more nutritious diet had fewer and small tumors that were not as widespread. Blaisdell, 45, changed his diet more than five years ago to eat “what our human ancestors ate.” He avoids processed food, bread, pasta, grains and food with added sugar. He eats meats, seafood, eggs, vegetables and fruits, and he has seen dramatic improvements in his health, both physically and mentally. “I’ve noticed a big improvement in my cognition,” he said. “I’m full of energy throughout the day, and my thoughts are clear and focused.” An expert in animal cognition, Blaisdell conducts research that addresses the relationship between health and lifestyle (diet and exercise) and the relationship between a junk food diet and cognitive impairments it may induce. “We are living in an environment with sedentary lifestyles, poor-quality diet and highly processed foods that is very different from the one we are adapted to through human evolution,” he said. “It is that difference that leads to many of the chronic diseases that we see today, such as obesity and diabetes.”

http://www.sciencedaily.com/  Science Daily

April 29, 2014

http://www.sciencedaily.com/releases/2014/04/140404221904.htm  Original web page at Science Daily

A new theory about the foods that can extend life is taking shape, and it’s sure to be a controversial one. Two studies out this week, one in mice and another primarily in people, suggest that eating relatively little protein and lots of carbohydrates—the opposite of what’s urged by many human diet plans, including the popular Atkins Diet—extends life and fortifies health. The research challenges other common wisdom, too. The authors of both studies believe that calorie restriction, a drastic diet that helps mice and other species live much longer than normal, may work not because it slashes calorie intake, but mostly because it cuts down on protein. They also speculate that the low-protein/high-carbohydrate balance that appears to extend life in the two studies, published in Cell Metabolism, could clarify why slightly plump people live longer on average than skinny ones—something epidemiologists have been hard-pressed to explain. “If these two studies are really correct, what people in general are trying to do” to get and stay thin “might be completely wrong in terms of maintaining health and even longevity,” says Shin-ichiro Imai, a molecular biologist at Washington University in St. Louis who studies aging. The “if” is a big one, however. The interplay between diet and health is extraordinarily complicated, and protein diets in particular have sparked confusion. On the one hand, some researchers have found a correlation between consuming lots of protein and heart disease. On the other, high-protein diets have been linked to improved metabolic profiles, such as lower blood glucose levels. Teasing out the role of protein versus total calories or carbohydrates is no easy task. “There are a whole lot of variables here,” says Cynthia Kenyon, who studies the biology of aging at the University of California, San Francisco.

An Australian group led by nutritional physiologist Stephen Simpson and biogerontologist David Le Couteur at the University of Sydney tried to clear up some of the confusion by assigning 858 mice to one of 25 diets with different mixes of protein, carbs, fats, and fiber. All were allowed to eat as much as they wanted. The mice whose diets included 5% to 15% protein and 40% to 60% carbohydrates lived the longest, up to 150 weeks compared with 100 weeks for those on a diet of about 50% protein. By comparison, Americans on average take in about 16% of their calories from protein. The animals on the low-protein/high-carb plan also had lower blood pressure, better glucose tolerance, and healthier cholesterol. (Levels of fat in their diet didn’t seem to make much difference.) Mice that ate lots of protein were skinnier—just as people on high-protein diets tend to be. But for these mice, slender translated to ill health and earlier death. This finding, Le Couteur says, supports the “concept of healthy obesity,” which has been raised by epidemiology studies of slightly overweight people. He suggests that if their diet is higher in carbohydrates and lower in protein than usual, that might be responsible. The second study, led by gerontology researcher Valter Longo and graduate student Morgan Levine at the University of Southern California in Los Angeles, focused on data from 6381 adults over 50 years old who were interviewed once about their diet as part of NHANES, a national survey of health and nutrition. Longo’s team used death records to conclude that those under 65 whose self-reported diets they classified as high-protein—the participants said at least 20% of their calories came from protein—were at much higher risk of illness and death than a group who took in 10% or fewer of their calories from protein. The high-protein eaters were more than four times as likely to die from cancer over the 18 years after they were surveyed, and 75% more likely to die of any cause.

