Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,245 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
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 don't do this. Show all posts
Showing posts with label don't do this. Show all posts
Monday, July 6, 2026
Wednesday, February 21, 2024
Dietary Thiamine Linked With Cognition — J-shaped curve emerges between vitamin B1 in diet and cognitive decline
Ask your competent? doctor PRECISELY what you should do with this. Don't try to figure this out yourself, your doctor is being paid to know this stuff. Your doctor should easily know how much thiamine you're getting in your hospital meals.
Dietary Thiamine Linked With Cognition J-shaped curve emerges between vitamin B1 in diet and cognitive decline
Dietary thiamine (vitamin B1) intake was linked with cognition in older adults, a longitudinal analysis in China suggested.
Over a median follow-up of 5.9 years, cognitive decline risk was minimal at dietary thiamine intake levels of 0.60 to 1.00 mg/day, reported Xianhui Qin, MD, of Southern Medical University in Guangzhou, and co-authors.
However, a J-shaped association emerged between intake of dietary thiamine and 5-year cognitive decline, with an inflection point at 0.68 mg/day (95% CI 0.56-0.80), the researchers wrote in General Psychiatryopens in a new tab or window.
Before the inflection point of 0.68 mg/day, thiamine intake was not significantly associated with cognitive decline. After the inflection point, each daily 1.0-mg increase in thiamine intake was associated with a drop of 4.24 points in global cognitive scores (95% CI 2.22-6.27) and 0.49 standard units in composite cognitive scores (95% CI 0.23-0.76) within 5 years (P<0.001 for both). Global cognitive scores could range from 0 to 27.
The association of dietary thiamine intake with cognitive decline beyond the inflection point appeared stronger in people with obesity or hypertension and in non-smokers, Qin and colleagues noted. After multiple test correction, the effect of hypertension and smoking became non-significant.
Food sources of thiamine include whole grains, meat, and fish. In the U.S., common thiamine sourcesopens in a new tab or window are cereals and bread. Several observational studies -- including a recent cross-sectional analysisopens in a new tab or window of National Health and Nutrition Examination Survey (NHANES) data -- have reported a linear relationship between dietary thiamine and cognitive function in older adults.
In animal models, thiamine deficiency produces many Alzheimer's-like changes, noted Gary Gibson, PhD, of the Burke Neurological Institute of Weill Cornell Medicine in White Plains, New York, who wasn't involved with the study.
"Evidence suggests that the decline is related to a reduced ability to transport thiamine," Gibson told MedPage Today. "Thus, brains of Alzheimer's disease patients and animal models can be thiamine-deficient despite normal intake."
In 2021, an exploratory clinical trialopens in a new tab or window led by Gibson suggested that pharmacological-grade benfotiamine, a thiamine prodrug not available commercially, may help people with mild cognitive impairment or mild Alzheimer's disease. A larger phase II studyopens in a new tab or window that randomizes people with early Alzheimer's disease to benfotiamine or placebo is underway.
In their analysis, Qin and co-authors used data from the China Health and Nutrition Surveyopens in a new tab or window. In 1997, 2000, 2004, and 2006, cognitively healthy participants ages 55 and older had assessments of mental acuity. Information about diet was collected in each survey round, supplemented by detailed data about dietary intake over 24 hours on 3 consecutive days, which were collected in person by trained investigators.
The study included 3,106 participants capable of completing repeated cognitive function tests who had at least two rounds of survey data. Mean age was 63, and the average dietary thiamine intake was 0.93 mg/day.
Cognitive decline was defined as the 5-year decline rate in global or composite cognitive scores based on a subset of items from the Telephone Interview for Cognitive Status-modified (TICS-mopens in a new tab or window), which can be administered by phone or in-person. The test included immediate and delayed recall of a 10-word list, counting backward from 20, and serial seven subtraction five times from 100 to evaluate verbal memory, attention, and calculation, respectively. Higher scores in each item indicated better function. The researchers also determined a composite score by averaging z scores of the test components.
Compared with participants with thiamine intake of 0.60 to less than 1.00 mg/day, β for 5-year decline rates in the composite cognitive score was 0.13, 0.15, and 0.33 in those with daily intake of less than 0.60 mg, 1.00 mg to less than 1.20 mg, and 1.20 mg or more, respectively. "Similar patterns were observed for the global cognitive scores," Qin and colleagues noted. "Moreover, multiple test correction had no significant effect on the results."
