Eating More Of This Fruit May Reduce Plaque Buildup In Arteries by mindbodygreen

 

 You can tell the competence of your doctor and hospital if they implemented watermelon in their hospitals from way back in November 2011. Is watermelon better than pomegrantes?  A competent? doctor would know that answer immediately!

Watermelon juice reverses hardening of the arteries  Nov. 2011

The latest here: 

Eating More Of This Fruit May Reduce Plaque Buildup In Arteries

 Pomegranates have long been considered a heart-healthy food, thanks to their high levels of plant compounds called polyphenols. But the real benefit might not come from the fruit itself. It may come from what your gut bacteria do with it after you eat it. A new study explored how one of these gut-made compounds affects1, with results that could change how we think about diet and heart disease.  

About the study

Pomegranates are packed with polyphenols, but your body can't absorb most of them directly because they're too large. Instead, your gut bacteria break them down into smaller molecules called urolithins. Researchers at Cardiff University wanted to figure out which of these compounds actually helps protect arteries. They tested the original pomegranate polyphenol along with several of its breakdown products on human cells in the lab, looking at whether these compounds could reduce cell damage, calm inflammation, and stop cells from absorbing harmful cholesterol. Urolithin A came out on top across the board. So the researchers took the next step: they gave urolithin A to mice that were prone to clogged arteries and fed them a high-fat diet for 12 weeks. Smaller plaques and less inflammation, without changing cholesterol. The mice that received urolithin A had noticeably less buildup in their arteries. Their plaques were smaller, and their arteries were less blocked compared to mice that didn't get the compound. What really stood out was what was happening inside those plaques. The urolithin A group had fewer immune cells, specifically the types that drive inflammation and make plaques more likely to rupture. At the same time, their plaques had more of the stabilizing components (muscle cells and collagen) that help keep them intact and at a lower risk of a dangerous break. None of this had anything to do with cholesterol levels. The mice showed no changes in total cholesterol, LDL, HDL, or triglycerides. The protection came entirely from reduced inflammation and less cell damage, not from lowering fats in the blood. 

What this means for humans

 This study was done in mice, so we can't say for certain that the same plaque-shrinking effects would happen in people. But there are reasons to be cautiously optimistic The dose the researchers used translates to roughly 4 mg/kg/day in humans, a level that's already being tested in clinical trials for other benefits like muscle health and aging. Human trials have used doses of around 1,000 mg/day for periods ranging from 28 days to four months, showing improvements in muscle function and mitochondrial health. So we know the compound is safe and bioavailable in people; we just don't have human data specifically on artery plaques yet. The mechanisms urolithin A affected (inflammation, oxidative stress, immune cell activity) are the same ones involved in human heart disease. And the fact that protection wasn't dependent on cholesterol changes is actually encouraging: it suggests a different, complementary route to heart protection beyond the standard "lower your cholesterol" approach. 

Why your gut bacteria may determine how much you benefit

 Urolithin A isn't actually in pomegranates. Your gut bacteria have to make it for you after you eat the fruit's polyphenols. And not everyone's gut does this equally well. Some people have the right bacteria to produce lots of urolithin A; others don't. This might explain why studies on pomegranate and heart health have had mixed results. The same fruit could have very different effects depending on who's eating it.Pomegranates are one of the richest dietary sources of the polyphenols that can be converted into urolithin A. While this study tested the isolated compound rather than whole fruit, the biological pathway is clear: pomegranate polyphenols are broken down by gut bacteria into urolithin A in certain individuals. For those who want a more direct route, urolithin A supplements have been tested in humans for muscle health and mitochondrial function, though not yet specifically for artery health.

The takeaway

This research suggests that pomegranate's heart benefits may depend less on the fruit itself and more on whether your gut can turn it into urolithin A. In mice prone to artery disease, the compound shrank plaques and reduced inflammation without touching cholesterol levels. Human studies on artery health are still needed, but the findings point to an intriguing gut-heart connection worth watching.https://www.mdpi.com/2076-3921/15/4/507

Midlife Vitamin D Levels Tied to Lower Tau Burden in Later Life

 Does this mean your competent? doctor will have EXACT supplement protocols for your use? Oh NO, NOTHING OF THE SORT!    

