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Mice fed a very high-salt diet showed accumulation of a protein in the brain linked with Alzheimer’s disease and other dementias
A diet high in salt is known to be a risk factor for high blood pressure, which in turn raises the risk of stroke and other health problems. Research has suggested that high salt intake may also be a risk factor for declining brain function with age. However, the mechanisms responsible for this link aren’t understood.
Previous studies suggested that high levels of salt in the diet can cause immune changes in the gut that lead to reduced blood flow in the brain and impaired cognition. In previous work, a team led by Dr. Costantino Iadecola at Weill Cornell Medicine found that mice fed a high-salt diet had reduced functioning of an enzyme called eNOS, which produces nitric oxide (NO).
NO helps direct blood vessels to relax, thereby increasing blood flow. Mice with a reduction in NO from the high-salt diet had reduced blood flow to the brain. These mice had trouble performing a standard set of cognitive tasks.
But the researchers suspected that the amount of reduced blood flow seen in these experiments wasn’t enough to directly affect cognition. In their new study, they explored how changes in the brain caused by a high-salt diet—and the resulting lowered NO production—might affect thinking and memory.
The team fed mice a very high-salt diet for 12 to 36 weeks. The mice underwent tests of cognitive function, and their brains were examined for molecular changes. The work was funded in part by NIH’s National Institute of Neurological Disorders and Stroke (NINDS). Results were published on October 23, 2019, in Nature.
The researchers found that high levels of dietary salt caused a chemical change to a protein called tau. This change—phosphorylation—can cause tau to clump together in the brain. Clumps of tau are linked with some dementias, such as Alzheimer’s disease.
As in their previous study, the team found that mice fed the high-salt diet had trouble recognizing novel objects and navigating through a maze. Mice with more phosphorylated tau in their brains had lower performance on these cognitive tasks.
When the mice were fed a high-salt diet supplemented with a compound that boosts NO production, they were protected against the accumulation of phosphorylated tau.
To confirm the link between salt intake, tau, and cognitive decline, the researchers fed the high-salt diet to mice that lacked tau. Those mice were protected from cognitive decline on the high-salt diet, even though they had reduced blood flow to the brain. Similar results were seen when tau was blocked in normal mice.
Further molecular studies showed that the effects of high salt on tau phosphorylation were mediated through NO levels, not through changes in blood flow.
“The take-home message here is that is that while there is a reduction in blood flow to the brains of mice that eat a high-salt diet, it really is tau that is causing the loss in cognitive abilities. The effect of reduced flow really is inconsequential in this setting,” Iadecola says.
The amount of salt fed to the mice was 8 to 16 times higher than that found in normal mouse chow. Most people wouldn’t approach such a high level in their diet. But the findings reveal a mechanism that might link high salt intake with reduced brain functioning. The results suggest that therapies targeting blood flow to the brain may not be enough to counter cognitive decline.
Ketogenic diet helps tame flu virus
Mice fed a ketogenic diet were better able to combat the flu virus than mice fed food high in carbohydrates, according to a new Yale University study published Nov. 15 in the journal Science Immunology.
The ketogenic diet -- which for people includes meat, fish, poultry, and non-starchy vegetables -- activates a subset of T cells in the lungs not previously associated with the immune system's response to influenza, enhancing mucus production from airway cells that can effectively trap the virus, the researchers report.
"This was a totally unexpected finding," said co-senior author Akiko Iwasaki, the Waldemar Von Zedtwitz Professor of Immunobiology and Molecular, Cellular and Developmental Biology, and an investigator of the Howard Hughes Medical Institute.
The research project was the brainchild of two trainees -- one working in Iwasaki's lab and the other with co-senior author Visha Deep Dixit, the Waldemar Von Zedtwitz Professor of Comparative Medicine and of Immunobiology. Ryan Molony worked in Iwasaki's lab, which had found that immune system activators called inflammasomes can cause harmful immune system responses in their host. Emily Goldberg worked in Dixit's lab, which had shown that the ketogenic diet blocked formation of inflammasomes.
The two wondered if diet could affect immune system response to pathogens such as the flu virus.
