ORGANIZATIONAL STRUCTURAL FAILURE #7: FAILURE OF AUTOPHAGY

Technology implications for infants and children:

The FIAF is made by our microbiome, our liver, muscles, and our small bowel wall and when food sources (think electrons and protons) are in short supply. This means we must ‘sense’ a paucity of electrons and protons across the entire gut system to create FIAF and subcutaneous fat that is common to our species to finish brain growth.  We know human evolution occurred in the East African rift zone and food from the ocean was plentiful.  This created a problem for the ancestral primate gut.  It changed because the environment around the primates changed as I laid out in Brain gut 3, 4, and 5.

FIAF builds the sub cutaneous fat mass in infant humans. FIAF grows subcutaneous fat when their is a scarcity signal from the vagus nerve in the gut.  This implies that the gut microbiota has to take a lot of the protons in food for themselves. This is also why the human gut shortened from primates.  When it shortened it created an ecologic island within the small bowel and in the colon.  Island bio-geography is a field within bio-geography that examines the factors that affect the species richness of isolated natural communities.  The field was started in the 1960s by the ecologists Robert MacArthur and E.O. Wilson,  as this theory predicts the number of species that would exist on a newly created island.  It turns out that when things are more isolated it fosters species diversity.  This is why the gut shortened before the mammalian body changed from primates to humans.  This is why bipedalism showed up in the skeleton of our species before the brain grew.

When this happened it fostered diversity and speciation in an oxygen free zone to pull protons from the marine food chain and left behind the electrons for us to absorb.  Limiting oxygen in the gut made the gut environment anaerobic and this allows us to recycle the carbon backbone in food stuffs.  This recycling effect lowers our energy costs for the ubiquination pathways which replace carbon backbones in proteins.

Anaerobic digestion within our gut saves carbon emissions twice over, by preventing the serious methane and nitrous oxide gases from reaching critical production within the lumen of our guts.  This ability is lost in people with SIBO or GERD, where molecular oxygen does get into the gut lumen and causes us to lose carbon recycling.  This has a huge energy cost to our GI tract.  This is another way we lose energy within this system to cause disease.  Another way for oxygen to enter the gut enterocytes is when DHA is lost in the gut lining’s cell membranes.  When this occurs it causes the cells to swell releasing zonulin into the lumen of the gut making it leaky.  This is how leaky gut can begin.  In the blood plasma, zonulin causes hemoglobin and free iron to be released from red blood cells into the lumen and into the gut cells themselves.  This has a chilling effect of the gut’s ability to function.  This effect causes oxygen, hemoglobin, and free iron to be released within the gut.  This causes the formation of haptoglobin which is an acute phase oxidant that lowers the redox state in the gut lining.   Note that this mechanism does not require any grains to be present.  All it requires is a lack of DHA in the gut cell membranes to occur.  Fixing a leaky gut should always have a DHA solution as part of its evolutionary Rx.  Very few see this mechanism.

 

The actions of limiting O₂ in our gut and shortening it had huge implication on the development of FIAF.  When the gut shortened,  it helped craft a strong FIAF signal to develop  the very unique subcutaneous fat mass human babies have to support post natal brain growth.

Our teeth are very different from other primates as well and do not allow us to chew as well even as adults. Babies have no teeth at birth.  In fact, children also have a primary dentition that really are underdeveloped that inhabit our mouth from age one to age six.  This is during the major post natal brain growth spurt and when major white mater tracts are being myelinated………

HAVE YOU EVER WONDER WHY  we humans  set of teeth from age 1-6??  Maybe now you can guess why we do.  The neocortex is extremely plastic from birth through 6 years old and then it becomes less plastic at its surface after 6 years old.  This is why before age  6, language acquisition in humans can still have the natural accents included in the speech.  After that age, the learning of a foreign language will not contain the native accents.

The human primary dentition is quite different than our adult teeth.  They look even more like a herbivore to generate more FIAF to develop the brain by decreasing our ability to chew our food.  It also explains why human children universally do not like vegetables but love protein and fat to deliver the best electron substrate to the microbiome to make FIAF.  That is because their growing brain is craving what it needs to mature.  Our social and cultural beliefs subjugate their quantum needs and desires.  When a small human eats fat and protein with a small set of poorly designed teeth more large undigested fragments of food gets delivered to a complex microbiome.  This is the perfect storm to make subcutaneous fat for brain growth by fostering growth of the perfect type of microbiota in our gut.  This brain growth continues until 25 years old in humans when the brain fully myelinates in the frontal lobes.

