New blood markers that reflect risk for Alzheimer’s disease (AD) are uncovering important modifiable risk factors to be aware of to dramatically reduce the likelihood of ever suffering from this cruel disease. The latest study shows that just one night of sleep disruption is associated with an increase in these blood markers.
The primary brain lesions of AD are the result of deposits of a substance known as beta-amyloid. Although the immune cells in the brain normally remove beta-amyloid and plaque, research is beginning to characterize a chronic and excessive inflammatory reaction to amyloid proteins in the brain in susceptible individuals that can promote AD. Blood measurements of a protein called tau that is formed from toxic beta-amyloid as well as a protein that acts as the internal skeleton of brain cells known neurofilament light chain (NfL) protein can predict neurodegeneration years before clinical symptoms appear in AD. When brain cells are damaged, tau and NfL are released into cerebrospinal fluid and then the blood.
Poor sleep quality is associated with a significant risk for Alzheimer’s disease. For example, researchers from the Washington University School of Medicine in St. Louis found that the inability to sleep through the night was associated with an increased risk the preclinical form of Alzheimer’s disease. Subjects who were the least efficient sleepers in the study were five times more likely to have preclinical form of Alzheimer's. While researchers are exploring the formation of the beta-amyloid as being the cause of the poor sleep quality, a more likely explanation is that the poor sleep quality is actually the cause of the beta-amyloid formation.
During the deeper levels of sleep the repair mechanisms and antioxidant system of brain cells are heightened. Sleeping pills seem to exacerbate this situation. Use of sedative hypnotic drugs (sleeping pills) was associated with a whopping 230% increase risk of AD over an eight-year period in a study in France while in a study in the U.K., the risk was even greater over a 22-year follow up study– a dramatic 294% increase. The link between sleeping pill usage and the dramatic increased risk for AD may be the result of the fact that these drugs typically negatively impact the ability to achieve deeper levels of sleep.
"Mental disorders often involve difficulty with complex cognitive functions, such as decision making, emotional self-regulation, or behavioral adaptation to changing circumstances. Those functions arise from the carefully timed and orchestrated synchrony of activity across multiple structures1—in other words, from network activity. It should therefore be possible to treat mental disorders by identifying abnormalities in that network activity and restoring them to healthy patterns. "
Targeting Cognition and Networks Through Neural Oscillations:Next-Generation Clinical Brain Stimulation
Alik S. Widge, MD, PhD; Earl K. Miller, PhD
Published Online: May 22, 2019. doi:10.1001/jamapsychiatry.2019.0740
A study published in the American Academy of Neurology demonstrated the neurophysiological and biochemical value of repeated compression using blood pressure cuffs on ones arm and leg for 5 minutes. Brain blood flow was improved for over 24 hours beginning 6 hours after the compression treatments were conducted.
This struck me as a relative benign and cost effective method of treatment for people with neurodegenerative and neurodevelopmental conditions, e.g, dementia and autism. I recalled the gowing evidence for intermittent hypoxia and hypocaloric interventions enhancing mental and physical and immune system functioniong. I've been made aware of its use in physical fitness training and want to explore how it could be developed into a safe, low-cost, noninvasive and rather useful 'outside in' treatment for older adults where blood flow is constrained by various forms of cardiovascular disease and impaired functioning.
Then I recalled Stan Grof's early work on what he termed basic perinatal matrices (Grof, 1976) where the fetus is compressed during the birth process and this confers important psychophysiological information that substnatively influences their future development. I saw a connection to Grof's insight about the challenges we experience in the birth process can carry forward into later life and manifesting as emotional and behavioral difficulties. Here we can see how the contraining of blood flow and then its sudden release repeats the experience of compression in the birth canal and subsequent release into progressively more independent, self-organizing and self-sustaining life. I then associated the paper's description of remote ischemic preconditioning to my use of Bioenergetic therapy as a psychophysiological way to enhance body-mind flexibility and self awareness.
Quietmind's current treatment model focuses on using photobiomodulation to increase cortical microcapillary perfusion, regional cerebral blood flow, ATP and specific chaperone proteins while reducing beta amyloid buildup. This is combined with brainwave biofeedback training to repair the dysregulated neural connectivity and functional medicine that can address any underlying infectious or metabolic sources of impaired immune response and systems-oriented Bioenergetic Analysis to re-establish and support more grounded emotional and interpersonal functioning.
Noninvasive non-drug treatment of dementia and other neurodegenerative disorders with photobiomodulation is getting more evidence of its effectiveness published in the traditional scientific literature. We are gratified and excited to see this approach gaining traction and hope this can lead to increased interest in Quietmind's integrated treatment model of photobiomodulation with infrared light and brainwave biofeedback training. This study builds on the work done at MIT with animals and shows how the pulsed light can influence neurochemistry and cellular communication processes to mitigate neurodegenerative activity.
