Low Vitamin K Intake Impairs Cognition, Neurogenesis, and Elevates Neuroinflammation in C57BL/6 Mice

 Ask your competent? doctor how to eat healthy if on warfarin and can't consume Vitamin K foods.  You do want good cognition and no inflammation, right? That requires a diet protocol and I bet your incompetent doctor doesn't have one for you! 

When taking warfarin, it is crucial to avoid foods that can interact with the medication and affect its effectiveness. Here are some foods to avoid: 

Foods High in Vitamin K: Green leafy vegetables (e.g., spinach, kale, broccoli, collard greens)

• Liver
• Brussels sprouts
• Asparagus
• Cauliflower

Foods Containing Flavonoids: grapefruit juice, green tea, and cranberry juice. Other Foods: alcohol, black licorice, turmeric, avocado, and olive oil

Low Vitamin K Intake Impairs Cognition, Neurogenesis, and Elevates Neuroinflammation in C57BL/6 Mice

Tong Zheng

, , , , , ,

https://doi.org/10.1016/j.tjnut.2025.01.023

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Abstract

Background

In addition to its important roles in blood coagulation and bone formation, vitamin K (VK) contributes to brain function. Low dietary VK intake, which is common among older adults, is associated with age-related cognitive impairment.

Objective

To elucidate the biological mechanisms underlying VK’s effects on cognition, we investigated the effects of low VK (LVK) intake on cognition in C57BL/6 mice.

Methods

Male and female 9-month old C57BL/6 mice (n=60) were fed a LVK diet or a control diet for 6 months. Behavioral tests were performed on a subset of animals (n=26) at 15 months and brain tissues were collected for follow-up analyses.

Results

Menaquinone-4 (MK4), the predominant VK form in the brain, was significantly lower in LVK animals compared to controls (15.6±13.3 vs 189±186 pmol/g, respectively, p<0.01). LVK animals showed reduced recognition memory in the novel object test by spending a lower percentage of time exploring the novel object compared to controls (47.45%± 4.17 vs. 58.08%±3.03, p=0.04). They also spent a significantly longer time learning the task of locating the platform in the Morris water maze test. Within the hippocampal dentate gyrus, LVK animals had a significantly lower number of proliferating cells, and fewer newly generated immature neurons compared to control animals. Additionally, more activated microglia cells were identified in the LVK animals.

Conclusion

Our data indicate that LVK intake reduced MK4 levels in brain tissues and impaired learning- and memory-related cognitive function. This impairment may be related to the observed reduced hippocampal neurogenesis and elevated neural inflammation.

Introduction

Within the next decade, it is estimated that there will be more Americans over the age of 65 years than under the age of 18 years [1], and many of these older adults will develop age-related cognitive impairments [2]. Modifiable factors, such as nutrition, have been implicated as important modulators for cognition [3], [4]. Growing evidence has shown that low vitamin K may have a role in age-related cognitive decline [5]. Green leafy vegetables are the main source of phylloquinone (PK), the primary form of dietary vitamin K [6], [7]. Concerningly, most adults do not consume the recommended quantity of these foods, leading to inadequate phylloquinone intake, especially among older adults in the U.S. [8]. Mostly known for its role in blood coagulation, phylloquinone is believed to also have important functions in the nervous system [9], [10]. Through recent and novel stable isotope experiments in rodent models, it has been shown that manipulation of dietary vitamin K causes rapid changes to the concentration of menaquinone-4 (MK4), which is the predominant form of vitamin K in the brain [11]. We also now know that all dietary forms of vitamin K convert to MK4 [12].

Observational data from the Rush Memory and Aging Project (MAP) demonstrated that higher postmortem brain levels of MK4 were associated with better cognitive function proximate to death. Further investigation of neuropathologically-defined outcomes also revealed that higher brain MK4 concentrations were associated with lower global dementia pathology, specifically fewer neurofibrillary tangles [13]. While these findings are encouraging, MK4 in the brain may simply be tracking healthy dietary patterns associated with higher vegetable intakes. Furthermore, the underlying biological mechanisms have yet to be elucidated. Thus, there is a critical need to establish the biological mechanism(s) underlying the cognition-protective effects of vitamin K in an animal model to overcome the limitations of observational data. Given that: 1) inflammation, which is closely associated with aging and neurodegeneration, impairs hippocampal neurogenesis; and 2) age-related cognitive decline is accompanied by reduced neurogenesis in the hippocampus, we propose that vitamin K’s protective effects on cognition and brain resilience may function through maintaining hippocampal neurogenesis and anti-inflammation.