Other variables -- age, sex, alcohol consumption, and dietary intake of fat, protein, or carbohydrate -- did not significantly change the findings, the researchers added.
The analysis relied on dietary intake recalled over 24-periods, which may not be fully accurate, Qin and co-authors acknowledged. It assessed data about cognitively healthy older adults in China only and findings might not apply to others.
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Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow
Disclosures
This study was funded by the National Key Research and Development Program of China and the National Natural Science Foundation of China.
Qin and co-authors reported no conflicts of interest.
Gibson reported relationships with the National Institute on Aging.
Primary Source
General Psychiatry
Source Reference: opens in a new tab or windowLiu C, et al "J-shaped association between dietary thiamine intake and the risk of cognitive decline in cognitively healthy, older Chinese individuals" Gen Psychiatr 2024; DOI: 10.1136/gpsych-2023-101311.
Friday, July 21, 2023
My stroke rehab schedule
This is not something any of you reading this should follow. None of this is sanctioned by any medical staff
I try to do this daily.
Since moving to an apartment in East Lansing, MI I have the ability to setup stroke stations and leave them up permanently. I work my way around the room.
Bosu, round side down - in the corner so I can touch the wall for balance. At the gym when I first started this I used a railing.10-15 minutes just rolling the Bosu under your feet. Excellent for strengthening your ankles and general balance.
Cane1 - handle in bad hand, good hand on rubber tip, push left hand straight out in front, then over the head and back down behind me, completing a complete circle. For my spasticity.
Cane2 - sitting in chair, bad hand on grip. Extend the arm directly out in front of you, pull it back in, 50 reps. When done, arm straight out, let it drop to the left, bring it upright, let it drop to the right, bring it upright. 25 times each.
Theraband progressive hand trainer sheets
with prepunched holes for your fingers. You put the sheet into an embroidery hoop, the one that comes with the kit doesn't work, so buy a 7 or 9 inch embroidery hoop. none of the individual sheets were strong enough to keep my fingers open, so I used all six that came in the red refill pack and put them into one hoop. I can get this on in 30 seconds. Not only can you work flexion, also spreading/unspreading your fingers.
Saebo flex -Because the Saebo takes me 20 minutes to get on I don't use it very much.
Passive flexing and unflexing the fingers - This is done anytime my right hand is not in use for daily tasks.
Hand Helper - I received one of these from my OT and would spend minutes willing my hand to relax. Getting the rubber bands on requires a two-handed person.
eStim -
Splitting wedge - This needs to be done on a carpeted floor, its too dangerous anywhere off the ground. I force the top end into my left hand and just balance it pointed side down, at first with my elbow on the floor, don't try this unless you have the ability to release your hand before it tips and hits the floor, its quite painful otherwise.
Gripmaster I bought a couple of light resistance ones but they don't work for me because I can't separate my fingers enough to use them.
Hamstring work, sitting in regular kitchen chair pull your bad leg underneath you.
Laundry basket carrying I load it up with clothes, if the left hand releases the falling to the floor does not hurt anything. Forcing my hand open to grab/release the handle will eventually(1 million tries later?) tell my extensors to work.
I try to do this daily.
Since moving to an apartment in East Lansing, MI I have the ability to setup stroke stations and leave them up permanently. I work my way around the room.
Bosu, round side down - in the corner so I can touch the wall for balance. At the gym when I first started this I used a railing.10-15 minutes just rolling the Bosu under your feet. Excellent for strengthening your ankles and general balance.
Cane1 - handle in bad hand, good hand on rubber tip, push left hand straight out in front, then over the head and back down behind me, completing a complete circle. For my spasticity.
Cane2 - sitting in chair, bad hand on grip. Extend the arm directly out in front of you, pull it back in, 50 reps. When done, arm straight out, let it drop to the left, bring it upright, let it drop to the right, bring it upright. 25 times each.
Theraband progressive hand trainer sheets
with prepunched holes for your fingers. You put the sheet into an embroidery hoop, the one that comes with the kit doesn't work, so buy a 7 or 9 inch embroidery hoop. none of the individual sheets were strong enough to keep my fingers open, so I used all six that came in the red refill pack and put them into one hoop. I can get this on in 30 seconds. Not only can you work flexion, also spreading/unspreading your fingers.
Saebo flex -Because the Saebo takes me 20 minutes to get on I don't use it very much.
Passive flexing and unflexing the fingers - This is done anytime my right hand is not in use for daily tasks.
