Posts tagged diet
Articles and news from the latest research reports.
Male and female brains aren’t equal when it comes to fat
Researchers have found that male and female brains respond in remarkably different ways to high-fat meals. Those differences in the brain lead to greater inflammation and increased health risks in males that indulge on fatty foods in comparison to females, a new study in mice shows. The findings reported in the Cell Press journal Cell Reports on October 16th may help to explain observed differences in obesity outcomes between women and men – premenopausal women carrying extra weight fare better than men do – and suggest that dietary advice should be made more sex-specific.
"Our findings, for the first time, suggest that males and females respond to high-fat diets differently," said Deborah Clegg of the Cedar-Sinai Diabetes And Obesity Research Institute in Los Angeles. "The data would suggest that is probably ‘ok’ for females to occasionally have a high-fat meal, where it is not recommended for males.
"The way we treat patients and provide dietary and nutritional advice should be altered. We might be less concerned about an occasional hamburger for women, but for men, we might more strongly encourage avoidance, especially if they have pre-existing diseases such as heart disease or type 2 diabetes."
Earlier data from Clegg’s team and others had suggested that inflammation in the brain is tied to overeating, blood sugar imbalances, and increased inflammation in other parts of the body, including fat tissue. Those effects can be triggered, in males in particular, by short-term exposure to a high-fat diet.
The researchers say they were initially shocked to discover that male and female brains differ in their fatty acid composition. When they manipulated male mouse brains to have the fatty acid profile of females, they found that those animals were protected from the ill effects of a diet high in fat.
When males with average male brains entered an inflammatory state after eating diets high in fat, they also suffered from reduced cardiac function in a way that female animals in the study did not. Those sex differences in the brain’s response to fat are related to differences between females and males in estrogen and estrogen receptor status.
Clegg says her team is now working out a strategy to confirm whether the findings in mice apply to people too. If they do, there will be some very immediate practical implications for what men and women should put on their plates.
"We have always had ‘one size fits all’ with respect to our nutritional information and our pharmaceutical approach," Clegg said. "Our data begin to suggest that sex should be factored in, and men should be more closely monitored for fat intake and inflammation than women."
(Image: Shutterstock)
Low-fat diet helps fatigue in people with MS
People with multiple sclerosis who for one year followed a plant-based diet very low in saturated fat had much less MS-related fatigue at the end of that year — and significantly less fatigue than a control group of people with MS who didn’t follow the diet, according to an Oregon Health & Science University study being presented today at the American Academy of Neurology’s annual meeting in Philadelphia, Pa.
The study was the first randomized-controlled trial to examine the potential benefits of the low fat diet on the management of MS. The study found no significant differences between the two groups in brain lesions detected on MRI brain scans or on other measures of MS. But while the number of trial participants was relatively small, study leaders believe the significantly improved fatigue symptoms merited further and larger studies of the diet.
"Fatigue can be a debilitating problem for many people living with relapsing-remitting MS," said Vijayshree Yadav, M.D., an associate professor of neurology in the OHSU School of Medicine and clinical medical director of the OHSU Multiple Sclerosis Center. "So this study’s results — showing some notable improvement in fatigue for people who follow this diet — are a hopeful hint of something that could help many people with MS."
The study investigated the effects of following a diet called the McDougall Diet, devised by John McDougall, M.D. The diet is partly based on an MS-fighting diet developed in the 1940s and 1950s by the late Roy Swank, M.D., a former head of the division of neurology at OHSU. The McDougall diet, very low in saturated fat, focuses on eating starches, fruits and vegetables and does not include meat, fish or dairy products.
The study, which began in 2008, looked at the diet’s effect on the most common form of MS, called relapsing-remitting MS. About 85 percent of people with MS have relapsing-remitting MS, characterized by clearly defined attacks of worsening neurological function followed by recovery periods when symptoms improve partially or completely.
The study measured indicators of MS among a group of people who followed the McDougall Diet for 12 months and a control group that did not. The study measured a range of MS indicators and symptoms, including brain lesions on MRI brain scans of study participants, relapse rate, disabilities caused by the disease, body weight and cholesterol levels.