Those leaping to grab a breadstick instead of sausage should note, however, that as the NHANES cohort aged, protein became more important. In the over-65 crowd, those who ate lots of protein survived longer, on average, than those who ate less. Geriatricians, Longo says, have long extolled the value of protein in older people, and “they’re right.” Longo and Imai speculate that elderly individuals may be less likely to absorb the protein they take in, so need more of it. The findings do fit with some molecular clues. Cutting protein intake is known to reduce levels of a growth factor called IGF-1, and lower IGF-1 levels are linked to longer lifespan and reductions in the risk of cancer and diabetes. Limiting protein intake also reduces levels of a protein called mTOR, and lower mTOR extends life in mice. The Australians saw the mTOR effect in their animals. Longo’s team, testing stored samples from the survey participants, saw that higher IGF-1 levels correlated with more dietary protein. “There’s certainly some truth to this relationship” between protein consumption and lifespan, says Matt Kaeberlein, a molecular biologist at the University of Washington, Seattle, who studies longevity. “But it’s probably overly simplistic to say that everyone should go on a low-protein diet at this point.” Among the many caveats, for example, is that the mouse study used a single strain, though different strains can have different reactions to diets such as calorie restriction. Kaeberlein also thinks it’s unlikely that reduced protein alone explains the dramatic impact of calorie restriction on lifespan. Le Couteur wants to find out for sure: He and his colleagues are planning a study that pits a low-protein/high-carb diet head-to-head with restricted calories, to see which mice live the longest.

http://news.sciencemag.org/sciencenow  ScienceNow

March 18, 2014

http://news.sciencemag.org/biology/2014/03/low-protein-diet-may-extend lifespan  Original web page at ScienceNow

New research findings indicate that an early onset of dietary treatment may slow down the progression of Alzheimer’s disease. The study was conducted on mice, and the results will be published in the February issue of Journal of Nutritional Biochemistry. Researchers from the University of Eastern Finland played a key role in the study, which was carried out as part of the LiPiDiDiet project funded by the European Union. According to current understanding, Alzheimer’s disease develops slowly and it may take up to 20 years before the first obvious symptoms occur. With the development of early diagnostics of the disease, the question of which treatments to offer to completely healthy people with an increased risk of developing Alzheimer’s becomes of key importance in the field of medicine. Various dietary treatments seem a promising alternative. Several epidemiological studies suggest that docosahexaenoic acid (DHA), an omega-3 fatty acid found in fatty fish, might reduce the risk of Alzheimer’s disease. Experimental studies have also observed a positive — although modest — association between DHA and several processes behind Alzheimer’s disease. This recently published study investigated whether the efficacy of DHA treatment can be enhanced by additional nutrients.

The study used transgenic female mice carrying APP and PS1 mutations linked with familial Alzheimer’s disease, and wild-type mice. All the mice began the dietary intervention at 5 months and continued on the diet until 13 months old. The fat content of the control chow was increased to better correspond to human diets. In addition to the control chow, some of the APP/PS1 mice were fed three experimental chows enriched with fish oil and having a similar fat content as the control chow: fish oil supplement only, plant sterol supplement or Fortasyn supplement, which contains uridine-monophosphate, phospholipids, B- vitamins, and antioxidants. As expected, APP/PS1 mice performed significantly poorer than wild-type mice in the Morris swim navigation task, which measures long-term spatial memory. Among transgenic mice on the experimental diets, the mice on the Fortasyn diet performed equally well as the wild-type mice, whereas other dietary treatments showed no improvement. However, all test diets reversed the memory deficit of the APP/PS1 mice in the odour recognition task. The levels of accumulated amyloid-β protein in the brain were examined at the end of the study. A significant reduction in the amyloid-β levels was observed in the plant sterol group while other experimental diets showed no effect. However, why was a substantial reduction in brain amyloid-β levels not accompanied by a positive memory effect in the spatial task in the plant sterol group? One explanation is that the plant sterol diet increased formation of reactive oxygen species in the hippocampus, whereas the Fortasyn diet, which yielded the best results in the spatial memory task, tended to have an opposite effect.

The results indicate that even slight changes in the composition of the diet may, under a sufficiently long period of time and at an early stage of the disease process, lead to significant changes in brain metabolism and improved memory performance. On the other hand, the mere brain amyloidosis in Alzheimer’s disease involves several mechanisms and it is unlikely that a single cocktail of nutrients will provide an optimal outcome. According to the researchers, the results definitely encourage further development of dietary treatments for Alzheimer’s disease. The now studied Fortasyn supplement is found in the medical nutrition formulation Souvenaid that just was introduced in Finland. In the light of the present results, the product can be warmly recommended for the treatment of mice suffering from mild cognitive impairment (pre-Alzheimer’s), but will it work as efficiently in humans, too? We will probably get the answer in a year, as results from a parallel clinical study of the LiPiDiDiet project become available. The study is coordinated by the Brain Research Unit at the Clinical Research Centre of the University of Eastern Finland.

http://www.sciencedaily.com/ Science Daily
February 18, 2014

http://www.sciencedaily.com/releases/2014/01/140124082558.htm Original web page at Science Daily