Doing This May Lower Blood Pressure More Than a Workout

 Along with this your competent? doctor told you about all the benefits of heat shock proteins, right?

• heat shock proteins (12 posts to April 2013)

NO? So, fucking incompetence exists in your doctor and hospital? And the board of directors is so incompetent they can't recognize incompetence in their own hospital! Time to reconstitute the hospital! 

Doing This May Lower Blood Pressure More Than a Workout

According to a study published in the European Journal of Applied Physiology, a nice, relaxing hot bath is genuinely relaxing enough that it might lower your blood pressure more than an intensive 30-minute workout.

Researchers at the University of Western Australia gathered 25 overweight or obese adults aged 45 to 70 and subjected them to two distinct tests, spaced at least three days apart. In one session, participants spent 30 minutes chest-deep in a tub of 104°F water. In the other, they spent 30 minutes pedaling on a stationary bike at a moderate pace.

When scientists scanned the tiny blood vessels beneath the participants’ skin using optical coherence tomography, the tub beat the bike across the board. Turning a bathtub into a you-flavored soup caused bigger increases in blood vessel diameter and blood flow speed, along with more overall microvascular density than pedaling a bike.

That 30-minute soak even produced slightly larger drops in both systolic and diastolic blood pressure, which you might otherwise know as the numerical values after getting your blood pressure checked.

Your Evening Bath Could Have a Benefit Beyond Relaxation

The idea here is that when your core body temperature goes up when you’re soaking in a hot tub, your circulatory system enters a kind of overdrive state in an attempt to dissipate heat, thereby dilating blood vessels through a process called vasodilation, surging blood through your skin. When you’re on a bike, your heart rate spikes due to muscle contraction, but your blood vessels are experiencing the same kind of extreme thermal strain.

None of this means that you should replace your cycling routine with a tub soak, since the benefits of a hot bath versus cycling begin and end at lowering blood pressure. When you’re exercising, you’re building muscle and burning calories, all while strengthening your heart, all stuff that a bath will never be able to replicate.

If you’re young, pedal away and then soak in a hot bath for 30 minutes afterward if you really want to get your blood pressure down. Older adults and anyone dealing with mobility issues can turn to a steaming hot bath to reap the apparently legitimate low-effort blood pressure benefits.

Neuroplasticity Biomarkers and Neurotransmitter Modulation in Post-Ischemic Stroke Rehabilitation: A Narrative Review

 You know nothing about how to make neuroplasticity repeatable on demand, so a useless word salad!

When your incompetent? doctor/researcher uses this word ask them to EXPLAIN EXACTLY what needs to happen for a neuron to drop a current task and take on a neighbors! 

NO explanation; PURE FUCKING INCOMPETENCE! Not knowing that makes neuroplasticity non repeatable on demand!

Neuroplasticity Biomarkers and Neurotransmitter Modulation in Post-Ischemic Stroke Rehabilitation: A Narrative Review

-Ischemic Stroke Rehabilitation: A Narrative Review

,

,

and

1

Department of Neurology, Dr. K. Jonscher Muncipal Medical Centre in Lodz, Milionowa 14, 93-113 Łódź, Poland

2

Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Łódź, Poland

3

Department of Neurological Rehabilitation, Medical University of Lodz, Milionowa 14, 93-113 Łódź, Poland

*

Authors to whom correspondence should be addressed.

J. Clin. Med.2026, 15(20), 8091;https://doi.org/10.3390/jcm15208091

This article belongs to the Special Issue Cerebrovascular Disease: Symptoms, Diagnosis and Current Treatment—Second Edition

Version Notes

Order Reprints

Abstract

Background/Objectives: 

Recovery after stroke is a complex process involving structural and functional reorganization of the nervous system. Neuroplasticity plays a key role in functional recovery, while biomarkers and neurotransmitter systems may reflect or modulate the biological processes underlying rehabilitation and adaptation after stroke. The aim of this review was to summarize the current evidence regarding biomarkers of neuroplasticity and neurotransmitter modulation in post-stroke rehabilitation, with a particular focus on their potential importance for functional recovery and rehabilitation outcomes. 

Methods: 

This narrative review synthesized evidence identified through searches of PubMed/MEDLINE, Scopus, and Web of Science, supplemented by reference-list screening. The literature was qualitatively analyzed according to the main themes of the review. 