It found no difference between the diet group and the control group in the number of MS-caused brain lesions detected on the MRI scans. It also found no difference between the two groups in relapse rate or level of disability caused by the disease. People who followed the diet did lose significantly more weight than the control group and had significantly lower cholesterol levels. People who followed the diet also had higher scores on a questionnaire that measured their quality of life and overall mood.
The study’s sample size was relatively small. Fifty-three people completed the study, with 27 in the control group and 22 people in the diet group who complied with the diet’s restrictions.
"This study showed the low-fat diet might offer some promising help with the fatigue that often comes with MS," said Dennis Bourdette, M.D., F.A.A.N., chair of OHSU’s Department of Neurology, director of OHSU’s MS Center and a study co-author. "But further study is needed, hopefully with a larger trial where we can more closely look at how the diet might help fatigue and possibly affect other symptoms of MS."
(Source: eurekalert.org)
Diet Can Predict Cognitive Decline
The importance of long-chain polyunsaturated fatty acids (PUFAs) to brain health has been demonstrated in multiple studies. To assess whether lower dietary intake of alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexanoic acid (DHA) were risk factors for cognitive decline, Tammy Scott, PhD, a scientist at the Jean Mayer USDA Human Nutrition Research Center on Aging (USDA HNRCA) at Tufts University recently conducted a longitudinal, observational study using the Boston Puerto Rican Health Study cohort. Alice Lichtenstein, DSc, also from the USDA HNRCA at Tufts University, and Katherine Tucker, PhD, the cohort director from the University of Massachusetts-Lowell, were co-authors of the study, which has been published as an abstract.
“The participants were put through an intensive series of cognitive tests such as memory tests using a list of words, an attention test to repeat lists of numbers forward and backward, and a test of organization and planning involving copying complex figures,” said Dr. Scott. To determine the participants’ intake of PUFAs they were given a questionnaire. The results were determined after comparing baseline test numbers with a 2 year follow up.
The researchers found that the intake of omega-3 PUFAs in the study sample of 895 participants was low. The 2010 U.S. Dietary Guidelines recommended an intake of 8 or more ounces of seafood per week (less for young children) to ensure an adequate intake of the very long chain omega-3 fatty acids (EPA and DHA). This translates to about 1,750 mg of EPA and DHA per week, which averages to 250 mg per day. Scott’s group reported that only 27% of the participants in their study met or exceeded that recommendation. The major source of EPA and DHA in their diets appeared to be from canned tuna. Based on the scientists’ findings, being in the lowest four quintiles of EPA and DHA intake was predictive of cognitive decline over 2 years.
What is the takeaway from this research? There is growing evidence that very long chain omega-3 fatty acids are beneficial for maintaining cognitive health, and many Americans do not have an adequate intake of these nutrients. “While more research is needed to determine whether intake of fatty fish such as salmon, tuna and trout can help prevent against cognitive decline, our preliminary data support previous research showing that intake of these types of fish have health benefits,” Scott said.
(Image: Fotolia)
Zinc Supplementation Shows Promise in Reducing Cell Stress After Blasts
Each year, approximately 2 million traumatic brain injuries (TBIs) occur in the USA, according to the Centers for Disease Control and Prevention. That number includes troops wounded in Iraq and Afghanistan, for whom TBI is considered an invisible wound of war, one that has few successful treatments. “We have nothing beyond ibuprofen for most TBIs,” said Dr. Angus Scrimgeour, who has been investigating the effects of low zinc diets on cell stress following a blast injury. “The adult brain does not self-repair from this kind of trauma.”
Scrimgeour works for the US Army Research Institute of Environmental Medicine and recently looked at the effects of 5-weeks of low and adequate zinc diets on a specific protein in muscle cells called MMP. The study recreated blast injuries in 32 rats similar to what soldiers experience from IEDs, including loss of consciousness. An equal number of rats served as a control group. Results suggest that zinc supplementation reduces blast-induced cell stress. He presented the results of his research at the American Society for Nutrition’s Scientific Sessions & Annual Meeting at EB on Sunday, April 27.
