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Sunlight is a gift that brings immunity to many pathogens. It just so happens the one everyone is interested in now, C-19 is one of those pathogens who has a strict seasonal variability.

A recent study has shown that Intrinsic Photosensitivity Enhances Motility of T Lymphocytes to improve motility to improve immune protection from pathogens.

Until recently, photoreception in mammals was believed to be restricted to the eye. Since 2017 we now know it is also a property of the skin.

The largest amount of T cells are found in the skin followed by the gut lining.

Normal skin contains a high density of T lymphocytes performing immune surveillance, and the total number of T cells resident in skin is estimated to be double of that in circulation

In this study it is shown that T cells possess intrinsic sensitivity to blue and UV light. Blue light links to T cell hypoxia and UV light decreases hypoxia by increasing oxygen to these cells to create a large free radical pulse to destroy pathogens.

1. Blue light increases [Ca^2+] in T cells which diminishes your immunity = increased C19 risk

Blue-light irradiation of Jurkat T cells triggers an increase in intracellular [Ca^2+] as measured by Fluo4 fluorescence which was followed by extension of lamellipodia

2. Irradiance and spectral dependence of T-cell photosignaling

Data shows that the light response depends on the total number of photons rather than irradiance flux or time and this observation supports the existence of a photon-counting mechanism.

3. Light generates Ca^2+ signals via a Src kinase/PLC-γ1 pathway

Blue-light dose-dependently stimulated phosphorylation of Lck, the dominant Src kinase in Jurkat cells.

4. Light generates H2O2 in T cells to fight viruses*

Flavins are readily photoreduced leading to the generation of ROS including H2O2. Accordingly, they confirmed that blue light irradiation of flavin-containing solutions, at similar doses (600 mJ cm^−2) used on T cells, produced H2O2 in vitro.

To directly and selectively monitor H2O2 levels they transfected Jurkat cells with the genetically-encoded H2O2 reporter, HyPerRed29. The researchers found that a low dose of blue light (300 mJ cm−2, 30 mW) was sufficient to trigger H2O2 production in Jurkat cells.

5. Therefore, we can now say definitively that the light in your environment can enhances T-cell motility* if it is solar based. We can also say that is decreases T cell function if the light you live under is man made.

The researchers observed that blue-light irradiation altered the morphology of T cells, inducing the extension of lamellipodia. Since motile lamellipodia are associated with cell migration they measured effects of light on T-cell motility by tracking the movement of activated CD8+ T cells across a fibronectin-coated surface. Low levels of blue light (120 mJ cm^−2) increased random T-cell motility and the peak surface area (reflecting spreading lamellipodia), an effect that persisted following irradiation. Thus, T cells exhibit photokinetic behavior.

Next, they measured effects of light on chemotaxis. Figure 5d shows that irradiation with white light (1–5 J cm^−2) enhanced migration of Jurkat T cells towards the T-cell chemokine, stromal-derived factor. Light increased chemotaxis in a dose-dependent manner with a peak 100% increase observed at irradiances greater than 2 J cm^−2.

REMEMBER: There is not a politician on this planet that is going to save you. Wearing a mask for a nanoscopic virus is pseudoscientific as the recent Danish study showed. The LA Times seems to have a reading comprehension problem.

This shows you the main stream media is another step closer to George Orwell’s Ministry of Truth (“1984”):

The LA Times tweet above was referring to the Danish mask RCT, ???????????????????? ???????????????????????? ???????????????? ???????????????????? ???????????? ???????????? ????????????????????????????????????, blatantly lies and reports the exact opposite conclusion!

A new low is made every day to get control of your behavior and life.

Lock downs are also pseudoscientific. Politicians could care less about biology; their only interest is in how much control you’re willing to give them by decree.

Don’t be fooled — you are responsible for yourself. This is a Black Swan mitochondriac axiom. Politicians need to live this axiom: Integrity is not a 90% thing, not a 95% thing; either you have it or you don’t.

#medicine #sunlight #aheadofthecurve #electromagnetic

CITES:

https://lnkd.in/g-vVDyB

Wow. BlackRock CIO of Fixed Income Rick Rieder talking about Bitcoin replacing gold on CNBC this morning. pic.twitter.com/9KZR0muJVp

— Pomp ???? (@APompliano) November 20, 2020

Black Swans need to pay attention to this topic. Many of you may not understand how health and wealth are linked but in the world being built right now by politicians that linkage in a few years will be undeniable and dangerous for those who fail to heed the warnings I am sharing now. This will be the antidote to the medical algorithms you’ll face from the aftermath of this pandemic. The relationship between health and wealth is called “gradient”: the health improves when the income grows, and the poor has worse health than the rich, what means the higher the gradient the better the health.

Now I want you to look at what a leading UK politician recently said to the news below.

^^^^The thinker who is linear will find this argument compelling.  But the thinker who plays 4D chess when everyone else is playing checkers will know the data behind these ideas show us something else.

This blog series is about the relationship between health and wealth. The goal is to show that they are connected to each other, and that improving health can lead to improve of wealth.
The first part discusses the effect of health on wealth and vice versa. It shows that better wealth is connected to better health and health increase lead to the wealth increase.  This is opposite to what the politician says above.

Then there is a theoretical model by Grossman (1972) and which was modified by Jacobson (2000). The model shows that the health is seen as “a stock” and that individual can invest into the health during the lifetime. The model shows also the change, when there is a family without children (partners can invest into each other’s health) and the family with a child (parents invest into child’s health).

The wage and education effect is shown and developed by Grossman (1972). The increase in wage leads to increase in health, individual has more money to visit the doctors who can give the correct answers to problems and not the ones designed in a government algorithm which goal is to limit government costs.  The algorithm is not optimized to your health. This is why it is given away in free healthcare systems.

Why should you come to this site or become my member longer term?  I will improve your health and wealth in ways few of you understand now.  Any increase in education should also leads to increase in health, but in this case individual gets more information on healthy lifestyle and follows it.

Many literature reviews show how education, social status, early childhood, family and nutrition affect the health span. The better educated (mitochondriacs) have better health and higher income over time. An additional year of education increases the life. I am going to tell that only corresponds to those who get the RIGHT education that marries to ideas that follow nature’s laws.

Lower socioeconomic status increases the probability of consuming unhealthy goods and being less educated. Medical algorithms are built to educate the masses for the benefit of govenrment, not for the public’s good.  This defines what a medical tyrrany is.

The subjective social status affects the childhood, the mental health and the income. Family plays a crucial role: the mother’s health, parents education, family’s socioeconomic status effect the health of a child and the future income. The low birth weight, mental health problems in childhood and bad nutrition lead to problems in health in the future and lower income.

When the connection between health and wealth, and factors affecting the health become known, it is easier to implement policies to increase the total health and wealth. The healthy individual is more productive and it eventually leads to economic growth.  Right now the world is imploding economically because of virtual reality pandemic built by politicians to bail out a failing monetary policy that is happening globally.

As I mentioned above the relationship between health and wealth is called “gradient”: the health improves when the income grows, and the poor has worse health than the rich, what means the higher the gradient the better the health. Poor health decreases the time available for working and decreases the earnings, at the same time it increases medical expenses, all of these lead to even poorer life than before.

I believe that increasing the health is one way to increase the wealth.  Here is an example to support my contentions above.

Candeias (2016) studied the effect of diabetes on the economic growth. The number of people having diabetes is rising. In 2010 around 11.6% of the total health expenditures in the world were spent on diabetes. Candeias writes: “Diabetes, and other preventable non-communicable diseases, can lead to increased absenteeism and reduced productivity while at work, inability to work as a result of disease-related disability, and lost productive capacity due to early mortality and exclusion from the workplace to take care of sick family members.”

Candeias (2016) concludes that preventing diabetes will help to prevent other diseases, like cardiovascular diseases and cancer, and the households can spend more money on other goods and services.

The relation between health and wealth

James P. Smith (1999) made calculations using data from Panel Study of Income Dynamics (PSID). His researches are based on the data from the United States of America. He made a table (Table 1) for different age groups and 3 different years (1984, 1989, 1994), where he showed the correlation between self-reported general health status and income (in 1996 dollars). He noticed that those in excellent health in 1984 have 74 percent more wealth than respondents in fair or poor health do. This difference in income is also related to schooling, “median incomes of 1984 college graduates were $77 000 compared to $ 28 000 among high school dropouts – virtually the same as the income gradient from excellent to poor health.”(Smith, 1999).

According to Smith, changes in health lead to changes in income. Among those in the age group 35- 44, who reported excellent health in 10 years (from 1984 to 1994) the medium income almost increased by $100 000, at the same time the income of those who reported fair or poor health increased only by less than $10 000. So, if the person’s self-estimated health increased from 1984, his or her income also increased.

The other factors which influence health are risk behaviors – like smoking, eating unhealthy food, drinking alcohol etc. These risk behaviors are more common in lower socioeconomic groups. For example, Marmout (1999) has found that the percentage of those with lower incomes or less education smoking is higher than of those who are well educated or earn more. In 1995, 40 percent of men who had not studied in a high school smoked, while only 14 percent of male college graduates smoked. Similar health patterns exist for other risk behaviors.

It is also important to mention that periods of poor health in the middle age has a negative impact on retirement. If the earnings are reduced in the middle age, it will lead to reducing of the pension and social benefits later on. Smith (1999): “Since health status is positively correlated even across quite distant ages, a correlation of retirement income and current health may flow from past health to current retirement income”.

