Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label alpha linolenic acid. Show all posts
Showing posts with label alpha linolenic acid. Show all posts

Wednesday, May 22, 2024

Mediterranean Diet May Slow Brain Aging

Pretty much totally useless, there is NOTHING SPECIFIC about the Mediterranean diet. So you likely will guess wrong  and thus you yourself can be blamed for not following the diet properly, rather than blaming your doctors, hospital and researchers for not providing specifics. If we had any leadership anywhere we would get specific amounts of these nutrients

Mediterranean Diet May Slow Brain Aging

Summary: A new study finds that specific nutrients, similar to those found in the Mediterranean diet, may play a crucial role in slowing down brain aging. The study combined blood biomarker analysis, brain imaging, and cognitive assessments to identify a nutrient profile associated with slower brain aging in cognitively healthy older adults.

These findings suggest that a diet rich in fatty acids, antioxidants, carotenoids, vitamin E, and choline could promote healthy brain aging and cognitive function.

Key Facts:

  • A specific nutrient profile is associated with slower brain aging in older adults.
  • This profile aligns with nutrients found in the Mediterranean diet.
  • The study combined blood biomarkers, brain imaging, and cognitive assessments.

Source: University of Nebraska Lincoln

Scientists have long been studying the brain with a goal of aiding healthier aging. While much is known about risk factors for accelerated brain aging, less has been uncovered to identify ways to prevent cognitive decline.

There is evidence that nutrition matters, and a novel study published in Nature Publishing Group Aging, from the University of Nebraska–Lincoln’s Center for Brain, Biology and Behavior and the University of Illinois at Urbana-Champaign further signals how specific nutrients may play a pivotal role in the healthy aging of the brain.

This shows olive oil and tomatoes.
The researchers will continue to explore this nutrient profile as it relates healthy brain aging. Credit: Neuroscience News

The team of scientists, led by Aron Barbey, director of the Center for Brain, Biology and Behavior, with Jisheng Wu, a doctoral student at Nebraska, and Christopher Zwilling, research scientist at UIUC, performed the multimodal study — combining state-of-the-art innovations in neuroscience and nutritional science — and identified a specific nutrient profile in participants who performed better cognitively.

The cross-sectional study enrolled 100 cognitively healthy participants, aged 65-75. These participants completed a questionnaire with demographic information, body measurements and physical activity.

Blood plasma was collected following a fasting period to analyze the nutrient biomarkers. Participants also underwent cognitive assessments and MRI scans. The efforts revealed two types of brain aging among the participants — accelerated and slower-than-expected. Those with slower brain aging had a distinct nutrient profile.

The beneficial nutrient blood biomarkers were a combination of fatty acids (vaccenic, gondoic, alpha linolenic, elcosapentaenoic, eicosadienoic and lignoceric acids); antioxidants and carotenoids including cis-lutein, trans-lutein and zeaxanthin; two forms of vitamin E and choline.

This profile is correlated with nutrients found in the Mediterranean diet, which research has previously associated with healthy brain aging.

“We investigated specific nutrient biomarkers, such as fatty acid profiles, known in nutritional science to potentially offer health benefits. This aligns with the extensive body of research in the field demonstrating the positive health effects of the Mediterranean Diet, which emphasizes foods rich in these beneficial nutrients,” Barbey, Mildred Francis Thompson Professor of Psychology, said.

“The present study identifies particular nutrient biomarker patterns that are promising and have favorable associations with measures of cognitive performance and brain health.”

Barbey noted that previous research on nutrition and brain aging has mostly relied on food frequency questionnaires, which are dependent on participants’ own recall. This study is one of the first and the largest to combine brain imaging, blood biomarkers and validated cognitive assessments.

“The unique aspect of our study lies in its comprehensive approach, integrating data on nutrition, cognitive function, and brain imaging,” Barbey said.

“This allows us to build a more robust understanding of the relationship between these factors. We move beyond simply measuring cognitive performance with traditional neuropsychological tests.

“Instead, we simultaneously examine brain structure, function, and metabolism, demonstrating a direct link between these brain properties and cognitive abilities. Furthermore, we show that these brain properties are directly linked to diet and nutrition, as revealed by the patterns observed in nutrient biomarkers.”

The researchers will continue to explore this nutrient profile as it relates healthy brain aging. Barbey said it’s possible, in the future, that the findings will aid in developing therapies and interventions to promote brain health.

