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From my initial post mortem of data I have gathered from my contacts on the front line in New Orleans this virus is hijacking hemoglobin’s ability to carry oxygen to tissues.  The lung tissue then responds to this in a reactive way via imaging studies.

HYPERLINK

I don’t think this paper above is getting enough publicity right now in this pandemic. It helps explain why the COVID 19 hypoxia is unique in its presentation.  

The paper theorizes how and why coronavirus reduces blood O2 and causes “crushed glass” lung imagery. This happens because the virus attacks the beta chains of hemoglobin and this binding appears to kick out heme from RBCs rendering them unable to deliver oxygen to mitochondria. The risk factors of high A1C, blood sugar, high LDH and ferritin, and why certain treatments work. (Hydroxychlorquine)

One clinical pearl I have heard from all my MD friends on the front line in NOLA is “Very often, extreme fatigue hits first.” PEEP and blood transfusions are not helpful. My bet is RBC transfusion won’t work well in patients who are actively shedding virus because the virus will immediately attack the new transfused RBC mimicking graft versus host disease response. COVID viral genes 1 and 8 have been predicted to interfere with heme synthesis.

Heme synthesis first step occurs in the mitochondria. So if it is disrupted this virus compounds the situation. Heme is the red compound in blood and in cytochrome C oxidase, and catalase that carries oxygen and CO2.   When mitochondrial oxygen consumption slows more dissolved oxygen in the cell rises and this excess oxygen become substrate to make free radicals that further destroy the lipid membranes of mitochondria and RBCs to lead to the early fever, and cytokine storm seen in COVID19 via the NFLR3 inflammasome.

This destroys ATP formation by the ATPase and this causes extreme hypoxia that mimics suffocation or high altitude pulmonary exposure (HAPE). It appears once the virus attacks it acts by kicking out the iron and this gives a specific phenotype in the blood that mimics malaria. This explains why chloroquine seems effective as a treatment. Why would azithromycin help augment hydroxychloroquine? Azithromycin appears to be effective in the treatment of COPD through its suppression of inflammatory processes.  Azithromycin prevents bacteria from growing by interfering with their protein synthesis. It binds to the 50S subunit of the bacterial ribosome, thus inhibiting translation of mRNA. Nucleic acid synthesis is not affected.

During a viral sepsis acid base balance is altered and most people become very acidotic. Azithromycin is an acid-stable antibiotic so its efficacy would not be altered in the face of metabolic or respiratory acidosis. This is why it has efficacy in COVID 19. It is one of the few antibiotics that can work in low pH environments. Due to its high concentration in phagocytes, azithromycin is actively transported to the site of infection. During active phagocytosis, large concentrations are released. The concentration of azithromycin in the tissues can be over 50 times higher than in plasma due to ion trapping and its high lipid solubility.

The damage to the beta chains of hemoglobin by COVID mimics malaria. Malaria also causes an inactivation of RBC to carry oxygen to mitochondria.  Malaria is an acute form of hemolytic anemia.  These types of anemia have symptoms that are similar to other forms of anemia (fatigue and shortness of breath), but in addition, the acute breakdown of red cells leads to jaundice and increases the risk of particular long-term complications, such as gallstones and pulmonary hypertension.

It appears COVID 19 happens so fast jaundice and gallstone do not have enough time to form but the pulmonary hypertension manifests as the key feature of the disease acutely.  The hemolysis can occur inside the vessels or outside the vessels.  I believe in COVID 19 it is an extravascular hemolysis that is operational.  Extravascular hemolysis refers to hemolysis taking place in the liver, spleen, bone marrow, and lymph nodes.  In this case very little hemoglobin escapes into blood plasma.

This is why no one is reporting jaundice in COVID 19 patients.

Pulmonary hypertension is a condition of increased blood pressure within the arteries of the lungs.  Symptoms include shortness of breath, syncope, tiredness, chest pain, swelling of the legs, and a fast heartbeat.

All of these symptoms are found in COVID 19 patients.

Extreme fatigue is a sign of HYPOXIA = HIF-alpha-1 = serious over use of thiamine which is a beacon of a loss of mitochondrial redox power no TCA use = lack of delta psi.  Without delta psi no new heme can be to replace hemoglobin or cytochrome C oxidase or catalase.  This explains why people present the way they do in the ER.

Here is a report from a NOLA ER doc who graduated LSU in 1998.

Clinical course is predictable.

“2-11 days after exposure (day 5 on average) flu like symptoms start. Common are fever, headache, dry cough, myalgias(back pain), nausea without vomiting, abdominal discomfort with some diarrhea, loss of smell, anorexia, fatigue.

Day 5 of symptoms- increased SOB, and bilateral viral pneumonia from direct viral damage to lung parenchyma.

Day 10- Cytokine storm leading to acute ARDS and multiorgan failure. You can literally watch it happen in a matter of hours.

81% mild symptoms, 14% severe symptoms requiring hospitalization, 5% critical.

Patient presentation is varied. Patients are coming in hypoxic (even 75%) without dyspnea. I have seen Covid patients present with encephalopathy, renal failure from dehydration, DKA. I have seen the bilateral interstitial pneumonia on the xray of the asymptomatic shoulder dislocation or on the CT’s of the (respiratory) asymptomatic polytrauma patient. Essentially if they are in my ER, they have it. Seen three positive flu swabs in 2 weeks and all three had Covid 19 as well. Somehow this VIRUS has told all other disease processes to get out of town. This shows you how the virus is causing a loss of medical capacity inside the hospital.

China reported 15% cardiac involvement. I have seen covid 19 patients present with myocarditis, pericarditis, new onset CHF and new onset atrial fibrillation. I still order a troponin, but no cardiologist will treat these heart attacks (STEMI) no matter what the number in a suspected Covid 19 patient. Even our non covid 19 STEMIs at all of our facilities are getting TPA in the ED and rescue PCI at 60 minutes only if TPA fails.

Diagnostic

CXR- bilateral interstitial pneumonia (anecdotally starts most often in the RLL so bilateral on CXR is not required). The hypoxia does not correlate with the CXR findings. Their lungs do not sound bad. Keep your stethoscope in your pocket and evaluate with your eyes and pulse ox.

Labs- WBC low, Lymphocytes low, platelets lower then their normal, Procalcitonin normal in 95%

CRP and Ferritin elevated most often. CPK, D-Dimer, LDH, Alk Phos/AST/ALT commonly elevated.

Notice D-Dimer- I would be very careful about CT PE these patients for their hypoxia. The patients receiving IV contrast are going into renal failure and on the vent sooner.

Basically, if you have a bilateral pneumonia with normal to low WBC, lymphopenia, normal procalcitonin, elevated CRP and ferritin- you have covid-19 and do not need a nasal swab to tell you that.

A ratio of absolute neutrophil count to absolute lymphocyte count greater than 3.5 may be the highest predictor of poor outcome. the UK is automatically intubating these patients for expected outcomes regardless of their clinical presentation.

An elevated Interleukin-6 (IL6) is an indicator of their cytokine storm. If this is elevated watch these patients closely with both eyes.

Other factors that appear to be predictive of poor outcomes are thrombocytopenia and LFTs 5x upper limit of normal.

Disposition

I had never discharged multifocal pneumonia before. Now I personally do it 12-15 times a shift. 2 weeks ago we were admitting anyone who needed supplemental oxygen. Now we are discharging with oxygen if the patient is comfortable and oxygenating above 92% on nasal cannula. We have contracted with a company that sends a paramedic to their home twice daily to check on them and record a pulse ox. We know many of these patients will bounce back but if it saves a bed for a day we have accomplished something. Obviously we are fearful some won’t make it back.

We are a small community hospital. Our 22 bed ICU and now a 4 bed Endoscopy suite are all Covid 19. All of these patients are intubated except one. 75% of our floor beds have been cohorted into covid 19 wards and are full. We are averaging 4 rescue intubations a day on the floor. We now have 9 vented patients in our ER transferred down from the floor after intubation.