As was mentioned before, health has an important influence on wealth, if the person experience poor health it may reduce the savings and the current income, at the same time it may increase out- of pocket savings. In this sense, the Black Swan should look at “health is a stock“, which has potential effects on future income, consumption and medical expenses.

Smith (1999) made a table using the data from Health and Retirement Survey (HRS) and from the Asset and Health Dynamics of the Oldest Old Survey (AHEAD). The table consists of two households, ages 51-61 and ages 70+, and distributions of out-of-pocket medical expenses separately for those who experienced severe, mild or no new chronic diseases. Smith explained that severe conditions were defined as cancer, heart condition, stroke, and disease of the lung. All other onsets defined as mild.

The results show that the expenses with severe new chronic diseases for average 70+ aged individual are almost double compare to the one with no new chronic disease. And in the age group 51-61 the difference in expenses is more than double. And in both age groups 2 percent with new chronic diseases spent more than $30 000.

Smith argues that these results can be helpful to understand savings behavior that “some current wealth may have been accumulated to deal with today’s health problems”.

The problems in health reduce also the labor supply. In case of family, the spouse can work more and invest into the partner; this can be seen in section 3. But anyway the current health problems may reduce the household income in the retirement period.

Another way when health affects savings is when the individuals want to consume more when they are healthy than during the period when they are sick. So it can be that savings rise if the individual expect himself to get sick.

Smith (1999) also made an empirical model which estimates effects of new chronic health problems on household wealth accumulation and the pathways through which savings effects take place. The data he used was from panel surveys of HRS and AHEAD, he used the ordinary least square regression models and the results are in table 3. The table has 3 columns (dependent variables), which shows “between-wave” (there were several surveys conducted in three different years, and Smith calls these surveys as “waves”) changes in total household wealth, OOP=out-of-pocket medical expenses and total medical expenses. The results are mean estimates.

The table 3 shows that even with the mild onset in ages 51-61 with total medical expenditures $2 555, and the out-of-pocket expenditures are $635, the household wealth is lowered by $3 620. But with the severe onset diseases, when the out-of-pocket medical expenditures are not yet that high, the wealth is lowered by $16 846. The change in wealth is even more dramatic for the household with above median income, the household wealth is lowered by $25 371. There are alsoresults showing that health insurance doesn’t affect much on the incomes lowering, the difference is $175.

Because there was not enough data available for AHEAD, there is no information for mild and severe onset separated. The table 3 shows that any disease lows the income by $10 481. There is no information on total medical expenditure in AHEAD, that’s why Smith put NA in the column. In case of households ages 70+ the income is also has a dramatic lowering for the ones with above median income – $17 040.

Because table 3 doesn’t show the reasons behind the income lowering, except the health conditions, Smith made calculations using “empirical models of the alternative pathways though which wealth accumulation can change – out-of-pocket and total medical expenses, changes in labor supply and household income, changes in bequest intentions, and changes in mortality expectations. Three waves of HRS and two waves of AHEAD were used with separate models estimated for changes observed between each survey wave”. Table 4 shows the results.

From the table 4 can be seen that the out-of-pocket medical expenses are over $1 600, what is low enough compare to the total medical expenses. So the out-of-pocket expenses are not the main reason for the low income. When the new health problem is severe – the change in weekly hours is about 4 hours per week and a 15 percent point decline in the probability of staying at work. And there is no evidence if the person returns to normal weekly hours. The change in own earnings is lowered by around $2 600. The table 4 also shows that with new health “shocks” the person also changes the expectation in probability of living to 75.

Where does BTC, the new stock for the Black Swan fit in this story?

At the same time Smith agreed that these results create a puzzle for us to solve, the out-of-pocket medical expenditures are not that high compare to the total medical expenditures, and the change in income own earnings is not that big, but the total change in wealth, shown in table 3, can be dramatic.   This is where the idea of BTC comes in to build your future health.  

Smith explained that it can be caused by “measurement issues that understate medical costs or household income changes, or that overstate changes in household wealth. Out-of-pocket medical costs may well understate the full financial costs of an illness.   Becoming chronically ill is devastating to wealth, more than any other factor I have researched including taxes.  There are expenditures associated with an illness of a family member – transportation, reconfiguration of home care environments, and so on – which people may not think of as medical costs and are often not reimbursed.

“Although household wealth is notoriously difficult to measure, it is not apparent why any errors should be systematically related to health events unless estimates of wealth shift from optimistic to pessimistic with the onset of an illness.”

At the same time with the reduction of income, there is possibility for rising consumption of household; Lillard and Weiss (1993) found out that the marginal utility of consumption increases in periods of poor health. Also people may “invest” in their siblings or consume at a very high rate.  So if you begin to spend a lot this will draw down your savings.  Relocation to optimal environments is a key health span cost that Black Swans rarely plan for.

The case for membership with me is about education and thinking.

The day this picture was lifted out of the paper BTC was at 14K dollars.  Today, it is close to 19K and today is only two weeks later.  I told all my members at my July 4th, 2020 event the single greatest thing I could do to help their health right now was to make the case for them to buy any amount of BTC before the election closed in November.  On July 4, BTC was below 10K per BTC.  Why did I say it?  What did I see coming that too few saw coming?

I believe Black Swan mitochondriac education will also help to train people for decision making and problem-solving, to get information about healthy lifestyle and possible treatments. This will help them avoid medical algorithms designed to harm them.  Under a Biden regime medical algorithms will take center stage in American healthcare to limit costs by taking care out of healthcare.

Moreover, we know education may have biological effects on the brain.

The other important factor which affects health in the future is the childhood. What will our kids look like in a technocracy going forward? Blue light has a massive effect on embryonic health and this implies the cost of having children is going to skyrocket.

Barker (1997) wrote that the health of an embryo has an effect of the future health problems. For example, the lack of natural light and lowered oxygen tensions for an embryo leads to the low birth weights and to the disproportionate growth in different parts of the body and these can lead to the coronary heart diseases 50 or 60 years later.

Another effect on health during lifetime is stress related to the job and family. In a technocratic society that is limiting our freedoms to gather, celebrate, and live, this has driven the cortisol melatonin axis in health to dangerous levels. This is why suicide and diseases have climbed tremendously this year. More people are dying now of non covid diseases because of policy changes instituted by govenments. None of the policies are sceintfic. When you lose control of freedom you better have a stable of value to support you in a storm. This is why this series is being written. The time is now……..not later to make changes to your life. You may never get this opportunity again.

When the person is under the stress or threat, the level of adrenaline can increase which allows body to perform at higher levels. The trade off is it destroys dopamine and melatonin and sets up the stage for chronic health demise.  Increased adrenaline provides simultaneous challenges for blood pressure, heart rate and the immune system. In the short-run this changes are not dangerous, but when the stress occurs too often, the results can lead to disease, like high blood pressure, diabetes or poor sleep.

Income inequality is also one of the key factors which affect health. A common idea is that the social inequality raises levels of psycho-social stress which negatively affects adrenaline and immunological processes. In industrial countries the material level matters less than the fact being at the bottom in the social ranking. (Smith, 1999).  Many of you may not understand these linkages but I want you all to know that this doctor does understand it and I want you all to know that talking to your doctor about wealth is a health discussion.

THE TAKE HOME FOR THE MITOCHONDRIAC:  Three most important comments made in interview above:

Does he own BTC? No. This means his bias is low.

Is it worth the price today? He says, I don’t know.   That is an honest answer.

Is it a durable asset class, that is trackable and has the potential to replace gold? Yes.  That tells us he sees the thermodynamic value of BTC to generate wealth to increase our health span.

Black Rock controls 7 Trillion dollars for clients.   This tells us, that the Cheif information officer at a behemoth sees the case this asset.

The present reality is now flipping before our eyes my swans – everything will eventually settle in Bitcoin.  Data is the new dollar in a post COVID world.   Oil -> Bitcoin-> <Bitcoin -> Fiat -> Next commodity Gold -> Bitcoin-> <Bitcoin -> Fiat -> Next commodity.  That is the new flow chart.

My parting shot comes from current Kruse Longevity Center member Johan Lindstrom:  He made this statement yesterday to me at the pool in Tulum yesterday after he arrived from Norway.   “Jack, my family initially thought it was nuts for me to pay out of pocket to see a physician in the USA when I am in pretty good shape, but the results of my visit have not only helped my health, you have helped me create a new wealth platform that has paid for my membership many times over in less than a year.  That ability to think outside the box is extremely valuable to me and my family and I appreciate it.”

Health is a function of how well we are able to think.

Johan, a father of three young children now sees how health and wealth are linked.  This makes me happy that a citizen of an EU country sees the forrest through the trees.

It is time for some of you to begin to think in non-linear fashion as well.  Are you ready?  Join my tribe.  kruseatdestin.com

CITES: 

Grossman M (1972) On the Concept of Health Capital and the Demand for Health. Journal of Political Economy, 80: 223-255

Grossman M (2015) The Relationship between Health and Schooling: What’s new? Nordic Journal of Health Economics, 3(1): 7-17

Jacobson L (2000) The Family as Producer of Health – an Extended Grossman Model. Journal of Health Economics 19: 611-637

Smith JP, Healthy Bodies and Thick Wallets: The Dual Relation between Health and Economic Status, 1999

Candeias V (2016) 5 Reasons why Tackling Diabetes will Boost Economic Growth. https://www.weforum.org/agenda/2016/04/5-reasons-why-tackling-diabetes-boosts-economic- growth/

Strulik H (2018) The Return to Education in Terms of Wealth and Health. The Journal of the Economics of Ageing, 12: 1-14

https://cryptoticker.io/en/bitcoin-over-gold-investment-bank/

LUKE’S PRESCRIPTION: Where observation and epiphany collided at this years member event.