“We know that soldiers’ brain tissue cannot repair on low zinc diets,” said Scrimgeour. “And they are losing zinc through diarrhea and sweating.” The question moving forward is whether prevention through diet supplementation or post-blast treatment works best to repair behavioral deficits associated with mild TBI.
Scrimgeour added that further research is planned to investigate nutrient combinations for treating mild TBI, including omega-3, vitamin D, glutamine and/or zinc. Although the Army is conducting this research, the results can be applied outside of the military, according to Scrimgeour. “As the blast impact experienced by Soldiers are similar to those experienced during head injuries received in a car accident or during an NFL concussion, these findings could translate from the Soldier to the civilian population.” Scrimgeour cautioned, however, that what works in animals doesn’t always work in soldiers, which is why more research is needed.
(Source: newswise.com)
Children’s preferences for sweeter and saltier tastes are linked to each other
Scientists from the Monell Chemical Senses Center have found that children who most prefer high levels of sweet tastes also most prefer high levels of salt taste and that, in general, children prefer sweeter and saltier tastes than do adults. These preferences relate not only to food intake but also to measures of growth and can have important implications for efforts to change children’s diets.
Many illnesses of modern society are related to poor food choices. Because children consume far more sugar and salt than recommended, which contributes to poor health, understanding the biology behind children’s preferences for these tastes is a crucial first step to reducing their intake.
"Our research shows that the liking of salty and sweet tastes reflects in part the biology of the child," said study lead author Julie Mennella, PhD, a biopsychologist at Monell. Biology predisposes us to like and consume calorie-rich sweet foods and sodium-rich salty foods, and this is especially true for children. "Growing children’s heightened preferences for sweet and salty tastes make them more vulnerable to the modern diet, which differs from the diet of our past, when salt and sugars were once rare and expensive commodities."
In the study, published online at PLOS ONE, Mennella and colleagues tested 108 children between 5 and 10 years old, and their mothers, for salt and sweet taste preferences. The same testing method was used for both children and their mothers, who tasted broth and crackers that varied in salt content, and sugar water and jellies that varied in sugar content. The method, developed by Mennella and her colleagues at Monell, scientifically determines taste preferences, even for very young children, by having them compare two different levels of a taste, pick their favorite, and then compare that favorite with another, over and again until the most favorite is identified.
Mennella and colleagues also had mothers and children list foods and beverages they consumed in the past 24 hours, from which daily sodium, calorie, and added sugar intakes were estimated. Subjects then gave a saliva sample, which was genotyped for a sweet receptor gene, and a urine sample to measure levels of Ntx, a marker for bone growth. Weight, height, and percent body fat were measured for all subjects.
Analyses of all these data showed that not only were sweet and salty preferences correlated in children, and higher overall than those in adults, but also children’s taste preferences related to measures of growth and development: children who were tall for their age preferred sweeter solutions, and children with higher amounts of body fat preferred saltier soups. There was also some indication that higher sweet liking related to spurts in bone growth, but that result needs confirmation in a larger group of children.
Sweet and salty preferences were correlated in adults as well. And in adults, but not in children, sweet receptor genotype was related to the most preferred level of sweetness. “There are inborn genetic differences that affect the liking for sweet by adults,” says collaborator Danielle Reed, PhD, “but for children, other factors – perhaps the current state of growth – are stronger influences than genetics.”
Both children and adults who preferred higher levels of salt in food also reported consuming more dietary salt in the past 24 hours, but no such relationship was found between sweet preferences and sugar intake. This difference may reflect parents exerting greater control in their children’s diet for added sugar than for added salt. Or it could reflect increased use of non-nutritive sweeteners in foods geared for children – in other words, the sweetness of some foods doesn’t reflect their sugar content.
Current intakes of sodium and added sugars among US children are well in excess of recommendations. For almost all 2- to 8-year-olds, added sugars account for more than half of their discretionary calories (130 total discretionary calories are allowed for children of this age). For 4- to 13-year-olds, sodium intake is more than twice adequate levels (1200-1500 mg/day is allowed for children of this age). The children studied by Mennella and colleagues, two-thirds of whom were overweight or obese, also consumed twice adequate levels of sodium, and their added sugar intake averaged almost 20 teaspoons, or 300 calories, each day.
