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.

Thursday, October 31, 2024

Post-stroke osteoporosis: Mechanisms, treatments, and recent advances

 We've known of this problem for over a decade, why haven't you figured out how to prevent it?
  • Osteoporosis (3 posts to November 2013)
  • Laziness? Incompetence? Or just don't care? NO leadership? NO strategy? Not my job? Not my Problem?

    Post-stroke osteoporosis: Mechanisms, treatments, and recent advances

    Liu, Zezhong MMa; Liu, Xiaoguang MMa; Wang, Congcong MMa; Sun, Quanxiang MMb; Zhang, Lan MMb; Wang, Jun PhDc

    Author Information
    Journal of Aging and Rehabilitation 1(3):p 59-67, September 2024. | DOI: 10.1097/jagr.0000000000000015
    • Open

    Abstract

    Post-stroke osteoporosis (PSO) is a common complication encountered in patients after stroke, characterized by a rapid decline in bone mass and disruption of bone microarchitecture, which significantly elevates the risk of fracture. The pathogenesis of PSO is multifaceted, encompassing factors, such as oxidative stress, inflammatory responses, neurological damage, extended immobilization, and hormonal imbalances, culminating in a dysregulation of bone metabolism. Treatment strategies encompass pharmacological interventions, nutritional supplementation, physical exercise, and rehabilitative training. Emerging therapies, such as stem cell therapy and exosome therapy, are being explored for their potential to promote cellular regeneration and modulate inflammatory responses in the treatment of PSO. Future therapeutic approaches should integrate a comprehensive understanding of the multifactorial pathogenesis of PSO to develop tailored treatment plans, aiming to optimize treatment efficacy and improve patients’ quality of life.

    Introduction

    The current state of stroke

    Stroke, as one of the leading causes of death and disability worldwide, poses a significant challenge to public health that cannot be overlooked. In China, it is particularly prominent, ranking first in terms of disease burden.1 Stroke is primarily categorized into hemorrhagic and ischemic types, with ischemic stroke being the focus of research and treatment due to its higher incidence rate, accounting for ∼85% of cases.2 The occurrence of ischemic stroke is a complex process involving various factors and mechanisms, including inflammatory responses, apoptosis, changes in extracellular ion concentrations, and alterations in the permeability of the blood-brain barrier.

    Currently, the main methods for treating ischemic stroke include thrombolytic therapy and endovascular thrombectomy. Thrombolytic therapy, which utilizes recombinant tissue plasminogen activator, is considered one of the most effective treatment modalities available.3,4 However, the efficacy of thrombolytic therapy is limited, with studies indicating that up to two-thirds of patients do not benefit from it,5 and ∼10% of patients experience hemorrhagic transformation.6 Endovascular thrombectomy, although an effective treatment method, is also constrained by time window limitations and scope of application restrictions.

    In recent years, stem cell therapy and exosome therapy have emerged as hot topics of research. Stem cell therapy has shown therapeutic potential by promoting cellular regeneration and inhibiting post-stroke inflammatory responses. Exosomes, as nanoscale vesicles containing various bioactive molecules, play a key role in intercellular communication due to their low immunogenicity, no risk of vascular obstruction, and ability to cross the blood-brain barrier, providing new insights for the treatment of ischemic stroke.

    The occurrence of post-stroke osteoporosis

    Post-stroke osteoporosis (PSO) is a frequently overlooked but highly significant clinical issue. It is a distinct type of osteoporosis characterized by an impact on both bone mass and quality.7 Compared with age-matched individuals without stroke, the risk of femoral neck fracture in stroke patients is increased fourfold.8 This type of osteoporosis can lead to disability and even death, becoming one of the major causes of mortality in stroke patients.9

    The occurrence of osteoporosis is associated with an imbalance in bone metabolism. Under normal conditions, bone resorption and bone formation are in equilibrium, maintaining skeletal health. However, after a stroke, this balance is disrupted, leading to bone loss and a decrease in bone quality.10 Changes in bone metabolism in stroke patients may be related to neurological impairment, prolonged immobilization, malnutrition, and endocrine disorders.11 These factors not only promote excessive activity of osteoclasts but also affect the function of osteoblasts, resulting in decreased bone quality and increased bone fragility.