Luckily we are part of a larger hospital group. Our main teaching hospital repurposed space to open 50 new Covid 19 ICU beds this past Sunday so these numbers are with significant decompression. Today those 50 beds are full. They are opening 30 more by Friday. But even with the “lockdown”, our AI models are expecting a 200-400% increase in covid 19 patients by 4/4/2020. “

That is the clinical view from New Orleans now.

If the patient isn’t showing signs of respiratory difficulty but has extreme fatigue, one thing to question is whether the oxygen is getting from lungs to body tissues.

This would lead to organ and tissue death, roughly in the same way as if a patient were being suffocated.

Even when a patient can breath (fill lungs with air), the oxygen isn’t getting to the colony of mitochondria in the cells in their body.

Similiarities between COVID 19 and High Altitude Pulmonary Edema

HAPE symptoms similar to covid: “HAPE was misdiagnosed for centuries, as evidenced by frequent reports of young, vigorous men suddenly dying of “pneumonia” within days of arriving at high altitude.”

HAPE’s mechanism results from low amounts of ambient atmospheric oxygen, so the subject’s blood is unable to bring enough oxygen to the body.

Nothing is “attacking” the lungs, but the lungs show similar inflammatory symptoms to COVID, because O2 in blood is low. Remember UV light exposure increases venous O2.

This would lead to organ and tissue death, roughly in the same way as if a patient were being suffocated.

Even when a patient can breath (fill lungs with air), the oxygen isn’t getting to the cells in their body.

The inflammation in the lungs results from the lungs not being able to perform the oxygen/CO2 exchange, and would therefore appear to be a SECONDARY result of the hijacking of the blood.

The lungs not working is a result of lack of O2 in blood, not the cause of it.  It might be a disease of heme.  

The reason why technology use exacerbates the disease because it also causes defects in RBC synthesis by blocking heme formation by causing mitochondrial damage. (pic below)

Several paper reviewed on drug models the behavior of chloroquine and faviparavir as well, which appear to bind to the non-structural viral proteins that hijack the heme groups, thus inhibiting them from knocking out the iron and wrecking the O2-carrying ability of the red blood cells.

This also explains the observation made by various ER docs that patients tend to have elevated ferritin: ferritin is used to store excess iron released from the RBC damage. If a lot of iron is knocked out of heme groups and floating around, the body produces more ferritin.

In humans, it acts as a buffer against iron deficiency and iron overload. This overlaod happens hyperacutely in COVID19.   Ferritin is found in most tissues as a cytosolic protein, but small amounts are secreted into the serum where it functions as an iron carrier. Plasma ferritin is also an indirect marker of the total amount of iron stored in the body; hence, serum ferritin is used as a diagnostic test for iron-deficiency anemia. This anemia can happen acutely or chronically.

If this mechanism of damage is true, this implies we need to think a lot differently than we are now:

1. Starting drug treatment while symptoms are mild keeps virus from hijacking too much of the RBC and cytochrome C oxidase, or catalase, enabling a still-healthy body to mount an immune response. Plasma therapies should be done before RBC transfusions.

This explains why early drug treatment (first week of symptoms) is often successful. It stabilizes iron metabolism and stabilzes CO2/O2 delivery early on and maintains mitochondrial function via cytochrome C oxidase. This preserves ATP function. Red light therapy would augment this affect.  Nitric oxide mimicry might save cytochrome c oxidase.  This might be why UV light helps limit COVID 19 cases.  UV light increases the production of nitric oxide and this shuts down the use of cytochrome c oxidase.

This would explain why all coronavirus seem to be inactive in summer months.

2. Drug treatment and intubation once patient is critical these option will rarely work because tissues/organs are already damaged by viral destruction of the beta chain of hemoglobin; therefore, blood can’t carry O2, and the body is too weak to produce new red blood cells able to carry iron (and thus oxygen/CO2) even if drugs inhibit more hijacking.

3. Thus: start severe patients on drug treatment upon hospital intake to suppress further hijacking of blood by the virus, then give them a blood transfusion of new red blood cells immediately that are unhijacked.

4. If heme/hemoglobin is involved, a higher hemoglobin count may be protective to the disease process.  This may explain why nicotine helps.  It maybe that’s why smokers are so underrepresented in the data.  Their chronic hypoxia from smoking increases their hemoglobin counts.   This also would also predict less severe acute mitochondrial failure from COVID 19 disease in high altitude populations.  The Johns Hopkins map supports this.  Nairobi is untouched. 

5. Hypoxia explains the loss of taste and smell too.  We know that the human olfactory receptor becomes less sensitive under hypoxic hypoxia.  HYPERLINK

CONCLUSIONS:

If all this is true, we would see rapid patient improvement with the use of plasma first. The reason for many cases of recrashing with COVID might be due to an inability to recovery the ability to make new heme because of the mitochondrial damage. People forget heme synthesis begins in the mitochondrial matrix. This implies we should consider RBC transfusion later in the disease during recovery.

These ideas should be very testable in the hospital environment now.

Also, if it’s true, we’re gonna need a lot of blood donations after the acute phase of viral attack.

So far as I know, there are no studies where we’ve tried transfusing blood from a patient who HASN’T had or recovered from COVID-19.

We can verify/disprove this by comparing outcomes between plasma-only and full blood transfusion (and control), or just between blood transfusion vs control (both should be given hydroxychloroquine. It appears the hydroxychloroquin is a heme salvage operation before acute infection and beta chain destruction.

So for ER/ICU/hospitalists MD’s handling incoming severe patients with multi-organ system failure that we consider early plasma therapies to protect all heme proteins and later blood transfusion with supportive care to deliver oxygen to mitochondria in tissues that are undergoing acute mitochondrial colony failure.  

CITES:

1. https://www.click2houston.com/news/local/2020/03/29/houston-methodist-first-in-nation-to-be-approved-by-fda-to-transfuse-donated-plasma-from-recovered-covid-19-patient/

2. https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surface_Glycoprotein_Inhibit_Heme_Metabolism_by_Binding_to_Porphyrin/11938173

3. https://jamanetwork.com/journals/jama/fullarticle/2763983

4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617508/

The media and politicians are obsessed about the number of ventilators available.  Is this wise?

Obsession is the single most wasteful human activity, because with an obsession you keep coming back and back and back to the same question and never get an answer. An obsession is a way for damaged people to damage themselves more.

What about these ideas:  are they worth considering now?

1. What about the number of people who are skilled to manage ventilated patients?  it is not a basic medical skill?

2. Have you ever contemplated what the sheer quantity of analgesics, sedatives and paralytics needed to treat ventilated patients is in a pandemic?  The public has no clue what a loss of medical capacity looks like much less what it feels like to a person on the front line.  Beware of false knowledge; it is more dangerous than ignorance. Ignorance is always afraid of adaptation, because thinking is heavy lifting for the unripe mind.  The data shows us that already our beliefs might be wrong…….about what is really afoot in the world tonight

3.  This year we are told the interventions we use to stabilize folks are not “safe” if have Covid 19. We won’t know result for 24hrs due to testing constraints. So in this situation should we deny life saving treatment? In a true disaster-yes. But is this axiom still true in a flattened curve situation?

4. Instead of black and white situation we’re  dealing with 150 shades of grey.  No one has an answer because too few can think about the asymmetry of the situation clearly.   The surreal part of this pandemic, I think, comes when you’re thrown into a situation that you’ve never been in before. It’s extremely disorienting to those who expect normalcy.   Right now, many of the patterns we know and love have been obliterated. We can’t go to happy hour, we can’t get toilet paper when we want it, we can’t plan our annual vacation getaway.

5. Highest number of nurses = lowest death rate = Germany.  Note it is nurses and not doctors that are the key to your survival in some areas.

6. The study of the surreal has mostly concerned Dali’s paintings and Kafka’s writings. But there are psychological reasons why every day during a pandemic seems so otherworldly.  What happens when all of a sudden the whole world follows the same narrative as the plot unfolds and nobody has a clue what the next scene is gonna be like, or what the end will be?

7. It’s like there’s no future, because we cannot plan for a future in abject chaos.  People are afraid of chaos.  Few see opportunity in its randomness.  The upending of our normal lives also obliterated the routines, however mundane, that keep the average person levelheaded.  Why do so many shoot for average in life? A man who wants to lead the orchestra must turn his back on the crowd and their beliefs at times.