Results: 

Current data point to BDNF, VEGF, and MMPs as promising biomarkers associated with post-stroke neuroplasticity and functional recovery. Neurotransmitter modulation, particularly involving GABA, glutamate, dopamine, and serotonin, may influence neuronal excitability, synaptic plasticity, and motor learning after stroke. The combination of biomarker assessment and rehabilitation-based modulation of these pathways may provide a more comprehensive approach to understanding and monitoring post-stroke recovery. 

Conclusions: 

Current evidence supports the role of neuroplasticity-related biomarkers and neurotransmitter modulation as potential tools for understanding biological responses to post-stroke rehabilitation. However, their clinical relevance and usefulness in guiding individualized rehabilitation require further validation in future clinical studies.

Application of artificial intelligence in the prediction and management of stroke rehabilitation

 Putting three useless items for stroke in one research paper has got to be the PINACLE OF STUPIDITY!

• Artificial intelligence doesn't do any good until the underlying exact protocols for recovery exist!
• Predictions DO NOTHING FOR DELIVERING RECOVERY!
• Management does nothing useful!

Application of artificial intelligence in the prediction and management of stroke rehabilitation

Stroke is a major cause of long-term disability, and recovery varies substantially across motor, cognitive, communication, and activities-of-daily-living domains, making continuous assessment and individualized rehabilitation essential. However, current rehabilitation decisions still rely heavily on periodic clinical scales, clinician experience, and local resources, which may not fully capture differences in lesion characteristics, baseline function, comorbidities, and recovery trajectories. Access is also limited by geographic barriers, uneven service capacity, and intermittent follow-up. Artificial intelligence is increasingly being explored for stroke imaging, early prognosis, rehabilitation-outcome prediction, movement and physiological assessment, robot- and virtual-reality-assisted training, brain–computer interfaces, wearable monitoring, and telerehabilitation, offering new opportunities for more adaptive and continuous care. “Yet acute diagnosis, early prognostication, and rehabilitation-specific outcomes are often discussed together despite addressing different clinical questions, and many rehabilitation applications remain supported mainly by small datasets, internal validation, or early feasibility studies. Technical performance therefore should not be equated with rehabilitation benefit.” said the author Weihua Song, a researcher at Capital Medical University, “This creates a need for a structured review that maps AI applications to their clinical decision points, rehabilitation relevance, validation maturity, and readiness for clinical translation.”

This study used a structured narrative review design, systematically searching PubMed/MEDLINE, IEEE Xplore, Web of Science, and Scopus for studies on artificial intelligence and stroke rehabilitation published from January 2010 to March 2025, with a PRISMA-style process used to improve transparency. The database searches identified 1,247 records, and after deduplication, title and abstract screening, and full-text assessment, 108 publications were included in the thematic synthesis. The reviewers extracted information on study design, AI technique, sample size, rehabilitation domain, outcomes, model performance, validation methods, and reported limitations. Evidence was organized into four major themes: AI for rehabilitation-outcome prediction, rehabilitation assessment and monitoring, therapeutic intervention and management, and integration of AI with robotics, virtual reality, brain–computer interfaces, wearable technologies, and telerehabilitation. Importantly, the review distinguishes acute diagnostic or prognostic evidence from rehabilitation-specific outcomes and evaluates each application according to validation quality, clinical relevance, and implementation barriers

One of the major applications of artificial intelligence in stroke rehabilitation is the prediction of subsequent functional recovery using clinical scales, imaging, EEG, wearable-sensor data, and demographic information. Existing studies have explored prediction of 90-day functional status, changes in Barthel Index, motor-function scores, language and cognitive recovery, quality-of-life improvement, and long-term mortality, using machine learning, deep learning, and explainable models to identify factors associated with recovery trajectories. Acute imaging and early prognostic models can provide baseline information on lesion burden, initial severity, and treatment response that may inform later rehabilitation planning, whereas rehabilitation-specific prediction focuses more directly on changes in motor function, activities of daily living, participation, and patient-reported outcomes over time. However, most studies remain retrospective, small, or single-center and rely mainly on internal validation, while independent multicenter external validation and prospective clinical-impact studies are still uncommon. Therefore, strong predictive accuracy indicates potential for risk stratification, but does not by itself demonstrate that AI-guided treatment improves rehabilitation outcomes.

