QUINTAIS IMORTAIS

University of South Australia. "Fewer fats over the festive season may be the perfect formula for men's fertility: Egg whites and whey protein boost testosterone." ScienceDaily. ScienceDaily, 23 December 2019. <www.sciencedaily.com/releases/2019/12/191223122907.htm>.

Plant-rich diet protects mice against foodborne infection

Date: December 23, 2019 Source: UT Southwestern Medical Center Summary: Mice fed a plant-rich diet are less susceptible to gastrointestinal (GI) infection from a pathogen such as the one currently under investigation for a widespread E. coli outbreak tied to romaine lettuce, UT Southwestern researchers report.

Mice fed a plant-rich diet are less susceptible to gastrointestinal (GI) infection from a pathogen such as the one currently under investigation for a widespread E. coli outbreak tied to romaine lettuce, UT Southwestern researchers report. A strain of E. coli known as EHEC, which causes debilitating and potentially deadly inflammation in the colon with symptoms such as bloody diarrhea and vomiting, is implicated in several foodborne outbreaks worldwide each year.

"There has been a lot of hearsay about whether a plant-based diet is better for intestinal health than a typical Western diet, which is higher in oils and protein but relatively low in fruits and vegetables," says Vanessa Sperandio, Ph.D., professor of microbiology and biochemistry at UT Southwestern. "So we decided to test it."

Her study on a mouse model of EHEC is published this week in Nature Microbiology.

"Plant-rich diets are high in pectin, a gel-like substance found in many fruits and vegetables. Pectin is digested by the gut microbiota into galacturonic acid, which we find can inhibit the virulence of EHEC," she adds.

"This is relevant to public health because EHEC outbreaks lead to hemorrhagic colitis, which is debilitating and sometimes causes death, particularly in the very young and the elderly," she says.

Intestinal pathogens like EHEC sense the complex chemistry inside the GI tract to compete with the gut's resident microbiota to establish a foothold, Sperandio says. Over centuries, the pathogens have developed different strategies to compete against the so-called good, or commensal, microbes that normally line the gut.

Those commensals include harmless strains of E. coli living in the colons of humans and other mammals, where they help the host's normal digestion process, she adds. The word commensal means "eating at the same table" and that is what the symbiotic bacteria that make up the gut's microbiota do.

The commensals that line the gut present a significant barrier to intestinal pathogens, Sperandio explains. EHEC and similar gram-negative bugs overcome that barrier by deploying a secretion system called T3SS.

T3SSs act like molecular syringes to inject a mix of virulence proteins into the cells lining the host's colon, setting off inflammation and symptoms of infection. Because mice are unaffected by EHEC, researchers use a similar pathogen, Citrobacter rodentium, in mouse studies, Sperandio explains.

"Our study finds first that the good E. coli and the pathogenic ones like EHEC use different sugars as nutrients," she says, adding that the two types of E. coli may have evolved to avoid competing for the same energy sources. "Second, we find that dietary pectin protects against the pathway the pathogenic EHEC uses to become more virulent."

Another type of commensal gut bacteria breaks down dietary pectin from fruit and vegetables, creating galacturonic acid, a sugar acid that the EHEC and C. rodentium use in two ways. Initially, the pathogen uses that sugar acid as an energy source to expand in the gut, Sperandio says.

"Once the sugar acid becomes depleted, the pathogen changes its survival strategy, almost like flipping a switch," she says. Instead of using the galacturonic acid for nourishment, the infectious bacteria employs it in a signaling pathway that increases the EHEC's and similar bacteria's virulence using the syringe-like T3SS.

In the study, mice fed pectin for about a week withstood infection. Comparing the colons of six mice fed a chow diet with 5 percent extra pectin from citrus peel with four mice on a typical diet, the researchers found a much lower rate of infection in the pectin-eating mice, Sperandio says.

The amount of bacteria in the mouse gut was measured by daily stool checks and by analysis of the amount of bacteria in a pouch at the juncture of the small and large intestines, called the cecum, at the experiment's end.

The researchers found that mice on the pectin-enriched chow had about 10,000 bacteria in the cecum compared to 1 million bacteria in mice on the typical diet. The pectin group also had fewer symptoms, she says, adding that a pectin level of 5 percent appears to prevent the pathogen from activating its virulence repertoire.

She stresses that the research is one step in a journey to define the molecular mechanisms that govern how the commensal species in the gut impact the virulence of intestinal pathogens.

"This is not translatable to humans yet. We hope a better understanding of how intestinal disease develops will lead to strategies to reduce the incidence or, at least, the symptoms caused by these gram-negative pathogens, possibly through new vaccines or drugs," she says.

Story Source:

Materials provided by UT Southwestern Medical Center. Note: Content may be edited for style and length.

