Monday, March 21, 2016

BDNF Increases Trigger Memory and Brain Network Improvement

This article notes that BDNF is the trigger for better memory and long term potentiation.
The investigators confirmed increased BDNF with transcranial direct current stimulation.
My cursory reading shows that actions, supplements and treatments that increases BDNF also increases HRV heart rate variation index.

Conjecture: a fast brain like a race car has more horsepower or bandwidth through parallel processing of fuel AND must have an antagonist or braking system that is similarly stronger.
Therefore autonomic nervous system strength measured by increased HRV indicates strong central sympathetic drivers and increased central parasympathetic vagal tone that varies with respiration and baroceptor response would show similar strength.  The later would be analogous to pumping the brakes to maintain control on the racetrack.  Increased vagal tone is associated with decreased central TNF alpha, cortisol and increased BDNF.

Additionally, prayer, meditation, yoga, tai chi, Amy Cuddy's power posing for two minutes and two minutes of slow paced breathing as in biofeedback increase vagal tone, BDNF and HRV.  I suspect that vagal nerve stimulators might also brake the redlining brain.

As people age they lose parasympathetic tone (or recovery braking) and may develop network damage from glutaminergic toxicity and the exhaust of TNFalpha and other inflammatory cytokines.  

Brief stress strengthens a system that adapts, hormesis.
Chronic stress weakens and kills a system, all spending and no investment.
There is likely a limit to growth (acceleration and sympathetic tone) and a limit to decline (braking, recovery and parasympathetic tone.)
The body then is like a business that grows within the safe range, fast but not too fast, with stored or accessible reserves of capital to weather a downturn or financial cycle.
Jim Collins books Good to Great and Great By Choice: Uncertainty, Chaos and Luck- Why Some Thrive Despite Them All   are excellent books that examine business like a system such as ourselves.

Better memory through electricity

Friday, March 18, 2016

Network Age based on Heart Rate Variation Index

Table 2 in article below shows the range of HRV for age.  The index is the number between 1-99 reported as HRV. 
 I expect the number of the mean index per decade would correspond to the 50%.
Therefore one could relatively calculate a HRV index age roughly.

Table 2. Aging Effects on 24-h Heart Rate Variability and Heart Rate by Decade
Age (yr)SDNN (ms)SDANN (ms)SDNN Index (ms)rMSSD (ms)pNN50 (%)HR (beats/min)
10–19176 ± 38159 ± 3581 ± 2053 ± 1725 ± 1380 ± 10
20–29153 ± 44137 ± 4372 ± 2243 ± 1918 ± 1379 ± 10
30–39143 ± 32a130 ± 3364 ± 15a35 ± 11a13 ± 9a78 ± 7
40–49132 ± 30a116 ± 31a60 ± 13ab31 ± 11ab10 ± 9a78 ± 7
50–59121 ± 27a106 ± 27a52 ± 15ab25 ± 9ab6 ± 6ab76± 9
60–69121 ± 32a111 ± 31a42 ± 13abcd22 ± 6ab4 ± 5ab77 ± 9
70–79124 ± 22a114 ± 20a43 ± 11abcd24 ± 7ab4 ± 5ab72 ± 9
80–99106 ± 23abc95 ± 24abc37 ± 12abcd

From the above an index score of 77 in a 35 year old corresponds to an 18 year old.
From the above an index score of 64 in a 62 year old corresponds to a 35 year old.

I conjecture that, like lung age, function follows the HRV index age for walking speed, working memory and balance in the aging individual because the brain network speed determines these parameters in other studies.
I further conjecture that network integrity and speed is determined by BDNF levels that protect synapticity, function and integrity of neurons at small scale and memory, mood and metabolism at a larger scale.

Prior studies show that increased IQ processing speed and working memory delays symptoms and signs of dementia.
Other studies show that advanced degrees and lifetime learning also delays symptoms and signs of dementia by building a larger, more robust network.

Dementia or network disconnection syndrome harms smaller and slower networks to levels of symptomatic degradation  sooner than larger or faster networks.
As dementia reflects loss of 2 or more cognitive domains (intelligence, memory, affect, judgement and orientation) and cognitive impairment affects only memory, these are simply later and earlier stages of disconnection syndrome respectfully.

http://www.sciencedirect.com/science/article/pii/S0735109797005548


Joseph Thomas (Tony) Liverman,

Saturday, March 5, 2016

Melatonin in the Morning and More Melatonin in the Evening is the Fountain of Health and Youth

Great article with old and new insights about melatonin which is more than a nighttime hormone related to sleep. It is a metabolic regulator essential to reduce inflamaging or aging.  Melatonin production declines with age unless optimized with diet, exercise, lifestyle and supplementation.