Artificial intelligence is increasingly being used to automate the assessment and continuous monitoring of motor function, posture, gait, and rehabilitation progress after stroke, complementing conventional clinical scales and periodic follow-up. Existing systems combine EEG, EMG, wearable sensors, motion tracking, and home-monitoring data to quantify movement patterns, exercise quality, and functional changes, while machine learning can identify abnormal movements or estimate clinical motor scores. Wearable and remote-monitoring technologies can further extend assessment into the home, providing longitudinal information on rehabilitation adherence and progression. However, many studies still focus primarily on technical feasibility, classification accuracy, or short-term surrogate outcomes, and commonly involve small samples, single-center datasets, and limited independent external validation. Heterogeneity in devices, data formats, and assessment schedules also restricts generalizability. Future work should therefore establish more standardized outcome measures and data pipelines and use multicenter, long-term, prospective studies to determine whether AI-based monitoring can meaningfully improve rehabilitation decisions and patient outcomes.

Beyond prediction and monitoring, artificial intelligence is increasingly being explored to support rehabilitation adjustment and the coordinated use of assistive technologies after stroke. Current approaches aim to adapt training intensity, task difficulty, and feedback frequency according to motor performance, cognitive status, and sensor-derived information, while integrating AI with rehabilitation robots, virtual reality, brain–computer interfaces, wearable devices, and telerehabilitation platforms. Robotic systems can provide standardized assisted movement, virtual reality emphasizes interactive task practice and augmented feedback, and BCIs can use neural signals to control external feedback or assistance when voluntary movement is severely limited. However, these technologies currently function mainly as rehabilitation adjuncts, with much of the evidence coming from small samples, short follow-up, and exploratory or single-arm studies; convincing evidence of superiority over conventional rehabilitation remains limited. A key future direction is the development of patient-centered closed-loop systems in which EEG, EMG, and wearable-sensor signals dynamically adjust robotic assistance, extended-reality tasks, and remote feedback while maintaining clinical supervision, interoperability, affordability, and compatibility with routine rehabilitation workflows.

Despite the growing potential of artificial intelligence for stroke rehabilitation prediction, assessment, and assisted intervention, clinical translation remains constrained by challenges in data, modeling, and implementation. Rehabilitation datasets are often small, heterogeneous, and inconsistently sampled, while multimodal clinical and sensor data remain difficult to standardize, increasing the risk of overfitting and limiting cross-institutional generalizability. In addition, the “black-box” nature of complex models can reduce clinical interpretability and trust, and improved predictive accuracy alone does not guarantee better treatment decisions or patient outcomes. Wearable monitoring, home rehabilitation, and remote-care platforms also raise concerns regarding privacy, security, data sharing, and device reliability. Future research should emphasize multicenter external validation and prospective clinical trials while developing genuinely closed-loop rehabilitation systems that combine clinical information, imaging, EEG, EMG, and wearable-sensor data to dynamically adjust robotic assistance, extended-reality training, and remote feedback. “Greater attention to explainability, interoperability, cost-effectiveness, and fairness will also be essential, with AI positioned as an adjunct to multidisciplinary care rather than a replacement for clinicians.” said Weihua Song.

Authors of the paper include Weihua Song, Shuai Si, Yinghui Wang, Hong Chang, and Xiaoying Tang.

This work was supported by the National Science and Technology Major Project (2023ZD0503800 and 2023ZD0503803), the Capital’s Funds for Health Improvement and Research (2024-1-2011), the Key R&D Program of China (2023YFC3605200 and 2023YFC3605201), the Project for Innovation and Development of Beijing Municipal Geriatric Medical Research Center (No. 11000025T000003320658), the Beijing “Young Seedling Program” for High-Level Innovative and Entrepreneurial Leading Talents (No. 2-1-008-0260), and the 2023 Special Nursing Project of Xuanwu Hospital, Capital Medical University (HLZD2023002).

The paper, “Application of Artificial Intelligence in the Prediction and Management of Stroke Rehabilitation” was published in the journal Cyborg and Bionic Systems on Oct 8, 2026, at https://doi.org/10.34133/cbsystems.0702.

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Journal

Cyborg and Bionic Systems

This Common Eating Habit Was Linked To 30% Lower Odds Of Frailty by mindbodygreen

 Will your competent? doctor GUARANTEE  this gets into your diet protocols(both hospital and home)?

This Common Eating Habit Was Linked To 30% Lower Odds Of Frailty

Scientists uncover a sleep-brain connection that could be the key to halting cognitive decline

 Your incompetent? doctor missed this well over a decade ago, right? Why don't you get them fired? There are no excuses for such massive incompetence!

