Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,370 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 neuronsthatDIEeach day because there areNOeffective 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.
Natural remedies in the treatment of health conditions are an
appealing option for many individuals. Previous studies reported that
fermented and unfermented rooibos tea have considerable
anti-inflammatory and antioxidative properties. Most of this knowledge,
however, originates from animal and cell culture studies. The aims of
this review are to evaluate the existing, but limited, body of knowledge
regarding rooibos tea interventions in humans and to identify the gaps
in the literature. The PRISMA extension for Scoping Reviews (PRISMA-ScR)
guidelines were followed in the collation of this scoping review. Among
the databases searched were Google Scholar, PubMed, Cochrane Library,
Scopus, and Web of Science. This review comprised 18 publications, with
half (50%) of the studies being conducted in South Africa. There were
488 participants in all, ranging in age from six to 83 years, in the
investigations. Rooibos tea was either fermented, unfermented, or black
in 62% of the studies. Doses ranging from 200 to 1,200 ml were employed.
In both healthy and at-risk individuals, rooibos has been shown to
enhance lipid profiles, boost antioxidant status, and lower blood
glucose levels. The existing findings suggests that rooibos consumption
demonstrated to improve lipid profiles, boost antioxidant status, and
lower blood glucose levels in both apparently healthy, and individual
at-risk individuals or diagnosed of chronic conditions. Thus, it can be
presumed that rooibos tea provides some health benefits, yet these
findings are based on a limited number of human intervention studies and
a small total sample size. Additionally, a variety of rooibos dosages
and types of tea in the experiments had inconsistent results that were
probably impacted by the amount consumed. Future studies should include a
dose-response study in humans, as well as large scaled clinical trials
to evaluate the health effects of Rooibos.
Ask your competent? doctorPRECISELY which glucose monitor to get and what to track. This is all just guidelines(NOT PROTOCOLS!) which tell you nothing actionable.
If you've been thinking about your brain health, you might already be tracking sleep, stress, or your omega-3 intake. But a large new study suggests there's another number worth paying attention to, one most people only associate with diabetes risk.
Blood
glucose. And according to researchers, it may be the single most
important metabolic marker when it comes to how fast your brain ages.
About the study
We've
known blood sugar affects the body, but its specific relationship to
brain aging, across a general population, is still being mapped. This
study set out to do exactly that.
Here's how it worked:
Brain age predictions:
Researchers used machine learning to analyze brain MRI scans from
healthy participants, training a model to estimate how old a brain looks
based on its structure.
Brain age gap:
They applied those predictions across 37,458 people to calculate each
person's "brain age gap" (how much older or younger your brain appears
compared to your actual age). A positive gap means your brain is aging
faster than expected.
Blood marker analysis: From there, they looked at blood data from more than 21,000 people to find which markers were most closely tied to that gap.
All data came from the UK Biobank, one of the largest health research databases in the world.
Glucose came out on top
Out of nine blood markers that showed a meaningful connection to brain aging, glucose stood out the most.
To
make sure this wasn't just a coincidence, researchers used a technique
called Mendelian randomization, basically a way of using people's
genetic data to test whether one thing is actually causing another, rather than just happening to appear alongside it.
The result?
There's real evidence that elevated glucose may be actively driving faster brain aging, not just tagging along for the ride.
Higher
glucose levels were also linked to shrinkage across 80 different brain
regions, areas tied to memory, movement, and mood. And people with
higher glucose tended to score lower on tests of thinking ability,
physical function, and mental health.
The brain conditions connected to glucose
The findings didn't stop at brain aging in general. Higher blood glucose was linked to seven specific brain-related conditions:
All-cause dementia: an umbrella term for all types of dementia
Vascular dementia: dementia caused by reduced blood flow to the brain
Parkinson's disease: a progressive condition that affects movement and coordination
Stroke: when blood supply to part of the brain is cut off
Depression: a mood disorder with well-established connections to brain structure
Anxiety: closely tied to changes in brain function over time
That's
a wide-ranging list, spanning memory disorders, movement conditions,
and mental health, which suggests blood sugar's impact on the brain goes
far beyond any one condition.
This isn't just a diabetes story
You don't need a diabetes diagnosis for blood sugar to matter to your brain.