Midlife Vitamin D Levels Tied to Lower Tau Burden in Later Life

Higher levels of vitamin D in early midlife were associated with significantly lower levels of tau deposition 16 years later in adults without dementia.

Results of a prospective, community-based cohort of nearly 800 adults showed those with higher serum 25-hydroxyvitamin D [25(OH)D] levels measured at age 39 showed lower global and regional tau burden on follow-up brain imaging.

However, there was no such association between midlife vitamin D levels and subsequent amyloid burden, a hallmark of Alzheimer’s disease (AD). This suggests that vitamin D may be more closely linked to tau-related pathways in the earlier stages of the disease rather than amyloid accumulation.

“These results suggest that higher vitamin D levels in midlife may offer protection against developing these tau deposits in the brain and that low vitamin D levels could potentially be a risk factor that could be modified and treated to reduce the risk of dementia,” lead investigator Martin David Mulligan, MB BCh BAO, of the University of Galway in Galway, Ireland, said in a news release. “Of course, these results need to be further tested with additional studies.”

The study was published online on April 1 in Neurology Open Access.

Vitamin D and Preclinical AD Risk

Vitamin D deficiency has previously been associated with cognitive decline and an increased risk for dementia in older adults.

Prior meta-analyses have shown a dose-dependent relationship, with lower 25(OH)D levels associated with a higher AD risk.

However, most studies have focused on vitamin D levels measured later in life, which limits the ability to determine whether earlier exposure affects preclinical disease processes.

Advances in neuroimaging now allow for the detection of early AD changes in asymptomatic individuals. While both tau and amyloid deposition are key AD biomarkers, tau accumulation may appear earlier and is closely tied to neuronal injury and cognitive impairment.

For the current study, investigators wanted to determine whether vitamin D levels in early midlife are associated with subsequent tau and amyloid deposition in later years among individuals who are dementia free.

The study included 793 participants (mean age, 39.2 years; 53.8% female) from the Framingham Heart Study Generation 3 cohort who were dementia free at the time of imaging.

Serum 25(OH)D levels were measured between 2002 and 2005 in a subset of 435 participants, followed by PET imaging between 2016 and 2019. The average follow-up was 16 years.

Tau imaging data were available for 369 participants, whereas amyloid imaging data were available for 424 participants.

At baseline, the mean vitamin D level was 38 ± 15 ng/mL. Approximately 34% of participants had levels < 30 ng/mL, and only 5% reported vitamin D supplementation.

The investigators used flortaucipir PET to assess tau burden across both global cortical regions and regions particularly vulnerable in early AD, including the entorhinal cortex, parahippocampal gyrus, fusiform gyrus, amygdala, and temporal cortices.

The Pittsburgh compound-B PET was used to measure amyloid burden across multiple cortical regions as a comparative baseline against tau deposition.

The researchers conducted multivariable linear regression analyses to adjust for a range of potential confounders, including age, sex, time from blood draw to imaging, depression, season, smoking status, systolic blood pressure, antihypertensive use, diabetes, cardiovascular disease, and BMI.

Link to Tau but Not Amyloid

Results showed higher midlife vitamin D levels were independently linked to lower tau deposition on PET imaging 16 years later.

In fully adjusted models, higher 25(OH)D levels were associated with lower global tau burden (beta-coefficient, -0.022; 95% CI, -0.040 to -0.004; P = .010). A similar association was seen for tau deposition in regions most vulnerable to early AD (beta-coefficient, -0.023; 95% CI, -0.043 to -0.003; P = .016).

These associations remained after adjusting for age, sex, time to imaging, depressive symptoms, season, and cardiometabolic risk factors.

Across sensitivity analyses, the findings were consistent, including models excluding participants taking vitamin D supplements.

Notably, no significant relationship was observed between vitamin D levels and amyloid burden (beta-coefficient, 0.001; 95% CI, -0.024 to 0.024; P = .987).

In analyses that used a clinical cutoff < 30 ng/mL vs ≥ 30 ng/mL, no statistically significant associations with tau burden were found in fully adjusted models. This suggests a gradual dose-dependent relationship between vitamin D rather than a threshold effect.