This ketogenic template in children has another big brain development factor few talk about.  During  ketosis, the hormonal status  in children  should be a high glucagon/insulin ratio, in combination with hypoglycemia.  This  promotes excessive lipid mobilization from the child’s subcutaneous fat to mature the brain.  It also creates a  greater hepatic removal of fatty acids and switches the liver to a higher rate of ketogenesis for active myelination of the brain.  Glucagon is a hormone that enhances macroautophagy,  especially in younger mammals.  This ability is lost in older mammals.  It is believed a fetal protein called REST mediates this autophagy effect.  REST is a regulator that switches off certain genes, is primarily known to keep younger neurons in an immature state until they develop to perform brain functions under the direction of melatonin and BDNF.  REST protein changes are firmly tied to neuro-degeneration risk’s.  Both of these hormones are destroyed by blue light in the brain as well.  In older people with Alzheimer’s and other dementias, the REST protein is sharply depleted in key brain regions.  This links blue light toxicity to neuro-degeneration.  This alters their ability to clear mis-folded proteins in neurons.  This alters the brain’s optics and thermodynamics.

Because glucagon is normally high in sleep, fasting, and ketotic states,  it also augments autophaphy during these times to construct and organize Hebbian circuitry in the brain as it matures.  Young humans need to sleep more to grow their brains.  Autophagy is critical in growing and maintaining the neocortex size of humans.  The quality of their sleep is also critical because it maximizes autophagy and does not deplete our stem cells in the recycling process.  The more efficient autophagy is the more you protect your stem cell supply and the longer you can live.  Autophagic efficiency is linked directly to energy mass equivalence.  The more electrons you have in your brain the more autographic efficiency you will have.  All cells created in the young humans brain are newly minted post mitotic cells.  Autophagy augments longevity in all post mitotic cells in 5 ways:

The 5 cytoprotective effects of autophagy:

1. Reduced accumulation of toxic protein aggregates or misfolded proteins
2. Destroying bad mitochondria via mitophagy
3. Reduced apoptosis to prevent stem cell depletion
4. Reduced necrosis
5. Improved hormesis by increasing the redox stickiness of semiconductors made of collagen and water.

This is why children sleep more than adults and why it is why autophagic efficiency is higher in younger mammals with a better redox potential.  Many people report poor sleep with ketosis and this is tied to the type of ketosis they employ.  This will be covered in OSF #8.  Contrary to modern belief’s not all ketotic templates are equivalent thermodynamically.  It also points out how fasting, sleep, ketosis, and autophagy all couple together to add in healthy development and exceptional longevity in the human neocortex.  DHA content in your cell membranes increase your ability to engage autophagy.

POOR MASTICATION AND IMMATURE TEETH ARE ADVANTAGOUS

When children chew a ketogenic template less well because of their immature dentition, this delivers more unprocessed food to this diverse microbiome in our shorter gut,  which makes things for us that drive organ health in many places to continue to under process food for the growing brain to provide it with a massive influx of electrons and not PROTONS.  PROTONS are for the expansion of gut bugs when O₂ is not present in the lumen of the intestines.   The protons provide energy and information to help develop other human organ systems using the power of our gut bugs as leverage.  It turns out simple life forms can handle protons better than complex life forms can.  They developed on Earth when oxygen was rare.  We developed when oxygen was present.  This is why we recruited them in our gut when no oxygen was available.

As the various bacterial cells  and human gut cells are colluding, they are likely trading energy and  information using subatomic particles as their language with cells in another realm.  The quantum realm using entanglement, spintronics, and protonicity within the exclusion zone (EZ) of water.  The micro-organisms in the mouth, skin, respiratory system, urogenital tract, stomach and digestive system all play distinctive roles with their host. Each microbe has its own set of genes, which can interact with those in the human body by exchanging quantum and molecular signals to direct molecular actions of tissues within us.

