Light Energy Increases Cell Energy; and Cell Production Efficiency

Light Energy Increases Cell Energy; and Cell Energy Production Efficiency.

ATP is the currency of cellular energy in man and animals.  Death of microbes (single celled organisms) can be confirmed by the absence of ATP which is transiently made to power the cell.  It is like the "manna from heaven" in that it provides energy sustenance transiently because it so readily discharges the energy to make heat or heat and  cellular activity.  90% of the oxygen used by the body is consumed by mitochondria, the cellular energy factory, in making and storing energy in the phosphate bonds of ATP and ADP.  The predominant source of that energy is the sun transferred to our planet as light energy.  It warms the earth with heat and provides the source of energy for plant photosynthesis.  All animals consume plants on earth or plankton in the ocean.  Energy from the sun directly from plants or indirectly from animals that eat only plants.  For warm blooded man, sunlight = warm environment + ATP.

Does light energize the cell directly?  Yes, but only in small amounts.

The red and near infrared frequency are absorbed by cytochrome c in the mitochondria and absorb the energy as an electron and send the power to make ATP through the electron chain transport system that makes power or ATP for the cell.

How is this useful?  It is useful in the same way that heater strips are useful in heat pumps.  When the mitochondria becomes degraded and inefficient, light energy is the most efficient way to make ATP, just as heater strips make energy more efficient because the available temperature gradient is narrow.

In effect, aging inefficient mitochondria cannot make enough energy to refurbish and improve cellular functions to fight aging, senescence and cell death.  Light therapy empowers the cell to heal and regenerate!

What evidence is there for light regeneration of cell, organs and organisms?

Rabbits underwent posterior knee deconstructive surgery damaging ligaments and  cartilage.  The post-op knees were treated with sham light and red near infrared light separately.  The sham light treated knees were damaged after healing.  The red near infrared light knees were not damaged after healing.

Knees treated with red near infrared light checked before and after treatment have reductions in synovial fluid inflammatory markers including COX2, TNF alpha and IL-6 levels.  These are the targets for inflammatory treatments NSAID such as ibuprofen and TNF blockers such as Humira used in rheumatoid arthritis.

In rodents who have their bilateral sciatic nerves interrupted by removing a short length of the nerve but connecting the two ends by placing them in a sheath treated with and without red near infrared light; greater healing and less oxidation radicals occurred within the sheath of light treated side.

In cell culture, red near infrared treated cells have shifted ADP/ATP ratios indicating greater production of ATP.

The Willow Curve is a commercially available red near infrared laser treatment of knees, hips and shoulders with endorsements of pain relief and improved function that resulted in delay of scheduled surgical joint replacement.

Red LED light has successfully treated acne with and without blue wavelength light to disrupt the bacteria responsible for acne.

There are an abundance of LED devices.  Examples include the LED devices sold by Elixa.com.  These have single or double arrays.  I use the dual array of red near infrared 120 array device that delivers 1J/CM2/Min.  Published treatments of joints used 10-22 joules of energy daily.  Published treatments of cells in culture used 2-10 joules of energy.  Therefore I would use red only 2-10 Joules for skin or superficial structures (protecting or shielding the eyes and thyroid) and use red near infrared 10-22 Joules in two divided doses for joints or deeper structures.

One could use adjunctive light treatments for joint pain, wound healing, inflammatory acne and neuropathy.

Moreover, there is research on local light treatment and distal effects, a so called abscompal effect.  In traumatic brain injury animal subjects treating the normal side of the brain improved the opposite untreated sided.  In two genetic rodent models of Alzheimer's disease, treatment of the lower leg with 22 joules of red near infrared light resulted in prevention and delayed onset of dementia.  In another animal model of drug induced Parkinson's disease leg treatment with 22 joules of red near infrared light prevented Parkinson's disease.

Could one prevent or delay neurodegenerative disease with light treatment of the tibia the lower leg bone?  The distant tissue improvement was the result of activating adult mesenchymal stem cells in bone marrow.  When activated or energized, the stem cells migrate to tissue secreting inflammatory cytokines ie. brain tissue.  They remain stem cells and do not make new brain cells.  They message or increase local  healing growth factors to do the protecting or healing.

Intermittent Fasting Reduces Aging; and Systemic Sclerosis?

Intermittent fasting reduces aging;  and systemic sclerosis!  See commentary and article below.