8. The imaginary of nature capabilities is what tends to become real in life.  We must begin to realize the black swan event is normal and not an outlier.  Normalcy is so toxic it’s made a majority of people in the modern world “normally” unhealthy, “normally” neurotic, “normally” gullible…long before this crisis.  Normalcy never was, never will be your friend.   QUESTION IT.

9.  Nothing that surrounds us is objective, and all around us is subjective to the environment we have created in the zipcode we inhabit by choice.  We are deluded by routine.  Most believe their routine is the scaffolding of life, because it’s how we organize information and our time. And without it, we can feel really lost.  People hate feeling lost.  The truth is stranger than our beliefs.  Just because someone stumbles and loses their path, doesn’t mean they’re lost.  They maybe acutely lost but they are not lost forever.  There’s always time to change the road your on, even in total chaos.

10.  Reality is obtained by Nature by slightly bending physical and chemical laws using probabilities.  This is why quantum mechanics is Nature’s language.

Rather than imagining life is a solo performance, Begin to create a tune that becomes part of a vast choral production the Universe has been singing since our primitive ancestors first looked towards the heavens. Realize our lives were part of a vocal symphony directed by a “cosmic composer” who is putting together a grand concert from musical threads supplied by every individual. Living optimally is a team game. Individuals may win the game at times, but teams win championships in life.  We’re all in this chaos together.

What is the ultimate cure of all diseases? Increasing your redox power via sunlight. We all need some Purple rain (UV/IR-A) from the sun to come upon us. Never forget it my Black Swans.

Here is the truth about life…..your current situation is never permanent. It is what you make of it from your choices. Life is not solid it is fluid and it always changes.

Night Swans……….

It is difficult to get modern humans to understand something when THEIR addiction to its use depends on THEM not understanding it.

This blog is about that very issue.  Does technology create an altered immune state in modern humans that lead them open to a myriad of diseases?

Yes.

Did you know that taking exogenous melatonin thins your retina and makes you fatter, yet endogenous melatonin production seems to help us maintain leptin sensitivity?  Ask your food gurus and your supplement sellers why this is the case before you ever give them a cent.

Pinealectomy induces circadian arrhythmia and has interesting effects on adipose tissue biology.  Did you know that blue light/nnEMF exposure through the eye and skin mimics the physiologic effects of the removal of the pineal gland?

Why is this important in the modern world?

Doctors are IMPOTENT to explain the rise of diabetics who are SKINNY.  Those diabetics who are skinny break the rules doctors are taught in med school and residency because educators of doctors have always believed diabetes was only caused by eating too many carbohydrates.  What did they not know?  Imbibing technology screen blue light and nnEMF is EQUIVALENT to eating carbs 24/7, but the damage it causes to your mitochondria and adipocytes is radically different because of how nnEMF/blue light DEMOLISH melatonin production in the pineal gland.  THAT is the key mode of creating a skinny diabetic.  Skinny diabetics are also more prone to cataract formation, myopia, and AMD.  Did you know that?  Have you ever thought to ask yourself why that might be?  It is because thin diabetics are hypoxic.

Skinny diabetics are also very hypoxic and they tend to get massive amounts of peripheral artery diseases and intracranial artery diseases that lead to early CABG, stroke, dementia, and melanopsin damage to the retina.  This leads to cataracts and AMD too.  All these diseases are spiking today.    What is the fundamental driver of this process?  A chronic mix of low melatonin production, low NO production, and chronic thiamine deficiency acting all at once.

Adipocytes isolated from pinealectomized animals in cite one below all exhibited lower glucose uptake, higher glucose oxidation, and lower de novo lipogenesis.  Collectively, these results suggest frank MASSIVE melatonin deficiency, that has long-lasting impacts on adipocyte biology which manifest as failure to conserve energy.  You need melatonin to have a normal fat mass.  It turns out blue light and nnEMF via CHRONIC overexposure of your eyes/skin can chronically cause you to massively lose fat while becoming a metabolic train wreck and push you to an early death.

Clinicians need to pay attention to different metrics in tech abusers.

In those people we should see an intial period where blue light fattened the patient follwed by some time elapse, when mitochondrial failure occurs.  What should we be looking for as clinicians in these patients?  Their glucose and insulin levels in the fed and fasted states usually aren not affected, but glucocorticoids on hormone panels are dramatically chronically elevated.  Cortisol levels usually become very abnormal and then leptin levels plummet in chronic fashion to a significantly greater degree when the patient screen time is excessive.  This is a different picture than one sees in acute leptin resistance.

Why is this mechanism important for clinicians to understand?  When leptin levels drop adiocytes atrophy and a very thin phenotype occurs.

The chronic fall in leptin became interesting to me because it should have predicted patients would have an enhanced energy conservation because they were thin, but this isn’t what happened because their fat cells were non functional.  Glucocorticoids usually rise at night when the circadian mechanism is intact, after melatonin peaks at 2AM.  When the circadian mechanism is chronically disrupted,  melatonin levels crater in the night,  and this seems to exacerbate the increase in glucocorticoids we see.  Blue light and nnEMF also boost insulin levels and blood glucose.  Why is this a problem for creation of the skinny diabetic?

Insulin alone has little direct effect on leptin secretion in mammals, but glucocorticoids are super- stimulatory to blood glucose release, and this is enhanced by insulin production.  This is often why in history taking we often find skinny diabetics used to be heavier in their life before they became more metabolic derranged.  It also explains why skinny diabetic go undiagnosed longer than obese diabetics.  Doctors are not taught to look for these signs in normal to slightly elevated BMI cases.  This should change in a tech abusing world.

As a result, light, and melatonin as light’s protein proxy, appears to negatively regulate this hormonal axis and boost the anabolic potential of adipocytes. This makes fats cells store fat. It appears the levels of melatonin in the central retinal pathways and the skin hypothalamic axis predict who will go on to become a skinny diabetic. This infographic is critical to understand this very complex light phenomena.

Interestingly, the slide on melatonin creation by AM UVA/UVB exposure points out why both type 1 and 2 diabetics show a latitude effect in their disease course (see below two figures).

WHAT HAPPENS IN THE MATRIX WHEN THIS OCCURS?

NAD+ drops with SIRT1 and UCP-2 mechanism in mitochondrial becomes radically permeable just as RBC become super permeable to lactate as you learned in Hypoxia #5 blog.

WHAT DOES UCP-2 do?

UCP2 controls the carburetor mix of fuel in the matrix, namely, oxygen & hydrogen mix (from stored fat or from hydrogen in foods) in mitochondria and deuterium leakage in a circadian/seasonal manner to stimulate growth & ELF-UV release = broken UCP2 leads to cancer generation.  When UCP-2 is leaky eukaryotic cells leak massive quantities of ELF-UV.  Functional UCP2 lowers mitochondrial heteroplasmy by controlling how much deuterium enters the TCA cycle to control the anions it moves. UCP2 does this by varying the light released and reduced ROS from cytochrome II to stimulate ketogenic substrates in TCA = based on temperature & light signals from the light environment you choose to live under and not simply by what you eat.  This is the food guru fallacy. This also points out why food cannot solve quantum diseases.  Think cancer generation.

To achieve optimal ketosis you need to be fasting & be in daily solar red light whilst barefoot grounding to program proton spin = this properly recycles the hydrogens in DNA/RNA backbones to make seasonally responsive to light variations and DNA expression. If you eat carbs out of season or expose yourself to nnEMFs/ALAN over the winter you will increase blood glucose levels and turn off fat burning because of the effects of insulin. UCP function depends on leptin sensitivity = light/dark.  Taking exogenous melatonin ACTS to increases blood glucose/AMPk/ and makes UCP-2 non functional.  This maybe why skinny diabetics have poor outcomes with cancers, cardiovascular diseases and strokes.

These people will be at risk for many infectious diseases in the modern world.

Today’s parting thought:

The Earth is recovering……….