Journal Reference:

Angel G. Jimenez, Melissa Ellermann, Wade Abbott, Vanessa Sperandio. Diet-derived galacturonic acid regulates virulence and intestinal colonization in enterohaemorrhagic Escherichia coli and Citrobacter rodentium. Nature Microbiology, 2019; DOI: 10.1038/s41564-019-0641-0

Cite This Page:

UT Southwestern Medical Center. "Plant-rich diet protects mice against foodborne infection." ScienceDaily. ScienceDaily, 23 December 2019. <www.sciencedaily.com/releases/2019/12/191223122851.htm>.

sábado, 21 de dezembro de 2019

Fatty meal interrupts gut's communication with the body, but why?

If that second helping of prime rib stuns your gut into silence, is that good or bad?

Date: December 17, 2019 Source: Duke University Summary: Gut cells that normally tell the brain and the rest of the body what's going on after a meal shut down completely for a few hours after a high-fat meal, a team of researchers discovered in zebrafish. Enteroendocrine cells normally produce at least 15 different hormones to send signals to the rest of the body. The finding could be a clue to insulin resistance that leads to Type 2 diabetes.

A high-fat meal can silence communication between the intestine and the rest of the body, according to a new Duke University study in zebrafish.

While using the fish to examine cells that normally tell the brain and the rest of the body what's going on inside the gut after a meal, a team of Duke researchers discovered that a high-fat meal completely shuts down that communication for a few hours.

The cells they were looking at are the enteroendocrine cells, which occur sparsely throughout the lining of the gut, but play a key role in signaling the body about the all-important alimentary canal. In addition to releasing hormones, the cells also have a recently-discovered direct connection to the nervous system and the brain.

These cells produce at least 15 different hormones to send signals to the rest of the body about gut movement, feelings of fullness, digestion, nutrient absorption, insulin sensitivity and energy storage.

"But they fall asleep on the job for a few hours after a high-fat meal, and we don't yet know if that's good or bad," said John Rawls, an associate professor of molecular genetics and microbiology in the Duke School of Medicine.

Since enteroendocrine cells are key players in digestion, the feeling of being full and subsequent feeding behavior, this silencing may be a mechanism that somehow causes people eating a high-fat diet to eat even more.

"This is a previously unappreciated part of the postprandial (after-meal) cycle," Rawls said. "If this happens every time we eat an unhealthy, high-fat meal, it might cause a change in insulin signaling, which could in turn contribute to the development of insulin resistance and Type 2 diabetes."

To understand the silencing better, the researchers tried to break the process down step by step in zebrafish.

After they first sense a meal, the enteroendocrine cells trigger a calcium burst within seconds, initiating the signaling process. But after that initial signal there's a delayed effect later in the after-meal period. It's during this later response that the silencing occurs, said Rawls, who also directs Duke's Microbiome Center.

The silenced cells change shape and experience stress in their endoplasmic reticulum, a structure that assembles new proteins. It seems that these enteroendocrine cells, which are specialized to synthesize and secrete proteins like hormones and neurotransmitters, become overstimulated and exhausted for a while.

The team tried the high-fat diet on a line of germ-free zebrafish raised in the absence of any microbes, and found they didn't experience the same silencing effect. So they began looking for gut microbes that might be involved in the process.

After screening through all the kinds of bacteria found in the gut, they saw that the silencing appeared to be the work of a single type of gut bacteria, called Acinetobacter. These bugs are normally less than 0.1 percent of the total gut microbiome, but they increased 100-fold after a high-fat meal and were the only bacteria able to induce the silencing effect.

"Next we want to understand how Acinetobacter evokes this interesting response," said Lihua Ye, a postdoctoral fellow and lead author on this paper. "We also suspect other bacteria might also have this capability."

Rawls said they aren't sure why silencing occurs, nor whether it has any positive effect on the fish. It might be a way to prevent excessive signaling about the fat, but by being silenced completely like this, the cells won't be communicating anything else either.

"We don't understand yet what the long-term impact of enteroendocrine silencing would be on metabolic health," Rawls said. "This may be a maladaptive response to high-fat feeding that impairs the normal regulatory functions of these cells, leading to metabolic disorders like insulin resistance. But it's also possible that the silencing is a beneficial adaptation to protect the animal from over-stimulation of the gut cells."

Story Source:

Materials provided by Duke University. Note: Content may be edited for style and length.