IgA responds to native magnetic fields and this links it to seasonal viral illness and to gut abnormalites. How does this occur?

There is a clinical correlation between an allergic patient’s ability to resist the development of symptoms that would have resulted from an allergenic challenge, the magnitude of geomagnetism at a geographic site, and (3) the amount of solar energy falling on that site. It is suggested that the digestive membrane has an electronic gatekeeper that “decides” electronically which molecules to allow or not allow to pass on to the absorptive surface. The unique bipolar structure of secretory immunoglobulin A (IgA), having a central secretory piece and the resultant unique electronic function of this polarized molecule, allows it to function as an electronic transistor, producing an electronic gatekeeper in the form of an electronic sieve.

High-gradient magnetic fields (HGMFs) have steadily gained the increased attention of researchers from different disciplines, such as cell biology, cell therapy, targeted stem cell delivery and nanomedicine because magnetic fields change cell structure and size. Recent theoretical framework has provided a fundamental understanding of the effects of HGMFs on intracellular processes. It appears altered magnetic fields have huge impacts on IgA creation and destruction. This science highlighs new directions for the study of living cell machinery: changing the probability of ion-channel on/off switching events by membrane magneto-mechanical stress, suppression of cell growth by magnetic pressure, magnetically induced cell division and cell reprograming, and forced migration of membrane receptor proteins. By deriving a generalized form for the Nernst equation, we find that a relatively small magnetic field (approximately 1 T) with a large gradient (up to 1 GT/m) can significantly change the membrane potential of human cell and thus have a significant impact on not only the properties and biological functionality of cells but also cell fate.

^^^^^  This is the most detailed model of a human cell to date, obtained using x-rays, nuclear magnetic resonance, and cryoelectron microscopy data sets.  Source and Credit: Transformation of the Cellular Landscape through a Eukaryotic Cell, by Evan Ingersoll Ingersoll Gael McGill ~ Digizyme’s Custom Maya Molecular Software—-Biología Al Instante

Current antibody tests for COVID-19 test only IgM and IgG, and assume that IgM represents a recent infection, while IgG will represent a recent or distant infection. IgM comes first, followed by IgG. IgM disappears rather rapidly, while IgG stays elevated for a very long time. Therefore, IgM suggests recent infection whether IgG is present or not, while IgG alone suggests an infection in the more distant past. In the first week, there are nearly twice as many people who are positive for IgA to the spike protein than those who are positive for either of the other antibodies. IgA continues to be most prevalent in the second week, and it is almost as prevalent as IgG in the third and fourth weeks. IgM is never the most prevalent, and it drops off in the fifth week just like IgA. Only IgG remains prevalent in the fifth week. IgA antibodies were five times more effective than IgG antibodies at neutralizing SARS-CoV-2, the coronavirus that causes COVID-19.

The patients whose IgA had the greatest ability to neutralize the virus were the ones who had the highest levels of IgA against the spike protein.  this means those who can harness the magnetic flux of the sun best have the lowest risk of C19.  It also means these are the people who won’t have gut issues from other causes.

Secretory immunoglobulin A is the dominant antibody isotype in mucosal secretions and plays an essential role in defense against pathogenic microorganisms bacterial and viral. However, even in the absence of infection, the body produces approximately four grams of IgA daily, more than all other antibody isotypes combined. Much of this IgA is secreted into the intestinal lumen, where it binds to and ‘coats’ specific members of the gut microbiota—the trillions of bacteria/viruses that constitutively colonize the human intestinal tract.

The gastrointestinal mechanism responsible for sorting molecules that were to be absorbed or rejected appeared to be related to the subject of electronics. The sorting process could be explained by the existence of an electronic sieve created via a massing of electronically enabled secretory immunoglobulin A (IgA) molecules, each acting as an electronic transistor. This electronic transistor function of secretory IgA can be achieved because of its bipolar structure and unique mid-secretory piece.

Secretory IgA plays a crucial role in shaping the composition and function of the gut microbiota in animals. It appears IgA responds to the varying magnetic fields on Earth between day and night.

Selective IgA deficiency (sIgAd), defined as a serum IgA concentration of less than 7 mg/dl with normal levels of serum IgG and IgM in subjects greater than four years of age, is the most common primary immunodeficiency in humans. Its incidence varies by geographical region, ranging from 1:700 in individuals of European descent to 1:18,500 in Japan. Location on Earth is linked to magnetic field strength variation. While IgA deficiency is often described as “asymptomatic,” sIgAd subjects exhibit increased incidences of infectious, allergic, and autoimmune disorders including inflammatory bowel disease. Secretory IgM can partially compensate for the lack of IgA in sIgAd subjects but not completely. Latitude and location seem to be the key to understanding the seasonality or the risk of electromagnetic pollution in many diseases.

UNCLE JACK’S TAKE HOME FOR LUKE: It appeared that the higher the geomagnetic properties of the area you live in, the more resistant the patient was to known allergens.  It appears if you live in a state with a lot of gas or oil deposits where drilling or fracking occur the more likely you will be to have gut issues. If you want an antidote move to the rim of the crater in PDC and Tulum and see how your symptoms respond. You might become able to turn on your electronic IgA transitor properly.

The gut mitohacker should investigation using the USGS color aeromagnetic anomaly map of the contiguous United States should be a top priority.

You should expect a sunset effect and seashore effect because of how magnetic flux varies at these times daily. You will crash at sunset and you will do better at the seashore with respet to all your allergens.

At the seashore or at a water fall you get a huge “Lenard effect”. This is when net negative ions are added to the air. This makes you more sensitive to magnetic flux and should improve your symptoms. An increase in ambient atmospheric negative air ions clinically appears to have a salubrious effect on a patient’s ability to successfully deal with a challenge from a known food allergen or from an altered microbiome.

Those with gut issues or weakened immune system should struggle with Faraday cage effects. If you use devices or a field-free room (Faraday cage) you might get worse. Within minutes after entering these rooms I have noticed over the years individuals experienced weakness and severe fatigue as a result. This told me IgA was their problem.

It appears to me as if the energy of the sun is capable to changing the magnetic suceptibilty of the gut and immune system. Observation of several of the Kruse Longevity cases over the last two years have given me this insight.

The final piece of the puzzle came for this October 2020 when I observed Luke over 4 days. I saw an amazing effect of a hurricane in the Gulf on Destin Fla Gulf and then observed changes at Morrison Creek and began to put things together. The eureka moment happened during a small speach from Luke in front of many where he came apart.  Sometimes we have to come apart to fall back together.

I realized that the sun’s magnetic flux was being absorbed in a kind of electronic “alimentation” that provided free energy to reverse entropy and allow for the accumulation of properly sized particles on one side of the digestive membrane, thus allowing secretory IgA to act like a kind of Maxwell’s demon.

Was this an evolutionary mechanism that animals developed to capture free solar energy just as plants developed photosynthesis as their mechanism for capturing free solar energy? I now suspect that secretory IgA is such a device that enabled this energy-capturing process to take place in the gut by acting as an electronic transistor to sculpt the microbiome and its immunologic response.  Could this a be a magnetic control gate for the brain?

Might gut IgA be the brain’s main protector.?

IgA cells that originate in the gut play a role appear to have neuroprotective properties against diseases associated with neuroinflammation, such as meningitis or viral infection.

The membranes surrounding our brains (dura) are in a never-ending battle against deadly infections, as germs constantly try to elude watchful immune cells and sneak past a special protective barrier called the meninges. In a study involving human autopsy tissue, researchers at the National Institutes of Health and Cambridge University have shown that some of these immune cells are trained to fight these infections by first spending time in the gut.

It appears gut-educated antibody-producing cells inhabit and defend regions that surround the central nervous system.   Without a proper IgA response the brain becomes attacked and mental and cognitive changes become more likely.

The central nervous system (CNS) is protected from pathogens both by a three-membrane barrier called the meninges and by immune cells within those membranes. The CNS is also walled off from the rest of the body by specialized blood vessels that are tightly sealed by the blood brain barrier. This is not the case, however, in the dura mater, the outermost layer of the meninges. Blood vessels in this compartment are not sealed, and large venous structures, referred to as the sinuses, carry slow moving blood back to the heart. The combination of slow blood flow and proximity to the brain requires strong immune protection to stop potential infections in their tracks.

The immune system has invested heavily in the dura mater. The venous sinuses within the dura act like drainage bins, and, consequently, are a place where pathogens can accumulate and potentially enter the brain. It makes sense that the immune system would set up camp in this vulnerable area to protect its Ferrari engine.

IgA cells had not been shown to reside in the dura mater under steady state conditions.  Now we know they do.

A recent study by the NIH (Cite two) discovered something surprising: there were many immune cells previously educated to make antibodies against specific microbes and viruses. These antibody-producing cells, called IgA cells, are typically found in other barriers such as the mucous membranes of the bronchial tree of the lungs and gut.