Hormone Shots Aid Cognition in Older Adults August 2012

Scientists uncover a sleep-brain connection that could be the key to halting cognitive decline

The study monitored and recorded the brain activity of mice through electrode brain implants. Researchers stimulated neurons located in the hypothalamus, including the growth-hormone-releasing hormone (GHRH) neurons and two types of somatostatin neurons responsible for the regulation of the growth hormone release during the sleep-wake cycle. 

Once those hormones are released, they increase activity in the brainstem region that affects attention, arousal, and cognition. This region, called the locus coeruleus, has also been associated with several neurological and psychiatric issues, such as PTSD and depression. 

In this study, researchers found that GHRH stimulates growth hormone release while somatostatin suppresses it, essentially functioning like an accelerator and brake system in the brain. They also discovered that these peptides behave differently in REM and non-REM sleep states. During a non-REM state, somatostatin levels dropped while GHRH activity rose, promoting growth hormone release. “This suggests that sleep and growth hormone form a tightly balanced system: Too little sleep reduces growth hormone release, and too much growth hormone can in turn push the brain toward wakefulness,” said Daniel Silverman, a postdoctoral fellow at UC Berkeley and a co-author of the study.

Eventually, this finding could help researchers better understand and potentially develop treatments for various conditions, including sleep disorders, degenerative diseases like Parkinson’s and Alzheimer’s, and even metabolic conditions like diabetes.

“Sleep drives growth hormone release, and growth hormone feeds back to regulate wakefulness, and this balance is essential for growth, repair, and metabolic health,” Silverman said. 

This post originally appeared at inc.com.

Who is more prone to Alzheimer’s? Scientists might have found a clue

 

With your risk of dementia post stroke, what will your competent? doctor do with this to prevent those problems? 

Parkinson’s Disease May Have Link to Stroke March 2017 

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

Oh, sorry; NOTHING AT ALL! In my opinion your doctor is completely incompetent in not using research to get you recovered!

Who is more prone to Alzheimer’s? Scientists might have found a clue

A slight difference in DNA could shape some peoples’ susceptibility to developing Alzheimer’s disease, researchers have found.

Experts based at various institutions in Hong Kong found that Chinese participants with longer repeats of a specific gene sequence in their DNA were more likely to have the disease. The association was also noted among European participants, although it was much weaker.

The study was published in the journal Nature Neuroscience on October 12.

Researchers have previously identified several genetic variants that are believed to be associated with Alzheimer’s risk, and it is understood that those who have a parent or sibling diagnosed with the disease are more likely to develop it than people without those links—although this doesn’t mean that person will develop Alzheimer’s, it only increases the odds.

That said, Alzheimer’s does not have a single genetic cause, and is believed instead to be influenced by a combination of genetic, lifestyle and environmental factors.

What the experts set out to understand in this study was whether repeats of certain genetic sequences—rather than specific genetic variants—could influence risk.

Rudolph Tanzi, a professor of neurology at Harvard University, told Newsweek that the “potentially important” study “goes beyond the normal single-base genome variants that are tested in the many genome-wide association studies of Alzheimer’s disease.”

 Related video: New study identifies possible early sign of dementia (Welltica+)

“We know that the common DNA variants that show association with Alzheimer’s in genome-wide association studies account for less than 50 percent of the heritability of Alzheimer’s disease. So finding these types of DNA repeat variants in the genome is very important,” he said.

Dr. Michael Guo, an assistant professor of neurology and genetics, and a clinician in the University of Pennsylvania Memory Center, told Newsweek: “This is an exciting study that highlights the importance of studying diverse populations and expanding our analyses to include broader sets of spelling errors in our DNA.”

“Their work may help improve our ability to predict Alzheimer’s disease risk,” he added. “Ultimately, by identifying a new gene linked to Alzheimer’s disease, this could spur further work into how FAM193B causes disease and whether it may serve as a drug target.”

A Chinese cohort of over 3,000 people were included in the study—around half of whom had Alzheimer’s disease—as well as genetic data and records obtained from UK Biobank (around 2,600 with Alzheimer’s and almost 23,000 controls) to see whether the findings were the same among different ancestries.

From 11 of the Chinese participants, the researchers built a more detailed reference of different structural DNA sets and then analyzed the collections of the other DNA readings.

They noticed that the CCG DNA string could have repeats from between four to 30 among the participants, and found that those with at least 18 repeats had twice the odds of having Alzheimer’s disease than those with no more than 11 repeats. This indicates that repeated strands of the sequence could increase likelihood of having the disease, not a person’s lifetime risk of developing the disease.