The signaling these microbes do is complex and this makes the process ideally suited for a quantum mechanism.  They send metabolic signals to each other; and they are sending chemicals and electromagnetic signals out constantly that are stimulating our biological processes.  That process is called quorum sensing.

People in different geographical locales and “zip codes” can harbor different microbial ecosystems.  This can happen within the same house hold.  In 2010, scientists reported evidence that the Japanese microbiome has acquired a gene for a seaweed-digesting enzyme from a marine bacterium.  The gene is not found in the guts of North Americans, and may aid in the digestion of Nori seaweed wrappers.

Modern diets consist of processed foods that are made of fake fats, altered protein and simple starch, all of which are digested and absorbed before reaching the colon. These simplified foods produce a simple and less diverse gut flora that may also produce more colonization factor antigens (CFA) rather than feces forming gut bacteria.

The underpinning thought here is when you are human: you are designed to isolate your microbiome by shortening your gut for the species development which fosters a complex flora.   Poor mastication of your diet facilitates this process by developing a more diverse gut flora.  This was the first key environmental change that crafted humans before they became encephalized primates.  Chimp dentition and gut anatomy are radically altered compared to humans.  Remember we have 98.9 % identical genes.  These anatomic differences crafted by compliant design changes meant we did not have to utilize the genome to craft these changes.  It implies you can only do this well when the food sources come with a dense source of electrons consistently that shape protein changes to get the desired result quickly.  The dense diverse speciation in human microbiota needs protons from these organisms to do its job.

MODERN MISMATCHES

The modern diet breaks this evolutionary design.  Electrons are what the marine food chain provides densely.   DHA is the only lipid that can capture electrons well from our diet.  You first have to capture electrons in your cell membranes before you can assimilate or use them properly.  This is why human evolution began in the East African rift adjacent to the ocean.  The electron is a nearly massless subatomic particle that can carry various amounts of energy and information at a low thermodynamic cost,  compared to a proton.  Protons have mass (1900 times more than an electron), and as such makes them less energy efficient.  The fact that a proton has mass,  limits it ability to carry more energy or information than an electron or photon.  This is why mitochondria organized around moving electrons and photons on its membranes to reduce oxygen to liberate even more electrons for a complex system to use.  Protons are used by Archea and Prokaryotes.  Eukaryotes use electrons exquisitely in their mitochondria and cell membranes.  When you move away from electrons illness just follows you.

The photoelectric effect can raise or lower the energy and information within electrons.  Protons do not have this ability.  This is why humans have built their most complex systems, namely the brain and immune system, around electron collection and not protons.   Protons are used to signal things within cells.  Protons are the subatomic mitochondrial signals that reproduce what the present environmental conditions are for cells to read and react too.  Mitochondria decipher these signals and send that information through the collagen cytoskeleton to all other cells using the piezoelectric signals within collagen when it is deformed by compression due to a volume change in mitochondria.  These signals direct cellular homeostasis everywhere in the cell.  The signals are all coherent within a cell.  These signals even tell the cytochromes how to process foods to electrons.  The food electrons are funneled in cytochrome 1 or 2 based upon their energy content, information, and spin of the electron.  This is how a mitochondria deciphers what season it is,  in our environment.  It samples the data in photons and electrons from foods to generate the correct answer for mitochondria.

The other cytochromes are used to signal the “change programs” in mitochondria, namely autophagy and apoptosis,  by opening a pore in the mitochondrial membrane to increase or decrease mitochondrial size and volume.  Apoptosis removes cells and mitochondria directly by cell suicide programs.  Apoptosis also uses a compliant design mechanism to work by altering protein shape and size.  Autophagy is the only way to remove our older broken down mitochondrial engines and recycle them,  as I mentioned above.   Autophagy is the best way to get rid of bad mitochondria without killing the cell.  This process is called “mitophagy.” Since bad mitochondria produce most of the “supra-hormetic doses of ROS and RNS”, this is quite important.

This is why the developing brain and healthy brain seek  ketones for their fuel source for maturation from our subcutaneous fat. Ketones shrink mitochondrial size and select for autographic efficiency to build and maintain a healthy brain.