Journal Reference:

Lihua Ye, Olaf Mueller, Jennifer Bagwell, Michel Bagnat, Rodger A Liddle, John F Rawls. High fat diet induces microbiota-dependent silencing of enteroendocrine cells. eLife, 2019; 8 DOI: 10.7554/eLife.48479

Cite This Page:

Duke University. "Fatty meal interrupts gut's communication with the body, but why? If that second helping of prime rib stuns your gut into silence, is that good or bad?." ScienceDaily. ScienceDaily, 17 December 2019. <www.sciencedaily.com/releases/2019/12/191217141551.htm>.

quinta-feira, 21 de novembro de 2019

Low-carb diet may reduce diabetes risk independent of weight loss

Researchers report reversal of metabolic syndrome in some cases

Date: June 20, 2019 Source: Ohio State University Summary: A low-carb diet may have benefits for people at risk of developing type 2 diabetes even if they don't lose any weight, a new study suggests.

A low-carb diet may have benefits for people at risk of developing type 2 diabetes even if they don't lose any weight, a new study suggests.

Researchers at The Ohio State University wanted to know what happens to obese people with metabolic syndrome, a precursor to diabetes, when they eat a diet low in carbohydrates but don't shed any pounds. They found that more than half of study participants no longer met the criteria for metabolic syndrome immediately following a four-week low-carb diet.

The new study included 16 men and women with metabolic syndrome, a cluster of factors that also put people at higher risk of heart disease and stroke. The conditions that contribute to metabolic syndrome include high blood pressure, high blood sugar, excess body fat around the waist and abnormally low 'good' HDL cholesterol or high triglyceride levels. About a third of American adults have the syndrome, according to the American Heart Association.

After eating a low-carb diet, more than half the participants -- five men and four women -- saw their metabolic syndrome reversed even though they were fed diets that intentionally contained enough calories to keep their weight stable.

Previous work in the Ohio State lab and elsewhere has shown that low-carb diets can be beneficial for people with metabolic syndrome and diabetes, but nutrition scientists and others have debated whether that's a product of the diet or a product of the weight loss typically seen when people reduce carbs, said the study's senior author, Jeff Volek, a professor of human sciences at Ohio State.

"There's no doubt that people with metabolic syndrome and type 2 diabetes do better on low-carb diets, but they typically lose weight and one of the prevailing thoughts is that the weight loss is driving the improvements. That was clearly not the case here," Volek said.

"Our view is that restricting carbs even without weight loss improves a host of metabolic problems. Obviously, quality of diet matters because quantity is locked down in this experiment."

The study appears today (June 20) in the Journal of Clinical Investigation Insight.

Over about four months, each study participant ate three month-long controlled diets -- high-carb, moderate-carb and low-carb -- with a two-week break between diets. The order in which the participants ate the diets was randomly assigned.

The research team, led by research scientist Parker Hyde, ensured that the participants would not lose weight by providing them with pre-prepared meals that contained an amount of calories equal to their energy expenditure.

After eating the low-carb diet, the participants had a variety of significantly improved health measures, particularly lower triglycerides and improved cholesterol readings. Despite the fact that the low-carb diet contained 2.5 times more saturated fat than the high-carb diet, it decreased saturated fat in the bloodstream and was associated with an increase in the size of cholesterol particles in the blood, which decreases the risk of cardiovascular disease, Hyde said.

The researchers also report evidence of increased fat-burning efficiency after a low-carb diet and an improvement in blood sugar. They did not see statistically significant improvements in blood pressure or insulin resistance.

Three participants no longer had metabolic syndrome after the moderate-carbohydrate diet and one no longer had the syndrome after the high-carb diet. Volek said that those results are likely explained by the fact that even these study diets -- particularly the moderate-carb diet -- represented a shift toward fewer carbs for study participants.

"Even a modest restriction is carbs is enough to reverse metabolic syndrome in some people, but others need to restrict even more," he said.

Because of the study design, waist circumference was not factored in as a contributor to metabolic syndrome. Had the participants been permitted to lose weight, it is likely that several more would have been considered free of the condition after the low-carb diet, Volek said.

This research doesn't address the potential long-term benefits and challenges of adopting a low-carbohydrate diet, and the researchers suggest that future long-term diet studies on people with metabolic syndrome need to include low-carb diets.

The research was supported by the National Dairy Council and the Dutch Dairy Association.

Story Source:

Materials provided by Ohio State University. Original written by Misti Crane. Note: Content may be edited for style and length.

Journal Reference:

Parker N. Hyde, Teryn N. Sapper, Christopher D. Crabtree, Richard A. LaFountain, Madison L. Bowling, Alex Buga, Brandon Fell, Fionn T. McSwiney, Ryan M. Dickerson, Vincent J. Miller, Debbie Scandling, Orlando P. Simonetti, Stephen D. Phinney, William J. Kraemer, Sarah A. King, Ronald M. Krauss, Jeff S. Volek. Dietary carbohydrate restriction improves metabolic syndrome independent of weight loss. JCI Insight, 2019; 4 (12) DOI: 10.1172/jci.insight.128308

Cite This Page:

Ohio State University. "Low-carb diet may reduce diabetes risk independent of weight loss: Researchers report reversal of metabolic syndrome in some cases." ScienceDaily. ScienceDaily, 20 June 2019. <www.sciencedaily.com/releases/2019/06/190620100036.htm>.