Pathogens present in the gut were important in educating meningeal IgA.

This new data provide more compelling evidence that the brain is protected by immune cells that are educated in the gut and lungs.

IgA is a magnetic transitor that needs to be present and active to repair the gut and brain.  Where you live matters deeply in this electronic dance with Nature.

 CITES

https://www.nature.com/articles/s41598-019-49923-2

“Gut-educated IgA plasma cells defend the meningeal venous sinuses” by Zachary Fitzpatrick, Gordon Frazer, Ashley Ferro, Simon Clare, Nicolas Bouladoux, John Ferdinand, Zewen Kelvin Tuong, Maria Luciana Negro-Demontel, Nitin Kumar, Ondrej Suchanek, Tamara Tajsic, Katherine Harcourt, Kirsten Scott, Rachel Bashford-Rogers, Adel Helmy, Daniel S. Reich, Yasmine Belkaid, Trevor D. Lawley, Dorian B. McGavern & Menna R. Clatworthy. Nature

Here is a brief history lesson time for those who do not understand how Bitcoin finance links to medical risk.

YOU SHOULD WATCH THE VIDEO ABOVE FIRST

PRESENT MOMENT:  WW2 uncovered a massive problem in financing using conventional banks in the post war period.  The baby boomers are driving massive use in healthcare because they are older and sicker.  1 million people per day become 65 years old in 2020.  Because of this, the USA is on track for a medical/retirement bankruptcy soon in the USA.

So anything that limits population size above the age of 60 will become excellent public policy because of what Nixon did in 1971.

Do you think this is hyperbole?

Do you want to continue to play checkers while some of us want to teach you to play 4D chess?

Our population is very ill  and OLD and the system is not able to handle their costs.  I see a bankruptcy of California and NY coming quite soon because of policy decisions.  Presidential decree and Congressional bailout are required to bail out a state.  Once this happens, money will be printed at will to pay the debt.   When did the US dollar become a FIAT currency?  1971 under Nixon.  This was done when Nixon announced the War on Cancer with Alton Ochsner.  The link for my members should now be obvious.  It was linked to the polio virus contamination with SV-40.  The government knew that there would be a coming chronic disease pandemics and had to do something to react to it.

President Nixon said to the Nation during his January 1971 State of the Union address: “I will also ask for an appropriation of an extra $100 million to launch an intensive campaign to find a cure for cancer, and I will ask later for whatever additional funds can effectively be used. The time has come in America when the same kind of concentrated effort that split the atom and took man to the moon should be turned toward conquering this dread disease. Let us make a total national commitment to achieve this goal.”

As part of this national effort, in October 1971, the Army’s Fort Detrick, Maryland, biological warfare facility was converted to a cancer research center, eventually becoming the Frederick Cancer Research and Development Center, an internationally recognized center for cancer and AIDS research.  That last part should perk your ears up.  AIDS is linked to the SIV for those who do not know.  Those of you who attended my July 4, 2019 event should really be perking up about now.  It was at this event that you heard me speak about the polio virus and the coupling to Bitcoin for the first time for my members.   I know it left many of you asking questions but this blog series will begin to close that gap.

On December 23, 1971, President Nixon followed through on his promise as he signed the National Cancer Act into law, declaring, “I hope in the years ahead we will look back on this action today as the most significant action taken during my Administration.”

The National Cancer Act (P.L. 92–218), “The War on Cancer,” gave the NCI unique autonomy at NIH with special budgetary authority. We see that unique behavior now born out in how Dr. Anthony Fauci has run free during the C19 pandemic.  Not even a president can keep a lid on his behavior.  You must ask yourself why this is the case.  I am asking you to look back to 1971 to understand what is really going on today.

The Cancer Chemotherapy National Service Center (CCNSC) increased its efforts to acquire new compounds for testing with the awarding of an acquisition and inventory contract responsible for the collection and documentation of test agents.

What else did they do at the same time?

Nixon created a shock wave for the economy.  The Nixon shock was a series of economic measures undertaken by United States President Richard Nixon in 1971, in response to increasing inflation, the most significant of which were wage and price freezes, surcharges on imports, and the unilateral cancellation of the direct international convertibility of the United States dollar to gold.

While Nixon’s actions did not formally abolish the existing Bretton Woods system of international financial exchange, the suspension of one of its key components effectively rendered the Bretton Woods system inoperative. While Nixon publicly stated his intention to resume direct convertibility of the dollar after reforms to the Bretton Woods system had been implemented, all attempts at reform proved unsuccessful. By 1973, the Bretton Woods system was replaced de facto by the current regime based on freely floating fiat currencies.

Since President Nixon’s decision to decouple the US dollar from gold in 1971, a system of national fiat currencies has been used globally.   My Black Swan who get this coupling are now talking about it privately.  My Farm members get more of this wisdom and insight than any other.  This is why I spoke about it publically for the first time in July of 19.

What is FIAT money?

Fiat money can be:

Any money declared by a government to be legal tender.

State-issued money which is neither convertible by law to anything else, nor fixed in value in terms of any objective standard.

Intrinsically valueless money used as money because of government decree.

An intrinsically useless object that serves as a medium of exchange.  Before fiat money the US dollar was pegged to the gold standard.  When and how?  The Bretton Woods system of monetary management established the rules for commercial and financial relations among the United States, Canada, Western European countries, Australia, and Japan after the 1944 Bretton Woods Agreement. The Bretton Woods system was the first example of a fully negotiated monetary order intended to govern monetary relations among independent states. The chief features of the Bretton Woods system were an obligation for each country to adopt a monetary policy that maintained its external exchange rates within 1 percent by tying its currency to gold and the ability of the International Monetary Fund (IMF) to bridge temporary imbalances of payments. Also, there was a need to address the lack of cooperation among other countries and to prevent competitive devaluation of the currencies as well.

Preparing to rebuild the international economic system while World War II was still raging, 730 delegates from all 44 Allied nations gathered at the Mount Washington Hotel in Bretton Woods, New Hampshire, United States, for the United Nations Monetary and Financial Conference, also known as the Bretton Woods Conference. The delegates deliberated during 1–22 July 1944, and signed the Bretton Woods agreement on its final day. Setting up a system of rules, institutions, and procedures to regulate the international monetary system, these accords established the IMF and the International Bank for Reconstruction and Development (IBRD), which today is part of the World Bank Group. The United States, which controlled two thirds of the world’s gold, insisted that the Bretton Woods system rest on both gold and the US dollar. Soviet representatives attended the conference but later declined to ratify the final agreements, charging that the institutions they had created were “branches of Wall Street”.  These organizations became operational in 1945 after a sufficient number of countries had ratified the agreement.

On 15 August 1971, the United States unilaterally terminated convertibility of the US dollar to gold, effectively bringing the Bretton Woods system to an end and rendering the dollar a fiat currency.

FED policy since 1971 was tied to control of the money supply without any grounded basis.  This has given central banks extraordinary control over public policy.  The major driver of costs in the USA budget since 1971 has been healthcare driven by the aging baby boomer.

So what do I see in the future?

What do I see? The Fed under Biden will only have two moves left to control the money supply : Print more cash or go to negative bond rates. Do you know what both of those things mean to you medical future? How about your financial future?

What do I see as option three? Is there a lift raft awaiting the Black Swan who plays 4D chess when everyone else is focused on the wrong metrics? I believe there is. There is one algorithm that is designed to fight the algorithms that are being built in corporate medicine which are designed to harm you.

I see a new Bretton Woods happening in the USA and Bitcoin will be that standard. I think medical bankruptcy by medicare and the two state defaults as the replacement for Bretton Woods during WW2 to replace the fiat currency.

THOUGHTS?  Leave me a comment below if you are a patron.

If you are a member of KruseatDestin.com I have more for you.

If you want to begin packing your own parachute or life raft open a BlockFi account here: https://blockfi.com/?ref=34f06254

This is advice I have given my Farm members.  I will be discussing this during this months Q and A for members.  I plan on opening the Q and A for all groups this month because this topic is now critical given the election results in the USA.

This is why your circle of six matters. Consider this my friendly reminder to you, you better have the right sets of eyes looking out for you in the future.

Thyroid function is like a relay race, with hormones passing the baton from the hypothalamus in the brain to the pituitary gland beneath it, then to the thyroid gland, to the liver, and finally to cells throughout the body.

The hypothalamus delivers messages to the pituitary gland via the chemical messenger thyrotropin releasing hormone (TRH). Once TRH delivers its message, the pituitary gland releases thyroid stimulating hormone (TSH).

TSH goes straight to the thyroid gland where it triggers the production of a protein called thyroglobulin. The thyroglobulin joins up with four molecules of iodine to produce the thyroid hormone T4, or thyroxine.

About 94 percent of the hormone made in the thyroid gland is T4. The remaining 6 percent is triiodothyronine (T3), named for its three molecules of iodine.

These thyroid hormones hitch a ride through the bloodstream on thyroid-binding proteins, during which they are referred to as “bound.” When they are dropped off at the cells for active duty, they are called “free” hormones.

Although the thyroid gland secretes only a little T3, it is the most active form the body can use. T4 must be converted to T3 before the body can use it. Most of this conversion happens in the liver, but also take place in cells of the heart, muscle, gut, and nerves. These cells convert T4 to T3 with an enzyme called tetraidothyronine 5’ deiodinase, which removes one molecule of iodine.

