New research shows that people who experience big dips in blood sugar levels, several hours after eating, end up feeling hungrier and consuming hundreds more calories during the day than others.
A study published today in Nature Metabolism, from PREDICT, the largest ongoing nutritional research program in the world that looks at responses to food in real life settings, the research team from King’s College London and health science company ZOE (including scientists from Harvard Medical School, Harvard T.H. Chan School of Public Health, Massachusetts General Hospital, the University of Nottingham, Leeds University, and Lund University in Sweden) found why some people struggle to lose weight, even on calorie-controlled diets, and highlight the importance of understanding personal metabolism when it comes to diet and health.
The research team collected detailed data about blood sugar responses and other markers of health from 1,070 people after eating standardized breakfasts and freely chosen meals over a two-week period, adding up to more than 8,000 breakfasts and 70,000 meals in total. The standard breakfasts were based on muffins containing the same amount of calories but varying in composition in terms of carbohydrates, protein, fat and fibre. Participants also carried out a fasting blood sugar response test (oral glucose tolerance test), to measure how well their body processes sugar.
Participants wore stick-on continuous glucose monitors (CGMs) to measure their blood sugar levels over the entire duration of the study, as well as a wearable device to monitor activity and sleep. They also recorded levels of hunger and alertness using a phone app, along with exactly when and what they ate over the day.
Previous studies looking at blood sugar after eating have focused on the way that levels rise and fall in the first two hours after a meal, known as a blood sugar peak. However, after analyzing the data, the PREDICT team noticed that some people experienced significant ‘sugar dips’ 2-4 hours after this initial peak, where their blood sugar levels fell rapidly below baseline before coming back up.
Big dippers had a 9% increase in hunger, and waited around half an hour less, on average, before their next meal than little dippers, even though they ate exactly the same meals.

A new probe into the lingering impacts of the COVID-19 pandemic revealed correlations to six unhealthy eating behaviors, according to a study by the University of Minnesota Medical School and School of Public Health. Researchers say the most concerning finding indicates a slight increase or the re-emergence of eating disorders, which kill roughly 10,200 people every year — about one person every 52 minutes.
U of M Medical School’s Melissa Simone, PhD, a postdoctoral research fellow in the Department of Psychiatry and Behavioral Sciences, collaborated with School of Public Health professor and head of the Division of Epidemiology and Community Health, Dianne Neumark-Sztainer, PhD, MPH, to learn from study participants in Neumark-Sztainer’s Project EAT between April and May 2020.
“The COVID-19 pandemic has resulted in the rapid implementation of public health policies to reduce transmission of the virus. While these protections are necessary, the disruptions to daily life associated with the ongoing pandemic may have significant negative consequences for the risk of eating disorders and symptoms,” said Simone, who is the lead author of the study. “Eating disorders have one of the highest mortality rates across all psychiatric health concerns, and therefore, it is important to try to make links between the consequences of the pandemic and disordered eating behaviors.
The study aimed to understand potential associations between stress, psychological distress, financial difficulties and changes in eating behaviors during the COVID-19 pandemic through the analysis of both qualitative and quantitative data. Simone’s findings, published in the International Journal of Eating Disorders, found six key themes of eating behavior changes: Mindless eating and snacking; Increased food consumption; Generalized decrease in appetite or dietary intake; Eating to cope; Pandemic-related reductions in dietary intake; And, a re-emergence or marked increase in eating disorder symptoms.Approximately 8% of those studied reported extreme unhealthy weight control behaviors, 53% had less extreme unhealthy weight control behaviors and 14% reported binge eating. The study revealed that these outcomes were significantly associated with poorer stress management, greater depressive symptoms and moderate or extreme financial difficulties.
“There has been a lot of focus on obesity and its connection with COVID-19. It is also important to focus on the large number of people who have been engaging in disordered eating and are at risk for eating disorders during and following the pandemic,” said Neumark-Sztainer, who is the principal investigator of Project EAT. “The majority of the young adults in our study are from diverse ethnic/racial and lower income backgrounds, who often do not receive the services they need. To ensure health inequities do not increase, we need to meet the needs of these populations.”
Simone added, “The economic consequences of the COVID-19 pandemic will likely persist long beyond the dissemination of a vaccine. Because our findings suggest that moderate or severe financial difficulties may be linked with disordered eating behaviors, it is essential that eating disorder preventive interventions and treatment efforts be affordable, easily accessible and widely disseminated to those at heightened risk. As such, online or mobile-based interventions may prove to be effective and accessible modes for targeted intervention efforts.”