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Advancing stroke rehabilitation: the role of wearable technology according to research experts

 In simple words; the complete stroke medical world is totally fucking incompetent for not already having protocols on wearables! 

With all this information out there who thinks this shows any sign of competence in your stroke medical 'professionals'? No one from the stroke medical world has ever contacted me to tell me I'm full of shit. I'm happily waiting for that day, it will be fun.

 wearable (39 posts to April 2012)

wearable EMG (1 post to January 2024)

wearable arms (1 post to May 2013)

wearable computing (3 posts to August 2013)

wearable devices (38 posts to October 2015)

wearable electronic device (1 post to July 2020)

wearable exoskeletons (1 post to April 2022)

Wearable inertial measurement units (2 posts to June 2019)

wearable inertial sensor (2 posts to June 2023)

wearable motion-tracking (1 post to July 2023)

wearable robotics (1 post to July 2022)

wearable sensors (26 posts to January 2018)

Advancing stroke rehabilitation: the role of wearable technology according to research experts

Amelia Cain

,

Tanisha Gunby

,

Carolee Winstein

&

Marika Demers

Received 27 Sep 2024, Accepted 22 Jan 2025, Published online: 28 Jan 2025

• Cite this article
• https://doi.org/10.1080/17483107.2025.2459326
• CrossMark

 

Abstract

Background

Advancements in wearable technology have created new opportunities to monitor stroke survivors’ behaviors in daily activities. Research insights are needed to guide its adoption in clinical practice, address current gaps, and shape the future of stroke rehabilitation. This project aims to: (1) Understand stroke rehabilitation researchers’ perspectives on the opportunities, challenges, and clinical relevance of wearable technology for stroke rehabilitation, and (2) Identify necessary next steps to integrate wearable technology in research and clinical practice.

Methods

Using a phenomenological qualitative design, two 90-minute focus groups were conducted with 12 rehabilitation researchers. The focus groups consisted of semi-structured, open-ended questions on functional movement behavior, motor performance and benefits and pitfalls of wearable technology. The transcribed focus groups were analyzed using inductive thematic analysis.

Results

Three main themes were derived from the analysis: (1) Assessing activity performance is critical to inform interventions, (2) The demonstrated benefit is not commensurate with the added hassle, (3) Collaboration is needed between the industry, academia and end-users. Necessary future steps were recognized including the identification of intuitive and actionable metrics, and the integration of sensor-derived data with electronic health records and into clinical workflow to support self-management strategies.

Conclusion

Wearable technology shows great potential to complement and support stroke rehabilitation. Many key barriers to clinical adoption remain(Well solve them! LEADERS WOULD SOLVE THEM! You're not leaders, are you?) which underscore the necessity to foster collaborations between industry, academia, and the participants we serve.

IMPLICATIONS FOR REHABILITATION

• Wearable technology provides critical information about activity performance to understand stroke survivors’ behavior and inform interventions.

• Concerted efforts of interdisciplinary research teams in partnerships with users and the industry are essential to accelerate clinical and research adoption.

Mushrooms, Microdosing, and Mental Illness: The Effect of Psilocybin on Neurotransmitters, Neuroinflammation, and Neuroplasticity

 Didn't your competent? doctor already put you on mushrooms and microdosing? NO? So, you DON'T have a functioning stroke doctor, do you?

Didn't your competent doctor already add Lion's Mane mushrooms and magic mushrooms to your diet protocol already? 

magic mushrooms (29 posts to October 2014)

• mushrooms (14 posts to October 2014)

• edible mushrooms (1 post to April 2023

microdosing (4 posts to March 2022)

Lion's Mane Mushroom (2 posts to September 2021)

 

The latest here:

Mushrooms, Microdosing, and Mental Illness: The Effect of Psilocybin on Neurotransmitters, Neuroinflammation, and Neuroplasticity

Authors Kinderlehrer DA 

Received 11 October 2024

Accepted for publication 17 January 2025

Published 29 January 2025 Volume 2025:21 Pages 141—155

DOI https://doi.org/10.2147/NDT.S500337

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Roger Pinder

Download Article [PDF] 