In the end, only about 60 percent of T4 is converted into usable T3. Twenty percent becomes reverse T3 (rT3), an inactive form the body cannot use. Levels of rT3 can become too high in times of major trauma, surgery, or severe chronic illness. Another 20 percent of T4 can be converted to T3 by healthy gut bacteria in the digestive tract.

HOW DOES ALTERED T3 LEAD TO HYPOXIA IN ILLNESS?  

A key discovery during the coronavirus H1N1 pandemic of 2009, … victims’ lungs lacked T3, a thyroid hormone that would normally be detectable. T3 reduces inflammation and coaxes epithelial cells in the lungs to absorb fluids.   Since AM sunlight creates T3 the antiviral link of sunlight should now be apparent.  This can be seen in the pic below.

In non-thyroidal illness (NTI) plasma T3 is often decreased and plasma rT3 increased; plasma FT4 is still in the normal range depending on the severity of the disease. The changes in plasma T3 and rT3 are explained by a diminished conversion of T4 to T3 and of rT3 to 3,3-T2 by D1 in the liver.

Most plasma T3 is derived from the peripheral conversion of T4.  Viral diseases are known to act as mitochondrial toxins that can lower oxidative phosphorylation and subsequent ATP production.  This causes a relative pseudohypoxia to develop in the colony of mitochondria during a viral illness.

T3 increases mitochondrial ATP production in oxidative muscle despite increased expression of UCP2 and -3.  So a lack of T3 would exacerbate mitochondrial hypoxia in illness.  This is what we have seen clinically in C19 patients who became symptomatic.  Those with mitochondrial dysfunction before infection are at the highest risk of C19 sequela.  Their Vitamin D levels have acted as a predictive lab for clinicians because solar exposure is critical in making Vitamin D3 and T3 in humans photosynthetically.

Since H1N1 is an RNA virus that shows homology to SARS_CoV_2 #COVID19 it should be obvious why T3 drugs are now being tested clinically in high latitude cities in the USA where the sun has lost its power.

As solar power is lost what happens in mitochondria?  Oxygen tensions change, and this causes changes in energy production and alterations in ROS because dissolved oxygen in cells increase as ATP drops.

Recall that ATP production is increased by exposure to red light. Sunlight is 43% red light. Here is another link of sunlight to energy production.

Thyroid hormone is indispensable for the normal development and metabolism of most cells and tissues. Thyroid hormones are metabolized by different pathways: glucuronidation, sulfation, and deiodination, the latter being the most important. Three enzymes catalyzing deiodination have been identified, called type 1 (D1), type 2 (D2), and type 3 (D3) iodothyronine deiodinases. D1 and D2 have outer ring deiodinase activity, converting the prohormone T4 to its bioactive form T3 and degrading rT3 to 3,3’-T2. D3 has inner ring deiodinase activity and degrades T4 to rT3 and T3 to 3,3’-T2.

The most remarkable feature of all three iodothyronine deiodinase is that they are selenoproteins, i.e. they contain a selenocysteine (Sec) residue in the center of the amino acid sequence.  Seafood is loaded with selenoproteins.  It is also loaded with iodine.  This is why seafood is also another antihypoxic C19 strategy because it has a huge supply of selenium and iodine involved in T3 optimization to improve mitochondrial function.

D1 is largely expressed in the liver and kidney. Its main role is clearance of rT3 from the circulation and it also contributes to the production of plasma T3. D2 is importantly expressed in the central nervous system, pituitary, brown adipose tissue, and muscle and, generally, its expression reciprocally responds to changes in thyroid state. D2 serves to adapt cellular thyroid state to changing physiological needs. D3 is importantly expressed in fetal tissues and in adult brain tissue. In addition, D3 can be re-expressed under certain pathological conditions such as critical illness or in specific cancers and infectious diseases.

CITES:

https://www.startribune.com/hormone-boost-could-be-covid-19-key/572944532/

Bianco AC, Salvatore D, Gereben B, Berry MJ, Larsen PR. Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases. Endocr Rev. 2002 Feb;23(1):38-89.

Larsen PR, Zavacki AM. Role of the Iodothyronine Deiodinases in the Physiology and Pathophysiology of Thyroid Hormone Action. Eur Thyroid J. 2012.

More on the science of masks.

The Science is Conclusive: Masks and Respirators do NOT Prevent Transmission of Viruses
Comment: The following review of the scientific literature on wearing surgical and other facemasks as a means of preventing the transmission of SARS-CoV-2 and thus preventing contraction of ‘Covid-19’ was published a month ago. And absent some miraculous suspension of decades of hard science on the transmission of viruses, it’s settled…

Abstract
Masks and respirators do not work for viral illnesses. There have been extensive randomized controlled trial (RCT) studies, and meta-analysis reviews of RCT studies, which all show that masks and respirators do not work to prevent respiratory influenza-like illnesses, or respiratory illnesses believed to be transmitted by droplets and aerosol particles.
Furthermore, the relevant known physics and biology, which I review, are such that masks and respirators should not work. It would be a paradox if masks and respirators worked, given what we know about viral respiratory diseases: The main transmission path is long-residence-time aerosol particles (< 2.5 μm), which are too fine to be blocked, and the minimum-infective-dose is smaller than one aerosol particle.

The present paper about masks illustrates the degree to which governments, the mainstream media, and institutional propagandists can decide to operate in a science vacuum, or select only incomplete science that serves their interests. Such recklessness is also certainly the case with the current global lockdown of over 1 billion people, an unprecedented experiment in medical and political history.

If masks worked as our experts said they did, why hasn’t the homeless population been wiped out? They don’t wear masks. They don’t social distance. And they live in unsanitary conditions for the most part.  But they do live outside where the sun is.  Is this a clue to us?

Review of the Medical Literature
Here are key anchor points to the extensive scientific literature that establishes that wearing surgical masks and respirators (e.g., “N95”) does not reduce the risk of contracting a verified illness:
Jacobs, J. L. et al. (2009) “Use of surgical face masks to reduce the incidence of the common cold among health care workers in Japan: A randomized controlled trial”, American Journal of Infection Control, Volume 37, Issue 5, 417 – 419.
N95-masked health-care workers (HCW) were significantly more likely to experience headaches. Face mask use in HCW was not demonstrated to provide benefit in terms of cold symptoms or getting colds.
Cowling, B. et al. (2010) “Face masks to prevent transmission of influenza virus: A systematic review”, Epidemiology and Infection, 138(4), 449-456. doi:10.1017/S0950268809991658
None of the studies reviewed showed a benefit from wearing a mask, in either HCW or community members in households (H). See summary Tables 1 and 2 therein.
bin-Reza et al. (2012) “The use of masks and respirators to prevent transmission of influenza: a systematic review of the scientific evidence”, Influenza and Other Respiratory Viruses 6(4), 257-267.
“There were 17 eligible studies. […] None of the studies established a conclusive relationship between mask ⁄ respirator use and protection against influenza infection.”
Smith, J.D. et al. (2016) “Effectiveness of N95 respirators versus surgical masks in protecting health care workers from acute respiratory infection: a systematic review and meta-analysis”, CMAJ Mar 2016, cmaj.150835; DOI: 10.1503/cmaj.150835
“We identified 6 clinical studies … In the meta-analysis of the clinical studies, we found no significant difference between N95 respirators and surgical masks in associated risk of (a) laboratory-confirmed respiratory infection, (b) influenza-like illness, or (c) reported work-place absenteeism.”
Offeddu, V. et al. (2017) “Effectiveness of Masks and Respirators Against Respiratory Infections in Healthcare Workers: A Systematic Review and Meta-Analysis”, Clinical Infectious Diseases, Volume 65, Issue 11, 1 December 2017, Pages 1934-1942, https://doi.org/10.1093/cid/cix681
“Self-reported assessment of clinical outcomes was prone to bias. Evidence of a protective effect of masks or respirators against verified respiratory infection (VRI) was not statistically significant”; as per Fig. 2c therein:
Clinical Infectious Diseases, Volume 65, Issue 11, 1 December 2017, Pages 1934–1942, https://doi.org/10.1093/cid/cix681
Radonovich, L.J. et al. (2019) “N95 Respirators vs Medical Masks for Preventing Influenza Among Health Care Personnel: A Randomized Clinical Trial”, JAMA. 2019; 322(9): 824-833. doi:10.1001/jama.2019.11645
“Among 2862 randomized participants, 2371 completed the study and accounted for 5180 HCW-seasons. … Among outpatient health care personnel, N95 respirators vs medical masks as worn by participants in this trial resulted in no significant difference in the incidence of laboratory-confirmed influenza.”
Long, Y. et al. (2020) “Effectiveness of N95 respirators versus surgical masks against influenza: A systematic review and meta-analysis”, J Evid Based Med. 2020; 1- 9. https://doi.org/10.1111/jebm.12381
“A total of six RCTs involving 9 171 participants were included. There were no statistically significant differences in preventing laboratory-confirmed influenza, laboratory-confirmed respiratory viral infections, laboratory-confirmed respiratory infection and influenza-like illness using N95 respirators and surgical masks. Meta-analysis indicated a protective effect of N95 respirators against laboratory-confirmed bacterial colonization (RR = 0.58, 95% CI 0.43-0.78). The use of N95 respirators compared with surgical masks is not associated with a lower risk of laboratory-confirmed influenza.”