    Currently, the treatment and prevention of PSO, in addition to routine treatment for stroke, also include proper nutritional supplementation, appropriate physical exercise, and necessary pharmacological interventions. Particularly for patients who are bedridden for extended periods, the prevention and treatment of osteoporosis should be emphasized to reduce the risk of fractures.12

    More at link

    From passenger to driver: an interview study on person-centeredness in clinical reasoning during stroke rehabilitation

    You haven't addressed the problem of the stroke medical 'professionals' using the tyranny of low expectations to reduce survivor expectations of recovery and absolve them of their failure to provide full recovery to survivors!

     From passenger to driver: an interview study on person-centeredness in clinical reasoning during stroke rehabilitation

    Received 19 Dec 2023, Accepted 30 Sep 2024, Published online: 16 Oct 2024

    Abstract

    Purpose

    To explore how stroke survivors experience and prefer to participate in clinical reasoning processes in the subacute phase of stroke rehabilitation.

    Methods

    An explorative qualitative design was used. Individual interviews were conducted with 10 stroke survivors (4 women and 6 men, mean age 68 years) 4 weeks after their stroke, and follow-up interviews were conducted with 6 of them after 10 weeks. The interview settings were the patient’s home during their home rehabilitation, an inpatient and an outpatient rehabilitation unit. A reflexive thematic analysis was performed.

    Results

    Four themes were identified: discharge as a critical point for participation, describing a stressful time with varying involvement; supportive actions and context as crucial for participation, describing collaboration with the stroke team, the team’s consideration of the stroke survivor’s resources and needs, and a supportive home environment; the importance of goals and follow-up, describing goals as motivational and an unstructured use of goals; and difficulties in participation, describing a lack of dialogue with the stroke team and undetected resources and needs.

    Conclusions

    The stroke survivors experienced changes in their participation in the clinical reasoning process as their rehabilitation progressed. They moved from perceiving themselves as passengers at the time of their hospital discharge to gradually seeing themselves as the driver of their rehabilitation process. Some person-centered attributes, such as respectful relationships and a health focus, were incorporated into the clinical reasoning, while others, such as a holistic view and shared goal-setting(the only goal in stroke is 100% recovery and don't let your stroke medical 'professional' talk you down from that!), required further emphasis for improved person-centeredness in stroke rehabilitation.

    Introduction

    In the last decade, person-centered care (PCC) has been strongly advocated in health care [Citation1], although difficulties still exist regarding its implementation in rehabilitation practices. Challenges concern e.g. to enact a holistic approach and not only individualised care considering personal needs and preferences [Citation2]. Health care professionals’ lack of person-centered knowledge and skills, negative attitudes towards shared decision-making, time constraints, and lack of a coordinated and empowering work environment are examples of barriers to implementing PCC [Citation3].

    PCC is defined as a partnership between patients, their relatives, and health care professionals and emphasises the importance of knowing the person in the patient role – including the patient’s values, preferences, and needs. Sharing of information, shared deliberation, and shared decision-making are core to the active inclusion of patients in their care [Citation4]. PCC is well aligned and accepted as an espoused means of achieving the goals of stroke care and rehabilitation [Citation5]. More specifically, it is seen as a means to reach the goal of allowing stroke survivors to influence, participate in, and make personal choices regarding their care [Citation6].

