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Viruses can inflame and disrupt connections between the olfactory system, which governs the sense of smell, and the part of the brain associated with memory and learning, possibly accelerating the onset of Alzheimer’s disease, according to a new study from researchers at the University of Colorado Anschutz Medical Campus.
The findings, published Tuesday in the journal Neurobiology of Aging, could lead to new therapies that detect Alzheimer’s disease (AD) earlier while helping to illuminate the role that viruses and the olfactory system play in driving the illness.
“We know that one of the early signs of Alzheimer’s disease is losing the sense of smell,” said the study’s lead author Andrew Bubak, PhD, assistant research professor in the division of neurology at the University of Colorado School of Medicine.
Bubak’s team focused on the olfactory tract, olfactory bulb and the hippocampus, the area of the brain which manages memory and learning.
They examined messenger RNA in the brain tissue of six individuals from Colombia who had Familial Alzheimer’s disease (FAD) and tissue from a control group without AD. They found signatures of viral infection in the olfactory bulbs of the FAD group and inflammation in the olfactory tract which carries information to the hippocampus. They also discovered altered myelination in the olfactory tract. Myelin is a protective fatty layer around nerves that allows electrical impulses to move quickly and smoothly. If it’s damaged, signaling stalls.
“These findings raise the possibility that viral infection and associated inflammation and dysregulation of myelination of the olfactory system may disrupt hippocampal function, contributing to the acceleration of FAD progression,” the study said.
The study’s senior author, Diego Restrepo, PhD, professor of cell and developmental biology at the CU School of the Medicine, said viruses have long been suspected of playing a role in cognition problems. Some studies have associated the SARS-CoV-2 virus, which causes COVID-19, with dementia. The virus, which travels through the nose, causes some of those infected to lose their sense of smell.
At the same time, the varicella zoster virus which causes shingles and the herpes simplex virus can deposit amyloid beta, a protein critical to the development of AD, in the olfactory bulb. The viruses often linger for years even after symptoms have disappeared.
“Our hypothesis is that some viruses accelerate Alzheimer’s disease,” Restrepo said. “Does the loss of smell specifically accelerate Alzheimer’s? That’s the question.”
Bubak and Restrepo suspect inflammation and the amyloid deposits in the olfactory system interrupt communication with the hippocampus. Without sensory input, they believe, the hippocampus begins to degenerate.
“The whole olfactory pathway goes to the hippocampus. If you decrease the signaling along that pathway then you get less signaling to the hippocampus,” Bubak said. “If you don’t use it, you lose it.”
The researchers hope to next focus on better understanding the relationship between the olfactory system and the hippocampus in the context of viral susceptibility and neurodegeneration.
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Materials provided by University of Colorado Anschutz Medical Campus. Original written by David Kelly. Note: Content may be edited for style and length.

In a study published recently in the journal Clinical Cancer Research, researchers at Baylor College of Medicine found that treating patients who have resectable malignant pleural mesothelioma, meaning that their tumor can be removed with surgery, with immunotherapy ahead of surgery resulted in favorable clinical outcomes. The study lays the groundwork for neoadjuvant immunotherapy in mesothelioma.
“Mesothelioma is a devastating disease with low survivability,” said Dr. Bryan Burt, professor and chief of the David J. Sugarbaker Division of Thoracic Surgery in the Michael E. DeBakey Department of Surgery at Baylor and senior author of the paper. “Traditionally, this disease has defeated all standard therapies.”
Immune checkpoint inhibitors are drugs that activate the immune system to fight cancer. They have revolutionized the treatment of cancer in general, but only recently have been recognized to have some efficacy in mesothelioma. Recent research on the efficacy of immunotherapy for patients with unresectable mesothelioma showed favorable outcomes, which led Burt and colleagues to study this approach in patients with resectable mesothelioma.
“Surgery itself may not be curative, however combining surgery with some other modality of therapy often provides benefit,” said Burt, who also is a member of the Dan L Duncan Comprehensive Cancer Center at Baylor. “Our trial is an important step to evaluate whether checkpoint inhibitors are safe and feasible to give before surgery.”
