HRV/BDNF Improves or, by absence, Degrades Balance, Endurance and Working Memory

In this study balance (fall prevention) and endurance (metabolic health) correlated to processing speed and working memory.  All were either good or not good on a continuum on the same parallel curves indicating a common determinant.

I believe all three (balance, endurance and working memory)  are  related by and directly proportional to BDNF and, by proxy, HRV or autonomic control using accelerator or brakes for control of physiological functions.

More BDNF indicates preserved structure, function and network plasticity.

Stay active physically, mentally and limit stress with a goal of optimum BDNF and optimum HRV.

Aging well: Processing speed inhibition and working memory related to balance and aerobic endurance - Zettel-Watson - 2015 - Geriatrics & Gerontology International - Wiley Online Library

http://onlinelibrary.wiley.com/doi/10.1111/ggi.12682/abstract?systemMessage=Wiley+Online+Library+will+be+unavailable+on+Saturday+27th+February+from+09%3A00-14%3A00+GMT+%2F+04%3A00-09%3A00+EST+%2F+17%3A00-22%3A00+SGT+for+essential+maintenance.++Apologies+for+the+inconvenience.&userIsAuthenticated=false&deniedAccessCustomisedMessage=

Autonomic Dysfunction ( Reduced HRV ) Precedes Rheumatoid Artritis and Presumptively Other Systemic Metabolic Diseases

In this study autonomic dysfunction, a physiological correlate of neurodegeneration or unchecked brain inflammation, precedes joint inflammation.

In effect early changes of of inflammation damage sensitive nerve tissues before attacking synovial tissues.  The functioning autonomic nerve system is the accelerator and brake pathways  the brain uses to control peripheral somatic physiology.

When the brakes are broken, Humira and Methitrexate are peripheral brakes which slow down the runaway body and preventing synovial dysfunction and damage.

I propose that lifestyle changes to increase BDNF and HRV along with  anti inflammatory strategies such as Melatonin and DHA along with monitoring of HRV heart rate variability would prevent 75% of the diseases we treat at a late macro fractal stage rather than "preventing it in the bud" or early fractal stage.  Think how a microscopic bacteria initiates a sepsis autonomic dysfunction up to 70 hours before it becomes macroscopic with fever, tachypnea, tachycardia, vascular collapse and end organ failure.

Because CSF cleansing of the brain during sleep removes inflammatory stimulants, I want to add sleep to my health plan.   Norepinephrine,a glymphatic flow antagonist reduces the glymphatic flow that cleanses the brain waste. I would avoid stress, exercise and sympathetic tone within one hour of bedtime.  Adding sleep is likely unnecessary to a plan that restores autonomic tone before disease and thereby restores sleep.  I believe that 2 minutes of slow paced breathing that reduces brain cortisol and TNF alpha would improve quality of sleep especially if performed right at bedtime.

Do you find this as exciting and logical as I suspect this approach to become?  I further conjecture that optimizing HRV because it is low cost, self testing feedback for right tract wrong track will be widely beneficial in prevention and treatment of disease.  It also is a an early warning sign of early fractal change that results in large fractal disease symptoms and signs.

http://www.sciencedirect.com/science/article/pii/S2352396416300688

Autonomic Dysfunction Precedes Development of Rheumatoid Arthritis: A Prospective Cohort Study

Cellular, Organ and Organism Level Network Resilience

This article explores the importance of a system resilience in maintaining health and function.

The cell is a network.  The body is a network.  The cell, organ and organism must have similar systems of resilience.

Conceptually every system has an accelerator and a braking system to remain stable.  

Dysfunction precedes loss.  

That is why resilience systems are vital.  BDNF and HRV heart rate variability are likely at the core of resilience.  They decline and predict system failure in cells, organs and organisms.

A midlife sympathetic tone dysfunction precedes cognitive, mood and body decline by 20 years.  Those who delay this decline maintain memory, mood and metabolism or system resilience.

We do not know what the limits of these hormetic or resilience actions, but they are substantial and worth participating in a healthy lifestyle.

HRV is proxy for this resilience.  I plan to measure my resting heart rate variability with a a $50 Bluetooth heart rate monitor and IPad app to calculate.  I hope to be able to demonstrate that lifestyle efforts to raise BDNF will increase HRV and by extension resilience and health; improved memory, mood and metabolism; reduced mortality.