– Air pollution is slowing down

– Water pollution is clearing up

– Natural wildlife returning home

Coronavirus is Earth’s vaccine

We’re the virus.

Mother Nature is teaching us what karma is when we use parts of the electromagnetic sptrum she told us not to use.

Humans should be mentally preparing themselves for this to be a marathon, not a sprint. Mother Nature has been aiming to beat our asses and now she has them.

CITES:

https://www.ncbi.nlm.nih.gov/pubmed/15305231

Due to the increased bandwidth demands and the scarcity of microwave frequency allocations, the wireless communications industry is beginning to focus on higher, previously unallocated portions of the spectrum in the millimeter wave frequencies from 40GHz to 300GHz.  This is the range of 5 and 6 G communications in the world today.

Due to the high levels of atmospheric RF energy absorption, the millimeter wave region of the RF spectrum is not usable in the long haul, wireless communications segments. However, for short haul, “last mile” segments, the expanded RF data bandwidth available in the millimeter wave region makes it ideal for interference-free, fiber speed connectivity.

At the millimeter wave frequency of 60GHz, the absorption is very high, with 98 percent of the transmitted energy absorbed by atmospheric oxygen. This is the oxygen plants make and mitochondria need for respiration. Oxygen is brought to the mitochondria by our blood which has hemoglobin. 60GHz RF signaling is capable of causing an inability to hemoglobin and oxygen reacting properly all the time. This implies that hypoxia or a pseudohypoxia could exist in people around these frequencies. This also implies that 40-80GHZ is where thiamine deficiency will be at its maximum for causing mitochondrial heteroplasmy.  This is why I believe 5G is an extinction possible event.  Much like an asteroid, the damage is hidden from most experts perspectives now.  But today we are seeing massive changes in people in 5G cities.  Most of them have varying degrees of thiamine deficiency and resultant mitochondrial damage.

Please remeber what oxygen does in your mitochondria. It accepts the electrons from food that have had all of their light removed from them and that stolen light is added to the respiratory proteins electrons and the electrons of free radicals so that the light maybe shared all over your body to ionize other proteins to action. This is how life works at the most fundamental levels.

What is life really?

Life is built around the complexity of how light powers electrons. Life is all about ionization. Ionization is the process by which an atom or a molecule in a cell acquires a negative or positive charge by gaining or losing electrons. This often in conjunction with other chemical changes from the action of electron movements and alterations in their charge. Light excites or powers electrons to do some unusual things that cells depend upon. This is how the physiology or the work of living gets done.

While oxygen absorption at 60GHz severely limits range, it also eliminates interference between same frequency terminals. 5G spans 3 GHz -90 GHz in the electromagnetic spectrum. A 60GHz communications system must overcome the effects of oxygen absorption because of the effects it will have on the living. When someone asks you why 5G is different than any other ediction of network power I want you to remember this blog and I want you to tell them why nature never used this part of the spectrum naturally. It is because this part of the spectrum make life imcompatible with her recipes.

So let us make this real simple in picture format so you get what it means when the cornerstone reactions are altered by 60GHz millimeter waves.

When more oxygen in cells is present and not able to be used all hell breaks loose. This is why I predicted all the diseases we are seeing in ER’s now. Sadly, few doctors understand cell biology at this levels so the diseases like POTS/EHS/CFS/LYME/AUTOIMMUNITY/CANCER go treated incorrectly. This why these diseases are exploding. The more we use technology the worse this will get.

What else happens in the mitochondrion when more oxygen is not used? Thiamine gets depleted and then this equation becomes critical to understand.

Pyruvate cannot be used so it is turned into lactate. Lactate is not what you think either. Lactate rises because thiamine is absent. In particular, metabolites, like lactate are emerging in the literature as active players in driving immunosuppression. This is why cancer and autoimmunity are exploding in places where technology is used. Lactate is a potent signaling molecule that promotes stabilization of hypoxia inhibitory factor alpha (HIF-α) & this increases vascular EGF expression and angiogenesis. Lactate is massively taken up by damaged RBC’s by nnEMF. When Pyruvate cannot be used because thiamine is absent lactate rises and at the same time NAD+ drops like a rock. What is the effect of redox potential when that happens? See below.

Why do I use peripheral blood smears at Kruse Longevity Center to detect how bad your exposure to nnEMF really are?

How and why does this happen? So far my 2019 Farm members know this answer because they visited me and I showed most of them their bad RBC’s and explained to them what it meant to their lives.

Now this blog post explains to you what I really am doing at Kruse Longevity Center.

What are your RBC’s in your blood?

This is Nature’s Wifi systems of how life operates with the sun and your colony of mitochondria.

A more GEEKIER version of this idea is now here:

The effects of electromagnetic fields (EMFs) upon genes, proteins and enzyme kinetics on a molecular level have been recognized and investigated in the literature. This is information few clinicians read and this is why they remain clueless about where our modern diseases begin fundamentally.

The mechanisms responsible for these EMF-induced effects and not fully understood by modern medicine and have been the subject of ignorant debate in academia and on the internet. This is especially true in functional medicine. When you understand that nnEMF makes RBC’s more permeable to things in foods and supplements you become acutely aware of how bad an idea it is to recommend exogenous chemicals to people who are living in a 2G-5G city. Lactate become even more permeable to RBC’s ruining their morphology and it also ruins mitochondrial size and shape (IMJ’s of mitochondria below) effecting energy production by lowering the redox power.

 

It is thought that the effects of EMF are diverse and dependent on the strength, frequency, and duration of the EMF exposures because this is the belief of physics.  That belief does not go far enough for Black Swan clinicians like me.   Why do I say this?  Most American cities are now using 3GHz – 25GHz frequencies right now.  What does this range do to us?

The EMF microwave effects in GHz frequencies have been studied recently and it was reported that multiple 18 GHz EMF exposures, with specific energy absorption rate (SAR) values between approximately 3.0 and 5.0 kW kg−1, induced permeabilization of live bacterial cells and yeast.   Y’all remember where your mitochondria came from huh?  

It is an ancient bacteria/archea.  This means that mitochondrial permeability is also at risk at these lower power densities.  Do you understand yet why my ideas seem counterintuitive to allopathic and functional medicine paradigms?  That is why the next meme was made.

My understanding of the situation goes way deeper than their knowledge base because of the biophysics at play.  This blog is your playbook to hand to any skeptic who thinks this is hyperbole.  IT IS OUR MODERN REALITY.

Recent data has shown in the lab bacteria uptake high molecular weight chemicals in alien fields.  The uptake of high molecular weight dextran (150 kDa) and silica nanoparticles (23.5 and 46.3 nm in diameter) was shown for several cell types, including the prokaryotic organisms Branhamella catarrhalis, Escherichia coli, Kocuria rosea, Planococcus maritimus, Staphylococcus aureus, Staphylococcus epidermidis, Streptomyces griseus, and a unicellular eukaryotic yeast Saccharomyces cerevisiae.  

YOUR COLONY OF MITOCHONDRIA HAS A PROKARYOTE ORIGIN FOLKS.

^^^^^ALL modern diseases have a mitochondrial basis. Why?

How is your colony of mitochondria supposed to operate?

If you are following this blog well this next meme should be uber-intuitive.

Why are doctors impotent in helping the public today?

They continue to look in the nuclear genome for modern disease answers and I am saying it loud and clear they won’t find any cures in RNA or DNA.

They will find it in the mitochondrial genome and biology. Mitochondria were stolen to operate within the visible range of light with oxygen. That is how evolution built them.

So what happens to the air we breath on Earth when we used 5G?

At 60GHz, the extremely high atmospheric absorption level is due primarily to the molecular composition of the atmosphere. For millimeter waves, the primary absorption molecules are H2O, O2, CO2, and O3. Since the presence of O2 is fairly consistent at ground level, its effect on 60GHz radio propagation is easily modeled for margin budgeting purposes.

What might some of the collateral damage effects be in a 60GHz system on humans?

We should expect nitric oxide (NO) and thiamine depletion. This means cardiovascular disease and brain diseases should begin to kill humans at unprecedented levels.  That began in the 1940’s when we started using radar.  Why?