Hand Helper - I received one of these from my OT and would spend minutes willing my hand to relax. Getting the rubber bands on requires a two-handed person.
eStim -
Splitting wedge - This needs to be done on a carpeted floor, its too dangerous anywhere off the ground. I force the top end into my left hand and just balance it pointed side down, at first with my elbow on the floor, don't try this unless you have the ability to release your hand before it tips and hits the floor, its quite painful otherwise.
Gripmaster I bought a couple of light resistance ones but they don't work for me because I can't separate my fingers enough to use them.
Hamstring work, sitting in regular kitchen chair pull your bad leg underneath you.
Laundry basket carrying I load it up with clothes, if the left hand releases the falling to the floor does not hurt anything. Forcing my hand open to grab/release the handle will eventually(1 million tries later?) tell my extensors to work.
Thursday, September 22, 2022
Study finds potential link between daily multivitamin and improved cognition in older adults
Ask your doctor if the upside potential outweighs the downsides. Don't do anything with this until your doctor informs you of their analysis. Of course you have no clue what is in the vitamins you take.
The supplements in the US have zero guarantee of purity or efficacy due to the fucking stupidity of the US Congress passing the Dietary Supplement Health and Education Act of 1994 (DSHEA).
Study finds potential link between daily multivitamin and improved cognition in older adults
(CNN)Taking a daily multivitamin might be associated with improved brain function in older adults, a new study says, and the benefit appears to be greater for those with a history of cardiovascular disease.
The findings did not surprise the researchers -- rather, they were shocked, said Laura Baker, an author of the study and professor of gerontology and geriatric medicine at Wake Forest University in North Carolina.
"I have to use the word 'shocked,' " Baker said.
The
researchers -- from the Wake Forest University School of Medicine, in
collaboration with Brigham and Women's Hospital in Boston -- analyzed
cognitive function in older adults who were assigned to take either a
cocoa extract supplement containing flavonoids, a multivitamin or a
placebo every day for three years. No one, not even the researchers,
knew who was assigned to which daily routine until the results were
revealed.
"We
really believed that the cocoa extract was going to have some benefits
for cognition based on prior reports of cardiovascular benefit. So we're
waiting for that big reveal in our data analysis -- and it was not
cocoa extract that benefited cognition but rather the multivitamin,"
Baker said. "We are excited because our findings have uncovered a new
avenue for investigation -- for a simple, accessible, safe, inexpensive
intervention that could have the potential to provide a layer of
protection against cognitive decline."
But
she added that she and her team are not ready to recommend that older
adults immediately add a daily multivitamin to their routine based on
these results alone.
The findings, published Wednesday in Alzheimer's & Dementia: The Journal of the Alzheimer's Association, are not definitive and cannot be generalized to the public. More research is needed to confirm them.
"It's too soon to make these recommendations," Baker said. "I feel like we need to do this in one other study."
Finding connections in brain health
The
new study included 2,262 people, 65 and older, who were enrolled
between August 2016 and August 2017 and followed for three years. The
participants completed tests over the phone annually to evaluate their
cognitive function. They were scored on recalling stories, showing
verbal fluency and ordering digits, among other tests.
The
researchers analyzed function, based on test scores, among those who
took cocoa extract daily compared with a placebo, and among those who
took the daily multivitamin compared with a placebo.
The
researchers found that three years of taking the multivitamin appeared
to have slowed cognitive aging by 1.8 years, or 60%, compared with the
placebo. Daily cocoa extract supplementation for three years did not
affect cognitive function, the researchers wrote.
The
study -- supported by the National Institute on Aging of the National
Institutes of Health -- also found that multivitamins were most
beneficial for older adults who had a history of cardiovascular disease.
"It's
well-known that those with cardiovascular risk factors could have lower
levels in their blood of vitamins and minerals. So supplementing those
vitamins and minerals could improve cardiovascular health and, by virtue
of that, improve cognitive health -- and we know that there's a strong
connection between cardiovascular health and brain health," said Dr.
Keith Vossel, a professor of neurology and director of the Mary S. Easton Center for Alzheimer's Research and Care at the University of California, Los Angeles.
Thanks
to that connection between cardiovascular and brain health, taking
steps to prevent cardiovascular disease or other chronic diseases --
such as maintaining a healthy diet and exercise -- can benefit the brain
too, said Vossel, who was not involved in the new study.