Guidelines from leading authorities, including the World Health Organization, American Heart Association, U.S. Department of Agriculture, and Institute of Medicine, recommend significantly cutting sugar and salt intake for children, but this can be a daunting task. Commenting on the implications of her research, lead author Mennella noted, “The present findings reveal that the struggle parents have in modifying their children’s diets to comply with recommendations appears to have a biological basis.”
Understanding the basic biology that drives the desire for sweet and salty tastes in children illustrates their vulnerability to the current food environment. But on a positive note, Mennella observed, “it also paves the way toward developing more insightful and informed strategies for promoting healthy eating that meet the particular needs of growing children.”
Your gut’s what you eat, too
As the saying goes, you are what you eat. But new evidence suggests that the same may also be true for the microbes in your gut.
A Harvard study shows that, in as little as a day, diet can alter the population of microbes in the gut — particularly those that tolerate bile — as well as the types of genes expressed by gut bacteria.
“What we are really excited about is we and others have shown in animal models that diet can rapidly have major effects on the microbes that are in the gut,” said Peter Turnbaugh, a Bauer Fellow at the Center for Systems Biology in the Faculty of Arts and Sciences. He is senior author of the paper, which appeared in Dec. 11 edition of the journal Nature.
“But it still wasn’t clear how fast the microbes in the human gut respond to changes in diet, and to what degree those changes would be similar in different people. This study is really the first time we’ve seen that, over the course of days, a new diet can reshape the microbial community, and that those changes are consistent and reversible.”
Obesity ballooning in developing world: report
The number of obese and overweight people in the developing world nearly quadrupled to almost a billion between 1980 and 2008, a think-tank report said on Friday.
There are now far more obese or overweight adults in the developing world than in richer countries, the Overseas Development Institute (ODI) said.
The London-based institute said more than a third of all adults around the world — 1.46 billion people — were obese or overweight.
Between 1980 and 2008, the numbers of people affected in the developing world rose from 250 million to 904 million. In the developed world, the figure rose from 321 million to 557 million.
This represented a rise from 23 percent to 34 percent of the world population.
"The growing rates of overweight and obesity in developing countries are alarming," said ODI research fellow Steve Wiggins, who co-authored the Future Diets report.
"On current trends, globally, we will see a huge increase in the number of people suffering certain types of cancer, diabetes, strokes and heart attacks, putting an enormous burden on public healthcare systems."
The report said overweight and obesity rates have almost doubled in China and Mexico since 1980, and risen by a third in South Africa.
The study said the rise in obesity was down to diets changing in developing countries where incomes were rising, with people shifting away from cereals and tubers to eating more meat, fats and sugar.
The over-consumption of food, coupled with increasingly sedentary lives, was also to blame.
The report found that North Africa, the Middle East and South America saw overweight and obesity rates increase to a level similar to Europe, around 58 percent.
At 70 percent, North America still has the highest percentage of overweight adults.
The report said there seemed to be little will among the public and leaders to take action on influencing diet in the future.
"Governments have focused on public awareness campaigns, but evidence shows this is not enough," said Wiggins.
"The lack of action stands in stark contrast to the concerted public actions taken to limit smoking in developed countries.
"Politicians need to be less shy about trying to influence what food ends up on our plates. The challenge is to make healthy diets viable whilst reducing the appeal of foods which carry a less certain nutritional value."
The report gave the example of South Korea as having made efforts to preserve healthy elements of the country’s traditional diet, via public campaigns and education, providing large-scale training for women in preparing healthy, traditional food.
The report said it was “only a matter of time” before people would begin to accept and even demand stronger and more effective measures to influence diets.
Why One Cream Cake Leads to Another
Continuously eating fatty foods perturbs communication between the gut and brain, which in turn perpetuates a bad diet.
A chronic high-fat diet is thought to desensitize the brain to the feeling of satisfaction that one normally gets from a meal, causing a person to overeat in order to achieve the same high again. New research published today (August 15) in Science, however, suggests that this desensitization actually begins in the gut itself, where production of a satiety factor, which normally tells the brain to stop eating, becomes dialed down by the repeated intake of high-fat food.