One reason to give a therapy that increases the immune reactivity to a tumor pre-operatively is that the immunotherapy can activate an immune response that will persist after the tumor is resected. If the tumor tries to recur, the body has an existing memory immune response to fight it.
For this trial, participants with resectable mesothelioma were divided into two groups. The first received a single cycle of durvalumab, which blocks the PD-L1 checkpoint. The other group received a single cycle of a dual agent immunotherapy regimen, which included durvalumab plus tremelimumab, which blocks the CTLA-4 checkpoint. Both groups received the immunotherapy about three weeks ahead of surgery.
Surgeons biopsied the tumor before any treatment, then gave immunotherapy and removed more tissue during the resection procedure to evaluate how the drugs influenced the tumor microenvironment and to see how the drugs modulated the immune cells within the tumor.
The authors found that combination immunotherapy with durvalumab plus tremelimumab resulted in significant and favorable changes to the tumor microenvironment. The dual agent immunotherapy increased the number of important types of CD8 T cells in the tumor, which serve as the “soldiers” of the immune response that kill and remember the tumor. Although this trial was not designed primarily to investigate efficacy, a provocative signal in increased overall survival was found in the dual agent immunotherapy group.
The researchers continue to follow the participants in the study, who received the treatment more than three years ago.
As a next step to this research, Burt and Baylor mesothelioma surgeon Dr. R. Taylor Ripley have designed a larger study that will compare the dual agent immunotherapy with a chemo-immunotherapy.
Other authors on the study include Hyun-Sung Lee, Hee-Jin Jang, Maheshwari Ramineni, Daniel Y. Wang, Daniela Ramos, Jong Min Choi, Taylor Splawn, Monica Espinoza, Michelle Almarez, Leandria Hosey, Eunji Jo, Susan Hilsenbeck, Christopher I. Amos and R. Taylor Ripley, all with Baylor College of Medicine.
This work was supported by AstraZeneca, an NIH R37 MERIT Award, a Cancer Prevention and Research Institute of Texas grant, Michael E. DeBakey Department of Surgery seed grant and the Gutenstein Family Foundation. This project was also supported by the Cytometry and Cell Sorting Core at Baylor College of Medicine with funding from the NIH and CPRIT. This research was performed in the Flow Cytometry & Cellular Imaging Facility, which is supported in part by the National Institutes of Health through M.D. Anderson’s Cancer Center Support Grant CA016672, the NCI’s Research Specialist 1 R50 CA243707-01A1, and a Shared Instrumentation Award from the CPRIT RP121010. Dr. Amos is a CPRIT Research Scholar, supported by RR170048.

Research from the lab of Fangqiong Ling at Washington University in St. Louis showed earlier this year that the amount of SARS-CoV-2 in a wastewater system was correlated with the burden of disease — COVID-19 — in the region it served.
But before that work could be done, Ling needed to know: How can you figure out the number of individuals represented in a random sample of wastewater?
A chance encounter with a colleague helped Ling, an assistant professor in the Department of Energy, Environmental and Chemical Engineering at the McKelvey School of Engineering, develop a machine learning model that used the assortment of microbes found in wastewater to tease out how many individual people they represented. Going forward, this method may be able to link other properties in wastewater to individual-level data.
The research was published in the journal PLOS Computational Biology.
The problem was straightforward: “If you just take one scoop of wastewater, you don’t know how many people you’re measuring,” Ling said. This is counter to the way studies are typically designed.
“Usually when you design your experiment, you design your sample size, you know how many people you’re measuring,” Ling said. Before she could look for a correlation between SARS-CoV-2 and the number of people with COVID, she had to figure out how many people were represented in the water she was testing.

Patients with treatment resistant depression have a 23 per cent higher risk of death than other depressed patients. They also have twice as much outpatient care and spend three times the number of days in inpatient care. These are findings of a new study published in JAMA Psychiatry by researchers from Karolinska Institutet and elsewhere, who conclude that it is important to identify patients at risk of developing treatment resistant depression.   