There were no significant interactions observed by sex or apolipoprotein E epsilon 4 carrier status, which suggests that the association was consistent across key subgroups.

Study limitations included its reliance on a single measurement of vitamin D, potential residual confounding, and a predominantly White cohort, which may limit the generalizability of the findings, the investigators noted.

“Low vitamin D in midlife may represent a potentially modifiable target to mitigate the risk of neuroimaging signs of preclinical dementia,” the investigators wrote.

They cautioned, however, that the findings are observational and warrant further investigation. “Our results do require validation in other cohorts of younger to middle-aged adults with follow-up data on markers of preclinical dementia.”

Taken together, the researchers suggest vitamin D levels may be a potential window for early intervention but highlight the need for randomized clinical trials to determine whether vitamin D supplementation can meaningfully reduce tau accumulation or dementia risk.

The study was funded by the National Institutes of Health, National Institute on Aging, National Institute of Neurological Disorders and Stroke, Irish Research Council, and Health Research Board of Ireland. Disclosure information for study authors is available in the original study publication.

Gut Bacteria’s Link to Alzheimer’s Explored

 Hopefully your competent? doctor will give exact amounts of probiotics and nutritional supplements and the type to buy.

Gut Bacteria’s Link to Alzheimer’s Explored

Summary: Researchers are investigating the connection between gut bacteria and Alzheimer’s disease. They believe harmful metabolites from bad bacteria can travel to the brain, causing inflammation and potentially triggering dementia.

The study aims to develop drug therapies to block these metabolites and explore the use of probiotics and nutritional supplements to promote gut health and potentially prevent or slow down Alzheimer’s progression.

Key Facts:

• Harmful gut bacteria may trigger and accelerate Alzheimer’s disease.
• A poor diet, aging, and lack of exercise can contribute to unhealthy gut bacteria.
• Probiotics and nutritional supplements could help combat bad bacteria and protect the brain.

Source: University of South Australia

The phrase ‘you are what you eat’ was coined almost a century before Alois Alzheimer made his breakthrough in identifying brain disease, but the evidence is now clear that diet, as well as age, influences the brain.

A growing body of research suggests a correlation between Alzheimer’s disease and an unhealthy gut, and Australian scientists are hoping to take this a step further by exploring how harmful gut bacteria access the brain and lead to dementia.

Most types of bacteria are harmless—many are even essential for our survival—but bad bacteria create biofilms which cause gastrointestinal infections, chronic diseases, bowel cancer and brain diseases. Credit: Neuroscience News

University of South Australia nano bio-scientist Dr. Ibrahim Javed says tiny metabolites released by bad bacteria in the gut can travel to the brain, causing inflammation and triggering Alzheimer’s disease, for which there is no cure.

In younger people, this is less likely because the blood-brain barrier is much stronger, but this weakens as people age, allowing harmful substances to damage neurons. When the microbiome in the gut ages, it also loses the ability to fight disease.

By identifying how metabolites released by bad bacteria damage neurons—and hopefully developing new drug therapies to block them—Dr. Javed says it should be possible to slow down or halt the progression of Alzheimer’s.

A second aim of the three-year research project is to investigate how probiotics and nutritional supplements, both of which contain friendly bacteria, can stamp out bad bacteria and stop metabolites from escaping from the gut.

This follows on from several international clinical research studies that have demonstrated that probiotics improve digestive and cognitive issues in people with acute and chronic COVID-19.

Did you know that a poor diet can accelerate your chances of developing Alzheimer’s disease?

An unhealthy gut produces bad bacteria, which releases tiny metabolites that travel to the brain, causing inflammation.

Scientists at the University of South Australia are exploring how probiotics and nutritional supplements – both of which contain friendly bacteria – can stamp out bad bacteria and stop metabolites from escaping the gut and accessing the brain. A poor diet is just one of several factors that harms gut bacteria.

Aging, lack of exercise, exposure to pesticides and genetics also play a role. Credit: University of South Australia

“Our research indicates that harmful gut bacteria can trigger early onset dementia as well as accelerate dementia in patients already battling the neurodegenerative disease,” Dr. Javed says.

“A poor diet is one of several factors that harms gut bacteria, increasing your chances of developing dementia. Aging, lack of exercise, exposure to pesticides and genetics also play a role, although the latter is responsible for a very small number of cases. In most cases, dementia is preventable.”