Think
of it less like an on/off switch and more like a dial. The lower you
can keep that dial, the more you may be protecting your brain for the
long haul.
How to keep your glucose working in your brain's favor
Blood sugar balance
is one of the most modifiable numbers in your health profile, and the
habits that support it aren't complicated. A few evidence-informed
places to start:
Prioritize proteinat every meal:
Protein slows digestion and softens the blood sugar spike that follows
eating; aim to include a quality source (eggs, fish, legumes, poultry)
at every meal.
Add fiber to your plate:
Fiber from vegetables, legumes, and whole grains slows how quickly
glucose enters your bloodstream, helping keep levels steadier throughout
the day; for foods that support blood sugar balance, there are some well-researched options worth knowing.
Move after meals:
Even a 10-minute walk after eating can reduce the blood sugar spike
that follows a meal; it doesn't have to be a workout, just movement.
Pair your carbs:
Eating refined carbohydrates on their own sends glucose levels surging;
pairing carbs with fat, fiber, or protein softens that response.
Consider tracking your glucose:
Continuous glucose monitors (CGMs) are small wearable sensors that
track your blood sugar in real time and can show you exactly how your
body responds to specific foods, sleep, and stress.
The takeaway
Of
all the metabolic markers researchers tested, glucose had the strongest
link to how fast the brain ages, and the connection extended to seven
brain-related conditions, from dementia to depression.
That makes blood sugar one of the most compelling levers for brain health, and one of the most actionable.
Your competent? doctor already told you of the benefits of living at a high altitude, right? NOPE? So, you finally figured out you DON'T have a functioning stroke doctor, didn't you?
What the fuck will prevent this poor outcome? You're so blitheringly stupid, you can't solve the problem in front of your face! Describing a problem is useless without a solution! And your mentors and senior researchers are just as stupid?
Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China
Background: Stress hyperglycemia is common in acute ischemic stroke (IS) and has been linked to adverse outcomes. The fasting glucose-to-glycated hemoglobin (HbA1c) ratio (GAR) has been proposed as a simple marker reflecting stress hyperglycemia relative to chronic glycemic status. Still, its prognostic value in patients undergoing endovascular treatment (EVT) remains unclear. This meta-analysis aimed to evaluate the association between GAR and 90d-day functional outcomes in these patients.
Methods: PubMed, Embase, Web of Science, Wanfang, and Chinese National Knowledge Infrastructure (CNKI) were systematically searched through May 29, 2025. Studies reporting the association between GAR and poor functional outcome, defined as a modified Rankin Scale (mRS) score of 3–6 at 90 days, were included. Odds ratios (ORs) with 95% confidence intervals (CIs) were pooled using a random-effects model accounting for heterogeneity.
Results: Twelve datasets from 10 retrospective cohort studies involving 3,878 patients were analyzed. The pooled analysis showed that a high GAR was significantly associated with an increased risk of poor functional outcome at 90 days after EVT (OR: 2.94, 95% CI: 2.22–3.88, p < 0.001; I2 = 14%). Meta-regression indicated that the proportion of diabetic patients showed a trend toward explaining the observed heterogeneity (coefficient = −0.0088, p = 0.08; I2 residual = 0%), whereas other factors showed no significant influence. Subgroup analyses yielded consistent results across age, sex, diabetes status, National Institutes of Health Stroke Scale (NIHSS), GAR cutoffs, and study quality (p for subgroup difference all > 0.05). The certainty of evidence for the primary outcome was rated as moderate according to the GRADE framework, mainly due to the retrospective design.
Conclusion: High GAR may independently predict poor 90-day functional outcomes(What will prevent that poor outcome; why wasn't that your research?) after EVT in patients with IS, supporting its potential prognostic value in clinical practice.
My high blood pressure didn't occur until 8 years after the stroke, no glucose problems, no clue on cholesterol since inflammation is the problem, NOT CHOLESTEROL!
A
2015 TIME article titled "Know Right Now: Why Cholesterol Isn't as Bad as We
Thought" suggested that dietary cholesterol might not be as problematic
as previously believed, aligning with shifts in dietary guidelines at
the time.