"If we can really eliminate or really prevent chronic diseases, we could prevent dementias," he said. "Roughly up to 40% of dementia could be prevented with just better preventative measures throughout life's span."
The
specific factors driving this link between a multivitamin and cognitive
function are unclear and require more research, but Baker and her team
think the findings might be connected to the way multivitamins can
benefit people who might be lacking in micronutrients such as vitamin C, vitamin E, magnesium or zinc.
"With
aging, the situation can get worse. A lot of our older adults do not
have adequate nutrition for a number of reasons," Baker said.
"As
we get older, we are more likely to have medical conditions that can
compromise micronutrient sufficiency," she said. "The medications that
we take for these conditions can also affect micronutrient sufficiency
by interfering with the body's ability to absorb these essential
nutrients from the diet."
'We've been down this road a little before'
Other
studies have had mixed results in the association between certain
vitamins and supplements and dementia risk, Vossel warned.
"We've
been down this road a little before with vitamins and dementia
research. For many years, dementia specialists were recommending vitamin
E based on some early promising results with vitamin E and cognition, and especially those with Alzheimer's disease. But then, the results have been mixed since then," Vossel said.
Older adults should talk to their primary care physician before starting a vitamin or supplement routine, he added.
"Supplementing
is usually safe, but it needs to be monitored carefully, especially for
those who have memory loss, because overdosing with vitamins can be
very dangerous," Vossel said. "Even with vitamin E overdosing or taking
high levels of vitamin E can increase the risk of bleeding. So these are
just some considerations."
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Overall,
the new study's findings are encouraging, said Heather Snyder, vice
president of medical and scientific relations at the Alzheimer's Association.
"There's
certainly follow-up work that we need to see happen -- particularly
independent confirmation in studies that are in larger and more diverse
populations -- but this is encouraging," she said. "There is more
research that needs to be done to understand what it might be in the
multivitamin that may have a benefit."
Friday, August 19, 2022
Statins, Enzyme CoQ10 Supplement Use, and Cognitive Functioning
Well, CoQ10 is listed in this; but unless your doctor prescribes don't do anything.
Top 7 Vitamins for Stroke Recovery, Backed by Science from Flint Rehab
February 2020
The latest here:
Statins, Enzyme CoQ10 Supplement Use, and Cognitive Functioning
Abstract
Objective:
The current study assessed the effects of statin and CoQ10 supplement use on changes in cognitive functioning in the Wisconsin Registry for Alzheimer’s Prevention study.
Methods:
1,573 subjects were administered medical histories, the Mini-Mental State Examination (MMSE), Rey Auditory Verbal Learning Test (RAVLT), Wechsler Memory Scale, Logical Memory subtest, and the Trail Making Test, Parts A (TMT-A) and B (TMT-B) 3-4 times over 5-10 years.
Saturday, July 2, 2022
Modulation of DNA methylation and protein expression in the prefrontal cortex by repeated administration of D-lysergic acid diethylamide (LSD): Impact on neurotropic, neurotrophic, and neuroplasticity signaling
DO NOT DO THIS! This is in mice and human testing likely will never occur. I see no proof this actually helped neuroplasticity. Neuroplasticity signaling doesn't mean neuroplasticity actually occurred.
Modulation of DNA methylation and protein expression in the prefrontal cortex by repeated administration of D-lysergic acid diethylamide (LSD): Impact on neurotropic, neurotrophic, and neuroplasticity signaling
Highlights
- •
Repeated LSD administration affects the DNA methylation level of genes involved with neurotropic, neurotrophic, and neuroplasticity signaling.
- •
Repeated LSD administration affects the protein level of genes involved with neurotropic, neurotrophic, and neuroplasticity signaling.
- •
Repeated LSD administration increases the transcription level of genes involved with neurotropic, neurotrophic, and neuroplasticity signaling detected as both differentially methylated, and differentially expressed.
- •
This could represent a core mechanism mediating the effects of psychedelics.
Abstract
Aim
Psychedelic compounds elicit relief from mental disorders. However, the underpinnings of therapeutic improvement remain poorly understood. Here, we investigated the effects of repeated lysergic acid diethylamide (LSD) on whole-genome DNA methylation and protein expression in the mouse prefrontal cortex (PFC).
