
What don’t they know about protons and how they relate to our relationships?
The way we think and feels about people in our life comes down to the redox state in our central nervous system.
The base of redox state is built by proton gradients and in humans newer systems in mitochondria and cells set the ceiling of the redox state to -400mV.
That system is built around glutathione which replaced the melatonin and Vitamin C system in lower eukaryotes as seen below. -200mV defines cytochrome C oxidase and the ATPase redox potential and this is the BASE that cells need to survive on Earth. I mentioned this in the video above. After 3.8 billion years we added other systems to build the redox potential of our cells to -400 mV to form complex life as the picture shows below.
The centerpiece of Nature’s conceptual idea for life lies in the novel use of natural proton gradients created in the ancient seas on Earth and they surround the story of water and light from the sun to do something remarkable around protons. Four billion years ago, alkaline fluids bubbled into what would then have been mildly acidic oceans (CO2 levels were about a thousand times higher than they are today, and CO2 forms carbonic acid in solution, rendering the oceans mildly acidic). Acidity is just a measure of proton concentration, which was about four orders of magnitude (four pH units) higher in the oceans than in vent fluids. That difference gave rise to a natural proton gradient across the vent membranes that had the same polarity (outside positive) and a similar electrochemical potential (about 200 millivolts [mV] across the membrane) as modern cells have. This is where the base of the redox potential of modern human cells come from. It is remarkable that no food guru understands the basic biophysics of this planet well enough to see why food is not the driver of health. An optimized proton gradient, however, is critical to it because it forms the base of the redox potential of cells.
The equation that defines this idea behind proton movements with IR-A light from the sun is below.
The H+ in NADH must be a proton and never a deuteron (deuterium isotope of hydrogen). When this substitution occurs life cannot be maintained far from equilibrium over a long time span. This is when illness enters and when your partners redox drops and your relationships begin to fail as you grow apart.
Drinking high pH water does nothing for your health or your relationships when you have functional kidneys.
When your redox drops in your body your ability to make the chemicals that bond us together as humans also drop. Those major chemicals are dopamine, melatonin, oxytocin.
Dopamine is a catecholamine.
The catecholamines, of which dopamine and adrenalin is the best known example, and the aminochromes, of which adrenochrome is the best known example, are intimately involved in stress reactions. Stress is well known to DESTROY relationships. What is not well known is how stress does it by ZAPPING your redox in the process of destroying the neurochemicals that bonds us as humans and that control our behaviors and emotions.
Therefore to moderate the influence of stress or to negate it, the orthomolecular belief is that we must use compounds which prevent these substances from damaging the body. THAT IS 180 degrees oposite of my belief. We need the sun and rebuild the redox before we need any substrates. The orthomolecular idea that Vitamin B-3 is a specific antidote to NAD+, dopamine, or adrenalin is old and a half truth. The reason for this opinion is it only takes the substrate biochemical view point and never considers the affect of light on these substrates in how their electrons get programmed by light to create their proper physiologic effect. This is what I was hinting at above in the video with Luke Storey.
The ortho molecular belief that exogenous antioxidants with the use of exogenous catecholamines is wise is just not supported. We see the effect in people with Parkinson’s diseease who use exogenous L-DOPA get tachyphyllaxis from the drug. Adding antioxidants such as vitamin C, Vitamin E, beta carotene, selenium and others DO NOT protect the body against the effect of the free radicals just by removing them more rapidly from the body is not a well thought out plan because it has no biophysical supports.
Any disease or condition which is stress related ought therefore to respond to the combined use of vitamin B-3 and these antioxidants, but the literature is filled with papers that show they do not. None of these papers have been repeated when using these drugs with solar redox strategies and this may show a huge change in outcome if it does get studied. I can tell you in my life and my practice experience it makes all the difference in the world.
Why do I think this orthomolecular supplement based strategy fails us so often?
Is this the same reason why adovcating a ketogenic diet for low NAD+ states is pure lunacy?
Yep. Why Uncle Jack?
When you eat a ketogenic diet guess what else happens? It is believed we bypass complex one at the inner mitochondrial membrane and enter FADH2. I used to believe this but I no longer do because of technology light. You heard about this in the Quantum electron blog post at JackKruse.com………but what did not I tell you in that POST?