Vanilla makes milk beverages seem sweeter

Date: June 20, 2019 Source: Penn State Summary: Adding vanilla to sweetened milk makes consumers think the beverage is sweeter, allowing the amount of added sugar to be reduced, according to new researchers, who will use the concept to develop a reduced-sugar chocolate milk for the National School Lunch Program.

Adding vanilla to sweetened milk makes consumers think the beverage is sweeter, allowing the amount of added sugar to be reduced, according to Penn State researchers, who will use the concept to develop a reduced-sugar chocolate milk for the National School Lunch Program.

"We are utilizing a learned association between an odor and a taste that will allow us to reduce the added sugar content," said Helene Hopfer, assistant professor of food science. "Reducing added sugar in products, just like reducing fat and salt, is the holy grail of food science."

The idea that congruent or harmonious odors enhance certain tastes is not new, explained Hopfer, whose research group in the College of Agricultural Sciences has been experimenting with these "cross-modal interactions" in food since she came to Penn State three years ago. Her goal is to see them actually incorporated into foods.

In a blind taste test that provided new insights into taste enhancement by an aroma, participants -- who did not know vanilla had been added to the milk -- consistently indicated that samples with vanilla were significantly sweeter than their added sugar concentrations could explain.

The subjects' responses indicate that with the addition of vanilla, the added sugar content in flavored milk could potentially be reduced by 20 to 50 percent, suggested lead researcher Gloria Wang, and people should not be able to perceive the beverage as less sweet.

"We maintain the sweetness perception by having this congruent odor -- this learned, associated odor -- basically trick the brain into thinking that there is still enough sweetness there," she said. "Based on our results, taste-aroma interaction is a robust effect."

Wang, now an associate scientist in product development with Leprino Foods Co. in Colorado, conducted the research at Penn State as part of her master's degree thesis in food science. She tested not only congruent taste-aroma combinations but incongruent combinations as well. It turned out that even a beef odor in milk slightly enhanced sweetness for study participants.

Given widespread concerns about sugar intake and health, manufacturers are reformulating their products to help address consumer demand, Wang noted. She believes the findings of the research, recently published in Food Quality and Preference, offer them a workable option to reduce added sugar in their products and retain the sweetness consumers demand.

The study was novel because it did not ask participants to rate individual attributes of the milk such as sweetness, intensity of vanilla odor or milk taste. Instead, participants took a more holistic approach and simply selected the best match for the vanilla milk from four differently sweetened milk choices.

Later this summer, Hopfer's lab in the Department of Food Science will start working on a two-year project, funded by the National Dairy Council, aimed at developing a reduced-sugar chocolate milk for the National School Lunch Program. The effort, based on the recent research using the synergistic actions between vanilla and sugar to reduce the added sugar content, will be a challenge because of the inherent bitterness of cocoa.

"The amount of sugar in chocolate milk is quite high because cocoa is very bitter, so you need some sugar to decrease the bitterness of the cocoa and then more to make it sweet," Hopfer said. "We are hoping to utilize what we found with odors to reduce the added sugar content by experimenting to find the sweet spot between cocoa powder, sugar content and vanilla flavor. We know that if it isn't sweet, children won't drink it."

Also involved in the research were Alyssa Bakke, staff sensory scientist in food science, and John Hayes, associate professor of food science and director of the Penn State Sensory Evaluation Center.

The U.S. Department of Agriculture's National Institute of Food and Agriculture supported this work.

Story Source:

Materials provided by Penn State. Original written by Jeff Mulhollem. Note: Content may be edited for style and length.

Cite This Page:

Penn State. "Vanilla makes milk beverages seem sweeter." ScienceDaily. ScienceDaily, 20 June 2019. <www.sciencedaily.com/releases/2019/06/190620121410.htm>.

Omega-3 fatty acids fight inflammation via cannabinoids

Date: July 18, 2017 Source: University of Illinois at Urbana-Champaign Summary: Chemical compounds called cannabinoids are found in marijuana and also are produced naturally in the body from omega-3 fatty acids. A well-known cannabinoid in marijuana, tetrahydrocannabinol, is responsible for some of its euphoric effects, but it also has anti-inflammatory benefits. A new study in animal tissue reveals the cascade of chemical reactions that convert omega-3 fatty acids into cannabinoids that have anti-inflammatory benefits - but without the psychotropic high.