The finding was also weaker—though still identified—among the European participants’ records from UK Biobank, meaning that the estimate among the Chinese cohort cannot be translated directly across different ancestral groups.

“This isn’t unexpected, many genetic variants including APOE have different effect sizes in populations of different ancestries,” Michael Lutz, a professor of neurology and pathology at Duke University, told Newsweek. APOE is the gene that has been associated with Alzheimer’s, and its variant APOE4 is the strongest known genetic risk factor for the disease.

What’s Behind The Association?

Reasons for this association could be down to FAM193B expression. The experts found that more repeats of the CCG sequence resulted in higher FAM193B expression, and that increased activity was separately found to result in nerve cell DNA damage and cellular harm.

The researchers also noted that FAM193B protein “directly interacts” with the enzymes GSK3alpha and GSK3beta, which is notable as they said when these enzymes dysregulate it can result in increased beta-amyloid and tau—the two proteins associated with Alzheimer’s disease.

“Analyses of postmortem human brains and cultured neuronal cells showed that elevated neuronal FAM193B expression is associated with DNA damage and cell death-related pathways which are key pathways involved in Alzheimer’s disease pathophysiology,” Lutz said.

“These findings establish the common FAM193B-CCG repeat as an Alzheimer’s disease risk genetic factor and highlight the contribution of common structural variants to Alzheimer’s disease heritability,” he added.

The experts emphasized that this does not mean that longer repeats of CCG damage neurons for certain or explain the association entirely.

What This Means For Alzheimer’s

Lutz said that it is “early to consider the impact of the findings on Alzheimer’s disease prevention and treatment,” but that the “most immediate application of the finding would be for Alzheimer’s disease risk prediction.” This is because the paper provides “support that including the structural variant, with the caveat of ancestral-specific risk, will improve lifetime disease risk prediction in clinical settings.”

He added that “as is pointed out in the paper, the biological function of the FAM193B gene is unclear, so further research would be needed to understand the biochemical and physiological impact of the repeat.”

Tanzi also said that the CCG variant association was found in a “relatively small Chinese population and will need to be replicated in larger populations.”

He added that the gene implicated here is “very interesting as one can imagine how it might affect tau tangle pathology downstream of amyloid deposition (by affecting the enzyme GSK3beta).”

“Functional studies along these lines are now warranted as well as replication of the genetic association with Alzheimer’s disease in larger populations,” he said.

Reference

Cao, H., Fu, Y., Zhou, X. et al. (2026) Genome-wide analysis of common structural variants in Alzheimer’s disease identifies a risk-associated regulatory CCG repeat in FAM193B. Nature Neuroscience. https://doi.org/10.1038/s41593-026-02481-z

Contact Newsweek editors on this story: Kara Dolman and Tony Phillips.

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Psilocybin Tied to Lower Inflammation in Parkinson's Trial

 Is your competent? doctor ready with this to try to prevent Parkinsons after your stroke? Sorry, your doctor doesn't even know of your Parkinson's risk! 

Parkinson’s Disease May Have Link to Stroke March 2017 

Haven't you gotten that INCOMPETENT DOCTOR FIRED YET?

Isn't your doctor already prescribing psilocybin for stroke recovery? Oh NO, you DON'T have a functioning stroke doctor, do you? 

psilocybin (59 posts to May 2014) 

Psilocybin Tied to Lower Inflammation in Parkinson's Trial

Key Takeaways

• Psilocybin therapy was associated with reduced inflammation in a small trial of Parkinson's patients with mood dysfunction.
• An inflammatory index remained lower through 30 days, but mitochondrial stress marker reductions were transient.
• Findings require confirmation in larger randomized controlled trials.

Markers of systemic inflammation and mitochondrial stress were reduced after psilocybin therapy in Parkinson's disease patients with mood dysfunction, a small nonrandomized trial showed.

Relative to baseline, an inflammatory index was significantly lower at all follow-up time points after psilocybin was administered, reported Ellen Bradley, MD, of the University of California San Francisco (UCSF), and co-authors.

The standard mean difference (SMD) was -0.72 (adjusted P=0.003) 1 day after 10 mg of psilocybin, Bradley and colleagues wrote in a JAMA Psychiatry research letter.

One day after 25 mg of psilocybin, the SMD was -0.60 (adjusted P=0.02), and 30 days after 25 mg, the SMD was -0.62 (adjusted P=.047).