They showed that mice fed a ketogenic diet and infected with the influenza virus had a higher survival rate than mice on a high-carb normal diet. Specifically, the researchers found that the ketogenic diet triggered the release of gamma delta T cells, immune system cells that produce mucus in the cell linings of the lung -- while the high-carbohydrate diet did not.
When mice were bred without the gene that codes for gamma delta T cells, the ketogenic diet provided no protection against the influenza virus.
"This study shows that the way the body burns fat to produce ketone bodies from the food we eat can fuel the immune system to fight flu infection," Dixit said.
Sugar binges increase risk of inflammatory bowel disease
In a study published in Scientific Reports, U of A researchers found that mice had an increased susceptibility to chemically induced colitis and more severe symptoms after only two days of a high-sugar diet compared with those eating a balanced diet.
Karen Madsen, who specializes in diet and its effects on inflammatory bowel disease, said the results echo what many patients with colitis have been saying for a long time: small changes in their diet can make their symptoms flare up.
"It's been previously shown that the type of diet that you are on can change your susceptibility to disease," said Madsen, who led the new study.
"We wanted to know how long it takes before a change in diet translates into an impact on health. In the case of sugar and colitis, it only took two days, which was really surprising to us. We didn't think it would happen so quickly."
What could drive such a significant change in such a short time? It turns out it's all about gut bacteria and the impact food has on them.
Fibre-rich foods act as fuel for the "good" bacteria that live in the gut and produce short-chain fatty acids, which are critical for an efficient immune response. Eating high-sugar diets and decreasing intake of fibre feeds "bad" microbes, such as E. coli, that are associated with inflammation and a defective immune response.
Madsen's study showed that the mice on the high-sugar diet had greater intestinal tissue damage and a defective immune response. These problems were alleviated when their diet was supplemented with short-chain fatty acids normally produced by good bacteria.
"Surprisingly, our study shows that short-term sugar consumption can really have a detrimental impact, and so this idea that it's OK to eat well all week and indulge in junk food on the weekend is flawed," Madsen explained.
Followup studies could pave the way to possibly using short-chain fatty acids as dietary supplements, she noted.
"Changing someone's diet is one of the hardest things to do, even if you tell them that it will fix their health problems," she said.
"People want to eat what they want to eat, so short-chain fatty acids could possibly be used as supplements to help protect people against the detrimental effects of sugar on inflammatory bowel disease."
Madsen and her colleagues also showed that just two days on the high-sugar diet and the absence of short-chain fatty acids caused an increase in gut permeability, opening interesting avenues of research on how diet may affect the bacteria in our gastrointestinal tract and brain health.
"There is an increasing amount of evidence that suggests there's a link between the bacteria present in our gut and neurodegenerative diseases such as Alzheimer's and Parkinson's," explained Madsen.
"Because our study showed that gut permeability increased quite dramatically in the mice on the high-sugar diet--which means that bacterial products are free to move from the gut, where they normally stay, to the rest of the body--it raises the possibility that this phenomenon might be driving these diseases, but this needs to be looked into."
Frying oil consumption worsened colon cancer and colitis in mice
Foods fried in vegetable oil are popular worldwide, but research about the health effects of this cooking technique has been largely inconclusive and focused on healthy people. For the first time, UMass Amherst food scientists set out to examine the impact of frying oil consumption on inflammatory bowel disease (IBD) and colon cancer, using animal models.
In their paper published Aug. 23 in Cancer Prevention Research, lead author and Ph.D. student Jianan Zhang, associate professor Guodong Zhang, and professor and department head Eric Decker showed that feeding frying oil to mice exaggerated colonic inflammation, enhanced tumor growth and worsened gut leakage, spreading bacteria or toxic bacterial products into the bloodstream.
"People with colonic inflammation or colon cancer should be aware of this research," says Jianan Zhang.
Guodong Zhang, whose food science lab focuses on the discovery of new cellular targets in the treatment of colon cancer and how to reduce the risks of IBD, stresses that "it's not our message that frying oil can cause cancer."