Chemical compounds called cannabinoids are found in marijuana and also are produced naturally in the body from omega-3 fatty acids. A well-known cannabinoid in marijuana, tetrahydrocannabinol, is responsible for some of its euphoric effects, but it also has anti-inflammatory benefits. A new study in animal tissue reveals the cascade of chemical reactions that convert omega-3 fatty acids into cannabinoids that have anti-inflammatory benefits -- but without the psychotropic high.

The findings are published in the Proceedings of the National Academy of Sciences.

Foods such as meat, eggs, fish and nuts contain omega-3 and omega-6 fatty acids, which the body converts into endocannabinoids -- cannabinoids that the body produces naturally, said Aditi Das, a University of Illinois professor of comparative biosciences and biochemistry, who led the study. Cannabinoids in marijuana and endocannabinoids produced in the body can support the body's immune system and therefore are attractive targets for the development of anti-inflammatory therapeutics, she said.

In 1964, the Israeli chemist Raphael Mechoulam was the first to discover and isolate THC from marijuana. To test whether he had found the compound that produces euphoria, he dosed cake slices with 10 milligrams of pure THC and gave them to willing friends at a party. Their reactions, from nonstop laughter, to lethargy, to talkativeness, confirmed that THC was a psychotropic cannabinoid.

It wasn't until 1992 that researchers discovered endocannabinoids produced naturally in the body. Since then, several other endocannabinoids have been identified, but not all have known functions.

Cannabinoids bind to two types of cannabinoid receptors in the body -- one that is found predominantly in the nervous system and one in the immune system, Das said.

"Some cannabinoids, such as THC in marijuana or endocannabinoids can bind to these receptors and elicit anti-inflammatory and anti-pain action," she said.

"Our team discovered an enzymatic pathway that converts omega-3-derived endocannabinoids into more potent anti-inflammatory molecules that predominantly bind to the receptors found in the immune system," Das said. "This finding demonstrates how omega-3 fatty acids can produce some of the same medicinal qualities as marijuana, but without a psychotropic effect."

Story Source:

Materials provided by University of Illinois at Urbana-Champaign. Original written by Steph Adams. Note: Content may be edited for style and length.

Journal Reference:

Daniel R. McDougle, Josephine E. Watson, Amr A. Abdeen, Reheman Adili, Megan P. Caputo, John E. Krapf, Rodney W. Johnson, Kristopher A. Kilian, Michael Holinstat, Aditi Das. Anti-inflammatory ω-3 endocannabinoid epoxides. Proceedings of the National Academy of Sciences, 2017; 201610325 DOI: 10.1073/pnas.1610325114

Cite This Page:

University of Illinois at Urbana-Champaign. "Omega-3 fatty acids fight inflammation via cannabinoids." ScienceDaily. ScienceDaily, 18 July 2017. <www.sciencedaily.com/releases/2017/07/170718142909.htm>.

Using omega 3 fatty acids to treat Alzheimer's and other diseases?

Date: July 18, 2017 Source: Louisiana State University Health Sciences Center Summary: Understanding how dietary essential fatty acids work may lead to effective treatments for diseases and conditions such as stroke, Alzheimer's disease, age-related macular degeneration, Parkinson's disease and other retinal and neurodegenerative diseases. The key is to be able to intervene during the early stages of the disease.

Understanding how dietary essential fatty acids work may lead to effective treatments for diseases and conditions such as stroke, Alzheimer's disease, age-related macular degeneration, Parkinson's disease and other retinal and neurodegenerative diseases. The key is to be able to intervene during the early stages of the disease. That is the conclusion of a Minireview by Nicolas Bazan, MD, PhD, Boyd Professor and Director, and Aram Asatryan, PhD, postdoctoral researcher, at the Neuroscience Center of Excellence at LSU Health New Orleans School of Medicine published in the Journal of Biological Chemistry's Thematic Minireview Series: Inflammatory transcription confronts homeostatic disruptions.

Docosahexaenoic acid (DHA), a key essential Omega-3 fatty acid, produces signaling molecules called docosanoids in response to disruptions in the state of equilibrium within cells caused by injury or disease. Neuroprotectin D1 (NDP1) is a docosanoid that the Bazan lab discovered and found protects neurons by controlling which and how certain genes in the retina and brain respond.

Research shows that the preclinical events in Alzheimer's disease including neuroinflammation, damage to dendritic spines -- small doorknob-shaped protrusions that help transmit electrical signals to the cell -- and problems with cell-to-cell communication coincide with decreased DHA content in the brain. The neuroprotective bioactivity of NPD1 includes inflammatory modulating properties as well as features that promote cell survival, both of which contribute to restoring a stable state of equilibrium, or homeostasis, within the cell.