Warning signs like high blood pressure, elevated cholesterol or glucose levels precede almost all heart attack and stroke cases, according to a study challenging the belief that these strike without warning.
Above-optimal levels of blood pressure, cholesterol, glucose or smoking almost always precede these cardiac events, say researchers from Yonsei University College in South Korea, who call for greater attention to early detection and control of these modifiable risks.
Scientists assessed health records for over nine million people in South Korea and nearly 7,000 in the US, following their health status for up to two decades.
The researchers looked for the presence of four major risk factors before a heart attack, stroke or heart failure – high blood pressure, cholesterol, blood sugar and smoking.
Non-optimal levels included past tobacco use, blood pressure over 120/80 mm Hg, total cholesterol over 200 mg/dL, fasting glucose over 100 mg/dL, and diagnosis of diabetes.
They also examined higher thresholds for elevated risk: blood pressure over 140/90, cholesterol above 240, glucose levels above 126, and current smoking.
They found that 99 per cent of those who had a major heart event during the study had non-optimal levels of at least one factor, and 93 per cent had two or more.
“We think the study shows very convincingly that exposure to one or more non-optimal risk factors before these cardiovascular outcomes is nearly 100 per cent,” said study co-author Philip Greenland from Northwestern University, US.
“The goal now is to work harder on finding ways to control these modifiable risk factors rather than to get off track in pursuing other factors that are not easily treatable and not causal.”
High blood pressure – or hypertension – was the most common, affecting over 95 per cent of patients in South Korea and over 93 per cent in the US.
Even among women under 60 – the group often assumed to be at the lowest risk – more than 95 per cent still had at least one of these factors before heart failure or stroke.
At least 90 per cent of patients had at least one major high-risk factor before their first cardiac event, the study found.
1Department of Neurology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China
2Department of Cardiology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China
Introduction: Acute ischemic stroke
(AIS) patients admitted to the intensive care unit (ICU) have a high
mortality rate, necessitating the early identification of those at risk
of a poor prognosis. This study investigated the association between the
blood glucose-to-potassium ratio (GPR) and the prognosis of AIS
patients.
Methods: We conducted a retrospective
cohort study using data from the Medical Information Mart for Intensive
Care IV (MIMIC-IV) database. The primary outcomes were 28-day, 90-day,
and 1-year mortality rates following ICU admission. Multivariate Cox
proportional hazards regression models were used to estimate adjusted
hazard ratios (HRs) with 95% confidence intervals (CIs). Subgroup
analyses, Kaplan–Meier survival curves, and restricted cubic spline
models were employed to further evaluate the relationship between the
GPR and mortality in AIS patients.
Results: A total of 2,636 AIS patients
were included in the study, with a mean age of 69.4 ± 15.6 years. The
1-year mortality rate was 36.8% (n = 969). After adjusting for
confounders, compared with the first quartile (Q1, GPR ≤ 1.39), the
1-year mortality risks for the second quartile (Q2, 1.39 < GPR ≤
1.74), third quartile (Q3, 1.74 < GPR ≤ 2.25), and fourth quartile
(Q4, GPR ≥ 2.25) were HR = 1.17 (95% CI: 0.95–1.43, p = 0.132), HR = 1.42 (95% CI: 1.17–1.73, p < 0.001), and HR = 1.61 (95% CI: 1.33–1.96, p
< 0.001), respectively. Similar trends were observed for 28-day and
90-day mortality. Kaplan–Meier (KM) analysis revealed that groups with
higher GPRs had higher mortality rates at 28 days, 90 days, and 1 year.
Non-linear analysis further confirmed the presence of an inflection
point in the association between the GPR and 365-day mortality, which
was identified at GPR = 2.75. At ratios less than this threshold, the
risk of mortality increased significantly with increasing GPR (HR:
1.466; 95% CI: 1.239–1.735; p < 0.001). However, above this
ratio, the association plateaued and was no longer statistically
significant (HR: 0.899; 95% CI: 0.726–1.113; p = 0.095).
Conclusion: The GPR is an independent
predictor of poor prognosis in AIS patients admitted to the ICU. Higher
GPRs are associated with increased 28-day and 90-day mortality rates,
highlighting the potential utility of this ratio in risk stratification
and clinical decision-making. A non-linear relationship was observed
between the GPR and 365-day mortality, with an inflection point
identified at GPR = 2.75.