Depression is the leading cause of functional disability the world over. The most common treatments are antidepressants or psychotherapy. Many sufferers need care for months or years, but a significant share of patients never recover despite two well-implemented treatment attempts. They have what is commonly called treatment resistant depression.   
Researchers at Karolinska Institutet and the Centre for Psychiatric Research have now examined the effects of treatment resistant depression in Region Stockholm at both an individual and societal level, something that has not been studied to the same extent previously.  
Examined patients around Stockholm
In the population-based observation study, the researchers used data from several sources, including Region Stockholm’s administrative healthcare database and the Swedish Social Insurance Agency. Over 145,000 patients with depression in the Stockholm region were included in the study.   
Having identified 158,000 depressive episodes in these patients between 2012 and 2017, of which in excess of 12,000 were of a treatment-resistant nature, the researchers were able to draw a number of conclusions about what characterises patients with treatment resistant depression.   
“We found that the treatment-resistant group used outpatient resources twice as much, had twice the amount of sick leave, spent three times the number of days in hospital and had a 23 percent higher mortality rate than patients with treatment-responsive depression,” says Johan Lundberg, adjunct professor of psychiatry at the Department of Clinical Neuroscience and head of the mood disorder section at the Northern Stockholm Psychiatry Clinic.   

Some species of gut-dwelling bacteria activate nerves in the gut to promote the desire to exercise, according to a study in mice that was led by researchers at the Perelman School of Medicine at the University of Pennsylvania. The study was published today in Nature, and reveals the gut-to-brain pathway that explains why some bacteria boost exercise performance.
In the study, the researchers found that differences in running performance within a large group of lab mice were largely attributable to the presence of certain gut bacterial species in the higher-performing animals. The researchers traced this effect to small molecules called metabolites that the bacteria produce — metabolites that stimulate sensory nerves in the gut to enhance activity in a motivation-controlling brain region during exercise.
“If we can confirm the presence of a similar pathway in humans, it could offer an effective way to boost people’s levels of exercise to improve public health generally,” said study senior author Christoph Thaiss, PhD, an assistant professor of Microbiology at Penn Medicine.
Thaiss and colleagues set up the study to search broadly for factors that determine exercise performance. They recorded the genome sequences, gut bacterial species, bloodstream metabolites, and other data for genetically diverse mice. They then measured the amount of daily voluntary wheel running the animals did, as well as their endurance.
The researchers analyzed these data using machine learning, seeking attributes of the mice that could best explain the animals’ sizeable inter-individual differences in running performance. They were surprised to find that genetics seemed to account for only a small portion of these performance differences — whereas differences in gut bacterial populations appeared to be substantially more important. In fact, they observed that giving mice broad-spectrum antibiotics to get rid of their gut bacteria reduced the mice’s running performance by about half.
Ultimately, in a years-long process of scientific detective work involving more than a dozen separate laboratories at Penn and elsewhere, the researchers found that two bacterial species closely tied to better performance, Eubacterium rectale and Coprococcus eutactus, produce metabolites known as fatty acid amides (FAAs). The latter stimulate receptors called CB1 endocannabinoid receptors on gut-embedded sensory nerves, which connect to the brain via the spine. The stimulation of these CB1 receptor-studded nerves causes an increase in levels of the neurotransmitter dopamine during exercise, in a brain region called the ventral striatum.
The striatum is a critical node in the brain’s reward and motivation network. The researchers concluded that the extra dopamine in this region during exercise boosts performance by reinforcing the desire to exercise.
“This gut-to-brain motivation pathway might have evolved to connect nutrient availability and the state of the gut bacterial population to the readiness to engage in prolonged physical activity,” said study co-author, J. Nicholas Betley, PhD, an associate professor of Biology at the University of Pennsylvania’s School of Arts and Sciences. “This line of research could develop into a whole new branch of exercise physiology.”
The findings open up many new avenues of scientific investigation. For example, there was evidence from the experiments that the better-performing mice experienced a more intense “runner’s high” — measured in this case by a reduction in pain sensitivity — hinting that this well-known phenomenon is also at least partly controlled by gut bacteria. The team now plans further studies to confirm the existence of this gut-to-brain pathway in humans.