In experimental models of stroke, researchers at LSU Health New Orleans Neuroscience Center led by Bazan have shown that the administration of NPD1 reduces the size of stroke damage and also saves tissue in the rim surrounding the stroke core, which remains viable for a short time.

Research has demonstrated that DHA from the liver is also retained and concentrated in photoreceptor cells and that retinal degeneration occurs when photoreceptor cells fail to capture DHA. When a gene that regulates the uptake of DHA is turned off, photoreceptor cells die and a single amino acid mutation in this receptor can cause retinitis pigmentosa.

Cells die through a variety of mechanisms. Contributors include a family of reactive oxygen species -- compounds formed continuously as by-products of aerobic metabolism such as from reactions to drugs and environmental toxins, or when the levels of antioxidants are diminished creating oxidative stress, as well as inflammation and the disease process. Cell death is considered to be reversible until a first "point of no return" checkpoint is passed. The authors describe how NPD1 acts to stop cells from passing that checkpoint in cell death activation pathways including apoptosis, necrosis, necroptosis, pyroptosis, and pyronecrosis, among others.

The Minireview summarizes the effects of the essential fatty acid family member DHA and its bioactive derivative NPD1 in the context of a specific target of gene regulation. The authors also describe the mechanism of a pathway of regulation by a bioactive lipid that has a significant impact on cellular homeostasis -- how NPD1 activates pro-survival genes and suppresses pro-death genes.

"The organizational and functional complexity of the brain raises new questions regarding how the cellular events described here operate in response to disrupted homeostasis to attain neuroprotection in pathological conditions," notes Bazan. "It is our hope that this knowledge will contribute to managing early stages of such devastating diseases as Alzheimer's, stroke, traumatic brain injury, age-related macular degeneration, Parkinson's and others."

Story Source:

Materials provided by Louisiana State University Health Sciences Center. Note: Content may be edited for style and length.

Journal Reference:

Aram Asatryan, Nicolas G. Bazan. Molecular mechanisms of signaling via the docosanoid neuroprotectin D1 for cellular homeostasis and neuroprotection. Journal of Biological Chemistry, 2017; jbc.R117.783076 DOI: 10.1074/jbc.R117.783076

Cite This Page:

Louisiana State University Health Sciences Center. "Using omega 3 fatty acids to treat Alzheimer's and other diseases?." ScienceDaily. ScienceDaily, 18 July 2017. <www.sciencedaily.com/releases/2017/07/170718124732.htm>.

sexta-feira, 15 de novembro de 2019

Health benefits of the Mediterranean diet are confirmed, but just for the upper class

Only the most advantaged people actually benefit from the Mediterranean diet, Italian study says

Date: August 1, 2017 Source: Istituto Neurologico Mediterraneo Neuromed I.R.C.C.S. Summary: The Mediterranean diet reduces the risk of cardiovascular disease but only if you are rich or highly educated. This is the surprising finding by researchers who performed a study on over 18,000 subjects.

The Mediterranean diet reduces the risk of cardiovascular disease but only if you are rich or highly educated. This is the surprising finding by researchers from the Italian I.R.C.C.S. Neuromed, who performed a study on over 18,000 subjects recruited within the Moli-sani study and published in the International Journal of Epidemiology.

Cardiovascular advantages associated with the Mediterranean diet are well-known but now the Italian study, conducted by a team of researchers at the Department of Epidemiology and Prevention led by Giovanni de Gaetano, reveals that such benefits are strongly influenced by the socioeconomic position of people. Basically, given a comparable adherence to this eating pattern, the study has shown that the reduction in cardiovascular risk is observed only in people with higher educational level and/or greater household income. No actual benefits were observed for the less advantaged groups.

"The cardiovascular benefits associated with the Mediterranean diet in a general population are well known -- says Marialaura Bonaccio, researcher at the Department of Epidemiology and Prevention and first author of the study -- Yet for the first time our study has revealed that the socioeconomic position is able to modulate the health advantages linked to Mediterranean diet. In other words, a person from low socioeconomic status who struggles to follow a Mediterranean model, is unlikely to get the same advantages of a person with higher income, despite the fact that they both similarly adhere to the same healthy diet."

Neuromed researchers went further and tried to unravel the possible mechanisms underlying such disparities.

"Given a comparable adherence to the Mediterranean diet, the most advantaged groups were more likely to report a larger number of indices of high quality diet as opposed to people with low socioeconomic status -- explains Licia Iacoviello, head of the Laboratory of nutritional and molecular Epidemiology at the Department -- For example, within those reporting an optimal adherence to the Mediterranean diet (as measured by a score comprising fruits and nuts, vegetables, legumes, cereals, fish, fats, meat, dairy products and alcohol intake) people with high income or higher educational level consumed products richer in antioxidants and polyphenols, and had a greater diversity in fruit and vegetables choice. We have also found a socioeconomic gradient in the consumption of whole-grain products and in the preferred cooking methods. These substantial differences in consuming products belonging to Mediterranean diet lead us to think that quality of foods may be as important for health as quantity and frequency of intake."