Daniel A Kinderlehrer

Private Practice, Denver, CO, USA

Correspondence: Daniel A Kinderlehrer, Email kinderlehrer@gmail.com

Abstract: The incidence of mental health disorders is increasing worldwide. While there are multiple factors contributing to this problem, neuroinflammation underlies a significant subset of psychiatric conditions, particularly major depressive and anxiety disorders. Anti-inflammatory interventions have demonstrated benefit in these conditions. Psilocin, the active ingredient of mushrooms in the Psilocybe genus, is both a potent serotonin agonist and anti-inflammatory agent, increases neuroplasticity, and decreases overactivity in the default mode network. Studies using hallucinogenic doses of psilocin under the supervision of a therapist/guide have consistently demonstrated benefits to individuals with depression and end-of-life anxiety. Microdosing psilocybin in sub-hallucinogenic doses has also demonstrated benefit in mood disorders, and may offer a safe, less expensive, and more available alternative to full doses of psilocybin for mood disorders, as well as for other medical conditions in which inflammation is the principal pathophysiology.

Keywords: Psilocybin, psilocin, microdose, depression, anxiety, neuroinflammation, anti-inflammatory

Introduction

The incidence of mental health disorders is increasing worldwide, and are a leading cause of disability.¹ Mental illness was more prevalent than heart disease, cancer, and diabetes even before the emergence of the COVID-19 pandemic. This trend was exacerbated by the pandemic, with a significant increase in the prevalence of depression and anxiety disorders in all age groups.^2,3 Mental health issues have been particularly severe in adolescents: in 2021, the World Health Organization (WHO) reported that 15% of all youth globally suffered from a mental health disorder.⁴ Treatment success of neuropsychiatric disorders varies; current antidepressants have limited efficacy in many patients.⁵ There is clearly a need for more effective interventions.

This review describes the pathophysiology of mental health conditions with an emphasis on the immune dysregulation and neuroinflammation associated with depression and anxiety disorders, and analyzes emerging research that demonstrates the potential of psilocybin to address the physiologic dysregulation associated with mental illness. Psilocybin may offer a safe, therapeutic alternative to the present pharmacopeia.

Stress and Inflammation

For most of the twentieth century, Western medicine subscribed to the tenets of mind-body dualism proposed by René Descartes in the 17^th century; namely, that mental phenomena are non-physical, and therefore the mind and body are separate and distinct.⁶ This premise was challenged in 1975 when Robert Ader and Nicholas Cohen at the University of Rochester performed a groundbreaking experiment. They fed rats cyclophosphamide in saccharin-flavored water and documented suppression of immune function. Once the rats were thereby conditioned, they were fed the saccharin-flavored water without cyclophosphamide; the rats again exhibited a decrease in antibody production. Ader and Cohen labeled this observed connection between the brain and immune system “psychoneuroimmunology” (PNI).⁷

Understanding the connection between mind and body has greatly expanded in the ensuing five decades, and with it an appreciation of the bidirectional connectivity between psychological stress and nervous, endocrine, and immune function, referred to as Psycho-Neuro-Endocrine-Immunology (PNEI). Stress leads to stimulation of the sympathetic nervous system (SNS) and activation of the hypothalamic-pituitary-adrenal (HPA) axis. The former leads to the release of catecholamines (CAs) from the adrenal medulla, while the latter leads to the release of glucocorticoids (GCs) from the adrenal cortex. CAs act on adrenergic receptors and GCs act on glucocorticoid receptors; collectively these receptors are expressed on virtually all cells in the body with sweeping consequences. These include the promotion of energy production, suppression of digestive and reproductive function, and modulation of immune function.^8,9

However, there is a significant difference in the downstream physiological consequences of stress based on the intensity and duration of the stressor and on individual susceptibility. Acute stress leads to the release of pro-inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-α), with activation of innate and adaptive immune function.⁹ This pro-inflammatory response is tempered by the release of anti-inflammatory cytokines IL-4, IL-10 and IL-13, as well as an increase in circulating cortisol. The sum total impact of acute, short-lived stress in an otherwise healthy, well-resourced individual is immunoprotection.^8,9

The same is not true for individuals who are chronically stressed, have underlying health problems, or have a history of prior trauma. In these individuals the impact of stress on immune function leads to unchecked inflammation owing to a multitude of factors. Activation of nuclear factor-kappa B (NF-κB) leads to maximal transcription of pro-inflammatory cytokines, thereby increasing levels of IL-6 and TNF-α. The release of GCs, while normally anti-inflammatory, can become pro-inflammatory due to decreased GC-receptor levels, amplification of inflammasome NLRP3 activity promoting the release of IL-1β and IL-18, and increased production of prostaglandin E2 (PGE2). The overall result of chronic stress is an increase in inflammation and the suppression of immune function.^8–10

Rapid Blood Test Can Improve Stroke Treatment

 Telling us nothing about how fast it is! Is it faster than this one?