1 Introduction
Stroke is a life-threatening and prevalent condition and is the second leading cause of death worldwide (1).
Patients with severe stroke often experience systemic organ failure,
which presents significant challenges for subsequent treatment (2).
Early identification of key prognostic factors and timely intervention
are crucial for improving patient outcomes. However, there is currently
no universally recognized objective indicator for predicting the
prognosis of patients with severe strokes. Research has shown that
during the acute phase of stroke, blood glucose levels can significantly
increase (3).
In patients with severe acute stroke, dysregulated glucose metabolism
can lead to infarct expansion and impaired neurological recovery (4).
Additionally, blood potassium levels have been shown to influence the
prognosis of stroke. A study involving 421 stroke patients revealed that
lower plasma potassium levels were associated with worse clinical
outcomes. This may be due to hypokalemia impairing brain cell function,
exacerbating ischemic injury, and increasing the risk of arrhythmia (5).
Therefore, the coexistence of hyperglycemia and hypokalemia is
associated with a poorer stroke prognosis. The ratio of serum glucose to
potassium (GPR) has been explored in clinical practice. Previous
studies have identified the GPR as a risk factor for aneurysmal
subarachnoid hemorrhage (6) and an important biomarker in traumatic brain injury (7).
Recent research further suggested that the GPR may serve as a
prognostic indicator for intracerebral hemorrhage and coronary artery
disease (8, 9).
Previous studies have suggested that the
glucose-to-potassium ratio (GPR) may serve as an indicator of the
short-term prognosis of ischemic stroke patients (10).
However, these studies were limited by small sample sizes and a focus
solely on short-term mortality. The impact of the GPR on the long-term
prognosis of patients with severe ischemic stroke remains unclear, and
no studies have specifically investigated its association with mortality
in ICU-admitted acute ischemic stroke (AIS) patients. Therefore,
utilizing the MIMIC-IV database, this study included ICU patients with
severe AIS to examine the relationship between the GPR and all-cause
mortality at 28 days, 90 days, and 1 year in critically ill AIS
patients. Our goal was to evaluate whether the GPR could serve as a
biomarker for predicting the prognosis of severe AIS patients.
1Academy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin, China
2Tianjin Neurological Institute, Tianjin Huanhu Hospital, Tianjin, China
3Department of Clinical Laboratory, Tianjin Huanhu Hospital, Tianjin, China
4Department of Neurology, Xianyang Central Hospital, Xianyang, China
5Department of Neurology, Second Hospital of Tianjin Medical University, Tianjin, China
6Department of Neurosurgery, Hengshui Fifth People’s Hospital, Hengshui, China
Objective: To analyze the effect of fasting blood
glucose levels after reperfusion of acute large vessel occlusion (ALVO)
on patient functional prognosis.
Methods: Retrospectively included ALVO patients
from three large stroke centers in China, all of whom achieved vascular
reperfusion after mechanical thrombectomy or bridging thrombolysis. The
prognosis scores of all patients at 90 ± 7 days post-recanalization were
categorized into a good prognosis group (mRS 0–2) and a poor prognosis
group (mRS 3–6). The relationship between mean blood glucose levels at
72 h post-recanalization and prognosis was explored using multivariable
logistic regression analysis. Then we measured the area under the ROC
curve for all factors to assess their predictive performance.
Results: (1) Totally 2,056 patients were included
in the study, with 1,488 males and 568 females. There were 1,370
patients in the good prognosis group (mRS 0–2) and 686 in the poor
prognosis group (mRS 3–6). (2) The two groups exhibited significant
differences in terms of age, preoperative mRS score, history of
diabetes, and mean fasting blood glucose (MFBG) (p < 0.001).
(3) With 90-day mRS as the outcome variable, all independent variables
were included in Univariate and multivariate regression analyses
analysis, and the results showed that: age, preoperative mRS score,
history of diabetes, and MFBG are all independent predictors of
prognosis after recanalization of ALVO, with MFBG demonstrating a higher
predictive power than the other factors (AUC = 0.644).