"Our results should promote a serious consideration of socioeconomic scenario of health -- comments Giovanni de Gaetano, director of the Department -- Socioeconomic disparities in health are growing also in access to healthy diets. During the very last years, we documented a rapid shifting from the Mediterranean diet in the whole population, but it might also be that the weakest citizens tend to buy 'Mediterranean' food with lower nutritional value. We cannot be keeping on say that the Mediterranean diet is good for health -- de Gaetano concludes -- if we are not able to guarantee an equal access to it."

The Moli-sani Project

Started in March 2005, it involves about 25,000 citizens living in the Molise region. The aim is to learn about environmental and genetic factors underlying cardiovascular disease, cancer and degenerative pathologies. Moli-sani study, now based in I.R.C.C.S. Neuromed, has transformed an entire Italian region in a large research lab.

Story Source:

Materials provided by Istituto Neurologico Mediterraneo Neuromed I.R.C.C.S.. Note: Content may be edited for style and length.

Journal Reference:

Marialaura Bonaccio, Augusto Di Castelnuovo, George Pounis, Simona Costanzo, Mariarosaria Persichillo, Chiara Cerletti, Maria Benedetta Donati, Giovanni de Gaetano, Licia Iacoviello on behalf of the Moli-sani Study Investigators. High adherence to the Mediterranean diet is associated with cardiovascular protection in higher but not in lower socioeconomic groups: prospective findings from the Moli-sani study. International Journal of Epidemiology, 2017 DOI: 10.1093/ije/dyx145

Cite This Page:

Istituto Neurologico Mediterraneo Neuromed I.R.C.C.S.. "Health benefits of the Mediterranean diet are confirmed, but just for the upper class: Only the most advantaged people actually benefit from the Mediterranean diet, Italian study says." ScienceDaily. ScienceDaily, 1 August 2017. <www.sciencedaily.com/releases/2017/08/170801171047.htm>.

On the path to vitamin A in rice

Date: July 21, 2017 Source: Albert-Ludwigs-Universität Freiburg Summary: Biochemists have elucidated the structure of an enzyme that supplies carotenoid, investigators report. The lack of vitamin A in food is a major cause of health problems worldwide and can lead to blindness and even death. This is especially a problem in threshold or third-world countries, where children are likely to suffer from a lack of vitamin A or its precursor beta-carotene due to malnourishment.

The lack of vitamin A in food is a major cause of health problems worldwide and can lead to blindness and even death. This is especially a problem in threshold or third-world countries, where children are likely to suffer from a lack of vitamin A or its precursor beta-carotene due to malnourishment. Among their many functions, carotenoids are responsible for the bright orange color of sweet potatoes as well as their namesake, the carrot. Thanks to its intense color, beta-carotene is used in the food industry in soft drinks, yoghurts, and other food and is known as food coloring E160. Rice, which is the most important basic nutrient in Asia, has no beta-carotene in its kernel, but there are carotenoids in the leaves of the rice plant. These long, fat-soluble pigments are used by the plant not only in photosynthesis, during which the plant generates energy and oxygen, but in other processes as well.

One of the first precursors to beta-carotene is phytoene, which is colorless and not water-soluble and can be found in the lipid bilayer of plastid organelles -- in other words, in the outer layer of these closed cellular compartments, which is involved in many processes including photosynthesis. Here, the enzyme phytoene desaturase (PDS) transforms the phytoene into the next intermediate of synthesis, which already has a yellowish color. Researchers in the labs of Prof. Dr. Peter Beyer at the Faculty of Biology and Prof. Dr. Oliver Einsle at the Faculty of Chemistry and Pharmacy of the University of Freiburg have successfully elucidated the three-dimensional structure of phytoene desaturase in rice, along with the mechanism of phytoene transformation. In order to achieve this, Dr. Sandra Gemmecker and Anton Brausemann had to isolate the highly pure enzyme and crystalize it, so they could obtain a three-dimensional structural image through diffraction experiments with X-rays. They then discovered that the PDS becomes partially immersed in the lipid bilayer of the plastid organelles and contains a hydrophobic tunnel that leads into its interior. Catalysis begins when the phytoene molecule enters this tunnel and reaches the reaction center of the enzyme, where one half of the phytoene molecule is transformed into the next intermediary carotenoid stage. After this intermediary product leaves the tunnel the same way it came, it enters another PDS enzyme right next to the first, where it is completely transformed. A helper molecule known as a quinone then regenerates the enzyme. The quinone accesses the enzyme through the same tunnel and takes up excess electrons, thereby preparing the enzyme for the next reaction cycle.