Contrast this with the sick human brain:  People with T2D,ME/CFS, AD,PD generally generate excessive amounts of superoxide in the brain as the cause of their disease because they eat too much sugar; doing so does not allow them to make a lot of ATP (38 vs 147) and not being able to make a lot of ATP, is why they crave carbs to fast recycle ATP as I mentioned in EMF 4. They can not make ketones well because high insulin levels block ketone production in the liver. It also lowers glucagon.  This destroys autophagy.  One of autophagy’s main goals is to clear unfolded or misfolded proteins marked for clearance by the ubiquitin system.  When autophagy is impaired these misfolded proteins remain in neurons and are not cleared.

When this happens,  superoxide rises……….a lot.

Neurons in the developing brain try to avoid superoxide generation at all costs.  Neurons usually attempt to increase lactate production as a result to offset superoxide generation to use lactate as a secondary fuel source to ketones.  CSF lactate is a signal.  This signal is sent through the CSF and into the circumventricular organs to get to the hypothalamus. This is where the leptin receptor senses the redox potential in neurons things from our environment.  This signal is destroyed by a lack of DHA in the cell membranes in these neurons and by the local redox changes in these cells.  This redox signal alters the 4 channel proteins in the leptin receptor to vary its physiologic functions.  Excess baseline ROS /RNS from poorly functioning mitochondria induces many different mitophagy programs directly via other signals.  Telomere shortening and redox imbalance have been related to the aging process.  I will cover this later in the series.  The mechanism is the same but the trigger of the mechanism is very varied with respect to autophagy.  

NORMAL BRAIN = NORMAL AUTOPHAGY

For post mitotic cells like brain cells, heart cells, and most other cells that we all want to “hang on to”, mitophagy is probably the most important anti-aging benefit within autophagy.  This is how we replace bad mitochondria them without losing them permanently.  Older, damaged,  and poor working mitochondria are phosphorylated by the kinase called  PINK1.  Then these bad mitochondria are marked for death and ubiquinated by the E3 ligase Parkin.  The ubiquinated “poor functioning mitochondria” are then selectively destroyed by mitophagy, which is a form of macroautophagy.

All bad mitochondria are tagged for removal,  by their cell volumes and size how many protons they contain and few electrons they process.  This is what makes up their redox potential.  A poorly functioning mitochondria has a poor redox potential and will leak a lot of lactate into the CSF.  The redox potential is buried in the ratio of electrons to protons produced by this mitochondria and it is transmitted in the CSF.  When there are more protons in CSF to electrons the brain swells.  When a cell/mitochondria swell,  it is due to a lack of electrons to protons, and this is the signal we begin the process.  Leptin resistance states are all inflammatory states within the CSF.  When this happens leptin can not enter the Blood Brain Barrier at is receptor site.  This is how leptin resistance fundamentally develops.  A loss of DHA in cell  membranes is always tied to leptin resistance.

HOW DOES KETOSIS REVERSE CIRCADIAN MISMATCHES?

Increased volumes are a sign of a low energy efficiency,  and decreased size is what we see in mitochondria in ketosis.  In fact, a ketogenic diet is a potential technique for clearing out deleterious heteroplasmic mitochondrial sub populations.  This all works based upon Einstein’s mass equivalence equation.  This equation defines the overall thermodynamics of the mitochondrial efficiency.  Dr. Doug Wallace video talks about this here.

Heteroplasmy fosters lower mitochondrial volumes because it drives electrons through cytochrome 2 toward oxygen at the end of electron chain transport,  and this makes us more energy efficient.  It also decreases brain swelling.  This helps to self select these types of mitochondria within a cell to lower mitochondrial swelling, over other ones who use more of cytochrome 1, which favors carbohydrate electrons from food.  Carbohydrate electrons carry different energy, information, and spintronics than electrons from fat or protein.

Carbohydrate electrons from cytochrome one cause the mitochondria to increase in size and volume increases and this decreases mitochondrial energy efficiency further.  To offset the change in energy, the use of carbohydrates allows for a faster recycling of ATP.  I covered this in detail in EMF 4 blogpost.  What should be more eye opening to you is that long lived humans, called centenarians have been found to have high levels of heteroplasmy in their mitochondria.  The more heteroplasmy one exhibits shows more metabolic flexibility is present in your cells.  Heteroplasmy should be built upon a lifetime of seasonal circadian signaling changes, not modern manipulation of your macronutrients based upon your beliefs.