Rather, the new research suggests that eating fried foods may exacerbate and advance conditions of the colon. "In the United States, many people have these diseases, but many of them may still eat fast food and fried food," says Guodong Zhang. "If somebody has IBD or colon cancer and they eat this kind of food, there is a chance it will make the diseases more aggressive."
For their experiments, the researchers used a real-world sample of canola oil, in which falafel had been cooked at 325 F in a standard commercial fryer at an eatery in Amherst, Massachusetts. "Canola oil is used widely in America for frying," Jianan Zhang says.
Decker, an expert in lipid chemistry performed the analysis of the oil, which undergoes an array of chemical reactions during the frying process. He characterized the fatty acid profiles, the level of free fatty acids and the status of oxidation.
A combination of the frying oil and fresh oil was added to the powder diet of one group of mice. The control group was fed the powder diet with only fresh oil mixed in. "We tried to mimic the human being's diet," Guodong Zhang says.
Supported by grants from the U.S. Department of Agriculture, the researchers looked at the effects of the diets on colonic inflammation, colon tumor growth and gut leakage, finding that the frying oil diet worsened all the conditions. "The tumors doubled in size from the control group to the study group," Guodong Zhang says.
To test their hypothesis that the oxidation of polyunsaturated fatty acids, which occurs when the oil is heated, is instrumental in the inflammatory effects, the researchers isolated polar compounds from the frying oil and fed them to the mice. The results were "very similar" to those from the experiment in which the mice were fed frying oil, suggesting that the polar compounds mediated the inflammatory effects.
While more research is needed, the researchers hope a better understanding of the health impacts of frying oil will lead to dietary guidelines and public health policies.
"For individuals with or prone to inflammatory bowel disease," Guodong Zhang says, "it's probably a good idea to eat less fried food."
In their paper published Aug. 23 in Cancer Prevention Research, lead author and Ph.D. student Jianan Zhang, associate professor Guodong Zhang, and professor and department head Eric Decker showed that feeding frying oil to mice exaggerated colonic inflammation, enhanced tumor growth and worsened gut leakage, spreading bacteria or toxic bacterial products into the bloodstream.
"People with colonic inflammation or colon cancer should be aware of this research," says Jianan Zhang.
Guodong Zhang, whose food science lab focuses on the discovery of new cellular targets in the treatment of colon cancer and how to reduce the risks of IBD, stresses that "it's not our message that frying oil can cause cancer."
Rather, the new research suggests that eating fried foods may exacerbate and advance conditions of the colon. "In the United States, many people have these diseases, but many of them may still eat fast food and fried food," says Guodong Zhang. "If somebody has IBD or colon cancer and they eat this kind of food, there is a chance it will make the diseases more aggressive."
For their experiments, the researchers used a real-world sample of canola oil, in which falafel had been cooked at 325 F in a standard commercial fryer at an eatery in Amherst, Massachusetts. "Canola oil is used widely in America for frying," Jianan Zhang says.
Decker, an expert in lipid chemistry performed the analysis of the oil, which undergoes an array of chemical reactions during the frying process. He characterized the fatty acid profiles, the level of free fatty acids and the status of oxidation.
A combination of the frying oil and fresh oil was added to the powder diet of one group of mice. The control group was fed the powder diet with only fresh oil mixed in. "We tried to mimic the human being's diet," Guodong Zhang says.
Supported by grants from the U.S. Department of Agriculture, the researchers looked at the effects of the diets on colonic inflammation, colon tumor growth and gut leakage, finding that the frying oil diet worsened all the conditions. "The tumors doubled in size from the control group to the study group," Guodong Zhang says.
To test their hypothesis that the oxidation of polyunsaturated fatty acids, which occurs when the oil is heated, is instrumental in the inflammatory effects, the researchers isolated polar compounds from the frying oil and fed them to the mice. The results were "very similar" to those from the experiment in which the mice were fed frying oil, suggesting that the polar compounds mediated the inflammatory effects.
While more research is needed, the researchers hope a better understanding of the health impacts of frying oil will lead to dietary guidelines and public health policies.
"For individuals with or prone to inflammatory bowel disease," Guodong Zhang says, "it's probably a good idea to eat less fried food."
from Health News Report https://ift.tt/2qKzlyG - health news
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