Apart from possibly offering cheap, safe, diet-based ways of getting ordinary people running and optimizing elite athletes’ performance, he added, the exploration of this pathway might also yield easier methods for modifying motivation and mood in settings such as addiction and depression.
The study was led by Penn Medicine scientist Lenka Dohnalová. Other Penn Medicine authors include: Patrick Lundgren, Jamie Carty, Nitsan Goldstein, Lev Litichevskiy, Hélène Descamps, Karthikeyani Chellappa, Ana Glassman, Susanne Kessler, Jihee Kim, Timothy Cox, Oxana Dmitrieva-Posocco, Andrea Wong, Erik Allman, Soumita Ghosh, Nitika Sharma, Kasturi Sengupta, Mark Sellmyer, Garret FitzGerald, Andrew Patterson, Joseph Baur, Amber Alhadeff, and Maayan Levy.
The study was supported in part by the National Institutes of Health (S10-OD021750, DP2AG067492, R01-DK-129691, , P01-DK119130 and R01-DK115578), the Pew Charitable Trust, the Edward Mallinckrodt, Jr. Foundation, the Agilent Early Career Professor Award, the Global Probiotics Council, the IDSA Foundation, the Thyssen Foundation, the Human Frontier Science Program, and Penn Medicine, including the Dean’s Innovation Fund.

Published1 day agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty Images/VCGBy Kerry AllenBBC MonitoringChina is facing problems with stockpiling after it relaxed its most severe Covid-19 policies last week. People have been rushing to buy ibuprofen, cold medicines and Covid testing kits amid reports of shortages. Products for home remedies are now largely unavailable online, including lemons and canned peaches rich in vitamin C, and electrolysed water. Hoarding has been a common global issue but this may be the first instance of it after lockdowns were eased. In China, as elsewhere in the world, it has been common to see people sharing pictures online of bare grocery aisles in major cities ahead of strict “stay at home” orders being imposed. But now the country has eased track-and-trace rules, and has allowed people to self-isolate at home and self-test for the virus, people appear to be panic-buying medicines in anticipation of a winter wave. Local governments have been urged to upgrade their ICU units and open fever clinics by the end of the month “in preparation for waves of infection”. And there are already signs that the health system is being quickly overwhelmed. Video has circulated this week of patients being hooked up to IV drips from their cars “as clinics are full”. Patients in China were getting treated while hooked up to IV drips in their cars because local clinics in several provinces are fully-booked. pic.twitter.com/xVVp2aKrge— South China Morning Post (@SCMPNews) December 14, 2022
The BBC is not responsible for the content of external sites.View original tweet on TwitterChina Daily reports on how there has been an “explosive growth in demand” for pain-relief medicines, vitamins and cold/flu drugs. Some outlets have shared pictures of empty pharmacy aisles, and media have been running stories throughout the week on how production lines at pharmaceutical firms are now working “full capacity” to deal with the surge of demand. The China Daily newspaper noted that panic-buying had been so rife that the government in the city of Guangzhou had called for “sensible purchasing”. “There is no need for hoarding them in large quantities,” it said in a statement. Guangzhou is the city that has seen the highest number of cases of the virus in recent weeks. Last week, the Global Times newspaper also observed that the turnover for Covid-19 detection kits had increased more than 300% in line with China’s new eased Covid policies. It said that kits quickly became out of stock on leading platforms like JD Health. Frequently labelled ‘out of stock’ News website The Paper adds that “consumer demand for vitamin C has skyrocketed”. Image source, Sina WeiboIt reports that lemons have sold out on some shopping platforms, as well as “lemon-flavoured tea, lemon-flavoured sweets and lemon-flavoured sparkling water”. China Daily observes a similar trend with tinned peaches. It notes that as the products are “rich in vitamin C” and “have a longer shelf life”, they have become coveted products both online and offline. “On some online shopping platforms, the demand for canned yellow peaches is rising so sharply that they are frequently labelled ‘out of stock’,” the newspaper says. Sina News says that rumours have spread online that they can “relieve symptoms” of Covid-19. Image source, Future PublishingDoctors, however, have disputed this, with some appearing on leading broadcaster CCTV warning people not to take vitamin C “in excess”. Some have even warned that excessively eating peaches could “aggravate a cough”. Other therapies have also quickly been tipped to follow suit in selling out online. Pear Video observed a surge of people rushing to buy electrolyte water, after it was marketed