I found a paper https://www.ncbi.nlm.nih.gov/pubmed/21459521
Med Hypotheses. 2011 Jun;76(6):769-73. doi: 10.1016/j.mehy.2011.01.020. Epub 2011 Apr 2.Tardive dysphoria: the role of long term antidepressant use in-inducing chronic depression.El-Mallakh RS1, Gao Y, Jeannie Roberts R.
This provoked me to inquire of my colleagues as to why there'd been no further exploration of this issue to be found in teh literature since 2011 and I got this reply from Robert Thatcher a neuroscientist and developer of the Neuroguide EEG analysis software that we use at Quietmind for our clnical and research activities. It is clear that the continued use of SSRI medications is now getting more critical attention now 30 years after the arrival of Prozac. Neurofeedback and other treatment methods are able to provide similar results without side effects and that last long after the training process has been completed. Here's Dr. Thatcher's reply:
This post concerns he science and publications showing negative effects after long term use of antidepressants. The negative effect of the antidepresssants is called Tardive Dysphoria which is chronic depression induced by long term use of antidepressants. There are several interesting studies on this topic if one does a simple Google search as well as a search of the National Library of Medicine database, e.g., https://www.ncbi.nlm.nih.gov/pubmed/30199999Tardive dysphoria: the role of long term antidepressant use in-inducing chronic depression
A common hypothesis is that anti-depressants inhibit re-uptake that results in increased serotonin in the extracellular space however over time there are compensatory mechanisms that remove serotonin faster than the drug can block re-uptake or different re-uptake mechanisms develop that result in a worse and chronic outcome.
Ketamine has a different mode of action, e.g., midline thalamus de-coupling to the medial frontal lobes and hippocampus that appears to disrupt a cyclic dynamic and sort of refreshes the circuity for a while,e.g., Cortical-brainstem (nu. Raphe) regulatory control mechanisms. A search of the National Library of Medicine database using the search terms "Depression Brain Network" results in 2,875 citations. There is good agreement about the hubs of this network between different imaging modalities such as fMRI, PET and EEG/MEG. Therefore, a reasonable idea is to measure the brain networks related to depression using QEEG and LORETA as a baseline assessment and then use NFB to reinforce increased stability and efficiency of the nodes and connections between the hubs of the depression network as well as to use QEEG to assess the relative effectiveness of non-SSRI treatment.. As Wes stated, exercise and good diet (Typtophan is a precursor of serotonin) and lifestyle changes and perhaps also Ketamine. However, given the risk of doing harm based on the over use of anti-depressant drugs as published in the scientific literature points toward considering alternative treatments.
Bob Thatcher, PhD Applied Neuroscience Inc.
It is now becoming more evident to traditional neuroscientists that there are ways to influence brain activity
This new study shows that transcranial alternating current stimulation can help restore memory functions in people with dementia. This is one of the techniques we use in our integrated memory restoration and protection program at Quietmind Fdn. Please call for details and to setup a consultation.
Assessing Alzheimer's and Parkinson’s Development Risk with Near-Infrared Photobiomodulation & Quantitative EEG in Adults Diagnosed with TBI/Post Concussion Syndrome
This Powerpoint slide show outlines the TBI/concussion treatment protocol that Quietmind Foundation is preparing to conduct. Funding support and research partnerships are being developed to support this multi-site research effort.
The above article supports the value of low-level infrared light stimulation using sophisticated blood oxygenation and imaging technology. We used similar though less advanced tools in our 2012 study 28 days of 6-minute, transcranial and intraocular 1065-1075nm photobiomodulation of subjects struggling with probable Alzheimer's disease. The current study using the same device is now 56-days with more powerful lLED stimulation.
This recent article by my colleague Michael Hambin, PhD offers a well organized and rather complete review of the current state of the science related to the clinical application of low level light stimulation. The edited volume on the subject Photobiomodulation and the Brain has recently been published by Elsevier and contains a chapter on the integration of neurofeedback photobiomodulation by myself, Trent Nichols, MD and our colleagues Jason Huang MD and Damir Nizmutdiinov MD PhD from Baylor Scott & White Research Institute.
We are seeing terrific results within our clinic using these tools and are excited by the future applications that are being created based on this and other research.
Our approach to treatment is aligned with Dr. Perlmutter, Bredesen and supports the Institute for Functional Medicine's model for clinical intervention by boosting the capacity for recovery and healing. Photobiomodulation stimulates mitochondria to produce more ATP and thereby improve the brain's ability to function efficiently. Neurofeedback adds an important component to this process by improving the neural connectivity that allows for continued improvement by having renormalized brain network functioning. Functional medicine works to remove the underlying bacterial, viral and toxic contributors to neurophysiological deterioration.
Our team regularly publishes articles and blog posts on the latest research and news coming out of our group and the field in general.