Conclusion regarding masks that do not work
No RCT study with verified outcome shows a benefit for HCW or community members in households to wearing a mask or respirator. There is no such study. There are no exceptions. Likewise, no study exists that shows a benefit from a broad policy to wear masks in public (more on this below).
Furthermore, if there were any benefit to wearing a mask, because of the blocking power against droplets and aerosol particles, then there should be more benefit from wearing a respirator (N95) compared to a surgical mask, yet several large meta-analyses, and all the RCT, prove that there is no such relative benefit. Masks and respirators do not work.

Precautionary Principle turned on its head with masks
In light of the medical research, therefore, it is difficult to understand why public-health authorities are not consistently adamant about this established scientific result, since the distributed psychological, economic and environmental harm from a broad recommendation to wear masks is significant, not to mention the unknown potential harm from concentration and distribution of pathogens on and from used masks.
In this case, public authorities would be turning the precautionary principle on its head (see below).

Physics and Biology of Viral Respiratory Disease, and why masks do not work
In order to understand why masks cannot possibly work, we must review established knowledge about viral respiratory diseases, the mechanism of seasonal variation of excess deaths from pneumonia and influenza, the aerosol mechanism of infectious disease transmission, the physics and chemistry of aerosols, and the mechanism of the so-called minimum-infective-dose.

In addition to pandemics that can occur anytime, in the temperate latitudes there is an extra burden of respiratory-disease mortality that is seasonal, and which is caused by viruses. For example, see the review of influenza by Paules and Subbarao (2017). This has been known for a long time, and the seasonal pattern is exceedingly regular.

For example, see Figure 1 of Viboud (2010), which has “Weekly time series of the ratio of deaths from pneumonia and influenza to all deaths, based on the 122 cities surveillance in the US (blue line). The red line represents the expected baseline ratio in the absence of influenza activity,” here:
The seasonality of the phenomenon was largely not understood until a decade ago. Until recently, it was debated whether the pattern arose primarily because of seasonal change in virulence of the pathogens, or because of seasonal change in susceptibility of the host (such as from dry air causing tissue irritation, or diminished daylight causing vitamin deficiency or hormonal stress). For example, see Dowell (2001).

In a landmark study, Shaman et al. (2010) showed that the seasonal pattern of extra respiratory-disease mortality can be explained quantitatively on the sole basis of absolute humidity, and its direct controlling impact on transmission of airborne pathogens.

Lowen et al. (2007) demonstrated the phenomenon of humidity-dependent airborne-virus virulence in actual disease transmission between guinea pigs, and discussed potential underlying mechanisms for the measured controlling effect of humidity.

The underlying mechanism is that the pathogen-laden aerosol particles or droplets are neutralized within a half-life that monotonically and significantly decreases with increasing ambient humidity. This is based on the seminal work of Harper (1961). Harper experimentally showed that viral-pathogen-carrying droplets were inactivated within shorter and shorter times, as ambient humidity was increased.

Harper argued that the viruses themselves were made inoperative by the humidity (“viable decay”), however, he admitted that the effect could be from humidity-enhanced physical removal or sedimentation of the droplets (“physical loss”): “Aerosol viabilities reported in this paper are based on the ratio of virus titre to radioactive count in suspension and cloud samples, and can be criticized on the ground that test and tracer materials were not physically identical.”

The latter (“physical loss”) seems more plausible to me, since humidity would have a universal physical effect of causing particle / droplet growth and sedimentation, and all tested viral pathogens have essentially the same humidity-driven “decay”. Furthermore, it is difficult to understand how a virion (of all virus types) in a droplet would be molecularly or structurally attacked or damaged by an increase in ambient humidity. A “virion” is the complete, infective form of a virus outside a host cell, with a core of RNA or DNA and a capsid. The actual mechanism of such humidity-driven intra-droplet “viable decay” of a virion has not been explained or studied.

In any case, the explanation and model of Shaman et al. (2010) is not dependant on the particular mechanism of the humidity-driven decay of virions in aerosol / droplets. Shaman’s quantitatively demonstrated model of seasonal regional viral epidemiology is valid for either mechanism (or combination of mechanisms), whether “viable decay” or “physical loss”.
The breakthrough achieved by Shaman et al. is not merely some academic point. Rather, it has profound health-policy implications, which have been entirely ignored or overlooked in the current coronavirus pandemic.
In particular, Shaman’s work necessarily implies that, rather than being a fixed number (dependent solely on the spatial-temporal structure of social interactions in a completely susceptible population, and on the viral strain), the epidemic’s basic reproduction number (R0) is highly or predominantly dependent on ambient absolute humidity.

For a definition of R0, see HealthKnowlege-UK (2020): R0 is “the average number of secondary infections produced by a typical case of an infection in a population where everyone is susceptible.” The average R0 for influenza is said to be 1.28 (1.19-1.37); see the comprehensive review by Biggerstaff et al. (2014).

In fact, Shaman et al. showed that R0 must be understood to seasonally vary between humid-summer values of just larger than “1” and dry-winter values typically as large as “4” (for example, see their Table 2). In other words, the seasonal infectious viral respiratory diseases that plague temperate latitudes every year go from being intrinsically mildly contagious to virulently contagious, due simply to the bio-physical mode of transmission controlled by atmospheric humidity, irrespective of any other consideration.
Therefore, all the epidemiological mathematical modelling of the benefits of mediating policies (such as social distancing), which assumes humidity-independent R0 values, has a large likelihood of being of little value, on this basis alone. For studies about modelling and regarding mediation effects on the effective reproduction number, see Coburn (2009) and Tracht (2010).
To put it simply, the “second wave” of an epidemic is not a consequence of human sin regarding mask wearing and hand shaking. Rather, the “second wave” is an inescapable consequence of an air-dryness-driven many-fold increase in disease contagiousness, in a population that has not yet attained immunity.

If my view of the mechanism is correct (i.e., “physical loss”), then Shaman’s work further necessarily implies that the dryness-driven high transmissibility (large R0) arises from small aerosol particles fluidly suspended in the air; as opposed to large droplets that are quickly gravitationally removed from the air.
Such small aerosol particles fluidly suspended in air, of biological origin, are of every variety and are everywhere, including down to virion-sizes (Despres, 2012). It is not entirely unlikely that viruses can thereby be physically transported over inter-continental distances (e.g., Hammond, 1989).
More to the point, indoor airborne virus concentrations have been shown to exist (in day-care facilities, health centres, and onboard airplanes) primarily as aerosol particles of diameters smaller than 2.5 μm, such as in the work of Yang et al. (2011):

“Half of the 16 samples were positive, and their total virus concentrations ranged from 5800 to 37 000 genome copies m−3. On average, 64 per cent of the viral genome copies were associated with fine particles smaller than 2.5 µm, which can remain suspended for hours. Modelling of virus concentrations indoors suggested a source strength of 1.6 ± 1.2 × 105 genome copies m−3 air h−1 and a deposition flux onto surfaces of 13 ± 7 genome copies m−2 h−1 by Brownian motion. Over 1 hour, the inhalation dose was estimated to be 30 ± 18 median tissue culture infectious dose (TCID50), adequate to induce infection. These results provide quantitative support for the idea that the aerosol route could be an important mode of influenza transmission.”

Such small particles (< 2.5 μm) are part of air fluidity, are not subject to gravitational sedimentation, and would not be stopped by long-range inertial impact. This means that the slightest (even momentary) facial misfit of a mask or respirator renders the design filtration norm of the mask or respirator entirely irrelevant. In any case, the filtration material itself of N95 (average pore size ~0.3−0.5 μm) does not block virion penetration, not to mention surgical masks. For example, see Balazy et al. (2006).

Mask stoppage efficiency and host inhalation are only half of the equation, however, because the minimal infective dose (MID) must also be considered. For example, if a large number of pathogen-laden particles must be delivered to the lung within a certain time for the illness to take hold, then partial blocking by any mask or cloth can be enough to make a significant difference.
On the other hand, if the MID is amply surpassed by the virions carried in a single aerosol particle able to evade mask-capture, then the mask is of no practical utility, which is the case.

Yezli and Otter (2011), in their review of the MID, point out relevant features:
most respiratory viruses are as infective in humans as in tissue culture having optimal laboratory susceptibility it is believed that a single virion can be enough to induce illness in the host the 50%-probability MID (“TCID50”) has variably been found to be in the range 100−1000 virions there are typically 103−107 virions per aerolized influenza droplet with diameter 1 μm − 10 μm
the 50%-probability MID easily fits into a single (one) aerolized droplet

For further background:

A classic description of dose-response assessment is provided by Haas (1993).

Zwart et al. (2009) provided the first laboratory proof, in a virus-insect system, that the action of a single virion can be sufficient to cause disease.

Baccam et al. (2006) calculated from empirical data that, with influenza A in humans, “we estimate that after a delay of ~6 h, infected cells begin producing influenza virus and continue to do so for ~5 h. The average lifetime of infected cells is ~11 h, and the half-life of free infectious virus is ~3 h. We calculated the [in-body] basic reproductive number, R0, which indicated that a single infected cell could produce ~22 new productive infections.”