This study was funded by the National Heart, Lung, and Blood Institute (R01HL116892, R35HL139853: Principal Investigator: D. Neumark-Sztainer), the National Center for Advancing Translational Sciences (TL1R002493, UL1TR002494), and the National Institute of Mental Health (T32MH082761).
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Non-alcoholic fatty liver disease (NAFLD) is the most common liver disorder worldwide, affecting as much as a quarter of humanity. It is characterized by fat accumulation in liver cells and may progress to inflammation, cirrhosis and liver failure. Now, researchers at the University of Tsukuba reveal the positive effects, beyond the expected weight-loss benefit, of exercise on the liver.
NAFLD is associated with unhealthy behaviors such as overeating and a sedentary lifestyle. In Japan 41% of middle-aged men have NAFLD and 25% will progress to non-alcoholic steatohepatitis (NASH) and hepatic dysfunction.
Weight reduction is fundamental to NAFLD management. Unfortunately, achieving a targeted bodyweight without supervision is difficult, and maintaining this over time even more so. Hitherto, exercise was considered adjunctive to dietary restrictions for weight loss but the other benefits such as reduced hepatic steatosis (fatty change) and stiffness are being increasingly recognized. However, the underlying mechanisms remain unclear.
“We compared data from obese Japanese men with NAFLD on a 3-month exercise regimen with those on dietary restriction targeting weight loss,” senior author Professor Junichi Shoda explains. “We tracked hepatic parameters, reduction in adipose tissue, increase in muscle strength, reductions in inflammation and oxidative stress, changes in organokine concentrations, and expression of target genes of Nrf2, an oxidative stress sensor.”
The researchers found that exercise preserved muscle mass better, though with modest decrease of body and fat mass. Remarkably, ultrasound elastography revealed that the exercise regimen reduced liver steatosis by an additional 9.5%, liver stiffness by an additional 6.8%, and the FibroScan-AST Score (a measure of liver fibrosis) by an additional 16.4% over the weight-loss regimen.
Additionally, the exercise regimen altered the circulating concentrations of specific organokines and apparently induced anti-inflammatory and anti-oxidative stress responses through activation of the Nrf2 (nuclear factor E2-related factor 2), an oxidative stress sensor. It also enhanced the phagocytic capacity of Kupffer cells which help maintain liver function.
Professor Shoda explains the relevance of their findings. “Our research shows how exercise prevents liver steatosis and fibrosis in NAFLD and clarifies that this benefit is compounded by preservation of muscle mass and is independent of weight changes. Patients on exercise regimens may become demotivated and drop out if they do not experience significant weight loss. Therefore, moderate to vigorous intensity exercise should be integrated in all NAFLD therapeutic regimens, and patients at risk for NASH should be encouraged to persevere with moderate to high intensity exercise regardless of whether or not they lose weight.”
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Humans cannot live on protein alone — even for the ancient indigenous people of the Pacific Northwest whose diet was once thought to be almost all salmon.
In a new paper led by Washington State University anthropologist Shannon Tushingham, researchers document the many dietary solutions ancient Pacific Coast people in North America likely employed to avoid “salmon starvation,” a toxic and potentially fatal condition brought on by eating too much lean protein.
“Salmon was a critical resource for thousands of years throughout the Pacific Rim, but there were a lot of foods that were important,” said Tushingham the lead author of the paper published online on April 8 in the American Journal of Physical Anthropology. “Native people were not just eating salmon. There’s a bigger picture.”
Some archeologists have contended for years that prehistoric Northwest people had an “extreme salmon specialization,” a theory primarily based on the amount of salmon bone found at archeological sites.
Tushingham and her co-authors argue that such a protein-intensive diet would be unsustainable. They point to nutritional studies and a global database of hunter-gatherer diets that indicate people have dietary limit on lean protein of around 35%. While it can vary by individual, exceeding that ceiling can be physically debilitating within a few days and fatal within weeks. Early explorers in the U.S. West subsisting on lean wild game discovered this problem the hard way and called it “rabbit starvation” or “caribou sickness.”
This toxic situation can apply to any lean meat, including salmon, Tushingham said. To avoid “salmon starvation,” early Pacific Coast people had to find ways to get other nutrients, especially for children and nursing mothers who have even lower dietary thresholds for lean protein.