New Device Quickly Assesses Brain Bleeding in Head Injuries - 5-10 minutes April 2017

The latest here:

Rapid Blood Test Can Improve Stroke Treatment

FRIDAY, Jan. 31, 2025 (HealthDay News) -- A rapid blood test could speed treatment for people who’ve suffered a stroke related to brain bleeding, a new study says.

Stroke victims with brain bleeds have nearly seven times higher blood levels of a brain protein called glial fibrillary acidic protein, or GFAP, compared to patients with strokes caused by a blood clot, researchers found.

A blood test that detects GFAP during emergency transport could kick off effective treatment for these patients before they even get to the hospital, potentially reducing their brain damage from stroke, researchers said Thursday ahead of the American Stroke Association’s (ASA) annual meeting in Los Angeles next week.

“It is crucial to differentiate these two types of stroke because they need opposite treatments,” lead researcher Dr. Love-Preet Kalra, a neurology resident at the RKH Hospital Klinikum Ludwigsburg in Germany, said in an ASA news release.

“In ischemic stroke, you need to open the blocked blood vessel with clot-busting drugs or physically remove the clot,” Kalra added. “In contrast, in a bleeding stroke, you need to lower increased blood pressure and give medication to reverse the effects of certain blood-thinning drugs.”

The more time that elapses before a stroke is diagnosed and treated, the more brain tissue is irreparably damaged, researchers said in background notes.

Currently, doctors use imaging scans to distinguish between bleed-based versus clot-caused strokes, researchers said.

Unfortunately, those scans can be delayed for hours while a patient is being stabilized, evaluated in the emergency room and then sent on to radiology, researchers noted. All the while, brain cells are dying.

The research team figured that GFAP might be useful in detecting a brain-bleed stroke. The protein is released into the bloodstream when brain cells are damaged and destroyed, and it’s already used when assessing traumatic brain injuries.

The study involved 353 patients treated within six hours of the onset of stroke symptoms.

Blood samples were taken on the way to the emergency room and tested for GFAP levels using a portable blood analyzer.

Brain imaging at the hospital revealed that bleeding strokes had occurred in 76 people, clot-caused strokes in 258 people, and conditions that mimic stroke like seizures or migraine in 19 people.

GFAP levels were nearly seven times higher in bleeding stroke patients compared to those with clot-caused strokes, and more than four times higher in people with a bleeding stroke than a stroke-mimicking condition, results show.

Researchers were able to predict which patients had a bleeding stroke with up to 95% accuracy when age was taken into account, according to their presentation.

In addition, GFAP levels were higher in bleeding stroke patients who were taking blood thinners.

If these results are confirmed in larger studies, the blood test could revolutionize treatment of stroke, Kalra said.

“Treatment to lower blood pressure and reverse blood-thinning medications could be performed in the prehospital setting, leading to a huge change in clinical practice,” Kalra said. “In the future, even blood thinners or clot-busting treatment might be applied before people reach the hospital.”

American Heart Association volunteer Dr. Louise McCullough agreed that the study results need to be verified in studies involving more people.

“The study had a relatively small sample size, and for the test to be effective, both the patient's blood and the GFAP test must be available as a “point of care” test in the field,” McCullough, chief of neurology at Memorial Hermann Hospital-Texas Medical Center in Houston, said in a news release.

“Currently, most ambulances and emergency medical services do not have access to this blood test,” McCullough pointed out, who was not involved in the study.

Findings presented at medical meetings should be considered preliminary until published in a peer-reviewed journal.

This Personality Trait Could Triple Your Dementia Risk - cynicism

 This one might be hard for your doctor to change.

Is your doctor going to work on your cynicism while also preventing your 33% dementia chance post-stroke from an Australian study 
Is your doctor doing anything at all to prevent dementia?

This Personality Trait Could Triple Your Dementia Risk

The trait has already been linked with worse physical health, but what is it doing to the brain?

People with high levels of cynicism are more likely to develop dementia.

It’s already been found that those who believe others are mainly motivated by selfish concerns — the definition of cynical distrust — have worse physical health; for example, cynicism has been linked to heart disease.