Brooke et al. (2013) showed that, contrary to prior modeling assumptions, although not all influenza-A-infected cells in the human body produce infectious progeny (virions), nonetheless, 90% of infected cell are significantly impacted, rather than simply surviving unharmed.

All of this to say that: if anything gets through (and it always does, irrespective of the mask), then you are going to be infected. Masks cannot possibly work. It is not surprising, therefore, that no bias-free study has ever found a benefit from wearing a mask or respirator in this application.

Therefore, the studies that show partial stopping power of masks, or that show that masks can capture many large droplets produced by a sneezing or coughing mask-wearer, in light of the above-described features of the problem, are irrelevant. For example, see such studies as these: Leung (2020), Davies (2013), Lai (2012), and Sande (2008).

Why there can never be an empirical test of a nationwide mask-wearing policy
As mentioned above, no study exists that shows a benefit from a broad policy to wear masks in public. There is good reason for this. It would be impossible to obtain unambiguous and bias-free results:

Any benefit from mask-wearing would have to be a small effect, since undetected in controlled experiments, which would be swamped by the larger effects, notably the large effect from changing atmospheric humidity.
Mask compliance and mask adjustment habits would be unknown.
Mask-wearing is associated (correlated) with several other health behaviours; see Wada (2012).

The results would not be transferable, because of differing cultural habits.
Compliance is achieved by fear, and individuals can habituate to fear-based propaganda, and can have disparate basic responses.

Monitoring and compliance measurement are near-impossible, and subject to large errors.

Self-reporting (such as in surveys) is notoriously biased, because individuals have the self-interested belief that their efforts are useful.

Progression of the epidemic is not verified with reliable tests on large population samples, and generally relies on non-representative hospital visits or admissions.

Several different pathogens (viruses and strains of viruses) causing respiratory illness generally act together, in the same population and/or in individuals, and are not resolved, while having different epidemiological characteristics.

Unknown aspects of mask-wearing

Many potential harms may arise from broad public policies to wear masks, and the following unanswered questions arise:

Do used and loaded masks become sources of enhanced transmission, for the wearer and others?

Do masks become collectors and retainers of pathogens that the mask wearer would otherwise avoid when breathing without a mask?

Are large droplets captured by a mask atomized or aerolized into breathable components? Can virions escape an evaporating droplet stuck to a mask fiber?

What are the dangers of bacterial growth on a used and loaded mask?

How do pathogen-laden droplets interact with environmental dust and aerosols captured on the mask?

What are long-term health effects on HCW, such as headaches, arising from impeded breathing?

Are there negative social consequences to a masked society?

Are there negative psychological consequences to wearing a mask, as a fear-based behavioral modification?

What are the environmental consequences of mask manufacturing and disposal?

Do the masks shed fibres or substances that are harmful when inhaled?

Conclusion
By making mask-wearing recommendations and policies for the general public, or by expressly condoning the practice, governments have both ignored the scientific evidence and done the opposite of following the precautionary principle.

In an absence of knowledge, governments should not make policies that have a hypothetical potential to cause harm. The government has an onus barrier before it instigates a broad social-engineering intervention, or allows corporations to exploit fear-based sentiments.

Furthermore, individuals should know that there is no known benefit arising from wearing a mask in a viral respiratory illness epidemic, and that scientific studies have shown that any benefit must be residually small, compared to other and determinative factors.

Otherwise, what is the point of publicly-funded science?

The present paper about masks illustrates the degree to which governments, the mainstream media, and institutional propagandists can decide to operate in a science vacuum, or select only incomplete science that serves their interests. Such recklessness is also certainly the case with the current global lockdown of over 1 billion people, an unprecedented experiment in medical and political history.

SUMMARY:

The true effectiveness of masks is psychological and economic. They work in that they provide a false sense of security that will get people to go out and buy things, and slightly buffer the economy at the expense of people’s health.

CITES:
Baccam, P. et al. (2006) “Kinetics of Influenza A Virus Infection in Humans”, Journal of Virology Jul 2006, 80 (15) 7590-7599; DOI: 10.1128/JVI.01623-05
Balazy et al. (2006) “Do N95 respirators provide 95% protection level against airborne viruses, and how adequate are surgical masks?”, American Journal of Infection Control, Volume 34, Issue 2, March 2006, Pages 51-57. doi:10.1016/j.ajic.2005.08.018
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Purines are a natural substance found in the body. They are also found in many foods such as liver, shellfish, and alcohol. They can also be formed in the body when DNA is broken down. When purines are broken down to uric acid in the blood, the body gets rid of it when you urinate or have a bowel movement.  This removal process allows humans and birds to conserve mitochondrial water.

Parkinson’s disease patients suffer from hypoxia of their pigmented neurons in the brain.  This leads to melanin breakdown and lowered levels of endogenous dopamine.  Uric acid, a metabolite of purine biochemistry protects neurons from melanin degeneration and dopamine loss.  In primates, having a higher level of uric acid is protective of hypoxia in dopamine producing neurons.  It appears evolution knew what it was doing when it altered the uric acid pathways in the big brained primate clade.

Parkinson’s Disease (PD) patients have been found to have significantly lower levels of serum Uric Acid than controls (p = 0.000) in published research.  This fact is not well known in clinical medicine.  In fact, in patients on L-dopa the situation is even more dire and shows us why Big Pharma solutions often run contrary to nature’s recipes.  In patients with PD serum UA levels were mush lower in the groups under L-Dopa + dopamine agonist treatment.

Uric acid (urate) is often referred to as a waste product of purine metabolism (Johnson et al., 2009; Rock et al., 2013) by people who just do not understand its impact in big brained primates. Normally, it circulates at high levels in humans and other hominoids due to mutations in the gene encoding the urate-catabolizing enzyme urate oxidase (UOx) during primate evolution (Wu et al. 1992, Oda et al. 2002).

In our species its circulating concentrations are so high they approach the limits of solubility.  Urate is best known clinically for the pain and damage that results when these limits are exceeded and urate crystallizes. When this occurs in joints it results in gout, a form of inflammatory arthritis triggered by urate crystals. Similarly, when urate (or more typically its acid form, uric acid) crystallizes in the urine then it can cause kidney stones.  People who have gout usually have serious blue light toxicity and melanopsin damage that lead to PD.  In fact, anyone with gout is a serious clue to me the quantum clinician that they have serious risks in their environment for damage to all melanin regions of the brain and skin.

To illustrate this point, I’d like to tell you about one of my Kruse Longevity Farm patients I treated in the last year. This person had many symptoms of undiagnosed mild Parkinson’s Disease. They came to me with many unusual symptoms that functional medicine doctors could not make sense of. This particular patient had went to the Kresser Institute and had 9300 dollars of testing over a 9 month period of time and never received an answer about their neurologic and gut issues he had.

After my nurse performed a review of systems and asked 45 minutes of questions I set down to review all the labs/tests that were ordered by 4 other clinicians. Once I reviewed the history, I noticed two things. The patient complained of a 3 year history of tinnitus, biannual bouts of gout, and a significant ENT history of cerumin accumulation and pale skin. This caused severe ear pain and reddened ear drums and multiple rounds of prescription antibiotics. After the first year, the person changed jobs and worked at night as an IT professional. During the first year of symptoms, gut issues and sleep became hugely disrupted no matter what interventions were done. As sleep worsened so did his cognition and motor abilities. He noticed changes to his emotions as well. He developed a worsening ringing in his ears and began to have balance issues.

When the patient arrived at my facility I asked pointed questions about the patients work environment after looking in their ears. Upon looking in the ears I saw cerumin accumulation on one side compared to the other but there was significant erythema of both ear drums. He was also sensitive to artificial light. I removed the ear wax and noted the area underneath it was pale. I also noted the pinna and external auditory canal were very pale and devoid of pigment. I examined his skin and noticed some uneven melanosis in places.

Immediately I asked about their use of cell phones, blue tooth, and nnEMF. Then I got my answer. The patient told me he used to use his cell phone to the ear 100% of the time but then his ENT physician convinced him to use wireless earbuds because of his ear problems to avoid putting the cell phone to his affected ear. Within 3 months of using the ear pods the patients symptoms of mild tinnitus progressed to mild Meniere’s disease with vertigo hearing loss and balance issues. This got worse when he shifted to night time consulting work. During this time he developed abnormal white skin patches over his torso and legs.

I asked him if he had the ear pods during his visit with me. He did. He told me he used them frequently in his car or when he traveled for business. I had him put them in the ear and we measured the nnEMF they emitted. The picture below shows you what I found. On his labs done at the Kresser Institute I noted three draws where his uric acids levels were off the charts. The patient also had high blood pressure every time he had his uric acid drawn according to the chart review.

This level of nnEMF was unbelievable. The amount of radiation delivered to the ear, ear drum, cochlea, and brainstem. The brain stem is where the vagal nuclei are that control the flow of autonomic information from the brain to the gut. His eye exam showed an abnormal blink reflex, and his pupils hardly reacted to blue LED during direct eye exam, while reacting briskly to red LED during the eye exam. This told me that there was a serious lack of dopamine in the pupillary mechanism. The eye exam revealed a pale retina. There was no change in refraction noted by the patient. When I consolidated all these findings, my advice to them were to eliminate the ear buds, quit the night shift, begin a serious increase of building the solar callus every AM, use of PBM/LLLT to the ears and head, and begin using my survivor’s soup patreon recipe every day. I also got him to wear blue blocking glasses with 550 BI tints anytime he was around blue light or in indoors behind glass. He has used Luciaeyes,com blue blockers for the last 7 months.