This can occur via reaction with oxy-Hemoglobin (Hb), leading to nonfunctional and toxic metHb. Once this occurs we should expect to see closely-linked hypertension develop in humans. So far no one has tested 5G for this effect. If this frequency of 5G is used biology better get ready to genetically engineer the Hb in order to slow down its reaction with NO.

Besides NO, the deoxy and especially the met forms of Hb also interact with reactive oxygen species (ROS) such as superoxide (O2•-) or hydrogen peroxide (H2O2). These processes yield ferryl (Fe^IV) Hb. This nasty molecule is a highly oxidizing species which not only degrades the Hb peptide and heme proteins but also amplifies the stress response by attacking other biomolecules and accidentally generating others (e.g., prostaglandins). This liberation of prostaglandins also causes deuterium to be released from the cell membrane in a stress response. When deuterium is unleashed from the cell membranes adjacent to the mitochondria it is capable of ruining Kreb’s bicycle kinetics as my previosu blog series have showed. I would remind you that cytochrome C oxidase is a heme protein too. This means apoptosis would be completely destroyed by a 5G 60GHz wave. The May 2018 webinar explains what this means and now you know why I predicted a massive amplification of cancer autoimmune conditions in cities using this technology. This is a small example of what 5G is capable of doing to your mitochondrial biology at a 60GHz frequency.

It turns out at Kruse Longevity Center I have found several novel ways to offset these 5G risks for some of clients. In 2020, expect more interesting changes to come out of my center at Destin.

Recall that sunlight is 42% infrared and this is nature’s version of photodynamic therapy. UV/IR combo light in sunlight is your vaccine to cancer. Amongst all the different types of cancer treatment, photodynamic therapy (PDT)- where light in is used to destroy malignant cells – might have one of the strangest side effects: patients are often better able to see in the dark.  Why?  with PDT red light is used to lyse cancer cells.  The same red light stimulates the repair of the photoreceptors in the eye and affects how retinal acts with those photoreceptors.

Normally in the retina, the combo of UV/IR light from the sun regenerate the photoreceptors in the eye to optimize the function of ipRGC’s and many other photoreceptors in the central retinal pathway.  This pathway also controls the neurohormone response in humans and that is why PDT and the sun can be used to treat different cancers.

For example, the intrinsically photosensitive retinal ganglion cells (ipRGCs) exhibit several important functions including circadian photoentrainment, pupillary light reflex, alertness, and phototaxis. We now have definitive evidence that ipRGCs regulate other physiological activities via the autonomic nervous system.  These autonomic ganglia are highly dependent upon the TCA cycle and thiamine dynamics to work optimally.

The sympathetic system uses acetylcholine at the proximal ganglion and norepinephrine at the distal terminal ganglion.

The parasympathetic, or craniosacral outflow, opposes the actions of the sympathetic system. It uses acetylcholine at both the proximal and distal ganglia. Increased tone in one system is modulated by the decreased tone in the other, an essential balance that results in a continuous adaptation to the environment. The concept of homeostasis is more aptly seen as homeodynamics, a continuous reaction between the environment and the adaptive status of the organism.

It has been shown in the literature that external light stimulation can activate hair follicle stem cells through the central retinal pathways semiconductive circuits via an ipRGC–suprachiasmatic nucleus–sympathetic nervous circuit. Immediately after ipRGCs are stimulated by light, the systemic sympathetic activities are activated in the brain stem that synapse in ganglia that innervate the skin. In the skin, the local release of the biogenic amine norepinephrine (made of tyrosine another aromatic amino acid) which is the key stimulus that activates hair follicle stem cells to regenerate and grow hair. This neural circuit in the retina enables prompt communication between peripheral tissues and the external environment just using light via the retina.  This tells us wearing glasses, contacts, or sunglasses has to affect the physiology of the system.  It also is really bad news for those who have permanently implanted intraocular lenses.   Due to the systemic activation of sympathetic activities, this circuit can also allow for timely responses to external light in other organs in the body to perform many autonomic tasks.  This highlights how a 5G topologic effect on the eye or skin can lead to chronic thiamine deficiency and the development of autonomic instability associated with EHS or POTS. It also highlights a function of ipRGCs in regulating autonomic nervous activity in the body.

The sympathetic nervous system plays an important role in the regulation of adipose tissue lipolysis. This is why blue light fattens humans and obese humans and diabetics often have evidence of thiamine deficiency when we look for it.

Chronic exposure to moderate and severe hypoxia increases the activity of the sympathetic nervous system and adrenal medulla. This is associated with chronic thiamine deficiency and low levels of Vitamin A and high level retinol binding protein in the blood. These are all markers of nnEMF/blue light toxicity and thiamine deficiency. Vitamin A is a retinal derivative in humans. Blue light and nnEMF alter Vitamin A levels and thiamine levels to cause hypoxia and lowered levels of oxygen consumption at the inner mitochondrial membrane. It also slows the turn rate of the TCA cycle and lowers ATP formation at the ATP synthase.

One of the important observations made in studying patients with thiamine deficiency is that arterial oxygen saturation in the regions of the body innervated by the sympathetic ganglia is relatively low in the disease when venous oxygen concentration is relatively high.  This tells us that the mitochondria in that region are not extracting oxygen well because of altered TCA dynamics due to the lack of thiamine.  Blue light and nnEMF decrease thiamine stores. The same phenomenon has been reported in sleep apnea and has been reported numerous times in the literature to be related to glucose dysregulation.

What explains humans’ ability to improve night time vision with IR-A light?  Does this somehow affect melanopsin and thiamine metabolism?

The answer is yes.

Recently, researchers have figured out why red light therapy during cancer treatment improves night time vision and can act as a chemotherapeutic agent against cancer: rhodopsin, a light-sensitive protein in the retinas in our eyes for night vision, interacts with a photosensitive compound called chlorin e6, a crucial component of this type of cancer treatment.

The work builds on what scientists already know about the organic compound retinal, which is found in the eye and usually isn’t sensitive to infrared light.  It is very sensitive to blue light frequencies.  When this chemical is liberated it is known to cause photoreceptor damage.

Visible light triggers retinal to separate from rhodopsin. Blue light causes retinal to separate from melanopsin due to its weak covalent bond. IR-A light does not have enough power to do this. The addition of chlorin e6 makes retinal very sensitive to red light – When retinal separates from rhodopsin this action converts light energy into the electrical signal our brains interpret to see. While we don’t get much visible light at night, it turns out this mechanism can also be triggered with another combination of light and chemistry when we employ it.

Under infrared light and with a chlorin injection, retinal changes in the same way as it does under visible light.

This explains the increase in night-time visual acuity. As chlorin e6 absorbs the infrared radiation, it interacts with the oxygen in the eye tissue, transforming it into highly reactive singlet oxygen – as well as destroying cancer cells, by creating singlet oxygen. In cases where thiamine is deficient, more oxygen is available in the blood as shown above and an abnormally large ROS singlet signal is made and this can lead to more damage to photoreceptors. In cases, without significant thiamine deficits, this free radical can also react with retinal and enable a boost in night vision.

This is why in patients undergoing photodynamic therapy with cancer, many have reported seeing silhouettes and outlines in the dark. This example also illustrates how thiamine and retinal physiology are intertwined with light frequencies.

People have remarked how could medicine not understand how powerful circadian biology and the sun are for humans?  How did we swing and miss on thiamine, deuterium, and mitochondrial biology?

Might it be how we collect our evidence in medicine?

I think so.

Why?  When I went through my own awakenings in 2004 and 2005 a key paper came out in the literature.

In 2005, Dr. John Ioannidis, a well-known meta-researcher, published an article in PLoS Medicine called Why Most Published Research Findings Are False. This article caused a splash and has been making waves in the medical research community ever since.

When I first read his article, I wasn’t the least bit shocked as a clinician because my patients were not getting better with any Evidence Based Medicine recipe that was published up until this.  This raises the question, if our evidence is bad, what could possibly go right in healthcare for patients?   The article left me begging the clinical question for my patients, what should I do now for my patients?