    Rehabilitation includes interventions to optimise individuals’ functioning and reduce disability in interaction with the environment [Citation7]. Different phases can be identified in stroke rehabilitation in which interdisciplinary stroke teams gather bio-psycho-social information, interpret findings, assess rehabilitation needs, and make decisions on treatment and management [Citation5]. These processes represent ‘a [context-dependent] way of thinking and decision-making in professional practice to guide practice actions’ encapsulated in the concept of clinical reasoning [Citation8]. Considerations and actions in the clinical reasoning process will influence health professionals’ clinical behaviours. Recent developments in clinical reasoning research emphasise contextual factors and a shared process between the professional and the patient [Citation9–12], which aligns with the PCC approach. Person-centered clinical reasoning implies a focus on the individual patient in a certain context and point of time [Citation9], thus, forming the core of person-to-person interactions for health care professionals [Citation11,Citation13,Citation14]. Lately, clinical reasoning has also been studied at the collaborative level, in which clinical reasoning within professional teams forms the unit of analysis [Citation15]. Thus, the current clinical reasoning literature contributes knowledge on professionals’ thinking and clinical actions whereas further research can benefit of addressing the concept of PCC. Contributions from clinical reasoning research can, thus, shed new light on how PCC can be enacted by contributing knowledge on how staff interact and how patients participate in the reasoning process. Integration of PCC attributes in clinical reasoning processes in rehabilitation has demonstrated positive patient outcomes, such as improved satisfaction, acceptance [Citation6], motivation [Citation16], goal achievement, functional capability [Citation17], and occupational performance [Citation6].

    However, such integration challenges the traditional biomedically oriented clinical reasoning, which focus on the task and diagnostic reasoning, thereby risk failing to acknowledge holistic and person-centered processes [Citation18]. PCC expands the biomedical dimension by including a biopsychosocial perspective on health, relationship building, respecting the patient as a person, empowering patients to participate in decision-making on their care, and coordination of care [Citation19] to enable patients to live a meaningful life [Citation20]. A PCC approach implies a clinical reasoning process shared by health care professionals and patients in which the patient’s experiences and needs and the health care professionals’ judgements contribute to analyses of findings, management planning and decision-making [Citation9,Citation21]. At present, the literature on patient participation in these aspects is scarce.

    Stroke care and rehabilitation is related to the stroke survivor’s recovery time, from the stroke onset, and continuing through the acute inpatient care phase (1–7 days), the subacute rehabilitation phase (7 days to 6 months), and the chronic phase (> 6 months) [Citation22]. Thus, stroke survivors’ needs of care and treatment change over time, requiring that information and management decisions are adapted accordingly [Citation5]. The hospital discharge and the first following months of rehabilitation are critical timepoints, as the stroke survivor experiences new difficulties in their daily life, new social interactions including the stroke team, and sometimes these changes also occur in a new environment [Citation23]. Consequently, the clinical reasoning of stroke teams must acknowledge the stroke survivor’s situation and needs in the various phases and adapt to these changes. A previous study [Citation24] demonstrated that stroke survivors in the acute phase surrendered themselves to care and medical expertise; and as they progressed during the first week of their care, they sought to be more actively involved in the clinical reasoning through information exchange, being asked about their personal needs, and being invited to shared decision-making. Previous studies [Citation16,Citation25–28] during the subacute and rehabilitation phases examined different aspects of patient participation in stroke care and rehabilitation. Their results indicate that key dimensions of patient participation, which are necessary for PCC, such as identification of personal needs, person-centered goal-setting, and shared decision-making do not sufficiently occur in everyday care.

    Despite the acknowledged values of PCC, lack of knowledge is a prevailing barrier for PCC and is prevalent on patient, staff and organisational levels [Citation16]. Thus, to overcome this barrier and shed light on how PCC enact in clinical reasoning practice we need to scrutinise clinical reasoning in everyday practice with a focus on how stroke survivors participate in phases of their care and recovery. To reach this, the stroke survivors’ views need to be considered. Therefore, the present study aims to explore how stroke survivors experience and prefer to participate in clinical reasoning processes in the subacute phase of stroke care and rehabilitation [Citation6,Citation16,Citation17].

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    Impact of selective reporting bias on stroke trials: potential compromise in evidence synthesis - A cross-sectional study

     Shouldn't our non-existent stroke leadership be all over this and cracking down? But since there is NO leadership in stroke, NOTHING WILL OCCUR!

