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

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.

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