The answer was to go back and look how the evidence was collected and then try to link it back to nature’s laws.

I think we must increase value by reducing waste in research.  Too many studies are being funded in areas that are useless to move the needle for the public good.  The reason this happens is because Big Pharma is paying the bill for RCT’s.

Nature doesn’t make mistakes – but people sure do with poor choices around light.  None of this is reflected in our evidence.  THIS IS A PROBLEM.

Modern evidence based medicine (EBM) via algorithms is a flawed process. The data that were sent to clinicians from the researchers are nothing more than fruit from a poison tree. How good is evidence if you are asking the wrong question and using a flawed metholodology in your data collection and testing? The process now used by medicine to harvest research data to make guidelines is scientific illegitimate, therefore it is clinically inappropriate.

Why EBM does not work is illustrated by Michel Accad having (mis)quoted the definition of EBM as “the conscientious, explicit, and judicious use of best evidence in making decisions about the care of individual patients”, in cite one below.

The correct quote should be:

“Evidence based medicine is the conscientious, explicit, and judicious use of CURRENT best evidence in making decisions about the care of individual patients”.

Most of today’s EBM is based on the drug cartel ideas of what we should study so they can gain more customers while they remain sick and untreated. Vested interests, such as the drug and medical device companies, often fund medical research. This means quality marks or guidelines based on this research may not represent the best clinical practice but rather the treatment option that benefits these companies.

The laudable goal of making clinical decisions based on evidence can be impaired by the restricted quality and scope of what is collected as “best available evidence.” The “authoritative aura” given to the collection alone, however, may lead to major abuses that produce inappropriate guidelines or doctrinaire dogmas for clinical practice. Today medicine’s algorithms are run by these horrendous ideas. This is why the public is getting a small benefit from healthcare today.

This illustrates the reasons why EBM is broken by those who use it:

1. Evidence comes in quality and selective reporting, either by publication bias or post-hoc subgroup analysis to obtain statistically and clinically significant results. It is quite common to use the examples illustrated by ISIS-2 study researchers to warn against frivolous subgroup analysis, in this case astrological signs, in blind pursuit of the holy grail of statistical significance.

2. Misquotation or taking the conclusion out of context is another expected way of forming the wrong basis for change in practice. The classic example for this is the conclusion drawn from NASCIS 2 involving the use of corticosteroids in spinal cord injury. This has been a huge issue in neurosurgery and spine care my entire career.

3. Garbage in, garbage out. This is my favorite reason why EBM is today’s best example of HOT GARBAGE. Most research today is not worth the paper it is written on. They ask the wrong questions and never serve the public good by helping lower diseases. This is why human epidemics are running wild. There are increasingly more observational studies in which causative links are suggested when the link can only be concluded as associative. These studies are retrospective research on prospectively collected data which is often flawed in certain aspect and cannot be used for anything other than what is it originally intended for.

4. Slow and out of date. Guidelines are often EBM in concept but can be biased due to institutional support, financial or material conflict of interest by various members of the committee and quickly out of date after publication. It is not unusual for various national clinical network to take 5+ years to form a consensus which itself is soon overtaken by new revelations and technology. The new guideline for AHA ACLS training come to mind. Over 330 new guidelines and only three have class one evidence? WHY ARE WE CHANGING A THING IN THIS CASE?

5. Bias in researchers/opinion makers: conscious and unconscious. Except for triple-blind studies, most results can be influenced (to various extents) by the conduct of the study which is dependent on researchers. Unconscious bias can occur based on individual outlook, professional training and past experience when a group of experts come to consider inclusion or exclusion of prospective studies to base their recommendations on.

6. The temple of Meta-analysis and Randomized Controlled Trials (RCTs) and their worshippers. Many EBM converts enthusiastically proclaim that without RCT or Meta-analysis, all treatments warrant review. THIS IS LUDICROUS. Workman’s compensation guideline use this to block PBM/LLLT treatments to people with TBI. However, many questions cannot have RCT to be performed due to rarity of the conditions or ethical issues. Some questions (for example, benchmarking diagnostic tests) do not need RCT to be performed. Well-conducted RCTs are often expensive, labor-intensive and take time to perform and reach their conclusion, sometimes being overtaken by other technological and social changes. TBI is one such area.

7. No evidence of effect is not the same as evidence of no effect. Many confuse the state of having no studies showing effect as the same as having studies showing no effect. Some suggest that certain treatment should be stopped when there are no high quality studies showing effectiveness of a therapy; that may be a valid assertion but as suggested by the definition of EBM, we ‘make do’ with whatever CURRENT evidence is available until something better comes along (we should remain vigilant for new knowledge). However, when there is high quality evidence of no effect, it is unethical to persevere with treatment proven to make no difference.

8. What matters to you does not necessarily matter to me. The recent move towards Patient Reported Outcome Measures (PROMs) and Patient Reported Experience Measures (PREMs) when designing new studies may still not be relevant to patients. Various studies looked at outcomes when the treatment was never intended to solve the problem. A recent example found paracetamol ineffective in long term back pain underlies the common sense that short acting symptom-relieving paracetamol was never meant to be used as a disease modifying drug. Evidence-based guidelines often map poorly to complex cases where the patient has multiple co-morbidities. Most specialist care cases fall here.

9. Ask the right questions, do the right maths in statistics. Today, this methodology is vastly ignored. It is often perplexing when considering large studies where some researchers appear to demonstrate lack of care in the most important aspects of the study both asking the question that is clinically relevant, choosing the right outcome indicators to measure, and harnessing the skills of a clinical statistician to determine what is needed to be done. 2 meta-analyses published with 12 months of each other can reach opposite conclusions; the difference lies in what question is really (and not reportedly) asked, which studies are chosen for analysis. Statistically significant benefits of one treatment over another may be marginal in clinical practice, but this information may not be included in CDS or other tools.

10. Academic and Institutional integrity of Centers and Hosptals must be questioned because of how they are using guideline to police clinicians. Inflexible treatment recommendations from evidence-based medicine tools may produce care that is management-driven rather than patient-centered. Clinicians can be punished by hospitals for not doing their dirty profitable work that never suits the patient.

Moreover, often times 2 apparently similar studies reach different conclusion in spite of similar setting and control; chance occurs providing conflicting answers. On the other hand, there are times when deliberate acadmic misconduct occurs and it can take years to identify the culprits of the misdeed. Being aware of websites like https://retractionwatch.com keeps people up to date but all researchers should be considered with some initial suspicion; even the work of a scientific icon like Mendel has been considered by some as ‘prescient’. No authors should be immune to the vigors of scientific curiousity and testing.

Does evidence based medicine adversely affect clinical judgment?

Yes, but only because the clinicians allow this to occur. In the age of information overload and excesses, it is important for clinicians to be professional is their approach to evidence, be it single landmark studies or national guidelines.

If the evidence is important enough to change your practice, then make sure the quality of research is high, the analysis is correct, the conclusions are reasonable and the relevance is current and applicable. If clinicians want to ignore the study conclusion or guideline recommendation, the onus is still on them to prove without bias why this should be.

The obligation rests with clinicians who are in direct therapeutic relationship with patients; hence they have the ultimate responsibility as learned sentinels advising the patient.

11. The current volume of evidence, especially clinical guidelines, has become almost unmanageable for ANY CLINICIAN.

Oculi tanquam speculatores altissimum locum obtinent = The eyes, like sentinels, occupy the highest place in the body.

Consistent with hypoxia/ischemia, thiamine deficiency stabilizes and activates Hypoxia Inducible Factor-1α (HIF-1α) under physiological oxygen levels.  Oxygen levels and thiamine control the intake and outtake systems of the mitochondrial matrix…………How did medicine miss these basics?

This series will continue to abolish more of your beliefs.

The reality is this:  the induction of HIF-1α mediated transcriptional up-regulation of pro-apoptotic/inflammatory signaling contributes to astrocyte cell death in the CNS and PNS during thiamine deficiency.  This destruction begins in the mitochondria and destroys neurons everywhere in your body.

Maybe now we can see why the evidence and treatment guideline has not yet supported why our modern environment is causing neurodegeneration? 