To wit., more melatonin is produced in the gut (and locally used or consumed) than the pineal gland!
And melatonin stimulates repair of pancreatic tissue and by extension other tissue with regeneration potential. Especially note the improvement in bone marrow cell lineage.  It is widely noted that immune function is either over expressed or under expressed in the aged leading to collateral tissue damage or increased vulnerability to inflammatory diseases or infections.

Two gut enzymes are responsible for producing more melatonin from dietary or consumed L-tryptophan.  Perhaps everyone who is aging should consume tryptophan rich foods or take a supplement of L-tryptophan to reduce oxygen radicals that accelerate aging.  Particularly relevant to persons with diseases associated with inflammation such as metabolic syndrome and its comorbidities that are often thought of as accelerated aging.

See bolded text below.

For sleep issues,  previous studies  in Japanese children showed sleep improvement with the following: 
tryptophan rich breakfast, 
one hour of bright sunlight before noon, and 
Blue blocking sunglasses at night to reduce inhibition of melatonin production during the dark photoperiod.

Based on the evidence below regarding daytime gut production of locally used and locally consumed melatonin at low tissue levels of 5-10 and the pulsed brain levels during darkness of 150 the following conjecture:

Gut produced melatonin protects the soma or bodily production of oxygen radicals related to normal mitochondrial and digestive functions during the day and that nighttime pulses during rest allows the melatonin to optimize the tissue regenerative effect during restorative sleep.

Levels of 5-10 turn down the metabolic stove from burning hot to simmer, and levels of 150 during nighttime rest and sleep turns the stove almost off to maximize healing and recharging of enzymatic antioxidant systems within all cells.

Note that daytime melatonin turns off TNF alpha and other inflammatory cytokines and elevates Il-10 a marker of reduced inflammation!

The full article is available at the link below.

Protective Effect of Melatonin on Acute Pancreatitis

Abstract

Melatonin, a product of the pineal gland, is released from the gut mucosa in response to food ingestion. Specific receptors for melatonin have been detected in many gastrointestinal tissues including the pancreas. Melatonin as well as its precursor, L-tryptophan, attenuates the severity of acute pancreatitis and protects the pancreatic tissue from the damage caused by acute inflammation. The beneficial effect of melatonin on acute pancreatitis, which has been reported in many experimental studies and supported by clinical observations, is related to: (1) enhancement of antioxidant defense of the pancreatic tissue, through direct scavenging of toxic radical oxygen (ROS) and nitrogen (RNS) species, (2) preservation of the activity of antioxidant enzymes; such as superoxide dismutase (SOD), catalase (CAT), or glutathione peroxidase (GPx), (3) the decline of pro-inflammatory cytokine tumor necrosis α (TNFα) production, accompanied by stimulation of an anti-inflammatory IL-10, (4) improvement of pancreatic blood flow and decrease of neutrophil infiltration, (5) reduction of apoptosis and necrosis in the inflamed pancreatic tissue, (6) increased production of chaperon protein (HSP60), and (7) promotion of regenerative process in the pancreas. Conclusion. Endogenous melatonin produced from L-tryptophan could be one of the native mechanisms protecting the pancreas from acute damage and accelerating regeneration of this gland. The beneficial effects of melatonin shown in experimental studies suggest that melatonin ought to be employed in the clinical trials as a supportive therapy in acute pancreatitis and could be used in people at high risk for acute pancreatitis to prevent the development of pancreatic inflammation.

Friday, March 4, 2016

Reducing Inflammation to Controlled Hormetic Challenges Shifts Inflamaging to Living

Inflammation control, not telomere length, is the key to long life.  Uninflamed or inactivated white blood cells with reduced innate immunity markers have longer telomeres in old age.  This is analogous to a retirement capital account that yields 4% and lasts seemingly forever.  Greater spending or inflammation shortens telomere length and the life of the account and account holder.

Melatonin, DHA, Slow paced breathing, Vitamin D3, Vitamin K2, increased BDNF and HRV, Klotho   Gene expression and improved parasympathetic braking  tone altogether contribute to decreased markers of inflammation.

CRP, brain cortisol, TNF alpha, Cox2, Il-6  are a few predictive inflammatory markers that decline with healthy lifestyle, supplements and diet.  I suspect that because HRV heart rate variation declines with age, inflamaging and mortality, then higher HRV indicates a reduced global inflammatory status.  Even the daily variation in high and low frequency bands within HRV associated with component sympathetic and parasympathetic tone respectfully would indicate that stresses such as exercise, fasting and illness all produce hormetic or recovery boosting stress in a stress and recover stronger and younger paradigm.