    Impact of selective reporting bias on stroke trials: potential compromise in evidence synthesis - A cross-sectional study

    Abstract

    Background

    Accurate reporting of outcomes is crucial for interpreting the results of randomized controlled trials (RCTs). However, selectively reporting outcomes in publications to achieve researchers’ anticipated results still occurs frequently. This study aims to investigate the prevalence of selective reporting of outcomes in RCTs on treating acute ischemic stroke (AIS), identify factors contributing to this issue, and assess its potential impact on the degree and direction of intervention effect.

    Methods

    A search was conducted in MEDLINE, Embase, and the Cochrane Library to collect interventional RCTs on AIS published from 2020 to 2022. Full texts of RCTs were reviewed, and only those reporting International Clinical Trials Registry Platform primary registry numbers were included. Registration information of the RCTs was extracted from the registry platforms and compared with the publications’ details to assess the selective reporting of outcomes. Bayesian multilevel logistic regression was used to analyze the reasons behind selective reporting.

    Results

    Among the total of 159 AIS RCTs identified, 82 (51.6%) were ultimately included, as they reported registration numbers, which encompassed 819 outcomes. Among them, 72 RCTs (87.8%) and 497 outcomes (60.7%) exhibited selective reporting. Omission-type selective reporting (downgrading, omitting, or ambiguously reporting) accounted for 36.4%, while addition-type selective reporting (upgrading, adding, or altering the measurement scope of outcomes) comprised 63.6%. Omission-type selective reporting correlated with negative results (OR: 7.39; 95% CI: 4.08—13.44), whereas addition-type selective reporting correlated with positive results (OR: 2.07; 95% CI: 1.34—3.26) and publication in journals that are not in the top quartile of the Journal Citation Reports (OR: 2.48; 95% CI: 1.15—5.38).

    Conclusions

    Registered interventional AIS RCTs still face significant issues regarding selective reporting of outcomes. Therefore, it is necessary to further evaluate the influence of selective reporting bias on the positive results obtained from individual AIS RCTs and the systematic reviews based on these RCTs.

    Peer Review reports

    Background

    Globally, stroke ranks as the second leading cause of death and the third leading cause of disability [1]. Acute Ischemic Stroke (AIS), characterized by acute focal neurological deficits due to vascular occlusive lesions, garners considerable attention among stroke types owing to its prevalent occurrence, notable disability rate, elevated mortality risk, and substantial economic burden [2,3,4,5,6,7]. Effective and timely treatments, such as intravenous thrombolysis and mechanical thrombectomy, are crucial in reducing mortality and disability rates, as well as in mitigating the economic burden of AIS [4, 8]. In the field of AIS treatment research, a substantial body of Randomized Controlled Trials (RCTs) and Systematic Reviews (SRs) provides a solid theoretical foundation for the formulation of treatment protocols [9,10,11,12,13,14,15,16]. These studies not only disclose the preferred treatment options under various circumstances but also highlight the optimal timing for intervention, offering crucial guidance for clinical practice.

    However, the quality of RCTs may be compromised by the presence of potential biases such as measurement bias, attrition bias, and selective reporting bias, which ultimately could impair the quality of evidence produced [17]. Among these, selective reporting bias is a common source of bias at the time of publication, leading to inaccurate estimations of intervention effects and the production of biased evidence [18]. To enhance the transparency of clinical research, organizations such as the World Health Organization (WHO) and The International Committee of Medical Journal Editors (ICMJE) have been advocating for the registration of clinical trials since 2004 [19]. Clinical trial registration is regarded as a tool for detecting selective reporting. Existing studies indicate that discrepancies are common between publications in fields such as dentistry, dermatology, and psychology and their registered information [20,21,22,23,24].

    Prior research has predominantly investigated the occurrence of selective outcome reporting in specific fields [20,21,22,23,24,25]. However, there is a lack of in-depth research analyzing the factors influencing different types of selective reporting. Therefore, this study aims to investigate the occurrence of selective reporting of outcomes in recently published RCTs on AIS treatment, analyze the factors influencing different types of selective reporting, and assess the potential impact on the degree and direction of outcome effects. This research endeavors to provide insights for the evaluation and utilization of evidence in AIS therapeutic studies.