Now you can add dementia to the list.

In the study, conducted in Finland, 1,449 people were given tests of their cynicism that included questions like:

• “I think most people would lie to get ahead.”
• “It is safer to trust nobody.”
• “Most people will use somewhat unfair reasons to gain profit or an advantage rather than lose it.”

The more people endorsed these statements, the stronger their cynical distrust was deemed to be.

They were also given tests of dementia and other factors that might affect their risk of developing dementia later on, like smoking and high cholesterol levels.

Eight years later, people were tested again to see if they had developed any symptoms of dementia.

The study was published in the journal Neurology (Neuvonen et al., 2014).

Motor modules are largely unaffected by pathological walking biomechanics: a simulation study

 Ask your competent? doctor how this information is going to recover your walking ability. In my case since most of my motor and pre-motor cortex is dead, nothing here is useful. My dead brain destroyed any possible synergy there was. WHAT IS THE FIX?

Motor modules are largely unaffected by pathological walking biomechanics: a simulation study

• Mohammad Rahimi Goloujeh &
• Jessica L. Allen 

Journal of NeuroEngineering and Rehabilitation volume 22, Article number: 16 (2025) Cite this article

• Metrics details

Abstract

Background

Motor module (a.k.a. muscle synergy) analysis has frequently been used to provide insight into changes in muscle coordination associated with declines in walking performance, to evaluate the effect of different rehabilitation interventions, and more recently, to control exoskeletons and prosthetic devices. However, it remains unclear whether changes in muscle coordination revealed via motor module analysis stem from abnormal walking biomechanics or neural control. This distinction has important implications for the use of motor module analysis for rehabilitation interventions and device design. Thus, this study aims to elucidate the extent to which motor modules emerge from pathological walking biomechanics, i.e. abnormal walking biomechanics commonly observed in individuals with neurological disease and/or injury.

Methods

We conducted a series of computer simulations using OpenSim Moco to simulate pathological walking biomechanics by manipulating speed, asymmetry, and step width in a three-dimensional musculoskeletal model. We focused on these spatiotemporal metrics because they are commonly altered in individuals with Parkinson’s disease, stroke survivors, etc. and have been associated with changes in motor module number and structure. We extracted motor modules using nonnegative matrix factorization from the muscle activations from each simulation. We then examined how alterations in walking biomechanics influenced the number and structure of extracted motor modules and compared the findings to previous experimental studies.

Results

The motor modules identified from our simulations were similar to those identified from previously published experiments of non-pathological walking. Moreover, our findings indicate that the same motor modules can be used to generate a range of pathological-like waking biomechanics by modulating their recruitment over the gait cycle. These results contrast with experimental studies in which pathological-like walking biomechanics are accompanied by a reduction in motor module number and alterations in their structure.

Conclusions

This study highlights that pathological walking biomechanics do not necessarily require abnormal motor modules. In other words, changes in number and structure of motor modules can be a valuable indicator of alterations in neuromuscular control and may therefore be useful for guiding rehabilitation interventions and controlling exoskeletons and prosthetic devices in individuals with impaired walking function due to neurological disease or injury.

Background

Motor module (a.k.a. muscle synergy) analysis has emerged over the last few decades as a useful method to characterize the complex coordination of the numerous muscles involved in movements such as walking. Motor modules reflect coordinated patterns of muscle activity that can be flexibly combined to meet the goals of different movement behaviors [1]. It is hypothesized that motor modules reflect an underlying nervous system strategy to overcome the complexity of controlling movement by grouping muscles into functional units. As such, many researchers are using motor modules to evaluate the effect of different rehabilitation interventions on neuromuscular control [2,3,4,5,6,7,8,9,10,11,12] and even to control exoskeletons and prosthetic devices [13,14,15,16,17,18,19,20,21]. However, since motor modules are identified from experimentally-recorded electromyography (EMG) data using numerical decomposition techniques such as principal component analysis or nonnegative matrix factorization [1, 22, 23], there is ongoing debate regarding whether they truly represent an underlying neural strategy or simply emerge from the biomechanics of the recorded movement. Incorporating EMG-derived motor modules into rehabilitation interventions and/or into controllers for exoskeletons and prosthetics introduces additional complexity compared to recording only movement biomechanics. If motor modules are simply emergent from movement biomechanics, then there may be no need to incorporate such complexity into these settings. Therefore, it is critical to understand to what extent EMG-derived motor modules reflect an underlying neural strategy to support their use in identifying neuromuscular deficits limiting walking function, guiding rehabilitation efforts, and facilitating control of exoskeleton and prosthetic devices.