Why does a ketogenic diet work in T1D, T2D, and help us lose weight, but does not help all metrics in health? When you lose water conduction at the inner mitochondrial membrane (cytochrome c oxidase due to deuterium) you lose the ability of proper nanoscopic protein folding of cytochrome 1 (NAD+). This throws off the nanoscopic precision (size and shape) required for quantum tunneling and this cause increased ROS and metabolic syndrome……..This is also why exogenous niacin can work in these diseases because it is a ketone mimic drug (sans artificial blue light). Why?
Niacin also known as vitamin B3 (above), nicotinic acid and vitamin PP, is an organic compound with the formula C6H5NO2 and one of the 40 to 80 essential human nutrients. In fact, when niacin deficiency is present it is one of 5 vitamins that causes a pandemic disease condition called pellagra.
But it can be used to bypass a “broken” cytochrome 1 when misfolding (due to a chronic ATP deficiency think EMF 7 blog post now). But why ? Why am I tormenting you with this science?…….because you need to think about things you are missing……..and you will see where QED takes us……….Vitamin B3 can help activate PPP when we are broken for some reason when we are ketotic from a dietary standpoint using vast amounts of coherent water as I laid out in the quantum electron blog post. Yes, niacin is a precursor to NAD+/NADH (cytochrome 1) and NADP+/NADPH (the magic of the PPP), which play essential metabolic roles in all living cells as I showed in EMF 4. What most people do not know is tryptophan the aromatic amino acid that absorbs UV light forms the base of all these chemicals. Without UV light to program them all none of them work as they should in cells.
Niacin cannot be directly converted to nicotinamide, but both compounds could be converted to NAD+ and NADP+ in vivo PROVIDED THE REDOX POTENTIAL IS GREATER THAN -200mV and this information is very valuable when you have liver leptin resistance, metabolic syndrome, or epilepsy. Your food gurus never tell you this. I do.
In 2010 Leonid Sazanov deciphered the crystalline structure of NAD+/NADH which is complex 1 respiratory complex in mitochondria. It is an the enormous protein in physical size and quite complex. You can read about it in Efremov et al .2010. Again, the atomic structure betrays the biophysical mechanism at play in NAD+ — in this case not a rotary motor as it is in the ATPase but, even more surprisingly, it uses a lever mechanism not unlike the piston of a steam engine. This is why I have told people that mitochondria really mimic Carnot Theorem in thermodynamics.
Red light stimulates cells to replace defective mitochondrial engines. Blue light damages them as the slide shows below.
When cytochrome 1 has misfolded electron transport proteins due to poor redox (ie:quinolone issue of CoEnQ10) you need to bypass it MOST of the time by eating fats that feed into FADH2 predominately because if you don’t, your mitochondria begin to make massive ROS that overwhelms the cells redox potentia dropping it from -400mV and this raises blood retinal levels while lowering vitamin D levels. It also causes pregnenolone steal syndrome which lowers all hormones. This is one of a myriad of ways your relationship can fail as your hormone panels crash.
Chronic pregnenolone steal syndrome will eventually shorten our telomeres to cause cellular signaling problems that lead to either senescence or advanced early aging. This also destroys our relationships.
The chronic loss of NAD+is the critical sign of a loss of negative feedback control of the ubiquitin cycle. This data scales directly to our molecular circadian clock and our peripheral clock genes (CCG’s). So this implies a loss of relationships is also related to poor circadian biology. All things lead back to the light we chose to live under. Few can fathom these links because they never look deeply into the life and how we work.
As our redox drops NAD+ builds up in relation to NADH levels on a per unit basis. There is a special case for blue light where a ketogenic diet can fatten you if you are chronically destroying cytochrome 1 because your REDOX is below -200mV. When redox drops below this threshold it tells us there is a proton problem and that problem is usually related to having too much deuterium leaking into the matrix via the UCP-2 mechanism I laid out in my webinars for members in the past 18 months.
Then a fat-laden diet during spring and summer can make you very obese when this situation occurs. See Jimmy Moore as a classic example.
Increasing the NAD+ endogenously (not via a supplement) in comparison to NADH changes a most of the mechanistic downstream signaling in protein kinase B pathways of cells. Why is that big issue? The AKT pathway is also known as protein kinase B (PKB). It is a serine/threonine-specific protein kinase that plays a key role in multiple cellular processes such as glucose metabolism, apoptosis, cell proliferation, transcription and cell migration.
Akt1 is involved in cellular survival pathways, by inhibiting apoptotic processes. This is how the brain shrinks in PD, AD, ALS, FTD, and in diabetes. It also is a huge problem in TBI’s which are concussions.