    Impact of fasting blood glucose on prognosis after acute large vessel occlusion reperfusion: results from a multicenter analysis

     

    So you described something, but DID NOTHING USEFUL THAT WILL HELP STROKE PATIENTS RECOVER. 

    Impact of fasting blood glucose on prognosis after acute large vessel occlusion reperfusion: results from a multicenter analysis

    Bin Luo,,&#x;Bin Luo1,2,3Yi Xiang&#x;Yi Xiang4Fanlei Meng&#x;Fanlei Meng5Yubo WangYubo Wang3Zhenzhong ZhangZhenzhong Zhang6Hecheng RenHecheng Ren3*Lin MaLin Ma3*
    • 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 (37). 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 (911). 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) (35). 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.

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    Stress, Meditation, and Alzheimer’s Disease Prevention: Where The Evidence Stands

     9 years and I bet your incompetent doctor still doesn't have a meditation protocol for you post stroke! My definition of competence is keeping up-to-date on all research in your field, which means learning beyond what you got in medical school. What's yours?

    Oops, I'm not playing by the polite rules of Dale Carnegie,  'How to Win Friends and Influence People'. 

    Telling your supposedly smart doctor they know nothing about stroke is a no-no even if it is true. 

    Politeness will never solve anything in stroke. Yes, I'm a bomb thrower and proud of it. Someday a stroke 'leader' will try to ream me out for making them look bad by being truthful, I look forward to that day. 

    Send me hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and my response in my blog. Or are you afraid to engage with my stroke-addled mind? I would like to know why you haven't created a mediation protocol.

    Stress, Meditation, and Alzheimer’s Disease Prevention: Where The Evidence Stands

    . 2015 Aug 28;48(1):1–12. doi: 10.3233/JAD-142766

    Editor: J Wesson Ashford
    PMCID: PMC4923750  PMID: 26445019

    Abstract

    Although meditation is believed to be over five thousand years old, scientific research on it is in its infancy. Mitigating the extensive negative biochemical effects of stress is a superficially discussed target of Alzheimer’s disease (AD) prevention, yet may be critically important. This paper reviews lifestyle and stress as possible factors contributing to AD and meditation’s effects on cognition and well-being for reduction of neurodegeneration and prevention of AD. This review highlights Kirtan Kriya (KK), an easy, cost effective meditation technique requiring only 12 minutes a day, which has been successfully employed to improve memory in studies of people with subjective cognitive decline, mild cognitive impairment, and highly stressed caregivers, all of whom are at increased risk for subsequent development of AD. KK has also been shown to improve sleep, decrease depression, reduce anxiety, down regulate inflammatory genes, upregulate immune system genes, improve insulin and glucose regulatory genes, and increase telomerase by 43%; the largest ever recorded. KK also improves psycho-spiritual well-being or spiritual fitness, important for maintenance of cognitive function and prevention of AD. KK is easy to learn and practice by aging individuals. It is the premise of this review that meditation in general, and KK specifically, along with other modalities such as dietary modification, physical exercise, mental stimulation, and socialization, may be beneficial as part of an AD prevention program.

    Keywords: Alzheimer’s disease, lifestyle, meditation, memory loss improvement, prevention, stress, psychospiritual well-being, reduction of risk factors

    LIFESTYLE AND ALZHEIMER’S DISEASE PREVENTION

    This is a critically important time in the field of Alzheimer’s disease (AD) prevention. As the search for a drug to prevent and/or cure AD continues to be elusive [], low cost lifestyle measures that create high levels of brain health, stop ongoing degeneration, repair neuronal damage, and prevent the type of cognitive disability that could lead to AD, are at the forefront of the discussion of AD prevention. Emerging research suggests that lifestyle choices can make a difference, when it comes to AD prevention []. In a recent study of lifestyle modification, The Finnish Geriatric Intervention Study To Prevent Cognitive Impairment and Disability (The FINGER Study), the effects of a 2-year multi-domain intervention targeting several lifestyle and vascular risk factors were studied simultaneously. FINGER included 1,260 participants aged 60–77 years. The initial study, which ended in 2014, will continue with an extended 7 year follow up period. FINGER indicated that utilizing nutritional intervention, physical exercise, cognitive training, and social activities together resulted in a significant beneficial effect on overall cognitive performance. The study was the first large randomized controlled trial that suggested that it is possible to prevent cognitive decline and thus delay or prevent AD using an integrative medical program among older, at-risk individuals [].