as “helpful with hydration after sweating or a fever”. The Global Times also adds that that rumours have circulated online that “drinking high quantities of alcohol”, can “prevent” or “kill the virus” and has warned people that there are only health dangers at doing so.China Covid: Hospitals under strain in wave of infectionsChina abandons key parts of zero-Covid strategy after protestsPapers are saturated with warnings from doctors at the moment against people “blindly” buying drugs, mixing medicines, or taking more than is necessary. Image source, Getty Images/VCGChina’s Food and Drink Administration has urged drug-related companies to “ensure the quality, safety and supply” of Covid-19 therapies. It has vowed strengthened supervision over the production and circulation of such products. Market supervisory authorities are warning consumers not to buy touted Covid-19 therapies online unless livestreamers have proper medical qualifications. Advice is being given to people to buy products through credited channels, so that they do not buy “counterfeit drugs”.Outlets are also stressing that “health kits” are being arranged to ensure that especially vulnerable patients are not left more vulnerable. China Daily reports that elderly residents and those with chronic diseases are receiving packs that contain medicines, antigen tests and throat syrups in the city of Wuhan, China’s original Covid-10 epicentre. Follow Kerry on Twitter: @kerrya11enMore on this storyCovid wave batters China’s overstretched hospitals1 day agoChina abandons key parts of zero-Covid strategy7 December

In a new study, researchers have taken a close look at three treatment approaches that have been widely believed to slow the aging process. However, when tested in mice, these treatments proved largely ineffective in their supposed impact on aging. “There is no internal clock of aging that you can regulate with a simple switch — at least not in the form of the treatments studied here,” concludes Dr. Dan Ehninger of the DZNE, the initiator of the study. The team has developed a new analytical approach to make influences on aging processes measurable.
The study, the results of which have now been published in the journal Nature Communications, involved researchers from DZNE, Helmholtz Munich and the German Center for Diabetes (DZD). “We chose three regulators for our interventions that many experts believe slow down aging,” explains Prof. Dr. Martin Hrab? de Angelis, head of the Institute of Experimental Genetics and director of the German Mouse Clinic at Helmholtz Munich, who also drove the project with his team. One of them is intermittent fasting, in which the calories consumed are reduced. Number two targets a central node of cell metabolism (mTOR), which is also the target of the supposed “anti-aging drug” rapamycin. Number three, in turn, interferes with the release of growth hormone. Similar treatments are also used by humans, although their efficacy with regard to aging has not been sufficiently proven.
For the assessment in mice, the scientists developed a new answer to the question of how to measure aging. “Many researchers in recent decades have used lifespan as an indirect measure of aging,” explains Dan Ehninger, who is a senior scientist at DZNE. So, for example, how old do mice get — and how can that lifespan be extended? “It is often assumed that if they just live longer, they will also age more slowly. But the problem is that mice, like many other organisms, do not die from general old age, but from very specific diseases,” says Ehninger. For example, up to 90 percent of mice die from tumors that form in their bodies at an advanced age. “So, if you were to look at the whole genome for factors that make mice become long-lived, you would like find many genes that suppress tumor development — and not necessarily genes that play a general role in aging.”
For their study, the scientists therefore chose an approach that does not emphasize lifespan, but rather focused on a comprehensive investigation of age-related changes in a wide range of bodily functions. “You can think of it as a complete health status survey,” says Martin Hrab? de Angelis: “The health check results in a compendium of hundreds of factors covering many areas of physiology” — an exact description of the state of the animal at the moment of examination. That’s exactly the approach the researchers applied to the animals subjected to one of the three treatment approaches that supposedly slow aging. Across different life stages, they were analyzed and compared: How much does each parameter typically change at a given stage of life? And, do parameters change more slowly when the mice are given one of the three treatments? This study design makes it possible to determine precisely whether the natural aging process can be slowed, and with it the deterioration of important physiological functions.