The Trajectory of Life.  Decreasing Physiological Network Complexity Through Changing Fractal Patterns.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4451341/pdf/fphys-06-00169.pdf

Brain Network Function improved by Higher BDNF relative to Klotho Variant Status

Here in abstract below is the evidence for the Klotho gene variant rs1207568 homozygous requiring highest levels of BDNF, the absence of Klotho gene variant requiring intermediate levels of BDNF and the heterozygous Klotho variant require lower levels of BDNF to have normal mood (and cognition.)

"we confirmed a significant improvement of depressive symptoms after treatment in patients carrying at least one minor allele at rs1207568 and a worse response in patients homozygous for the minor allele at rs9536314. Our results were the first that suggested a possible role of KL in the complex pathway of SSRI response in late-life MDD."

Klotho polymorphism affects SSRI response in late life depression.

GT. high response.

TT  normal response

GG. Low response.

Klotho gene /normal gene as heterozygous pair amplifies BDNF effect via GluN2b receptor increase.  Absence of this amplifier status for BDNF then requires more BDNF to achieve an antidepressant response in TT homozygous normal gene and even higher BDNF levels for homozygous GG.

Hence my statement,  all patients need BDNF but some need it more is confirmed.  Depression is a low BDNF state.  SSRI work to increase BDNF levels.  Response to SSRI is therefore a function of Klotho variant gene status and BDNF level achieved with treatment.

The addition of lifestyle to optimally raise BDNF will improve response rates above SSRI alone.  Higher BDNF levels further improve mood, memory and metabolism.

http://link.springer.com/article/10.1007/s12035-016-9711-y

Two BDNF Producing Activities are Better , How about Five or More?

This abstract shows that exercise and cognitive brain gaming improved cognitive function in older individuals.

I believe this verifies that exercise and cognitive training increases BDNF more than exercise alone , improving cognition/memory, mood and metabolism.  A proxy for serum BDNF level is heart rate variability which is a function of noradrenalin produced during exercise of both body and mind and its effect on Vagal neurons that promote greater heart rate variability. 

This partially answer the question, would other combinations of lifestyle changes increasing BDNF be synergistic resulting in greater improved memory, mood and metabolism and its proxy resting respiratory heart rate variability?

I think this will be proved! 

 Conjecture:  resting heart rate variability will become a measurable proxy for BDNF and prevent overtraining due to over exertion or age related intolerance in persons of all ages.

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=10033638&fileId=S1355617715001083

Journal of the International Neuropsychological Society

Aerobic and Cognitive Exercise (ACE) Pilot Study for Older Adults: Executive Function Improves with Cognitive Challenge While Exergaming

Nicole Barcelos^a1, Nikita Shah^a1, Katherine Cohen^a1, Michael J. Hogan^a2, Eamon Mulkerrin^a3, Paul J. Arciero^a4, Brian D. Cohen^a1, Arthur F. Kramer^a5 and Cay Anderson-Hanley^a1 

BDNF; Aging and Anti-Aging

Noradrenalin up regulates the Muller cell ( a retinal glial or helper cell of retinal nerves and nerve endings) production of BDNF (brain derived neurotrophic factor). Retinal degeneration occurs in elderly persons, the same age group cohort that develops other neurodegenerative diseases that BDNF prevents.

Noradrenalin is produced in high levels by HIIE (high intensity interval exercise.)

An early defect, preceding Alzheimer's disease by 20 years, is intracranial sympathetic (noradrenalin) tone loss that is associated with reduced heart rate variability, low BDNF levels and lower aerobic exercise capacity.  

Increased BDNF level, especially associated with noradrenalin increase, should protect the retina and brain.  HIIE of 4 minutes increases noradrenalin by 17 fold and last 19 minutes post exercise.  The use of green tea extract, an o methyl transferase inhibitor (enzyme that degrades stimulants) prolongs the basal (resting) rate of noradrenalin and may also be helpful.  Lastly, endothelial (blood vessel lining cells) cells produce BDNF, and taste bud receptor cells produce BDNF and is responsible for the continuous synapticity or connection hookup of the nerve to the taste bud.  Noradrenalin may up regulate the mRNA (DNA template that makes gene product proteins) of BDNF directly.  Green tea extract will be an indirect agonist (increases action) by increasing noradrenalin duration of activity by blocking its enzymatic break down.  HIIE would pulse or strengthen the effect of both.