Converging evidence suggests that recruiting a reduced number of motor modules to control walking contributes to impaired walking function. Several studies have identified that between four to six motor modules are needed to describe muscle activity in unimpaired walking [24,25,26]. Comparatively fewer motor modules are required to describe muscle activity in people with neurological deficits (e.g., stroke [7, 24, 27, 28] cerebral palsy [29] and Parkinson’s disease [30,31,32]) and musculoskeletal conditions such as osteoarthritis [33]. Given that each module in unimpaired walking is organized around producing biomechanical functions such as leg swing control and forward propulsion [34, 35], it is not surprising that individuals with a reduced number of motor modules typically walk with impaired walking function. For example, reduced motor module number in stroke survivors is associated with slower walking speeds and more asymmetrical steps [24, 27] and an inability to change speed, cadence, step length, and step height [28]. Moreover, increases in motor module number that occur with rehabilitation are associated with improved walking function [10, 36]. While the prevailing interpretation of these studies is that a decrease in motor module number causes impaired function, an alternative explanation is that the observed reduction in motor modules may be a consequence of the altered walking biomechanics rather than the cause.

Musculoskeletal modeling and simulation offer a means to disentangle the effects of neural control and biomechanics on motor modules in a carefully controlled manner. For example, Falisse et al., demonstrated a reduction in motor module number alone could not produce the crouch gait biomechanics often observed in cerebral palsy [37]. Moreover, Mehrabi et al., found that normal walking biomechanics could not be achieved with reduced motor module number [38]. Conversely, a recent experimental study provided some evidence that healthy individuals could emulate crouch gait patterns commonly observed in children with cerebral palsy without reducing motor module number [39]. Taken together, these studies suggest that although biomechanics may have some influence on motor modules, there remains room for them to have a neural basis. However, a limitation of these studies is their focus on a single gait type, preventing insights into the extent of biomechanics versus neural control on motor module structure across the diverse walking biomechanics often observed in populations with neurological disease and/or injury.

The purpose of this study was to explore the extent to which motor modules are emergent from pathological walking biomechanics. Or in other words, does pathological walking biomechanics require a reduced number and/or altered structure of motor modules. Inspired by the work of De Groote et al. [26] in which motor modules were extracted from individual muscle-driven simulations of unimpaired walking identical to how motor modules are identified experimentally from EMG, we compared motor modules extracted from 27 muscle-driven simulations of pathological gait biomechanics. We use the term “pathological walking biomechanics” to refer to measurable gait characteristics such as spatiotemporal parameters, kinematics, and kinetics resulting from injury or disease. In this study, we focused on the effect of varying speeds, step length asymmetry, and step widths commonly observed in populations with neurological disease or injury such as stroke survivors, persons with Parkinson’s disease, etc. We hypothesized that motor modules cannot be explained by biomechanics alone and thus reflect to some extent an underlying neural control strategy. Based on this hypothesis, we predicted that the number and structure of motor modules would not differ across simulations with different pathological walking biomechanics.

More at link.

Flossing may reduce risk for stroke and irregular heart rhythm

 But are sonic water flossers better? Why don't you know?

Flossing may reduce risk for stroke and irregular heart rhythm

Flossing regularly may lower the risk of some strokes as well as a type of irregular heart rhythm that can increase stroke risk, new research suggests.

The findings, which will be presented Wednesday at the American Stroke Association's International Stroke Conference in Los Angeles, show people who flossed at least once a week had a lower risk for strokes caused by blood clots coming from the heart and for an irregular heart rhythm called atrial fibrillation, or AFib, that can lead to a stroke. The findings are considered preliminary until the full results are published in a peer-reviewed journal.

"I wouldn't say dental flossing is the only thing you need to do to prevent a stroke, but our findings suggest it is one more thing to be added to a healthy lifestyle," said lead researcher Dr. Souvik Sen, a professor and chair of the neurology department at the University of South Carolina in Columbia.

Sen said prior studies have shown a link between oral health, oral infection and damage to white matter and small blood vessels in the brain, as well as to a buildup of plaque in the arteries that supply blood to the brain.

The new study included 6,278 participants who had answered questions about home use of dental floss. About 65% of the participants reported flossing at least once a week.