Conclusion: Various factors are correlated with
the prognosis in patients who have undergone ALVO recanalization.
Notably, the MFBG level demonstrates a significant predictive value for
outcomes within the first 72 h following the recanalization procedure.
1 Background
Although mechanical thrombectomy (MT) has achieved
higher rates of vascular recanalization in patients with acute large
vessel occlusion (ALVO), the issue of reperfusion injury to brain tissue
after vascular recanalization has always been a challenge that scholars
and clinicians cannot avoid. Approximately 20–50% of ALVO patients may
experience stress-induced hyperglycemia, caused by the release of
cortisol and adrenaline leading to elevated blood glucose levels, a
phenomenon commonly seen even in non-diabetic patients (1, 2).
Patients undergoing MT procedures need to consider factors such as
surgery-related stress, and hyperglycemia has been associated with
adverse clinical outcomes in ALVO patients (3–7).
Hyperglycemia levels can further exacerbate the hypoxic status of
midbrain cells in the ischemic penumbra, leading to increased acidosis,
mitochondrial dysfunction, and even failure (8).
Besides, elevated blood glucose levels are associated with the
formation of free radicals and activation of matrix metalloproteinases,
which can further worsen brain edema (9–11). The 2018 American Heart Association/American Stroke Association (AHA/ASA) guidelines recommend (12)
targeting blood glucose levels to 140–180 mg/dL (7.8–10.0 mmol/L), but
this standard lacks a higher level of objective evidence due to limited
supporting data (1).
Our team’s previous research findings showed:
hyperglycemia is an independent risk factor for poor prognosis in ALVO
patients after vascular recanalization. The good prognosis rate in the
low blood glucose group was 1.62 times higher than that in the
hyperglycemia group; and for every 1 mmol/L decrease in blood glucose,
the rate of poor prognosis decreased by 7.2% [OR: 0.928, 95% CI (0.879,
0.979), p = 0.007] (2).
Other studies have shown the opposite: However, other studies have
yielded conflicting results, with no significant difference in the
90-day modified Rankin Scale (90ds-mRS) between patients on intensified
glucose lowering (4.44–7.22 mmol/L) and patients at standard glucose
levels (4.44–9.93 mmol/L) (3–5). Further research is needed to determine whether different blood glucose levels affect the 90ds-mRS in patients.
Taking into account the above factors, we conducted a
retrospective study on the fasting blood glucose levels of 2,056 post-MT
patients with ALVO from three different medical centers, analyzing the
relationship between MFBG levels and 90ds-mRS.
Large vessel occlusion stroke may be particularly vulnerable to the effects of hyperglycemia.
•
We analyzed intracerebral hemorrhage severity as a result of hyperglycemia-induced
toxicity.
•
Increasing blood glucose was associated with increasing severity of intracerebral
hemorrhage.
•
Future study is needed to determine if glycemic control improves outcomes in this
population.
ABSTRACT
Objectives
Hyperglycemia is associated with poor outcome in large vessel occlusion (LVO) stroke,
with mechanism for this effect unknown.
Materials and Methods
We used our prospective, multicenter, observational study, Blood Pressure After Endovascular
Stroke Therapy (BEST), of anterior circulation LVO stroke undergoing endovascular
therapy (EVT) from 11/2017-7/2018 to determine association between increasing blood
glucose (BG) and intracerebral hemorrhage (ICH). Our primary outcome was degree of
ICH, classified as none, asymptomatic ICH, or symptomatic ICH (≥4-point increase in
National Institutes of Health Stroke Scale [NIHSS] at 24 hours with any hemorrhage
on imaging). Secondary outcomes included 24-hour NIHSS, early neurologic recovery
(ENR, NIHSS 0-1 or NIHSS reduction by ≥8 within 24 hours), and 90-day modified Rankin
Scale (mRS) using univariate and multivariable regression.
Results
Of 485 enrolled patients, increasing BG was associated with increasing severity of
ICH (adjusted OR, aOR 1.06, 95% CI 1.02-1.1, p<0.001), higher 24-hour NIHSS (aOR 1.22,
95% CI 1.11-1.34, p<0.001), ENR (aOR 0.90, 95% CI 0.82-1.00, p<0.002), and 90-day
mRS (aOR 1.06, 95% CI 1.03-1.09, p<0.001) when adjusted for age, presenting NIHSS,
ASPECTS, 24-hour peak systolic blood pressure, time from last known well, and successful
recanalization.