“An important next step involves conducting randomized controlled trials. In these trials, we will isolate specific nutrients with favorable associations with cognitive function and brain health, and administer them in the form of nutraceuticals,” Barbey said.

“This will allow us to definitively assess whether increasing the levels of these specific nutrient profiles reliably leads to improvements in cognitive test performance and measures of brain structure, function, and metabolism.”

Barbey is also co-editing an upcoming special collection for the Journal of Nutrition, “Nutrition and the Brain — Exploring Pathways to Optimal Brain Health Through Nutrition,” which is currently inviting submissions for consideration, and articles will begin publishing next year.

“There’s immense scientific and medical interest in understanding the profound impact of nutrition on brain health,” Barbey said.

“Recognizing this, the National Institutes of Health recently launched a ten-year strategic plan to significantly accelerate nutrition research. Our work directly aligns with this critical initiative, aiming to contribute valuable insights into how dietary patterns influence brain health and cognitive function.”

About this diet and brain aging research news

Author: Leslie Reed
Source: University of Nebraska Lincoln
Contact: Leslie Reed – University of Nebraska Lincoln
Image: The image is credited to Neuroscience News

Original Research: Open access.
Investigating nutrient biomarkers of healthy brain aging: a multimodal brain imaging study” by Aron Barbey et al. Nature Aging

Tuesday, January 25, 2022

The nutraceutical potential of omega-3 alpha-linolenic acid in reducing the consequences of stroke

 You can't do anything with this until maybe 50 years from now when your doctor finally gets around to reading this research and creates protocols from it. Hope you aren't dead yet.

These failures of clinical trials have been known for years. WHOM  is cataloging and solving them to make the next ones better?

This is not going to be easy as Dr. Michael Tymianski, of the Toronto Western Hospital Research Institute in Canada states;  over the last half-century, there have been more than 1,000 drugs (So what are they?)aimed at preventing brain damage that have failed to work in people, even though they worked well in mice or rats.

The nutraceutical potential of omega-3 alpha-linolenic acid in reducing the consequences of stroke

Affiliations

Abstract

Stroke is a worldwide major cause of mortality and morbidity. Preclinical studies have identified over 1000 molecules with brain-protective properties. More than 200 clinical trials have evaluated neuroprotective candidates for ischemic stroke yet, to date almost all failed, leading to a re-analysis of treatment strategies against stroke. An emerging view is to seek combinatory therapy, or discovering molecules able to stimulate multiple protective and regenerative mechanisms. A pertinent experimental approach to identify such candidates is the study of brain preconditioning, which refers to how the brain protects itself against ischemia and others stress-inducing stimuli. The recent discovery that nutrients like alpha-linolenic acid (ALA is an essential omega-3 polyunsaturated fatty acid required as part of our daily diet), may be an efficient brain preconditionner against stroke fosters the novel concept of brain preconditioning by nutraceuticals. This review stresses the underestimated role of nutrition in preventing and combating stroke. Although there is a consensus that increased consumption of salt, fatty foods and alcoholic beverages may promote pathologies like hypertension, obesity and alcoholism - all of which are well known risk factors of stroke - few risk factors are attributed to a deficiency in an essential nutrient in the diet. The ALA deficiency observed in the Western modern diets may itself constitute a risk factor. This review outlines how ALA supplementation by modification of the daily diet prevented mortality and cerebral damage in a rodent model of ischemic stroke. It also describes the pleiotropic ability of ALA to trigger responses that are multicellular, mechanistically diverse, resulting in neuronal protection, stimulation of neuroplasticity, and brain artery vasodilation. Overall, this review proposes a promising therapeutic opportunity by integrating a nutritional-based approach focusing on enriching the daily diet in ALA to prevent the devastating damage caused by stroke.

Keywords: Brain preconditioning; Functional food; Ischemia; Neurogenesis; Neuroprotection; Synaptogenesis.

 

Thursday, January 10, 2019

Dietary intake of alpha-linolenic acid and risk of fatal ischemic heart disease among women

I'm making a giant leap of faith here that this might also help in preventing stroke. But what do I know, I'm not medically trained. Is your doctor medically trained and able to extrapolate this to helping for stroke? 20 years and I bet your doctor has completely failed in getting you a diet protocol for this. 

Dietary intake of alpha-linolenic acid and risk of fatal ischemic heart disease among women

  1999 May;69(5):890-7.

Abstract

BACKGROUND:

Experimental studies in laboratory animals and humans suggest that alpha-linolenic acid (18:3n-3) may reduce the risk of arrhythmia.