If systemic sclerosis is both autoimmune and innate immunity related and the macrophage is the bridge between the two systems, INCREASING the macrophage's ability to phagocytosis or eat and destroy superfluous inflammatory inciters in their cytoplasm would regulate or re-regulate the inflammation of both systems!

Aging also degrades macrophage through reduced AUTOPHAGY leading to reduced protective function and increased degenerative function. 

One activity known to increase phagocytosis is INTERMITTENT FASTING or fasting once a week for 23-24 hours.  Restricting  carbohydrate and protein, but not fat, is required because the action of gene switching follows lowering of insulin and insulin growth factor 1.  I have performed weekly fasting for over 2 years.  On fasting days I substitute modified bulletproof coffee (containing coconut oil) i.e. coffee without glucose or protein, (stevia, heavy cream and 30 mls of MCT or coconut oil) for the 2 missed meals and snacks.  This provides beta hydroxybutyrate for brain energy needs that supplements stored glucose release from the liver.  This brief fasting turns on genes of longevity and regeneration, increases helper proteins called chaperones to correct misfolded proteins such as enzymes and lastly takes any superfluous trash or misfolded proteins and loose mRNA and recycles them through PHAGOCYTOSIS into usable elements that are harmless and not able to incite the inflamasome and degrade the macrophage cell purpose.

Increased PHAGOCYTOSIS is the opposite of reduced AUTOPHAGY ; improvement preserves the function of macrophages despite age, disease or disorder.  See abstract below.

Innate immune system involves toll like receptors and the inflamasome and is generally considered a form of individual cell immunity.  Adaptive immunity is the immune system to protect the organism such as antibodies and cellular immunity of macrophages and T lymphocytes.

Tony Liverman

http://www.karger.com/Article/Abstract/370112

Abstract

Macrophages provide a bridge linking innate and adaptive immunity. An increased frequency of macrophages and other myeloid cells paired with excessive cytokine production is commonly seen in the aging immune system, known as ‘inflamm-aging'. It is presently unclear how healthy macrophages are maintained throughout life and what connects inflammation with myeloid dysfunction during aging. Autophagy, an intracellular degradation mechanism, has known links with aging and lifespan extension. Here, we show for the first time that autophagy regulates the acquisition of major aging features in macrophages. In the absence of the essential autophagy gene Atg7, macrophage populations are increased and key functions such as phagocytosis and nitrite burst are reduced, while the inflammatory cytokine response is significantly increased - a phenotype also observed in aged macrophages. Furthermore, reduced autophagy decreases surface antigen expression and skews macrophage metabolism toward glycolysis. We show that macrophages from aged mice exhibit significantly reduced autophagic flux compared to young mice. These data demonstrate that autophagy plays a critical role in the maintenance of macrophage homeostasis and function, regulating inflammation and metabolism and thereby preventing immunosenescence. Thus, autophagy modulation may prevent excess inflammation and preserve macrophage function during aging, improving immune responses and reducing the morbidity and mortality associated with inflamm-aging.
© 2015 S. Karger AG, Basel

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Article / Publication Details

Received: 6/13/2014 8:13:00 PM
Accepted: 11/25/2014
Published online: 3/10/2015
Issue release date: June 2015
Number of Print Pages: 17
Number of Figures: 6
Number of Tables: 2
ISSN: 1662-811X (Print)
eISSN: 1662-8128 (Online)
For additional information: http://www.karger.com/JIN

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Open Access License / Drug Dosage / Disclaimer

Open Access License: This is an Open Access article licensed under the terms of the Creative Commons Attribution 3.0 Unported license (CC BY 3.0) (www.karger.com/OA-license-WT), applicable to the online version of the article only.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

Mind Body Age = Cellular Energy + Regenerative Gene Expression6 - Degenerative Inflammation Activation

Energy + Regenerative Gene Expression - Degenerative Inflammation Activation = Metabolic Resilience OR Organism/Organ/Cell Age

Read first the conclusion of the paper linked below.

http://onlinelibrary.wiley.com/doi/10.1111/imr.12295/pdf

The conclusion wrongly implicates obesity and not macrophage and micro glia (brain macrophage) activation or cellular innate immunity activation as the culprit in degeneration even though they showed evidence that calorie restriction and intermittent fasting blocked the activation of inflammatory macrophages ( whether fat or not, young or old.)  They also showed that NLRP3 knock out mice did not get age related inflamaging.