Age related conditions are negatively impacted by BDNF neurodegenerative change.  

First in sympathetic and autonomic systems.  

Second in their end organs, 

retina, macular neuro-degeneration, 

taste, lack of connection or hook up of nerves to taste buds, 

appetite, a function of bone marrow produced BDNF, 

brain, mood and cognitive disconnection syndrome, and

heart, where low BDNF levels reduces the relaxation and contraction limits of the heart muscle cell and reduces the pump function of the heart reducing activity levels.

Conjecture.

Aging is degeneration of the network within and between cells.

Lack of BDNF allows degeneration.

Normal or increased BDNF reverses, stabilizes or slows degeneration.

A negative BDNF lifestyle and inflammation within cells and between cells degrades the individual's memory, mood and metabolism.

A positive BDNF lifestyle and anti-inflammatory strategy could reverse, stabilize or slow the disconnection syndrome that degrades the individual's memory, mood and metabolism. (Vision, hearing, taste, appetite, cardiac output)

Conjecture 2.

The elderly during and post autonomic, sympathetic intracranial nerve function decline might be rescued with supplementation of lifestyle agonist known to increase BDNF.

Noradrenalin; green tea extract, stimulant therapy.

Lactate; LR iv, Mag Lactate. (Lactate producing exercise increase BDNF production )

Intermittent weekly fasting; MCT oil. Axona to provide beta hydroxybutyrate.

HIIE; blood restricted exercise to produce lactic acid with low intensity exercise.

The core of this can be accomplished with my 3,2,1 plan at LivermanHealthAdvice.blogspot.com.

Müller Cells as a Source of Brain-derived Neurotrophic Factor in the Retina: Noradrenaline Upregulates Brain-derived Neurotrophic Factor Levels in Cultured Rat Müller Cells - Springer

http://link.springer.com/article/10.1007%2Fs11064-005-7936-7

Abstract

Müller cells, the predominant glial cells in the retina, are thought to play important roles in the survival of retinal neurons. Previous studies have demonstrated that Müller cells express brain-derived neurotrophic factor (BDNF), which has a pronounced neurotrophic effect on retinal ganglion cells. In this study, we investigated whether Müller cells express and release BDNF in culture. Reverse transcriptase-PCR, immunocytochemistry and Western blotting revealed that Müller cells produce BDNF mRNA and protein. Using the enzyme-linked immunosorbant assay, BDNF protein levels in Müller cells and their conditioned medium were quantified, demonstrating that Müller cells produce and release high levels of BDNF. Noradrenaline administration caused an upregulation of BDNF mRNA and protein expression by cultured Müller cells. These results suggest that Müller cells may act as an endogenous source of BDNF in the retina. Furthermore, induction of BDNF expression by adrenergic agonists may provide a therapeutic approach to retinal neurodegenerative disorders.

Other Bipolar Disorders, Anorexia Nervosa and Bulimia, Opiate and Stimulant Addictions

Here is an enlightened article showing how cognitive training (which increases BDNF, synapticity, nerve function and nerve cell integrity)  potentially allows better decision making by activating cognitive and salience networks via working memory and cognitive training.

This results in better choices, less denial and greater levels of BDNF (that has been shown to rise in 26 weeks of opiate addiction recovery to levels below normal controls).  Perhaps cognitive brain training will increase BDNF levels above normal and provide more resilience!  Perhaps other BDNF increasing lifestyle interventions would further improve central executive function, promote brain plasticity and result in above average serum BDNF levels establishing resilience against relapse and global improvement in performance status of mental, emotional and physical resilience in general.

A debate on working memory and cognitive control: can we learn about the treatment of substance use disorders from the neural correlates of anorexia nervosa? | BMC Psychiatry | Full Text

http://bmcpsychiatry.biomedcentral.com/articles/10.1186/s12888-016-0714-z

Joseph Thomas (Tony) Liverman, Jr. MD