OBJECTIVE:

The objective was to examine the association between dietary intake of alpha-linolenic acid and risk of fatal ischemic heart disease (IHD).(ischemia because of a build-up or blockage in your arteries)

DESIGN:

This was a prospective cohort study. The intake of alpha-linolenic acid was derived from a 116-item food-frequency questionnaire completed in 1984 by 76283 women without previously diagnosed cancer or cardiovascular disease.

RESULTS:

During 10 y of follow-up, we documented 232 cases of fatal IHD and 597 cases of nonfatal myocardial infarction. After adjustment for age, standard coronary risk factors, and dietary intake of linoleic acid and other nutrients, a higher intake of alpha-linolenic acid was associated with a lower relative risk (RR) of fatal IHD; the RRs from the lowest to highest quintiles were 1.0, 0.99, 0.90, 0.67, and 0.55 (95% CI: 0.32, 0.94; P for trend = 0.01). For nonfatal myocardial infarction there was only a modest, nonsignificant trend toward a reduced risk when extreme quintiles were compared (RR: 0.85; 95% CI: 0.61, 1.19; P for trend = 0.50). A higher intake of oil and vinegar salad dressing, an important source of alpha-linolenic acid, was associated with reduced risk of fatal IHD when women who consumed this food > or =5-6 times/wk were compared with those who rarely consumed this food (RR: 0.46; 95% CI: 0.27, 0.76; P for trend = 0.001).

CONCLUSIONS:

This study supports the hypothesis that a higher intake of alpha-linolenic acid is protective against fatal IHD. Higher consumption of foods such as oil-based salad dressing that provide polyunsaturated fats, including alpha-linolenic acid, may reduce the risk of fatal IHD.

Comment in

PMID:
10232627
DOI:
10.1093/ajcn/69.5.890
[Indexed for MEDLINE]

Thursday, August 31, 2017

Alpha-Linolenic Acid Treatment Reduces the Contusion and Prevents the Development of Anxiety-Like Behavior Induced by a Mild Traumatic Brain Injury in Rats

Don't do this without a doctors prescription. 

Alpha-Linolenic Acid Treatment Reduces the Contusion and Prevents the Development of Anxiety-Like Behavior Induced by a Mild Traumatic Brain Injury in Rats


  • Taiza H. Figueiredo
  • Carolina L. Harbert
  • Volodymyr Pidoplichko
  • Camila P. Almeida-Suhett
  • Hongna Pan
  • Katia Rossetti
  • Maria F. M. Braga
  • Ann M. Marini
  • Taiza H. Figueiredo
    • 1
  • Carolina L. Harbert
    • 1
  • Volodymyr Pidoplichko
    • 1
  • Camila P. Almeida-Suhett
    • 1
  • Hongna Pan
    • 2
  • Katia Rossetti
    • 1
  • Maria F. M. Braga
    • 1
  • Ann M. Marini
    • 2
  1. 1.Department of Anatomy, Physiology and GeneticsUniformed Services University of the Health SciencesBethesdaUSA
  2. 2.Department of Neurology and Program in NeuroscienceUniformed Services University of the Health SciencesBethesdaUSA
Article

Abstract

Approximately, 1.7 million Americans suffer a TBI annually and TBI is a major cause of death and disability. The majority of the TBI cases are of the mild type and while most patients recover completely from mild TBI (mTBI) about 10% result in persistent symptoms and some result in lifelong disability. Anxiety disorders are the second most common diagnosis post-TBI. Of note, TBI-induced anxiety disorders are difficult to treat and remain a chronic condition suggesting that new therapies are needed. Previous work from our laboratory demonstrated that a mild TBI induced an anxiety-like phenotype, a key feature of the human condition, associated with loss of GABAergic interneurons and hyperexcitability in the basolateral amygdala (BLA) in rodents 7 and 30 days after a controlled cortical impact (CCI) injury. We now confirm that animals display significantly increased anxiety-like behavior 30 days after CCI. The anxiety-like behavior was associated with a significant loss of GABAergic interneurons and significant reductions in the frequency and amplitude of spontaneous and miniature GABAA-receptor-mediated inhibitory postsynaptic currents (IPSCs) in the BLA. Significantly, subchronic treatment with alpha-linolenic acid (ALA) after CCI prevents the development of anxiety-like behavior, the loss of GABAergic interneurons, hyperexcitability in the BLA and reduces the impact injury. Taken together, administration of ALA after CCI is a potent therapy against the neuropathology and pathophysiological effects of mTBI in the BLA.