CITES:

Sackett DL, Rosenberg WMC, Gray JA, Haynes RB, Richardson WS. Evidence based medicine: what it is and what it isn’t. BMJ1996;312:71-2

David H. Freedman (November, 2010) Lies, Damned Lies, and Medical Science, The Atlantic

Ebrahim S, Sohani ZN, Montoya L, et al. “REanalyses of Randomized Clinical Trial Data.” JAMA 312, no. 10 (September 10, 2014): 1024–32. doi:10.1001/jama.2014.9646.

Ioannidis, John P. A. “Why Most Published Research Findings Are False.” PLoS Med 2, no. 8 (August 30, 2005): e124. doi:10.1371/journal.pmed.0020124.

Ioannidis JA, and Khoury MJ. “Assessing Value in Biomedical Research: The Pqrst of Appraisal and Reward.” JAMA 312, no. 5 (August 6, 2014): 483–84. doi:10.1001/jama.2014.6932.

Young, Neal S, John P. A Ioannidis, and Omar Al-Ubaydli. “Why Current Publication Practices May Distort Science.” PLoS Med 5, no. 10 (October 7, 2008): e201. doi:10.1371/journal.pmed.0050201.

The poem above was written for me by Anna P., a college freshman at Spring Hill University in Mobile Alabama..  

There’s a reason why the first thing we often ask someone when we meet them, right after we learn their name, is “where’s home for you?”

For me home is 100% in Nature.  It does not require a house for me.  This makes my perspective unique in the West.  

We may use our homes to help distinguish ourselves, but the dominant Western viewpoint is that regardless of location, the individual remains unchanged. It wasn’t until I stumbled across the following notion, mentioned in passing in a book about a Hindu pilgrimage by William S. Sax, that I began to question that idea:  People and the places where they reside are engaged in a continuing set of exchanges; they have determinate, mutual effects upon each other because they are part of a single, interactive system.

What I learned from Eastern philosophy is that while in the West we may feel sentimental or nostalgic attachment to the places we’ve lived, in the end we see them as separate from our inner selves. Most Westerners believe that your psychology, and your consciousness and your subjectivity don’t really depend on the place where you live, They come from inside — from inside your brain, or inside your soul or inside your personality. But for many Eastern cultures, a home isn’t just where you are, it’s who you are.

I realized I am relentless chaos years ago.  That is where my home is built.

In the modern Western world, perceptions of home are consistently colored by factors of economy and choice. There’s an expectation in our society that you’ll grow up, buy a house, get a mortgage, and jump through all the financial hoops that home ownership entails.

The endless options can leave us constantly wondering if there isn’t some place with better schools, a better neighborhood, more green space, and on and on. We may leave a pretty good thing behind, hoping that the next place will be even more desirable.

In some ways, this mobility has become part of the natural course of a life for this Black Swan. The script is a familiar one: you move out of your parents’ house, maybe go to college, get a place of your own, get a bigger house when you have kids, then a smaller one when the kids move out. It’s not necessarily a bad thing. Even if we did stay in one place, it’s unlikely we would ever have the same deep attachment to our environment as those from some South Asian communities do. It just doesn’t fit with our culture.

But in spite of everything — in spite of the mobility, the individualism, and the economy — on some level we do recognize the importance of place. The first thing we ask someone when we meet them, after their name, is where they are from, or the much more interestingly-phrased “where’s home for you?” We ask, not just to place a pushpin for them in our mental map of acquaintances, but because we recognize that the answer tells us something important about them. My answer for “where are you from?” is usually NYC, but “where’s home for you?” is a little harder for me to answer because I do not resonate with the concrete jungle any longer.

That environment taught me what not to seek in a home.

Home is where my heart beats well in Nature, then by its most literal definition, my home is wherever I am at that moment. I make the best of it because I a confident that I am making the choices of where I should be living for me.

Home is where I have all my skin in my own game.

And the truth is, the location of your heart, as well as the rest of your body, does affect who you are. The differences may seem trivial (a new subculture means new friends, more open spaces make you want to go outside more), but they can lead to lifestyle changes that are significant.

Memories, too, are cued by the physical environment we choose these days. We remain clueless about how the nnEMF footprint changes our feelings about the place we live now. When you visit a place you used to live and feel the difference now, these cues can cause you to revert back to the person you were when you lived there. You realize for the first time just how relative time is.

The rest of the time, different places are kept largely separated in our minds. The more connections our brain makes to something, the more likely our everyday thoughts are to lead us there. But connections made in one place can be isolated from those made in another, so we may not think as often about things that happened for the few months we lived someplace else. Looking back, many of my homes feel more like places borrowed than places possessed, and while I sometimes sift through mental souvenirs of my time there, in the scope of a lifetime, I was only a tourist in my own journey.

I can’t possibly live everywhere I once labeled home, but I can frame these places on my walls. My decorations can serve as a reminder of the more adventurous person I was in New York City, the more carefree person I was in Connecticut, and the more ambitious person I was in New Orleans. I can’t be connected with my home in the intense way Easterns are, but neither do I presume my personality to be context-free. No one is ever free from their social or physical environment. This is ever more true in todays social media terroir. And whether or not we are always aware of it, a home is a home because it blurs the line between the self and the surroundings, and challenges the line we try to draw between who we are and where we are.

For me right now as a soloist, home isn’t a place. It is a person. And I think I am finally getting home right.

I live in my own little world. But its ok for me. It appears they know me here well and I like that discomfort.

Reading Anna’s poem made me realize discomfort is the price of admission to a meaningful life………….I rather like that.

Thiamine, also known as vitamin B1, is now known to play a fundamental role in energy metabolism.  When we are deficient in B1 the mitochondrial matrix suffers from pseudohypoxia.   Its discovery followed from the original early research on the ‘anti-beriberi factor’ found in rice polishings. After its synthesis in 1936, it led to many years of research to find its action in treating beriberi, a lethal scourge known for thousands of years, particularly in cultures dependent on rice as a staple.

Thiamine pyrophosphate (TPP) is the active co-enzyme form of thiamine and it is abundant in human RBC’s.  For this reason it is a reasonable marker that we can use in mitochondrial matrix failure associated with higher heteroplasmy states.  When we see abnormal peripheral smears in patients it signifies that we might want to clinically assess TPP activity and thiamine levels in our patients.  Some disease states associated with high mitochondrial density show these clinical features more often than not because certain organs have higher mitochondrial capacity.

When TPP is abnormal so is transketolase in RBC’s.  Transketolase is an enzyme of both the pentose phosphate pathway in all organisms and the Calvin cycle of photosynthesis.

When RBC transketolase is abnormal this is a beacon that RBC might not have a high fidelity signal connecting the sun to our colony of mitochondria.  This fosters the development of heteroplasmy in an insiduous way.  If one is not looking for it, a relative thiamine deficiency can manifest in many disease or non disease states.

In humans, transketolase connects the pentose phosphate pathway (EMF 4) to glycolysis, feeding excess sugar phosphates into the main carbohydrate metabolic pathways. Its presence is necessary for the production of NADPH (PPP), especially in tissues actively engaged in biosyntheses, such as fatty acid synthesis by the liver and mammary glands, and for steroid synthesis by the liver and adrenal glands. Thiamine diphosphate is an essential cofactor, along with calcium as a co-factor.

THE KEY LINK:

Thiamine Pyrophosphate (TPP) is the cofactor needed for the following reactions, Thiamine is required for only 4 biochemical reactions in the body  1. Pyruvate dehydrogenase 2. α ketoglutarate dehydrogenase  3. Branched-chain ketoacid dehydrogenase  4. Transketolase  TPP is involved in energy metabolism. Deficiency of TPP will affect the link reaction and TCA cycle. This leads to reduced ATP production and can alter function of the Pentose phosphate pathways I wrote about in EMF 4 blog post.  Red light from the sun can augment this ATP loss from thiamine deficiency.