Participants were followed for 25 years to see if they developed AFib or had an ischemic stroke, which occurs when a blood vessel to the brain is blocked. The researchers also looked at the risk of specific types of ischemic stroke: thrombotic strokes, caused by a blood clot in large arteries in the brain; cardioembolic strokes, caused by a clot traveling to the brain from the heart; and lacunar strokes, clots that occur in small arteries deep in the brain.

Compared to non-flossers, people who flossed experienced a 22% lower risk of an ischemic stroke, a 44% lower risk of a cardioembolic stroke, and a 12% lower risk of AFib, which developed in 20% of study participants. The analysis showed no link between flossing and thrombotic or lacunar strokes.

"Dental flossing reduces oral infections and gum disease, which are linked to inflammation," Sen said. Because inflammation can contribute to the risk for stroke, "it would make sense that if people flossed regularly, it might also reduce the risk of stroke and AFib."

Dr. Karen Furie, neurologist-in-chief at Brown University Health in Providence, Rhode Island, said she wasn't surprised that flossing might help reduce stroke risk.

"Flossing does help get debris out from between teeth that brushing alone might miss," said Furie, who also is chair of neurology at the Warren Alpert Medical School of Brown University. "Things that cause inflammation to the gums might be retained food or seeds, things that if not removed might inflame the gums and contribute to a systemic inflammatory state that might affect the health of the blood vessels."

But Furie, who was not involved in the study, was surprised the investigation found no association between flossing and thrombotic strokes, because of their link to inflammation and atherosclerosis, the buildup of plaque in the arteries.

"I would have thought this type of stroke would have been the most reduced," she said. "It's possible that people who have thrombotic strokes, which you can anticipate because you can see evidence of atherosclerosis in the arteries, were being managed more vigorously than people who had cardioembolic strokes, which come out of the blue."

The lower stroke risk could stem from "something fundamentally different about people who floss," Furie said. "The 65% who floss may be people who follow the recommendations of their dentists and doctors and are attentive to the small details of health maintenance. They might be different than the 35% who don't floss, who might not be as compliant or might have other lifestyle or medical factors that reduce their compliance."

Managing blood pressure and cholesterol, maintaining a healthy weight, staying physically active, eating a healthy diet and getting enough sleep are all important steps people can take to help prevent strokes, Furie said, but the new study "shows good dental health also matters. That is an important message and something people don't appreciate. Many neglect their oral hygiene, and hopefully this calls attention to it being an important aspect of total good health."

A common mouth and gut bacteria may be linked with increased stroke risk

 Is your competent? doctor ready to detect and prevent this problem in the next month? I doubt you have a functioning stroke doctor that will get that done.

Do you prefer your doctor incompetence NOT KNOWING? OR NOT DOING?

A common mouth and gut bacteria may be linked with increased stroke risk

             American Stroke Association International Stroke Conference 2025 - Abstract 106

Research Highlights:

• Increased levels of Streptococcus anginosus, a common type of bacteria that usually lives in the mouth and gut, was found in the gut of recent stroke survivors in Japan.
• Over two years, stroke patients with a significant amount of Streptococcus anginosus bacteria in their gut were more likely to die or have another major cardiovascular event than stroke patients without Streptococcus anginosus in the gut.
• The results suggest that analyzing mouth and gut bacteria may someday help determine stroke risk, and that targeting these harmful bacteria with new therapies and proper dental hygiene may help prevent stroke.
• Note: The study featured in this news release is a research abstract. Abstracts presented at the American Heart Association’s scientific meetings are not peer-reviewed, and the findings are considered preliminary until published as full manuscripts in a peer-reviewed scientific journal.

Embargoed until 4 a.m. CT/5 a.m. ET, Thursday, Jan. 30, 2025

DALLAS, Jan. 30, 2025 — A common bacteria usually found in the mouth and gastrointestinal tract, Streptococcus anginosis, may be abundant in the guts of people with stroke and is associated with a worse prognosis and increased risk of death, according to a preliminary study to be presented at the American Stroke Association’s International Stroke Conference 2025. The meeting is in Los Angeles, Feb. 5-7, 2025 and is a world premier meeting for researchers and clinicians dedicated to the science of stroke and brain health.

“In the future, if there was a quick test to detect harmful bacteria in the mouth and gut, we could use the information to help calculate stroke risk. Targeting these specific harmful oral bacteria may help prevent stroke,” said Shuichi Tonomura, M.D., lead author of the study and staff physician in the department of neurology at the National Cerebral and Cardiovascular Center in Osaka, Japan.