The results were unambiguous: Although the researchers were able to identify individual cases in which old mice looked younger than they actually were it was clear that “this effect was not due to slowing down aging, but rather due to age-independent factors,” says Dan Ehninger. “The fact that a treatment already has its effect in young mice — prior to the appearance of age-dependent change in health measures — proves that these are compensatory, general health-promoting effects, not a targeting of aging mechanisms.”
The DZNE and Helmholtz Diabetes Center teams have now set their sights on the next goal: They want to investigate other treatment approaches that experts believe can slow aging. The researchers’ hope: The new research method will provide a more comprehensive picture of possible treatment approaches and their effectiveness.
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Materials provided by DZNE – German Center for Neurodegenerative Diseases. Note: Content may be edited for style and length.

Alzheimer’s disease (AD) is the fifth leading cause of death in adults over 65 years old. While many potential treatments for the neurodegenerative disease focus on developing drugs to target key culprits, a relatively new approach aims to more directly treat the brain. Deep brain stimulation (DBS) is a neurosurgical technique of electrically exciting brain circuits to alleviate symptoms of disorders such as Parkinson’s disease and obsessive-compulsive disorder. Preliminary use of DBS in AD patients has produced mixed results, with variation in cognitive outcomes. These different outcomes may be due to discrepancies in electrode placements across patients. Researchers from Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system, compared DBS targets in AD patients previously treated at seven international sites, finding that stimulating the intersection of two particular brain networks correlated with better patient outcomes than stimulating nearby sites. Findings are published in Nature Communications.
“Not many Alzheimer’s patients have been treated with DBS, and so isolating a targetable network and showing that it could be predictive of patient outcomes was exciting,” said corresponding author Andreas Horn, MD, PhD, of the Center for Brain Circuit Therapeutics. “We refined an optimal DBS site, which future clinical trials of DBS may now use, going forward. If more patients are stimulated at this region, we may see clearer evidence across the group supporting the effectiveness of DBS.”
With the collaboration of colleagues from Toronto Western Hospital and six other centers, forty-six patients with mild AD treated with DBS to the fornix (fx-DBS) were included in this study. The fornix is an essential structure involved in memory formation. Brigham researchers developed a software capable of precisely registering fx-DBS sites from individual patients into a standardized map of the brain. From there, the researchers calculated the target associated with optimal clinical outcomes and determined what modulations of local tracts and whole-brain networks led to best results. Cognitive improvement was associated with DBS to the direct interface between the fornix and bed nucleus of the stria terminalis (involved in emotional and behavioral responses), with tract connections to the circuit of Papez playing a role as well (this circuit connects to the hippocampus, a major center for memory formation).
Using an approach inspired by the machine-learning literature, the researchers validated their findings in a test cohort of 18 patients, whose data had been excluded from the initial stages of the research. They developed a model that was able to accurately determine clinical outcomes in these 18 patients based on where electrodes had been placed during their fx-DBS procedures.
The authors emphasize that this was a retrospective study, and prospective validation is required to further confirm their findings. They emphasize that neurodegeneration will progress even in patients who respond well to fx-DBS, but the procedure can potentially ameliorate symptoms.
As clinical trials of DBS continue, the researchers are looking to collaborate further with centers that conduct DBS to better define targetable networks for AD. They are also interested in further studying the exact circuits involved in memory formation based on stroke lesions that lead to cognitive decline.
“The data we used in this study are unique, and it was an honor that the team entrusted us with it so that we could apply methods we have developed over the past ten years to identify the sites in the brain that matter most for DBS in AD,” Horn said. “This is still basic science, but it may give hope in terms of potential treatments that, if applied correctly, could lead to symptomatic improvements.”