The results support the researchers' parent trial, which showed an association between psilocybin therapy and reduced depression, anxiety, and motor symptoms in Parkinson's patients.

"To our knowledge, this is the first report of changes in these types of markers after psychedelic treatment in people with a neurodegenerative disease," Bradley told MedPage Today. "That gives us and other researchers super-interesting biological questions to pursue: What could be producing these changes, are they consistent in larger groups of people, and do they have anything to do with clinical benefits people with Parkinson's might experience with psilocybin?"

This research comes as part of a series of studies examining the biological effects of psychedelics as potential therapeutics for non-psychiatric conditions, said Albert Garcia-Romeu, PhD, of the Johns Hopkins University School of Medicine in Baltimore, who wasn't involved with the study. It also comes on the heels of work showing that psilocybin appeared to block nerve damage related to chemotherapy in mice, he pointed out.

Much of the work looking at psilocybin or LSD has focused squarely on mental health conditions like depression, anxiety, or addiction, Garcia-Romeu noted. "However, this study is in patients with a neurological condition -- Parkinson's disease -- and shows evidence that psilocybin may have impacted biological markers of inflammation and mitochondrial stress," he told MedPage Today.

"These new data suggest biological effects of psychedelics could be driving potential benefits in patients and pave the way for more work to better understand how psilocybin might be a useful therapeutic both in psychiatric and non-psychiatric conditions," he added.

In their open-label trial, Bradley and colleagues studied 12 people with mild-to-moderate Parkinson's disease ages 40 to 75. Participants received 10-mg and 25-mg doses of oral synthetic psilocybin approximately 2 weeks apart.

The researchers collected plasma samples from nine participants at four time points: baseline, 1 day after each psilocybin administration, and 30 days after the 25-mg dose.

The primary outcome to assess systemic inflammation was a proinflammatory index calculated as the mean z score of interleukin (IL)-6, IL-8, tumor necrosis factor alpha, interferon gamma, and high-sensitivity C-reactive protein concentrations. Mitochondrial stress was evaluated with growth differentiation factor 15 (GDF-15) and fibroblast growth factor 21 (FGF-21) measurements.

Components of the index, including IL-6, were significantly lower 1 day after the 10-mg dose but at no other time points. IL-10 was significantly higher 1 day after the 10-mg dose but not at other times.

GDF-15 was significantly lower relative to baseline 1 day after each psilocybin administration, but not from baseline 30 days after the 25-mg dose. FGF-21 was higher 1 day after each psilocybin administration, but this finding was not significant.

This was a small study of psilocybin therapy and results must be interpreted cautiously, noted co-author Aoife O'Donovan, PhD, also of UCSF. "However, the results are highly promising and suggest that more research in this area is warranted," she told MedPage Today. "We are already following this study up with more in-depth analyses of the effects of psilocybin therapy on inflammation and mitochondrial stress in a randomized controlled trial in patients with Parkinson's disease."

Work from Garcia-Romeu's lab also is studying psilocybin in a trial of people with mild cognitive impairment or early-stage Alzheimer's disease and depression. "To date, we've treated 18 individuals in that study, and enrolled 19 of a targeted 20 patients," he said. "We plan to complete the trial and publish our findings next year."

AHA issues framework to work toward better blood pressure control

 What is your competent? doctors' EXACT BLOOD PRESSURE MANAGEMENT  post stroke?

Doesn't have one I bet; so, COMPETELY FUCKING INCOMPETENT!

Not having one allows many more neurons to die! Charge your doctor $1000 for each dead neuron! That might get your doctor to solving stroke!

A framework is NOT A PROTOCOL So, the AHA  is pushing incompetence!

AHA issues framework to work toward better blood pressure control

Key takeaways:

• The American Heart Association issued a framework of necessary investments to improving BP control in the U.S.
• Investments included research, policy, education, clinical care and community.

The American Heart Association issued a science advisory statement outlining a framework for the investment of resources and funding to address the high prevalence of uncontrolled blood pressure in the U.S.

Investment in research and policy, education, clinical care and community and workplace were identified as the primary domains by which long-term change in the prevalence of uncontrolled BP can be affected, according to the scientific advisory published in Hypertension.

Approximately 122.4 million U.S. adults are estimated to have hypertension with only approximately 20.7% reaching BP control, according to the advisory.