Methods
Whole genome bisulphite sequencing (WGBS) and proteomics profiling of the mouse prefrontal cortex (PFC) were performed to assess DNA methylation and protein expression changes following 7 days of repeated LSD administration (30 μg/kg/day); a treatment we previously found to potentiate excitatory neurotransmission and to increase dendritic spine density in the PFC in mice. qRT-PCR was employed to validate candidate genes detected in both analyses.
Results
LSD significantly modulated DNA methylation in 635 CpG sites of the mouse PFC, and in an independent cohort the expression level of 181 proteins. Gene signaling pathways affected are involved in nervous system development, axon guidance, synaptic plasticity, quantity and cell viability of neurons and protein translation. Four genes and their protein product were detected as differentially methylated and expressed, and their transcription was increased. Specifically, Coronin 7 (Coro7), an axon guidance cue; Penta-EF-Hand Domain Containing 1 (Pef1), an mTORC1 and cell cycle modulator; Ribosomal Protein S24 (Rps24), required for pre-rRNA maturation and biogenesis of proteins involved with cell proliferation and migration, and Abhydrolase Domain Containing 6, Acylglycerol Lipase (Abhd6), a post-synaptic lipase.
Conclusions
LSD affects DNA methylation, altering gene expression and protein expression related to neurotropic-, neurotrophic- and neuroplasticity signaling. This could represent a core mechanism mediating the effects of psychedelics.
Data availability
Data will be made available on request.
Cited by (0)
- 1
Current address: Vita-Salute San Raffaele University, Division of Neuroscience, Milan, Italy.
Promising Action of Cannabinoids on ER Stress-Mediated Neurodegeneration: An In Silico Investigation
Don't read between the lines and think that cannabidiol or marijuana would suffice in duplicating the benefits. You're going to have to wait 50 years before anything gets defined for layperson use. Hope you last that long.
Promising Action of Cannabinoids on ER Stress-Mediated Neurodegeneration: An In Silico Investigation
Volume 41,
Issue 4, 2022,
pp. 39-54
DOI: 10.1615/JEnvironPatholToxicolOncol.2022040055
Get access
Fathima Hajee Basha
School of Life Sciences, B.S Abdur Rahman Crescent Institute of Science of Technology, Vandalur, Chennai 600048, Tamil Nadu, India
School of Life Sciences, B.S Abdur Rahman Crescent Institute of Science of Technology, Vandalur, Chennai 600048, Tamil Nadu, India
Mohammad Waseem
School of Life Sciences, B.S Abdur Rahman Crescent Institute of Science of Technology, Vandalur, Chennai 600048, Tamil Nadu, India
School of Life Sciences, B.S Abdur Rahman Crescent Institute of Science of Technology, Vandalur, Chennai 600048, Tamil Nadu, India
Hemalatha Srinivasan
School of Life Sciences, B.S Abdur Rahman Crescent Institute of Science of Technology, Vandalur, Chennai 600048, Tamil Nadu, India
School of Life Sciences, B.S Abdur Rahman Crescent Institute of Science of Technology, Vandalur, Chennai 600048, Tamil Nadu, India
ABSTRACT
Neurodegeneration has been recognized as a clinical episode characterized by neuronal death, including dementia, cognitive impairment and movement disorder. Most of the neurodegenerative deficits, via clinical symptoms, includes common pathogenic features as protein misfolding and aggregation. Therefore, the focus highlights the cellular organelle endoplasmic reticulum (ER) critically linked with the quality control and protein homeostasis. Unfolded protein response (UPR) or ER stress have also been considered as hallmarks for neurodegenerative disorders. It has been implicated that the levels of endocannabinoids (ECB) could rise at the platform of neurodegeneration. In addition, phytocannabinoids (PCB) including cannabidiol (CBD) could also initiate the IRE1, PERK, XBP-1, and ATF6, pathways that could lead to the degradation of the misfolded proteins and termination of protein translation. Thus, our aim was to determine if cannabinoids bind to these ER arm proteins involved in UPR by molecular docking and therefore determine its drug resemblance through ADME analysis. In our study, three cannabinoid receptors (CB1, CB2, and CB3) were considered to demonstrate their neuroprotective actions. The chosen ligands were screened as PCB (Δ9-tetrahydrocannabinol or THC), CBD, and two ECB, anandamide (AEA) and 2-arachidonoylglycerol (2-AG). The current findings have advocated that the cannabinoids and their molecular targets have shown considerable binding and their ADME properties also reveals that they possess moderate drug-like properties making it as a valuable option for the treatment and management of neurodegenerative diseases.
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