The evidence herein shows how BHB beta hydroxybutyrate from calorie restriction and/or coconut oil inhibits activation of damaging macrophages and microglia which prevents organ damage in the body and brain respectfully. 

Moreover, intermittent weekly fasting reduced many of the age related inciters of the innate immune system or inflamasome, through auto phagocytosis of waste in lysozymes rendering the molecules unable in their reduced elements to incite NLRP3, thereby prolonging quality of life and length of life.  This occurs at the beginning of a prolonged fast which has three actions, make essential proteins, activate cellular chaperones or folding helper proteins to correctly fold misfolded proteins and recycling of persistently misfolded proteins in lysosomes or chemical bags that convert molecules into elements for recycling.

The article more than hints that both "disease and conditions" are improved by blocking the inflamasome  of which NLRP3 is the initiator.  Moreover it also implicated crystals and clearing of crystals as important whether they be cholesterol, Uric acid or beta amyloid crystals in preserving cell, organ and organism integrity.  

The section on Vitamin D was also revealing as an agent to modify inflammatory response in all tissues and not just in bone osteoclasts.  The combination of vitamin D3 and K2 removes calcium crystals from atheromatous plaques thereby blocking the NLRP3 activation leading to atherosclerosis, ruptured plaques and/or aneurysmal rupture.

http://onlinelibrary.wiley.com/doi/10.1111/imr.12295/pdf

Alzheimer's Review Article Prescription for Action.

Brain metabolic health and Body metabolic health are linked through shared metabolism, inflammation and repair pathways.  

Therefore improving the metabolism of the body or brain helps both.  

Inhibiting the inflamasome cascade helps both brain and body.  

Promoting the repair and longevity gene expression in brain and body cells builds resilience for both.  

What would supply evidence of increased physical resilience?

A body with increased aerobic capacity for exercise?

A body with increased lean body mass?

A body that metabolizes fat into ketones after an overnight 10 hour fast?

Increased beat to beat heart rate variability?

More good HDL cholesterol?

Less bad LDL cholesterol?

LDL cholesterol particles that are larger, with lower particle count and hence are less atherogenic?

Increased BDNF, GDNF and NGF?

Increased insulin sensitivity?

Increased sympathetic, parasympathetic tone?

Increased subcortical and cortical brain speed for auditory and visual processing speed?

ALL the above RESULT FROM THE FOLLOWING PRESCRIPTION that increases BDNF.

1. Mediterranean diet with supplemental MCT and coconut oil. 30 ml once daily for low dose and up to 4 doses daily for high dose.

2.  HIIE 4 minutes daily 5 or more days per week.  Resistance training once per week (low dose) or 3-5 times per week (high dose)

3.  Brain training up to 40 hours or 90 percentile.  Note that subcortical sensory processing is the most improved part of the brain, the automatic non thinking part of responding to brain exercises. Alzheimer's is believed to begin in the brain stem and degrade noradrenergic neurons antegrade to the higher cortex.

4.  2 minutes of slow paced breathing 5 secs in and 5 secs out for two minutes twice daily.

5.  VLS#3 a commercial probiotic has recently been shown in mice to reduce inflammation in the brain by its effect on modulating the gut-brain axis and increasing BDNF either directly or indirectly by inhibiting micro glia action in the brain.  These bacteria may increase short chained fatty acids in the gut from unrestricted starch such as the fiber of nuts.

Alzheimer's Review Article Summarized

Alzheimer's has a decade long phase of Glucose hypo-metabolism (reduced metabolism) in the brain. Ketone body (a special derivative of fat) metabolism remains unaffected and intact. 

Sub cortical (the root level, reactive non-thinking base of the brain) damage precedes  Alzheimer's. 

Beta-amyloid protein (an abnormal cell waste product) is toxic.

Micro glia (immune function cells in the brain) inflame and degrade neurons (nerve cells) and astrocytes (nerve support cells.)

Impaired astrocyte function degrades cognitive function from damaged energy metabolism for the neuron (nerve cell) and decreased inhibition of micro glia action to destroy nerve cells and their connections. 

Mitochondrial DNA is inherited from the mother in humans. 

Glucose hypometabolism (inability to use glucose for energy) is more severe with 2 demented parents, intermediate with only demented mother and least with only demented father. 

