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    Home > Biochemistry News > Natural Products News > Several studies have shown that intermittent fasting can treat a variety of diseases!

    Several studies have shown that intermittent fasting can treat a variety of diseases!

    • Last Update: 2020-06-17
    • Source: Internet
    • Author: User
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    , June 6, 2020 /PRNewswire-Bio ValleyBIOON/-- For followers of popular science news or the latest diet craze, the word "intermittent fasting" is undoubtedly a trendEvery time you talk about a diet plan, it leads to more insight into the health benefits it can bringin the past six months alone, new studies have linked fasting to a reduced risk ofdiabetes, heart disease and many chronic inflammatory diseasesRegular fasting may also improve symptoms of multiple sclerosis and inflammatory bowel diseaseA study has found that 24 hours of rapid exercise can promote the regeneration ofstem cells in aging miceWhat's behind the potential benefits of these occasional non-eating? Research from Yale University shows that sugar-free foods have many benefits of fastingIt can prevent or reduce inflammation that causes or exacerbates many diseasesMoreover, each potential health benefit of eliminating sugar may come from different mechanismsto eat with a virus infection,bacteriato be hungry for infection?When DrAndrew Wang and Dr Ruslan Medzhitov discuss how they feed their children when they are sick, they begin to think about the reasons behind this old adage: "It's bad to eat, fever is good for hunger." "All animals, from worms to flies to dogs to dogs , do this , " Otto SteinerWhen we get seriously infected, we lose our appetite, and people have been wondering for a long time why this is the case," said Wang, an assistant professor in medicine (rheumatology) andof immunologythe two of them wanted to find out the potential benefits of fasting during illnessIn their 2016 study, published in the journal Cell, they force-fed an animal that was fighting a listeria infection, abacteriainfection, and diedFeeding animals that are struggling with influenza, a viral infection, can help them recoverwhen researchers break down food into the main ingredients -- protein, fat and sugar -- they found that sugar was the active ingredientInfected mice need glucose to adapt to the stress of antiviral inflammation and prevent cell death caused by stressHowever, inbacterialinfections, glucose blocks the action of ketogenic, which is necessary to combat oxidative stress in antibacterial inflammation, however, Wang said, "As a doctor, I don't want to simply say, 'If you think you're infected withbacteria
    go hungry, and if you think it's a virus, don't go hungry." and Wang has good reason to give this advice The role of glucose in inflammation is much more complex A lack of glucose may actually prepare the body for the flu before it is infected, new research suggests In fact, glucose promotes adaptation to inflammation after influenza infection, and a November 2019 study published in Science Immunology showed that mice with ketogenic effects were already better able to fight the flu in the study, mice on a high-fat, low-carbohydrate ketogenic diet who ate the flu were more likely to survive than those on a normal, high-carbohydrate diet The study found that a very low-carbohydrate diet activates a group of T cells in the lungs that were previously unrelated to the immune system's response to the flu T cells increase the production of mucus in airway cells and trap the virus while these studies point to the opposite effect of glucose in viral inflammation, they also raise different questions "Our 2016 study," Wang said, "askwhy animals eat less when they get the flu." So we feed them after they get infected and see what the impact is The new study raises the question' 'How does an animal affect its response to an influenza infection if it is in a ketogenic state?' 'I think it's clear from both studies that the metabolic state of the body before, during infection, and possibly during recovery is a key determinant of the body's overall prognosis in infection "
    glucose also plays a role in parasitic infections Wang and Medzhitov explored the relationship in a study published in 2018 in the Proceedings of the National Academy of Sciences (PNAS) When they stopped the sugar enzyme seislacofing mice with malaria, the mice did not develop into cerebral malaria glucose deficiency did not make mice resistant to malaria In fact, in both groups of mice, parasite burden, nerve inflammation, blood-brain barrier permeability, and anemia were the same However, blocking glucose makes mice more resistant to the disease Or, the study's authors argue that inhibiting glycoenzyme can reduce the parasite's own harm In any case, the mice had fewer micro-blood clots (tiny blood clots) in their brains, preventing the infection from spreading to the brain burning fat and delaying aging
    of course, inflammation is not just an acute response to new infections Almost all diseases of old age are associated with persistent inflammation If regulating glucose can alter the process of acute infection, does it also interfere with the life-long process of aging? "Most cells in the body work mainly on glucose, " says Dixit So, we want to know what happens when glucose is limited "The answer is more indicative of the health benefits of fasting and low-carbohydrate diets, such as ketogenic diets when the body does not have glucose as fuel, it burns fat as energy This process occurs during endurance exercise after fasting, hunger and the depletion of sugar reserves This can also happen on a low-carbohydrate diet picture source: Cell
    brain and heart are the biggest drains of energy from the body But when the body converts fat into long-chain fatty acids, they can't cross the blood-brain barrier As a result, the body converts it into short-chain fatty acids, especially a ketone metabolite called beta-hydroxybutyric acid, for use by the brain Dixit and his team wondered what happens to the function of immune cells when the body is fueled by fat Macrophages are mobile white blood cells that gather at the site of infection and feed on glucose when they become inflamed "If macrophages do not see glucose but are exposed to alternative fuels, how does this affect their activation?" "
    Dixit and his team found that beta-hydroxybutyrate can block an inflammatory protein complex called NLRP3 inflammatory small cells Right now, NLRP3 isn't all bad It plays an important role in the inflammatory response of acute infection However, Dixit explains, "If it is chronically activated, it can lead to a variety of chronic diseases, which are associated with the whole process of aging." "
    when the researchers injected inflamed mice with beta-hydroxybutyric acid, the ketone metabolites blocked the inflammatory glin, and the mice did not develop several age-related chronic diseases findings may help explain why the health benefits of popular diets such as intermittent fasting and ketones outweigh the of weight loss "Because when a person fasts," Dixit says, "the body has to burn fat, and the added metabolites in this process may reduce inflammation." "
    a spoonful of sugar a deeper understanding of the role of sugar in inflammation could lay the foundation for dietary recommendations and various inflammatory drugs that regulate glucose doesn't mean sugar is harmful "What we need is the right amount of food," Dixit said "
    no diet is for everyone "Different types of inflammation require different things," Wang says "So you have a lot of changeable parts, and finding a combination that gives you the best clinical results is not easy." " ( References: Ketostasis: Nature's Sweet Spot
    2- Ruslan Medzhitov et al.
    Specific sequences of the disease siel to secondary hemophoagocytic lymphohistiocis-like disease in mice PNAS 2019 DOI:
    3: Emily L Goldberg et al.
    Ketogenic diet activates sr t cell responses against influenza virus Science Immunology 15 Nov 2019: Vol 4, Issue 41, eaav2026 DOI: 10.1126/sciimmunol.aav2026
    4 Andrew Wang et al.
    Opposing Effects of The Saarings on The Tissue Tolerance in The and Viral Cell DOI:
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