“We have effective treatments and strong guidelines, so the gap is about delivering care consistently and reaching the people most affected. The American Heart Association already does a great deal of work in this space, through Target: BP — part of the National Hypertension Control Initiative — public awareness campaigns, policy advocacy and community partnerships. We wanted to show how these efforts fit together and how they are expected to lead to measurable improvements in BP control while giving other organizations a framework they can adapt,” Yvonne Commodore-Mensah, PhD, MHS, RN, FAHA, professor and associate dean for research at Johns Hopkins School of Nursing and Johns Hopkins Bloomberg School of Public Health, department of epidemiology (joint appointment), told Healio. “No single intervention will close the BP control gap. Clinical quality improvement is essential, but so are the conditions people live in, including access to care, medication costs, food insecurity and transportation. I hope health systems see that their work is strongest when connected to community partners, and that policymakers recognize how much policy matters. Medicaid coverage for home BP monitors and reimbursement for patient training, for example, still varies widely by state. Disparities in BP control are largely driven by modifiable factors, which means they can be addressed.”

AHA BP Control Logic Model

The logic model is designed to outline what investment must be done, what each input in to each component produces and how those activities support short-, medium- and long-term changes in population-level BP control.

For the first step of the model, the authors identified the current BP situation in the U.S. — nearly half of adults have high BP and less than one-quarter have controlled BP — and items to prioritize: equitable health, culturally and linguistically appropriate interventions, multisector collaboration and community.

Next, the authors identified resources and capabilities, including staff and volunteers, research networks, scientific evidence and more, as well as funding sources that included philanthropies and corporate sponsors.

“Starting points will vary by setting, but the closest thing to a universal first step is knowing your own data,” Commodore-Mensah told Healio. “Look at your current BP control rate and break it down by race, ethnicity, age, insurance and geography to see where the gaps are. That baseline tells you where to focus. Then map what you are already doing onto the model’s four strategy areas: research and policy, education, clinical care, and community and workplace. Most organizations will find they are strong in one or two areas and thin in others, which shows where new investments or partnerships would add the most value.”

Investment of resources for long-term successes

The authors identified four domains that may benefit from these inputs — research and policy, education, clinical care and community and workplace — and explained how their outputs could impact long-term outcomes in BP control.

“Organizations should define specific, measurable indicators for each outcome. ‘Improved BP control’ might mean the percentage of patients below 130/80 mm Hg, with a target such as 70% or higher and a timeline based on your starting point,” Commodore-Mensah told Healio. “The model also lets institutions track earlier progress, such as clinicians trained, adoption of treatment protocols, social needs screening, and use of home BP monitoring. This kind of measurement works: Health centers in the National Hypertension Control Initiative improved BP control by 9.8 percentage points from 2020 to 2023, compared with 6.9 points at other health centers. Institutions should also track results across population groups, since overall gains can mask persistent gaps.”

Investment of resources, capabilities and funding into BP research and policy could produce scientific publications, professional guidelines, policy recommendations and advocacy materials. In the long term, these outputs may institutionalize evidence-based policies, establish a supportive regulatory environment and create sustainable funding and change health system infrastructure, according to the advisory.

The authors added that investment in education could produce culturally and linguistically appropriate educational materials, public education campaigns and patient resources, which may lead to long-term changes such as sustained behavioral changes.

Investment in the domain of clinical care could lead to the creation of professional training programs, clinical toolkits, best-practice protocols, evidence-based guidelines, quality improvement initiatives and achievement awards. In the long term, these outcomes could result in increased hypertension control, reduced disparities and reduced CV events and CV mortality, according to the advisory.

The authors wrote that investment in community and workplace may produce community partnership programs and technical assistance resources that, together with investment in clinical care, may improve social needs screening and connect community with clinical care.

“BP control is a shared responsibility. Clinicians, including nurses, pharmacists and community health workers, can deliver team-based care. Public health professionals can lead population-level strategies, community organizations can build trust and connect people to care, employers can support wellness and funders can sustain what works,” Commodore-Mensah told Healio. “Prevention also needs to start early, beginning with maternal health and continuing through childhood. Finally, we still need to learn which strategies work best, for whom, and in what settings. I hope this model encourages organizations to measure, share what they learn, and build that evidence together.”

For more information:

Yvonne Commodore-Mensah, PhD, MHS, RN, FAHA, can be reached at ycommod1@jhu.edu and on X at @ycommodore.

Cardiometabolic risk factors in midlife impact risk for dementia in late life

 Between 40-50 my BMI was great. My midlife exercise capability(50-69) was almost reduced to nothing because my incompetent? doctor had nothing to get me 100% recovered.