“There were ingenious nutritional and cultural solutions to the circumstances in the Northwest,” said Tushingham. “Yes, salmon was important, but it wasn’t that simple. It wasn’t just a matter of going fishing and getting everything they needed. They also had to think about balancing their diet and making sure everybody could make it through the winter.”
The researchers point to evidence in California that people offset stored salmon protein with acorns; in Oregon and Washington, they ate root crops like camas as well as more fat-heavy fish such as eulachon. Further north, where plants are more limited, communities often ate marine mammals with high fat content such as seals and walrus. In far north interior, where there are few plants and the salmon runs can go thousands of miles inland, this was particularly challenging. Lean dried salmon was an important food source, and people circumvented salmon starvation through trading for oil with coastal peoples or obtaining fat through processing bone marrow from caribou and elk.
The authors focus on the limits of salmon, which used to be considered a “prime mover” of Pacific Northwest populations, but their analysis also has implications for the study of historical human nutrition. If their argument is correct, it is unlikely that any human society was fully driven by pursuit of protein alone as their diets had to be more complex.
“People try to come up with one ‘paleo-diet,’ but there was no one specific ideal diet,” said Tushingham. There were nutritional baselines that they had to cover, and nutritional limits that they couldn’t exceed. There were many good solutions. It depended on where you lived and the history of your community.”
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Materials provided by Washington State University. Original written by Sara Zaske. Note: Content may be edited for style and length.

Humans are exposed to many types of bacteria daily, the majority of which are harmless. However, some bacteria are pathogenic, which means they can cause disease. An extremely common pathogenic bacterial infection is Helicobacter pylori (H. pylori) in the stomach, where it can lead to chronic inflammation (gastritis), ulcers, and even cancer. A group of researchers from Osaka University have determined a specific molecular mechanism that H. pylori uses to adapt to growing in the human stomach for long periods of time.
In a report published in Nature Communications, this group found that a small RNA molecule called HPnc4160 plays a key role in how H. pylori invades the stomach and leads to disease.
Previous studies showed that HPnc4160 is conserved in different strains of H. pylori, suggesting that it has an important function. Yet, the amount of this molecule produced in the bacteria is variable among strains. Genetic analysis revealed that a specific part of the H. pylori gene, called the T-repeat region, varied in length from strain to strain. The researchers became interested in how this region affected HPnc4160 expression. Additionally, they were curious how these fluctuations would allow some strains to colonize the human stomach more efficiently than others.
“Slight differences in the genetic sequence of H. pylori can sometimes give certain strains advantages over others that allow it to grow better,” says lead author of the study Ryo Kinoshita-Daitoku. “We were interested in the genetic and molecular reasons behind why particular strains are more pathogenic and can live in the stomach for decades, leading to cancer development.”
To address these questions, the researchers infected gerbils and mice with wild type (normal) H. pylori for 8 weeks, then extracted and genetically characterized the mutant strains that appeared. They discovered that strains with a higher number of T-repeats had lower expression of HPnc4160.
“We found that the H. pylori strains with low HPnc4160 levels were more infectious,” explains Hitomi Mimuro, senior author. “When this RNA was completely absent, the amounts of several bacterial pathogenic factors significantly increased and the strain showed stronger colonization within the rodent stomach.”
One of the pathogenic factors was the bacterial protein CagA, which is known as an oncoprotein because it can promote cancer development.
“Interestingly, we observed longer T-repeat regions, lower levels of HPnc4160, and higher levels of CagA in gastric cancer patients compared with those not suffering from cancer,” describes Kinoshita-Daitoku.
These novel findings provide crucial information regarding the molecular and genetic landscape of highly pathogenic H. pylori and may assist in the development of innovative therapeutics for the treatment of H. pylori related illnesses, including gastric cancer.
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Researchers at the University of Calgary and The Hospital for Sick Children (SickKids), in Toronto, have discovered genetic risk factors for OCD that could help pave the way for earlier diagnosis and improved treatment for children and youth.
“Our group made the first finding of a genome-wide significant risk gene relevant to childhood OCD,” says Dr. Paul Arnold, MD, PhD, co-principal investigator, a professor and director of The Mathison Centre for Mental Health Research & Education at the Cumming School of Medicine. “We’ve known that OCD runs in families, but we hadn’t identified and validated specific genetic risks of OCD symptoms in children and youth until now.”