    This review will initially focus on a lifestyle factor common today: chronic stress. Stress, via the cortisol connection, causes neurotoxic damage to cells in the hippocampus and elsewhere in the brain which may increase AD risk. Beyond that, stress has a causative association with multiple risk factors for AD, including inflammation, calcium dysregulation, cardiovascular disease including hypertension, diabetes/insulin resistance, depression, anxiety, physical inactivity, sleep deprivation, and smoking []. A recent study of 1,796 elderly people with AD compared to 7,184 without an AD diagnosis highlighted the direct connection between anxiety, insomnia, benzodiazepine use, and AD []. Previously, a number of these drugs were shown to turn on AD promoting genes [].

    How meditation acts to reduce stress and cortisol levels and improve multiple aspects of health and cognition will then be reviewed. Beyond the basics of this discussion, this article will discuss research on a simple, twelve-minute, meditation technique called Kirtan Kriya (KK), that positively impacts brain and memory function, cellular health, genetic expression, and well-being. Moreover, KK may reverse memory loss in subjects with subjective cognitive decline (SCD) and mild cognitive impairment (MCI), both of which may progress to dementia [].

    STRESS, AGING, AND NEURON DEATH

    According to leading stress researcher Robert Sapolsky Ph.D., a stressor can be defined physiologically as any perturbation from the outside world that disrupts homeostasis []. Beyond the physical, stress can also be psychological or emotional and the potency and pathogenicity of psychological stress cannot be ignored, as it may increase the risk of developing AD [].

    Modern stress research is considered to havebegun in the last century with the work of Walter B. Cannon [], and later recognized as the first stage of Selye’s general adaptation syndrome []. This work led Sapolsky and others to appreciate that while acute stress actually heightens cognition, these same responses are highly deleterious when activated chronically [].

    Furthermore, aging is a time of decreased ability to handle stress and, untreated, chronic stress accelerates many of the degenerative aspects of aging, including cognitive decline. In contrast, meditation may counter-balance many aspects of the stress response and protect the brain specifically from the ravages of aging combined with stress overload [].

    Stress may injure hippocampal cells via the release of the hormone cortisol from the adrenal gland in response to hypothalamic and pituitary stimulatory signals, such as CRF and ACTH. Such injury could lead to dysfunction and atrophy of that critically important memory and emotional brain structure []. Beyond that, hippocampal cellular loss is dramatically exacerbated because of the destruction of the specific neurons that control cortisol secretion from the adrenal gland [].

    This loss of feedback inhibition may lead to a persistent toxic cortisol level, thus causing the further injury or death of hippocampal cells by activating NMDA receptors, which may allow excessive extracellular calcium ion to pass through now open channels, flooding the interior of the cell with markedly excessive calcium ion. This excessive intracellular calcium leads to cytosolic injury, mitochondrial damage, severe oxidative stress, and possibly inflammation, which may ultimately lead to significant cognitive decline []. Current research also indicates that chronic stress arousal activates multiple inflammatory mediators, including the NF-κB system, leading to widespread brain inflammation, especially in the hippocampus []. These disturbances of central inflammation have been shown to be a hallmark of AD [].

    The negative effects of chronic stress are considerable. Beyond cognitive decline and memory loss, stress also affects numerous neurobehavioral phenomena, from anxiety to depression to various abnormal behaviors and unconscious self-defeating compulsive actions. Some of these behaviors may lead to premature cognitive decline and AD []. Significantly, Lupien argues that it is not simply isolated episodes of stress that do damage to the brain. Rather, it is the magnitude of cortisol exposure over the lifetime, especially middle age and beyond, that is linked to AD and promotes emotional and cognitive dysfunction, including disruption of hippocampal-dependent selective attention and explicit short term memory loss, SCD, MCI, and AD [].