Glucose hypometabolism leads to less hexokinasei (an enzyme used in glucose metabolism) binding of mitochondrial anion channels (energy requiring revolving door of the mitochondrial wall) which prevents escape of untreated and damaging ROS (reactive oxygen species analogous to rust particles). More cellular ROS activates oxidative stress (rust) and inflamasomes (chemical committee or molecule that degrades cells). Beta-amyloid in the mitochondria increases ROS production that can escape from the mitochondria into the cell and cause inflammation. 

APP or amyloid precursor protein is produced by neurons, astrocytes and microglia. The latter 2 can rapidly produce APP when stimulated by neuronal injury. 

When cleaved (separated into 2 parts) to an active form by alpha secretase (enzyme= protein that alters another protein), it is soluble and neuroprotective (useful during development)

When alternatively cleaved by beta secretase (an enzyme) it is soluble but not neuroprotective. Further action by gamma secretase (enzyme) makes soluble beta amyloid and a generator of ROS and inflamasone activation. With increasing and concentrated amounts, beta amyloid precipitates in cells and forms non-soluble aggregates. 

Dementia correlates best with soluble Beta amyloid which is the toxic form. The precipitates and plaques of beta amyloid are only non-soluble residues of the invisible soluble toxins that have already damaged the cell and brain. (Analogous to radioactive precipitates or aggregates after a nuclear blast, the damage is done and only the contamination remains)

This leads to oxidative stress, release of stimulating glutamate (a brain chemical that 

activates, energizes or over energizes) which causes extra synaptic NMDA receptor 

activation and synaptic loss. (Analogous to a power surge that damages the function)

The  damage by soluble beta amyloid (which blocks glucose uptake, oxygen uptake and astrocytes mitochondrial depolarization producing a dead battery/mitochondria) is blocked or prevented by addition of pyruvate, the end product of glucose metabolism in the cell outside of the mitochondria which next becomes fuel for the mitochondria. 

Beta hydroxybutyrate, a ketone energy chemical derived from medium chain triglycerides such as coconut oil, also blocked soluble beta amyloid damage.  

Energy supplied, in the form of pyruvate, prevented cognitive decline (synaptic signaling or long term potentiation and synaptic loss) without reducing amyloid precipitates and plaques in a mouse model of Alzheimer's. 

Conjecture:  since a small level of supplemental energy 4mM of beta hydroxybutyrate like pyruvate 5mM inhibits soluble beta amyloid damage; and because beta hydroxybutyrate binds NLRP3 to prevent activation of the inflamasone which leads to cell death;  improved metabolic health represented by ketosis after 10 hour fast, high BDNF levels (which amplifies metabolism and promotes neuroplasticity and repair) plus low glycemic Mediterranean diet supplemented with MCT and Coconut oil (which makes beta hydroxybutyrate and improves cell membrane function and integrity) plus DHA 900 mg (the omega 3 fatty acid in the brain that demonstrably 

improves language acquisition in the young, improves short term memory by 50% in mild cognitive impairment, a precursor of dementia in the elderly and also improves measurable synaptic and phospholipid membrane functions) would treat both 1.the hypometabolic glucose energy deficit in the cell (ketone such as beta hydroxybutyrate for mitochondrial fuel) and 2. Beta hydroxybutyrate blocks NLRP3 and damage from increased ROS (activation of NLRP3) that results from reduced glucose use for energy in the cell fluid leading to expulsion of ROS from mitochondria. 

Dementia may begin in the subcortex (the brain stem or root level of brain below the cortex) first, an antegrade degeneration originating in the brainstem (root) and secondarily affecting the brain cortex (tree)

The brain stem sends noradrenergic (a stimulant chemical) projections to the cortex. The same system responsible for heart rate variability, indirectly; is directly responsible for beta adrenergic receptor (the target of noradrenalin and adrenalin) stimulation that suppresses the activity of inflammatory transcription factors (gene switches in the DNA) causes alterations in nuclear localization of proteins (chaperones that help fold proteins into their optimum shape for action), and induces gene expression via cAMP-response element binding protein activation (creb =an active protein made by DNA with help from chaperone proteins) which are neuroprotective and anti-inflammatory.   1. These creb proteins increase expression of neurotrophic substances including BDNF (brain derived neurotrophic protein),GDNF (glia derived neurotrophic protein) and nerve growth factor. The absence of these factors are 

permissive for dementia. 2.Noradrenergic enhances metabolism. It promotes glycogenolysis the release of glucose from liver and muscle stores.  It also enhances the rate that NAD and cytochrome can increase the production of ATP with increased demand or intensity of movement or cellular work.