Mitochondria that use cytochrome 1 excessively,  do not have as long lifespans,  as those that use cytochrome two.  This process is controlled by autophagy and apoptosis change programs built into mitochondria in their interaction with the collagen cytoskeleton inside a cell to react to minute changes in mitochondria sizes and volumes.  This is how ketosis helps foster heteroplasmy in  mitochondria in human centenarians.  It has been shown that mitochondria swell in summer and they tend to be smaller in winter in wild animals. Wild animals are forced by life to follow natures design, while modern humans are the only animal that can create its own rules for their environment.  It is also fundamentally why carbohydrates shorten your life if you make them your primary fuel source consistently.  They are designed to be used seasonally in long light cycles only.

It is now clear to anyone without bias that mitochondria are subject to selection pressures within the body directed by the environment they are in.  The same selection pressure also affects the gut flora.  This process is controlled by quorum sensing which is also controlled by the redox chemistry within the gut.  Remember the gut should be anaerobic and lack O₂ by evolutionary design, and as such,  this favors a proton rich environment that gut bacteria do well in.  This creates the signal to make FIAF for the human host benefit.  The electrons left in foodstuffs are then reserved for human use.  Our mitochondria then direct these electrons to certain cytochrome’s for processing.  This implies that mitochondrial cytochromes also work by circadian signaling.  When you understand this process, you begin to see why long lifespans are associated with low gene defects in our mitochondrial DNA lines.

This observation was an initial shock to most obesity researchers’ because they perceived the etiology of obesity as an energy excess state.  One would expect using their current paradigm that excessive ROS/RNS from the mitochondria would lead to more mitochondrial gene defects.  However the observations made in experiment showed they do not accumulate at high rates in obese humans. The defective mitochondria are weeded out by autophagy quickly.  Obesity researchers are still looking at these genes for their answers.  It is a foolish place too look, in my opinion.  The issue is a metabolic redox shift in the mitochondria.

Most research today remains gene centric.  It would appear that defected genes cause all of our diseases and maladies. Gene expression levels are directly tied to covalent modification of biomolecules (by electrons).  This is an example of an electron can alter the biochemical responses that lead to cellular or organelle heterogeneity.  The key point missed in this discussion is that current mitochondrial signaling research is telling biology that the mitochondrial wiring diagram yokes the cell membrane voltage to the inner mitochondrial membrane redox potential.  Both voltages are controlled by electronic induction by electrons on proteins in both places.  This quantum mechanism was discussed at length in OSF 3 blog.

Centenarians tend to have a lot of heteroplasmy within their mitochondria.  This supports looking at the mitochondria and away from the nuclear genes.  This implies heteroplasmy must be good, when you have a basic understanding of this complex quantum event.  Nick Lane has made the key point of differentiation in several recent reviews in the literature that there are tissues where heteroplasmy may in fact, be bad.  For example, cells with high ATP demands, tend to do poorly with heteroplasmy?  Why is that?  It is because water is lacking in these cells for some reason.  He is pointing out,  what I have,  in the EMF 4 blog post.  The answer is found in thermodynamics.

All thermodynamic problems are basically mass equivalence issues at their core.  That last statement is foundational to my Quilt document.  Nothing in life is really a biologic process, they are all quantum thermodynamic ones.  Doug Wallace, an NIH mitochondrial researcher is saying this loud and clear, but biology folks do not understand what he is really implying. Biology does not understand how mass equivalence links directly to cellular bioenergenics yet. Changes in mass and volume of cells are direct energy efficiency signals that trigger metabolic variations in pathogenic steps in cancer, viral infection, or variable drug responsiveness in diseases.

Mitochondria are organized according to the statistical nature of the Second Law of Thermodynamics, and as such, it deals directly with the mass equivalence relationships of energy everywhere in cells.  Since an electron has no mass effectively, it is by far the most favorable sub atomic particle for life to organize around because it carries a small thermodynamic cost.  This is why the human brain can operate on just 20 watts of power. This makes it the choice subatomic particle of the evolution of complex life.  This is also why DHA has never been replaced in 600 million years of eukaryote evolution.  This is why the input to human mitochondria is called electron chain transport.