Akt1 is also able to induce protein synthesis pathways (urea cycle), and is, therefore, a key signaling protein in the cellular pathways that lead to skeletal muscle hypertrophy, and general tissue growth.
Since it can block apoptosis (mitochondrial disease risks and cancer risk), and thereby promote cell survival, Akt1 has been implicated as a major factor in many types of cancer. Akt (now also called Akt1) was originally identified as the oncogene in the transforming retrovirus, AKT8. UVA light can help restore apoptosis. In a mouse (nocturnal) which is null for Akt1 but normal for Akt2, glucose homeostasis is unperturbed, but the animals are smaller, consistent with a role for Akt1 in growth.
In contrast, mice which do not have Akt2, but have normal Akt1, have mild growth deficiency and display a diabetic phenotype (insulin resistance/ T2D), again consistent with the idea that Akt2 is more specific for the insulin receptor signaling pathway. The role of Akt3 is less clear, though it appears to be predominantly expressed in the brain. It has been reported that mice lacking Akt3 have small brains. This is what causes brain shrinkage in all the neurodegenerative disorders I mentioned above that are linked to cytochrome 1 size and shape issues. PCOS is tied to this early one before the more chronic diseases come to the forefront. This will also change you moods, alertness, your cognitive ability, and your behavior.
Akt2 is an important signaling molecule in the Insulin signaling pathway and you do not need food inputs to effect it. Alien light in your environment can do it without any food stimulus. It is required to induce glucose transport. TBI induces AMpK pathways and increase blood glucose because of the lack of circadian control of this process.
The follow through? AKT1 is involved in the PI3K/AKT/mTOR pathway and other signaling pathways. These all cause massive changes in cell cycle signaling and in cellular communication. mTOR is huge in longevity and in cancer progression via the dys-regulation of the p53 gene. If the high oxygen pathways are defective for any reason metabolic mitochondrial diseases are likely. (TCA/urea cycle)
What else is more likely to occur in your life when all this hard core biochemistry and biophysics fail in your cells?
YOUR RELATIONSHIPS WITH OTHER HUMANS WON’T BE AS GOOD AS THEY USED TO BE EITHER.
This might be a tough swallow for some of you, but it is the truth according to what Nature is telegraphing us.
Now you can see why when this pathway is activated many bad things can happen that are common to T1D, T2D, most cases of leptin resistance with elevations in hs-CRP. These steps are stops on the way to either final pathway and we call them neolithic diseases due to chronic mitochondrial failure and collapse.
Why do relationships really fail? What is the foundational science problem?
A LACK OF CELLULAR REDOX POTENTIAL IS THE ANSWER.
Relationships are not about passive agreements and merely spending time together: they are living, breathing entities, and if you don’t actively take care of them, they will suffer and die. If you want your relationship to be strong, you can’t just hope for it — you need to put in the work. The work you need to put in is below in PICTURE FORM.
We often wonder why couples fight, lose interest or seem to lose the ability to communicate even when they love each other as redox drops. Why do dirty dishes or apparently innocuous words become triggers for such heated arguments?
Relationship conflict is a result of one or both partners feeling that their attachment is threatened and that psychologic issues is underpinned by how our stress hormones are acting under the direction of mitochondria in cells.
Most of us don’t see this connection because the symptoms have purely emotional roots and those emotions are built by the light that control our mitochondria to make chemicals in neurons.
This is why anxienty and mood changes are linked to poor mitochondrial function as laid out in CITE 1 below.
So, why do we need secure attachment so much?
According to research, it’s because the lack of it can actually be a literal threat to our survival.
Researchers at Case Western Reserve University asked men with a history of angina and high blood pressure whether their wives “showed their love.” The ones who said no, suffered twice as many angina episodes during the next five years.
Another study found that women who had had a heart attack showed a 3x higher risk of having another if there was conflict in their marriage.
Being able to trust and be trusted (dopamine/melatonin/oxytocin), to love and be loved in your relationship is not just helpful: it’s crucial for you and your partner’s health, happiness, and overall quality of life.
Trust is a function of the neuro-chemicals built in these stress pathways by the redox power in your cells. This is why relationships fail fundamentally. If we trace the steps back it always comes back to couples who have differing redox states compared to one another. Its shocking, but the links are laid out here in this blog for you to examine for yourself.
CITES:
1. https://medicalxpress.com/news/2019-09-anxiety-disorders-linked-disturbances-cells.html