Most types of bacteria are harmless—many are even essential for our survival—but bad bacteria create biofilms which cause gastrointestinal infections, chronic diseases, bowel cancer and brain diseases.

Alzheimer’s disease affects up to 55 million people worldwide and with an aging population, this number is expected to double every 20 years, according to Alzheimer’s Disease International.

Early onset dementia—under the age of 65—is becoming more common in the global population, attributed to preventable factors such as a poor diet and a sedentary lifestyle, smoking, excessive alcohol consumption, social isolation, exposure to pesticides and air pollution.

Dr. Javed’s team is also collaborating with UniSA neuroscientist Associate Professor Larisa Bobrovskaya on a potential link between stress and Alzheimer’s disease, and whether women are more at risk.

About this Alzheimer’s disease and microbiome research news

Author: Ibrahim Javed
Source: University of South Australia
Contact: Ibrahim Javed – University of South Australia
Image: The image is credited to Neuroscience News

Nutritional Supplementation in Stroke Rehabilitation: A Narrative Review

So use in recovery for regular persons is not warranted.

Nutritional Supplementation in Stroke Rehabilitation: A Narrative Review

Sung-Hwa Ko,1,2 and Yong-Il Shin1,2
1Department of Rehabilitation Medicine, Rehabilitation Hospital and Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan, Korea.
2Department of Rehabilitation Medicine, Pusan National University School of Medicine, Yangsan, Korea.
Correspondence to Yong-Il Shin. Department of Rehabilitation Medicine, Rehabilitation Hospital and Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital and Department of Rehabilitation Medicine, Pusan National University School of Medicine, 20 Geumo-ro, Mulgeum-eup, Yangsan 50612, Korea. Email: rmshin01@gmail.com ,Email: rmshin@pusan.ac.kr
Received March 14, 2022; Revised March 16, 2022; Accepted March 17, 2022.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Malnutrition is associated with increased mortality and poor functional recovery after stroke. Most guidelines for stroke rehabilitation strongly recommend nutritional screening for malnutrition. Nutritional status after stroke is related to long-term outcomes, and nutritional supplementation is recommended for stroke patients with malnutrition and those at risk of malnutrition. However, routine nutritional supplementation in stroke patients, regardless of nutritional status, is not correlated with improved functional outcomes, and nutritional supplementation is not recommended if the nutritional status is adequate. Nutritional supplementation with protein, amino acids, vitamins, and minerals positively affects recovery after stroke, with improvements seen in motor function, cognition, activities of living, and mood. However, the evidence is insufficient due to the small number of studies and the lack of well-designed randomized controlled studies. Therefore, nutritional supplementation for stroke patients in rehabilitation should not be uniform, and individual nutritional interventions based on an assessment of the patient’s nutritional status should be provided.
Highlights
• In stroke rehabilitation, nutritional supplementation for malnutrition is required. • Nutritional supplementation may affect positive outcomes after stroke.

Keywords: Dietary Supplements; Malnutrition; Nutritional Status; Stroke; Rehabilitation

Go to: INTRODUCTION

Stroke, which is one of the most common and severe neurological diseases, is among the leading causes of death and disability worldwide. Stroke patients are at risk for dehydration and malnutrition due to dysphagia, cognitive impairment, and decreased consciousness.

Nutritional status may deteriorate during the acute phase after stroke for various reasons, including surgery and energy consumption, and malnutrition is associated with increased mortality and poor functional recovery in stroke patients [1, 2, 3, 4]. Malnutrition can also persist after stroke if it is not managed effectively. The key components of nutritional management include nutritional screening, assessment, and supplementation. Many guidelines for stroke rehabilitation recommend screening for malnutrition and providing nutritional supplementation [5, 6, 7, 8, 9]. Herein, we review nutritional supplementation in stroke rehabilitation for functional recovery, with a focus on general nutritional supplementation with protein/amino acids, vitamins, and minerals.

Brain Neurorehabil. 2022 Mar;15(1):e3. English. Published online Mar 25, 2022.  https://doi.org/10.12786/bn.2022.15.e3

Copyright © 2022. Korean Society for Neurorehabilitation