This is fundamentally why apoptosis and autophagy are directly linked to cell volumes and mass as well. Taking the scale further we can see where changes in mass directly affect longevity because of the effect of mass on time.  In physics, Richard Feynman said that time is a direct function of mass.  Time gains its direction in life because of the redox potential.  The more “electron life” can organize around the longer life will live.  This directly links changes in mass to alterations in telomere lengths of chromosomes in biology.

Ketosis increase telomerase action in cells.  Ketosis also decreases heteroplasmy in tissues as we age allowing us to get more use out of the mitochondria we have by making them more efficient by controlling their size best.  Moreover, this mechanism allows us to recover our mitochondrial DNA protein synthesis.  This occurs because ketosis provides the most dense source of electrons to our mitochondria while lower delta psi.  Since electrons  are the only source of “massless energy”, It would stand to reason why electrons have the most favorable thermodynamic profile of all subatomic particles.

This is why proteins associated directly with cell mass and size are deadly to humans.  For example, consider defects  in the protein laminin.  This defect kills people with a disease called progeria.   CFTR defects cause kids with Cystic Fibrosis to die earlier.  Cells lose the tensegrity of their collagen cytoskeleton and get larger. Anything that gets larger is losing electrons and has more protons.  More protons means a higher atomic mass and mass requires more energy to organize around.  Protons have a mass, and electrons have 1/2000 of their mass. Electrons impart the piezoelectric current present in collagen to limit its size.  So do you still think life is about genes or about electrons and protein thermodynamic changes?

A study in 2004 in Nature Genetics by Alan Wright has shown why the “gene centric’ approach in biology maybe wrong.  He showed that if you could extend lifespan,  you could simultaneously postpone all the disease of aging with an ingenious experiment.  He asked a simple question.  What happens to different animals with different lifespans when you knock out the same nuclear DNA gene?  He looked at Huntington’s, Parkinson’s, and Alzheimer’s disease in this experiment among seven others.  They found a tight correlation between disease progression and the leakiness of the mitochondria in all these diseases.  It was irrespective of the nuclear gene deletion!  It is now clear to us that our old beliefs about nuclear DNA dominance is no longer applicable.  It appears that  disease onset is married to the cellular physiology of longevity built into the mitochondria.  In all degenerative diseases,  it appears cells are lost by apoptosis and mitochondrial leakiness and volume changes are what determines this cellular fate with respect to cytochrome C action.  This was a correlative study and not a causative one,  but the linkage was very tight.  Later in 2004,  another study appeared in Nature,  from the Karolinska Institute that suggested strong causation.  I suggest you read about them in Nick Lane’s book , Power, Sex, and Suicide.  Since that time the it is clear the change in volume,  links directly to mass equivalence and thermodynamics.  No one in medicine or paleo seems to know this.   Moreover, these findings requires no RCT because it is a universal physical law.  E=mc² is the law everywhere.    This is also lost on many researchers.

If an organ has mostly defective mitochondria, the organs function will be suboptimal, but the organ can amplify the least damaged mitochondria for years using autophagy and apoptosis programs. Mitochondrial fusion and fission, together with autophagy, have been proposed and shown to form a quality-maintenance mechanism that facilitates the removal of damaged mitochondria from the cell, a process that is particularly important to forestall aging and organ failure.  This is commonly seen in kidney and heart failure.  Both kidney and heart sizes also increase when they fail.  Interestingly, the human heart fails most commonly by autophagy with diastolic failure.

Mitochondria usually last about 3 weeks in most cell lines.  The choice for mitochondria in life is limited;  divide or die.  In this fashion,  defective power plants are constantly weeded out.  Let me give you an example.  Take a brain neuron.  They usually are as old as we are and are rarely replaced.  Their function does not crash if there is a power plant mutation.  Instead, its function is diminished to a very small degree over time.  The more defective mtDNA is,  the more oxidation will be found in the cell. Oxidation is an electron steal phenomena and this results in an enlargement of the tissue in question.  Oxidation destroys the DHA content in cell membranes.  Blue light is a form of non native EMF and it oxidizes DHA.  When this happens vitamin D and A levels are altered in the nervous system.  When DHA is lost, electrons are lost.  When electrons are lost things swell.  When things swell in a cell it also cause enzymatic fluxes to slow and signaling is altered.  All energy dynamics begin to become inefficient.  