“It’s really fantastic work,” said Paul Kenny, a professor of molecular therapeutics at The Scripps Research Institute in Jupiter, Florida, who was not involved in the study. “It could be a so-called missing link between gut and brain signaling, which has been something of a mystery.”
While pork belly, ice cream, and other high-fat foods produce an endorphin response in the brain when they hit the taste buds, according to Kenny, the gut also sends signals directly to the brain to control our feeding behavior. Indeed, mice nourished via gastric feeding tubes, which bypass the mouth, exhibit a surge in dopamine—a neurotransmitter promoting reinforcement in the brain’s reward circuitry—similar to that experienced by those eating normally.
This dopamine surge occurs in response to feeding in both mice and humans. But evidence suggests that dopamine signaling in the brain is deficient in obese people. Ivan de Araujo, a professor of psychiatry at the Yale School of Medicine, has now discovered that obese mice on a chronic high-fat diet also have a muted dopamine response when receiving fatty food via a direct tube to their stomachs.
To determine the nature of the dopamine-regulating signal emanating from the gut, Araujo and his team searched for possible candidates. “When you look at animals chronically exposed to high-fat foods, you see high levels of almost every circulating factor—leptin, insulin, triglycerides, glucose, et cetera,” he said. But one class of signaling molecule is suppressed. Of these, Araujo’s primary candidate was oleoylethanolamide. Not only is the factor produced by intestinal cells in response to food, he said, but during chronic high-fat exposure, “the suppression levels seemed to somehow match the suppression that we saw in dopamine release.”
Araujo confirmed oleoylethanol’s dopamine-regulating ability in mice by administering the factor via a catheter to the tissues surrounding their guts. “We discovered that by restoring the baseline level of [oleoylethanolamide] in the gut … the high-fat fed animals started having dopamine responses that were indistinguishable from their lean counterparts.”
The team also found that oleoylethanolamide’s effect on dopamine was transmitted via the vagus nerve, which runs between the brain and abdomen, and was dependent on its interaction with a transcription factor called PPAR-a.
Oleoylethanolamide levels are also reduced in fasting animals and increase in response to eating, communicating with the brain to stop further consumption once the belly is full. Indeed, oleoylethanolamide is a known satiety factor. Therefore, when chronic consumption of high-fat food diminishes its production, the satisfaction signal is not achieved, and the brain is essentially “blind to the presence of calories in the gut,” said Araujo, and thus demands more food.
It is not clear why a chronic high-fat diet suppresses the production of oleoylethanolamide. But once the vicious cycle starts, it is hard to break because the brain is receiving its information subconsciously, said Daniele Piomelli, a professor at the University of California, Irvine, and director of drug discovery and development at the Italian Institute of Technology in Genoa.
“We eat what we like, and we think we are conscious of what we like, but I think what this [paper] and others are indicating is that there is a deeper, darker side to liking—a side that we’re not aware of,” Piomelli said. “Because it is an innate drive, you can not control it.” Put another way, even if you could trick your taste buds into enjoying low-fat yogurt, you’re unlikely to trick your gut.
The good news, however, is that “there is no permanent impairment in the [animals’] dopamine levels,” Araujo said. This suggests that if drugs could be designed to regulate the oleoylethanolamide–to-PPAR-a pathway in the gut, Kenny added, it could have “a huge impact on people’s ability to control their appetite.”
(Source: the-scientist.com)
Study of Dietary Intervention Examines Proteins in Brain
The lipidation states (or modifications) in certain proteins in the brain that are related to the development of Alzheimer disease appear to differ depending on genotype and cognitive diseases, and levels of these protein and peptides appear to be influenced by diet, according to a report published Online First by JAMA Neurology, a JAMA Network publication.
Sporadic Alzheimer disease (AD) is caused in part by the accumulation of β-amyloid (Αβ) peptides in the brain. These peptides can be bound to lipids or lipid carrier proteins, such as apolipoprotein E (ApoE), or be free in solution (lipid-depleted [LD] Αβ). Levels of LD Αβ are higher in the plasma of adults with AD, but less is known about these peptides in the cerebrospinal fluid (CSF), the authors write in the study background.