3 years post stroke at a physical I had a resting heart rate of 54 at age 53, level of an athlete. My doctor asked what exercises I was doing, 'I've done no exercises for the past 3 years'. So now after 20 years of little exercise I'm no longer that athlete.

Cardiometabolic risk factors in midlife impact risk for dementia in late life

Key takeaways:

• Controlling cardiometabolic risk factors can help prevent dementia and Alzheimer’s disease.
• Implementing lifestyle modifications can delay the onset of cognitive decline.

BOSTON — Vascular pathology and changes in midlife play a major role in brain health later in life, suggesting that reducing cardiometabolic risk factors may lower risk for dementia and Alzheimer’s disease, according to a speaker.

“We now know with advances in neuroimaging that most people diagnosed with Alzheimer’s disease also have vascular injury and vice versa,” Rachel Whitmer, PhD, professor of public health sciences and neurology at the University of California, Davis, said during a presentation at the Cardiometabolic Health Congress. “So, this is a multifactorial process with multiple pathways leading to it, which can get complicated when you’re thinking about how to reduce risk and precision medicine, but it also opens up the idea that there are multiple ways to actually lower risk. So, we do a lot of work looking at risk factors over the life course.”

Data derived from Whitmer R. Keynote: 25 years of dementia prevention: From risk factor discovery to prevention trials. Presented at: Cardiometabolic Health Congress; Oct. 14-17, 2026; Boston.  

High BMI between age 40 and 50 years is associated with elevated risk for Alzheimer’s disease late in life, as is smoking in midlife, Whitmer said.

Cardiometabolic risk factors and dementia odds

“There is a midlife dementia risk score that was published in 2006 out of Finland, which shows a combination of mostly modifiable cardiovascular risk factors in middle age are strongly associated with future risk for dementia,” Whitmer said. “We replicated this in Kaiser Permanente in a diverse group of people, and it predicted quite well across different racial and ethnic groups. If you’re looking at midlife, increasing odds of dementia go up the more risk factors that you have, and both of these studies look at high cholesterol, hypertension, diabetes or prediabetes and obesity in midlife.”

The relationship extends throughout the life course, as one study showed that people with CV risk factors early in life had worse cognitive performance later in life, even if they did not have dementia, Whitmer said.

A Lancet commission on dementia prevention, intervention and care identified 14 modifiable risk factors that could greatly reduced risk for dementia and Alzheimer’s if controlled: diabetes, high BP in midlife, obesity in midlife, high LDL cholesterol, physical inactivity, depression, smoking, low education, hearing loss, vision loss, traumatic brain injury, high alcohol consumption, social isolation and air pollution, Whitmer said.

“We know that dementia is a multifactorial process,” Whitmer said. “The thinking was, what can we do when we target several things at once, which of course is challenging to do.”
the U.S. POINTER study of 2,111 older adults to determine whether lifestyle interventions could improve brain health and prevent dementia. Participants were aged 60 to 75 years, had suboptimal diet, did not exercise regularly and had risk for cognitive decline but did not have dementia at baseline.

Participants were assigned to a self-guided intervention in which they met with a study navigator three times per year to receive lifestyle education and support and tools to implement it or to a structured intervention in which they conducted physical activity at a community facility while wearing a Fitbit, received encouragement to follow the MIND diet, underwent home-based computer cognitive training and regular participation in engaging activities and met with a medical advisor once every 6 months.

Both groups improved in cognitive function at 2 years, but the structured intervention group improved to a greater degree, Whitmer said.

‘Wonderful to see’

“And this was the part that was so wonderful to see: It was the same effect whether you were male vs. female,” Whitmer said. “It was the same effect no matter what age group you were in. It was the same effect whether or not you had the APOE4 genotype. And it was the same effect given your heart health. The magnitude of the effect of the study was the same or larger than a lot of the drug trials that are looking at change in cognitive function with medications for Alzheimer’s disease. So in thinking about that change over 24 months, we think about what could that be in a longer lifetime if someone incorporates some of these lifestyle changes.

“I get asked the question, what can you do? You can’t change your family history. You can’t change your genetics,” Whitmer said. “But I want to remind people that you can do things to at least delay the onset. And that’s very powerful as a clinical tool, speaking from a personal level, a health level, and then also on a population level for our community and our world and our country. So if you can delay, it would give huge benefits just in terms of valuing the economics, but also in what you are specifically experiencing.”