The research drew on the Spit for Science study, a research project led by SickKids looking at how genes interact with the environment to impact physical and mental health. Participants from the community were recruited via an innovative research design run out of the Ontario Science Centre, which has generated a diverse sample of 23,000 participants thus far. Participants provide a DNA sample through their saliva, do a cognitive task, and complete questionnaires on their health, lifestyle and behaviours.
In this study, saliva samples from over 5,000 children and youth were scanned and compared to participant responses using the Toronto Obsessive-Compulsive Scale (TOCS). The TOCS is a questionnaire used to evaluate obsessive-compulsive traits developed by Dr. Arnold and the team at SickKids. After looking across millions of genetic variants from the saliva samples, the team identified that children and youth with a genetic variant in the gene PTPRD had a greater risk for more obsessive-compulsive traits. The findings are published in Translational Psychiatry.
“Discovering the genes involved in OCD is critical to help improve patients’ lives. It is still early days, but our hope is these findings will lead us to understand the causes of OCD, which in turn could help identify people with OCD sooner and develop better treatments,” says Dr. Christie Burton, PhD, lead author and research associate in the Neurosciences & Mental Health program at SickKids.
The research team, which also includes co-principal investigators, Drs. Jennifer Crosbie, PhD, Clinical Psychologist at SickKids, and Russell Schachar, MD, Psychiatrist at SickKids, highlight that a greater understanding of the underlying genetics may eventually be an important complement to clinical assessment and could help guide treatment options in the future.
“OCD can present very differently and at various ages in each individual, adding to the challenge of treatment and diagnosis,” says Crosbie, who is also an associate scientist in the Neurosciences & Mental Health program at SickKids. “Studies like this one are an important step towards developing precision medicine approaches for mental health.”
Sam, 17, lives with OCD and with therapy and medication, he says he has been able to face his obsessions and compulsions, ride out the anxiety and control his actions. Looking back at his childhood, Sam says he had some OCD tendencies as early as elementary school, but neither he nor his family realized he had a mental illness. The researchers hope that by understanding the genetics of OCD they can develop better treatments, improve outcomes and diagnose youth like Sam earlier.
“At first I wasn’t sure what to do with the diagnosis, it was very foreign, I didn’t want to perceive myself as having a mental health issue,” says Sam. “But, knowing I have OCD helped me overcome the challenges. With therapy and medication, I’ve stopped OCD from overtaking my life and taken back control.”
Sam is a real teenager, but Sam isn’t his real name. He says due to the stigma around OCD he would prefer to remain anonymous.
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Materials provided by University of Calgary. Original written by Kelly Johnston. Note: Content may be edited for style and length.

People with early-onset dementia are often mistaken for having depression and now Australian research has discovered the cause: a profound loss of ability to experience pleasure — for example a delicious meal or beautiful sunset — related to degeneration of ‘hedonic hotspots’ in the brain where pleasure mechanisms are concentrated.
The University of Sydney-led research revealed marked degeneration, or atrophy, in frontal and striatal areas of the brain related to diminished reward-seeking, in patients with frontotemporal dementia (FTD).
The researchers believe it is the first study to demonstrate profound anhedonia — the clinical definition for a loss of ability to experience pleasure — in people with FTD.
Anhedonia is also common in people with depression, bipolar disorder and obsessive-compulsive disorder and can be particularly disabling for the individual.
In the study, patients with FTD — which generally affects people aged 40-65 — displayed a dramatic decline from pre-disease onset, in contrast to patients with Alzheimer’s disease, who were not found to show clinically significant anhedonia.
The results point to the importance of considering anhedonia as a primary presenting feature of FTD, where researchers found neural drivers in areas that are distinct from apathy or depression.
The findings were published today in the leading neuroscience journal, Brain.
The paper’s senior author, Professor Muireann Irish from the University of Sydney’s Brain and Mind Centre and School of Psychology in the Faculty of Science, said despite increasing evidence of motivational disturbances, no study had previously explored the capacity to experience pleasure in people with FTD.
“Much of human experience is motivated by the drive to experience pleasure but we often take this capacity for granted.
“But consider what it might be like to lose the capacity to enjoy the simple pleasures of life — this has stark implications for the wellbeing of people affected by these neurodegenerative disorders.