The remainder of the patients extensive work up at the Kruse Longevity Center under my care showed no other sigficant abnormalities.  The patient instituted all my protocols and advice the symptoms for the most part improved within 3 weeks.  His Bristol stool score went from a 7 to a 4 in two weeks and all the GI symptoms improved quickly when he eliminated tech use to his ears and used more light from the sun and his red light I recommended.  His tinnitus improved over 6 months.  He grade his tinnitus at 7 out of ten at his initial visit, and at his 6 month follow up he reported it was now a 1 of 10.    His Meniere’s symptoms resolved in 4 months 100%.  The patient was taught how to improve his skin’s melanosis with sensible solar behavioral change and I used my light hygiene protocol to augment this result.  That protocol is devoid of any Big Pharma solutions.  His cognition and sleep improved over 3 months, and his uric acid levels normalized over the last year.  This case illustrates how nnEMF can destroy melanosis and cause abnormal neurologic symptoms, skin changes, and gut issues that lead to many low dopamine symptoms and disease phenotypes.

WHY DID ALL THIS MAKE SENSE TO ME? 

Most people think high uric acid levels are pathologic.  This is not always true.  Many times people with electromagnetic sensitivities have high levels of uric acid to compensate for cellular hypoxia.

Uric acid has been studied in several cardiorespiratory processes that produce hypoxia since this condition leads to increased catabolism of purines. In this sense, uric acid has shown me to be a useful as a prognostic marker of hypoxia from many causes.  This includes electromagnetic hypersensitivity, blue light toxicity,  heart failure, pulmonary thromboembolism, viral illness,  and primary pulmonary hypertension.  A higher uric acid level is a subtle sign of significant mitochondrial heteroplasmy from an unknown source linked to hypoxia.  So is a higher level of homocysteine.  Tissue hypoxia contribute to a sequence of events by leading to the depletion of adenosine triphosphate (ATP) and activation of purine nucleotide degradation to uric acid.

It appears this patients previous care givers did not know about these links.  That is why they missed it.  Uric acid is vilified by functional medicine practitioners because they are ignorant of how evolution has used it in primates.  It carries a negative connotation for many clinicians, but as a neurosurgeon, I am acutely aware that high levels of uric acid also are protective in traumatic brain injury, CNS trauma, and this is best seen in people with Parkinson’s disease.  Uric acid has a significant potential for helping people with Parkinson’s disease and other neurodegenerative diseases that are exploding in this tech driven world.

Despite the known and theoretical adverse effects of higher uric acid levels in medical books, the evolutionary biology and biochemistry of uric acid suggests that its salubrious actions has a deep evolutionary purpose for large brained primates.  Uric acid appears to offset and possibly outweigh its detrimental effects (Álvarez-Lario & Macarrón-Vicente, 2010). Gout maybe a disease Nature gives is because uric acid protects us from cognitive decline and motor degeneration of low dopamine states.  I have also noted uric acid levels being higher in those with depression and bipolar disorder.  I believe this is a protective evolutionary response to a poor environment.  It turns out the uric acid-elevating inactivation of the urate oxidase enzyme in chimpanzees, gorillas, and humans can be attributed to multiple independent mutations in UOx during the speciation of primates (Wu et al. 1992, Oda et al. 2002).  This is unique to our evolutionary family.

This is why many doctors have reported acute gout flare ups in patients with PD who were put on receiving L-dopa in combination with a decarboxylase inhibitor. It appears blockade of decarboxylation leads to major changes in the pattern of L-dopa metabolites.

As such, the Black Swan clinician should reasonably presume that uric acid elevation conveys a critical survival advantage to our ancestors, with respect to their large brains. The discovery that uric acid possesses strong antioxidant properties, with a comparable or greater activity than ascorbate at their physiological concentrations in humans (Ames et al., 1981), suggested potential benefits of protection against oxidative stress. Uric acid decreases neuro-degeneration risks and this is likely why all primates have traded the higher levels of gout to protect their larger brains.

Might this be linked to the Warburg metabolism via glutamine?  Yes.  Glutamine enters the Krebs uric acid cycle. This move generates excess uric acid, and ammonia-N is excreted as uric acid-N. When this occurs cells require large inputs of glycine into the urea acid cycle along with, serine, and threonine, which serve as glycine precursors.  This is why I recommended the use of the survivor soup recipe to this patient.  That soup recipe is a glycine replacement mechanism for those who are tech addicted.  It is also why I recommended something called an Optimal Cocktail that I created at Kruse Longevity Center at Destin.

This is an oral trouche we’ve created with one of my pharmacist Farm member’s to offset low glycine states that appears with low dopamine states by taking advantage of the serine glycine interconversion pathway.

Every mole of uric acid synthesized as the end-product of N metabolism requires one mole of glycine, and the loss of glycine incurs a loss of 12.5 ATP molecules.  This amount of ATP stresses mitochondrial function which is underperforming in a low dopamine disease.  This increase need for ATP is why red light therapy helps the low dopamine state.

Since mitochondrial energy in the form of ATP is required to dispose of excess ammonia, it is apparent that ATP must be available for the urea cycle to properly function in low dopamine states. Thus, the urea cycle has to be closely linked physiologically to the citric acid cycle, which derives one of its nitrogens from the transamination of oxaloacetate to form aspartate and returns fumarate to the cycle while recycling metabolic water.  It was discovered in biochemical research that urea cycle disorders not only disturbe the metabolism of amino acids involved in the urea cycle but it also induce the accumulation of ammonia detoxification, but also interfered with the metabolism of amino acids related to some nervous systems, such as pipecolic acid and N-acetylaspartic acid.

SUMMARY

Is urea and uric acid the same thing?

In contrast, mammals (including humans) produce urea from ammonia; however, they also form some uric acid during the breakdown of their nucleic acids. In this case, uric acid is excreted in urine instead of in feces, as is done in birds and reptiles. Uric acid is a compound similar to purines found in nucleic acids.  Since the end product nitrogen metabolism is ammonia in birds, in which ammonia cannot be synthesized by urea; thus, birds and humans are prone to the accumulation of uric acid.  Birds, like humans have high mitochondrial capacity.  This is no coincidence.  What else does uric acid reserve for birds and humans?  Water.  Metabolic water to be exact.   In birds and reptiles, and in some desert dwelling mammals (such as the kangaroo rat), uric acid also is the end-product of purine metabolism, but it is excreted in feces as a dry mass on purpose to conserve water.. This involves a complex metabolic pathway that is energetically costly in comparison to processing of other nitrogenous wastes such as urea (from the urea cycle) or ammonia, but has the advantages of reducing water loss and preventing dehydration.  Water is the key electromagnetic capacitor in cells that have high mitochondrial capacity.  Recall that mitochondria make metabolic water from metabolism.

Purines are found in high concentration in meat and meat products, especially internal organs such as liver, shellfish, and kidney. In general, plant-based diets are low in purines.  This is another reason why a vegan diet stresses primates with a large brain and massive mitochondrial capacity.

Aside from the crucial roles of purines (adenine and guanine) in DNA and RNA, purines are also significant components in a number of other important biomolecules, such as ATP, GTP, cyclic AMP, NADH, and coenzyme A.

There are many naturally occurring purines. Adenosine is one of the major ones that signals the onset of sleep.  This is why the patient above could not sleep well.  Some common human purines are the nucleobases adenine  and guanine . In DNA, these bases form hydrogen bonds with their complementary pyrimidines, thymine and cytosine, respectively.  You saw those appear in the last blog.   This is called complementary base pairing. In RNA, the complement of adenine is uracil instead of thymine.  It is also a purine.

Other notable purines are hypoxanthine , xanthine, theobromine, caffeine, uric acid  and isoguanine.

Hans Kornberg wrote a paper entitled ‘Krebs and his trinity of cycles’ commenting that every school biology student knows of the Krebs cycle, but few know that Krebs discovered two other cycles in biology. These are (1) the ornithine cycle (urea cycle), (2) the citric acid cycle (tricarboxylic acid or TCA cycle), and (3) the glyoxylate cycle that was described by Krebs and Kornberg. Ironically, Kornberg, codiscoverer of the ‘glyoxylate cycle’, overlooked a fourth Krebs cycle – (4) the uric acid cycle.  This cycle is critical in low dopamine states.  Anytime dopamine levels are lowered by blue light and nnEMF we should expect higher levels of uric acid to protect dopamine stores in pigmented cells in our body.

The patient spent over 20,000 dollars in 3 years and got no answers.  He became a Farm member and with in 6 months he found his answer and got better without any need of a drug.  His cost of membership was much lower than he spent to solve this problem.

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     Ames BN, Cathcart R, Schwiers E, Hochstein P.  Uric acid provides an antioxidant defense   in humans against oxidant- and radical-caused aging and cancer: a hypothesis.Proc Natl Acad Sci U S A. 1981 Nov; 78(11):6858-62.

Serum uric acid levels and freezing of gait in Parkinson’s disease.Ou R, Cao B, Wei Q, Hou Y, Xu Y, Song W, Zhao B, Shang H.Neurol Sci. 2017 Jun;38(6):955-960. doi: 10.1007/s10072-017-2871-3. Epub 2017 Mar 1.PMID: 28251464

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