Conclusions
In the BEST study, increasing BG was associated with greater odds of increasing ICH
severity. Further study is warranted to determine whether treatment of will decrease
ICH severity following EVT.
Will
this prompt your stroke hospital to create protocols for testing this
and then followup protocols to prevent cognitive decline from happening?
Or is your hospital incompetent in not even knowing about this?
Do you prefer your doctor and hospital incompetence NOT KNOWING? OR NOT DOING?
Higher
cumulative glucose levels may contribute to faster cognitive decline in
stroke survivors, representing a potential treatment target to preserve
cognition after stroke, according to a study published in JAMA Network Open.
“Having a stroke increases a person’s risk of dementia up to 50-fold,
but we lack a comprehensive treatment approach that could reduce this
risk, other than preventing a second stroke,” said Deborah A. Levine,
MD, University of Michigan Medical School, Ann Arbor, Michigan. “These
findings suggest that higher cumulative blood sugar levels after stroke
contribute to faster cognitive decline, and hyperglycaemia after stroke,
regardless of diabetes status, could be a potential treatment target to
protect post-stroke cognition.”
Dr. Levine and colleagues evaluated associations of post-stroke
systolic blood pressure (BP), glucose, and low-density lipoprotein (LDL)
cholesterol levels with cognitive decline by conducting a meta-analysis
of 4 US cohort studies (conducted 1971-2019) that included 982
dementia-free individuals (48.9% female; 29.4% Black).
The median age at incident stroke was 74.6 years. Cumulative mean
post-stroke systolic BP and LDL cholesterol levels were not associated
with any cognitive outcome. However, after accounting for cumulative
mean post-stroke systolic BP and LDL cholesterol levels, higher
cumulative mean post-stroke glucose level was associated with faster
decline in global cognition (-0.04 points/y faster per each 10 mg/dL
increase; P = .046) but not executive function or memory.
After restricting to 798 participants with apolipoprotein E4 (APOE4)
data and controlling for APOE4 and APOE4 × time, higher cumulative mean
post-stroke glucose level was associated with a faster decline in global
cognition in models without and with adjustment for cumulative mean
post-stroke systolic BP and LDL cholesterol levels (-0.05 points/y
faster per 10 mg/dL increase, P = .01; -0.07 points/y faster per 10 mg/dL increase, P = .002) but not executive function or memory declines.
Dr. Levine noted that the new study suggests the need for clinical
research to test whether tight glycaemic control in stroke survivors
reduces post-stroke cognitive decline and dementia in those with and
without diagnosed diabetes.
Tight glycaemic control has been shown in people with diabetes to
reduce small blood vessel complications in the eyes, kidney, and nerves,
and may have the potential to also decrease small blood vessel disease
in the brain, but this is unproven.
Yun Cai1,2†, Hongtao Zhang1†, Qiang Li2 and Peilan Zhang3*
1Clinical College of Neurology, Neurosurgery and Neurorehabilitation, Tianjin Medical University, Tianjin, China
2Department of Neurology, Affiliated Hospital of Hebei University, Baoding, China
3Department of Neurology, Tianjin Huanhu Hospital, Tianjin, China
Objective: To investigate the effects
of blood glucose variability on early therapeutic effects after
intravenous thrombolysis with alteplase and the levels of serum
inflammatory factors in patients with acute ischemic stroke (AIS).
Methods: We enrolled AIS patients who
received intravenous thrombolysis within 4.5 h of the onset of symptoms.
Clinical data, including the National Institutes of Health Stroke Scale
(NIHSS), glycosylated hemoglobin, mean blood glucose, standard
deviation of blood glucose, mean amplitude of glycemic excursion, mean
variation coefficient of blood glucose, interleukin-6 (IL-6), active
matrix metalloproteinase-9 (MMP-9), tumor necrosis factor α (TNF-α), and
hypersensitive C-reactive protein (hs-CRP) levels, were compared
between a group who showed improvement (the improvement group) and a
group who did not show improvement (the non-improvement group). Relevant
factors for early neurological improvement after thrombolysis with
alteplase were analyzed by using multivariate logistic regression
models. A Pearson linear correlation analysis was also performed on
blood glucose variation and inflammatory factor levels within the two
groups.