“Our findings also reflect the workings of a complex network of regions in the brain, signaling potential treatments,” said Professor Irish, who also recently published a paper in Brain about moral reasoning in FTD.
“Future studies will be essential to address the impact of anhedonia on everyday activities, and to inform the development of targeted interventions to improve quality of life in patients and their families.”
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In a new study led by Yale Cancer Center, researchers have advanced a tumor-targeting and cell penetrating antibody that can deliver payloads to stimulate an immune response to help treat melanoma. The study was presented today at the American Association of Cancer Research (AACR) virtual annual meeting.
“Most approaches rely on direct injection into tumors of ribonucleic acids (RNAs) or other molecules to boost the immune response, but this is not practical in the clinic, especially for patients with advanced cancer,” said Peter M. Glazer, MD, PhD, Chair of the Department of Therapeutic Radiology at Yale, Chief of Radiation Oncology at Smilow Cancer Hospital, and senior author of the study. “In this study, we can deliver immune stimulatory RNA to tumors in vivo following systemic administration.”
RNA is a nucleic acid present in all living cells. Its principal role is to act as a messenger to carry instructions from DNA to control the synthesis of proteins, although in some viruses RNA rather than DNA carry the genetic information. In this study, using mice with melanoma tumors, members of the Glazer lab at Yale achieved almost complete tumor suppression upon intravenous injection of antibody/RNA complexes.
“These results are very encouraging,” added Glazer. “They highlight a novel approach for the systemic delivery of immunostimulatory RNAs in a targeted manner that may one day offer therapeutic advantages for difficult to treat cancers like melanoma, over current approaches.”
The lead author of the study from Yale is Elias Quijano, and a co-author, also from Yale, is Yanfeng Liu, along with Bruce Turner and Stephen Squinto of Gennea Bio.
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KAIST researchers have developed a novel nanofiber production technique called ‘centrifugal multispinning’ that will open the door for the safe and cost-effective mass production of high-performance polymer nanofibers. This new technique, which has shown up to a 300 times higher nanofiber production rate per hour than that of the conventional electrospinning method, has many potential applications including the development of face mask filters for coronavirus protection.
Nanofibers make good face mask filters because their mechanical interactions with aerosol particles give them a greater ability to capture more than 90% of harmful particles such as fine dust and virus-containing droplets.
The impact of the COVID-19 pandemic has further accelerated the growing demand in recent years for a better kind of face mask. A polymer nanofiber-based mask filter that can more effectively block harmful particles has also been in higher demand as the pandemic continues.
‘Electrospinning’ has been a common process used to prepare fine and uniform polymer nanofibers, but in terms of safety, cost-effectiveness, and mass production, it has a several drawbacks. The electrospinning method requires a high-voltage electric field and electrically conductive target, and this hinders the safe and cost-effective mass production of polymer nanofibers.
In response to this shortcoming, ‘centrifugal spinning’ that utilizes centrifugal force instead of high voltage to produce polymer nanofibers has been suggested as a safer and more cost-effective alternative to the electrospinning. Easy scalability is another advantage, as this technology only requires a rotating spinneret and a collector.
However, since the existing centrifugal force-based spinning technology employs only a single rotating spinneret, productivity is limited and not much higher than that of some advanced electrospinning technologies such as ‘multi-nozzle electrospinning’ and ‘nozzleless electrospinning.’ This problem persists even when the size of the spinneret is increased.
Inspired by these limitations, a research team led by Professor Do Hyun Kim from the Department of Chemical and Biomolecular Engineering at KAIST developed a centrifugal multispinning spinneret with mass-producibility, by sectioning a rotating spinneret into three sub-disks. This study was published as a front cover article of ACS Macro Letters, Volume 10, Issue 3 in March 2021.
Using this new centrifugal multispinning spinneret with three sub-disks, the lead author of the paper PhD candidate Byeong Eun Kwak and his fellow researchers Hyo Jeong Yoo and Eungjun Lee demonstrated the gram-scale production of various polymer nanofibers with a maximum production rate of up to 25 grams per hour, which is approximately 300 times higher than that of the conventional electrospinning system. The production rate of up to 25 grams of polymer nanofibers per hour corresponds to the production rate of about 30 face mask filters per day in a lab-scale manufacturing system.