Ironically, this oxidation does not effect energy delivery from the diet, in the cell as we once thought.  Studies have been done in damaged organs and cannot find evidence for increased oxidative damage.  What is changed in these cells,  is the generation of transcription factors and genes by the new cellular redox state.  This redox state is the warning system for the cell of possible impending doom over time.  This is tied to the ratio of electrons to protons within the mitochondria and on its inner cell membrane.  This is why the redox potential is the most critical factor in human life.

Nuclear regulatory factors 1 and 2 get activated (NRF 1 and 2).  NRF1 is what signals the nucleus of the cell to manufacture of new mitochondria and NRF2 is the signal that shuts it off.  This signaling system accounts for the chronic inflammation due to oxidation that underscores aging and disease propagation in humans.  The level of oxidation chronically resets itself depending upon the current cellular terroir.  This implies the redox state within the cell is the biggest factor in how protein signaling occurs within a cell.

We know in humans that this state can exists for decades.  I follow these trend with a battery of labs I spoke about in the Redox Rx, which tells us what is likely going on at the mitochondrial levels from electron transport.

When the redox state is low, we may notice we have less energy, we take longer to recover from exercise, but it generally won’t kill us.  With this explanation,  it should be clear that the trade-off for removing bad mitochondria is long-term organ failure.  this happens, however,  slowly over time by depleting stem cells from our subcutaneous fat stores.  We call this aging today.

The better the redox potential on the inner mitochondrial membrane the more heteroplasmy we see because it tells us the organism is best able to handle the changing signals in the environment. When the redox potential is not as good,  our mitochondria use too much apoptosis or cell suicide, and not enough autophagy.  When this situation exists on a chronic basis,  we deplete stem cells, organ failure is more common, and life shortens.

Where do the human stem cells come from?  The most plastic human stem cell is in human subcutaneous fat.  This is why plastic surgeons use fat transfers in their work on the human face.  We talk about this tissue later in this series.  Einstein’s mass equivalence equation tells you why life organized around what it did…..the redox potential. Electrons = a high redox potential and excess protons lower it. Electrons build complexity. Protons do not. They are the signaling subatomic particles from the environment to the mitochondria.  You gain electrons from having DHA in every cell membrane of your body.

What did I say in the April 2014 webinar Q & A about oxygen? Oxygen allowed complexity because it has electrons within its  atoms, O₂.

Electrons carry a massless form of energy and information to reduce oxygen.  More oxygen generates more electrons in the CSF.

Electrons build complexity, because they are free of the thermodynamic constraints of mass.  Mass requires more energy thermodynamically.

What do humans have within their skulls,  that primates do not?

Where do we develop that complexity?

Still think macronutrients and calories matter?

Only a simple mind does………….

It is the reservation of electrons for construction of the brain and immune system that separates us from our nearest ancestors. How do we capture electrons best as humans?  DHA.  How do we assimilate them best?  When DHA, water, collagen, and cell membrane chemistry are all working properly together.

 

CITES

http://www.ncbi.nlm.nih.gov/pubmed/18256136

http://www.ncbi.nlm.nih.gov/pubmed/2240203

http://www.ncbi.nlm.nih.gov/pubmed/17618960

http://www.ncbi.nlm.nih.gov/pubmed/17823426

http://chemse.oxfordjournals.org/content/30/suppl_1/i182.long

An obesity-associated gut microbiome with increased capacity for energy harvest.
Vol 444 | 21/28 December 2006 | doi:10.1038/nature05414

http://www.fbmc.fcen.uba.ar/materias/ga/seminarios/Gut_environ_genomics.pdf

http://www.ncbi.nlm.nih.gov/pubmed/15389892

http://www.ncbi.nlm.nih.gov/pubmed/24499129

http://www.ncbi.nlm.nih.gov/pubmed/20940129

http://www.ncbi.nlm.nih.gov/pubmed/24605246