Everyone has trillions of bacteria in their gut, collectively known as the gut microbiota. There is also another community of bacteria in the mouth called oral microbiota. Most of these bacteria positively affect the body and assist with normal body processes, such as digestion. However, when the helpful and unhelpful types of bacteria get out of balance, illness can happen, Tonomura noted.

Previously, these researchers found that a different bacteria that causes tooth decay, Streptococcus mutans, was associated with a higher risk of bleeding inside the brain. In this new study, conducted at the largest stroke center in Japan, researchers quantified all detectible bacteria in both the saliva and guts of people who had recently had any type of stroke, comparing them to people without a stroke of similar age undergoing routine medical checkups.

The researchers found that one species of bacteria, Streptococcus anginosus, was significantly more abundant in the saliva and gut of people with acute stroke than in the control group of people who had not had a stroke.

An analysis of various groups of bacteria found:

• Streptococcus anginosus in the gut was independently associated with 20% higher odds of stroke after controlling for vascular risk factors, while Anaerostipes hadrus (a gut bacteria associated with beneficial effects) was associated with a drop in risk by 18% and Bacteroides plebeius (a gut bacteria common in the Japanese population) was associated with a drop in risk by 14%.
• Over the two-year follow-up, stroke survivors with Streptococcus anginosus in the gut had a significantly higher risk of death and major cardiovascular events over the two-year follow-up period.
• Increased risk of death and poor outcomes was not noted in stroke survivors with Anaerostipes hadrus and Bacteroides plebeius compared to controls.

“Our findings offer new insights into the connection between oral bacteria and the risk of stroke, as well as potential strategies for stroke prevention. Both Streptococcus mutans and Streptococcus anginosus are bacteria that contribute to tooth decay by producing acids that break down tooth enamel. This highlights the importance of preventing tooth decay, which can be achieved by reducing sugar intake and using toothpaste that targets these bacteria. Maintaining good oral hygiene is essential,” Tonomura said.

The researchers hope to conduct similar studies in people who have not experienced a stroke, but have risk factors for stroke.

“Extending the analysis to populations at risk of stroke is crucial for understanding broader implications and developing potential preventive strategies for those susceptible to stroke,” Tonomura said.

Because the study was conducted in a Japanese population with a relatively small sample size (189 stroke patients and 55 non-stroke participants), the findings may not be fully generalizable to other populations or larger, more diverse groups.

“The oral and gut microbiome is strongly affected by lifestyle. Other bacteria may be main players in stroke in other countries,” Tonomura said.

“Poor oral health can lead to inflammation and may increase the risk of stroke. The increased levels of Streptococcus anginosus found in the gut of patients with recent stroke is intriguing, and the fact that levels were linked to increased mortality two years after stroke suggests that it may play a role in ongoing stroke risk,” said Louise D. McCullough, M.D., P.H.D., FAHA, who is the Roy M. and Phyllis Gough Huffington Distinguished Chair of Neurology at McGovern Medical School; chief of neurology at Memorial Hermann Hospital-Texas Medical Center and co-director of UTHealth Neurosciences, all in Houston, who was not involved in the study. “Since this study was conducted after a stroke occurred, examining a larger group of people who have not yet had a stroke but do have risk factors could enhance our understanding of how these bacteria are related to stroke risk. This knowledge could help improve prevention strategies.” McCullough also coauthored the commentary Stroke and the Microbiome published in the Jan. 2024 issue of the American Heart Association Stroke journal.

Study details, background or design:

• The study included 250 people (average age 70, 40% female, all Japanese). Two hundred patients diagnosed (using brain imaging) with a stroke (either bleeding or clot-caused) within the past seven days were compared with 50 people the same age without a history of stroke who were receiving a routine medical checkup. The control group may have other medical problems such as high blood pressure, diabetes or high cholesterol.
• Stroke patients were seen at the National Cerebral and Cardiovascular Center in Osaka, Japan’s largest stroke center. Controls were participants in the ongoing population-based Suita study, which examines cardiovascular risk factors in middle-aged and older people.
• Researchers analyzed the oral and gut microbiomes using saliva and stool samples obtained from the stroke patients and controls between July 2020 to July 2021. Over a two-year follow-up period, they observed how many of the stroke patients died or had new cardiovascular events.

Co-authors, disclosures and funding sources are listed in the manuscript.  

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