By integrating the mass-produced polymer nanofibers into the form of a multi-component fiber web, the researchers were able to fabricate mask filters that have comparable filtration performance with the filters used in KF80 and KF94 face masks that are currently available in the Korean market. The KF80 and KF94 masks have been approved by the Ministry of Food and Drug Safety of Korea to filter out at least 80% and 94% of harmful particles respectively.
“When our system is scaled up from the lab scale to an industrial scale, the large-scale production of centrifugal multispun polymer nanofibers will be made possible, and the cost of polymer nanofiber-based face mask filters will also be lowered dramatically,” Kwak explained.
This work was supported by the KAIST-funded Global Singularity Research Program for 2020.

Older adults with more harmful than healthy bacteria in their gums are more likely to have evidence for amyloid beta — a key biomarker for Alzheimer’s disease — in their cerebrospinal fluid (CSF), according to new research from NYU College of Dentistry and Weill Cornell Medicine. However, this imbalance in oral bacteria was not associated with another Alzheimer’s biomarker called tau.
The study, published in the journal Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring, adds to the growing evidence of a connection between periodontal disease (gum disease) and Alzheimer’s. Periodontal disease — which affects 70 percent of adults 65 and older, according to CDC estimates — is characterized by chronic and systemic inflammation, with pockets between the teeth and gums enlarging and harboring bacteria.
“To our knowledge, this is the first study showing an association between the imbalanced bacterial community found under the gumline and a CSF biomarker of Alzheimer’s disease in cognitively normal older adults,” said Angela Kamer, DDS, PhD, associate professor of periodontology and implant dentistry at NYU College of Dentistry and the study’s lead author. “The mouth is home to both harmful bacteria that promote inflammation and healthy, protective bacteria. We found that having evidence for brain amyloid was associated with increased harmful and decreased beneficial bacteria.”
Alzheimer’s disease is characterized by two hallmark proteins in the brain: amyloid beta, which clumps together to form plaques and is believed to be the first protein deposited in the brain as Alzheimer’s develops, and tau, which builds up in nerve cells and forms tangles.
“The mechanisms by which levels of brain amyloid accumulate and are associated with Alzheimer’s pathology are complex and only partially understood. The present study adds support to the understanding that proinflammatory diseases disrupt the clearance of amyloid from the brain, as retention of amyloid in the brain can be estimated from CSF levels,” said the study’s senior author Mony J. de Leon, EdD, professor of neuroscience in radiology and director of the Brain Health Imaging Institute at Weill Cornell Medicine. “Amyloid changes are often observed decades before tau pathology or the symptoms of Alzheimer’s disease are detected.”
The researchers studied 48 healthy, cognitively normal adults ages 65 and older. Participants underwent oral examinations to collect bacterial samples from under the gumline, and lumbar puncture was used to obtain CSF in order to determine the levels of amyloid beta and tau. To estimate the brain’s expression of Alzheimer’s proteins, the researchers looked for lower levels of amyloid beta (which translate to higher brain amyloid levels) and higher levels of tau (which reflect higher brain tangle accumulations) in the CSF.
Analyzing the bacterial DNA of the samples taken from beneath the gumline under the guidance of NYU College of Dentistry microbiologist Deepak Saxena, PhD, the researchers quantified bacteria known to be harmful to oral health (e.g. Prevotella, Porphyromonas, Fretibacterium) and pro-oral health bacteria (e.g. Corynebacterium, Actinomyces, Capnocytophaga).
The results showed that individuals with an imbalance in bacteria, with a ratio favoring harmful to healthy bacteria, were more likely to have the Alzheimer’s signature of reduced CSF amyloid levels. The researchers hypothesize that because high levels of healthy bacteria help maintain bacterial balance and decrease inflammation, they may be protective against Alzheimer’s.
“Our results show the importance of the overall oral microbiome — not only of the role of ‘bad’ bacteria, but also ‘good’ bacteria — in modulating amyloid levels,” said Kamer. “These findings suggest that multiple oral bacteria are involved in the expression of amyloid lesions.”
The researchers did not find an association between gum bacteria and tau levels in this study, so it remains unknown whether tau lesions will develop later or if the subjects will develop the symptoms of Alzheimer’s. The researchers plan to conduct a longitudinal study and a clinical trial to test if improving gum health — through “deep cleanings” to remove deposits of plaque and tartar from under the gumline — can modify brain amyloid and prevent Alzheimer’s disease.
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