If the PDS enzyme in a plant does not function properly, for example due to a reaction to a herbicide, then the plant's seedlings become pale and whitish instead of green and the plant dies within a few days. Since the early twentieth century, scientists worldwide have been working to reveal the exact mechanisms of carotene synthesis. This has proven difficult, however, due to the complicated composition of various enzyme complexes and because of their relatively low numbers in plant cells. The researchers from the University of Freiburg were able to elucidate the structure of the PDS enzyme using a specialty: They added a molecule of norflurazon, an herbicide developed in the 1970s, during the isolation of PDS. Due to the presence of norflurazon, PDS is deactivated and thus no longer available to the growing plant, causing it to bleach and die. Knowledge about the position and orientation of this bleaching herbicide within the enzyme can therefore be useful to researchers when developing new agents in the future. It is now also possible to induce specific changes in the sequence of the enzyme and use biotechnological procedures to give crops an advantage over weeds.

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Journal Reference:

Anton Brausemann, Sandra Gemmecker, Julian Koschmieder, Sandro Ghisla, Peter Beyer, Oliver Einsle. Structure of Phytoene Desaturase Provides Insights into Herbicide Binding and Reaction Mechanisms Involved in Carotene Desaturation. Structure, 2017; DOI: 10.1016/j.str.2017.06.002

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Albert-Ludwigs-Universität Freiburg. "On the path to vitamin A in rice." ScienceDaily. ScienceDaily, 21 July 2017. <www.sciencedaily.com/releases/2017/07/170721090111.htm>.

quinta-feira, 14 de novembro de 2019

Too much vitamin A may increase risk of bone fractures

Date: October 9, 2018 Source: Society for Endocrinology Summary: Consuming too much vitamin A may decrease bone thickness, leading to weak and fracture prone bones, according to a new study in mice.

Consuming too much vitamin A may decrease bone thickness, leading to weak and fracture prone bones, according to a study published in the Journal of Endocrinology. The study, undertaken in mice, found that sustained intake of vitamin A, at levels equivalent to 4.5-13 times the human recommended daily allowance (RDA), caused significant weakening of the bones, and suggests that people should be cautious of over-supplementing vitamin A in their diets.

Vitamin A is an essential vitamin that is important for numerous biological processes including growth, vision, immunity and organ function. Our bodies are unable to make vitamin A but a healthy diet including meat, dairy products and vegetables should be sufficient to maintain the body's nutritional needs. Some evidence has suggested that people who take vitamin A supplements may be increasing their risk of bone damage. Previous studies in mice have shown that short-term overdosing of vitamin A, at the equivalent of 13-142 times the recommended daily allowance in people, results in decreased bone thickness and an increased fracture risk after just 1-2 weeks. This study is the first to examine the effects of lower vitamin A doses that are more equivalent to those consumed by people taking supplements, over longer time-periods.

In this study, Dr Ulf Lerner and colleagues from Sahlgrenska Academy at the University of Gothenburg, report that mice given lower doses of vitamin A, equivalent to 4.5-13 times the RDA in humans, over a longer time period, also showed thinning of their bones after just 8 days, which progressed over the ten week study period.

Dr Ulf Lerner commented, "Previous studies in rodents have shown that vitamin A decreases bone thickness but these studies were performed with very high doses of vitamin A, over a short period of time. In our study we have shown that much lower concentrations of vitamin A, a range more relevant for humans, still decreases rodent bone thickness and strength."

Next, Dr Ulf Lerner intends to investigate if human-relevant doses of vitamin A affect bone growth induced by exercise, which was not addressed in this study. Additionally, his team will study the effects of vitamin A supplementation in older mice, where growth of the skeleton has ceased, as is seen in the elderly.

Dr Ulf Lerner cautions: "Overconsumption of vitamin A may be an increasing problem as many more people now take vitamin supplements. Overdose of vitamin A could be increasing the risk of bone weakening disorders in humans but more studies are needed to investigate this. In the majority of cases, a balanced diet is perfectly sufficient to maintain the body's nutritional needs for vitamin A."

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Materials provided by Society for Endocrinology. Note: Content may be edited for style and length.

Journal Reference:

Vikte Lionikaite, Karin L Gustafsson, Anna Westerlund, Sara H Windahl, Antti Koskela, Juha Tuukkanen, Helena Johansson, Claes Ohlsson, Herschel H Conaway, Petra Henning, Ulf H Lerner. Clinically relevant doses of vitamin A decrease cortical bone mass in mice. Journal of Endocrinology, 2018; DOI: 10.1530/JOE-18-0316

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