Transketolase is an enzyme that uses a thiamine pyrophosphate (TPP) as its KEY cofactor to conduct a 2 carbon transfer from ketoses onto aldoses in humans. In the Pentose Phosphate Pathway (EMF 4 blog), it performs both a transfer of carbons from xylulose-5-P onto Ribose-5-P and onto Erythrose-4-P, setting them up for reaction with transaldolase.

Transketolase activity is decreased in deficiency of thiamine and can be used as a marker of heightened heteroplasmy by enlightened physicians.

RBC transketolase activity is reduced in deficiency of vitamin B1, and may be used in the diagnosis of Wernicke’s encephalopathy and other B1-deficiency syndromes if the diagnosis is in doubt. Apart from the baseline enzyme activity (which may be normal even in deficiency states), acceleration of enzyme activity after the addition of thiamine pyrophosphate may be diagnostic of relative thiamine deficiency from any causes.  This altered activity can be quantified as follows:

a. 0-15% normal

b. 15-25% deficiency

c. >25% severe deficiency

CENTRAL LEPTIN RESISTANCE:  LONG LOOP OF BAZAN

Liver disease is one such disease state that causes central leptin resistance (Leptin resistance Part Deux blog).  Most cases of liver disease have central leptin resistance associated with them due to damage of the long loop of Bazan (image below).  This limits the reincorporation of DHA into human cell membranes and fosters inflammation because the elvanoids cannot be made to curtail the inflammatory cascade.

 

Simultaneously, thiamine can be depleted because of altered matrix functioning.   There is brisk evidence that thiamine deficiency is found in many liver diseases.  The literature reports 58% of patients with chronic liver disease have B1 deficiency, moreover, the incidence is higher in alcoholic than in non-alcoholic hepatic patients. It has also been shown that daily supplementation with high doses of thiamine hydrochloride (200 mg/day) for one week can restores levels of thiamine pyrophosphate (TPP) in most cases.  Since TPP is the active co-enzyme form of thiamine, it also stimulates synthesis of the enzyme transketolase. Because of the essential role of TPP as a co-factor in intermediary metabolism of carbohydrates, lipids, and protein it can be a proxy marker for mitochondrial matrix dysfunction.  It maybe a NOVEL new way for us to indirectly measure heteroplasmy levels in humans.

THE LINK TO TECHNOLOGY:

Because thiamine is a major factor in the metabolism of glucose, it has long been known that ingestion of simple carbohydrates, processed in the body mainly to glucose, automatically increases the need for dietary thiamine. Since Frey and Volkow work, we know exposure to nnEMF also increase AMPK and glucose metabolism it should be clear that technology use and abuse can mimic nutritional problems historically associated with Vitamin B1.  Thus, high calorie malnutrition and technology abuse should be commonly associated with a chronic relative thiamine deficiency, irrespective of its fortification in food substances or the diet of any patient.  This relative deficit might lead to unusual presentations of disease linked to elevated heteroplasmy in humans.

QUICK SUMMARY:

Thiamine is normally present in pastured  lean pork and other meats, wheat germ, liver and other organ meats, poultry, eggs, fish, beans and peas, nuts, and whole grains. It is lower in foods like those mentioned above that have been altered by man’s input into food webs.  Blue light screens and nnEMF field deplete cells of thiamine because of how they affect AMPk pathways and glucose metabolism to mimic high calorie malnutrition.  Modern dairy products, fruit and vegetables are not good sources of B1.  In fact most of them deplete thiamine stores.  Humans only have the ability to store 14-18 days of this essential vitamin.  This storage ability is decreased by technology abuse and by vegan/vegetarian diets.   The RDA is 0.5 mg per 1000 kcal, adequate for a healthy individual consuming a healthy diet. Considerable losses occur during cooking or other heat-processing of food. Polyphenolic compounds in coffee and tea inactivate thiamine so that heavy use of these beverages could compromise thiamine stores in tissues.  

CITES:

http://jackkruse.com/emf-4-why-might-you-need-carbs-for-performance/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6435462/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6459027/

When a wise person speaks he understands fully the intent of the words, but what the ignorant person hears is subject to their present set of knowledge. There is an inherent disconnect. There is always a loss of information and energy transfer in this case which is why social media is not the ideal place to explain yourself in order to teach.

This requires the student having skin in the game to understand things well and it is best done in person. Where misunderstanding dwells, misuse will not be far behind in the under-educated mind. It is far safer and wiser for the quantum biologist to remain on the solid ground of the physics of light and eschew the shifting sands of philosophic extrapolations found in modern physics. The ignorant among us can know things, but the point of life is to understand how all things link back to the fabric of nature and life.

Life also has another surprise for those with natural wisdom: When we talk sense to a fool they often try to label you foolish only because of their own ignorance. If your audience is not wise this can lead to meme creation and control of many other lean minds. The goal is to make the curious wise with nature’s wisdom quickly to overcome the wasteful inertia of a paradigm’s core beliefs. This is why I am allergic to a closed mind who buries curiosity. What is the core message for a curious mind? Just because you don’t understand it, doesn’t mean or imply that the truth is not being delivered to you. Your wisdom myopia does not trump the deep truths buried in nature’s laws. There is a science of light out there to understand, and to bring it to biology is to brighten everyone’s perspectives. Today, biology is in the dark ages of understanding how light works with and within cells and innovates life from abiotic atoms.

This must change if medicine is to advance. An age in science is called dark, not because the light fails to shine, but because people refuse to see what is already published in the literature but still have yet to understand how it links back to life. Their educational myopia allows them to remain in the dark because they continue to misunderstand the implications of this data.

Your friends and family might not understand your new found ideas so this might help you help them to improve your relationships with in your circle of six.

I covered this in Levee 25 of the Quilt long ago and now this series will visit this in depth:

Hypoxia/pseudohypoxia.  Hypoxia is a cellular state that disrupts normal oxygen supply to the tissue (mitochondria), causing cellular dysfunction. Examples of t 25.his are altitude sickness at high elevations and clots in a blocked artery in an organ causing an organ to fail and die. Apoptosis and autophagy allow cells to adapt over their lifespan to many situations. Hypoxia is directly toxic to mitochondrial energy production. In humans, when oxygen is in short supply we can shift to anaerobic energy production, but it is not as efficient as mitochondrial energy production. Athletes with proper training can perform well in anaerobic conditions but it does appear that they pay a steep price for this adaptation by depleting their stem cell supply.  The gateway in mitochondria for hypoxia is pseudohypoxia by blockade of pyruvate which sits atop the TCA cycle inside the matrix.  The gatekeeper of the creation of Acetyl-CoA from pyruvate is thiamine.  It is the major controller of substate movements in the matrix.  As it drops we lose control of UCP-2 and this alters the matrix concentration of hydrogen isotopes.

Thiamine deficiency causes a relative pseudohypoxia and is closely linked to heteroplasmy rate elevation in aging.  Coffee and polyphenols destroy thiamine levels.  As this occurs there is massive signaling to the SIRT system to affect mitochondrial biology.

As a consequence of pseudohypoxia, NAD+ levels drop and this funnels all the way back to how the aromatic amino acid tryptophan is catabolized in cells.  It has multiple pathways it can travel and the pathway chosen will lead to the cell’s fate.

Hypoxia plays a role in aging because as one age the amount of blood to organs declines as the heart fails to deliver the same amount of blood through a stiffened arterial tree throughout the body. THIS IS A PROTECTIVE STATE FOR POOR MITOCHONDRIAL FUNCTION = higher heteroplasmy rate.

This causes cellular oxygen levels to fall and usually is a signal to mitochondrial biogenesis to offset the deficits. As one age, this signaling system is not as accurate in sensing changes to the oxygen level. This can be measured in the pyruvate/lactate levels. Low oxygen tension is a signal to autophagic pathways that normally help repair cells. If this gets impaired, signaling autophagy becomes less effective as we age and results in more organ failure and diseases of aging. Hypoxia is critical signaling in the cell for repair processes. This is disordered in heart disease and in sleep abnormalities such as sleep apnea. Hypoxia decreases cell mass and improves leptin resistance by forcing a calorie restriction via a relative thiamine deficiency state. This only operates well if the person remains in a strong solar environment.

This, below, is the deep lesson of levee 25.