Improving BDNF is Improving Metabolic Health

Improving BDNF is Improving Metabolic Health

I recommend a fitness regimen that enhances BDNF, (brain derived neurotrophic factor), which increases brain neuroplasticity and metabolic efficiency peripherally in body cells and centrally in brain cells.

Higher BDNF reduces fatigue. 
Lower BDNF, secondary to aging or insults, increases fatigue. 
BDNF is increased by High intensity exercise, resistance training, deep breathing involving the diaphragm and vagal nerve and brain training.
Therefore I recommend the following:

4 minutes of high-intensity Tabata intervals e.g. Timer app for iPhone performed on exercise bike 5 or more days per week. Other exercises can substitute, sprinting, jumping.

2 minutes twice daily of slow paced breathing, 5 secs in 5 secs out, preferably belly inhalation and slow forceful chest exhalation using a power pose as in video below. Maximum movement out of diaphragm while breathing in and maximal movement of sternum in on breathing out.

Brain training at BrainHQ.com 20 minutes daily up to 40 total hours. 

All 3 training exercises above increase BDNF, heart rate variability and stamina; which increases RESILIENCE of physical, mental and emotional domains. 

Bonus weekly resistance exercise to improve and reduce Sarcopenia or lean muscle loss mentioned previously on this blog.

My conjecture about the difference in power and submissive posing effects on testosterone and cortisol is related to differences in breathing i.e. Slow diaphragmatic versus fast chest breathing. The former stimulates vagal  tone, the latter stimulates sympathetic tone. The former decreases Il-6, a blood marker of inflammation cascade activation; the latter increases Il-6 especially hyperventilation. 

https://m.youtube.com/watch?v=Ks-_Mh1QhMc

Preventing Cognitive Decline

Mild cognitive impairment improvement plan with goal of reversing the strong probability of future dementia.

WHAT:

1.  DHA alga 900 mgs two capsules daily.  

2.  L-methylfolate 10 mgs daily. 

3.  Methylcobalamin 5,000 mcgs sublingually daily.  

4.  B100 complex vitamin daily.  

5.  Liquid coconut oil and MCT oil.  Mix 15 ml or 20 ml of each for 30 -40 ml total in chocolate mousse or other and consume 4 times daily.

6.  BrainHQ.com brain training daily to achieve 90% or 40 hours total.

7.  Melatonin 3 mgs two hours before bedtime.

8.  One hour of bright light every morning before noon.

WHY:

1.  Studies show DHA 900 mgs improved short-term memory 50% over eight weeks. This is also important for developing and preserving synaptic connections.

2.  L-methylfolate is required to maximally produce and preserve neurotransmitters that keep the brain healthy. Specifically serotonin, norepinephrine, Dopa and GABA.  

3.  Methylcobalamin is the active form of the B12 vitamin and the oral mucosa can absorb a small amount every day that is useful in repairing the brain and nervous tissue along with the l-methylfolate.

4.  B100 complex vitamins assure there is an adequate supply of the vitamins necessary to transport the other vitamins actively across the blood brain barrier and also provides the precursors for energy producing NADH.

5.  This combination of coconut oil and it's derivative supplies adequate ketones for the cells of the brain that are unable to use glucose, the normal substrate for energy used by the brain.

http://aanddjournal.net/article/S1552-5260(14)01112-1/abstract

http://www.youtube.com/watch?v=I3UfgQ9vkr0

6.  Daily brain exercises increases the speed of seeing and hearing and improves short-term memory significantly. The following book explains this in more detail.

http://www.amazon.com/Soft-Wired-Science-Brain-Plasticity-Change-ebook/dp/B00EB48ZDU/ref=sr_1_sc_1?s=digital-text&ie=UTF8&qid=1425331259&sr=1-1-spell&keywords=Michael+mezernich

7 and 8.  Sleep is vitally important for a person having abnormal alpha beta amyloid protein deposition in the brain associated with dementia. It is during high quality sleep that the cerebrospinal fluid rinses out the toxins produced in the brain.  One hour of bright light using the visor before noon and the melatonin supplement to initiate sleep at the proper time. Melatonin is also a first rate antioxidant.

http://www.npr.org/blogs/health/2013/10/18/236211811/brains-sweep-themselves-clean-of-toxins-during-sleep