Results: A total of 146 patients were
included, 63 of which had early symptom improvement (43.15%). The
diabetes ratio, atrial fibrillation ratio, baseline NHISS score, random
blood glucose at admission, and glycosylated hemoglobin of patients in
the improvement group were significantly lower than those in the
non-improvement group (P < 0.05 in all cases). The mean blood
glucose, standard deviation of blood glucose, mean amplitude of glycemic
excursion, and mean blood glucose variation coefficients of patients in
the improvement group were significantly lower than those in the
non-improvement group (P < 0.05). Serum inflammatory factor
levels, including IL-6, MMP-9, TNF-α and hs-CRP, were significantly
lower in patients in the improvement group compared to patients in the
non-improvement group (P < 0.05). Multivariate logistic regression analysis showed that baseline NIHSS scores (OR = 1.28, 95% CI = 1.05–1.62, P = 0.02), glycosylated hemoglobin scores (OR = 2.57, 95% CI = 1.78–3.98, P = 0.0005), diabetes (OR = 13.10, 95% CI = 1.63~131.45, P = 0.021), the mean amplitude of glycemic excursion (OR = 2.98, 95% CI = 1.92–5.00, P < 0.0001), and the mean variation coefficient of blood glucose (OR = 1.40, 95% CI = 1.26–1.60, P
= 0.0078) were significantly correlated with early symptom improvement
after thrombolysis. Pearson linear correlation analysis showed that the
standard deviation of blood glucose, mean amplitude of glycemic
excursion, and the mean variation coefficient of blood glucose were
significantly positively correlated with IL-6, MMP-9, TNF-α and hs-CRP
levels (P < 0.01).
Conclusions: Blood glucose variability
is correlated with early neurological improvement after intravenous
thrombolysis with alteplase in AIS patients. With the increase of blood
glucose fluctuation range, the inflammatory response is enhanced, which
affects the prognosis of patients.
Stroke is the disease with the highest incidence,
disability, and mortality in China, with ischemic stroke accounting for
70% of disease burden. At present, the most effective treatment is
intravenous thrombolytic therapy with recombinant tissue plasminogen
activators (rt-PA) at early stages of the disease (<4.5 h) (1).
Early improvement in neurological function after thrombolytic therapy
is a marker of vascular recanalization and is independently predictive
of good prognoses at 3 months. However, the efficacy of intravenous
thrombolytic therapy is not always satisfactory. This may be due to many
factors. Blood glucose and blood glucose variability are important risk
factors for cardiovascular and cerebrovascular diseases, and blood
glucose variation can induce the occurrence or aggravation of
inflammatory responses. Recent studies have confirmed that blood glucose
variability is an important prognostic factor that can independently
predict death in critically ill patients. However, there is still no
consensus about the influence of blood glucose variability on the
effects of early thrombolytic therapy and inflammatory responses in AIS
patients. Here, we studied AIS patients that were treated with
intravenous thrombolytic therapy with alteplase. While strictly
controlling for blood glucose levels and reducing the incidence of
hypoglycemia, we evaluated the correlation between blood glucose
variation levels, the early treatment effects of intravenous
thrombolytic therapy with alteplase, and levels of serum inflammatory
factors. We hope to guide effective blood glucose-based interventions,
and to improve the therapeutic effects of intravenous thrombolysis in
patients experiencing AIS.
Researchers studying Australians with type 2 diabetes found those taking
the first-line treatment medication metformin had significantly slower
cognitive decline compared to those who did not. Learn more.
Metformin is the first-line treatment for most cases of type 2 diabetes
and one of the most commonly prescribed medications worldwide, with
millions of individuals using it to optimise their blood glucose levels.
A new research study, conducted over six years in the Sydney Memory and
Ageing Study in 1037 Australians (aged 70 to 90 years old at baseline),
has revealed an additional effect: individuals with type 2 diabetes who
used metformin experienced slower cognitive decline with lower dementia
rates than those who did not use the medication.