Angela J. Hanson, M.D., Veterans Affairs Puget Sound Health Care System and the University of Washington, Seattle, and colleagues studied 20 older adults with normal cognition (average age 69 years) and 27 older adults with amnestic mild cognitive impairment (average age 67 years).
The patients were randomized to a diet high in saturated fat content (45 percent energy from fat, greater than 25 percent saturated fat) with a high glycemic index or a diet low in saturated fat content (25 percent of energy from fat, less than 7 percent saturated fat) with a low glycemic index. The main outcomes the researchers measured were lipid depleted (LD) Αβ42 and Αβ40 and ApoE in cerebrospinal fluid.
Study results indicate that baseline levels of LD Αβ were greater for adults with mild cognitive impairment compared with adults with normal cognition. The authors also note that these findings were more apparent in adults with mild cognitive impairment and the Ɛ4 allele (a risk factor for AD), who had higher LD apolipoprotein E levels irrespective of cognitive diagnosis. Study results indicate that the diet low in saturated fat tended to decrease LD Αβ levels, whereas the diet high in saturated fat increased these fractions.
The authors note the data from their small pilot study need to be replicated in a larger sample before any firm conclusions can be drawn.
“Overall, these results suggest that the lipidation states of apolipoproteins and amyloid peptides might play a role in AD pathological processes and are influenced by APOE genotype and diet,” the study concludes.
Editorial: Food for Thought
In an editorial, Deborah Blacker, M.D., Sc.D., of the Massachusetts General Hospital/Harvard Medical School, Boston, writes: “The article by Hanson and colleagues makes a serious effort to understand whether dietary factors can affect the biology of Alzheimer disease (AD).”
“Hanson et al argue that the changes observed after their two dietary interventions may underlie some of the epidemiologic findings regarding diabetes and other cardiovascular risk factors and risk for AD. The specifics of their model may not capture the real underlying biological effect of these diets, and it is unclear whether the observed changes in the intermediate outcomes would lead to beneficial changes in oligomers or plaque burden, much less to decreased brain atrophy or improved cognition,” she continues.
“At some level, however, the details of the biological model are not critical; the important lesson from the study is that dietary intervention can change brain amyloid chemistry in largely consistent and apparently meaningful ways – in a short period of time. Does this change clinical practice for those advising patients who want to avoid dementia? Probably not, but it adds another small piece to the growing evidence that taking good care of your heart is probably good for your brain too,” Blacker concludes.
(Source: media.jamanetwork.com)
Researchers define key events early in the process of cellular aging
For the first time, scientists at Fred Hutchinson Cancer Research Center have defined key events that take place early in the process of cellular aging.
Together the discoveries, made through a series of experiments in yeast, bring unprecedented clarity to the complex cascade of events that comprise the aging process and pave the way to understanding how genetics and environmental factors like diet interact to influence lifespan, aging and age-related diseases such as cancer and neurodegenerative disorders.
The findings, including unexpected results that link aspects of aging and lifespan to a mechanism cells use to store nutrients, are described in the Nov. 21 issue of Nature by co-authors Daniel Gottschling, Ph.D., a member of the Hutchinson Center’s Basic Sciences Division, and Adam Hughes, Ph.D., a postdoctoral fellow in the Gottschling Lab.
The work began with Hughes and Gottschling searching for the source of age-related damage in mitochondria.
“Normally, mitochondria are beautiful, long tubes, but as cells get older, the mitochondria become fragmented and chunky,” said Gottschling, also an affiliate professor in the Department of Genome Sciences at the University of Washington. “The changes in shape seen in aging yeast cells are also observed in certain human cells, such as neurons and pancreatic cells, and those changes have been associated with a number of age-related diseases in humans.”
What causes mitochondria to become distorted and dysfunctional as cells age had long been a mystery, but Gottschling and Hughes have discovered that specific changes in the vacuole lead directly to their malfunctioning.The researchers found the acidity of a structure in yeast cells known as the vacuole is critical to aging and the functioning of mitochondria – the power plants of the cell. They also describe a novel mechanism, which may have parallels in human cells, by which calorie restriction extends lifespan.