    Further evidence links decreased memory performance and a greater risk of AD in people reporting higher levels of work-related stress, having stress-prone personalities, enduring early childhood stress such as abuse, trauma, and neglect and/or suffering from midlife stress as well. In a study specific to women, for each additional stressor reported, the risk of later developing AD increased 20% [].

    In a study by Wilson, those subjects who scored high in distress proneness (90th percentile) had twice the risk of developing AD than those in low distress proneness (10th percentile) suggesting that an increased vulnerability to psychological distress may be a risk factor for AD.

    A randomized, double blind, placebo controlled comparison of two fixed oral doses of cortisol (40 mg/d and 160 mg/d using split doses to approximate circadian rhythm) in volunteers over four days to a matched group of healthy subjects (n = 51) showed reversible impaired verbal, declarative, and short term memory in those subjects receiving the higher or stress dose of cortisol []. Additionally, Wang showed that psychological stress in the workplace as manifest by low job control and high job strain was associated with increased risk of AD in late life, independent of other risk factors []. Chronic stress is associated with multiple brain anatomic abnormalities, including a decreased size of the anterior cingulate cortex, which leads to impaired hypothalamic-pituitary-adrenal axis regulation and perhaps an increased vulnerability to the effects of chronic stress [].

    Finally, recent stress research by Epel and Blackburn shows that stress has a pronounced negative effect on genetic health, diminishing telomerase levels, the enzyme responsible for maintenance of telomere length, the protective cap of DNA. Shorter telomeres are associated with inflammation, accelerated aging, and AD []. Moreover, telomeres are shorter in those with childhood maltreatment [].

    MEDITATION AS ALZHEIMER’S DISEASE PREVENTION MEDICINE

    In 1949, Swiss physiologist Walter Hess, PhD, was awarded the Nobel Prize in Medicine and Physiology for his description of two centers in the hypothalamus of the cat []. One of the points, which he called the ergotrophic center, when stimulated electrically, produced the typical physiological features of the sympathetic stress response: rise in blood pressure, increase in pulse, faster respiratory rate, and an increase in oxygen consumption or MVO2. He broke new ground when he demonstrated anadditional point in the hypothalamus that, when stimulated, caused the exact opposite of the stress response. He called it the trophotrophic center, which was associated with parasympathetic activation, relaxation, sleepiness, and withdrawal from activities. The trophotrophic system protects against stress overload and allows for recovery and regeneration []. This dichotomy suggests that there exists an innate, natural way to reduce the deleterious effects of stress.

    Approximately twenty years later, Herbert Benson, MD, further elucidated the physiological underpinnings of the trophotrophic center. First he described what he called “The Four States”: awake, sleep, dream, and the fourth state. The difference between the first three states and the fourth state is that the first three happen spontaneously, while specific actions are required to enter into the fourth state or what Benson initially called “eliciting the relaxation response(RR)” []:


    Comfort: Sit easily in a chair or on the floor.

    Quiet: Be alone in a spot where you will not be disturbed, i.e., no texts, emails, cell phones, etc., while eliciting the relaxation response.

    Tool: Focus on a word, thought, breathing, sound, or short prayer.
    Attitude: When other thoughts enter your mind, re-focus on your tool to the exclusion of everything else for 10 to 20 minutes twice a day.

    Meditation is not blanking out your mind, for that is virtually impossible. Rather, it is a wakeful, hypo-metabolic state that is produced by following these four steps, especially the last one []. Recently, Benson modified his original approach to two steps required to elicit the RR: Repetition of a word, sound or movement and the passive disregard of everyday thoughts when they come to mind during the practice of the chosen technique. Through four decades of research, Benson and colleagues have shown that the RR impacts genomic, structural, physical, psychological, and functional outcomes [].

    Other meditation techniques that have been studied prominently include the Transcendental Meditation technique (TM) as taught by Maharishi Mahesh Yogi, which uses a secret, silent, prescribed sound or mantra as its tool, and mindfulness meditation or Mindfulness Based Stress Reduction (MBSR), a Buddhist approach with the focus on the breath as its tool.