Funding: Horn is supported by the National Institutes of Health (R01 13478451, 1R01NS127892-01 & 2R01 MH113929), the New Venture Fund (FFOR Seed Grant), the German Research Foundation (424778381 — TRR 295), and the EU Joint Programme — Neurodegenerative Disease Research.
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Materials provided by Brigham and Women’s Hospital. Note: Content may be edited for style and length.

After an intermittent fasting diet intervention, patients achieved complete diabetes remission, defined as an HbA1c (average blood sugar) level of less than 6.5% at least one year after stopping diabetes medication, according to a new study published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.
Intermittent fasting diets have become popular in recent years as an effective weight loss method. With intermittent fasting, you only eat during a specific window of time. Fasting for a certain number of hours each day or eating just one meal a couple of days a week can help your body burn fat. Research shows intermittent fasting can lower your risk of diabetes and heart disease.
“Type 2 diabetes is not necessarily a permanent, lifelong disease. Diabetes remission is possible if patients lose weight by changing their diet and exercise habits,” said Dongbo Liu, Ph.D., of Hunan Agricultural University in Changsha, China. “Our research shows an intermittent fasting, Chinese Medical Nutrition Therapy (CMNT), can lead to diabetes remission in people with type 2 diabetes, and these findings could have a major impact on the over 537 million adults worldwide who suffer from the disease.”
The researchers conducted a 3-month intermittent fasting diet intervention among 36 people with diabetes and found almost 90% of participants, including those who took blood sugar-lowering agents and insulin, reduced their diabetes medication intake after intermittent fasting. Fifty-five percent of these people experienced diabetes remission, discontinued their diabetes medication and maintained it for at least one year.
The study challenges the conventional view that diabetes remission can only be achieved in those with a shorter diabetes duration (0-6 years). Sixty-five percent of the study participants who achieved diabetes remission had a diabetes duration of more than 6 years (6-11 years).
“Diabetes medications are costly and a barrier for many patients who are trying to effectively manage their diabetes. Our study saw medication costs decrease by 77% in people with diabetes after intermittent fasting,” Liu said.
The other authors of this study are Xiao Yang of Hunan Agricultural University, the State Key Laboratory of Subhealth Intervention Technology and Changsha and Tourism College in Changsha, China; Jiali Zhou of Hunan Agricultural University and the Department of Shizi Mountain Primary Care in Changsha, China; Huige Shao and Bi Huang of Changsha Central Hospital in Changsha, China; Xincong Kang of Hunan Agricultural University, the National Research Center of Engineering Technology for Utilization Ingredients From Botanicals and the Hunan Provincial Engineering Research Center of Medical Nutrition Intervention Technology for Metabolic Diseases in Changsha, China; Ruiyu Wu of Hunan Agricultural University and the State Key Laboratory of Subhealth Intervention Technology Achievement Application Center in Changsha, China; Fangzhou Bian of the University of California Irvine in Irvine, Calif.; and Minghai Hu of Central South University in Changsha, China.
The study received funding from the National Natural Science Foundation of China.
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Materials provided by The Endocrine Society. Note: Content may be edited for style and length.

It is well-known exercise has many benefits, but new Edith Cowan University (ECU) research has revealed just how critically important it can be — even for people with advanced cancer.
Previous work from ECU’s Exercise Medicine Research Institute has shown men with advanced prostate cancer can change the chemical environment of their body over six months of exercise training to suppress growth of cancer cells.
The team observed increased levels of proteins called ‘myokines’ which are produced by skeletal muscles and can suppress tumour growth and even help actively fight cancerous cells by stimulating a range of anti-cancer processes in the body.
But a new EMRI study has shown a single bout of exercise can elevate myokines even further and induce additional cancer suppression.
Importantly, this exercise induced medicine occurs in patients with incurable, advanced cancer where the disease has well and truly taken hold and patients have already received extensive treatment over many years.
Nine patients with late-stage prostate cancer performed 34 minutes of high intensity exercise on a stationary cycle, with blood serum collected immediately before and after, and then again 30 minutes post-workout.