The findings provide new hope for a means of reducing the risk of
dementia in individuals with type 2 diabetes, and potentially those
without diabetes who number nearly 47 million people worldwide.
The study was led by researchers at the Garvan Institute of Medical
Research and the Centre for Healthy Brain Ageing (CHeBA), UNSW Sydney,
and published in the journal Diabetes Care.
"We've revealed the promising new potential for a safe and widely used
medication, which could be life-changing for patients at risk of
dementia and their families. For those with type 2 diabetes, metformin
may add something extra to standard glucose lowering in diabetes care: a
benefit for cognitive health," says first author Professor Katherine
Samaras, Leader of the Healthy Ageing Research Theme at the Garvan
Institute and endocrinologist at St Vincent's Hospital Sydney.
Protecting brain function
Type 2 diabetes occurs when the body can no longer produce enough
insulin to meet its needs, leaving affected individuals unable to
maintain blood glucose levels within a normal range. This can lead to
long-term health complications, including cognitive decline.
"As they age, people living with type 2 diabetes have a staggering 60%
risk of developing dementia, a devastating condition that impacts
thinking, behaviour, the ability to perform everyday tasks and the
ability to maintain independence. This has immense personal, family,
economic and societal impacts," says Professor Samaras.
The researchers of this study investigated data from participants of
CHeBA's Sydney Memory and Ageing Study. In this cohort, 123 study
participants had type 2 diabetes, and 67 received metformin to lower
blood sugar levels. The researchers tested cognitive function every two
years, using detailed assessments that measured cognition over a number
of capabilities, including memory, executive function, attention and
speed, and language.
The findings revealed individuals with type 2 diabetes taking metformin
had significantly slower cognitive decline and lower dementia risk
compared to those not taking metformin. Remarkably, in those with type 2
diabetes taking metformin, there was no difference in the rate of
decline in cognitive function over 6 years compared to those without
diabetes.
New use for a common medication
Metformin has been used safely to treat type 2 diabetes for 60 years. It
works by reducing the amount of glucose released from the liver into
the blood stream and allows the body's cells to better respond to blood
glucose levels.
Studies over the last decade have revealed evidence of metformin's
benefit in cancer, heart disease, polycystic ovary syndrome and weight
management. While the current study suggests metformin may have
cognitive benefits for people living with type 2 diabetes, the
researchers say it may also benefit those at risk of cognitive decline
more broadly.
"This study has provided promising initial evidence that metformin may
protect against cognitive decline. While type 2 diabetes is thought to
increase dementia risk by promoting degenerative pathways in the brain
and nerves, these pathways also occur in others at risk of dementia and
it is possible insulin resistance may be the mediator," says Professor
Samaras.
"To establish a definitive effect, we are now planning a large,
randomised controlled trial of metformin in individuals at risk of
dementia and assess their cognitive function over three years. This may
translate to us being able to repurpose this cheap medication with a
robust safety profile to assist in preventing against cognitive decline
in older people."
CHeBA's Sydney Memory and Ageing Study is an observational study of
older Australians that commenced in 2005 and researches the effects of
ageing on cognition over time.
Professor Perminder Sachdev, senior author of the study and Co-Director
of CHeBA, says: "While an observational study does not provide
conclusive 'proof' that metformin is protective against dementia, it
does encourage us to study this and other anti-diabetic treatments for
dementia prevention. Metformin has even been suggested to be
anti-ageing. The intriguing question is whether metformin is helpful in people in those with normal glucose metabolism. More work is clearly needed."
Article continued below...
MORE INFO:
The study was supported by Australia's National Health and Medical Research Council (Grant number 510124).
Katherine Samaras, Steve Makkar, John D. Crawford, Nicole A.
Kochan, Wei Wen, Brian Draper, Julian N. Trollor, Henry Brodaty,
Perminder S. Sachdev. Metformin Use Is Associated With Slowed
Cognitive Decline and Reduced Incident Dementia in Older Adults With
Type 2 Diabetes: The Sydney Memory and Ageing Study. Diabetes Care, 2020; dc200892 DOI: 10.2337/dc20-0892
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